Snail and Slug Baits

Metaldehyde is a polymer of acetaldehyde and is often used as snail and slug bait. Commercial products are available in various forms, such as granules, pellets, and liquids, and are designed to be used in and around gardens (Figure 31-1). Toxicosis is more common in dogs, which are more likely to ingest bait in a garden or from an improperly stored container. The minimum lethal dose of metaldehyde in cats is not known; however, in dogs it is 100 mg/kg.⁴² Serious adverse effects occur at much lower doses. Although the mechanism of action of metaldehyde is not known, its effects are well established. Both metaldehyde and its metabolite, acetaldehyde, will distribute widely in the body and cross the blood–brain barrier.

FIGURE 31-1 Pelleted slug and snail bait is often placed under plant foliage in gardens, either scattered loosely or in small traps. Nontoxic slug and snail bait containing ferric phosphate is readily available.

After ingestion affected animals have signs of tachycardia, nervousness, sensitivity to light and noise, panting, drooling, ataxia, hyperthermia, tremors, and seizures.⁴² Onset of clinical signs in dogs generally occurs within 3 to 5 hours of ingestion but can occur in as soon as 30 minutes. Clinical signs can last for up to 5 days but will lessen over 12 to 72 hours with appropriate treatment.⁵¹ Metabolic acidosis often occurs with toxicity, and in some cases hepatic failure may occur within 2 or 3 days after exposure.⁴²

The diagnosis of metaldehyde toxicosis is based on history of exposure and associated clinical signs. If necessary, serum and urine can be assayed for acetaldehyde. Lesions on necropsy are generally nonspecific.

Treatment includes early decontamination, supportive care, and seizure control. Emesis can be induced in appropriate patients, or gastric lavage may be used under sedation or anesthesia. Activated charcoal may help inhibit metaldehyde absorption. Methocarbamol has been used successfully to control tremors and seizures from metaldehyde toxicosis in dogs (Table 31-1).⁴² Other options for seizure control include diazepam, barbiturates, and inhalant anesthesia. Affected animals should be monitored for metabolic acidosis and hyperthermia. Intravenous fluid therapy is indicated to combat hyperthermia and dehydration. Metabolic acidosis may be treated with bicarbonate if necessary. A warm, quiet, comfortable environment helps lessen anxiety and nervousness. Treatment should continue until clinical signs are resolved, which may take several days.

TABLE 31-1 Selected Drugs Useful in the Treatment of Toxicoses in the Cat

Drug	Indication	Dose
Acetylcysteine	Acetaminophen toxicity	140 mg/kg PO for initial dose, then 70 mg/kg PO every 4 hours for 3-5 treatments
Activated charcoal	Adsorbent for ingested toxicants	2-5 g/kg PO; slurry made with 1 g per 5-10 mL water
Ascorbic acid	Acetaminophen toxicity	20-30 mg/kg, PO, every 6 hours
Atropine	OP, carbamate toxicity	0.2-0.5 mg/kg; given IV, remainder IM or SC; every 4-8 hours as needed
Cimetidine	Acetaminophen toxicity	5-10 mg/kg PO or IV, every 6 to 8 hours
Dapsone	Brown recluse spider envenomation	1 mg/kg PO, once daily for 14 days
Diazepam	Control of seizures	0.25-0.5 mg/kg IV or rectally; repeat as needed
Ethanol (20%): add 250 mL 100% ethanol to 1 L crystalloid fluids	Ethylene glycol toxicity	5 mL/kg, CRI over 1 hour; every 6 hours for 5 treatments, then every 8 hours for 4 treatments
Kaolin/pectin	Gastrointestinal protectant	1-2 mL/kg PO, every 6 hours
Methocarbamol	Control of tremors, muscle fasciculations	55-200 mg/kg IV or PO, every 8 hours; maximum 330 mg/kg/day
Misoprostol	Gastric protectant, NSAID toxicity	1-3 µg/kg PO, every 12 hours
Pamidronate	Cholecalciferol toxicity	1.3-2 mg/kg IV, diluted with saline and given over 2 hours
Phenobarbital	Control of seizures	2-6 mg/kg IV bolus, repeat up to 2 times at 20-minute intervals
Pralidoxime chloride (2-PAM)	OP toxicity (not for carbamate toxicity)	10-15 mg/kg IM or SC, every 8-12 hours
Sodium sulfate	Cathartic	250 mg/kg PO
Sorbitol (70% solution)	Cathartic	1-2 mL/kg PO
Sucralfate	Oral, esophageal, gastric, duodenal ulceration	0.25-0.5 g/cat PO, every 8 to 12 hours
Vitamin K1	Anticoagulant rodenticide toxicity	3-5 mg/kg PO or SC, every 8 to 12 hours with food
For Induction of Emesis*	Comments	Dose
Apomorphine	Dissolve 6 mg tablet in water or saline; flush conjunctival sac after emesis; antagonized with yohimbine (0.1 mg/kg, IV or 0.5 mg/kg SC or IM)	0.04 mg/kg IV or 0.25 mg/kg, conjunctival sac
Hydrogen peroxide (3%)	Take care to avoid aspiration	2 mL/kg PO; maximum 10 mL/cat
Xylazine	May cause respiratory depression, reversed with yohimbine (0.1 mg/kg IV or 0.5 mg/kg SC or IM)	0.44-1.1 mg/kg IM

