Background: There are two types of intoxicated patient that present to veterinary practices: the asymptomatic patient with a known exposure and the patient with clinical signs that may (or may not) be due to a toxin or poison. Deciding when (or if) to treat these patients is often an inexact science and the decision must be made based on numerous risk factors, the owner’s level of comfort with risk and any financial constraints.
Aim of the article: This article is the first in a series of four and aims to provide a basic overview of the approach to decontamination of an asymptomatic patient presented with a known intoxication. It also outlines therapies that may be considered in both symptomatic and asymptomatic patients, and these will be discussed in more detail in future articles.
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Karen Humm graduated from Cambridge university in 2001. She is a senior lecturer in small animal emergency and critical care at the Royal Veterinary College.
Tom Greensmith graduated from the Royal Veterinary College in 2010. He is a lecturer in small animal emergency and critical care at the Royal Veterinary College.
Key learning outcomes
After reading this article, you should understand:
The structured approach to deciding whether a potentially intoxicated patient should be treated;
Techniques for decontamination and when they should and should not be used;
Additional supportive care for intoxicated patients;
When it may be appropriate to undertake haematology and biochemistry testing;
Antidotes available for specific toxicants.
Although these terms are often used interchangeably, a ‘poison’ or a ‘toxicant’ is defined as any agent that may have harmful effects upon an organism, while the term ‘toxin’ should be reserved for a poison of biological origin.
Whether a patient is at risk following an intoxication depends on numerous factors, including the dose, drug formulation, route of exposure, species affected, the speed with which treatment is administered, patient co-morbidities that affect toxicant metabolism and clearance (such as chronic kidney disease or hepatopathy), and any concurrent medications the animal may be receiving.
With the exception of agents that are directly irritating to tissue (corrosive or caustic toxicants such as bleach), toxicants need to be absorbed by some route into the body. The most common route of exposure is oral ingestion. Once absorbed, the toxicant is often (but not always) metabolised before being excreted. Metabolism may detoxify the compound, or (as with ethylene glycol and paracetamol) result in the formation of more toxic metabolites.
The major powerhouse of toxicant metabolism is the liver, with common routes of excretion from the body being renal and biliary excretion. Knowledge of how each toxicant is metabolised and excreted can be clinically useful, as it allows assessment of whether treatment may need to be adjusted due to patient co-morbidities. In-depth understanding is not essential for most toxicants encountered in small animal practice; however, pertinent details that may affect treatment (such as whether the toxicant undergoes enterohepatic recirculation) are always important to be aware of.
Taking a history
Telephone triage and taking a history are important aspects of the care of animals with potential intoxication (Box 1). If an owner believes their pet has been exposed to a toxicant, every effort should be made to determine the realistic likelihood of this. Owners often believe intoxication may be the cause of their pet’s illness. Therefore, targeted questions are necessary to validate or negate this theory, including when the potential exposure was likely to have occurred, any evidence of access to toxicants (turned over bins, chewed tablet boxes, etc) and any clinical signs noted so far.
Guidance for telephone triage of an owner contacting a practice about a potentially intoxicated pet
Obtain signalment of patient.
Suspected timing of ingestion/exposure
Advise that the pet should be brought to the practice immediately if appropriate based on the information provided.
Determine likely time of arrival.
If the toxicant is on the skin or coat, instruct the owner to place an Elizabethan collar or wrap the pet in a towel to prevent further ingestion.
For ocular contamination the owner can be instructed to rinse the corneal surface with tap water (if they consider that it is safe to attempt this).
Instruct the owner to bring any packaging of the suspected toxicant.
While the owner is en route, the rest of the clinical team can be informed to allow preparation.
Poison information services can be contacted and if it is determined decontamination is not required, then the owner can be contacted.
This approach prevents wasted time while information is gathered as the more rapidly emesis is induced, the more effective it is likely to be.
