Page 684 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Alcohols and Glycols Chapter | 49 649

VetBooks.ir could occur (Means, 2003). Hypothermia may develop, (Bischoff, 2006a). Diagnosis can be made by history and
measurement of blood methanol concentrations (or formic
and alterations in hydration, electrolyte, and acid base
acid in primates).
status should be corrected (Richardson, 2006).
Treatment in nonprimates is symptomatic and similar
Methanol Toxicosis to treatment for ethanol toxicosis. Primates are treated
with 4-methylpyrazole to compete with ADH to inhibit
Methanol (methyl alcohol or wood alcohol, CH 3 OH) is the bioactivation of methanol (Barceloux et al., 2002) or,
widely used as a solvent, fuel (Sterno), gasoline additive, alternatively, with ethanol. It is probably inappropriate to
antifreeze, and windshield washer fluid (30 40% metha- treat methanol toxicosis in nonprimates with ethanol
nol). The minimum lethal dose (MLD) in dogs is between because ethanol contributes to the sedation, and the meta-
3.9 and 8.9 g/kg, and in rats, rabbits, rhesus monkeys, and bolites of methanol do not cause blindness in nonpri-
human beings it is 9.5, 7, 3, and 0.99 g/kg, respectively, mates, as they do in primates. Hemodialysis is also used
indicating a variation in species susceptibility to methanol to remove formic acid. Folic acid is given i.v. to enhance
toxicosis (Valentine, 1990; Gilger and Potts, 1955). formic acid metabolism.
Methanol toxicosis is rare in dogs, but it has been
reported in a dog that chewed open a bottle of 98% meth-
anol antifreeze (Hurd-Kuenzi, 1983). Isopropanol Toxicosis
Isopropanol (isopropyl alcohol or IPA, CH 3 CH(OH)CH 3 )
Toxicokinetics
is found in rubbing alcohol (70%), antifreeze, detergents,
Ingested methanol is absorbed quickly from the GI tract, window cleaning products, and disinfectants. Ingestion is
and peak methanol concentrations occur within the usual cause of poisoning in humans, although toxicity
30 60 min following ingestion (Barceloux et al., 2002). from inhalation and topical absorption has been reported.
Toxicosis has also been reported following inhalation or Isopropanol toxicosis is rare in domestic animals, possibly
dermal absorption. The rate of elimination of methanol due to its bitter taste. It has been reported in a horse that
from the blood is slower than that of ethanol. Methanol is was mistakenly administered isopropanol via nasogastric
metabolized by ADH to formaldehyde, which is oxidized intubation for colic; the isopropanol was mistaken for
to formic acid by formaldehyde dehydrogenase mineral oil (Somerville and Plumlee, 1996).
(Fig. 49.1). In mammals other than primates, formic acid
is detoxified relatively rapidly to yield carbon dioxide and
water. Formic acid is metabolized less efficiently in pri- Toxicokinetics
mates. This may lead to the accumulation of formic acid, Isopropanol is approximately twofold more toxic than eth-
which plays a major part in the development of acidosis anol in dogs, rabbits, and rats (Lehman and Chase, 1944)
observed in primates. Consequently, methanol is more and about as toxic as methanol when taken orally. On the
toxic to humans and nonhuman primates that it is to other other hand, it is safer after dermal exposure as it does not
mammals. pass through the skin as easily as methanol. It is rapidly
absorbed from the GI tract, and approximately 80% is
Mechanism of Action metabolized to acetone, which is also a CNS depressant,
but acetone has a much longer half-life (16 20 h) than
Formic acid is responsible for ocular and CNS lesions in
does alcohol (Fig. 49.1). Acetone is further metabolized
primates as a result of the inhibition of cytochrome oxi-
to CO 2 . The metabolism of IPA appears equivalent across
dase (Roe, 1982). Blindness and permanent neurological
species.
abnormalities are common sequelae in primates.
Diagnosis and Treatment Diagnosis and Treatment
Clinical signs in animals other than primates are similar Clinical signs associated with isopropanol toxicosis are
to those seen with ethanol toxicosis and are primarily similar to those for ethanol toxicosis and include CNS
related to CNS depression. Vomiting and abdominal pain depression, hypotension, vomiting, and abdominal pain
may be seen. In primates, following the initial nausea and due to severe gastritis, which is secondary to direct irrita-
CNS depression, a latent period of approximately tion. The breath of patients who have ingested isopropa-
12 24 h is followed by metabolic acidosis and impaired nol has a characteristic acetone-like odor (Somerville and
visual function. Coma, other CNS signs, and death Plumlee, 1996). Treatment is supportive and includes
(20 30 h) may follow after significant exposures. fluids, correction of acid-base abnormalities, and assisted
Laboratory findings in primates include hyperosmolality, respiration, if necessary (Oehme and Kore, 2006).
increased anion gap, and severe metabolic acidosis Hemodialysis is effective in removing isopropanol and