Vitamin K is an essential cofactor for the activation of factors II, VII, IX, and X. These factors are synthesized as precursors, and require post-translational carboxylation by gamma glutamyl carboxylase. Reduced vitamin K is required as a cofactor for this reaction. In its absence, the secreted factors are inactive, and the extrinisic pathway is affected.
Normalizes INR within 24 hrs after administration.
Vitamin K in liver disease
Phytomenadione is a fairly benign substance. The argument may be, why not give it? In liver disease, there may be not much liver left to build clotting factors, but the addition of vitamin K to the substrate is unlikely to be harmful. Liver disease patients are also likely to be suffering from nutritional deficiencies of all sorts, and therefore it may be valuable to supplement them.
However, it is not the drug of choice to treat massive haemorrhage. An article by Lisman et al (2010) doesn't even mention it in the table describing options for medical control of severe acute bleeding in liver disease.
Vitamin K in reversing warfarin
The administration of vitamin K depends to a significant extent on whether the patient is bleeding or not, and at what sort of risk they are thought to be.
- INR 4.5 – 10.0 and high risk of bleeding: Vitamin K (1 – 2 mg orally or 0.5 – 1.0 mg iv).
- If the patient is acutely bleeding, use a high dose of Vitamin K - 5-10mg IV.
The patients with a high INR, even if they are at an elevated risk of bleeding, should only ever receive 0.5-2mg of Vitamin K; this is enough to return their INR to a more tolerable state. In contrast, the profusely bleeding warfarinised patient will require at least 5-10mg of Vitamin K.