PO, By mouth; OP, organophosphate; IV, intravenously; IM, intramuscularly; SC, subcutaneously; CRI, constant-rate infusion; NSAID, nonsteroidal antiinflammatory drug.

* Emesis should not be induced in patients that have ingested corrosive or caustic substances or substances that may cause aspiration pneumonia. In addition, induction of emesis is contraindicated in animals with decreased consciousness or those that have or are likely to have seizures.

Fly Bait

Methomyl is an extremely toxic carbamate insecticide that is found in certain fly baits. The mechanism of action of carbamates is through the inhibition of both acetylcholinesterases and pseudocholinesterases.³ Almost immediately after ingestion, seizures and pulmonary edema occur. The signs occur rapidly and are so severe that most cases are fatal.³ Atropine, a cholinergic agent, is antidotal for methomyl toxicity.³ In addition, seizure control is recommended. Because the clinical signs occur so quickly, decontamination is usually not an option.

Anticoagulant Rodenticides

Anticoagulant rodenticides include the short-acting warfarin and long-acting chemicals such as pindone, diphacinone, difethialone, chlorophacinone, brodifacoum, and bromadiolone. They are readily available in many formats, including pellets and powders, from several sources, including feed stores and home and garden stores. One of the first rodenticides marketed was warfarin, but resistance rapidly developed in target species, so newer generation compounds have been developed. Anticoagulants act by blocking the recycling of vitamin K₁ in the liver, which results in a coagulopathy. Dysfunctional forms of clotting factors II, VII, IX, and X are released into circulation.³¹

Clinical signs of an anticoagulant toxicity include ecchymoses, petechiae, frank hemorrhage, pale mucous membranes, weakness, exercise intolerance, lameness, dyspnea, coughing, and swollen joints. Early signs may be vague, such as lethargy and anorexia.²¹ The most common clinical presentation is acute onset of dyspnea caused by bleeding into the thoracic cavity.²⁴ Other presentations include otic bleeding, hematoma, melena, and hematochezia.²¹ Sudden death without preceding clinical signs is also possible. Clinical signs are seen several days after the bait is ingested because of the time needed to completely block the coagulation pathways. The duration of action, and thus the length of treatment required, is highly variable, ranging from 14 days to several weeks, depending on the chemical involved.²⁴

Commonly used coagulation tests include bleeding time, activated clotting time (ACT), prothrombin time (PT), and activated partial thromboplastin time (APTT). ACT and APTT measure the intrinsic clotting cascade. PT measures the extrinsic coagulation pathway. Anticoagulant rodenticides affect both the extrinsic and intrinsic pathways. When vitamin K is depleted, the first clotting factor to be affected is factor VII of the extrinsic coagulation pathway. In early cases of toxicoses (36 to 72 hours after ingestion), the PT will be prolonged, but the animal will still appear clinically normal because the other pathways are functioning.³⁰ However, after 72 hours factor IX becomes depleted and shuts down the intrinsic pathway, prolonging other coagulation tests, at which time hemorrhage is possible.

