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This article is the third in an eight-part series on canine hip dysplasia (CHD). What follows is written from the perspective that the readers of the series are conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary medical texts, it is a relatively in-depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading it you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.
Conclusions from Part I: Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it either is dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.
Conclusions from part II: While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog.
This third article deals with the abnormal hip and how to diagnose it. Though CHD can afflict all breeds, it is more common in the large and giant breeds. There is far more to a proper diagnosis than first meets the eye. Anecdotal evidence has shown that canine hip dysplasia is one of the most over-diagnosed and misdiagnosed problems afflicting dogs. Many clinicians may depend too often on only subjective radiographic interpretation in the diagnosis of CHD. Physical examination techniques are helpful, and one can often pick up on concurrent conditions that could be otherwise overlooked. Initially, this article will focus on the clinical signs of hip dysplasia, the specific methods used by the experienced practitioner to make the diagnosis and the problems associated with the classic hips-extended, Orthopedic Foundation for Animals-approved X-ray positioning for radiographic study. The latter part of the article will be devoted to important new developments that hold promise for predicting the probability of phenotypic expression of CHD.
In the second article in the series, we said that canine hip dysplasia can be conveniently categorized into two major types. The first is severe and is seen early in the afflicted dog’s life. The second, and far more common type, is the insidious chronic form that develops over a period of time. It is therefore useful to separate dogs by age classification when describing the clinical signs of hip dysplasia. A reasonable classification that takes into account maturity, puberty and attaining adult height, if not near adult weight, would be dogs less than one year in age and those more than one year in age. This gives time for atrophy and extraordinary musculature to develop as clinically recognizable signs. In the young dog, the first symptoms appear to be decreased activity, sometimes accompanied by joint pain. 1 If a young dog is found to have a swaying or unsteady gait, or runs with both hind legs moving together - often referred to by breeders as the "bunny hop" - it is worth further investigation. Acute episodes of lameness with both or only one side affected can also occur after exercise or minor trauma. These signs can also be the result of infections in joints, lack of synovial fluid or the result of trauma. As CHD progresses, the dog may also have difficulty rising from a lying or sitting position and will frequently balk at going up or down stairs.
TYPE OF MOVEMENT | RANGE IN DEGREES |
---|---|
Flexion | From Neutral to 70 to 80 |
Extension | From Neutral to 80 to 90 |
Adduction | From Neutral to 30 to 40 |
Abduction | From Neutral to 70 to 80 |
Internal Rotation | From Neutral to 50 to 60 |
Internal to External | From Neutral to 80 to 90 |
Two clinical signs that most often appear together in the older dog are well-developed muscles in the forelimbs and shoulders due to shifting weight forward. 2 As the disease progresses, hypertrophy (over-development) of the front end is accompanied by symmetrical or non-symmetrical atrophy of the pelvic muscles. Such animals appear weak in the pelvic region, are reluctant to exercise, generally prefer sitting to standing and exhibit extreme discomfort when their forelimbs are lifted off the ground.
Remember also that the affected dog may exhibit none of these symptoms. A
substantial
number of dogs with radiographic signs of hip dysplasia show no clinical
signs of the
disease. Explanations of this phenomenon are as varied as they are
controversial. Quite
a few practitioners believe that a dog radiographically positive for hip
dysplasia but
clinically negative for signs is just a dog in an intermediate stage of the
disease
progression. This period may last for months, even years, until the onset of
substantial
degenerative joint disease. It is not uncommon for an afflicted (genetically
predisposed)
dog to die of old age before any non-radiographic signs develop.
We repeat again the warning issued in the preceding articles: You cannot
tell if a dog is
genetically predisposed to hip dysplasia by its movement. Reject the false
wisdom of
the old-time breeder who emphatically states that if his or her dogs had hip
dysplasia he
or she would be able to see it. Hip dysplasia is a polygenic, multifactorial
disease.
Before a definitive diagnosis of CHD can be made, other problems must be
ruled out. 3
Thorough medical, orthopedic and neurological examinations must be made in
order to
rule out other disorders of the hip and spine. Multiple joint involvement
may be the case.
