Alcoholic Ketoacidosis StatPearls NCBI Bookshelf

Subsequent fluid resuscitation and monitoring were instituted. Further biochemical investigation after treatment showed a rapid decline in the level of ketones and normalization of pH. I often get consults because the patient history was a solid AKA story (drink everyday, don’t make time to eat, denies toxic alcohols), but the UA doesn’t have the impressive ketones that the treating team expected. While testing for acetoacetate and acetone is certainly helpful in identifying DKA, the predominance of BHB in AKA makes many UA assays misleading. Learn about what alcohol withdrawal syndrome is, the symptoms, treatments, and who’s most likely to experience it. Each of these situations increases the amount of acid in the system.

  • The diabetic form of ketoacidosis may have a sweet and fruity smell rather than one like acetone.
  • If you chronically abuse alcohol, you probably don’t get as much nutrition as your body needs.
  • The presence of a large osmolal gap suggests acute isopropyl, ethanol, methanol, or ethylene glycol ingestion.
  • Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin.
  • But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol.

Elevation in ketones in most cases is considered favorable, as they provide energy and are efficient in fueling the body’s energy needs. Recent literature demonstrates a plausible link between elevated levels of circulating ketones and oxidative stress, linking hyperketonemia to innumerable morbid conditions. Ketone bodies are produced by the oxidation of fatty acids in the liver as a source of alternative energy that generally occurs in glucose limiting conditions. Regulation of ketogenesis and ketolysis plays an important role in dictating ketone concentrations in the blood. Hyperketonemia is a condition with elevated blood levels of acetoacetate, 3-β-hydroxybutyrate, and acetone.

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Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide . This goal can usually be achieved through the administration of dextrose and saline solutions.

An elevated anion gap metabolic acidosis and ketosis is the classic present. However, a mixed acid-base disorder may be present especially if vomiting is contributing to a hypochloremic alkalosis.

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Electrolyte imbalances, specifically hypokalaemia, should be corrected. Thiamine supplementation is often included to prevent Wernicke encephalopathy. Fulop M, Bock J, Ben‐Ezra al Plasma lactate and 3‐hydroxybutyrate levels in patients with acute ethanol intoxication. 4.Matsuzaki T, Shiraishi W, Iwanaga Y, Yamamoto A. Case of alcoholic ketoacidosis accompanied with severe hypoglycemia.

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Additional and complications may require extra care. Patients often need hydration, potassium repletion and dextrose injections to stimulate insulin production. Every patient is different, and careful monitoring is essential during the treatment process. Another common sign of ketoacidosis is a distinct breath smell. The alcoholic ketoacidosis smell is like acetone or nail polish remover, noticeable when someone exhales ketone molecules. The diabetic form of ketoacidosis may have a sweet and fruity smell rather than one like acetone. The elevated L/P ratio also explains why lactate levels rise in AKA, just as they do in DKA.


Table and chapter 15, Acid-Base Disorders, list the most important causes of metabolic acidosis that should be excluded to diagnose alcoholic ketoacidosis. Those with glucose intolerance and/or pancreatic insufficiency from chronic pancreatitis may even be somewhat hyperglycemic. But when hypoglycemia is present, the high NADH/NAD ratio in the presence of fasting/starvation is the main problem.

Neurologically, alcoholic ketoacidosis are often agitated but may occasionally present lethargic on examination. Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated. However, if an AKA patient is lethargic or comatose, an alternative cause should be sought. Potassium, phosphate, and magnesium are often low in patients with AKA and should be repleted along with glucose.

Patients often have a recent bout of heavy drinking before the period of relative starvation, with persistent vomiting and abdominal pain contributing to their inability to tolerate PO intake. Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having “alcoholic ketoacidosis” because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L.


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