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Wrangling on the Range #141

Laminitis - founder

                        
WRANGLING ON THE RANGE #141

FROM NORTHERN HORSE REVIEW - SEPTEMBER 2005

LAMINITIS

The Second Largest Killer of Horse

It is much easier to prevent laminitis and founder than it is to
treat it. Even Secretariat's caregivers could not keep him from
succumbing to this painful condition.

by Heather McCutcheon


One of the longest identifiable afflictions of horses, laminitis,
has confounded veterinarians and horse owners for hundreds of
years. With most cases, the damage is already done before we are
even aware of it, making the condition difficult to treat in a
timely and effective manner. Although laminitis is considered
irreversible, there are management techniques that can be used
based on the stage and severity of it.
According to research done by Dr. Chris Pollitt at the Australian
Equine Laminitis Research Unit (AELRU), "Laminitis remains the
second biggest killer of horses, after colic."

Laminitis is commonly referred to as "founder." As testament to
the history of the ailment, documentation records evidence of
laminitis being referred to as 'Gout' and 'Barley Disease' by the
Romans. According to Dr. David Ramey is his book, "Concise Guide
to Laminitis in the Horse," - "Some people have tried to make the
distinction between the terms laminitis and founder. For example,
for a while, laminitis was the veterinarian's term and founder
was the term used by everyone else. Others have tried to say that
a foundered horse is one in which there is chronic lameness,
accompanied by changes in the anatomical structures of the foot.

Such distinctions really aren't particularly useful and they can
be quite confusing. In fact, they're all simply just different
degrees of the same thing.

THE BEAUTIFUL ENGINEERING OF THE EQUINE FOOT

The anatomy of the foot is fairly simple to understand. The
coffin bone fits into the hoof and is attached to the inner hoof
wall by structures called the laminae and the basement membrane.
As any horse owner knows, a horse's hoof grows constantly. If
these structures connect the coffin bone and the hoof wall, how
does the foot grow?
"The hoof wall of a mature horse is in a constant state of
growth, much like your fingernails," says Dr. Pollitt. "With each
footstep, your horse wears down the part of the hoof that is in
contact with the ground - so his hoof must continually grow from
the coronet band down to replace wear and tear. The hoof wall
obviously needs to move while the coffin bone remains stationary.
What happens is a 'slipping' of the hoof wall along the coffin
bone at a molecular level through constant movement and
regeneration of the laminellar and basement membrane
connections." Enzymes are constantly at work within the foot to
assist this movement by helping to break down connections and
rebuild them.

Also important, the deep digital flexor tendon (DDFT) runs down
behind the knee or hock, cannon bone, fetlock and finally
attaches to the bottom tip of the coffin bone. The DDFT's
function is to exert a pull that lifts the horse's foot off the
ground with each step. This tendon remains tight and helps to
counterbalance the immense weight that a horse puts on its coffin
bone and the laminae with each step - unfortunately it is this
characteristic that later helps increase the damage of laminitis.

The blood supply to a horse's foot has special functions that
make it a very unique creation. There are two arteries that bring
oxygenated blood to capillaries that run throughout the foot. As
your high school biology teacher may have told you, all living
tissues - which include bone and muscles - require oxygen to
survive. The capillaries distribute the oxygenated blood
throughout all tissues of the foot. This blood is then returned
to the heart through two large veins that run parallel to the
arteries at the back of the foot. Your horse actually helps this
circulation occur with every footfall. It's toug to pump blood
uphill into the legs and back to the heart - a reason why many
horses become, stocked up when they stand in their stalls for too
long. But what really distinguishes the horse's hoof from other
animals is the system of shunts that are found just above the
hairline of the foot. These shunts connect the veins and arteries
along the coronary band and act as flow gates to the blood that
goes in and out of the foot - they can actually allow the blood
to bypass the foot completely.

"Normally, blood doesn't bypass the foot," writes Dr. Ramey, "but
the shunts do serve a useful purpose in certain circumstances. It
is thought that the shunts are there to help the horse regulate
the temperature of its feet. They allow the horse to adjust the
flow of the warm blood to the hoof, allowing for more or less
blood as environmental temperatures dictate."

