Long-term corticosteroid use has been shown to increase the occurrence of peripheral vasoconstriction in horses. As in the above cases, peripheral vasoconstriction causes ischemic necrosis of the laminae and allows the third phalanx to tear away from the laminae and rotate downward.
New Theory bacterial involvement causing an increase in blood supply to the foot.
Overgrowth of , exotoxin G+ thermolosin, in the hindgut leads to acidosis when carbohydrate overload has occured. When the bacteria enter the blood supply and reaches the structures of the foot, it targets the basement membrane of the laminae and begins to disintegrate it. Some research has sited the increased activity of the enzyme metalloproteinase to the breakdown of the lamellar junction. This enzyme functions to facilitate the breakdown of desmosomes between adjacent cells and has been shown to play a role in decreasing the integrity of the lamellar junction. Predispositions for laminitis include: over-weight horses, pony breeds, Cushings disease, high impact exercise on hard footing, long-term corticosteroid use, sudden increases in the richness of diet, excessive water intake, short and upright pasterns, tension on or contraction of the deep digital flexor tendon, and systemic infection. Laminitis is more common to occur in the fore feet, bilaterally but can occur in the hind feet as well. in the foot (feet), bounding digital pulse, reluctance to move, recumbency, standing with weight shifted back onto the heel, heel-first landing of foot, increased temperature, pulse and blood pressure and positive reaction for pain when hoof testers are applied over the front of the sole. In the acute stage laminitis presents as In the chronic stage laminitis is seen as downward rotation of the third phalanx (founder), separation of the hoof from the pastern at the coronary band, dishing of the dorsal aspect of the hoof wall, diverging growth visible on hoof wall, the tip of the third phalanx visible protruding through the sole, and osteomyelitis of the third phalanx. Diagnosis can generally be made by the clinical signs and symptoms of laminitis though radiology is necessary to determine the degree of founder that has occurred. Thermography may be useful in diagnosing the acute stage of mild cases of laminitis, while blood analysis (ELISA) may be used in cases related to bacterial invasion. Treatment of laminitis depends on the stage of the disease. In the acute stage the administration of NSAID’s with the removal of any suspected initiating factors is used. hydrotherapy is critical in the acute stage to help manage inflammation and pain as it slows the enzyme activity therefore slowing the breakdown of tissues. In the chronic stage the oral administration of a NSAID such as phenylbutazone (Bute) on a daily schedule is recommended in combination with
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