Alcoholic Ketoacidosis: Signs, Symptoms, and Treatment

Without enough insulin, the body begins to break down fat as fuel. This causes a buildup of acids in the bloodstream called ketones. If it’s left untreated, the buildup can lead to diabetic ketoacidosis. Arrange follow-up to evaluate patients after the resolution of symptoms, in order to detect other complications of chronic alcohol abuse.

Signs and symptoms

You may get vitamin supplements to treat malnutrition caused by excessive alcohol use. Untreated, diabetic ketoacidosis can lead to loss of consciousness and, eventually, death. If you feel ill or stressed or you’ve had a recent illness or injury, check your blood sugar level often. You might also try a urine ketone test kit you can get at a drugstore. 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.

• Restoration of volume status and correction of the acidosis may be difficult to accomplish in the emergency department (ED).
• One complication of alcoholic ketoacidosis is alcohol withdrawal.
• Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels.
• The resulting increase in the NADH/NAD+ ratio inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid.

Alcoholic Ketoacidosis: Signs, Symptoms, and Treatment

The condition is an acute form of metabolic acidosis, a condition in which there is too much acid in body fluids. Alcoholic ketoacidosis is the buildup of ketones in the blood due to alcohol use. Ketones are a type of acid that form when the body breaks down fat for energy. There are many ways to prevent diabetic ketoacidosis and other diabetes complications.

Management of Alcohol Withdrawal Syndrome

Specifically look for nystagmus, confusion, ataxia, confabulation, and restriction of extraocular movements. Strongly consider providing thiamine supplementation to patients with alcohol dependence even without signs of thiamine deficiency. 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.

In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis. During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. 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. If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help.

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 alcoholic ketoacidosis 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. Dextrose stimulates the oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH) and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+).

What are the complications of alcoholic ketoacidosis?

• These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal.
• Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid.

• Note information about the patient’s social situation and the presence of intoxicating agents besides alcohol.
• Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA.
• If you develop any of these symptoms, seek emergency medical attention.
• 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.