Toxicology cases in veterinary medicine are not as commonly seen in primary practice as infectious disease or trauma. However, veterinary nurses or technicians should have a working knowledge of the common toxicants in order to know what pertinent questions to ask when taking a patient's history, anticipate what clinical signs they can expect to observe in their patient during nursing care, and help provide medically correct answers to common questions owners may ask about the poison. The focus of this article is on some of the toxicants commonly identified with small animal patients.
General concepts of toxicology as it applies to veterinary nursing
A toxicant is any poison, while a toxin is a poison that comes from a biological origin (e.g. tetanus toxin and toad toxin). Most toxicants produce an acute onset of clinical signs, although there are some exceptions to the rule. One example are anticoagulant rodenticides and ethylene glycol (antifreeze), which cause toxicity after being metabolised to a more toxic ingredient or produce a secondary physiological effect that manifests as toxic signs. Therefore, if a patient was fine in the morning and now is ill in the afternoon, toxicants and trauma (physical or biological, such as a ruptured splenic tumor) should be at the top of the differential list for causes (Gupta, 2007). Even relatively rapidly appearing infectious diseases usually have prodromal clinical signs before the onset of significant disease noticed by the owner. During admission of the patient, this chronology of clinical signs (clinically normal in the morning, ill by afternoon) should prompt the veterinary nurse or technician to ask questions about the animal's environment, opportunities to access potentially toxic agents (e.g. access to a garage, unsupervised outside, etc), human medications in the household to which the pet may have access, and any other questions that can help the veterinarian identify the potential for toxicity.
Owners need to be advised to bring in any suspected material that the animal may have contacted or ingested. A chewed medication bottle, a foil tablet strip, a part of a chewed rodenticide bait or a prescription medication bottle can enable the veterinarian to identify more accurately the potential toxicant and the amount of toxicant ingested or contacted.
Because the progression of many toxicants is so rapid compared with infectious diseases, and because most intoxications produce vague clinical signs early on (e.g. vomiting and lethargy), the history plays one of the most critical roles in arriving at an early diagnosis. Failure to ask the correct question to gain a key piece of patient information may delay both the diagnosis and the correct intervention needed to prevent progression of the intoxication (Schildt and Jutkowitz, 2009).
Many orally ingested toxicants produce vomiting. The contents of such vomitus may contain the toxicant and thus may provide a valuable clue to the cause of the clinical signs. Whoever handles the initial client contact by telephone or on presentation of the patient should advise the owner to bring in the vomitus if at all possible. The presence of grain, granules or coloured dye are all clues of potential oral ingestion of a common toxicant (Schildt and Jutkowitz, 2009).
As a general rule, owners should not spend time trying to induce vomiting of the suspected oral toxicant if the veterinary practice is within a few minutes' drive of their location. It is more important to have the animal admitted, evaluated and medically determined if induced vomiting will provide more benefit than risk. Ingestion of corrosives (e.g. strong acids, alkalies or oxalates), light petroleum products (e.g. gasoline) or other compounds that either burn the oesophagus or create a significant risk for aspiration are reasons not to induce vomiting. If the animal is semi-comatose, has depressed gag reflexes or has ingested a medication that has anti-emetic properties, vomiting poses a greater risk for aspiration of acidic stomach contents than benefits if the owner were to attempt induction of vomiting (Hackett, 2000).
Most toxicants do not have an antidote. Thus, treatment for intoxication is targeted towards decreasing absorption, increasing elimination and supporting body system functions long enough for the poison to clear the body and the animal to recover. Because of the paucity of effective antidotes, a philosophy in treating toxicants is to treat the animal, not the poison.
As intoxications may result from malicious poisoning, it is critical that any physical evidence (e.g. vomitus, physical injury, toxicant containers, boxes or bottles, partially chewed rodenticide baits) be kept or documented, along with a detailed physical examination and history. In the event of litigation, veterinary records in their original form may be subpoenaed as court evidence, and any attending veterinary team members called to appear or submit a disposition of their observations (Gwaltney-Brant, 2013).
Other general principles for stabilising an intoxicated patient include the use of charcoal or other adsorbents (compounds that cause toxicants to adhere to their surface) and the use of emetic drugs and cathartics, all of which are covered in greater detail in other veterinary sources (Dorman, 1997; Cope, 2004).
