eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Alkalosis, Metabolic: Treatment & Medication

Author: Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Coauthor(s): Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Contributor Information and Disclosures

Updated: Aug 13, 2008

Treatment

Medical Care

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 is approximately 7.55 mmol/L and 40 mmol/L, respectively, 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 is limited 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.
  • Acetazolamide may help patients with chloride-resistant metabolic alkalosis and has been safely used for treatment of diuretic induced metabolic alkalosis in pediatric cardiac patients.2,3
  • 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 ECF volume contraction occasionally require sodium and potassium administration. If continued diuretic use is indicated, potassium salt supplements may help avoid metabolic alkalosis.
  • Manage the specific disease that led to metabolic alkalosis.

Surgical Care

Children with pyloric stenosis require surgical intervention (pyloromyotomy) following intravascular fluid expansion and correction of metabolic abnormalities.

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.

Diet

Tailor dietary changes to the underlying disease.

Medication

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

Chloride solutions

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)

Amount required to correct metabolic alkalosis is determined by estimating the amount of pH deficit, the volume, and the infusion rate of HCl solution.
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. May also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity).
Typical preparation contains 0.1 N solution (ie, 100 mmol H+/L [mEq/L]) in D5W or 0.9% NaCl).

Adult

IV via central venous catheter: H+ ion deficit (mEq) = 0.3 X weight (kg) X (measured HCO3 - desired HCO3 [mEq/L])
Rate of H+ replacement: 0.1-0.2 mEq/kg/h
For example, 0.1 N solution IV at 100 mL/h provides about 10 mEq/h

Pediatric

Not established, limited data have been reported

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use HCl solutions with concentrations >0.2 N (increased venous irritation and potential hemolysis); concentrations >0.1 N have been reported to cause corrosive effects, even when administered through a central venous catheter; injection of HCl into a peripheral vein may cause extravasation and can produce severe tissue necrosis; monitor ABGs and serum electrolyte levels


Ammonium chloride (NH4Cl)

Administer to correct severe metabolic alkalosis related to chloride deficiency. NH4 Cl is converted to ammonia and HCl by the liver. By releasing HCl, NH4 Cl may help correct metabolic alkalosis.
Available as 500-mg tabs and 26.75% parenteral for IV use. Parenteral contains 5 mEq/mL (267.5 mg/mL).

Adult

8-12 g/d PO divided q6h
1.5 g IV q6h; dilute solution to concentration <0.4 mEq/mL; not to exceed infusion rate of 1 mEq/kg/h

Pediatric

75 mg/kg/d PO/IV divided q6h; not to exceed 6 g/d and an infusion rate of 1 mEq/kg/h; dilute solution to concentration <0.4 mEq/mL

May reduce levels of aspirin, chlorpropamide, ephedrine, methadone, pseudoephedrine, spirolactone, and para-aminosalicylic acid (PSA)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use with extreme caution in infants; may produce acidosis and hyperammonemia with encephalopathy; may cause GI irritation; monitor chloride levels, serum ammonia levels, and acid-base status


Potassium chloride (Clor-Con, K-Tab, K-Dur)

Essential for transmission of nerve impulses, contraction of cardiac muscle, and maintenance of intracellular tonicity, skeletal and smooth muscles, and normal renal function.

Adult

20-120 mEq PO qd
Up to 20 mEq/dose IV; dilute in >500 mL IV fluid for peripheral line infusion or >100 mL for central line infusion; not to exceed administration rate of 10 mEq/h unless cardiac monitoring in place

Pediatric

0.5-1 mEq/kg/dose IV; dilute in adequate IV fluid before administering by either peripheral or central IV; not to exceed administration rate of 10 mEq/h unless cardiac monitoring in place; may be prudent to not exceed 10 mEq in any one total dose, regardless if per Kg calculation indicates higher dose; recheck level, and administer additional dose as needed

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; caution if discontinuing potassium administration in patients maintained on digoxin (hypokalemia may result in digoxin toxicity)

Hyperkalemia; renal failure; conditions in which potassium retention is present; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not rapidly infuse; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration >40 mEq/L is infused, local pain and phlebitis may also follow

Carbonic anhydrase inhibitors

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


Acetazolamide (Diamox)

A carbonic anhydrase inhibitor that blocks HCO3 reabsorption in the proximal renal tubules. A recent study demonstrated that acetazolamide 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 ECF volume that frequently accompanies chloride-resistant metabolic alkalosis.

Adult

5-10 mg/kg/d PO/IV divided q6h

Pediatric

5 mg/kg PO qd/qod
8-30 mg/kg/d IV/IM divided q6-8h; not to exceed 1 g/d

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution with respiratory acidosis and diabetes mellitus (may increase blood glucose); IM administration is painful

More on Alkalosis, Metabolic

Overview: Alkalosis, Metabolic
Differential Diagnoses & Workup: Alkalosis, Metabolic
Treatment & Medication: Alkalosis, Metabolic
Follow-up: Alkalosis, Metabolic
References
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References

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  2. 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. Feb 2006;10(1):R14. [Medline].

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

  4. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. Jan 8 1998;338(2):107-11. [Medline].

  5. Finberg L, Kravath RE, Hellerstein S. Metabolic Alkalosis. In: Water and Electrolytes in Pediatrics: Physiology, Pathophysiology, and Treatment. Philadelphia, Pa: WB Saunders; 1993:97-98.

  6. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. Feb 2000;11(2):369-75. [Medline].

  7. Kokko JP, Tannen RL, eds. Metabolic Alkalosis. In: Fluids and Electrolytes. 1990. Philadelphia, Pa: WB Saunders; 356-376.

  8. Maxwell MH, Kleeman CR, eds. Metabolic Alkalosis. In: Clinical Disorders of Fluid and Electrolyte Metabolism. New York, NY: McGraw-Hill; 1994:213-220.

  9. Naka T, Bellomo R. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy. Crit Care. Apr 2004;8(2):108-14. [Medline].

  10. Omron EM. Metabolic alkalosis and cystic fibrosis. Chest. Mar 2004;125(3):1169; author reply 1169-70. [Medline].

  11. Palmer BF, Alpern RJ. Metabolic alkalosis. J Am Soc Nephrol. Sep 1997;8(9):1462-9. [Medline].

  12. Shapiro BA, Harrison RA, Cane RD. Clinical application of blood gases. St. Louis, Mo: Mosby; 1989.

  13. Siberry GK, Iannone R. Formulary. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. St. Louis, Mo: Mosby; 2000:616, 629.

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

  15. [Best Evidence] Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. Jun 15 2006;354(24):2564-75. [Medline].

  16. Wong HR, Chundu KR. Metabolic alkalosis in children undergoing cardiac surgery. Crit Care Med. Jun 1993;21(6):884-7. [Medline].

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Further Reading

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Keywords

metabolic alkalosis, plasma bicarbonate, HCO3, acid-base abnormality, metabolic acidosis, chloride-responsive metabolic alkalosis, chloride-resistant metabolic alkalosis, primary aldosteronism, hypoxemia, arteriolar constriction, hypokalemia, vomiting, pyloric stenosis, primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, deoxycorticosterone excess syndromes, hypertension, hypermineralocorticoid state, cystic fibrosis, primary aldosteronism, Liddle syndrome, anorexia nervosa, hyperglucocorticoidism, milk-alkali syndrome, hypercalcemia, hypochloremia, hyponatremia

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Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, Canadian Medical Association, Ontario Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; 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, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

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, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

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, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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