The following is a condensed list of some of the more common conditions that
mimic or
may be concurrent with canine hip dysplasia:
Dr. William Inman a clinician in Washington state feels that canine hip
dysplasia is the
most over-diagnosed and misdiagnosed condition in the veterinary medical
practice. 4
While he feels that hip dysplasia is genetically predisposed, he remains
puzzled by
finding in his practice clinically dysplastic dogs with radiographically
normal hips and
symptom-free dogs with coxofemoral joints that look "like a bomb went off in
them."
Inman states, "Curiously, in all the young dogs we see with hip dysplasia
signs in the 5
to 18-month range, we always find a subluxation at T8-T10 [dislocation of
the Thoracic
vertebra 8 through Thoracic vertebra 10]." This is a potentially important
finding because
the T8 to T10 area "innervates the peraspinal muscles and the iliopsas
muscle, which
attaches to the femoral head and pulls it forward. Subluxation leads to
muscle spasming,
which causes continued anterior traction of the femur on the hip socket,
flattening the
joint…reduction of this subluxation reverses the progression of hip
dysplasia by curing the
musculo-skeletal dysfunction." Inman has relieved the symptoms of more than
3,500 dogs
with his procedure.
The conclusion that Inman has drawn from his practice is that the T8-T10
subluxation is a
physical condition that, unless dealt with immediately, will progress to the
joint capsular
fibrosis and muscle stricture associated with decreased range of motion. The
subsequent
skeletal changes that follow can only be addressed surgically. He recommends
early
intervention in dogs thus afflicted to halt this insidious process.
Inman’s theory appears radical, but it is not contrary to the concepts
previously presented.
He does not maintain that a genetic disease is not associated with hip
dysplasia, only
that a misdiagnosed physical condition mimics the disease process. Thus, the
incidence
of CHD may be lower than previously thought by other researchers.
Given that many other processes may be at play, the following are some of
the physical
techniques used in the diagnosis of CHD. While a tentative diagnosis can be
made on
the basis of history, clinical signs and the various palpation methods,
standard veterinary
practice requires radiographic signs of CHD. Diagnostic methods fall into
two general
categories: subjective and quantitative. We have found no method, subjective
or
quantitative, that is without its detractors or without serious controversy.
Observation. The first step in the diagnosis of a suspected case of
CHD is
orthopedic examination, which should include observation of the dog at rest,
walking,
running and a re-examination of the dog the day following vigorous
exercise.5, 6
Observation and neurologic examination should be conducted before
administering any
drugs, and especially before sedation or general anesthesia, which can
significantly
alter the dog’s neurologic status.
Range of motion. In an anesthetized dog, the coxofemoral joint’s
range of motion
is approximately 110 degrees. 7 With pathology, this range of
motion can be reduced
to as little as 45 degrees. When following a chronic patient, the clinician
uses changes in
the range of motion to quantify the progress of the disease and as an aide
when
determining treatment options. Figure 1 is a table of the clinical
categories by range of
motion.
Changes in gait patterns. A shortened length of stride is associated
with a loss in
range of motion. There is a considerable variance among animals, but as a
general rule,
shortened stride length does not appear until fully extended movement is
painful for the
dog. This is the case with severe degenerative joint disease. Similarly,
this type of gait
abnormality can occur if the joint capsule has become fibrous. The many
shapes and
sizes of dogs make it impossible to describe all the potential gait changes.
However,
the bunny hop, left to right shift of the pelvis or an elliptical swing of
the leg and hip are
common gait problems encountered.
Forced extension. Affected dogs will not only exhibit discomfort with
forced
extension of the hip, but will try to return the limb to a more relaxed
position. Depending
on the temperament of these animals, they may also vocalize or exhibit
aggressive
behavior in response to pain. Be aware that the fighting dogs and the
Northern breeds
tend to have high pain tolerance levels and are generally stoic with respect
to pain.
Downward pressure on the rear limb. When force is applied to the hips
of a
standing animal, the affected animal will show little or no resistance to
the pressure, and
will assume a sitting position. Several factors may simultaneously be
involved and
interrelated, such as pain, muscle weakness or atrophy.
