POS-087 ACUTE METABOLIC ACIDOSIS IN ALCOHOL ABUSERS IS HIGHLY ASSOCIATED WITH LACTIC ACIDOSIS

Abstract

It has long been known that alcohol abuse combined with dehydration and starvation causes acute metabolic acidosis. Recently, it has attracted attention because of its pathogenic similarity to SGLT2i-induced euglycemic ketoacidosis. In these conditions, the accumulation of acids, specifically lactic acid, other than ketones is considered rare except in special circumstances, such as sepsis and vitamin deficiencies. However, its incidence in clinical practice seems to be more frequent. Therefore, we reviewed the present situation at our hospital to determine the etiology of lactic acid accumulation. From January 2013 to June 2020, we extracted data of patients with blood gas conditions of pH <7.30 and HCO3 <18 mEq/l in our hospital. Then, we defined cases with documented illnesses suggestive of alcohol abuse and a clear indication of prior heavy drinking as the alcohol-related acidosis (AIA) group. To understand the direct effect of alcohol, cases with proven infection were excluded. As a control, diabetic ketoacidosis (DKA) patients >18 years of age with the same blood gas condition were included. In 7.5 years, 28,697 blood gas analyses were performed, of which 1404 met the defined blood gas conditions. Among them, 25 AIA and 20 DKA patients met the inclusion criteria. Urinary ketones were 90% and 67% positive in DKA and AIA patients, respectively. As expected, lactate was significantly higher in AIA than in DKA (16.4 ± 8.4 vs. 4.6 ± 2.7 mmol/l p<0.001). There was no difference in oxygenation or renal function between the two groups at the time of admission. However, blood pressure and blood glucose levels were lower and liver deviation enzymes were higher in the AIA group than in the DKA group. Although in AIA, lactic acid is thought to be a contributing factor for circulatory failure due to dehydration, there was no significant difference in the amount of fluid infused up to 6 h from the start of treatment between the two groups (2.6 L in AIA vs. 3.0 L in DKA, p=0.4). Additionally, there was no difference in the time from the start of treatment to improvement in acidosis (pH>7.3. 6.7 h in AIA and 7.5 h in DKA, p=0.5). Moreover, there was no correlation between the amount of fluid and time to improve acidosis in the 22 AIA patients who were treated with fluid alone (r = -0.004). Among study participants divided into two groups according to median fluid intake in the AIA group (mean 1.3. vs. 3.9 L / 6 hours, respectively; p<0.001), there was no difference in time to improvement in acidosis (7.0 vs. 6.2 hours, p=0.6) Acute metabolic acidosis that occurs in alcohol abusers was accompanied by a high frequency of lactic acid accumulation and ketones. Furthermore, the standard therapy of dehydration correction was not an effective treatment. Recently, in the area of sepsis, it is believed that the cause of elevated lactate is not circulating insufficiency but overproduction due to adrenaline stimulation or decreased excretion due to hepatic and renal damage; therefore, excessive fluid infusion should be avoided. These results suggest that alcohol-induced lactic acid accumulation may be due to similar reasons.