Poisons Flashcards
(253 cards)
1
Q
what resource can be useful when you are dealing with a poisoning case?
A
VPIS - veterinary poisons information service
2
Q
what does VPIS do?
A
available 24/7
has vet helpline to advise on antidotes or management of poisoning
owner support line
tox box services
3
Q
why is a ToxBox so useful?
A
some poisonings are very rare and antidotes not regularly kept in practice
4
Q
how rapid is the onset of symptoms in an intoxication case?
A
acute
5
Q
what can signs of intoxication be referable to?
A
the affected organ system (e.g. liver, kidneys, GI)
6
Q
how does poisoning often occur?
A
inadvertent or accidental
malicious poisoning is rare
7
Q
how may an animal be poisoned accidentally / inadvertently?
A
inappropriate use of human medications by well meaning owner
overdose of prescribed medication
exposure to products in the home environment
8
Q
via what route are most toxins ingested?
A
oral
9
Q
what are the less common routes of toxin ingestion?
A
topical or inhalation (among others)
10
Q
what questions should you ask during phone triage if intoxication is suspected?
A
what when what does (if owner knows) up to date bodyeight
11
Q
why is an up to date body weight needed?
A
to check if dose ingested is toxic or not
12
Q
what should be done if the suspected intoxicated patient is asymptomatic or has ingested and unknown or low risk product?
A
call VPIS who can offer specific advice
13
Q
what should be done if the suspected intoxicated patient is symptomatic or has ingested known high risk product?
A
requires immediate veterinary attention (even if no signs)
avoid house calls as this only takes up time for treatment
14
Q
what should the owner bring with them when attending the practice with their suspected intoxication patient?
A
product label or photo if possible
a sample of the product if the label is unavailable
an indication of approximate time of toxin ingestion and quantity ingested
15
Q
what should owners do if there is dermal contamination of toxic substance?
A
prevent self-grooming (and so ingestion)
buster collar may be useful
16
Q
what advice should be given to owners before they bring their intoxicated animal into practice?
A
ensure other pets/children to not have access to toxin or anything containing it (e.g. vomit)
do not follow internet remidies
17
Q
what should be done before the intoxicated patient arrives?
A
if dose/toxin/bodyweight already known then contact VPIS or other source for specific up-to date management advice (may already have been done
prepare for triage and initial management
18
Q
what should be done pending owner arrival at the practice with an intoxicated patient if dose/toxin/bodyweight already known?
A
consutl VPIS or other source for specific up-to-date management advice
19
Q
how should you prepare for triage / initial management of intoxicated patients?
A
prepare yourself
inform the vet if not already aware
prep hospital sheet/recording chart
IV catheter and fluid prepped
O2 supply can help in some cases so prepare
diagnostic supplies (e.g. blood tubes and needles)
decontaminents/emetics
20
Q
what should be avoided if anti-coagulant ingestion is suspected?
A
only blood sample from peripheral veins not jugular as pressure bandage is needed
21
Q
what should be involved in the history taken from the owner while their pet is triaged?
A
patient signalment
pre-exisiting medical history (signs day to day and any medication)
current issue
signed consent form
22
Q
how can the history taking be facilitated during triage?
A
delegation / team work
23
Q
what should be asked about the current condition when taking a history from an owner about toxin ingestion?
A
onset and progression of signs
specific information regarding the possible toxin
24
Q
when is a primary survey performed?
A
on all emergancy cases
25
what are the main stages of the primary survey?
```
respiratory
CVS
neurological
urogenital
other
```
26
what is assessed during the respiratory section of the primary survey?
```
is there apnoea
any URT obstruction
resp distress
cyanosis
abnormal lung sounds
```
27
what should happen if apnoea is found during the primary survey?
commence CPR straight away
28
what is assessed during the cardiovascular section of the primary survey?