Palpation. In humans, the most popular and reliable palpation
maneuver used to
identify congenital dislocation of the hip determines the presence or
absence of the
Ortolani sign. "A positive Ortolani sign confirms the diagnosis of
coxofemoral subluxation
in newborns prior to development of clinical signs or radiographic changes."
8 Many
veterinarians feel that the techniques have too much subjectivity and
variance to be of
much use. Nonetheless, the Ortolani sign still figures prominently in the
literature. 9-14
Animals to be examined must be anesthetized past the point where there is
still a
palpable response. Two basic approaches are used: dorsal recumbency and
lateral
recumbency, with dorsal recumbency being preferred for large dogs. Downward
pressure
is applied down the axis of the femur until the femoral head subluxates. The
leg is slowly
abducted while holding the stifle firmly. If the joint is loose, a distinct
clicking may be felt
and in some cases will be audible.
Other palpation methods have been proposed by Barlow and Bardens.
15,16 Barlow’s
Sign is essentially the first half of the Ortolani Test. Downward axial
pressure is applied
on the femur without abducting the leg. The Bardens’ Test places the dog on
its side, and
the leg is held perpendicular to the spine. Lifting pressure is applied to
the femoral shaft
without abduction. The examiner’s finger is placed on the greater
trochanter. Any
movement of the finger by more than one-fourth inch is considered a positive
sign for a
loose joint. Palpation has shown diagnostic use in human neonates, but is
controversial
and may have little diagnostic or prognostic utility in the dog. A caution:
In human infants,
it has been suggested that repetitive Barlow tests, and presumably Ortolani
and Bardens
as well, are capable of making infant hips unstable, thus giving a
false-positive result. 17
The Neurologic exam. During a normal physical examination, the
clinician will
observe both the posture and movement of the dog. Of the two observations
(gait and
posture), how the animal stands or its ability to return to a normal stance
tells more about
the neurological status. Some breeds have been selectively bred for a
characteristic
gait. Thus gaits may vary tremendously among breeds. A Borzoi moving as a
Bulldog
would be one sick Borzoi. A poor postural response may indicate a
proprioceptive
deficit.
Proprioception, or posture sense, is the ability to recognize the location
of limbs in
relation to the rest of the body without visual clues. An abnormally wide
stance is one
indication of a possible problem. The simplest method of evaluation is to
bend the paw
so the back of the foot is bearing the dog’s weight. The normal response is
to
immediately reposition the paw correctly. A problem in proprioception
positioning is
often an early indication of neurological problems, and most often precedes
motor
dysfunction (gait anomalies).
When evaluating the dog specifically for hip dysplasia, one needs to rule
out deficits in
the spinal-reflex arc. An example of the spinal-reflex arc where the neural
response is not
transmitted to the brain but returned (arcs back) is the familiar tap on the
knee with a
rubber hammer. (The neural response travels from the muscle to the spine and
returns to
the muscle, without traveling to the brain.) The absence of an involuntary
response or an
exaggerated response are indications of neurologic problems. Some variance
among
breeds is noted, as large dog responses tend to be less rapid than those in
smaller
breeds.
Routinely, the "knee jerk" (quadricep reflex) is tested first with the
normal reaction being
a single quick extension of the stifle. Next, the flexor reflex is evaluated
by gently
pinching the toes. The normal dog should pull the entire limb (hip, stifle
and hock) up
toward the belly. Although not strictly analogous, the extension toe reflex
has been
compared to the Babinski reflex in humans. The examiner will hold the hock
and gently
stroke the back surface from the hock down toward the pad. The normal animal
will either
exhibit no response or a slight flexion of the toes. The abnormal reaction
is the extension
and spreading of the toes. These tests, by no means comprehensive or
exhaustive,
constitute the minimal examination to rule out spinal problems in a dog
being evaluated
for hip dysplasia. 18
Hip-extended radiographic method. This traditional X-ray position has
been the
standard position, which has the dog sedated, on its back, with legs fully
extended and
patella facing upward, became the standard of the American Veterinary
Medical
Association Panel on Hip Dysplasia in 1961, and was adopted by the
Orthopedic
Foundation for Animals in 1966. University of Pennsylvania
studies have
been conducted that show interpretations are not highly consistent among
radiologists,
and are not highly consistent when the same radiologist reads the same deck
of X-rays
in shuffled order.19 OFA scores (excellent, good, fair,
borderline, mild, moderate and
severe) have wide acceptance but as subjective interpretations not readily
repeatable
with the same animal , nor likely to be interpreted consistently by
different radiologists.
