91 | The essential guide to toxicology part two: how to manage dietary toxins confidently as a veterinary nurse

NursingPodcastToxicologyEmergency + Critical Care
Written By Laura Jones

I’m willing to bet that most people listening have seen a dietary toxin case at some point in their career.

Dogs especially have a knack for raiding bins, cupboards, and kitchen counters. Thankfully most cases we see are mild, but they can be life-threatening and need intensive monitoring and nursing care. 

But what happens when our patients ingest these toxins? What signs do we see, and what nursing care do these patients need? Well, it varies depending on the toxin - but it’s often intensive.

Today, we’ll focus on three big dietary toxins: chocolate, grapes, and tremorgenic mycotoxins. We’ll talk about how they affect our patients, the signs to look out for, and how to treat and nurse these patients effectively. So you can spend less time on the phone to the poisons helpline, and more time caring for your patients.

Let’s start with canine chocolate toxicity.

Chocolate contains methylxanthines, specifically theobromine and caffeine. These compounds impact messenger molecules and transmitters within cells, causing stimulation. To get technical for just a second, they actually increase levels of something called cyclic AMP within the cells. cAMP is responsible for mediating levels of hormones, neurotransmitters, and other stimuli. The result of this increase? Huge catecholamine release - simply put, methylxanthines cause massive cardiovascular and central nervous system stimulation.

So what happens when a dog eats chocolate?

Well, the first thing to say is this: not every single chocolate toxicity case will get that massive surge of stimulation I just mentioned. 

The levels of theobromine significantly vary depending on the cocoa content within the chocolate. White chocolate has virtually none, milk chocolate has low-to-moderate levels, and dark chocolate (and cocoa powder) are the most dangerous, with very high theobromine concentrations.

When deciding how to manage a patient, we need to take into account not just the type of chocolate eaten, but the volume of it.

Toxic theobromine doses are reported to be from 20mg/kg, with severe signs noted at 40-50mg/kg, and seizures reported at 60mg/kg. Current recommendations are to treat patients who have consumed over 3.5g dark chocolate/kg bodyweight, or over 14g milk chocolate/kg bodyweight.

Dogs metabolise theobromine very slowly, with a half-life of up to 17.5 hours, so effects are prolonged. Cats are equally sensitive but less commonly affected, since most won’t seek out chocolate.

What signs do we see with chocolate toxicity in dogs?

Clinical signs usually appear within 6–12 hours of ingestion. Depending on the dosage, signs vary from mild GI signs, to significant neurological and cardiovascular signs such as:

  • Vomiting and diarrhoea

  • PU/PD

  • Hyperexcitability and restlessness

  • Tachycardia and arrhythmias

  • Tremors and seizures

  • Hyperthermia

So that’s the signs we see. What about treating (and nursing) these patients?

As we discussed in episode 90, patients should undergo gastrointestinal decontamination, assuming they’ve consumed the chocolate within an appropriate timeframe.

Theobromine is absorbed by activated charcoal, so after inducing emesis, repeated doses of activated charcoal are warranted. As the toxin can be recirculated between the liver and GI tract, it takes a long time to completely clear the toxin from the system, so prolonged activated charcoal treatment is required.

Aside from gastrointestinal decontamination, treatment is supportive. IV fluids may be used to support renal clearance of the toxin and manage any dehydration present. Anti-seizure medication may be needed depending on the patient’s clinical signs, and if arrhythmias are present (and interfering with cardiac output), antiarrhythmics may be required.

These patients need significant monitoring, particularly of their cardiovascular status, whilst minimising stimulation. These patients are often hyperexcitable, and need careful (but often intensive) management. 

What about grape and raisin toxicity?

Grapes - and dried grapes, including raisins, sultanas and currants - are a frustrating toxicity to manage, mostly because we don’t know why toxicosis occurs, and which patients are most susceptible.

Grapes contain levels of tartaric acid and potassium bitartrate, with varying concentrations depending on the variety and growing conditions. Dogs have a unique susceptibility to tartaric acid, and related organic acids - meaning dogs can have a severe reaction to even just a few grapes or raisins.

And that reaction? Acute kidney injury.

