Poisons

Question 1

When should we suspect intoxication?

Answer 1

Usually acute onset
Signs referable to affected organ system(s)
Often accidental/inadvertent
Usually oral ingestion

Question 2

How do we phone triage suspected poisoning cases?

Answer 2

What, when and dose? (need up-to-date bodyweight)
If asymptomatic/unknown or low-risk product - call VPIS
Symptomatic / known ingestion of high-risk product - immediate veterinary attention

Question 3

What instructions should we give the owner during phone triage?

Answer 3

Bring product label/photo/sample if label not available
Approximate time and quantity
If dermal contamination, try to prevent self-grooming - use buster collar if available
Ensure other pets/children do not have access
Do not follow online remedies

Question 4

How can we prepare for arrival of an intoxication patient?

Answer 4

If dose/toxin/bodyweight known, consult VPIS/other sources
Prepare for triage and initial management
Inform vet if not already aware, hospital sheet/recording chart, IV catheter/fluids, oxygen supply
Diagnostic samples - blood tubes/needle/syringe (if suspected anti-coagulant ingestion, use peripheral vein)
Decontaminants/emetics etc.

Question 5

What history can we collect on arrival of the intoxicated patient?

Answer 5

Patient signalment
Pre-existing medical history - signs, medications
Onset and progression of current signs
Specific information regarding possible toxin
Signed consent form

Question 6

What are the 5 stages of a primary survey?

Answer 6

Respiratory system
Cardiovascular system
Neurological system
Urogenital system
Other

Question 7

How can we diagnose an intoxication?

Answer 7

History of possible exposure
Clinical suspicion - acute onset signs, especially GI/renal/neuromuscular
‘Toxin panel’ analysis possible - rarely used except for legal reasons (suspected malicious poisoning)

Question 8

What are the general principles of managing intoxication?

Answer 8

Remove/eliminate toxin
Reduce ongoing absorption
Dilution of toxin

Question 9

When is admin of oral products/induction of emesis contraindicated?

Answer 9

Where there is risk of aspiration (i.e. obtundation, seizures, pre-existing laryngeal compromise, respiratory distress)

Question 10

In what ways can we remove/eliminate the toxin?

Answer 10

Induce emesis
Gastric lavage
Cutaneous decontamination
Haemodialysis

Question 11

Describe induction of emesis.

Answer 11

Emesis empties ~40-60% of gastric contents (may enhance effectiveness by feeding small meal immediately prior)
Indicated within 2-3hrs of oral ingestion of non-corrosive intoxicant
Possibly effective >3hrs post-ingestion with substances likely to coalesce in stomach, e.g. chocolate

Question 12

What are the three main reasons induction of emesis may be contraindicated?

Answer 12

If intoxicant is corrosive/irritant
Pre-existing aspiration risk
Specifically contraindicated if petroleum distillate is ingested (aspiration risk)

Question 13

What are the available emetic agents?

Answer 13

Dogs - Apomorphine SC
Cats - Xylazine IM (effective in <50% cats, use reversal agent afterwards) / other alpha-2 agonists if xylazine not available

Question 14

When would we consider gastric lavage?

Answer 14

Known significant intoxication within last hour or so
AND induction of emesis unsuccessful or contraindicated
AND benefits considered to outweigh risks
Unlikely to be of benefit if emesis has already occurred

Question 15

What are the potential complications with gastric lavage?

Answer 15

Anaesthesia-related
Aspiration
Gastro-oesophageal trauma/perforation

Question 16

How can we perform cutaneous decontamination?

Answer 16

Wear appropriate PPE
Clip affected regions in long-haired patients
Warm water
Mild shampoo/detergent (e.g. baby shampoo) or degreasing agents if especially greasy
Care to avoid ocular contamination and patient self-grooming post-bath
Do not attempt to neutralise acids/alkalis with the opposite
Do not use solvents/alcohol - likely to spread toxin

Question 17

Describe haemodialysis.

Answer 17

Extracorporeal therapy - renal replacement (for nephrotoxins) / toxin removal
Rarely used, limited access in UK

Question 18

In what two ways can we reduce ongoing absorption?

Answer 18

Enteric adsorbents (activated charcoal)
Intralipid IV

Question 19

Describe the use of enteric adsorbents.

