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]
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]
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 (e.g., mannitol) – leads to a combination of sodium and free water losses.
Water losses associated with extreme sweating.
Severe watery diarrhea (osmotic diarrhea results in hypotonic (dilute) watery diarrhea resulting in significant loss of free water and a higher concentration of sodium in the blood; this type of water loss can also be seen with viral gastroenteritis).
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.[11]
Mineralcorticoid excess due to a disease state such as Conn's syndrome usually does not lead to hypernatremia unless free water intake is restricted.
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 failure or corticosteroids in nephropathy also can be used.[19]
^ abcdefgLin, 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. PMID15982544.
^ abcMuhsin, 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. PMID27156758.
^Baselt, R. C. (2014). Disposition of Toxic Drugs and Chemicals in Man (10th ed.). Seal Beach, Ca.: Biomedical Publications. pp. 1855–1856. ISBN9780962652394.
^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. PMID24286605.