Alcohols are readily absorbed across the GI tract and skin. Alcohol intoxication can rapidly result in inebriation, metabolic acidosis, hypothermia, and CNS depression. Severe cases can result in coma, seizures, or death. There is no specific antidote; treatment entails attending to life-threatening clinical signs and providing supportive care.
Alcohols are readily absorbed across the GI tract and skin, where they can rapidly result in inebriation, metabolic acidosis, hypothermia, and CNS depression. Severe cases of alcohol intoxication can result in coma, seizures, or death. Blood alcohol concentrations can be determined, but in clinical practice they rarely are.
For toxicosis from ethylene glycol, see Ethylene Glycol Toxicosis.
Etiology of Alcohol Toxicoses in Animals
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, some alcohol-based hand sanitizers, and fermenting bread dough. Methanol is most commonly found in windshield washer fluids (sometimes known as "windshield antifreeze").
Alcohols are GI irritants, and ingestion can 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 can 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 the osmolal gap.
Hypothermia can develop as a result of peripheral vasodilation, CNS depression, and interference with thermoregulatory mechanisms. Hypoglycemia develops secondary to the alcohol-induced depletion of pyruvate, resulting in the inhibition of gluconeogenesis.
Toxicokinetics of Alcohol Toxicoses in Animals
Absorption: All alcohols are rapidly absorbed via the GI tract, and most are well absorbed through the skin. Toxicosis resulting from overspraying pets with alcohol-based flea sprays is not uncommon.
Pearls & Pitfalls
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Distribution: Alcohols reach peak plasma concentrations within 1.5–2 hours and are widely distributed throughout the body.
Metabolism: Alcohols 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 carbon dioxide. In humans 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 observed in primates.
Elimination: Alcohols are eliminated via the urine as parent compounds and as metabolites. In dogs, up to 50% of a dose of methanol can be eliminated, unchanged, via the lungs.
Lethal dose: The lethal oral dose of methanol in dogs is 4–8 mL/kg; however, notable clinical signs can occur at lower doses. Isopropanol is twice as toxic as ethanol and is found in rubbing alcohols, in some alcohol-based hand sanitizers, and in alcohol-based flea sprays for pets. An oral dose of isopropanol ≥ 0.5 mL/kg can result in serious clinical signs in dogs.
Clinical Findings of Alcohol Toxicoses in Animals
Clinical signs of alcohol toxicosis generally begin within 30–60 minutes after ingestion and include vomiting, diarrhea, ataxia, disorientation (inebriation), lethargy, tremors, and dyspnea. Severe cases can progress to coma, hypothermia, seizures, bradycardia, and respiratory depression. Death is generally due to respiratory failure, hypothermia, hypoglycemia, or metabolic acidosis. Pneumonia secondary to the aspiration of vomitus is possible.
Diagnosis of Alcohol Toxicoses in Animals
Clinical evaluation
Blood alcohol concentrations
Alcohol toxicosis is generally diagnosed on the basis of a history of exposure and compatible clinical signs. Determining blood alcohol concentrations can help to confirm the diagnosis.
Treatment of Alcohol Toxicoses in Animals
Control of life-threatening clinical signs
Supportive care
Stabilization of patients with severe clinical signs of alcohol toxicosis 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.
Provided that clinical signs have not yet developed, induction of emesis can be beneficial in the first 20–40 minutes 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 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 administered to stimulate respiration in comatose dogs with alcohol toxicosis.
Key Points
Alcohols are quickly absorbed from the GI tract, resulting in the rapid onset of clinical signs and a short window of opportunity for decontamination after ingestion.
Alcohol toxicosis results in notable metabolic and CNS disturbance, including inebriation, hypothermia, and CNS depression.
Most cases of alcohol toxicosis respond well to appropriate supportive care.
For More Information
Also see pet owner content regarding alcohol poisoning.
