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| field = [[Nephrology]]
| symptoms = Decreased ability to think, [[headache]]s, [[nausea]], poor [[Balance (ability)|balance]], confusion, [[seizures]], [[coma]]<ref name="babar" /><ref name=Wil2016/><ref name=Ann2015/>
| complications =
| onset =
| duration =
| types = [[hypovolemic|Low volume]], normal volume, [[hypervolemic|high volume]]<ref name=CMAJ2014/>
| causes =
| risks =
| diagnosis = Serum sodium < 135 mmol/L<ref name=Ann2015/>
| differential = [[Ethanol]] intoxication or withdrawal, [[hyperproteinemia|
| prevention =
| treatment = Based on underlying cause<ref name=CMAJ2014/>
| medication =
| prognosis =
| frequency = Relatively common<ref name=Ros2013/><ref name=Ball2016>{{cite journal |last1=Ball |first1=SG |last2=Iqbal |first2=Z |title= Diagnosis and treatment of hyponatraemia |journal= Best Practice & Research. Clinical Endocrinology & Metabolism |date=March 2016 |volume=30 |issue=2 |pages=161–73 |pmid= 27156756 |doi=10.1016/j.beem.2015.12.001}}</ref>
| deaths =
}}
<!-- Definition and symptoms -->
'''Hyponatremia''' or '''hyponatraemia''' is a low concentration of [[sodium]]
<!-- Cause and mechanism -->
The causes of hyponatremia are typically classified by a person's body fluid status into [[hypovolemic|low volume]], normal volume, or [[hypervolemic|high volume]].<ref name=CMAJ2014/> Low volume hyponatremia can occur from [[diarrhea]], [[vomiting]], [[diuretics]], and [[sweating]].<ref name=CMAJ2014/> Normal volume hyponatremia is divided into cases with [[concentration|dilute]] urine and [[concentration|concentrated]] urine.<ref name=CMAJ2014/> Cases in which the urine is dilute include [[adrenal insufficiency]], [[hypothyroidism]], and [[polydipsia|drinking too much water]] or [[potomania|too much beer]].<ref name=CMAJ2014/> Cases in which the urine is concentrated include [[syndrome of inappropriate antidiuretic hormone secretion]] (SIADH).<ref name=CMAJ2014/> High volume hyponatremia can occur from [[heart failure]], [[liver failure]], and [[kidney failure]].<ref name=CMAJ2014/> Conditions that can lead to falsely low sodium measurements include [[hyperproteinemia|high blood protein levels]] such as in [[multiple myeloma]], [[hyperlipidemia|high blood fat levels]], and [[hyperglycemia|high blood sugar]].<ref name=Fil2016/><ref name=Ros2013>{{cite book |last1= Marx |first1= John |last2= Walls |first2= Ron |last3= Hockberger |first3= Robert |title= Rosen's Emergency Medicine – Concepts and Clinical Practice |date= 2013 |publisher= Elsevier Health Sciences |isbn= 978-
<!--Prevent and treatment -->
Treatment is based on the underlying cause.<ref name=CMAJ2014/> Correcting hyponatremia too quickly can lead to complications.<ref name=Fil2016/> Rapid partial correction with [[3% normal saline]] is only recommended in those with significant symptoms and occasionally those in whom the condition was of rapid onset.<ref name=CMAJ2014/><ref name=Ros2013/> Low volume hyponatremia is typically treated with intravenous [[normal saline]].<ref name=CMAJ2014/> SIADH is typically treated by correcting the underlying cause and with [[fluid restriction]] while high volume hyponatremia is typically treated with both fluid restriction and a diet low in salt.<ref name="babar" /><ref name=CMAJ2014/> Correction should generally be gradual in those in whom the low levels have been present for more than two days.<ref name=CMAJ2014>{{cite journal |last1=Lee |first1=JJ |last2=Kilonzo |first2=K |last3=Nistico |first3=A |last4= Yeates |first4=K |title= Management of hyponatremia. |journal= CMAJ
<!-- Epidemiology and prognosis -->
