Alcoholic ketoacidosis

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. Toxicity from methanol or ethylene glycol is an important differential diagnosis. Toxic metabolites of both substances result in severe metabolic acidosis with wide anion gap and wide osmolal gap.18 Neither, however, causes alcoholic ketoacidosis ketosis.

Table 1 Metabolic factors affecting acid base balance in AKA .

Alcoholic ketoacidosis (AKA) is a common reason for investigation and admission of alcohol dependent patients in UK emergency departments. Although well described in international emergency medicine literature, UK emergency physicians rarely make the diagnosis of AKA. There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence.

Who Is at Risk for Alcoholic Ketoacidosis?

Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis. Lactic acidosis occurs when ethanol metabolism results in a high hepatic NADH/NAD ratio, diverting pyruvate metabolism towards lactate and inhibiting gluconeogenesis. In peripheral tissues, where NADH levels are lower, this lactate may be converted to pyruvate for metabolic needs.

• Generally, the physical findings relate to volume depletion and chronic alcohol abuse.
• Patients improved rapidly (within 12 hours) with intravenous glucose and large amounts of intravenous saline, usually without insulin (although small amounts of bicarbonate were sometimes used).
• Going on a drinking binge when your body is in a malnourished state may cause abdominal pain, nausea, or vomiting.
• Alcoholic ketoacidosis most commonly happens in people who have alcohol use disorder and chronically drink a lot of alcohol.

Signs and symptoms of alcoholic ketoacidosis

A person who isn’t eating properly and getting the nutrition the body needs from food because they’re drinking  heavy amounts of alcohol instead, starts to get a buildup of excessive amounts of ketones in the body. Most cases of AKA occur when a person with poor nutritional status due to long-standing alcohol abuse who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea, or vomiting. In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis. Alcoholic ketoacidosis most commonly happens in people who have alcohol use disorder and chronically drink a lot of alcohol. But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol. Alcoholic ketoacidosis doesn’t occur more often in any particular race or sex.

• When this happens, it can cause ketones, which are acids, to build up in your blood.
• Toxicity from methanol or ethylene glycol is an important differential diagnosis.
• Moreover, volume depletion increases the concentration of counter-regulatory hormones, further stimulating lipolysis and ketogenesis.
• 5, 12 Such accumulation is caused by the complex interaction stemming from alcohol cessation, decreased energy intake, volume depletion, and the metabolic effects of hormonal imbalance.
• This review covers definition, pathophysiology, clinical manifestations, diagnostic approach and treatment.

BOX 3 MANAGEMENT OF AKA

All chronic alcohol misusers attending the ED should receive intravenous B vitamins as recommended by The Royal College of Physicians.23 Strenuous efforts must be made to exclude concomitant pathology. The prevalence of AKA in a given community correlates with the incidence and distribution of alcohol abuse in that community. With timely and aggressive intervention, the prognosis for a patient with AKA is good. The long-term prognosis for the patient is influenced more strongly by recovery from alcoholism. Meetings are widely available at little-to-no cost in most communities. Support groups can be a valuable source of support and can be combined with medication and therapy.

Pyruvate and lactate are then maintained in steady state at much higher levels than normal. This results in a decrease in circulating lactic acid and an increase in acetoacetate. Patients improved rapidly (within 12 hours) with intravenous glucose and large amounts of intravenous saline, drug addiction usually without insulin (although small amounts of bicarbonate were sometimes used).

Clinical findings

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. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH). It can be helpful to understand the basic guidelines for alcohol consumption so you can determine whether you are drinking above recommended levels and engaging in potentially harmful alcohol use.

The evaluation consists of 11 yes or no questions that are intended to be used as an informational tool to assess the severity and probability of an alcohol use disorder. The test is free, confidential, and no personal information is needed to receive the result. Dehydration and volume constriction directly decrease the ability of the kidneys to excrete ketoacids. Profound dehydration can culminate in circulatory collapse and/or lactic acidosis. The resulting increase in the NADH/NAD+ ratio inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid. Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA.