Hypernatremia

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Hypernatremia
Na-TableImage.png
Sodium
Classification and external resources
Specialty Internal medicine
ICD-10 E87.0
ICD-9-CM 276.0
DiseasesDB 6266
eMedicine emerg/263
Patient UK Hypernatremia

Hypernatremia, also spelled hypernatraemia, is a high sodium ion level in the blood.[1] Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite.[2] Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain.[2][3] Normal serum sodium levels are 135 - 145 mmol/L (135 - 145 mEq/L).[4] Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L.[1] Severe symptoms typically only occur when levels are above 160 mmol/L.[2]

Hypernatremia is typically classified by a person's fluid status into low volume, normal volume, and high volume. Low volume hypernatremia can occur from sweating, vomiting, diarrhea, diuretic medication, or kidney disease. Normal volume hypernatremia can be due to fever, inappropriately decreased thirst, prolonged increased breath rate, diabetes insipidus, and from lithium among other causes.[2] High volume hypernatremia can be due to hyperaldosteronism, be health care caused such as when too much intravenous 3% normal saline or sodium bicarbonate is given, or rarely be from eating too much salt.[2][3] Low blood protein levels can result in a falsely high sodium measurement.[5] The cause can usually be determined by the history of events. Testing the urine can help if the cause is unclear.[2]

If the onset of hypernatremia was over a few hours, then it can be corrected relatively quickly using intravenous normal saline and 5% dextrose. Otherwise correction should occur slowly with, for those unable to drink water, half-normal saline. Hypernatremia due to diabetes insipidus as a result of a brain disorder, may be treated with the medication desmopressin. If the diabetes insipidus is due to kidney problems the medication which is causing it may need to be stopped.[2] Hypernatremia affects 0.3-1% of people in hospital. It most often occurs in babies, those with impaired mental status, and those who are old. Hypernatremia is associated with an increased risk of death but it is unclear if it is the cause.[3]

Signs and symptoms[edit]

The major symptom is thirst.[6][7] The most important signs result from brain cell shrinkage and include confusion, muscle twitching or spasms. With severe elevations, seizures and comas may occur.[6]

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 157 mmol/L[8] (normal blood levels are generally about 135–145 mmol/L for adults and elderly). [8] Values above 180 mmol/L are associated with a high mortality rate, particularly in adults.[9] However, such high levels of sodium rarely occur without severe coexisting medical conditions.[10] Serum sodium concentrations have ranged from 150–228 mmol/L in survivors of acute salt overdosage, while levels of 153–255 mmol/L have been observed in fatalities. Vitreous humor is considered to be a better postmortem specimen than postmortem serum for assessing sodium involvement in a death.[11][12]

Cause[edit]

Management of hypernatremia

Common causes of hypernatremia include:[6]

Low volume[edit]

In those with low volume or hypovolemia:

  • Inadequate intake of free water associated with total body sodium depletion. Typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates and also are sodium depleted. This is the most common cause of hypernatremia.
  • Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics - leads to a combination of sodium and free water losses.
  • Water losses associated with extreme sweating.
  • Severe watery diarrhea

Normal volume[edit]

In those with normal volume or euvolemia:

High volume[edit]

In those with high volume or hypervolemia:

  • Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body) with restricted free water intake. This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic and free water is not available. There are several recorded cases of forced ingestion of concentrated salt solution in exorcism rituals leading to death.[9]
  • Mineralcorticoid excess due to a disease state such as Conn's syndrome usually does not lead to hypernatremia unless free water intake is restricted.
  • Salt poisoning (this condition is most common in children).[14][15] It has also been seen in a number of adults with mental health problems.[9] Too much salt can also occur from drinking seawater or soy sauce.[16]

Treatment[edit]

The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. Water alone cannot be administered intravenously (because of osmolarity issue), but rather can be given with addition to dextrose or saline infusion solutions. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by a physician or other medical professional with experience in treatment of electrolyte imbalance, specific treatment like ACE inhibitors in heart failure and corticosteroids in nephropathy also can be used.[17]

See also[edit]

References[edit]

