Pediatric Metabolic Alkalosis Treatment & Management
- Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD more...
Mild or moderate metabolic alkalosis or alkalemia rarely requires correction. For severe metabolic alkalosis, therapy should address the underlying disease state, in addition to moderating the alkalemia. As with correction of any electrolyte or acid-base imbalance, the goal is to prevent life-threatening complications with the least amount of correction. The initial target pH and bicarbonate level in correcting severe alkalemia are approximately 7.55 mmol/L and 40 mmol/L, respectively, which are not values within the reference range.
Consider the severity of hypovolemia or hypokalemia and the degree of alkalosis when managing metabolic alkalosis due to chloride loss from vomiting or other GI losses. Children with protracted vomiting, whether due to pyloric stenosis or other causes, may develop hypovolemic shock. Intravascular volume expansion with isotonic crystalloid solution is needed, and monitoring of central venous pressure to determine adequacy of volume resuscitation may be indicated.
Administer potassium as a chloride salt to patients with hypokalemia to help replenish chloride losses. However, remember that using potassium chloride (KCl) alone to correct hypochloremia has limited utility because the KCl infusion rate cannot exceed prescribed safe levels.
For persistent severe metabolic alkalosis, administration of HCl or ammonium chloride (NH4 Cl) may be considered, but must be administered with care. Although uncommon, fatality from extravasated HCl has been reported.
Acetazolamide may help patients with chloride-resistant metabolic alkalosis. It has been safely used for treatment of diuretic-induced metabolic alkalosis in pediatric cardiac patients.[9, 10, 11]
Correction of metabolic alkalosis in patients with renal failure may require hemodialysis or continuous renal replacement therapy with a dialysate that contains high levels of chloride and low levels of HCO3.
Temporary discontinuation of chloruretic diuretics (eg, furosemide, bumetanide, ethacrynic acid) may help patients with metabolic alkalosis due to long-term diuretic use. Potassium-sparing diuretics and carbonic anhydrase inhibitors may be used in patients who require continued diuretic therapy. Patients with accompanying extracellular fluid (ECF) volume contraction occasionally require sodium and potassium administration. If continued diuretic use is indicated, potassium salt supplements may help avoid metabolic alkalosis.
Severe metabolic alkalemia should be monitored in an ICU setting with full noninvasive cardiopulmonary monitoring. Invasive monitoring and specialized vascular access may be necessary, depending on the overall clinical picture.
Monitor serum electrolyte levels and acid-base status when providing treatment for metabolic alkalosis, particularly when using chloride salts. Provide follow-up care specific to the disease that caused metabolic alkalosis.
Children with pyloric stenosis require surgical intervention (pyloromyotomy) following intravascular fluid expansion and correction of metabolic abnormalities.
Tailor dietary changes to the underlying disease.
Metabolic alkalosis may be avoided by judicious use of long-term diuretics with appropriate monitoring.
The role of a pediatric tertiary care center where appropriate subspecialists are available in the care of a child with metabolic alkalosis cannot be overemphasized. If the patient requires dialysis or has a renal disease, such as Bartter syndrome, transfer the patient to a nephrologist. An endocrinologist should manage primary aldosteronism and mineralocorticoid excess states. Children who develop hypovolemic shock or those with persistent severe and symptomatic metabolic alkalosis are best monitored in a critical care setting.
Respiratory status and oxygenation must be monitored. Failure to realize that severe metabolic alkalosis can lead to hypoventilation and consequent hypoxemia could delay treatment and result in hypoxic damage.
Hydrochloric acid can cause severe tissue necrosis if the solution extravasates into the tissues. In addition, use of high concentrations (ie, >0.1 N) of HCl can corrode central veins and venous catheters.
Physicians must be familiar with the complications associated with the use of chloride salts to treat severe metabolic alkalosis. Use of NH4 Cl can result in hyperammonemia and encephalopathy. Carefully weigh use of chloride salts against risks. Use chloride salts only when absolutely necessary.
Severe alkalemia should be initially managed in an ICU setting under the direction of a pediatric intensivist. Subsequent consultations should be obtained with specific specialists (eg, endocrinologist, nephrologist) to manage the underlying etiology responsible for the metabolic alkalosis.
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