TOXICOLOGY - Clinical Approach to Poisoning Flashcards
(138 cards)
1
Q
How do you manage a poisoning case?
A
- Stabilise the clinical signs
- Take a detailed history
- Prevent continual absorption of the toxin (decontamination)
- Give an antidote if available
- Removal of the toxin
2
Q
Which six paramaters should be included when establishing a database for investigating poison cases?
A
PCV/TS
Urea/creatinine (to investigate renal function)
Liver enzymes
Glucose
Electrolytes
Urinalysis
3
Q
Which decontamination techniques can you use to prevent further absorption of a toxin into the gastrointestinal tract?
A
Induce emesis
Gastric lavage
Absorbants
Enemas
Surgical removal
4
Q
What are the contraindications to inducing emesis?
A
Patients with neurological dysfunction
Corrosive ingestion
Patients predisposed to aspiration
If toxin was ingested over 4 hours ago (emesis won’t be helpful at this point)
If patients have already vomited the toxin
Ingestion of button batteries
5
Q
Why is inducing emesis contraindicated in patients with neurological dysfunction?
A
Patients with neurological dysfunction are at an increased risk of aspirating
6
Q
What can you use as a decontamination technique instead of emesis in patients with neurological dysfunction?
A
Gastric lavage
7
Q
Why is inducing emesis contraindicated in patients that have ingested button batteries?
A
If you induce emesis and the batteries get stuck in the oesophagus, they can establish an electrical current and cause oesophageal necrosis
8
Q
Which toxins prevent the induction of emesis?
A
Cannibus
Codeine
9
Q
Which emetic drug is most commonly used in dogs?
A
Apomorphine
10
Q
What classification of drug is apomorphine?
A
Opioid
11
Q
What is the mechanism of action of apomorphine?
A
Apomorphine acts on the dopamine receptors in the chemoreceptor trigger zone to trigger emesis
12
Q
How should apomorphine be administered?
A
Subcutaneously
13
Q
How can the sedative effects of apomorphine be reversed?
A
You can reverse the sedative effect of apomorphine with naloxone
14
Q
Which emetic drug is most commonly used in cats?
A
Dexmedetomidine
15
Q
What classification of drug is dexmedetomidine?
A
α2-adrenoreceptor agonist
16
Q
What method is recommended to improve the effectiveness of dexmedetomidine?
A
Administer the dexmedetomidine followed by slowly spinning the cat on a chair
17
Q
How can the sedative effects of dexmedetomidine be reversed?
A
The effects of dexmedetomidine can be reversed with atipamezole
18
Q
How do you carry out a gastric lavage?
A
- Place your patient under general anaesthetic (making sure to intubate with a cuffed endotracheal tube to reduce the risk of aspiration)
- Advance a stomach tube and infuse with 5 - 10ml/kg of warm water
- Repeat until the water runs out clear
19
Q
What are contraindications for gastric lavage?
A
Corrosive ingestion
Patient is a high anaesthetic risk
If toxin was ingested over 4 hours ago (gastric lavage won’t be helpful at this point)
20
Q
Which methods can you use to administer activated charcoal?
A
In small volumes of food
Syringe
Stomach tube
21
Q
How often should you administer activated charcoal if your patient has ingested a toxin that undergoes enterohepatic recycling?
A
Administer activated charcoal every 4 hours for 24 - 48 hours
22
Q
Which toxins undergo enterohepatic recycling?
A
Paracetamol
Theobromine
Ibuprofen
23
Q
Why should you leave two hours between giving activated charcoal and oral medication?
A
The activated charcoal with absorb the oral medication
24
Q
What should you warn the owners of after administering activted charcoal?
A
Warn the owners activated charcoal will stain the faeces black
25
You can get formulations of activated charcoal with cathartics. What is the function of cathartics?
Cathartics speed up gut movement by pulling water into the gut - diluting the toxin as well as increasing gut motility
26
Which toxins are not absorbed by activated charcoal?
Xylitol
Ethylene glycol
27
Which decontamination techniques can you use to prevent further topical absorption of a toxin?
Washing
Ocular irrigation
28
What can you use to prevent the animal from grooming themselves when you're carrying out topical decontamination?
Buster collar
Shaving the fur
29
Why is it important to never wash an animal in an active seizure?
Animals in an active seizure are at risk of aspirating the water
30
How long should you carry out ocular irrigation to decontaminate the eye?