Hyponatremia is the most common type of [[electrolyte imbalance]], and is often found in older adults.<ref>{{Cite journal|last1=Valle|first1=Jana M.|last2=Beveridge|first2=Alexander|last3=Chróinín|first3=Danielle Ní|date=2022-02-16|title=Exploring hyponatremia in older hospital in-patients: management, association with falls, and other adverse outcomes|journal=Aging and Health Research|volume=2|language=en|page=100060|doi=10.1016/j.ahr.2022.100060|s2cid=246938773|issn=2667-0321|doi-access=free}}</ref><ref name=Din2017>{{cite journal|last1=Dineen|first1=R|last2=Thompson|first2=CJ|last3=Sherlock|first3=M|title=Hyponatraemia – presentations and management.|journal=Clinical Medicine|date=June 2017|volume=17|issue=3|pages=263–69|doi=10.7861/clinmedicine.17-3-263|pmid=28572229|pmc=6297575}}</ref> It occurs in about 20% of those admitted to hospital and 10% of people during or after an [[endurance sport]]ing event.<ref name=Ann2015/><ref name=Fil2016/> Among those in hospital, hyponatremia is associated with an increased risk of death.<ref name=Fil2016>{{cite journal |last1=Filippatos |first1=TD |last2=Liamis |first2=G |last3= Christopoulou |first3=F |last4=Elisaf |first4=MS |title= Ten common pitfalls in the evaluation of patients with hyponatremia.|journal=European Journal of Internal Medicine|date=April 2016 |volume=29 |pages=22–25 |pmid= 26706473 |doi=10.1016/j.ejim.2015.11.022|doi-access=free }}</ref> The economic costs of hyponatremia are estimated at $2.6 billion per annum in the United States.<ref>{{cite book |last1=Simon |first1=Eric E. |title=Hyponatremia: Evaluation and Treatment |date=2014 |publisher=Springer Science & Business Media |isbn=978-
== Signs and symptoms ==
Signs and symptoms of hyponatremia include [[nausea]] and [[vomiting]], [[headache]], [[short-term memory loss]], [[confusion]], [[lethargy]], [[fatigue (medical)|fatigue]], [[loss of appetite]], [[irritability]], [[muscle weakness]], spasms or [[cramp]]s, [[Epileptic seizure|seizures]], and decreased consciousness or [[coma]].<ref name="babar">{{cite journal |pmid=24259701 |date=October 2013 |last1=Babar |first1=S. |title=SIADH Associated With Ciprofloxacin. |volume=47 |url=http://aop.sagepub.com/content/47/10/1359.full.pdf |issue=10 |pages=1359–63 |issn=1060-0280 |journal=The Annals of Pharmacotherapy |doi=10.1177/1060028013502457 |s2cid=36759747 |access-date=November 18, 2013
[[Neurological]] symptoms typically occur with very low levels of plasma sodium (usually <115 mmol/L).<ref name="babar"/> When sodium levels in the blood become very low, water enters the brain cells and causes them to swell ([[cerebral edema]]). This results in increased [[intracranial pressure|pressure in the skull]] and causes ''hyponatremic encephalopathy''. As pressure increases in the skull, [[brain herniation|herniation of the brain]] can occur, which is a squeezing of the brain across the internal structures of the skull. This can lead to headache, nausea, vomiting, confusion, [[seizure]]s, [[brain stem]] compression and [[respiratory arrest]], and non-cardiogenic [[pulmonary edema|accumulation of fluid in the lungs]].<ref name=Moritz2003>{{cite journal |doi=10.1093/ndt/gfg394 |title=The pathophysiology and treatment of hyponatraemic encephalopathy: An update |year=2003 |last1=Moritz |first1=M. L. |last2=Ayus |first2=J. C. |journal=Nephrology Dialysis Transplantation |volume=18 |issue=12 |pages=2486–91 |pmid=14605269|doi-access=free }}</ref> This is usually fatal if not immediately treated.
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Symptom severity depends on how fast and how severe the drop in blood sodium level is. A gradual drop, even to very low levels, may be tolerated well if it occurs over several days or weeks, because of neuronal adaptation. The presence of underlying neurological disease such as a seizure disorder or non-neurological metabolic abnormalities, also affects the severity of neurologic symptoms.
