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== Signs and symptoms ==
== 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 cramps, [[seizures]], and decreased consciousness or [[coma]].<ref name="babar">{{cite journal |pmid=24259701 |quote= |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 |accessdate=November 18, 2013 |publisher=Sage Publishing |pmc= |deadurl=no |archiveurl=https://web.archive.org/web/20150501034854/http://aop.sagepub.com/content/47/10/1359.full.pdf |archivedate=May 1, 2015 |df= }}</ref> The presence and severity of signs and symptoms are related to the level of salt in the blood, with lower levels of plasma sodium associated with more severe symptoms. However, emerging data suggest that mild hyponatremia (plasma sodium levels at 131–135&nbsp;mmol/L) is associated with numerous complications or subtle, presently unrecognized symptoms<ref name="autogenerated185"/> (for example, increased falls, altered posture and gait, reduced attention).<ref>{{cite journal |doi=10.1016/j.amjmed.2006.05.013 |title=Is Asymptomatic Hyponatremia Really Asymptomatic? |year=2006 |last1=Decaux |first1=Guy |journal=The American Journal of Medicine |volume=119 |issue=7 |pages=S79–82 |pmid=16843090}}</ref>
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|cramps]], [[seizures]], and decreased consciousness or [[coma]].<ref name="babar">{{cite journal |pmid=24259701 |quote= |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 |accessdate=November 18, 2013 |publisher=Sage Publishing |pmc= |deadurl=no |archiveurl=https://web.archive.org/web/20150501034854/http://aop.sagepub.com/content/47/10/1359.full.pdf |archivedate=May 1, 2015 |df= }}</ref> The presence and severity of signs and symptoms are related to the level of salt in the blood, with lower levels of plasma sodium associated with more severe symptoms. However, emerging data suggest that mild hyponatremia (plasma sodium levels at 131–135&nbsp;mmol/L) is associated with numerous complications or subtle, presently unrecognized symptoms<ref name="autogenerated185"/> (for example, increased falls, altered posture and gait, reduced attention).<ref>{{cite journal |doi=10.1016/j.amjmed.2006.05.013 |title=Is Asymptomatic Hyponatremia Really Asymptomatic? |year=2006 |last1=Decaux |first1=Guy |journal=The American Journal of Medicine |volume=119 |issue=7 |pages=S79–82 |pmid=16843090}}</ref>


[[Neurological]] symptoms typically occur with very low levels of plasma sodium (usually <115&nbsp;mmol/L).<ref name="babar"/> When sodium levels in the blood become very low, water enters the brain cells and causes them to swell. 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}}</ref> This is usually fatal if not immediately treated.
[[Neurological]] symptoms typically occur with very low levels of plasma sodium (usually <115&nbsp;mmol/L).<ref name="babar"/> When sodium levels in the blood become very low, water enters the brain cells and causes them to swell. 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}}</ref> This is usually fatal if not immediately treated.

Revision as of 14:46, 25 September 2018

Hyponatremia
Other namesHyponatraemia, low blood sodium
Sodium
SpecialtyInternal medicine
SymptomsDecreased ability to think, headaches, nausea, poor balance, confusion, seizures, coma[1][2]
TypesLow volume, normal volume, high volume[3]
Diagnostic methodSerum sodium < 135 mmol/L[2]
Differential diagnosisHigh protein levels, high blood fat levels, high blood sugar[4][5]
TreatmentBased on underlying cause[3]
FrequencyRelatively common[5][6]

Hyponatremia is a low sodium level in the blood.[3] It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEql/L.[2][7] Symptoms can be absent, mild or severe.[1][8] Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance.[2] Severe symptoms include confusion, seizures, and coma.[1][8]

