eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Alkalosis, Metabolic: Follow-up

Author: Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
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
Contributor Information and Disclosures

Updated: Aug 13, 2008

Follow-up

Further Inpatient Care

  • Severe metabolic alkalemia should be monitored in an ICU setting with full noninvasive cardiopulmonary monitoring. Invasive monitoring and specialized vascular access may be necessary, depending on the overall clinical picture.
  • Monitor serum electrolyte levels and acid-base status when providing treatment for metabolic alkalosis, particularly when using chloride salts.
  • Provide follow-up care specific to the disease that caused metabolic alkalosis.

Further Outpatient Care

  • Outpatient care depends on the underlying disease process.

Transfer

  • The role of a pediatric tertiary care center where appropriate subspecialists are available in the care of a child with metabolic alkalosis cannot be overemphasized.
  • If the patient requires dialysis or has a renal disease, such as Bartter syndrome, transfer the patient to a nephrologist.
  • An endocrinologist should manage primary aldosteronism and mineralocorticoid excess states.
  • Children who develop hypovolemic shock or those with persistent severe and symptomatic metabolic alkalosis are best monitored in a critical care setting.

Deterrence/Prevention

  • Metabolic alkalosis may be avoided by judicious use of long-term diuretics with appropriate monitoring.

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 existing mechanical ventilation.
  • Metabolic alkalosis can also lead to neuromuscular excitability and, if accompanied by hypocalcemia, can result in tetany, seizures, and life-threatening ventricular arrhythmias.
  • Intracellular shift of potassium in severe alkalemia may lead to life-threatening arrhythmias or cardiac arrest.

Prognosis

  • Overall prognosis depends on the underlying etiology.
  • Chloride-responsive metabolic alkalosis responds to volume resuscitation and chloride repletion.
  • Chloride-resistant metabolic alkalosis may be more difficult to control. Prognosis is good with prompt treatment and avoidance of hypoxemia.

Patient Education

  • Educate patients placed on long-term diuretic therapy and those with diseases that can lead to metabolic alkalosis to recognize the symptoms of moderate-to-severe alkalosis; this knowledge allows them to promptly seek medical care.

Miscellaneous

Medicolegal Pitfalls

  • Failure to realize that severe metabolic alkalosis can lead to hypoventilation that may result in hypoxemia could delay treatment and result in hypoxic damage.
  • Physicians must be familiar with the complications associated with the use of chloride salts to treat severe metabolic alkalosis. Hydrochloric acid can cause severe tissue necrosis if the solution extravasates into the tissues. In addition, use of high concentrations (ie, >0.1 N) of HCl can corrode central veins and venous catheters.
  • Use of NH4 Cl can result in hyperammonemia and encephalopathy.
  • Carefully weigh use of chloride salts against risks. Use chloride salts only when absolutely necessary.
 


More on Alkalosis, Metabolic

Overview: Alkalosis, Metabolic
Differential Diagnoses & Workup: Alkalosis, Metabolic
Treatment & Medication: Alkalosis, Metabolic
Follow-up: Alkalosis, Metabolic
References
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References

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  2. 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].

  3. 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].

  4. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. Jan 8 1998;338(2):107-11. [Medline].

  5. Finberg L, Kravath RE, Hellerstein S. Metabolic Alkalosis. In: Water and Electrolytes in Pediatrics: Physiology, Pathophysiology, and Treatment. Philadelphia, Pa: WB Saunders; 1993:97-98.

  6. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. Feb 2000;11(2):369-75. [Medline].

  7. Kokko JP, Tannen RL, eds. Metabolic Alkalosis. In: Fluids and Electrolytes. 1990. Philadelphia, Pa: WB Saunders; 356-376.

  8. Maxwell MH, Kleeman CR, eds. Metabolic Alkalosis. In: Clinical Disorders of Fluid and Electrolyte Metabolism. New York, NY: McGraw-Hill; 1994:213-220.

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  13. Siberry GK, Iannone R. Formulary. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. St. Louis, Mo: Mosby; 2000:616, 629.

  14. 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].

  15. [Best Evidence] Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. Jun 15 2006;354(24):2564-75. [Medline].

  16. Wong HR, Chundu KR. Metabolic alkalosis in children undergoing cardiac surgery. Crit Care Med. Jun 1993;21(6):884-7. [Medline].

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Further Reading

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Keywords

metabolic alkalosis, plasma bicarbonate, HCO3, acid-base abnormality, metabolic acidosis, chloride-responsive metabolic alkalosis, chloride-resistant metabolic alkalosis, primary aldosteronism, hypoxemia, arteriolar constriction, hypokalemia, vomiting, pyloric stenosis, primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, deoxycorticosterone excess syndromes, hypertension, hypermineralocorticoid state, cystic fibrosis, primary aldosteronism, Liddle syndrome, anorexia nervosa, hyperglucocorticoidism, milk-alkali syndrome, hypercalcemia, hypochloremia, hyponatremia

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Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, 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.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

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.

 
 
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