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T H E
S T A N D A R D S
O F
JANUARY 2012
UPCOMING CONTINUING EDUCATION
LECTURES FOR DOCTORS &
TECHNICIANS
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soon. Please go to www.IVGHospitals.com and
follow the links for veterinary teams and
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V E T E R I N A R Y
C A R E
VOLUME 12, ISSUE 1
Diagnosis and Treatment of
Bradycardia
Written by John MacGregor, DVM, DACVIM (Cardiology)
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Corneal Transplants
Written by Nicholas Cassotis, DVM, DACVO
SAVE THE DATE
5TH ANNUAL IVG SYMPOSIUM
|6|
Join us on Sunday April 29 for our 5th Annual
Symposium.
The day will consist of dry-labs, wet-labs
and expanded lecture content, offering both
doctors and technicians the opportunity to
create a personalized learning plan of up to
6 CE credits from 18 total hours of RACE
approved CE. More information will be
posted online soon.
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Tarsal Osteochondrosis
Written by Robert B. Hillman, DVM, MS, DACVS
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Our newest 24 hour emergency
& specialty referral hospital:
IVG MetroWest is now open in
Natick, MA. If you’re in the
neighborhood, drop in for a tour!
Diagnosis and Treatment of
Bradycardia
ABNORMAL BRADYCARDIA IN DOGS CAN BE DUE TO
primary cardiac causes or can be caused by factors
outside the heart. Broadly, the causes could be related
to a pathologic arrhythmia, external causes such as
hypothermia, metabolic causes (which might include
an Addisonian crisis or urinary obstruction, among
other potential causes), or vagally mediated
bradycardia. Care must be taken not to confuse a
sinus bradycardia, which can be as low as 30 bpm in a
dog in deep sleep or 50 bpm in an awake dog, with a
pathological rhythm. Additionally, most bradycardias
are not treated unless they result in clinical signs.
Clinical signs generally consist of collapse, episodic
weakness or lethargy. Treatment for metabolic and
external causes of bradycardia consists of correcting the
primary conditions and will not be discussed further.
DIAGNOSIS OF BRADYCARDIA
Often an “in-room” ECG can determine the cardiac
rhythm that results in bradycardia. However, bradycardia
can be intermittent and sometimes more extensive
testing is required. A normal in-room ECG does not rule
out bradycardia as the cause for a collapse. A 24 hour
ambulatory ECG monitor (Holter monitor) or an event
recorder could be used to determine if a bradycardia
exists. A Holter monitor records 24-72 hours of
continuous ECG data. This data is recorded either on a
cassette tape, or digitally. The patient has 5-7 electrodes
placed on their skin and carries the monitor for the
duration of the testing period (figure 1). The data from the
monitor is analyzed and a catalogue of the rhythm is
generated via a computer program. A Holter monitor is
most useful for determining the severity of arrhythmia
present in the testing period, or in determining efficacy of
anti-arrhythmic therapy. In contrast, an external event
loop recorder (figure 2) has two electrodes and is worn for
up to one week at a time. It records continuously, but
does not save data until a button on the recorder is
pressed by the pet owner during an event. The recorder
then saves an ECG loop. Since the data saved is a loop, it
contains ECG recording for several seconds prior to the
button being pushed, the ECG when the button was
pushed and the ECG for several seconds after the button
was pushed. This enables the event recorder to “reach
|2|
John MacGregor, DVM, DACVIM (Cardiology)
Dr. John MacGregor practices at
Massachusetts Veterinary
Referral Hospital in Woburn, MA
and Port City Veterinary Referral
Hospital in Portsmouth, NH.
back in time” to capture the ECG that was most likely to
be associated with the clinical signs exhibited by the
patient. These event recorders can be worn for up to a
week at a time, and are most useful when the patient is
having two or more events per week, but has a normal
rhythm most times. The final option is an implantable
loop recorder (figure 3). This is a device that is implanted
subcutaneously, and can be programmed to record all low
and high heart rate events. The data is read and
programmed via an external unit, and can be utilized to
determine whether rhythm events are the cause of rare
collapse events.