Irrigate the eye for at least 15 minutes with water or saline
31
What can you use to check the eye for corneal ulcers?
Fluoroscein
32
Which methods can be used to help remove a toxin from the body?
IV fluids
IV lipid emulsion
33
How can intravenous lipid emulsions be used to help remove toxins from the body?
Intravenous lipid emulsions can be used to eliminate lipophilic toxins and toxins with a short half life
34
Which toxins can be removed from the body with intravenous lipid emulsions?
Permethrin
Cannibis
Ibuprofen
35
What is important to note when using intravenous lipid emulsions?
Intravenous lipid emulsions are off-liscence drugs and thus should only be used for severe toxicosis when recognised treatments have been unsuccessful
36
What are the possible adverse effects of intravenous lipid emulsions?
Pancreatitis
Fluid overload as they act as colloid solutions
Coagulopathies
37
Why are cats so susceptible to paracetomal toxicity?
Cats lack the enzyme glucoronyl transferase which makes them particularly susceptible to paracetamol toxicity as this enzyme usually metabolises the toxic by-product of paracetomal metabolism - N-acetyl-p-benzoquinone which causes hepatocellular necrosis, oxidative damage to red blood cells resulting in methaemaglobinaemia and heinz body anaemia
38
Which organ metabolises paracetamol?
Liver metabolises paracetamol
39
What are the clinical signs of paracetamol toxicity in the first 24 hours?
Anaemia
Cyanosis or muddy brown mucous membranes
Tachycardia
Tachypneoa
Lethargy
Facial and paw oedema
Vomiting
40
What are the four clinical signs of paracetamol toxicity 24 hours **after** ingestion?
Signs of liver failure
Icterus
Seizures
Haematuria/haemoglobinuria
41
What is a rare clinical sign of paracetamol toxicity?
Kerratoconjunctivitis sicca
42
At what dose of paracetamol ingestion should you begin treatment for paracetamol toxicity in cats?
If the cat has ingested more than 10mg/kg of paracetamol you should begin treatment for paracetamol toxicity in cats
43
At what dose of paracetamol ingestion should you begin treatment for paracetamol toxicity in dogs?
If the dog has ingested more than 50 - 100mg/kg of paracetamol you should begin treatment for paracetamol toxicity in dogs
44
Which decontamination techniques can you use for paracetamol toxcicity?
Emesis
Activated charcoal *(remember to repeat doses due to enterohepatic recycling)*
45
Within how many hours after paracetamol ingestion would it still be effective to induce emesis?
Within 2 hours following paracetamol ingestion
46
What supportive care should you provide patients with paracetamol toxicity?
IV fluid therapy
Oxygen supplementation
Blood transfusion
Antiemetics
Antioxidants *(SAMe, N-acetylcysteine)*
Ascorbic acid
Analgesia
47
What is the function of ascorbic acid?
Ascorbic acid can be used to reverse methaemaglobinaemia
48
What is the toxic component found in slug bait?
Metaldehyde
49
(T/F) Metaldehyde poisoning has a slow onset
FALSE. Metaldehyde poisoning has a rapid onset of between 30 minutes and 3 hours
50
What are the four main clinical signs of metaldehyde poisoning?
Tremors
Seizures
Hyperthermia
Hyperaesthesia
51
What is hyperaesthesia?
Hyperaesthesia is excessive physical sensation
52
How can metaldehyde poisoning progress and cause death?
Metaldehyde poisoning can progress to severe seizures, respiratory arrest and disseminated intravascular coagulation (DIC) - which can all result in death
53
Which decontamination techniques can you use for metaldehyde poisoning?
Emesis *if they have not started with tremors or seizures*
Activated charcoal
Gastric lavage
54
What supportive care should you provide patients with metaldehyde poisoning?
IV fluid therapy
Antiepileptic drugs
Muscle relaxant
55
Which muscle relaxant drug can you give to patients with metaldehyde poisoning?
Methocarbamol
56
How can you administer methocarbamol if you are unable to administer them orally (i.e. if they are in active seizures) in patients with metaldehyde poisoning?
You can crush methocarbamol tablets and give them via an enema
57
What is the mechanism of action for anticoagulant rodenticides?
