INTRODUCTION
Despite the recent advances in breeding, nutrition and farm management, flexure deformities continue to be seen at an alarmingly high rate. Flexure deformities have been traditionally referred to as "contracted tendons." Since tendons lack the ability to contract, the primary defect is a shortening of the musculotendinous unit rather than a shortening of just the tendon portion, making the descriptive term "flexure deformity" the preferred one. This shortening of the musculotendinous unit produces a structure of insufficient length for normal limb alignment and results in variable clinical signs ranging from an upright pastern angle to club feet. The focus of this article will be on flexure deformities involving the deep digital flexor tendon (DDFT) and involving the distal interphalangeal joint (DIP). Flexure deformities can be divided into congenital or acquired deformities.

ANATOMY
The deep digital flexor tendon lies directly on the caudal aspect of the radius (forearm) and is covered by the superficial digital flexor tendon and the flexors of the carpus (knee). It consists of three muscle bellies (the humoral head, radial head and ulnar head) which form a common tendon just above the knee. This tendon, along with the superficial digital flexor tendon passes through the carpal canal, continues down the palmer aspect of the limb, perforates the tendons of the superficial digital flexor tendon below the fetlock and inserts on the palmer surface of the third phalanx (P3). A strong tendinous band known as the inferior check ligament originates from the deep palmer carpal ligament and joins the deep flexor tendon at the middle of the metacarpus (Figure 1). It is obvious from the anatomy that any prolonged shortening of the musculotendinous unit will affect the DIP joint, pulling it forward into a flexed position. The resultant changes in the hoof capsule follow rapidly. It can also be noted that resecting the check ligament will result in a lengthening of the musculotendinous unit.

CONGENITAL FLEXURE DEFORMITIES
Congenital flexure deformities are characterized by abnormal flexion with inability to extend the joints of the distal limb are present at birth. They are thought to result from uterine mal-positioning of the fetus, nutritional management of the mare during gestation, exposure to influenza virus or possibly a genetic link¹. The foal will walk on his toe, unable to place the heel on the ground (Figure 2). Treatment of foals with congenital flexure deformity will vary with the severity of the deformity. Repeated intervals of brief exercise in a small paddock for the first few days of life may be all that is necessary. Physical therapy in the early stages, which involves manually straightening the limb two-to-three times daily, may also be helpful. If the condition has not improved by the third day post-foaling, every-other-day administration of oxytetracycline under the supervision of a veterinarian is frequently beneficial, along with the application of a toe extension. The toe extension is cut out of a thin piece of aluminum upon which the foal's foot has been traced along with the amount of extension needed. The toe extension is then taped on the foot with Elastikon®. In severe cases, splints can be combined with the toe extension, but we rarely find this necessary.

ACQUIRED FLEXURE DEFORMITIES
Acquired flexure deformities usually develop between two and six months of age. The cause of this deformity is still elusive with genetics, nutrition (excessive carbohydrates (energy) and unbalanced minerals) and exercise thought to play roles. It is this author's opinion that this syndrome is not part of the developmental orthopedic disease (DOD) complex but, in many cases, is caused by a response to pain. Any discomfort in the foot or lower limb will initiate the flexure withdrawal reflex which causes the flexor muscles above the tendon to contract, leading to altered positions of the distal joint. Since, in this case, the flexure deformity is secondary to discomfort, the source of any lameness that accompanies a flexure deformity should be investigated with physical evaluation, local anesthesia and radiographs.

A genetic component must also be considered for acquired flexure deformities, as, year after year, some mares will consistently produce foals that develop flexure deformities in the same limb. With any flexure deformity, an attempt should always be made to determine the cause and correct it immediately.

The initial clinical sign may only be abnormal wear of the hoof at the toe. Closer investigation may reveal an increased hoof wall angle. The heels may not contact the ground after trimming. A prominent coronary band may or may not be present at this stage. The foal will usually have a normal pastern angle. Heat in the affected foot and hoof tester pain will usually be present as a result of trauma to the toe. This is the time for conservative treatment such as restricted exercise to reduce trauma, judicious use of anti-inflammatory agents to relieve pain and the administration of oxytetracycline which will cause muscle relaxation, resulting in lengthening of the musculotendinous unit. At the same time, the heels are lowered and Equilox® can be applied to the dorsal hoof wall to form a toe extension. The Equilox-impregnated fiberglass is continued over the solar surface to protect that area from further bruising. The toe extension will serve as a lever arm for the toe.