```
mm colour
CRT
HR
pulse quality
are extremities cold (perfusion check)
BP if possible
```
29
what should you do if unsure about any respiratory issues (aside from apnoea!!)?
provide O2 therapy
30
what is assessed during the neurological section of the primary survey?
mentation (dull, stuporous or comatose)
anisocoria
seizures
paresis/paralysis
31
what is assessed during the urogential section of the primary survey?
bladder (present and size)
any prolapse
priapism
pregnancy, whelping or dystocia
32
what is assessed after all other systems during the primary survey?
hyper/hypothermia
suspected toxicity
pain
obvious trauma or haemorrhage
33
what should be done once the primary survey is completed?
treat any abnormalities found
34
how can any issues from the primary survey be addressed?
provide O2 and establish airway
address hypoperfusion if any
manage any neurological impairment
35
how can hypoperfusion be addressed?
hypovolaemia - IVFT
| cardiac rhythm disturbances / myocardial failure - treat as appropriate
36
how is neurological impairment found on the primary survey treated?
manage seizures
ensure respiratory function is adequate (may be affected by muscle weakness)
protect against aspiration
37
what happens during the secondary survey?
review all areas of primary survey and ensure stabilised
| give more in depth exam
38
how is an intoxication diagnosed?
history of possible exposure
clinical suspicion
toxin panel analysis is possible also
39
what clinical signs would lead you to suspect toxin exposure?
acute onset signs
| especially GI, renal and neuromuscular
40
what is the issue with toxin panel analysis?
takes time
| not often used as clinical diagnosis can be made without
41
what can be used to perform a toxin panel?
ingested substance
gastric contents (lavage or vomit)
blood or urine samples
42
when may a toxin panel be used?
when required for legal reasons (e.g. owner suspects malicious poisoning)
43
what are the 3 main principles of managing intoxication?
remove or eliminate toxin
reduce ongoing absorption
dilution of toxin
44
when is administration of oral products or induction of emesis contraindicated?
where there is a risk of aspiration
45
what conditions increase the risk of aspiration?
obtundation
seizures
pre-exisiting laryngeal compromise
respiratory distress
46
what can be done to reduce or eliminate a toxin?
induce emesis
gastric lavage
cutaneous decontamination
haemodialysis (limited availability)
47
how much of the gastric contents is emptied by emesis?
40-60% of gastric contents
48
what can enhance the effectiveness of emesis in clearing toxins from the stomach?
feed small meal immediately prior to induction of emesis
49
when is emesis indicated?
within 2-3 hours of oral ingestion of a non-corrosive intoxicant
50
when can emesis be possibly effective >3 hours post ingestion?
with substances likely to coalesce in the stomach (e.g. chocolate)
51
when is emesis contraindicated?
in intoxicant is corrosive or irritant
pre-existing aspiration risk
specifically contraindicated if petroleum distillate is ingested
52
what is the main emetic agent used in dogs?
apomorphine
53
via what route is apomorphine given?
SC although can be given via other methods if correct solution used
54
how effective is apomorphine in dogs?
typically very effective
55
what emetic agent is used in cats?
xylazine
56
via what route is xylazine given?
IM
57
how effective is xylazine in inducing emesis in cats?
works in less than 50% of cats
58
what can be used if xylazine is not available to induce emesis in cats?
other alpha 2 agonists
59
what should be used after an alpha 2 agonist is administered and has had emetic effect?
appropriate reversal agent
60
what is the main side effect of xylazine?
sedation as it is asedative
61
what is found in the home that could be used if the owner is absolutely unable to come to the practice?
washing soda 9sodium carbonate)
62
what is gastric lavage?
washing out of stomach
63
is gastric lavage commonly used?
no
64
when should gastric lavage be considered?
known significant toxin ingestion within the last hour or so
and induction of emesis is unsuccessful or contraindicated
and benefits considered to outweigh risks
65
when is gastric lavage unlikely to be of benefit?
if emesis (voluntary or involuntary) has already occurred
66
what are the potential complications of gastric lavage?
anaesthesia related
aspiration
gastro-oesophageal trauma or perforation
67
how should the patient be prepared for gastric lavage?
anaesthetised
| intubated with cuffed ET tube
68
what is the issue with cuffing ET tubes in cats?
can lead to tracheal necrosis
69
what position should animals be placed in for gastric lavage?
lateral recumbancy (left is standard)
70
how should the stomach tube be measured for gastric lavage?
nares to last rib
71
what should be done with the stomach tube tip before it is inserted?
lubricated
72
how much fluid is used to lavage the stomach?
