Laboratory Studies
When hypernatremia is discovered in a patient, obtain urine osmolality and sodium levels. Check serum glucose level to ensure that osmotic diuresis has not occurred.
The kidneys' normal response to hypernatremia is excretion of a minimal amount of maximally concentrated urine. If urine osmolarity is high, suspect extrarenal hypotonic fluid losses (eg, vomiting, low sodium diarrhea, sweat, evaporation from burns, low sodium ostomy output). The urine also is concentrated in salt overload states, although the total volume should increase.
Isotonic urine osmolality can be observed with diuretics, osmotic diuresis (mannitol, glucose, urea), or salt wasting.
Hypotonic urine and polyuria are characteristic of DI. Note, however, that partial DI can occur in which some concentrating ability remains, especially in the absence of a water load.
Serum sodium level indications include the following:
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Serum sodium levels of more than 190 mEq/L usually indicate long-term salt ingestion
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Serum sodium levels of more than 170 mEq/L usually indicate DI
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Serum sodium levels of 150-170 mEq/L usually indicate dehydration
A study by Solak indicated that results from blood gas analyzers (BGAs), which may be used in the emergency department to measure sodium pending results from biochemistry laboratory autoanalyzers (BLAs), tend to significantly differ from BLA values. It was found that BLA serum sodium values tended to be higher than BGA results for hyponatremia, eunatremia, and hypernatremia, with an absolute mean difference of over 4 mmol/L for the three groups. [15]
Imaging Studies
Head CT scan or MRI is suggested in all patients with severe hypernatremia.
Traction on dural bridging veins and sinuses caused by movement of water from the brain and brain shrinkage can lead to intracranial hemorrhage, most often in the subdural space.
Hemoconcentration from total body water loss may lead to dural sinus thrombosis.
Imaging studies may indicate a central cause for hypernatremia.
Other Tests
Water deprivation test
With DI, water deprivation induces serum hyperosmolality and hypernatremia, but urine osmolality does not increase appropriately.
ADH stimulation
With nephrogenic DI, urine osmolality does not increase after ADH or desmopressin acetate administration.
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