Anticoagulant rodenticides are slowly absorbed by the gastrointestinal tract and mechanically inhibit an enzyme which is crucial for the production of vitamin K1, a necessary component for clotting factors II, VII, IX and X. When the production of these clotting factors in the liver is inhibited, prothrombin cannot be adequately converted to thrombin, and coagulopathy results
58
How long after ingestion does it usually take to see clinical signs of anticoagulant rodenticide poisoning?
1 to 5 days
59
What are the six main clinical signs of anticoagulant rodenticide poisoning?
Epistaxis
Body cavity haemorrhage *(haemothorax, haemoabdomen)*
Gastrointestinal bleeding *(meleana, haematemesis)*
Haemoarthrosis
Haematomas
Anaemia
| Signs of a coagulopathy
60
(T/F) Anticoagulant rodenticides can cause tracheal narrowing
TRUE. Anticoagulant rodenticides can cause tracheal narrowing due to a combination of intraluminal haemorrhage and mediastinal haemorrhage
## Footnote
Differential to consider in dog breeds presenting with upper respiratory signs but are not predisposed to tracheal collapse etc.
61
Which diagnostic tools can you use to help identify anticoagulant rodenticide poisoning?
Coagulation profile
Platelet count
Haematology
62
Which specific coagulation parameters should you look for when investigating anticoagulant rodenticide poisoning?
Prothrombin time (PT)
Activated partial prothrombin time (aPTT)
63
When will a patient typically present with a prolonged prothrombin time (Pt) after ingesting anticoagulant rodenticides?
A prolonged prothrombin (PT) time typically occurs within the first 36 hours of ingestion
64
When will a patient typically present with a prolonged activated partial thromboplastin time (aPTT) after ingesting anticoagulant rodenticides?
A prolonged activated patial prothrombin time (aPTT) typically occurs within the first 72 hours of ingestion
65
How will the platelet count be affected by anticoagulant rodenticide poisoning?
The platelet will be normal or decreased due to increased platelet consumption
66
Which decontamination techniques can you use for anticoagulant rodenticide poisoning?
Emesis
Activated charcoal
| Will only be effective within 4 hours of ingestion
67
What do you use to treat anticoagulant rodenticide poisoning?
Vitamin K1
68
How long should you treat patients with vitamin K1 for anticoagulant rodenticide poisoning?
Up to six weeks
69
Why is the treatment regime for anticoagulant rodenticide poisoning so lengthy?
Anticoagulant rodenticides have a very long plasma half-life and thus remain in the circulation for a long time
70
How do you administer vitamin K1?
Administer the first dose of vitamin K1 subcutaneously and then the rest can be given as an oral tablet
71
What can you advise owners to do to increase the bioavailability of oral vitamin K1 tablets?
Give oral vitamin K1 tablets with a fatty meal to increase their bioavailability
72
Why is it important **NOT** to blanket treat all patients with vitamin K1 for anticoagulant rodenticide poisoning?
Not all cases require vitamin K1 treatment and since the treatment regimen with vitamin K1 can be lengthy, it is important to determine if it is necessary to avoid any unnecessary inconvenience for the owner
73
How do you determine if a patient suspected of ingesting antigoagulant rodenticides requires vitamin K1 treatment?
1. If they are clinically affected begin immediate treatment
2. If they are not clinically affacted , determine if the patient ingested a toxic dose, if yes then begin treatment
3. If they are not clinically affected and haven't ingested a toxic dose, test their prothrombin time (Pt) 48 and 72 hours after ingestion. If their prothrombin time (Pt) is prolonged, begin treatment
74
When should vitamin K1 administration begin to work?
Coagulation factors are produced within 6–12 hours of implementing treatment, prothrombin time (Pt) and activated partial prothrombin time (aPPT) improve within 12–24 hours
75
What supportive care can you provide patients with symptomatic anticoagulant rodenticide poisoning?
Oxygen supplementation
Blood transfusion
Plasma transfusion
76
What are the clinical signs of ethylene glycol poisoning within the first 12 hours of ingestion?
Neurological signs
Gastrointestinal signs
Metabolic acidosis
77
What are the clinical signs of ethylene glycol poisoning 12 to 24 hours after ingestion?
Tachycardia
Tachypneoa
Pulmonary oedema
Shock
Metabolic acidosis
| i.e. cardiorespiratory signs
78
What are the six clinical signs of ethylene glycol poisoning 24 to 72 hours after ingestion?