Generally, the hoof is the same temperature as the environment,
however in situations of intense cold conditions, the temperature
of the hoof will hover one to two degrees above freezing.
Conversely, if it is really hot outside, the shunts may allow
less blood to enter the foot. "Shunts can become very important
in the horse with laminitis ... it's fair to say that the unique
and special features th characterize the blood circulation to the
horse's foot also make it a target for the numerous problems that
occur in laminitis."

The structures within the foot that researchers now know are
intimately involved in laminitis are the laminae and the basement
membrane. Dr. Ramey describes these structures in his book:


"The hoof and the coffin bone are connected. These connections
called the laminae are the only things that keep the the horse
from driving the coffin right on down into the ground. The
laminae link up like Velcrow; some of them arise from the inner
part of the hoof wall and others come from the living tissue
that's attached to the surface of the coffin bone. These
attachments between bone and hoof are simply thin little layers.
They interlock with each other in a manner not unlike the paper
that's around a popular peanut-butter and-chocolate candy cup.
There are hundreds of them inside each foot. A thin sheet of
tissue known as the basement membrane keeps these layers
attached. The basement membrane is the glue that holds the
laminae of the hoof to the laminae of the coffin bone. When
laminitis occurs, it's this basement membrane that seems to be
the target of the initial damage. When the basement membrane
starts to fall apart, the connections between the hoof and the
coffin bone may begin to give way, with some potentially
devastating consequences for the poor horse to which those
connections are attached."

WHAT GOES WRONG?

The physiology of what actually occurs in laminitis has not been
fully understood until the recent decade. It has been gleaned
mainly from research conducted by Dr. Pollitt who is regarded as
the leading researcher on laminitis. He describes laminitis as "a
spectacular disintegration of the laminae that attach the coffin
bone to the hoof."

But how does this disintegration begin? There are three main
theories of the causes of laminitis.

* Circulation Theory - The most widely held belief has been that
laminitis is caused by a triggered swelling in the foot that
results in a decrease in the normal blood flow to the foot. What
causes the swelling is unknown, as with the other theories. But
it is known that foot temperature decreases and there is no sign
of pain in the first stage of laminitis, suggesting a reduction
in the blood supply. However, microscopic sections taken from
horse's hooves in the first stage of laminitis show no blood
clots or swelling that should be there if this theory were
correct. As Dr. Ramey suggests, "there is little doubt that blood
flow to the foot is affected in laminitis but it's not known if
this is the primary cause."

It's one of those chicken or egg dilemmas. 

* Trauma Theory - More than just an injuries to the internal
tissues is what occurs under traumatic circumstance. Such is the
case in 'road founder,' - impact trauma can cause tearing in the
laminae in the hoof and blood vessel damage from excessive weight
trauma. It's different than normal laminitis in that it is a
mechanically induced version of laminitis. Dr. Pollitt states,
"When a horse has to bear a load constantly, the blood supply to
the foot is compromised to the point where laminitis is induced
by a lack of blood supply to the foot. Load, weight and the
unrelenting pull of the DDFT on the coffin bone causes this form
of laminitis. Supporting limb laminitis is also, seen in horses
that will not bear any weight on an injured limb. These horses
are prone to developing laminitis in the limb right next to it,
because that limb is bearing the most weight. Horses that hobble
or shuffle on the injured limb, periodically relieving the
weight-bearing foot are less prone."

* Enzyme Activation Theory - The third and most actively
researched theory has been a focus of Dr. Pollitt and the AELRU's
research. It is called the Enzyme Activation Theory and
challenges many of the previously held beliefs of the causes of
laminitis.

Initially there is a 'trigger event'. This can occur in any
system of the horse such as the intestine (too much grain),
reproductive (retained membranes), or circulatory (toxin or high
fever) systems. These events release something that researchers
call the trigger factor into the body. Currently the exact factor
is not known, but what is known is that this trigger factor
arrives to the foot via the circulation system and begins to
affect the basement membrane and laminae, eventually causing
their breakdown and hoof separation.

