What Is Alcoholic Ketoacidosis? The Impact of a Buildup of Ketones in Your Blood

The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. Ethyl alcohol oxidizes at a rate of 20 to 25 mg/dL per hour in most individuals. The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see. Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.

  • Meetings are widely available at little-to-no cost in most communities.
  • The prognosis for alcoholic ketoacidosis is good as long as it’s treated early.
  • Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones and by providing metabolic substrate.
  • The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body.
  • One complication of alcoholic ketoacidosis is alcohol withdrawal.

Metabolism of ethanol

When your liver uses up its stored glucose and you aren’t eating anything to provide more, your blood sugar levels will drop. During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue. The clinical and biochemical features of AKA are summarised in boxes 1 and 2. The classical presentation is of an alcoholic patient with abdominal pain and intractable vomiting following a significant period of increased alcohol intake and starvation. There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”.

alcoholic ketoacidosis

Alcoholic Ketoacidosis Symptoms

If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis. If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help. It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours. During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention.

alcoholic ketoacidosis

What are the complications of alcoholic ketoacidosis?

  • Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
  • But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol.
  • The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see.
  • Going on a drinking binge when your body is in a malnourished state may cause abdominal pain, nausea, or vomiting.

General literature reviews, single case reports, and letters were also excluded. All remaining papers were retrieved and the reference lists hand searched for any additional information sources. Patients generally do not need to be transferred to special facilities. Appropriately evaluate the patient for any life-threatening complications before a transfer is considered. American Addiction Centers (AAC) is committed to delivering original, truthful, accurate, unbiased, and medically current information. We strive to create content that is clear, concise, and easy to understand.

alcoholic ketoacidosis

The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis. Nausea, vomiting, and abdominal pain were by far the most commonly observed complaints. Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent. Both Wrenn et al6 and Fulop and Hoberman5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin. Arrange follow-up to evaluate patients after the resolution of symptoms, in order to detect other complications of chronic alcohol abuse.

However, if an AKA patient is lethargic or comatose, an alternative cause should be sought. The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase.

alcoholic ketoacidosis

Alcoholic Ketoacidosis Treatment & Management

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