Human medications
Perhaps because of the increase in prescribed human medications found in the typical household (e.g. antidepressants, treatments for chronic conditions such as arthritis or pain and cholesterol medications), the number of inquiries to veterinary poison control centres regarding accidental human medication intoxications has increased (Figure 1). The associate director of the Pet Poison Helpline in Minneapolis, Minnesota, USA, estimates that over 50% of the calls received in 2012 were regarding pet ingestion of human medications (Lee, 2013).
It is important for the veterinary nurse or technician to remember that dogs and cats can react very differently to medications compared with the equivalentsized human. The classic example is acetaminophen/paracetamol, which is toxic in cats but well tolerated in humans. Because the way cats and dogs absorb, metabolise and eliminate medications, an equivalent low mg/kg dosage of a human medication can potentially be lethal to a pet.
When such calls are received, the veterinarian needs to know how many tablets, capsules or what volume of liquid medication the veterinary patient potentially has received. By knowing the amount of drug ingested and the weight of the animal, the veterinarian or veterinary nurse may be able to compare the ingested dose of the toxicant to the toxicant's LD50 (dose as which 50% of animals die) or the maximum tolerated dose/minimum toxic dose (MTD). This will help in assessing the risk for toxicity and communicating the prognosis for recovery to the owner of the intoxicated animal.
Antidepressants
Antidepressants are a broad category of human drugs used for clinical depression, sleep disorders, anxiety and a wide variety of other disorders including attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD). The veterinary nurse may recognise antidepressants under their category names such as selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs) or monoamine oxidase inhibitors (MAOIs). Because these drugs work by altering the balance of neurotransmitters within the brain, intoxication in veterinary patients can appear as central nervous system (CNS) overstimulation (agitation, hyperactivity, tremors, tachycardia/tachyrhythmias, hypertension or hyperthermia from tremors/seizures) or paradoxically as profound sedation.
Identifying the medication is key to interpreting the clinical signs. Treatment is targeted towards reducing the clinical signs (e.g. reducing tachycardia or reducing seizures) or supporting body systems (e.g. supporting respiration if profound depression has occurred). Hyperactivity and overstimulation are often treated using major tranquilisers such as acepromazine (Wismer, 2000; Thomas et al, 2012; Lee, 2013). Successful treatment depends on sustaining the body systems and functions long enough for the drug to be metabolised and eliminated.
It is important to determine the brand name of the human prescription product ingested as some forms of the medications are sustained release, extended release or long acting, meaning that treatment for these medications will need to be extended beyond the typical 24 hours it takes to eliminate these drugs from the body. Long-acting versions of drugs typically have additional letters added to the trade name (e.g. XR, LA or SR) to indicate their difference from the base drug version.
Sleep aids
Sleep aids are medications that work by enhancing the inhibitory neuronal effects in the brain, producing sedation. In pets, these drugs typically produce ataxia and sedation to varying degrees depending on the dose. However, occasionally, these sedative-type products produce a paradoxical central nervous stimulation, resulting in the patient being agitated and hyperactive. As a general rule, these medications have a wide safety margin; for those animals with ataxia and sedation, the animal is typically given supportive care (e.g. intravenous fluids to maintain hydration and arterial blood pressure) and cage rest. The animals with agitation and hyperactivity should not be given a benzodiazepine tranquilizer (e.g. diazepam or midazolam), as the hyperactivity is a result of the sleep aid that either acts in a similar mechanism as the benzodiazepines or may actually be a benzodiazepine. Instead, phenothiazine tranquilisers such as acepromazine are sometimes used to relieve some of the agitation and hyperactivity (Lee, 2013).
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs are widely used as non-prescription products in human medicine (e.g. naproxen, ibuprofen, ketoprofen and diclofenac), whereas in animals they constitute a toxic threat because of the pet owner administering the drug to their pet rather than visiting the veterinarian. In addition, prescription forms of NSAIDs are used in both veterinary medicine and human medicine. As such, NSAID toxicity is a common toxicity that has been widely publicised in the veterinary literature (Villar et al, 1998).
More detailed information on treatment and supportive care is readily available in other publications (Talcott and Gwaltney-Brants SM,2013; Gupta, 2007), but the key point with NSAID toxicosis is the impact on the gastrointestinal (GI) tract and the kidney. NSAIDs decrease inflammation by blocking the formation of prostaglandins associated with the inflammatory response (redness, swelling and pain). However, by also blocking the formation of beneficial prostaglandins in the GI tract, which stimulate increased mucus production, reduce acid production and improve perfusion to the GI tract tissue, the NSAIDs predispose the GI tract to inflammation (gastritis and enteritis) and potentially ulcers.