Within the foot there are enzymes that help hooves grow and
repair themselves from injuries. Enzymes are essential for
natural hoof growth and, under normal circumstances, their
production along with the natural enzyme inhibitors, complete
just one of many chemical cycles that occurs in the horse. In the
case of a horse with laminitis, there is a sharp increase in the
production of a proteindissolving enzyme called proteinase which
is normally responsible for helping the hoof to grow while the
coffin bone stays in the same place. With its increase, the
basement membranes and laminae connections break down at a vastly
increased rate.
As this breakdown occurs, the connections stretch out and weaken.
The weight of the horse presses down on the skeletal structure,
pushing the coffin bone down. The tension of the DDFT, now with
less resistance as the anchoring connections are destroyed, pulls
the tip of the coffin bone towards ground. As laminitis
progresses, it is often measured in degrees of rotation of the
coffin bone away from the hoof wall.

Now in the circulation system, the blood vessels begin to be
affected as tearing occurs inside the foot. "The destruction of
the capillaries does two things," says Dr. Pollitt. "First, it
causes a tremendous increase in the resistance to the flow of
blood. This has implications for the diagnosis of laminitis; it
means that blood is going to have a hard time getting into the
foot, and you may even be able to feel that such a thing is
happening. Second, it causes blood to bypass the capillaries.
This may have implications for the treatment of diagnosis."

TREATMENT AND DIAGNOSIS

"The key to treating laminitis under the enzyme activation
scenario is to try to slow down the enzyme activity and to try to
keep the factors that start the process from getting to the foot
in the first place," explains Pollitt. "It implies quite a
different therapeutic approach in the developmental phase of
laminitis." Where proponents of the circulation theory suggest
that an increase in circulation helps a laminitic horse, this
suggests that slowing down the blood getting into the foot may in
fact, be a better idea. The less of the 'trigger factor' that
gets into your horse's foot during this crucial phase, the less
breakdown that will occur.

Dr. Pollitt's research at the AELRU has discovered that when cold
water is applied in a specific manner to laminitis-induced
horses, they will not develop laminitis. To further prove this
treatment, laminitis was induced on horses which then had cold
water treatment on one front leg, but not the other - and only
the foot that was untreated developed laminitis. The practical
applications of this treatment are not yet fully developed for
the lay-horseperson. If the water is too cold and applied for too
long, you can risk damage to the tissues of the leg. While on the
other hand, if it is applied too late in the developmental stage
of laminitis there is a chance it will have no effect. This
compounds the fact that there is no effective way to identify
that laminitis is occurring until there are clinical signs such
as lameness or a visible rotation of the coffin bone on an x-ray.

For horses in the acute stages of laminitis, there is still hope
for recovery and management, even in the most severely affected
horses. In those horses, with extreme pain and rotation of the
coffin bone, surgery has been conducted with optimism that a
veterinary surgeon could correct the rotation of the coffin bone
and hopefully, allow the connections of the hoof to repair
themselves. What has been attempted - with limited success - is a
surgical treatment called a deep flexor tenotomy. This is the
practice of cutting the digital flexor tendon so that it releases
the constant tension on the coffin bone that pulls the bone
towards the ground.

Myron McLane, a Certified Journeyman Farrier who recently spoke
at the Western Canadian Equine Practitioners Conference in
Calgary, Alberta, explains that in his opinion, "Proper frog
support is the key to correcting the rotation of the coffin
bone."
One of the most common tools he uses in this case is a wedge or
heart bar shoe. "It relieves weight from the hoof wall and places
it on the frog and it helps preserve that crucial blood supply to
the foot," says McLane. "I feel that temporary frog support is
necessary right away, even a roll of gauze taped onto the bottom
of the foot to provide that immediate, temporary support is vital
until your farrier can come put on a more permanent shoe. In most
cases, it is almost too late - a wedge or heart bar shoe should
have been put on yesterday in horses that are becoming laminitic
to best counteract the pressure effects of laminitis and
therefore, protecting the blood flow."

