U5 O3 - Toxicological Emergencies (Intoxications)

Question 1

What is the time frame within which most ingested compounds can be removed by emesis? Up to…

Select one:

a. 6 hours
b. 2 hours
c. 12 hours
d. 18 hours

Answer 1

The correct answer is: 2 hours

Question 2

Table salt should NOT be used as an emetic because

Select one:

a. It is unlikely to cause vomiting
b. It will result in sedation of the patient
c. It will cause vomiting in cats but not in dogs
d. It can cause salt toxicity ( hypernatraemia)

Answer 2

The correct answer is: It can cause salt toxicity ( hypernatraemia)

Question 3

A cathartic is a substance which:

Select one:

a. Irritates the stomach
b. Induces vomiting
c. Acts as a laxative
d. Activates the chemoreceptor trigger zone

Answer 3

The correct answer is: Acts as a laxative

Question 4

Cholecalciferol causes

Select one:

a. Hyperkalaemia
b. Hypercalcaemia
c. Hypomagnesia
d. Hypochloraemia

Answer 4

The correct answer is: Hypercalcaemia

Question 5

Which of the following drugs can be used as an antidote to cholinesterase inhibitor toxicity?

Select one:

a. Atropine
b. Glycopyrrolate
c. Charcoal
d. Xylazine

Answer 5

The correct answer is: Atropine

Question 6

Which of the following anticoagulants has the shortest half life?

Select one:

a. Brodifacoum
b. Warfarin
c. Bromadiolone
d. Defenacoum

Answer 6

The correct answer is: Warfarin

Question 7

Which of the following inhibits prostaglandin synthesis and can result in gastric ulceration?

Select one:

a. Ibuprofen
b. Metaldehyde
c. Lead
d. Cholecalciferol

Answer 7

The correct answer is: Ibuprofen

Question 8

Which of the following crystals may be found in the urine of an animal suffering from ethylene glycol poisoning?

Select one:

a. Oxalate
b. Struvite
c. Ammonium urate
d. Uric acid

Answer 8

The correct answer is: Oxalate

Question 9

Chocolate coloured mucous membranes may be associated with which poisoning in cats?

Select one:

a. Chocolate
b. Ethylene glycol
c. Paracetamol
d. Ibuprofen

Answer 9

The correct answer is: Paracetamol

Question 10

Ingestion of lilies ,by a cat, will result in damage to which body system?

Select one:

a. Gastrointestinal
b. Renal
c. Hepatic
d. Cardiovascular

Answer 10

The correct answer is: Renal

Question 11

Digitalis is found in which of the following?

Select one:

a. Poinsettia
b. Rhododendron
c. Foxglove
d. Lily of the valley

Answer 11

The correct answer is: Foxglove

Question 12

The disease state caused by something poisonous or toxic is called:

Select one:

a. toxicosis
b. toxigenic
c. intoxication
d. toxicity

Answer 12

The correct answer is: toxicosis

Question 13

Select all of the following that would expose an animal to lead, and increase the risk of them experiencing lead toxicity.

Select one or more:

a. Batteries
b. Tennis balls
c. Biro pens
d. Air pods
e. Shotgun pellets
f. Golf balls
g. Marbles
h. Lego figures
i. Electrical wires
j. Old paint
k. Plumbing materials
l. Fishing weights
m. Plastic toys

Answer 13

The correct answers are: Old paint, Batteries, Plumbing materials, Fishing weights, Shotgun pellets, Golf balls

Question 14

Of the following, the type of chocolate most toxic to dogs, containing the highest amount of theobromine is:

Select one:

a. milk chocolate
b. baking chocolate
c. cocoa powder
d. dark chocolate

Answer 14

The correct answer is: cocoa powder

Question 15

An example of a bezoar would be:

Select one:

a. mycotoxin
b. raisins
c. chewing gum
d. chocolate

Answer 15

The correct answer is: chewing gum

Question 16

Select the unwanted potential side effects of apomorphine administration .

Select one or more:

a. ataxia
b. vomiting
c. polyuria
d. respiratory depression
e. hyperthermia
f. diarrhoea
g. protracted vomiting
h. sedation
i. nystagmus

Answer 16

The correct answers are: sedation, ataxia, respiratory depression, protracted vomiting

Question 17

Which of the following is a gut protectant which could be administered following emesis to adhere to the gastric mucosa and support healing of erosions?

Select one:

a. sucralfate
b. rantidine
c. maropitant
d. omeprazole

Answer 17

The correct answer is: sucralfate

Question 18

When pre-measuring a stomach tube for gastric lavage, you measure from the external nares to the:

Select one:

a. 4th - 7th rib
b. 13th rib - umbilicus
c. 10th - 13th rib
d. 7th - 10th rib

Answer 18

The correct answer is: 10th - 13th rib

Question 19

The toxic dose of paracetamol in cats is:

Select one:

a. 50mg/kg
b. 75mg/kg
c. 100mg/kg
d. 25mg/kg

Answer 19

The correct answer is: 50mg/kg

Question 20

Cardiac arrhythmia is common following theobromine toxicity, showing as supraventricular tachycardia and/or:

Select one:

a. atrial fibrillation
b. ventricular tachycardia
c. sinus arrhythmia
d. ventricular premature contractions

Answer 20

The correct answer is: ventricular premature contractions

Question 21

Activated charcoal is to be administered to a 14kg dog following emesis. Calculate the volume required of a 20% solution to deliver a dose of 1g/kg.

Answer 21

The correct answer is: 70 ml

Question 22

Define toxicity?

Answer 22

Toxicity

The ability of a poison/ toxin to cause toxicosis

Question 23

Define toxicosis?

Answer 23

Toxicosis

The disease state caused by something poisonous/ toxic

Question 24

Define toxic?

Answer 24

Toxic

Poisonous substance

Question 25

Define poison?

Answer 25

Poison

A substance which can cause harm to a living organism

Question 26

Define toxin?

Answer 26

Toxin

A poisonous substance produced by a living organism

Question 27

Define intoxication?

Answer 27

Intoxication
The condition that arises due to ingestion of a chemical substance which results in altered consciousness, cognition or behaviour e.g. alcohol.

Question 28

Define intoxicant?

Answer 28

(In)toxicant

A substance which causes toxicosis or intoxication e.g. cleaning product or alcohol

Question 29

Define venom?

Answer 29

Venom
A toxin (produced by a living organism) which is injected from a living organism into another e.g. an Adder biting a dog

Question 30

Define antitoxin?

Answer 30

Antitoxin
A substance (antibody), produced by a living organism that counteracts/ neutralises a specific toxin e.g. tetanus antitoxin

Question 31

Define antivenom?

Answer 31

Antivenom
A substance (antibody), produced by a living organism that counteracts/ neutralises a specific venom e.g. adder antiserum

Question 32

Define antidote?

Answer 32

Antidote

A substance which counteracts a specific poison

Question 33

Define cathartic?

Answer 33

Cathartic

A substance which causes emptying of the GI tract = laxative.

Question 34

Define gavage/gastric lavage/

Answer 34

Gavage/ gastric lavage

Introducing material into the stomach via a stomach tube; washing out the stomach using a liquid.

Question 35

Define adsorption?

Answer 35

Adsorption

The adhesion of a substance to another surface.

Question 36

Define adsorbent?

Answer 36

Adsorbent
A substance that causes adsorption of another. In a poisoning case the action of an adsorbent (e.g. active charcoal) limits absorption of a poison into the body

Question 37

What approach is taken when a poisoned patient presents in ana emergency?

Answer 37

Approach to a poisoned patient- ▪ telephone triage ▪ primary triage assessment ▪ full clinical examination and history taking ▪ stabilisation +/- decontamination ▪ further treatment

Question 38

What is the aim when carrying out a telephone triage for an animal that has had a potential toxicity and after basic questioning and history taking what should be decided?

Answer 38

The aim of the initial telephone triage is to quickly identify a patient who is already showing serious signs and needs to be brought to the surgery immediately e.g. continuous seizure activity. Otherwise, some basic questioning and history taking should be performed to decide if
➢ the animal should be brought to the surgery for assessment and likely treatment
➢ further information is required before guidance can be required e.g. contact VPIS to see if the substance ingested is harmful
➢ home management is a reasonable approach

Question 39

What questions should be included when carrying out a telephone triage for an animal that has had a potential toxicity?

Answer 39

Questions include:
1. What is the poison and when did exposure occur?
2. What was the route of exposure i.e. was the poison ingested?
3. How much poison has the animal been exposed to?
4. Was exposure to the poison witnessed or is it suspected? Is there any evidence to be suspicious of poisoning – if so what is it?
5. Is the packaging for the poison available (e.g. household product, medication)?
If so it should be brought with the animal to the surgery.
6. If medication has been ingested, how much and what is the strength of the medication? Any other significant information e.g. long acting product
7. Patient details (species, breed, age, weight etc.)
8. Is the animal currently showing any signs- if so what are they?
9. Could any other animals be affected?
10. Has the owner already administered any treatment/ performed any first aid?
11. Is the animal on medication for any other condition?
12. What is the owner’s contact phone number?

Question 40

What guidance can be given to an owner of an animal that has a potential toxicity?

Answer 40

Other guidance to the owner could include-
➢ Ensure the animal cannot be further exposed to the poison e.g. remove packaging; prevent self-grooming
➢ Avoid administering any remedies at home e.g. salt water, mustard powder etc.
➢ Do not attempt to make the animal sick unless advised by the veterinary surgeon

If the owner is clear what the animal has been exposed to and poisoning is considered likely, they should be advised that their animal should be seen immediately. It is important to emphasise the need to come directly to the practice; and to give guidance on how to limit the absorption of any further poison e.g. wrap in towel to prevent grooming for topical poisons. If the animal is already showing clinical signs (e.g. seizures), appropriate guidance should be given on how it should be transported safely.
It some cases it may be more appropriate to speak to a veterinary surgeon in the first instance. In this situation, the owner’s phone number should be obtained, and they should be clearly informed of the time-scale (very short) in which they will be contacted to advise on the recommended course of action. A veterinary surgeon should be consulted IMMEDIATELY- they may suggest contacting the VPIS for guidance. It may be that the VPIS advise that the product is not poisonous; or that the dose ingested is unlikely to be harmful. In this case the risks of inducing emesis/decontamination would
be greater than the potential poisoning risk.

Question 41

What situations would emesis not be suitable following a potential toxic ingestion?

Answer 41

If induction of emesis is indicated, it is best performed within a veterinary practice. On rare occasions (e.g. nearest vet is over an hour away) an owner could be advised to attempt to induce emesis in a dog at home. This should only be considered if the dog
sounds to be clinically stable. Emesis is not appropriate and could be dangerous to the patient in the following situations-
➢ altered mentation
➢ respiratory distress or pre-existing respiratory conditions
➢ already vomiting
➢ ingestion of corrosive/ caustic substance

Question 42

If an owner had to be advised to make their dog vomit in the event that they ate something toxic but lived a distance from the veterinary practice?

Answer 42

There is a greater likelihood of a dog vomiting if it has eaten, so bread could be offered. The best way to induce emesis at home is by administering one crystal of washing soda (see below). If this method is used, however, it is essential, that the owner administers a washing soda crystal and not caustic soda (sodium hydroxide)
which is very corrosive and can cause very severe, potentially fatal, damage to the oropharyngeal and oesophageal mucosa. If there is any doubt, household products should NOT be advised.

Question 43

What concerns are there over using washing soda crystals as an emetic?

Answer 43

Woodmansey (2019) states that ‘Veterinary Poisons Information Service (VPIS) is alerting vets to a recent report highlighting the risks of using soda crystals (washing soda, sodium carbonate) as an oral emetic in dogs’. It is not known how washing soda acts as an emetic -it is thought that this could be ‘due to the direct alkaline irritant to the mucosa of the upper gastrointestinal tract’ (Woodmansey, 2019).
Washing soda ‘crystals’ are now available as a fine powder where previously they were individual crystals. It is suggested that this fine composition is likely to adhere to a larger area of the gastrointestinal and respiratory tract, causing direct damage to it; it is also less likely to be eliminated completely when the patient vomits and there may be a greater risk of aspiration of the powdered preparation than the crystal.
Because of this report VPIS no longer recommend using washing soda crystal for induction of emesis especially when there are effective licenced products

Question 44

What approach should be taken when managing a patient with a toxicity?

Answer 44

R - resuscitate/risk assessment
S - supportive care and monitoring
I -investigation

D - decontamination
E - enhanced elimination
A - Antidotes
D - Discharge

Question 45

What initial management should a patient with a toxicity receive?

Answer 45

As with all emergency patients, the initial patient assessment should focus on the major body systems (neurological, cardio-vascular and respiratory) and providing immediate life- saving measures if required. Following this the actual order in which the steps are followed will depend on the nature of the poisoning and the patient’s current clinical status e.g. if a patient presents with severe clinical signs, management
of these is the immediate priority. As stated by Jasani (2017) ‘…ultimately treatment is directed at the patient and not the poison’.
e.g. many poisoned patients will present with neurological signs (seizuring or tremors) that will need emergency management prior to investigation or decontamination.
A minimum data base may be obtained relevant to the patient’s condition. This could include all or some of- manual packed cell volume (PCV) and serum total solids (TS); blood glucose, electrolytes, urea and creatinine; lactate; blood smear; ECG and blood
pressure.
As soon as is feasible a full history should be obtained from the owner alongside performing a full clinical examination of the patient. Decontamination should be started promptly with the aim of limiting further systemic absorption of the poison. If available, an antidote may be administered at this stage (although frequently there is no antidote, with treatment usually being supportive and symptomatic). Further treatment aimed at increasing the rate of elimination of any
absorbed poison may be administered e.g. intravenous fluid therapy (IVFT). Ongoing intensive monitoring and evaluation of the patient’s condition and response to
treatment will be required. The patient’s nursing needs should be decided, with actual and potential problems being considered and anticipated. Appropriate, supportive nursing care should be provided throughout
When obtaining a history, it is important to identify features suggestive of poisoning e.g. sudden onset of dramatic clinical signs following exposure to an unknown substance is more suggestive of poisoning than low- grade vomiting and diarrhoea of
several days’ duration following a dietary change

Question 46

What should the primary triage assessment involve when assessing a patient with a toxicity?