Answer 19

Reduce ongoing absorption / facilitate faecal excretion of toxin (liquid/powder to increase surface area)
Activated charcoal - mix with wet food/syringe feed/via stomach tube following gastric lavage
AC not effective for all drugs
For drugs undergoing enterohepatic recirculation, repeated AC doses q4-8hrs for 2-3 days are indicated (e.g. NSAIDs, salicylates, theobromine, methylxanthines, digoxin, marijuana)
AC may cause GI irritation - contraindicated where caustic material ingested
Will cause black faeces +/- constipation

Question 20

Describe the use of Intralipid.

Answer 20

Lipid component of parenteral nutrition - give IV
Creates ‘lipid sink’ in intravascular space - sequesters lipophilic compounds
Used for lipophilic toxins, e.g. macrocyclic lactones, permethrin, LAs, calcium channel blockers
Usually used when other treatments have failed
Reported complications include fat embolization/overload and pancreatitis

Question 21

How can we supportively manage intoxication?

Answer 21

Specific antidote/therapy (if available)
Organ-specific care as needed
Maintain hydration and nutrition
Analgesia (opioids) where required
Manage nausea (antiemetics)
Recumbent patients - turn regularly, consider urinary management (i.e. urinary catheterisation/manual expression)
Patients with reduced blink - lubricate eyes q4-6hrs as needed

Question 22

What are the clinical signs associated with nephrotoxins?

Answer 22

Sudden onset (often within hours)
Relate to Acute Kidney Injury - inappetence, lethargy, vomiting, diarrhoea

Question 23

How can we diagnose nephrotoxins?

Answer 23

Azotemia with submaximally concentrated urine

Specific findings e.g. calcium oxalate monohydrate crystals in ethylene glycol toxicity

Question 24

What are some common nephrotoxins?

Answer 24

NSAIDs
Lilies (cats) - all parts of plant/flower
Grapes/raisins (dogs)
Ethylene glycol (antifreeze) - often also hypocalcaemia and may have severe tremors/seizures
Vitamin D analogues (causing renal calcification) - psoriasis creams, some houseplants

Question 25

How can we manage nephrotoxin patients?

Answer 25

Decontamination - GI = induce emesis / activated charcoal (no benefit in ethylene glycol), dermal e.g. lily pollen Specific antidotes for some, e.g. NSAIDs = misoprostol, ethylene glycol = 4-methylpyrazole / medical-grade ethanol

Question 26

What nursing considerations should we have for nephrotoxin patients?

Answer 26

Maintain euhydration and euvolaemia (renal perfusion) Monitor fluid ins/outs (ins may need to be reduced if oliguric/anuric) Antiemetics if nauseous, avoid development of food aversions Opioid analgesia if painful Hypertension common - monitor and treat BP

Question 27

What is the prognosis for nephrotoxin patients?

Answer 27

Variable - depends on toxin and extent of injury Polyuric = better, ethylene glycol = poor Dialysis available for refractory cases

Question 28

What are the clinical signs associated with neurotoxins?

Answer 28

``` Hyper-excitability, agitation May have cardiac stimulant effects (tachycardia/arrhythmias) Muscle tremors - risk of hyperthermia Seizures Obtundation, coma ```

Question 29

What are some common neurotoxins?

Answer 29

Theobromine (chocolate) - commonly causes cardiac stimulation Permethrin (spot-on) on cats Metaldehyde (slug pellets) Tremorogenic mycotoxins Cannabis - worse with ingestion vs inhalation

Question 30

How do we manage neurotoxin patients?

Answer 30

Decontamination - GI emesis often contraindicated (gag reflex, mental status) so can consider gastric lavage, dermal e.g. permethrin Muscle relaxants e.g. diazepam, methocarbamol Anti-epileptic therapies (ensure no hypoglycaemia/hypocalcaemia) Intralipid often valuable

Question 31

What nursing considerations should we have for neurotoxin patients?

Answer 31

Regular turning, padded bedding, monitoring for decubital ulcers Toileting considerations and nursing care Muscle tremors/seizures - monitor for and manage hyperthermia Respiratory function (neuromuscular toxins) - monitor resp. pattern and ETCO2 Monitor gag reflex - oral feeding/medications appropriate? IV fluids, nutritional support etc.

Question 32

What are some common hepatotoxins?

Answer 32

``` Xylitol (artificial sweetener) Mushrooms (e.g. Amanita spp.) Blue-green algae (Cyanobacteria) Aflatoxins Drugs e.g. phenobarbitone, paracetamol, azathioprine, doxycycline, lomustine (CCNU) ```

Question 33

How can we manage hepatotoxin patients?

