ABSTRACT: This article examines three of the most common toxins for cats in a home environment. Permethrin-based spot-on products are widely available and often used accidentally on cats, resulting in twitching or seizures. Lilies often result in vomiting and severe renal failure when only a very small amount is ingested, if not identified and treated promptly. Ethylene glycol, most commonly found in antifreeze products, often carries a grave prognosis of acute renal failure. Basic treatment, expected clinical signs and prognosis are outlined for each poison, along with general poisoning first aid advice

Toxicology is the study of adverse reactions that any living creature may have to chemicals. It not only includes the study of signs we can expect to see, but also the treatment to counteract them and the detection of the toxin in the first place. We should have an understanding not only of a range of toxins, but also of the important relationship between dose and level of toxicity.

Because their hepatic metabolic pathways differ from those of the dog – they are deficient in certain hepatic enzymes – cats are unable to break down some chemicals and are, therefore, more susceptible to poisoning than dogs. In addition, it is often more difficult to determine an accurate medical history for cats, as they may be left alone for long periods of time with little supervision from their owners and they are often allowed to roam outside of their home environment.

However, given that cats are expected to be more discriminating in their choice of food than their canine counterparts, how the exposure to toxins occurs at all can be quite puzzling. Cats, though, are also known for their curiosity, and not all toxins are unpleasant to taste, so cases are not as uncommon as expected (Table 1).

When dealing with a suspected poisoned feline patient, a thorough history from the owner may reveal clues that would otherwise seem irrelevant. Establishing whether the illness has been acute or chronic in onset, or if there has been any known or possible toxin exposure, are good starting points.

Bear in mind that, although the term ‘poisoning’ can evoke suspicion of malicious intent, in most cases the cause is very much accidental or may even be a result of well-meaning intentions, or simply just lack of owner awareness.

Table 1 gives a summary of the three most common causes of toxicity to cats. An understanding of the most common toxic household products will undoubtedly aid in nursing feline patients when they are under our care. Unfortunately poisoning cases are often undiagnosed until they are critically unwell, which makes their care considerably more challenging.


The use of permethrin-containing products is becoming more widespread in cats and a recent report by the UK Veterinary Poisons Information Service (VPIS) revealed that it is the most common toxic cause of death in cats.1

Permethrin is an insecticide used commonly in spot-on flea treatments meant for dogs but is often used by pet owners on their cats with no knowledge of the consequences (Figure 1). It is so potent to cats that even grooming a dog that has been recently treated with a permethrin-containing product can be enough to result in a toxic event.

Figure 1: Permethrin-containing products are becoming more readily available in pet shops and supermarkets, and are considerably cheaper than other products on the market

In cats, permethrin acts as a neurotoxin, binding and blocking open sodium channels on the surface of nerve cells. This results in disruption to normal nerve cell function, resulting in muscle tremors, twitching and even seizures. There are some anecdotal reports of dogs reacting in this way to permethrin, but cats seem to be much more sensitive.


Treatment for permethrin toxicity can be intensive and prolonged and consists mainly of supportive care, as there is no specific antidote. As with all spot-on treatments, permethrin is absorbed through the skin.

As spot-ons are often applied with no knowledge of their potential for harm, a large amount may already have been absorbed by the time clinical signs become apparent and medical attention is sought. However, thoroughly washing the patient with lukewarm water and a mild shampoo can stop any further absorption.

Seizure management is also important – using benzodiazepines, barbiturates or even sedation or anaesthesia in more severe cases, to allow the muscles to ‘relax’. General supportive care will include giving intravenous fluids and helping to maintain temperature control as necessary.


These beautiful flowers tend to be popular both in gardens and bouquets owing to their potent fragrance and striking appearance (Figure 2). Lilies, however, indeed all of the Lilium plant species, are known to be highly toxic to cats.

Figure 2: Popular because of their striking appearance and potent fragrance, lilies are deadly to cats

It is a common misconception that only their pollen is toxic; in fact, the entire plant is dangerous. Ingestion of less than one leaf can result in renal failure. Toxic effects will also occur from brushing up against the flowers and then grooming pollen from the contaminated fur.

The main clinical signs of lily toxicity are prolonged vomiting, along with depression and anorexia. In more severe cases, the prognosis is very poor owing to renal failure. Clinical signs are often apparent within hours.


Treatment for known lily poisoning patients consists of decontamination of the fur by thorough washing and supportive nursing, such as intravenous fluid therapy to offset the effects of vomiting and, if renal changes are present, monitoring for clinical signs.

