Approaches to Selected Toxicoses

Ethylene Glycol Toxicosis. Ethylene glycol is commonly used as an antifreeze. It is metabolized by alcohol dehydrogenase to mixed aldehydes, carboxylic acids, and 

Ethanol Toxicosis. Absorption of ethanol by the GI tract absorption is rapid. Peak levels can be reached 30 to 60 minutes after ingestion. As a rule of thumb, 1 ml of absolute ethanol per kilogram weight results in a level of 100 mg/100 ml (0.1%) in 1 hour. Supportive treatment is directed toward the control of acidosis and hypoglycemia. 

Since organophosphate toxicosis results in respiratory failure, the treatment approach for must include the maintenance of a patent airway. Artificial respiration may also need to be employed. The first pharmacological approach is the administration of atropine. Atropine competes with acetylcholine for its receptor site, thus reducing the effects of the neurotransmitter. N-methylpyridinium 2-aldoxime (2-PAM) is used in with atropine therapy as an effective means to restore the covalently bound enzyme to a normal state. It reacts with the phosphorylated cholinesterase enzyme removing the phosphate group. As previously mentioned, carbamates interact with cholinesterase by weak, ionic bonding thus 2-PAM is of no use to combat toxicosis caused by these compounds. However, atropine is effective to prevent the effects on respiration. 

Arsenic Toxicosis. Urine arsenic is the best indicator of current or recent exposure. Atomic absorption spectrophotometry is preferred as the detection method. Hair or fingernail sampling may also be helpful. Use of blood is useful if analyzed soon after exposure or in cases of continuous chronic exposure. After acute exposure, chelation therapy is instituted utilizing either (1) Dimercaprol BAL (British Anti-Lewisite) and analogues  

Chronic Exposure (Arsenic). Primarily symptomatic treatment is chosen. Chelation therapy is practiced, but its usefulness in cases of chronic exposure is still questionable. 

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