|
A Practical Approach To Treating Laminitis
Stephen E. O'Grady, DVM, MRCVS
Laminitis is among the most devastating and
crippling diseases that affect horses. This disease often
accompanies or follows a primary disease process that affects
another body system, such as the gastrointestinal,
respiratory, reproductive or musculoskeletal system. Many
different forms of therapy have been proposed over the last
twenty years, yet no one treatment appears to be consistently
effective. The primary disease process can lead to a
pathologic response within the foot, resulting in decreased
capillary perfusion, ischemia and necrosis of the laminae.
Common disease processes and other factors contributing to
laminitis include colic, enteritis, pleuritis, retained
placenta, grain overload, exhaustion, corticosteroid
administration and exposure to black walnut shavings. In
addition, vascular disruptions in the foot are occasionally
caused by direct hoof trauma, such as excessive concussion or
subsolar bruising from improper trimming.
Laminitis can be classified as uncomplicated or complicated,
depending on the horse's response to therapy1. Most cases of
laminitis are uncomplicated. In these cases, the horse
responds favorably regardless of the therapy. The remainder of
laminitis cases are complicated-the patient fails to respond
to prompt, aggressive medical treatment. These horses have a
guarded prognosis. The cause of the laminitis often determines
whether the case is complicated or uncomplicated. The severity
of the initial damage to the laminae is the most important
factor affecting the outcome of the case.
Pathogenesis
Recent research findings have increased our understanding of
the physiologic response within the foot during laminitis, but
a single agent has not been identified as the specific
mediator for triggering laminitis. The blood flow to the
dorsal laminae primarily moves in a palmar to dorsal and
distal to proximal direction. This flow against gravity
probably predisposes the dorsal laminae to ischemia. In
addition, the arteriovenous anastomoses, which are under
adrenergic neuronal control, will open, shunting blood away
from the capillaries and increasing blood flow to the foot.
The increase in blood flow accounts for the elevation in
digital pulse pressure and heat during the early phases of
laminitis.
Alterations in capillary perfusion may also be attributed to
venoconstriction caused by an unknown vasoactive mediator,
which acts to increase precapillary and particularly
postcapillary resistance. Increases in capillary bed vascular
resistance allow fluid afflux from the vasculature into the
interstitial tissue of the laminae. Increases in interstitial
pressure further impede capillary blood flow and lead to
ischemia4. Ischemia, impeded capillary blood flow, and
increases in interstitial pressure contribute to the
development of microthrombosis.
Dr. Chris Pollitt's latest work suggests the activation of a
lammelar enzyme ("MMP-2") may be responsible for the
separation in the secondary lamina.
These mechanisms (shunting of blood away from the laminar
capillaries, digital venoconstriction and toxic effects on the
lamina), which may be interrelated, lead to ischemia of the
secondary laminae, which results in laminitis. If the disease
process is allowed to continue, laminar necrosis will ensue
and disrupt the laminar bond between the hoof wall and the
distal phalanx, leading to a mechanical change within the hoof
capsule. The downward load through the bony column of the
affected limb, coupled with the distractive force of the deep
digital flexor tendon on the palmer aspect of the distal
phalanx, results in rotation, or distal displacement, of the
distal phalanx.
Radiographic Evaluation
Radiographic evaluation should be an integral part of the
management of a laminitis case. In order to detect subtle
changes within the hoof capsule, high-quality radiographs must
be obtained. A uniform technique should be used for the
initial and subsequent radiographs. Because variations in
technique affect subsequent interpretation of radiographs
(specifically the distance and angle measurements), it is
essential to standardize the radiographic procedure in order
to detect small changes that may occur between examinations.
For a lateromedial radiograph, I prefer using a 3-in thick
wooden positioning block with a wire embedded longitudinally
in the top.Another wire is taped vertically to the dorsal
surface of the hoof wall. These wires allow accurate
measurements to be determined within the hoof capsule. A
consistent focal spot-to-film distance will eliminate one
source of film exposure variability, and a line level placed
on top of the machine will maintain a level primary beam. The
primary beam is centered midway between the toe and heel, 2 to
3 cm above the bottom of the foot.
One of the earliest radiographic signs of developing laminitis
is an increased distance between the dorsal cortex of the
distal phalanx and the hoof wall. Tis distance should be less
than 18 mm in the normal horse. An increase in this distance
indicates laminar swelling and early laminar degeneration.
