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CVNT2 > Poisons > Flashcards

Poisons Flashcards

1
Q

what useful resources are available for poisoning/suspected poisoning cases?

A

veterinary poisons information service (VPIS) -vet/owner helplines, toxbox service

BSAVA/VPIS guide and online poison triage tool

textbooks (antidote tables)

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2
Q

when should you suspect intoxication?

A

usually acute onset

signs refer to affected organ system

often accidental/inadvertent, malicious poisoning is rare

usually oral

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3
Q

which organ systems are commonly affected by intoxication?

A

hepatic
renal
neurological
GI

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4
Q

how do poisonings accidentally/inadvertently occur in the home?

A

inappropriate use of human medications by well-meaning owner

overdose of prescribed medication

exposure to products in home environment

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5
Q

how do you phone triage a poison/suspected poison case?

A

ask what/when/dose - will need up to date body weight

if asymptomatic/unknown or low-risk product - call VPIS

if symptomatic/known ingestion of high-risk product - requires immediate veterinary attention, avoid house calls

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6
Q

what should the owner be advised to bring with them?

A

product label/photo
sample of product (if label not available)
approximate time, quantity

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7
Q

what other advice should be given to the owner?

A

if dermal contamination, try to prevent self-grooming (buster collar if poss)

ensure other pets/children do not have access

do not follow internet ‘remedies’

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8
Q

how can you prepare for triage and initial management pending patient arrival?

A

inform the vet if not already aware

have hospital sheet/recording chart ready

equipment for IV catheter, fluid therapy

oxygen supply

diagnostic samples - blood tubes/needle/syringe

decontaminants/emetics

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9
Q

what should be involved in taking patient history?

A

patient signalment

pre-existing medical history

onset and progression of signs

specific information regarding possible toxin

signed consent form

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10
Q

what should be involved in the respiratory section of the primary survey?

A

apnoea?

upper respiratory obstruction?

respiratory distress?

cyanosis?

abnormal long sounds?

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11
Q

what should be involved in the cardiovascular section of the primary survey?

A

abnormal MM colour?
abnormal CRT?
abnormal HR/pulse quality?
cold extremities?

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12
Q

what should be involved in the neurological section of the primary survey?

A

inappropriate mentation? (dull/stupor/coma)
anisocoria?
seizures?
paresis/paralysis?

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13
Q

what should be involved in the urogenital section of the primary survey?

A

bladder present? size?

prolapse (uterine)?

priapism?

pregnant/whelping/dystocia?

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14
Q

what should be involved in the ‘other’ section of the primary survey?

A

hyper/hypothermia
suspected toxicity
pain
obvious trauma/haemorrhage

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15
Q

how might you go about diagnosing an intoxication?

A

history of possible exposure

clinical suspicion - acute onset signs, especially GI/renal/neuromuscular

toxin panel analysis is possible

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16
Q

why isn’t toxin panel analysis carried out regularly?

A

clinical diagnosis can usually be made without it
takes too long to receive results for steering treatment
however, is useful if owner suspects malicious poisoning

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17
Q

what are the general principles of managing intoxication?

A

remove/eliminate toxin
reduce ongoing absorption
dilution of toxin

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18
Q

what is important to remember when managing intoxication?

A

administration of oral products/induction of emesis is contraindicated where there is a risk of aspiration (i.e. obtundation, seizures, pre-existing laryngeal compromise or respiratory distress)

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19
Q

what are the possible routes for removal/elimination of a toxin?

A

induce emesis
gastric lavage
cutaneous decontamination
haemodialysis (limited availability)

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20
Q

how much of the gastric contents are emptied by emesis?

A

40-60%

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21
Q

how can you improve effectiveness of emesis?

A

feed small meal immediately prior

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22
Q

when is emesis indicated?

A

within 2-3 hours of oral ingestion of non-corrosive intoxicant

possibly effective >3 hours post-ingestion with substances likely to coalesce in stomach (e.g. chocolate)

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23
Q

when in emesis contraindicated?

A

if intoxicant is corrosive/irritant

pre-existing aspiration risk

specifically contraindicated if petroleum distillate is ingested (aspiration risk)

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24
Q

what emetic agent is used in dogs?

A

apomorphine (subcut usually) - effective

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25
Q

what emetic agent is used in cats?

A

xylazine (intramuscular)
only effective in <50% cats

can use powdered sodium carbonate (washing powder) if owner cannot afford to/is unable to get to clinic

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26
Q

when should gastric lavage be considered?

A

when there was a known significant intoxication within the last 1 hour or so

and induction of emesis unsuccessful/contraindicated

and benefits considered to outweigh risks

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27
Q

what are the potential complications of gastric lavage?

A

anaesthesia-related complications
aspiration
gastro-oesophageal trauma/perforation

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28
Q

how do you perform a gastric lavage?

