3. Pesticide poisoning Flashcards
Fumigation
Only done by trained person
CO2, HCN, zinc or aluminium phosphide gases are used
Pulmonary oedema
Bait
- anticoagulant rodenticides
- powdered corn cob (agricultural waste) - highly hydroscopic -> lots os water coming to GIT -> severe hypovolemia and hypovolemic shock
Anticoagulant rodenticides. Source
- sweet clover (coumarin) -> dicoumarol
Coumarin is used in food industry, On its own doesn’t have hurtful effect
But during storage some coumarin will change to dicoumarol but it’d not be enough to cause problem.
From dicoumarol warfarin was produced. And belongs to 1st generation of anticoagulants. Rn is obsolete
Warfarin should be taken for several days to cause an effect. Resistance is developing.
2nd generation of anticoagulants
- Brodifacoum
- Bromadiolone
- Difenacoum
- Difethialon
- Difacinon
Can be taken only once for effect. Toxicity is also higher comparing to 1st generation. Have longer half-life -> longer treatment in case of poisoning needed
Comparing to volume of product there is small amount of active ingredient
BUT
If product is flavoured, animal can consume product repeatedly -> consuming of enough amount of active substance to cause poisoning
Toxicity of anticoagulant
In case of repeated consumption LD is much lower! More dangerous!
LD50 of different anticoagulants
Brodifacoum is the most toxic !
If consumed more than 0.02 ml/bwkg -> observe
Check PTT. If ok -> check next day, if ok -> check in 3 days, if ok -> no need to treat
In first several days usually no signs
Toxicokinetics
Absorption
- lipophilic, can be absorbed dermally
- accumulation in liver (esp. brodifacoum)
- high albumin binding
Metabolism, excretion
- long-half life (albumin, liver, EHC)
-
Dose of activated charcoal for poisoning
1 GRAM per body weight
Mechanism of action of anticoagulant rodenticides
Inhibition of blood coagulation factor activation ->
blood coagulation problems
Vitamin K should be reactivated after activation coagulation factors. Rodenticides inhibit work of reactivating enzyme => no active vit K -> coagulation factors are not activated
Damage of capillary endothel -> bleeding, haematomas, hypovolaemia
PT increase (24h)
Clotting time increase (in 4-6 days after poisoning)
Endothelial damage! (after some days)
Clinical sign of anticoagulant poisoning
ACUTE:
Usually 3-6 days
- severe anaemia
- coagulation time increase (possibly icterus)
- bleeding (injuries, body cavities, eye, nose, gingiva, haematomas; damage of vessels in pregnant animal, rupture of vessels -> uterine bleeding, abortion)
Death of hypovolaemic shock
Pathological changes
- inadequate clotting of blood
- anaemia
- haematomas, bleeding everywhere
Diagnosis
Anamnesis + progressive blood clotting problems
Lab additional examinations:
- thoracic radiograph
- thoracic ultrasound
- blood clotting parameters
Lab tests
- prothrombin time (PTT) elevated
- PIVKA (proteins induced by vit K antagonism)
- bleeding time
- clotting time
- activated partial thromboplastin time (APTT)
- trombocyte count is normal!!
Treatment
- inducing emesis (<4h) (..morphine, xylazine,ropinirol)
- blood transfusion (or serum) 15-20ml/bwkg
- activated charcoal
- vitamin K1 (no vit K3!!)
Symptomatic therapy:
- vit C - for vessels
- Ca++ supplementation - for vessels
- tranexamic acid - inhibition of the fibrinolysis