Etiology

• Rodenticides are widely used on farmland and may be stored in large quantities.
• Grain may be dressed with anticoagulant rodenticide to reduce damage and loss through rodent infestation. It will be readily eaten by cattle if they gain access.
• Large acute ingestion and low level chronic exposure may cause toxic effects.

Predisposing factors

General

• These compounds have long half-lives and animals with recent exposure will be at increased risk of bleeding if re-exposed.

Specific

• Animals with liver disease may be more at risk because of inability to synthesize clotting factors and decreased metabolism of the rodenticide.

Pathophysiology

• Vitamin K is a cofactor in the activation of clotting factors II (prothrombin), VII, IX and X. Without vitamin K these coagulation proteins remain in a non-functional state.
• Anticoagulants act by inhibiting hepatic vitamin K₁ epoxide-reductase, the enzyme responsible for conversion of vitamin K₁ epoxide to vitamin K₁.
• There is gradual depletion of the body stores of vitamin K₁ needed to convert precursor coagulation proteins to their activated forms.
• There is a reduction in Factors II (prothrombin), VII, IX and X and therefore inhibition of prothrombin synthesis within the liver.
• Once vitamin K₁ and the clotting factors have been depleted bleeding occurs. Hence the lag-time before onset of signs.

Timecourse

• Variable; several days after acute large ingestion, and longer after low dose chronic exposure.

Epidemiology

• Rarely reported in cattle, but may be underdiagnosed.