Emergent Treatment of Alcoholic Ketoacidosis: Overview, Prehospital Care, Emergency Department Care

The choice of oral vs. IV replacement depends on the severity of the abnormality and the ability of the patient to tolerate PO. 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.

These https://ecosoberhouse.com/ acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal. Mortality specifically due to AKA has been linked to the severity of serum beta-hydroxybutyric acid in some studies. It should be used as an indicator of the severity of the disease.Identifying these high-risk patients can help set the intensity of monitoring required for the patient to ensure optimal patient outcomes are achieved. The etiology of Alcoholic ketoacidosis stems from the patient’s inability to ingest, absorb and utilize glucose from their diet.

History

Insulin is of no proven benefit and can even be dangerous, as patients often have depleted glycogen stores and normal or low glucose levels. Sodium bicarbonate is not indicated unless patients are severely acidemic, with a pH . Severe acidemia is unlikely to be explained by alcoholic ketoacidosis alone. Mildly elevated osmolal gaps can exist, but it is important to consider co-ingestions, or other causes of anion gap acidosis, if the gap fails to close with ongoing fluid and carbohydrate treatment.

• These changes are further enhanced as ethanol is metabolized to acetaldehyde and acetyl-CoA, leading to an increased NADH/NAD+ ratio.
• Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, seizures, or delirium.
• In general, exogenous insulin is contraindicated in the treatment of AKA, because it may cause life-threatening hypoglycemia in patients with depleted glycogen stores.
• Mitochondrial NAD is reduced to NADH during this process.13 In liver tissue exposed to alcohol, this mitochondrial NADH accumulates, increasing the NADH/NAD ratio, and interfering with mitochondrial metabolic activity.

The presence of a mixed alcoholic ketoacidosis-base disturbance suggests a comorbid disorder. Common concurrent illnesses are dehydration and electrolyte disturbances from vomiting and reduced intake, pancreatitis, gastritis or upper GI bleeding, seizures, alcohol withdrawal, pneumonia, sepsis, and hepatitis. Insulin release from the pancreatic beta cells might be abnormally sensitive to catecholamine inhibition. The pivotal variable appears to be a relative deficiency of insulin. Individuals with higher insulin levels are more likely to present with the syndrome of alcohol-induced hypoglycemia without ketoacidosis.

Diabetes

Acetyl CoA can be further oxidized through the Krebs cycle, used to synthesize fatty acids, or used in ketogenesis. Mechanism and significance of carbohydrate intolerance in chronic alcoholism. The first 24 hours of acute pancreatitis—changes in biochemical and endocrine homeostasis in patients with pancreatitis compared with those in control subjects undergoing stress for reasons other than pancreatitis.

If you are diagnosed with alcoholic ketoacidosis, your recovery will depend on a number of factors. Seeking help as soon as symptoms arise reduces your chances of serious complications. Treatment for alcohol addiction is also necessary to prevent a relapse of alcoholic ketoacidosis. If your blood glucose level is elevated, your doctor may also perform a hemoglobin A1C test.

BOX 1 PRESENTING FEATURES OF AKA

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