The PIVKA (protein induced in vitamin K antagonism) test (Thrombotest; Axis-Shield PoC, Oslo, Norway) is a newer diagnostic tool for anticoagulant rodenticide toxicosis. It evaluates the extrinsic and common pathways.²² However, if the PT is prolonged, the PIVKA test adds no further information. PIVKA times are also prolonged in any vitamin K₁–responsive coagulopathy.

Decontamination is helpful only with early recognition of ingestion. Vomiting may be induced if ingestion occurred within the previous 4 hours.²⁴ Activated charcoal may be useful if a significant amount of chemical has been ingested. Other treatment is aimed at providing functional clotting factors. PT and PIVKA are monitored at baseline and 48 and 73 hours later.²⁴ Because PT elevates before clinical signs occur, it is a useful indicator of when vitamin K₁ therapy is indicated. Testing for both PT and PIVKA must be performed before vitamin K₁ is administered to prevent false-negative results.

In some cases initial treatment may require transfusion of fresh frozen plasma or whole blood to supply clotting factors.²¹ Oral vitamin K₁ (phytonadione) therapy is antidotal for anticoagulant rodenticides. Injectable vitamin K₁ is not recommended because of the risk of anaphylactic reactions. Vitamin K₃ is contraindicated because it is not effective and may induce hemolytic anemia.³⁰ Treatment should continue as long as necessary, depending on the type of rodenticide (e.g., 14 days for warfarin, 21 days for bromadiolone, 30 days for other compounds). Confirming a normal PT 48 to 72 hours after the last dose of vitamin K₁ can ensure that it is not needed further. The prognosis is generally good if the toxicity is recognized and treated early.

Bromethalin

Bromethalin has been sold since the 1980s and is typically available in grain-based pellet form. Bromethalin is an uncoupler of oxidative phosphorylation and causes a reduction of adenosine-5’-triphosphate (ATP), decreasing nerve impulse conduction.¹² After ingestion absorption is rapid and peak plasma levels are reached in a few hours.³⁰ Clinical signs can occur at any time from 24 hours after ingestion to 2 weeks later and include muscle tremors, seizures, hyperexcitability, forelimb extensor rigidity, ataxia, depression, loss of vocalization, paresis, paralysis, and death.^11,12,30 Low-dose exposure causes slow development of clinical signs, starting with hindlimb ataxia and paresis, with hindlimb paralysis following.¹¹ Affected animals also show decreased conscious proprioception, loss of deep pain, and upper motor neuron bladder paralysis.¹¹ The most common postmortem lesions include cerebral and spinal cord edema and a spongy appearance to the cerebellum.¹²

Diagnosis is based on history of exposure and compatible clinical signs. Because there is no antidote to this rodenticide and the clinical effects can be extremely severe, early aggressive decontamination is critical. If ingestion occurred recently (within 2 hours of presentation), emetics, activated charcoal, and a cathartic should be administered.¹¹ Activated charcoal may be required every 4 to 8 hours for at least 3 days. Cats with cerebral edema may be treated with mannitol (250 mg/kg intravenously, every 6 hours) and dexamethasone (2 mg/kg intravenously, every 6 hours).¹¹ Seizures may be managed with diazepam or phenobarbital. Unfortunately, treatment of such severely affected animals is often futile. Mildly affected animals may recover in 1 to 2 weeks. More severely affected animals may require prolonged nutritional support and nursing care.