Answer 33

Antioxidant support (SAMe/silybin, NAC) If encephalopathic - lactulose (oral/enema) Normal electrolytes esp. potassium Supplement glucose if hypoglycaemic If coagulopathic (PT/aPTT prolongation) and clinically bleeding, consider plasma

Question 34

What are the clinical signs of xylitol intoxication?

Answer 34

Stimulates endogenous insulin release Causes hypoglycaemia (within 2hrs) Causes lethargy, weakness, ataxia, collapse, seizures Hepatotoxic

Question 35

How can we manage xylitol-intoxicated patients?

Answer 35

GI decontamination - emesis, activated charcoal Hypoglycaemia - IV supplementation (bolus in emergency, CRI 1.25-5% if not), feeding (little and often, high fibre complex carbohydrates)

Question 36

What are the clinical signs of anticoagulant rodenticide intoxication?

Answer 36

``` Witnessed ingestion (pre-symptomatic - takes 2-5 days to develop symptoms) Symptomatic = severe coagulopathy (haemoabdomen/haemothorax, collapsed, hypovolaemic +/- anaemic) ```

Question 37

How can we manage pre-symptomatic witnessed ingestion of anticoagulant rodenticide [patients?

Answer 37

GI decontamination - emesis, activated charcoal Measure clotting times (PT/aPTT) at that time and 48hrs post-decontamination, diagnosis based on prolonged PT +/- aPTT Need treating if abnormal clotting times at any point - vitamin K1 therapy for 4 weeks, repeats PT/aPTT post-treatment

Question 38

How can we manage symptomatic cases of anticoagulant rodenticide ingestion?

Answer 38

Urgent veterinary attention Handling and sampling considerations - coagulopathic Too late for decontamination Vitamin K1 therapy (oral, SC) Plasma if bleeding life-threatening - rapid replacement of clotting factors May need red blood cells

Question 39

How does paracetamol toxicity manifest in dogs vs cats?

Answer 39

Dogs (less of a problem) typically hepatic injury as main problem Cats typically methaemoglobinaemia as main problem

Question 40

Describe methaemoglobinaemia in paracetamol toxicity in cats.

Answer 40

RBC oxidative damage causes Fe3+ haem (cannot bind oxygen) Leads to discolouration of MMs - chocolate-coloured or dark/dusty cyanotic Diagnosis = drop of blood, >10% methaemoglobinaemia noticeable brown discolouration

Question 41

What can methaemoglobinaemia in cats lead to?

Answer 41

Reduced tissue O2 delivery, signs of shock Cardiorespiratory distress Neurological signs (reduced oxygen to brain), death Facial and limb oedema

Question 42

What is the treatment and prognosis for paracetamol intoxication in cats?

Answer 42

Induce emesis (if ingestion <1hr ago and no contraindications) Activated charcoal Antioxidants - preferably N-acetylcysteine slow IV, can use vitamin C/SAMe Highly toxic, guarded prognosis

Question 43

What are the clinical signs of an adder bite?

Answer 43

``` Usually develop within 2hrs Look for puncture wounds Swelling local to bite +/- severe bruising Altered mentation - depressed Panting, pyrexia +/- arrhythmias ```

Question 44

How can we treat adder bites?

Answer 44

Keep dog quiet and calm, leave bite area alone Antivenom - recommended for facial bites/patients with systemic signs Opioid analgesia Do not use steroids No need for antibiotics IV fluid therapy Prognosis reasonably good with treatment

Question 45

What are some common irritants/caustics?

Answer 45

``` Alkali Batteries Benzalkonium chloride Petroleum distillate Washing tablet ```

Question 46

What are clinical signs of irritant/caustic poisoning?

Answer 46

Oral ulceration - pain, hypersalivation, anorexia Oesophageal ulceration - regurgitation Gastric ulceration - vomiting Dermal alopecia/burns/ulceration

Question 47

How can we treat patients with irritant/caustic poisoning?

Answer 47

If battery ingestion, radiograph to assess location and whether intact Gut decontamination contraindicated! Dermal decontamination if recent dermal exposure - warm water rinse only Opioid analgesia Maintain hydration - IV fluids Tube feeding (bypass ulcerated area) Prognosis depends on severity of burns