Owners who have witnessed toxicant ingestion or exposure, or are highly suspicious about exposure to a particular substance, should be asked to bring in the container of the toxicant if this is possible, as this will provide clarity about the exact toxicant and possibly the dose ingested. It is also vital to ask if the owners have already attempted any treatment themselves (such as administration of salt water to induce vomiting), as in some cases these methods can be more dangerous than the toxicant in question.
Practitioners should advise that any pet with acute-onset clinical signs severe enough to concern an owner should be brought to the veterinary practice for examination. Such signs may or may not be attributable to a toxic exposure, but only with a thorough history and physical examination can the index of suspicion for intoxication be ascertained.
On presentation, a major body systems assessment (triage) should be performed. This fast and focused examination assesses the three main body systems responsible for life, namely the neurological, cardiovascular and respiratory systems. Marked abnormalities in any of these three systems require rapid intervention and stabilisation as otherwise the patient is at risk of rapid deterioration and death. Management of intoxicated patients with major body system instability will be discussed in the later articles in this series.
To determine the likelihood of toxicant exposure being the cause of the patient’s clinical signs, clinical and historical information should be gathered, which can then be assessed objectively. Intoxicated pets with overt clinical signs often have a peracute onset of signs attributable to one or more organ systems. The specific constellation of clinical signs (and in some cases haematological and biochemical abnormalities) may aid the clinician in deriving a list of likely toxicants. Targeted questions can then be asked to determine the likelihood of exposure. ‘Could your pet have been exposed to a poison?’ is less useful than ‘Do you have any slug pellets in your home, garage or garden?’ for example, particularly as owners may well be unaware of many of the possible toxicants in their households.
The time course of clinical signs can also be useful – is the patient deteriorating, improving or has it remained static? This information can help in narrowing a differential diagnoses list for the toxicant involved and in guiding the ongoing therapy and providing a prognosis.
It is important to note that confirmation of intoxication is not required before starting supportive care. Depending on the organ system involved, more specific tailored therapy may be required as the clinical signs progress.
In asymptomatic cases it is likely that the exposure was either witnessed, or at least very strong evidence of access to the toxicant has been noted by the owner (such as finding chewed tablet packets). In these cases, the primary aim of the veterinary surgeon should be to assess the possible consequences of intoxication to determine if it is necessary to see the pet. If in doubt, the animal should be examined. Some common non-toxic agents are listed in Box 2, but if unsure a reliable source (such as the Veterinary Poisons Information Service – www.vpisglobal.com) should be contacted for further advice.
common low toxicity or non-toxic agents
Borax (found in many ant and insect powders)
Ivy, holly, mountain ash, mistletoe and hyacinth
Oral contraceptive pills
Statins, proton pump inhibitors
Many fertilisers (including bone meal)
* While commonly considered to be toxic, cases of severe intoxication are extremely rare. Local oral/gastrointestinal irritation are the most likely sequelae to exposure.
The dose of the toxicant to which a patient has been exposed is often unknown, and in this situation it is safer to assume a ‘worst case’ scenario than to be conservative in any evaluation. In cases where the dose is considered enough to cause the patient clinical concerns, decontamination and supportive care are indicated.
In the majority of cases, toxicants are ingested and therefore gastrointestinal decontamination is required. This is a broad term that includes the induction of emesis, gastric lavage and whole bowel irrigation. Induction of emesis is the most commonly employed of these techniques, and when used appropriately can reduce the dose ingested and potentially avoid serious consequences of oral toxicant ingestion.
While sources vary on the appropriate time frame to induce emesis, the sooner emesis can be performed after toxicant ingestion the better – in several canine studies recovery of toxicant from the stomach was between 17 and 62 per cent of the total dose ingested if emesis was induced within one hour (Lee 2019). This may well require prioritising these patients over others in the waiting room and rapidly obtaining a history and performing a physical examination to maximise the efficacy of emesis induction.
Some toxicants can be rapidly absorbed from the stomach (such as alcohols and xylitol powder), whereas others may remain present for many hours (grapes/raisins, extended-release pharmaceutical formulations, drugs that amalgamate, such as aspirin or xylitol-containing gum, and chocolates).