Answer 46

The primary triage assessment has been discussed previously (Outcome 1.1). The cardiovascular assessment should focus on assessing the perfusion status of the patient and identifying any cardiac arrythmias (a relative common consequence of
poisoning).
The respiratory assessment should focus on identifying signs of respiratory compromise/ distress and recognising any signs suggestive of aspiration (Jasani,
2017). Immediate oxygen supplementation should be provided to a patient with respiratory distress.
The neurological assessment should focus on the patient’s mentation status and identifying signs suggestive of neurological involvement e.g. tremors, twitching etc.
Altered mentation could influence the method of decontamination that is chosen for this patient e.g. emesis will be contraindicated in a patient with altered consciousness.
The patient’s body temperature should be checked as the harmful effects of several poisonous compounds can result in hypothermia or hyperthermia i.e. seizures, muscle tremors. Immediate emergency treatment for these may be required. N.B. Emergency treatment may be indicated prior to performing decontamination
depending on the patient’s clinical status e.g. treatment of seizures/ severe muscle tremors; hypoglycaemia or serious cardiac arrythmias

Question 47

What methods of decontamination of toxicity can occur in an animal?

Answer 47

How decontamination is performed depends on the route of poisoning but could include ocular, dermal, inhalation, gastro-intestinal, renal excretion or, occasionally, surgical removal.

Question 48

How does the approach to human poisoning differ to that of veterinary.

Answer 48

The approach to human poisoning has changed in recent years with less focus on decontamination (e.g. inducing emesis, administering activated charcoal etc.) and more focus on using specific treatments e.g. antidote, haemodialysis. However, in veterinary cases decontamination is still likely to be the first line approach for practical (e.g. access to facilities) and financial reasons

Question 49

Explain what type of decontamination is most common in veterinary patients and how this is carried out?

Answer 49

Many veterinary patients are poisoned by ingestion meaning that gastrointestinal decontamination is often indicated. Gastric decontamination usually involves some method of gastric emptying - with the method being dictated by the patient and poison e.g. mentation status, species, non-corrosive versus corrosive. Following gastric emptying, an adsorbent (e.g. activated charcoal) may be administered to limit further absorption of the poison. Administration of a cathartic (e.g. a laxative) is rarely performed in most poisoning cases currently.
As explained by Jasani (2017) there is no real evidence base to support using one method of gastric decontamination in a veterinary patient over another. There are varying opinions as to what method and treatments should/ should not be used e.g. some clinicians advocate administration of activated charcoal following gastric decontamination and others do not. Some advocate administration of activated
charcoal rather than induction of emesis.
Decontamination is frequently a first consideration in toxicosis cases, but induction of emesis or administration of activated charcoal may not always be indicated and in some cases, it can be harmful

Question 50

After ingestion of a toxin, ideally when should emesis occur?

Answer 50

Emesis should, generally, only be induced if ingestion of the poison/toxin has occurred within the past two hours - ideally sooner than this as stomach emptying may be complete within 1.5 to 2 hours.

As many poisons/ toxins are ingested, gastrointestinal decontamination is the mainstay of treatment for most poisonings in dogs and cats. Emesis should, generally,
only be induced if ingestion of the poison/toxin has occurred within the past two hours - ideally sooner than this as stomach emptying may be complete within 1.5 to 2 hours. The longer the lag period following ingestion, the less likely it is that induction of emesis will be successful at removing the poison. With some poisons (e.g. grapes, chocolate) which may remain longer in the stomach, inducing vomiting may still be effective even
several hours later (Merola, 2013). Jasani (2017) states that clinical experience demonstrates that induction of emesis up to six hours following ingestion of poison
can be effective. However, Babyak and Lee (2018) advise that delayed induction of emesis should only be attempted if the patient is asymptomatic and the poison is one that is known to remain for a longer period within the stomach (chocolate, raisins, bezoar of e.g. chewing gum). Even with successful induction of emesis, some poison may remain within the stomach. Merola (2013) states that no clear benefit of inducing emesis over activated charcoal administration alone has been demonstrated despite its routine use in the emergency management of poisoning.

Question 51

What are the contraindications to inducing emesis?

Answer 51

Contraindications to inducing emesis include the following:
1. Cardiovascularly unstable patient
2. Inability to protect airway
a. Neurologically inappropriate (CNS depression)
b. Absent gag reflex
c. Laryngeal disease
3. Respiratory distress
4. (Risk of) raised intracranial pressure, seizures or altered mentation
5. Caustic or corrosive substances e.g. petroleum/ bleach N.B. consumption of milk or water by the patient may help to dilute corrosive/ caustic poisons if there
is no contraindication to this.
6. Solid materials that could cause patient damage during emesis

Induction of emesis should NOT be considered in a species that is unable to vomit e.g. rabbit
If the patient has already vomited several times, further emesis is unlikely to be of benefit and may increase the risks associated with fluid and electrolyte loss.

Question 52

What following substances may be used to induce emesis in a patient following toxicity?

Answer 52

The following substances may be used to induce emesis in the patient (although there is debate about the safety/ efficacy of some) -
➢ Apomorphine – the licenced product is administered via the subcutaneous route (it is not licenced for cats).
➢ Hydrogen peroxide (3% only) for dogs
➢ Medetomidine or xylazine can be used in cats but there is potential for cardiorespiratory depression.

Dogs typically respond predictably (within 20 minutes) to systemic administration of apomorphine. Higher doses can be associated with sedation, respiratory depression and ataxia – naloxone can be administered to manage this. The vomiting can occasionally be excessive.

Question 53

What following substances may be used to induce emesis in a cat following toxicity

Answer 53

Medetomidine or xylazine can be used in cats but there is potential for cardiorespiratory depression.

Question 54

Can cats be given apomorphine to induce emesis?

Answer 54

Unfortunately, cats do not respond predictably to apomorphine - a safe and effective dose has not been established in cats. Therefore, apomorphine use in cats is not recommended, although there are some anecdotal reports of its successful use

Question 55

What can be the side effects to using hydrogen peroxide to induce emesis?

Answer 55

Hydrogen peroxide is reported to cause protracted vomiting, gastro-intestinal ulceration and, in cats especially, haemorrhagic gastritis

Question 56

What can be given to cats to induce emesis and how soon should emesis occur after administration?

Answer 56

Xylazine is a potent emetic in cats - a single subcutaneous dose is reported to be rapidly effective in >75% of cats (BSAVA 2017). However, Thawley and Drobatz suggest that dexmedetomidine may be more effective at inducing emesis in a cat.

Question 57

What products have been used anecdotally to induce emesis without evidence to support their use?

Answer 57

In the unlikely situation that parenteral administration of an agent that induces emesis is not possible, alternative products could be considered e.g. one crystal of washing soda (N.B. see previous 2019 update re washing soda) or 3% hydrogen peroxide (maycause severe or bloody vomiting). There are several products that have been used anecdotally but have no evidence to support their use and could cause harm to the
patient e.g. salt solution, mustard powder (Garcia, 2012). Oral administration is not well tolerated by cats. Administration of liquid, dishwashing detergent, table salt or mechanical stimulation of the pharynx (to cause gagging) is not recommended. As effective veterinary products are available they should be used in preference. A veterinary nurse should always consult a veterinary surgeon before advising that an owner administers a product intended to induce emesis.

Question 58

Following administration of an anti-emetic what medication may be required?

Answer 58

Once the animal has vomited, gastro-protectants and anti-emetics may be required to prevent prolonged vomiting, protect the stomach and reduce the risk of gastritis and ulceration using e.g. antacids (e.g. omeprazole, cimetidine, misoprostol or ranitidine);
protectants (e.g. sucralfate); and anti-emetics (e.g. metoclopramide and maropitant).
Because metoclopramide is a dopamine antagonist, it may be the most effective product for stopping vomiting caused by the dopamine agonist effect of apomorphine

Question 59

When should activated charcoal be administered following ingestion of a toxin?

Answer 59

Medical grade activated charcoal can be administered per os or via stomach tube before or after gastric lavage. If appropriate, it should be administered as soon as possible after ingestion of a suspected/ actual poison although it may still beneficial up to six hours after ingestion

Question 60

How does activated charcoal work with toxicity?

Answer 60

Activated charcoal
has a large surface area which some poisons can bind to. Adsorption of organic compounds promotes their removal from the intestinal tract without absorption. Some formulations also contain sorbitol which is an osmotic cathartic

Question 61

What conditions are contraindicated with activated charcoal?

Answer 61

this should not be administered to a patient with diabetes mellitus or dehydration
Whilst activated charcoal might not be effective for some poisonings,

Activated charcoal should not be used in a patient that is actively vomiting; has any disorder with increased likelihood of aspiration e.g. megaoesophagus/ laryngeal paralysis; has CNS depression or is seizuring; or is dehydrated. If there is a possibility of gastro-intestinal (GI) perforation, GI obstruction, ileus or if it is anticipated that endoscopy or GIT surgery may be required, activated charcoal should not be
administered

Babyak and Lee (2018) advise that if there is a high chance that a patient has ingested a potentially poisonous substance and it is not known what the substance is, a single dose of activated charcoal could probably be administered. It depends on the material
that has been ingested as to how well it is adsorbed by activated charcoal- some products will not be removed.

Question 62

What toxins are not considered to be affected by activated charcoal?

Answer 62

Activated charcoal is not considered to be effective
against alcohols (e.g. ethanol), ethylene glycol, xylitol or heavy metals e.g. iron tablets

Question 63

What toxins is activated charcoal contraindicated with?

Answer 63

It is contraindicated in cases of
➢ salt toxicosis (could contribute to/ worsen hypernatraemia)
➢ corrosive or caustic product ingestion e.g. alkalis (lack of efficacy)
➢ petroleum compounds (lack of efficacy)
➢ mineral acids e.g. hydrochloric acid and sulphuric acid (lack of efficacy)

Question 64

What precautions should be taken when administering activated charcoal under anaesthetic and what is the major risk of doing this?

Answer 64

If activated charcoal is administered to an unconscious patient (e.g. under general anaesthetic), a cuffed endotracheal tube must be in place and the
patient must be monitored very closely on recovery from anaesthesia. Poli (2017) reports that some animals will vomit activated charcoal on recovery meaning there is a risk of aspiration

Question 65

What side effects may there be from repeated doses of activated charcoal?

Answer 65

Vomiting or constipation may be a result of repeated doses and theoretically, hypernatraemia is a potential complication of activated charcoal administration

Question 66

What is the dose of activated charcoal? and how often can it be administered?

Answer 66

Charcoal is usually administered at 1-2g/kg orally as a slurry (approximately 1g charcoal per 5ml water) and repeated at 4-6 hours intervals. Activated charcoal can
induce vomiting, particularly at higher dosages. Repeat doses every 4-6 hours have been recommended for toxins that undergo enterohepatic recirculation

Question 67

What monitoring should be carried out when administered repeated doses of activated charcoal and why?

Answer 67

Electrolyte levels should be monitored after multiple doses of activated charcoal (ideally after single doses too) due to the potential for electrolyte disturbances
(i.e., hypernatremia, hypermagnesemia, hypokalemia)

Question 68

When might gastric lavage be indicated over inducing emesis?

Answer 68

Gastric lavage is an alternative to induction of emesis and could be used when induction of vomiting has been unsuccessful; or is contra-indicated due to the risks e.g. patient is unconscious, airway cannot be protected.

Question 69

In what situations may gastric lavage be beneficial with toxicity?

Answer 69

Situations where gastric lavage may be of benefit include-
➢ recent ingestion of highly toxic material if presented very soon after ingestion (10 to 30 minutes)
➢ toxic material that causes delayed gastric emptying
➢ slowly released toxin (due to low solubility of ingested material)
➢ where the toxin forms a gastric concretion (e.g. chocolate, chewing gum, cat litter)
➢ massive ingestion that could lead to foreign body obstruction (e.g. unbaked bread dough, bone meal)
➢ extremely toxic substances where even a small decrease in the amount of toxin absorbed will help the patient e.g. lily and paracetamol ingestion in cats
➢ drugs/ products with a very narrow safety margin and/or very severe associated clinical signs (e.g. calcium channel blockers, baclofen, metaldehydes)

Question 70

What are the contraindications to gastric lavage following toxicity?

Answer 70

As with induction of emesis, there are some situations where gastric lavage is also contraindicated-
➢ following ingestion of sharp, volatile, caustic or corrosive substances
➢ if the poison could cause severe aspiration pneumonia e.g. petroleum products/ hydrocarbons
➢ where the airway cannot be protected
➢ where there is a high risk of gastric perforation
➢ and/or where the risks of general anaesthesia are considered unacceptable

Question 71

When is Gastric lavage not likely to be of benefit following toxicity?

Answer 71

Gastric lavage is not likely to be of benefit if the toxin was ingested more than two hours previously (some exceptions); or if the toxin is rapidly absorbed (e.g. ethanol, propanol, isopropanol, ethylene glycol and aspirin).

Question 72

How soon should gastric lavage take place following toxicity and briefly describe how it is carried out?

Answer 72

If gastric lavage is to be performed, it should be as soon as possible whilst the poison is still in the stomach e.g. ideally within 1 -2 hours of ingestion. The patient should be anaesthetised with a cuffed endotracheal tube in place to reduce the risk of aspiration.
Samples of gastric contents may be kept and submitted to a toxicology laboratory for analysis. The stomach should be lavaged with warmed water. To avoid
hyponatraemia, warmed 0.9 % saline or 0.45% saline could be used but the risk of hypernatraemia must be considered if large volumes are used. Following lavage,
activated charcoal and cathartics may be placed within the stomach, via the stomach tube, to further reduce absorption of the toxin.

Question 73

What equipment is required for gastric lavage?

Answer 73

Equipment for gastric lavage

1. Anaesthetic agent and equipment
2. Anti-emetic e.g. maropitant/ ondansetron
3. Stomach tube and pen to mark- separate ingress and egress tubes or a commercial twin-lumen tube can be used
4. Gag
5. Lubricant
6. Warmed fluids
7. Mouth gag
8. Sample pots
9. Bucket/ large container
10. Activated charcoal

Question 74

Describe the procedure for performing a gastric lavage?