Another early radiographic indication of laminitis is a change
in the position of the coronary band. On a lateral radiograph
of a normal foot, the coronary band is positioned over the
hoof wall. With the laminitic changes, a soft tissue
depression appears on the radiograph at the usual site of the
coronary band7. Ventral rotation of the tip of the distal
phalanx away from the hoof wall and distal displacement of the
extensor process with respect to the coronary groove can also
be seen radiographically in laminitic horses.
The phases of laminitis and corresponding treatment
Laminitis can be arbitrarily divided into three phases:
developmental, acute and chronic. Specific therapy can be
directed toward each phase.
The developmental phase The developmental phase begins
when the horse is affected by one of the primary disease
processes or factors previously discussed and ends when
clinical signs of lameness appear. Treatment during the
developmental phase attempts to prevent clinical laminitis.
During this phase of the disease, there are few clinical signs
other than an increased digital pulse and warm hooves. The
radiographic signs are usually normal during this phase.
Treatment is therefore based upon the probability that
laminitis will occur.
Therapy during the developmental phase is directed toward
eliminating the inciting cause and increasing blood flow to
the secondary laminae. Using some form of foot support to
protect the laminae should be considered.
Removal of the inciting cause may entail dietary changes or
the administration of mineral oil, antibiotics, intravenous
fluids or hyperimmune anti-endotoxin serum. Anti endotoxin
serum has been successful in preventing the onset of laminitis
when administered at the same time carbohydrate overload is
induced in experimental horses9.
Vasodilation of the secondary laminae may be accomplished with
the use of alpha-adrenergic antagonists such as acepromazine
and phenoxybenzamine for three to five days, unless signs of
the acute phase appear. In my experience, acepromazine appears
to be effective at a dosage of 0.06 mg/kg intramuscularly,
three times daily. Phenoxybenzamine provides prolonged action,
but is not readily available. When this drug is administered
intravenously at a dosage of 0.66 mg/kg, diluted in sterile
saline solution, vasodilatation will last 12 to 24 hours. (If
hypovolemia and shock are present, it is imperative that these
conditions be treated appropriately [e.g. isotonic intravenous
fluid administration] before vasodilator therapy is
initiated.)
Heparin (40 to 70 units/kg given subcutaneously b.i.d.) has
been effective in preventing laminitis when administered
during the initial stages of the disease5. Aspirin (5 to 10
mg/kg every other day) can be administered for its
antiplatelet effect. Flunixin meglumine may be beneficial when
used at the anti-endotoxin dose of 0.25 mg/kg given
intravenously four times a day.
The acute phase The acute phase of laminitis begins
just after the onset of clinical signs of lameness. These may
include a marked digital pulse, warm hooves, a painful
response to a hoof tester examination, the characteristic
laminitic stance and lameness, which is classified using the
Obel grading system.
With Obel grade 1 lameness, the horse constantly shifts its
weight from one leg to the other. Lameness is not noticed at a
walk. But at a trot, the horse's gait is stiff and stilted.
Obel grade 2 lameness is characterized by a stiff, stilted
gait at both a walk and a trot. A front foot may be lifted of
the ground without difficulty. With Obel grade 3 lameness, the
horse exhibits a markedly stiff, stilted gait; is reluctant to
move; and resists attempts to lift a front foot. When Obel
grade 4 lameness is present, the horse refuses to move unless
forced and spends much of its time recumbent.
Lameness in the acute stage is due to pain and inflammation
from ischemia of the secondary laminae. The severity of the
lameness relates to the severity of the damage to the laminae.
The acute phase lasts 48 hours or until movement of the distal
phalanx occurs10.
Therapy (medication and foot care) during the acute phase is
directed toward relieving pain and preventing rotation of the
distal phalanx.
Drug therapy Since systemic hypertension and peripheral
vasoconstriction are coincident with the pain, it is important
to begin or continue vasodilator therapy in the acute phase.
In addition, anti-inflammatory therapy is important in
decreasing laminar edema, easing pain, and therefore
indirectly aids circulation. Nonsteroidal anti-inflammatory
drugs (NSAIDs) are the most effective drugs for treatment of
acute laminitis. Phenylbutazone and flunixin meglumine are
most commonly used.
