Unilateral Stump Foot (Club Foot) in Horses

by
James Rooney, D.V.M. and Ray Miller

This concerns only the unilateral condition sometimes described as "contracture" of the deep flexor tendon or club foot both of which are misnomers. The condition may be better called stump foot or goat foot or even stilt foot. Club foot is a human condition not comparable to the condition in the horse. Also, contracture^[1] is a misnomer; the condition to be described is a shortening of the deep flexor tendon towards its rest length; tendons do not contract and, so, are not subject to contracture.

I have written on this subject a number of times in the past and always, unhappily, either incorrectly or incompletely (or both). The earlier errors and omissions have been corrected, but the story is not completely clear even yet, and the work goes on.

Bilateral shortening of the flexor tendons and suspensory of the newborn and the bilateral shortening of the tendons of the weanling/yearling during the first year or so of life are not considered here.

Pain can cause unilateral, deep flexor shortening as the result of reducing the weight borne on the affected foot. With such weight reduction the equilibrium of moments at the coffin joint,^[1], Figure.1, is disturbed. F, the applicable body weight, is smaller and the tension in the deep flexor, DF, is reduced, and the deep flexor tendon shortens.

Foals which were kept in boxes during bad weather and pawed the ground obsessively developed deep flexor shortening, Owen (1975)^[2]. He related this to excessive wearing of the toe of the foot while the heel grew out. This observation was made in the 1800s by a number of German authors who saw "stelzfuss" in animals on pasture, particularly dry pasture in drought years^[3].

There is a class of deep flexor shortening not related to either of the recognized causes above. The salient characteristics include:

1. apparently begins early in life though may not detected until later
2. the right fore is more frequently involved than the left
3. contra Lungwitz deep flexor shortening rarely involves the hind feet
4. the horse usually "stands back" - the affected foot placed farther to the rear than normal
5. There is anecdotal evidence of a genetic component in many cases.

Mechanics

The moments (turning forces) at the coffin joint suggest that " weakness", lack of sufficient tensile strength of the common extensor tendon and/or extensor branches of the suspensory could be a cause of deep flexor shortening (shortening). Looking at the moment equation, [1], Figure 1: if CE, the tensile strength of the common extensor plus extensor branches, is decreased, DF, the tensile force in the deep flexor tendon, must decrease in order to reestablish equilibrium. If DF decreases, the tendon shortens. This is basically the same pathogenesis given for lack of weight bearing with F decreased while in this case CE is decreased. CEc and Fa are clockwise moments and DFb is a counterclockwise moment (a usual convention in mechanics).

DFb-(Fa+CEc)=0             [1]

Figure1: The equilibrium of moments at the coffin joint. A moment is the linear force such as F, DF, CE multiplied by its perpendicular distance (moment arm) from the center of rotation of the system which is in the distal end of P2. Thus, Fa is the clockwise moment generated by the ground reaction force, F, acting around the perpendicular distance,a,from the center of rotation in the distal end of P2. Cec is the clockwise moment generated by the tensile force in the common extensor tendon and the extensor branches of the suspensory acting around, c, the perpendicular distance to the center of rotation. DFb, now, should be obvious. It is the counterclockwise moment which balances the two clockwise moments.

A suggestive observation is that luxation of the pastern joint (palmar flexion) results in so-called bear foot, Figure 2. Such luxation can follow transection of the extensor branches of the suspensory ligament. Transection is, obviously, the ultimate case of weakness of the extensor branches. Obviously, with luxation, the deep digital flexor tendon can shorten, the load on the heels is decreased, the heels grow out, and the stump foot develops.

Figure2: The normal digit to the left and the bear foot to the right.

Usually, when the deep flexor shortens, the heels grow out (increased angle at the toe) and the horse "stands back." The mechanism for this is shown in Figure 3.

Figure3: With increased heel, in red, the foot moves back (shown as the body moving forward).

Data

Data concerning the strength of the extensor branches of the suspensory ligament is crucial for the hypothesis presented above. Ray Miller, a Wisconsin farrier, has been generous spirited and helped me in this regard. At my request he and an assistant measured the width of the medial and lateral branches of the extensor branches of the normal foot and the stump foot with calipers in eight affected individuals. Three were a Rocky Mountain mare and two of her offspring; there were two Arabians, and three Quarterhorses. The absolute means and standard deviations of the measurements after combining medial and lateral branches (which showed little or no differences) are given in Table 1. The measurements in fractions were converted to decimals. Data for the individual horses is not shown but in all cases showed the same qualitative differences as the mean values.

Normal foot means that both feet were on the ground. Normal foot unilateral means the stump foot was held up off the ground. Similarly, stump foot means both feet were on the ground while stump foot unilateral means the normal foot was held up off the ground.

Certainly no claim is made that measurement of width absolutely defines the strength, the tensile force, capability of the extensor branches. It is, however, a function of the cross section area which is a function of tensile strength and can, therefore, be used as a marker or indicator. The data shows a clear-cut difference between the stump and the normal extensor branches of the same individual and that does not falsify the hypothesis that less strength of the extensor branches is a factor in the pathogenesis of stump foot. Obviously, the common extensor has not been measured and is even more difficult to measure with reasonable accuracy in the live horse than the extensor branches. Also, there would be other clinical signs associated with laxity of the common extensor - notably tripping or stubbing the toe when moving.

