Alcohol toxicosis results in metabolic acidosis, hypothermia,
and CNS depression. All species are susceptible.
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). 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
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.
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.
Last full review/revision May 2013 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT