Download Conditions of the Foot Causing Lameness Part 1

Conditions of the Foot Causing Lameness
Part 1
Jim Schumacher
University of Tennessee
Navicular Disease
Navicular disease is a chronic lameness of one or usually both thoracic limbs associated
with pain arising from the navicular (distal sesamoid) bone and/or closely related structures,
including the collateral ligaments of the navicular bone, the impar (distal sesamoidean) ligament,
the navicular bursa, and that portion of the deep digital flexor tendon lying adjacent to the
navicular bone. Navicular disease, which was first described over 230 years ago, has been
estimated to be responsible for one third of chronic lameness. The nature of disease is not
understood but is characterized by signs of pain that can be localized to the foot by using
regional or synovial analgesia.
Anatomy and function
The articular surface of the navicular bone is covered w/ hyaline cartilage and articulates
with distal aspect of the middle phalanx. The flexor surface of the bone is covered with
fibrocartilage to provide a gliding surface for the deep digital flexor tendon, which also has a
fibrocartilaginous surface where it contacts the navicular bone. The proximal border of the
navicular bone is attached to the dorsal portion of joint capsule of the proximal interphalangeal
joint by the proximal suspensory ligament of the navicular bone, and distal border of the
navicular bone is attached to the palmar aspect of the distal phalanx by the impar ligament. The
distal border contains synovial invaginations, visible on radiographs, that were once considered
to be vascular channels. The navicular bone acts as a fulcrum to decrease the work of deep
digital flexor tendon, which exerts compressive force on the distal one-third of the bone. The
greatest force is on the bone during the propulsion phase of the stride.
Pathological changes of the navicular bone
Pathological changes of the navicular bone include adhesions between flexor surface and
the adjacent portion of the deep deep digital flexor tendon; erosions of the fibrocartilage of the
flexor surface, particularly over median ridge; and osseous metaplasia of proximal suspensory
ligament and the impar ligament. Some consider an increase in the diameter and number of
synovial fossae on distal border of the bone to be pathological changes, whereas others do not.
Theories of cause of navicular disease:
The pathogenesis of navicular disease is not known, but theories of its cause include the
vascular, or ischemic, theory and the biomechanical stress theory. The vascular theory, which
has never been substantiated, supposes that thrombosis or arteriosclerosis of distal navicular
arteries causes ischemia, which in turn, causes pain and may lead to necrosis of subchondral
bone. In response to ischemia, the number of vessels within the bone increases leading to
osteoporosis. The vascular theory is difficult to substantiate because pathological changes in the
navicular bone and clinical signs of navicular disease have not been reproduced by occluding
blood supply to the bone.
The biomechanical theory of navicular disease supposes that repetitious pressure of the
deep digital flexor tendon against the navicular bone or vibration between the deep digital flexor
tendon and the navicular bone that occurs during locomotion damages the fibrocartilage on the
flexor surface of the bone and inflames the navicular bursa. The hyperemia caused by bursitis
causes the navicular bone to demineralize.
Risk Factors
Navicular disease occurs in performance horses of all types, but the incidence is highest
in thoroughbreds, American quarter horses, and European warmbloods. The incidence is lowest
in Arabian horses and ponies. Although the disease can occur in horses 3 to 4 years old, it is
diagnosed most commonly in horses 7 to 14 years old. Geldings are most frequently affected.
Horses used for jumping or horses working on hard surfaces, such as carriage horses, seem to be
at increased risk of developing navicular disease. The incidence of navicular disease in highlevel competition horses appears to be lower than that in horses subjected to less demanding
athletic endeavors.
The shape of the navicular bone apparently affects the likelihood of occurrence of
navicular disease. Navicular disease is less likely to occur if the proximal articular border is
straight or convex. Horses with an undulating or concave proximal articular border have a
propensity to developing the disease. The foot conformation often associated with navicular
disease includes small feet, long toes, a broken-back hoof-pastern axis, under-run heels, and
sheared heels.
Diagnosis of navicular disease
Criteria on which navicular disease is diagnosed are controversial. Diagnosis is based on
history, clinical signs, a positive response to diagnostic tests, results of synovial and regional
analgesia, findings of diagnostic imaging, and rarely, results of endoscopic examination of the
navicular bursa. Navicular disease can be diagnosed most reliably by using magnetic resonance
imaging. Navicular disease often begins as intermittent lameness of one or both thoracic limbs
or a change in performance. Lameness caused by navicular disease may first become apparent
after a period of enforced rest. Lameness is generally most noticeable after the affected horse
engages in heavy work, but the lameness often improves with rest. The affected horse usually
performs worse on rough or hard surfaces.
The disease is manifested usually as lameness of both thoracic limbs but may be mistaken
as lameness of only one, because usually, one thoracic limb is more severely affected. The gait is
short and choppy (i.e., a “pottery” gait), and affected horses have a tendency to stumble. Horses
with navicular disease also have a tendency to land on the toes of the thoracic feet, which is
probably the result of increased contraction of the deep digital flexor muscle. Landing on the toe
increases the force in the deep digital flexor muscle and hence increases the compressive force
on the navicular bone.
Lameness caused by navicular disease is accentuated by turning the horse in a tight circle
on a hard surface, especially when the lamer limb is on the inside of the circle. Less commonly
lameness is accentuated when the lamer limb is on the outside of the circle. The horse may stand
pointing one thoracic foot and may alternate the foot that is pointed. The horse may pack
bedding beneath its heels and may even sit on objects, such as a manger, to decrease weight on
the thoracic feet. If lameness is consistently worse on one thoracic limb, the shape of the affected
feet may become asymmetrical. The lamer foot becomes narrower and has a longer heel.
Horses lame because of navicular disease often show a response to hoof testers applied
over the navicular area, but a lack of response does not rule out navicular disease, and a response
does not necessarily indicate that the horse has navicular disease. A horse lame because of
navicular disease may show signs of pain when hoof testers are applied to the toe if the horse has
been repeatedly overloading the toe. Lameness caused by navicular disease may be exacerbated
by hyperflexing the distal portion of the limb, but exacerbation of lameness is not pathognomic
for navicular disease, and lack of exacerbation does not rule out navicular disease.
Lameness caused by navicular disease is ameliorated by anesthetizing the palmar digital
nerves or by instilling local anesthetic solution into the distal interphalangeal joint or the
navicular bursa. Navicular disease cannot be diagnosed based solely on response to these blocks
because amelioration of lameness is not specific for navicular disease. Anesthesia of the palmar
digital nerve desensitizes the entire foot, except perhaps for the dorsal laminae, and anesthesia of
the distal interphalangeal joint also desensitizes the entire foot, provided 10 mL or more of local
anesthetic solution is instilled into the joint. Anesthesia of the navicular bursa desensitizes not
just the navicular bone and associated structures, it also desensitizes the toe of the foot and often
that portion of the deep digital flexor tendon located within the foot.
Nuclear scintigraphic examination of the foot has been used to detect disease of the
navicular bone, but its ability to detect soft-tissue injury is poor, and its accuracy is inversely
proportional to the amount of bone that is diseased. Radiographic examination of navicular bone
may aid diagnosis of navicular disease, but like nuclear scintigraphic examination of the foot, it
is unable detect abnormalities of soft tissue. Three common radiographic views are the lateral
view; the 60-degree, high coronary view or the similar, 80-degree, upright pedal view; and the
palmaroproximal-palmarodistal view.
Radiographic changes often seen include mineralization of proximal suspensory
ligament, which is seen as spurs on the wings of the bone; remodelling of the proximal and distal
borders; enlarged fossae on the distal border, which seems to be most significant if seen along
the wings of the bone; cysts; thinning or erosion of flexion cortex; and loss of the
corticomedullary junction. Contrast radiography of the navicular bursa may reveal thinning or
erosion of the flexor fibrocartilage, loss of dye column caused by adhesions between the deep
digital flexor tendon and the navicular fibrocartilage, and filling defects on the palmar aspect of
the bursa caused by fibrillation of the deep digital flexor tendon. The more the number of
radiological changes present in all radiographic projections, the more likely it is that the horse
has clinically evident navicular disease, but the absence of radiological abnormalities of the
navicular bone does not preclude the presence of pain associated with the navicular bone.
Computed tomographic imaging and magnetic resonance imaging of the foot are more
sensitive than radiographic imaging of the foot, but to use these methods of diagnostic imaging,
the horse often must often be anesthetized, and the equipment is often unavailable or too
expensive to use. One of the earliest and most reliable changes detected in the navicular bone of
horses with navicular disease by magnetic resonance imaging is accumulation of fluid within the
navicular bone. Endoscopic evaluation of the navicular bursa permits evaluation of the
fibrocartilage on the flexor surface of the navicular bone, the navicular bursa itself, the overlying
dorsal surface of the deep digital flexor tendon, and a portion of the impar ligament.
Treatment of horses for navicular disease
Treatment of horses for navicular disease is varied and controversial. Horses with
navicular disease can only be managed. They cannot be cured. Although lameness usually
improves with rest, rest is often not useful because lameness quickly recurs when the horse is
returned to exercise. One of the most common treatments is a change in shoeing. The horse
should be encouraged to land normally, rather than toe first, to avoid increased forces on the
navicular bone from the deep digital flexor tendon. Abnormalities of the foot causing
dorsopalmar and mediolateral imbalance should be corrected. Strain on the flexor tendon is
decreased by increasing the hoof angle by 2 to 4 degrees. Elevating the heels by 6% has been
shown to reduce the maximal force on the navicular bone by 24%. Egg-bar shoes provide
support for the heel and a greater surface area through which forces are transmitted and are
particularly useful if horse has run-under heels. Rolling the toes eases break-over and, therefore,
compression of the navicular bone by the deep digital flexor tendon. The Tennessee (navicular)
shoe, by nature of the rails on the palmar aspect of its branches, moves the point of breakover to
just dorsal to the apex of the frog. The owner should be made aware that improvement in gait
after corrective trimming and shoeing may take weeks and that if the horse already has a wellconformed foot, little is like to be achieved with changes in shoeing.
