The United Kingdom Horse Shoers Union
The voice of the farrier.
Posterior Third Lameness.
A series of articles by Peter N Baker.
An in depth study of posterior third lameness of the equine front foot. To a greater degree a predictable condition, which by good farriery, husbandry and attention to hoof capsular shape can be arrested if not reversed.
Part Two:
Having established the capsule shapes and suggested their locomotive roles, we must now look at the internal changes which result in a shortening of stride and an "ouchy" progression.
6. Pre-navicular Syndrome ( Caldwell )
10. Bar - Buckling and Laminitis
11. Cartilage and Circulatory Changes
12. Tight Heels - Type 1 Navicular Changes
13. Low Weak Heel, Type 2 Navicular Changes
The first signs are clearly defined by Caldwell, (FWCF Thesis ) as pre-navicular syndrome. At this stage clear visible indicators are not usually present, but the use of hoof testers gives a positive test result when the heels of the horse are compressed.
7. Corns.
Shortly after the onset of pre-navicular syndrome, a bruised area near
the seat of corn will appear. This bruise may not be of the diffuse type;
mostly it manifests itself as linear bruising following the solar edge
of the bars. It has long been considered that this corn condition was
a contusion of the sensitive sole. Under certain circumstances this may
be
the case, as in the short shoe on the vastly overgrown foot. It is more
probable that this comes about as a result of the animals heels being
pulled/driven forwards, distorting the solar papillae, tearing the papillae
of the white zone, and compressing the laminae of the heel quarter and
the bars. We must also consider disruption of the blood supply to the
coronary plexus, and compression of the papillae of the hoof wall due
to shunting. Irregular growth and bruising of the hoof wall is regularly
seen in horses that are moving " heel sore ".
8. Laminal Bed Necrosis.
The dry bruise " corn " condition will soon progress to a moist state as the damage compounds itself. Abscessation often ensues and may result from rejection of debris resulting from physical changes and laminal tearing in this area (Fisher 1991, personal communication). At this stage the heel is usually opened, and a lesion is found to be present, which closely resembles a laminitis lesion found in the white zone of the toe in the normal dorsal wall condition.
9. Heel Laminitis.
It is suggested that this heel laminal condition can be correctly described as heel laminitis. To emphasise this, consider that we have all encountered heels which have burst open, sometimes these are presented as over reaches - an incorrect assumption due to the presence of deep localised necrosis, this consequence will leave a horizontal scar to grow downwards with the new heel horn. These scars are often present when hunters and N/H horses return from grass, and indicate abscess break out due to laminal disruption during the previous working season.
10. Bar Buckling and Laminitis
Close examination of the bar will show a definite distortion. The bar
will not be straight, but buckled about a third of the way along its length
from the heel. At the angle of the buckle will be found a crack. These
cracks extend deep into the foot, and up the bar structure. A bruise will
be found in the apex of this bend and in the most severe cases active
bleeding will be observed. Abscessation is not uncommon. Probably the
bar buckle and bar crack are not unrelated to the condition referred to
as quarter crack, albeit that this is located in a different area. The
underlying tissue in the bar laminae is damaged and sensitive. Surely
this condition could correctly be described as bar laminitis ?
The laminal bed of the bars are closely related to the distal edge of the cartilage of P3. The cartilage in this area actually reflect upwards to form a type of barb appearance. Buckling of the bars undoubtedly causes constriction of the distal edge of the lateral cartilages. It is noted that animals exhibiting these features rapidly loose their free flowing forwards movement.
To recap and consider points 7 to 10 above, it can be seen that the lateral cartilages and the laminal bed in the posterior third of the equine foot are now twisted, compressed and stressed, and in extreme cases physically "sheared". The cartilages are resilient, and to a greater degree they are considered devoid of blood vessels. The stressing effect to the actual structure is therefore asymptotic.
11. Circulatory Changes.
Interlacing through, over and around the cartilage are arteries, veins and nerves. It is the stressing and trauma to these which causes bleeding and pain. When the cartilages distort, the angles of their vascular channels alter and some impingement of the nerves and blood vessels takes place. As time passes, these channels greatly enlarge.The cartilage is seen to dramatically thicken at its border with the distal phalanx. Soon the vascular channels will deviate and form crazy angles within the structure of the cartilages. The cartilages now begin to loose their flexibility.
The three types of foot previously mentioned are clearly identifiable, namely, the animal with tight upright heels, those with flatish open weak heels, and the hybrid foot that has one heel that is open or flatish, and the other heel is driven upwards, forwards, and maybe folded under, with the heel growth on the distorted side twisted, the horn tubes are not straight. Without doubt this third type of hoof capsule is related to a medial / lateral imbalance of P3 within the hoof capsule. The progression of posterior third lameness moves forwards in three distinct directions.