==
The specific causes of hyponatremia are generally divided into those with [[low tonicity]] (lower than normal concentration of [[solutes]]), without low tonicity, and falsely low sodiums.<ref name=Din2017/> Those with low tonicity are then grouped by whether the person has high fluid volume, normal fluid volume, or low fluid volume.<ref name=Din2017/>
===High volume===
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* [[Congestive heart failure]]<ref name=Din2017/>
* [[Nephrotic syndrome]] in the kidneys<ref name=Din2017/>
* Excessive
===Normal volume===
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* [[Hypothyroidism]]<ref name=Din2017/>
* Not enough [[ACTH]]<ref name=Din2017/>
* [[Beer potomania]]
* Normal physiologic change of [[pregnancy]]<ref>{{cite book |last1=Plant |first1=Tony M. |last2=Zeleznik |first2=Anthony J. |title=Knobil and Neill's Physiology of Reproduction |date=2014 |publisher=Academic Press |isbn=978-
*
===Low volume===
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* Diuretic use (due to the diuretic causing a volume depleted state and thence [[anti-diuretic hormone|ADH]] release, and not a direct result of diuretic-induced urine sodium loss)<ref name=Din2017/>
* [[Addison's disease]] and [[congenital adrenal hyperplasia]] in which the [[adrenal gland]]s do not produce enough steroid hormones (combined glucocorticoid and [[mineralocorticoid deficiency]])<ref name=Din2017/>
* [[Isolated hyperchlorhidrosis]] (Carbonic anhydrase XII deficiency), a rare [[genetic disorder]] which results in a lifelong tendency to lose excessive amounts of sodium by sweating.
* [[Pancreatitis]]<ref name=Din2017/>
* Prolonged exercise and sweating, combined with drinking water without electrolytes is the cause of [[exercise-associated hyponatremia]] (EAH).<ref name=Fil2016/><ref>{{cite journal|last=Bennett|first=BL|author2=Hew-Butler, T |author3=Hoffman, MD |author4=Rogers, IR |author5= Rosner, MH |title=Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia.|journal=Wilderness & Environmental Medicine|date=Sep 2013|volume=24|issue=3|pages=228–40|pmid=23590928|doi=10.1016/j.wem.2013.01.011|doi-access=free}}</ref> It is common in marathon runners and participants of other endurance events.<ref>{{cite journal |doi=10.2215/CJN.02730806 |title=Exercise-Associated Hyponatremia |year=2006 |last1=Rosner |first1=M.H. |last2=Kirven |first2=J. |journal=Clinical Journal of the American Society of Nephrology |volume=2 |pages=151–61 |pmid=17699400 |issue=1|doi-access=free }}</ref>
* The use of [[MDMA]] (ecstasy) can result in hyponatremia.<ref>{{cite journal|title=High incidence of mild hyponatraemia in females using ecstasy at a rave party|journal=Nephrology Dialysis Transplantation|volume=28|issue=9|pages=2277–83|doi=10.1093/ndt/gft023|pmid=23476039|year=2013|last1=Van Dijken|first1=G. D.|last2=Blom|first2=R. E.|last3=Hene|first3=R. J.|last4=Boer|first4=W. H.|doi-access=free}}</ref>
===Medication===
[[Antipsychotics]] have been reported to cause hyponatremia in a review of medical articles from 1946 to 2016.<ref>{{cite journal | title=Hyponatremia in Association With Second-Generation Antipsychotics: A Systematic Review of Case Reports |
Available evidence suggests that all classes of [[psychotropics]], i.e., [[antidepressants]], [[antipsychotics]], mood stabilizers, and sedative/[[hypnotics]] can lead to hyponatremia. Age is a significant factor for drug induced hyponatremia.
===Other causes===
Miscellaneous causes that are not included under the above classification scheme include the following:
* False or pseudo hyponatremia
* Hyponatremia with elevated tonicity can occur with [[high blood sugar]], causing a shift of excess free water into the serum.<ref name=Din2017/>
== Pathophysiology ==
The causes of and treatments for hyponatremia can only be understood by having a grasp of the size of the [[body fluid]] compartments and subcompartments and their regulation; how under normal circumstances the body is able to maintain the sodium concentration within a narrow range ([[homeostasis]] of [[body fluid]] [[osmolality]]); conditions can cause that [[feedback]] system to malfunction ([[pathophysiology]]); and the consequences of the malfunction of that system on the size and solute concentration of the fluid compartments.<ref>Sterns (2013).
