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Veterinary Nursing > Poisons > Flashcards

Poisons Flashcards

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1
Q

When should we suspect intoxication?

A

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

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2
Q

How do we phone triage suspected poisoning cases?

A

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

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3
Q

What instructions should we give the owner during phone triage?

A

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

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4
Q

How can we prepare for arrival of an intoxication patient?

A

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.

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5
Q

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

A

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

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6
Q

What are the 5 stages of a primary survey?

A 
Respiratory system
Cardiovascular system
Neurological system
Urogenital system
Other
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7
Q

How can we diagnose an intoxication?

A

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)

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8
Q

What are the general principles of managing intoxication?

A

Remove/eliminate toxin
Reduce ongoing absorption
Dilution of toxin

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9
Q

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

A

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

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10
Q

In what ways can we remove/eliminate the toxin?

A

Induce emesis
Gastric lavage
Cutaneous decontamination
Haemodialysis

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11
Q

Describe induction of emesis.

A

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

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12
Q

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

A

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

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13
Q

What are the available emetic agents?

A

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

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14
Q

When would we consider gastric lavage?

A

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

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15
Q

What are the potential complications with gastric lavage?

A

Anaesthesia-related
Aspiration
Gastro-oesophageal trauma/perforation

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16
Q

How can we perform cutaneous decontamination?

A

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

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17
Q

Describe haemodialysis.

A

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

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18
Q

In what two ways can we reduce ongoing absorption?

A 
Enteric adsorbents (activated charcoal)
Intralipid IV
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19
Q

Describe the use of enteric adsorbents.

A

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

20
Q

Describe the use of Intralipid.

A

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

21
Q

How can we supportively manage intoxication?

A

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

22
Q

What are the clinical signs associated with nephrotoxins?

A 
Sudden onset (often within hours)
Relate to Acute Kidney Injury - inappetence, lethargy, vomiting, diarrhoea
23
Q

How can we diagnose nephrotoxins?

A

Azotemia with submaximally concentrated urine

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

24
Q

What are some common nephrotoxins?

A

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

25
Q

How can we manage nephrotoxin patients?

A

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

26
Q

What nursing considerations should we have for nephrotoxin patients?

A

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

27
Q

What is the prognosis for nephrotoxin patients?

A

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

28
Q

What are the clinical signs associated with neurotoxins?

A 
Hyper-excitability, agitation
May have cardiac stimulant effects (tachycardia/arrhythmias)
Muscle tremors - risk of hyperthermia
Seizures
Obtundation, coma
29
Q

What are some common neurotoxins?

A

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

30
Q

How do we manage neurotoxin patients?

A

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

31
Q

What nursing considerations should we have for neurotoxin patients?

A

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.

32
Q

What are some common hepatotoxins?

A 
Xylitol (artificial sweetener)
Mushrooms (e.g. Amanita spp.)
Blue-green algae (Cyanobacteria)
Aflatoxins
Drugs e.g. phenobarbitone, paracetamol, azathioprine, doxycycline, lomustine (CCNU)
33
Q

How can we manage hepatotoxin patients?

A

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

34
Q

What are the clinical signs of xylitol intoxication?

A

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

35
Q

How can we manage xylitol-intoxicated patients?

A

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)

36
Q

What are the clinical signs of anticoagulant rodenticide intoxication?

A 
Witnessed ingestion (pre-symptomatic - takes 2-5 days to develop symptoms)
Symptomatic = severe coagulopathy (haemoabdomen/haemothorax, collapsed, hypovolaemic +/- anaemic)
37
Q

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

A

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

38
Q

How can we manage symptomatic cases of anticoagulant rodenticide ingestion?

A

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

39
Q

How does paracetamol toxicity manifest in dogs vs cats?

A

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

40
Q

Describe methaemoglobinaemia in paracetamol toxicity in cats.

A

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

41
Q

What can methaemoglobinaemia in cats lead to?

A

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

42
Q

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

A

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

43
Q

What are the clinical signs of an adder bite?

A 
Usually develop within 2hrs
Look for puncture wounds
Swelling local to bite +/- severe bruising
Altered mentation - depressed
Panting, pyrexia
\+/- arrhythmias
44
Q

How can we treat adder bites?

A

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

45
Q

What are some common irritants/caustics?

A 
Alkali
Batteries
Benzalkonium chloride
Petroleum distillate
Washing tablet
46
Q

What are clinical signs of irritant/caustic poisoning?

A

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

47
Q

How can we treat patients with irritant/caustic poisoning?

A

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

Veterinary Nursing (65 decks)

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