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Laminitis
Trinity Consultants
Equine Nutrition Research & Development
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This publication is prepared for private clients of Trinity Consultants for information purposes. However as with all scientific research there are differences of opinion, we are not able to cover all of these differences in a short publication. Whilst every effort is made to keep it accurate and up to date, it is not intended to be the definitive article on laminitis.
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To understand laminitis it is necessary to understand how the inside of the foot is constructed and how horses bear weight. The force created by the horses weight is transmitted down through the bones of the leg to the coffin bone (third phalanx or P3), which sits within the hoof wall. The force is transferred from the bone to the wall, and then from the wall to the ground. The laminae (or laminar junction) connect the outside of the coffin bone to the inside of the hoof wall: it is their presence that prevents the bone from descending through the sole. In effect, the coffin bone (and therefore the horse’s weight) is suspended from the inside of the wall by these delicate structures.
Each lamina runs from the top of the foot to the bottom, one set of laminae projecting out as thin sheets of tissue from the coffin bone, a second set projecting inwards from the hoof wall. The main laminae are called primary laminae. Each primary lamina has lots of mini-laminae projecting from its surface, known as secondary laminae. The end result of all these primary and secondary laminae is a great increase in the surface area bonding the outside of the bone and the inside of the wall. This increase in surface area reduces the stress across the junction. The laminar junction contains specialised blood vessels known as arterio-venous anastomoses (AVAs) which allow blood to pass rapidly from arteries to veins without passing through the small blood vessels (capillaries) of the foot. It is only when blood is in the capillaries that it can nourish the tissues. AVAs are probably present in the foot to act as pressure-relief valves so that the capillaries do not burst when the foot hits the ground.
Laminitis is a weakening or destruction of the laminae, thought to result from lack of blood supply to the affected region. The development of the disease is not completely understood, however, and other mechanisms may prove to be involved. The lack of blood supply may result from inappropriate prolonged opening of AVAs which shunt blood away from the capillaries. Mild cases of laminitis may go unnoticed, with no permanent damage to the foot. In more severe cases, the lack of blood supply causes the laminae on the outside of the bone to unzip from the laminae on the inside of the hoof wall. In the worst cases, the weakened laminar junction can no longer support the weight of the horse, and the coffin bone moves relative to the wall.
Movement of the bone can further reduce blood supply to the laminae by squashing blood vessels, compounding the damage. The coffin bone can move in two main ways: if the laminae at the front of the foot are affected more severely than those at the heels (a common finding) the bone will rotate. If the entire laminar junction is affected the bone may move directly downwards. This is a sinker. The position of the bone can (and should) be determined by X-ray. Both rotation and sinking may cause the bone to penetrate the sole of the foot.
Causes of Laminitis Occasionally a horse or pony will get laminitis for no obvious reason. These are the exceptions, however. The factors listed below all significantly increase the chances of an animal becoming affected.
Excessive feed intake, Toxaemia, Trauma, Excessive weight-bearing, Steroids, Stress, Cancer of the pituitary gland (older horses).
The maintenance of a stable, optimum local pH within the gut is of paramount importance in the prevention of Laminitis. Sudden changes such as environmental status, increases in available protein and calorie intake cause intestinal pH to vary due to subtle and sometimes dramatic changes to microflora balance. As a result of this, the burden of cell wall fragments crossing into the blood becomes unacceptable (endotoxaemia) and a chain reaction of Catecholamines (venal restrictors) causes changes in blood pressure particularly at the extremities. These changes in turn create arterial shunts initially causing inflammation, heat and concentrated pain as nutrient flow is restricted. Finally as capillary blood supply diminished finally bypasses critical areas of the foot cell necrosis occurs and rotation of the pedal bone occurs through lack of support.