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The 10 most common toxicoses in catsValentina Merola, DVM, DABT, and Eric Dunayer, MS, VMD, DABT
Cats are sensitive to many toxic agents, sometimes in barbiturates, propofol, or both can be used. Diazepam is
ways unique to their species. In addition, cats are
generally ineffective for the tremors but should be used if
less likely than dogs to expose themselves through
curious ingestions, but cats will nibble on potentially deadly
Additional care should include monitoring the patient’s
agents, such as lilies. Cats also can jump to high places and
body temperature and administering intravenous fluids to
obtain materials assumed to be out of reach. And because of
protect the kidneys from myoglobinuria due to muscle
their grooming behavior, cats with dermal exposure are
breakdown. Atropine is not antidotal for permethrin; no true
antidote exists. The prognosis is generally good with aggres-
In this article, we describe 10 common toxicoses in cats.
The agents discussed were selected based on the 10 mostfrequent feline exposures reported to the ASPCA Animal Poi-
son Control Center (APCC) in the past four years.
Besides permethrin products, manyother flea control products are on the
pyriproxyfen, which have low oral and dermal toxic poten-
tial in mammals. Insecticide ingredients may include
organophosphates or carbamates, pyrethroids, imidacloprid,
in spot-ons and 3% or more permethrin in dips, are applied
fipronil, and selamectin, all of which when used appropri-
to cats accidentally or by individuals who ignore the warn-
ately (including low-concentration pyrethroid products) have
ings on the label. In some instances, cats have developed
a low risk of causing serious problems.4,5
signs of permethrin toxicosis after being in close contact with
In general, topical flea control products applied according
(sleeping near or grooming) a dog recently treated with a
to label directions will not cause systemic effects in cats.4,5 Any
permethrin spot-on product. Initial signs may appear within
topically applied product can cause either dermal irritation or a
a few hours but can take 24 to 72 hours to manifest. Full-
dermal hypersensitivity-like reaction. If dermal signs appear,
body tremors are the most common finding, although
wash the product off with a mild detergent. If the irritation is
seizures may also occur.1 Other pyrethroids, including phe-
localized, the contents of a vitamin E capsule or a corticosteroid
nothrin and etofenprox, can cause a similar syndrome in cats
cream can be applied. If the irritation is more widespread, cor-
ticosteroids or antihistamines may be used systemically.
Treatment consists of bathing the cat in a liquid hand
If a cat licks a topically applied product, a taste reaction—
dishwashing detergent (e.g.
Dawn Dishwashing Liquid—
characterized by hypersalivation, agitation, and occasionally
Procter & Gamble) to remove the sebum in which the prod-
vomiting—may develop. These signs are simply a reaction to
uct is distributed. If the cat is symptomatic, delay the bath
the bitter taste and can sometimes be quite dramatic. Remov-
until the tremors have been controlled. The tremors are best
ing the product from the tongue by giving the cat milk or liq-
treated with slow intravenous boluses of methocarbamol
uid from a tuna fish can should resolve the signs.
(Robaxin-V—Fort Dodge Animal Health; total initial dose 55to 220 mg/kg).1 Repeat the methocarbamol as needed, but
do not exceed a dose of 330 mg/kg/day or respiratory de-
pression may occur.3 If methocarbamol is not effective, then
Wyeth) is a bicyclic antidepressant avail-able in tablets and capsules of 25, 37.5,50, 75, 100, and 150 mg. Venlafaxine acts
“Toxicology Brief” was contributed by Valentina Merola, DVM, DABT,and Eric Dunayer, MS, VMD, DABT, ASPCA Animal Poison Control Center,
1717 S. Philo Road, Suite 36, Urbana, IL 61802. The department editor
take inhibitor as well as a weak dopamine reuptake in-
is Petra A. Volmer, DVM, MS, DABVT, DABT, College of Veterinary
hibitor. Cats seem to readily eat venlafaxine capsules (ASPCA
Medicine, University of Illinois, Urbana, IL 61802.
APCC Database: Unpublished data, 2003-2005). Less than one37.5-mg capsule is enough to cause mydriasis, vomiting,
tachypnea, tachycardia, ataxia, and agitation (ASPCA APCC
veals elevated creatinine, blood urea nitrogen (BUN), and
Database: Unpublished data, 2002-2005). Signs generally
phosphorus concentrations; the creatinine concentration is
begin within one to eight hours after exposure (later if an
often elevated disproportionately to the BUN concentration.7
extended-release formulation was ingested).
