General Approach to Intoxication
Ahna Brutlag, DVM, MS, DABT, DABVT, Pet Poison Helpline, Minneapolis, Minnesota
Suspicion of poisoning in dogs and cats is typically based on known exposure to a potentially dangerous substance, as well as patient history and clinical presentation. Determining timing, dose of toxicant ingested, testing, treatment, and risk/benefit analysis are key in these patients.
Background & Pathophysiology
Any compound, no matter how seemingly safe, can be toxic if the dose is high enough. It is critical—though potentially difficult—to first determine whether the patient was exposed to a toxic dose. Toxic doses vary widely depending on the specific toxicant, route of exposure, species, breed, age, health/disease status, reproductive status, concomitant medications, and other related factors (eg, prior exposure to the toxicant). For example, dogs are considerably more sensitive than cats to the effects of brodifacoum, an anticoagulant rodenticide, of which the minimum acute toxic dose for a 10-lb (4.5-kg) dog is 4.5 g of bait (brodifacoum, 0.005%) and the minimum acute toxic dose for a 10-lb (4.5- kg) cat is >500 g of bait.1 Many veterinary toxicology textbooks and online references are available, and specialists at animal poison control centers (see Suggested Reading) can provide immediate tailored advice to both pet owners and clinicians.
History & Clinical Signs
Patient history is important in cases of suspected poisoning.
For patients exposed to a toxicant, the pet owner should be asked to bring in the product container, plant, or food or provide photos of the toxicant and exposure site to help the clinician identify the involved material, active ingredient, medication name, concentration, dose, and/or quantity. Asking the owner detailed questions about the exposure can help determine whether it was witnessed or is suspected. If exposure is suspected, the owner should be asked what evidence (eg, disturbed compost pile, overturned trash can, plant material in vomitus) is involved. A timeline of exposure and onset/progress of clinical signs should be established. Owners should also be questioned whether clinical signs appear to be improving or worsening and whether new signs have emerged since exposure. Of note, owners may be reluctant to provide details regarding exposure to an illicit substance.
For patients presented with illness that the owner does not recognize as having a potential toxicologic cause, it can be helpful to ask about specific exposure to a toxin versus generally asking whether the patient has been exposed to any toxins. For example, the owner of a dog presented with acute kidney injury can be asked if the dog had exposure to grapes or raisins, as owners may not realize these common foods can be harmful to dogs and may be less likely to offer this information without prompting.
Poisoning should be suspected in the following circumstances:
A healthy animal becomes acutely ill or dies suddenly with no evidence of infectious disease
Exposure to a new or changed environment (eg, recent change of indoor/outdoor residence, construction in the home)
Recent ingestion of indoor/outdoor plants or newly introduced plants/flower bouquets
Introduction of a new food or container of food with no other changes
An animal was uncharacteristically left outdoors or in a garage/outbuilding for an extended period of time
Recent application of a lawn, garden, or home pesticide
Unintentional exposure to oral or topical medications or an owner administers medication without consulting a veterinarian
Recent exposure to garbage or compost
Sudden illness occurs after an animal may have had access to a guest’s purse or luggage or was offered food by the guest
Threats of malicious poisoning
Diagnostic Testing & Clinical Monitoring
If the patient was exposed to a known toxicant, diagnostic and laboratory testing should be focused on monitoring for abnormalities associated with the specific toxicant and/or confirmation of exposure to a toxic dose. For example, if a patient ingested ethylene glycol (EG), measuring the amount of EG in the serum can confirm exposure to a toxic dose. If signs consistent with EG poisoning (eg, “drunkenness,” ataxia, vomiting, tachypnea, polyuria, polydipsia) develop, laboratory monitoring for metabolic acidosis, electrolyte abnormalities, and azotemia are needed.
In patients with suspected intoxication from an unknown substance that cannot be confirmed based on history or clinical presentation, a wider variety of diagnostics are needed. Serum chemistry profile, CBC, and urinalysis can help identify impacted organ systems; this can narrow the list of potential toxicants and focus treatment. Consultation with an animal poison control center or toxicologist at a veterinary diagnostic laboratory can also help guide clinical decision-making.
Tailored toxicologic analysis can be of significant value. Although there is no universal test for toxins, samples of vomitus, gastric lavage contents, feces, urine, whole blood, and serum should be sent to a veterinary diagnostic laboratory. All samples should be frozen, except whole blood, which should be refrigerated.2 If the patient’s food or water source is a suspected source of intoxication, the owner should be advised to preserve samples; keep dry food in a cool, dry place; freeze canned/moist food; and refrigerate water. If the patient dies, a full-body necropsy should be performed by a board-certified pathologist.
WHEN & HOW TO DECONTAMINATE THE GI TRACT
The following questions can help identify the risk/benefit standpoint before GI decontamination is initiated.