The causes of hyponatremia are typically classified by a person's body fluid status into low volume, normal volume, or high volume.[3] Low volume hyponatremia can occur from diarrhea, vomiting, diuretics, and sweating.[3] Normal volume hyponatremia is divided into cases with dilute urine and concentrated urine.[3] Cases in which the urine is dilute include adrenal insufficiency, hypothyroidism, and drinking too much water or too much beer.[3] Cases in which the urine is concentrated include syndrome of inappropriate antidiuretic hormone secretion (SIADH).[3] High volume hyponatremia can occur from heart failure, liver failure, and kidney failure.[3] Conditions that can lead to falsely low sodium measurements include high blood protein levels such as in multiple myeloma, high blood fat levels, and high blood sugar.[4][5]

Treatment is based on the underlying cause.[3] Correcting hyponatremia too quickly can lead to complications.[4] 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.[3][5] Low volume hyponatremia is typically treated with intravenous normal saline.[3] SIADH is typically treated with fluid restriction while high volume hyponatremia is typically treated with both fluid restriction and a diet low in salt.[3] Correction should generally be gradual in those in whom the low levels have been present for more than two days.[3]

Hyponatremia occurs in about 20% of those admitted to hospital and 10% of people during or after an endurance sporting event.[2][4] Among those in hospital, hyponatremia is associated with an increased risk of death.[4] The economic costs of hyponatremia are estimated at $2.6 billion in the United States.[9]

Signs and symptoms

Signs and symptoms of hyponatremia include nausea and vomiting, headache, short-term memory loss, confusion, lethargy, fatigue, loss of appetite, irritability, muscle weakness, spasms or cramps, seizures, and decreased consciousness or coma.[10] The presence and severity of signs and symptoms are related to the level of salt in the blood, with lower levels of plasma sodium associated with more severe symptoms. However, emerging data suggest that mild hyponatremia (plasma sodium levels at 131–135 mmol/L) is associated with numerous complications or subtle, presently unrecognized symptoms[11] (for example, increased falls, altered posture and gait, reduced attention).[12]

Neurological symptoms typically occur with very low levels of plasma sodium (usually <115 mmol/L).[10] When sodium levels in the blood become very low, water enters the brain cells and causes them to swell. This results in increased pressure in the skull and causes hyponatremic encephalopathy. As pressure increases in the skull, 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, seizures, brain stem compression and respiratory arrest, and non-cardiogenic accumulation of fluid in the lungs.[13] This is usually fatal if not immediately treated.

Symptom severity depends on how fast and how severe the drop in blood salt level. 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.

Chronic hyponatremia can lead to such complications as neurological impairments. These neurological impairments most often affect gait (walking) and attention, and can lead to increased reaction time and falls.[citation needed] Hyponatremia, by interfering with bone metabolism, has been linked with a doubled risk of osteoporosis and an increased risk of bone fracture.[14]

Causes

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.[15] Those with low tonicity are then grouped by whether the person has high fluid volume, normal fluid volume, or low fluid volume.[15] Too little sodium in the diet alone is very rarely the cause of hyponatremia.

High volume

Both sodium and water content increase: Increase in sodium content leads to hypervolemia and water content to hyponatremia.

Normal volume

There is volume expansion in the body, no edema, but hyponatremia occurs[16]

Low volume

The hypovolemia (extracellular volume loss) is due to total body sodium loss. The hyponatremia is caused by a relatively smaller loss in total body water.[16]

Other causes

Miscellaneous causes that are not included under the above classification scheme include the following:

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.[22]

Normal homeostasis

There is a hypothalamic-renal 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), (also called vasopressin).[23] 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.[24] 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 renal tubule. Also, no thirst is experienced. These two act in concert to raise the serum sodium to the normal range.[25][26][27]

Hyponatremia

Hyponatremia occurs 1) when the hypothalamic-renal 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.[26] If the feedback system is overwhelmed, this is water intoxication with maximally dilute urine and is caused by 1) pathological water drinking ("psychotic 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-mediated, 3) congestive heart failure, 4) cirrhosis, 5) nephrosis, 6) spinal cord disease, 7) Addison's disease, 8) cerebral salt wasting, and 9) syndrome of inappropriate antidiuretic hormone secretion (SIADH). If the feed-back system is normal, but an impairment of urine diluting ability unrelated to ADH occurs, this is 1) oliguric renal failure, 2) tubular interstitial renal disease, 3) diuretics, or 4) nephrogenic syndrome of antidiuresis.[26]

