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Pediatric Metabolic Acidosis Workup

  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Jan 06, 2015
 

Approach Considerations

An arterial blood gas (ABG) measurement reveals the acidemia.

Basic laboratory tests for a child with metabolic acidosis should include measurements of electrolytes, BUN, creatinine, and serum glucose levels, as well as a urinalysis.

Echocardiography is performed if a left-sided, obstructive lesion in a neonate or a new occurrence of a cardiomyopathy presenting with a lactic acidosis is suggested.

Computed tomography (CT) scans for an infectious source or ischemic bowel should be performed, if indicated.

Go to Metabolic Acidosis in Emergency Medicine and Metabolic Acidosis for complete information on these topics.

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Imaging Studies

Imaging studies may be required depending on the presumed underlying etiology for the acidosis.

Echocardiography is performed if a left-sided, obstructive lesion in a neonate or a new occurrence of a cardiomyopathy presenting with a lactic acidosis is suggested.

CT scans for an infectious source or ischemic bowel should be performed, if indicated.

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Determining Respiratory Compensation

As previously mentioned, an ABG measurement reveals the acidemia. In addition, it shows the degree of respiratory compensation. To determine whether respiratory compensation is adequate or a mixed metabolic and respiratory acidosis is present, the Winter formula can be applied:

Expected PaCO2 = (1.5 X [HCO3-]) + 8 ± 2

A PaCO2 that is significantly higher than the level indicated by the Winter formula indicates that the patient is unable to compensate appropriately. This condition may be caused by a depressed mental state, airway obstruction, or fatigue. The inability to compensate may be especially important in patients with diabetic ketoacidosis who are at risk for cerebral edema.

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Other Laboratory Tests

Basic laboratory tests for a child with a metabolic acidosis should include measurements of electrolytes, blood urea nitrogen (BUN), creatinine, and serum glucose levels, as well as a urinalysis.

Calculate the anion gap from the electrolyte levels. This guides the initial diagnostic approach (ie, for a normal or elevated anion gap).

The serum potassium level is often abnormal. Patients with a metabolic acidosis may have a low serum potassium level due to excessive body losses of potassium or an elevated serum potassium level secondary to renal insufficiency, tissue breakdown, and shift of potassium from the intracellular space to the extracellular space as a result of acidemia.

Patients with renal insufficiency have elevated BUN and creatinine levels. A BUN-to-creatinine ratio greater than 20:1 supports the diagnosis of prerenal azotemia and hypovolemia.

Hypoglycemia associated with a metabolic acidosis can be caused by adrenal insufficiency or liver failure.

Hyperglycemia, glycosuria, ketonuria, and a metabolic acidosis support the diagnosis of diabetic ketoacidosis.[5] Less commonly, this combination of findings can be secondary to an inborn error of metabolism.

Normoglycemia, glycosuria, and a metabolic acidosis can occur in children with type II renal tubular acidosis (Fanconi syndrome).

Starvation causes ketosis, but a metabolic acidosis may be absent or mild (bicarbonate level >18).

The serum lactate level can be monitored as an adjunct to evaluate the response to therapy.

The osmole gap may be helpful in diagnosing a suspected ingestion of a toxic substance. An elevated osmole gap (>20 mOsm/L) with a metabolic acidosis can suggest the presence of osmotically active agents such as methanol, ethylene glycol, or ethanol. The osmole gap and serum osmolality can be measured as follows:

Osmole Gap = Measured Serum Osmolality - Estimated Serum Osmolality

Estimated Serum Osmolality = 2(Na+) + [Glucose /18] + [BUN /2.8]

Normal serum osmolality is 280-295 mOsm/L

Hypoalbuminemia is the most common cause of a low anion gap. Albumin represents about half of the total unmeasured anion pool; for every decrease of 1 g/dL of the serum albumin level, the serum anion gap decreases by 2.5 mEq/L.

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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.

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.

Acknowledgements

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.

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Approach for evaluating metabolic acidosis.
 
 
 
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