Shortening Tendons in the Young Horse
(so-called contracted tendons)

by
James Rooney, D.V.M.

It has become apparent that many of the questions I receive about stump foot (so-called clubfoot) are really concerned with so-called contracted tendons in foals, weanlings, and yearlings. These are really two different phenomena even though they may appear, at a glance, to be the same. Before trying to sort this out, it is necessary to emphasize, and emphasize strongly, that tendons do not contract. At least they do not contract enough to account for the clinical picture of either shortening tendons (as I shall call “contracted tendons”) or stump foot^[1]. The process in stump foot is a shortening of the deep flexor tendon towards its normal rest length – rest length being the length of a tendon which is experiencing no strain, no loading. Shortening tendons is a shortening towards the rest length of primarily the superficial flexor tendon and the interosseus tendon (suspensory ligament). When the process is sufficiently advanced, the deep flexor tendon, too, will shorten towards its rest length.

Newborn foal

a. physiological tendon shortening: This is caused, one presumes, by crowding of the foal in the uterus during the last weeks of pregnancy. The foal, helped to its feet if necessary, usually walks out of this shortening in a few days or a week or so.

b. pathological tendon shortening: The foal is born with variably severe shortening of the forelegs and occasionally the hind legs as well. This is often accompanied by a wry nose distortion of the head and scoliosis. The condition is described in some detail in Equine Pathology and in The Lame Horse (see bibliography). The basic lesion is partial hypoplasia of the distal end of Mc3 and some intervertebral articulations. I have suggested this is an atavism – a throwback to the condition of Mc3 in Equids about 20/25 million years ago.

Postnatal foals, weanlings, yearlings

There are two conditions as already indicated: shortening tendons and stump foot.

a. Shortening tendons: This is an almost invariably bilateral problem of both forelegs. The average appearance is indicated in Figure 1.

The pastern moves upward and forward and the front (dorsal) angle of the fetlock increases while the foot remains flat on the ground, suggesting that the superficial flexor and interosseus are shortening while the deep flexor is not. (This has often been called superficial flexor contracture.) As already mentioned, in the later stages the deep flexor tendon shortens as well, and the heels may be lifted from the ground. The first signs to be noticed are often a trembling or instability of one or both fetlocks with eventual knuckling forward of the knee.

Figure 1

The cause of this condition remains in dispute though disrepair might be a better term. My interpretation is that too rapid gain of weight of the young horse causes mashing down of the heels, decreasing the hoof angle, as measured at the toe. In effect the rapid weight gain outstrips the rate of maturation and toughening of the horn of the hoof wall and this will be particularly marked with the thin walled heels. This tendency for load-related decreased hoof angle is, of course, exacerbated by the all too common tendency to trim young feet to an adult appearance. The hoof angle should be greater in the young animal, decreasing to the normal of about 50⁰ by about a year of age as the animal reaches near-mature weight.

There appears to be a genetic predisposition in some cases at least, and this predisposition could be either a tendency to gain weight rapidly or too slow horn maturation or both.

By a clear-cut mechanical process this leads to the shortening of the tendons^[2]. It is known, though it is astonishing how many do not know it yet, that reducing the hoof angle, as by cutting down the heels, causes the pastern to gradually move upward and the fetlock front angle to increase, as one sees in Figure 1. This is a perfectly normal phenomenon and, in the normal animal, can readily be reversed by raising the heels, thereby increasing the hoof angle, and allowing the pastern to move downward.

Treatment for the affected animal is obvious but may take some time and may fail if the condition is too far advanced before treatment is begun. Immediately reduce food intake: eliminate grain and rich hay in favor of modest or even poor quality grass hay. Rasp the bearing edge of the hoof wall in the toe area. If necessary use shoes with heel wedges to increase the hoof angle.

Some animals may begin this process and then return to normal without human intervention. There are two reasons: first the hobbling, affected animal does not move around as readily and does not eat as much, slowing or stopping rate of gain. Second, the heels mash down in the first place because the horn of the hoof wall is insufficiently mature and strong enough to handle the rapid weight gain. As the process of shortening goes on and the deep flexor begins to shorten, the heels experience less loading while the horn continues to mature and strengthen.

In the final, desperate case tendon cutting salvage may be used. It has become fashionable to treat these animals with tetracycline with, of course, claims of wonderful results. There has not, however, been a single, logical, and properly controlled study undertaken to establish the value of such treatment. Such a study is needed because of the self-curing describe in the preceding paragraph.

b. Stump foot: Figure 2: This condition has been discussed in detail in two other essays on this site. While I believe I have learned a good deal about it, the full story – a complete theory – still eludes me. The condition may appear at any time during the first year of life, like the shortening tendons already discussed. The important distinctions are the appearance of the affected leg – the deep flexor tendon alone is shortening - and the unilateral occurrence of stump foot, most often though not invariably the right foreleg.

Figure 2

The drawings are after Lungwitz (1884).

Bibliography
Rooney JR (1998) The Lame Horse. Meerdink. Neenah, Wisconsin.

Rooney JR and Robertson JL (1996) Equine Pathology. Iowa State Univ. Press. Ames, Iowa
Lungwitz A (1884) Horseshoeing. Facsimile Edition. Oregon State Univ. Press. Corvallis.

^[1] On average tendons are stretched by maximum loading to about 4% of their starting length. They can recover, then, about 4% of that stretching when the load is removed.

^[2] I have discussed the mechanics in numerous papers and shall spare you a reprise since I know the overwhelming majority will not read it. If there is, by chance, any kindred soul who would like to see it, please let me know, and I shall oblige.

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