Poisons and Toxins Flashcards
Define a poison
A substance that is capable of causing the illness or death of a living organism when introduced or absorbed
What are classified as natural poisons?
Plants
Animals
Fungi
Inorganic material
What are classified as chemical poisons?
Drugs and medicines (human or veterinary)
Pesticides (domestic or agricultural)
Household chemicals
Industrial chemicals
What is the mechanism of paracetamol toxicity?
Saturation of metabolic pathways - toxic metabolite conjugated by glutathione which is promptly depleted
Cats lack the metabolic capacity to detoxify paracetamol
What are the early clinical manifestations of paracetamol toxicity?
Progressive cyanosis
Brown/blue MM
Weakness and lethargy
What are the clinical manifestations of paracetamol toxicity between 4 and 24 hours?
Facial and paw oedema
Vomiting
Depression
Dark brown blood - mtheaemoglobinemia
What are the clinical manifestations of paracetamol toxicity that appear after a day has passed?
Severe methaemoglobinemia
Hepatic necrosis
What are the signs of methaemoglobinaemia?
Blue or brown mucous membranes
Arterial blood is chocolate brown in colour and remains dark on aeration
Cyanosis fails to respond to oxygen therapy
What level of paracetamol is toxic to dogs and cats?
Dogs = 150mg/kg Cats = 20mg/kg
What is the treatment for paracetamol toxicity?
Emesis with apomorphine in dogs and xylazine in cats
Activated charcoal
Antidote is acetylcysteine which is a precursor of glutathione
SAMe 90mg twice daily for 3 d the 90mg daily for 14 d
Ascorbic acid 30-40mg/kg every 6 hrs for at least 36 hrs
What is the dosing of acetylcysteine in cats?
For 20-60mg/kg paracetamol 140mg/kg by slow IV infusion over 6 hours
For >60 mg/kg paracetamol or if evidence of metHb 280mg/kg orally or by slow IV over 6 hours
After 6 hours 70mg/kg orally or IV over 20 minutes every 6 hours for 2-4 days
What is the dosing of acetylcysteine in dogs?
> 150mg/kg paracetamol or evidence of metHb 280mg/kg orally or by slow IV over 6 hours then 70mg/kg orally every 6 hours for 2-4 days
What should be monitored after paracetamol poisoning?
For 1 week liver function, clotting, renal function and full blood count
Why does NSAID toxicity occur?
Mainly due to COX-1 inhibition
What are the early manifestations of NSAID toxicity?
Gastrointestinal erosion, ulceration an possibly perforation
Vomiting and diarrhoea both may be bloody
Rarely CNS symptoms (ataxia, lethargy, drowsiness)
What are the late manifestations of NSAID toxicity?
Renal failure
Hepatic failure
What is the treatment for NSAID toxicity?
Decontamination using emesis or activated charcoal
Prevention of gastric ulceration using H2 receptor antagonists, proton pump inhibitors or ulcer healing or coating agent
Prostaglandin supplementation with Misoprostol
Maintenance of renal function with IVFT
What are the clinical effects of theobromine (chocolate) poisoning?
Vomiting, diarrhoea, polydipsia, salivation - dehydratioin
CNS/myocardial stimulation - tremor, convulsions, tachycardia, hypertension, arrhythmia
Renal failure
Fatal cases due to severe convulsions/circulatory failure
How is theobromine toxicity managed?
Emesis, repeat dose activated charcoal, adequate rehydration, surgery observation for up to 72 hours
Monitor vital signs, ECG, benzodiazepines for CNS stimulation, treatment of arrhythmia is lidocaine
Where do tremorgenic mycotoxins come from?
Food waste and rubbish, mouldy bread, mouldy rice, dairy products, mouldy cream cheese, mouldy macaroni cheese, mouldy blue cheese and blue cheese, mouldy fallen fruit and nuts, silage, compost
What is the mechanism of tremorgenic mycotoxin toxicity?
Penitrem A may interfere with release of neurotransmitters
May act synergisitically
What are the clinical effects seen within 3 hours of tremorgenic mycotoxin ingestion?
Vomiting, ataxia, whole-body muscle tremors, rigidity with hyperextension of extremities, hyperactivity, hyperaesthesia, tachycardia, panting, tachypnoea, nystagmus and blepharospasm
What are the clinical effects seen in severe cases of tremorgenic mycotoxin ingestion?
Severe tremors and opisthotonus, convulsions and coma with paddling
Rarely aspiration
Increased muscular activity - hyperpyrexia, exhaustion, rhabdomyolysis, dehydration and hypoglycaemia
How is tremorgenic mycotoxin ingestion managed?
Decontamination by emesis, gastric lavage and activated charcoal
Anticonvulsants such as benzodiazepines, barbiturates, methocarbamol
Supportive care - rehydration, cooling measures, ventilation, antiemetics, observe for 24-48 hours
What allium species are poisonous?