TYPES OF BRADYARRHYTHMIAS
Vagal stimulation to the heart and blood vessels can
result in bradycardia and hypotension (i.e. reflex cardiac
slowing +/- peripheral vasodilation). In dogs, these
episodes are typically brought on by either coughing,
exertion or excitement. This can occur in normal healthy
animals or in animals with cardiac disease. It commonly
occurs in small breed dogs with advanced mitral valve
disease. An atropine response test can be used to
determine the influence of parasympathetic (vagal) tone
on the heart rate and rhythm. Atropine is a competitive
antagonist of the muscarinic acetylcholine receptors that
acts as a parasympatholytic and as such abolishes or
diminishes the influence of the vagus nerve on heart rate.
This leads to increased firing of the sinus node and can
increase conduction through the AV node if this is being
inhibited by high vagal tone. In this test, a baseline ECG is
recorded and then 0.04 mg/kg of atropine is administered
intravenously. Ten to fifteen minutes later a follow up ECG
is recorded. If the rhythm abnormality is due to high vagal
tone, the heart rate in follow up ECG should be
significantly faster and the abnormalities should
normalize; often the result is sinus tachycardia. In this
patient, atropine administration did result in sinus
Figure 1. 24 Hour Ambulatory
tachycardia (figure 4).
ECG Monitor. Note cassette tape
Bradycardia can also be caused by atrioventricular (AV)
block. In first degree AV block, the atrial impulse is
abnormally delayed resulting in a prolonged P-R interval
and does not result in bradycardia. In second degree AV
block one or more of the atrial impulses does not pass
through the AV node. There are two types of second
degree AV block – Mobitz type I and Mobitz type II. In
Mobitz type I second degree AV block there is successive
prolongation of the P-R interval with each beat until one P
wave is blocked completely. First degree AV block and
Mobitz type I AV block do not cause clinical signs and
generally are not treated. In Mobitz type II second degree
AV block, prolongation of the P-R interval does not occur
prior to the P wave being blocked. Mobitz type II second
degree AV block can be described by the ratio of total P
waves to conducted P waves. As an example, when only
every 9th P wave is conducted, it is called 9:1 second
degree AV block (figure 5). Mobitz type II second degree
AV block can cause clinical signs depending on the
severity of the AV block.
In third degree AV block, none of the P waves are
conducted through the AV node (figure 6). Ventricular
depolarization occurs secondary to development of an
“escape rhythm” that emanates from pacemaker cells
either in the more distal part of the AV junction (the His
bundle), or in the ventricles. When the escape rhythm
emanates from the AV node or Bundle of His the QRS
complexes are narrow with an escape rate of 40 to 60
bpm. When the escape pacemaker is in the ventricular
myocardium, the QRS complexes appear wide and
bizarre, and the escape rate is 20 to 40 beats/minute.
Third degree AV block is more common in older animals,
but can occur at any age. Patients may present for
lethargy, exercise intolerance or collapse. At times it is
difficult to distinguish between high grade second degree
AV block and third degree AV block, calling it advanced AV
block suffices as it describes both conditions.
Sinus arrest is defined as a failure of a normal impulse to
be formed in the sinus node owing to a depression of
automaticity in the sinus node (figure 7). This is often
where ECG data is stored,
battery compartment and ECG
cable. The ends of the ECG leads
are attached to self adhering
electrode patches on either side
of the thoracic cavity at the level
of the 4-6th intercostal spaces.
Figure 2. External Event Loop
recorder. Note two electrodes that
are attached to self adhering
electrode patches on either side of
the thorax. Electrodes are placed
over the heart in the middle of the
thorax. Note “Record” button in
center of recorder. In the event of a
collapse episode, the patient’s
owner presses the button and the
ECG loop that was recorded is
stored. This data is then transferred
transtelephonically and an ECG is
generated.
Figure 3. Implantable loop
recorder. Note the US dime (18
mm) placed in picture for size
reference. The event recorder is
placed subcutaneously and stays
in the patient for many months.
The event recorder can be
programmed to record high and
low heart rate incidents, and a
remote control device can be
utilized by the owner to mark
events in the memory.
difficult to distinguish from sinus node block in which the
impulse is formed normally, but a conduction abnormality
exists preventing the impulse from reaching the rest of
the heart. Both result in pauses where no P wave is seen.