Systemic administration of anti-inflammatory drugs, such as phenylbutazone, may enable
the horse to remain in work. Treatment with this drug, or any other, may not be an option if the
horse is tested for drugs before or after competition. Warfarin therapy, which increases
coagulation time, used to be a popular, though dangerous treatment for horses with navicular
disease. Overdosing of warfarin or concomitant administration of warfarin and other drugs may
lead to severe and often fatal hemorrhage. This drug is rarely administered for treatment for
navicular disease because of complications associated with its use and because its efficacy in
ameliorating lameness has not been proven.
Isoxsuprine hydrochloride, a beta agonist that increases blood-flow by dilating the
peripheral vasculature, is sometimes used treat horses for navicular disease. Isoxsuprine’s mode
of action in the treatment of horses for navicular disease is unknown, but it may decrease pain by
improving the impaired venous drainage from the congested medullary spaces in the diseased
navicular bone. This drug may also have some anti-inflammatory or hemorheologic properties.
The treatment appears to be most effective in horses with no or mild radiological abnormalities.
Its use has waned because of lack of proof of efficacy and because studies have shown that orally
administered isoxsuprine may not achieve a therapeutic concentration in the circulation. The
usual oral dose is 0.6 mg/kg, administered twice daily for 30 days. If no response is seen within
30 days, the dosage can be increased to 0.9 mg/kg. Treatment with isoxsuprine should be
considered ineffective if the horse does not respond to the higher dosage within 30 days.
One of the most common medical treatments of horses for navicular disease is periodic
administration of a corticosteroid into the distal interphalangeal joint or the navicular bursa. The
results of this treatment may eventually become short-lasting. Instilling a corticosteroid into the
navicular bursa results in more horses becoming sound and staying sound for a longer time than
does instilling the corticosteroid into the distal interphalangeal joint. If the first injection of
corticosteroid is effective in alleviating lameness, regardless of whether it is placed into the distal
interphalangeal joint or into the navicular bursa, subsequent injections tend to be effective as
well, but lameness tends to recur after a shorter time with subsequent injections. Eventually,
horses become non-responsive to injection of the corticosteroid. Occasionally, a horse may show
signs of pain immediately after the navicular bursa has been injected, but horses showing signs
of pain can usually be managed by administering a non-steroidal, anti-inflammatory drug. Some
horses experience transient lameness at 3 to 4 days after injection, possibly because tearing of
adhesions in the bursa after improvement in lameness. Temporary resolution of lameness after
injection may be followed by occurrence of a more severe lameness because of severe
exacerbation of tendinopathy of the deep digital flexor tendon, which perhaps was unrecognized
at the time of injection, due to increased weight-bearing after improvement of lameness.
Sarapin, a suspension of powder from the pitcher plant (Sarracenia purpurin), has been
injected around the palmar digital nerves to provide temporary relief from pain caused by
navicular disease, but scientific evidence of the efficacy of this drug in ameliorating sensory
innervation to painful regions is lacking. Bisphosphonate drugs, such as tiludronate, regulate
metabolism of bone by inhibiting bone reabsorption by inhibiting the action of osteoclasts.
Tiludronate has been used in horses to help prevent the excessive bone reabsorption associated
with navicular disease, identified on radiographic images of the navicular bone as radiolucent
areas. Tiludronate has been dosed intravenously at 0.1 mg/kg daily for 10 days (total dose, 1
mg/kg), but more commonly, the total dose of 1 mg/kg is administered as a single injection.
Optimal improvement of lameness is observed between 2 and 6 months after the onset of
treatment. If improvement in lameness is insufficient, a second treatment is administered. The
effect of treatment tends to diminish after 6 months. Some practitioners administer 1/10 to 1/3 of
the systemic dose by regional, intravenous perfusion into a palmar vein at the level of the pastern
or the proximal sesamoid bones. This allows similar concentrations to be achieved locally for
less expense. The more recent the onset of clinical signs at the time of treatment, the greater is
the efficacy of the drug. This drug is unavailable in the USA.
Surgical treatments for horses with navicular disease include sectioning the proximal
suspensory ligaments of the navicular bone and palmar digital neurectomy. Sectioning the
proximal suspensory ligaments of the navicular bone supposedly decreases stress on the
navicular bone, but its effect may be from cutting sensory nerves to navicular bone that traverse
these ligaments. Palmar digital neurectomy is usually performed as a last resort to relieve
lameness caused by navicular disease. Complications include failure to alleviate lameness,
recurrence of lameness from regrowth of nerve, formation of a painful neuroma, failure to
recognize subsolar infection, and rupture of deep digital flexor tendon, resulting in subluxation
of the distal interphalangeal joint. Slough of the hoof capsule has also been reported, but this
complication occurs only after one or more subsequent surgeries to transect the palmar digital
nerves. The simple guillotine technique results in the longest period of desensitization and less
likelihood of formation of a painful neuroma compared to the technique of epineural capping and
dividing the nerves using a carbon dioxide laser. Neurectomy provides relief from lameness in
approximately 65% to 70% of horses for approximately 12 to 18 months.