Hypernatremia treatment: Difference between revisions
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Oral intake of water or IV 5% dextrose solutions can be used to replace water loss in euvolemic hypernatremia. | Oral intake of water or IV 5% dextrose solutions can be used to replace water loss in euvolemic hypernatremia. | ||
** Acute hypernatremia should be treated by rapid replacement of water losses. The remainder of the deficit could be administered over 24 to 48hours after the neurologic manifestations resolve. | ** Acute hypernatremia should be treated by rapid replacement of water losses. The remainder of the deficit could be administered over 24 to 48hours after the neurologic manifestations resolve. | ||
** '''Overly rapid correction of chronic 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 especially in patients with chronic hypernatremia, 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. The rate of chronic hypernatremia correction should be '''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 imbalance]]s. | ** '''Overly rapid correction of chronic 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 especially in patients with chronic hypernatremia, 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. The rate of chronic hypernatremia correction should be '''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 imbalance]]s. | ||
** Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate. | ** 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. | ** Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet. | ||
Revision as of 14:33, 12 December 2011
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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
Correcting sodium level is vital in order to prevent any permanent brain damage. Free water replacement is required and the amount is calculated using a formula mentioned below. The management of any other condition causing hypernatremia should be adressed as well.
Treatment
- Three factors should be considered when treating hypernatremia: the volume status, the severity of the patient's symptoms and the time over which hypernatremia has occured.
- The cornerstone of treatment is administration of free water to correct the relative water deficit.
- Water can be replaced orally or intravenously (IV).
- Patients with hypovolemic hypernatremia (ie, patients with GI losses (diarrhea, vomiting), skin losses (burn patients) or renal losses (loop diuretics or osmotic diuresis)): water and sodium deficit should be replaced with isotonic normal saline (0.9%) solutions because there is concomitant loss of both sodium and water. when the patient is hemodynamically stable, 0.45% saline solutions should be used to replace the remainder of the sodium and water deficit.
- Patients with euvolemic hypernatremia (ie, patients with renal losses due to diabetes insipidus (both neurogenic and nephrogenic) or extrarenal losses (sweating, fever, mechanical ventilation, defective thirst mechanism) with no replacement of the water deficit): water losses can be calculated by the following formula:
Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[Sodium]/140)-1).
Oral intake of water or IV 5% dextrose solutions can be used to replace water loss in euvolemic hypernatremia.
- Acute hypernatremia should be treated by rapid replacement of water losses. The remainder of the deficit could be administered over 24 to 48hours after the neurologic manifestations resolve.
- Overly rapid correction of chronic 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 especially in patients with chronic hypernatremia, 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. The rate of chronic hypernatremia correction should be 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.
- 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.
- Patients with hypervolemic hypernatremia: These patients have excess sodium with an increased total body volume; diuretics should be administered to remove the excess sodium.