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