Poisons Flashcards
what useful resources are available for poisoning/suspected poisoning cases?
veterinary poisons information service (VPIS) -vet/owner helplines, toxbox service
BSAVA/VPIS guide and online poison triage tool
textbooks (antidote tables)
when should you suspect intoxication?
usually acute onset
signs refer to affected organ system
often accidental/inadvertent, malicious poisoning is rare
usually oral
which organ systems are commonly affected by intoxication?
hepatic
renal
neurological
GI
how do poisonings accidentally/inadvertently occur in the home?
inappropriate use of human medications by well-meaning owner
overdose of prescribed medication
exposure to products in home environment
how do you phone triage a poison/suspected poison case?
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
what should the owner be advised to bring with them?
product label/photo
sample of product (if label not available)
approximate time, quantity
what other advice should be given to the owner?
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’
how can you prepare for triage and initial management pending patient arrival?
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
what should be involved in taking patient history?
patient signalment
pre-existing medical history
onset and progression of signs
specific information regarding possible toxin
signed consent form
what should be involved in the respiratory section of the primary survey?
apnoea?
upper respiratory obstruction?
respiratory distress?
cyanosis?
abnormal long sounds?
what should be involved in the cardiovascular section of the primary survey?
abnormal MM colour?
abnormal CRT?
abnormal HR/pulse quality?
cold extremities?
what should be involved in the neurological section of the primary survey?
inappropriate mentation? (dull/stupor/coma)
anisocoria?
seizures?
paresis/paralysis?
what should be involved in the urogenital section of the primary survey?
bladder present? size?
prolapse (uterine)?
priapism?
pregnant/whelping/dystocia?
what should be involved in the ‘other’ section of the primary survey?
hyper/hypothermia
suspected toxicity
pain
obvious trauma/haemorrhage
how might you go about diagnosing an intoxication?
history of possible exposure
clinical suspicion - acute onset signs, especially GI/renal/neuromuscular
toxin panel analysis is possible
why isn’t toxin panel analysis carried out regularly?
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
what are the general principles of managing intoxication?
remove/eliminate toxin
reduce ongoing absorption
dilution of toxin
what is important to remember when managing intoxication?
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)
what are the possible routes for removal/elimination of a toxin?
induce emesis
gastric lavage
cutaneous decontamination
haemodialysis (limited availability)
how much of the gastric contents are emptied by emesis?
40-60%
how can you improve effectiveness of emesis?
feed small meal immediately prior
when is emesis indicated?
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)
when in emesis contraindicated?
if intoxicant is corrosive/irritant
pre-existing aspiration risk
specifically contraindicated if petroleum distillate is ingested (aspiration risk)
what emetic agent is used in dogs?
apomorphine (subcut usually) - effective
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
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
what are the potential complications of gastric lavage?
anaesthesia-related complications
aspiration
gastro-oesophageal trauma/perforation
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
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
which methods are available to reduce ongoing absorption?
enteric adsorbents (activated charcoal) intralipid IV
how can you administer activated charcoal?
mix with wet food
syringe
stomach tube following gastric lavage
how often should activated charcoal be given for drugs undergoing enterohepatic recirculation?
repeat doses q4-8 hours for 2-3 days
which toxins under enterohepatic recirculation?
NSAIDs
salicylates (aspirin)
theobromine (chocolate)
methylxanthines (stimulants)
digoxin (cardiac medication)
marijuana
what are the limitations of using activated charcoal?
may cause GIT irritation
contraindicated where caustic material ingested
will cause black faeces +/- constipation
how do intralipids work to reduce ongoing absorption?
creates ‘lipid sink’ in intravascular space which sequesters lipophilic compounds
what are intralipids used for?
lipophilic toxins - macrocyclic lactones, permethrin, LAs, calcium channel blockers
usually used where other treatments have failed
what are the limitations of intralipid IV?
reported complications include fat embolisation/overload and pancreatitis (rarely seen)
what is the first line treatment of intoxication?
specific antidote/therapy (if available/indicated)
plus supportive/organ specific care as needed (case dependent)
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)
what type of damage do nephrotoxins cause to the kidneys?
acute onset azotemia
what are the clinical signs of AKI due to nephrotoxins?
oliguria/anuria (polyuria less commonly)
sudden onset (hours)
inappetence, lethargy, vomiting, diarrhoea
how is AKI due to nephrotoxicity diagnosed?
azotemia with submaximally concentrated urine
specific findings - calcium oxalate monohydrate crystals with ethylene glycol toxicity
what type of crystals form with ethylene glycol toxicity?
calcium oxalate monohydrate
what are some of the common nephrotoxins?
