Page 683 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

648 SECTION | IX Gases, Solvents and Other Industrial Toxicants

VetBooks.ir beverages. Ethanol toxicosis in dogs has been associated (BEC). Clinical signs include ataxia, lethargy, sedation,
hypothermia, metabolic acidosis, vomiting, diarrhea, and
with ingestion of bread dough (Thrall et al., 1984a; Suter,
poor breathing (Kovalkovicova et al., 2009). Levels of
1992; Means, 2003). Uncooked bread dough contains
Saccharomyces cerevisiae (common brewer’s and baker’s 2 4 mg/mL in adult dogs have produced clinical signs
yeast) that metabolizes carbohydrate substrates to ethanol ranging from ataxia and coma (Valentine, 1990). The
and carbon dioxide. Ethanol poisoning in dogs has also time of onset of clinical signs is dependent on the dose
been associated with rotten apples (Kammerer et al., 2001) ingested and the amount of food present in the GI tract,
and alcoholic beverages (van Wuijckhuise and Cremers, but it usually occurs within an hour of ingestion.
2003). Ethanol is also an ingredient in many liquid formula-
tions of various medications; some products contain as Mechanism of Action
much as 25% ethanol (Papich, 1990). Although it is
The mechanism of action of alcohol on the CNS is related
unlikely that a pet would ingest enough ethanol from these
in part to its interactions with biomembranes and its prob-
preparations to produce ethanol toxicosis, the alcohol may
able inhibition of gamma-aminobutyric acid receptors
augment the depressive effects of other ingredients. Ethanol
(Valentine, 1990).
toxicosis can also occur in dogs and cats when ethanol is
given intravenously (i.v.) as a competitive substrate to treat
EG toxicosis (Thrall et al., 1998). Ethanol intoxication was Diagnosis and Treatment
also reported in a litter of 6-week-old puppies shampooed
A diagnosis can be made based on history, clinical signs,
with an alcohol-based detergent (Del Mar, 1984). The increased plasma osmolality and osmole gap, metabolic
median lethal dose (LD 50 ) of 100% ethanol in dogs is acidosis, and BEC. If rapid BEC cannot be obtained, the
4.1 4.9 g/kg after ingestion (Du Jardin-Beaumet, 1875). animal has to be treated based on clinical signs. It is
important to differentiate EG toxicosis from alcohol toxi-
cosis as the clinical signs and early laboratory findings
Toxicokinetics can be similar. However, patients with EG toxicosis must
Ethanol is rapidly absorbed from the gastrointestinal (GI) be given ADH inhibitors such as 4-methylpyrazole to pre-
tract; the rate of absorption can be slowed by the presence vent the formation of toxic metabolites, whereas patients
of food in the stomach or small intestine. Most of the eth- with ethanol toxicosis can be treated supportively. Heart
anol is metabolized in the liver to acetaldehyde (a toxic and respiratory rate should be monitored. Respiratory
metabolite) by ADH and then to acetate by aldehyde depression may require the administration of Doxapram
dehydrogenase (Fig. 49.1). The end products of ethanol (a respiratory stimulant) or in severe cases mechanical
metabolism are carbon dioxide and water. ventilation. Emesis should not be induced in dogs or cats
Clinical findings in dogs and cats with ethanol intoxi- with severe ataxia or CNS depression as the animal could
cation can be correlated with blood ethanol concentration become recumbent or comatose quickly and aspiration

FIGURE 49.1 Pathways of formation of toxic meta-
bolites for methanol, ethanol, and isopropyl alcohol.