In sinus block, the R-R length of the pause is an exact
multiple of R-R intervals preceding the pause, whereas in
sinus arrest, the pause can be any length greater than
two R-R intervals. In practice, it is often quite difficult,
and clinically irrelevant, to distinguish between the two
underlying causes of lack of P wave formation and the
resultant ECG is simply called sinus arrest. Sinus arrest
is sometimes a component of sick sinus syndrome (aka
bradycardia/tachycardia syndrome) in which periods of
sinus arrest alternate with periods of sinus tachycardia.
TREATMENT OF BRADYARRHYTHMIAS
If there is a positive response to atropine, several oral
medications may be utilized to help normalize the
rhythm. Propatheline bromide is a quaternary
antimuscarinic anticholenergic that can be given orally
three times daily at a dose starting at 7.5 mg/patient q 8
|3|
>continued
Diagnosis and Treatment of Bradycardia
Figure 4. ECG obtained 15 minutes after atropine administration as part of atropine response test. (lead II, 25
mm/sec, 1mV = 10 mm). Heart rate is 150 beats per minute and rhythm is sinus tachycardia. This indicates a
positive response to atropine and demonstrates that the arrhythmia was at least partially due to high vagal tone.
Figure 5. Example of 9:1 second degree
AV block. (lead II, 25 mm/sec, 1mV = 10
mm). Single headed arrows indicate P
waves and arrow heads indicate QRS
complexes. Double headed arrows
demonstrate the P-R interval from the
conducted (ninth) P waves.
Figure 6. Third degree AV block. (lead II,
25 mm/sec, 1mV = 10 mm). Single
headed arrows indicate P waves. Double
headed arrows demonstrate the P-R
interval. Note variable P-R interval that
is consistent with third degree (complete)
AV block.
Figure 7. ECG (lead II, 25 mm/sec, 1mV =
10 mm) Arrows indicate P waves that are
blocked (no QRS complex follows the P
waves). Arrow head demonstrates a
ventricular escape beat. The “A” distance
is a period of sinus arrest of 3.6 seconds.
Complex “B” is a premature
supraventricular complex.
Figure 8. ECG obtained after 1 week of propantheline bromide therapy. (lead II, 25 mm/sec, 1mV = 10 mm). Heart rate is
75-150 beats per minute and rhythm is sinus tachycardia with Mobitz type II second degree AV block present. Arrows
represent blocked P waves.
|4|
Figure 9 Pacemaker generator (GEN) and lead (Lead). Note active fixation, screw in
type tip (AF) and bipolar sites (arrows).
10.b
10.a
Figure 10 Thoracic radiographs post-pacemaker implantation. a. Right lateral thoracic radiograph showing the pacemaker generator
(Gen) within the right lateral neck. The pacemaker lead then courses from the generator through the subcutaneous tissues, right
jugular vein (Right Jugular), cranial vena cava (CrVC), right atrium (RA) and finally into the right ventricular apex (RV) where the lead
tip comes into contact with the right ventricular endocardium. b. Dorsoventral radiograph showing the same features with the labels
identifying the same structures.
hours. This can be increased to 30 mg/patient q 8 hours
as needed. Common side effects are dry mouth and eyes,
anxious behavior and GI signs. Hycosamine, an
anticholinergic alkaloid, can also be utilized at 0.003 to
0.006 mg/kg q 8 hours (figure 8).
In most cases of advanced AV-block, pacemaker therapy
is required. Positive chronotropic medications can be
administered such as theophylline (5-15 mg/kg PO BID of
the extended release formulation) or terbutaline (0.2
mg/kg PO BID-TID). However, response is variable and
almost always unrewarding with third degree AV-block.
The critical components of a pacing system include a
pulse generator, which has been programmed
appropriately, and a pacing lead (figure 9). The cardiac
pacemaker functions as an electrical circuit whereby the
pulse generator (battery) provides electrical stimulation
that travels through the pacing lead to the myocardium
and then back to the battery to form a complete circuit. All
pacemaker systems have two poles. Bipolar pacemaker
leads are most commonly used and create a smaller
circuit with both poles located near the end of the
pacemaker lead. Unipolar leads have one pole located
near the end of the lead with the other pole encompassing
the metal of the pacemaker generator. Unipolar leads
therefore contain a larger circuit of electricity and can
trigger activation of surrounding musculature. Bipolar
leads only trigger stimulation of the ventricular
myocardium and are less likely to pick up stray signals
from the environment. In dogs, transvenous pacemakers
are utilized almost exclusively (figure 10), whereas in cats,
epicardial pacemakers are used more frequently due to
increased potential for chylothorax in this species.