Is decontamination medically necessary?
Was the patient exposed to a toxic dose?
If not, decontamination is rarely warranted, as, regardless of method, decontamination is not benign, and adverse effects can occur.3
When did the exposure occur?
Was the exposure recent enough for the patient to benefit from decontamination? For example, emesis induction should typically be performed within 30 to 60 minutes of ingestion to be effective.3 If the ingestion was more than 60 minutes before presentation, skipping emesis and administering activated charcoal may be more beneficial.
Is decontamination safe for the patient?
Is the patient stable enough for decontamination?
In general, if the patient shows clinical signs, inducing emesis is not advised. For example, patients with CNS depression may have a depressed gag reflex or lowered seizure threshold and, therefore, have a greater risk for aspiration when emesis is induced. In addition, if the patient is showing signs consistent with the toxicant, it may be too late for effective decontamination, and the patient would instead benefit more from other, more specific treatments.3 For example, due to the rapid onset of hypoglycemia in dogs following xylitol ingestion, blood glucose should be checked first unless emesis can be induced within a few minutes following exposure.
Could decontamination worsen prognosis or clinical signs?
Some toxicants may cause additional harm if vomited,3 like caustic substances that can result in further chemical damage to the esophagus and oro- and nasopharynx or volatile, low-viscosity hydrocarbons (eg, gasoline, tiki torch fluid) that are easy to aspirate.
Activated charcoal is contraindicated if the patient is hypernatremic, dehydrated, or ingested toxicants (eg, paintballs) that increase the risk for free-water shift into the gut.3,7
Does patient signalment or an underlying issue preclude safe decontamination?
For example, it may not be safe to induce vomiting in neonatal animals or dogs with a history of laryngeal paralysis or megaesophagus.3
Can the toxicant pose a risk to humans?
If so, can the risk be mitigated by use of personal protective equipment or decontamination of the patient outside?
Which decontamination agents or procedures are appropriate for this toxicant and species?
Is the correct emetic agent being used for the species?
Emetic agents for cats and dogs are not the same (see Emetic Agents for Cats vs Dogs).
Does the toxicant bind to activated charcoal? Most nonpolar toxicants bind to activated charcoal. Examples of toxicants that do not bind well to charcoal include alcohol (eg, ethanol, isopropanol, methanol, ethylene glycol, propylene glycol), most heavy metals (eg, iron, lead, zinc), hydrocarbons (eg, fossil fuels, mineral oil), sodium chloride, and xylitol.3,7
Should activated charcoal be given with a cathartic (eg, sorbitol)? The intent of giving a cathartic is to decrease transit time through the GI tract, thereby reducing risk of the toxicant separating from the activated charcoal and being absorbed by the body. Typically, activated charcoal administration with a cathartic is advised; however, a cathartic is contraindicated in patients with severe diarrhea, dehydration, recent intestinal surgery, volume depletion, and/or electrolyte imbalances.7
Does the toxicant undergo enterohepatic recirculation? If so, multiple doses of activated charcoal may be beneficial. Examples of these toxicants include bromethalin, cholecalciferol (ie, vitamin D3), ibuprofen, tea tree oil (ie, melaleuca oil), and theobromine.8,9
Could the toxicant be removed using extracorporeal therapies (eg, hemodialysis, hemofiltration, hemoperfusion, therapeutic plasma exchange)?
Is the toxicant lipophilic, and, if so, would IV lipid emulsion be appropriate?
Treatment & Management
Appropriate decontamination procedures are often paramount to successful treatment and are typically the first approach that should be considered in most intoxication cases (see When & How to Decontaminate the GI Tract) in which the patient was exposed to a toxic dose. The decision to decontaminate is based on time since exposure, specific toxicant, dosage, and presentation and signalment of the patient; methodology depends on the route of exposure. In some cases, decontamination is contraindicated (eg, emesis induction when a caustic agent was ingested, administration of activated charcoal to a hypernatremic patient), as it may worsen prognosis or clinical signs.3
GI decontamination is the most common procedure because most cases involve ingestion of toxic substances.
In general, emesis induction should be performed within 30 to 60 minutes of substance ingestion for maximum effect; however, for certain substances (eg, chocolate, grapes/raisins), emesis induction several hours postingestion can be beneficial. Emesis induction should only be performed in clinically unaffected patients and is contraindicated in patients with subtoxic ingestion, neurologic impairment (due to increased risk for aspiration), and ingestion of certain toxicants (eg, volatile hydrocarbons [eg, gasoline]). Likewise, extra care should be taken if the ingested toxicant may result in rapid-onset clinical signs (eg, xylitol inducing hypoglycemia in dogs, antidepressant or attention deficit hyperactivity disorder medications resulting in CNS signs). If spontaneous emesis has already occurred, the need for forced emesis induction should be carefully considered. If the patient has vomited or shows clinical signs of intoxication, gastric lavage may still be effective after the patient is stabilized if the ingestion was recent (ie, <60 minutes prior to presentation), a large amount of substance was ingested and is still located within the stomach, or the ingested substance (eg, tricyclic antidepressants) results in delayed gastric emptying. Selecting the correct emetic agent for the species is also important (see Emetic Agents for Cats vs Dogs).
