Emergency Veterinary Toxicology Reference

How to Use This Reference

This emergency toxicology reference is designed for rapid clinical lookup during initial triage and stabilization of toxin-exposed patients. It covers the 20 most commonly encountered pet toxin exposures in small-animal practice, organized by category: food-based, medications, plants and environmental agents, and household chemicals.

For each toxin you will find the toxic dose threshold (where established), time to onset of clinical signs, key symptoms to monitor, and first-line treatment protocols. The decontamination and antidote sections provide quick-reference dosing for emergency procedures.

Navigation tip: Use the table of contents on the left (desktop) or above (mobile) to jump directly to the toxin category or protocol you need. Each toxin entry is self-contained so you can reference it independently during a case.

Initial Triage Protocol

When a toxin-exposed patient presents, follow a structured triage approach before focusing on the specific substance. The first minutes are critical for determining whether decontamination is still viable and whether the patient requires immediate stabilization.

Step 1: Stabilize the Patient (ABCs)

Assess Airway, Breathing, and Circulation before all else. Secure the airway if the patient is obtunded or actively seizing. Establish IV access early, as many toxicoses require aggressive fluid therapy, and having a patent catheter allows rapid administration of anticonvulsants, antidotes, or vasopressors if needed.

• Seizures: Diazepam 0.5-1 mg/kg IV or midazolam 0.1-0.3 mg/kg IM/IN as first-line seizure control.
• Bradycardia: Atropine 0.02-0.04 mg/kg IV if symptomatic bradycardia present (oleander, organophosphates).
• Hypotension: Isotonic crystalloid bolus 10-20 mL/kg IV over 15-20 minutes, repeat as needed.

Step 2: Obtain a Targeted History

Gather the following information as quickly as possible from the owner while the patient is being stabilized:

• Substance: Exact product, including brand name if available. Have the owner bring the packaging or take a photo.
• Amount: How much was ingested, applied, or inhaled? Even a rough estimate helps calculate toxic dose.
• Time since exposure: This determines whether decontamination (emesis, activated charcoal) is still within the effective window.
• Body weight: Essential for toxic dose calculation. Weigh the patient if the owner is unsure.
• Species and breed: Some toxins have species-specific effects (acetaminophen in cats, xylitol primarily in dogs) and certain breeds have known sensitivities (e.g., MDR1 mutation in collies).

Step 3: Determine the Decontamination Window

For most oral ingestions, decontamination via emesis is most effective within 1 to 2 hours of ingestion. After 2 hours, most of the substance has transited the stomach and emesis yields diminishing returns. Activated charcoal can be considered up to 4-6 hours post-ingestion for substances that undergo enterohepatic recirculation. See the Decontamination Protocols section for specific agents and dosing.

Step 4: Calculate the Toxic Dose

Determine whether the estimated exposure exceeds the published toxic dose threshold for the specific substance. For substances with established dose-response relationships (chocolate, NSAIDs, xylitol), this calculation helps guide triage decisions. For idiosyncratic toxins (grapes and raisins), any ingestion warrants treatment regardless of amount.

Food-Based Toxins

Chocolate (Theobromine / Caffeine)

Chocolate toxicosis is the most commonly reported canine poisoning in North America. The toxic component is theobromine (and to a lesser extent caffeine), with concentration varying dramatically by chocolate type.

• Cocoa powder / baking chocolate: 130-450 mg theobromine/oz. Toxic dose: approximately 0.5 oz/lb body weight (1 oz/kg). This is the most dangerous form.
• Dark chocolate (60-70% cacao): 150-160 mg theobromine/oz. Toxic dose: approximately 1-1.5 oz/lb.
• Milk chocolate: 44-64 mg theobromine/oz. Toxic dose: approximately 3-4 oz/lb. Large amounts needed for severe signs.
• White chocolate: Negligible theobromine (0.25 mg/oz). Not a methylxanthine risk but high fat content poses pancreatitis risk.