Cholecalciferol

Cholecalciferol (vitamin D₃) is metabolized in the liver to calcifediol (25-hydroxycholecalciferol). Calcifediol is then metabolized by the kidney to calcitriol (1,25-dihydroxycholecalciferol). Cholecalciferol increases intestinal absorption of calcium, stimulates bone resorption, and enhances renal tubular reabsorption of calcium. Toxic ingestion results in hypercalcemia, which can lead to renal failure, cardiovascular abnormalities, and tissue mineralization. Plasma phosphorus and calcium increase within 72 hours of ingestion. The (calcium × phosphorus) product may exceed 130 mg²/dL² (10.5 mmol²/L²), well above the level at which soft tissue mineralization occurs.²⁹ Other laboratory abnormalities include increased blood urea nitrogen (BUN) and creatinine, hyperkalemia, acidosis, and decreased urine specific gravity.³⁰

Clinical signs usually occur 18 to 36 hours after ingestion and include vomiting, diarrhea, inappetence, depression, polyuria, polydipsia, and cardiac arrhythmia.^29,30 With high doses renal failure results from the deposition of calcium in the kidney and occurs in 24 to 48 hours.²⁹ Death is often due to acute renal failure, and animals that survive may have permanent loss of renal function and other abnormalities. Cholecalciferol is highly lipid soluble and is eliminated slowly from the body.²⁹ Clinical signs, and therefore duration of treatment, may last for weeks.

Diagnosis is based on a history of exposure and compatible clinical signs. Other causes of hypercalcemia must be ruled out. Assessment of serum parathyroid hormone, parathyroid hormone–related polypeptide, and 25-hydroxycholecalciferol levels may be helpful in the differential diagnosis.

Decontamination is recommended with early exposures. Emesis may be induced in appropriate patients. Activated charcoal should be administered concurrently with a cathartic. Baseline and serial monitoring of serum BUN, creatinine, phosphorus, and calcium is necessary. In cats that develop clinical signs or changes in laboratory parameters, diuresis with intravenous 0.9% saline is indicated. Furosemide is added to the therapy once the cat is hydrated to increase renal calcium excretion.²⁹ Oral prednisone may be used to decrease serum calcium by decreasing bone resorption, decreasing intestinal absorption, and increasing renal excretion.

Severely affected cats or those that relapse after initial therapy may require treatment with a bisphosphonate. Pamidronate (see Table 31-1) inhibits osteoclastic bone resorption and has been used successfully to treat exposures in combination with fluid therapy and supportive care.²⁹ Once calcium levels are normal, they should be monitored daily for 4 days. Retreatment may be required.

Strychnine

Strychnine is an alkaloid derived from the nux vomica tree that is used to kill rodents and also other pests, including coyotes.³⁰ Strychnine is considered a restricted pesticide in many states. It is often, but not always, found as red-colored grain-based pellets. Cats are less commonly affected than dogs but may be poisoned by accidental or malicious exposure. Strychnine is a glycine antagonist in the central nervous system (CNS) and results in excessive neuronal activity, causing muscle spasms and severe convulsions.⁵² The lethal dose in cats is 2 mg/kg.⁵² Early signs of toxicity (within minutes) include apprehension and stiffness, progressing to tonic extensor rigidity, especially in response to stimulation (light, sound, touch).³⁰ Clinical signs affect the face, neck, and limb muscles first.⁵² Convulsions with opisthotonos can appear quickly. Death may occur as a result of hypoxia from impaired respiration as soon as 10 minutes after ingestion or up to 24 to 48 hours later.⁵² The differential diagnosis includes a wide variety of possibilities, including rabies and other intoxications.

