It is a sad sight when it happens. The newly born foal struggles to its feet and stands there wobbling on forelimbs and/or hindlimbs that can't seem to bear the weight. There might be a knuckling over at the pastern with the foal literally walking on the dorsal portion of the hoof, or the flexion might be radically the other way so that the youngster is literally walking on the bulbs of its heels or pastern.
For some foals with flexural deformities, the prognosis is very good. For others, it isn't. A lot depends on whether the deformity was congenital (born with it) or acquired (developing after birth).
"These deformities," says Gayle Trotter, DVM, MS, Diplomate ACVS, of Colorado State University, "are commonly referred to as contracted tendons, even though true tendon contracture is unlikely the cause of the problem. However, with flexural deformities, the soft tissue structures on the forelimb and, less commonly, the hindlimb, are affected to the point that the bones align in varying degrees of flexion.
"The true cause and method of development of flexural deformities remain unknown, although horses with acquired deformities often share similar factors to those associated with the developmental orthopedic disease complex."
First, a look at a worst-case scenario involving congenital deformity. When this occurs, the foal might be compromised to the point where it dies in utero. Unfortunately that is not the end of the problem. The mare is also at serious risk because ankylosed (locked limbs) can make a normal delivery impossible.
M. Phyllis Lose, VMD, in her book, Blessed Are The Foals, described this devastating condition thusly:
"When a fetus in utero is involved, characteristically the spinal cord, skull, and limbs become severely contracted and distorted into a mass almost unrecognizable. One consistent finding is a scoliosed (curved) spinal cord associated with foals aborted or delivered. Although difficult to determine by physical examination, scoliosis of the thoracic (chest) area is believed by some researchers to exist in all foals or horses manifesting a single contracted limb. This is not to be confused with nutrition contraction, where two or more limbs are involved.
"In a truly contracted fetus, the contorted members ankylose and are rigidly fixed into position. The immovable joints and joint structures cease to develop, are incomplete, and so are never functional, regardless of remedial measures or heroic surgical attempts at restoration.
"In a near-term fetus, when intrauterine death occurs and abortion is imminent, the rigid mass cannot be delivered unassisted; the only exception is the small, undersized fetus that succumbs early in gestation, permitting adequate passage through the mare's birth canal. Unfortunately, most cases of contraction are discovered late in gestation and more often at the time of parturition.
"Ninety-five percent of all difficult births (dystocias) suffered by broodmares are caused by some variation of contraction. These contracted or ankylosed foals-to-be are frequently found in aborted masses. But, extreme trouble begins when an affected fetus continues to live and grow inside the uterus, with no feasible way to get out."
The problem in such cases often rests with the foal's forelimbs. The only way it can travel through the birth canal is for both front legs to be fully extended with the neck and head also extended along the forelimbs.
If the front limbs are locked into a bent position, there is no way the birth canal can accommodate a normal delivery. This means that delivery by Caesarean section or a fetotomy is the only alternative.
What causes this hideous misshapen development in our worst case scenario? No one knows for sure, other than the likelihood that multiple factors may be involved.
Trotter puts it this way: "Many factors can be involved in congenital deformities. These include intrauterine positioning, ingestion of certain toxins by the mare such as locoweed or hybrid Sudan grass, collagen cross-linking defects, equine hypothyroidism/goiter, and unidentified predisposing genetic factors. Multiple factors may be involved in a given case. Congenital flexural deformities can be due to hyperflexion, or, less commonly, hyperextension due to flaccid or relaxed flexor muscles and tendons."
There are some researchers who think the mare's diet might be implicated. An overfed mare on a super-high protein diet might increase the risk factor over that of a mare on a balanced diet of moderate proportions.
Fortunately, all cases of congenital flexural deformities are not as severe as our worst-case scenario discussed above. What follows is a rundown of some of the congenital deformities and what can be done to correct them. Much of this information comes from a paper published on the subject by Trotter.
