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

NursingPodcastToxicologyEmergency + Critical Care
Written By Laura Jones

Today we’re continuing our toxicology mini-series with another group of very common, and often very critical, toxins - human medications.

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.

Some of these toxins will be seen due to accidental ingestion of a caregiver’s medication, and others may be well-meaning attempts at pain management from unknowledgeable caregivers. But regardless of how the toxicosis occurs, the impact on our patient is the same - and in some cases, it can be life threatening.

These patients also need a whole host of nursing support. We’re essential in the management of these cases, where prompt triage and stabilisation is vital, as is intensive monitoring.

To do that confidently, we need to understand how each of these toxins impact our patients, and the signs we see as a result - so we can spot them, and care for the patient accordingly.

And that’s exactly what you’ll find in this episode. So whether you’re on the way into the clinic for a shift, walking the dog, catching up on some CPD or just sitting with a cuppa in the break room, let’s take the panic out of poisons and manage these patients together.

Let’s start by looking at paracetamol (acetaminophen) toxicity in cats.

Paracetamol is one of the most common and most dangerous accidental toxins in cats. Often given by well-meaning caregivers trying to help their pet with pain, even a single standard 500mg tablet can be fatal.

Paracetamol has largely replaced drugs like aspirin and salicylates as a human analgesic - and it’s probably the most common over-the-counter painkiller we use. It’s available worldwide in a variety of formulations, from oral liquids to tablets, capsules, gel capsules and even suppositories.

Once ingested, paracetamol is rapidly absorbed from the gastrointestinal tract. Peak plasma concentrations are usually seen at about an hour post-ingestion, though this may be longer with extended-release formulations.

After it hits the bloodstream, it metabolised by the enzyme cytochrome P450, and after this it undergoes either glucuronidation or sulfation. In simple terms, this means that either a glucuric acid molecule or a sulfate molecule is attached to the drug, respectively, to help the body eliminate it.

And that process works - for most species, but not all of them.

Cats have a very limited capacity to metabolise anything via glucuronidation, because they have very low levels of glucuronyl transferase - the enzyme that attaches glucuric acid to the drug. 

So this means that cats are especially sensitive to paracetamol toxicity, as they have a severely reduced ability to eliminate it correctly. Instead, the body has to use alternative methods to metabolise paracetamol, and when this happens, a highly reactive compound called NAPQI (N-acetyl-p-benzoquinone imine) is produced as a result. 

Normally, NAPQI is detoxified by the antioxidant glutathione. However, cats have a very limited ability to do this, meaning that severe oxidative damage to the liver and red blood cells occurs as a result. 

This leads to two major syndromes: methaemoglobinaemia, where haemoglobin is oxidised and can’t carry oxygen, and hepatic necrosis, causing acute liver failure.

What signs do we see when a cat ingests paracetamol?

Clinical signs can develop very quickly - even after just a few hours. Whilst toxicosis generally occurs with ingestions of around 40-50mg/kg, some patients will present with clinical signs after ingesting just 10mg/kg. These signs commonly include:

  • Dyspnoea

  • Tachypnoea

  • Lethargy

  • Anorexia

  • Vomiting

  • Hypersalivation

  • Hypothermia

Icterus and other signs of hepatic toxicosis are usually seen only in very large ingestions. In dogs, however, hepatic signs are more common.

Clinical examination often reveals muddy or chocolate brown-coloured mucous membranes due to methaemoglobinaemia.

Ok, so that’s the signs we see, but how is paracetamol toxicity diagnosed?

Diagnosis is mostly made based on things like the patient’s history, witnessed, known or suspected ingestion of paracetamol, muddy or brown mucous membrames, and supportive findings on bloodwork.

These include Heinz body anaemia on a blood smear (since Heinz bodies are associated with oxidative injury), elevated methaemoglobin levels (if measured - some blood gas analysers can do this) and in severe cases, evidence of hyperbilirubinaemia and hepatic injury.

Other bloodwork changes may be seen associated with dehydration, vomiting and anorexia. For example, haemoconcetration due to dehydration and hypokalaemia due to anorexia.

And once we know our patient has paracetamol posioning, it’s time to talk treatment and nursing care.

That treatment focuses on three things: decontamination, antidote administration, and supportive care. 

If ingestion was within 1-2 hours and the cat is stable, emesis may be attempted (assuming the patient is stable enough to do so), though many are already symptomatic and may have already vomited. Activated charcoal can be given, though paracetamol absorption is often rapid and its use may therefore be limited.

The main component of treatment is N-acetylcysteine (NAC). 