10-30 ml/kg
73
how is gastric lavage performed?
10-30ml/kg of warmed water/isotonic saline is instilled into stomach down tube via gravity
then allowed to run out by lowering tube into bucket
74
what can be instilled into the stomach tube following gastric lavage?
activated charcoal if indicated
75
how should the stomach tube be removed safely after lavage?
kink tube or cover end prior to removal and maintain this until tube is fully removed
76
what should be done after gastric lavage before anaesthetic recovery?
suction oropharynx
77
what must have returned prior to extubation after gastric lavage?
swallow reflex
78
when is cutaneous decontamination needed?
toxin or substance on skin
| ingestion occuring via absorption or ingestion after grooming
79
what should you wear when performing cutaneous decontamination?
appropriate PPE
80
what should be done with long haired patients during cutaneous decontamination?
clip affected regions
81
what should be used to wash the fur/skin during cutaneous decontamination?
warm water
mild shampoo / detergent (e.g. baby shampoo)
degreasing agents (e.g. swarfega) if especially greasy
82
what should be avoided when performing cutaneous decontamination?
occular contamination and patient grooming post bath
83
how can patient grooming post cutaneous decontamination be prevented?
buster collar
84
what should you not do when performing cutaneous decontamination?
attempt to neutralise acids or alkali with the opposite
| use solvents or alcohol as are likely to spread toxin
85
what is haemodialysis?
treatment used as renal replacement (in kidney damage) to filter out nephrotoxins or for solute (toxin) removal
86
is haemodialysis often used?
no - only one in UK at RVC
87
what is the weight restriction for haemodialysis?
>2.5kg
88
how can ongoing toxin absorption be reduced?
```
enteric absorbents (activated charcoal)
intralipid (IV)
```
89
what is the role of enteric absorbents?
reduce ongoing absorption and facilitate faecal excretion of toxin by binding it
90
what form is activated charcoal given in?
liquid or powder for large surface area
91
how can activated charcoal be administered?
mixed with wet food
syringed
stomach tube following gastric lavage
92
is activated charcoal effective for all drugs?
no
93
how often should activated charcoal be given for drugs undergoing enterohepatic re-circulation?
every 4-8 hours for 2-3 days
94
what drugs is activated charcoal effective for?
```
NSAIDs
salicylates (asprin)
theobromine (chocolate)
mathylxanthines (stimulants)
digoxin
marijuana
```
95
what may be caused by activated charcoal?
GI irritation
96
when is activated charcoal contraindicated?
where caustic material has been ingested
97
what effect can activated charcoal have on faeces?
cause them to go black after 1-2 days and may lead to constipation
98
what is the role of intralipid therapy in treating toxin ingestion?
creates 'lipid sink' in intravascular space where fat soluble toxins will bind and then can no longer be taken up into organs
99
what is intralipid therapy used for?
lipophilic toxins
100
what are the main lipophilic toxins that may be treated with intralipid?
macrocyclic lactones
permethrin
LA
calcium channel blockers
101
when is intralipid therapy most often used?
where other treatment has failed
102
what are the reported side effects of intralipid therapy?
fat embolisation / overload
| pancreatitis
103
are side effects of intralipid therapy often seen?
no - rare
104
what is involved in the supportive management of intoxication?
specific antidote/therapy if available or indicated
supportive/organ specific care as needed (depending on case)
nursing and symptomatic care
105
what is involved in the nursing and symptomatic care of treatment of intoxication?
```
maintain hydration and nutrition
analgesia where required
manage nausea with anti-emetics
correct management of recumbent patients
manage eyes if reduced blink
```
106
what analgesia is usually given to intoxication cases?
opioids
107
how should the recumbent patient be managed?
