Hypochloremic Alkalosis Follow-up

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

Further Inpatient Care

  • Assess hydration status and electrolyte levels in patients with hypochloremic alkalosis.
  • Obtain a full nutritional assessment, calculate energy intake, and ensure adequate energy intake through oral or nasogastric methods.
  • Educate the caregiver regarding the primary disease and how to prevent recurrence of dehydration.
  • Ask the clinical pharmacist to discuss the importance and methods of drug administration, timing, and adverse effects with the caregiver, in addition to storage of medications at home.
  • Discharge medication instructions should be clearly written, and a supply sufficiently large to last until the patient is seen in the outpatient clinic should be prescribed.
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Further Outpatient Care

  • Patients should receive regular follow-up examinations by a physician and nurse clinician at least once every month in infants and less frequently in older children and children who are more stable.
  • Review medications at each visit. Refill medications and adjust doses depending on clinical status and laboratory results.
  • Preclinic laboratory workup includes a biochemical profile and monitoring of urine electrolytes.
  • Patients with chronic diseases, such as Bartter syndrome, chloride-losing diarrhea (CLD), and cystic fibrosis, should have lifelong follow-up care.
  • Repeat radiologic studies as required. For example, kidney ultrasonography may be needed to assess the degree of nephrocalcinosis in children with Bartter syndrome.
  • Assess growth parameters and evaluate the need for growth hormone therapy in consultation with a pediatric endocrinologist.
  • Assess renal function and minimize the use of nephrotoxic agents if possible.
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Deterrence/Prevention

  • In patients with CLD, encourage fluid intake to prevent renal damage resulting from recurrent dehydration.
  • Instruct patients or caregivers to avoid long periods of exposure to hot climates, which may exacerbate dehydration episodes.
  • Treat constipation in patients with Bartter syndrome.
  • Treat any intercurrent febrile illnesses, especially urinary tract infections, to prevent further renal damage.
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Complications

  • Disease-related complications
    • Nephrocalcinosis and nephrolithiasis may occur in patients with Bartter syndrome and in patients with CLD.
    • In patients with cystic fibrosis, liver damage and recurrent chest infection may lead to hepatic and pulmonary failure, respectively.
    • End-stage renal disease (ESRD) may occur in patients in whom compliance is poor. ESRD can occur in all conditions mentioned, including Bartter syndrome and CLD.
  • Drug-related complications
    • Indomethacin-induced nephrotoxicity should be carefully assessed.
    • Acetazolamide treatment may compromise respiratory function in children with lung disease.
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Prognosis

  • Prognosis is usually good for patients with Bartter syndrome, provided the patient complies well with treatment. Children who receive effective treatment have minimal risk of severe renal damage.
  • In patients with CLD, renal failure and ESRD may complicate the picture if diagnosis and treatment are delayed.
  • In patients with cystic fibrosis, prognosis depends on the severity of lung and liver involvement.
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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/.

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  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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