Intoxication acute ethanol

Corongiu, F.P., Lai, M. and Milia, A. (1983). Carbon tetrachloride, bromotrichloromethane and ethanol acute intoxication. New chemical evidence for lipid peroxidation in rat tissue microsomes. Biochem. J. 212, 625-631. 

The treatment goals for acute intoxication of ethanol, cocaine/amphetamines, and opioids include (1) management of psychological manifestations of intoxication, such as aggression, hostility, or psychosis, and (2) management of medical manifestations of intoxication such as respiratory depression, hyperthermia, hypertension, cardiac arrhythmias, or stroke. 

The treatment goals for acute intoxication due to ethanol, cocaine/amphetamines, and opioids include (1) management of... 

Eventually these reactions result in the oxidative destruction of cellular membrane and serious tissue damage in the liver even though <0.5% of CCI4 is ever metabolized. An essential involvement of lipid peroxidation in the events leading to death of hepatocytes has been proved in the acute intoxication as well as with other haloalkanes such as bromotrichloromethane (CBrCls), dibromoethane, and halothane. Lipid peroxidation is also involved in the hepatotoxicity of ethanol, allyl alcohol, and some drugs like adriamycin. 

Ethanol is a widely used and often abused chemical substance. Consequently the measurement of ethanol is one of the more frequently performed tests in the toxicology laboratory. Although less frequently encountered, it is important to include methanol, isopropanol, and acetone (a metabolite of isopropanol) in a test battery for alcohols for proper evaluation of the acutely intoxicated patient. 

Ethanol is usually ingested through the gastrointestinal tract, but can be absorbed as vapor by the alveoli of the lungs. Ethanol is oxidized metabolically more rapidly than methanol, first to acetaldehyde, then to CO2. Ethanol has numerous acute effects resulting from central nervous system depression. These range from decreased inhibitions and slowed reaction times at 0.05% blood content of ethanol, through intoxication, stupor and—at more than 0.5% blood ethanol—death. 

In the above discussion, we have defined several directions for biochemical correction xmder acute intoxication with FA and suggested suitable preparations for therapeutic complexes (i) competitive inhibition of FA and CoA interaction, (ii) competitive inhibition of FC and aconitase interaction, (iii) replenishment of the TCA cycle distally of aconitase, and (iv) utilization of accumulating citrate. In previous publications, we presented the first data on effectiveness of therapeutic complexes named METIS (Concharov et al., 2006, 2009). These consisted of ethanol, methylene blue (MB), sodium glutamate (SC), and glycerol trinitrate (CT). Indices of therapeutic efficiency (ratio for different... 

Bautista, A.P. and Spitzer, J.J. (1992). Acute ethanol intoxication stimulates superoxide anion production by in situ perfused rat liver. Hepatology 15, 892-898. 

Boe, D. M., Nelson, S., Zhang, P. et al., Acute ethanol intoxication suppresses lung che-mokine production following infection with Streptococcus pneumoniae, J. Infect. Dis., 184, 1134, 2001. 

Kutob SD, Plaa GL. 1962. The effect of acute ethanol intoxication on chloroform-induced liver damage. J Pharmacol Exp Ther 135 245-251. 

Ethanol produces central nervous system depression over a wide range of doses. Its effects are additive or sometimes more than additive with other central nervous system depressants. Symptoms often associated with acute alcohol intoxication include increase in self-confidence, loss of inhibitions, euphoria, and loss of judgment. With increasing doses motor and intellectual impairment become prominent. Chronic abuse of ethanol leads to severe liver impairment (see Chapter 35). 

The most important goals in the treatment of acute alcohol intoxication are to prevent severe respiratory depression and to prevent aspiration of vomitus. Even with very high blood ethanol levels, survival is probable as long as the respiratory and cardiovascular systems can be supported. The average blood alcohol concentration in fatal cases is above 400 mg/dL however, the lethal dose of alcohol varies because of varying degrees of tolerance. 

Sukul NC, De A, Sinhababu SP, Sukul A. 2003. Potentized Mercuric chloride and Nux vomica facilitate water permeability in erythrocytes of a freshwater catfish Clarius batrachus under acute ethanol intoxication. J Alt Comp Med 9 719-725. 

Ethanol has a range of acute effects, normally expressed as a function of percent blood ethanol. In general, these effects are related to central nervous system depression. Mild effects such as decreased inhibitions and slowed reaction times begin to appear at about 0.05% blood ethanol. Most individuals are clinically intoxicated at a level of 0.15 to 0.3% blood ethanol in the 0.3 to 0.5% range, stupor may be produced and at 0.5% and above, coma and often death occur. 

Valenzuela, A. Lagos, C. Schmidt, K. Videla, L.A. Sily-marin protection against hepatic lipid peroxidation induced by acute ethanol intoxication in the rat. Biochem. Pharmacol. 1985, 34, 2209-2212. 

Intoxication with depressants (e.g., acute ethanol intoxication), organophosphates, carbon monoxide, or nerve gas Lambert-Eaton syndrome... 

There are severe acute and chronic concerns around pediatric medicines containing ethanol. Hepatic metabolism of ethanol involves a nonlinear saturable pathway. Young children have a limited ability to metabolize and thereby detoxify ethanol. Ethanol intoxication has been recorded in children with blood levels as low as 25 mg/dL. Alcohol has a volume of distribution of approximately 0.65 L/kg. Ingestion of 20 mL of a 10% alcohol solution will produce a blood level of 25 mg/dL in a 30-lb. child. The American Academy of Pediatrics (AAP) Committee on Drugs recommends that pharmaceutical formulations intended for use in children should not produce ethanol blood levels of >25 mg/dL after a single dose. In general, manufacturers have voluntarily complied with the recommendations. In 1992 the Nonprescription Drug Manufacturers Association established voluntary limits for alcohol content of nonprescription products (65). 

Foo and Lemon (1997) assessed the acute effects of kava, alone and in combination with alcohol, on subjective measures of impairment and intoxication and on cognitive performance. This was a placebo-controlled study, with ten subjects in each of four conditions placebo, kava, alcohol, and kava plus alcohol. The placebo was pure fruit juice and fruit juice was added to kava and alcohol as well to maintain double blind conditions. A battery of tests was included to measure outcomes, including subjective measures of impairment and intoxication, and visual-motor and cognitive performance. These measures were performed before (time = 0), and 30, 60 and 90 minutes after consumption of the drinks. Each test trial took about 12 minutes. Kava consumption produced no significant effects on perceived or measured competence, while alcohol caused motor and cognitive impairments. However, when kava and alcohol were combined, kava potentiated both the perceived and measured impairment produced by the alcohol alone. This potentiation effect is in accord with the findings of Jamieson and Duffield (1990) on the positive interaction of ethanol and kava resin in mice. 

---