The renal toxicity effect comes primarily from the use of NSAIDs at the same time as the animal is hypotensive. The beneficial prostaglandins normally produced in the kidney keep the renal blood supply dilated and adequate blood flowing to the kidney tissue even under conditions of low blood pressure. However, under the influence of NSAIDs, these beneficial prostaglandins are blocked from being produced, and the vasodilatory effect under hypotension is similarly blocked. Thus, under hypotension, parts of the kidney tissue may not receive adequate blood supply, resulting in ischaemia and cell death, a condition referred to as renal papillary necrosis. Treatment for NSAID intoxication is targeted towards maintaining normal blood pressure to circumvent hypotension and renal damage, and protecting the GI tract (Talcott and Gwaltney-Brant, 2013).
It is important for veterinary nurses and veterinary technicians to emphasise to clients to keep chewable veterinary NSAID products away from their pets, as the enhanced flavouring of the tablets are attractive to animals, especially dogs. Numerous reports in the veterinary literature attest to dogs gaining access to veterinary NSAID products and ingesting large quantities, producing severe NSAID toxicosis.
Acetaminophen/paracetamol
Acetaminophen/paracetamol is widely found in nonprescription pain relief and ‘cold and flu’ medications. Because it is not an inhibitor of peripheral prostaglandins like the NSAIDs, it is promoted as being better for its lack of GI side-effects in humans. Although descriptions of this poisoning in cats are widely disseminated in veterinary literature, dogs can also experience toxicity. In both species, toxicity results from overwhelming the ability of the liver to remove a toxic intermediate metabolite that is produced in the normal metabolism of acetaminophen/paracetamol in mammals, including humans. The cat's reduced capacity to metabolise makes the cat more susceptible to this toxicity at a far lower dose than the toxic dose in dogs; in cats, one 500 mg tablet can be lethal (Roder, 2004). Cats manifest with brown discolouration of the mucous membranes and blood as a result of the toxic metabolite's conversion of haemoglobin to met-haemoglobin and the corresponding change of colour of the blood. As a result of the change in the oxygen-carrying capacity of the haemoglobin, the cat may appear in respiratory distress or rapidly breathing (tachypnoea). Swelling of the paws and face is reported in both species. The toxic metabolite is also hepatotoxic, thus signs of liver injury or failure are seen, especially in dogs. While hepato-toxicosis also occurs in cats, the rapid progression of clinical toxicosis owing to compromise of the oxygen-carrying capacity of the blood results in death before clinical signs of liver disease have the opportunity to develop (Sellon, 2013).
Household products
Chocolate
The toxicity of chocolate (theobromine and caffeine) and its GI signs (vomiting and diarrhoea), cardiovascular signs (tachycardia, hypertension and arrhythmias) and CNS hyperactivity signs (pacing, agitation, tremors and seizures) are widely published elsewhere in the veterinary nursing and veterinary medical literature (Meadows and Gwaltney-Brant, 2006). The key points are that the amount of methylxanthines, theobromine and caffeine vary according to type of chocolate, with milk chocolate having the least at about 60 mg theophylline per oz of milk chocolate (2.1 mg/g), dark chocolate about 150 mg/oz (5.3 mg/g) and baking chocolate having the most at 450 mg/oz (15.9 mg/g) (Gwaltney-Brant, 2001). Generally, GI tract signs appear at the lowest dose exposures, cardiovascular responses occur at slightly higher doses and CNS signs appear with the most severely intoxicated (Meadows and Gwaltney-Brant, 2006).
Treatment is targeted towards preventing absorption by elimination of the chocolate from the GI tract (Figure 2), reducing the methylxanthine stimulatory effects on the cardiovascular system through use of beta-blocker anti-arrhythmic drugs (e.g. metoprolol or propranolol) and reducing the CNS stimulatory effects with benzodiazepines (e.g. diazepam or midazolam) (Gwaltney-Brant, 2001). Because renally excreted methylxanthines can be reabsorbed from the urine through the bladder wall, it is often recommended to use a urinary catheter to keep the bladder empty of urine.
