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Club Foot

From: lbm@avs.com (Linda B. Merims) Subject: Club Foot (Long) Date: 29 Nov 1993 23:58:55 GMT Organization: Advanced Visual Systems Inc.

Jonas Herbertsson wrote: :I have a 9 yo Swedish WB mare with a strange front foot. I haven't :found out why this foot is different from the other but have some :theories about it. Has anyone else seen this phenomenon and/or :have any theories about it? : :- The right front foot is slightly smaller than the left one. : :- It grows significantly faster than the left one. : :- It has a slightly concave side profile at the toe. : :- If left unattended by the shoer the heel will be too high and : the back of the foot will be very narrow.

This is, alas, something I know all too much about. The condition is called "club foot." It is widely thought to be an inherited defect, though it can easily skip generations. No studies have been done that document and describe its heritability. Indeed, the entire state of formal research on this defect is abysmal. This may change as it is becoming a significant problem in thoroughbred racing lines.

I know about it because the weanling Morgan filly I purchased began to display this defect at about 9 months of age. This set me off on a long, confusing, discouraging, but ultimately somewhat enlightening search for information. This included a literature search through the Cornell Vet School library.

WHAT IS IT?

You will never get anybody who can tell you exactly what is wrong. All you will get is a description of the phenomena, to whit:

                               ||
                               ||_      canon bone (base--fetlock)
                              //
   Normal foot               //_        first distal phalanx (P1--pastern)
                            //_         second distal phalanx (P2--short pastern)
                           //           third distal phalanx (P3--coffin bone)


                               ||
                               ||_      canon bone
                              //
   Club foot                 //_        first distal phalanx (P1--pastern)
                            //_         second distal phalanx (P2--short pastern)
                           ||           third distal phalanx (P3--coffin bone)

The third distal phalanx (P3--coffin bone) is not in a smooth line with the first two phalanxes. It is rotated to _some_ degree behind the line it should be. Therefore, the bottom of the coffin bone is not parallel to the ground. The horse is therefore standing to some degree on its toe.

Appearance and Onset

• Age at clear manifestation is about 9 months. Problem worsens for two to six months, then stabilizes. After this period, the horse doesn't become "more" club footed. Onset is probably earlier, but only becomes obvious to the casual observer at about 9 months.

• It doesn't appear to be caused or mitigated by anything in the horse's environment.

• For reasons nobody knows, 80% of club feet are in the off fore. Only 20% occur in the near fore.

• The foot takes on a dished profile. It is upright and boxy. The heel grows faster than the toe, and the rear bulbs of the hoof are round and full.

• Though rotated, the coffin bone starts out wholly and correctly attached to the front hoof wall.

• The club footed horse cannot extend its coffin bone (and hence point its hoof) to normal limits during a stride. Depending upon the degree of club footedness, the horse travels short on that leg. Sometimes it isn't even noticeable. Sometimes the horse is clearly uneven, tied in, even limping.

There are degrees of club-footedness. The best article I ever saw on this was by a research vet named Rooney at the University of Kentucky at Lexington, published in _The Blood Horse_ about three years ago. Rooney taxonomized the condition like this:

• Grade I -- slight rotation, may not even be apparent from the outside.

• Grade II -- marked rotation, dished profile.

• Grade III -- rotation more pronounced. Significant misalignment also occuring in P1 and P2 as they are "pushed up" by P3. Profile of front rim of coffin bone visible as a crescent on the bottom of the hoof.

• Grade IV -- front of coffin bone is vertical or behind the vertical.

Grades I's and mild II's can often compete without "the bad stuff" starting to occur. Racehorse Easy Goer has a Grade I-II club foot (which ain't going to help his value at stud). Grade III's are likely to have have significant problems with anything more than the very lightest use. Grade IV's are in very bad shape. Rooney said that an estimated 20% of thoroughbreds foaled now display club footedness to some degree.

Club Foot Not the Same As Contracted Tendons

A club foot is _NOT_ the same thing, though it is similar, to contracted tendons. (Contracted tendons are bilateral instead of unilateral, occur earlier in the foal's development (about 6 months), are affected by environment, and are more amenable to corrective surgery. This is also an inherited tendancy. For example, in Morgans, it is rampant in the Waseekas In Command horses.) Vets will, however, often refer to a club foot as "a contracted tendon," or "deep flexor contracture." Get them to clarify which they mean. Unilateral is the tip-off. Also be aware that there is something called a contracture of the superficial flexor tendon--but that's a different story.

WHAT IS REALLY WRONG?

