History

The onset of acidosis may be rapid (ie, within minutes to hours) or progressive (ie, over a period of several days).

Lactic acidosis frequently occurs during strenuous exercise in healthy people, bearing no consequence. However, development of lactic acidosis in disease states is ominous, often indicating a critical illness of recent onset. Therefore, a careful history should be obtained to evaluate the underlying pathophysiologic cause of shock that contributed to lactic acidosis. Furthermore, a detailed history of ingestion of various prescription drugs or toxins from the patient or a collateral history from the patient's family should be obtained.

The clinical signs and symptoms associated with lactic acidosis are highly dependent on the underlying etiology. No distinctive features are specific for hyperlactatemia.

Lactate acidosis is present in patients who are critically ill from hypovolemic, septic, or cardiogenic shock.

Lactate acidosis always should be suspected in the presence of elevated anion gap metabolic acidosis.

Lactic acidosis is a serious complication of antiretroviral therapy. A history of antiretroviral treatment should be obtained.

Children who have a relatively mild form of congenital lactic acidosis may develop firmament metabolic acidosis during an acute illness such as respiratory infection. These patients have a deficiency in the activity of pyruvate dehydrogenase, and the stress-induced increases in the glycolytic rate may result in severe metabolic acidosis.

D-lactic acidosis, a unique form of lactic acidosis, can occur in patients with jejunoileal bypass or small bowel resection causing short bowel syndrome. In these settings, the glucose and carbohydrates are metabolized in the colon into D-lactic acid, which is absorbed into systemic circulation. The overgrowth of gram-positive anaerobes such as lactobacilli is able to produce lactate from carbohydrates. These patients develop confusion, ataxia, slurred speech, and altered mental status.

Physical Examination

The clinical signs usually indicate tissue hypoperfusion. Severe hypotension, oliguria or aneuria, deteriorating mental status, and tachypnea always are present when the cause of lactic acidosis is tissue hypoxemia.

Clinical signs of impaired tissue perfusion include the following:

Hypotension
Alteration in sensorium
Peripheral vasoconstriction
Oliguria

Findings that may be late manifestations of shock and that are relatively insensitive indicators of hypoperfusion are as follows:

Tachypnea
Hypotension
Deteriorating mental status

Kussmaul hyperventilation (deep sighing respiration) may be observed if the severity of the acidosis is sufficient to elicit a degree of respiratory compensation.

Because sepsis accounts for most cases of lactic acidosis, fever (>38.5°C) or hypothermia (35°C) commonly is present in addition to symptoms and signs indicating the organ where the sepsis originated.

Differential Diagnoses

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Pathophysiologic classification of lactic acidosis.

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Author

Kyle J Gunnerson, MD Associate Professor, Departments of Emergency Medicine, Anesthesiology, and Internal Medicine, University of Michigan Health System; Chief, Division of Emergency Critical Care; Medical Director of the Emergency Critical Care Center, University of Michigan Health System

Kyle J Gunnerson, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Medical Association, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Carrie E Harvey, MD, MS Assistant Professor, Department of Emergency Medicine, Michigan Medicine

Carrie E Harvey, MD, MS is a member of the following medical societies: Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Thoracic Society, European Society of Intensive Care Medicine, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Baxter Medical, Exostat, LiDCO<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED.

Additional Contributors

Cory Franklin, MD Professor, Department of Medicine, Chicago Medical School at Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Sat Sharma, MD, FRCPC, to the development and writing of the source article.

Lactic Acidosis Clinical Presentation

History

Physical Examination

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