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. |