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 polar structure too large to pass through the cell membrane: "channels" or "pumps" are required. Cell swelling also produces activation of volume-regulated anion channels which is related to the release of taurine and glutamate from astrocytes.[28]

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.[29] The history and physical exam are necessary to help determine if the patient is hypovolemic, euvolemic, or hypervolemic, which has important implications in determining the underlying cause. An assessment is also made to determine if the patient is experiencing symptoms from their hyponatremia. These include assessments of alertness, concentration, and orientation.

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 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 high blood triglyceride level (most common) or paraproteinemia 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.[30]

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(ADH), which in turn leads to water retention. Hypervolemic hyponatremia is most commonly the result of congestive heart failure, 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" 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).

Acute versus chronic

Chronic hyponatremia is when 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.[11]

Acute hyponatremia is when sodium levels drop rapidly, resulting in potentially dangerous effects, such as rapid brain swelling, which can result in coma and death.

Treatment

The treatment of hyponatremia depends on the underlying cause.[15] How quickly treatment is required depends on a persons symptoms.[15] Fluids is typically the cornerstone of initial management.[15] In those with severe disease an increase in sodium of about 5 mmol/L over one to four hours is recommended.[15]

Fluids

Options include:[citation needed]

  • Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.[31]
  • 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.
  • Severe hyponatremia or severe symptoms (confusion, convulsions, or coma): consider hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h. Hypertonic saline may lead to a rapid dilute diuresis and fall in the serum sodium. It should not be used in those with an expanded extracellular fluid volume.[citation needed]

Medications

American and European guidelines come to different conclusions regarding the use of medications.[32] In the United States they are recommended in those with SIADH, cirrhosis, or heart failure who fail limiting fluid intact.[32] In Europe they are not generally recommended.[32]

There is tentative evidence that vasopressin receptor antagonists (vaptans), such as conivaptan, may be slightly more effective than fluid restriction in those with high volume or normal volume hyponatremia.[3] They should not be used in people with low volume.[15] Their use in SIADH is unclear.[8]

Demeclocycline, while sometimes used for SIADH, has significant side effects including potential kidney problems and sun sensitivity.[33][15] In many people it has no benefit while in others it can result in overcorrection and high blood sodium levels.[15]

Daily use of urea by mouth, while not commonly used due to the taste, has tentative evidence in SIADH.[33][15] It, however, is not available in many areas of the world.[15]

Precautions

Raising the serum sodium concentration too rapidly may cause central pontine myelinolysis.[34] Avoid correction that leads to a serum sodium rise of more than 12 mEq/L/day.[35]

Epidemiology

Hyponatremia is the most commonly seen water–electrolyte imbalance.[15] The disorder is more frequent in females, the elderly, and in people 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 people who are hospitalized have a serum sodium level (salt blood level) of less than 130 mmol/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 inhibitors.[11]

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.[36]