Onset: 6-12 hours. Clinical signs: Vomiting, diarrhea, hyperactivity, polydipsia, polyuria, tachycardia, muscle tremors, hyperthermia. At high doses: seizures, cardiac arrhythmias, death.

Treatment: Induce emesis if within 2 hours of ingestion. Administer activated charcoal (1-2 g/kg PO) — repeated doses every 4-6 hours may be beneficial as theobromine undergoes enterohepatic recirculation. IV fluid therapy to support renal excretion. Diazepam for seizures. Monitor ECG for arrhythmias. Theobromine half-life in dogs is approximately 17.5 hours, so clinical signs may persist 24-72 hours.

Xylitol (Birch Sugar / Sugar Alcohol)

Xylitol is an increasingly common sugar substitute found in sugar-free gum, candies, baked goods, peanut butter, and dental products. It is profoundly toxic to dogs but does not appear to cause the same effects in cats.

• Hypoglycemia dose: >0.1 g/kg (100 mg/kg). A single piece of xylitol gum may contain 0.3-1.0 g of xylitol.
• Hepatotoxicity dose: >0.5 g/kg (500 mg/kg). Liver failure typically develops 24-72 hours post-ingestion.

Onset: Hypoglycemia within 30-60 minutes (can be as rapid as 10 minutes). Hepatic failure: 24-72 hours.

Clinical signs: Vomiting, weakness, ataxia, collapse, seizures (from hypoglycemia). With hepatotoxic doses: icterus, coagulopathy, hepatic encephalopathy.

Treatment: Check blood glucose immediately. If hypoglycemic: dextrose bolus (0.5-1 mL/kg of 50% dextrose IV, diluted 1:3 with sterile saline). Maintain on dextrose-supplemented fluids (2.5-5% dextrose CRI). Monitor blood glucose every 1-2 hours for 12-24 hours. For hepatotoxic doses: liver protectants (SAMe, silymarin), monitor liver enzymes, PT/PTT, and bilirubin every 12-24 hours. Prognosis for uncomplicated hypoglycemia is good with prompt treatment. Prognosis for hepatic failure is guarded to poor.

Grapes and Raisins

Grape and raisin toxicosis causes acute kidney injury (AKI) in dogs. The toxic principle was recently identified as tartaric acid and potassium bitartrate, which explains the variable toxicity between grape cultivars. Cats and ferrets may also be susceptible.

• Toxic dose: Not reliably established due to individual and cultivar variability. Some dogs develop AKI after ingesting as few as 4-5 grapes, while others tolerate larger quantities. All ingestions should be treated as potentially toxic.
• Raisins: More concentrated than grapes — a smaller quantity carries higher risk.

Onset: Vomiting within 6-12 hours. AKI signs at 24-72 hours. Clinical signs: Vomiting, diarrhea, lethargy, anorexia, abdominal pain, oliguria/anuria, elevated BUN and creatinine.

Treatment: Induce emesis if within 2 hours. Activated charcoal (1-2 g/kg). Aggressive IV fluid diuresis at 2-3x maintenance for 48-72 hours. Monitor renal values (BUN, creatinine, phosphorus), urine output, and electrolytes every 12-24 hours. If oliguric/anuric AKI develops, consider peritoneal dialysis or hemodialysis if available. Prognosis with early, aggressive treatment is generally good; prognosis with established anuric renal failure is poor.

Onions and Garlic (Allium Species)

All members of the Allium genus (onions, garlic, leeks, chives, shallots) contain organosulfur compounds that cause oxidative damage to red blood cells, leading to Heinz body formation and hemolytic anemia. Cats are more sensitive than dogs.

• Toxic dose (dogs): >15-30 g/kg for onions. Garlic is approximately 5 times more concentrated than onions on a per-gram basis.
• Toxic dose (cats): >5 g/kg. Cats have higher susceptibility due to their hemoglobin structure.