```
turn regularly (prevent decubital ulcers)
consider urinary management
```
108
how should patients with a reduced blink be managed?
lubrication of eyes every 4-6 hours depending on need
109
why is eye lubrication needed in patients with reduced blink?
prevention of corneal drying and ulceration
110
what may be caused by nephrotoxins?
acute kidney injury (AKI)
111
what are the main signs of AKI?
acute onset azotemia
olig or anuria
less commonly polyuria
112
what are the clinical signs of intoxication with nephrotoxin?
```
sudden onset (within a few hours)
AKI related - inappetance, lethargy, vomiting and diarrhoea
```
113
how is intoxication with nephrotoxins diagnosed?
azotemia with sub-maximally concentrated urine
| specific findings
114
what specific findings are there for nephrotoxins?
calcium oxalate monohydrate crystals seen with ethylene glycol toxicity
115
what are the common nephrotoxins?
```
NSAIDs
Lillies (cats)
Grapes and raisins (dogs)
ethylene glycol (antifreeze)
vitamin D analogues
```
116
why can NSAIDs cause nephrotoxicity?
COX inhibition meaning that prostaglandins are unable to manage RPF and perform protective GI function.
117
when is NSAID toxicity more profound?
if patient is inappetant
dehydrated
hypotensive
due to reduced protection for the stomach and reduced renal plasma flow
118
what parts of the lily are toxic to cats?
all parts of the plant and flower
119
why are grapes/raisins toxic?
idiosyncratic although dried fruits are worse
120
why are dried fruits more toxic to dogs?
more are eaten as smaller and often more palatable
121
what is caused by ethylene glycol?
crystals form in the renal tubules
122
what other effects, aside from AKI may be caused by ethylene glycol toxicity?
may be hypocalcaemic and have severe tremors or seizures
123
why may patients who have ingested ethylene glycol be hypocalcaemic?
due to the formation of crystals
124
what do vitamin D analogues cause?
renal calcification
125
what in the blood may indicate ingestion of vitamin D analogues?
Ca2+ and phosphate levels will increase
126
where are vitamin D analogues found in the home?
psoriasis creams
| some house plants
127
what is the effect of renal calcification caused by vitamin D analogues?
normal renal byproducts are not removed so build up and lead to AKI
128
how is nephrotoxin ingestion managed?
decontamination
| specific antidotes available for some toxins
129
what is involved in GI decontamination of nephrotoxins?
induce emesis
| give activated charcoal
130
for what nephrotoxin is activated charcoal of no benefit?
ethylene glycol
131
when is dermal contamination of a nephrotoxin needed?
if lily pollen on skin
132
what nephrotoxins have specific antidotes?
NSAIDs
| ethylene glycol
133
what is the specific antidote for NSAID toxicity?
misoprostal - prostaglandin analogue
134
why must care be taken when administering misoprostal?
is abortative in humans
135
what is the specific antidote for ethylene glycol?
4-methylpyrazole (in reality often use medical grade ethanol)
136
what is the role of 4-methylpyrazole in treating ethylene glycol toxicity?
minimises the production of toxic metabolites
137
what are the nursing considerations for patients with nephrotoxin intoxication?
```
maintain euhydration and euvolaemia
monitor fluid ins and outs and titrate fluid given accordingly
anti-emetics given as often nauseous
opioid analgesia if painful
monitor for and treat hypertension
```
138
how can the development of food aversions be avoided?
control any nausea before feeding
139
what is the prognosis for a patient with nephrotoxin intoxication?
variable - depends on the toxin and the extent of the injury
polyuric is better
ethylene glycol is poor
140
what is available for refractory nephrotoxin patients?
dialysis
141
what are the clinical signs of neurotoxin ingestion?
```
hyper-excitability
agitation
muscle tremors
seizures
obtundation or coma
```
142
what effects can neurotoxins have on the heart?
cardiac stimulation (as neurostimulants) leading to tachycardia or arrhythmias
143
what is the risk if a patient with a neurotoxin has muscle tremors?
if enough muscle mass is involved they could develop hyperthermia
144
what are the common neurotoxins?
