Toxin Season: A Practical Guide for Veterinary Professionals

It’s March. The daffs are out. The chocolate’s everywhere. The hot cross buns are “cooling on the side” (they’re not).

Which means one thing in practice: toxin season is back.

In this bonus episode, we wanted to pull together a practical, basic GP-friendly approach to common toxicities we see in practice. Not a pharmacology lecture. Just:

• How they present

• What to do first

• When to induce vomit

• When not to vomit

• When charcoal helps

• When intralipids are worth the risk

• And a CRI calculation shortcut you’ll thank us for later

  
  

Let’s get stuck in.

First Principles: Before You Reach for the Apomorphine

Toxin cases usually come in one of two ways:

1. “He’s eaten something.”

2. Unexplained symptoms.

   
   

The second group is trickier. Collapse? Tremors? Vomiting? Hyperexcitability? Unexplained tachycardia?

As ever:

HISTORY. HISTORY. HISTORY.

• What was accessible?

• When?

• How much?

• Any remnants of packaging?

• Any human meds missing?

• Asthma inhaler chewed?

• Rat bait in the shed?

• What was in the vomit? Any clues?

• Neighbours putting anything down?

  
  

Then the usual triage:

• Stable vs unstable?

• Shocky?

• Tremoring vs seizuring?

• Can they maintain their airway?

  
  

If unstable: stabilise first. Oxygen. IV access. Fluids (supportive, not “flushing”). Seizure control. Analgesia where appropriate.

Some neuro cases can look awful but have very stable cardiovascular parameters and are not nearly as concerning as they initially appear.

Decontamination: Vomit, Wash or Wait?

Inducing vomiting can be very useful if a toxin has been ingested recently. In general, this is most effective within the first 3–4 hours. However, it may still be worthwhile later for substances that slow gastric emptying or form gastric masses — chocolate and raisins are classic examples.

It’s usually not helpful for rapidly absorbed toxins, such as paracetamol, where significant systemic absorption can occur within a short period.

DO NOT induce vomiting if:

• They can’t maintain their airway

• They’re dyspnoeic

• They’re actively seizuring

• They’ve ingested caustic or sharp material

  
  

Dogs

• Apomorphine (some of us use lower than licensed doses to reduce sedation)

• Clevor® eye drops (Ropinirole)

  
  

You can combine if needed. Both work within 15 minutes and can be reversed with maropitant if vomiting is overly protracted.

Cats

Medetomidine or xylazine (if available, tradename Rompun) can be used. Use at lower doses to help achieve emesis without too much sedation. Try medetomidine at 5-10ug/kg any route. In my experience, younger, growing cats seem more sensitive to medetomidine and usually need lower dose rates.

(And yes… spinning cats in their basket can help!)

Don’t Forget the Coat and Mouth

Especially:

• Lilies in cats – clip, wash, remove all pollen.

• Rodenticide – check the oral cavity. Charlotte has found bits of rodenticide sticking in between the teeth!

• Dermal decontamination matters more than we sometimes remember.

  
  
  
  

Activated Charcoal: When It Actually Helps

• Carbodote® is common stock in practice.

• Liquid dose typically ~5 ml/kg.

• Repeat every 4–6 hours for toxins with:

- Stops enterohepatic recirculation

- Extended-release formulations

- Long half-lives

If repeating doses, avoid using the prime carbadote, which contains a cathartic.

If you can’t remember which toxins need repeating (because honestly, who can?), Domes Pharma (formerly TVM) have practical toxicity guides available via their vet portal. These can be popped into a file at work or on your phone. A genuinely useful quick-reference resource.

Intralipids: The Lipid Sink

Useful for lipophilic toxins:

• Marijuana

• Macrocyclic lactones (ivermectin, selamectin)

• Some antidepressants

• Certain cardiac drugs (e.g. some beta blockers, diltiazem, lidocaine)

  
  

Mechanism:

• Creates a “lipid sink”

• May support cardiac myocytes

  
  

Typical approach with 20% solution:

• 1.5 ml/kg bolus over 5–15 mins

• Then 0.25 ml/kg/min for 30–60 mins

  
  

While generally safe, there are risks:

• Pancreatitis

• Fat embolism

• Corneal lipaemia

• Drug binding (can reduce the efficacy of things like benzodiazepines, propofol, maropitant)

  
  

Always warn owners.