McLane has gone so far as to create the Myron McLane Emergency
Wedge that fits between the hoof and a regular shoe to provide
that temporary, but crucial and immediate relief. "Remove all but
the toe nails on the foot, wedge this contraption in between the
shoe and the foot, and duct tape it on. This instantly provides
extra frog support."

Many vets, while agreeing that shoeing can be important in
managing laminitis, understand that no single approach is
the best for managing the condition. "Some horses do seem to
benefit transfer of weight to the frog, and there are
many ways to do that including pads or rolls of gauze," says Dr.
Ramey. "However, for some horses, heart bar shoes can make it
more painful although we are not sure why. Regardless, the heart
bar shoe does not somehow resist rotation of the coffin bone as
some have proposed."

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are "the most
commonly used drugs in the treatment of laminitis," writes Dr.
Ramey. First of all, they control the pain that a horse will feel
in the acute stages of laminitis. Secondly, they help to control
the inflammation and swelling that is occurring in the foot as
the basement membrane and lamellae tear apart. "In a rigid
structure such as the foot, there is no where for the swelling to
go and this can cause a number of problems."

Laminitis seems to be an individually treatable disease. There is
no one way to treat a laminitic horse. Some can cope with
medication, some with shoeing, while some will get better
"...despite our attempts to treat them," as Dr. Ramey intones.
"There is no best way for every horse. There's the way that seems
appropriate for each individual horse and a lot of that depend on
the experience of the person doing the treatment."

If your horse is in the acute stage of laminitis, Dr. Ramey
suggests you discuss the case with your veterinarian immediately
and consider, "Icing the feet, pulling the shoes, giving your
horse Phenylbutazone ('bute') and putting him in a stall with
deep sand. There is some percentage of horses that get better
with no treatment at all. So as long as you don't mess things up
with the treatment, they're going to get better. There are also
some horses that are going to do terribly no matter what you do.
In the former case, you can't ascribe success to a treatment and
in the latter case you can't ascribe failure to a treatment."

While treatment options can be confusing, owners need to seek out
the advice of an experienced veterinarian and an experienced
farrier before determining what the best course of action may be.


Get everyone working together and between the three of you, a
course of action will be established.

THE FUTURE OF LAMINITIS RESEARCH

The future is bright, claims Dr. Pollitt who continues to pursue
research opportunities relentlessly from his home in Brisbane,
Australia. The Australian Equine Laminitis Research Unit he
founded is currently researching the theory on laminitis that
basically states laminitis occurs when trigger factors produced
elsewhere in the body (gastro-intestinal tract, uterus, muscle),
travel via circulation to the feet. These factors trigger enzyme
activation that degrades hoof-coffin bone attachment apparatus.
"We hope to continue research in the future utilizing Magnetic
Resonating Machines (MRMs) and we hope that within three to four
years we will have a blood test to test for trigger factors that
is similar to the PSA test for prostrate screening in humans that
tests for prostate cancer markers." By developing a screening
test, veterinarians would be able to determine whether or not the
laminitis trigger factors were present in a horse's bloodstream
and therefore take action before any damage is done.

Phases of Laminitis 

Three distinct phases of laminitis are identified in afflicted
horses. 

Phase 1: Developmental - The separation of the laminae attaching
the coffin bone to the hoof begins. There are no obvious clinical
signs. This phase can last from around 12 hours in the case of a
toxin-caused laminitis or as long as 40 hours in the case of a
grain induced laminitis. 

Phase 2. Acute - This stage lasts from the first clinical signs
to when changes are visible on x-rays, or when the horse gets
better. It is a continuation of the disintegration of the laminae
and includes downward rotation of the coffin bone.

Phase 3: Chronic - This phase lasts indefinitely and ranges from
persistent and mild lameness to severe and unrelenting pain.

Horses do not recover from this phase though they can have their
pain managed.

..........


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