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Poisons Flashcards

(85 cards)

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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
what emetic agent is used in cats?
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
26
when should gastric lavage be considered?
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
27
what are the potential complications of gastric lavage?
anaesthesia-related complications aspiration gastro-oesophageal trauma/perforation
28
how do you perform a gastric lavage?
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
29
how is cutaneous decontamination carried out?
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
30
which methods are available to reduce ongoing absorption?
``` enteric adsorbents (activated charcoal) intralipid IV ```
31
how can you administer activated charcoal?
mix with wet food syringe stomach tube following gastric lavage
32
how often should activated charcoal be given for drugs undergoing enterohepatic recirculation?
repeat doses q4-8 hours for 2-3 days
33
which toxins under enterohepatic recirculation?
NSAIDs salicylates (aspirin) theobromine (chocolate) methylxanthines (stimulants) digoxin (cardiac medication) marijuana
34
what are the limitations of using activated charcoal?
may cause GIT irritation contraindicated where caustic material ingested will cause black faeces +/- constipation
35
how do intralipids work to reduce ongoing absorption?
creates 'lipid sink' in intravascular space which sequesters lipophilic compounds
36
what are intralipids used for?
lipophilic toxins - macrocyclic lactones, permethrin, LAs, calcium channel blockers usually used where other treatments have failed
37
what are the limitations of intralipid IV?
reported complications include fat embolisation/overload and pancreatitis (rarely seen)
38
what is the first line treatment of intoxication?
specific antidote/therapy (if available/indicated) | plus supportive/organ specific care as needed (case dependent)
39
what are the general nursing considerations for intoxication management?
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
what type of damage do nephrotoxins cause to the kidneys?
acute onset azotemia
41
what are the clinical signs of AKI due to nephrotoxins?
oliguria/anuria (polyuria less commonly) sudden onset (hours) inappetence, lethargy, vomiting, diarrhoea
42
how is AKI due to nephrotoxicity diagnosed?
azotemia with submaximally concentrated urine specific findings - calcium oxalate monohydrate crystals with ethylene glycol toxicity
43
what type of crystals form with ethylene glycol toxicity?
calcium oxalate monohydrate
44
what are some of the common nephrotoxins?
``` NSAIDs lilies (cats) - all parts grapes, raisins (dogs) - dried worse ethylene glycol vitamin D analogues ```
45
how are NSAIDs a nephrotoxin?
cause COX inhibition - COX involved in maintaining kidney perfusion especially nephrotoxic if combined with inappetence/dehydration/hypotension
46
why are vitamin D analogues nephrotoxic?
cause renal calcification
47
other than nephrotoxicity, what effect can ethylene glycol have?
hypocalcaemia, severe tremors/seizures
48
how do you decontaminate nephrotoxins?
GI - induce emesis, activated charcoal warm water dermal decontamination if lily pollen
49
are there any specific antidotes available for nephrotoxins?
NSAIDs - misoprostol ethylene glycol - 4-methylpyrazole (usually use medical grade ethanol)
50
what are the nursing considerations for nephrotoxicity?
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
what is the prognosis for nephrotoxicity?
variable - depends on toxin and extent of injury polyuric better ethylene glycol poor
52
what treatment is available for refractory cases of nephrotoxicity?
dialysis
53
what are the clinical signs of neurotoxicity?
hyper-excitability, agitation cardiac stimulant effects muscle tremors - risk of hyperthermia seizures obtundation, coma
54
what are some of the common neurotoxins?
``` theobromine (chocolate) permethrin (cats) - spot-on metaldehyde (slug pellets) tremorogenic mycotoxins cannabis (worse with ingestion) ```
55
how can ingestion of neurotoxins be managed?
induce emesis, activated charcoal | gastric lavage where emesis contraindicated
56
why is emesis often contraindicated in neurotoxin patients?
gag reflex and mental status may be compromised
57
how is permethrin contamination managed?
bathing affected cat in warm water
58
what other therapies can be useful in management of neurotoxins?
muscle relaxants (diazepam, methocarbamol) anti-epileptic therapies - ensure no hypoglycaemia/hypocalcaemia first intra-lipid frequently available
59
what ambulatory-related nursing considerations are there for neurotoxins?
regular turning, padded bedding, monitoring for decubitus ulcers toileting considerations and nursing care
60
what are the other important nursing considerations for neurotoxicity patients?