===Normal homeostasis===
There is a hypothalamic-kidney feedback system which normally maintains the concentration of the serum sodium within a narrow range. This system operates as follows: in some of the cells of the [[hypothalamus]], there are [[osmoreceptors]] which respond to an elevated serum sodium in body fluids by signalling the posterior pituitary gland to secrete [[antidiuretic hormone]] (ADH) ([[vasopressin]]).<ref>{{cite journal|last1=Antunes-Rodrigues|first1=J|last2=de Castro|first2=M|last3=Elias|first3=LL|last4=Valença|first4=MM|last5=McCann|first5=SM|title=Neuroendocrine control of body fluid metabolism.|journal=Physiological Reviews|date=January 2004|volume=84|issue=1|pages=169–208|pmid=14715914|doi=10.1152/physrev.00017.2003}} {{Update inline|date=September 2017}}</ref> ADH then enters the bloodstream and signals the kidney to bring back sufficient solute-free water from the fluid in the kidney tubules to dilute the serum sodium back to normal, and this turns off the osmoreceptors in the hypothalamus. Also, thirst is stimulated.<ref>{{cite journal|last1=Baylis|first1=PH|last2=Thompson|first2=CJ|title=Osmoregulation of vasopressin secretion and thirst in health and disease.|journal=Clinical Endocrinology|date=November 1988|volume=29|issue=5|pages=549–76|doi=10.1111/j.1365-2265.1988.tb03704.x|pmid=3075528|s2cid=10897593}} {{Update inline|date=September 2017}}</ref> Normally, when mild hyponatremia begins to occur, that is, the serum sodium begins to fall below 135 mEq/L, there is no secretion of ADH, and the kidney stops returning water to the body from the kidney tubule. Also, no thirst is experienced. These two act in concert to raise the serum sodium to the normal range.<ref>{{cite journal |vauthors=Ball SG, Iqbal Z| year = 2016 | title = Diagnosis and treatment of hyponatraemia | journal = Best Practice & Research. Clinical Endocrinology & Metabolism | volume = 30 | issue = 2| pages = 161–73 | pmid = 27156756 | doi=10.1016/j.beem.2015.12.001}}</ref><ref name="Elsevier Science">{{cite book|last1=Sterns|first1=RH|last2=Silver|first2=SM|last3=Hicks|first3=JK|editor1-last=Alpern|editor1-first=Robert J.|editor2-last=Moe|editor2-first=Orson W.|editor3-last=Caplan|editor3-first=Michael|title=Seldin and Giebisch's The Kidney Physiology & Pathophysiology.|date=2013|publisher=Elsevier Science|location=Burlington|isbn=978-
===Hyponatremia===
Hyponatremia occurs 1) when the hypothalamic-kidney feedback loop is overwhelmed by increased fluid intake, 2) the feedback loop malfunctions such that ADH is always "turned on", 3) the receptors in the kidney are always "open" regardless of there being no signal from ADH to be open; or 4) there is an increased ADH even though there is no normal stimulus (elevated serum sodium) for ADH to be increased.
Hyponatremia occurs in one of two ways: either the osmoreceptor-aquaporin feedback loop is ''overwhelmed'', or it is ''interrupted''. If it is interrupted, it is either ''related'' or ''not related'' to ADH.<ref name="Elsevier Science"/> If the feedback system is overwhelmed, this is water intoxication with maximally dilute urine and is caused by 1) pathological water drinking ([[Primary polydipsia|psychogenic polydipsia]]), 2) [[beer potomania]], 3) overzealous intravenous solute free water infusion, or 4) infantile water intoxication. "Impairment of urine diluting ability related to ADH" occurs in nine situations: 1) arterial volume depletion 2) hemodynamically
If the feed-back system is normal, but an ''impairment of urine diluting ability unrelated to ADH'' occurs, this is 1) oliguric kidney failure, 2) tubular interstitial kidney disease, 3) diuretics, or 4) nephrogenic syndrome of antidiuresis.<ref name="Elsevier Science"/>
Sodium is the primary positively charged ion outside of the cell and cannot cross from the interstitial space into the cell. This is because charged sodium ions attract around them up to 25 water molecules, thereby creating a large [[Polarity (chemistry)|polar structure]] too large to pass through the cell membrane: "channels" or "pumps" are required.
