As long as bacterial synthesis in the intestinal tract remains functional and dog and cat foods contain animal by-products rich in vitamin K (e.g., liver and fish meal), supplementary dietary vitamin K is not necessary. Supplementary vitamin K has not been proven to be beneficial to dogs and cats unless they have consumed a source of anticoagulants such as dicumarol.
When dogs and cats accidentally consume a dicumarol-based rat poison (e.g., warfarin), vitamin K should be administered subcutaneously or orally. When vitamin K1 is given it takes six to 12 hours for clinically significant synthesis of clotting factors to occur after vitamin therapy (Squires, 1993). Warfarin intoxication can usually be adequately treated with 1 mg/kg/day vitamin K1 orally or subcutaneously for a week. Second-generation, long-acting anticoagulants may require 2.5 to 5.0 mg/kg/day vitamin K1 orally or subcutaneously for up to six weeks. Two days after cessation of vitamin K1 administration for both short- and long-acting anticoagulant rodenticide intoxication, coagulation function should be checked (ideally, by measurement of prothrombin time). In dogs receiving warfarin, vitamin K1 administered orally or parenterally reduced prothrombin time, but vitamin K3 (menadione) was less effective. In treating warfarin poisoning in dogs, menadione compared to vitamin K1 is not as prompt, not as potent and not as prolonged in action (Kerr, 1986). However, on a weight basis, menadione is about as effective as vitamin K1 in preventing prolongation of clotting time, whereas it may take several times as much menadione as K1 to cure an existing deficiency (NRC, 1985). Marks (1975) observed that the most common cause of vitamin K deficiency in veterinary practice is the accidental poisoning of animals with warfarin.
Antagonists other than dicumarol promote vitamin K deficiency. Mycotoxins are toxic substances produced by molds. Vitamin K supplementation may be helpful in correcting vitamin K deficiency induced by mycotoxins. Use of sulfa drugs, antibiotics and other medications will likely reduce intestinal synthesis of the vitamin. Various diseases or conditions affecting the gastrointestinal tract that require oral administration of certain antimicrobial drugs will decrease synthesized vitamin K.
To assure proper vitamin K nutrition, supplementation of pet foods with vitamin K is advisable. For dogs it may be prudent to provide 22 µg menadione (or vitamin K equivalent) per kg (10 µg per lb) of body weight daily for adult maintenance and 44 µg per kg (20 µg per lb) of body weight during growth (NRC, 1985). This would be more than supplied by a dry diet concentration of 1.0 mg menadione per kg (0.45 mg per lb).
For cats, a supplemental level of 100 µg per kg (45.5 µg per lb) is suggested by NRC (1986) and at least 1 mg per kg (0.45 mg per lb) by Ralston Purina (1987). AAFCO (1992) recommends a minimum of 0.1 mg per kg (0.045 mg per lb) vitamin K for cat foods. This recommendation relates to added vitamin K activity required for cat diets containing more than 25% fish on a dry-matter basis, since fish oil contains antivitamin K activity (Corbin, 1996).
For prevention or treatment of a vitamin K deficiency, both dietary and injectable sources are used. Stability of the naturally occurring sources of vitamin K is poor. However, stability of the water-soluble menadione salts is satisfactory in multivitamin premixes unless trace minerals are present (Frye, 1978). Basic pH conditions also accelerate the destruction of menadione salts; thus, soluble or slightly soluble basic mineral substances should not be included in multivitamin premixes containing menadione. Gadient (1986) concludes that vitamin K in the form of menadione sodium bisulfite (MSB) or menadione sodium bisulfite complex (MSBC) is very sensitive to moisture and trace minerals, sensitive to light and basic pH, and moderately sensitive to reduction and acid pH. Choline chloride is particularly destructive to vitamin K with an average monthly loss of 34% to 38% for MSBC and menadione dimethylpyrimidinol bisulfite (MPB) when stored in a vitamin premix with choline (Gadient, 1986). Less water-soluble forms or coated K3 forms exhibit superior stability as compared to uncoated MSB. At higher temperatures uncoated MSB preparations lost about 60% activity (Gropp and Mehringer, 1990). Heat, moisture and trace minerals increase the rate of destruction of menadione salts in both pressure-pelleted and extruded feeds (Hoffmann-La Roche, 1981). For these reasons, greater quantities of vitamin K3 are recommended in premixes that contain large quantities of choline chloride and certain trace minerals, especially when premixes are exported or stored for an extended period of time (Schneider, 1986).
