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Veterinarian Technician April 2013 (Vol 34, No 4)

Toxicology Brief: Ethanol Toxicosis in Dogs

by Carrie Lohmeyer-Mauzy, CVT, BS

    Ethanol (ethyl alcohol) is a type of alcohol commonly found in alcoholic beverages (i.e., beer, wine, and spirits).1 Depending on the type of beverage, the concentration of ethanol can be 4% to 40% or higher. Ethanol is used as a solvent in perfumes and cosmetics and can be found in oral hygiene rinses, windshield-washer fluids, glass and multisurface cleaners (1% to 10% ethanol), hand sanitizers, and antifreeze.2–4 Ethanol is produced by yeast when bread dough rises.5 Pets can be exposed to ethanol by consuming any of the products mentioned above. Ethanol is also used to treat ethylene glycol toxicosis in veterinary patients.6

    After ingestion, ethanol is rapidly absorbed from the gastrointestinal tract, possibly resulting in clinical signs within 1 hour after exposure.1,7 Once clinical signs develop, they can last up to 12 hours or longer, depending on the amount of the product ingested and the concentration of ethanol.8 Ethanol is metabolized in the liver and excreted unaltered in the breath, urine, and feces.4 Ethanol toxicosis can cause severe central nervous system (CNS) depression, coma, and acidosis in dogs. The depressant effects are thought to be due to the sensitivity of certain ion channels and proteins in the CNS.7 Common clinical signs of ethanol toxicosis are lethargy, sedation, depression, ataxia, gastrointestinal signs (vomiting and diarrhea), disorientation, respiratory depression, vocalization, coma, and seizures. Diagnostic findings include hypothermia, acidosis, hypoglycemia, and hypotension.


    Management of ethanol toxicosis consists of early decontamination and good supportive care. Because clinical signs can be observed within minutes of the initial exposure, decontamination through emesis is only indicated in healthy asymptomatic patients within 30 minutes of ethanol exposure. Although the use of activated charcoal is recommended by many clinicians, its efficacy is questionable. Activated charcoal is associated with a high risk of aspiration, especially in symptomatic patients (those that are comatose or vomiting), and it is hypothesized that activated charcoal may not be effective at binding ethanol due to the small size of ethanol molecules.1,3

    For patients exposed to ethanol, the recommended laboratory work may include a complete blood count, a blood chemistry profile, and a blood gas analysis to detect dehydration, hypoglycemia, acidosis, and anoxia. To determine whether ethanol exposure has occurred, a veterinary patient’s blood alcohol level can be checked at a human diagnostic laboratory, which may provide results more quickly than a veterinary diagnostic laboratory. Calculating the anion gap is effective for confirming exposure to ethanol.3 The patient’s heart rate, blood pressure, electrocardiogram, and temperature should be monitored to detect reflex tachycardia, hypotension, premature ventricular contractions, and hypothermia.

    Isotonic solutions such as lactated Ringer solution, Normosol-R (Hospira, Inc., Lake Forest, IL), or Plasma-Lyte (Baxter Healthcare Corporation, Deerfield, IL) may need to be administered intravenously at two times the maintenance rate for supportive care. The fluid rate may need to be adjusted if hypotension develops. Dextrose and sodium bicarbonate can be added to the fluids if hypoglycemia or acidosis is expected or confirmed.

    In cases involving cardiac arrest, epinephrine can be used. Valium is generally effective for managing seizures. Lidocaine can be used to treat premature ventricular contractions. In comatose patients or patients with severe respiratory depression, yohimbine or naloxone can be tried as a possible reversal agent.4,5 Comatose patients may require mechanical ventilation. Endotracheal intubation is recommended to help decrease the risk of aspiration.

    Case Study

    A 1-year-old, 7-lb, spayed miniature dachshund ingested 7 oz of a mixed beverage containing soda and whiskey. The patient started showing clinical signs approximately 20 minutes after exposure: depressant effects progressed to recumbency, nonresponsiveness, miosis, vomiting, and hypothermia (97.0°F; normal: 100.5°F to 102.5°F) in less than 1 hour.

    Treatment of ethanol toxicosis began at an emergency clinic 45 minutes after the initial ingestion. The patient was administered intravenous fluids containing dextrose and B vitamins as well as a dose of naloxone. (In cases involving severe depression, dextrose can be given to help maintain blood sugar; B vitamins were administered because ethanol decreases thiamine absorption.) Body temperature was monitored, and warming devices were used as needed. Blood pressure and oxygen saturation were monitored. Blood glucose and blood gases were monitored for hypoglycemia and acidosis, respectively.

    Ten hours after ethanol exposure, the patient was sternal and responsive, with a body temperature of 99.5°F, but signs of ataxia and depression were still evident. Supportive and symptomatic care continued for 4 hours until the patient was stable enough to be discharged from the hospital. The patient recovered fully.

    The Technician’s Role

    To help manage patients with acute ethanol intoxication, veterinary technicians may be responsible for obtaining a toxicologic history and implementing supportive care. A toxicologic history involves obtaining the client’s name and contact information, the patient’s signalment and clinical status at presentation, information on the toxic agent, and the exposure history (i.e., the source of ethanol, the product’s brand name, the concentration of ethanol, the amount ingested, the time of exposure, the onset time of clinical signs, signs observed by the owner, and home treatments). Because managing patients with ethanol toxicosis largely involves supportive care, technicians should closely monitor the patient’s heart rate, blood pressure, hydration status, respiration, electrocardiogram, body temperature, and overall clinical progress and status. Significant changes should be reported to the attending veterinarian.

    Ms. Lohmeyer-Mauzy is employed by the ASPCA Animal Poison Control Center, Urbana, Illinois.

    1. Thrall MA, Hamar DW. Alcohols and glycols. In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. New York, NY: Elsevier; 2007:605-606.

    2. Spyker DA, Sullivan JB. Oxygenated compounds: alcohols, glycols, ketones and esters. In: Sullivan JB, Krieger GR, eds. Hazardous Materials Toxicology. Baltimore, MD: Williams and Wilkins; 1992:1105-1106.

    3. Brutlag AG. Chemical toxicities. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Saunders and Elsevier; 2010:571-572.

    4. Ethanol. POISINDEXSystem[intranet database]. Version 5.1. Greenwood Village, CO: Thomson Reuters (Healthcare).

    5. Means C. Bread dough toxicosis in dogs. J Vet Emerg Crit Care 2003;13(1):39-41.

    6. Plumb DC. Ethanol, alcohol, ethyl, ethyl alcohol. In: Veterinary Drug Handbook. 5th ed. Ames, IA: Blackwell Publishing; 2005:314.

    7. Fleming M, Mihic SJ, Harris RA. Ethanol. In: Brunton LL, Lazo JS, Parker KL, eds. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. New York, NY: McGraw-Hill; 2006:592-593, 600.

    8. Unpublished data. ASPCA Animal Poison Control Center.

    References »

    NEXT: Case Report: Pyelonephritis and Chronic Renal Insufficiency in a Cat


    Did you know... After ingestion, ethanol is rapidly absorbed from the gastrointestinal tract, possibly resulting in clinical signs within 1 hour after exposure.Read More

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