Cell swelling also produces activation of [[volume-regulated anion channel]]s which is related to the release of [[taurine]] and [[glutamate]] from astrocytes.<ref>{{Cite book|last=Diringer|first=M.|title=Critical Care Neurology Part II|date=2017|chapter=Neurologic manifestations of major electrolyte abnormalities|
== Diagnosis ==
The history, physical exam, and laboratory testing are required to determine the underlying cause of hyponatremia. A blood test demonstrating a serum sodium less than 135 mmol/L is diagnostic for hyponatremia.<ref>{{
===False hyponatremia===
False hyponatremia, also known as spurious, pseudo, hypertonic, or artifactual hyponatremia is when the lab tests read low sodium levels but there is no [[Tonicity|hypotonicity]]. In hypertonic hyponatremia, resorption of water by molecules such as glucose (hyperglycemia or diabetes) or [[mannitol]] (hypertonic infusion) occurs. In isotonic hyponatremia a measurement error due to [[hypertriglyceridemia|high blood triglyceride level]] (most common) or [[paraprotein]]emia occurs. It occurs when using techniques that measure the amount of sodium in a specified volume of serum/plasma, or that dilute the sample before analysis.<ref>{{cite web|title=Ask the Expert: May 2016 Investigating Hyponatremia |url=https://www.aacc.org/publications/cln/articles/2016/may/investigating-hyponatremia |work=American Association for Clinical Chemistry |access-date=16 September 2013
===True hyponatremia===
True hyponatremia, also known as hypotonic hyponatremia, is the most common type. It is often simply referred to as "hyponatremia." Hypotonic hyponatremia is categorized in 3 ways based on the person'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:
* '''High volume hyponatremia''', wherein there is decreased [[effective circulating volume]] (less blood flowing in the body) even though total body volume is increased (by the presence of [[edema]] or swelling, especially in the ankles). The decreased effective circulating volume stimulates the release of anti-diuretic hormone ([[Vasopressin|ADH]]), which in turn leads to water retention. Hypervolemic hyponatremia is most commonly the result of [[congestive heart failure]], [[cirrhosis|liver failure]], or kidney disease.
* '''Normal volume 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, that is, [[syndrome of inappropriate antidiuretic hormone hypersecretion]] (SIADH). Often categorized under euvolemic is hyponatremia due to inadequate urine solute (not enough chemicals or electrolytes to produce urine) as occurs in beer potomania or "[[Tea and toast syndrome|tea and toast]]" hyponatremia, hyponatremia due to [[hypothyroidism]] or central [[adrenal insufficiency]], and those rare instances of hyponatremia that are truly secondary to excess water intake.
* '''Low volume hyponatremia''', wherein ADH secretion is stimulated by or associated with volume depletion (not enough water in the body) due to decreased effective circulating volume.
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The treatment of hyponatremia depends on the underlying cause.<ref name=Din2017/> How quickly treatment is required depends on a person's symptoms.<ref name=Din2017/> Fluids are typically the cornerstone of initial management.<ref name=Din2017/> In those with severe disease an increase in sodium of about 5 mmol/L over one to four hours is recommended.<ref name=Din2017/> A rapid rise in serum sodium is anticipated in certain groups when the cause of the hyponatremia is addressed thus warranting closer monitoring in order to avoid overly rapid correction of the blood sodium concentration. These groups include persons who have hypovolemic hyponatremia and receive intravenous fluids (thus correcting their hypovolemia), persons with adrenal insufficiency who receive [[hydrocortisone]], persons in whom a medication causing increased ADH release has been stopped, and persons who have hyponatremia due to decreased salt and/or solute intake in their diet who are treated with a higher solute diet.<ref name="Filippatos2016"/> If [[polyuria|large volumes of dilute urine]] are seen, this can be a warning sign that overcorrection is imminent in these individuals.<ref name="Filippatos2016"/>
Sodium deficit = (140 – serum sodium)
Total body water = kilograms of body weight
===Fluids===
Options include:
* Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 millilitres per day (mL/d) of water with adjustments based on serum sodium levels. Long-term [[fluid restriction]] of 1,200–1,800 mL/d may maintain the person in a symptom-free state.<ref>{{cite book |last1=Schürer |first1=Ludwig |last2=Wolf |first2=Stefan |last3=Lumenta |first3=Christianto B. |chapter=Water and Electrolyte Regulation |pages=[https://archive.org/details/neurosurgery00lume_223/page/n602 611]–15 |doi=10.1007/978-3-540-79565-0_40 |editor1-first=Christianto B. |editor1-last=Lumenta |editor2-first=Concezio |editor2-last=Di Rocco |editor3-first=Jens |editor3-last=Haase |editor4-first=Jan Jakob A. |display-editors = 3 |editor4-last=Mooij |year=2010 |title=Neurosurgery |url=https://archive.org/details/neurosurgery00lume_223 |url-access=limited |isbn=978-3-540-79565-0 |series=European Manual of Medicine}}</ref>
* Moderate and/or symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of [[furosemide]] and replacing sodium and potassium losses with 0.9% saline.