Answer 74

The patient should be lightly anaesthetised, the endotracheal tube tied in place and the cuff of the endotracheal tube carefully inflated. An anti-emetic could be administered to decrease the risk of vomiting and aspiration following extubation.
1. Place the patient in sternal/ right lateral recumbency
2. Place a mouth gag or use a roll of bandage
3. Pack the back of the pharynx to avoid aspiration
4. Pre-measure the stomach tube(s) from the external nares to the level of the 10th -13th rib/ xiphoid process and lubricate (N.B. different sources give different
guidance as to where the tube is measured to. It is important that the tube is not positioned too far into the stomach to avoid damage)
5. The patient’s oral cavity should be kept lower than stomach
6. Introduce the lubricated tube(s) with care (wide bore egress tube followed by narrow ingress, if using 2 tubes) – gentle, twisting motions help placement of the
tube. Gentle blowing into the tube can help the passage into the stomach
7. Correct tube positioning can be confirmed byI. Palpating two tube like structures in the neck (trachea and stomach tube in the oesophagus)
II. Palpating the end of the tube through the abdominal wall
III. The presence of gastric contents/ gas in the tube
IV. Introducing a small volume of air and listening for gastric sounds
8. Introduce warmed tap water/saline (10 ml/kg) and allow to run out through the tube passively. Samples can be obtained for toxicological analysis.
9. Repeat the lavage until the fluid runs clear (could be up to 15-20 cycles). The patient may be carefully rolled from left to right side between gavages.
10. The stomach should be carefully palpated, frequently, to ensure it is not over distended; palpation of the stomach can also help the process of gastric
emptying
11.At the end of the lavage, activated charcoal may be administered carefully via the stomach tube
12.The end of the tube should be kinked prior to removal to prevent accidental aspiration. Once kinked the tube should be removed quickly in one clean
movement.
13.The patient must be carefully monitored throughout the procedure until fully recovered. It is essential that any material used to pack the pharynx is removed at
the end of the procedure before the patient is woken up.
14.The patient should be positioned in sternal recumbency with its head elevated. The endotracheal tube should not be removed until a strong gag reflex is present

Question 75

What is a cathartic and what should it be used alongside?

Answer 75

Cathartics such as sorbitol can decrease the absorption of substances by accelerating
their transit through the GI tract. Sorbitol can be administered with the activated charcoal- it increases the palatability, as well as increasing the rate of passage of activated charcoal

Question 76

How often should a cathartic be administered following toxicity and what are the contraindications?

Answer 76

A cathartic should only be administered once to avoid inducing dehydration due to the osmotic effect. A cathartic should not be administered if an animal has diarrhoea, ileus or possible intestinal obstruction

Question 77

How do you perform topical decontamination in a patient with a toxic substance?

Answer 77

Topical decontamination
If an animal is poisoned via the skin, washing is advised- to remove as much poison as possible and so limit percutaneous absorption; and to minimise skin irritation. It is important to wash with something that will neither increase absorption of the poison nor cause skin irritation. Mild soap or detergent solution is generally used- this must then be rinsed off using large volumes of warm water (too cold could cause
hypothermia; too hot could cause burns and increase absorption of some poisons).
The patient should be dried thoroughly following washing and rinsing.
For heavy contamination, especially of long-haired animals, clipping may be required.
On welfare grounds, chemical restraint is preferred for this (e.g. eye protection).
General anaesthesia with placement of an endotracheal tube may be indicated to prevent aspiration (Jasani, 2017). Using butter or margarine can help to soften and
remove oily and sticky substances – these must be removed thoroughly by washing in soapy water, rinsing and drying. Liquid paraffin, vegetable oil or a commercial product e.g. Swarfega ® could be considered for oily substances. However, if used, Swarfega ® must be removed thoroughly after use. Powdered substances could be removed using a vacuum cleaner. Staff involved in skin decontamination should wear appropriate personal protective equipment (PPE)

Question 78

If a patient has been exposed to a caustic or corrosive substance on the skin or in the eye what action can be taken?

Answer 78

If a patient has been exposed to a caustic or corrosive substance (skin or eye), copious washing with a non-irritant solution is recommended e.g. warmed 0.9% saline or tap water (Jasani, 2017). Attempts to neutralise can be counter-productive- it is possible that the wrong substance could be used and, in an attempt to neutralise, more acid could actually be added to an acid burn or more alkali added to an alkaline burn.
Additionally, Jasani (2017) advises that the chemical reaction involved in neutralising something could potentially lead to skin burns. Pain assessment and provision of analgesia is also an important consideration for patients exposed to corrosive or
caustic substances

Question 79

is intravenous fluid therapy indicated following toxicity and why? What monitoring should take place?

Answer 79

Intravenous fluid therapy is commonly instituted in patients following poisoning. It may be administered as supportive treatment to patients that are dehydrated,
hypovolaemic or hypotensive; to increase cardiac output and ensure adequate oxygen delivery to cells; to increase renal perfusion and support kidney function especially where the poison could be a nephrotoxin; to encourage excretion of the poison or to manage electrolyte abnormalities. The patient’s fluid requirements should be calculated and delivered at an appropriate rate. If relatively large volumes of fluids are
being administered to stimulate diuresis and rapid renal elimination of the poison, it is essential that the patient is monitored very carefully for signs of over infusion.
Perfusion parameters and the hydration status of any patient receiving intravenous fluid therapy should be closely monitored. Too rapid infusion of large volumes of intravenous fluids could lead to cerebral and pulmonary oedema. Forced diuresis should only be used where there is a specific indication e.g. nephrotoxins including lilies, grapes and ethylene glycol. The aim is to increase the excretion of nephrotoxins or their metabolites

Question 80

What fluid rate can be administered to promote diuresis?

Answer 80

a rate of 1-4 ml/kg/ hr, in addition to calculated fluid requirements, could possibly be administered to promote diuresis.

Question 81

What type of fluids are usually indicated with toxicity?

Answer 81

The use of specific acidifying and alkalinising agents, to increase elimination, risks causing dangerous patient acidosis or alkalosis. Generally, only balanced, isotonic crystalloid solutions are indicated. In some poisonings, packed red blood cell or whole blood transfusions may be performed to restore oxygen carrying capacity. In such patients, additional monitoring for any signs of a transfusion reaction is warranted

Question 82

What are the extracorporeal methods of toxin removal in veterinary patients?

Answer 82

Extra-corporeal methods of removing some toxins (e.g. barbiturates, ethylene glycol), through haemodialysis and haemoperfusion, have been used. These options are only available in a small number of veterinary hospitals currently

Question 83

What is the difference between haemodialysis and haemoperfusion?

Answer 83

Haemodialysis can be performed in several ways to ‘clear urea, metabolic waste products, toxins, and excess fluid from the blood’
Haemoperfusion is a different, blood purifying process ‘in which whole blood is exposed directly to sorbent materials with the capacity to selectively or nonselectively bind endogenous or exogenous toxins’

Question 84

What is the main indication for a lipid infusion (e.g. Intralipid®) ?

Answer 84

The main indication for a lipid infusion (e.g. Intralipid®) is for total or partial parenteral nutrition, in veterinary or human patients; or as a vehicle for drug delivery (e.g.
propofol) in human patients). However, intravenous lipid emulsion therapy is increasingly used, off-licence, in the management of some veterinary poisonings.
There are currently no evidence-based trials to support the use of ILE in veterinary poisonings but there are increasing anecdotal reports of its successful use. It was originally demonstrated to shift the dose-response of bupivacaineinduced cardiac arrest in rats (Weinberg, et al. 1998). Several human and, increasingly, veterinary case reports have been published on the clinical use of ILE in neurological, cardiac and other poisonings.

Question 85

What is the main mechanism of action of intralipid emulsion therapy?

Answer 85

It acts as a ‘lipid sink’ i.e. lipophilic drug/ poison binds to it meaning there is less free drug/ poison in plasma to bind to target receptors on the patient’s cells.
Lipophilic drug/ poison is thought to be sequestered into a lipid compartment within the intravascular space - with a consequent reduction in tissue distribution of the drug. The extent to which a drug/poison is sequestered into this lipid compartment is dependent on its lipophilicity. Theoretically therefore, any intoxication from a highly lipophilic drug could benefit from lipid rescue.
Provides cardiac myocytes with increased energy (free fatty acids). The increased cardiac energy supply is thought to improve myocardial/ cardiac performance.
• Additionally, myocardial function is improved by increasing intracellular calcium concentration.

Question 86

What toxins can potentially be treated with intra-lipd emulsion therapy?

Answer 86

Intravenous lipid emulsion (ILE) can be used as a ‘lipid sink’ to bind lipid soluble toxins such as macrocyclic lactones (e.g. ivermectin, moxidectin/ milbemycin); pyrethroids/ permethrins in cats, lipophilic GABA receptor agonists (e.g. baclofen), lipophilic beta- blockers (e.g. propranolol), metaldehyde, calcium channel blockers (e.g. diltiazem), marijuana, NSAIDs (e.g. ibuprofen, naproxen), local anaesthetics (e.g. lidocaine) and psychotropics (e.g. selective serotonin reuptake inhibitors (SSRIs), selective serotonin and norepinephrine reuptake inhibitors (SSNRIs), cyclic antidepressants)
Macrocyclic lactones (e.g. ivermectin, moxidectin/ milbemycin) can cause acute neurological intoxications; local anaesthetic e.g. lidocaine can cause cardiotoxicity. As discussed by Kormpou et al. (2018) tremorgenic mycotoxins are lipophilic and so ILE may be of benefit in these patients.

Question 87

What concentrations are intra-lipid available in ?

Answer 87

ILE is available as a 10% or 20% emulsion- its use in veterinary poisoning cases is currently off-licence (Jasani, 2017). The preparation that is generally used in veterinary practice is (Intralipid 20%) a soybean-oil-based emulsion

Question 88

What are the suggested protocols for intra-lipid administration? What cases have been successful following these protocols?

Answer 88

Jasani (2017) suggests a protocol where Intralipid 20% is administered at 1.5 ml/kg as a slow IV bolus over 2-3 minutes N.B. 20% ILE is preferred to 10% and being
isotonic it can be administered through a peripheral intravenous catheter. The bolus is followed with a CRI of 0.25 ml/kg/min for 30-60 minutes. The serum should be monitored every two hours for evidence of lipaemia. If the patient remains symptomatic, the bolus followed by infusion can be repeated, when the serum
becomes clear again (non-lipaemic). If there is no improvement after three doses (bolus + infusion), ILE treatment should be discontinued; no more ILE should be administered to a patient if the serum appears very orange or yellow. The patient should be monitored until the clinical signs have resolved and the serum is no longer lipaemic. The ideal duration of the infusion has not been established, with the timeframe being dependent on factors such as the half-life of the poison (Jasani, 2017).
N.B. If the poison has a long half-life, it is possible that toxicity signs could return once the ILE has been metabolised (clear serum).

BSAVA (2017) suggest 1.5 – 5 ml/kg of 20% lipid emulsion (e.g. Intralipid® 20%) as an IV bolus dose; followed by an IV infusion of 0.25- 0.5 ml/kg/min for 30-60 minutes. A bolus of 1.5 ml/kg can be repeated. An infusion of 0.5 ml/kg/min can be administered for a maximum of 24 hours corresponding to the maximum
recommended cumulative dose of 12 mL/kg. ILE is generally administered for 30 minutes initially and then repeated once or twice if no improvement.

Canine cases, reported to have improved following treatment had infusions of 30, 60 or 90 minutes respectively (Reineke, 2014). Reineke (2014) also states that the only report of successful ILE therapy in a cat with lidocaine intoxication describes improvement in clinical signs following 1.5 mL/kg over 30 minutes.

Question 89

How long does intra-lipid last for once opened?

Answer 89

Strict aseptic protocols must be adhered to when using ILE to prevent bacterial contamination and destabilisation of the emulsion. Once opened ILE should be refrigerated and must be used within 24 hours- any excess should be discarded due
to the risk of bacterial contamination. If therapy is required for longer than 24 hours, a new bag or vial must be used

Question 90

What are the side effects to intra-lipid administration?

Answer 90

Because of the high lipid content of ILE, hypertriglyceridaemia and lipaemia will occur
following administration. However, this is usually short-term and of no clinical consequence. The main potential side-effect is local or systemic infection is due to bacterial contamination caused due to poor handling or aseptic technique. N.B. The total volume of ILE that is likely to be administered to a poisoned
patient is significantly less than the volume that would be administered to another patient receiving parenteral nutrition. There are occasional reports of anaphylactic type reactions and pancreatitis is considered to be a rare possibility in veterinary patients

Question 91

What treatment might be administered to a patient with tachycardia following chocolate toxicity?

Answer 91

Additional miscellaneous treatment may
be administered for certain poisonings e.g. beta blockers may be considered if the
patient has severe tachycardia due to chocolate poisoning

Question 92

What is an antidote?

Answer 92

Antidotes are substances that can be used in certain poisonings – they act specifically either to neutralise a poison or to antagonise the harmful effects

Question 93

What is the antidote for lead, anticoagulant rodenticides, organophosphate poisoning and ethylene glycol?

Answer 93

EDTA can be used to chelate lead in a case of lead poisoning to neutralise the poison; vitamin K is a specific antidote to the anticoagulant rodenticides which helps to promote haemostasis; atropine is an antidote to organophosphate poisoning and fomepizole is an antidote to ethylene glycol poisoning

Question 94

What are the mechanisms of action for anticoagulant rodenticide?

Answer 94

There are various preparations of rodenticide. The anticoagulant rodenticides interfere with vitamin K activation - leading to coagulopathy and haemorrhage (see also Unit 3
Outcome 1 for more information). Active vitamin K is required for the activation of several clotting factors (II, VII, IX and X) (Babyak and Lee, 2018). Cats are more
resistant to the effects of the anticoagulant rodenticides than dogs

Question 95

Give some examples of anticoagulant rodenticides?

Answer 95

Examples of anticoagulant rodenticides include

1. Brodifacoum (2nd generation coumarin type - ‘super warfarin’)
2. Bromadiolone (2nd generation coumarin type)
3. Difenacoum (2nd generation coumarin type)
4. Diphacinone (2nd generation indandione type)
5. Warfarin (1st generation coumarin type)

Question 96

What generation of rodenticide is considered to be more toxic?

