Hypernatremia history and symptoms: Difference between revisions
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Revision as of 20:28, 7 February 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Assistant Editor(s)-In-Chief: Jack Khouri
Overview
The symptoms of hypernatremia are subtle and include weakness or lethargy. With more severe elevations of the sodium level, seizures and coma may occur.
History
A detailed history is important for the diagnosis of the etiology of hypernatremia. It should be directed at obtaining a history of diabetes insipidus, hyperaldosteronism, Cushing's disease, neurologic disease, seizure disorder, malabsorptive disease and ingestion of excess sodium salts. A recent history of diarrhea, burns, exercise (increased sweating), polyuria and polydypsia should be obtained. A thorough drug history should include diuretic use or ingestion of osmotic agents (eg, mannitol or lactulose).
Symptoms
Clinical manifestations of hypernatremia can be subtle, consisting of lethargy, weakness, irritability, 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 158 mEq/L, which corresponds to an osmolar gradient of 30-35 mEq/kg between plasma and brain. Beyond that level, the rapid reduction of brain volume can cause rupture of cerebral veins leading to intracerebral and subarachnoid hemorrhage. Values above 180 mEq/L are associated with a high mortality rate, particularly in adults. However such high levels of sodium rarely occur without severe coexisting medical conditions.
To note that if hypernatremia progresses over more than 24 hours, the brain adapts rapidly to plasma hyperosmolarity by the intracellular accumulation of many osmolytes such as amino acids (eg, glutamate).