The United Kingdom Horse Shoers Union

The voice of the farrier.

Posterior Third Lameness.

Part Four: the progression of posterior third lameness.

Quarter cracks must now be considered. They always seem to appear in a similar place on the hoof wall "not varying much from one horse to another" ( Redden 1989, personal communication ). It seems this point is near to where the primary laminal attachment transfers from the distal phalanx to its cartilage, (specifically this location may vary depending upon whether bony changes are or have taken place). There may be some relationship between sub-clinical quarter cracks, loss of flexibility of the cartilage, physical shearing, and the early development of a side bone. Undoubtedly this causes localised pain.

CASE HISTORY 1:

A very interesting feature was found when an active competition horse with an advanced unilateral side bone was examined. The side bone had remained flexible. The modified cartilage extended above the coronary band
but its base was not fused to the wings of the distal phalanx. This incomplete junction caused some lameness during the development stage, although the horse continued to compete at the highest level, eventually being killed in a competition. Later post mortem examination of the junction showed a massive formation of sponge bone, which had abrasively eroded what remained of the laminal attachment.

Axially the exostosis constricted the internal cavity of the hoof and impinged upon the wings of the distal sesamoid bone, causing remodelling to its extremities, thus altering the terminal attachment points of its navicular suspensory ligaments.

Distally the exostosis formed a bony enlargement on the solar surface of the retrossal process. This projection was similar in shape and size to a small walnut shell, and must have in life compromised the corium of the sole, its connective tissue and the digital cushion.

There is some evidence of downwards bony projections, and spurring on the tips of the third phalanx in the development stage of side bone disease. The author wonders if these bony changes to the base of the distal phalanx
play a part in the development stage pain, and the chronic change of form seen in the heels of upright feet, or the contracted heel of the chronic hybrid foot?

There is a point that is important to note before attempting to correct the conformation and balance of mis-matched front feet, especially when they have been long standing. The distal phalanxes within these types of feet consistently vary in size and shape to each other. The upright foot will have an upright pedal bone, an the flat foot will have a flatter wider bone configuration. The general conformation of these bones mimics their hoof capsules or visa versa ; " pintoed hoof capsules, equal pin-toed pedal bones ". Further to this observation, examination of the middle an proximal
phalanxes of a similarly affected horse found the sides of the shafts of these bones to be of differing lengths, they being longer laterally. The articular surfaces were therefore not parallel to each other, compounding the toe in effect.

So far only the direct progression of posterior third lameness has been discussed. There are variations of this dilemma and jump in stages.

CASE HISTORY 2:

A worth while observation was made when working on an American riders horse which was considered foot sound prior to a 18 hour air journey, the animal was very tight heeled, with a broken back hoof pastern axis (HPA). Three days after its journey, it came up bilateral lame. The only indication of pain was when its heels were compressed with hoof testers. A series of x-rays over a four week period showed changes taking place in the navicular bones. Several synovial fossae enlarged and a cyst appeared on the cortex of the tendon surface of this bone. At this time the coronary crown and the wall of the heel quarters became very mobile, and a concave area was present proximo- distally on all four heel quarters of the front feet. Even after the HPA was realigned degeneration continued. The animal was chronically lame and showed pain across its heels, and up the previously mentioned flexible area of the wall, and in the coronary crown above this weakened area. The horse was truly a posterior third lameness case. Travel trauma had caused the horse to go lame and set up a progression at a very rapid pace.

CASE HISTORY 3:

During the summer of 1991, the author was fortunate enough to work on a 2 year old Thoroughbred filly which had developed an infection in the muscle in the right hand side of its chest. The animal had systemic laminitis in all four feet, and for 30 days was extremely lame on her right fore leg. This condition caused her to bear most of her weight on her left fore foot. The left fore was fitted with a lily pad, and later with a glue on heart bar shoe; even so the distal phalanx prolapsed through the solar plate.

The animal was near to death. It took thirty days to deal with the chest muscle infection, at which stage a steel heart bar shoe was fitted to her right fore, only at this point did she start to bear weight on this foot. The laminitis went into and remained in remission.

The animal continued to be shod in the same type of shoes. Some six months later, it was noted that the feet of this filly had changed shape, The right fore was a flat open type of foot, which the author feels relates to a vertical displacement of the pedal bone within its capsule. The left fore was of the upright type which is felt to relate to a forwards rotation of the distal phalanx, within its capsule, remember this bone prolapsed through the solar plate.

The animal developed mis-matched feet as a result of a laminitic crisis.

It is felt that the above clearly defined progression closely relates to the much slower insidious developing mis-matched feet in the performance horse, as previously described, and that both relate to laminitis, the laminitic condition in the performance animal being mechanically induced, and of a much lower grade.

The onset of the condition of insidiously developing mis-matched feet is not exclusive to mechanical induction. Many cases start as simply as a serious thrush outbreak in the central cleft of the frog, leading to the rotting away of the width support structures, and causing heel collapse. The heels tighten up, and the mis-matched foot condition will develop over a period of months or years.

The next article will look at what can be done to help arrest the progression of posterior third lameness.

First published in Forge Magazine 1998. Copyright Peter N Baker.

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