Xylitol
Xylitol is a common artificial sweetener ingredient found in many sugar-free gums (concentrations can vary widely), candy, baked goods, sugar-free drinks, mouthwashes, toothpastes and sugar-free vitamins. Although an overdose of ingested xylitol typically produces an osmotic diarrhoea in humans, xylitol can produce severe hypoglycaemia and hepatotoxicosis in dogs (Dunayer and Gwaltney-Brant, 2006). At lower doses, the toxicity is related to the massive release of insulin caused by the xylitol. The spike of insulin results in blood glucose levels plummeting within 10–30 minutes of ingestion (Dunayer, 2004).
A dog with a sudden onset of depression and lethargy with possible exposure to sugar-free items should have a statutory blood glucose check to help confirm xylitol ingestion. At higher doses, xylitol is hepatotoxic, but signs of hepatotoxicity (icterus, haemorrhage as a result of the liver's inability to produce clotting factors or liver enzyme elevation on blood chemistries) may not occur until days after the ingestion (Dunayer, 2006). The clinical signs of hepatotoxicity can occur without a hypoglycaemic episode. It is important to remember that activated charcoal commonly used to adsorb (adhere to) toxicants and prevent absorption into the body will not work with xylitol because it will not adhere to the charcoal.
Treatment is targeted towards control of the blood glucose levels, removal of xylitol from the GI tract by inducing vomiting and the use of laxatives, and supportive care for the liver for up to 2 weeks after the intoxication, using drugs such as S-adenosyl-L-methionine (SAMe).
Grapes, raisins, currants and sultanas
Grapes, raisins, currants and sultanas emerged as a potential toxicant in dogs around 1999 (Eubig et al, 2005). Toxicity can occur from either ingestion of the fruit or dried fruit, or from fruit cakes that contain the dried grape products (Sutton et al, 2009). The mechanism and toxic agent have yet to be identified, and as such there is little explanation for the widely varying sensitivity to the toxicity of grapes or raisins (Morrow et al, 2003; Mazzaferro et al, 2004).
The clinical signs most commonly seen are initial vomiting, often containing macerated grapes or raisins, followed by diarrhoea and lethargy (Eubig et al, 2005). The unknown toxicant is a nephrotoxin and produces acute renal damage and failure. As the actual toxicant is not known, the toxic dose is not established. However, documented toxicity has occurred at doses of 9–18.5 g (0.32 to 0.65 oz) grapes or raisins per kg bodyweight (Mazzaferro et al, 2004). The acute renal failure can occur any time after 24 hours, with clinical signs (e.g. lethargy, inappetence or polyuria) and laboratory values (e.g. increased blood urea nitrogen, creatinine and fixed-range specific urine specific gravity) reflecting renal compromise or failure (Gwaltney-Brant et al, 2001; Morrow et al, 2003).
Treatment is targeted towards decontamination through induced emesis and activated charcoal, followed by intravenous fluid diuresis to help reduce the impact of the nephrotoxicity (Campbell and Bates, 2003). If caught early, the prognosis is good for recovery; however, if the animal is presented with anuria or after significant renal signs have appeared, the prognosis is far more guarded (Mazzaferro et al, 2004; Eubig et al, 2005).
Permethrin
Permethrin is a type II pyrethroid insecticide and repellent included in topically applied ‘dog-only’ flea products. The high concentration of permethrin in these products (45–65%) and the poor metabolism of permethrin by the feline liver results in toxic accumulation when the product is inadvertently applied to a cat, or a cat comes in contact with the permethrin application site on the dog (Volmer, 2004; Linnett, 2008; Merola, 2006). Because permethrin is a neurotoxicant, initial signs appear within a few hours and include full body tremors progressing to seizures. Treatment is targeted towards reducing seizures or tremors using methocarbamol, and decontaminating the cat's exposure by bathing in a liquid hand-dishwashing detergent, which can remove the oily sebum on the cat's skin where the insecticide is distributed (Richardson, 1999; Sutton et al, 2007). More recently, the use of intravenous lipid emulsion has been shown to be an effective adjunct therapy for treatment of cats with permethrin toxicosis (Kuo and Odunayo, 2013). Permethrin toxicosis is one poisoning that can be prevented by the veterinary nurse or technician emphasising the need and the rationale for why this canine insecticide needs to be kept away from any cats in the household.