Specifically, these compounds can cause proximal tubular necrosis in the nephrons, leading to significant renal dysfunction.

There is a huge variation in the susceptibility between individual dogs; evidence in this area is lacking, and we still do not fully understand why some dogs react severely to relatively small amounts of toxin.

The lowest reported dosages to cause AKI are 19.6g/kg weight for grapes, and 2.8g/kg weight for raisins. However, even just a few grapes can be fatal in small dogs.

Alongside AKI, neurological and gastrointestinal signs are also reported following grape ingestion.

What signs do we see in grape toxicity, and how do we diagnose it?

Clinical signs are varied and non-specific, and usually appear within 6–24 hours of ingestion. They include:

  • Vomiting

  • Diarrhoea

  • Lethargy

  • Ataxia

  • Recumbency

  • Anorexia/inappetence

  • Abdominal pain

  • PU/PD initially, then oliguria or anuria as renal injury develops

  • Uraemic signs such as halitosis, oral ulceration

Diagnosis is usually made based on clinical history and examination, potential or confirmed ingestion, and evidence of acute kidney injury on bloodwork.

Biochemistry tends to reveal increased BUN and creatinine, increased phosphate, and potentially hyperkalaemia. Hypercalcaemia may be seen, as the high sugar levels in grapes can stimulate calcium absorption.

And urinalysis often reveals isosthenuria (SG 1.008-1.015) with proteinuria.

Ok, so that’s how we diagnose grape ingestion in dogs - but what about treating and nursing it?

We need to treat grape ingestion aggressively, regardless of the dose our patient ingests - because we can’t make direct correlations between how much a patient consumes and the severity of their clinical signs.

If emesis is possible (based on ingestion time and the patient’s presenting signs) then this should be performed. Activated charcoal is not super effective, so is generally not as essential; instead, the mainstay of treatment is IV fluid diuresis to promote renal clearance of the toxin. Baseline renal parameters should be re-evaluated after 12 hours, 24 hours and 48 hours of treatment depending on the individual patient.

Alongside this, antiemetics and gastroprotectants are often indicated in patients with gastrointestinal signs.

In patients with severely compromised renal function, advanced renal support therapies may be required. We can’t keep pushing IV fluids into a patient with failing kidneys and decreasing urine output - as we’ll end up giving them fluid overload. So, in those patients, our focus instead aims on either replacing renal function (with dialysis) whilst the kidneys recover, or attempting to increase urine output with diuretics.

For nurses, this is where our skills really come in. Monitoring and supporting AKI is very nursing-intensive, particularly when it comes to fluid therapy and preventing overload. Accurately assessing fluid balance, measuring urine output, weighing patients regularly and adjusting fluid rates to match urine output are essential.

Alongside this, regular monitoring of renal parameters and electrolytes are key, alongside nutritional support, elimination management, close monitoring, and general supportive nursing care.

Client communication is also a huge part of our role. Caregivers are often shocked that such a small amount of raisins could require days of hospitalisation, so providing appropriate advice and support, and managing their expectations, is also important.

Our last canine dietary toxin is tremorgenic mycotoxin… commonly caused by mouldy food.

We don’t tend to think of these as a classic dietary toxin, but they’re more common than you think. In fact, a tremorgenic mycotoxin was the first ever emergency I got called out to help with as a student nuse. A dog had raided the bin and eaten mouldy bread, and next thing you know… he’s on a propofol CRI.

Tremorgenic mycotoxins are produced by certain fungi found in mouldy food, spoiled dairy products, and compost. Often dogs will present with signs after raiding the bin, eating mouldy bread, or rummaging through a compost heap.

The toxins work by interfering with inhibitory neurotransmitters such as GABA in the central nervous system. This leads to CNS stimulation and uncontrolled firing of neurons.

There are several different tremorgenic mycotoxin species, such as penitrem A, produced by penicillum mould, roquefortine C, and penitrem C, produced by some species of both penicillum and aspergillus moulds. Regardless of the toxin type ingested, we tend to see similar clinical signs.

What signs do we see in dogs who have ingested tremorgenic mycotoxin?!

Depending on the amount ingested, patients will present with varied neurological signs, lasting from hours to days. These signs can develop very quickly, within 30 minutes to 2 hours of ingestion.

