93 | The essential guide to toxicology part four: how to manage rodenticide and pesticide toxicities as a veterinary nurse

NursingPodcastToxicologyEmergency + Critical CareNeurology
Written By Laura Jones

In this episode, we’re continuing our miniseries on toxicology with some of the common pesticide poisonings we see - specifically anticoagulant rodenticide, metaldehyde and organophosphate toxicity.

There are a whole host of different medication toxicities we see, and in this episode I’m going to walk you through 4 big ones: paracetamol toxicity in cats, NSAID toxicity in both cats and dogs, inhaler ingestion or overdose, and ingestion of antidepressants and ADHD medications.

These common pesticides and biotoxins cause severe, often life-threatening signs in our patients, and as veterinary nurses and technicians, we’re often the ones responsible for advising our clients, triaging and stabilising these patients, and providing intensive nursing care as they recover.

And to do that well, we need to understand exactly how these toxins affect our patients, the complications and clinical signs they cause, and the treatment and nursing care these patients need. Which is exactly what we’re covering in this episode.

Starting with probably the most common pesticide we encounter… anticoagulant rodenticide toxicity.

Anticoagulant rodenticides are widely used worldwide and can cause significant harm to mammals, birds and wildlife. Patients may be exposed via direct ingestion of the specific rat bait toxin, or ingestion of prey or scavenged target animals resulting in relay toxicity.

How do anticoagulant rodenticides work, and what happens if a dog eats rat poison?

Anticoagulant rodenticides are available in various formulations, each with different active ingredients. We can break these down into first-generation anticoagulants (which include warfarin, pindone, chlorphacinone and diphacinone) and second-generation anticoagulants (such as brodifacoum, bromadiolone, and difenacoum).

First-generation anticoagulants aren’t as potent as second-generation. In fact, target species generally need to ingest the toxin multiple times for it to be fatal. Second-generation anticoagulants, on the other hand, are more potent. They have median lethal doses between 2.5x and 200x lower than first-generation varieties, meaning lower doses will cause significant clinical signs.

In dogs and cats, the toxic dose is generally accepted as 1/10th of this median lethal dose - depending on the individual active ingredient.

Anticoagulant rodenticides inhibit the vitamin K epoxide reductase enzyme, a protein critical for producing vitamin K.

Since vitamin K is a vital component of many clotting factors - particularly factors II, VII, IX and X - the body can’t make sufficient clotting factors, and coagulopathy results. 

The onset of this coagulopathy is delayed, since the body will have a supply of clotting factors to use before bleeding becomes apparent. Circulating supplies of these factors are exhausted around 24-64 hours after ingestion, meaning that clotting times remain normal for the first couple of days.

So that’s how rat poison impacts our patients - but what signs do we see in affected cases?

We don’t necessarily always see clinical signs, and in fact, if the patient’s ingestion was witnessed, that’s the ideal time to intervene. However, if the ingestion was missed, or treatment is delayed, clinical signs will develop around 3-5 days after ingestion of a toxic dose.

These signs are associated with coaglopathy and bleeding, and the cardiovascular impact severe haemorrhage has.

Patients commonly present with:

  • Lethargy

  • Weakness

  • Epistaxis

  • Bruising

  • Haematoma

  • Petechial haemorrhage

  • Haematemesis

  • Melena

  • Haematochezia

Pleural haemorrhage (haemothorax) and pulmonary haemorrhage (potentially causing haemoptysis) are also common; both of these will have significant impact on ventilation and oxygenation, causing marked respiratory signs.

Rarely, joint haemorrhage and CNS haemorrhage can also occur, causing joint pain and lameness and neurological signs, respectively. And where haemorrhage is severe, significant hypovolaemia and anaemia will result - causing cardiovascular signs such as pale mucous membranes, tachycardia or bradycardia, and weak pulses.

What about diagnosis and decontamination?

Decontamination is vital in non-clinically affected patients who have known or suspected recent ingestion. Because the onset of clinical signs is so delayed, patients with any of the signs listed above are not suitable for decontamination - instead, our focus is on rapid diagnosis, stabilisation and treatment.

If appropriate, emesis should be induced. Activated charcoal may be considered, though it is often not used, due to the widespread use and availability of the antidote - vitamin K1.

In all patients, regardless of clinical signs, coagulation testing should be performed. This should include:

  • Baseline PCV measurement and total solids levels

  • Haematology

  • Prothrombin time

  • Activated partial thromboplastin time

An elevated PT is commonly seen in these patients, since this test evaluates the vitamin-K-dependent clotting factors within the body. This will typically elevate first, and aPTT will increase shortly after. By the time a patient presents with bleeding, both will be elevated.

