Pediatric Metabolic Acidosis Clinical Presentation

  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Feb 17, 2012
 

History

The etiology of a metabolic acidosis is often apparent from the patient’s history and physical examination. The following factors are assessed in a complete investigation of the patient's history:

  • Anorexia, nausea, vomiting, or diarrhea - In pediatric patients, diarrhea is the most common cause of a metabolic acidosis
  • Metabolic acidosis associated with seizures, a depressed sensorium, or both in a neonate - This warrants consideration of an inborn error of metabolism, or neonatal sepsis
  • History of depressed mental status, lethargy, and poor feeding in a neonate - Left-sided, obstructive cardiac lesions should be considered (eg, aortic coarctation or hypoplastic left heart syndrome)
  • Failure to thrive suggestive of chronic metabolic acidosis - This can be seen in renal insufficiency or RTA
  • New onset of polyuria, polydipsia, and weight loss - This could signify undiagnosed diabetes mellitus and diabetic ketoacidosis in a child
  • Possible ingestion of a toxin or other form of intoxication - Inquire as to what medications are in the home; suspect a poisoning in a healthy child who quickly develops a metabolic acidosis; possible agents are ethanol, ethylene glycol, salicylates, and methanol
  • History of trauma, hives, or fever
  • History of states associated with a lactic acidosis secondary to shock from hypovolemia, sepsis, cardiac failure, anaphylaxis, or spinal shock
  • Chronic medical or surgical issue - Examples to be concerned with include chronic renal failure, presence of a ureterosigmoidostomy, or diabetes mellitus
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Physical Examination

Clinical findings generally depend on the etiology and severity of the metabolic acidosis.

Hyperventilation or Kussmaul breathing may often be the first sign of a metabolic acidosis in a child. Breath sounds are often clear to auscultation (“quiet tachypnea”).

Patients with metabolic acidosis secondary to shock may have signs reflective of single- or multiple-organ dysfunction, as follows:

  • CNS manifestations may include lethargy, coma, and seizures
  • Respiratory manifestations may include tachypnea, respiratory distress, and hypoxemia
  • Cardiovascular signs may include poor perfusion, weak pulses, tachycardia, hypotension, murmurs, or a gallop
  • Nonspecific abdominal symptoms and signs may be present such as nausea, pain, vomiting, and altered appetite
  • Signs of dehydration may include tachycardia, dry mucous membranes, and delayed capillary refill
  • Patients with diabetic ketoacidosis may present with fruity odor to their breath
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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 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.

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.

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; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

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.

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.

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

  1. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. May 2010;6(5):274-85. [Medline].

  2. Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. Jan 25 2001;344(4):264-9. [Medline].

  3. Hodson E. Metabolic acidosis and growth in children. Nephrology. Dec 2005;10(S5):S221-2. [Full Text].

  4. Han JJ, Yim HE, Lee JH, Kim YK, Jang GY, Choi BM, et al. Albumin versus normal saline for dehydrated term infants with metabolic acidosis due to acute diarrhea. J Perinatol. Jun 2009;29(6):444-7. [Medline].

  5. Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. Jan 2000;117(1):260-7. [Medline].

  6. Manthous CA. Lactic acidosis in status asthmaticus : three cases and review of the literature. Chest. May 2001;119(5):1599-602. [Medline].

  7. Agarwal B, Kovari F, Saha R, Shaw S, Davenport A. Do Bicarbonate-Based Solutions for Continuous Renal Replacement Therapy Offer Better Control of Metabolic Acidosis than Lactate-Containing Fluids. Nephron Clin Pract. Feb 23 2011;118(4):c392-c398. [Medline].

 
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Approach for evaluating metabolic acidosis.
 
 
 
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