Onset: Clinical anemia typically develops 3-5 days post-ingestion (delayed). Clinical signs: Lethargy, pale or icteric mucous membranes, tachycardia, tachypnea, hemoglobinuria (red-brown urine), vomiting, diarrhea.

Treatment: Emesis if recent ingestion. Activated charcoal. Monitor CBC with reticulocyte count and blood smear for Heinz bodies daily for 5-7 days. Transfusion if PCV drops below 15-18% or the patient is hemodynamically unstable. IV fluid support. Most cases resolve with supportive care over 1-2 weeks as red blood cells regenerate.

Macadamia Nuts

Macadamia nut toxicosis is reported exclusively in dogs. The toxic mechanism is unknown. The condition is generally self-limiting.

• Toxic dose: >2.4 g/kg. Clinical signs typically appear after ingestion of 2-60 g/kg.

Onset: 6-24 hours. Clinical signs: Weakness (especially hind limb), vomiting, ataxia, tremors, hyperthermia, joint swelling or pain.

Treatment: Largely supportive. IV fluids, anti-emetics if vomiting persists, pain management (avoid NSAIDs if concurrent chocolate ingestion). Most dogs recover fully within 24-48 hours. If co-ingested with chocolate (common in macadamia chocolate products), treat for both toxicoses.

Medication Toxins

NSAIDs (Ibuprofen, Naproxen)

Over-the-counter NSAIDs are among the most frequently ingested human medications by pets. Ibuprofen and naproxen are the most commonly involved. Dogs are more frequently affected, but cats are far more sensitive on a per-kilogram basis.

• Ibuprofen toxic doses (dogs): GI effects at >25 mg/kg, renal effects at >100 mg/kg, CNS effects at >400 mg/kg, potentially fatal at >600 mg/kg.
• Cats: Toxic at much lower doses due to impaired glucuronidation. As little as 50 mg total can be toxic.

Clinical signs: Vomiting (often hematemesis), melena, abdominal pain, anorexia, lethargy. At higher doses: acute kidney injury, seizures, coma.

Treatment: Decontamination if within 2 hours. GI protectants (sucralfate 0.5-1 g PO q8h, omeprazole 1 mg/kg PO/IV q12-24h). IV fluid therapy to protect renal function. Monitor BUN, creatinine, and fecal occult blood. Serial abdominal imaging if GI perforation suspected.

Acetaminophen (Paracetamol / Tylenol)

Acetaminophen is extremely dangerous in cats and can also cause serious toxicity in dogs at higher doses. Cats lack adequate glucuronyl transferase activity, making them exquisitely sensitive.

• Cats: Toxic at >10 mg/kg. A single regular-strength tablet (325 mg) can be fatal in an average cat.
• Dogs: Hepatotoxicity at >100 mg/kg, methemoglobinemia at >200 mg/kg.

Clinical signs (cats): Methemoglobinemia (chocolate brown mucous membranes, cyanosis), facial and paw edema, respiratory distress, depression, death. Dogs: hepatotoxicity (vomiting, icterus, elevated liver enzymes) at moderate doses; methemoglobinemia at higher doses.

Treatment: N-acetylcysteine (NAC) is the specific antidote: loading dose 140 mg/kg PO or IV, then 70 mg/kg q6h for 5-7 additional treatments. Ascorbic acid (vitamin C) 30 mg/kg PO/IV q6h as adjunctive methemoglobin reducer. SAMe for hepatoprotection. Oxygen supplementation. Monitor methemoglobin levels, liver enzymes, and coagulation.

Human SSRIs (Sertraline, Fluoxetine, Citalopram)

Selective serotonin reuptake inhibitors are commonly prescribed human antidepressants. Ingestion by pets can cause serotonin syndrome, a potentially life-threatening condition.

Clinical signs of serotonin syndrome: Agitation, vomiting, diarrhea, hyperthermia, tachycardia, tremors, myoclonus, hyperreflexia, dilated pupils, seizures. Signs can appear within 1-4 hours of ingestion.