Urinalysis may show cellular casts beginning about 18 hours
Emesis may be initiated in asymptomatic patients. Acti-
vated charcoal is effective; repeat the dose in four to six
Treatment consists of immediate decontamination, in-
hours if the animal was exposed to an extended-release for-
cluding emesis and activated charcoal. Start fluid diuresis as
mulation. Be sure to monitor heart rate and blood pressure.
soon as possible, and continue it for at least 48 hours. The
Cyproheptadine (1.1 mg/kg orally or rectally up to three or
prognosis is good with prompt, aggressive treatment. Once
four times a day) can be used as a serotonin antagonist, and
renal failure develops, some recovery is possible but may
acepromazine or chlorpromazine can be used to treat agita-
take weeks, and the cat may require peritoneal dialysis for
tion. Generally, the prognosis is good with close monitoring
support.7 The development of oliguria or anuria is a poor
contain a liquid that glows in the dark.
fur if exposed to a spill. Liquid potpourri
July and at Halloween. Cats frequently bite into the jewelry.
may contain high concentrations of cationic detergents, es-
The main ingredient is dibutyl phthalate, an oily liquid that
sential oils, or a combination of both.9 Cationic detergents
has a wide margin of safety with an oral LD in rats of
are corrosive to the oral mucosa and can cause severe gas-
greater than 8 g/kg.6 So ingesting the contents of a piece of
trointestinal upset, drooling, central nervous system (CNS)
glow jewelry should not cause any serious effects. The
depression, and hypotension. Cats may exhibit dermal irrita-
chemical has an extremely unpleasant taste, and most cats
tion and ulceration as well as severe corneal ulceration if
will not ingest more than a small amount.
skin or eye exposure occurs. Essential oils may cause gas-
Almost immediately after biting into a piece of glow jew-
trointestinal and oral irritation and CNS depression.9
elry, cats exhibit signs of a taste reaction, including hypersali-
If the exposure is detected quickly, dilution with milk or
vation, agitation, and, occasionally, vomiting. The behavioral
water should be performed; do not induce vomiting or admin-
changes are likely due to the cat’s reacting to the unpleasant
ister activated charcoal. Hospitalize symptomatic cats. Sucralfate
taste. A tasty treat such as milk, liquid from a tuna fish can,
slurries can be used to coat and protect oral and esophageal le-
or other palatable food can ameliorate the taste reaction. Re-
sions while they heal. Pain management with opioids can
move any liquid on the fur with a wet washcloth to prevent
make the cats more comfortable. Monitor the white blood cell
re-exposure; take the cat into a darkened room to help you
count and begin antibiotics if signs of infection are evident.
Give intravenous fluids for hydration. Cats may be anorectic forseveral days, so forced feeding or alimentation through a feed-
ing tube may be needed until the cats recover. Endoscopy may
be required to evaluate esophageal damage, but be sure to
avoid further damage to or perforation of a devitalized esopha-
, renal failure has been seen
gus. The prognosis with supportive care is good unless
only with Lilium
lilies, Stargazer lilies, tiger lilies, Asiatic
lilies, Oriental lilies) and Hemerocallis
species (day lilies).7
Ingesting any part of the plant (including the pollen) may
cause signs, and even the smallest of exposures should be
After ingesting lilies, cats generally develop vomiting and
rarely, by self-ingestion, often with ca-
depression within two to four hours. Often the cats seem to
recover and then begin to deteriorate rapidly about 24 to 72
can cause gastrointestinal upset, including vomiting, diar-
hours after the exposure with signs of polyuria, polydipsia,
rhea, ulceration, hemorrhage, and ulcer perforation. Acute
and more severe depression.8 A serum chemistry profile re-
renal failure can occur at higher dosages. Some NSAIDs
have been associated with CNS signs such as seizuresand comas at high doses in cats. The more commondrugs that can cause this syndrome include carprofen,ibuprofen, deracoxib, naproxen, etodolac, meloxicam,and indomethacin.10,11
In general, cats have a low tolerance for NSAIDs. For
example, cats are thought to be at least twice as sensitiveto ibuprofen as dogs are.10 Gastrointestinal ulceration canoccur in cats exposed to 4 mg/kg of carprofen; acuterenal failure can develop at doses greater than 8 mg/kg(ASPCA APCC Database: Unpublished data, 2001-2005).