NAC replenishes glutathione stores, allowing detoxification of NAPQI. If you’ve heard me chat about this drug before, it’s because NAC isn’t just used for paracetamol toxicity - we use it in acute hepatic failure, too. 

And if you don’t know it by name, you may by smell, because this drug absolutely stinks of rotten eggs. It’s given IV (diluted in 5% dextrose) as a 6-hour CRI in repeated doses over 2-3 days, until 6-8 treatments have been completed. 

Alongside this, patients require supportive treatment including IV fluids and electrolytes to replenish losses, antiemetics to manage ongoing nausea or vomiting, and careful monitoring.

Speaking of that monitoring, careful respiratory assessment, alongside general nursing care, is vital. SpO2 will not be representative due to the presence of methaemoglobin, so instead monitor mucous membrane colour, respiratory rate, pattern and effort, and consider blood gas evaluation if needed.

Alongside this, monitoring hepatic function, including blood glucose where needed, is also important. These patients often need regular sampling, repeated IV infusions and medications, and are at risk of bleeding - so careful line management is an important nursing consideration.

Next, we’re talking about NSAID toxicity in dogs and cats.

And whilst we commonly use NSAIDs safely, there are many human medications that fall under this umbrella, too. Drugs like ibuprofen, naproxen and diclofenac are common culprits - even at small doses. And even accidental overdoses of meloxicam or carprofen can have the same negative impact on our patients.

So what happens when our patient eats ibuprofen?

All NSAIDs work by inhibiting cyclooxygenase (COX) enzymes, reducing prostaglandin production. 

We want them to do this, because, at therapeutic doses, that’s useful for inflammation and pain. However, prostaglandins aren’t just responsible for inflammation - we have protective prostaglandins too, particularly in the GI tract and the kidney.

At toxic doses, these protective prostaglandins are also inhibited - resulting in things like gastrointestinal ulceration and acute kidney injury. At very high doses, CNS effects such as seizures may occur.

Toxicosis affects both dogs and cats, and whilst toxic doses vary by individual drug, toxicosis in cats occurs at approximately half of the toxic dose for dogs.

And the signs we see when our patients ingest NSAIDs vary.

They include signs of gastrointestinal ulceration, including vomiting, diarrhoea, haematemesis and melena, alongside things like anorexia, lethargy and abdominal pain.

If renal injury develops, patients often present with dehydration, lethargy, anorexia and varied changes to their urination - polyuria initially, and then oliguria and anuria as renal injury progresses.

Seizures or ataxia may also be seen at very high doses.

Like paracetamol, NSAID toxicity is usually diagnosed using a combination of clinical examination findings and a history of supportive clinical signs, with known or suspected evidence of NSAID ingestion. Bloodwork changes are usually nonspecific, and may include azotaemia and electrolyte abnormalities in kidney injury, or anaemia secondary to GI ulceration and bleeding.

So that’s what NSAID ingestion does, and how we diagnose it. But what about treatment?

Treatment depends on timing. Within 1-2 hours, emesis and activated charcoal are indicated. Because many NSAIDs undergo enterohepatic recirculation, multiple doses of charcoal may be required.

In cases of severe ingestion causing neurological signs, intravenous lipid emulsion has been successfully used. There are many protocols for this, with most including an initial loading/bolus dose over 5-15 minutes, followed by a CRI over several hours.

After that, it’s all about supportive care. This includes IV fluids to maintain renal perfusion (tailored to meet urine production), gastroprotectants like omeprazole, pantoprazole, or sucralfate, and antiemetics such as maropitant or ondansetron. 

Patients with severe oliguric or anuric kidney injury may need additional treatments, such as renal replacement therapy and therapeutic plasma exchange.

And when it comes to nursing, these patients need intensive monitoring, particularly of their fluid balance and renal function. This means regular weight checks, calculating urine output, and tracking ins and outs carefully. Alongside this, we need to monitor these patients carefully for signs of further gastrointestinal haemorrhage or worsening anaemia.

Our next medication toxicity is a true emergency: salbutamol inhaler toxicosis.

This occurs more commonly than you think, and it’s a much bigger problem for your patient than it might initially seem. We see these cases when a dog bites into a human asthma inhaler, releasing a massive, concentrated dose of medication.

Most inhalers contain bronchodilator medications belonging to the beta-2 agonist category, like salbutamol or albuterol. These medications are also available in liquid ampoules for nebulisation, or oral formulations. Regardless of the variety, each has the same result - these drugs act on the beta-2 adrenoregic receptors, causing relaxation of the smooth muscle lining the airway, and bronchodilation. 

However, when massive beta-2 adrenergic stimulation occurs, we see significant cardiovascular and electrolyte changes.