Clinical signs of an acute renal injury (AKI)
79
What treatment option should you consider if you see a cat exhibiting renal signs following ethylene glycol ingestion?
Euthanasia
80
Which diagnostic tools can you use to diagnose ethylene glycol poisoning?
Haematology
Biochemistry
Urinalysis
Ultrasound
81
What are the characteristic changes of ethylene glycol poisoning on biochemistry?
Metabolic acidosis
Azotaemia
Hyperkalaemia
Hypocalcaemia
Hyperglycaemia
Hyperphosphataemia
82
What are the characteristic changes in urinalysis that can indicate ethylene glycol poisoning?
Calcium oxalate crystals in the urine
Urine casts
Low urine specific gravity (USG)
Glycosuria
Proteinuria
Urine pH of less than 6.5
83
What is the medullary rim sign?
The medullary rim sign is a distinct hyperechoic zone in the outer renal medulla seen on ultrasound indicative of ethylene glycol poisoning
84
What supportive care can you provide patients with ethylene glycol poisoning?
IV fluid therapy
Antiepileptic drugs
Oxygen supplementation
85
What is the antidote for ethylene glycol poisoning?
20% ethanol
86
Which methods can you use to administer 20% ethanol?
Intravenous (IV)
Stomach tube
87
What is the toxic component of chocolate?
Theobromine
88
What dose of theobromine causes low dose theobromine toxicity?
20mg/kg theobromine
89
What are the clinical signs of low dose theobromine toxicity?
Vomiting
Diarrhoea
Hyperactivity
Panting
Shaking
90
What dose of theobromine causes moderate dose theobromine toxicity?
40mg/kg theobromine
91
What is the main clinical sign of moderate dose theobromine toxicity?
Signs of cardiotoxicity such as arrthythmias
92
What dose of theobromine causes high dose theobromine toxicity?
60mg/kg theobromine
93
What is the main clinical sign of high dose theobromine toxicity?
Seizures
94
At what dose of milk chocolate should you treat for theobromine toxicity?
Over 14g/kg of milk chocolate
95
At what dose of dark chocolate should you treat for theobromine toxicity?
Over 3.5g/kg of dark chocolate
96
What calculation can you use to determine the accurate theobromine content in dark chocolate?
Theobromine content (mg/kg) = % Cocoa x 0.16
97
Which decontamination techniques can you use for theobromine toxicity?
Emesis
Activated charcoal *(remember to repeat doses due to enterohepatic recycling)*
Gastric lavage *(for patients presenting with neurological dysfunction)*
98
What supportive care should be provided for theobromine toxicity?
IV fluid therapy
Constant ECG and seizure monitoring
Antiemetics
Antiepileptics
Urinary catheterisation
99
Which two arrhythmias can be seen with theobromine toxicity?
Supraventricular arrhythmias
Ventricular tachycardia
100
What can you use to treat supraventricular arrhythmias?
β-blocker
101
What can you use to treat ventricular tachycardia?
Lidocaine
102
Give an example of an anti-emetic you can provide animals with theobromine toxicity
Maropitant
103
Why may you consider placing a urinary catheter in a patient with theobromine toxicity?
Theobromine is renally excreted and thus will sit in the urine in the bladder where is can be absorbed into the bladder wall and re-enter the circulation
104
What is the mechanism of action of xylitol?
Xylitol stimulates insulin release which moves glucose from the circulation into the cells, resulting in hypoglycaemia. When glucose moved into the cells, potassium and phosphate move with it resulting in hypokalaemia and hypophosphataemia
105
At what dose of xylitol ingestion will animals develop hypoglycaemia?
Over 100mg/kg of xylitol
106
How long after xylitol ingestion will an animal develop hypoglycaemia?
Animals will develop hypoglycaemia 30 minutes after xylitol ingestion
107
At what dose can xylitol ingestion cause hepatic necrosis?
Over 500mg/kg of xylitol can cause hepatic necrosis which also results in coagulopathies
| Remember the liver produces the coagulation factors
108
Which three parameters should you monitor in animals with xylitol poisoning?
Blood glucose levels
Liver parameters
Clotting time
109
What supportive care can you provide patients with xylitol poisoning?
IV fluid therapy
IV dextrose CRI
Antioxidants *(SAMe)*
Manage coagulopathies
110
(T/F) Raisins/grapes are toxic to all dogs
FALSE. Raisins/grapes have an idiosyncratic reaction with only 10% of dogs experiencing raisin/grape toxicity
111
What is the toxic component of raisins/grapes?