|5|
Corneal Transplants
Nicholas Cassotis, DVM, DACVO
THE BEAUTY OF THE CORNEA IS IN ITS
clarity. This avascular, thin, anterior-most
tissue of the eye serves functional and
structural roles. Functionally it allows
light/image entry and begins the focusing
process of the image. Without clarity of the
cornea image distortion occurs and vision
becomes compromised. Diseases/traumatic
processes that put the clarity of the cornea at
risk must be halted early to prevent the onset
of disruptive wound healing steps.
Corneal fibrosis, pigmentation, and vascularization
are examples of healing responses that can help
stabilize a wound, but in the process rob the patient
of vision. The structure of the cornea protects the
intraocular environment. Despite its thin measure,
it imparts incredible strength. Because of the
strength of the stroma it is able to withstand blunt
trauma and degenerative processes (to a point)
before rupture.
The goals of treating corneal disease are to restore
both functional and structural roles of the cornea.
Rapid wound healing of superficial ulcerations
without vascularization is one example. Another is
instituting aggressive treatment to resolve infectious
or inflammatory disease as to prevent the onset of
scar tissue or stromal thinning.
Corneal disease resulting in defects within the
corneal stroma are a common part of ophthalmic
practice. The loss of the structural stroma is
worrisome as it raises the risk of rupture (figure 1).
When this occurs procedural options should
embrace the goals of structure and clarity as much
as possible. Various corneal grafting techniques are
available; however when a central visual field lesion
occurs, the option of corneal transplantation must
be considered.
The most common type of corneal restructuring
graft is the conjunctival pedicle/advancement flap.
The techniques are suited primarily for restoring the
|6|
Dr. Nick Cassotis practices at
Port City Veterinary Referral
Hospital in Portsmouth, NH.
corneal strength (marginal at best though), but is a
very poor optical choice. These grafts rarely result in
clarity (figure 2). Their value however lies in the rapid
vascular supply to a degenerating wound that either
has perforated or is at high risk of rupture. In
wounds that are stable and non-progressive other
techniques should be considered.
A variation of the conjunctival graft that allows the
surgeon to bring optical clarity and reconstructive
strength to central corneal lesions is the
corneocon-junctival transposition (CCT). This
procedure uses the disease free peripheral cornea
for reconstruction of the central wound. The
resulting peripheral wound is then filled in with
limbal and conjunctival tissue. Rejection of the graft
is very uncommon since it is autogenous tissue.
Additionally autogenous partial thickness grafting is
used when a region of significant thinning is present
centrally and peripheral clear is available. This
ultimately results in two partial thickness defects
within the same cornea. Again the advantage of the
procedure is that of acceptance of autogenous
transferred tissue, clarity and improved strength
(figures 3 and 4).
If the disease or trauma results in large (wide and
deep) defects in the corneal stroma, use of
autogenous tissue is not an option. Corneal
transplants from like species becomes an excellent
alternative. Most commonly in veterinary surgery
Figure 1: Descemetocele.
Figure 2: Persistent vascularization following
conjunctival grafting.
partial thickness grafting techniques are available
and are limited only by the availability of donor
tissue. Donor corneal tissue comes from animals
who have passed on and whose guardians have
given permission for collection. The donors have
been screened to ensure prior corneal disease was
not present. Donations are greatly appreciated gifts
for patients who are in need.
Currently transplanted corneal tissue is used for
reconstruction of corneal sequestra (figure 5),
descemetoceles (figure 1), deep corneal defects, and
severe central corneal scarring. For patients with
descemetoceles or epithelialized deep corneal
defects (severe stromal thinning), the use of partial
thickness tissue transplants is ideal. These partial
thickness grafts are especially desired when the
defects involve the cornea within the visual axis. Full
thickness techniques are rarely used in veterinary
surgery.
