Common hazards for cats (Proceedings)

Permethrin

Permethrin, a synthetic type I pyrethroid, is found in many flea and tick shampoos, dips, foggers, spot-ons, and sprays as well as many household and yard insecticide formulations. While permethrins have a relatively wide margin of safety in dogs, cats appear to be more sensitive to the toxicity of concentrated permethrins. The low-concentration products (sprays, foggers) approved for use on cats contain 0.05–0.1% permethrin and do not cause the clinical syndrome that has been associated with the inappropriate use of concentrated (45–65% permethrin) spot-on products on cats. Permethrin toxicity usually occurs when the concentrated dog product is applied to cats, but cats that actively groom or engage in close physical contact with recently treated dogs may also be at risk of toxicity.

Clinical signs of permethrin toxicosis in cats include hypersalivation, depression, ear twitching, facial twitching, generalized muscle tremors or fasciculations, hyperthermia, vomiting, anorexia, seizures, and possibly death. The onset of clinical signs is usually within a few hours of exposure but may be delayed up to 24 hours. The severity of clinical signs often varies among individual cats.

Treatment of permethrin toxicosis should include control of tremors, supportive care, and decontamination. Methocarbamol (50–150 mg/kg slow IV; do not exceed 330 mg/kg/day) is preferred to control the tremors. If no injectable methocarbamol is available, the oral form may be dissolved in water and administered rectally. If the cat is actively seizing, barbiturates or inhalant anesthesia may be needed. Given alone, diazepam may actually exacerbate the tremors, but once methocarbamol has been used to reduce the tremor activity, diazepam is sometimes useful at reducing hyperesthesia. The use of atropine is not indicated in pyrethroid exposures and should be avoided.

Once tremors are under control, cats should be bathed to remove the product from the haircoat and skin. Liquid dishwashing soap (e.g. Dawn®) should be used to bathe the entire cat. Thermoregulation is very important in these cases, as tremoring cats often present hyperthermic only to develop hypothermia following tremor control and bathing. Hypothermic cats may experience recrudescence of tremors as well as decreased metabolism of the permethrin due to decreased metabolic rate. Permethrins appear to have no direct action on the liver or kidneys, but fluids may be helpful in protecting the kidneys from myoglobin breakdown products in severely tremoring or seizing cats. Potential complications to permethrin toxicosis in cats include disseminated intravascular coagulopathy and rhabdomyolysis due to prolonged seizure activity and/or hyperthermia. The prognosis for mildly tremoring cats is usually good, but treatment may be required for up to 24–48 hours. The prognosis for severely seizuring cats is guarded, although many of these will make full recoveries if given aggressive veterinary care.

Lily plants

Easter lilies (Lilium longiflorum), tiger lilies (Lilium tigrinum), rubrum or Japanese showy lilies (Lilium speciosum and Lilium lancifolium), and various day lilies (Hemerocallis species) have been incriminated in causing acute renal failure and death in cats. The toxic principle is unknown. Even minor exposures (a few bites on a leaf, ingestion of pollen, etc.) may result in toxicosis, so all feline exposures to lilies should be considered potentially life-threatening and merit aggressive clinical intervention. It should be noted that not all plants with "lily" in the name are members of Liliaceae, e.g. calla lily (Zantedeschia spp. see oxalate-containing plants) or lily of the valley (Convallaria spp., see cardiac glycosides-containing plants).

Affected cats often vomit within a few hours of exposure to lilies, but the vomiting usually subsides after a few hours, during which time the cats may appear normal or may be mildly depressed and anorexic. Within 24 to 72 hours of ingestion, oliguric to anuric renal failure develops, accompanied by vomiting, depression, anorexia, dehydration, and hypothermia; additionally, disorientation, ataxia, facial and paw edema, dyspnea, and seizures have been less commonly reported.

Elevations in blood urea nitrogen (BUN), creatinine, phosphorus and potassium are detectable as early as 12 hours post ingestion. Creatinine elevations may be especially striking, with levels as high as 44 mg/dl reported. In some cases, hypoglycemia and mild liver enzyme elevations may occur. Abundant casts, proteinuria, glucosuria, and isosthenuria are usually detectable on urinalysis within 24 hours of ingestion, reflecting lily-induced damage to renal tubular cells. In severe cases, death or euthanasia due to acute renal failure generally occurs within 3 to 6 days of ingestion.

When initiated within 18 hours of ingestion, decontamination (emesis, oral activated charcoal, and cathartic) and fluid diuresis using lactated Ringer's solution at twice maintenance infusion rate for 48 hours have been effective in preventing lily-induced acute renal failure. Conversely, delaying treatment beyond 18 hours frequently results in death or euthanasia due to severe renal failure. Baseline renal values should be obtained upon presentation and then repeated at 12, 24, 36 and 48 hours.