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===Medications===
American and European guidelines come to different conclusions regarding the use of medications.<ref name=Rondon2017/> In the United States they are recommended in those with SIADH, cirrhosis, or heart failure who fail limiting fluid intake.<ref name=Rondon2017/> In Europe they are not generally recommended.<ref name=Rondon2017>{{cite journal|last1=Rondon-Berrios|first1=Helbert|last2=Berl|first2=Tomas|title=Vasopressin Receptor Antagonists in Hyponatremia: Uses and Misuses|journal=[[Frontiers in Medicine]]|volume=4|
There is tentative evidence that [[vasopressin receptor antagonist]]s (vaptans), such as [[conivaptan]], may be slightly more effective than fluid restriction in those with high volume or normal volume hyponatremia.<ref name=CMAJ2014/> They should not be used in people with low volume.<ref name=Din2017/> They may also be used in people with chronic hyponatremia due to SIADH that is insufficiently responsive to fluid restriction and/or sodium tablets.<ref name="Filippatos2016">{{cite journal |last1=Filippatos |first1=TD |last2=Liamis |first2=G |last3=Elisaf |first3=MS |title=Ten pitfalls in the proper management of patients with hyponatremia |journal=Postgraduate Medicine |date=June 2016 |volume=128 |issue=5 |pages=516–22 |doi=10.1080/00325481.2016.1186488 |pmid=27153450|s2cid=6237667 }}</ref>
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===Precautions===
Raising the serum sodium concentration too rapidly may cause [[Central pontine myelinolysis|osmotic demyelination syndrome]].<ref name="Bernsen">{{cite journal |last1=Bernsen |first1=HJ |last2=Prick |first2=MJ |title=Improvement of central pontine myelinolysis as demonstrated by repeated magnetic resonance imaging in a patient without evidence of hyponatremia. |journal=Acta Neurologica Belgica |date=September 1999 |volume=99 |issue=3 |pages=189–93 |pmid=10544728}}</ref><ref name="pmid11430268">{{cite journal |last1=Ashrafian |first1=H. |last2=Davey |first2=P. |title=A review of the causes of central pontine myelinosis: yet another apoptotic illness? |journal=European Journal of Neurology |volume=8 |issue=2 |pages=103–09 |year=2001 |pmid=11430268 |doi=10.1046/j.1468-1331.2001.00176.x |s2cid=37760332 }}</ref><ref name="Abbott">{{cite journal |last1=Abbott |first1=R |last2=Silber |first2=E |last3=Felber |first3=J |last4=Ekpo |first4=E |title=Osmotic demyelination syndrome. |journal=BMJ (Clinical Research Ed.) |date=8 October 2005 |volume=331 |issue=7520 |pages=829–30 |doi=10.1136/bmj.331.7520.829 |pmid=16210283|pmc=1246086 }}</ref> Rapid correction of sodium levels can also lead to [[Central pontine myelinolysis|central pontine myelinolysis (CPM)]].<ref>{{Cite web|title=Central Pontine Myelinolysis Information Page|url=https://www.ninds.nih.gov/Disorders/All-Disorders/Central-Pontine-Myelinolysis-Information-Page#:~:text=Definition,pulls%20water%20from%20brain%20cells.|website=National Institute of Neurological Disorders and Stroke}}</ref> It is recommended not to raise the serum sodium by more than 10 mEq/L/day.<ref name="Auth2012">{{cite book|author=Patrick C. Auth|title=Physician Assistant Review|url=https://books.google.com/books?id=P5wxOR3mCKIC&pg=PA245|year=2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-4511-7129-7|pages=245–|via=Google Books}}</ref>
== Epidemiology ==
