U5 O3 - Toxicological Emergencies (Intoxications) Flashcards

Question

Define poison?

Answer 1

Poison | A substance which can cause harm to a living organism

Answer 2

Toxin | A poisonous substance produced by a living organism

Answer 3

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

Answer 4

(In)toxicant | A substance which causes toxicosis or intoxication e.g. cleaning product or alcohol

Answer 5

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

Answer 6

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

Answer 7

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

Answer 8

Antidote | A substance which counteracts a specific poison

Answer 9

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

Answer 10

Gavage/ gastric lavage | Introducing material into the stomach via a stomach tube; washing out the stomach using a liquid.

Answer 11

Adsorption | The adhesion of a substance to another surface.

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

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?

Answer 16

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.

Answer 17

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

Answer 18

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.

Answer 19

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

Answer 20

R - resuscitate/risk assessment S - supportive care and monitoring I -investigation D - decontamination E - enhanced elimination A - Antidotes D - Discharge

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

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.

Answer 27

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.

Answer 28

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.

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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.

Answer 33

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.

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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.

Answer 38

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

Answer 39

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)

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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)

Answer 44

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.

Answer 45

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)

Answer 46

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

Answer 47

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).

Answer 48

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.

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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)

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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

Answer 59

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’

Answer 60

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.

Answer 61

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.

Answer 62

``` 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. ```

Answer 63

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

Answer 64

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.

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

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)

Answer 72

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

Answer 73

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

Answer 74

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.

Answer 75

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

Answer 76

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

Answer 77

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.

Answer 78

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.

Answer 79

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

Answer 80

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

Answer 81

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

Answer 82

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.

Answer 83

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

Answer 84

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

Answer 85

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.

Answer 86

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

Answer 87

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.

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

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.

Answer 92

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.

Answer 93

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).

Answer 94

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).

Answer 95

``` 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 ```

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

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

Answer 100

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.

Answer 101

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

Answer 102

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.

Answer 103

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.

Answer 104

``` 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.

Answer 105

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.

Answer 106

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.

Answer 107

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

Answer 108

``` 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 ```

Answer 109

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.

Answer 110

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

Answer 111

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

Answer 112

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.

Answer 113

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.

Answer 114

``` 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 ```

Answer 115

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.

Answer 116

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.

Answer 117

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.

Answer 118

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.

Answer 119

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 1. lethargy 2. hyperexcitability 3. ataxia 4. convulsions 5. nystagmus 6. blindness 7. coma. If lead encephalopathy is present, the prognosis is poor.

Answer 120

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.

Answer 121

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.

Answer 122

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.

Answer 123

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.

Answer 124

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.)

Answer 125

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

Answer 126

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

Answer 127

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

Answer 128

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)

Answer 129

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)

Answer 130

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

Answer 131

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.

Answer 132

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.

Answer 133

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

Answer 134

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.

Answer 135

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.

Answer 136

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

Answer 137

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.

Answer 138

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

Answer 139

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.

Answer 140

``` 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 ```

Answer 141

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

Answer 142

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

Answer 143

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

Answer 144

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

Answer 145

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.

Answer 146

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

Answer 147

``` 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 ```

Answer 148

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

Answer 149

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.

Answer 150

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.

Answer 151

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

Answer 152

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

Answer 153

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

Answer 154

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

Answer 155

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

Answer 156

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.

Answer 157

``` 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 ```

Answer 158

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.

Answer 159

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.

Answer 160

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

Answer 161

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

Answer 162

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).

Answer 163

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.

Answer 164

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

Answer 165

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

Answer 166

``` 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 ```

Answer 167

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.

Answer 168

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

Answer 169

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.

Answer 170

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

Answer 171

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).

Answer 172

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

Answer 173

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.

Answer 174

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.

Answer 175

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.

Answer 176

``` 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) ```

Answer 177

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

Answer 178

``` 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 ```

Answer 179

``` 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. ```

Answer 180

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

Answer 181

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

Answer 182

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.

Answer 183

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

Answer 184

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

Answer 185

``` 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 ```

Answer 186

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.

Answer 187

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.

Answer 188

Foxglove Cardiac glycoside (digitalis) Cardiac arrhythmias Gastric lavage/ activated charcoal gavage. Management of cardiac arrhythmias.

Answer 189

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.

Answer 190

Lily of the valley Alkaloids GI irritation, cardiac arrhythmias Gastric lavage/ activated charcoal gavage. Management of cardiac arrhythmias

Answer 191

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

Answer 192

Yew Taxine (an alkaloid) Cardiac toxin, Vomiting, diarrhoea, ataxia, seizures, coma, bradycardia, respiratory failure Gastric lavage/ activated charcoal gavage. Management of cardiac arrhythmias.

Answer 193

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

Answer 194

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.

Answer 195

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.

Answer 196

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

Answer 197

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.

Answer 198

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.

Answer 199

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

Answer 200

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

Answer 201

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.

Answer 202

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

Answer 203

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

Answer 204

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.

Answer 205

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

Answer 206

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.

Answer 207

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

Answer 208

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.