Hypernatremia: Difference between revisions
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==[[Hypernatremia differential diagnosis|Differential Diagnosis]]== | ==[[Hypernatremia differential diagnosis|Differential Diagnosis]]== | ||
== | ==[[Hypernatremia history and symptoms|History and Symptoms]]== | ||
==Labs and Procedures== | ==Labs and Procedures== | ||
Revision as of 19:54, 9 December 2011
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Hypernatremia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Hypernatremia On the Web |
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American Roentgen Ray Society Images of Hypernatremia |
| Hypernatremia | |
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| Sodium | |
| ICD-10 | E87.0 |
| ICD-9 | 276.0 |
| DiseasesDB | 6266 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-In-Chief: Jack Khouri
Overview
Pathophysiology
Causes
Differential Diagnosis
History and Symptoms
Labs and Procedures
- Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urinewith a urine osmolality >800 mosmol/kg.
- Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
- Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
- Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.
- The water deprivation test
- The objective of this test is to distinguish the origin of diabetes insipidus (DI).
- Desmopressin (AVP), a synthetic analogue of vasopressin, is effective in patients with central DI.
- Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
- Patients with central DI have intact kidney response to vasopressin and will have a substantial increase in urine osmolarity in response to water deprivation and desmopressin administrarion.
- Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
- Patients with partial central DI show an increase in urine osmolarity of >10%.
Treatment
- The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously.
- Overly rapid correction of hypernatremia is potentially very dangerous. As we mentioned before, 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 (cerebral edema). This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Central pontine myelinolysis can also occur with over rapid correction of the sodium which should be about 0.5 meq/l/hour and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a physician or other medical professional with experience in treatment of electrolyte imbalances.
- Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[Sodium]/140)-1)
- Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate.
- Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet.