Hypochloremic Alkalosis Treatment & Management

  • Author: Abbas AlAbbad, MD; Chief Editor: Bruce Buehler, MD   more...
 
Updated: Mar 30, 2012
 

Medical Care

  • Acute emergency management (0-6 h) of hypochloremic alkalosis
    • Assess dehydration status to determine if it is chronic or superimposed by acute dehydration. If the patient is in shock, treatment should be directed toward aggressive resuscitation with isotonic fluid, preferably normal saline.
    • Always remember to obtain blood and urine samples for testing of electrolytes before any form of therapy; this is of great help in differentiating etiologic factors in new cases.
    • Initial management includes assessment of dehydration status and severity of hypochloremia, hypokalemia, hyponatremia, and metabolic alkalosis.
    • Always remember not to treat chronic acid-base disturbances rapidly because more serious complications may be prevented by meticulous and slow correction. For example, initial blood work shows the following results: 120 mmol/L sodium, 2 mmol/L potassium, 80 mmol/L chloride, 40 mmol/L bicarbonate, and pH 7.5. In this child, assess cardiac function; if dysrhythmia is absent, rapid correction of this severe hypokalemia is not needed. In this case, 5% dextrose in 0.9 isotonic sodium chloride solution plus potassium chloride 20 mEq/L administered at a maintenance rate per 24 hours can be a safe measure.
  • Maintenance management (over the next 72 h) of hypochloremic alkalosis
    • Maintenance therapy depends on how much improvement occurred after 6 hours of initial fluid and electrolyte administration.
    • The aim is to increase the serum potassium concentration very slowly as the serum bicarbonate level drops. This helps prevent a sharp increase in serum potassium concentration and its subsequent detrimental effects on cardiac conductivity.
  • Long-term management (after 72 h) of hypochloremic alkalosis
    • Intravenous fluids can be discontinued. The physician should calculate the average amounts of chloride, sodium, and potassium administered per day that was required to correct the serum electrolyte levels. The total amount can then be orally administered in 3-4 divided doses per day. In most patients, the average chloride dose required is 4-10 mEq/kg/d in the form of sodium and potassium salts.
    • Other management procedures depend on the primary cause of hypochloremic alkalosis.
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Surgical Care

  • Surgical intervention is usually unnecessary. If ileus is suspected in a child with severe hypokalemia, treatment is potassium chloride administration and not surgical intervention.
  • If the cause of hypochloremic alkalosis is an upper gastrointestinal tract abnormality, such as gastroesophageal reflux or pyloric stenosis, surgical or endoscopic intervention is indicated.
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Consultations

  • Pediatric nephrologist - Should always be consulted in these acid-base disorders
  • Pediatric gastroenterologist
  • Genetic counselor
  • Social workers
  • Pediatric nutritionist
  • Pediatric endocrinologist - To exclude other causes of growth failure
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Diet

  • Kilojoule intake should meet the patient's catabolic status, usually 100-150% of the recommended daily allowance (RDA).
  • Additional protein should be ingested to prevent malnutrition.
  • Fat requirements depend on the individual patient. For example, if the patient has cystic fibrosis, special dietary needs should be followed.
  • Provide multivitamins and hematinics as required.
  • Provide supplemental trace elements (eg, zinc) in patients with deficiency, such as some patients with chloride-losing diarrhea (CLD).
  • High sodium and potassium diets are required for all children with chronic metabolic alkalosis secondary to Bartter syndrome or CLD.
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Activity

  • Normal activity should be recommended in children unless CNS damage is severe, which requires special restrictions.
  • Children with refractory severe hypokalemia should avoid extended exposure to heat, especially in hot climates. Exposure to heat may cause dehydration and may exacerbate the condition.
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Contributor Information and Disclosures
Author

Abbas AlAbbad, MD  Consultant Pediatric Nephrologist, Section of Pediatric Nephrology, Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

Specialty Editor Board

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.

Leonard G Feld, MD, PhD, MMM, FAAP  Sara H Bissell and Howard C Bissell Endowed Chair in Pediatrics, Chief Medical Officer, Levine Children's Hospital, Carolinas Medical Center

Leonard G Feld, MD, PhD, MMM, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Physician Executives, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Juvenile Diabetes Foundation International

Disclosure: Nothing to disclose.

Paul D Petry, DO, FACOP, FAAP  Consulting Staff, Freeman Pediatric Care, Freeman Health System

Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Bruce Buehler, MD  Professor, Department of Pediatrics and Genetics, Director RSA, University of Nebraska Medical Center

Bruce Buehler, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Pediatrics, American Association on Mental Retardation, American College of Medical Genetics, American College of Physician Executives, American Medical Association, and Nebraska Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

The author would like to thank Gloria Matthews (University of Texas Health Science Center at San Antonio Pediatrics) for her expert assistance with grants administration.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Pinar Ozand, MD, PhD, to the development and writing of this article.

References

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  11. Jacobson HR. Chloride-responsive metabolic alkalosis. In: Seldin DW, Gieb G, eds. The Regulation of Acid-Base Balance. Lippincott-Raven; 1989:431-57.

  12. Rose BD. Causes of metabolic alkalosis. UpToDate. Available at http://www.uptodate.com/.

  13. Rose BD. Treatment of metabolic alkalosis. UpToDate. Available at http://www.uptodate.com/.

  14. Rose BD. Urine electrolytes in diagnosis of metabolic alkalosis. UpToDate. Available at http://www.uptodate.com/.

  15. Simon DB, Karet FE, Hamdan JM, et al. Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2. Nat Genet. Jun 1996;13(2):183-8. [Medline].

  16. Wang J, Cortina G, Wu SV, et al. Mutant neurogenin-3 in congenital malabsorptive diarrhea. N Engl J Med. Jul 20 2006;355(3):270-80. [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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