The technique for a lamellar keratoplasty involves
removal of the anterior portion of the donor corneal
stroma and epithelium. The thickness of the donor
graft depends fully on the depth of the recipient’s
wound. Therefore deep anterior lamellar
keratoplasty involves dissection to the level of, but
does not include) Descemet’s membrane. Lamellar
keratoplasties are for less deep defects. Prior to the
transfer, the recipient bed was prepared and
measurements taken to ensure proper fit. The
Figure 3: Use of partial thickness corneal
autograft to repair a descemetocele.
Figure 4:
Customized fit of
corneal autograft.
donor tissue is then transferred onto the
anesthetized patient’s cornea. The corneal graft is
sutured in position with 9-0 Ethilon and less
commonly with absorbable 9-0 Vicryl to ensure
stability during recovery (figures 6 and 7).
Post operative care for the transplant patient is no
more complicated than that of other corneal
procedures. Topical antibiotics and oral pain
medications are commonly dispensed. The initial
goal is to ensure the graft is not at risk of infection.
Epithelialization of the graft helps to keep surface
bacterial contamination to a minimum. The next
phase of recovery is to limit the degree of
vascularization in order to maintain the clarity of the
graft (figure 8). This may require longer term
medication, but life time medications are rare.
Ultimately the clarity of the graft can be excellent
and supersede the results of vascularized grafts
(figure 9).
|7|
>continued
Corneal Transplants
Figure 6: Deep lamellar
graft from donor being
placed after excision of
the corneal sequestrum.
Figure 5: Feline corneal
sequestrum prior to surgery.
Figure 7: Immediate post-op appearance of deep lamellar corneal
allograft.
Figure 8: Post operative appearance with keratitis.
|8|
Figure 9: Post transplant clarity.
Tarsal Osteochondrosis
Robert B. Hillman, DVM, MS, DACVS
THE MOST COMMON CAUSES OF PELVIC LIMB
lameness in adult dogs are cruciate disease and hip
dysplasia. But when puppies present with lameness,
we must avoid tunnel vision. Our differential list
should be prioritized based on signalment.
Dr. Robert Hillman practices at
Port City Veterinary Referral
Hospital in New Hampshire, NH.
The following is a brief discussion of tarsal
osteochondrosis including etiology and pathogenesis,
clinical signs, diagnostics, treatment and prognosis. It
is a combination of literature review and editorial
based on clinical impression.
ETIOLOGY AND PATHOGENESIS
Osteochondrosis (OC) is a developmental orthopedic
disease commonly observed in rapidly growing, largeand giant-breed, dogs, typically between five and ten
months of age. Normally, the process of endochondral
ossification involves physiologic calcification of the
cartilage at the osteochondral junction and replacement
by bone. When this fails to occur, a thickened focal area of
degenerative cartilage results, outgrowing its nutrient
supply. This area of necrotic cartilage is vulnerable to
shearing forces encountered during normal weight
bearing. This lesion is referred to as osteochondritis
dissecans (OCD) when fissures are formed and joint fluid
dissects (the dissecans part of OCD) between the
cartilage and underlying bone, forming a flap. Cartilage
degradation products reach the synovial fluid when a flap
forms, causing synovitis, effusion, joint pain, and
lameness. The cartilage flap may remain in situ and
potentially reattach to subchondral bone or may dislodge
forming a joint mouse. Joint mice may be resorbed in
synovial recesses or remain in the joint, causing synovitis
and osteoarthritis. The cause of OC has not been
determined, but a combination of factors, including
genetics, rapid growth, over nutrition and excess dietary
calcium, trauma, ischemia, and hormonal influences, has
been implicated.
The typical patients are puppies from predisposed breeds
- typically large compared to littermates, having rapid
growth rates, and are often on high planes of nutrition.
The disease is most common in dogs that reach an adult
weight of greater than 20 kg and tends to occur during
periods of rapid growth. Puppies from small breeds of
dogs are rarely affected with OC.
After the shoulder and elbow, the tarsal joint is the third
most common site of OC in the dog. While male dogs are
more commonly affected than female dogs with OC in
other sites, this sex difference has not been seen with
tarsal OC. All of the patients treated for tarsal OCD at
Port City in the last two years were young female
Labradors. Like OC in other sites, it is usually noted
between six to twelve months of age. Lesions are bilateral
40 % of the time. Right and left limbs are equally affected.
