The definition of laminitis is: inflammation of the sensitive lamina of the hoof. This can lead to disruption of the attachment between the coffin bone and the inner hoof wall. A horse has founder when the lamellae of the inner hoof wall, which normally suspend the coffin bone from the inner surface of the hoof capsule, degenerate and fail. Without the coffin bone properly attached to the inside of the hoof, the weight of the horse and the forces of movement drive the bone down into the hoof capsule. This process causes severe pain which is characterized by acute lameness.
During normal hoof growth, attachments between the hoof wall and the hoof capsule are constantly being broken down and then reformed. It is proposed that the cell-cell and cell-basement membrane attachments are released under the influence of active matrix metalloproteinases (MMPs). MMPs have been isolated from normal lamellar tissues and are increased in lamellar tissues of horses affected by laminitis.
The enzymatic theory of laminitis based on lamellae MMP activation challenges the alternative view that laminitis develops because of vascular changes to the circulation of the foot. Traditionally, it was suggested that vasoconstriction and compartment syndrome decreased the flow of blood in the lamellar microcirculation to induce severe damage and death of epidermal lamellae. Collectively, these results suggest that in the acute phase of laminitis, the enzymatic effect might be the earliest and most influential effect on laminar structures.
The most common predisposing factors with laminitis include excessive ingestion of carbohydrates (grain overload), grazing of lush pastures (especially in ponies) and excessive exercise in adult horses. It also may occur secondary to post-parturient metritis, endotoxemia, colic, enteritis, or administration of excess corticosteroids.
Clinical signs of laminitis are often only noted after the disease has progressed and, by that time, the inciting factor may be difficult to ascertain. Once clinical signs of laminitis are present, the clinical course of the disease is typically correlated to the degree of laminar damage. Horses with mild laminar damage have less severe signs and usually respond quickly to therapy. Horses with extensive laminar changes have more severe signs and either respond less quickly or not at all to medical therapy. In general, the acute laminitis affects both front feet, but all four feet could be involved. On palpation, heat may be present over the hoof wall and coronary band. An increased bounding digital pulse is evident. The degree of pain may be reflected by an increased heart rate, muscle tremors, and sweating. In severe cases, examination is difficult since the horse will often not allow the feet to be picked up to be examined. The picture to the right is of a horse with severe laminitis; note how the horse places its hind feet further under to try and relieve the weight and pressure for the front feet.
The diagnosis of laminitis is based on clinical signs, physical examination and radiography. Examination with a hoof tester will reveal pain over the sole, particularly at the toe, and tapping on the hoof wall may also cause pain. Radiographs should be taken at the first sign of cute laminitis to develop a baseline for continuous radiographic comparison. Early radiographic signs in laminitis include mild bony reaction along the front of the coffin bone, in addition to widening the distance between the coffin bone and the hoof wall. Rotation of the coffin bone away from the hoof wall confirms the diagnosis of laminitis.
The goals of treatment are:
1) To prevent the further progression of laminitis
2) To reduce the pain
3) To prevent movement of the coffin bone (rotation or sinking)
Acute laminitis should be considered a medical emergency, and treatment should be initiated as soon as possible, preferably before clinical signs develop. Since circulating endotoxin and infectious processes are found in cases of laminitis, treatment for endotoxemia and sepsis should be attempted. When a horse is suspected of grain overload, one gallon of mineral oil by stomach tube acts as a laxative and tends to prevent absorption of toxic material from the gastrointesinal tract. Some recommended treatments include intravenous fluids, antibiotics, flunixin meglumine (Banamine) or phenylbutazone (Bute). Additional laminitis-preventative measures include the administration of anti-inflammatory drugs, vasodilator, heparin, oral aspirin, and placement of the horse in the stall. Some cases need trimming of the hoof. Laminitis will cause abnormal and sometimes accelerated hoof growth.
The outcome of horses with laminitis is difficult to predict. It correlates with predisposing factors, degree, if any of rotation or sinking, and ability of the owner to work through the management of the condition.