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Hypernatremia

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Hypernatremia
SpecialtyNephrology, endocrinology Edit this on Wikidata

Hypernatremia or hypernatraemia is an elevated sodium level in the blood, specifically a serum level above 145 mEq/L.[1] Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body. For this reason, hypernatremia often coincides with dehydration.

Water is lost from the body in a variety of ways, including perspiration, imperceptible losses from breathing, and in the feces and urine. If the amount of water ingested consistently falls below the amount of water lost, the plasma sodium level will begin to rise, leading to hypernatremia. Rarely, hypernatremia can result from massive salt ingestion,[2][3] such as may occur from drinking seawater or excessive amounts of a salty liquid like soy sauce.[4][5] When the total protein concentration is low in serum, a falsely high sodium measurement (pseudohypernatremia) tends to occur with the usual assay method, indirect potentiometry, an artifact explained by the electrolyte exclusion effect.

Ordinarily, even a small rise in the plasma sodium concentration above the normal range results in a strong sensation of thirst, an increase in free water intake, and correction of the abnormality. Therefore, hypernatremia most often occurs in people such as infants, those with impaired mental status, or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water.

Signs and symptoms

Clinical manifestations of hypernatremia can be subtle, consisting of lethargy, weakness, irritability, neuromuscular excitability, and edema. With more severe elevations of the sodium level, seizures and coma may occur.

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 157 mEq/L[6] (normal blood levels are generally about 135-145 mEq/L for adults and elderly) [6] Values above 180 mEq/L are associated with a high mortality rate, particularly in adults.[2] However such high levels of sodium rarely occur without severe coexisting medical conditions.[7] Serum sodium concentrations have ranged from 150-228 mEq/L in survivors of acute salt overdosage, while levels of 153-255 mEq/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.[8][9]

Cause

Management of hypernatremia

Common causes of hypernatremia include:

  • Hypovolemic
    • 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
  • Euvolemic
  • Hypervolemic
    • 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.[2]
    • 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).[11][12]

Treatment

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.[13]

See also

References

  1. ^ Lewis, J. L. (March 2013). "Hypernatremia". Merck Manual of Diagnosis and Therapy. Medical Library Association. Retrieved 25 December 2015.
  2. ^ 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.
  3. ^ Hédouin, V.; Révuelta, E.; Bécart, A.; Tournel, G.; Deveaux, M.; Gosset, D. (1999). "A case of fatal salt water intoxication following an exorcism session". Forensic Sci. Int. 99: 1–4. doi:10.1016/S0379-0738(98)00179-0. PMID 10069018.
  4. ^ Ghose, T. (7 June 2013). "Soy Sauce Overdose Sends Man Into Coma". Huffington Post. Retrieved 26 December 2015.
  5. ^ 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.
  6. ^ 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.
  7. ^ Shier, D.; Butler, J.; Lewis, R. (2006). Hole's Human Anatomy and Physiology (11th ed.). McGraw-Hill Companies. ISBN 9780073256993.
  8. ^ Coe, J. I. (1993). "Postmortem chemistry update. Emphasis on forensic application". Am. J. Forensic Med. Pathol. 14 (2): 91–117. PMID 8328447.
  9. ^ Baselt, R. C. (2014). Disposition of Toxic Drugs and Chemicals in Man (10th ed.). Seal Beach, Ca.: Biomedical Publications. pp. 1855–1856. ISBN 9780962652394.
  10. ^ 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.
  11. ^ 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.
  12. ^ 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.
  13. ^ Adrogué, H. J.; Madias, N. E. (2000). "Hypernatremia". N. Engl. J. Med. 342: 1493–1499. doi:10.1056/NEJM200005183422006. PMID 10824078.
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