Ayşe Sümeyye ARI^a , Gülhan KURTOĞLU ÇELİK^a

^aAnkara Bilkent City Hospital, Clinic of Emergency Medicine, Ankara, Türkiye

ABSTRACT
Alcoholic ketoacidosis (AKA) is a syndrome observed in individuals who engage in excessive alcohol consumption and have inadequate nutrition, typically triggered by the abrupt cessation of alcohol intake. Patients with AKA are both nutritionally deficient due to reduced oral intake and dehydrated owing to the diuretic effect of alcohol. When glycogen stores are depleted, metabolism shifts towards the breakdown of fat and protein. Additionally, reduced oral intake leads to decreased insulin levels and a significant increase in lipolysis. Insulin deficiency further enhances hormone-sensitive lipase activity, promoting the conversion of ethanol to acetaldehyde and acetyl-CoA. In each acetaldehyde-toacetyl-CoA conversion, NAD+ is transformed into NADH. The shift in the NAD+/NADH ratio towards NADH causes hypoglycemia, increased lactate, and elevated beta-hydroxybutyric acid. Patients typically present with nonspecific symptoms such as nausea, vomiting, and abdominal pain. Metabolic acidosis may occur, necessitating an increased respiratory rate and Kussmaul breathing for compensation.Blood ethanol and glucose levels may be normal or decreased due to inadequate oral intake. Malnutrition may lead to hypokalemia and hypomagnesemia. Evaluation for Wernicke’s encephalopathy (encephalopathy, ataxia, ophthalmoplegia) is crucial. AKA is primarily diagnosed clinically, with the exclusion of other causes of metabolic acidosis, most notably diabetic ketoacidosis. Fluid resuscitation is paramount in treatment, and solutions containing dextrose, thiamine, and early transition to oral intake are crucial. Correction of identified electrolyte abnormalities is essential for comprehensive management.
Keywords: Ethanol; metabolic acidosis; diyabetic ketoacidosis