Alcoholic Ketoacidosis

The alcoholic ketoacidosis is a metabolic complication at the confluence of alcohol abuse and starvation conditions, which is characterized by a hyperketonaemia and metabolic acidosis with anion gap without relevant hyperglycemia. The alcoholic ketoacidosis causes nausea, vomiting and abdominal pain. The diagnosis is made by means of the history and the evidence of ketoacidosis without hyperglycemia. The treatment consists of infusion of saline and dextrose.

The alcoholic ketoacidosis occurs due to the combination of the impact that alcohol and starvation on glucose metabolism.

The alcoholic ketoacidosis is a metabolic complication at the confluence of alcohol abuse and starvation conditions, which is characterized by a hyperketonaemia and metabolic acidosis with anion gap without relevant hyperglycemia. The alcoholic ketoacidosis causes nausea, vomiting and abdominal pain. The diagnosis is made by means of the history and the evidence of ketoacidosis without hyperglycemia. The treatment consists of infusion of saline and dextrose. The alcoholic ketoacidosis occurs due to the combination of the impact that alcohol and starvation on glucose metabolism. Pathophysiology alcohol reduces hepatic gluconeogenesis and leads to reduced secretion of insulin, increased lipolysis, impaired fatty acid oxidation and consequently to ketogenesis, which leads to an elevated metabolic acidosis with anion. Against regulatory hormones are increased and can further impair insulin secretion. The plasma glucose levels are low usually, but occasionally you can also see a mild hyperglycemia. Typically, symptoms and complaints introduces excessive alcohol consumption to vomiting and adjusting the alcohol and food intake for ? 24 hours. During this period of starvation, the vomiting continues, and it developed an abdominal pain that causes the patient seek medical help. Pancreatitis can also occur. Diagnosis Clinical evaluation Determination of anion exclusion of other diseases Diagnosis requires a strong attention. Like symptoms in alcoholic patients can result from acute pancreatitis, a methanol or ethylene glycol poisoning or diabetic ketoacidosis (DKA). In patients with suspected alcoholic ketoacidosis serum electrolytes should be (including magnesium), urea nitrogen and creatinine, glucose, ketones, amylase, lipase and plasma osmolality measured. The urine should be tested for ketones. In patients who appear clearly ill and those with positive ketones a blood gas analysis and serum lactate measurement should be performed. The absence of hyperglycemia makes it unlikely that there is a DKA. Patients with mild hyperglycemia may have evincing by elevated levels of glycosylated hemoglobin (HbA1c) underlying diabetes mellitus. Typical laboratory values ??are metabolic acidosis with a large anion, a ketosis and low values ??for potassium, magnesium and phosphate. Evidence of acidosis can be complicated by a concurrent metabolic alkalosis due to vomiting, as this leads to a relatively normal pH, and this is the most important indicator of the increased anion gap. If the history does not exclude a toxic alcohol consumption as a cause of increased anion gap, the methanol and ethylene glycol levels should be checked. Calcium oxalate crystals in the urine also suggest an ethylene glycol poisoning. Lactate levels are often elevated due to hypoperfusion and impaired balance of reduction and oxidation reactions in the liver. Treatment Intravenous thiamine and other vitamins, as well as magnesium Intravenous 5% dextrose in 0.9% saline solution The treatment starts with an infusion of 5% dextrose in 0.9% saline solution, in conjunction with a previous infusion of 100 mg thiamine, to prevent the development of Wernicke encephalopathy or Korsakoff’s psychosis. The initial i.v. Liquids should water soluble vitamins and magnesium are added with potassium supplementation as needed. The ketoacidosis and gastrointestinal symptoms respond rapidly to therapy. The use of insulin is only indicated if the possibility of atypical DKA exists or hyperglycemia develops> 300 mg / dl (16.7 mmol / l).

Health Life Media Team

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