Because of this sensitivity, most exposures require aggres-sive treatment.
Initial treatment should consist of gastric decontamina-
tion. If spontaneous vomiting has not begun and the in-gestion was less than four hours earlier, induce emesis.
Then administer activated charcoal and give repeateddoses when exposure involves an NSAID that undergoesenterohepatic recirculation. To prevent gastrointestinal ul-ceration, administer an acid reducer such as an H2blocker (e.g.
ranitidine or famotidine) or proton-pump in-hibitor (e.g.
omeprazole), as well as sucralfate and miso-prostol (1 to 3 µg/kg orally b.i.d.)12 for seven to 10 days.
Monitor the cat for signs of gastrointestinal hemorrhage,such as melena or a decreased packed cell volume. Initi-ate fluid diuresis at twice the maintenance rate for at least48 hours to prevent renal damage, and monitor the re-sults of renal function tests.11
As with NSAIDs, acetaminophen isoften administered to sick cats bytheir owners. Acetaminophen has anarrow margin of safety in cats. Oneadult tablet (325 to 500 mg) could
be lethal. Clinical signs such as depression, vomiting,dyspnea, brown discoloration of the mucous mem-branes and blood due to methemoglobinemia, respira-tory distress, swelling of the face and paws, and hepaticnecrosis can develop at almost any level of exposure.11Signs of methemoglobinemia generally occur withinhours of exposure, and liver damage may take a coupleof days to manifest.
In asymptomatic cats, emesis may be initiated and ac-
tivated charcoal administered. If methemoglobinemia ispresent, start oxygen therapy combined with a bloodtransfusion or polymerized bovine hemoglobin solution(Oxyglobin—Biopure) administration. Begin N
Mucomyst—Bristol-Myers Squibb)therapy immediately in any case of acetaminophen expo-sure in a cat. Dilute the N
-acetylcysteine solution to a 5%concentration with 5% dextrose or sterile water; this will
■ Circle 107
on Reply Card
yield a 50-mg/ml solution. The loading dose is 140 mg/kg
followed by 70 mg/kg every six hours for seven additional
doses. Administer N
-acetylcysteine orally unless either a bac-
teriostatic filter or a sterile solution of N
pression, attention deficit disorder, and
(Acetadote—Cumberland Pharmaceuticals) is available. Ad-
junctive therapy includes intravenous fluids, cimetidine (to in-
hibit CP450 liver enzymes that activate acetaminophen to the
amphetamine, methamphetamine, and 3,4-methylene-
toxic metabolite), and ascorbic acid, which may be used to
dioxymethamphetamine (MDMA), also known as Ecstasy
help reduce methemoglobin to hemoglobin.11 The prognosis
phetamines act as CNS stimulants by increasing catecholamine
release, inhibiting catecholamine reuptake, and increasing re-lease of serotonin.15 Almost any exposure in a cat can result
in clinical signs such as agitation, hyperthermia, tremors,
seizures, tachycardia, hypertension, cardiac arrhythmias, and
coma (ASPCA APCC Database: Unpublished data, 2002-2005).
Treatment should include gastric decontamination if the
neurotoxin) or cholecalciferol (a vitamin
animal is asymptomatic, but a rapidity in the onset of clinical
signs may limit the possibility for this. Monitor cardiovascular
lants can cause coagulopathy by inhibiting the recycling of
and CNS signs closely. Also monitor body temperature, and
vitamin K and blocking the synthesis of clotting factors II,
maintain it in a normal range. Administer acepromazine or
VII, IX, and X. Clinical signs generally occur three to seven
chlorpromazine for agitation, and barbiturates may be used to
days after exposure when circulating clotting factors are de-
control seizures.16 Cyproheptadine may be used as a serotonin
pleted. Bleeding may occur in any location, so signs may be
antagonist. Treat cardiac arrhythmias as needed (e.g.
