2 下列何者可用為當犬貓誤食抗凍劑ethylene glycol 中毒時之解毒劑？
(A) ascorbic acid
(B) ethanol
(C) penicillamine
(D) vitamine K

EG is rapidly absorbed from the GI tract; in dogs, peak blood concentrations of EG occur within 3 hr of ingestion. Approximately 50% of ingested EG is excreted unchanged by the kidneys; however, a series of oxidation reactions in the liver and kidneys metabolize the remaining EG. Toxic metabolites of EG cause severe metabolic acidosis and renal tubular epithelial damage.
 

The prognosis varies inversely with the amount of time that elapses between ingestion and initiation of treatment. Treatment is aimed at decreasing absorption of ingested EG, increasing excretion of unmetabolized EG, preventing metabolism of EG, and correcting the metabolic acidosis that occurs with EG metabolism. Further absorption of EG is prevented by induction of emesis or gastric lavage (or both) within 1–2 hr of ingestion, although the rapidity of EG absorption from the GI tract suggests these procedures may not be beneficial. Vomiting should not be induced in a dog or cat exhibiting neurologic signs because of increased risk of aspiration. Activated charcoal is not likely to reduce absorption of EG from the GI tract. Once absorption has occurred, excretion of EG is increased by fluid therapy designed to correct dehydration and increase urine production. To prevent metabolism of EG, the activity of alcohol dehydrogenase is decreased by direct inactivation or by competitive inhibition. 4-Methylpyrazole (4-MP, fomepizole) effectively inactivates alcohol dehydrogenase in dogs without the adverse effects of ethanol and is the treatment of choice. The dose of 4-MP (5% solution [50 mg/mL]) is 20 mg/kg body wt, IV, initially, followed by 15 mg/kg, IV, at 12 and 24 hr, and 5 mg/kg, IV, at 36 hr. Commercial formulations of 4-MP are available. If 4-MP is not available, an ethanol regimen (5.5 mL of 20% ethanol/kg body wt IV every 4 hr for five treatments and then every 6 hr for four additional treatments) is recommended.

In cats, 4-MP is ineffective at the canine dosage, and either a higher, extra-label dosage (125 mg/kg initially, followed by 31.3 mg/kg at 12, 24, and 36 hr after the initial dose) or ethanol is used. The recommended dosage is 5 mL of 20% ethanol/kg body wt diluted in IV fluids and given as a drip over 6 hr for five treatments, and then over 8 hr for four more treatments.

The metabolic acidosis associated with metabolism of EG is corrected by administration of sodium bicarbonate. The formula 0.3 − (0.5 × kg body wt) × (24 − plasma bicarbonate) is used to determine the dose, in mEq of bicarbonate. One-half of this dose should be given IV slowly to prevent overdose, and plasma bicarbonate concentrations should be monitored every 4–6 hr. Additional doses of bicarbonate based on the above formula are frequently necessary. Monitoring urine pH may also be helpful, with a goal of maintaining the urine pH between 7.0 and 7.5.

In dogs and cats with azotemia or in oliguric acute renal failure, inhibition of alcohol dehydrogenase is of little benefit, because almost all of the EG has already been metabolized. The prognosis for these animals is guarded to poor. Treatment should include correction of fluid, electrolyte, and acid-base disorders and, if possible, induction of diuresis.