```
theobromine (chocolate)
permethrin (spot on)
Metaldehyde (slug pellets)
tremorogenic mycotoxins
cannabis
```
145
what signs are commonly caused by theobromine ingestion?
cardiac stimulation as well as neuro signs
146
what animals is Permethrin toxic to?
cats
147
should Permethrin be used in cat containing households?
no as it is so toxic
148
what can metaldehyde intoxication lead to?
seizures as it is so toxic
149
where are tremorogenic mycotoxins found?
in mould
150
what can cannabis intoxication lead to?
ataxia
incontinence
seizures
coma
151
how may cannabis be taken in by an animal?
ingestion or inhalation
152
what method of intake makes cannabis toxicity signs worse?
ingestion
153
how does theobromide concentration differ between different types of chocolate?
the darker the chocolate the more theobromide and so more toxic it is
154
how should neurotoxins be managed?
decontamination where possible
muscle relaxants
anti-epileptic therapies
intra-lipid therapy
155
how can GI decontamination of neurotoxins be performed?
induce emesis
| activated charcoal
156
is induction of emesis often indicated in neurotoxin patients?
no - due to gag reflex absence or altered mental status which increases the risk of aspiration pneumonia
157
when is gastric lavage useful for neurotoxin patients?
if there has been recent ingestion of high toxicity substance (e.g. metaldehyde) as the benefit will outweigh the risk
158
when may dermal decontamination for a neurotoxin be used?
permethrin
159
what muscle relaxants may be used for management of neurotoxins?
diazepam
| methcarbamol
160
why are muscle relaxants needed in the management of neurotoxins?
ongoing seizures or tremors can lead to hyperthermia
161
what should you ensure you have checked if a patient who has ingested a neurotoxin is seizing?
ensure no hypoglycaemia or hypocalcaemia and if present, treat
162
why is intra-lipid therapy often used for neurotoxins?
many neurotoxins are lipid soluble
163
what are the main nursing considerations for patients with neurotoxin intoxication?
assess ambulatory capacity
monitor for and manage muscle tremors and seizures and associated hyperthermia
monitor respiratory function if a neuromuscular toxin has been ingested
monitor gag reflex to see if feeding or oral medication is appropriate
IVFT, nutrition where appropriate
164
what are the main areas to be managed if a patient is non-ambulatory?
```
decubital ulcers are a risk - regular turning, padded bedding
toileting considerations (catheter or manual expression)
```
165
how should respiratory function of neurotoxin patients be monitored?
monitor resp pattern and EtCO2 using capnography
166
what are the common hepatotoxins?
```
xylitol (artificial sweetener)
Mushrooms
blue green algae
aflatoxins (food contamination)
drugs
```
167
what drugs can be hepatotoxic?
```
phenobarbitone
paracetamol
azathioprine
doxycycline
lomustine (CCNU)
```
168
what are the main supportive measures for hepatotoxins?
antioxidant support
treat encephalopathy if present
treat hypoglycaemia if present
treat coagulopathies if presnet
169
what antioxidant support can be given to hepatotoxic intoxication patients?
SAMe/silybin
| NAC
170
what support can be given to encephalopathic hepatotoxic intoxication patients?
lactulose orally or via enema
| ensure electrolytes are normal (especially K+) as this exacerbates signs
171
what do encephalopathy and hypoglycaemia indicate?
extreme liver dysfunction
172
what support can be given to hypoglycaemic hepatotoxic intoxication patients?
supplementation of glucose
173
what support can be given to coagulopathic hepatotoxic intoxication patients?
consider plasma
174
how can you tell if a patient is coagulopathic?
PT / aPTT prolonged
| clinically bleeding
175
what is the effect of xylitol in the body?
stimulates endogenous insulin release
| hepatotoxic
176
what does endogenous insulin release due to xylitol lead to?
```
hypoglycaemia within 2 hours
lethargy
weakness
ataxia
collapse
seizures
(as muscles and brain deprived of oxygen)
```
177
how should xylitol intoxication be managed?
GI decontamination
| management of hypoglycaemia
178
how is GI decontamination performed in patients who have ingested xylitol?
emesis
activated charcoal
(assuming not contraindicated)
179
how is hypoglycaemia managed?
