The Correlation of Concentration of Plasma Lactates and Blood Alcohol Concentration in Patients Acutely Intoxicated by Alcohol
Franceski, Tanja, Karlovic, Dalibor, Kovak-Mufic, Ana, Madzarac, Vedran, Torre, Robert, Alcoholism
The aim of this paper was to examine the correlation of concentration of plasma lactates and blood alcohol concentration in patients acutely intoxicated with alcohol. Since alcohol inhibits gluconeogenesis and lactate is its main substrate, an increase of serum lactates with a possible development of acidosis by lactic acid is expected in acutely intoxicated persons.
All the patients detoxicated at the Department of Psychiatry, University Hospital Sestre milosrdnice, in the first five months in 2006 were included in the study. We excluded all the patients with a somatic diagnosis. The diagnosis of acute alcohol intoxication was made according to ICD-10 criteria. We analyzed consciousness as well as plasma concentrations of glucoses, urea, lactates, ethyl alcohol, AST, ALT and GGT There was a statistically significant correlation between the concentration of plasma lactates and blood alcohol concentration in patients acutely intoxicated with alcohol (Spearman's correlation = 0.537 and p = 0.01). In conclusion, the results of this study show that alcohol-intoxicated patients risk the occurrence of lactic acid, so this fact should be taken into account while monitoring actively alcohol-intoxicated patients.
Keywords: plasma lactates; blood alcohol concentration; acute alcohol intoxication
Lactates are the final product of anaerobic glycolysis, especially in muscles, erythrocytes, intestines and brain. The formed lactate converts itself into glucose by gluconeogenesis in liver, and partly in the kidney cells.1 Ethanol inhibits the processes of gluconeogenesis in several points by decreasing the intake of glucose precursor from liver and kidneys. It directs the precursors towards other metabolic paths (it limits the entrance in the gluconeogenesis paths), directly limits gluconeogenesis enzymes, and by use of metabolic products decreases cofactors (NAD) and mitochondrion oxidative processes which help gluconeogenesis.2 Since lactate is one of the main gluconeogenesis substrates, an increase of plasma lactates with a possible occurrence of acidosis induced by lactic acid is expected to occur due to acute alcohol intoxication.
Alcohol intoxication occurs by a single intake of an alcoholic beverage, and in proportion to the quantity of the alcohol intake it leads to the consciousness level disorder, cognition disorder, perception disorder, mood disorder and other forms of behavior disorders. While a mild intoxication can cause the patient to become relaxed, talkative, and euphoric, a severe intoxication often leads to severe disorders, such as aggression, labile mood, erroneous judgment and social and working inability.3-5
The intoxicated persons show at least one of the following symptoms: irregular and incomprehensible speaking, coordination disturbances, nystagmus, memory disorder, somnolence, sopor, and coma.
Complications in acute drunkenness are head injuries (subdural, epidural and intracranial hematoma), fractures of other bone systems, inhaling the thrown up content, traffic accidents, crimogene behavior, homicides and suicides. Complications, especially changes of consciousness to which the development of lacteal acidosis can contribute, are a special problem.67
The aim of this paper was to examine the correlation of concentration of plasma lactates and blood alcohol concentration in patients acutely intoxicated with alcohol.
SUBJECTS AND METHODS
The study was structured as prospective-observational and it included all the patients acutely intoxicated with alcohol detoxicated at the Department of Psychiatry, University Hospital Sestre milosrdnice, in the first five months of 2006 (N = 73). All the patients with a somatic diagnosis (N = 50) were excluded from the study. The final sample consisted of 23 patients. There were 18 male and 5 female patients. The subjects' mean age was (mean ± SD; 45.9 ± 9.82) years (from a minimum of 32 to a maximum of 65 years of age). …