A 2-year old spayed American Staffordshire Bull Terrier that weighs 30 kg is brought into your clinic by her concerned owners after they witnessed her ingesting some rat bait 30 minutes ago. On further questioning, the owner states the dog has ingested an entire wax block and produces a photo of the packaging which clearly reads “Racumin Rat And Mouse Blocks” which contain 0.37 g/kg Coumatetralyl. As per the photo, each block weighs 30 g.
There is 0.37 g, or 370 mg in 1000 g of bait. The dog has ingested 30 g of bait. The dog has therefore ingested 11.1 mg which is equivalent to 0.37 mg/kg.
There is 0.37 g, or 370 mg in 1000 g of bait. The dog has ingested 30 g of bait. The dog has therefore ingested 11.1 mg which is equivalent to 0.37 mg/kg.
There is 0.37 g, or 370 mg in 1000 g of bait. The dog has ingested 30 g of bait. The dog has therefore ingested 11.1 mg which is equivalent to 0.37 mg/kg.
The density of the block is not required as we already know that the total block weight is 30 g and the concentration of coumatetralyl is 0.37 g/kg.
The dog appears well with no signs of bleeding. Given that the dog has ingested an entire block recently, you decide to induce emesis with apomorphine. Emesis is induced effectively within minutes, which retrieves a large amount of blue waxy material. It is difficult to tell if the entire wax block has been removed from the gastrointestinal tract so once vomiting settles, you give a single dose of activated charcoal which the dog readily drinks. The owner appears very concerned about their dog, lives nearby and appears reliable.
This is a reasonable treatment option, however a study published in the Journal of Veterinary Emergency and Critical care in 2008 (Pachtinger G et al, Incidence of prolonged prothrombin time in dogs following gastrointestinal decontamination for acute anticoagulant rodenticide ingestion) indicates that prophylactic vitamin K may not be necessary. This research shows that most dogs (>90%) who receive gastrointestinal decontamination within 6 hours of ingesting an anticoagulant rodenticide do not develop coagulopathy. This patient has also had approximately 100X less than the reported coumatetralyl acute oral LD50 in dogs of 35 mg/kg.
A study published in the Journal of Veterinary Emergency and Critical care in 2008 (Pachtinger G et al, Incidence of prolonged prothrombin time in dogs following gastrointestinal decontamination for acute anticoagulant rodenticide ingestion) indicates that the majority of dogs (>90%) who receive gastrointestinal decontamination within 6 hours of ingesting an anticoagulant rodenticide do not develop coagulopathy. This patient has also had approximately 100X less than the reported coumatetralyl acute oral LD50 in dogs of 35 mg/kg.
This patient has had approximately 100X less than the reported coumatetralyl acute oral LD50 in dogs of 35 mg/kg, and the risk of coagulopathy is very low. Coagulopathy is typically noted once Factor VII is exhausted (has the shortest half-life of the vitamin K dependent factors), and this would be evident within 48-72 hours post ingestion. The owner also lives nearby and appears reliable, so there is no reason to believe the dog will not be brought back to the clinic for assessment of coagulation at 2-3 days post ingestion.
Given that the dog has had approximately 100X less than the reported LD50 of coumatetralyl, it is likely that the risk of significant coagulopathy will be low if the animal receives no further treatment. However, given that death or serious harm are risks of missing coagulopathy, the Australian Animal Poisons Centre recommends assessment of blood clotting at 48-72 hours post-ingestion.
You advise the owner to take the animal home and to re-present in 2 days’ time for assessment of blood clotting. You warn the owner of signs of coagulopathy and if any of these signs are noted to return immediately for assessment. 2 days later, the patient is returned to your clinic asymptomatic with a PT/aPTT that has not increased from baseline values.
A normal PT/aPTT at 48-72 hours essential excludes toxicity and there is no need to alarm the owner to observe for delayed onset of symptoms or to advise on rest.
Factor VII has the shortest half-life of all vitamin K dependent clotting factors. Whilst it may be subclinical, you would expect some rise in PT/aPTT at 48 hours post ingestion if toxicity was going to occur.
Normal coagulation studies at 48 hours post-ingestion exclude toxicity. There is no need to provide ongoing Vitamin K.
Whilst many of the anticoagulant rodenticides do undergo enterohepatic circulation, multiple dose activated charcoal has not been shown to be beneficial. In addition, given the dog has normal coagulation parameters at 2 days post-ingestion, she has not ingested a toxic dose and there is no role for ongoing therapy or further investigation.
Anticoagulant rodenticides are toxic in their bait form and do not require moisture to activate or convert them into toxic compounds.
Anticoagulant rodenticides can be absorbed through the skin, but it is not really possible to develop toxicity from skin exposure to market preparations due to their very low concentration. As an example, the dermal LD50 for brodifacoum in rabbits is reported to be 0.25-0.36 mg/kg.
It is very unlikely that a dog or cat will ingest a sufficient quantity of an anticoagulant rodenticide by ingesting a poisoned rodent. Long acting anticoagulants can however bioaccumulate, and therefore repeated feeding of rodents poisoned by long acting anticoagulants can result in coagulopathy. This has been seen in some predator bird species that regularly feed on rodents in locations where long acting anticoagulants have been laid.
It is true that most (but not all) long acting anticoagulant rodenticides available in Australia contain 0.05 g/kg of active ingredient. An intervention criteria of 0.2 mg/kg for dogs and cats however is too high and the Animal Poisons Centre recommends veterinary assessment at doses of 0.02 mg/kg for all long acting anticoagulant rodenticides.