If this condition is allowed to persist, severe changes in the foot and DIP joint will occur. A prominent bulge at the coronary band with a broken-forward pastern angle, an increase in the length of the heel relative to the toe of the hoof and heels that are unable to contact the ground. Eventually, the foot develops a boxy tubular shape with a dish along the dorsal surface of the hoof wall (Figure 3).

At this point, conservative treatment is generally of little benefit. Elevating the heels has been used to reduce tension on the DDFT and to promote weight bearing on the hoof. Although it makes the animal more comfortable initially, we have not been able to lower the heel later or to remove the wedge and establish a normal hoof angle. Once the DIP joint has been pulled forward into a flexed position, surgical intervention in the form of an inferior check ligament desmotomy is indicated (Figure 4,5).
 

INFERIOR CHECK LIGAMENT DESMOTOMY
It is my contention that for consistently successful results, the surgery and foot care must go hand in hand. The addition of a toe extension at the time of surgery will increase the surface area of the foot, promote weight bearing on the heels of the foot and protect the toe portion of the hoof that is usually bruised. We have found it beneficial to do both procedures at the same time. The foal is placed under general anesthesia and the surgery is performed in a routine manner (Figure 6,7).

As soon as the bandage is in place, the farrier addresses the foot. The heels are lowered from the point of the frog palmarly, until the sole adjoining the hoof wall becomes soft. The dorsal hoof wall and ground surface of the foot in front of the frog is prepared for Equilolx® using a rasp or Dremel tool. Deep separations are explored and filled with Keratex® putty if necessary. The foot is washed with solvent and dried with a heat gun. Foals undergoing this procedure are usually between two and five months. The size and weight of the foal makes reinforcing the toe extension necessary. Fiberglass is pulled apart or cut in thin strips and mixed with the composite. The composite is applied to the dorsal hoof wall and extended onto the solar surface of the foot to the apex of the frog. The composite is molded into the desired shape, usually extending one-half to three-quarters inch in front of the foot. A piece of 1/8 inch aluminum (1.5 inch x 1.5 inch) with multiple holes drilled in it, is now placed in the composite with half the width under the foot and the other half extending in front of the hoof. The aluminum is pushed down so that the composite material extrudes through the holes. The aluminum plate is then covered with additional Equilox® (Figure 8,9).

This reinforcement allows the older foals to be walked daily without the toe extension breaking or wearing out.

AFTERCARE
Following surgery, the medical aftercare is the preference of the attending veterinarian. Along with the medical care, we feel controlled exercise in the form of daily walking is essential. With regards to farrier care, the foal is trimmed at two to four week intervals, depending on the amount of hoof growth, the object being to normalize the hoof capsule (Figure 10 ). The toe extension is maintained for two months following the surgery. The heels are lowered as necessary and the toe is backed up from the front until the desired conformation is attained. We remove no sole anterior to the frog. When the desired effect is reached, we trim the foot normally. It is important to emphasize that when the hoof capsule returns to normal, we still only remove that sole which is shedding-any discomfort in the solar area can revert to some degree of the original deformity.

CONCLUSIONS
It is important for the farrier to recognize subtle changes in the foal's limbs as they are often the first one to examine the foal when it is presented for its routine trim. With early recognition, the foal may be treated with conservative treatment without having to resort to surgery. If the surgery is indicated and performed early, it should not affect the future athletic performance of the animal in any way². Interaction between the veterinarian and farrier is necessary for a successful outcome when treating flexure deformities, regardless of whether treatment is conservative or surgical (Figure 10: Flexure deformity post surgery. This is the same foal as pictured in Figure 4. Note the hoof pastern axis and the toe extension.) .


REFERENCES
1. Hunt RJ, Current Therapy in Equine Medicine, Vol. 4, Philadelphia, W.B. Saunders 1997, 623-624.

2. Stick JA, et al, Long-term effects of desmotomy of the accessory ligament to the deep digital flexor muscle in Standardbreds: 23 cases (1979-1989). J Am Vet Med Assoc 1992; 200: 1131-1132.