In addition to this, patients with supportive clinical signs require additional testing, including blood typing +/- cross-matching in preparation for transfusion, thoracic and abdominal imaging (eg. point-of-care ultrasound) to look for evidence of bleeding.

So once the vet has confirmed the rat poison ingestion diagnosis, it’s time to start treatment.

Thankfully, treatment is simple and the antidote - vitamin K1 - is widely available.

Our treatment (and nursing care) depends on whether the patient is showing clinical signs at the time of presentation, and if so, how stable they are.

All patients require treatment with vitamin K1, regardless of whether bleeding is apparent. A prolonged course (typically 4 weeks) of oral vitamin K is given in most cases, though subcutaneous administration in hospital may be used initially. Medication should be given with food, since vitamin K is a fat-soluable medication, and clotting times should be repeated 24-48 hours after initiating treatment. Vitamin K acts quickly, and both PT and aPTT should improve within 12-24 hours.

If our patient is showing signs of haemorrhage or has prolonged clotting times, additional treatment will be required. This may include a fresh frozen plasma or frozen plasma transfusion to replace the lost clotting factors, or a whole blood transfusion where significant haemorrhage has occured.

Alongside this, supportive care, antiemetics and oxygen may be required, and patients should be kept calm, rested and handled carefully until they are no longer coagulopathic.

Our role in managing these patients as nurses and technicians is vast. We’ll be calculating and administering transfusions, performing careful venepuncture to minimise haemorrhage, providing respiratory support and monitoring things like bruising, melena and other signs of bleeding. We can also use tools like serial POCUS to check for free fluid, and alert the vet if bleeding progresses.

Outcomes are generally good for most anticoagulant rodenticide patients, providing we catch it early and intervene quickly - and nurses play an essential role in this.

The next toxin we’re looking at is metaldehyde - aka slug bait toxicity - in dogs.

These patients are often significantly unwell and their disease progresses rapidly. 

I’ll never forget the last few I saw - in fact, one evening in 2020 lockdown in the ICU we had two arrive at the same time. One ended up on a ventilator very quickly and the other didn’t look great either. 

I passed a nasogastric tube and started draining the stomach under the vet’s direction, and low and behold, out of my tube comes bright blue fluid - classic for metaldehyde.

Metaldehyde is the active ingredient in molluscicide agents - the drugs used to control slugs and snails. They’re used mostly in wet or coastal areas worldwide, and I say this as someone living in the south of England, recording this in a very rainy November - peak slug season!

Once slug pellets (and similar formulations, such as powder or liquid) are laid, they have a long duration of effect - metaldehyde can remain active for up to 10 days. Additionally, other agents such as carbamate insecticides are sometimes added to slug pellets to increase their effectiveness, meaning more severe signs for our patients.

What happens when a patient ingests slug pellets (or an affected slug or snail?)

Slug bait is highly palatable, so most patients present having consumed large quantities, and high doses. Most birds and mammals are susceptible to its effect, but we tend to see far more dogs than other species. Depending on the species, lethal doses range from 100-600mg/kg,

After the patient ingests metaldehyde, it is partially broken down in the stomach to acetaldehyde. Both metaldehyde and acetaldehyde are readily absorbed from the GI tract, and the severity and onset of clinical signs will depend on the stomach contents at time of ingestion, and the patient’s gastric emptying time.

Metaldehyde and its derivatives decrease inhibitory neurotransmitters within the body, causing significant CNS stimulation and excitation. Serotonin and noradrenaline levels also decrease, lowering the seizure threshold. Muscle tremors also occur, and the result of all of this is hyperthermia, severe electrolyte and fluid imbalances and metabolic acidosis.

What clinical signs do we see in affected patients?

After slug bait ingestion, patients will rapidly develop dose-dependent neurological signs. These are seen around 1-3 hours after ingestion, and include:

  • Severe tremors

  • Anxiety/agitation

  • Ataxia

  • Hyperaesthesia

  • Tachycardia

  • Hyperthermia

  • Depression

  • Hyperventilation

  • Continuous tonic seizures

  • Obtunded mentation with no response to external stimuli

  • Vomiting

  • Diarrhoea

  • Hypersalivation

  • Abdominal pain

  • Cyanosis

As you can see from these signs, patients are often critically unwell and require intensive supportive and nursing care to recover.