Treatment: Decontamination if recent. Cyproheptadine (serotonin antagonist) 1.1 mg/kg PO or rectally in dogs, 2-4 mg/cat PO q4-6h as needed. IV fluids. Active cooling if hyperthermic (target temp <103.5 F). Methocarbamol 55-220 mg/kg IV for severe tremors. Benzodiazepines for seizures. Monitor for 24-72 hours.

Benzodiazepines (Alprazolam, Diazepam, Lorazepam)

Benzodiazepine ingestion causes CNS and respiratory depression. While rarely fatal as a sole ingestion, significant CNS depression can lead to aspiration or respiratory compromise.

Clinical signs: Profound sedation, ataxia, weakness, disorientation, respiratory depression. Paradoxical agitation or dysphoria can occur in some animals.

Treatment: Flumazenil 0.01-0.02 mg/kg IV is the specific reversal agent (onset 1-2 minutes). Use cautiously — redosing may be necessary as flumazenil has a shorter duration than most benzodiazepines. Supportive care: maintain airway, oxygen supplementation, IV fluids, monitor respiratory rate and oxygen saturation. Most cases resolve within 12-24 hours.

ADHD Medications (Amphetamines, Methylphenidate)

Prescription stimulants (Adderall, Ritalin, Vyvanse, Concerta) are increasingly common in households and represent a serious ingestion risk for pets. Extended-release formulations are particularly dangerous.

Clinical signs: Hyperactivity, agitation, tremors, tachycardia, hypertension, hyperthermia, mydriasis, seizures, cardiac arrhythmias. Extended-release formulations may cause prolonged (12-24 hour) duration of signs.

Treatment: Decontamination if recent and patient is not already showing CNS stimulation. Do not induce emesis if the patient is already agitated or hyperthermic. Acepromazine (0.05-0.1 mg/kg IM) or chlorpromazine for sedation. Benzodiazepines for seizures. Beta-blockers (propranolol 0.02 mg/kg IV slowly) for severe tachycardia. Active cooling. IV fluids. ECG monitoring for 12-24 hours (longer for extended-release).

Plant & Environmental Toxins

Lilies (Cats) — Lilium and Hemerocallis Species

True lily exposure is one of the most lethal toxicoses in feline medicine. All parts of the plant (petals, leaves, pollen, stem, and even the water in the vase) are nephrotoxic to cats. The toxic principle has not been definitively identified.

Onset: Vomiting within 1-3 hours. AKI develops at 24-72 hours. Clinical signs: Initial vomiting and depression, followed by apparent improvement, then progressive renal failure — anorexia, vomiting, polyuria transitioning to oliguria/anuria, dehydration, seizures.

Treatment: Induce emesis if within 2 hours. Activated charcoal (less proven efficacy for lily toxin but generally recommended). Aggressive IV fluid diuresis at 2-4x maintenance for a minimum of 48-72 hours. Monitor renal values every 12 hours. If oliguric/anuric renal failure develops despite fluids, hemodialysis is the only viable option. Prognosis is good if treatment begins within 6 hours; prognosis is poor to grave with established anuric renal failure.

Sago Palm (Cycas revoluta)

Sago palms are popular ornamental plants found in homes and yards throughout warmer climates. All parts are toxic, but the seeds (nuts) contain the highest concentration of cycasin, a potent hepatotoxin.

• Toxic dose: As little as 1-2 seeds can be fatal in a medium-sized dog. Mortality rates of 50% or higher are reported even with treatment.

Onset: GI signs within 15 minutes to several hours. Hepatotoxicity at 24-72 hours. Clinical signs: Vomiting (often bloody), diarrhea, abdominal pain, followed by icterus, hepatomegaly, coagulopathy (petechiae, ecchymoses, frank hemorrhage), hepatic encephalopathy, and DIC.