Tartaric acid
112
What are the clinical signs of raisin/grape toxicity?
Gastrointestinal signs
Clinical signs of acute kidney injury (AKI)
113
(T/F) It is recommended to only treat a dog for raisin/grape toxicity if they have ingested more than one raisin/grape
TRUE. There have been no reported cases of dogs experiencing clinical signs after eating only one raisin/grape
114
Which decontamination techniques can you use for raisin/grape toxicity?
Emesis
Activated charcoal
115
What supportive care can you provide patients with raisin/grape toxicity?
IV fluid therapy
116
What is the mechanism of action for lily toxicity?
The toxic principles of lily toxicity are unknown, however the renal failure caused by lily toxicity is due to necrosis of the renal tubular epithelial cells. *However, the basement membrane remains intact which means that prompt treatment can result in regeneration of tubular epithelial cells*
117
Which lillies are nephrotoxic to cats?
True lillies
Day lillies
118
Which components of the lily plants are toxic to cats?
All components of the lily plant are toxic
119
What are the five main clinical signs of lily toxicity within the first 6 hours of ingestion?
Hypersalivation
Vomiting
Anorexia
Lethargy
Depression
| Initial signs of lily ingestion are due to gastrointestinal irritation
120
When should vomiting associated with lily toxicity resolve?
Vomiting associated with lily toxicity should resolve within 12 hours of ingestion
121
What are the clinical signs of lily toxicity within the first 12 - 30 hours of ingestion?
Clinical signs of acute kidney injury (AKI)
122
Which decontamination techniques can you use for lily toxicity?
Emesis
Activated charcoal
Bathe to remove pollen
123
(T/F) Gastrointestinal decontamination is required for all animals that have ingested lilies
FALSE. Gastrointestinal decontamination is only required in cats
124
What supportive care can you provide patients with lily toxicity?
Manage as an AKI case
125
Which two diagnostic tools can you use to diagnose lily toxicity?
Biochemistry
Urinalysis
126
What is the prognosis for lily toxicity?
There is a good prognosis if there has been rapid decontamination and fluid diuresis. However the prognosis will be poor if the animal is presented 18 hours after ingestion or develops anuria
127
What is the mechanism of action for ibuprofen toxicity?
Ibuprofen is an NSAID. NSAIDs inhibit the cyclooxygenase (COX) enzymes and the subsequent production of prostaglandins. This inhibiton accounts for the majority of the clinical signs seen as a result of ibuprofen toxicity
128
Which species is more susceptible to ibuprofen toxicity?
Dogs
129
What are seven of the clinical signs of gastrointestinal ulceration due to ibuprofen toxicity?
Vomiting
Haematemesis
Diarrhoea
Meleana
Abdominal pain
Anorexia
Pale mucous membranes
130
How do you determine the dose of ibuprofen that has been ingested?
Dose of ibuprofen = (mg per tablet x number of tablets ingested) / Body weight (kg)
131
At what dose of ibuprofen will you sees signs of gastrointestinal ulceration?
Over 10 - 25mg/kg of ibuprofen
132
At what dose of ibuprofen will you sees signs of acute kidney injury?
Over 100 - 150mg/kg of ibuprofen
133
At what dose of ibuprofen will you sees signs of neurological dysfunction?
Over 400mg/kg of ibuprofen
134
Which decontamination techniques can you use for ibuprofen toxicity?
Emesis
Activated charcoal *(remember to repeat doses due to enterohepatic recycling)*
Gastric lavage *(for patients presenting with neurological signs)*
135
How to you manage and treat ibuprofen toxicity?
Gastroprotectants
Antiemetics
IV fluid therapy
136
Which gastroprotenctants can you administer to patients with ibuprofen toxicity?
Omeprazole
Misoprostol
Surfactants
137
What is the contraindication to administering misoprostol?
Misoprostol is an abortion drug so shouldn't be administered to pregnant animals, of be handled by pregnant owners
138
What is the prognosis for ibuprofen toxicity?
- Prognosis is goood in animals that present soon after acute ingestion and have treatment started promptly
- Late-presenting animals are at greater risk of toxic effects
- Animals with a large acute overdose with rapid onset of neurological signs, gastrointestinal perforation or chronic exposure to ibuprofen have a more guarded prognosis
