My pet ate something Flashcards
List the basic principles when dealing with known ingestion/exposure to toxin
Decontamination
Assessment of effects
Treatment of symptoms
List 3 ways toxins are absorbed
eaten- absorbed either across mucous membranes or absorbed across intestinal mucosa
via skin exposure
via inhalation
Many compounds are not inherently toxic until they have been metabolised
what is the window of opportunity with an ingested toxin
2-8 hours dogs
2-12 hours cats
can we do decontamination if the toxin is absorbed across the MM
no - this is incredibly quick so we often are too late
you can attempt to wash the mouth out but may be pointless
can we do decontamination if the toxin is eaten and absorbed across the GIT
yes - we can induce emesis or do gastric decontamination
Describe how we use to make dogs vomit
apomorphine
what do we use to make cats vomit
alpha-2 agonists e.g. xylazine or medetomidine (decent number won’t vomit)
list 2 situations should we not induce emesis with toxin ingestion
Avoid neurologically compromised patients e.g. obtunded due to aspiration risk
avoid caustic substances
why do we not make patients vomit if they have eaten a caustic substance
it can cause more of an issue on the way back up
e.g. causing oesophagitis
how to do gastric decontamination
flush warmed crystalloid fluid down a tube into the stomach, remove the fluid - repeat
when doing a stomach lavage what do we need to be careful of
removing the tube and leaking fluid - aspiration risk
if a toxin has been eaten and the window of opportunity for vomiting has passed, what can we do
give activated charoal
how does activated charcoal help in toxic cases
it is an incredibly porous substance - this means it is very good at allowing molecules to react and bind - this helps it to remove substances from the GIT before they are absorbed
how can we decontmainate after skin exposure to toxins
gently wash the skin with water, activated charcoal or washing up liquid
care when drying- absorption through abrasions
prolonged washing can increase absorption of some chemicals
how can we decontaminate after inhalation of toxins
Very rare, but realistically decontamination for your patient is not possible.
appropriate PPE
how can we decontaminate if a toxin is only toxic after metabolism
the solution to pollution is dilution
IVFT
lipid infusions
why does fluid therapy help with toxins
Increase GFR and promote renal excretion- if renally excreted
Increased organ perfusion and transit of compounds- decreasing opportunity for toxins to damage organs
what fluid rate do we give toxin patients
2 x Maintenance in the normally hydrated patient
how do lipid infusions prevent toxicities
works well for lipid soluble compounds
lipid soluble toxin is sequesteres into fat and metabolised as part of the fat
what are the side effects of lipid infusions
pulmonary lipid embolus - clump of fat gets stuck and leads to lack of perfusion to a section of lung
if we don’t know what toxin was ingested or what that toxin does, what do we do
assess all body systems
how do we treat toxin exposures post decontamination attempts
symptomatic treatment based on what systems are affected
how do we control seizures
diazepam IV - can give 3 doses- should see affect within 10 mins
phenobarbital/levetiracetam IV- if diazepam not working
propofol CRI - causes an induced coma- if the other fail
how can we support the liver after toxin ingestion
anti-oxidants
how can we support the kindey after toxin ingestion
IVFT (keep up there losses) +/- diuretics depending on urine output (need to be well hydrated- need to be careful)
dialysis if required
what do we give to ventricular tachycardic patients
lidocaine
what do we give to supraventricular tachycardic patients
beta-blockers
e.g. propranolol
what do we give to bradycardic patients
Atropine - should see quick response
may need to readminister because short half-life
if toxin affected vagal tone
how do we maintain a good BP
IVFT
vasopressors
what do we give if BP too high
anti-hypertensives (e.g. amlodipine)
do we want to stop vomiting in acute phase of toxin ingestion
no
what do we give to V/D patients after toxin ingestion
IVFT
GIT diet
anti-emetic (e.g. maropitant, metoclopramide, ondansetron) if vomiting won’t stop after prolonged period
treatment for toxin patients with clotting dysfunction
vitamin K
plasma (fresh frozen plasma- because got lots of clotting factors in)
how do ibuprofen/ NSAIDs cause toxicity
they reduce prostaglandin production (COX inhibitors) - this can damage the kidneys and GIT
List the clinical signs of NSAID toxicity
Haemorrhagic vomiting / diarrhoea
AKI
Describe the treatment for NSAID toxicity
H2 blockers (ranitidine/ cimetidine)
proton pump inhibitors (omeprazole)
prostaglandin analogue (misoprostol)- not in pregnant animals
intralipid infusion
why is aspirin toxicity different to NSAID toxicity
it can have a greater effect on thromboxane which can lead to thrombocytopathy (because it is important for platelet function) on top of the other clinical signs
List the clinical signs of asprin toxicity
Thrombocytopathy – bleeding e.g. prolonged BMBT
haemorrhagic V+/D+
AKI
describe how to treat asprin toxicity
Treatment as for NSAIDs.- proton pump inhibitor, prostaglandin analogue, intralipid infusion
Bleeding is unlikely to be significantly associated with death before other damage.