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
what are some of the common hepatotoxins?
``` xylitol mushrooms blue green algae (cyanobacteria) aflatoxins some drugs (phenobarbitone, paracetamol) ```
62
what are the general management considerations for hepatotoxins?
antioxidant support (SAMe/silybin) lactulose if encephalopathic ensure normal electrolytes (esp K) supplement if hypoglycaemic consider plasma if coagulopathic
63
how is xylitol a hepatotoxin?
directly hepatotoxic stimulates endogenous insulin release, causing hypoglycaemia, lethargy, weakness, ataxia, collapse, seizures
64
how do you decontaminate after xylitol ingestion?
emesis and activated charcoal
65
how do you manage hypoglycaemia resulting from xylitol ingestion?
IV supplementation - bolus in emergency, CRI if not | feed little and often, high fibre complex carbohydrates (avoid simple sugars)
66
how do rodenticides cause coagulopathy?
inhibit the enzyme which reduces vitamin K so that it is unable to activate the inactive clotting factors
67
how does rodenticide ingestion present?
witnessed ingestion -takes 2-5 days to develop symptoms severe coagulopathy if symptomatic - haemoabdomen/haemothorax present collapsed, hypovolaemic +/- anaemic
68
how should pre-symptomatic rodenticide ingestion be managed?
Gi decontamination - emesis, activated charcoal measure clotting times presently and 48hrs post-decontamination need treating if clotting times abnormal at either time point
69
how should pre-symptomatic witnessed ingestion of rodenticide be treated?
4 weeks of vitamin K1 therapy - repeat clotting test post-treatment
70
how should symptomatic cases of rodenticide ingestion be treated?
require urgent veterinary attention too late for decontamination vitamin K1 therapy (oral/subcut) plasma if bleeding life-threatening may need RBCs
71
how does paracetamol toxicity manifest differently in dogs vs cats?
cats typically MetHb is main problem | dogs typically hepatic injury is main problem
72
what is methaemoglobinaemia?
elevated methaemoglobin in blood (Fe3+)
73
how is methaemoglobinaemia caused?
oxidative damage to RBCs - iron in haem not in correct form to bind oxygen
74
what effect does methaemoglobinaemia have on the mucous membranes?
chocolate coloured or dark/dusky cyanotic
75
how is methaemoglobinaemia diagnosed?
drop of blood - if >10% MetHb there will be a noticeable brown discolouration esp compared to normal deoxygenated blood
76
why are cats susceptible to paracetamol toxicity?
lack pathways required for metabolism of paracetamol --> accumulate highly oxidative metabolites
77
what are the clinical signs of methaemoglobinaemia?
altered mm cardiorespiratory distress neurological signs (reduced oxygen to brain), death facial and limb oedema (cats)
78
what is the treatment for paracetamol toxicity?
induce emesis in ingested <1 hour ago and no contraindications activated charcoal anti-oxidants (N-acetylcysteine slow IV, vitamin C)
79
what is the prognosis for paracetamol toxicity?
guarded - highly toxic
80
what are the clinical signs of an adder bite?
``` usually within 2 hours look for puncture wounds swelling local to bite +/- severe bruising altered mentation, depressed panting, pyrexia +/- cardiac arrhythmias ```
81
how are adder bites treated?
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
what is the prognosis for an adder bite?
reasonably good with treatment
83
what are some of the common irritant/caustic substances?
``` alkali battery benzalkonium chloride (hand sanitiser) petrolleum distillate washing tablets ```
84
what are the signs of irritant/caustic ingestion?
oral ulceration - pain, hypersalivation, anorexia oesophageal ulceration - regurgitation gastric ulceration - vomiting
85
how should irritant/caustics exposure be treated?
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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