Hyponatremia

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Hyponatremia
hyponatraemia
Na-TableImage.png
Classification and external resources
Specialty Internal medicine
ICD-10 E87.1
ICD-9-CM 276.1
DiseasesDB 6483
MedlinePlus 000394
eMedicine emerg/275 med/1130 ped/1124
Patient UK Hyponatremia
MeSH D007010

Hyponatremia, also spelled hyponatraemia, is a low sodium level in the blood.[1] Symptoms can vary from none to severe.[2][3] Mild symptoms include a decreased ability to think, headaches, nausea, and an increased risk of falls.[4] Severe symptoms include confusion, seizures, and coma.[2][3] Normal serum sodium levels are 135 - 145 mEq/liter (135 - 145 mmol/L).[5] Hyponatremia is generally defined as a serum sodium level of less than 135 mEq/L and is considered severe when the level is below 120 mEq/L.[4]

The cause of hyponatremia is typically classified by a person's fluid status into low volume, normal volume, and high volume. Low volume hyponatremia can occur from diarrhea, vomiting, diuretics, and sweating. Normal volume hyponatremia is divided into cases with dilute urine and concentrated urine. Cases in which the urine is dilute include adrenal insufficiency, hypothyroidism, and drinking too much water or too much beer. Cases in which the urine is concentrated include syndrome of inappropriate antidiuretic hormone secretion (SIADH). High volume hyponatremia can occur from heart failure, liver failure, and kidney failure.[1] Conditions that can lead to falsely low sodium measurements include high protein levels such as in multiple myeloma, high blood fat levels, and high blood sugar.[6][7]

Treatment is based on the underlying cause.[1] Correcting hyponatremia too quickly can lead to complications.[6] 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.[1][7] Low volume hyponatremia is typically treated with intravenous normal saline. SIADH is typically treated with fluid restriction while high volume hyponatremia is typically treated with both fluid restriction and a diet low in salt. Correction, in those in whom the the low levels have been present for more than two days should generally be gradual.[1]

Hyponatremia is one of the most commonly seen water–electrolyte imbalances.[7][8] It occurs in about 20% of those admitted to hospital and 10% of people during or after an endurance sporting event.[6][4] Among those in hospital hyponatremia is associated with an increased risk of death.[6] The economic costs of hyponatremia are estimated at $2.6 billion in the United States.[9]

Signs and symptoms[edit]

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 mEq/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 mEq/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[edit]

The specific causes of hyponatremia are generally divided into those that occur with high fluid volume, those with normal fluid volume, and those with low fluid volume. Too little sodium in the diet alone is very rarely the cause of hyponatremia.

High volume hyponatremia[edit]

Both sodium & water content increase: Increase in sodium content leads to hypervolemia and water content to hyponatremia. Total body water and sodium are regulated independently.[15]

Normal volume hyponatremia[edit]

Video explanation of SIADH

There is volume expansion in the body, no edema, but hyponatremia occurs[15]

  • states of severe pain or nausea
  • in the setting of trauma or other damage to the brain
  • SIADH (and its many causes)
  • Hypothyroidism
  • Glucocorticoid (steroid) deficiency

Low volume hyponatremia[edit]

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.[15]

Prolonged periods of exercise may be a cause, known as exercise-associated hyponatremia (EAH).[16][6] It is common in marathon runners and participants of other endurance events.[17] The use of MDMA can result in hyponatremia.[18] This likely occurs as a result of fluid loss via sweating and replacement with water without electrolytes.

Other causes[edit]

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

Diagnosis[edit]

The history, physical exam, and laboratory testing are required to diagnose and determine the underlying cause of hyponatremia. A blood test demonstrating a serum sodium less than 135 mEq/L is diagnostic for hyponatremia.[19] 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[edit]

False hyponatremia, also known as spurious, pseudo, hypertonic, or artifactual hyponatremia is when the lab tests reads 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.[20]

True hyponatremia[edit]

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-diurectic hormone(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).
  • 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 (that is, extreme psychogenic polydipsia)
  • Low volume hyponatremia, wherein ADH secretion is stimulated by or associated with volume depletion (not enough water in the body).

Acute versus chronic[edit]

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.

Pathophysiology[edit]

Sodium is the primary positively charged ion in the environment outside of the cell and cannot freely cross from the interstitial space into the cell. Charged sodium ions attract up to 25 water molecules around them thereby creating a large polar structure too large to pass through the cell membrane.

Treatment[edit]

The treatment of hyponatremia depends on the underlying cause and whether the person's blood volume status is high, normal, or low.

Fluids[edit]

In the setting of hypovolemia, intravenous administration of normal saline (salt) is usual, care being taken not to raise the serum sodium level (salt level in the blood) 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 are 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 is usually treated by addressing the underlying heart or liver failure. If it is not possible to do so, the treatment becomes the same as that for euvolemic hyponatremia (that is, fluid restriction and/or use of a vaptan drug).

