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44.e2 Alcohol Intoxication (Ethanol, Isopropyl Alcohol, and Methanol)

Alcohol Intoxication (Ethanol, Isopropyl Alcohol, and Methanol)
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chain and a hydroxyl group miscible with
BASIC INFORMATION
water, ether, and chloroform. TREATMENT
Definition Mechanism of toxicosis: Treatment Overview
Acute toxicosis associated with accidental • Hypothesized mechanism of action: dis- Induce emesis if asymptomatic and ingestion
ingestion of alcoholic beverages, alcohol-con- solution of lipid biomembranes affecting < 30 minutes prior, and stabilize patients that
taining household products (windshield wiper ion channels and their proteins, causing are showing clinical signs. Provide supportive
fluid), liquid medications, perfumes, or bread CNS depression. Ethanol can also augment care until alcohol is metabolized and eliminated
dough (enteric fermentation) is characterized gamma-aminobutyric acid–mediated synaptic from the body.
by vomiting, lethargy, ataxia, weakness, coma, inhibition and changes in chlorideions.
and acidosis. Improper dosing or rate of • Ethanol is metabolized by alcohol dehydro- Acute General Treatment
administration of ethanol for ethylene glycol genase to acetaldehyde, then acetate. Decontamination of the patient (p. 1087):
toxicosis can also result in ethanol toxicosis. • Isopropanol is converted to acetone, then • Emesis indicated in patients within 30
to acetate, formate, and carbon dioxide. minutes of exposure if not showing clinical
Synonyms • Methanol in nonprimates is metabolized by signs of toxicosis
• Ethanol: grain alcohol, ethyl alcohol catalase peroxidase to formaldehyde, then • Activated charcoal is not recommended
• Isopropyl alcohol: rubbing alcohol (70% to formate, and then to carbon dioxide and because it does not bind well to ethanol.
isopropanol) water. Primates metabolize methanol by The risk of aspiration is significant because
• Methanol: wood alcohol, Manhattan or alcohol dehydrogenase to formaldehyde, then vomiting is frequently seen in toxicosis.
colonial spirit to formate, carbon dioxide, and water. Supportive care:
Primates accumulate formate because of low • Fluid diuresis: isotonic fluids if normogly-
Epidemiology levels of tissue folate, leading to acidosis and cemia. If hypoglycemia is present, use
SPECIES, AGE, SEX ocular toxicosis (blindness). dextrose-containing fluids (e.g., 2.5% dex-
• Dogs and cats of both sexes and all breeds trose: add 50 mL of 50% dextrose per liter
and ages are susceptible. DIAGNOSIS of fluids) and add B vitamins.
• Dogs are more likely to ingest alcoholic • Mechanical ventilation may be necessary in
beverages or alcohol-containing household Diagnostic Overview comatose patients.
products. A tentative diagnosis is based on history of • Thermoregulation (judicious rewarming for
exposure and appropriate clinical signs (seda- hypothermia)
GEOGRAPHY AND SEASONALITY tion, ataxia, vomiting). • Cardiovascular support: monitor ECG and
Toxicosis more likely to occur in winter months perfusion. If ventricular arrhythmias are
(windshield washer fluid) and during holiday Differential Diagnosis present, check serum potassium and other
season (alcoholic beverages and holiday baking) • Ethylene glycol intoxication possible triggers (pp. 1033 and 1457).
• Marijuana intoxication • Yohimbine (0.1 mg/kg IV) or naloxone
ASSOCIATED DISORDERS • Uremia (0.02-0.04 mg/kg IV) may help reverse
Gastric dilation +/− volvulus possible when • Diabetic ketoacidosis alcohol-induced coma.
ethanol is from fermentation (e.g., bread dough • Hepatic encephalopathy Correct acid-base abnormalities:
−
ingestion) • Medications including opiates, benzodiaz- • Correct acidosis if severe (HCO 3 <
epines, barbiturates 12 mEq/L) and persistent despite rehydration
Clinical Presentation • Primary CNS disease (inflammation, neo- and good perfusion. Sodium bicarbonate
HISTORY, CHIEF COMPLAINT plasia, other) 1-3 mEq/kg IV as needed
• History of exposure to alcohol-containing
beverage or household products or circum- Initial Database Possible Complications
stances favoring exposure (e.g., recent social • CBC: generally unremarkable • Aspiration pneumonia
gathering without supervision of the pet) • Serum chemistry profile: some electrolyte • Acute kidney injury associated with myo-
• Acute vomiting, lethargy, central nervous abnormalities and azotemia possible second- globinuria (rare)
system (CNS) depression, ataxia, disorientation, ary to vomiting and dehydration; hypo- • Acute hepatic injury (rare)
vocalization, or excitability (“drunkenness”) glycemia may be present
• In severe cases, dyspnea, tremors, seizures, • Urinalysis: generally unremarkable Recommended Monitoring
and coma are possible. • Blood gas analysis: may be consistent with Acid-base status, ECG, blood pressure, heart
metabolic acidosis, often with a high anion rate, temperature, blood glucose
PHYSICAL EXAM FINDINGS gap (>25 mEq/L)
• Vomiting, signs of abdominal pain • Serum osmolality: may be increased (osmole PROGNOSIS & OUTCOME
• Hypotension gap > 20 mOsm/kg); major differential
• Tachycardia diagnosis is ethylene glycol intoxication Good prognosis in most cases; fair if
• CNS depression, ataxia, vocalization, dis- • Electrocardiogram (ECG): may reveal cardiac complications
orientation, or coma arrhythmias (p. 1096)
• Dehydration • Arterial blood pressure: rule out hypotension PEARLS & CONSIDERATIONS
• Hypothermia (p. 1065)
Comments
Etiology and Pathophysiology Advanced or Confirmatory Testing • Ethanol: oral lethal dose in dogs is 5.5-7.9 g/
Source: Serum or blood alcohol levels can be kg 100% ethanol
• Alcohols are transparent, colorless, mobile, requested from a human hospital to confirm • Methanol causes blindness and neuronal
volatile liquids composed of a hydrocarbon exposure. necrosis in primates. This is not an issue in

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