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Hypernatremia (serum sodium > 145 meq/L) develops from excess water loss, frequently accompanied by an impaired thirst mechanism (eg, dehydration, lactulose or mannitol therapy, or diabetes insipidus). Hypokalemia, hypercalcemia, or sickle cell anemia can cause nephrogenic diabetes insipidus. Rarely, excessive sodium intake may cause hypernatremia (eg, accidental intravascular injection of hypertonic saline used for induction of abortion or use of large doses of sodium bicarbonate therapy during cardiac arrest). Since total body sodium content is the major determinant of extracellular fluid volume, one must determine if the hypernatremia is accompanied by a normal, decreased, or increased extracellular fluid volume.
A. Symptoms and Signs: Intact thirst usually prevents hypernatremia, and thus its presence is commonly associated with conditions in which access to water is limited, eg, cerebrovascular disease. Orthostatic hypotension and oliguria are typical. Hyperthermia, delirium, and coma may be seen with severe hyperosmolality.
B. Laboratory Findings:
1. Urine osmolality > 400 mosm/kg–Renal water-conserving ability is functioning.
a. Nonrenal losses–Hypernatremia will develop if water ingestion fails to keep up with hypotonic losses from excessive sweating, exertional losses from the respiratory tract, or through stool water. Lactulose causes an osmotic diarrhea with loss of free water.
b. Renal losses–While diabetic hyperglycemia can cause pseudohyponatremia (see above), progressive volume depletion from the osmotic diuresis of glycosuria can result in true hypernatremia. Osmotic diuresis can occur with the use of mannitol or urea.
2. Urine osmolality < 250 mosm/kg–A dilute urine with osmolality less than 250 mosm/kg with hypernatremia is characteristic of central and nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus, seen with lithium or demeclocycline therapy or after relief of prolonged urinary tract obstruction, or with interstitial nephritis, results from renal insensitivity to ADH.
Treatment of hypernatremia is directed toward correcting the cause of the fluid loss and replacing water and, as needed, electrolytes. In response to increases in plasma osmolality, brain cells synthesize solutes—or idiogenic osmoles—which increase osmotic flow of water back into the brain cells to regulate their volume. This begins 4–6 hours after dehydration and takes several days to reach a steady state. If hypernatremia is too rapidly corrected, the osmotic imbalance may cause water to preferentially enter brain cells, causing cerebral edema and potentially severe neurologic impairment. Fluid therapy should be administered over a 48-hour period, aiming for a decrease in serum sodium of 1 meq/L/h (1 mmol/L/h). Potassium and phosphate may be added as indicated by serum levels; other electrolytes are also monitored frequently.
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