nonspecific and include weakness, lethargy, and dyspnea.13
nolol if tachycardia is present). Intravenous fluids will help
Hemorrhage is most common in the lungs, so cough or res-
promote elimination. Consider administering ammonium chlo-
piratory difficulty is a common finding.14 Frank hemorrhage
ride or ascorbic acid to acidify the urine and promote elimina-
or ecchymoses may be seen. Lameness may occur if bleed-
tion if acid-base balance can be monitored. The half-life of the
ing occurs in a joint, and various neurologic signs may be
drug and the duration of signs depend on the urinary pH, and
noted if bleeding occurs in the brain or spinal cord.13
signs may be seen for 12 to 48 hours or more.16 The prognosis
Anticoagulant rodenticide poisoning can be diagnosed
with aggressive supportive care is good in most cases.
by measuring the prothrombin time (PT). PIVKA (proteinsinduced by vitamin K absence or antagonism) and
Richardson JA. Permethrin spot-on toxicoses in cats. J Vet Emerg Crit
Thrombotest (Axis-Shield) time are other screening tests
for anticoagulant toxicosis. PT and PIVKA tests are most
Volmer PA. Pyrethrins and pyrethroids. In: Plumlee KH, ed. Clinical
. St. Louis, Mo: Mosby, 2004;188-190.
sensitive to depletions of factor VII because it has the
Plumb DC. Veterinary drug handbook
. 5th ed. Ames: Iowa State Uni-
Meerdink GL. Anticholinesterase insecticides. In: Plumlee KH, ed.
If performed within two to four hours of exposure, de-
Clinical veterinary toxicology
. St. Louis, Mo: Mosby, 2004;178-180.
contamination by inducing emesis and administering acti-
Wismer T. Novel insecticides. In: Plumlee KH, ed. Clinical veterinary
. St. Louis, Mo: Mosby, 2004;183-186.
vated charcoal is effective at reducing the amount absorbed
Rosendale ME. Glow jewelry (dibutyl phthalate) ingestion in cats. Vet
systemically. Otherwise, treatment with vitamin K (3 to 5
Volmer PA. Easter lily toxicosis in cats. Vet Med
mg/kg orally divided twice daily) is antidotal. Vitamin K1
Rumbeiha WK, Francis JA, Fitzgerald SD, et al. A comprehensive study
should be given for 14 days after warfarin exposure, for 21
of Easter lily poisoning in cats. J Vet Diagn Invest
Richardson JA. Potpourri hazards in cats. Vet Med
days after bromadiolone exposure, and for 30 days after
Villar D, Buck WB, Gonzalez JM. Ibuprofen, aspirin, and acetaminophen
brodifacoum and all other anticoagulant exposure or un-
toxicosis and treatment in dogs and cats. Vet Hum Toxicol
Roder JD. Analgesics. In: Plumlee KH, ed. Clinical veterinary toxicol-
. St. Louis, Mo: Mosby, 2004;282-284.
Also test the PT or PIVKA about 48 hours after cessation of
Boothe DM, Jenkins W. In: Adams HR, ed. Veterinary pharmacology
. 7th ed. Ames: Iowa State University Press, 1995;1025.
vitamin K treatment to determine whether the patient was
Means C. Anticoagulant rodenticides. In: Plumlee KH, ed. Clinical vet-
treated long enough. If an animal presents in hemorrhagic
. St. Louis, Mo: Mosby, 2004;444-446. 14.
Merola V. Anticoagulant rodenticides: deadly for pests, dangerous for
crisis, treatment is generally supportive and should consist of
whole blood or plasma transfusions and stabilization as
Hoffman BB, Lefkowitz RJ. Catecholamines, sympathomimetic drugs,
and adrenergic receptor antagonists. In Hardman JG, Limbird LE, Molinoff
needed as well as vitamin K .13 If treatment is started before
PB, et al
, eds. Goodman & Gilman’s the pharmacological basis of thera-
coagulopathy, the prognosis is excellent. The prognosis is
. 9th ed. New York, NY: McGraw-Hill, 1996;219-221. 16.
Volmer PA. Drugs of abuse. In: Peterson ME, Talcott PA, eds. Small an-
guarded if the patient is already bleeding.
. Philadelphia, Pa: WB Saunders Co, 2001;198-201. ■
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