Written By Dr. Kris Hiney

This month we will wrap up our discussion of the fat soluble vitamins with a vitamin that is not discussed all that often in regards to horses, vitamin K.  Vitamin K is actually a family of fat soluble vitamins from both plant and animal origins. Vitamin K in the diet occurs in the form of phylloquinone,  which is found in plants.  Phylloquinone can be converted to menaquinone via intestinal bacteria, or by other tissues within the animal.  Menaquinone is the active form of the vitamin for animals.  Most people recognize vitamin K’s role in blood clotting, but it is also a part of bone metabolism, vascular health, and even brain metabolism.

Vitamin K acts to cause the carboxylation of glutamate (an amino acid) in proteins.  This carboxylation reaction allows proteins to bind to Ca.  This is a key part of the cascade of events which occur during blood clotting.  Vitamin K deficiency is typically seen as a decreased ability to clot blood, or internal hemorrhaging.  Vitamin K is also important for the action of osteocalcin, which is a hormone needed for bone metabolism.  It is thought that supplementing vitamin K may help with osteoporosis in the elderly. Luckily in horses, deficiencies of vitamin K from consuming a nutritionally inadequate diet have not been reported.  The amount of phylloquinones present in green forages combined with the menaquinone production in the body leave little reason for supplementation.  If supplementation is desired, both phylloquinones and menaquinones have wide safety margins.  However, menadione has been linked with toxicity issues when given at manufacturer’s recommendations.  Typically vitamin K would only need to be administered to horse’s if they are on a therapeutic regimen of warfarin, an anti-clotting drug.

However, it is possible for horses to become vitamin K deficient by consuming substances which interfere with vitamin K.  Dicoumarol is a substance which is an antagonist of vitamin K, and blocks the blood clotting cascade.   Coumarin is the original chemical which is converted to dicoumarol by fungi. Clovers naturally contain a high content of coumarin, which in and of itself has no ability to affect coagulation. It is only through the action of fungi which transforms coumarin to dicourmarol.  Thus, moldy sweet clover hays are to be avoided.  Unfortunately the mold may not always be visually detectable.  Luckily, this syndrome, often referred to as sweet clover poisoning, rarely occurs on pasture.  It is important when creating clover hay that adequate drying time is achieved, which decreases the likelihood of molding.  However, this is often difficult when drying clovers due to their coarser stem.  Crimping may help decrease drying time and help to avoid molding.  Large round bales, especially the outer layer of hay, tend to be much higher in mold content.  Overall, sweet clover poisoning is seen much more commonly in cattle than it is in horses, but is not unheard of.  Unfortunately, as dicoumarol poisoning results in internal bleeding, it is often hard to detect in animal which has been exposed.  Stiffness of gait may be an indicator due to bleeding within the muscle.  Unfortunately it is often death that results in diagnosis.  As it is almost impossible to determine visually if sweet clover hay contains dicoumarol it is often recommended to be avoided.  If not, sweet clover hay can be fed intermittently with a high quality alfalfa which is high in vitamin K.   Feeding sweet clover hay for a period of no more than 7-10 days is recommended. No animals which may soon undergo surgery or parturition should be given sweet clover hay for the period of four weeks prior.  Overall, it may just be easier to forego sweet clover hay altogether.

Next month we will begin discussion of the many water soluble vitamins, their functions, and requirements by the horse.