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Role of Nutrition in Causes and Treatment of Laminitis in Horses By Kentucky Equine Research Staff · March 4, 2014

Laminitis is any inflammation of the laminae that interdigitate between the hoof wall and the inner structures of the hoof. These laminae can become inflamed in any generalized systemic condition which can affect peripheral circulation. These conditions include endotoxemia, septicemia, severe dehydration, and cardiovascular shock. Other causes include mechanical stress, endocrine disease, steroids, and genetic predisposition as seen in some ponies.

Nutrition can play a role in initiating laminitis, either through precipitating an abrupt change in bacterial flora and releasing an endotoxic shower or directly through a carbohydrate overload. It is also necessary to nutritionally manage the laminitic horse to increase hindgut fermentation.

Laminitis in rarely seen in neonates, seldom seen in weanlings, and commonly seen in adult horses. Ponies are prone to laminitis as are heavily muscled stallions, obese horses, and endotoxic adults. Treatment is most effective if it occurs very early in the disease process or even prophylactically. Medical treatment is aimed at decreasing blood viscosity, improving vasodilation, and decreasing systemic inflammation. Nutritional treatment tries to effect a decreased absorption of endotoxin from the gastrointestinal (GI) tract, repopulation of the bacterial flora of the gut, and increased transit time of ingesta through the hindgut via increased fiber content and less acidic pH in the colon.

Some of the most common cases of laminitis occur secondarily to diarrhea, especially colitis which compromises the gut mucosa and allows for absorption of endotoxin from the GI tract. As increased endotoxin is absorbed into the circulation, the blood supply to the foot changes and the small laminae are compromised through poor circulation and ischemia (deprivation of oxygen) to their tissues. Once signs of laminitis are obvious, the pathological process of ischemia and vessel endothelial damage due to venoconstriction or microthrombosis is already in effect. The most successful intervention that can be offered is a prophylactic one aimed at preventing the onset of the process.

Any therapies directed towards abating the effects of inflammatory mediators and circulatory changes have a therapeutic potential. Primarily used are cold therapy, anti-inflammatories such as flunixin meglumine or phenylbutazone (Bute), vasodilators such as acepromazine for short term or isoxsuprine for long term therapy, anticoagulants such as heparin, and pentoxifylline which blocks the production of tumor necrosis factor and decreases the viscosity of the blood. In cases of diarrhea/colitis with laminitis as a sequela, the prevention of absorption of endotoxin from the gut may address the potential cause. Experimentally, however, sublethal doses of endotoxin have not been shown to induce laminitis. The myriad of treatments that need to be used for laminitis indicate the limited success of any one treatment modality.