Answer 96

The first-generation rodenticides are relatively less toxic than the second generation - usually requiring repeated ingestion to cause clinical signs. Most of the second-generation rodenticides are dyed a blue-green colour in the UK

Question 97

What effect does vitamin K have following anticoagulant rodenticide?

Answer 97

Vitamin K is necessary for the hepatic synthesis (γ-carboxylation of vitamin K dependent) of coagulation factors (factors II, VII, IX, X); and vitamin K-dependent
anticoagulants (protein C and protein S). Without activated vitamin K, these coagulation factors are depleted and clinical haemorrhage may occur within three to five days ingestion of the poison. The haemorrhage will typically be into a body cavity
(unlike haemorrhage caused by thrombocytopaenia), from the nose (epistaxis), into the gastrointestinal tract, into the pericardium, into joints or into the lungs

Question 98

What will clinical signs of anticoagulant rodenticide toxicity be dictated by?

Answer 98

Clinical signs will be dictated by the volume and site of haemorrhage - they will often be those of acute haemorrhage (hypovolaemia and decreased oxygen delivery by the blood to tissues) and related to the site of the haemorrhage – e.g. haemorrhage into
the pleural space will cause respiratory distress and haemorrhage into the joints will cause lameness.

Question 99

What are the clinical signs of anticoagulant rodenticide toxicity?

Answer 99

Clinical signs
These can include -
1. signs of hypovolaemia/ haemorrhagic shock (tachycardia, pale mucous
membranes, prolonged CRT, altered mentation etc.)
2. mucosal (e.g. episcleral) / skin haemorrhage (e.g. ecchymosis -bruising)
3. haemoptysis
4. tachypnoea, respiratory distress
5. lameness
6. epistaxis
7. melaena

the most common signs relate to blood
loss and breathing difficulties; with melaena, epistaxis, bleeding from the gums and ecchymoses being less common

Question 100

What might a PCV/TP with anticoagulant rodenticide poisoning be consistent with?

Answer 100

A minimum database may be consistent with acute haemorrhage (low total solids with low or normal packed cell volume).

Question 101

Why might a patient with anticoagulant poisoning be thrombocytopaenic?

Answer 101

Patients with anticoagulant rodenticide poisoning
may be thrombocytopaenic because of consumption of platelets secondary to the massive haemorrhage that can occur. Every patient with evidence of severe
haemorrhage should be evaluated for objective measures of coagulation.

Question 102

Why will Anticoagulant rodenticides cause prolonged prothrombin time (PT) before the activated partial thromboplastin time (aPTT)?

Answer 102

Anticoagulant rodenticides will cause prolonged prothrombin time (PT) before the activated partial thromboplastin time (aPTT) is prolonged. This is because factor VII, which is involved in the extrinsic pathway, has the shortest half-life of the vitamin K
dependant clotting factors- the extrinsic pathway is assessed by measuring PT. aPTT assesses the intrinsic system and the common clotting pathways - it will be prolonged once factors II, IX, and X are also depleted; and from consumption of other factors, if
haemorrhage occurs. The activated clotting time (ACT) also reflects the intrinsic pathway and will therefore not be prolonged until overall factor depletion is severe.

Question 103

Is anticoagulant redenticide poisoning likely if a patient has a prolonged PT with clinical signs of bleeding (and normal/ mildly increased aPTT)?

Answer 103

Therefore, if a patient has a prolonged PT with clinical signs of bleeding (and normal/ mildly increased aPTT), anticoagulant rodenticide poisoning is likely.

Question 104

Is anticoagulant redenticide poisoning likely if a patient has a severe prolongation of the aPTT and a mild prolongation of the PT?

Answer 104

anticoagulant rodenticide poisoning is unlikely in a patient with a severe prolongation of the aPTT and a mild prolongation of the PT.

Question 105

Is anticoagulant redenticide poisoning likely if a patient has both the PT and the aPTT are severely prolonged?

Answer 105

If both the PT and the aPTT are severely prolonged, then a diagnosis of anticoagulant rodenticide poisoning is more difficult.

Question 106

How would you treat a patient that has eaten the poison recently (less than 2 hours)?

Answer 106

If the patient has eaten the poison recently (less than 2 hours) then decontamination by inducing emesis is indicated. This can then be followed by administration of activated charcoal. If decontamination is performed promptly, the risk of coagulopathy is low and therefore
treatment with vitamin K1 is not likely to be required- prothrombin time can be monitored however.

Question 107

What is the recommended treatment plan for a patient that has ingested and probably absorbed anticoagulant
rodenticide?

Answer 107

In patients who have ingested and probably absorbed anticoagulant rodenticide, clinical signs of haemorrhage usually develop within 72 hours of ingestion (up to 5-7 days (BSAVA, 2019). In such a patient, however, the PT is likely to be prolonged after ~ 48 hours after ingestion. Therefore, there is a 24-hour window when PT is likely to be prolonged but clinical signs (haemorrhage) have not yet developed.
Therefore, starting 36- 48 hours after known ingestion of rodenticide, PT should ideally be tested daily for at least 3 days. If it remains within the normal reference range, no treatment/follow-up is likely to be necessary. N.B. A small gauge needle and peripheral vein should be used for blood sampling. If the PT is prolonged, then vitamin K1 treatment is required usually twice daily for one month. A final prothrombin time (PT) should be assessed 2-3 days after the last planned treatment.
If the PT remains prolonged, another 2 weeks of vitamin K1 therapy is indicated. Following this PT should again be performed 2-3 days after the last vitamin K1 treatment

Question 108

What is the recommended treatment plan for anticoagulant rodenticide poisoning even if no signs/ likelihood of coagulopathy i.e. small volume/ prompt
decontamination?

Answer 108

Some concerned owners may prefer that their pet has vitamin K1 treatment even if no signs/ likelihood of coagulopathy i.e. small volume/ prompt decontamination. As above, prothrombin time (PT) should be assessed 2-3 days after the last planned treatment. If the PT is prolonged (unlikely in this case), another 2 weeks of vitamin K1 therapy is indicated followed by another check of PT 2-3 days
after the last vitamin K1 treatment

Question 109

Why is a single, prophylactic administration of

vitamin K1 to a patient that has ingested anticoagulant rodenticide is not advised?

Answer 109

a single, prophylactic administration of vitamin K1 to a patient that has ingested anticoagulant rodenticide is not advised. This would affect the results of the 36- 48-hour PT test. PT could appear normal, in a patient
who has absorbed anticoagulant rodenticide, due to this one-off vitamin K1 administration. Because of this ‘normal’ result no further vitamin K1 treatment would
be administered leaving the patient at risk of haemorrhage once the vitamin K1 injection is fully metabolised. If a single, prophylactic treatment of vitamin K1 is administered, the patient will then require vitamin K1 treatment for a further month.

Question 110

How do you treat a case of anticoagulant rodenticide associated haemorrhage?

Answer 110

In the case of anticoagulant rodenticide associated haemorrhage, vitamin K1 treatment will be required to allow activation of the coagulation factors. The actual
treatment regime depends on the type of rodenticide ingested and the results of blood tests to assess clotting function (as above). However, as it will take at least 12 hours for new clotting factors to be produced by the patient, a plasma transfusion (either
frozen or fresh frozen) may be required initially to provide an emergency supply of these. If the patient is anaemic, then packed RBCs may be administered as well; or a whole blood transfusion may be performed. The half-life of clotting factors is short so
a second plasma transfusion may be required. Careful
handling of a patient with a coagulopathy is necessary to minimise further haemorrhage and bruising. If the patient is hypovolaemic, it should be fluid resuscitated - further administration of packed red blood cells, plasma (fresh-frozen or frozen) or whole blood may be required

Question 111

What vitamin K treatment will known first-generation rodenticide toxicity require?

Answer 111

A lower dose of vitamin K1 and a shorter course of treatment will be needed for a patient with known first-generation rodenticide toxicity (BSAVA, 2017). Vitamin K1 is administered initially by subcutaneous injection (there is a risk of anaphylaxis with intravenous injection). The subcutaneous injection sites should be alternated and the patient’s activity restricted during this period to prevent the chance of haemorrhage. Follow up doses are then given at 12-hour intervals either SC or PO.

Question 112

What vitamin K treatment will known second-generation rodenticide toxicity require?

Answer 112

Modern, second generation rodenticides, such as brodifacoum, have prolonged halflives, remaining active in the body for a relatively long period- thus a longer course of vitamin K1 therapy may be needed – (up to 3-4 weeks in most cases). Whilst parenteral vitamin K1 is used for the initial treatment, oral vitamin K1 can be administered for the remainder of the treatment. A final prothrombin time (PT) should be assessed 2-3 days after the last planned treatment.
If the PT is prolonged, another 2 weeks of vitamin K therapy is indicated. Following this PT should again be performed 2-3 days after the last vitamin K treatment

Question 113

What is bromethalin? and how does it affect an animal?

Answer 113

Pathogenesis

This rodenticide is a neurotoxin which causes oedema of the central nervous system.

Question 114

What are the clinical signs of bromethalin?

Answer 114

Clinical signs
Clinical signs can be acute or chronic depending on how much toxin is ingested. They are associated with central nervous system dysfunction and can include1. seizures
2. muscle tremors
3. ataxia
4. weakness
5. coma.
Cats are reported to develop a paralytic syndrome irrespective of the dose ingested

Question 115

How can rodenticide toxicity be diagnosed?

Answer 115

The history may indicate consumption of this poison. Clinical signs may be suggestive, but analysis of the contents of gastric lavage may be required for definitive diagnosis.

Question 116

How do you treat bromethalin toxicity?

Answer 116

If the poison has recently been ingested, emesis or gastric lavage is indicated followed by activated charcoal administration, to reduce further absorption. Due to enterohepatic recirculation, repeated doses of activated charcoal may be administered.
There is no recognised antidote so treatment is symptomatic and aimed at controlling CNS clinical signs and reducing cerebral oedema. This may include the use of mannitol, sedatives and anticonvulsants as for any neurological patient. Treatment may be required for days to weeks.

Question 117

What is cholecalciferol and what can it result in?

Answer 117

Cholecalciferol is a rodenticide which causes vitamin D overdose. This results in hypercalcaemia, acute renal failure and mineralisation of soft tissues (including the
blood vessels, heart and kidneys).

Question 118

What can vitamin D poisoning in pets be caused by?

Answer 118

Vitamin D poisoning could be caused by exposure to rodenticides, vitamin preparations, cod liver oil, veterinary medicines, growth promoters and human
medicines (especially psoriasis creams).

Question 119

What are the clinical signs of vitamin D toxicity and how soon after ingestion do these develop?

Answer 119

Clinical signs usually develop within 6-12 hours of ingestion.
These can include
1. depression
2. muscle weakness
3. convulsions
4. vomiting
5. diarrhoea
6. polydipsia
7. polyuria

Question 120

How do you diagnose cholecalciferol poisoning?

Answer 120

Diagnosis
History and detection of high serum calcium and phosphorus levels, with normal parathyroid levels, is suggestive of cholecalciferol poisoning.

Question 121

What treatment and nursing care is required for cholecalciferol poisoning?

Answer 121

There is no specific antidote. Early decontamination with emesis and/or activated charcoal administration is required. A treatment regime to encourage excretion of the toxic metabolites, support renal function and limit the harmful effects of hypercalcaemia is required – intravenous fluid therapy will be the mainstay of
treatment. 0.9% NaCl is the fluid therapy of choice for hypercalcaemia. Specific additional measures to reduce serum calcium levels may be used e.g. furosemide,
prednisolone and bisphosphonates will be necessary; gastro-protectants are also of benefit.
Renal function and serum electrolytes, especially calcium, should be monitored regularly

Question 122

What is metaldehyde?

Answer 122

This is present in molluscocides and is toxic to cats and dogs. It is also found in camping stove fuel packs

Question 123

How does metaldehyde cause toxicity?

Answer 123

Metaldehyde is thought to work by increasing excitatory neurotransmitters and / or decreasing inhibitory neurotransmitters. Decreased brain levels of gamma aminobutyric acid (GABA) causes CNS clinical signs. The exact pathogenesis is unclear as other side-effects are seen without altered GABA activity

Question 124

What are the clinical signs of metaldehyde toxicity and how soon after ingestion do clinical signs occur?

Answer 124

Clinical signs
Clinical signs may develop within 30 minutes of ingestion of the poison. The central nervous system is mainly affected.
Signs can include
1. hyperaesthesia
2. seizures
3. salivation
4. hyperthermia
5. muscle tremors, spasms and rigidity
6. respiratory signs
7. liver damage (2-3 days post exposure but less common)
8. tachycardia
9. nystagmus and dilated pupils
10.temporary blindness may occur (usually resolves after 2-3 weeks)
Typically, it is the clinical signs of ‘shake and bake’ i.e. tremors and hyperthermia that
are classical for this poisoning. Tabor (2014) discusses the pathophysiology and management of hyperthermia. Hyperthermia can lead to disseminated intravascular coagulation and organ failure.

Question 125

How is metaldehyde toxicity diagnosed?

Answer 125

Diagnosis
The history of exposure to slug/snail bait, along with the above clinical signs is suggestive. Detection of metaldehyde in the stomach contents or green diarrhoea (many preparations are dyed green) is also possible. Metaldehyde pellets are radiopaque so abdominal radiography may be useful for diagnosing

Question 126

What treatment and nursing care is required for metaldehyde toxicity?

Answer 126

Decontamination with induction of emesis, if no contraindication, followed by activated charcoal administration is advised. Gastric lavage may be
performed if sedation/ anaesthesia is required to control seizuring.
Neurological signs can be treated with muscle relaxants (e.g. methocarbamol) and anticonvulsants (e.g. benzodiazepines, phenobarbitone or propofol). N.B. anaesthesia may be required for up to 24 hours.
Anticonvulsant therapy will help to lower body temperature but management of potentially life-threatening hyperthermia (fans, IV fluids etc.) may also be required.
Supportive intravenous fluid therapy (IVFT) will be required to minimise renal damage associated with muscle damage secondary to excessive activity.
Metaldehyde poisoning may cause an acidosis so monitoring of acid-base balance is important; the coagulation profile may need to be monitored if the patient develops DIC secondary to hyperthermia.

Question 127

What is paraquat and how does it cause toxicity?