Treatment: Aggressive decontamination (emesis + multiple doses of activated charcoal). Hepatoprotectants (SAMe 20 mg/kg PO daily, silymarin 5 mg/kg PO q12h). IV fluids, anti-emetics, GI protectants. Monitor liver enzymes, bilirubin, glucose, and coagulation panels every 12 hours. Fresh frozen plasma or whole blood for coagulopathy. Prognosis is guarded even with aggressive therapy.

Marijuana / THC (Cannabis)

With increasing legalization, cannabis exposures in pets have risen sharply. Pets are most commonly exposed through edibles, which may also contain chocolate or xylitol (compounding the toxicity).

Clinical signs: CNS depression or agitation (dose dependent), ataxia, disorientation, mydriasis, hypersalivation, urinary incontinence, hypothermia, bradycardia. In severe cases: prolonged coma, respiratory depression, aspiration risk.

Treatment: Largely supportive. Anti-emetics if vomiting. IV fluids. Intralipid emulsion (1.5 mL/kg IV bolus, then 0.25 mL/kg/min CRI for 30-60 minutes) may be considered in severe cases, as THC is highly lipophilic. Maintain body temperature. Prevent aspiration in obtunded patients. Most cases resolve within 24-72 hours. Ask owners directly about cannabis exposure — many owners are reluctant to volunteer this information.

Mushrooms (Wild)

Wild mushroom toxicity ranges from mild GI upset to fatal hepatic and renal failure depending on the species. In practice, definitive species identification is often not possible, and a conservative approach is warranted.

• Amanita phalloides (Death Cap): Amatoxin causes delayed-onset (6-24 hours) severe hepatotoxicity. Mortality 50-90% without aggressive treatment.
• Inocybe / Clitocybe spp.: Muscarinic effects — SLUDDE signs (salivation, lacrimation, urination, defecation, dyspnea, emesis). Treat with atropine.
• Most yard mushrooms: Cause self-limiting GI upset (vomiting, diarrhea) within 1-6 hours.

Treatment: If species unknown, treat as potentially hepatotoxic. Decontamination, activated charcoal, IV fluids. Monitor liver enzymes, renal values, and coagulation at 12 and 24 hours. For confirmed Amanita: silymarin (silibinin) 20-50 mg/kg/day IV if available, high-dose penicillin G (300,000-1,000,000 U/kg/day IV), NAC, aggressive fluid support.

Oleander (Nerium oleander)

Oleander is an ornamental shrub containing cardiac glycosides (oleandrin, neriine) in all parts of the plant. Even small ingestions can cause life-threatening cardiac arrhythmias. Dried plant material retains toxicity.

Clinical signs: Vomiting, diarrhea, abdominal pain (early), followed by cardiac abnormalities — bradycardia, heart block (1st, 2nd, or 3rd degree), ventricular tachycardia, ventricular fibrillation. Hyperkalemia is common and contributes to cardiac dysfunction.

Treatment: Decontamination if recent. Activated charcoal (multiple doses due to enterohepatic recirculation). Atropine for symptomatic bradycardia (may require higher than standard doses).Digoxin-specific Fab antibody fragments (Digibind) are the definitive antidote — dose based on estimated glycoside load (typically 1-2 vials for small animals). Correct hyperkalemia with insulin/dextrose, calcium gluconate, and sodium bicarbonate. Continuous ECG monitoring for a minimum of 24 hours.

Household & Chemical Toxins

Rodenticides

Rodenticide toxicosis is one of the most common and dangerous household exposures. There are four major categories, each with a completely different mechanism and treatment:

1. Anticoagulant Rodenticides (brodifacoum, bromadiolone, warfarin, chlorophacinone): Inhibit vitamin K-dependent clotting factor synthesis. Onset of clinical bleeding is delayed 2-5 days as existing clotting factors are consumed.

• Signs: Lethargy, dyspnea, pallor, hematomas, hemothorax, hemoabdomen, hematuria, epistaxis, prolonged bleeding from wounds.
• Treatment: Vitamin K1 (phytonadione) 2.5-5 mg/kg PO q12h with a fatty meal (NOT vitamin K3). Duration: 30 days for second-generation anticoagulants. Check PT at 48 and 72 hours after discontinuing Vitamin K1 to confirm coagulation has normalized.

