ETHANOL TOXICITY

Ethanol (ethyl alcohol) is simply a colourless, volatile and flammable liquid. Ethanol (EtOH), also called alcohol or ethyl alcohol, is the main type of alcohol found in alcoholic beverages, produced by the fermentation of sugars by yeasts. As an alcohol, it’s described as a neurotoxic and psychoactive drug. It can cause alcohol poisoning when it’s overused. Ethyl alcohol is used in thermometers and as antifreeze due to its low freezing point. Additionally, we can use ethanol as a solvent, antiseptic and fuel.

Generally, Ethanol toxicity results from the ingestion of large quantities of ethanol. This can be caused by ingesting ethanol as beverage, commonly known as alcohol and non-beverage ethanol found in items such as mouthwash, cologne and daily medicine. Alcohol is the most common form of ethanol. The signs and symptoms are associated with alcohol toxicity depending on the blood alcohol concen-tration (BAC). As the BAC increases, so does the severity of the symptoms. Ethanol poisoning results in turbidity in consciousness. Ethyl alcohol toxicity can be occurred in both acute and chronic settings, representing two distinct disease spectrums.

Acute ethanol toxicity results from ingesting ethanol faster than it can be metabolized by the liver and eliminated, which leads to accumulation of ethyl alcohol and its metabolites in the blood. Ethanol intoxication presents with variable manifestations progressing from mild (e.g., incoordination, ataxia and altered sensorium) to severe (e.g., coma, tumour and respiratory depression) with increas-ing blood ethanol concentrations. Acute toxicity is diagnosed by clinical presentation and DSM-5 crite-ria. Ancillary studies may be required depending on individual presentation (e.g., electrolytes, glucose, blood or breath ethanol levels). The main treatment for acute alcohol poisoning is supportive treat-ment. The patient should be kept on a close watch util being clinically stable.

In the second place, with chronic ethanol use, the number of Gamma-aminobutyric acid (GABA) receptors is increased, requiring more and more alcohol to create the same level inhibition. This is a phenomenon known as tolerance. The number of NMDA receptors and their glutamate sensi-tivity are increased in patients with alcohol use disorder. Because of the increased sensitivity of these receptors, patients with alcohol use disorder are at risk of seizures and hallucinations when alcohol is discontinued.

To sum up, as I mentioned above, exposure to ethanol a colourless, volatile and flammable substance, is a serious problem for our body. Since, ethyl alcohol poisoning causes changes in the state of consciousness, direct intervention should be done.

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REFERENCES https://www.acilcalisanlari.com/etanol-zehirlenmeleri.html https://elsevier.health/en-US/preview/acute-ethanol-toxicity#synopsis https://www.ncbi.nlm.nih.gov/books/NBK557381/#:~:text=Ethanol%20toxicity%20re-sults%20from%20the%20ingestion%20of%20ethanol%2C%20usually%20in,%2C%20co-logne%2C%20and%20cough%20medicine