A

anaesthetised patient, intubated with cuff (not cats), left lateral recumbency

measure nares to last rib, lubricate tube tip

lavage with 10-30ml/kg warmed water/isotonic saline instilled via gravity

follow lavage with activated charcoal if indicated

kink tube end prior to removal and maintain until fully removed

suction oropharynx prior to recovery

ensure swallow reflex returned prior to extubation

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29
Q

how is cutaneous decontamination carried out?

A

clip affected regions in long-haired patients

warm water and mild shampoo/detergent

care to avoid ocular contamination and patient grooming post-bath

do not attempt to neutralise acid/alkali with opposite

do not use solvent/alcohol - likely to spread toxin

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30
Q

which methods are available to reduce ongoing absorption?

A 
enteric adsorbents (activated charcoal) 
intralipid IV
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31
Q

how can you administer activated charcoal?

A

mix with wet food
syringe
stomach tube following gastric lavage

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32
Q

how often should activated charcoal be given for drugs undergoing enterohepatic recirculation?

A

repeat doses q4-8 hours for 2-3 days

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33
Q

which toxins under enterohepatic recirculation?

A

NSAIDs

salicylates (aspirin)

theobromine (chocolate)

methylxanthines (stimulants)

digoxin (cardiac medication)

marijuana

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34
Q

what are the limitations of using activated charcoal?

A

may cause GIT irritation
contraindicated where caustic material ingested
will cause black faeces +/- constipation

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35
Q

how do intralipids work to reduce ongoing absorption?

A

creates ‘lipid sink’ in intravascular space which sequesters lipophilic compounds

36
Q

what are intralipids used for?

A

lipophilic toxins - macrocyclic lactones, permethrin, LAs, calcium channel blockers

usually used where other treatments have failed

37
Q

what are the limitations of intralipid IV?

A

reported complications include fat embolisation/overload and pancreatitis (rarely seen)

38
Q

what is the first line treatment of intoxication?

A

specific antidote/therapy (if available/indicated)

plus supportive/organ specific care as needed (case dependent)

39
Q

what are the general nursing considerations for intoxication management?

A

maintain hydration and nutrition

analgesia where required

manage nausea (antiemetics)

turn recumbent patients regularly and consider urinary management

lubricate eyes in patients with reduced blink (q4-6 hours)

40
Q

what type of damage do nephrotoxins cause to the kidneys?

A

acute onset azotemia

41
Q

what are the clinical signs of AKI due to nephrotoxins?

A

oliguria/anuria (polyuria less commonly)

sudden onset (hours)

inappetence, lethargy, vomiting, diarrhoea

42
Q

how is AKI due to nephrotoxicity diagnosed?

A

azotemia with submaximally concentrated urine

specific findings - calcium oxalate monohydrate crystals with ethylene glycol toxicity

43
Q

what type of crystals form with ethylene glycol toxicity?

A

calcium oxalate monohydrate

44
Q

what are some of the common nephrotoxins?

A 
NSAIDs 
lilies (cats) - all parts 
grapes, raisins (dogs) - dried worse 
ethylene glycol 
vitamin D analogues
45
Q

how are NSAIDs a nephrotoxin?

A

cause COX inhibition - COX involved in maintaining kidney perfusion

especially nephrotoxic if combined with inappetence/dehydration/hypotension

46
Q

why are vitamin D analogues nephrotoxic?

A

cause renal calcification

47
Q

other than nephrotoxicity, what effect can ethylene glycol have?

A

hypocalcaemia, severe tremors/seizures

48
Q

how do you decontaminate nephrotoxins?

A

GI - induce emesis, activated charcoal

warm water dermal decontamination if lily pollen

49
Q

are there any specific antidotes available for nephrotoxins?

A

NSAIDs - misoprostol

ethylene glycol - 4-methylpyrazole (usually use medical grade ethanol)

50
Q

what are the nursing considerations for nephrotoxicity?

A

maintain euhydration and euvolaemia

monitor fluid ins/outs

consider antiemetics - often nauseous, avoid development of food aversions

consider opioid analgesia

hypertension common - monitor and treat BP

51
Q

what is the prognosis for nephrotoxicity?

A

variable - depends on toxin and extent of injury
polyuric better
ethylene glycol poor

52
Q

what treatment is available for refractory cases of nephrotoxicity?

A

dialysis

53
Q

what are the clinical signs of neurotoxicity?

A

hyper-excitability, agitation

cardiac stimulant effects

muscle tremors - risk of hyperthermia

seizures

obtundation, coma

54
Q

what are some of the common neurotoxins?

A 
theobromine (chocolate) 
permethrin (cats) - spot-on 
metaldehyde (slug pellets)
tremorogenic mycotoxins 
cannabis (worse with ingestion)
55
Q

how can ingestion of neurotoxins be managed?

A

induce emesis, activated charcoal

gastric lavage where emesis contraindicated

56
Q

why is emesis often contraindicated in neurotoxin patients?

A

gag reflex and mental status may be compromised

57
Q

how is permethrin contamination managed?

A

bathing affected cat in warm water

58
Q

what other therapies can be useful in management of neurotoxins?