When considering whether to induce emesis, we suggest a risk-benefit calculation. Emesis should not be performed if there are any contraindications (Box 3), and while for some toxicants data suggest that emesis may not be useful unless performed within one to two hours of ingestion, if the patient has no clinical signs associated with intoxication and has no contraindications, it may still be beneficial to induce emesis even after an extended period. However, induction of emesis more than four to six hours after ingestion is unlikely to be beneficial.
Contraindications to induction of emesis
Caustic/corrosive agent ingestions (eg, bleach)
Hydrocarbon ingestion (eg, petroleums)
High risk of aspiration (reduced mentation, poor/absent gag reflex, laryngeal paralysis, megaoesophagus, severe brachycephalic obstructive airway syndrome)
Patients that have already experienced protracted vomiting after toxicant ingestion
Ingestion of a non-toxic/very low toxicity substance or dose
Severe acid-base or electrolyte derangements that could become life-threatening if worsened by gastrointestinal fluid loss
Options for inducing emesis are described in Table 1. Apomorphine is the only licensed drug for inducing emesis in dogs and there is no licensed option for cats. Apomorphine has a rapid action and is considered to be consistently effective in most cases. Sodium hydroxide (caustic soda) crystals have a similar name and appearance to sodium carbonate (washing soda) crystals but are very caustic and can cause marked tissue injury, so care should be taken to ensure the correct product is chosen. In addition, the use of sodium carbonate powder rather than crystals has been reported to cause severe ulceration with adverse gastrointestinal and respiratory adverse effects (Watson and Indrawirawan 2019).
Other agents previously recommended to induce emesis that are no longer recommended include salt/salt water (as it can cause life-threatening hypernatraemia), mustard, syrup of ipecac and hydrogen peroxide. Although hydrogen peroxide was shown to have minimal adverse effects in one retrospective study (Kahn and others 2012), a prospective experimental study found significant overt and histopathological gastric lesions in dogs after administration of 3 per cent hydrogen peroxide (Niedswecki and others 2017) and severe necroulcerative haemorrhagic gastritis has been described in a cat after its use (Obr and others 2017).
Restricting the animal to an area prepared with newspaper or incontinence pads (Fig 1) is advisable once the emetic agent has been given, but it is important they can get away from their vomitus and that it is quickly removed once produced to prevent patient distress, soiling and repeat ingestion. It is also beneficial to examine the vomitus for the presence of the suspected toxicant (Fig 2) to allow confirmation of the supposed diagnosis, an understanding of the likely proportion of toxicant eliminated and reassurance for the owner. These patients also benefit from gentle handling and some tender loving care during this period as their nausea can be extreme and is likely distressing.
Gastric lavage (Fig 3) is not commonly employed in intoxicated human patients, with studies showing that recovery of gastric contents declines rapidly after one hour from ingestion. Animal studies suggest a similar time frame with documented mean toxicant recovery after one hour of between 8.6 and 13 per cent (Lee 2019). Therefore, there is no benefit to performing lavage over standard emesis in most patients. Gastric lavage is only indicated in animals with recent ingestion of a known lethal dose of a toxicant that have contraindications to the induction of emesis or in which emesis is not successfully induced. Toxicants that have a strong antiemetic action may also be considered candidates for gastric lavage. The technique for performing gastric lavage is outlined in Box 4.
technique for gastric lavage
Induce general anaesthesia and place a cuffed endotracheal tube with a good seal to protect the airway.
Pass a well-lubricated large bore stomach tube (measured from the mouth to the last rib [Fig a]) down the oesophagus into the stomach.
Instil 10 to 15 ml/kg of warm water (ideally close to body temperature) via the tube, while the stomach is gently agitated by turning the patient between lateral recumbencies. In smaller patients electrolyte disturbances are more common and so lavage with normal saline (0.9% NaCl) rather than water may be more appropriate.