A notable and significant feature is that the narrowing when in unilateral support is greater for the normal extensor branches (about 23%) than for those of the stump foot (about 7%), see the graph above. The narrowing of the extensor branch as the branch is stretched, elongated, is known as the Poisson effect^[5], and there is a definite relationship between the elongation and the narrowing, known as the Poisson ratio. Since the normal extensor branch narrows more under increased (unilateral) loading, it is lengthening more than the extensor branch of the stump foot. This suggests that the stump foot extensor branch is already stretched nearer its elastic limit^[6] before the unilateral increase of loading.

More Questions

The next problem, of course, is why the extensor branches of the affected foot are narrower and weaker than those of the normal foot. There appear to be three possibilities:

1. The narrower and longer extensor branches of the stump foot are the result of the deep flexor shortening rather than the cause. This implies, of course, some cause other than the one I propose here.
   
   Such causes have been suggested in a considerable literature in German on stelzfuss (literally, stilt foot or stump foot). A frequent observation, summarized by Schwendimann 1934^[7], was that there were two forms of unilateral shortening, most often of the foreleg. The first was tendinous in origin and said to be the result of scarring and subsequent shortening of the check ligament of the deep flexor tendon without lesions in the deep flexor tendon proper. Pathological descriptions could not be found, and many authors did not find lesions in postmortem cases. The second form, much less common, was associated with severe damage in and around digital joints with scarring and thickening of ligaments and damage to articular cartilage.
   
   The second, articular form is certainly not related to the common stump foot seen in modern times. The first, tendinous form, is plausible and, if true, would falsify the hypothesis which I offer here. There are no pathological descriptions of this tendinous form, however, and cases with chronic scarring and damage to the check ligament that I have seen at postmortem did not present as stump foot. Further, it is difficult to accept that scarring of the check ligament would cause significant shortening of that ligament and tendon which are constantly in tension in the standing horse.
2. The extensor branches of one forefoot are congenitally/genetically weaker (narrower). This is possible but highly unlikely.
3. Horses can and do stand preferentially on one diagonal or the other (data from the Hoof Research Project at Texas A&M, Dr. David Hood). It is at least plausible that such preference is basically genetic. If the young horse stands preferentially on the right fore/ left hind diagonal during the period in which the extensor branches are maturing and cross-linking, the extensor branches could be stretched and "necked," reducing the cross section area of the branches and maturing in this longer and weaker configuration. The problem, then, would be set in stone before shortening of the deep flexor became apparent. Todd (2001)^[8] pointed out that he and his trainer noted that the stump foot horse stands with the body weight shifted unto the clubfoot side with the other foreleg "propped" or standing out to the side. No reason was given for this observation, but it is consistent with what has been said above. Regular, careful foot care (as with most Standardbreds) could obviate this predisposition to stump foot becoming apparent until later in life when the horse was retired and/or the feet were no longer being well cared for.
   
   As already noted there appears to be a genetic propensity for this condition and that propensity could operate through preferential weight-bearing as discussed just above. Unfortunately, there is little information on this point beyond the observations of Hood mentioned above. Additional studies of preferential weight-bearing in the standing horse would clearly be of considerable interest.

Summary

An hypothesis is presented for the pathogenesis of unilateral stump foot, shortening of the deep flexor tendon, usually of the right fore foot. The hypothesis suggests that loss of static equilibrium of moments at the coffin joint is caused by inadequate tensile strength of the extensor branches of the suspensory ligament. This loss of equilibrium leads inevitably to shortening of the deep flexor tendon.

The inadequate tensile strength of the extensor branches may be caused early in life by genetically preferential weight-bearing on the affected leg, stretching and necking the extensor branches before they are mature and cross-linked.

^[1] I may forget and use contracture on occasion in deference to common usage even though it is incorrect. As noted the tendons SHORTEN towards their rest length. They do not contract. The rest length is that length of the tendon without any tension in the tendon.

^[2] Owen J M (1975) Abnormal flexion of the corono-pedal joint of “contracted tendons” in unweaned foals. Equine Veterinary Journal 7: 40-5

^[3] A review of the old literature was made with the indispensable help of Susanne Whitaker of the Flower-Sprecher Library at Cornell University. Most of the literature reviewed is referenced in: Habacher F (1942) Beitrag zum erworbenen “Stelzfuss” älterer Fohlen. Wiener Tierärtliche Monatsschrift 29: 385-95.

^[4] No further statistical analyses were done since the numbers are small and the differences in the data are clear.

^[5] Fairman, S and Cutshall, CS (1953) Mechanics of Materials. Wiley. New York.

^[6] The elastic limit is the limit of elongation before a permanent deformation of the tissue occurs. See reference in footnote 5.

^[7] Schwendimann, F (1934) Der Beschlag des Stelzfusses ertwachsener Pferde. Schweiz. Hufschmied 19: 97-102.

^[8] This is in an exchange of comments on a bulletin board at: www.horseshoes.com. Use the Search function .for: Todd.

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