Alcohol toxicosis results in metabolic acidosis, hypothermia, and CNS depression. All species are susceptible.
Etiology:
Ethanol, methanol, and isopropanol are the alcohols most frequently associated with toxicosis in companion animals. Ethanol is present in a variety of alcoholic beverages, some rubbing alcohols, drug elixirs, and fermenting bread dough ( see Bread Dough Toxicosis in Animals). Methanol is most commonly found in windshield washer fluids (windshield “antifreeze”). The lethal oral dose of methanol in dogs is 4–8 mL/kg, although significant clinical signs may be seen at lower dosages. Isopropanol is twice as toxic as ethanol and is found in rubbing alcohols and in alcohol-based flea sprays for pets. Oral dosages of isopropanol ≥0.5 mL/kg may result in significant clinical signs in dogs.
Pathogenesis:
All alcohols are rapidly absorbed via the GI tract and most are well absorbed dermally; toxicosis from overspraying pets with alcohol-based flea sprays is not uncommon. Alcohols reach peak plasma levels within 1.5–2 hr and are widely distributed throughout the body. They are metabolized in the liver to acetaldehyde (ethanol), formaldehyde (methanol), and acetone (isopropanol); these intermediate metabolites are then further converted to acetic acid, formic acid, and/or carbon dioxide. (In people and some other primates, accumulation of formic acid after methanol ingestion results in retinal and neuronal damage; nonprimates are efficient at eliminating formic acid and therefore do not develop the blindness and cerebral necrosis seen in primates.) Alcohols are eliminated via the urine as parent compound as well as metabolites. In dogs, up to 50% of a dose of methanol may be eliminated unchanged via the lungs.
Alcohols are GI irritants, and ingestion may result in vomiting and hypersalivation. Alcohols and their metabolites are potent CNS depressants, affecting a variety of neurotransmitters within the nervous system. Metabolites such as acetaldehyde may stimulate the release of catecholamines, which can affect myocardial function. Metabolic acidosis results from the formation of acidic intermediates, and both parent compounds and metabolites contribute to increases in osmolal gap. Hypothermia may develop due to peripheral vasodilation, CNS depression, and interference with thermoregulatory mechanisms. Hypoglycemia develops secondary to alcohol-induced depletion of pyruvate, resulting in inhibition of gluconeogenesis.
Clinical Findings and Diagnosis:
Signs generally begin within 30–60 min of ingestion and include vomiting, diarrhea, ataxia, disorientation (inebriation), depression, tremors, and dyspnea. Severe cases may progress to coma, hypothermia, seizures, bradycardia, and respiratory depression. Death is generally due to respiratory failure, hypothermia, hypoglycemia, and/or metabolic acidosis. Pneumonia secondary to aspiration of vomitus is possible.
The determination of blood alcohol levels may help to confirm the diagnosis of alcohol intoxication.
Treatment:
Stabilization of severely symptomatic animals is a priority. Adequate ventilation should be maintained, and cardiovascular and acid-base abnormalities should be corrected. Seizures can be controlled with diazepam (0.5–2 mg/kg, IV) as needed. For asymptomatic animals, induction of emesis may be of benefit in the first 20–40 min after ingestion. Activated charcoal is not thought to appreciably bind small-chain alcohols and is not often recommended. Bathing with mild shampoo is recommended for significant dermal exposures. Supportive care, including thermoregulation and fluid diuresis to enhance alcohol elimination, should be administered. Anecdotally, yohimbine (0.1 mg/kg, IV) has been used to stimulate respiration in severely comatose dogs with alcohol toxicosis.