How do we diagnose, treat and nurse these patients?

Metaldehyde poisoning is made based on a history of exposure to slug bait, with supportive clinical signs. This diagnosis may be confirmed by analysing gastric contents; in some cases, metaldehyde concentrations can be measured, though this is often not performed since the disease progresses rapidly, and the test is not easy or quick.

Treatment is supportive - with decontamination, tremor management and supportive care.

There is no specific treatment for metaldehyde toxicity, and instead aggressive management is indicated. Patients should be anaesthetised and undergo gastric lavage and activated charcoal administration as soon as possible.

Intravenous lipid emulsion can also be used to create a ‘lipid sink’ and absorb free-circulating toxin, since it is lipophilic. Alongside this, sedation or anaesthesia, muscle relaxants (such as methocarbamol) and fluid therapy is required.

Nursing is intensive. These patients are recumbent and anaesthetised, so close monitoring, recumbency care, special sense care and temperature monitoring and management are essential. We also need to balance their need for intensive care with their hyperaesthesia and stimulation risk - minimising further stimulation or excitation that could trigger worsening neurological signs.

Thankfully, metaldehyde has a short half-life of around 27 hours, and provided we can support them through the period of toxicity, recovery is quick. Nursing makes all the difference in these challenging cases, and though they can be stressful, they’re incredibly rewarding to care for.

Our last toxin today is organophosphate toxicity.

Organophosphates are widely used in insecticides around the world. There are hundreds of different organophosphate compounds, each varying in toxicity, residue levels and excretion.

These toxins work by inhibiting acetylcholinesterase enzyme. This significantly increases levels of acetylcholine in the body.

Acetylcholeine is a neurotransmitter responsible for transmitting nerve impulses to muscles at the neuromuscular junction. When levels increase, muscarinic and nicotinic acetylcholine receptors become overstimulated, leading to a cholinergic crisis.

These patients develop hypersecretion (eg. hypersalivation, lacrimation, diarrhoea and urination), convulsions, and rapid muscle twitches/tremors known as fasciculations.

Seizures and even death can occur, and the ongoing muscular twitches and activity causes oxidative inflammation and damage to the brain. Ultimately, this can result in respiratory failure.

What signs do we see in organophosphate toxicity?

These pesticides generally have a low margin of safety and patients present with signs of cholinergic overstimulation. This is divided into three main categories: muscarinic signs, nicotinic signs, and central signs.

Muscarinic signs include changes to heart rate, hypersalivation, miosis, frequent urination, vomiting, diarrhoea, and dyspnoea due to increased airway secretions.

Nicotinic signs, on the other hand, include muscle fasciculations and weakness. And central signs include nervousness, ataxia, agitation and seizures.

Depending on the specific organophosphate toxin, we’ll see varying combinations and severities of these signs - for example, some agents do not cross into the brain as easily, limiting the neurological signs we see.

Patients will usually present with rapid-onset signs, depending on the volume ingested and the route of exposure. In most cases, signs develop minutes-to-hours after exposure, though delayed signs are also possible.

What about diagnosing, treating and nursing these patients?

Diagnosis is usually made using a combination of supportive clinical signs and potential exposure risk. 

Measuring acetylcholinesterase levels is also recommended, though elevated levels do not necessarily correlate with the severity of poisoning, and the test often takes a long time to perform.

Due to the rapid and progressive nature of toxicity, prompt and aggressive treatment is indicated. This includes antimuscarinics like atropine to counteract the effects of the toxin, and cholinesterase-reactivating medications such as pralidoxime. Intravenous lipid emulsion has also been successfully used as an adjunctive treatment, though its effectiveness varies depending on timing, and the specific organophosphate toxin.

Decontamination is also essential; like metaldehyde, emesis or gastric lavage (depending on the patient’s neurological status) should be performed in cases of recent ingestion, and dermal exposure should be decontaminated ASAP.

Just like metaldehyde toxicity, these patients need intensive nursing care. Thorough monitoring, reducing stimulation, careful cardiovascular and respiratory monitoring, temperature management and recumbency care are all vital nursing considerations for these patients.

So there you have it - an overview of some of the common pesticide toxicities that we see, and the nursing care they need. Depending on the individual toxin, there’s a LOT of nursing to do with these patients - from decontamination, to line placement, to intensive monitoring, recumbency care and lots more. But with that comes a lot of skills for us to use, and a reminder of just how important we are in toxin management.


Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
Next

92 | The essential guide to toxicology part three: how to manage common medication toxicities as a veterinary nurse