Phenylbutazone may be the most effective of the NSAIDs for the
treatment of acute laminitis. The initial dose is 4.4 mg/kg
given orally or intravenously twice a day. After the pain has
lessened and other clinical signs have improved, the horse is
then maintained on 3 g of phenylbutazone divided into two
daily doses to reduce the possibility of gastrointestinal or
renal damage. Flunixin meglumine can be administered at a dose
of 1.1 mg/kg orally or intravenously, twice a day for three to
five days. Dimethyl sulfoxide (DMSO) is another potent
anti-inflammatory agent that can be administered once or twice
daily for three days. DMSO (1 g/kg diluted in 3 liters of
saline) administered by nasogastric tube may reduce edema in
the laminae. It may also be helpful in reducing laminar
inflammation because of its activity as an oxygen or hydroxyl
radical scavenger. The use of 2 percent nitroglycerine patches
placed on the palmar or plantar aspect of the pastern to
dilate the digital vessels have been described. The benefit of
these patches has not been proven. Gloves must be worn during
the application of the nitroglycerine ointment, as it is a
potent vasodilator in humans as well, and can be absorbed
through the skin. Because of the implications for
contamination of the person applying the drug, liability
issues may make it unwise to dispense nitroglycerine for owner
use. The use of aspirin is initiated or continued at the dose
of 5 to 10 mg/kg every other day.
Foot Care The horse must be confined to a stall.
Methods of foot care at this stage are aimed at supporting and
protecting the compromised laminae. Shoes are never used at
this stage. Removing excess toe length (beveling the hoof wall
at the toe back to the white line) will decrease the bending
force or lever arm exerted on the laminae. Foot support should
utilize all of the structures in the caudal part of the foot,
but secondary support can also be helpful in the solar area.
Sand has always been a readily available, inexpensive and
often-effective form of foot support. It provides even support
over the entire ground surface of the foot and allows the
animal to angle his toes down into the sand, changing the
angle of the fetlock and decreasing the tension on the deep
digital flexor tendon.
Recently, the use of 3-in industrial styrofoam has become
popular as a form of foot support. (See" how to" apply foot
support) It is easy to apply, very forgiving and provides good
support. The emphasis of the weight bearing is placed on the
structures of the heels, which allows support to be placed
under the sole. Another easy method of foot support is to use
a 4o wedge pad. Draw the outline of the foot on a wedge pad,
extending to the bulbs of the heels. Cut the wedge pad
following the outline. Fill the bottom of the foot with dental
impression material and place the pad on the foot using a few
small nails or tape. This method provides the best heel
elevation.
A third method of foot support is to use 3-M Custom Support
Foam®. The roll of foam is folded in layers the width of the
bottom of the foot, ending up with more folds in the heel
area. The foam is then placed in water and the horse is then
made to stand on it so that it forms a contour to the bottom
of the foot. After it dries, it is trimmed around the
perimeter and taped to the bottom of the foot.
All of the above methods are easy to apply, provide firm but
forgiving support and allow easy removal to examine the bottom
of the foot. All three methods can be used to provide mild
heel elevation, which is important in that it reduces one of
the distractive forces caused by the deep flexor tendon.
The horse should remain on one of the above forms of support
until it becomes comfortable and medication is reduced or
eliminated. Only at this point should shoes be applied. The
use of foot support allows medical therapy to be more
effective in relieving pain and increasing capillary
perfusion.
The chronic phase The chronic phase of laminitis begins
when rotation of the distal phalanx occurs. Therapy at this
stage depends on the severity of the damage to the laminae
within the digit. Therapeutic shoeing to re-establish correct
alignment of the distal phalanx and hoof capsule and to
establish appropriate support of the skeletal column is
imperative. If the damage to the laminae is extensive and the
patient is unresponsive to therapeutic trimming and shoeing, a
deep digital flexor tenotomy can be performed.
Conclusion Currently, there is no single treatment that
can be recommended for all cases of laminitis. The severity of
the laminar damage cannot be predicted in the initial phases
of the disease. If the ischemic insult is severe enough, no
systemic treatment or foot therapy will prevent rotation of
the distal phalanx. I believe systemic treatment instituted
before the appearance of clinical signs of laminitis to be the
best hope for preventing severe laminar damage. Successful
therapy of laminitis requires teamwork between the owner,
veterinarian and farrier. When this group is willing to spend
the time and effort, treatment of these cases can be
rewarding. However, without their joint dedication, treatment
is frustrating and usually ends with euthanasia of the horse.
|
|
|
