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Pediatric Metabolic Alkalosis Clinical Presentation

  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Jan 03, 2016
 

History

Obtain historical data to pinpoint the nature of the disease causing metabolic alkalosis. Ask about vomiting, other gastric fluid loss, and diuretic use. Loss of gastric fluid and HCl due to vomiting is the most common cause of metabolic alkalosis. Vomiting may be caused by pyloric stenosis or ulcers. Occasionally, it may be self-induced. Significant gastric fluid loss can occur via long-term nasogastric (NG) tube drainage.

Diuretic use may lead to increased chloride losses. It may also result in potassium loss, and hypokalemia may lead to metabolic alkalosis.

Obtain information about specific disease states such as primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, and deoxycorticosterone (DOC) excess syndromes.[5, 6]

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Physical Examination

Signs and symptoms observed with metabolic alkalosis usually relate to the specific disease process that caused the acid-base disorder. Increased neuromuscular excitability (eg, from hypocalcemia) sometimes causes tetany or seizures. Generalized weakness may be noted if the patient also has hypokalemia.

Patients who develop metabolic alkalosis from vomiting can have symptoms related to severe volume contraction, with signs of dehydration that include tachycardia, dry mucous membranes, decreased skin turgor, postural hypotension, poor peripheral perfusion, and weight loss.

Although diarrhea typically produces a hyperchloremic metabolic acidosis, diarrheal stools may rarely contain significant amounts of chloride, as in the case of congenital chloride diarrhea. Children with this condition present at birth with watery diarrhea, metabolic alkalosis, and hypovolemia.

Weight gain and hypertension may accompany metabolic alkalosis that results from a hypermineralocorticoid state.

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Complications

Severe metabolic alkalosis can lead to hypoventilation; the resultant hypoxemia is compounded by a shift of the oxygen-hemoglobin dissociation curve to the left. In extreme cases, hypoventilation may be severe enough to require mechanical ventilation or to interfere with weaning from current mechanical ventilation.

Intracellular shift of potassium in severe alkalemia may lead to life-threatening arrhythmias or cardiac arrest.

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Contributor Information and Disclosures
Author

Lennox H Huang, MD, FAAP Associate Professor and Chair, Department of Pediatrics, McMaster University School of Medicine; Chief of Pediatrics, McMaster Children's Hospital

Lennox H Huang, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD Associate Professor of Clinical Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania; 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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

References
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  2. Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. 1980 Dec. 8(12):725-8. [Medline].

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

  4. Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and surgical patients. South Med J. 1987 Jun. 80(6):729-33. [Medline].

  5. Fretzayas A, Gole E, Attilakos A, Daskalaki A, Nicolaidou P, Papadopoulou A. Expanding the spectrum of genetic mutations in antenatal Bartter syndrome type II. Pediatr Int. 2013 Jun. 55(3):371-3. [Medline].

  6. Ishimori S, Kaito H, Matsunoshita N, Otsubo H, Hashimoto F, Ninchoji T, et al. SLC26A3 gene analysis in patients with Bartter and Gitelman syndromes and the clinical characteristics of patients with unidentified mutations. Kobe J Med Sci. 2013 Apr 18. 59(2):E36-43. [Medline].

  7. Mathew JT, Bio LL. Injectable ammonium chloride used enterally for the treatment of persistent metabolic alkalosis in three pediatric patients. J Pediatr Pharmacol Ther. 2012 Jan. 17(1):98-103. [Medline]. [Full Text].

  8. Buchanan IB, Campbell BT, Peck MD, Cairns BA. Chest wall necrosis and death secondary to hydrochloric acid infusion for metabolic alkalosis. South Med J. 2005 Aug. 98(8):822-4. [Medline].

  9. 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. 2006 Feb. 10(1):R14. [Medline].

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

  11. Andrews MG, Johnson PN, Lammers EM, Harrison DL, Miller JL. Acetazolamide in critically ill neonates and children with metabolic alkalosis. Ann Pharmacother. 2013 Sep. 47(9):1130-5. [Medline].

  12. Bhardwaj S, Pandit D, Sinha A, Hari P, Cheong HI, Bagga A. Congenital chloride diarrhea - novel mutation in SLC26A3 gene. Indian J Pediatr. 2015 Dec 5. [Medline].

  13. Heble DE Jr, Oschman A, Sandritter TL. Comparison of arginine hydrochloride and acetazolamide for the correction of metabolic alkalosis in pediatric patients. Am J Ther. 2014 Nov 6. [Medline].

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Algorithm for metabolic alkalosis.
 
 
 
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