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Hypochloremic Alkalosis Treatment & Management

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

Approach Considerations

Hydration status and electrolyte levels must be assessed. Replacement of electrolytes with chloride salts is the most important mode of therapy for hypochloremic alkalosis. A full nutritional assessment should be obtained, energy intake calculated, and adequate energy intake ensured through oral or nasogastric methods.

Nonsteroidal anti-inflammatory drugs (NSAIDs; eg, indomethacin) are used in patients with Bartter syndrome. Hydrochloric acid (HCl) and carbonic anhydrase inhibitors (eg, acetazolamide) may be used in some acute situations. Potential complications of pharmacotherapy include the following:

  • Indomethacin-induced nephrotoxicity
  • Acetazolamide treatment compromising respiratory function in children with lung disease

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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Medical Correction of Hypochloremic Alkalosis

Acute emergency management (6 hours or less)

Initial management includes assessment of dehydration status and severity of hypochloremia, hypokalemia, hyponatremia, and metabolic alkalosis. If the patient is in shock, treatment should be directed toward aggressive resuscitation with isotonic fluid, preferably normal saline. Blood and urine samples for testing of electrolytes should always be obtained before any form of therapy is initiated; this is of great help in differentiating etiologic factors in new cases.

Chronic acid-base disturbances must not be treated too rapidly; more serious complications may be prevented by meticulous and slow correction. For example, consider the case of a child whose initial blood work shows the following results:

  • Sodium 120 mmol/L
  • Potassium 2 mmol/L
  • Chloride 80 mmol/L
  • Bicarbonate 40 mmol/L
  • pH 7.5

In this child, assessment of cardiac function is indicated. If there is no dysrhythmia, rapid correction of this severe hypokalemia is unnecessary. Administration of 5% dextrose in 0.9 isotonic sodium chloride solution plus potassium chloride 20 mEq/L at a maintenance rate can be a safe measure.

Maintenance management (7-72 hours)

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 hours)

For long-term management, intravenous (IV) fluids can be discontinued. The physician should calculate the average daily amounts of chloride, sodium, and potassium that were required to correct the serum electrolyte levels. The total amounts can then be administered orally in 3-4 divided doses per day. In most patients, the average chloride dose required is 4-10 mEq/kg/day in the form of sodium and potassium salts.

Other management procedures depend on the primary cause of hypochloremic alkalosis.

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Surgical or Endoscopic Intervention

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

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Diet

Kilojoule intake should be appropriate for 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, patients with cystic fibrosis have special dietary needs that should be met.

Multivitamins and hematinic agents should be provided as required. Supplemental trace elements (eg, zinc) should be provided to patients with a trace-element 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 for children with hypochloremic alkalosis unless central nervous system (CNS) damage is severe, in which case special restrictions are required.

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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Prevention

In patients with CLD, fluid intake should be encouraged so as to prevent renal damage resulting from recurrent dehydration. Patients or caregivers should be instructed to avoid long periods of exposure to hot climates, which may exacerbate dehydration episodes.

Constipation must be treated in patients with Bartter syndrome. Any intercurrent febrile illnesses, especially urinary tract infections, must be treated to prevent further renal damage.

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Consultations

The following may be consulted as necessary:

  • Pediatric nephrologist (in all cases)
  • Pediatric gastroenterologist
  • Genetic counselor
  • Social workers
  • Pediatric nutritionist
  • Pediatric endocrinologist (to exclude other causes of growth failure)
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Long-Term Monitoring

Patients should receive regular follow-up examinations by a physician and nurse clinician. Such examinations should take place at least once every month in infants but may be less frequent in older children and children who are more stable.

The preclinic laboratory workup includes a biochemical profile and monitoring of urine electrolytes. The pharmacotherapeutic regimen should be reviewed at each visit. Medications should be refilled and dosages adjusted in accordance with the patient’s clinical status and laboratory results.

Diagnostic imaging studies should be repeated as necessary. For example, kidney ultrasonography may be needed to assess the degree of nephrocalcinosis in children with Bartter syndrome.

Growth parameters should be assessed, and the question of whether growth hormone therapy is needed should be evaluated in consultation with a pediatric endocrinologist. Renal function should be assessed, and every effort should be made to minimize the use of nephrotoxic agents if possible.

Patients with chronic diseases, such as Bartter syndrome, chloride-losing diarrhea (CLD), and cystic fibrosis, should have lifelong follow-up care.

Future pregnancies in women with a child with hypochloremic alkalosis should be monitored in a tertiary care center so that early diagnosis and intervention are available at delivery.

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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
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  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].

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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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