Diagnosis is based on a history of exposure, compatible clinical signs, and strychnine testing (on urine, tissues, or stomach contents). If exposure is recent and the patient’s status is stable, activated charcoal may be administered to reduce further absorption. Emetics should be used with care insofar as they may precipitate violent muscle or convulsive activity.⁵² It may be safer to perform gastric lavage on a sedated or anesthetized patient. Seizure control in most cases is difficult but may include the use of methocarbamol, propofol, or barbiturates. Diazepam is usually not recommended because its efficacy for strychnine-induced seizures is variable.³⁰

Respiration should be monitored closely and mechanical ventilation initiated if severe respiratory depression occurs. Supportive care includes intravenous fluid therapy and provision of a quiet, dark environment. Most poisoned animals require hospitalization for 24 to 72 hours. Patients presented late in the progression of the disease are at higher risk of death.

Zinc Phosphide

Zinc phosphide is commonly found in mole and gopher baits at concentrations up to 5% and is highly toxic.¹ It is used for vermin control in areas where rodents have become resistant to other chemical control methods and is usually a restricted-use pesticide. Dogs and cats are the species most likely to suffer accidental ingestion and toxicosis. Cats that eat very recently poisoned rodents may also be at risk of toxicity from zinc phosphide still in the gastrointestinal tract of the target animal.¹ For most species a lethal dose is 20 to 40 mg/kg.¹

After ingestion, phosphide is converted to phosphine gas by stomach acid.¹ Released phosphine gas causes severe irritation to the pulmonary tissues, which results in respiratory distress and death occurring secondary to respiratory failure. Clinical signs are typically seen in 15 minutes to 4 hours, depending on when the animal last ingested a meal.¹ Early signs of toxicosis include anorexia and depression, followed by rapid and deep respirations.¹ Vomiting is common and often contains blood.

Treatment includes early decontamination (induction of emesis or gastric lavage, activated charcoal with a cathartic) and supportive care for the associated clinical effects (e.g., acidosis, respiratory compromise, depression). Some animals suffer liver failure.¹ There is no specific antidote for zinc phosphide. Because the conversion of zinc phosphide to phosphine gas is enhanced with gastric acidity, treatment with antacids is highly recommended.

The phosphine gas emitted from the affected animal is a human health hazard and can be dangerous to hospital personnel even at levels that cannot be detected by smell. Therefore precautions such as adequate ventilation should be taken to protect staff members.¹

Pyrethrins and Pyrethroids

Pyrethrins are naturally derived from chrysanthemum flowers, whereas pyrethroids are synthetic analogs. These compounds modify the sodium channels in nervous tissue and muscle cell membranes, causing repetitive discharging of the cell and clinical signs of neurotoxicity. Most insecticidal products labeled for use in cats contain low levels of pyrethrin and, if used appropriately, are relatively safe for cats.³⁷

Permethrin is derived from a combination of esters that are extracted from dried chrysanthemum flowers and is further classified as a type I pyrethroid.³⁷ This insecticide is used in spot-on flea treatments for dogs but is contraindicated in cats because of the high risk of toxicity. Cautionary labeling on canine products may not be visible enough or adequate to prevent inappropriate use, and risk awareness among pet owners may be low. Cats are highly sensitive to the effects of permethrin, probably because of their deficiency of hepatic glucuronidase transferase.⁶ Permethrin toxicity is one of the most commonly reported feline toxicities.^28,50

Cats are most commonly exposed to concentrated permethrin compounds inappropriately or accidentally through exposure to topical flea products intended for canine use only. These spot-on products can contain 45% to 65% permethrin or more. The most commonly seen clinical signs include tremors, muscle fasciculations, ear twitching, facial twitching, hyperesthesia, ataxia, ptyalism, pyrexia, mydriasis, and seizures.⁶ Clinical signs may occur with exposure to only a few drops of the concentrated solution and may occur within a few hours or several days. In general, clinical signs will continue for 24 to 72 hours but may last up to 7 days.^37,50 Death occurs in about 10% of cases.⁵⁰

Diagnosis of permethrin toxicity is based on a history of recent exposure and typical clinical signs. Differential diagnoses include other causes of seizures and tremors. Treatment should focus on seizure control, decontamination, and supportive care (Box 31-2). With recent exposures to permethrin, the cat should be bathed completely using lukewarm water and mild hand dishwashing detergent or shampoo to remove any residual product. Hot water should not be used because it may increase dermal perfusion and uptake of permethrin. Seizures and tremors typically respond to methocarbamol (see Table 31-1).³⁷ Other options for seizure control include propofol, barbiturates, diazepam, and inhalant anesthetics. In addition, supportive care, including maintaining normal body temperature, supplying intravenous fluids, and providing nutritional support, is needed.

