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Pediatric Metabolic Alkalosis Treatment & Management

  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Jan 03, 2016
 

Approach Considerations

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.[7] Although uncommon, fatality from extravasated HCl has been reported.[8]

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.

Transfer considerations

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.

Other considerations

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.

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Consultations

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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Contributor Information and Disclosures
Author

Lennox H Huang, MD, FAAP Associate Professor and Chair, Department of Pediatrics, McMaster University School of Medicine; Chief of Pediatrics, McMaster Children's Hospital

Lennox H Huang, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD Associate Professor of Clinical Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia

Margaret A Priestley, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

References
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  2. Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. 1980 Dec. 8(12):725-8. [Medline].

  3. van Thiel RJ, Koopman SR, Takkenberg JJ, Ten Harkel AD, Bogers AJ. Metabolic alkalosis after pediatric cardiac surgery. Eur J Cardiothorac Surg. 2005 Aug. 28(2):229-33. [Medline].

  4. Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and surgical patients. South Med J. 1987 Jun. 80(6):729-33. [Medline].

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  6. Ishimori S, Kaito H, Matsunoshita N, Otsubo H, Hashimoto F, Ninchoji T, et al. SLC26A3 gene analysis in patients with Bartter and Gitelman syndromes and the clinical characteristics of patients with unidentified mutations. Kobe J Med Sci. 2013 Apr 18. 59(2):E36-43. [Medline].

  7. Mathew JT, Bio LL. Injectable ammonium chloride used enterally for the treatment of persistent metabolic alkalosis in three pediatric patients. J Pediatr Pharmacol Ther. 2012 Jan. 17(1):98-103. [Medline]. [Full Text].

  8. Buchanan IB, Campbell BT, Peck MD, Cairns BA. Chest wall necrosis and death secondary to hydrochloric acid infusion for metabolic alkalosis. South Med J. 2005 Aug. 98(8):822-4. [Medline].

  9. Moviat M, Pickkers P, van der Voort PH, van der Hoeven JG. Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients. Crit Care. 2006 Feb. 10(1):R14. [Medline].

  10. Moffett BS, Moffett TI, Dickerson HA. Acetazolamide therapy for hypochloremic metabolic alkalosis in pediatric patients with heart disease. Am J Ther. 2007 Jul-Aug. 14(4):331-5. [Medline].

  11. Andrews MG, Johnson PN, Lammers EM, Harrison DL, Miller JL. Acetazolamide in critically ill neonates and children with metabolic alkalosis. Ann Pharmacother. 2013 Sep. 47(9):1130-5. [Medline].

  12. Bhardwaj S, Pandit D, Sinha A, Hari P, Cheong HI, Bagga A. Congenital chloride diarrhea - novel mutation in SLC26A3 gene. Indian J Pediatr. 2015 Dec 5. [Medline].

  13. Heble DE Jr, Oschman A, Sandritter TL. Comparison of arginine hydrochloride and acetazolamide for the correction of metabolic alkalosis in pediatric patients. Am J Ther. 2014 Nov 6. [Medline].

 
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