Alcoholic Ketoacidosis: Causes, Symptoms, and Diagnosis
Determination of serum lactic acid level and serum osmolality also may be helpful. Diagnosis is made by the criteria listed in Table 226-1, with metabolic acidosis, positive serum ketones, elevated anion gap, and a low or mildly elevated serum glucose level. Patients frequently have hypophosphatemia, hyponatremia, and/or hypokalemia. Most patients also will have elevated bilirubin and liver enzyme levels due to liver disease from a long history of chronic ethanol use. The nitroprusside reagent used to measure urine and serum ketones measures acetoacetate. So, the initial ketone levels may be low or negative in alcoholic ketoacidosis.
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 https://ecosoberhouse.com/ with ongoing fluid and carbohydrate treatment. Hypophosphatemia is common in alcoholics and can retard the resolution of acidosis because phosphorus is necessary for mitochondrial utilization of glucose for oxidation of NADH.
The patient presented with acute shortness of breath, generalised abdominal pain, and vomiting. Blood gas analysis indicated severe high anion gap metabolic acidosis with elevated serum ketones and modest hyperglycaemia which was initially treated as diabetic ketoacidosis . A diagnosis of AKA was later made after obtaining a thorough history of his binge drinking. The patient subsequently responded well to thiamine and aggressive fluid resuscitation. This case highlights the importance of a well-documented patient history and in-depth knowledge of ketoacidosis.
Base administration has also been postulated to increase renal excretion of formate and glycolate . The delivery of base with dialysis might be preferred to lessen complications of base therapy . Folic acid to enhance the metabolism of formate and pyridoxine or thiamine alcoholic ketoacidosis to promote the conversion of glyoxylate to glycine, and glycolic acid to ά-hydroxy-β-ketoadipate, respectively has also been recommended . Basic principles underlying treatment of methanol, ethylene glycol, and diethylene glycol intoxications are summarized in Table 4.
Treatment of Alcoholic Ketoacidosis
Learn about what alcohol withdrawal syndrome is, the symptoms, treatments, and who’s most likely to experience it. It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Following resuscitation, our patient had plasma electrolyte levels corrected, nutritional supplementation provided and completed an alcohol detoxification regimen. Given the early recognition of AKA and concurrent management, our patient had a good outcome. The need to correct pH actively depends on the severity of the pH imbalance, the compensatory capabilities of the patient, the patient’s overall clinical condition, and the potential harm caused by alkali administration.
- Therefore, continuous observation of the heart rate is recommended, as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids once levels fall below 5.3 mmol/L.
- People with alcoholic ketoacidosis are usually admitted to the hospital, often to the intensive care unit .
- Assess for clinical signs of thiamine deficiency (Wernicke-Korsakoff syndrome).
- Serum sodium is usually relatively low because of shifts of solvent from the intracellular to extracellular spaces because of the osmotic pull of hyperglycemia.
- Prevention of alcoholic ketoacidosis involves the treatment of chronic alcohol abuse.
- After drinking too much alcohol without taking enough food for a long period of time.
As rehydration progresses and adequate renal function is established, consider electrolyte replacement, giving particular attention to potassium and magnesium. 2.Gerrity RS, Pizon AF, King AM, Katz KD, Menke NB. A Patient With Alcoholic Ketoacidosis and Profound Lactemia.