Char’s CRI Formula (The One Worth Screenshotting)

Formula:

BW (kg) × CRI dose (mg/kg/hr) × bag volume (ml)

DIVIDED BY

Fluid rate (ml/hr) × drug concentration (mg/ml)

EQUALS

mls of drug to add to the bag.

Remember:

• Remove that volume from the bag first.

• Run fluids at the same rate used in your equation.

  
  

It saves brain melt at 2am. It's worth cross-checking your calculation with one of the online calculators or eyeballing the dose given over an hour to see if it seems about right.

The Easter Offenders

This blog post is intended as a basic educational guide only. Clinical decisions should always be made based on the individual patient. Please consult organisations such as the Veterinary Poisons Service (UK) or equivalent services within your country of practice for specific case advice.

Chocolate (Theobromine)

Early Signs:

• Vomiting, diarrhoea

  
  

Then:

• Tachycardia

• Arrhythmias

• Hyperexcitability

• Tremors/seizures

  
  

Use the Vets Now chocolate calculator to help assess risk.

Management:

• Emesis if appropriate

• Repeated charcoal

• IV fluids (supportive)

• Frequent walks to encourage urination (methylxanthines like theobromine and caffeine are reabsorbed via the bladder, so ‘flushing’ really does help in this situation!)

  
  
  
  

Grapes / Raisins / Sultanas

• Potentially nephrotoxic in a minority of dogs.

• The toxic component is likely tartrate within the fruit, as toxicity symptoms resemble those seen in tartrate ingestion (a baking ingredient called cream of tartar).

  
  

Clinical signs often delayed 24–72 hours:

• Vomiting first

• Then PUPD

• Then possible AKI

  
  

Lowest reported toxic doses:

• Grapes: ~1 g/kg

• Raisins: ~2.8 g/kg

  
  

Management:

• Emesis is important, certainly up to 6 hours from ingestion.

• Baseline bloods are not wrong.

• The use of IV fluids in grape and raisin toxicity remains somewhat controversial. Many toxicology resources and clinicians recommend hospitalisation and fluid therapy following ingestion to support renal perfusion and monitor kidney function.

• In practice, IV fluids are clearly indicated in patients that are vomiting, dehydrated, or not drinking due to nausea, where maintaining circulating blood volume is important.

• However, some clinicians question whether aggressive fluid therapy is always necessary in well patients with normal renal parameters. There is a theoretical concern that excessive fluid administration could worsen renal injury by contributing to interstitial oedema within the kidney, which sits inside a relatively non-expandable capsule.

• As a result, fluid therapy is often individualised, based on the patient’s clinical status, bloodwork, and ability to maintain hydration.

• Monitor renal parameters.

  
  

Prognosis:

Excellent with appropriate management.

Daffodils

Lycorine + calcium oxalate crystals. Typically, eating bulbs, either during or shortly after planting.

Mild:

• Vomiting

• Hypersalivation

  
  

Severe (usually bulbs):

• Tremors

• Arrhythmias

• Collapse

  
  

Treatment:

• Emesis

• Single charcoal dose

• IV fluids as needed

  
  
  
  

The Regular Offenders

Marijuana

Classic Signs:

• Lethargic

• Urinary incontinence

• Ataxic

• “Stoned” 😂

  
  

Management:

• Emesis (if early)

• Repeated charcoal

• Supportive care

• Consider intralipids

  
  
  
  

NSAIDs (Including Human Ones)

Dose dependent:

Lower doses:

• GI upset

  
  

Higher doses:

• Ulceration

• AKI

  
  

Diagnostics:

• Bloods every 6-24 hours in symptomatic cases or high dose ingestions.

• Check for hypoproteinaemia, anaemia.

• POCUS if worried about perforation.

  
  

Treatment:

• These cases often look mild at first, but deterioration can be delayed — early treatment and monitoring are key.

• IV fluids to maintain hydration and blood volume.

• Omeprazole.

• Sucralfate if available.

• Consider misoprostol.

• Referral for haemodialysis or other extracorporeal therapies if deteriorating or not responding to treatment.

  
  

Prognosis worsens significantly with azotaemia/anuria.

Rodenticides

Anticoagulants block vitamin K production. Clinical signs only appear 3–5 days later when no vitamin K is left:

• Bleeding (especially internally into cavities, joints, mucosal surfaces).