Vomiting is usually seen initially, and can be helpful as it will limit the severity of the intoxication. After this, patients tend to develop:

  • Vocalisation

  • Salivation

  • Blepharospasm

  • Fasciculations

  • Localised or generalised tremors

  • Hyperaesthesia

  • Ataxia and incoordination

  • Tachycardia and hyperthermia due to muscle activity

  • Seizures, which can escalate to status epilepticus

  • Respiratory signs (in the case of aspiration pneumonia)

Patients who have ingested lower concentrations of toxin generally have fine muscle tremors that last for hours to days, whereas larger-scale intoxication cases generally present with seizures, and can even be fatal.

A key clinical feature of tremorgenic mycotoxicity is that stimulation worsens signs. Dogs may appear quiet when left alone but tremor violently when touched or disturbed. This is important for us to note, as it means our nursing care must focus heavily on reducing external stimulation.

Ok, that’s the signs we see - what about diagnosing these patients?

Like most other toxicity cases, diagnosis is made based on supportive clinical signs and a history of potential or confirmed exposure to mouldy food or compost. 

We don’t tend to see specific changes on bloodwork or diagnostic imaging, though elevated CK (due to muscle activity) is commonly seen, and changes associated with things like inflammation and aspiration also may be present.

And when it comes to treating these patients, there’s a LOT of nursing care to think about.

If the patient has presented early, is stable and does not have significant neurological compromise, decontamination is indicated. This includes inducing emesis where appropriate, administering activated charcoal (if possible, depending on the patient’s neurological status and aspiration risk) and potentially considering gastric lavage if the patient’s neurological status indicates.

After decontamination, treatment is aimed at controlling seizures and muscle tremors. Benzodiazepines, methocarbamol and propofol CRIs are commonly used to do this.

Intravenous lipid emulsion (ILE) has been used successfully in some tremorgenic mycotoxin cases, though evidence is limited. Intravenous lipid emulsions such as intralipid act as a ‘lipid sink’ or ‘lipid shuttle’, meaning that highly lipophilic agents become sequestered in these lipid molecules, rather than absorbed by the body.  Penitrem A, for example, is a lipid-soluble compound, meaning ILE can be used in patients with severe signs not responding to standard therapy.

Alongside controlling the neurological signs, fluid therapy is generally required to support hydration and perfusion status, antiemetics are used to control vomiting and minimise the risk of aspiration. 

Temperature management is an essential nursing consideration for these patients; most are hyperthermic due to persistent muscle/seizure activity, so active cooling is necessary. 

Reducing stimulation is also key - house these patients in a quiet, dimly-lit area but one where they can still be monitored closely. Keep their monitoring as hands-off as you possibly can, utilising multiparameter monitoring to observe their vitals from a distance, and avoid handling them as much as possible.

Aside from this, recumbency care is a huge part of their nursing. We need to balance their hyperaesthesia and stimulation risk with the fact they’re sedated - managing bladder and bowel function, and turning when necessary. We also need to be mindful of aspiration - particularly if repeated doses of activated charcoal are needed. It may be better to place something like a nasogastric feeding tube in these patients, and administer the charcoal via that if possible.

Nursing care is intensive, but rewarding. With good nursing care, most patients recover relatively quickly - within 24-72 hours. However, low-level signs such as ataxia can persist for months-to-years in some cases, so ongoing supportive care and caregiver support is essential.

So there you have it - a refresher on three of the biggest dietary toxins we see in dogs.

Whether it’s tremorgenic mycotoxins, chocolate, or grapes and raisins, our role as nurses and technicians is critical in managing toxicology patients, and it cannot be overloooked.

We’re the ones triaging these patients, arranging decontamination, monitoring their sedation (if needed) and providing that ongoing monitoring and supportive care in the hospital.

So when you’re nursing one, monitor them closely (but hands-off), reduce stimulation where needed, and pay careful attention to things like cardiovascular signs, fluid balance, and neurological status, and be prepared to intervene quickly if your patient deteriorates.

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
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90 | The essential guide to toxicology part one: how to decontaminate poisoned pets as a vet nurse