Pediatric Metabolic Alkalosis Clinical Presentation

  • Author: Lennox H Huang, MD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jun 8, 2011
 

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.

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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  Chair, Department of Pediatrics, McMaster University School of Medicine; Chief of Pediatrics, McMaster Children's Hospital

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

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD  Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; 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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

G Patricia Cantwell, MD, FCCM  Professor of Clinical Pediatrics, University of Miami, Leonard M Miller School of Medicine; Chief, Division of Pediatric Critical Care Medicine, Medical Manager, Urban Search & Rescue, South Florida TF-2, Medical Director, Holtz Children's Hospital Palliative Care Team, Medical Director, Tilli Kids – Pediatric Initiative of Hospice Care of SE Florida, Director, Pediatric Critical Care Transport, Holtz Children's Hospital/Jackson Memorial Hospital

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, and Wilderness Medical Society

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.

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, and 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, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

References

  1. Caltik A, Akyuz SG, Erdogan O, Bulbul M, Demircin G. Rare presentation of cystinosis mimicking Bartter's syndrome: reports of two patients and review of the literature. Ren Fail. Jan 2010;32(2):277-80. [Medline].

  2. Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. Dec 1980;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. Aug 2005;28(2):229-33. [Medline].

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

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

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

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

 
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Algorithm for metabolic alkalosis.
 
 
 
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