Leeks, onions, shallots, spring onions, garlic and chive
What animals are susceptible to allium toxicity?
Dogs, cats, sheep, cattle and goats
What is the mechanism of action of allium toxicity?
Organosulphoxides in plants convert to organic sulphur compounds (n-propyl disulphide G6PD) when traumatised which enters erythrocytes and reduces the protective effect of glutathione
Mixed sulphide bond forms between Hb and glutathione resulting in Heinz bodies
Damaged erythrocytes removed from the circulation inducing anaemia
What are the clinical effects of allium toxicity?
Signs of haemolysis can be delayed for 1-5 days
GI effects (vomiting, inappetance, onion smelling breath)
Heinz body anaemia (lethargy, pale MM, tachycardic, tachypnoeic)
Haematuria and haemoglobinurea
Urine may smell of onions
Mild methaemoglobinaemia
In severe cases icterus due to haemosiderin in the liver
What is the toxic does of allium?
Not known as seems to vary
How is allium toxicity managed?
Emesis, activated charcoal
Monitor haematology, IV fluids
High protein diet may promote restoration of glutathione stores
Supplement oxygen and oxyglobin may be given in severe cases or a blood transplant
What is the mechanism of toxicity of anticoagulant rodenticides?
Vitamin K is essential for production of factors II, VII and X which are essential for the production of fibrin
Anticoagulants inhibit Vitamin K epoxide reductase so there is a depletion of Vitamin K and therefore a reduction in factors II, VII and X
What are the clinical effects of rodenticide toxicity?
Rare as clotting factors have long half life so there is a delay between exposure and clinical effects
Elevation of clotting or PTT
Main effect is haemorrhage but may present with dyspnoea, lethargy, weakness or anorexia
Bruising, bleeding from gums, nose, GI tract and wounds
How is rodenticide toxicity managed?
Decontamination if <2 hours previously
Blood tests
Vitamin K therapy if symptomatic or elevations in PTT
What is the dose of Vitamin K used to treat rodenticide toxicity?
2-5mg/kg IM or SC daily at multiple injection sites until PT normalises
Once PT normalised Vitamin K orally for 2-3 weeks 2-5mg/kg in divided doses gradually reducing
What important information needs to be collected to assess the severity/likely severity of rodenticide toxicity?
Full trade name/active ingredient Household or commercial product Lifestyle Concentration % Acute/chronic exposure Amount eaten
What are the different types of molluscicides?
Metaldehyde
Methiocarb
Aluminium sulphamate
Ferric phosphate
What is the mechanism of toxicity of molluscicides?
Not fully understood
Increase in muscular activity leading to hyperthermia
Rapid cellular necrosis and metabolic acidosis
What are the clinical effects of molluscicide toxicity?
Hypersalivation, vomiting, diarrhoea, ataxia, panting, tremors, convulsions, hyperthermia
Respiratory and cardiac effects less common
How is molluscicide toxicity managed?
Emetics? Gastric lavage? Activated charcoal
Managements of convulsions using benzodiazepines or propofol CRI
What are the mechanisms of toxicity of European adder poisoning?
Significant morbidity but low mortality
Hypovolaemia and oedema due to increased vasular permeability due to release of mediated histamine, serotonin, bradykinin and prostaglandin
Local haemorrhage due to cytolytic and haemolytic factors
Cardiac effects due to impaired cirulation and poor perfusion of the myocardium
Renal impairment due to hypovolaemic shock
What are the local clinical effects of European Adder poisoning?
Localised painful swelling
Swelling oedema may last days
Necrosis is rare
What are the systemic clinical effects of European Adder poisoning?
Shock, collapse and hypotension Pain, panting, hypersalivation, mental status change, hyperthermia, bruising, pale MM, tachypnoea, lameness Coagulopathy Renal effects Hepatic effects Cardiac effects
How is European Adder toxicity managed?
Keep animal still and quiet IVFT Antivenom BP, pulse, respiration, temperature ECG Check for coagulopathy, renal and hepatic parameters
What are the indications for using antivenom to treat European Adder poisoning?
Any animal with bite to face or with severe swelling
Swelling beyond the next major joint proximal to bite
Hypotension unresponsive to IVFT
Evidence of coagulopathy
Any ECG abnormality
What is the dose of European Adder antivenom used?
10ml ampoule diluted in 2-3 volumes of isotonic saline by slow IV injection or by IV infusion over 30 minutes
What are the two types of adverse reaction to antivenom?
Anaphylactic reactions - urticaria, vomiting, fever and tachycardia. In severe cases hypotension and bronchospasm
Serum sickness occurs days later characteristed by fever, urticaria, joint pain and lymphadenopathy
What are other treatment options that could be used instead/as well as antivenom?
Analgesia
Antibiotics
Antihistamines
Steroids