If the toxicant binds to charcoal, activated charcoal (1-3 g/kg PO) with a cathartic (eg, sorbitol) may also be administered to adsorb toxicants and accelerate GI transit time.4 If the ingested toxicant undergoes enterohepatic recirculation (eg, bromethalin) or is a sustained-release formula, multiple doses of activated charcoal (1-2 g/kg without a cathartic every 6-8 hours for 24 hours) may be beneficial. The most common adverse effect is hypernatremia; thus, concurrent administration of IV fluids and monitoring of serum sodium concentrations is advised.
In patients with ocular exposure, the eyes should be flushed ideally with eye wash solution or warm tap water (saline can also be used if needed). To remove topical toxicants (eg, essential oils, concentrated pyrethroid products in cats), the patient should be bathed with a follicle-flushing or degreasing shampoo5; dishwashing liquid will also suffice.
EMETIC AGENTS FOR CATS VS DOGS
Apomorphine (0.03 mg/kg IV; preferred)10
Alternatively, a 6.25 mg tablet (whole or crushed; not available in the United States) can be placed under the conjunctiva, or a crushed tablet (typically 6.25 mg) can be dissolved in a saline solution (0.9% NaCl) and instilled in the conjunctival sac. The tablet should be removed and rinsed with water or saline solution after emesis, resulting in a dose to effect.10
Hydrogen peroxide 3% (1-2 mL/kg PO; maximum dose, 60-70 mL total); food in the stomach increases the chance for success11
In some cases, hydrogen peroxide 3% can also be used to induce vomiting at home provided the patient is stable, ingestion was recent, and owner is given proper instruction and administration information. This is the only at-home emetic agent recommended in dogs.
Ropinirole ophthalmic solution (1-8 eye drops/dog)12
Ophthalmic formulation FDA-approved to induce vomiting in dogs 4.5 months of age and older and weighing at least 1.8 kg (4 lb)17
Although all 3 of these agents are ≈95% effective, hydrogen peroxide poses a greater risk for gastric irritation and should be used judiciously if the ingested toxin (eg, aspirin, NSAIDs, iron) may also cause gastric damage.12,13
Emetics that are no longer recommended in dogs or cats include syrup of ipecac, table salt, and liquid soap.
Dexmedetomidine (7-10 µg/kg IM)14
Hydromorphone (0.1 mg/kg SC)15
Xylazine (0.44 mg/kg IM)16
Medications can be reversed as needed with atipamezole (eg, dexmedetomidine, xylazine) or naloxone (eg, hydromorphone).
Hydrogen peroxide, apomorphine, and ropinirole should not be used in cats.
No emetics are safe or recommended for use in cats at home.
Antidotes & Supportive Care
Relatively few antidotes are available, considering the number of potential poisons. Common examples of antidotes used in dogs and cats include antivenom for snake and spider bites, atropine for cholinesterase inhibitors, bisphosphonates for vitamin D3/cholecalciferol, chelating agents for heavy metals, fomepizole or ethanol for ethylene glycol, naloxone for opioids, and vitamin K1 for certain anticoagulants (eg, rodenticides). Due to the limited number of antidotes, treatment for most poisonings should be focused on preventing clinical complications and providing supportive care based on clinical signs, trending laboratory values, and the specific toxicant ingested (if known). For example, NSAID toxicosis is common in both cats and dogs. Understanding the mechanism of NSAIDs allows treatment to be focused on prevention of downstream effects (eg, GI ulceration, acute kidney injury) by administering gastroprotectants and IV fluids before clinical signs are observed.6 Although neither of these treatments is truly antidotal, they contribute to a good outcome.
Clinical follow-up and monitoring should be based on the specific toxicant, secondary organ damage that may have resulted from the poisoning, and severity of the patient’s signs. Recheck examinations and laboratory monitoring to assess organ function following hospital discharge can help detect long-lasting damage or dysfunction and guide therapy.
It is important that clinicians treat the patient, not the poison. This emphasizes the importance of considering whether the patient was exposed to a toxic dose and, if so, how much time has passed since exposure to help determine whether treatment is medically necessary.
Editor's note: The originally published version of this article noted that ropinirole ophthalmic solution is not available in the US. This article has been updated to reflect recent information on ropinirole as of September 24, 2021.