IV supplementation
| feeding
180
what IV glucose supplementation is used in an emergency?
bolus (i.e seizing)
181
what IV glucose supplementation is used if it is not an emergency?
CRI of 1.25-5% infusion
182
how can feeding be used to manage hypoglycaemia?
little and often
high fibre
complex carbs
183
what should be avoided when feeding the hypoglycaemic patient?
simple sugars
184
where are clotting factors activated in the body?
in liver
185
what clotting factors are activated within the liver?
II
VII
IX
X
186
how are clotting factors activated?
oxidation of vitamin K which makes the clotting factors become carboxylated
187
how do anticoagulant rodenticides work?
interfere with the enzyme vitamin k-epoxide reductase which reactivates vitamin K
188
how long does it take for symptoms of anticoagulant rodenticide ingestion to present?
2-5 days
189
is indirect anticoagulant rodenticide toxicity common?
no - dog/cat would have to consume over half their body weight in poisoned rats for there to be any effect
190
what are the main reasons patients present with anticoagulant rodenticide ingestion?
witnessed ingestion and so pre-symptomatic
| symptomatic - severe coagulopathy
191
what is the presentation of symptomatic anticoagulant rodenticide intoxication?
haemoabdomen/haemothorax
collapse
hypovolaemic
+/- anaemia
192
why does anticoagulant rodenticide toxicity present as a severe coagulopathy?
due to lack of clotting factors
193
how should pre-symptomatic witnessed ingestion of anticoagulant rodenticides be treated?
GI decontamination - emesis and activated charcoal
| measure clotting times at admission and 48 hours post decontamination
194
what is diagnosis of anticoagulant rodenticide intoxication based on?
prolonged PT +/- aPTT
195
when should clotting times of asymptomatic anticoagulant rodenticide intoxication be taken?
at admission and 48 hours after decontamination
196
what will indicate if GI contamination has been effective in preventing anticoagulant rodenticide intoxication?
normal clotting times 48hrs post treatment
197
what must happen if clotting times are abnormal when tested?
treatment required
198
how is asymptomatic anticoagulant rodenticide intoxication treated?
vitamin K therapy - 4 weeks
199
what should be repeated after vitamin K treatment?
PT/aPTT testing
200
when must symptomatic cases of anticoagulant rodenticide intoxication be seen?
urgently by vet
201
what must be considered when handling and performing diagnostic tests on anticoagulant rodenticide intoxication patients?
care with handling and blood sampling as they have coagulopathy
no jugular vein samples
202
is decontamination indicated in symptomatic anticoagulant rodenticide intoxication cases?
no as 2-3 days will have passed
203
how is symptomatic anticoagulant rodenticide intoxication treated?
vitamin K1 therapy
plasma if life threatening bleeding
RBC if needed
204
how can vitamin K1 therapy be administered?
oral
| SC
205
how long does vitamin K1 therapy take to work?
12 hours
206
why may plasma be needed in symptomatic anticoagulant rodenticide intoxication patients that have serious bleeding?
rapid replacement of clotting factors
207
in what species is paracetamol toxicity more of a problem?
cats
208
can paracetamol toxicity occur in dogs?
yes but is also used therapeutically so is related to overdose
209
what do cats with paracetamol toxicity present with?
methaemoglobinaemia as main issue
210
what do dogs with paracetamol toxicity present with?
hepatic injury is main issue
211
what state must the iron in haem be in to bind oxygen?
Fe2+
212
what is the effect of RBC oxidative damage on haem?
leads to creation of Fe3+ which leads to methaemoglobin and an inability to bind oxygen
213
what is the main clinical sign of methaemoglobinaemia?
discolouration of MM
| usually chocolate coloured but may be dark/dusky cyanotic
214
how is methaemoglobinaemia diagnosed?
drop of blood onto tissue
| if >10% MetHb there is noticeable brown discolouration
215
how does non-methaemoglobinaemia blood appear when exposed to air (oxygen)?
bright red
216
why are cats so susceptible to paracetamol toxicity?
they lack pathways required for the metabolism of paracetamol and therefore accumulate highly oxidative metabolites
217
what signs do patients with methaemoglobinaemia present with?
signs of shock (tachycardia, tachypnoea)
cardio respiratory distress
neurological signs due to reduced O2 supply to the brain
facial and limb oedema (cats only)
218
what is the main effect of methaemoglobinaemia?
reduced delivery of O2 to tissues
219
how is paracetamol toxicity treated?
