What is the acidosis associated with alcohol (ethanol) consumption?

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Last updated: March 26, 2025View editorial policy

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From the Guidelines

Alcohol consumption is primarily associated with alcoholic ketoacidosis, a condition characterized by the production of excessive ketone bodies leading to an acidic blood pH. The acidosis associated with alcohol consumption is a result of the body's response to heavy drinking and reduced food intake, which depletes glycogen stores and inhibits gluconeogenesis, forcing the body to metabolize fatty acids for energy [1]. This condition is distinguished from other causes of metabolic acidosis, such as diabetic ketoacidosis, lactic acidosis, or toxic ingestions, by clinical history and plasma glucose concentrations, which in alcoholic ketoacidosis range from mildly elevated to hypoglycemia [1]. Key features of alcoholic ketoacidosis include:

  • Dehydration and electrolyte imbalances due to poor intake and vomiting
  • Production of NADH, which promotes ketone body formation while impairing their utilization
  • Serum bicarbonate concentration can be lower than 18 mEq/l, distinguishing it from starvation ketosis [1]
  • Patients typically present with nausea, vomiting, abdominal pain, and sometimes altered mental status Treatment involves intravenous fluids with dextrose, electrolyte replacement, and thiamine supplementation to prevent Wernicke's encephalopathy [1].

From the Research

Acidosis Associated with Alcohol Consumption

  • Alcoholic ketoacidosis (AKA) is a common presentation in emergency departments, characterized by metabolic acidosis and ketosis in patients with alcohol use 2, 3, 4.
  • The underlying pathophysiology of AKA is related to poor glycogen stores and elevated nicotinamide adenine dinucleotide and hydrogen, resulting in metabolic acidosis with elevated beta-hydroxybutyrate levels 2.
  • Patients with AKA often present with a history of alcohol use, poor oral intake, gastrointestinal symptoms, and ketoacidosis on laboratory assessment, and are generally dehydrated with variable serum glucose levels 2, 3, 4.
  • Laboratory evaluation typically reveals an anion gap metabolic acidosis with ketosis and electrolyte abnormalities 2, 3, 5.
  • Management of AKA includes fluid resuscitation, glucose and vitamin supplementation, electrolyte repletion, and evaluation for other conditions 2, 3, 4, 5.

Types of Acidosis

  • Metabolic acidosis in alcoholics can be due to lactic acidosis, ketoacidosis, and acetic acidosis, with varying degrees of each condition 5.
  • Alcoholic ketoacidosis is characterized by the predominance of beta-hydroxybutyrate compared to acetoacetate, which can lead to negative or slightly positive serum Acetest measurements of ketones 4.
  • Mixed acid-base disturbances can occur, with metabolic acidosis and metabolic alkalosis present simultaneously 5.

Diagnosis and Treatment

  • Diagnosis of AKA should be considered in chronic alcoholic patients with ketoacidosis, even in the absence of hyperglycemia or glycosuria 6.
  • Treatment of AKA should include sodium, chloride, potassium, phosphorus, magnesium, and thiamine replacements, along with attention to concomitant clinical problems 2, 3, 4, 5.
  • Insulin should be withheld unless life-threatening acidemia is present or expected, and glucose need not be given immediately unless hypoglycemia is present 4, 5.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management.

The Journal of emergency medicine, 2021

Research

Metabolic acidosis in the alcoholic: a pathophysiologic approach.

Metabolism: clinical and experimental, 1983

Research

Ketoacidosis and trace amounts of isopropanol in a chronic alcoholic patient.

Clinica chimica acta; international journal of clinical chemistry, 2013

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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