* Digital Hyperextension--These are foals which are born with weak flexor tendons. When the tendons are flaccid, the foal's toes will elevate off the ground during weight bearing, and they will walk on the bulbs of their heels or pastern. In severe cases, this brings an attendant problem. Walking on the bulbs or pastern can cause soft tissue abrasion injuries.
To correct the problem, Trotter says, temporary heel extensions might need to be applied until muscle and tendon tone improve.
* Ruptured Common Digital Extensor Tendon--This condition might be either congenital or acquired, Trotter tells us, and the cause is unknown. Affected foals have characteristic swellings over the tendon sheath at the dorsolateral aspect of the knee. Foals might also appear to be bowlegged and they tend to knuckle over at the fetlock when walking. When standing, they often will appear to be over at the knee. Again, if not corrected, the problem can be exacerbated by abrasions and soft tissue injury as the foal hobbles around on knuckled-over pasterns.
Normally, the problem can be corrected with the application of temporary splints.
"Presumably," reports Trotter, "the tendon ends fibrose or scar down, because functionally these foals become normal."
* Congenital Carpal Deformities--These deformities are often severe and, in many cases, only one limb is involved.
"Manual correction is often impossible," Trotter says. "Careful evaluation of these cases should be undertaken to determine whether surgical correction is even feasible. Many cases have sufficient contracture of the carpal joint capsule and ligaments to prevent correction, even after transection of all carpal flexor tendons. For less severe forms, temporary splinting is effective."
* Congenital Flexural Deformities of the Foot and Fetlock--Affected foals either stand on the toe or knuckle forward at the level of the fetlock.
Trotter offers this assessment and recommendation: "Careful palpation of the flexor tendons should be completed in both the weight bearing and non-weight bearing positions to determine which of the flexor tendons is most involved. Involvement of both superficial and deep digital flexor tendon to a similar degree is sometimes seen.
"If the foal can stand and the limbs can be manually extended into a normal position, the prognosis is favorable for resolution with temporary splinting. More severe forms may require check ligament desmotomy (more about that shortly) for correction.
"More recently, the use of oxytetracycline has been advocated for some of these deformities. The initial description was for correction of deformities involving the foot only, although some success has been realized for fetlock deformities as well. The dose recommended was 3 grams given intravenously, followed by a second injection if correction was not observed. Success has also been seen using half this dose, and one case of renal toxicity has been reported in a foal after the use of this drug. The mechanism of action is unknown, but is thought to relate to calcium chelating properties of the antibiotic."
"There are many potential causes for acquired flexural deformities," Trotter informs us, "and those factors important in the development of osteochondrosis are also the same factors that are important here. Flexural deformities seem to occur most commonly in fast-growing individuals, and often those that are on a high plane of nutrition. Other factors that can be involved include pain, which results in the flexion withdrawal reflex and an altered stance. The source of pain could be OCD, joint infections, physitis, or some other form of acute trauma. If the altered stance is maintained, a flexural deformity will result. It has also been noticed that foals on a poor plane of nutrition that are then introduced to good quality feed often develop flexural deformities.
"The cause(s) of these deformities seem to be multifactorial, with nutrition and rapid growth rate being factors that are commonly present. If the problem occurs frequently on a given premise, careful evaluation of the feeding program needs to be done."
There appear to be two age groups of foals that develop acquired flexural deform-ities. Foals developing deformities of the coffin joint are usually one to four months of age. Foals which develop fetlock joint de-formities are usually 12 to 14 months of age.
"This age relationship," says Trotter, "is thought to be related to the effects of the accessory or check ligaments of the deep digital and superficial flexor tendons, respectively, and the fact that limb growth at the distal limb is largely completed by three months of age, but continues at the level of the carpus or knee for a much longer period of time. There is no evidence to suggest that true contracture or shortening of the tendons occurs, but the check ligaments may restrict passive elongation of their respective flexor tendons during periods of rapid bone growth at the more distal or proximal locations.