These patients develop severe tachycardia, arrhythmias, hypotension, tremors, restlessness and panting. Severe hypokalaemia also occurs, as the drug causes potassium to shift out of the bloodstream and into the cells.

Clinical signs develop within minutes, and patients are often collapsed, weak, and require emergency stabilisation.

Thankfully, the diagnosis is usually straightforward if the history is clear. Patients will often have been seen to chew an inhaler, and supportive clinical signs and examination findings, alongside hypokalaemia on bloodwork, confirm the diagnosis.

These patients require intensive, prompt and careful stabilisation and nursing.

Continuous ECG monitoring, IV fluid therapy, and potassium supplementation is vital. Potassium levels must be corrected carefully, avoiding supplementation past the maximum safe level of 0.5mmol/kg/hour.

Depending on the patient’s heart rate, blood pressure and ECG trace, beta-blockers may be administered under the direction of the veterinary surgeon.

The patient’s condition can change rapidly and deterioration can occur quickly, so intensive monitoring and spotting subtle changes early is vital.

Recovery is usually seen within 8-24 hours, though rarely signs may persist for up to 36-48 hours. As nurses and technicians, our priority is to provide intensive supportive care and monitoring throughout that period, until signs resolve.

The last medications we’ll look at this episode are human psychiatric medications, like antidepressants and ADHD medication.

These are increasingly common sources of toxicity in pets simply because they’re so widely prescribed - and they have significant effects on our patients.

What happens if a dog ingests antidepressants?

Most human antidepressants belong to a class of medications called selective serotonin reuptake inhibitors or SSRIs. These medications include fluoxetine, sertraline, citalopram, and they work by increasing serotonin levels within the body. Other types of antidepressants, such as trazodone, mirtazapine and amitriptyline, also block serotonin reuptake.

We’re no stranger to these medications in veterinary medicine, either. Mirtazipine is, I’m sure, something we’ve all used to manage inappetence in cats, and other antidepressants are sometimes prescribed for inappropriate urination, cognitive dysfunction, separation anxiety and other behavioural conditions.

Overdose of these medications can cause serotonin syndrome - a condition where excessive serotonin stimulates the central nervous system and causes autonomic dysfunction.

Patients with serotonin syndrome present with things like agitation, vocalisation, hyperthermia and tremors. Tachycardia, hypertension and arrhythmias are also common.

But we don’t just see these signs with antidepressants - stimulant toxicity is another problem we face in our patients.

Many ADHD medications, such as methylphenidate or amphetamine-based medications, cause marked cardiovascular changes in our patients. These medications are stimulants, and when ingested, can cause dose-dependent hyperactivity, tremors, tachycardia, hypertension and even seizures. As well as being stimulants, many of these drugs are serotonin-releasing agents, meaning they also contribute to serotonin syndrome. 

So how do we manage these patients?

Where appropriate, decontamination is the first step. Emesis or gastric lavage is often indicated, following by administration of activated charcoal.

After that, it’s all about supportive care. Sedation with benzodiazepines, acepromazine, or dexmedetomidine helps manage agitation, tremors and hyperthermia. Seizures may need anticonvulsants like levetiracetam or propofol. Active cooling is indicated in hyperthermic patients, and in cases of severe tremors which persist despite sedation, neuromuscular blockade and ventilation may even be required.

Intravenous lipid emulsion has been documented in human case reports, but not in veterinary medicine; and whilst IV fluids will support cardiovascular and renal function, they will not clear these drugs from the sytem, as most are highly protein-bound.

Antidotes such as chlorpromazine or cyproheptadine (periactin) can be used in cases of serotonin syndrome. These drugs are serotonin receptor antagonists, and have been shown to prevent the onset and severity of clinical signs associated with serotonin syndrome.

Nursing care of these patients is demanding; they require careful and regular assessment of their cardiovascular status, temperature, neurological status and sedation levels (in some cases). Minimising stimulation is important, so keep the patient housed in a quiet, calm area but one where you can still monitor them closely. For patients receiving aggressive supportive treatment, most clinical signs will resolve within 36 hours.

So what’s the takeaway for us as nurses and technicians?

Medication toxicities are some of the most dramatic cases we see, but also some of the most rewarding to treat. Our role starts at that first triage call and ends at discharge - these patients need intensive nursing throughout.

We calculate toxic doses, administer antidotes, set up CRIs, monitor ECGs, meticulously monitor our patients, and support anxious caregivers. We’re the eyes and ears for our patients spotting changes before they escalate, and alerting the vet to prevent our patient from deteriorating, so never underestimate your role in managing these patients in the hospital.


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

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