Hypernatremia history and symptoms: Difference between revisions
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==History== | ==History== | ||
A detailed history is important for the diagnosis of the etiology of hypernatremia. | A detailed history is important for the diagnosis of the etiology of hypernatremia. Patients having hypernatremia may have a positive history of | ||
* [[diabetes insipidus]] | |||
* [[hyperaldosteronism]] | |||
* [[Cushing's disease]] | |||
* Neurological disorder | |||
* Seizure disorder | |||
* [[malabsorptive disease|Malabsorption]] | |||
* Ingestion of excess sodium salts. | |||
Hypernatremic patients can also have a recent history of the following diseases: | |||
* [[diarrhea]] | |||
* [[burns]] | |||
* [[exercise]] ([[increased sweating]]) | |||
* [[polyuria]] | |||
* P[[polydypsia|olydypsia]] | |||
==== Drug history: ==== | |||
Patients on the following drugs can also have high sodium levels: | |||
* [[diuretic|Diuretics]] | |||
* Lactulose | |||
==Symptoms== | ==Symptoms== | ||
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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. | 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. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 03:13, 8 May 2018
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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. Patients having hypernatremia may have a positive history of
- diabetes insipidus
- hyperaldosteronism
- Cushing's disease
- Neurological disorder
- Seizure disorder
- Malabsorption
- Ingestion of excess sodium salts.
Hypernatremic patients can also have a recent history of the following diseases:
Drug history:
Patients on the following drugs can also have high sodium levels:
- Diuretics
- 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.