Answer 127

This herbicide is available as a liquid or granules although it has been banned in the UK since 2007 - it is highly poisonous producing free radicals which
cause cell damage. Some preparations may be absorbed through the skin. Paraquat concentrates in the lungs and causes severe respiratory distress.

Question 128

What are the clinical signs of paraquat toxicity?

Answer 128

Clinical signs
These are associated with local irritation of the gastrointestinal tract, respiratory and neurological signs including
1. mucosal and skin irritation e.g. nose, eyes, oral cavity and facial skin
2. vomiting and GIT signs
3. hyperexcitability
4. ataxia
5. depression
6. respiratory distress
7. cyanosis

The initial clinical signs of paraquat poisoning are due to its irritant effects - later clinical signs are due to progressive pulmonary pathology.

Question 129

How do you diagnose paraquat toxicity and how soon after are clinical signs seen following ingestion?

Answer 129

Diagnosis
As this poisoning is rare, the following information is mainly for interest - Clinical history of exposure to this herbicide, along with clinical signs may be suggestive. Paraquat levels may be measured in the blood. There is also a urine spot test where 1ml of urine is added to 1ml of a mixture of 100mg sodium dithionite in 10ml
of sodium hydroxide (1 molar concentration). If the mixture turns blue-green, this indicates the presence of paraquat. This may only occur, however, within the first two days post ingestion. Radiography of the lungs often fails to show changes that reflect severity of the condition observed clinically.

Question 130

What treatment and nursing care is required for paraquat toxicity?

Answer 130

Treatment and nursing care
Absorption of paraquat from the GIT is slow. As there is no specific antidote, decontamination with activated charcoal and a cathartic should decrease absorption
and increase removal from the GI tract. N-acetylcysteine may be administered to help to neutralise free radicals, although little data exists to prove the efficacy of this
treatment.
Management of pulmonary oedema with oxygen therapy, diuretics and nursing interventions may be required. GI protectants, e.g. sucralfate and antacids; and antiemetics are also helpful to reduce GIT mucosal irritation and vomiting.

Question 131

What are Pyrethrums and pyrethroids and how do they cause toxicity?

Answer 131

Pyrethrins are naturally-derived parasiticides/pesticides, from Chrysanthemum species, used primarily for flea, and other insect, control and treatment; pyrethroids are the synthetic equivalent. They are an increasingly common cause of poisoning in cats- cats are more sensitive to these compounds than dogs, due to their
metabolism.
Pyrethrins and pyrethroids are used in household insecticides and topical/ spot-on flea and tick preparations for dogs. The most common cause of toxicity in cats is, accidental, administration of a product intended for dogs.
Permethrins are neurotoxins which cause rapid firing of neurons leading to CNS clinical signs. Toxic levels of metabolites accumulate more rapidly in cats due to their
poor liver glucuronide conjugation

Question 132

What are the clinical signs of pyrethrum/pyrethroid toxicity?

Answer 132

Clinical signs
These are neurological in origin and include
1. hypersalivation
2. agitation
3. tachypnoea
4. vomiting
5. muscle tremors
6. weakens/ ataxia
7. seizures
Secondary hyperthermia may develop and some affected cats die. Dogs are less likely to be affected – affected dogs are less likely to show CNS signs, showing skin related signs instead e.g. dermal paraesthesia, pruritus, rubbing and chewing

Question 133

How do you diagnose pyrethrum/pyrethroid toxicity?

Answer 133

Diagnosis
History is important as poisoning may have been caused by exposure to -
• a household insecticide or environmental flea control product
• a topical preparation (e.g. shampoo, spot-on, shampoo, powder, collar)
• a recently treated animal, its bedding or discarded packaging
There is often a history of accidental exposure to or treatment with a product designed for dogs. In conjunction with the clinical signs, this is often diagnostic.

Question 134

What is the treatment and nursing care for pyrethrum/pyrethroid toxicity?

Answer 134

Treatment and nursing care

There is no antidote so the treatment is aimed at early decontamination - absorption can be oral and percutaneous.

Question 135

If no neurological signs have developed after pyrethrum/pyrethroid toxicity, how do you carry out skin decontamination and prevention of grooming?

Answer 135

If no neurological signs have developed, dermal contamination should be performed to remove the product, thus limiting absorption- immediate by washing with a mild detergent e.g. soap and warm water. Following skin decontamination, the area should be rinsed and dried to limit further absorption. An Elizabethan collar can be applied to prevent grooming. If the product was ingested (less likely) then gastric lavage could be performed

Question 136

If neurological signs have developed after pyrethrum/pyrethroid toxicity, What treatment is required?

Answer 136

If neurological clinical signs (e.g. seizures, tremoring and hyperaesthesia) have developed, immediate supportive therapy is required to manage these. An intravenous cannula should be placed. A muscle relaxant (e.g. methocarbamol) or an anticonvulsant can be administered (e.g. benzodiazepine, phenobarbitone)
Benzodiazepines e.g. diazepam or midazolam may be enough in mild cases but more severe cases can be treated with methocarbamol (a sedative with muscle relaxant properties) administered as an intravenous bolus or CRI (BSAVA, 2017). However, there is currently no injectable preparation of methocarbamol available in the UK.
Tablets for oral administration can be crushed and dissolved in water for administration via an orogastric or nasogastric tube in a patient that is conscious but unable to swallow; or it can be administered per rectum using a feeding tube or a Foley catheter
(Jasani, 2017). The dose of methocarbamol should not exceed 330mg/kg/day. A propofol infusion can be used to control seizures and reduce muscular activity – this cannot be used for a prolonged period in a cat (> 12 hours) due to the risk of Heinz body anaemia. An alfaxalone infusion could also be performed. Intravenous lipid emulsion (ILE) therapy is increasingly used in patients with reported good results.
Supportive therapies e.g. intravenous fluid therapy, temperature control and recumbency management should be also provided as appropriate to the case and stage e.g. hyperthermia can arise due to seizures/ tremors however following sedation hypothermia is more of a potential issue. Blood glucose should be monitored as hypoglycaemia could arise secondary to prolonged muscle tremors/ seizures.
With appropriate management and intensive nursing care, most affected patients do well.

Question 137

What are Organophosphate / carbamate insecticides and how do they cause toxicity?

Answer 137

These parasiticides/insecticides (garden, household or agricultural) are neurotoxins which work by inhibiting cholinesterases in the central nervous system.
Cholinesterases are required to breakdown acetylcholine which is a predominant neurotransmitter. Lack of acetylcholinesterase results in excess levels of acetylcholine binding to nicotinic and muscarinic receptors, resulting in over-stimulation, especially
of the parasympathetic nervous system. The clinical signs of poisoning are associated with neurological dysfunction.
Agricultural products are more concentrated and therefore more toxic.

Question 138

What are the clinical signs of Organophosphate / carbamate insecticides toxicity and how soon after ingestion are these signs usually seen?

Answer 138

Clinical signs usually arise within 12-24 hours of exposure
They include
1. vomiting
2. diarrhoea
3. hypersalivation
4. alterations in muscle tone, tremors, twitching and restlessness
5. CNS signs (hyperaesthesia, ataxia, depression or seizures)
6. hyperthermia +/- DIC
Other signs may include:
1. bradycardia
2. miosis
3. respiratory depression
4. urinary incontinence

Question 139

How do you diagnose Organophosphate / carbamate insecticides toxicity?

Answer 139

Diagnosis
Clinical signs and a history of contact with organophosphates (sheep dips etc.) are suggestive. Lowered blood cholinesterase levels (anything greater than 50% depression of cholinesterase levels) are pathognomic.

Question 140

What treatment is required for Organophosphate / carbamate insecticides toxicity?

Answer 140

Gastric or skin decontamination should be performed, depending on the method of poisoning and the time scale. Some agricultural products may also contain petroleum products.
Atropine sulphate is generally administered to effect - it is an antidote which prevents acetylcholine attaching to receptors, thus blocking its actions.
In severe cases pralidoxime hydrochloride (2-PAM) may be administered, in addition to atropine, as soon as possible post exposure - this prevents irreversible binding of the organophosphate to the cholinesterases. Pralidoxime hydrochloride (2-PAM) is not effective against carbamates, however.
Additional treatment is symptomatic e.g. management of seizures, if present, using standard anti-convulsant medication.

Question 141

How are pets most commonly exposed to lead?

Answer 141

Dogs are most often affected by lead poisoning but other species, including birds, may be affected. The commonest sources of poison include lead fishing weights, lead shot, lead flashing and lead paint.

Question 142

How does lead cause toxicity?

Answer 142

Lead interferes with certain essential enzymes and sulphydryl groups e.g. those associated with haemoglobin synthesis. It also has CNS effects, due to interfering with intracellular calcium levels; and increasing the fragility of capillaries which can lead to
spontaneous haemorrhage.

Question 143

What are the clinical signs of lead toxicity?

Answer 143

Clinical signs
The clinical signs depend on the age of the animal, type of lead compound and length of exposure. Young animals are at greater risk of poisoning.
These include

1. local irritation
2. GI signs e.g. anorexia, vomiting, hypersalivation, diarrhoea, constipation,
   abdominal pain
3. anaemia
4. haemorrhage
5. polyuria and polydipsia
6. weight loss (chronic)
   In acute cases there are often neurological signs including
7. lethargy
8. hyperexcitability
9. ataxia
10. convulsions
11. nystagmus
12. blindness
13. coma.
    If lead encephalopathy is present, the prognosis is poor.

Question 144

How do you diagnose lead toxicity?

Answer 144

Diagnosis
The history of access to lead items e.g. lead fishing weights, lead shot, lead toys, lead painted wood in the house is suggestive. Radiography may show radio-dense particles in the GIT. Blood levels of lead can be measured- mammals normally have no
measurable lead in the blood.
Haematological changes may be present- red blood cells may be nucleated and show basophilic stippling with Giemsa/Romanowsky stains.

Question 145

What treatment and nursing care is required for lead toxicity?

Answer 145

Treatment and nursing care
If possible, surgery should be performed to remove any large lead objects/ particles, but only once the animal has been stabilised. It may be possible, if the lead has
recently been ingested, to perform gastric lavage. However, patients usually do not show clinical signs until the lead has moved into the small intestine. A cathartic could be used if there is evidence of lead in the GIT. Activated charcoal is not effective for
lead poisoning (ASPCAPro, 2019).
If the patient is showing clinical signs or serum lead levels are elevated, administration of a chelating agent is indicated i.e. a compound that binds the lead in the blood stream allowing it to be excreted. The main chelating agent used for lead is calcium disodium
edetate (Ca-EDTA) although dimercaptosuccinic acid (DMSA) may be used instead, as it may be less toxic. Calcium disodium edetate needs to be diluted to a 1% solution (10 mg/ml) using 5% dextrose in water. It is administered by 6 hourly subcutaneous injections for 2-5 days. Animals must be closely monitored as it is reversibly nephrotoxic.

Question 146

How can zinc cause toxicity in animals and what can this result in?

Answer 146

Zinc is an essential trace metal that is essential for numerous body enzyme functions.
Animals may be poisoned, however, by ingestion of zinc containing products which form zinc salts in the acid pH of the stomach – because these salts are caustic, they
damage the gastric and intestinal mucosa thus increasing systemic absorption. Therefore, the longer the object is in the stomach’s acidic environment, the more zinc is absorbed systemically (Medici and Grigsby, 2013). Zinc toxicosis can cause intravascular haemolysis, pancreatitis, coagulopathies, acute renal failure, and neurotoxicity.

Zinc containing compounds including galvanised screws and nails; zinc-coated furnishings; batteries; coins (common cause); zinc-oxide cream and zinc supplements.
Consumption may lead to zinc poisoning. N.B. chronic ingestion of zinc oxidecontaining products, applied to a patient’s skin, can cause toxicosis following low-dose
chronic ingestion over a few days or longer. Zinc attacks similar enzyme pathways to lead causing GIT signs (including pancreatitis); haemolytic anaemia; convulsions and multiple organ (particularly liver and kidney) dysfunction/failure. Zinc poisoning is less frequently reported in the cat - possibly more due to their more selective feeding habits than their susceptibility.

Question 147

What are the clinical signs of zinc toxicity?

Answer 147

Clinical signs
These include
1. vomiting and other GIT signs
2. CNS depression or convulsions
3. anaemia (due to intravascular haemolysis), jaundice and haemoglobinuria
4. multiple organ failure (liver, kidney, heart)
Gastrointestinal irritation is usually intense with signs including vomiting and anorexia,
diarrhoea, and melaena. Intravascular haemolysis can occur within a few hours of
consumption of significant amounts of zinc leading to lethargy, anaemia, haemoglobinuria and icterus.

Question 148

How do you diagnose zinc toxicity?

Answer 148

Diagnosis
Clinical signs and history are suggestive (although there is often no known history of ingestion). Radiography may confirm the presence of a metallic foreign body;
haematological changes may be suggestive. Blood zinc levels may be measured - normal values in the dog are 0.7-2ppm. In poisoning the level usually exceeds 10ppm.
Haematology is helpful with signs of regenerative anaemia but no signs suggestive of immune-mediated haemolytic anaemia (e.g. no spherocytes, agglutination etc.)

Question 149

What treatment and nursing care is required for zinc toxicity?

Answer 149

Treatment and nursing care
Treatment is mainly supportive - if zinc foreign material is suspected, it should be removed as soon as the animal is stable (endoscopy/ surgery). Symptomatic treatment should be provided e.g. anti-emetics, antacids and gastroprotectants; activated charcoal is not effective at adsorbing zinc products. Intravenous fluid therapy can be administered to support renal function and promote diuresis. Administration of blood
products e.g. packed RBCs may be required in acute cases with severe intravascular haemolysis.
The use of chelating agents is controversial, calcium disodium edetate could be used as the chelation agent if the patient does not have acute kidney injury; however, DMSA will not chelate zinc. Zinc levels, however, should decrease once the zinc object has
been removed.
Other reported poisonings have included copper, mercury and fluoride

Question 150

How can paracetomol cause toxicity in pets?