Cholinesterase Inhibitors

Cholinesterase inhibitors include carbamates and organophosphates. These compounds have been widely used in agricultural and veterinary medicine for decades. Cats may be exposed accidentally or by inappropriate use of products. Organophosphates are very toxic to cats and not recommended in this species. Carbamates (e.g., carbaryl) are less toxic and are found in several insecticides marketed for use in cats in various formulations (e.g., shampoos, powders, collars). These compounds bind to and inhibit cholinesterases, causing excess accumulation of acetylcholine and resulting in cholinergic excitation and muscarinic and nicotinic signs.²⁷ Organophosphates have higher binding affinity than carbamates and are often called irreversible inhibitors.

Clinical signs result from overstimulation of the cholinergic nervous system, as well as skeletal muscle and the CNS, and appear within minutes to hours after exposure.⁵³ Clinical signs of toxicity include classic muscarinic signs often referred to as SLUDGE signs: salivation, lacrimation, urination, defecation, gastrointestinal upset, and emesis.²⁷ Nicotinic signs include ataxia, weakness, tremors, and muscle fasciculations. Cholinesterase inhibitors can also cause seizures, increased bronchial secretions, pulmonary edema, and bradycardia.²⁷

Diagnosis is based on history of exposure and compatible clinical signs. To confirm exposure to a cholinesterase inhibitor, whole blood, serum, or plasma cholinesterase enzyme activity (ACHE test) can be evaluated through an accredited veterinary laboratory. The diagnosis is confirmed if the cholinesterase activity is less than 25% of normal. In addition, the insecticide can be detected in stomach contents and tissues. Changes on complete blood cell count, serum chemistry panel, and urinalysis are generally nonspecific.⁵³

Patients affected by organophosphate or carbamate toxicity may deteriorate quickly so treatment must be initiated as soon as possible. Respiratory failure is the main cause of death, so artificial respiration may be required. Treatment also includes control of seizures. The specific antidote for organophosphate toxicity is pralidoxime chloride (2-PAM; Protopam, Ayerst Laboratories), which releases cholinesterase from the organophosphate. 2-PAM will control nicotinic signs and is most effective when given as soon as possible after exposure (preferably within 24 to 48 hours). Clinical improvement should occur within 3 to 4 days, and treatment is continued as long as needed. This drug is usually not recommended for carbamate toxicity.⁵³

Although atropine is often considered an antidote to cholinesterase inhibitors insofar as it blocks the effects of the excess acetylcholine at the neuromuscular junction, it should be used with caution. If muscarinic signs are present, a test dose (0.02 mg/kg intravenously) can be given to determine if the signs are due to organophosphate or carbamate toxicity versus other causes. If the heart rate increases and the pupils dilate in response to the test dose, the clinical signs are probably not due to organophosphate or carbamate toxicity. This is because the atropine dose required to resolve clinical signs caused by insecticide toxicity is about 10 times the preanesthetic dose of the drug. If insecticide toxicity is confirmed, atropine can be administered to control muscarinic signs (see Table 31-1). The dose is adjusted by monitoring response, especially heart rate and secretion production.

Activated charcoal may be used to bind insecticide in the gastrointestinal tract, and bathing with soap and water can be used for cats with dermal exposure to prevent further absorption. Additional treatments may include methocarbamol, diazepam, or phenobarbital to control seizures and muscle tremors.⁵³ Good supportive and nursing care, including intravenous fluid therapy and nutritional management, is essential.