Details of osmolal gap are discussed in chapter 17, Fluids and Electrolytes. In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Symptoms result not only from an anion gap metabolic acidosis but also from coexisting disorders, like withdrawal from alcohol and the acute effects of binge drinking. We present a 64-year-old female who presented with generalized abdominal pain, nausea, vomiting and shortness of breath. Arterial blood gas analysis showed significant acidaemia with a pH of 7.10, bicarbonate of 2.9 mmol/l and lactate of 11.7 mmol/l.

• The metabolism of alcohol itself is a probable contributor to the ketotic state.
• AKA is a diagnosis of exclusion, and many other life-threatening alternative or concomitant diagnoses present similarly, and must be ruled out.
• This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA.
• Excess alcohol intake, as demonstrated by recent binge by our patient, therefore can lead to a significant and severe metabolic acidosis.
• Mechanism and significance of carbohydrate intolerance in chronic alcoholism.

When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. A heightened adrenergic state and volume depletion worsen ketosis and inhibits gluconeogenesis, creating a state that favors the creation and maintenance of a ketotic milieu. Alcohol ingestion, compounded with decreased caloric intake and dehydration, favors a ketotic state. This case highlights the importance of diagnosing patients with AKA and providing the appropriate treatment. With early diagnosis and appropriate treatment, patients improve rapidly and serious complications are prevented. AKA typically begins with a low ethanol level, so plasma alcohol level is often low or not detectable.

Deterrence and Patient Education

When glycogen stores are depleted in a patient stressed by concurrent illness or volume depletion, insulin secretion is also suppressed. Under these same conditions, glucagon, catecholamine, and growth hormone secretion are all stimulated. This hormonal milieu inhibits aerobic metabolism in favor of anaerobic metabolism and stimulates lipolysis. Acetyl coenzyme A is metabolized to the ketoacids, β-hydroxybutyrate (βHB) and acetoacetate. Patients improved rapidly with intravenous glucose and large amounts of intravenous saline, usually without insulin . Metabolic Panel – The basic metabolic panel will likely be abnormal.

Jenkins et al2 suggested that alcohol induced mitochondrial damage might account for AKA. Alcohol produces structural changes in human liver mitochondria within days.

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Recipients may need to check their spam filters or confirm that the address is safe. Thomsen J L, Simonsen K W, Felby S.et al A prospective toxicology alcoholic ketoacidosis analysis in alcoholics. 2.Gerrity RS, Pizon AF, King AM, Katz KD, Menke NB. A Patient With Alcoholic Ketoacidosis and Profound Lactemia.

• He is one of the founders of theFOAMmovement (Free Open-Access Medical education) and is co-creator oflitfl.com, theRAGE podcast, theResuscitologycourse, and theSMACCconference.
• Fulop and Hoberman5 argued that a functional abnormality is more likely to be responsible, as even severe AKA usually improves rapidly with treatment.
• Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea.
• Abdominal pain is commonly present, although it may be secondary to alcoholic gastritis or pancreatitis.