Ethylene glycol
Ethylene glycol found in antifreeze and de-icing compounds continues to be a source of toxicosis in small animals, despite the introduction of safer formulated and more bitter tasting propylene glycol antifreeze products (Rowland, 1987). The high toxicity of ethylene glycol, its sweet, attractive taste and the progression of clinical signs relative to the rate at which the compound becomes highly nephrotoxic to the kidneys all contribute to the poor prognosis for recovery of animals presenting with clinical signs of this toxicity. While ethylene glycol produces signs similar to ‘alcohol intoxication’ (e.g. vomiting, ataxia or drunken gait), by itself these effects are not typically life threatening; because this stage of intoxication may resolve to some degree within a few hours, owners may perceive the animal as improving, thus delaying taking their pet to the veterinarian. Unfortunately, during this period of time the liver is metabolising ethylene glycol to the far more toxic metabolites that result in metabolic acidosis and acute renal disease and failure. Clinical signs of renal failure are typically evident within 36–72 hours post ingestion in dogs and 12–24 hours post ingestion in cats (Thrall et al, 2013). Calcium oxalate crystals do not appear in the urine until the ethylene glycol has been metabolised to the toxic metabolites including oxalic acid, which combines with calcium to produce the characteristic crystals in the urine (Grauer et al, 1984).
Treatment is focused primarily on support of renal function, as by the time the animal is presented 24-48 hours after ingestion, the ethylene glycol has been fully absorbed and the metabolism of ethylene glycol to the more toxic metabolites has already occurred. Still, if an animal is presented sufficiently early, typically immediately after being observed to drink from a puddle of antifreeze, decontamination by induction of emesis can be tried, and administration of compounds that inhibit or reduce the effectiveness of the enzymes used to metabolise the ethylene glycol to toxic metabolites can be implemented (Thrall et al, 2013). Ethanol (ethyl alcohol) can be administered intravenously and binds to the same enzyme (alcohol dehydrogenase) that metabolises ethylene glycol to the toxic compounds. If the ethanol can ‘tie up’ the enzyme, the ethylene glycol itself may be eliminated by the kidneys before it is converted to the toxic metabolites. However, this intervention must occur within a few minutes to hours to be effective (Thrall et al, 2013).
Fomepizole is another compound that inhibits the alcohol dehydrogenase enzyme, and can likewise prevent the formation of toxic metabolites. It is expensive, not widely available and did not have much clinical evidence that it improved survivability over ethanol, especially in cats. However, some more recent evidence does suggest that higher doses used within 3 hours of ingestion may be more effective than ethanol (Connally and Thrall, 2010). Regardless of treatment, the best ‘treatment’ is prevention of exposure in the first place, and that is something the veterinary nurse or technician can do through client education and public service information opportunities (e.g. television, radio media and printed materials).
Poisonous plants
A total review of toxic plants commonly affecting small animals is beyond the scope of this article, but there are certain principles all veterinary nurses or technicians should know related to toxic plants in general. The number of systemically toxic plants is relatively small compared with the far larger number that can produce a mild gastric irritation and vomiting as a result of their physical presence in the GI tract. Identification of plant toxicity is often complicated by the fact that some plants have multiple common names used by the public, the suspected plants involved are often misidentified by owners and there are often ornamental variations with similar names to a toxic plant, but which possess no significant toxicity. Often an owner may only know of the general name for a group of similar plants such as ‘lily’, which exist in a wide variety of forms encompassing multiple genera of plants, some of which are toxic and some of which are not. Additionally, widely disseminated public information may be incorrect, including some plants, like the poinsettia, which have a ‘history’ of being reported as lethally toxic, when in actuality they are not especially toxic.
Additional challenges to correctly assessing the toxicity risk from plant ingestion includes the fact that many toxic plants may be poisonous to one species but not another, the plant may be toxic as a young sprout but not as an adult plant or vice versa, or only particular parts of the plant are toxic while others are relatively harmless. Thus, to properly assess the toxicity risk, the veterinary nurse or technician should instruct the owner to bring the suspected plant with them, if possible, for proper identification. Additionally, the veterinary professional should be familiar with the names and toxicity of those plants commonly found growing in their region or country, and know which plants are widely distributed in retail stores that sell indoor house-plants or outdoor ornamentals. Veterinary poison control centres often have information or links to additional online resources on their website, and multiple pictures of toxic plants for identification can be easily found on the internet.