At first it appeared that the seven-point scale was more discrete than
diagnostic protocol
warranted. When the seven-point scale was collapsed to a three-point scale
(normal,
borderline, dysplastic) agreement improved. The hips-extended positioning
has come
under criticism because it masks joint laxity. This positioning masks joint
laxity in two
ways both involving the joint capsule. With the hip extended, the fibers of
the joint
capsule tighten in such a way as to push the femoral head into the
acetabulum. This
position also leads to a lowering of the intra-articular pressure, which
combined with the
fixed synovial fluid volume causes invagination of the joint capsule. These
two
conditions limit the amount of sideways movement of the femoral head.
Similarly,
unsedated positioning may further mask joint laxity.
Norberg Angle method. The Norberg Angle radiographic method of
determining
joint laxity (subluxation) has been used more in Europe than in the United
States. The
standard OFA hip-extended radiographic projection is used (see figure 3).
Norberg
angles typically range from 55 degrees to 115 degrees, with the smaller
numbers
representing looser hips. Unfortunately, there is no common agreement as to
what
constitutes a normal angle, though 105 degrees may be used as a point
estimate for
normal joint laxity. Correlation with OFA interpretations is poor, which is
one reason the
Norberg Angle method is not well accepted as a diagnostic tool and is
considered
subjective at this time.
Compression/Distraction method. This new stress radiographic method
originated at the University of Pennsylvania School of Veterinary Medicine
and is
currently marketed by PennHIP®. What started as a look at the role of
passive
hip laxity in CHD has become a quantitative diagnostic protocol referenced
to an
extensive data base. In recent years joint laxity has been established in
the literature as
prognostic for degenerative joint disease. Initially, however little
statistical evidence
supported this contention. Now that a major data base has been developed for
purposes
of comparison and for determining probabilities, joint laxity can be used
as an indirect
variable with which to predict the probability of eventual phenotypic
expression of CHD.
Unfortunately for breeders, deep sedation is required in the
compression/distraction
method. The traditional OFA positioning was found inadequate. In the stress
radiographic method, the dog is laid on its back with its hips at a neutral
flexion/extension
angle. A compression view is taken with the femoral heads seated tightly in
the acetabula
congruency between
the two joint surfaces. A second, or distraction, view is taken showing the
maximum
separation distance of the femoral head center from the acetabular center
A special device is used to force the femoral head away from the acetabulum
for the
distraction view. This protocol has been shown at University of Pennsylvania
to reveal
2.5 times more joint laxity than the standard hip-extended radiograph.
The power of this method lies both in the new positions and in the
statistical significance
of the compression index (CI) and the distraction index (DI) as supported by
a data
base. 20 The indices range from 0 to 1, with "0 being a fully
congruent hip (as seen
in the compression radiographic view) and 1 representing the most extreme
joint laxity
as might be seen in the distraction view of hips that are virtually
luxated." 21 The
OFA scoring method is an ordinal scale, the Norberg Angle method is an
interval scale
and the DI is a ration scale. Thus the DI is intuitive in its meaning: A hip
with a DI of 0.5
has twice the laxity of a hip with a DI of 0.25. Similarly a DI of 0.5 can
be thought of as a
hip 50 percent luxated. The DI ratio scale is far more useful a rating than
the Norberg
Angle. See figure 2 for a comparison of scales.
Breeders are always looking for earlier detection of CHD, the earlier the
better for
determining which animals to keep and classify as show and breeding
hopefuls.
