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Hypochloremic Alkalosis Medication

  • Author: Abbas AlAbbad, MD; Chief Editor: Luis O Rohena, MD  more...
 
Updated: Mar 13, 2014
 

Medication Summary

Replacement of electrolytes with chloride salts is the most important mode of therapy for hypochloremic alkalosis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in patients with Bartter syndrome. Hydrochloric acid (HCl) and carbonic anhydrase inhibitors may be used in some acute situations.

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Electrolytes

Class Summary

Electrolytes are administered to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance. They are also given to reestablish osmotic equilibrium of specific ions.

Potassium chloride (K-Lor, Klor-Con, Micro-K, K-Vescent)

 

Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion or gastrointestinal (GI) loss or because of low intake.

Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition. Potassium depletion sufficient to cause a 1 mEq/L drop in the serum potassium level requires a loss of approximately 100-200 mEq of potassium from the total body store.

Sodium chloride hypertonic

 

Hypertonic sodium chloride is given to restore sodium ions in patients with restricted oral intake, especially those with hyponatremia states or salt-wasting syndromes.

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Nonsteroidal Anti-inflammatory Drugs

Class Summary

NSIADs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is unknown but may involve inhibition of cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also play a role, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Indomethacin (Indocin)

 

Indomethacin inhibits prostaglandin synthesis. It is rapidly absorbed and is metabolized in liver via demethylation, deacetylation, and glucuronide conjugation.

Ibuprofen (Motrin, Advil)

 

Ibuprofen is usually the drug of choice for mild to moderate pain, if no contraindications exist. This drug inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclooxygenase, which results in decreased prostaglandin synthesis.

Ketoprofen

 

Ketoprofen is used to relieve mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects; therefore, administer high doses with caution, and closely observe patient response.

Naproxen (Anaprox, Naprelan, Naprosyn)

 

Naproxen is indicated for the relief of mild to moderate pain. This agent acts by inhibiting inflammatory reactions and pain via decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

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Carbonic Anhydrase Inhibitors

Class Summary

The major pharmacologic action of agents in this class is noncompetitive inhibition of the enzyme carbonic anhydrase. Carbonic anhydrase is located at the luminal border of cells of the proximal tubule. Urine volume increases with enzyme inhibition (proximal tubule reabsorption of water is reduced by approximately one third), which promotes an alkaline pH. This results in a subsequent decrease in the excretion of titratable acid and ammonia. Increases in urinary excretion of bicarbonate and sodium lead to metabolic acidosis.

Acetazolamide (Diamox Sequels)

 

Acetazolamide may be used in loop or thiazide diuretic−induced metabolic alkalosis, especially in edematous states.

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Acidifying Agents

Class Summary

Consequences of severe metabolic alkalosis include increased susceptibility to ventricular arrhythmia and a left shift of the oxyhemoglobin dissociation curve. HCl is particularly useful in patients with hepatic or renal impairment, which often precludes more standard treatments.

Hydrochloric acid

 

Intravenous administration of HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when sodium chloride or potassium chloride 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, in cardiac arrhythmia, hepatic encephalopathy, or digoxin toxicity). HCl for IV use is not commercially available and must be extemporaneously compounded from concentrated HCl solution.

Dosing is based on the chloride deficit and base excess. Typically, concentration ranges from 0.1N to 0.15N (ie, H+ concentration of 100-150 mmol/L). Concentrations greater than 0.2N may be associated with an increased risk of hemolysis.

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Xanthine Oxidase Inhibitors

Class Summary

Xanthine oxidase inhibitors are effective for treating diuretic-induced hyperuricemia and renal complications resulting in hyperuricemia.

Allopurinol (Zyloprim, Aloprim)

 

Allopurinol inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. It reduces synthesis of uric acid without disrupting biosynthesis of vital purines.

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Contributor Information and Disclosures
Author

Abbas AlAbbad, MD Associate Professor, Alfaisal University College of Medicine; Acting Head and Consultant Pediatric Transplant Nephrologist, Section of Pediatric Transplant Nephrology, Department of Kidney and Pancreas Transplantation, Organ Transplant Center, King Faisal Specialist Hospital and Research Center, Saudi Arabia

Abbas AlAbbad, MD is a member of the following medical societies: American Academy of Pediatrics, International Pediatric Transplant Association, International Society for Peritoneal Dialysis

Disclosure: Nothing to disclose.

