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Contents

   



(Top)
 


1 Signs and symptoms  





2 Cause  



2.1  Low volume  





2.2  Normal volume  





2.3  High volume  







3 Diagnosis  





4 Treatment  





5 See also  





6 References  





7 External links  














Hypernatremia






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Hypernatremia
Other namesHypernatraemia
Sodium
SpecialtyHospital medicine
SymptomsFeeling of thirst, weakness, nausea, loss of appetite[1]
ComplicationsCardiac arrest, confusion, muscle twitching, bleeding in or around the brain[1][2]
TypesLow volume, normal volume, high volume[1]
Diagnostic methodSerum sodium > 145 mmol/L[3]
Differential diagnosisLow blood protein levels[4]
Frequency~0.5% in hospital[2]

Hypernatremia, also spelled hypernatraemia, is a high concentration of sodium in the blood.[3] Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite.[1] Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain.[1][2] Normal serum sodium levels are 135–145 mmol/L (135–145 mEq/L).[5] Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L.[3] Severe symptoms typically only occur when levels are above 160 mmol/L.[1]

Hypernatremia is typically classified by a person's fluid status into low volume, normal volume, and high volume.[1] Low volume hypernatremia can occur from sweating, vomiting, diarrhea, diuretic medication, or kidney disease.[1] Normal volume hypernatremia can be due to fever, extreme thirst, prolonged increased breath rate, diabetes insipidus, and from lithium among other causes.[1] High volume hypernatremia can be due to hyperaldosteronism, excessive administration of intravenous normal salineorsodium bicarbonate, or rarely from eating too much salt.[1][2] Low blood protein levels can result in a falsely high sodium measurement.[4] The cause can usually be determined by the history of events.[1] Testing the urine can help if the cause is unclear.[1] The underlying mechanism typically involves too little free water in the body.[6]

If the onset of hypernatremia was over a few hours, then it can be corrected relatively quickly using intravenous normal saline and 5% dextrose in water.[1] Otherwise, correction should occur slowly with, for those unable to drink water, half-normal saline.[1] Hypernatremia due to diabetes insipidus as a result of a brain disorder, may be treated with the medication desmopressin.[1] If the diabetes insipidus is due to kidney problems the medication causing the problem may need to be stopped or the underlying electrolyte disturbance corrected.[1][7] Hypernatremia affects 0.3–1% of people in hospital.[2] It most often occurs in babies, those with impaired mental status, and the elderly.[2] Hypernatremia is associated with an increased risk of death, but it is unclear if it is the cause.[2]

Signs and symptoms[edit]

The major symptom is thirst.[8][9] The most important signs result from brain cell shrinkage and include confusion, muscle twitching or spasms. With severe elevations, seizures and comas may occur.[8]

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 157 mmol/L[10] (normal blood levels are generally about 135–145 mmol/L for adults and elderly).[10] Values above 180 mmol/L are associated with a high mortality rate, particularly in adults.[11] However, such high levels of sodium rarely occur without severe coexisting medical conditions.[12] Serum sodium concentrations have ranged from 150 to 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.[13][14]

Cause[edit]

Common causes of hypernatremia include:[8]

Low volume[edit]

In those with low volume or hypovolemia:

Normal volume[edit]

In those with normal volume or euvolemia:

High volume[edit]

In those with high volume or hypervolemia:

Diagnosis[edit]

Hypernatremia is diagnosed when a basic metabolic panel blood test demonstrates a sodium concentration higher than 145 mmol/L.

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 issues leading to rupturing of red blood cells in the bloodstream), but rather can be given intravenously in solution with dextrose (sugar) or saline (salt). 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 treatments such as thiazide diuretics (e.g., chlorthalidone) in congestive heart failureorcorticosteroids in nephropathy also can be used.[19]

See also[edit]

References[edit]

  1. ^ a b c d e f g h i j k l m n o p 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 1410848. PMID 16565125.
  • ^ a b c d e f g 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.
  • ^ a b c 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.
  • ^ a b 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. Archived from the original on 2017-09-08.
  • ^ Kuruvilla, Jaya (2007). Essentials of Critical Care Nursing. Jaypee Brothers Publishers. p. 329. ISBN 9788180619205.[permanent dead link]
  • ^ Ranasinghe, Sudharma; Wahl, Kerri M.; Harris, Eric; Lubarsky, David J. (2012). Anesthesiology Board Review Pearls of Wisdom 3/E. McGraw Hill Professional. p. 6. ISBN 9780071773638.
  • ^ Khanna, A (May 2006). "Acquired Nephrogenic Diabetes Insipidus". Seminars in Nephrology (Review). 26 (3): 244–8. doi:10.1016/j.semnephrol.2006.03.004. PMID 16713497.
  • ^ a b c Lewis, J. L. (March 2013). "Hypernatremia". Merck Manual of Diagnosis and Therapy. Medical Library Association. Archived from the original on 27 December 2015. Retrieved 25 December 2015.
  • ^ Department of Health & Human Services, State Government of Victoria, Australia Better Health Channel: Salt Archived 2016-04-02 at the Wayback Machine Last updated: May 2014
  • ^ 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 1410848. PMID 16565125.
  • ^ 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. S2CID 20446209.
  • ^ Shier, D.; Butler, J.; Lewis, R. (2006). Hole's Human Anatomy and Physiology (11th ed.). McGraw-Hill Companies. ISBN 9780073256993.
  • ^ 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. S2CID 35536508.
  • ^ Baselt, R. C. (2014). Disposition of Toxic Drugs and Chemicals in Man (10th ed.). Seal Beach, Ca.: Biomedical Publications. pp. 1855–1856. ISBN 9780962652394.
  • ^ Leroy, C.; Karrouz, W.; Douillard, C.; Do Cao, C.; Cortet, C.; Wémeau, J. L.; Vantyghem, M. C. (2013). "Diabetes insipidus". Ann. Endocrinol. 74 (5–6). Paris: 496–507. doi:10.1016/j.ando.2013.10.002. PMID 24286605.
  • ^ 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.
  • ^ 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. S2CID 3212802.
  • ^ 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.
  • ^ Adrogué, H. J.; Madias, N. E. (2000). "Hypernatremia". N. Engl. J. Med. 342 (20): 1493–1499. doi:10.1056/NEJM200005183422006. PMID 10816188.
  • External links[edit]


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