how does paracetamol cause toxicity
paracetamol is metabolised by the liver - these pathways can become saturated, cytochrome P450 oxidses the excess to NAPQI (BAD)
NAPQI is then detoxified - but these pathways can become exhausted too, PAP can also be produced (ALSO BAD)
NAPQI and PAP cause clinical signs
NAPQI causes hepatic cell necrosis and nephrotoxicity
PAP causes methemoglobinaemia
List the clinical signs of paracetamol toxicity
Brown mm
jaundice
abdominal pain
lethargy
vomiting
AKI
signs of hypoxia to tissues- arrhythmias, peripheral oedema, resp distress
Describe how to treat paracetamol toxicity
N-acetyl cysteine (binds to toxic metabolites)
H2 receptor antagonists (rantidine - reduces CP450 oxidation)
ascorbic acid
antioxidants
IVFT
GI support
How does chocolate cause toxicity
Theobromine and caffeine (Methyl-xanthines) increase catecholamine release
this increases cAMP
which increases intracellular calcium in cardiac and skeletal muscles
it is also inhibits adenosine receptors
List the clinical signs of choclate toxicity
hyperactivity
V/D
arrythmias
seizures
coma
death
Describe the treatment of choclate toxicity
symptomatic treeatment
fluids
ECG and monitoring
how long do you need to give activated charcoal for following toxin ingestion
at least 24 hours
how does xylitol cause toxicity
it mimics glucose without calorific contribution
stimulates insulin release and is hepatotoxic
what is xylitol found in
chewing gum - sugar free
some peanut butters (check label)
List the clinical signs of xylitol ingestion
hypoglucaemia
elevated liver enzymes
weakness
collapse
seizures
coma
death
jaundice
Describe treatment of xylitol toxicity
IVFT
glucose infusion- oral or IV
- need to avoid causing further insulin spikes
antioxidants
these need constant glucose monitoring (every hour) for 24-48hrs
what can pyrethroids be found in
insecticides such as ‘raid’ and ant powders
in some old school flea products
List the clinical signs of pyrethroid toxicity
Primarily act on neural axons (Na channels)
Ataxia
tremours
disorientation
seizures
dyspnoea
respiratory arrest
hypersalivation
vomiting
AKI following rhabdomyolysis from uncontrolled seizuring
Describe the treatment for pyrethroid toxicity
IVFT
intralipid infusion- as it is highly lipophilic
diazepam for seizures
how do cleaning products commonly cause an issue
due to surface contact or mucosa contact
what is the worrying consequence of ingestion of a caustic agent
oesophagitis
how does anti-freeze cause toxicity
ethylene glycol is metabolised into glycolic acid, glycoaldehyde, oxalic acid
- glycoaldehyde is neurotoxic
- glycolic acid - produces a severe acidosis
- oxalic acid binds calcium leading to calcium oxalate formation in organs
Mortality is high - cats particularly susceptible
List the clinical signs of cleaning product toxicity
oral pain
dysphagia
regurgitation
vomiting
describe how to treat cleaning products toxicity
oral water - rinse out mouth as much as can
washing exposed surfaces with water
List the clinical signs of anti-freeze toxicity
<12 hours- vomiting, lethargy (looking drunk)
12-24 hours - tachyarrythmias, tachypnoea, hypocalcaemia
24-72 hours- AKI and death
can you test for ethylene glycol ingestion
there are tests but they are not great, some anti-freeze has fluorescein in so you can test the paws and mouth for its presence (with Woods lamp)
what is the prognosis like for animals after ingesting anti-freeze