Hyponatremia is corrected slowly, to lessen the risk of the development of central pontine myelinolysis (CPM), a severe neurological disease involving a breakdown of the myelin sheaths covering parts of nerve cells. In fact, overly rapid correction of hyponatremia is the most common cause of that potentially devastating disorder.[21] During treatment of hyponatremia, the serum sodium (salt level in the blood) is not allowed to rise by more than 8 mmol/L over 24 hours (that is, 0.33 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 is an abrupt water diuresis (an increase in urination since there is no longer any ADH acting to retain the water). A rapid and profound rise in serum sodium (salt level in the blood) can then occur. Should the rate of rise of serum sodium exceed 0.33 mmol/L/h over several hours, vasopressin may be administered to prevent ongoing rapid water diuresis (excessive urination).[22]

Medications[edit]

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.[1] They should not be used in people with low volume. There use is SIADH is unclear.[3]

Epidemiology[edit]

Hyponatremia is the most common electrolyte disorder. Electrolytes are sodium (salt), potassium, calcium, magnesium, chloride, hydrogen phosphate, and hydrogen carbonate. 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 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 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 readmisson. This is particularly the case in men and in the elderly.[23]

See also[edit]

References[edit]

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  2. ^ a b Williams, DM; Gallagher, M; Handley, J; Stephens, JW (July 2016). "The clinical management of hyponatraemia.". Postgraduate medical journal. 92 (1089): 407–11. PMID 27044859. 
  3. ^ a b c Ball, S; De Groot, LJ; Beck-Peccoz, P; Chrousos, G; Dungan, K; Grossman, A; Hershman, JM; Koch, C; McLachlan, R; New, M; Rebar, R; Singer, F; Vinik, A; Weickert, MO (2000). "Hyponatremia". PMID 25905359. Accessed 1 August 2016. 
  4. ^ a b c Henry, DA (4 August 2015). "In The Clinic: Hyponatremia.". Annals of internal medicine. 163 (3): ITC1–19. PMID 26237763. 
  5. ^ Kuruvilla, Jaya (2007). Essentials of Critical Care Nursing. Jaypee Brothers Publishers. p. 329. ISBN 9788180619205. 
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  7. ^ a b c Marx, John; Walls, Ron; Hockberger, Robert (2013). Rosen's Emergency Medicine - Concepts and Clinical Practice (8 ed.). Elsevier Health Sciences. p. 1639-1642. ISBN 1455749877. 
  8. ^ Ball, SG; Iqbal, Z (March 2016). "Diagnosis and treatment of hyponatraemia". Best practice & research. Clinical endocrinology & metabolism. 30 (2): 161–73. PMID 27156756. 
  9. ^ Simon, Eric E. (2014). Hyponatremia: Evaluation and Treatment. Springer Science & Business Media. p. 205. ISBN 9781461466451. 
  10. ^ a b Babar, S. (October 2013). "SIADH Associated With Ciprofloxacin." (PDF). The Annals of Pharmacotherapy. Sage Publishing. 47 (10): 1359–1363. doi:10.1177/1060028013502457. ISSN 1060-0280. PMID 24259701. Retrieved November 18, 2013. 
  11. ^ a b c Schrier, Robert W. (2010). "Does 'asymptomatic hyponatremia' exist?". Nature Reviews Nephrology. 6 (4): 185. doi:10.1038/nrneph.2010.21. PMID 20348927. 
  12. ^ Decaux, Guy (2006). "Is Asymptomatic Hyponatremia Really Asymptomatic?". The American Journal of Medicine. 119 (7): S79–82. doi:10.1016/j.amjmed.2006.05.013. PMID 16843090. 
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  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: Online first. doi:10.1210/jc.2015-4228. PMID 26913635. 
  15. ^ a b c Mange, Kevin; Matsuura, D; Cizman, B; Soto, H; Ziyadeh, FN; Goldfarb, S; Neilson, EG (1997). "Language Guiding Therapy: The Case of Dehydration versus Volume Depletion". Annals of Internal Medicine. 127 (9): 848–53. doi:10.7326/0003-4819-127-9-199711010-00020. PMID 9382413. 
  16. ^ Bennett, BL; Hew-Butler, T; Hoffman, MD; Rogers, IR; Rosner, MH (Sep 2013). "Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia.". Wilderness & environmental medicine. 24 (3): 228–40. doi:10.1016/j.wem.2013.01.011. PMID 23590928. 
  17. ^ Rosner, M.H.; Kirven, J. (2006). "Exercise-Associated Hyponatremia". Clinical Journal of the American Society of Nephrology. 2 (1): 151–61. doi:10.2215/CJN.02730806. PMID 17699400. 
  18. ^ "High incidence of mild hyponatraemia in females using ecstasy at a rave party". 
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  21. ^ Bernsen HJ, Prick MJ (September 1999). "Improvement of central pontine myelinolysis as demonstrated by repeated magnetic resonance imaging in a patient without evidence of hyponatremia". Acta Neurol Belg. 99 (3): 189–93. PMID 10544728. 
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External links[edit]