Ethylene glycol poisoning from

B. Other useful laboratory studies include electrolytes, lactate, ethanol, glucose, BUN, creatinine, calcium, hepatic transaminases, urinalysis (for crystals and Wood s lamp examination), measured osmolality, arterial blood gases, and ECG monitoring. Serum beta-hydroxybutyrate levels may help distinguish ethylene glycol poisoning from alcoholic ketoacidosis, which may also cause increased anion and osmolar gaps. (Patients with alcoholic ke-... 

Three stages of ethylene glycol overdose occur. Within the first few hours after ingestion, there is transient excitation followed by CNS depression. After a delay of 4-12 hours, severe metabolic acidosis develops from accumulation of acid metabolites and lactate. Finally, delayed renal insufficiency follows deposition of oxalate in renal tubules. The key to the diagnosis of ethylene glycol poisoning is recognition of anion gap acidosis, osmolar gap, and oxalate crystals in the urine in a patient without visual symptoms. 

Kidney failure from the metabolic formation of calcium oxalate has been especially common in cat species, which have voracious appetites for ethylene glycol in antifreeze. Deposits of solid calcium oxalate have also been observed in the liver and brain tissues of victims of ethylene glycol poisoning. 

Fortunately, treatment is possible, using alcohol (that is, ethyl alcohol), the same treatment as for ethylene glycol poisoning. The acidity is also treated with bicarbonate of soda. Methyl alcohol is eliminated from the body slowly, and so repeated intake, as in those who drink meths, could lead to cumulative poisoning. 

Wallman P, Hogg K. Towards evidence based emergency medicine best BETs from the Manchester Royal Infirmary. Management of acute ethylene glycol poisoning. Emerg Med J 2002 19(5) 431-2. 

Figure 23-2. The oxidation of alcohols by alcohol dehydrogenase results in the formation of metabolites that cause serious toxicities. Ethanol, a preferred substrate for ADH, is used in methanol or ethylene glycol poisoning to slow the rate of formafion of fhe toxic metabolites of these alcohols. Acetaldehyde formed from ethanol is oxidized rapidly by aldehyde dehydrogenase except in the presence of disuifiram.

Thousands of pets, and more than a few children and adults, die each year from ethylene glycol poisoning. Most of these deaths are accidental, but there are, unfortunately, many recorded cases in which ethylene glycol has heen used to poison an unsuspecting spouse or child. 

Most tj es of antifreeze used in cars are solutions of ethylene glycol. Every year, thousands of dogs and cats die from ethylene glycol poisoning because they consume improperly stored antifreeze or antifreeze that has leaked out of a radiator. The antifreeze has a somewhat sweet taste, which attracts a curious dog or cat. Young children are also at risk for ethylene glycol poisoning. 

The law of 1906 was only a beginning. It did not regulate the safety and effectiveness of drug formulations. This was no more evident than in the case of mass poisoning which resulted from the consumption of "elixir of sulfanilamide" produced by the S.E. Massengill Company of Bristol, Tennessee. Between September and October 1937 doctors had prescribed almost 12 gallons of a 10% solution of sulfanilamide in an ethylene glycol(antifreeze) solvent flavored with saccharin, caramel, amaranth, and raspberry extract. The company s chief chemist, Harold Watkins, was not aware of the toxicity of that concentration of the solvent. 

Alcohols occur widely in nature. Methanol is also known as wood alcohol because it can be obtained by distilling wood in the absence of air. It is very poisonous and can cause blindness or death if ingested. Ethanol is consumed in alcoholic beverages. Other simple alcohols, such as 2-phenylethanol from roses and menthol from peppermint, are constituents of natural flavors and fragrances. Alcohols are important intermediates in chemical synthesis. They are also commonly used as solvents for various chemical processes. Ethylene glycol is used in antifreeze and in the preparation of polymers such as Dacron. 

Poisoning by ethylene glycol (CH2OHCH2OH) is due to aldehydes, glycolate, oxalate, and lactate, resulting from an initial attack by alcohol dehydrogenase. This is similar to the activation of methanol to formaldehyde and subsequent oxidation by aldehyde dehydrogenase to formic acid. 

The ethylene glycol and methyl alcohol (see below), which is also sometimes found in antifreeze, are poisonous because they are converted into more toxic products. Once inside the body, the ethylene glycol in the antifreeze is changed by metabolism into first one, and then several other chemicals. This requires the same enzyme that metabolizes the alcohol we consume in alcoholic drinks (ethyl alcohol). The ethylene glycol is converted into oxalic acid which is poisonous, and other poisonous products are also produced. Oxalic acid is also found in rhubarb leaves, which is what makes them poisonous. The result of these metabolic conversions is that the acidity of the blood increases (the pH decreases) and normal metabolic processes are inhibited. The oxalic acid formed can crystallize in the brain and the kidneys, causing damage. The oxalic acid also reacts with calcium and removes it from the body. The reduction of calcium... 

Modifiers have also been used to influence the selectivity of vapor-phase partial hydrogenations of benzene. The presence of ethylene glycol increased reaction selectivity with a ruthenium black catalyst from 7% to 41% while the turnover frequency (TOF) decreased from 31 to 3. Pyridine also increased selectivity in the short term, but prolonged use poisoned the catalyst. Passivating a ruthenium black catalyst with caprolactam not only stabilized the catalyst toward deactivation but also increased reaction selectivity from 7% to 20%. 

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