Hyponatremia is the most commonly seen [[water–electrolyte imbalance]].<ref name=Din2017/> The disorder is more frequent in females, the elderly, and in people who are hospitalized. The number of cases of hyponatremia depends largely on the population. In hospital it affects about 15–20% of people; however, only 3–5% of people who are hospitalized have a sodium level less than 130 mmol/L. Hyponatremia has been reported in up to 30% of the elderly in nursing homes and is also present in approximately 30% of people who are depressed on [[selective serotonin reuptake inhibitor]]s.<ref name="autogenerated185">{{cite journal |doi=10.1038/nrneph.2010.21 |title=Does 'asymptomatic hyponatremia' exist? |year=2010 |last1=Schrier |first1=Robert W. |journal=Nature Reviews Nephrology |volume=6 |issue=4 |
People who have hyponatremia who require hospitalisation have a longer length of stay (with associated increased costs) and also have a higher likelihood of requiring readmission. This is particularly the case in men and in the elderly.<ref>{{cite journal|last1=Corona|first1=Giovanni|last2=Giuliani|first2=Corinna|last3=Parenti|first3=Gabriele|last4=Colombo|first4=Giorgio L.|last5=Sforza|first5=Alessandra|last6=Maggi|first6=Mario|last7=Forti|first7=Gianni|last8=Peri|first8=Alessandro|title=The Economic Burden of Hyponatremia: Systematic Review and Meta-Analysis|journal=The American Journal of Medicine|date=August 2016|volume=129|issue=8|pages=823–835.e4|doi=10.1016/j.amjmed.2016.03.007|pmid=27059386|doi-access=free}}</ref>
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== Further reading ==
* {{cite journal |author1=Sandy Craig |author2=Erik D Schraga |author3=Francisco Talavera |author4=Howard A Bessen |author5=John D Halamka |date=2010-04-13 |title=Hyponatremia in Emergency Medicine |url=http://emedicine.medscape.com/article/767624-overview |website=[[Medscape]]}}
* {{cite journal |vauthors=Kugler JP, Hustead T |title=Hyponatremia and hypernatremia in the elderly |url=http://www.aafp.org/afp/20000615/3623.html |journal=Am Fam Physician |volume=61 |issue=12 |pages=3623–30 |date=June 2000 |pmid=10892634 |access-date=2011-05-15 |archive-date=2011-06-06 |archive-url=https://web.archive.org/web/20110606054017/http://www.aafp.org/afp/20000615/3623.html }}
* {{cite web |author=James L. Lewis, III, MD |date=May 2009 |title=Hyponatremia |url=http://www.merckmanuals.com/professional/sec12/ch156/ch156d.html#CIHEIHHA |work=[[Merck Manual of Diagnosis and Therapy]] |access-date=2011-05-15 |archive-date=2011-01-11 |archive-url=https://web.archive.org/web/20110111045040/http://www.merckmanuals.com/professional/sec12/ch156/ch156d.html#CIHEIHHA }}
* {{cite web |author=Elizabeth Quinn |date=2011-03-07 |title=What Is Hyponatremia: Hyponatremia or water intoxication – Can Athletes Drink Too Much Water? |url=http://sportsmedicine.about.com/od/hydrationandfluid/a/Hyponatremia.htm |publisher=[[About.com]] |access-date=2009-08-16 |archive-date=2009-10-28 |archive-url=https://web.archive.org/web/20091028170546/http://sportsmedicine.about.com/od/hydrationandfluid/a/Hyponatremia.htm }}
== External links ==
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{{Medical resources
| DiseasesDB = 6483
| ICD10 = {{ICD10|E|87|1|e|70}}
| ICD9 = {{ICD9|276.1}}
| ICDO =
| OMIM =
| MedlinePlus = 000394
| eMedicineSubj = emerg
| eMedicineTopic = 275
| eMedicine_mult = {{eMedicine2|med|1130}} {{eMedicine2|ped|1124}}
| MeshID = D007010
}}
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[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Wikipedia neurology articles ready to translate]]
[[Category:
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