• Lethargy.

  
  

Management:

• Emesis.

• Repeated charcoal.

• Check prothrombin time (first one to lengthen).

• Vitamin K for 21+ days.

• Plasma or blood if bleeding.

  
  

Be aware of alternative rodenticides, though neither of us have yet to come across these in the UK ourselves… yet.

1. Bromethalin - Neuro signs.

2. Cholecalciferol - Severe hypercalcaemia → AKI.

   
   
   
   

Mycotoxins (Mouldy Food)

“Shake and bake” tremor dogs.

Signs:

• Tremors

• Hyperaesthesia

• Seizures

  
  

Treatment:

• Emesis or lavage.

• Repeated charcoal.

• Methocarbamol crushed and made into paste and given per rectum, or PO.

• Seizure control.

• Intralipid in severe cases worth trying.

  
  

Monitor for aspiration.

Paracetamol (Especially Cats)

Cats: toxic at ~10 mg/kg. Dogs: can be toxic at high doses. Consult other references.

Causes:

• Methaemoglobinaemia

• Oxidative injury

• Hepatic damage

  
  

Signs:

• Facial/paw swelling

• Brown mucous membranes

• Dyspnoea

  
  

Treatment:

• Activated charcoal.

• N-acetylcysteine (140 mg/kg loading, then 70 mg/kg q6h) is very effective.

• Oxygen.

• Blood products if severe.

  
  
  
  

The Ones You Don’t Want to Miss

Salbutamol Inhalers

Massive tachycardia + hypokalaemia. Surprisingly, I have heard of paramedics using beta-2 agonists to bring down potassium quickly in case of hyperkalemia in human patients.

Check:

• ECG

• Electrolytes

  
  

Treat:

• IV fluids.

• Potassium supplementation.

• Propranolol (carefully titrated).

  
  
  
  

Ethylene Glycol

Antifreeze. Used to be thought of as palatable to cats. Rapidly fatal if untreated. Typically, cats with access to antifreeze in a garage.

Cat usually presents with sudden onset ataxia and altered mentation. Essentially, they are very drunk. Bloodwork typically shows azotemia. This presentation should prompt suspicion of ethylene glycol toxicity.

Early:

• Drunken

• Vomiting

  
  

Later:

• AKI

  
  

Diagnosis aided by:

• Presence of hypocalcemia.

• Fluorescence in UV light (unreliable).

• Calcium oxalate monohydrate crystals in urine.

• High anion gap metabolic acidosis.

• Ethylene glycol blood test if available.

  
  

Treat BEFORE azotaemia develops, but tragically patients usually present too late for effective treatment.

Antidote:

• Ethanol (higher affinity for alcohol dehydrogenase). Better to use Fomepizole (4-MP) if available.

  
  

Once azotemia has occurred, clients should be warned that prognosis is poor.

Blue-Green Algae

• History or owner awareness of risk prompted suspicion.

• No antidote. Often fatal.

• Liver or neurologic injury.

• Supportive only.

• Prevention is key.

  
  
  
  

Slug Bait (Metaldehyde)

• “Shake and bake.”

• Tremors.

• Severe hyperthermia.

• Seizures.

  
  

Often need:

• Gastric lavage if appropriate.

• Charcoal.

• Methocarbamol.

• Heavy sedation helpful.

• Monitor and manage hyperthermia.

• Monitoring for DIC.

  
  
  
  

Final Thoughts

Toxin cases can feel chaotic. But the framework is usually simple:

1. Stabilise.

2. Decontaminate (if appropriate).

3. Support.

4. Targeted therapy or antidote.

5. Monitor.

   
   

And if unsure?

• Animal PoisonLine (owners).

• VPIS (vets).

  
  

You are not alone in this.

We hope this deep dive has been helpful — whether you’re the one placing the IV, calculating the CRI, washing pollen off a cat, or making your fifth dog vomit before lunchtime on Easter Sunday.

We’ll be back soon with more clinical deep dives — but until then, stay safe out there.

And maybe hide the hot cross buns.

Disclaimer

As always, everything we discuss on the podcast and within our blog is for general educational purposes for veterinary professionals. Individual cases can vary, so please use your own clinical judgement and check current guidelines where appropriate.