Lilies
Lilies of the genus Lilium, which includes Easter lilies, tiger lilies, stargazer lilies and Asiatic lilies, and lilies of the genus Hemerocallis, which includes day lilies, are very nephrotoxic to cats (Figure 4) (Merola, 2006; Campbell, 2007). All parts of the plant are considered potentially toxic, as is the water that accumulates in the pot saucer on the bottom of the plant's pot. Clinical signs include initial GI tract irritation (vomiting or anorexia), followed by signs of renal injury and nephrotoxicity 24–48 hours later (Rumbeiha et al, 2004). Polyuria and polydipsia progressing to anuria in advanced cases are characteristic of renal injury. Elevated blood urea nitrogen, creatinine and phosphorous are characteristic blood chemistry profile alterations indicating decreased glomerular function along with casts in the urinalysis reflecting injury to the renal tubules.
Treatment is targeted towards intravenous fluid diuresis to support the kidneys and reduce toxic injury. Because the basement membrane of the renal tubules may remain intact after the toxic injury, the renal tubules may be able to partially regenerate over several days to weeks if interventional treatment is successful in arresting the progression of the damage. Anuria confers a poor prognosis for recovery (Hadley et al, 2003; Hall, 2013).
The peace lily (Spathiphyllum species) and calla lily (Zantedeschia species) are not members of the Lilium genus and do not have nephrotoxic effects like the lily plants described above. Although these plants contain insoluble calcium oxalate crystals that produce gastric irritation and vomiting, they are not lethal. This is a good example of where the well-educated veterinary nurse or technician can help correctly identify whether a toxicosis risk is present or not.
Other toxic agents
Other agents of toxicologic concern reported in the veterinary literature include ingestion of human iron supplement tablets (hepatotoxic), lithium or alkaline batteries (corrosive, perforation of GI tract), paintballs (hypernatraemia causing swelling of the brain) (Donaldson, 2003; King and Grant, 2007), metaldehyde found in snail bait or slug bait (inhibition of the gamma-aminobutyric acid neurotransmitter causing seizures and respiratory failure) (Dolder, 2003), and various herbal remedies or supplements. This is obviously not a comprehensive list of possible small animal toxicants, and any substance or product ingested that is not readily found in the veterinary literature warrants a call to a local poison control centre for advice.
Other agents not of great toxicological concern
Many poison control centres receive telephone calls about many items that are not toxic or unlikely to produce severe toxicosis. These include insect bait stations, discs or chambers that typically have low doses of commonly used veterinary insecticides (e.g. avermectins or fipronil) or boric acid, plus an attractant (e.g. peanut butter). The attractant makes these items attractive to dogs, but the amount of insecticide ingested is unlikely to produce toxicosis. The plastic container of the bait station itself poses more of a threat as a foreign body than the insecticide contained.
Glow sticks and glow jewellery do contain an oily substance, dibutyl phthalate, that has the potential to be toxic if enough is ingested. However, the dibutyl phthalate has a low toxicity in general, and is so unpleasant tasting that the animal (typically the cat) rejects the object immediately and instead shows signs of salivation and agitation as a result of the taste itself. It has been suggested that, if possible, the cat be given tuna fish oil, milk or pleasant-tasting soft food to help remove the bitter taste (Rosendale, 1999).
The small silica gel packs shipped with items meant to be kept free of excessive moisture are for the most part non-toxic; they are composed of silica or sand and are usually non-reactive when ingested.
Topical insecticidal products containing insect growth regulators, such as methoprene or pyriproxyfen, or products specifically formulated for topical application on the cat have a low degree of toxicity to both dogs and cats (Wismer, 2004). Dermal reactions to a topical agent will show as excessive grooming of the area of application or redness of the skin. Grooming and oral ingestion of the product typically produces increased salivation, reflecting the bitter or unpleasant taste of the product and thereby limiting the amount ingested.
Fertiliser products generally have a wide margin of safety and produce self-limiting signs associated with GI irritation (e.g. vomiting, diarrhoea, salivation and lethargy). However, while the nitrogen, phosphorous and potassium of fertilisers have limited toxicity, herbicides or insecticides added to the fertiliser can produce toxicosis. Owners who suspect ingestion of a fertiliser product should present the container so the full extent of possible toxicosis from multiple ingredients can be evaluated.
Conclusion
By being vigilant to watch for suggestions of possible toxicant exposure in a patient presented to a veterinary hospital or discussed during a telephone conversation, the veterinary nurse or technician familiar with common toxicants can solicit information to assist the veterinarian in arriving at a diagnosis and can better communicate factual information to clients and the public regarding common small animal toxicants.