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Pediatric Metabolic Alkalosis Medication

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

Medication Summary

Metabolic alkalosis that results from chloride depletion and volume contraction can often be corrected with volume replacement. Persistent severe metabolic alkalosis may require more specific therapy directed at moderating the alkalemia.


Chloride Solutions

Class Summary

These solutions are the recommended therapeutic agents for rapid correction of severe metabolic alkalosis, especially metabolic alkalosis due to gastric losses of chloride.

Hydrochloric acid (HCl)


IV HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when NaCl or KCl cannot be administered because of volume overload or advanced renal failure. It may also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity).

The amount of HCl required to correct metabolic alkalosis is determined by estimating the amount of pH deficit, the volume, and the infusion rate of HCl solution. The typical HCl preparation contains 0.1 N solution (ie, 100 mmol H+/L [mEq/L]) in D5W or 0.9% NaCl).

Ammonium chloride (NH4Cl)


Ammonium chloride is administered to correct severe metabolic alkalosis related to chloride deficiency. NH4Cl is converted to ammonia and HCl by the liver. By releasing HCl, NH4Cl may help correct metabolic alkalosis.

This agent is available as 500-mg tabs and 26.75% parenteral formulation for IV use. The parenteral formulation contains 5 mEq/mL (267.5 mg/mL).

Potassium chloride (Epiklor, MicroK, Klor-Con)


Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, and maintenance of intracellular tonicity, skeletal and smooth muscles, and normal renal function. Metabolic alkalosis is often associated with hypokalemia.


Angiotensin-Converting Enzyme Inhibitors

Class Summary

ACE inhibitors block the conversion of angiotensin I to angiotensin II and prevent the secretion of aldosterone from the adrenal cortex. These agents are indicated in metabolic alkalosis due to hyperaldosteronism.



Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Enalapril (Vasotec)


A competitive inhibitor of ACE, enalapril reduces angiotensin II levels, decreasing aldosterone secretion.

Lisinopril (Prinivil, Zestril)


Lisinopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.


Carbonic Anhydrase Inhibitors

Class Summary

These agents may be used to treat chloride-resistant metabolic alkalosis.

Acetazolamide (Diamox)


Acetazolamide is a carbonic anhydrase inhibitor that blocks HCO3 reabsorption in the proximal renal tubules. It causes increased renal excretion of sodium vs chloride, causing a net increase in serum chloride. Acetazolamide is also a diuretic and, therefore, may help decrease extracellular fluid (ECF) volume that frequently accompanies chloride-resistant metabolic alkalosis.


Potassium-Sparing Diuretics

Class Summary

These agents may be used to correct potassium deficiency or fluid/electrolyte imbalance.

Triamterene (Dyrenium)


Triamterene interferes with potassium/sodium exchange (active transport) in the distal tubule, cortical collecting tubule, and collecting duct by inhibiting sodium/potassium adenosine triphosphatase (ATPase). This agent decreases calcium excretion and increases magnesium loss.

Spironolactone (Aldactone)


Spironolactone is an aldosterone antagonist that competitively inhibits binding to the aldosterone receptor. It competes for receptor sites in distal renal tubules and increases water excretion while retaining potassium and hydrogen ions needed to restore the acid-base balance.



Amiloride is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known potassium-conserving (antikaliuretic) or diuretic agents. It is an antikaliuretic drug, which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Contributor Information and Disclosures

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.


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.

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Algorithm for metabolic alkalosis.
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