Answer 150

Pathogenesis
Paracetamol is an anti-pyretic and analgesic drug commonly used in humans. ‘Most animals are exposed through accidental ingestion or uninformed owner administration’. A licenced veterinary preparation is available for acute pain of traumatic origin, post-operative analgesia and as a complementary treatment in pain associated with other conditions e.g. degenerative joint disease. Paracetamol can cause poisoning in both dogs and cats, but cats are most susceptible due to their metabolism. Paracetamol is metabolised in the liver by various processes including
conjugation with glucuronide. As cats have an inefficient glucuronide conjugation pathway, toxic metabolites can build up very quickly. Once the liver is unable to conjugate any more paracetamol, a toxic product known as N-acetyl-p-benzoquinone (NAPQI) is produced which damages liver cells and erythrocytes -
methaemoglobinaemia and Heinz body anaemia result. Toxic levels of paracetamol are ~ 600mg/kg for dogs and 50 mg/kg for cats. In dogs, acute hepatic necrosis is the most serious effect

Question 151

What are the clinical signs of paracetomol toxicity?

Answer 151

Clinical signs
A poisoned cat may present with severe, acute clinical signs within an hour of exposure. Signs can include facial and paw swelling and gastrointestinal signs (e.g.
anorexia, hypersalivation and vomiting), respiratory distress, brown mucous membranes, cyanosis, tachypnoea and respiratory distress. Dogs can present with similar signs but are more likely to present with signs of liver failure (24-48 hours following ingestion) than signs associated with methaemoglobinaemia. Signs of liver failure include lethargy, anorexia, vomiting, hypersalivation, elevated liver enzymes,
icterus, hepatic encephalopathy and death

Question 152

What are the clinical signs of paracetomol toxicity?

Answer 152

Clinical signs include

1. depression
2. weakness
3. anorexia
4. emesis
5. tachypnoea/respiratory distress
6. facial and paw oedema (cats more than dogs)
7. tachycardia
8. hypersalivation
9. brown discolouration of mucous membranes (due to methaemoglobin formation)
10. haemoglobinuria
11. +/- keratoconjunctivitis sicca in dogs (rare and may be caused by doses within the normal range)

Question 153

How do you diagnose paracetomol toxicity?

Answer 153

Diagnosis
The history and clinical signs and may be suggestive (particularly brown colouration of the mucous membranes, especially in cats). In dogs, signs associated with acute hepatic necrosis, possibly including jaundice may be suggestive. Haematology and
biochemistry will show signs compatible with methaemoglobinaemia (cats) and liver damage (dog)

Question 154

What treatment and nursing care is required for paracetomol toxicity?

Answer 154

Treatment and nursing care
Paracetamol is rapidly absorbed following ingestion (within 20 minutes). Babyak and Lee (2018) and BSAVA (2019) state that induction of emesis is not warranted due to the rapid absorption of paracetamol – they advise immediate administration of activated charcoal with a cathartic instead. Antioxidants, gastroprotectants and hepatoprotectants may also be administered.
There is a specific antidote to paracetamol, N-acetylcysteine (NAC) - it binds to toxic metabolites and acts as a glutathione precursor. Methionine may also be administered to replenish glutathione. Supportive therapy with intravenous fluid therapy and
medication to support liver function e.g. S adenosylmethionine (SAM-e) should be
given. Ascorbic acid, sodium sulphate and methylene blue have been suggested in the management of methaemoglobinaemia (Bates, n.d.). Blood products may be indicated if methaemoglobinaemia is severe. Otherwise treatment is supportive. The prognosis for affected animals depends on how much paracetamol was ingested and how rapidly decontamination/ treatment was instigated. The prognosis for patients with severe hepatotoxicity is poor

Question 155

How can schedule 1 drugs cause toxicity?

Answer 155

Pathogenesis
Most schedule 1 drugs e.g. heroin/cocaine are opioid based, acting on mu (OP3) receptors in the central nervous system, to causing CNS clinical signs e.g. euphoria and hyperexcitability. Seizures, depression and coma may develop along with profound respiratory depression. Cocaine is an ester of benzoic acid.

Question 156

How might animals be exposed to scedule 1 or class A drugs?

Answer 156

Schedule 1 / ‘Class A’ drugs
Exposure to these drugs may be accidental, malicious or unintentional - for the animal to get the most prompt and effective treatment, communication must be very effective.
For various reasons, including fear of prosecution, the history may be lacking, vague or inaccurate. It is important to encourage the owner to provide an accurate history by reinforcing that patient welfare is paramount.

Question 157

What may be the clinical signs for class A or schedule 1 drug toxicity?

Answer 157

Clinical signs
For opioid based drugs the clinical signs are usually neurological with mydriasis but can also be cardiovascular with arrythmias and hypertension
1. euphoria/dysphoria
2. hyperactivity, shaking, ataxia, panting, hyperthermia, seizures
3. mydriasis
4. respiratory depression
5. tachycardia/ arrythmias
6. GIT signs - vomiting, diarrhoea, constipation
7. hypertension

Question 158

How do you diagnose class A or schedule 1 drug toxicity?

Answer 158

Diagnosis
History and clinical signs may provide an indication of the cause. Blood serum assays for specific drugs are also available through many human laboratories. Blood glucose and liver enzymes may be elevated. Affected patients may have hyperglycaemia and elevated lactate levels.

Question 159

What treatment and nursing care is required for class A or schedule 1 drug toxicity?

Answer 159

Treatment and nursing care
Treatment is aimed at gastric decontamination (if appropriate) and CNS, cardiovascular, respiratory and GIT support.
If appropriate, emesis may be induced if there are no contraindications e.g. loss of consciousness. Gastric lavage may be preferred, followed by administration of
activated charcoal. To reverse the effects of opioid agonists, naloxone as a bolus or may be administered. Supportive therapy e.g. treatment with sedative or anxiolytic drugs including diazepam, midazolam, acepromazine and chlorpromazine or seizure
control with diazepam or propofol may be required. Respiratory support e.g. intermittent positive pressure ventilation may be required. IVFT will aid excretion; acid base and electrolyte abnormalities will need to be managed as well.

Question 160

What are the clinical aigns of ecstasy?

Answer 160

Ecstasy
This drug has sympathomimetic effects – clinical signs following exposure include CNS excitation, hyperexcitability, mydriasis, tachycardia etc. Treatment is supportive and symptomatic e.g. IVFT

Question 161

What are the clinical signs of Marijuana/Cannabis?

Answer 161

Marijuana is the dried material of the plant Cannabis sativa. These drugs act on a specific CNS receptor causing clinical signs which include- depression, ataxia,
bradycardia, hypothermia, vocalisation, hypersalivation, vomiting, diarrhoea, urinary incontinence, seizures, and coma (Merck, 2014). Urinary incontinence is a significant
finding suggestive of marijuana/ cannabis intoxication
Treatment is supportive and symptomatic. ASPCAPro (2019) state that decontamination is often not necessary and can do more harm than good.
It is likely that with increased use of legal highs, there will be increased incidence of veterinary related poisonings as well. ASPCAPro (2019) report a significant increase in veterinary patients reported due to marijuana toxicity.

Question 162

How do non-steroidal anti inflammatories cause toxicity in pets?

Answer 162

NSAIDs are routinely used in the management of chronic pain related to inflammation.
They have varying anti-pyretic, anti-inflammatory and analgesic properties. There are numerous preparations - many of which are licenced for veterinary use. They inhibit cyclooxygenase enzymes (COX) leading to decreased production of prostaglandins and inflammatory mediators. Products which selectively inhibit COX 2, rather than COX 1, are less likely, theoretically, to be associated with side-effects.
COX 1 enzymes promote prostaglandin synthesis. Prostaglandins protect the gastric mucosa; cause vasodilation and adequate renal perfusion; and platelet aggregation during haemorrhage.
Whilst most products are administered orally, toxicity may occur due to parenteral administration or from ingestion of topical preparations.
The toxic effects of NSAIDs are mainly due to their ability to inhibit prostaglandin synthesis leading to widespread vasoconstriction: this induces gastric ulceration, renal failure and haemorrhage tendencies.
Liver failure is another side-effect due to hepatocellular necrosis - certain NSAIDs are more prone to causing these effects i.e. the propionic acid derived NSAIDs such as carprofen

Question 163

How do dogs and cats show differential toxicity to non-steroidal anti-inflammatories?

Answer 163

Dogs and cats show differential toxicity to NSAIDs- with some more likely to cause toxicity than others e.g. ibuprofen is particularly toxic to dogs and cats. Furthermore, certain species (such as cats) are more sensitive to the toxic side-effects than others e.g. ibuprofen requires hepatic glucoronic conjugation which cats have limited ability to do. This leads to toxic levels of metabolites in the liver which cause liver damage.
Babyak and Lee (2018) state that for veterinary NSAIDs, > five times the therapeutic dose may lead to GIT signs; > ten times the therapeutic dose is likely to cause acute kidney injury.

Question 164

What are the clinical signs of non-steroidal anti inflammatory toxicity?

Answer 164

Clinical signs
Clinical signs are usually related to the toxic effects on the GIT, kidneys, liver and haemostasis.
They include:
1. vomiting, diarrhoea
2. nausea, anorexia, abdominal discomfort
3. melaena
4. haematemesis
5. polydipsia/polyuria (renal failure)
6. urticaria
7. liver failure/jaundice/ seizures
8. haemorrhage
9. ‘acute abdomen’ / septic peritonitis secondary to rupture of gastric ulcer

Question 165

How do you diagnose NSAID toxicity?

Answer 165

Diagnosis
History and clinical signs usually indicate the cause. NSAID assays can be performed on stomach contents and serum. Azotaemia, elevated liver enzymes, decreased platelets, hyperkalaemia and metabolic acidosis may be present; or clinical findings
associated with septic peritonitis e.g. free abdominal fluid containing toxic neutrophils with intracellular bacteria; increased lactate and decreased glucose levels etc

Question 166

What treatment and nursing care is required for NSAID toxicity?

Answer 166

Treatment and nursing care
Treatment is supportive and symptomatic. Gastric decontamination should be performed, if the poisoning has been recent and ingested - emesis or gastric lavage are important both for diagnosis and decreasing drug absorption. Activated charcoal may be used subsequently- multiple doses may be administered if the NSAID undergoes enterohepatic circulation Intravenous fluid therapy is the mainstay of therapy, aiming to reduce the likelihood of renal failure. Renal function, and often liver function, should be regularly assessed.
Antacids such as cimetidine and ranitidine (H2 antagonists), proton pump inhibitors e.g. omeprazole and mucosal protectants such as sucralfate may all be used to minimise and treat gastric ulcer development.
Misoprostol, a synthetic prostaglandin analogue, can be administered to increase gastric mucous production, mucosal blood flow and promote healing. However,
misoprostol has unknown efficacy in the prevention or treatment of gastric ulcers

Question 167

How cna baclofen cause toxicity in pets?

Answer 167

baclofen (a centrally acting muscle relaxant used in people with spinal issues or multiple sclerosis) – it is highly toxic and can cause neurological signs
(ataxia, disorientation and seizures), respiratory distress and respiratory arrest

Question 168

How do macrocylic lactones cause toxicity in pets?

Answer 168

macrocyclic lactones (e.g. ivermectin, moxidectin and selamectin). These drugs are used as antiparasitics in veterinary patients. Some breeds of dog are
genetically more susceptible to poisoning even at relatively low doses e.g. Border Collies (Babyak and Lee, 2018); other are poisoned by ingestion/
administration of a large overdose e.g. accidental ingestion of equine product.
Neurological signs develop - hyperaesthesia, ataxia, seizures and neuromuscular paralysis (respiratory depression). Decontamination should be
performed if possible (emesis or gastric lavage and multiple doses of activated charcoal). ILE may be effective. Otherwise treatment is symptomatic - IPPV
may be required

Question 169

How do anti-depressents cause toxicity in pets?

Answer 169

Antidepressants (e.g. SSRIs or SNRIs). These drugs are commonly prescribed. The clinical signs associated with poisoning depend on the specific drug but are often neurological. Decontamination should be performed if possible. Otherwise treatment is supportive and symptomatic.

Question 170

How does chocolate cause toxicity in pets?

Answer 170

Pathogenesis
Chocolate poisoning is common (Babyak and Lee, 2018). Chocolate contains theobromine - a methylxanthine plant alkaloid. Methylxanthine alkaloids stimulates increased CNS activity, diuresis, and myocardial contractility via inhibition of cyclic
nucleotide phosphodiesterases and sympathetic nervous system stimulation with release of catecholamines (Babyak and Lee, 2018). Dogs are more sensitive to the effects of the theobromine than cats due to their slower metabolism of the drug. Similar
clinical signs can be induced by ingestion of other sources of methylxanthines e.g. coffee beans, caffeine drinks, cocoa powder, body building supplements etc. Some chocolate products may contain raisins which are also toxic. The highest levels of theobromine are found in cocoa beans, dark chocolate, cocoa powder and cocoa shell garden mulches. White chocolate has minimal levels of theobromine.
The likelihood of signs of toxicity developing depends on the relative concentration and amount of theobromine which is ingested

Question 171

What clinical signs are seen with chocolate toxicity in pets?

Answer 171

Clinical signs
Clinical signs are related to CNS, cardiac and renal stimulation. They include
1. seizures
2. hyperexcitability/ agitation
3. hyperthermia
4. polydipsia/polyuria
5. hypersalivation, vomiting/diarrhoea
6. tachycardia
7. cardiac arrhythmias e.g. supraventricular tachycardia/ ventricular premature contractions
8. ataxia
9. renal dysfunction
10.high doses can result in death

Question 172

How do you diagnose chocolate toxicity in pets?

Answer 172

Diagnosis

The history and clinical signs are often suggestive. Blood pressure monitoring and ECG are useful.

Question 173

What treatment and nursing care is required for chocolate toxicity?

Answer 173

Treatment and nursing care
Prompt, aggressive decontamination, with induction of emesis or gastric lavage, to remove any retained chocolate; followed by repeated doses of activated charcoal (without a cathartic) to prevent further absorption caused by enterohepatic circulation
is recommended
Because chocolate can remain in the stomach for several hours, emesis can be induced several hours after ingestion if considered appropriate. Gastric lavage may be preferred if the patient is showing any neurological signs or aspiration is a concern.
Treatment is symptomatic and supportive. Intravenous fluids, anxiolytics (e.g. acetyl promazine), beta blockers (e.g. atenolol and metoprolol), muscle relaxants (e.g.
methocarbamol) and anticonvulsants (e.g. benzodiazepines and barbiturates) may all be required. Control of muscle activity and seizuring is essential - this will help to control hyperthermia but further therapy with fans, tepid water may be required
(Mazzaferro, 2015).
Intravenous lidocaine may be required if a serious ventricular arrhythmia develops in a dog.
Frequent walks (Babyak and Lee, 2018) and urinary catheterisation (Merck, 2013) have also been suggested as useful methods for increasing expulsion of methylxanthines, such as theobromine, which can be absorbed by the bladder epithelium.
Close patient monitoring is required with temperature, ECG, electrolyte, acid base and renal parameters being assessed.