Because the tubular injury from lily ingestion spares the renal tubular basement membrane, regeneration of damaged tubules may be possible. In severe cases, peritoneal dialysis may aid in managing renal failure until tubular regeneration occurs (10-14 days or longer).

Liquid potpourri

Liquid potpourri may contain essential oils and cationic detergents; because product labels may not list ingredients, it is wise to assume that any given liquid potpourri contains both ingredients. The majority of significant exposures to liquid potpourri in cats occur when the product is spilled, and cats get the product on their coats and groom it off.

Essential oils in liquid potpourris can cause mucous membrane and gastrointestinal irritation, central nervous system depression, and dermal hypersensitivity and irritation. Severe clinical signs can be seen with potpourri products that contain cationic detergents. Dermal exposure to cationic detergents can result in erythema, edema, intense pain, and ulceration. Clinical signs from ingestion of cationic detergents may not develop immediately, and it may require up to 12 hours for the full extent of tissue damage to become apparent. Signs resulting from ingestion of cationic detergents include depression, hypersalivation, anorexia, oral inflammation or ulceration, smacking of lips, tongue flicking, dysphagia, vomiting (+/- blood), abdominal pain, and melena. Significant hyperthermia (>104° F) may accompany oral inflammation. Esophageal and/or pharyngeal ulceration may occur. Inhalation of corrosive material may result in coughing, dyspnea, and moist lung sounds. Sequelae can include esophageal perforations or strictures and pleuritis or peritonitis from leakage of ingesta through perforated mucosa.

As with ingestion of any potentially corrosive agent, emesis should NOT be induced nor should activated charcoal be given. Complete evaluation of the oral cavity and pharynx for ulceration or irritation should be performed upon presentation of the cat to the veterinarian, although with very recent exposures the oral cavity may appear normal. Evidence of oral discomfort and inflammation generally develop within 2 to 4 hours, although the full extent of injury may not be evident until 12 hours post exposure.

It is important to remember that the absence of oral burns does not preclude the development of esophageal burns. Endoscopy may be elected for cases in which esophageal damage is a concern, although delaying endoscopy for 12 hours will allow the full extent of the burns to develop. Should mucosal burns develop, treatment should include antibiotics, pain medication as needed, gastrointestinal protectants (e.g. sucralfate slurries), anti-inflammatories (corticosteroid use is controversial) and general supportive care. In cases with severe oral burns or esophageal burns, placement of a gastrostomy tube will facilitate nutritional support while allowing for mucosal healing. Esophageal lesions may take weeks to heal and there may be risk of stricture formation, leading to impairment of esophageal function.

Glow-in-the-dark items

Glow-in-the-dark items are popular novelties that are sold at fairs, carnivals, novelty stores and skating arenas; they are most popular around the 4th of July and Halloween holidays. These items include glo-sticks and glow-in-the-dark jewelry (necklaces, bracelets, etc). The primary luminescent agent in these types of products is dibutyl phthalate (n-butyl phthalate), an oily liquid that is also used as a plasticizer and insect repellent. Dibutyl phthalate is of relatively low toxicity (LD50 >8000 mg/kg in rats). Pet exposures to glow-in-the-dark items are unlikely to cause serious problems due to the low toxicity, the extremely unpleasant taste and the small amounts of dibutyl phthalate in these types of items.

Exposures generally occur when cats bite into glo-sticks or jewelry. The extremely unpleasant taste of dibutyl phthalate is thought to be responsible for the clinical signs seen and to limit exposure to these items. Signs generally occur within seconds of the cat biting into the item, and cats will often have a much exaggerated reaction to the taste of dibutyl phthalate. They may display profuse salivation and foaming, with occasional retching and/or vomiting. More dramatic are the behavioral effects in cats from exposure to glow items, with neurological signs such as hyperactivity, aggression, head shaking, hiding, and agitation being reported. Rarely, transient panting, dyspnea, tremors and urinary incontinence have been reported in cats.

In spite of their initial intensity, signs from these items are generally self-limiting and should resolve once the cat gets the taste of the product out of its mouth. The goal of managing an exposure to glow items is to dilute the taste using milk or highly palatable food (e.g. canned tuna). Any chemical that has gotten on skin or fur should be bathed off to prevent re-exposure should the cat groom itself; taking the pet into a darkened room will aid in identifying the luminescent chemical on the skin or coat. For ocular exposure, copious flushing of the eyes is recommended. In most cases, once the disagreeable taste is dealt with, cats will return to normal with no further treatment needed.

