02.01.2020
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Page 1 of 15Imagine your best mare has just been observed to have colic. Your veterinarian diagnoses a large colon volvulus, a fatal twist of the large intestine if surgery is not completed immediately.

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After being encouraged by a successful abdominal surgery correcting the problem, four days later the surgeon calls with new problem, laminitis. Your mare is lame in all four feet, but particularly in the front feet. There is a bounding pulse in the arteries coursing to the feet and the feet are hot. The mare treads as if walking on eggs and postures with her front limbs stretched out in front of her. Radiographs of the front feet reveal a change in the coffin bone position within the hoof. The bone is separating from the hoof wall with the tip of the coffin bone angling down toward the ground.The pain is not relieved with pain relievers, special shoes or even surgery to relieve pull of the deep flexor tendon. The pain is constant and excruciating.

Even with the best of treatments the disease progresses with penetration of the bone through the bottom of the foot. Euthanasia is your only real choice. How did it start; how did it progress so quickly? Why can’t laminitis be prevented?

Too often this scenario is experienced by owners and veterinarians.Laminitis or inflammation and degeneration of the lamina in the horse’s foot is unique to the horse. The problem is both a physical problem due to the way the hoof lamina support the horses weight and the vascular system in the foot, which is particularly sensitive to systemic inflammation originating in the intestine or uterus.Research on equine laminitis has unraveled many of the physiologic responses that occur within the horse’s foot.

However, the exact cascade of events, which lead to damaged lamina with eventual separation of the coffin bone from the cornified hoof is not completely understood.Risk FactorsThe disease is most often associated with diet, diet changes, toxins or gastrointestinal disease. One constant with intestinal diseases is disruption of the intestinal mucosa by such diseases as Salmonellosis, Potomac Horse Fever, carbohydrate overload, or bowel infarction.1 As the mucosa is damaged, endotoxemia commonly occurs prior to the onset of laminitis 2 and specific amines are released into the circulation. 3 Other diseases including retained placenta also have endotoxemia as a common mediator of systemic shock and carry an increased risk for laminitis. Horses eating excessive amounts of grain, particularly a different feed than normally ingested are more likely to have laminitis. In cases of anterior enteritis horses with weights of 550 kg and those with bloody gastric reflux were more likely to have laminitis. 4 Horse with pituitary adenoma are at higher risk of laminitis as are ponies which have a tendency toward insulin resistance.

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5Horses with have excessive weight bearing on one limb compared to the contralateral limb are at risk for unilateral laminitis on the overloaded limb. This is most frequent after limb fractures, infectious arthritis or tenosynovitis. This form of laminitis appears to be a mechanical cause of laminitis.

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