Question 174

What effect do Grapevine products - Grapes / raisins/sultanas/ currents have when ingested?

Answer 174

Clinical signs of poisoning, including acute kidney injury/ anuric renal failure, have been reported in dogs which have ingested these products - dried products, as used in baking, are thought to be more harmful. The pathogenesis of this toxicity is not currently known. Not all dogs that eat grapevine products will be poisoned and the effects are not thought to be dose-dependent.

Question 175

What are the clinical signs of Grapes / raisins/sultanas/ currents toxicity?

Answer 175

Clinical signs
Clinical signs are those of acute kidney injury (AKI) and can include -
1. vomiting, diarrhoea, haematemesis,
2. anorexia
3. lethargy, depression, ataxia and weakness
4. polyuria/polydipsia which can than progress to oliguria/ anuria if AKI develops
5. uraemic halitosis
6. haematuria and pancreatitis may also occur
7. hypercalcaemia and hyperphosphatemia may develop within 24 hours of ingestion

Question 176

How do you diagnose Grapes / raisins/sultanas/ currents toxicity?

Answer 176

Diagnosis
Patient history, with sudden onset of clinical signs associated with renal failure, especially if vomiting of grapes/raisins has occurred, should be suggestive.

Question 177

What treatment and nursing care is required for grapes / raisins/sultanas/ currents toxicity?

Answer 177

Treatment and nursing care
There is no known antidote. Prompt gastric decontamination should be performed, with gastric lavage/induction of emesis, to remove grapes/raisins etc. IVFT should be administered, possibly at higher than the patient’s calculated requirement, to promote
diuresis provided. Otherwise therapy is supportive and symptomatic e.g. antiemetics, gastroprotectants etc. Additional treatment for acute kidney injury may be required.
The patient should be monitored carefully for signs of acute kidney injury developing (urine output, specific gravity, creatinine/ urea, electrolytes) and fluid overload (blood pressure).
(Babyak and Lee, 2018) state that anecdotally most dogs that are treated aggressively do not develop AKI but that the prognosis tends to be poor for those that develop oliguric / anuric AKI

Question 178

What are the clinical signs of macadamia nut toxicity?

Answer 178

Pathogenesis
Macadamia nuts have been associated with a non-fatal syndrome - dogs are the only species in which signs have been reported. The pathogenesis is unknown.

These include

1. muscle weakness
2. ataxia
3. vomiting
4. tremors
5. hyperthermia

Question 179

What treatment and nursing care is required for macadamia nut toxicity?

Answer 179

Diagnosis
The clinical history, clinical signs +/- vomiting nuts is suggestive.
Treatment and nursing care Gastric decontamination with induction of emesis/ gastric lavage could be performed followed by administration of activated charcoal.
Additional supportive and symptomatic therapy may be required e.g. IVFT, tremor control and hyperthermia management. (Mazzaferro, 2015). Affected patients tend to recover well within 48 hours

Question 180

How can mushrooms cause toxicity?

Answer 180

Mushrooms
Ingestion of poisonous mushrooms can cause liver failure, neurotoxicity or gastrointestinal irritation.
Pathogenesis
Amanitin (amatoxin) is the main chemical found in poisonous toadstools/mushrooms.
It causes significant hepatocyte damage which can lead to liver and then multiorgan failure. It may have a delayed effect, taking a few days to produce clinical signs.

Question 181

What are the clinical signs of mushroom toxicity?

Answer 181

Clinical signs
This is an uncommon toxicity seen mainly in dogs, as cats are unlikely to eat toadstools/ mushrooms. Clinical signs are related to liver and kidney failure; although
some mushrooms have hallucinogenic compounds as well.
Clinical signs include
1. vomiting
2. diarrhoea
3. jaundice
4. abdominal pain
5. polydipsia/polyuria
6. haemorrhage
7. bradycardia
8. ataxia

Question 182

How do you diagnose mushroom toxicity?

Answer 182

Diagnosis
The history may suggest mushroom poisoning although the clinical signs are nonspecific. Most poisonings are seasonal, generally occurring in the autumn - although
some mushrooms may be seen earlier in the year, during wet summers.
Hypoglycaemia and coagulopathy may arise as liver failure develops.

Question 183

What treatment and nursing care is required for mushroom toxicity?

Answer 183

Treatment and nursing care
Prompt gastric decontamination should be performed if recent ingestion has occurred;
followed by administration of multiple doses of activated charcoal. Supportive therapy for liver and kidney damage can be administered including IVFT and hepatic protectants e.g. milk thistle (silymarin) or S-Adenosyl-L-methionine (SAMe).
Once liver damage has occurred the prognosis is poor.

Question 184

How does the allium species cause toxicity?

Answer 184

Allium species e.g. Onions / garlic/ leeks/ chives
Pathogenesis
Thiosulphates in members of the onion/ garlic family cause oxidative damage to erythrocytes leading to Heinz body formation and haemolysis of affected cells- Heinz body anaemia. Cats are particularly susceptible to the harmful effect although are possibly less likely to voluntarily ingest onion/ garlic products. Onions are thought to be more toxic than other members of the family. Thiosulphates can also cause direct
irritation of the GI tract.
N.B. Propofol infusions, paracetamol, phenols and methylene blue may also cause Heinz body anaemia in cats

Question 185

What are the clinical signs of allium species (onion/garlic) toxicity?

Answer 185

These usually develop within 24 hours and the severity of the signs depends on how much of the toxic agent was ingested. The clinical signs are those of haemolytic anaemia and include

1. signs of anaemia – lethargy, depression, weakness, collapse
2. icterus
3. haemoglobinuria
4. vomiting
5. diarrhoea

Question 186

How do you diagnose allium species (onion/garlic) toxicity?

Answer 186

Diagnosis
Clinical signs of anaemia with a history of exposure to the likely toxin e.g. feeding meat (often mince) with onions/garlic is suggestive. The combination of clinical signs of anaemia and the presence of Heinz bodies, on a blood smear, in a significant number of red cells is not pathognomic but is suggestive. Changes associated with immunemediated haemolytic anaemia would not be expected on this slide. (N.B. refer to unit
three, outcome three).

Question 187

What treatment and nursing care is required for allium species (onion/garlic) toxicity?

Answer 187

Treatment and nursing care
Prompt gastric decontamination (induction of emesis) should be performed if recent ingestion has occurred - gastric lavage to remove any remaining plant material may be considered if induction of emesis is not appropriate. This can be followed by administration of activated charcoal. Further supportive therapy including oxygen therapy, IVFT and transfusion of blood products may be required.

Question 188

What is xylitol?

Answer 188

Xylitol is used as a sweetener/ sugar substitute in various products e.g. sugar-free
chewing gum, peanut butter, human medication and household products such as toothpaste

Question 189

What effect does xylitol have on the body?

Answer 189

Pathogenesis
Xylitol stimulates a large insulin release, within ~ 30 minutes of ingestion, leading to marked, rapidly occurring hypoglycaemia - it is also hepatotoxic especially if larger amounts are eaten

Question 190

What are the clinical signs of xylitol toxicity?

Answer 190

The signs of hypoglycaemia develop within ~ 2 hours of ingestion – however sign of
hepatotoxicity may not occur till later.
Signs caused by hypoglycaemia include
1. vomiting
2. lethargy
3. ataxia
4. stupor, collapse, coma and convulsions
5. tachycardia
Clinical signs of liver failure include
1. lethargy
2. collapse
3. GIT signs
4. coagulopathy
5. altered mentation +/- seizures due to hepatic encephalopathy

Question 191

How do you diagnose xylitol toxicity?

Answer 191

Diagnosis History of access to a product containing xylitol; and the clinical signs of hypoglycaemia +/- liver failure and coagulopathy are suggestive.
Blood glucose measurement will confirm hypoglycaemia. Biochemistry, haematology and clotting profiles may confirm liver damage and coagulopathy.

Question 192

What treatment and nursing care is required for xylitol toxicity?

Answer 192

Treatment and nursing care
Prompt gastric decontamination should be performed if recent ingestion has occurred and there are no signs of hypoglycaemia - induction of emesis. Activated charcoal is not thought to be effective at adsorbing xylitol so its use is not recommended. N.B. it
is essential to check blood glucose levels, prior to inducing emesis, to anticipate imminent hypoglycaemia induced altered consciousness.
If a patient presents with signs of hypoglycaemia, treatment with intravenous 50% dextrose diluted in 0.9% saline/ LRS should be started (the injection should be administered over 1-2 minutes) (Babyak and Lee, 2018). Thereafter induction of emesis could be performed if there is the possibility of a bezoar of e.g. chewing gum. A 2.5- 5% dextrose CRI should be continued until blood glucose returns to normal (~ 12-24 hours).
Blood glucose should continue to be monitored regularly; liver enzymes and clotting profiles should be monitored. Symptomatic treatment for liver failure could be provided if necessary e.g. IVFT and hepatoprotectants (e.g. silymarin/ SAMe). If coagulopathy occurs, then transfusion blood transfusions may be required

Question 193

How do pets come across tremorgenic mycotoxins?

Answer 193

Tremorgenic mycotoxins
Mycotoxins are produced because of fungal metabolism of food. They may be found in mouldy food, silage and compost. This type of poisoning is occurring more frequently due to scavenging and the increased use of food recycling bins. Bough (2019) discusses tremorgenic mycotoxicosis in dogs.

Question 194

What type of effect do tremorgenic mycotoxins have?

Answer 194

Pathogenesis
There are numerous mycotoxins- ~ 20 have been identified with penitrem A being the most frequently reported to have caused clinical signs. The pathogenesis is unclear but it is thought that the mycotoxins can cross the blood brain barrier due to their lipophilic properties and have a neuro-toxic effect

Question 195

What are the clinical signs of tremorgenic mycotoxin ingestion?

Answer 195

Clinical signs
These usually develop within 30 minutes of ingestion although are sometimes delayed by several hours. The main clinical findings are tremors and restlessness.
Clinical signs can include –
1. vomiting, diarrhoea
2. restlessness, irritability, hyperaesthesia, ataxia, convulsions, status epilepticus and coma
3. muscles tremors, rigidity and opisthotonus
4. tachycardia
5. tachypnoea
6. mydriasis, nystagmus
7. dehydration
8. hypoglycaemia
Hyperthermia might develop due to increased muscle activity; and/ or acute kidney injury with myoglobinuria secondary to muscle breakdown (rhabdomyolysis).

Question 196

How do you diagnose tremorgenic mycotoxin ingestion?

Answer 196

Diagnosis
History of recent access to decomposing materials is suggestive. The diagnosis could only be confirmed following laboratory analysis of stomach contents which is not immediate

Question 197

What treatment and nursing care is required for tremorgenic mycotoxin toxicity?

Answer 197

Treatment and nursing care
Prompt gastric decontamination should be performed, if recent ingestion has occurred - gastric lavage is advised rather than inducing emesis due to the rapid onset of clinical signs and the potential to trigger seizures (Bough, 2019). Activated charcoal is
effective at adsorbing mycotoxins so could be administered following lavage.
Management of the neurological signs is the main priority. The muscle relaxant, methocarbamol, is recommended initially- diazepam is reported to be fairly ineffective. If methocarbamol is not effective or convulsions occur, treatment with phenobarbitone or propofol may be required. Management of hyperthermia may be required – however if the patient is sedated/ anaesthetised, hypothermia may be an
issue. In this situation, appropriate nursing care for the anaesthetised, recumbent patient is required.
Kormpou et al. (2018) discuss the aetiology, presenting signs and management of tremorgenic mycotoxicosis. They conclude that treatment with ILE may be beneficial.

Question 198

What is ethylene glycol?

Answer 198

Ethylene glycol is an odourless, brightly coloured, sweet tasting product that is found in antifreeze, screen wash, brake fluid and coolants. It is also present in some printer inks and other household products e.g. bath sealant although these are reported to be
rare causes of toxicosis (Babyak and Lee, 2018). Cats, in particular, are susceptible to ethylene glycol poisoning – they may be poisoned by drinking from a gutter where antifreeze has leaked from a car radiator. Cats with chronic renal failure may be more at risk of poisoning due to their indiscriminate drinking habits and PUPD.

Question 199

How does ethylene glycol cause toxicity?

Answer 199

This is one of the commonest causes of toxicosis in cats and dogs. Ethylene glycol itself is not particularly toxic; it is the metabolites that cause the damage, especially glycolic and oxalic acid. Glycolic acid causes severe metabolic acidosis and oxalic acid combines with calcium to precipitate as calcium oxalate crystals in the small blood vessels and renal tubules. This leads to acute kidney injury, hypocalcaemia and calcium oxalate crystalluria.

Question 200

What are the clinical signs of ethylene glycol toxicity?

Answer 200

Clinical signs
These include the following -
1. ataxia, ‘drunkenness’, depression
2. GIT signs – hypersalivation, vomiting
3. tachycardia
4. tachypnoea
5. seizures
6. acute kidney injury (this may initially present as polyuria but anuria soon develops; depression, anorexia, abdominal pain, ptyalism, uraemic halitosis)

Question 201

How many phases are there with ethylene glycol toxicity?

Answer 201

The condition is commonest in cats and will often follow three distinct phases- although all the phases might not be observed by the owner.

Question 202

Describe phase 1 of ethylene glycol toxicity?

Answer 202

Phase 1 (1-4 hours post ingestion) - The clinical signs are due to ingestion of alcohol - ataxia, disorientation, convulsions, tachycardia, tachypnoea and dehydration
due to polyuria may be seen

Question 203

Describe phase 2 of ethylene glycol toxicity?