Acetaminophen

Acetaminophen (Tylenol®, non-aspirin pain reliever, APAP) is a synthetic non-opiate derivative of p-aminophenol. Acetaminophen's exact mechanism of action is unknown but it is believed to block production of prostaglandins from arachidonic acid by inhibiting COX-3. Acetaminophen acts primarily in the CNS to increase the pain threshold and may also inhibit chemical mediators that sensitize the pain receptors to mechanical or chemical stimulation. The antipyretic activity of acetaminophen is achieved by blocking the effects of endogenous pyrogens by inhibiting prostaglandin synthesis.

Acetaminophen is rapidly and almost completely absorbed from the GI tract. Peak plasma levels are seen at 10-60 minutes for regular products and at 60-120 minutes for extended release forms. Two major conjugation pathways are used to metabolize acetaminophen by most species (P-450 metabolism followed by glucuronidation or sulfation). Acetaminophen-induced hepatoxicity and nephrotoxicity is due to the formation of the metabolite, N-acetyl-para-benzoquinoneimine (NAPQI), in the liver and to a lesser degree in the kidney. NAPQI binds covalently to sulfhydryl groups on tissue macromolecules leading to cell necrosis. Glutathione can conjugate and neutralize NAPQI, but when glutathione stores are depleted, NAPQI binds to the hepatic cell membrane and damages the lipid layer. Large doses of APAP can cause nephrotoxicity characterized by proximal tubule necrosis. Another metabolite, para-aminophenol (PAP), has been show to damage the RBCs leading to methemoglobinemia and Heinz body formation.

Methemoglobin values increase within 2-4 hours, followed by Heinz body formation. Clinical signs seen with acetaminophen toxicity include depression, weakness, hyperventilation, icterus, vomiting, methemoglobinemia, hypothermia, facial or paw edema, death, cyanosis, dyspnea, and hepatic necrosis. Other possible clinical signs include metabolic acidosis, renal insufficiency/damage, myocardial damage, coma, thrombocytopenia, and vomiting. Liver necrosis is less common with cats than with dogs. Clinical signs of methemoglobinemia may last 3-4 days. Hepatic injury may not resolve for several weeks. Hepatotoxicity has been reported in dogs at 100 mg/kg and 200 mg/kg caused clinical methemoglobinemia in 3 out of 4 dogs. Doses of 40 mg/kg have resulted in KCS 72 hours after ingestion. Cats develop clinical signs at doses >40 mg/kg. No dose is safe in cats since they are deficient in glucuronyl transferase. Ferrets are considered to be as sensitive as cats.

Early decontamination is most beneficial. Emesis can be performed in the asymptomatic animal, unless contraindicated. Activated charcoal adsorbs acetaminophen and may need to be repeated, due to enterohepatic recirculation. A cathartic should also be used, unless the animal is dehydrated or has diarrhea. Monitor liver values and for the presence of methemoglobinemia. ALT, AST and bilirubin may rise within 24 hours after ingestion and peak within 48 to 72 hours. Serum albumin concentrations decrease significantly after 36 hours and continue to decrease during liver failure, providing a true index of liver function.

Symptomatic patients need initial stabilization, including oxygen if dyspneic. Treatment involves replenishing the glutathione stores and converting methemoglobin back to hemoglobin. N-acetylcysteine (Mucomyst®, NAC) is hydrolyzed to cysteine and becomes a precursor in the synthesis of glutathione or can also be oxidized to organic sulfate needed for the sulfation pathway. This provides sulfhydryl groups which bind with acetaminophen metabolites to enhance elimination. NAC is available in 10% and 20% solutions. An initial oral loading dose for NAC would be 140 mg/kg of a 5% concentration (can be diluted in 5% Dextrose or sterile water) and then 70 mg/kg PO QID for generally 7 treatments. With ingestion of massive quantities some authors suggest using 280 mg/kg for a loading dose and continuing treatment for 12 to 17 doses. Adverse effects of the oral route of NAC include nausea and vomiting. Not all NAC is labeled for IV use however the loading dose (diluted to 5%) could be given slow IV over a period of 15 to 20 minutes with use of a bacteriostatic filter (0.2 micron) in life-threatening cases. A two-to-three hour wait between activated charcoal administration and PO administration of NAC is recommended, since activated charcoal could adsorb NAC as well as acetaminophen. Fluid therapy is used to correct dehydration and for maintenance needs, not for diuresis. Whole blood transfusions or oxyglobin may be necessary to increase oxygen carrying capacity.

For hepatic injury, a new therapy that shows potential is s-adenosylmethionine (SAMe, Denosyl-SD4®) at 20 mg/kg/day. Early studies and anecdotal reports show a positive effect for treatment of acetaminophen toxicosis. OTC formulations of SAMe have variable potency; use a prescription quality, enteric coated product (round the dose to nearest whole pill and do not break pill). Steroids and antihistamines are contraindicated.

Prognosis is good if the animal is treated promptly. Animals with severe signs of methemoglobinemia or with hepatic damage have poor to guarded prognosis. Treatment may continue for weeks.