Infection or other illnesses such as pancreatitis can also trigger alcoholic ketoacidosis in people with alcohol use disorder. 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 ketosis. Both cause abdominal pain, with marked central nervous system depression, but methanol toxicity results in visual impairment, while ethylene glycol toxicity results in crystalluria, oliguria, and renal failure.
Clinical ReviewsAlcoholic Ketoacidosis: Etiologies, Evaluation, and Management
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. This literature review discusses the alcoholic ketoacidosis smell history, characterisation, pathophysiology, diagnosis, and management of AKA. One complication of alcoholic ketoacidosis is alcohol withdrawal. Your doctor and other medical professionals will watch you for symptoms of withdrawal.
- Treatment for alcohol addiction is also necessary to prevent a relapse of alcoholic ketoacidosis.
- Alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking.
Metabolic acidosis in the alcoholic: a pathophysiologic approach
Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. This case demonstrates the importance of considering AKA in the differential diagnosis of a patient presenting with non-specific symptoms, significant metabolic acidosis and a history of alcohol excess. It is essential to differentiate AKA from DKA to ensure that inappropriate insulin administration does not occur.
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Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance. Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. In the series from Fulop and Hoberman, seven patients were alkalaemic. In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.
Clinical Scenario
It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Alcoholic ketoacidosis is a problem caused by drinking a lot of alcohol without eating food. 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.
Treatment / Management
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. Patients typically present with non-specific features including nausea, vomiting and generalized abdominal pain. Vomiting and/or diarrhoea is common and can lead to hypovolaemia and potassium depletion. Signs of shock including tachycardia and hypotension can be complicated by overlap of alcohol withdrawal 2.
- Pyruvate and lactate are then maintained in steady state at much higher levels than normal.
- This process is catalyzed by the enzyme acetyl-CoA synthetase.
- AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness.
- Group meetings provide support for people trying to quit drinking.
- The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation.
Alcohol-Related Metabolic Emergencies
Calcium oxalate crystals in the urine also suggests ethylene glycol poisoning.
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