The stomach tube should then be lowered into a container and both fluid and gastric contents allowed to drain under gravity and the siphon effect.
Repeat until the gastric effluent is clear, at which point the stomach should be emptied as completely as possible before kinking the tube (to prevent fluid egress from the tube while it is removed) and gently removing it in one smooth motion.
The pharynx and oesophagus should be suctioned to remove any extraneous fluid before recovering the patient from anaesthesia.
In cases where the toxicant ingested may bind to activated charcoal the instillation of a charcoal slurry into the stomach before removing the gastric tube can be considered; however, we do not routinely recommend this due to the risk of aspiration on recovery.
Whole bowel irrigation
Whole bowel irrigation is a very rarely employed technique in the intoxicated patient, in some part due to the need for an osmotically balanced solution with which to lavage the gastrointestinal tract, but mainly because it is very rarely indicated. A polyethylene glycol electrolyte solution is the most commonly recommended solution and this is instilled continuously (common recommendations are as high as 500 ml/hr) via a nasogastric tube until the rectal effluent is clear. We recommend that whole bowel irrigation is only performed on the advice of a specialist, as it is of theoretical benefit in only a small number of toxicities. Whole bowel irrigation should not be used in cases of severe gastrointestinal disease, such as bowel obstruction, ulceration or perforation.
Activated charcoal is a commonly used agent in small animal intoxication, due to its ability to non-specifically bind to a variety of toxicants. This action is due to its large surface area; therefore, administering it as a slurry or powder is far more effective than as tablets. Not every agent will bind to activated charcoal (for example, alcohol and xylitol do not). In cases where the toxicant does bind, the activated charcoal should be administered as promptly as possible, although clearly this needs to be after emesis or gastric lavage has finished.
Activated charcoal is particularly useful in the treatment of patients that have ingested toxicants that undergo enterohepatic recirculation (such as NSAIDs). Repeated doses of activated charcoal may be more beneficial than a single dose in these cases (the exact dosing interval and time frame for repeated doses likely varies between toxicants and there is not much in the evidence base – we commonly dose every four to eight hours for a 48-hour period).
Many animals will eat activated charcoal when mixed with food and this does not decrease its efficacy by a clinically relevant level (Wilson and Humm 2013). Voluntary ingestion of activated charcoal is beneficial as it decreases the risk of aspiration associated with syringe administration.
Complications reported with the administration of activated charcoal include constipation and hypernatraemia (due to its osmotic action). Because activated charcoal slows gastrointestinal transit time, many preparations contain a cathartic (such as sorbitol), but these preparations should ideally only be given as a single dose, as repeated cathartic dosing may lead to dehydration, hypovolaemia and hypotension, so the make-up of the formulation should be checked carefully before use.
Activated charcoal should not be used in patients with gastrointestinal tract abnormalities (such as obstruction) or those with ongoing vomiting and should only be used in those with a reduced gag reflex, altered mental status or seizures if the patient has a cuffed endotracheal tube in place. Activated charcoal may also reduce the efficacy of orally administered antidotes, although it is difficult to quantify this effect.
Rarely, decontamination may require surgical or endoscopic intervention, including some cases of metal intoxication (such as zinc, heavy metals and iron) in which the toxicant cannot be fully removed from the gastrointestinal tract in another way. Iron tablets may amalgamate and adhere to the gastric lining and ingested coins may not be fully removed with emesis for example. In such cases, if after discussion with a poison advisory centre more aggressive therapy is recommended, the potential for surgical or endoscopic removal should be remembered.
Dermal decontamination is much less commonly required in dogs and cats. It is necessary for substances that have the potential to be absorbed through the skin, such as permethrin, or substances that could be toxic if licked off the coat or skin, such as ethylene glycol. Before presentation to the practice, the owner could be advised to place an Elizabethan collar if they have one so as to prevent ingestion. Then, on arrival, decontamination is generally fairly simple to perform by clipping affected sections of the coat and cleaning the area with warm soapy water to limit any ongoing reservoir for dermal absorption. It should be noted that for some compounds (such as oil) specific detergents may be more effective than generic soap; again, specialist advice is advised in such cases. All members of staff dealing with these patients should wear protective clothing to prevent any risk to them.
