Common hazards for cats (Proceedings)
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.
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).