2. Bromethalin: Uncouples oxidative phosphorylation, causing cerebral edema. No specific antidote.

• Signs: Tremors, ataxia, seizures, paralysis, depression, coma. Onset 2-24 hours (high dose) or 1-5 days (lower dose).
• Treatment: Aggressive decontamination (emesis + multiple doses of activated charcoal q4-8h for 24 hours). Mannitol 0.5-1 g/kg IV for cerebral edema. Supportive care. Prognosis is guarded once neurological signs develop.

3. Cholecalciferol (Vitamin D3): Causes hypercalcemia and hyperphosphatemia, leading to renal failure and soft tissue mineralization.

• Signs: Polydipsia, polyuria, anorexia, vomiting, lethargy, AKI. Onset 12-36 hours.
• Treatment: Decontamination. Aggressive IV saline diuresis. Furosemide 2-4 mg/kg IV q8-12h to promote calciuresis. Prednisone 1-2 mg/kg PO q12h (reduces calcium absorption). Pamidronate 1.3-2 mg/kg IV over 4 hours for refractory hypercalcemia. Monitor ionized calcium, phosphorus, and renal values every 12 hours. Hypercalcemia may persist for weeks.

4. Zinc Phosphide: Reacts with gastric acid to release phosphine gas. Signs include vomiting, dyspnea, abdominal distension, cardiovascular collapse. Treatment is supportive; minimize staff exposure to phosphine gas from vomitus.

Ethylene Glycol (Antifreeze)

Ethylene glycol toxicosis carries one of the highest mortality rates of any small-animal poisoning. The sweet taste is attractive to pets. Treatment is time-critical.

• Minimum lethal dose: Dogs: 4.4 mL/kg. Cats: 1.4 mL/kg (extremely low — less than 1 teaspoon for a cat).

Three phases of toxicity:

1. Stage 1 (30 min - 12 hours): "Drunk" appearance — ataxia, PU/PD, vomiting, CNS depression.
2. Stage 2 (12-24 hours): Apparent improvement. Tachycardia, tachypnea developing. Calcium oxalate crystalluria on urinalysis.
3. Stage 3 (24-72 hours dogs, 12-24 hours cats): Oliguric/anuric renal failure. Bilateral renomegaly. Severe metabolic acidosis.

Treatment: Fomepizole (4-MP) is the preferred antidote: Dogs — 20 mg/kg IV initially, then 15 mg/kg IV at 12 and 24 hours, then 5 mg/kg IV at 36 hours. Cats — 125 mg/kg IV initially, then 31.25 mg/kg IV at 12, 24, and 36 hours. Must begin within 8 hours in dogs, 3 hours in cats for best outcomes. Ethanol (20% solution, 5.5 mL/kg IV q4h for 5 treatments, then q6h for 4 treatments) is an alternative when fomepizole is unavailable but causes significant CNS depression. Aggressive IV fluid diuresis. Correct metabolic acidosis with sodium bicarbonate. Monitor renal values, blood gas, and urinalysis (calcium oxalate crystals). Hemodialysis if available and renal failure established.

Button Batteries and Disc Batteries

Battery ingestion is a dual hazard: caustic alkaline burns from electrical current generation and heavy metal toxicity (zinc, lithium, manganese) from casing breakdown.

Clinical signs: Hypersalivation, dysphagia, oral pain, vomiting, hematemesis, melena, esophageal or GI perforation (with lodged batteries). Zinc toxicosis from penny or battery ingestion causes hemolytic anemia, pancreatitis, and organ failure.

Treatment: Radiograph to locate battery. If lodged in esophagus: emergent endoscopic removal. If in stomach and intact: endoscopic removal recommended before casing erodes. Do not induce emesis (risk of caustic re-exposure to esophagus). For zinc toxicosis: chelation with CaEDTA (25 mg/kg SC q6h) or succimer (10 mg/kg PO q8h for 10 days). IV fluids, GI protectants, blood transfusion if hemolytic anemia develops.