Ocular decontamination may be required if a caustic liquid has splashed onto the eye. It is performed using either water (if performed by the owner as an emergency measure before presentation at the clinic) or 0.9 per cent sodium chloride (normal saline). Extended periods (more than 10 to 15 minutes) of ocular lavage are often needed, particularly if the compound involved is alkaline, given the high risk of severe corneal ulceration. The ocular surface pH can be measured using a urine dipstick at the planned end of flushing and if it is above 7.5 further flushing is recommended. Such thorough lavage may only be possible with sedation or anaesthesia in many animals. Once initial decontamination has been performed, an ocular examination should be undertaken, including fluorescein staining. It may be beneficial to consult with a veterinary ophthalmologist if evidence of corneal damage is present.
Routine haematology and biochemistry testing is not always indicated in asymptomatic patients and obtaining samples should not delay decontamination attempts. In many cases, these tests often have normal values. This could be due to insufficient time for toxicant absorption, or because the toxicant exerts its clinical effects without altering these values. Regardless, baseline values can sometimes be useful to assess for possible disease progression if measured parameters may change. For example, in cases of suspected ethylene glycol toxicity, it is useful to know a baseline creatinine level at initial assessment, as if it is found to be elevated after 24 hours, it may be unclear whether this is due to pre-existing underlying disease or the toxicant. Similarly, many cats can have a fairly high basal level of Heinz bodies and this can be confusing in cases of onion toxicity. Therefore, whether haematology and biochemistry testing is required should be determined by the specific suspected toxicant.
In symptomatic patients with a suspected but unspecified toxicant exposure, a complete blood count and biochemistry may help in narrowing the differential diagnoses for the toxicant. However, they are rarely able to provide a definitive answer. With these caveats in mind we would still recommend a minimum of packed cell volume/ total solids, blood glucose, electrolytes and renal/liver parameters in all symptomatic patients with suspected intoxication, as abnormalities in some may mandate immediate therapy (such as glucose administration in severe hypoglycaemia).
Urinalysis (assessing specific gravity, dipstick and microscopic evaluation to look for casts and crystals) may prove beneficial in some cases (such as suspected ethylene glycol ingestion) and should always be performed in patients with suspected or known exposure to nephrotoxicants, and in those with abnormal renal blood parameters.
More targeted testing could be indicated in some cases with a specific indication; animals with acute-onset bleeding disorders or known anticoagulant rodenticide exposure should ideally have prothrombin and partial thromboplastin times or activated clotting time assessed.
In some cases, analysis of samples may lead to a confirmatory diagnosis of the toxicant involved. Stomach contents, blood or urine can be submitted to a veterinary laboratory for analysis with large toxicology panels, which can provide results within 24 hours to 10 days depending on the toxicant involved. The advantage of these panels is that the individual toxicant does not need to be specified and many common intoxicants are tested for. Stomach contents produced either by lavage or emesis can be submitted and will be highly likely to give a positive result if the toxicant is present. False negative results can be obtained when urine is analysed early in the intoxication period, but generally by 12 hours after ingestion, the toxicant or its metabolites will be present. However, for some toxicants, by the time these results are available the patient may have either improved or died, but even in these cases, the results can provide some emotional relief for owners, and allow assessment of the risk to other pets that may be in the same environment as the exposed animal.
General supportive care
Intravenous fluid therapy is a cornerstone of general supportive care for intoxicated patients. They may have abnormal intravascular volume status, hydration status and/or electrolyte values, often due to gastrointestinal losses associated with vomiting or diarrhoea. Some toxicants that are renally excreted may benefit from an empiric increase in basal intravenous fluid rate (such as 4 ml/kg/hr instead of 2 ml/kg/hr) in excess of any dehydration deficit. This is considered forced diuresis; however, data on the efficacy of this technique are lacking for most toxicants. Contraindications to forced diuresis include toxicants that are not renally excreted, patients with known underlying heart disease, hypertension or oliguric/anuric renal failure. The excretion of some toxicants (such as aspirin) can be improved by urinary alkalinisation, but such measures should only be employed if the ability to monitor blood pH is available, as severe acid-base derangements can occur during therapy.