  1. ^ a b Muhsin, SA; Mount, DB (March 2016). "Diagnosis and treatment of hypernatremia.". Best practice & research. Clinical endocrinology & metabolism. 30 (2): 189–203. doi:10.1016/j.beem.2016.02.014. PMID 27156758. 
  2. ^ a b c d e f g Reynolds, RM; Padfield, PL; Seckl, JR (25 March 2006). "Disorders of sodium balance.". BMJ (Clinical research ed.). 332 (7543): 702–5. doi:10.1136/bmj.332.7543.702. PMC 1410848Freely accessible. PMID 16565125. 
  3. ^ a b c Lin, M; Liu, SJ; Lim, IT (August 2005). "Disorders of water imbalance.". Emergency medicine clinics of North America. 23 (3): 749–70, ix. doi:10.1016/j.emc.2005.03.001. PMID 15982544. 
  4. ^ Kuruvilla, Jaya (2007). Essentials of Critical Care Nursing. Jaypee Brothers Publishers. p. 329. ISBN 9788180619205. 
  5. ^ Kliegman, Robert M.; Stanton, Bonita M. D.; Geme, Joseph St; Schor, Nina F. (2015). Nelson Textbook of Pediatrics (20 ed.). Elsevier Health Sciences. p. 348. ISBN 9780323263528. 
  6. ^ a b c Lewis, J. L. (March 2013). "Hypernatremia". Merck Manual of Diagnosis and Therapy. Medical Library Association. Retrieved 25 December 2015. 
  7. ^ Department of Health & Human Services, State Government of Victoria, Australia Better Health Channel: Salt Last updated: May 2014
  8. ^ a b Reynolds, R.; Padfield, P. L.; Seckl, J. R. (2006). "Disorders of sodium balance". BMJ. 332 (7543): 702–705. doi:10.1136/bmj.332.7543.702. PMC 1410848Freely accessible. PMID 16565125. 
  9. ^ a b c Ofran, Y.; Lavi, D.; Opher, D.; Weiss, T. A.; Elinav, E. (2004). "Fatal voluntary salt intake resulting in the highest ever documented sodium plasma level in adults (255 mmol L−1) a disorder linked to female gender and psychiatric disorders". J. Intern. Med. 256 (6): 525–528. doi:10.1111/j.1365-2796.2004.01411.x. PMID 15554954. 
  10. ^ Shier, D.; Butler, J.; Lewis, R. (2006). Hole's Human Anatomy and Physiology (11th ed.). McGraw-Hill Companies. ISBN 9780073256993. 
  11. ^ Coe, J. I. (1993). "Postmortem chemistry update. Emphasis on forensic application.". Am. J. Forensic Med. Pathol. 14 (2): 91–117. doi:10.1097/00000433-199306000-00001. PMID 8328447. 
  12. ^ Baselt, R. C. (2014). Disposition of Toxic Drugs and Chemicals in Man (10th ed.). Seal Beach, Ca.: Biomedical Publications. pp. 1855–1856. ISBN 9780962652394. 
  13. ^ Leroy, C.; Karrouz, W.; Douillard, C.; Do Cao, C.; Cortet, C.; Wémeau, J. L.; Vantyghem, M. C. (2013). "Diabetes insipidus.". Ann. Endocrinol. (Paris). 74 (5-6): 496–507. doi:10.1016/j.ando.2013.10.002. PMID 24286605. 
  14. ^ Saunders, N.; Balfe, J. W.; Laski, B. (1976). "Severe salt poisoning in an infant.". J. Pediatr. 88 (2): 258–61. doi:10.1016/s0022-3476(76)80992-4. PMID 1249688. 
  15. ^ Paut, O.; André, N.; Fabre, P.; Sobraquès, P.; Drouet, G.; Arditti, J.; Camboulives, J. (1999). "The management of extreme hypernatraemia secondary to salt poisoning in an infant.". Paediatr. Anaesth. 9 (2): 171–174. doi:10.1046/j.1460-9592.1999.9220325.x. PMID 10189662. 
  16. ^ Carlberg, D. J.; Borek, H. A.; Syverud, S. A.; Holstege, C. P. (2013). "Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion". J. Emerg. Med. 45 (2): 228–231. doi:10.1016/j.jemermed.2012.11.109. PMID 23735849. 
  17. ^ Adrogué, H. J.; Madias, N. E. (2000). "Hypernatremia". N. Engl. J. Med. 342: 1493–1499. doi:10.1056/NEJM200005183422006. PMID 10816188. 

External links[edit]

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