The medial trochlear ridge is affected in 79 % of tarsal
OCD cases, and 21 % involve the lateral ridge.
Breeds at risk for OC of the tarsus are the Bullmastiff,
Labrador Retriever and Rottweiler. I.e., Bullmastiffs are
86 times more likely (odds ratio) to have tarsal OC than
mixed breed dogs. The true odds ratio is 95% likely to be
between 36 and 206 times (95% confidence interval).
Rottweilers and Labrador retrievers account for 70 % of
hock OCD cases.
Lesions may affect one or both trochlear ridges at
multiple sites. The most common location is the plantar
aspect of the medial trochlear ridge (80 % of cases).
Seventy percent of cases affecting the lateral trochlear
ridge involve the dorsal aspect. Rottweilers in one study
accounted for 80 % of cases of lateral ridge OCD and 63 %
of those cases had bilateral lesions.
CLINICAL SIGNS
It has been reported that half the dogs presenting with
tarsal OCD have a non-weight bearing lameness,
although this has not been my personal experience. I
mostly see pups with an intermittent but persistent
moderate pelvic limb lameness. Perhaps the primary care
vets in my area are more astute than most, and refer the
|9|
>continued
Tarsal Osteochondrosis
Figure 1. CT image of lateral
talar OCD lesion.
the CT examination helped to determine the exact site,
and the number and size of the fragments of bone.
A CT scan is extremely helpful, because 40% of cases
have bilateral lesions, lateral lesions can be difficult to
identify and localize with radiography alone, and because
the three dimensional image is invaluable in planning the
surgical approach.
cases before they become non-weight bearing. Lameness
for those cases bearing weight usually worsens with
exercise. There is typically palpable if not readily visible
joint effusion. The affected joints usually have a decreased
range of motion in flexion and may appear hyperextended.
DIAGNOSIS
A presumptive diagnosis is made based on signalment
and clinical signs. Tarsal OCD can be a difficult
radiographic diagnosis. OCD of the medial trochlear ridge
can be diagnosed on extended plain craniocaudal and
slightly flexed mediolateral radiographs. Findings
suggestive of medial OCD include increased joint space at
the OCD defect, joint effusion and presence of an
osteochondral fragment. A “sky-line” view of the tarsus
with the joint flexed to 90 degrees and the x-ray beam
directed perpendicular to the long axis of the tibia is often
required to visualize OCD of the lateral trochlear ridge.
Radiographic evaluation should include standard lateral,
flexed lateral, and dorsoplantar views of both tarsi.
Additional views are also helpful, including a craniocaudal
view of the proximal trochlear ridges, a
dorsolateral-plantomedial oblique view (D45 L-PLMO),
and a dorsomedial-plantolateral oblique view (D45
M-PLLO). The dorsal 45 degrees lateral-plantaromedial
oblique (D45 degrees L-PMO) projection was the most
useful in identifying the lateral lesions.
By the time you have taken six views of each tarsus, you
might as well have done a CT – yes, even when comparing
costs. One study compared a six-view study of each
tarsus to CT and arthroscopic findings. Although the
survey radiographs were sufficient to make a diagnosis,
| 10 |
One retrospective study compared the value of
radiographic CT imaging for the diagnosis of lateral
trochlear ridge talar OCD. The flexed dorsoplantar
sky-line and the plantarolateral-dorsomedial projections
were the most reliable for radiographic detection of OCD
fragments. While radiography detected OCD fragments in
8 of 11 joints, OCD fragments could be visualized and
exactly localized by CT in all 11 joints. The ability to
evaluate the talar ridges without superimposition of any
bony structures is key.
Clearly CT is superior to radiography for localizing OCD
fragments, especially on the lateral talar ridge. There are
certainly many cases, particularly those involving the
medial ridge, for which radiography would suffice for
localization. I perform a CT on all tarsal OCD cases
because of advantages in sensitivity and specificity and
lesion localization. It helps me chose the least invasive
approach to the lesion. Figure 1 is a CT reconstruction
image of a seven month-old female spayed Labrador with
a large lateral talar OCD lesion. In this case, the fragment
was too large to remove. A lateral approach using a
fibular osteotomy, sparing the lateral collateral ligament,
was used. The fragment was stabilized with a screw and
wires. The osteotomy was stabilized with two screws
(figures 2 and 3).