12. Tight Heels - Type 1: Navicular Changes - Bilateral Sidebone
Consider now the horse that has bi-laterally under run heels and upright
pasterns, This animal is a prime candidate for type one navicular changes
( as explained by Dr. Roy Pool, 3rd Laminitis Symposium Louisville 1989
), with the deep digital flexor tendon compressing the tendon surface
of the distal sesamoid, the active bone remodelling, the formation of
enlarged foramina, the fibrous changes within the bone channels of distal
sesamoid, the attendant venous hypertension, the cystic ulcers on the
tendon surface of the sesamoid bone, the resulting damage to the cortex
of
this bone, the bone tendon adhesions, and the extremely painful condition
navicular bursitis.
It is thought that this condition is triggered due to the weight of the horse falling behind the heel of the hoof when the animal is asked to do strenuous work with shoes that are to short for it. This configuration will allow the toe to lift off of the ground during the loading phase of the stride, thus stressing the heel area. Observations indicate that rapid changes now take place within the cartilages of the distal phalanx, and the onset of bilateral sidebone disease is evident as the nature attempts the lengthen the animals table of support within the hoof capsule. It is not unusual for this type of foot to be accompanied by a much flatter co-lateral foot to make up an asymmetric pair.
This animal has under-gone physiological changes to its feet although if it is given enough support, (length and width of shoe), the horse usually survives in a relatively sound state. It is noted in the racehorse if it has this foot configuration,. that it will perform better on a left or right handed track enabling it to lead with the open foot. This observation is also born out by dressage and event riders, who have indicated that certain animals are left or right handed. It follows that those with mismatched feet tend to prefer the open foot to be part of the natural lead leg.
13. Low Weak Heel, Type 2: Navicular Changes - Premature Breakover
Consider now the low, weak heeled foot that causes lameness problems.
Still observed is the a broken back hoof pastern axis and the attendant
compression of the cortex of the tendon surface of the distal sesamoid
bone by the deep digital flexor tendon. The toe will appear to be long,
and the centre of the foot appears to collapse. The horses natural physiological
response is to strengthen the solar plate in order to stabilise this solar
prolapsed. The frog is found to be strong, the bars are over-developed,
spew across the solar plate, and may even bridge the lateral sulci to
unite with the frog (Duckett Newmarket Symposium 1990). This bridging
corresponds with the widest part of the foot, which generally is vastly
expanded. Wall / laminae shearing and cavitation are common. The thickened
sole does not exfoliate in flakes as is normally the case. The solar plate
becomes much more rigid, and the wall posterior to the widest part reflects
inwards with abnormal rapidity. The wall midway between the coronary band
and the ground surface in the area of the solar bridge bulges outwards.
This bulging stresses the binding mechanism of the co-lateral cartilage
with
the pedal bone, triggering the laying down of new bone on the wings of
the wings of the distal phalanx, ( Bilateral side-bone disease ). Although
pain is some what rare in the quarter area of the low weak heeled flat
foot, when it does occur it is related to cartilage compression, wall
/ laminae shearing, and an ensuing yeast infection.
The greatest source of discomfort in the flat type of foot comes as a result of dorsal wall separation, Dorsal depression, ( Bailey Louisville Symposium 1988 ), and the attendant toe crack. The central dorsal area of the pedal bone will develop a flattened area extending in a triangular shape upwards towards the apex of the extensor process. This flattened area forms a defective base for the laminae membrane. This is a chronic condition and a permanent defect under the hoof wall will always be evident, with good husbandry however toe cracks in this area can be reunited and stabilised always providing that the laminal bed destruction is not to severe.
Run forwards heels always lead to dorsal depression of the toe area. The author suggests that this displacement of the dorsal wall, demonstrates that oblique forces across the solar plate are present. It is suggested that these forces may correspond to the lines drawn on ( Fig 1a ). The author feels that the points where these lines emerge across the ground surface of the dorsal wall, should relate to the placement and width of a correctly fitted rolled toe shoe, (See article Forge 1997 September issue).
A recent observation suggests that run forward heels and dorsal depression,
result from a condition referred to as Premature Breakover, when instead
of the heel lifting off the ground when the weight of the horse has passed
over it, the flexor group of muscles are required to elevate the heel
mechanically before the foot is fully unloaded. This modification of action
would account for the large number of horses suffering from frog shearing,
and the resulting
heel instability and decay of the centeral cleft. The abnormal early breakover
must require extra muscular effort, and would explain the heavy muscled
shoulders referred to earlier in these articles. The laminal tearing associated
with dorsal depression, is probably bought about as the physical effect
of the toe lifting forces of the flexor apparatus. Without doubt premature
breakover results from posterior third front foot pain, and is well illustrated
when horses are sore after having been worked in snow balling conditions,
or when a heel sore animal is asked to walk down a slight hill. It is
not clear whether the relationship between run forwards heels, and dorsal
depression results from a pulling
action of the toe or a pushing action from the heel, the fact it happens
is sufficient, the physical causes are for the scientist to establish.
The above described condition, (Premature Breakover), explains why dramatic
success is seen when a rolled toe shoe is used, and may explain the stated
benefit of the four point shoe.
The next article will look at the so called hybrid foot.
First published in Forge Magazine 1998. Copyright Peter N Baker.