```
induced emesis (if ingestion was <1hr ago and no contraindications)
activated charcoal
antioxidants
```
220
when is emesis indicated for paracetamol toxicity?
if ingestion <1 hr ago and no contraindications
221
what antioxidants may be given to paracetamol toxicity patients?
N-acetylcysteine (preferred)
| vitamin C and SAMe (less effective)
222
how is N-acetylcysteine administered to paracetamol toxicity patients?
slow IV injection
223
why must you take care when placing an IV catheter to give N-acetylcysteine?
can lead to phlebitis if extravasates
224
what is the prognosis of paracetamol toxicity?
guarded prognosis as highly toxic
225
what is the only UK venomous snake?
adder (protected species)
226
where are adders found?
moorlands, heaths, sands, peripheral woodlands
227
when are adders typically encountered?
the summer by inquisitive dogs
228
what are the effects of adder venom?
cytotoxic
cytolytic
can cause direct cardiovascular effects if it enters systemic circulation
229
when do clinical signs of adder bites usually present?
within 2 hours
230
what are the clinical signs of adder bites?
swelling local to bite +/- severe bruising
altered mentation (depressed) due to pain
panting
pyrexia
may have cardiac arrhythmias
231
how should adder bites be treated?
```
keep dog quiet and calm
leave bite area alone
give anti-venom
analgesia (opioids)
IVFT
```
232
what does of antivenom is needed for adder bites?
single dose per bite
233
when is antivenom recommended for adder bites?
facial bites and patients with systemic signs
234
are steroids indicated for adder bites?
no
235
are antibiotics needed for adder bites?
no unless there is clear evidence of concurrent infection (which is rare)
236
what is the prognosis of an adder bite?
reasonably good with treatment
237
why is it important to leave the adder bite area on the patient alone?
prevents any venom reaching systemic circulation
238
what irritants or caustic substances may animals ingest?
```
alkali
batteries
Benzalkonium chloride
Petrolleum distillate
washing tablets
```
239
what are the clinical signs of irritant/caustic ingestion?
varies depending on location of burns / irritation
| may be oral, oesophageal, gastric or dermal ulceration
240
what are the signs of oral ulceration following irritant/caustic ingestion?
pain
hypersalivation
anorexia
241
what are the signs of oesophageal ulceration following irritant/caustic ingestion?
regurgitation
242
what are the signs of gastric ulceration following irritant/caustic ingestion?
vomiting
243
what are the signs of irritant/caustic contact with the skin?
dermal alopecia
burns
ulceration
244
is gut decontamination indicated for irritant/caustic ingestion?
no
245
how should irritant/caustic ingestion / exposure be treated?
if battery, radiograph to assess location and if it is intact
dermal decontamination with warm water if recent dermal exposure
analgesia (opioids)
maintain hydration with IVFT
tube feeding often needed to bypass ulcerated areas
trail soft foods to see if animal will eat
246
what should be done if an animal has ingested a battery?
radiograph to assess location (obstruction risk) and if it is intact as this will alter treatment plan
247
what may happen if animals consume the contraceptive pill?
possible V/D
| may interrupt oestrus if contain progesterone
248
is treatment required for ingestion of the contraceptive pill?
no
249
is treatment required for ingestion of silica gel?
no - in this case do not eat warning just means it is a non-food item
250
is treatment required for catnip exposure?
no - cats may appear stimulated or that they are hallucinating but is is euphoria releated
251
is treatment required for ingestion of novelty luminous items?
may need other oral fluid or food to take away the taste but other than that none needed
252
what is usually found within novelty luminous items?
dibutyl phthalate (low toxicity)
253
what can be caused by ingesting novelty luminous items?
hypersalivation and occasional vomiting / hyperactivity