"In the case of the deep digital flexor tendon, a flexural deformity affecting the foot will be the end result, as this tendon attaches to the distal phalanx or coffin bone. With involvement of the superficial flexor tendon, the deformity will appear at the level of the fetlock joint."
Here's a look at two acquired flexural deformities.
* Acquired Flexural Deformity of the Coffin Joint--This condition is referred to by many horsemen as club foot. Foals which are severely afflicted display the signature upright or clubbed foot appearance. Foals which are less severely affected might not be "club-footed," but a dished appearance to the dorsal hoof wall will appear over time. In more severely affected foals, the heel will not contact the ground. Very severely affected foals often will walk on their dorsal hoof wall.
"If lameness is present," says Trotter, "the foot should be radiographed to evaluate the distal phalanx or coffin bone, as bone reabsorption or even infection at the toe portion of the foot can develop."
Trotter also recommends that dietary management be undertaken immediately. The mare also is involved as it might be necessary to limit milk production. If the foal is being creep fed, this should be immediately curtailed.
"Exercise should also be controlled," Trotter feels, "so that some exercise is given, but excessive exercise at pasture is eliminated. With less severely affected cases, a toe extension may be taped or glued to the foot, or a special glue-on shoe with a toe extension may be applied."
However, there will be cases that are so severe that mere manipulation of the diet or application of special shoes will not result in correction. In those cases, Trotter recommends consideration of a distal (carpal or inferior) check ligament desmotomy (cutting a ligament).
Desmotomy is performed just below the knee and in essence lengthens the affected tendon without touching tendon tissue or weakening the tendon. The inferior check ligament encompasses and lightly supports the deep digital tendon. By transecting the ligament, the tendon is released and lengthened by several centimeters. This means the heel can now rest comfortably on the ground and normal stance and stride are possible.
"The prognosis," reports Trotter, "is highly favorable with this surgery, although some soft tissue blemish often develops at the surgery site. The treatment works by relaxing the restraint normally placed on the deep digital flexor tendon by this ligament. Correction is usually observed immediately after surgery. Postoperative bandage care is important to limit the degree of the blemish. In very severe cases, transection or cutting of the deep flexor tendon proper may be required. Such cases are salvage cases not intended for athletic function."
* Acquired Flexural Deformity of the Fetlock Joint--Horses afflicted with this condition are usually in the 10- to 18-month age group. This deformity results in an upright conformation of the front legs. In severe cases, the horse will knuckle over at the fetlock joint.
"This deformity," says Trotter, "is thought to be related to rapid bone growth originating at the growth plate of the distal radius, and restriction to passive elongation of the superficial digital flexor tendon by the proximal (radial or superior) check ligament. However, involvement of the deep digital flexor tendon can also occasionally result in this type of deformity. Palpation of both flexor tendons should again be completed with the limb in both weight-bearing and non-weight-bearing positions to help determine which individual tendon, or whether both tendons, are involved."
Again, treatment begins with establishing an appropriate and balanced diet, but that might not be enough. Remedial steps with the foot itself might be necessary. Some horses, for example, will respond to elevation of the heel of the foot--with or without a toe extension.
"Although an initial tendency may be to try to lower the heel of the foot," Trotter says, "this will make the condition worse. More aggressive types of handcrafted shoes and splints designed to maintain the fetlock in a more normal position may be useful in selected cases. Exercise should be restricted and controlled, but should not be eliminated."
There will be cases where that approach is not enough to effect a remedy.
"If conservative treatment fails," Trotter reports, "transection of the proximal check ligament may be indicated. This procedure is designed to relieve the restrictive effect of this ligament on elongation of the superficial digital flexor tendon...Proximal check ligament desmotomy is technically more difficult to complete than distal check ligament desmotomy and post-operative seroma (a tumor-like collection of fluid in the tissues) formation at the surgery site is also a common complication. However, the procedure can be very useful in selected cases. Some cases will still need to have temporary splinting to maintain proper extension of the fetlock."