Answer 203

Phase 2 (4-6 hours post ingestion) - Anorexia, depression, vomiting, miosis, respiratory distress, coma and hypothermia due to metabolic acidosis and pulmonary oedema. Death may occur at this stage if the
dose consumed was large enough.

Question 204

Describe phase 3 of ethylene glycol toxicity?

Answer 204

Phase 3 (2-7 days post ingestion) - Acute oliguric/ anuric renal failure with azotaemia.

Question 205

How do you diagnose ethylene glycol toxicity?

Answer 205

Diagnosis
History may indicate access to a garage etc. Clinical signs of acute renal failure, often associated with irritation to the oral mucous membranes, is suggestive; and birefringent rosette shaped calcium oxalate crystals in the urine is almost pathognomic although crystalluria is temporary. Blood analysis is likely to demonstrate azotaemia as AKI develops and hypocalcaemia, hyperkalaemia and metabolic acidosis.
Commercial antifreeze contains a product that fluoresces when exposed to ultraviolet light. A Wood’s lamp may demonstrate fluorescence around the oral cavity, suggesting recent antifreeze ingestion/ ethylene glycol ingestion; or urine may fluoresce.
Ultrasound may demonstrate characteristic renal changes and a small bladder, if acute renal failure has developed. There are veterinary specific ethylene glycol test kits although these can give false positive results

Question 206

What is the treatment and nursing care for ethylene glycol toxicity?

Answer 206

Treatment and nursing care
Gastric decontamination (induction of emesis) is only likely to be useful if the poison has been ingested very recently, within the previous hour as the toxin is rapidly
absorbed from the GI tract. More than one-hour post ingestion, induction of emesis is not indicated. Activated charcoal is not effective for ethylene glycol toxicity.
There are antidotes to ethylene glycol- ethanol and fomepizole/ 4-methylpyrazole (4- MP). Both competitively inhibit alcohol dehydrogenase, which is responsible for metabolising ethylene glycol into its toxic metabolites. The aim of administering an
antidote in this poisoning is to prevent the metabolism of relatively non-toxic ethylene glycol to the toxic metabolites. For the best possible outcome, treatment must be started as soon as possible after poisoning- within three hours in cats and within eight
to twelve hours in dogs. It is reported (Connally et al.,2010 cited by Babyak and Lee, 2018) that if antidote treatment is delayed beyond three hours in cats, it will be ‘ineffective and is associated with almost 100% fatality’.
An initial loading dose of ethanol is usually administered followed by a CRI for 24-36 hours or until the ethylene glycol test is negative (Babyak and Lee, 2018). Ethanol can cause depression Fomepizole is reported to have fewer side effects be preferable to ethanol, particularly in dogs. Availability however is limited, and it is more expensive. In dogs an initial dose
is administered over 15-30 minutes; follow up treatment is administered every 12 hours until the plasma ethylene glycol levels drop, or the dog has recovered. In cats
the first dose is administered by slow IV injection followed by treatment at 12, 24 and 36 hours.
There are various protocols for administration of medical ethanol or fomepizole – a current, veterinary source should be consulted.
If medical grade ethanol/ fomepizole is not available, commercially available alcohol could be administered, with vodka being considered the safest (BSAVA, 2017).
Haemodialysis could be considered to remove ethylene glycol and the harmful metabolites although this is only available at a few institutions (Babyak and Lee, 2018).
For a patient already showing clinical signs the prognosis is poor- meaning that euthanasia on welfare grounds may be performed. However, if treatment is
considered, intensive management of acute kidney injury, electrolyte abnormalities and acidosis is necessary to ensure that the patient remains well hydrated and hypovolaemia is corrected. IVFT is the mainstay of treatment - if the patient is oliguric/anuric, care must be taken to avoid fluid overload. Fluids are often delivered in boluses as ‘fluid challenges’ with close patient monitoring. Urine output should be
monitored - ideally this should be 1-2 ml/kg/hr (International Cat Care, 2017) but is often less than this if the patient has acute kidney injury. The patient should be monitored closely for signs of fluid overload- increased weight, tachypnoea, crackles on auscultation, oedema of the axilla etc. Blood pressure monitoring should be performed. If acute renal failure persists, after fluid resuscitation, diuretics (furosemide or mannitol) may be administered in an attempt to stimulate urine production. If mannitol is administered the patient should be very carefully monitored for signs of fluid overload with this osmotic diuretic. Haemodialysis/ peritoneal dialysis could be considered. Unfortunately, however, once an animal has become azotaemic the
prognosis is very poor.

Question 207

How are dogs most commonly exposed to blue-green algae?

Answer 207

This is most commonly seen in dogs and is associated with drinking / swimming in contaminated ponds and lakes containing the algae/cyanobacteria involved. These bacteria proliferate, especially during periods of hot weather, producing colonies on water that have a blue-green appearance

Question 208

How does blue-green algae cause toxicity?

Answer 208

Small numbers of the bacteria produce
anatoxins (neurotoxins) and microcystins (hepatotoxins). These inhibit acetylcholinesterase and protein phosphatases respectively, leading to neurological
signs, severe hepatocellular necrosis and haemorrhage

Question 209

What clinical signs are seen with blue-green algae?

Answer 209

Clinical signs
Clinical signs may develop very rapidly (minutes to hours after exposure) and rapidly progress to respiratory failure and death in some cases.
Clinical signs mainly involve the GI tract and neurological system and include
1. vomiting, diarrhoea, anorexia, lethargy, nausea
2. abdominal pain
3. haemorrhagic gastroenteritis
4. liver failure
5. jaundice, haemoglobinaemia
6. coagulopathy
7. seizures
8. muscles spasms, paralysis
9. respiratory arrest
10. hypovolaemic shock
11. death

Question 210

How do you diagnose blue-green algae toxicity?

Answer 210

Diagnosis
A history of playing or swimming in or near water affected by blue-green algae/cyanobacteria (therefore more common in the summer months when these
blooms occur), with corresponding clinical signs, is suggestive. Liver enzymes may be elevated, clotting profiles may be abnormal and blood glucose decreased.

Question 211

What treatment and nursing care is required with blue-green algae toxicity?

Answer 211

Treatment and nursing care
There is no antidote and the signs may progress rapidly. Treatment is generally supportive and symptomatic.
Gastric lavage could be performed, if very soon after ingestion, followed by activated charcoal.
Atropine can be used for signs of neurotoxicity. Aggressive IVFT for hypovolaemic shock, along with ventilation in cases of respiratory depression, is essential. Treatment of seizures with diazepam/barbiturates/propofol may also be needed.
The prognosis is generally poor once clinical signs have started.

Question 212

What is the toxin, clinical signs and treatment for foxglove poisoning?

Answer 212

Foxglove

Cardiac glycoside
(digitalis)

Cardiac arrhythmias

Gastric lavage/ activated charcoal
gavage. Management of cardiac
arrhythmias.

Question 213

What is the toxin, clinical signs and treatment for lily poisoning?

Answer 213

Lilies

Unknown. All plant parts are
considered poisonous.

Acute renal failure in cats, polydipsia, polyuria, vomiting

Gastric lavage/ activated charcoal
gavage. IVFT and management
for acute renal failure.

Question 214

What is the toxin, clinical signs and treatment for lily of the valley poisoning?

Answer 214

Lily of the valley

Alkaloids

GI irritation, cardiac arrhythmias

Gastric lavage/ activated charcoal gavage. Management of cardiac arrhythmias

Question 215

What is the toxin, clinical signs and treatment for Rhododendron/ azaleas poisoning?

Answer 215

Rhododendron/ azaleas

Andromedatoxin

Oral ulceration, vomiting, diarrhoea, bradycardia,
seizures, coma, respiratory failure

Gastric lavage/ activated charcoal/ tea gavage (tea
contains tannins which can bind toxins). Atropine for bradycardia, aggressive IVFT

Question 216

What is the toxin, clinical signs and treatment for yew poisoning?

Answer 216

Yew

Taxine (an alkaloid)

Cardiac toxin, Vomiting, diarrhoea, ataxia, seizures, coma, bradycardia, respiratory failure

Gastric lavage/ activated charcoal gavage. Management of cardiac
arrhythmias.

Question 217

What is the toxin, clinical signs and treatment for Daffodil (concentrated especially in bulbs) poisoning?

Answer 217

Daffodil (concentrated especially in bulbs)

calcium oxalate crystals, alkaloids and glycosides

Vomiting, diarrhoea, abdominal discomfort, anorexia,
ataxia, bradycardia and seizures

Gastric lavage/ activated charcoal
gavage. IVFT. Supportive treatment

Question 218

What is the only native poisonous species of snake in the UK?

Answer 218

Snake bites
Aetiology and Pathogenesis
The only native poisonous species of snake is the European adder (Vipera berus). Adders only bite when provoked - this is more common during summer months when they may be basking and dogs attempt to pick them up. However, it is also possible that pet snakes could bite patients; and as the number of different species kept increases, so does the range of causes of poisoning.

Question 219

What are the clinical signs of a European snake bite?

Answer 219

Clinical signs
The clinical signs depend on the specific species of snake. In general pain, swelling/oedema at site of bite, hypotension, and allergic/anaphylactic reaction are the
main clinical features. Where a venomous snake has bitten the patient, other clinical signs that may be seen include erythema, petechiation, ecchymoses, cyanosis and sloughing of tissue. The European adder venom contains various active substances e.g. histamine, serotonin, bradykinin and prostaglandins which induce a marked localised inflammatory reaction leading to loss of function in the area. Coagulopathy may occur in some cases.

Question 220

How do you diagnose a European adder snake bite?

Answer 220

Diagnosis
Diagnosis is usually made on the history - an owner seeing the dog being bitten or having a snake in the house. However, it is possible for an animal to be bitten without being seen and in this case, it is possible that bite wounds may be visible alongside oedema. In some cases, an allergic reaction may be all that is present and the snake bite may only be a possibility

Question 221

What treatment and nursing is required for a European adder snake bite?

Answer 221

Treatment and nursing care
The patient should be kept as immobile as possible and transported for veterinary treatment. The bite wound should not be touched and no attempt should be made to withdraw the toxin.
Blood samples should be taken on admission to provide a baseline which further testing can be compared to. If the species of snake is known and antivenom is available, then this should be administered.
General supportive treatment e.g. fluid therapy for hypotension and hypovolaemia; and wound management should be instigated. Cardiovascular and respiratory systems, as well as clotting profiles, should be closely monitored. Steroids should not
be administered.

Question 222

How do you diagnose a wasp or bee sting?

Answer 222

Wasp and bee stings will clinically appear very similar – namely swelling, pain, and an allergic or anaphylactic reaction. If the sting affects the respiratory tract or mouth then any swelling may affect respiration. Diagnosis
Diagnosis is generally made on the history and clinical signs. It is possible that the sting may be present, but this is not always the case.

Question 223

What treatment and nursing care is required for a wasp or bee sting?

Answer 223

Treatment and nursing care
If possible, cold packs should be applied to the area affected by the sting. Antihistamines, and possibly corticosteroids, may be used to reduce inflammation.
Although many patients will recover uneventfully they should be monitored for possible problems especially any problems with respiration. Where anaphylaxis is present animals will need emergency treatment for shock

Question 224

What are the clinical signs of contact with an acid/alkali substance?

Answer 224

Clinical signs

Clinical signs are skin trauma, vomiting, GIT haemorrhage, pain and salivation.

Question 225

How do you diagnose a patient that has had contact with an acid/alkali substance?

Answer 225

Diagnosis
Diagnosis is based on the history and the clinical signs. If owners are aware of what the animal has come in contact with, then this will be helpful in making a diagnosis and providing appropriate treatment.

Question 226

What treatment and nursing care is required for contact with an acid/alkali substance?

Answer 226

Treatment and nursing care
Where patients have ingested acid/alkali, emetics should NOT be given, as they will cause more damage to the oesophagus during vomition. Attempts to neutralise a caustic acid by administering an alkali (or vice versus) are not advocated as the heat producing, exothermic reaction could cause further damage. Dilution with milk/ water shortly after ingestion may be of benefit but not if the patient is showing signs of GIT
damage/ nausea. GI protectants, such as antacids and sucralfate, can be administered to protect the gastrointestinal tract. Topical exposure should be managed by copious flushing with a pH neutral, non-irritant substance e.g. distilled water

Question 227

How do pets come into contact with phenols and what effects can these have?

Answer 227

Phenols are found in a variety of household compounds such as cleaning products and disinfectants; as well as coal tar shampoos. They can cause chemical burns to the skin and mucous membrane e.g. gastrointestinal tract and conjunctiva. They are also carcinogenic. The more concentrated the solution the greater the toxic effects

Question 228

What are the clinical signs of phenol toxicity?

Answer 228

Clinical signs
Topical exposure results in dermal necrosis; ingestion results in ulceration of upper GI tract and liver / kidney damage. Pain, panting, salivation, vomiting, diarrhoea, ataxia, depression, collapse and death may occur.

Question 229

What is the treatment and nursing care for phenol toxicity?

Answer 229

Treatment and nursing care
Where the skin has been damaged, treatment is indicated as for any other burn with copious lavage (Unit 6 Outcome 1). Where phenols have been ingested, inducing emesis and use of activated charcoal is NOT recommended - giving water, milk or eggs has been suggested to attempt to decrease absorption. GI protectants such as sucralfate and antacids can also be given. Medications such as acetylcysteine, can be given to reduce kidney and liver damage. Supportive IVFT and analgesia may also be indicated

Question 230

How can pets get carbon monoxide poisoning and effect can this have?

Answer 230

Carbon monoxide poisoning may occur following incomplete combustion of carbon products - old gas heaters etc.
When inhaled, carbon monoxide readily combines with haemoglobin to form carboxyhaemoglobin. Oxygen is displaced and the patient becomes hypoxic.

Question 231

What are the clinical signs for carbon monoxide toxicity?

Answer 231

Clinical signs include

1. lethargy
2. drowsiness
3. cherry-red mucous membranes
4. depression
5. vomiting
6. respiratory distress
7. collapse
8. death

Question 232

How do you diagnose carbon monoxide poisoning and what treatment is required?

Answer 232

Diagnosis
This is usually based on the history and clinical signs especially cherry-red mucous membranes.
Treatment
This is symptomatic and involves providing 100% oxygen. IVFT may also be administered to improve perfusion.