Poisons Flashcards
1
Q
when to suspect intoxication
A
- usually acute onset
- often accidental (human meds, overdose, exposure to toxins at home)
- usually oral ingestion, can be topical
2
Q
phone assessment questions
A
- what, when, dose
- up-to-date body weight
- call VPIS if needed
- avoid house calls
3
Q
owner instructions for emergency admit
A
- bring product label, photo
- sample of product
- try to prevent self grooming if dermal toxin
- do not follow internet remedies
4
Q
before owner arrival
A
- consult VPIS/others for up-to-date management advice
- prep for triage (catheter, oxygen, decontaminants, emetics)
5
Q
primary survey
A
- respiratory
- cardiovascular
- neurological
- renal/urogenital
- pain
6
Q
diagnosing intoxication
A
- history, clinical suspicion
- toxin panel (blood, gastric contents)
7
Q
managing intoxication general principles
A
- remove/eliminate toxin
- reduce ongoing absorption
- dilution of toxin
8
Q
options for removing/eliminating toxin
A
- induce emesis
- gastric lavage (reserved for patients where emesis doesn’t work)
- cutaneous decontamination
- haemodialysis
9
Q
induction of emesis
A
- empties 40-60% gastric contents
- indicated within 2-3hrs oral ingestion
- possibly effective >3hrs post-ingestion with substances that coalesce
10
Q
contraindications of inducing emesis
A
- if patient is seizing, unconscious
- if intoxicant is corrosive, irritant
- if petroleum distillate is ingested
11
Q
emetic agent for dogs
A
- apomorphine (subcut)
- long lasting (anti-emetic after)
12
Q
emetic agent for cats
A
- xylazine (IM) effective in <50%
- use reversal agent after
- used as sedative
13
Q
gastric lavage considerations
A
- uncommon
- known significant intoxication within the last 1hr
- and induction of emesis unsuccessful or contraindicated
14
Q
potential complications of gastric lavage
A
- induce anaesthesia (risks)
- aspiration pneumonia
- gastro-oesophageal trauma
15
Q
gastric lavage steps
A
- anaesthetised patient in left lateral recumbency
- measure nares to last rib, lube tube tip
- lavage with 10-30ml/kg warmed saline
- kink tube prior to removal to prevent spilling of contents
- suction oropharynx prior to recovery
- ensure swallow reflex returned prior to extubation
16
Q
cutaneous decontamination
A
- clip affected regions in long-haired patients
- warm water, mild shampoo
- degreasing agents if necessary
- avoid ocular contamination
- prevent patient grooming
- do not neutralise acids/alkali
- do not use alchol/solvents
17
Q
haemodialysis
A
- extracorporeal therapy
- renal replacement
- very unavailable
18
Q
reducing ongoing absorption methods
A
- enteric adsorbents (activated charcoal)
- intralipid (IV)
19
Q
enteric adsorbents
A
- reduces ongoing absorption and facilitates faecal excretion of toxin
- liquid/powder
- not effective for all toxins
- repeated admin for enterohepatic recirculation cases
20
Q
complications for enteric adsorbents
A
- not effective for all toxins
- can cause black faeces, constipation
- may cause GIT irritation
21
Q
intralipid IV
A
- creates lipid sink, holding lipids in intravascular space preventing its effect on the brain
- not effective for all toxins
22
Q
complications of intralipid (IV)
A
- toxin must be lipophilic
- can cause fat embolization, pancreatitis
23
Q
supportive care for poison patients
A
- specific antidote
- maintain hydration and nutrition
- manage nausea, pain
- turn recumbent patients regularly
- lubricate eyes for patients with reduced blink
24
Q
special considerations for neurotoxins
A
- manage seizures
- check no metabolic cause
- monitor gag reflex
25
which ingestants not to worry about
- contraceptive pill (GI upset)
- silica gel
- catnip exposure
- novelty luminous items (hypersalivation)
26
clinical signs of nephrotoxin ingestion
- sudden onset
- signs of AKI
- inappetence
- lethargy
- vom, diarrhoea
27
diagnosis of nephrotoxin ingestion
- azotemia
