Changes

Anticoagulant rodenticides inhibit vitamin K epoxide reductase, preventing the recyling of vitamin K and depriving the liver of the active, reduced form of the vitamin^1-5. Activation of factors II, VII, IX and X ceases, but there is a quantity of these already in the circulation that are not affected. A time-lag therefore exists between ingestion of anticoagulant rodenticide and the clinical manifestation of toxicity (unchecked haemorrhage), while the supply of still-viable, vitamin K-dependent clotting factors reach the end of their life span. This delay is around 5 days in length³.  

Anticoagulant rodenticides inhibit vitamin K epoxide reductase, preventing the recyling of vitamin K and depriving the liver of the active, reduced form of the vitamin^1-5. Activation of factors II, VII, IX and X ceases, but there is a quantity of these already in the circulation that are not affected. A time-lag therefore exists between ingestion of anticoagulant rodenticide and the clinical manifestation of toxicity (unchecked haemorrhage), while the supply of still-viable, vitamin K-dependent clotting factors reach the end of their life span. This delay is around 5 days in length³.  

Factor VII has the shortest half-life (6.2 hours), and thus it and the extrinsic pathway are the first to shut down. When this occurs, hemostasis is impaired slightly, and a mild degree of hemorrhage may occur, but clinical signs are usually not apparent, because the other pathway (intrinsic) is still operational and serves as a sort of "back-up." During this period of time, laboratory evaluation of the blood will reveal an abnormality in the now defunct (extrinsic) pathway. This abnormality is in the form of an elevated prothrombin time (PT).

Since factor VII has a half-life of only 6 hours, the extrinsic pathway is the first to be affected. This causes slight impatirement of haemostasis is impaired slightly giving a mild degree of haemorrhage, but the intrinsic pathway is still functional and is able to prevent the development of overt clinical signs.  

Once the lifespan of factor IX (in the back-up intrinsic path) is at an end (half-life 13.9 hours), that pathway will be shut down and be defunct. It is at this point that hemorrhage begins to go unchecked and the most common time that the first signs of observable clinical abnormalities are noted. It is also at this point that laboratory evaluation of the blood will reveal an elevated partial thromboplastin time (PTT or APTT) as representative of a defect within that particular (intrinsic) pathway. PT is still elevated. From this point, deterioration of the patient due to hemorrhage may be quite rapid (assuming that no more active vitamin K is added to the system).

Once the lifespan of factor IX (in the back-up intrinsic path) is at an end (half-life 13.9 hours), that pathway will be shut down and be defunct. It is at this point that hemorrhage begins to go unchecked and the most common time that the first signs of observable clinical abnormalities are noted. It is also at this point that laboratory evaluation of the blood will reveal an elevated partial thromboplastin time (PTT or APTT) as representative of a defect within that particular (intrinsic) pathway. PT is still elevated. From this point, deterioration of the patient due to hemorrhage may be quite rapid (assuming that no more active vitamin K is added to the system).