Metabolic Acidosis in Emergency Medicine Clinical Presentation

  • Author: Antonia Quinn, DO; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Nov 13, 2009
 

History

Metabolic acidosis can result in a variety of nonspecific changes in several organ systems, including, but not limited to, neurologic, cardiovascular, pulmonary, gastrointestinal, and musculoskeletal dysfunction. Symptoms are often specific to and a result of the underlying etiology of the metabolic acidosis.

Head, eyes, ears, nose, throat (HEENT) findings include the following:

  • Tinnitus, blurred vision, and vertigo can occur with salicylate poisoning.
  • Visual disturbances, dimming, photophobia, scotomata, and frank blindness can be seen in methanol intoxication.

Cardiovascular findings include the following:

  • Palpitations
  • Chest pain

Neurologic findings include the following:

  • Headache
  • Visual changes
  • Mental confusion

Pulmonary findings include subjective dyspnea from the patient's observation of hyperventilation.

GI findings include the following:

  • Nausea and vomiting
  • Abdominal pain
  • Diarrhea
  • Polyphagia

Musculoskeletal findings include the following:

  • Generalized muscle weakness
  • Bone pain
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Physical

Neurologic

Cranial nerve palsies may occur with ethylene glycol intoxication.

Retinal edema may be seen in methanol ingestions.

Lethargy, stupor, and coma may occur in severe metabolic acidosis, particularly when it is associated with a toxic ingestion.

Cardiovascular

Severe acidemia (ie, pH < 7.10) can predispose a patient to potentially fatal ventricular arrhythmias, and it can reduce cardiac contractility and the inotropic response to catecholamines, resulting in hypotension and congestive heart failure.

Pulmonary

Patients with acute metabolic acidosis demonstrate tachypnea and hyperpnea as prominent physical signs.

Kussmaul respiration, an extremely intense respiratory effort, may be present.

Hyperventilation, in the absence of obvious lung disease, should alert the clinician to the possibility of an underlying metabolic acidosis.

Musculoskeletal

Chronic metabolic acidosis (eg, uremia, renal tubular acidosis [RTA]) is associated with substantial bone disease from bone buffering of calcium carbonate.

Long bone malformations in pediatric patients (eg, vitamin D resistant, rickets) and fractures in adult patients are noted.

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Causes

Causes of inability to excrete the dietary H+ load are as follows:

  • Renal failure - Diminished NH4+ production
  • Hypoaldosteronism - Type 4 RTA
  • Diminished H+ secretion - Type 1 (distal) RTA

Causes of increased H+ load include the following:

  • Lactic acidosis - Numerous causes, including circulatory failure, drugs and toxins, and hereditary causes (see Lactic Acidosis)
  • Ketoacidosis - Diabetes, alcoholism, and starvation
  • Ingestions -Salicylates, methanol, ethylene glycol, isoniazid,[3]iron, paraldehyde, sulfur, toluene, ammonium chloride, phenformin/metformin,[4] and hyperalimentation fluids

GI HCO3- loss is caused by the following:

  • Diarrhea
  • Pancreatic, biliary, or intestinal fistulas
  • Ureterosigmoidostomy
  • Cholestyramine

Renal HCO3- loss may be caused by type 2 (proximal) RTA.

Acetazolamide may also be a cause of metabolic acidosis.

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Contributor Information and Disclosures
Author

Antonia Quinn, DO  Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate Medical Center/Kings County Hospital Center; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Antonia Quinn, DO is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO  Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Howard A Bessen, MD  Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Karen L Stavile, MD, to the development and writing of this article.

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