As has been suggested several times by Trotter, remedial help for the foal with a flexural deformity might be in the form of a cast or shoes with toe or heel extensions.
However, these remedies have some in-built problems. First of all, it is often difficult to nail a shoe to the small, thin, soft hoof of a youngster. The solution for this problem might be glue-on shoes, but here an expense factor can be involved, along with the shoe not allowing the hoof to expand properly as the foal grows.
A Simple Approach
During the AAEP annual gathering in Denver, farrier H. Joe Painter of Auburn University presented a down-to-earth solution when toe or heel extensions are called for--the use of polyvinylchloride (PVC) pipe.
Painter set the stage for his approach with PVC pipe this way: "Although the treatment of flexural deformities varies, depending on the age of the foal, the severity of the condition and the musculotendinous units of ligaments involved, toe extensions can be beneficial in the treatment of most foals with flexural deformity. Toe extensions force stretching of the shortened musculotendinous units or ligaments in the phase of the stride just before breakover.
"In the case of flexural deformity of the distal interphalangeal (coffin) joint, excessive heel should be trimmed; however, by shortening the heel, the weight-bearing surface of the foot is decreased and excessive wear of the toe may result. For these foals, toe extensions protect the toe and prevent excessive wear."
The toe extension device described by Painter is made from two- to four-inch PVC pipe. The diameter of pipe, he said, corresponds to the size of the foot. For most foals, two-inch pipe is appropriate.
Here is Painter's description of how he forms the device for a foal:
"With the use of a fine-toothed saw or an electric cast cutter, the pipe is cut from the end of a pipe at approximately a 50-degree angle (to correspond to the slope of the hoof). The cut extends through three-fourths of the circumference of the pipe. For the extension to be made, the cut is extended longitudinally until the desired length of extension is cut, usually three-fourths to one inch.
"The shape of the cuff thus created should correspond to the shape of the hoof wall from the toe to the heel region. The caudal portion of the cuff is removed. The extension is then heated by using a heat gun, and bent to the angle of the original cut. This is the edge that contacts the ground after the cuff is applied to the foot. Ten to 20 evenly spaced one-eighth- to one-fourth-inch holes are then drilled into the cuff. The edges of the cuff are rounded with a rasp.
"For the device to be molded to the contours of the foot, the sleeve is heated with the heat gun until it is malleable and applied to the hoof until it cools and hardens. The device is removed and the hoof is rasped and acetone is applied to it. The device is then attached to the foot with acrylic. The pre-drilled holes in the sleeve increase the surface area for bonding between the sleeve and hoof. When an extension is considered no longer necessary, a hoof nipper is used to pry the device from the hoof. The device can be reheated and reapplied if necessary."
Most of his experience with the device, Painter says, was associated with the treatment of foals with acquired flexural deformity of the coffin joint.
"We have used the device," he says, "in conjunction with inferior check ligament desmotomy, or as part of a non-surgical treatment of acquired flexural deformity of the distal interphalangeal joint. Foals that have recently acquired a mild deformity--within two to three weeks--respond favorably to trimming of excessive heel and application of the device. More chronically and severely affected foals are additionally treated by desmotomy of the inferior check ligament."
When the device is used to correct a flexural deformity problem without surgery being involved, progress should be manifested within seven days, he says. If there is no improvement in seven days, he told the group, it might mean that check ligament surgery is required.
"After two years of experience with the device, involving approximately 100 feet, we are unaware of problems associated with its use," he says. "The device does not separate from the hoof wall as long as the acrylic product mentioned (Acetone) is used, but other acrylic products may be equally effective.
"Because the device incompletely encompasses the hoof and because of the elastic nature of the acrylic, expansion of the foot as the foal grows does not appear to be significantly restricted. To minimize constriction of the hoof, however, one should generally remove the device in two to four weeks."
The PVC pipe, Painter says, can also be used to construct splints in correcting limb deformities.