What actually seems to be wrong here is that, for some reason, the deep flexor tendon, which attaches to the back of the coffin bone, is pulling the coffin bone back from where it should be. What's wrong? Nobody knows. Theories abound:

• - the tendon is too short, or doesn't develop evenly at that point in the foal's growth

• - the leg is longer than the other leg

• - the leg is shorter than the other leg

• - the foal grazed one-footed too long and shortened his tendon (the "grass foot" theory--markedly club footed horses always graze with the club foot beneath them and the non-club foot extended. They never exchange legs.)
• - the inferior check ligament which attaches the deep flexor tendon at its mid-point to the top of the canon bone is too short and the tendon can't stretch as much as it should

• - it is a secondary effect of other leg defects
  • - misshapen base of canon bone resulting in unstable flexor tendons, which "tighten up" in an effort to stabilize the leg
• - calf knee

• - my own off-the-wall theory is an ingrown frog

Two treatments exist:

• 1. The traditional treatment has been to carefully keep shaving down the horse's heel to bring P3 into more normal alignment. The idea is that you keep gently removing heel, letting the weight of the horse slowly "stretch" the deep flexor tendon back to where it should be.

• 2. The new treatment is desotonomy of the inferior check ligament. You cut this ligament (which acts as the emergency brake to prevent the coffin/deep flexor from hyperextending), thus letting the deep flexor "relax" and take the pull off the coffin bone.

Treatment 1 is now being discredited by research (that was one of the main points of _The Blood Horse_ article) as being counterproductive. However, that's what most farriers have been taught and you're going to have a devil of a time talking them out of it.

The Bad Stuff--What Eventually Goes Wrong with a Club Footed Horse?

The reason this therapy is being discredited has to do with all "the bad stuff" that can start happening to a club-footed horse undergoing use heavier than the leg can stand:

• - The front rim of the coffin bone is rotated. In Grade III's, it is even visible as a crescent in the bottom of the hoof. With heavy use, the leading edge of this coffin bone can chip and start to deteriorate. This is very serious for the eventual utility of the horse. It is essentially a broken foot.

• - Eventually, the laminae holding the coffin bone to the hoof wall begin to break down, and you get a mechanical founder--the coffin bone separates from the hoof wall.

The problem with Treatment 1 is that it rests on the theory of gently "stretching" the deep flexor tendon. An attractive theory. Rooney says this is nonsense. By shaving the heels:

• - you have removed the horse's base of support at the heels. The dynamics are complicated without a diagram, but essentially you have set up a tug-of-war between the laminae and deep flexor tendon. Rooney says the deep flexor tendon is going to win and you will get mechanical founder.

• - because the horse can no longer land flat on its foot, it is going to jab its toe into the ground at every stride, concussing the leading edge of the coffin bone.

I agree with Rooney. This is _exactly_ what happened to my filly (a Grade III) after her various "therapeutic" heel trims. After a trim, you could slip a piece of paper 3/4 of the way under her foot. She was standing on her toe. No deep flexor "stretching;" the rotten dynamics set up by this situation only slowly corrected itself as the heel grew out again. By 18 months she had coffin deterioration and separation from the hoof wall. By 2 she was a lame horse.

High Ringbone

The downside to letting the heels get long is another side effect:

• - P1 and P2 are also being pushed up out of alignment. You are likely to get progressive high ringbone (arthritic bone spurs on the outside, non-weight bearing parts of the joint) where P1 and P2 meet.

High ringbone, however, is not as serious as the effects of trimming heels too much.

Trim--But Not Too Much

You _do_ have to trim the heels on a club foot more often than on a normal foot. The trick is to only trim the excess and never so much that the horse is not bearing weight and landing unevenly on the foot. This way, you avoid putting strain on the deep flexor/laminae. Never try to "carve" a normal looking foot out of a club foot. Never try to make it match the other foot. (Good luck debating this with your farrier.) Honest, they do better with a long heel. (Jonas, if your horse is healthy and happy with how she's being trimmed now, great, don't change.)

Efficacy of Desotomy Questioned

Treatment 2, desotomy of the inferior check ligament, was originally developed as a treatment for bilateral contracted tendons. When performed when the horse is very young (before 2), it can help the situation. However, studies on the efficacy of the surgery have not distinguished between club foot and contracted tendons. It is now being thought that it is more effective for contracted tendons, and only moderately effective to ineffective for club feet. (It helped my filly only a little.) It is also questionable whether a horse without an inferior check ligament should be racing or jumping.

SUMMARY

A horse with mild club footedness can lead an active, athletic life. But, the greater the degree of rotation, the worse the skill exercised with heel trimming, the harder the use given the animal will all contribute to development of "the bad stuff." (I havn't heard of navicular problems being associated with this defect, but all that means is that I havn't heard it.) Too much bad stuff and you have an unusable horse.

• You take side x-rays to determine the degree of rotation, and of separation (if any) of the coffin from the hoof wall.

• You take bottom x-rays to determine the degree of chipping/degeneration in the leading edge of the coffin bone.

• Nerving for a horse in distress over the long term secondary effects of a club foot is available as a last resort. It really fixes nothing, but may alleviate the horse's distress.

If you breed such a horse, you may luck out and get a normal foal. But somebody down the line is going to start scratching their head when _their_ foal is about 9 months old when they begin to notice that one of their feet (probably the off fore) is starting to look awful funny.

Linda B. Merims Waltham, MA

(I guess you can tell this got to be a bit of an obsession with me.)