Alcoholic Ketoacidosis StatPearls NCBI Bookshelf

You just breathe it out (‘AOB’ really should be ‘acetone on breath’). It does, however, make that one nurse who shouts “we got a DKA patient in room 3” look clairvoyant. Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are reesterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis. Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages.

Diagnosis of AKA requires the detection of ketone bodies in the urine and serum. Urine can be tested with nitroprusside tablets or dipsticks, though this rapid test cannot indicate whether the degree of ketone accumulation can account for the total anion gap. Direct testing for beta-hydroxybutyrate in the serum is replacing nitroprusside tests.

Emergency Department Care

Potassium, phosphate, and magnesium are often low in patients with AKA and should be repleted along with glucose. The choice of oral vs. IV replacement depends on the severity of the abnormality and the ability of the patient to tolerate PO. 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. So, in the cytoplasm, high NADH/NAD ratios make us shunt towards lactate, while in mitochondria, the same high ratios make us shunt towards beta-hydroxybutyrate.

How do you fix alcoholic ketoacidosis?

Treatment of alcoholic ketoacidosis involves administering IV fluids, monitoring electrolyte levels, and administering thiamine followed by glucose, if needed. Medications (i.e., benzodiazepines) may be administered to minimize the risk of experiencing severe symptoms of alcohol withdrawal.

The hallmark of AKA is ketoacidosis without marked hyperglycemia; the serum glucose level may be low, normal, or slightly elevated. This finding can help to distinguish AKA from diabetic ketoacidosis . alcoholic ketoacidosis is usually triggered by an episode of heavy drinking. If you can’t eat for a day or more, your liver will use up its stored-up glucose, which is a type of sugar. When your liver uses up its stored glucose and you aren’t eating anything to provide more, your blood sugar levels will drop. Alcoholic ketoacidosis is a condition that can happen when you’ve had a lot of alcohol and haven’t had much to eat or have been vomiting.


The next important step in the management of AKA is to give isotonic fluid resuscitation. Dextrose is required to break the cycle of ketogenesis and increase insulin secretion. The dextrose will also increase glycogen stores and diminish counterregulatory hormone levels. It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci[itation. If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized. Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia.

Efficient and timely management can lead to enhanced patient outcomes in patients with AKA. However, after adequate treatment, it is equally essential to refer the patient to alcohol abuse rehabilitation programs to prevent recurrence and long-term irreversible damage from alcohol abuse. Dehydration causes an elevated heart rate and dry mucous membranes. A degree of alcohol withdrawal and agitation are likely to be present, resulting in an increased heart rate as well. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated.

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