Alcohol produces structural changes in human liver mitochondria within days. Fulop and Hoberman5 argued that a functional abnormality is more likely to be responsible, as even severe AKA usually improves rapidly with treatment. They attributed this to the administration of therapy (intravenous dextrose) rather than the withdrawal of the toxin, ethanol. After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management
Ethyl alcohol oxidizes at a rate of 20 to 25 mg/dL per hour in most individuals. The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see. Each of these situations increases the amount of acid in the system. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Sometimes it’s added deliberately and illegally during or after manufacturing as a cheaper way to increase the alcohol content in a drink.
The syndrome of alcoholic ketoacidosis
Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent. An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury. Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis. The presence of a high anion gap, although not specific, is suggestive of AKA in a patient with an appropriate clinical history 9. Additional measurements that may help determine the diagnosis of AKA include beta-hydroxybutyrate levels (high in AKA, low in DKA) and serum alcohol concentration (typically low or undetectable) 8.
- 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.
- Ethanol is metabolized into a chemical compound called acetaldehyde.
- AKA typically presents with a severe metabolic acidosis with a raised anion gap and electrolyte abnormalities, which are treatable if recognized early and appropriate management instituted.
- Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid.
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Ketones are a type of acid that form when the body breaks down fat for energy. You can prevent alcoholic ketoacidosis by limiting your alcohol intake. You can learn how to reduce your alcohol intake or eliminate it altogether. Joining a local chapter of Alcoholics Anonymous may provide you with the support you need to cope. You should also follow all of your doctor’s recommendations to ensure proper nutrition and recovery.
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. Generally, the physical findings relate to volume depletion and chronic alcohol abuse.
Symptoms
The key differential diagnosis to consider, and exclude, in these patients is DKA. Although DKA can also present with a severe metabolic acidosis, with a raised anion gap and the presence of ketones, the history and examination are quite distinct from that of someone presenting with AKA (Table 1). Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients. Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness.
- This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive a proper and timely diagnosis to obtain the correct treatment.
- Cells still need energy to survive, so they switch to a back-up mechanism to obtain energy.
- Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis.
Critical Care
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the alcohol acidosis unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world.
Medical
Signs of shock including tachycardia and hypotension can be complicated by overlap of alcohol withdrawal 2. Electrolyte abnormalities are common to this condition and can precipitate fatal cardiac arrhythmias 3, 4. Nausea, vomiting, and abdominal pain were by far the most commonly observed complaints. Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent. Both Wrenn et al6 and Fulop and Hoberman5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin.
Acute necrotizing esophagitis (black esophagus): An autopsy case with alcoholic ketoacidosis
Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. People who consume a lot of alcohol during one occasion often vomit repeatedly and stop eating. If the vomiting and starvation go on for a day or more, the liver’s normal stores of sugar (glucose) decrease.
What Is the Prognosis for Alcoholic Ketoacidosis?
American Addiction Centers (AAC) is committed to delivering original, truthful, accurate, unbiased, and medically current information. We strive to create content that is clear, concise, and easy to understand. Neurologically, patients are often agitated but may occasionally present lethargic on examination.