Essential Oils

The popularity of essential oil diffusers and topical products has increased pet exposure to concentrated plant oils. Cats are particularly vulnerable due to their lack of glucuronyl transferase activity, impairing metabolism of many phenolic and terpenoid compounds.

• High-risk oils for cats: Tea tree (melaleuca), peppermint, wintergreen, cinnamon, citrus (d-limonene), pine, eucalyptus, ylang-ylang, clove, pennyroyal.
• Signs: Drooling, vomiting, ataxia, tremors, respiratory distress, hepatotoxicity (elevated liver enzymes), hypothermia.

Treatment: Remove from source (ventilate room if diffuser exposure, bathe with dish soap if dermal exposure). IV fluids, liver protectants, anti-emetics, thermoregulation. Monitor liver enzymes for 72 hours. Most recover with supportive care. Caution owners against applying undiluted essential oils to pets or using diffusers in enclosed rooms with cats.

Cleaning Products (Alkalis and Acids)

Household cleaning agents cause chemical burns to the oral cavity, esophagus, and stomach. The management approach depends on whether the product is alkaline or acidic.

• Alkaline products (bleach, drain cleaners, oven cleaners, dishwasher pods): Cause liquefactive necrosis — deep, progressive tissue burns.
• Acidic products (toilet bowl cleaners, rust removers): Cause coagulative necrosis — typically more superficial.

Treatment: Dilution with water or milk if ingestion was very recent and the patient is cooperative (small amounts — do not force). GI protectants (sucralfate slurry). Pain management (opioids). NPO initially if significant oral burns present. Endoscopy within 12-24 hours to assess esophageal injury grade. Antibiotics if perforation suspected. Nutritional support (esophagostomy tube) may be needed for severe esophageal burns.

Decontamination Protocols

Inducing Emesis

Emesis is the first-line decontamination method for most oral ingestions when performed within the appropriate time window (generally 1-2 hours). Agent selection depends on species.

Dogs:

• Apomorphine: 0.03 mg/kg IV (preferred) or 0.04 mg/kg IM. Can also be placed in the conjunctival sac (0.25 mg/kg crushed tablet). Onset 2-5 minutes IV. Rinse conjunctival sac after emesis to prevent prolonged effect.
• Hydrogen peroxide 3%: 1-2 mL/kg PO (max 45 mL). Can repeat once if no emesis within 10-15 minutes. Less reliable than apomorphine. Do not use concentrations greater than 3%.

Cats:

• Dexmedetomidine: 7 mcg/kg IM. Induces reliable emesis in approximately 90% of cats within 5-10 minutes. Can be reversed with atipamezole after emesis is complete.
• Apomorphine is not reliable for inducing emesis in cats. Hydrogen peroxide is not recommended in cats due to risk of severe hemorrhagic gastritis.

Contraindications to emesis:

• Caustic or corrosive substance ingestion
• Petroleum distillate or hydrocarbon ingestion
• Sharp object ingestion
• Patient is already symptomatic (seizuring, obtunded, or comatose)
• Loss of gag reflex
• Known brachycephalic breed with high aspiration risk
• Greater than 2-3 hours post-ingestion (diminishing return)

Activated Charcoal

Activated charcoal adsorbs toxins in the GI tract and reduces systemic absorption. It is most effective when administered within 1-2 hours of ingestion but may provide benefit up to 4-6 hours for substances with delayed gastric emptying or enterohepatic recirculation.

• Dose: 1-2 g/kg PO. Administer as a slurry via syringe or orogastric tube.
• Sorbitol (cathartic): Include with the first dose only (sorbitol 70% at 1-2 mL/kg). Do not repeat sorbitol due to risk of hypernatremia and osmotic diarrhea.
• Repeat dosing: For substances with enterohepatic recirculation (chocolate, bromethalin, oleander), give activated charcoal without sorbitol every 4-8 hours for 24 hours.