Compression and distraction evaluations have been done on a sample of
8-week-old
German Shepherd Dog puppies without the results being conclusive. At 16
weeks, this
method becomes useful. Dr. Gale Smith, et. al., at the University of
Pennsylvania Hip
Improvement Program (PennHIP) recommended that dogs not be evaluated before
16
weeks and that follow-up radiography should be done at 6months or 1 year of
age. 22
In later articles in this series we will address the utility of the PennHIP
protocol for
prognosis.
Genetic (blood-based) diagnostic test. At this time, no biomechanical
or
metabolic differences have been identified in the dysplastic dog. Extensive
work
continues for an early blood marker for the condition. Finding such a marker
would be
ideal, as it would both allow the breeder to definitively screen breeding
stock, and help
the clinician identify appropriate treatment protocols. Parallel work is
being done in
determining genetic factors in humans for rheumatoid arthritis and
osteoarthritis.
Restriction Fragment Length Polymorphism (RFLP) linkage analysis has been
used to
identify genes associated with those diseases. Since there appears to be a
strong
genetic base for CHD, restriction fragments in the white blood cell DNA
should
correspond to the dysplastic phenotype. 23, 24
Conclusions: Canine Hip Dysplasia can be difficult to diagnose. Other
orthopedic,
neurological, autoimmune/infection and metabolic problems may mimic CHD or
may be
concurrent with CHD. Numerous palpation techniques (Ortolani, Bardens,
Barlow) have
been proposed; however, they remain subjective nonquantitative methods that
rely
heavily on the skill of the clinician. The standard in current veterinary
practice is to
confirm CHD radiographically. The traditional American Veterinary Medical
Association
and Orthopedic Foundation for Animals hip-extended radiographic view
distorts the
amount of joint laxity present by forcing the femoral head deeper into the
acetabular cup,
thus understating the amount of laxity present. University of Pennsylvania
(PennHIP)
protocols for stress radiography are coming to the forefront as a more
definitive way of
visualizing hip joint laxity. Canine hip dysplasia remains a polygenic,
multifactorial
disease.
The next article in this series will discuss the various hip dysplasia
registries, their
approaches to the problems of canine hip dysplasia and the importance of
having a
"tamper-proof" identification system.
RADIOGRAPHIC
METHOD
SCORES
TYPE OF
SCORING
TYPE OF
SCALE
7 Point Scale(OFA)
Excellent
Good
Fair
Borderline
Mild-HD
Severe-HD
Subjective
Oridinal
3 Point Scale
Normal
Borderline
Dysplastic
Subjective
Oridinal
Norberg Angle (NA)
Tight hip > 105 degrees
Loose Hip < 90 degrees
Quantitative
Interval
DJD Score
DJD Absent
NA
DJD Present
Subjective
Oridinal
Distraction Index
Index = 0 Tight Hip
NA
Index = 1 Loose Hip
Quantitative
Interval
An example of another condition masquerading as hip dysplasia is the
all-too-common
spinal degenerative myelopathy in German Shepherd Dogs. After reading the
preceding
list, you should realize that CHD is not an easy condition to diagnose with
great surety
unless a full examination is conducted. If you do not find radiographic
signs, that still
does not preclude some of the problems mentioned above.
Subjective Methods of Diagnosis
Subjective Diagnostic Radiographic Methods
Quantitative Diagnostic Radiographic Method
References
LINKS
A scientific study of the chromosomes in dogs. Also information about genetic disorders in dogs.
PRA . PRA Today: Current Research in Progressive Retinal Atrophy . by Gregory Acland and Gustavo Aguirre . CHD . Canine Hip Displasia . Go to the Home Page of The Dog Genome Project. . This page was
The Dog Genome Project at the Fred Hutchinson Cancer Research Center is working to develop resources necessary to map and clone canine genes. Some of the resources we are developing, and the stage of
Eliminating Genetic Diseases in Dogs: A Buyer's Perspective . Eliminating Genetic Diseases in Dogs: A Buyer's Perspective . Photo of Gary Mason's . "Canine vWD Poster Puppy" , .
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