AKA results from the accumulation of the hydroxybutyric acid, and acetoacetic acid , and acetone. Such accumulation is caused by the complex interaction stemming from alcohol cessation, decreased energy intake, volume depletion, alcoholic ketoacidosis and the metabolic effects of hormonal imbalance. 12.Jang HN, Park HJ, Cho HS, Bae E, Lee TW, Chang SH, Park DJ. The logistic organ dysfunction system score predicts the prognosis of patients with alcoholic ketoacidosis.

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In AKA, the increased ratio of NADH/NAD+ increases the proportion of beta hydroxybutyrate relative to acetoacetate. Generally, the physical findings relate to volume depletion and chronic alcohol abuse. Typical characteristics of the latter may include rhinophyma, tremulousness, hepatosplenomegaly, peripheral neuropathy, gynecomastia, testicular atrophy, and palmar erythema. The patient might be tachycardic, tachypneic, profoundly orthostatic, or frankly hypotensive as a result of dehydration from decreased oral intake, diaphoresis, and vomiting. In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early. Delayed presentation or diagnosis may result in end-organ damage such as acute renal failure with tubular necrosis. The long-term prognosis of patients diagnosed with AKA depends on the severity of their underlying alcohol abuse disorder rather than AKA itself.


An anxiety state and alcohol withdrawal further exacerbate the patient’s ability to eat. The lack of nutrients other than alcohol causes the formation of ketones and elevated gap ketoacidosis in the absence of diabetes. NAD+ is a coenzyme used to carry electrons in intracellular redox reactions. The reduction of NAD+ and consequential accumulation and imbalance of NADH in the metabolism of ethanol has several important consequences. BHB generation predominates over the production of ACA in this high NADH to NAD+ ratio. Pyruvate is a substrate used in numerous energy-producing pathways, but in alcoholic ketoacidosis, it is shifted from its normal metabolic pathways to others that increase lactate production.

How severe the alcohol use is, and the presence of liver disease or other problems, may also affect the outlook. AKA is a diagnosis of exclusion, and many other life-threatening alternative or concomitant diagnoses present similarly, and must be ruled out. Failure to make the diagnosis can result in severe metabolic abnormalities, https://ecosoberhouse.com/ acidosis, and shock. NADH from the metabolism of ethanol to acetaldehyde drives the equilibrium between acetoacetic acid and beta-hydroxybutyric acid towards beta-hydroxybutyric acid. Acetoacetic acid is the acid detected by several diagnostic tests for AKA, like the nitroprusside test, so false negatives may result.

What causes alcoholic ketoacidosis?

Alcoholic ketoacidosis is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking. It is a clinical diagnosis with patients presenting with tachycardia, tachypnea, dehydration, agitation, and abdominal pain. This activity illustrates the evaluation and treatment of alcoholic ketoacidosis and explains the role of the interprofessional team in managing patients with this condition. The cause of alcoholic ketoacidosis stems from the patient’s inability to ingest, absorb and utilize glucose from their diet 2. The vomiting and nausea prevent the patient from keeping foodstuffs in the gastrointestinal tract that can cross over and provide nourishment. The alcohol further depressed gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient’s ability to eat.

Patients with alcohol use disorder require 100 mg of thiamine IV or IM prior to glucose to decrease the risk of precipitating Wernicke’s encephalopathy. AKA typically begins with a low ethanol level, so plasma alcohol level is often low or not detectable. Ethanol is metabolized by hepatocytes to acetic acid, which is converted to acetyl CoA. Acetyl CoA can be further oxidized through the Krebs cycle, used to synthesize fatty acids, or used in ketogenesis. The prevalence of AKA in a given community correlates with the incidence and distribution of alcohol abuse in that community. The metabolism of alcohol itself is a probable contributor to the ketotic state.

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Elevated cortisol levels can increase fatty acid mobilization and ketogenesis. Growth hormone can enhance precursor fatty acid release and ketogenesis during insulin deficiency. Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis. 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.

alcoholic ketoacidosis pathophysiology

The remainder of the patient’s laboratory evaluation – including liver enzymes, amylase, and lipase – were within normal limits, and methanol, ethylene glycol, salicylate, and digoxin levels were negative. Of note in the table above, the patient’s INR was greater than 11, above the upper limit of the assay, and this was confirmed by repeating the test. Treatment includes administration of intravenous saline to rehydrate and 5% dextrose to turn off gluconeogenesis. Electrolyte imbalances, specifically hypokalaemia, should be corrected. Thiamine supplementation is often included to prevent Wernicke encephalopathy.