NSAIDs lilies (cats) - all parts grapes, raisins (dogs) - dried worse ethylene glycol vitamin D analogues
how are NSAIDs a nephrotoxin?
cause COX inhibition - COX involved in maintaining kidney perfusion
especially nephrotoxic if combined with inappetence/dehydration/hypotension
why are vitamin D analogues nephrotoxic?
cause renal calcification
other than nephrotoxicity, what effect can ethylene glycol have?
hypocalcaemia, severe tremors/seizures
how do you decontaminate nephrotoxins?
GI - induce emesis, activated charcoal
warm water dermal decontamination if lily pollen
are there any specific antidotes available for nephrotoxins?
NSAIDs - misoprostol
ethylene glycol - 4-methylpyrazole (usually use medical grade ethanol)
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
what is the prognosis for nephrotoxicity?
variable - depends on toxin and extent of injury
polyuric better
ethylene glycol poor
what treatment is available for refractory cases of nephrotoxicity?
dialysis
what are the clinical signs of neurotoxicity?
hyper-excitability, agitation
cardiac stimulant effects
muscle tremors - risk of hyperthermia
seizures
obtundation, coma
what are some of the common neurotoxins?
theobromine (chocolate) permethrin (cats) - spot-on metaldehyde (slug pellets) tremorogenic mycotoxins cannabis (worse with ingestion)
how can ingestion of neurotoxins be managed?
induce emesis, activated charcoal
gastric lavage where emesis contraindicated
why is emesis often contraindicated in neurotoxin patients?
gag reflex and mental status may be compromised
how is permethrin contamination managed?
bathing affected cat in warm water
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
what ambulatory-related nursing considerations are there for neurotoxins?
regular turning, padded bedding, monitoring for decubitus ulcers
toileting considerations and nursing care
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
what are some of the common hepatotoxins?
xylitol mushrooms blue green algae (cyanobacteria) aflatoxins some drugs (phenobarbitone, paracetamol)
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
how is xylitol a hepatotoxin?
directly hepatotoxic
stimulates endogenous insulin release, causing hypoglycaemia, lethargy, weakness, ataxia, collapse, seizures
how do you decontaminate after xylitol ingestion?
emesis and activated charcoal
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)
how do rodenticides cause coagulopathy?
inhibit the enzyme which reduces vitamin K so that it is unable to activate the inactive clotting factors
how does rodenticide ingestion present?
witnessed ingestion -takes 2-5 days to develop symptoms
severe coagulopathy if symptomatic - haemoabdomen/haemothorax
present collapsed, hypovolaemic +/- anaemic
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
how should pre-symptomatic witnessed ingestion of rodenticide be treated?
4 weeks of vitamin K1 therapy - repeat clotting test post-treatment
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
how does paracetamol toxicity manifest differently in dogs vs cats?
cats typically MetHb is main problem
dogs typically hepatic injury is main problem
what is methaemoglobinaemia?
elevated methaemoglobin in blood (Fe3+)
how is methaemoglobinaemia caused?
oxidative damage to RBCs - iron in haem not in correct form to bind oxygen
what effect does methaemoglobinaemia have on the mucous membranes?
chocolate coloured or dark/dusky cyanotic
how is methaemoglobinaemia diagnosed?
drop of blood - if >10% MetHb there will be a noticeable brown discolouration esp compared to normal deoxygenated blood
why are cats susceptible to paracetamol toxicity?
lack pathways required for metabolism of paracetamol –> accumulate highly oxidative metabolites
what are the clinical signs of methaemoglobinaemia?
altered mm
cardiorespiratory distress
neurological signs (reduced oxygen to brain),
death
facial and limb oedema (cats)
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)
what is the prognosis for paracetamol toxicity?
guarded - highly toxic
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
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
what is the prognosis for an adder bite?
reasonably good with treatment
what are some of the common irritant/caustic substances?
alkali battery benzalkonium chloride (hand sanitiser) petrolleum distillate washing tablets
what are the signs of irritant/caustic ingestion?
oral ulceration - pain, hypersalivation, anorexia
oesophageal ulceration - regurgitation
gastric ulceration - vomiting
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
