Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated. The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. 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.
An evidence-based narrative review of the emergency department evaluation and management of rhabdomyolysis
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. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking.
Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management
Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well). Emergency clinician knowledge of the evaluation and management of AKA is essential in caring for these patients. 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.
Alcoholic Ketoacidosis Treatment and Diagnosis
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. The absence of hyperglycemia makes diabetic ketoacidosis improbable. Patients with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C). Efficient and timely management can lead to enhanced patient outcomes in patients with AKA.
- The underlying pathophysiology is related to poor glycogen stores and elevated nicotinamide adenine dinucleotide and hydrogen.
- Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
- The length of your hospital stay depends on the severity of the alcoholic ketoacidosis.
- Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are reesterified to triglyceride.
It is a clinical diagnosis with patients presenting with tachycardia, tachypnea, dehydration, agitation, and abdominal pain. This activity illustrates the evaluation and treatment of alcoholic ketoacidosis and explains the role of the interprofessional team in managing patients with this condition. Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia.
- If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help.
- Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia.
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- This activity illustrates the evaluation and treatment of alcoholic ketoacidosis and explains the role of the interprofessional team in managing patients with this condition.
Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea. Limiting the amount of alcohol you drink will help prevent https://ecosoberhouse.com/ this condition. How severe the alcohol use is, and the presence of liver disease or other problems, may also affect the outlook.
- Exclude other causes of autonomic hyperactivity and altered mental status.
- Your doctor and other medical professionals will watch you for symptoms of withdrawal.
- Patients are generally dehydrated, and serum glucose can be low, normal, or mildly elevated.
Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment
