Metabolic Acidosis: Pathophysiology, Diagnosis and Management

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Box 1.

Tests useful in the DD of metabolic acidosis

Box 2.

Causes of metabolic acidosis

Box 3.

Recommendations for the treatment of acute metabolic acidosis

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Author(s)

Jeffrey A. Kraut, MD

Professor of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California; Chief of Dialysis, Division of Nephrology, Greater Los Angeles Veterans Administration Healthcare System, Los Angeles, California; Investigator, UCLA Membrane Biology Laboratory, Los Angeles, California

Disclosures

Disclosure: Jeffrey A. Kraut, MD, has disclosed no relevant financial relationships.

Nicolaos E. Madias, MD

Maurice S. Segal, M.D. Professor of Medicine, Tufts University School of Medicine, Boston, Massachusetts; Chairman, Department of Medicine, St. Elizabeth's Medical Center, Boston, Massachusetts

Disclosures

Disclosure: Nicolaos E. Madias, MD, has disclosed no relevant financial relationships.

Editor

Susan Allison

Editor, Nature Reviews Nephrology

Disclosures

Disclosure: Susan Allison has disclosed no relevant financial relationships.

CME Author(s)

Charles P. Vega, MD

Associate Professor; Residency Director, Department of Family Medicine, University of California, Irvine

Disclosures

Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

Sarah Fleischman

CME Program Manager, Medscape, LLC

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Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

CME

Metabolic Acidosis: Pathophysiology, Diagnosis and Management

Authors: Jeffrey A. Kraut, MD; Nicolaos E. Madias, MD
CME Released: 3/23/2010
THIS ACTIVITY HAS EXPIRED FOR CREDIT
Valid for credit through: 3/23/2011, 11:59 PM EST

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Target Audience and Goal Statement

This activity is intended for primary care physicians, intensive medicine specialists, nephrologists, and other physicians who care for patients with metabolic acidosis.

The goal of this activity is to describe the diagnosis and treatment of metabolic acidosis.

Upon completion of this activity, participants will be able to:

Describe the pathophysiology of metabolic acidosis
Diagnose the cause of metabolic acidosis effectively
Distinguish the causes of metabolic acidosis associated with an elevated anion gap
Treat metabolic acidosis effectively

Disclosures

Author(s)

Jeffrey A. Kraut, MD

Professor of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California; Chief of Dialysis, Division of Nephrology, Greater Los Angeles Veterans Administration Healthcare System, Los Angeles, California; Investigator, UCLA Membrane Biology Laboratory, Los Angeles, California

Disclosures

Disclosure: Jeffrey A. Kraut, MD, has disclosed no relevant financial relationships.

Nicolaos E. Madias, MD

Maurice S. Segal, M.D. Professor of Medicine, Tufts University School of Medicine, Boston, Massachusetts; Chairman, Department of Medicine, St. Elizabeth's Medical Center, Boston, Massachusetts

Disclosures

Disclosure: Nicolaos E. Madias, MD, has disclosed no relevant financial relationships.

Editor

Susan Allison

Editor, Nature Reviews Nephrology

Disclosures

Disclosure: Susan Allison has disclosed no relevant financial relationships.

CME Author(s)

Charles P. Vega, MD

Associate Professor; Residency Director, Department of Family Medicine, University of California, Irvine

Disclosures

Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

Sarah Fleischman

CME Program Manager, Medscape, LLC

Disclosures

Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

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Abstract and Introduction

Abstract

Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO₃ ^-) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO₂) of ~1 mmHg for every 1 mmol/l fall in serum HCO₃ ^- concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na+] - ([HCO₃ ^-] + [Cl^-]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular function and few complications.

Introduction

Metabolic acidosis is characterized by a primary reduction in the serum concentration of bicarbonate (HCO₃^-), a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO₂), and a reduction in blood pH. Metabolic acidosis frequently occurs as a part of mixed acid-base disorders, especially among the critically ill. Metabolic acidosis can be acute (lasting minutes to several days) or chronic (lasting weeks to years) in duration. Acute metabolic acidosis is relatively common among seriously ill patients, with one study showing that the disorder affected approximately 64% of patients in a large intensive care unit in the US.^[1] Chronic metabolic acidosis is less common; only 1.9% of more than 15,000 individuals surveyed in the NHANES III study^[2] had a serum HCO₃ ^-concentration below 22 mmol/l, although this value rose to 19% in patients with an estimated glomerular filtration rate (eGFR) within the range 15-29 ml/min/1.73 m². Therefore, the frequency of chronic metabolic acidosis might increase with the anticipated rise in chronic kidney disease (CKD) in our aging population. Metabolic acidosis—acute or chronic—can have considerable adverse effects on cellular function and can contribute to increased morbidity and mortality.^[1,3-5]

In this Review, we summarize current views on the pathogenesis, diagnosis, adverse effects, and management of metabolic acidosis. Owing to space constraints, we address the causes of this acid-base disorder only briefly.

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Pathophysiology of Metabolic Acidosis

CME Information

References

References

Disclaimer

The material presented here does not necessarily reflect the views of Medscape, LLC or companies that support educational programming on www.medscapecme.com. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity.

Disclaimer

The authors, the Journal Editor S. Allison and the CME questions author C. P. Vega declare no competing interests.

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References

Faculty and Disclosures

Author(s)

Jeffrey A. Kraut, MD

Nicolaos E. Madias, MD

Editor

Susan Allison

CME Author(s)

Charles P. Vega, MD

CME Reviewer(s)

Sarah Fleischman

CME

Metabolic Acidosis: Pathophysiology, Diagnosis and Management

Target Audience and Goal Statement

Disclosures

Author(s)

Jeffrey A. Kraut, MD

Nicolaos E. Madias, MD

Editor

Susan Allison

CME Author(s)

Charles P. Vega, MD

CME Reviewer(s)

Sarah Fleischman

Accreditation Statements

For Physicians

Instructions for Participation and Credit

Metabolic Acidosis: Pathophysiology, Diagnosis and Management

Abstract and Introduction

Abstract

Introduction

Table of Contents

Disclaimer