Laminitis and your horse
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Laminitis and your horse

Laminitis can be a career and life threatening disease. Recent research has led to the development of a variety of strategies involving medical treatment and shoeing. Even so, laminitis still is not fully understood.
This multi-faceted disease requires the professional support of both farrier and veterinarian. Together they must address the many complications and varying situations as they arise. Obviously, these professionals must have an effective working rapport with one another. They must work in harmony and share the same goal---helping the horse cure itself through therapeutic shoeing and medical intervention.
Choose a veterinarian and farrier that have past experiences with laminitis. Their combined knowledge and experience will help classify the damage and formulate a plan. Though results are often favorable, it is important to note that some cases of laminitis are non-responsive.
Throughout the years, a variety of medical and shoeing techniques have been performed on our own equine friends. Some medical treatments and farrier techniques seem to work well for some and fail with others. It is important to realize that, at this time, there are no miracle shoes or treatments.
I have worked on many laminitic and foundered horses throughout the past twelve years together with several different veterinarians. Some horses have simply given up the fight. Others have had severe insult to the hooves, and the aftercare and the monies involved became emotionally and financially draining for the owners. However, many horses do respond to treatment and this makes my work as a farrier extremely gratifying.
Laminitis is caused by a primary insult that causes a constriction of blood flow in the foot; the blood constriction leads to the cell death of the laminae. The laminae attach the coffin bone to the hoofwall (think of it as Velcro).
Some of the primary causes of laminitis are the following:
Endotoxmia ? A build-up of toxins consisting of cell walls of dead, gram-negative bacteria in the blood stream, causing dehydration, shock, and possibly death.
Examples:
  • A colic, such as that resulting from a twisted bowel, that causes an interruption of blood flow.
  • Edonmetritis, a uterine infection caused by a retained placenta.
  • Pleuropneumonia, a bacterial infection of the lungs and chest cavities.
  • Colitis, an inflammation of the large intestine that causes watery diarrhea.
  • Potamac Horse Fever, which causes colitis.
Carbohydrate overload
Overeating grain, sweet feed, lush pasture, and carbohydrate supplements can cause endotoxins to enter the bloodstream.
Severe Dehydration and Shock
Dehydration causes a reduction in blood volume and blood pressure, which translates to reduced blood flow to tissues. Shock is a circulatory collapse that results in a drop in blood pressure.
Pituitary Gland Dysfunction
The pituitary gland is located at the base of the brain. It produces hormones that dictate the function of other glands including the adrenal gland, which can produce too much cortisol (natural ?cortisone?) when a benign tumor forms.
Excessive load
When a limb has to bear more weight than normal, such as when there is prolonged lameness on the opposite limb.
Corticosteroid use
Corticosteroids may cause the blood vessels of the feet to be sensitive to catecholamines (hormones) such as adrenaline
It can take up to forty hours from the start of the insult, which triggered the upset of blood flow to the feet, to show signs of lameness. When the horse starts showing a shortness of stride and a reluctance to walk and has a strong digital pulse, it is time to call the veterinarian. Most important is to have the foot or feet radiographed to determine what is occurring.
The radiographs may show rotation. This is caused by the failure of the connective tissue between bone and hoofwall plus the pull of the deep flexor tendon, which is attached to the semi-lunar crest of the coffin bone. This tendon travels back over the navicular bone and up the back of the leg and attaches to a muscle at the back and distal end of the radius. This rotation process is what needs to be arrested. If not, continual tearing of the blood vessels that supply blood to the sensitive laminae will occur at the toe causing future rotation or sinking. Sinking refers to the coffin bone rotating downward.
Shoeing treatment consists initially of trimming the hoof wall parallel to the true frog. In the acute stage, a plastic cuff that is attached to two wedge pads along with a sole and frog support cushion may be used. The cushion is applied three-eights of an inch behind the true apex of the frog (towards the bulbs). Raising the heels will alleviate the pull of the deep flexor tendon on the coffin bone. The shoe incorporates a breakover point, which is set under the coffin bone. The breakover is located approximately three-quarter of an inch to one inch in front of the apex of the frog. It will also help to relive stress on the coffin bone.
In the chronic stage, a wedge shoe with sole and frog support cushions maybe utilized. Depending on the grade of lameness, a possible tenotomy and opening of the sole/wall junction may be required.
The wedge shoe is customized with a beveled, rounded toe to ease breakover. The wedge raises the heels of the foot and reduces the pull of the deep flexor tendon.
A tenotomy, or severing of the flexor tendon, is performed when favorable results are not being obtained. Once the tendon is severed, there will not be any pull on the coffin bone, reducing the tearing of the laminae, and coffin bone rotation thereby increasing the circulation in and around the coffin bone. The tendon will start reattaching itself seven to ten days following surgery and will firmly bridge with fibrotic tissue within two to three months. The tendon is functional in about six to eight months and fully recovered one year later. The horse is to be flat shod with a shoe that incorporates an easy breakover. This will allow the deep flexor tendon to be further apart at the severed ends, thus reducing the time it takes for the deep flexor to reconnect.
When and if the sole/wall junction is opened, serum may be present. This serum is caused by a migrating infection under the sole. It is simply left to drain and the opening is packed with sugardine (mixture of Betadine and sugar) and gauze and is bandaged.
In most severe cases, the horse is nerve-blocked in order for the horse to be shod.
Recovery times vary depending on the severity of the disease, from four weeks for a mild case to a year for serious cases. Some horses may only be pasture sound. Some may suffer additional attacks more or less on a yearly basis.