References

  1. ^ a b c Williams, DM; Gallagher, M; Handley, J; Stephens, JW (July 2016). "The clinical management of hyponatraemia". Postgraduate Medical Journal. 92 (1089): 407–11. doi:10.1136/postgradmedj-2015-133740. PMID 27044859.
  2. ^ a b c d e Henry, DA (4 August 2015). "In The Clinic: Hyponatremia". Annals of Internal Medicine. 163 (3): ITC1–19. doi:10.7326/aitc201508040. PMID 26237763.
  3. ^ a b c d e f g h i j k l m n o Lee, JJ; Kilonzo, K; Nistico, A; Yeates, K (13 May 2014). "Management of hyponatremia". CMAJ : Canadian Medical Association Journal. 186 (8): E281-6. doi:10.1503/cmaj.120887. PMC 4016091. PMID 24344146.
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  13. ^ Moritz, M. L.; Ayus, J. C. (2003). "The pathophysiology and treatment of hyponatraemic encephalopathy: An update". Nephrology Dialysis Transplantation. 18 (12): 2486–91. doi:10.1093/ndt/gfg394. PMID 14605269.
  14. ^ Upala, Sikarin; Sanguankeo, Anawin (25 February 2016). "Association Between Hyponatremia, Osteoporosis and Fracture: a Systematic Review and Meta-analysis". The Journal of Clinical Endocrinology & Metabolism. 101: Online first. doi:10.1210/jc.2015-4228. PMID 26913635.
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  21. ^ "High incidence of mild hyponatraemia in females using ecstasy at a rave party".
  22. ^ Sterns, Chapter 44, Antinatriureic peptides, in Seldin and Giebisch’s The Kidney, Fifth Edition. Page 1511-13. DOI:https://dx.doi.org/10.1016/B978-0-12-381462-3.00037-9. 2013 Elsevier Inc. (c) All rights reserved
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  25. ^ Ball SG, Iqbal Z (2016). "Diagnosis and treatment of hyponatraemia". Best practice & research. Clinical endocrinology & metabolism. 30 (2): 161–73. doi:10.1016/j.beem.2015.12.001. PMID 27156756.
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  27. ^ Kwon, TH; Hager, H; Nejsum, LN; Andersen, ML; Frøkiaer, J; Nielsen, S (May 2001). "Physiology and pathophysiology of renal aquaporins". Seminars in nephrology. 21 (3): 231–8. doi:10.1053/snep.2001.21647. PMID 11320486.
  28. ^ Diringer, M. (2017). "Neurologic manifestations of major electrolyte abnormalities". Handbook of Clinical Neurology. 141: 705–713. doi:10.1016/B978-0-444-63599-0.00038-7. ISSN 0072-9752. PMID 28190443.
  29. ^ Sabatine, [edited by] Marc S. (2014). Pocket medicine (Fifth ed.). [S.l.]: Aspen Publishers, Inc. ISBN 1451193785. {{cite book}}: |first1= has generic name (help)
  30. ^ "Ask the Expert: May 2016 Investigating Hyponatremia". American Association for Clinical Chemistry. Archived from the original on 8 June 2016. Retrieved 16 September 2013. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  31. ^ Schürer, Ludwig; Wolf, Stefan; Lumenta, Christianto B. (2010). "Water and Electrolyte Regulation". In Lumenta, Christianto B.; Di Rocco, Concezio; Haase, Jens; et al. (eds.). Neurosurgery. European Manual of Medicine. pp. 611–5. doi:10.1007/978-3-540-79565-0_40. ISBN 978-3-540-79565-0.
  32. ^ a b c Rondon-Berrios, Helbert; Berl, Tomas (2017). "Vasopressin Receptor Antagonists in Hyponatremia: Uses and Misuses". Frontiers in Medicine. 4. doi:10.3389/fmed.2017.00141. ISSN 2296-858X. PMC 5573438. PMID 28879182.{{cite journal}}: CS1 maint: unflagged free DOI (link) This article incorporates text available under the CC BY 4.0 license.
  33. ^ a b Zietse, R.; van der Lubbe, N.; Hoorn, E. J. (2009). "Current and future treatment options in SIADH". Clinical Kidney Journal. 2 (Suppl_3): iii12–iii19. doi:10.1093/ndtplus/sfp154. PMC 2762827. PMID 19881932.
  34. ^ Ashrafian, H.; Davey, P. (2001). "A review of the causes of central pontine myelinosis: yet another apoptotic illness?". European Journal of Neurology. 8 (2): 103–9. doi:10.1046/j.1468-1331.2001.00176.x. PMID 11430268.
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