Rat poison and dogs
Penny is a healthy, 3-year old Maltese who came to see us after possible ingestion of a small amount of Ramik, an anti-coagulant type of rodenticide. The active ingredient is diphacinone. It had been about a day since she may have gotten into it, so we couldn’t induce vomiting (wouldn’t have helped this late in the game). Instead, we started her on Vitamin K. She will take one 25 mg capsule for 25 days. After that course of treatment, we plan to check some of her clotting times.
By starting her on treatment BEFORE she shows signs of bleeding (such as bruising, bloody diarrhea, or lethargy), we have the best chance of preventing problems.
If you’re interested in understanding why vitamin K is helpful treatment with rodenticide poisoning, read on.
Here’s what normally happens when a blood vessel breaks and there’s bleeding:
- The blood vessel automatically constricts and spasms. This restricts the blood flowing to the damaged area and helps minimize blood loss.
- The exposed pipe attracts circulating platelets, cloud-like cells that circulate ready to assist in clotting should the need arise. Platelets clump together over the tear in the blood vessel forming a plug within the first 5 minutes of the injury. This is all a good thing, but the platelets will stay in place unless a substance called fibrin can be made to bind them.
- Platelets have on their surface binding sites for coagulation proteins, which also circulate normally in inactive forms. These coagulation proteins must be activated in order to produce fibrin. There are two ways to do this: a so-called intrinsic pathway and a so-called extrinsic pathway. There are twelve clotting factors involved between these two pathways and we will not confuse you by reviewing these steps, but suffice it to say that calcium is one of the factors as are four enzymes called serine proteases. It is the serine proteases that are relevant to rat poisoning. The end product of these pathways is protein fiber called fibrin, which binds the platelets and serves as a scaffolding for the permanent healing of the vessel tear.
Clotting factors are identified by number and the serine proteases (also called “K-dependent factors for reasons that are about to become clear) are factors II, VII, IX, and X. These factors are produced in an inactive state by the liver and go happily circulating through the bloodstream awaiting activation.
When a vessel tears and it becomes necessary to form a clot, these factors are activated in a process that requires Vitamin K (a fat soluble vitamin not as famous as its fat-soluble cousins Vitamins A and E). As the clotting factors are activated, Vitamin K is inactivated but later recycled by another set of enzymes to be ready to participate in clotting factor activation again later.
As long as there is plenty of Vitamin K, the serine proteases can be activated and clotting can proceed normally.
The anticoagulant rodenticides abolish Vitamin K recycling. This means that as soon as one’s active Vitamin K reserves are depleted, there can be no meaningful blood clotting.
In cases of poisoning one would expect symptoms to be nearly immediate, but in the case of anticoagulant rodenticide poisoning it takes several days to deplete Vitamin K. After that, even the smallest of jostles and traumas can lead to life-threatening bleeds.