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Acidosis, Metabolic: Differential Diagnoses & Workup

Author: 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: Jun 25, 2009

Differential Diagnoses

Adrenal Insufficiency
Myocarditis, Nonviral
Anemia, Acute
Myocarditis, Viral
Bacteremia
Necrotizing Enterocolitis
Cardiomyopathy, Dilated
Neonatal Sepsis
Chronic Kidney Disease
Neuroleptic Malignant Syndrome
Coarctation of the Aorta
Ornithine Transcarbamylase Deficiency
Dehydration
Phenylketonuria
Diabetic Ketoacidosis
Pneumococcal Bacteremia
Diarrhea
Sepsis
Hyperammonemia
Toxic Shock Syndrome
Hypoplastic Left Heart Syndrome
Toxicity, Ethanol
Interrupted Aortic Arch
Toxicity, Iron
Intestinal Volvulus
Toxicity, Isoniazid
Maple Syrup Urine Disease
Toxicity, Salicylate
Meningococcal Infections

Other Problems to Be Considered

Renal tubular acidosis
Lactic acidosis
Cyanide toxicity
Ethylene glycol toxicity
Methanol toxicity

Workup

Laboratory Studies

  • 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.
  • Basic laboratory tests for a child with a metabolic acidosis should include measurements of electrolytes, 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. 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.
    • 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.

Imaging Studies

  • 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.

More on Acidosis, Metabolic

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

  1. Glaser N, Barnett P, McCaslin I, 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].

  2. Han JJ, Yim HE, Lee JH, 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].

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

  4. Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. Aug 2005;23(3):771-87, ix. [Medline].

  5. Fall PJ. A stepwise approach to acid-base disorders. Practical patient evaluation for metabolic acidosis and other conditions. Postgrad Med. Mar 2000;107(3):249-50, 253-4, 257-8 passim. [Medline].

  6. Fattal-Valevski A, Kesler A, Sela BA, et al. Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. Pediatrics. Feb 2005;115(2):e233-8. [Medline].

  7. Levraut J, Grimaud D. Treatment of metabolic acidosis. Curr Opin Crit Care. Aug 2003;9(4):260-5. [Medline].

  8. Naka T, Bellomo R. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy. Crit Care. Apr 2004;8(2):108-14. [Medline].

  9. Szaflarski N, Hanson CW 3rd. Metabolic acidosis. AACN Clin Issues. Aug 1997;8(3):481-96. [Medline].

  10. Thauvin-Robinet C, Faivre L, Barbier ML, Chevret L, Bourgeois J, Netter JC. Severe lactic acidosis and acute thiamin deficiency: a report of 11 neonates with unsupplemented total parenteral nutrition. J Inherit Metab Dis. 2004;27(5):700-4. [Medline].

  11. Uchida H, Yamamoto H, Kisaki Y, Fujino J, Ishimaru Y, Ikeda H. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. J Pediatr Surg. Apr 2004;39(4):634-6. [Medline].

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Further Reading

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Keywords

metabolic acidosis, bicarbonate, anions, cations, hydrogen, anion gap, anion gap acidosis, normal anion gap metabolic acidosis, renal tubular acidosis, RTA, acid-base disorder, plasma bicarbonate, plasma bicarbonate level, acidemia, respiratory acidosis, respiratory failure, myocardial depression, diarrhea, inborn error of metabolism, neonatal sepsis, hypoplastic left heart syndrome, renal insufficiency, renal tubular acidosis, RTA, failure to thrive, hypoglycemia, hyperammonemia, treatment, diagnosis

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Contributor Information and Disclosures

Author

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 financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

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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