Contraindications: Not effective for alcohols, heavy metals, xylitol, petroleum products, or caustics. Do not administer if GI perforation is suspected or if the patient has impaired consciousness (aspiration risk — intubate first if charcoal is critical).

Gastric Lavage

Gastric lavage is reserved for cases where emesis is contraindicated or unsuccessful and a life-threatening dose has been ingested recently (within 1-2 hours). Requires general anesthesia with a cuffed endotracheal tube to protect the airway.

Procedure: Pass the largest possible orogastric tube. Lavage with warm water or saline in aliquots of 5-10 mL/kg, aspirating after each instillation. Continue until aspirate runs clear. Follow with activated charcoal administration through the tube before removal.

Antidotes Quick Reference

The following table summarizes specific antidotes for the most commonly encountered toxicoses. Stock availability varies by hospital — consider maintaining a toxicology emergency kit with critical antidotes.

Monitoring Parameters

Targeted monitoring helps detect organ injury early and guides treatment duration. The following table organizes monitoring recommendations by toxin category.

Renal Panel (BUN, Creatinine, Phosphorus, Urinalysis)

Monitor every 12-24 hours for toxins associated with acute kidney injury:

• Grapes and raisins — for a minimum of 72 hours
• Lilies (cats) — for a minimum of 72 hours
• Ethylene glycol — look for calcium oxalate monohydrate crystalluria on urinalysis
• NSAIDs at nephrotoxic doses
• Cholecalciferol rodenticides (also monitor ionized calcium)

Liver Panel (ALT, AST, ALP, Bilirubin, Albumin, Glucose)

Monitor every 12-24 hours for hepatotoxic exposures:

• Xylitol (hepatotoxic doses >0.5 g/kg) — onset 24-72 hours
• Sago palm — onset 24-72 hours, monitor for 5-7 days
• Acetaminophen — especially in dogs at hepatotoxic doses
• Amanita mushrooms — monitor for 5-7 days
• Essential oils in cats

Coagulation Panel (PT, PTT, ACT, Platelet Count)

• Anticoagulant rodenticides — baseline, then at 48 and 72 hours post-ingestion (before clinical bleeding onset), and 48-72 hours after completing Vitamin K1 therapy
• Sago palm — for DIC monitoring

Blood Glucose

• Xylitol — check immediately and every 1-2 hours for 12-24 hours

Methemoglobin Level / Pulse Oximetry

• Acetaminophen in cats — note that pulse oximetry may be inaccurate with methemoglobinemia
• Onion/garlic ingestion (Heinz body evaluation on blood smear)

ECG / Cardiac Monitoring

• Oleander and other cardiac glycoside plants
• Chocolate (at doses causing tachycardia or arrhythmias)
• ADHD medications (tachycardia, arrhythmias)
• Ethylene glycol (hyperkalemia-associated changes)

Free Toxicology Tools

VetGeni provides free digital tools to support toxicology triage in clinical practice:

VetGeni Toxin Checker

The VetGeni Toxin Checker is a free online tool that helps veterinary professionals and pet owners quickly assess the risk of a toxin exposure. Enter the substance, species, body weight, and estimated amount ingested to receive species-specific toxic dose ranges, expected clinical signs by dose category, recommended immediate actions, and guidance on whether emergency veterinary care is needed. No account or login is required.

Toxicology Demo

The VetGeni Demo showcases the AI-powered clinical documentation platform, including how toxicology cases can be documented with voice-to-SOAP note generation. See how AI structures the history, physical exam findings, diagnostic plan, and treatment protocol for a toxicology case in real time.

Emergency Contacts

Keep these numbers posted in your treatment area and saved in your phone for rapid access:

Both ASPCA and Pet Poison Helpline provide case numbers that allow your treating veterinarian to call back for ongoing toxicologist support throughout the case. The consultation fee is per incident (not per call), so follow-up calls regarding the same exposure are included.