What happens later in life to horses afflicted with flexural deformities at an early age? one might ask. Will their soundness and athletic abilities be compromised?
Trotter says there is no evidence that such will be the case. Foals with flexural deformities that are corrected, even with check ligament desmotomy, normally will develop into healthy, capable horses, he says.
Heritability Of Deformities
A bit more complicated is another question: How heritable is the tendency for flexural deformities?
Lose, in her book, and Trotter, in an interview, took different stances.
Lose was outspoken in her viewpoint when club-footedness is involved: "It is my strong conviction that club-footedness is of hereditary or congenital origin and will breed true. A mare or a stallion showing any degree or tendency toward club-footedness should never be bred, or you will see it in the offspring more often than not."
Trotter adopted a more moderate stance when addressing flexural deformities in general. Heredity might play a role in predisposing horses to the affliction, but there is no proof that it is the prime cause, he says.
For example, he points out, many fillies which developed a club foot and had the affliction remedied have grown into broodmares which have produced foals without the deformity.
The Role of Diet
While there are many factors that appear to be involved in either congenital or acquired flexural deformities, diet does appear to be strongly implicated.
To summarize in succinct fashion what has already been said, problems can occur when an overly aggressive feeding program results in bone growth outstripping tendon development.
Trotter was quoted earlier in this article as saying that horses with acquired deformities often share similar factors to those associated with the developmental orthopedic disease complex.
A colleague of Trotter's, C. Wayne McIlwraith, BVSc, PhD, Diplomate ACVS, in a paper on Developmental Orthopedic Disease (DOD), had this to report concerning the role of nutrition in the development of the disease:
"...The idea of over-nutrition as a cause of OCD (osteochondritis dissecans) has been extrapolated from work in dogs and pigs. There has been an increased incidence of OCD lesions noted in horses fed 130% of what the National Research Council (NRC) recommends for carbohydrate and protein. A second study in Australia by Dr. Kate Savage, which was very well controlled, showed that high-energy diets (120% NRC requirements) consistently produced lesions of osteochondrosis in weanling foals compared to a control diet based on 100% NRC requirements. Some people have focused on 'high protein' being a problem, but this has not been demonstrated.
"Various mineral imbalances have been implicated as causative factors with OCD, including high calcium, high phosphorus, low copper, and high zinc. Although high calcium levels have been implicated, experimental research in the horse with three times the NRC level of calcium in the diet failed to produce lesions of osteochondrosis. High phosphorous diets (five times NRC) did produce lesions of OCD in young foals.
"Low copper has been implicated as a cause. An epidemiologic study on clinical cases of DOD implicated low copper
levels as the most consistent factor. In experimental studies, it has been noted that a marked copper deficiency produced OCD-like lesions and flexural deformities. In another study in Thoroughbred foals
in which osteochondrosis developed before weaning, seven had serum copper and ceruloplasmin concentrations below normal. In a third controlled experiment in Canada with high (30 parts per million) and low (7 parts per million) copper diets, there was a much higher incidence of lesions seen in the foals fed the lower copper diet. However, it is to be noted that most of the changes were present in the cervical vertebrae rather than the limbs where we commonly see clinical problems.
"Excessive zinc intake has been related to equine osteochondrosis. Generalized osteochondrosis has been seen in foals raised near a zinc smelter. The relationship between zinc and copper (it has been suggested that high zinc suppresses copper levels) is still being elucidated."
McIlwraith's report tells us that research still hasn't uncovered all of the mysteries that surround these potentially crippling diseases that can afflict young horses.
One thing appears to be certain--more isn't better when designing rations for pregnant mares and young, growing foals.
The good news is that modern science and technology, involving both surgical techniques and constructing appropriate shoes, have improved the prognosis for many foals and young horses afflicted with certain congenital and acquired flexural deformities.
The bad news is that most cases involving severely contracted fetuses aren't discovered until late in pregnancy, which greatly increases the danger factor for the mare.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.