- calcium oxalate monohydrate crystals in ethylene glycol toxicity
28
common nephrotoxins
- NSAIDs
- lilies (cats)
- grapes, raisins (dogs)
- ethylene glycol (antifreeze)
- vitamin d analogues (renal calcification)
29
nephrotoxin management
- decontamination (induce emesis, activated charcoal, wash)
- specific antidotes for some toxins
30
nephrotoxin nursing considerations
- maintain euhydration and euvolaemia
- monitor fluid ins/outs
- often nauseous- antiemetics
- analgesia
- hypertension common
31
clinical signs of neurotoxins
- hyper-excitability, agitation
- tachycardia, arrhythmias
- muscle tremors (risk of hyperthermia_
- seizures
- obtundation
32
common neurotoxins
- theobromine (chocolate)
- permethrin (spot-on) on cats
- metaldehyde (slug pellets)
- tremorogenic mycotoxins (mould)
- canabis
33
management of neurotoxins
- decontaminate (emesis, activated charcoal, wash)
- muscle relaxants (diazepam)
- anti-epileptics
- ensure no hypoglycaemia, calcaemia
- intra-lipid treatment
34
neurotoxin nursing considerations
- regular turning for obtunded patients
- toileting considerations
- monitor for seizures, tremors
- monitor gag reflex
35
common hepatotoxins
- xylitol (artificial sweetner)
- mushrooms
- blue green algae
- alfatoxins (found in mould)
- drugs
36
considerations for hepatotoxins
- monitor for hypoglycaemia, coagulopathy
- may develop hepatic encephalopathy
37
how do anticoagulant rodenticides cause coagulopathies?
- impacting vitamin K dependant clotting factors (II, VII, IX, X)
- produced in the body in inactive form
- become active through carboxylation (Vit K)
- Vit K becomes inactive (oxidised)
- can be reduced through Vit K-epoxide reductase
- anticoagulant rodenticides block Vit K-epoxide reductase
- inactive clotting factors can no longer be activated
38
presentation of anticoagulant rodenticide
- pre-symptomatic- witnessed ingestion
- takes 2-5 days to develop symptoms) - symptomatic- severe coagulopathy
- haemoabdomen/haemothorax
- collapse, hypovolaemic, anaemic
- indirect toxicity due to ingestion of dead rats is unlikely
39
witnessed ingestion of rat bait- treatment
- GI decontamination (emesis, activated charcoal)
- measure clotting times (PT, aPTT) immediately and 48hrs after
- Vit K1 therapy
- repeat PT, aPTT post-treatment
40
treatment of symptomatic anticoagulant rodenticide
- care when taking bloods
- too late for decontamination
- Vit K1 therapy
- plasma, RBC, replacement of clotting factors
41
methaemoglobinaemia
- caused by paracetamol toxicity in cats
- oxidative damage to RBC
- iron should be Fe2+ state to bind to O2, oxidative damage causes Fe3+ (methaemoglobin)
42
clinical signs of methaemoglobinaemia
- chocolate coloured mucous membranes
- brown blood
43
clinical signs of paracetamol toxicity in cats
- methaemoglobinaemia- reduced O2 delivery, signs of shock
- cardiorespiratory distress
- neurological signs
- facial and limb oedema
44
treatment of paracetamol toxicity
- induce emesis if ingested <1hr, no contraindications
- activated charcoal
- anti-oxidants (N-acetylcysteine)
45
clinical signs of adder bite
- usually within 2hrs
- puncture wounds
- swelling, bruising local to bite
- altered mentation- depressed)
- panting, pyrexia
- +/- cardiac arrhythmias
46
treatment of adder bite
- keep patient quiet and calm
- leave bite well alone
- antivenom
- analgesia
- fluid therapy?
47
common irritant/caustic substances
- batteries
- benzalkonium chloride (disinfection)
- petrolleum distillate
- washing tablets
48
clinical signs of caustic substances
- oral ulceration- pain, hypersalivation, anorexia
- oesophageal ulceration- regurgitation
- gastric ulceration- vomiting
- dermal alopecia, burns, ulceration
49
treatment of caustic substances
- gut decontamination contraindicated
- dermal decontamination (warm water rinse)
- analgesia (opioids)
- maintain hydration
- tube feeding (bypass ulcerated areas)
- radiograph to locate battery