poor
can we treat anti-freeze toxicity
may be able to slow production of toxic metabolites by diluting with alcohol dehydrogenase for 3 days (basically vodka diluted with saline (20%), dialysis can help the outcome
what is ethically wrong with anti-freeze toxicity treatment
we are providing 3 days worth of alcohol to an animal
don’t know if worked at 7 day mark
how does warfarin cause toxicity
it inhibits vitamin K epoxide reductase - this inhibits vitamin K synthesis which inhibits the production of clotting factors
List the clinical signs warfarin toxicity
coagulopathies 36-72 hours post-ingestion
Describe how can we diagnose warfarin toxicity
PT prolonged
aPTT prolonged
caviatatory bleeds
Petechiae are unlikely to be present
Describe warfarin toxicity treatment
vitamin K injections and oral- up to 8 weeks (expensive)
fresh frozen plasma transfusion in severe cases
what is the toxic substance in raisins/grapes/sultanas/currants
unknown but thought to be tartaric acid
List the clinical signs of raisin/ grape toxicity
V+/D+
AKI- but unknown at what dose this will occur
What is the toxic dose of raisin/ grapes/ sultanas/ currants
no known toxic dose- so any exposure should be considered serious
Describe the treatment for raisin/ grape toxicity
IVFT- 48-72hrs is recommended because unknown toxic dose (expensive)
emetic
dialysis
Most dogs will be fine but some get AKI
List the clinical signs of cocaine toxicity
hyperactive
hyperthermia
tachyarrythmias
vomiting
ataxia
seizures
Describe treatment of cocaine toxicity
IVFT
cooling- depends on degree of hyperthermia you see
antidysrhymia drugs
seizure medication, etc
List the clincial signs marijuana toxicity
vomiting
‘paranoia’
ataxia
depression
coma
urinary incontinence
Describe treatment of marijuana toxicity
urinary catheter
IVFT
intralipid - may take a while to recover
List clinical signs of opiate toxicity
depression
lethargy
vomiting
constipation
hypoventilation
Describe treatment for opiate toxicity
IVFT
oxygen
naloxone reversal
may need ventilation
List the clinical signs of ketamine toxicity
ataxia
hallucinations
aggression
cataplexy
loss of patent airway
Describe treatment of ketamine toxicity
IVFT
intubation
ventilation
What is the toxic substance in lillies
Toxic substance not known (probably a steroidal glycoalkaloid
clinical signs of lily ingestion in cats
AKI
clinical signs of lily ingestion in dogs
GI signs
What part of a lily is toxic
Any part of the plant is toxic – including the stamen and pollen – which cats will play with because they are ‘floppy’
Describe treatment for lily ingestion
decontamination of fur
IVFT
treatment per AKI
How much Onions, Garlic, Leeks, Chives need to be ingested to be toxic
large quantities
cats may be more sensitive
how do onions/garlic/leeks/chives cause toxicity
sulphur containing compounds can cause haemolysis or heinz-body anaemia
List the clinical signs of onion/garlic/leek/chive ingestion
V+/D+
tachycardia
tachypnoea
pale MM (anaemia)
Describe how to treat Onions, Garlic, Leeks, Chives toxicity
general principles
keep an eye on PCV- transfusion if severe
why can mouldy foodds be toxic
fungal metabolites are neurotoxic
List the clinical signs of mould ingestion
muscle tremors
hyperaesthesia
seizure
coma
death
treatment for mould ingestion
IVFT
Diazepam is ineffective for muscle tremors- methocarbamol instead
intralipid infusion
if in doubt about a toxin, who do you call
VPIS