The most obvious way to avoid lily toxicity is for cat owners to prevent contact w
here at all possible. This can be important especially to house cats that may be bored and looking for stimulation within their home environment. Controlling contact for cats who are allowed outside is obviously much more difficult, but a passing knowledge of plants in neighbouring gardens would be very beneficial in these cases.

Ethylene glycol

Perhaps the most well known feline toxin is ethylene glycol, found not only in antifreeze products but also in car radiators and brake or transmission fluid. Ethylene glycol is either drunk directly – because it is sweet tasting – or groomed from contaminated paws or fur. Owing to its high toxic potential (only 1.4ml/kg is a fatal dose) prognosis is often grave and progression unpredictable.

Toxic products of the metabolism of ethylene glycol cause metabolic acidosis and renal tubular damage resulting in acute renal failure. The acidic and oxalate by-products result in the formation of calcium oxalate crystals, crystalluria and hypocalcaemia which have severe consequences. Initial signs within the first 12 hours of ingestion are usually severe vomiting and neurological signs, including ataxia, depression and incoordination.

Within the first 24 hours, renal damage will have begun, leading to acute renal failure. Usually, after 24 hours, marked acute renal failure will have developed, resulting in oliguria or anuria, continual vomiting and hyperkalaemia with associated bradycardia and ECG abnormalities in severe cases.

As ingestion of ethylene glycol is very rarely witnessed – and the early stages of toxicity progress quickly – diagnosis is often tricky and acute renal failure may often be the presenting sign. Diagnosing ethylene glycol toxicity is, therefore, based mainly on clinical findings: analysis of renal parameters to assess kidney function and urinalysis would normally show isosthenuria and the presence of calcium oxalate crystals.

Ethylene glycol blood levels can also be measured; but this test takes a long time to perform and is rarely used, because the significant time delay in receiving results isn’t beneficial when treating a suspected patient.


Treatment for patients who are known to have ingested the poison within the previous 12 hours should include gastric decontamination by inducing emesis or gastric lavage. Ethanol is known to inhibit the metabolism of ethylene glycol, thus delaying the formation of toxic by¬products when given intravenously. Either 20 per cent medical ethanol can be used or, if unavailable, plain vodka in an absolute emergency (a constant rate infusion of 1.25ml/hr can be used for up to 72 hours).

Treatment with any ethanol product after 12 hours is unlikely to help as acute renal failure will already have developed and so this will further impair renal function.

Supportive care in these cases is arduous and constant monitoring for further deterioration is of the utmost importance. Intravenous fluids are often at the forefront of treatment because renal perfusion will often need to be restored, so 0.9 per cent sodium chloride solution is recommended as hyperkalaemia may be present after considerable renal damage.

Urine production should be monitored closely, ideally by placing an in-dwelling urinary catheter, although bladder palpation is also helpful in oliguric or anuric patients. Care should be taken, when correcting renal perfusion, not to volume overload the patient and thoracic auscultation should be carried out regularly in the initial stages. Diuretics may be used to correct anuria, but not until volume deficits have been corrected and electrolytes should be monitored continually with regard to hyperkalaemia.

With severe cases, ECG abnormalities, namely spiked T-waves, are noted and treatment with intravenous calcium gluconate should be considered.

Peritoneal dialysis could also be considered as a last resort if azotaemia fails to improve despite treatment; however, the associated risk of infection and complications often outweigh the possible benefit and almost inevitably poor prognosis.


When giving advice for any suspected poisoning try to remember the following three points:

1.   Remove the patient from the toxic source, if known, and ask the owner to bring any packaging, plant or substance with them to the veterinary practice. Knowing with what toxin you’re dealing will lead to faster treatment and, therefore, a better overall prognosis.

2.   Prevent grooming if the fur is known to be contaminated. This can be done either by washing the patient thoroughly in lukewarm water using a mild shampoo, or wrapping it in a towel to prevent further grooming en route to the veterinary practice.

3.   When a known toxin has been ingested, inducing emesis is only advisable if the substance isn’t caustic, and this is best done at the veterinary practice under controlled conditions. This is especially important if mentation or consciousness is affected, as aspiration could occur. 


Angel Thompson RVN MBVNA

Angel Thompson, RVN, works at Dick White Referrals in Suffolk and has particular interests in internal medicine and oncology.

To cite this article use either

DOI: 10.1111/j.2045.0648.2012.00214.x or Veterinary Nursing Journal Vol 27 pp 344-346


1. Campbell. A. & Sutton. N. M. [2009] UK Veterinary Poisons Information Service [VPIS],

 • VOL 27 • September 2012 • Veterinary Nursing Journal