Coauthor(s)

Sunil Sinha, MD Assistant Professor, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Sunil Sinha, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Luis O Rohena, MD Chief, Medical Genetics, San Antonio Military Medical Center; Assistant Professor of Pediatrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Assistant Professor of Pediatrics, University of Texas Health Science Center at San Antonio

Luis O Rohena, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American College of Medical Genetics and Genomics, American Society of Human Genetics

Disclosure: Nothing to disclose.

Acknowledgements

Sadek Al-Omran, MD Consultant Of Pediatrics and Pediatric Nephrologist, Departments of Pediatrics and Pediatric Nephrology, Maternity and Children's Hospital-Al-Ahsa, Saudi Arabia

Disclosure: Nothing to disclose.

Robert J Ferry Jr, MD Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Eli Lilly & Co Grant/research funds Investigator; MacroGenics, Inc Grant/research funds Investigator; Ipsen, SA (formerly Tercica, Inc) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Grant/research funds Investigator; Bristol-Myers-Squibb Grant/research funds Other; Amylin Other; Pfizer Grant/research funds Other; Takeda Grant/research funds Other

Pinar Ozand, MD, PhD Head, Section of Inborn Errors of Metabolism, Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Saudia Arabia

Disclosure: Nothing to disclose.

Christian J Renner, MD Consulting Staff, Department of Pediatrics, University Hospital for Children and Adolescents, Erlangen, Germany

Disclosure: Nothing to disclose.

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.

References
  1. Akil I, Ozen S, Kandiloglu AR, Ersoy B. A patient with Bartter syndrome accompanying severe growth hormone deficiency and focal segmental glomerulosclerosis. Clin Exp Nephrol. 2010 Jun. 14(3):278-82. [Medline].

  2. Naesens M, Steels P, Verberckmoes R. Bartter's and Gitelman's syndromes: from gene to clinic. Nephron Physiol. 2004. 96(3):p65-78. [Medline].

  3. Al-Abbad A, Nazer H, Sanjad SA, Al-Sabban E. Congenital chloride diarrhea: A single center experience with ten patients. Ann Saudi Med. 1995 Sep. 15(5):466-9. [Medline].

  4. [Guideline] Grosse SD, Boyle CA, Botkin JR, et al. Newborn screening for cystic fibrosis: evaluation of benefits and risks and recommendations for state newborn screening programs. MMWR Recomm Rep. 2004 Oct 15. 53:1-36. [Medline].

  5. Aranzamendi RJ, Breitman F, Asciutto C, Delgado N, Castanos C. [Dehydration and metabolic alkalosis: an unusual presentation of cystic fibrosis in an infant]. Arch Argent Pediatr. 2008 Oct. 106(5):443-6. [Medline].

  6. Hoglund P, Haila S, Socha J, et al. Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea. Nat Genet. 1996 Nov. 14(3):316-9. [Medline].

  7. Makela S, Kere J, Holmberg C. SLC26A3 mutations in congenital chloride diarrhea. Hum Mutat. 2002 Dec. 20(6):425-38. [Medline].

  8. Simon DB, Bindra RS, Mansfield TA, et al. Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. Nat Genet. 1997 Oct. 17(2):171-8. [Medline].

  9. Hulka F, Campbell TJ, Campbell JR, Harrison MW. Evolution in the recognition of infantile hypertrophic pyloric stenosis. Pediatrics. 1997 Aug. 100(2):E9. [Medline].

 
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Infant with severe metabolic alkalosis resulting from congenital chloride-losing diarrhea.
Watery stool from an infant with congenital chloride-losing diarrhea. Chloride level was 205 mmol/L.
Renal ultrasonograph of an infant with congenital chloride-losing diarrhea showing diffuse sclerosis.
Severe nephrocalcinosis in a 2-year-old child with Bartter syndrome.
Visible bowel loops in an infant with congenital chloride-losing diarrhea.
 
 
 
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