Patients that have pain should receive appropriate analgesics – in the intoxicated patient it is often best to avoid NSAIDs in case of renal injury and instead opt for an opioid such as buprenorphine or methadone. Patients with intractable vomiting should be provided with antiemetics such as maropitant or metoclopramide, as well as gastroprotectants such as omeprazole or sucralfate to reduce the risk of oesophagitis and gastric mucosal damage. More specific therapeutics for given toxicants will be described in future articles in this series.
Specific antidotes and therapies
Some toxicants have antidotes available and a list of common antidotes is provided in Table 2. While some of these antidotes may not be habitually kept at the practice, they can often be obtained from an emergency veterinary clinic (the ToxBox collaboration between VetsNow and the Veterinary Poisons Information Service can provide antidotes to any veterinary practice), a local human pharmacy or a human hospital. Where a specific antidote exists, its use is strongly recommended to mitigate the severity of intoxication. Each antidote may have specific contraindications that should be taken into consideration.
Intravenous lipid emulsion therapy (IVLE) has been described as both a method of decontamination and as a non-specific antidote for the intoxicated patient. In recent years, IVLE has revolutionised the management of many forms of intoxication. While the exact mechanism of action is not fully understood, there are two main theories:
It provides a lipid phase within the blood, allowing reduced tissue concentration of any lipid-soluble toxicants.
It provides an alternative energy source in some specific cells (such as cardiomyocytes).
The risks associated with IVLE are considered to be very low, and so its use may be justified in cases where a lipid-soluble toxicant is suspected. Such risks include corneal lipidosis, fat overload syndrome and pancreatitis (Robben and Dijkman 2017).
IVLE should ideally be administered using an in-line 1.2 μm filter to reduce the risk of fat emboli. Repeated dosing can be performed if a clinical improvement is seen; however, before repeated dosing the patient should be assessed for lipaemia, and if it is present further doses should be withheld until the lipaemia resolves.
IVLE has been used for many toxicants – a list is provided in Box 5 although it is likely to be of use in the management of many other lipophilic toxicants not listed.
Toxicants potentially amenable to intravenous lipid emulsion therapy
Beta blockers (eg, esmolol, propranolol)
Calcium channel blockers (eg, amlodipine, verapamil, diltiazem)
Ivermectins and milbemycins (eg, moxidectin, avermectin)
Local anaesthetics (eg, lidocaine, bupivacaine, ropivacaine)
NSAIDs (eg, ibuprofen, naproxen)
Tricyclic antidepressants (eg, amitriptyline, mirtazapine)
Thiopental, phenobarbital, pentobarbital
Extracorporeal drug removal is not commonly available within the UK at this time, although it is useful in the management of many intoxications and is standard practice in people. Ideally the treatment is provided before the development of clinical signs, or in cases that are refractory to standard management. Three main treatment types exist: dialysis (for small compounds such as ethylene glycol), plasma exchange (for protein-bound toxicants such as NSAIDs) and charcoal haemoperfusion (which can be useful for both). While these therapies are not commonly employed, they are available at some referral institutions. A major difficulty is that the time from toxicant ingestion to presentation at a referral centre may be too long for these therapies to then be of use. Such modalities may increase as the technology becomes more widely available.
The management of the intoxicated patient can be both frustrating and rewarding. Knowledge of patient and toxicant factors help guide the decision as to whether therapy is indicated at all, and if it is deemed necessary then an understanding of the treatment options and supportive care in each case can affect the outcome. In this series of articles, we will highlight our clinical approach to intoxicated patients, with this basic overview to be followed by organ system-specific approaches in the upcoming articles.
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