A

muscle relaxants (diazepam, methocarbamol)

anti-epileptic therapies - ensure no hypoglycaemia/hypocalcaemia first

intra-lipid frequently available

59
Q

what ambulatory-related nursing considerations are there for neurotoxins?

A

regular turning, padded bedding, monitoring for decubitus ulcers
toileting considerations and nursing care

60
Q

what are the other important nursing considerations for neurotoxicity patients?

A

monitor for/manage hyperthermia (due to muscle tremors)

monitor respiratory pattern and ETCO2 (neuromuscular toxins)

monitor gag reflex - consider whether requires Iv fluids/nutritional support

61
Q

what are some of the common hepatotoxins?

A 
xylitol 
mushrooms 
blue green algae (cyanobacteria) 
aflatoxins 
some drugs (phenobarbitone, paracetamol)
62
Q

what are the general management considerations for hepatotoxins?

A

antioxidant support (SAMe/silybin)

lactulose if encephalopathic

ensure normal electrolytes (esp K)

supplement if hypoglycaemic

consider plasma if coagulopathic

63
Q

how is xylitol a hepatotoxin?

A

directly hepatotoxic

stimulates endogenous insulin release, causing hypoglycaemia, lethargy, weakness, ataxia, collapse, seizures

64
Q

how do you decontaminate after xylitol ingestion?

A

emesis and activated charcoal

65
Q

how do you manage hypoglycaemia resulting from xylitol ingestion?

A

IV supplementation - bolus in emergency, CRI if not

feed little and often, high fibre complex carbohydrates (avoid simple sugars)

66
Q

how do rodenticides cause coagulopathy?

A

inhibit the enzyme which reduces vitamin K so that it is unable to activate the inactive clotting factors

67
Q

how does rodenticide ingestion present?

A

witnessed ingestion -takes 2-5 days to develop symptoms
severe coagulopathy if symptomatic - haemoabdomen/haemothorax
present collapsed, hypovolaemic +/- anaemic

68
Q

how should pre-symptomatic rodenticide ingestion be managed?

A

Gi decontamination - emesis, activated charcoal

measure clotting times presently and 48hrs post-decontamination

need treating if clotting times abnormal at either time point

69
Q

how should pre-symptomatic witnessed ingestion of rodenticide be treated?

A

4 weeks of vitamin K1 therapy - repeat clotting test post-treatment

70
Q

how should symptomatic cases of rodenticide ingestion be treated?

A

require urgent veterinary attention
too late for decontamination

vitamin K1 therapy (oral/subcut)
plasma if bleeding life-threatening
may need RBCs

71
Q

how does paracetamol toxicity manifest differently in dogs vs cats?

A

cats typically MetHb is main problem

dogs typically hepatic injury is main problem

72
Q

what is methaemoglobinaemia?

A

elevated methaemoglobin in blood (Fe3+)

73
Q

how is methaemoglobinaemia caused?

A

oxidative damage to RBCs - iron in haem not in correct form to bind oxygen

74
Q

what effect does methaemoglobinaemia have on the mucous membranes?

A

chocolate coloured or dark/dusky cyanotic

75
Q

how is methaemoglobinaemia diagnosed?

A

drop of blood - if >10% MetHb there will be a noticeable brown discolouration esp compared to normal deoxygenated blood

76
Q

why are cats susceptible to paracetamol toxicity?

A

lack pathways required for metabolism of paracetamol –> accumulate highly oxidative metabolites

77
Q

what are the clinical signs of methaemoglobinaemia?

A

altered mm

cardiorespiratory distress

neurological signs (reduced oxygen to brain),

death

facial and limb oedema (cats)

78
Q

what is the treatment for paracetamol toxicity?

A

induce emesis in ingested <1 hour ago and no contraindications

activated charcoal

anti-oxidants (N-acetylcysteine slow IV, vitamin C)

79
Q

what is the prognosis for paracetamol toxicity?

A

guarded - highly toxic

80
Q

what are the clinical signs of an adder bite?

A 
usually within 2 hours 
look for puncture wounds 
swelling local to bite +/- severe bruising 
altered mentation, depressed 
panting, pyrexia 
\+/- cardiac arrhythmias
81
Q

how are adder bites treated?

A

keep quiet and calm, leave bite area alone

antivenom recommended for facial bites/systemic signs

analgesia (opioids)

IV fluid therapy

no evidence for antibiotics

82
Q

what is the prognosis for an adder bite?

A

reasonably good with treatment

83
Q

what are some of the common irritant/caustic substances?

A 
alkali 
battery 
benzalkonium chloride (hand sanitiser) 
petrolleum distillate 
washing tablets
84
Q

what are the signs of irritant/caustic ingestion?

A

oral ulceration - pain, hypersalivation, anorexia

oesophageal ulceration - regurgitation

gastric ulceration - vomiting

85
Q

how should irritant/caustics exposure be treated?

A

if battery, radiograph to assess location/whether intact

gut decontamination contraindicated

warm water rinse for dermal decontamination

analgesia - opioids

IV fluids

tube feeding to bypass ulcerated areas

CVNT2 (47 decks)

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