If you have a six month old Labrador, lame with a swollen
hock that has decreased flexion, a set of radiographs prior
to referral can be helpful, but is not essential. I am always
going discuss the option of a CT with your clients. The CT
is performed immediately pre-op, so there is only one
sedation/anesthesia episode.
TREATMENT
Removal of the flap via small arthrotomy or arthroscopy
and curettage of the bed is recommended. Some studies
report about 1/3 of tarsal OCD lesions can be managed via
arthroscopy alone. The rest require at least a
mini-arthrotomy. As previously mentioned, CT is
extremely helpful in planning the approach (medial or
lateral, dorsal or plantar? Will maximal flexion or
extension aid visualization? Will an osteotomy be
required?). Dogs with lameness and a large flap appear to
do better if operated early prior to the onset of DJD. Dogs
with small lesions appear to have a better long-term
prognosis. It has also been demonstrated that in dogs
with bilateral tarsal OCD lesions found on CT but
unilateral lameness, the nonclinical lesions were
significantly smaller. Similar lesion size/prognosis
correlations have been made with regard to OCD in the
canine shoulder. Loss of a big piece of the trochlear ridge
due to a large OCD defect or removal of excess bone
(curettage) at surgery may cause increased joint
instability and a poor prognosis.
In one study, sixteen joints with OCD treated with
arthroscopy resulted in 10/14 dogs with lameness after
exercise only, progression of DJD in most cases, and
chronic lameness when comparing operated to
unoperated limbs with force plate evaluation at a mean
follow-up of 35 months.
Medical management for tarsal OCD is recommended in
older dogs with severe regenerative changes. Most recent
reports suggest that surgical intervention is preferred for
treating tarsal OC. One study found no significant
difference in long-term outcome between joints treated
medically and those treated surgically, but that data is
from nearly 30 years ago. Use caution if basing clinical
decisions on old texts, and review articles citing review
articles. The lack of difference in surgically and medically
managed cases is more likely to be true in older dogs with
chronic and significant OA. Surgical exploration and
removal of the cartilage flap or osteochondral fragment
can allow in-growth of fibrocartilage from the underlying
subchondral bone.Early intervention with a minimally
invasive approach is preferred. Once the lesion is
exposed, the cartilage flap or osteochondral fragment is
excised. Overall function is better with minimal curettage.
There are some fragments that are simply too large to
remove (i.e, the resultant defect would lead to joint
instability). Large fragments can be stabilized with screw
or wire fixation.
PROGNOSIS
Time to maximal postoperative performance was 30 days
or less in one study. Most cases have some gait
Figure 2. Lateral post-op film
Figure 3. AP post-op
film.
abnormalities postoperatively, but are usually better than
they were preoperatively. Dogs with OCD of the medial
trochlear ridge seem to have more postoperative
lameness than dogs with lateral trochlear OCD. Lateral
OCD has less affect on the weight-bearing surface than
medial OCD. Medical management may be needed
long-term for treatment of DJD/OA.
The prognosis for OC of the tarsus after conservative
therapy is guarded. Most dogs have intermittent lameness
and moderate progression of OA. Even after surgery, OA
is likely and often requires medical therapy to control pain
and lameness. Despite the progression of OA noted
radiographically after surgery, many dogs are clinically
improved. Nevertheless, the prognosis remains guarded,
because joint pain and lameness may recur as the OA
progresses. One report sites faster recovery in dogs with
lesions involving the non–weight bearing dorsal aspect of
the lateral trochlear ridge. Several factors may influence
the success of medical and surgical treatment, including
the age of the dog, presence of OA, size of the
osteochondral defect, presence of joint instability, site of
the lesion, and whether the lesions are unilateral or
bilateral.
Even though my tarsal OCD caseload has been fairly
uniform in terms of signalment, I am surprised by the
diversity of lesions found. After the thorough orthopedic
exam, the consult involves discussing all options with the
clients. Ensuring they understand the variable prognosis
and different treatment options is important. While there
may be occasional cases best managed conservatively, I
am yet to have a client say they regret their decision to
pursue CT and surgery for their dog’s tarsal OCD.
| 11 |
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