Central pontine myelinolysis primary prevention
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To minimize the risk of central pontine myelinolysis developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected slowly. The primary goals of treating hypernatremia are estimating the magnitude of water deficit, determining the proper rate of correction, addressing the concurrent electrolyte or volume deficits and calculating the fluid deficit regimen using the estimated water deficit and desired rate of correction. Correcting sodium level is vital in order to prevent any permanent brain damage.
To minimize the risk of central pontine myelinolysis developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected slowly. The medical therapy of hypernatremia is as follows:
Rationale for therapeutic management of hypernatremia
- Estimating the magnitude of water deficit
- Determining the proper rate of correction
- Addressing the concurrent electrolyte or volume deficits
- Calculating the fluid deficit regimen using the estimated water deficit and desired rate of correction.
1.Estimation of water deficit:
Estimation of the water deficit is done using the following mathematical formula:
Water deficit = Current TBW x (Serum sodium|140 - 1)
2.Choice of rate of correction
3.Rate of correction in acute hypernatremia
- Serum sodium should be rapidly lowered to a near-normal level in less than 24 hours in patients with acute hypernatremia in order to prevent acute neuronal injury such as osmotic demyelination.
- The hourly infusion rate should exceed the water deficit divided by 24:
Hourly infusion rate (mL/hour) > Water deficit in mL ÷ 24 hours
4.Rate of correction in chronic hypernatremia
- The maximum rate at which the serum sodium concentration should be decreased is 12 mEq/L per day.
- To ensure safety, it can be lowered at 10 mEq/L per day.
5.Rate of correction in hypernatremia associated with hyperglycemia
- The hypertonicity as a result of hypernatremia in hyperglycemic patients is corrected slowly to prevent cerebral edema which is a major cause of morbidity and mortality in DKA patients.
- The rate of correction for the decrease in tonicity during correction of hyperglycemia should not be greater than 3 mosmol/kg per hour.
- The goal for blood glucose decrement should be 50 to 75 mg/dL per hour.
6.Treatment regimen in patients with concurrent electrolyte abnormalities
- In patients having concurrent electrolyte imbalance, sodium or potassium can be added to the intravenous fluid as necessary to simultaneously correct the water and electrolyte deficits.
- However, the addition of sodium or potassium to the replacement fluid decreases the amount of free water that is being given.
7.Remeasurement of sodium levels and modification of the regimen
- 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 occurred.
- The cornerstone of treatment is the 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 another medical professional with experience in the 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.
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