Page 1601 - Clinical Small Animal Internal Medicine

174 Developmental Orthopedic Diseases 1539

containing a gene or group of genes influencing the phe- stairs, and exercise intolerance. Hips are often very pain-
VetBooks.ir notypic expression of a trait) for CHD and hip OA have ful in these animals. Older dogs mostly present with
similar signs but with a more chronic presentation due to
been identified on multiple canine chromosomes.
Several upgraded genes like COX‐2, MIG‐6/Gene 33,
for these signs include panosteitis, iliopsoas myopathy,
DNCLl, LAMS, and ATF3 have been identified. Only the slow progression of arthritic changes. Differentials
genetically predisposed animals exposed to certain spe- bilateral cruciate disease, and lumbosacral disease.
cific environmental factors may develop clinical hip dys-
plasia, and dogs not predisposed but exposed to the Diagnosis
same environmental factors will not. Affected hip joints have a decreased range of motion
The hormones estrogen and relaxin have also been and pain on extension and abduction, and may exhibit
implicated as etiologic factors of CHD. Both are present crepitus on manipulation. There is often atrophy of the
in colostrum and may be absorbed from the puppy’s gas- large muscles round the thigh and hip joint. Hip laxity
trointestinal tract. Estrogen is probably not a strong etio- may be clinically assessed using the Ortolani test. With
logic factor, as estrogen fluctuations during the estrus this test, the presumed lax hip joint is first manually
cycle do not result in joint laxity changes. One of relax- subluxated and then reduced. If the joint is lax, the sub-
in’s functions prepartum is to relax the ligaments of the luxated hip will reduce with a palpable or audible clunk
maternal pubic symphysis, and in dogs and humans it is or click. This evidence of reduction is regarded as a
associated with joint laxity. However, the significance of positive Ortolani sign and is suggestive of hip laxity. In
relaxin in the etiology of CHD is unclear. the awake, unsedated patient, the Ortolani test can be
Rapid growth and body weight have been associated most easily performed with the dog in lateral recum-
with the development of CHD. In recent studies, heavier bency, affected side up. The test may induce pain and
puppies developed hip OA requiring treatment at a much should be performed humanely. In the sedated patient,
younger age than lighter littermates. Similarly, ad libitum the Ortolani maneuver also can be performed with the
feeding of Labrador retrievers accelerated the onset of hip patient in dorsal recumbency.
OA when compared to a control group fed a restricted diet. The diagnosis of CHD is confirmed using well‐posi-
High dietary concentrations of calcium and/or vitamin D3 tioned, ventrodorsal extended hip and lateral pelvic radi-
have also been implicated, but not conclusively proven, as ographs. The lateral pelvic view is mostly evaluated for
etiologic factors. A high dietary anion gap and vitamin C evidence of lumbosacral disease. The ventrodorsal hip‐
deficiency have also been proposed as causes of CHD, but extended (VD) view is assessed for hip joint laxity, osteo-
their clinical significance has not been demonstrated. phytes, hip remodeling, and enthesophytes of the lesser
trochanter suggestive of iliopsoas muscle injury. This
Epidemiology view is also helpful in identifying transitional vertebrae,
Hip dysplasia is the most commonly diagnosed canine for example sacralization of the last lumbar vertebra. Hip
orthopedic condition and in one North American epide- laxity is suspected if on the VD view less than 50% of the
miologic study of canine appendicular musculoskeletal femoral head is within the acetabulum or if the cranial
disorders, it comprised 9.6–12.8% of all patients. In this half of the joint space is not uniformly wide and diverges
population, the incidence of CHD ranged from 21.1 to medially. Unfortunately, with this technique actual hip
28.1 per 1000 patients, but incidences as high as 50–70% laxity may be present in the absence of radiographic
in some large breeds have been reported. Hip dysplasia signs. Thus this technique has limited sensitivity for the
in cats is thought to be uncommon. detection of hip laxity as false‐negative results may be
obtained. Early nonspecific osteoarthritic signs can be
Signalment found around the femoral head (circumferential femoral
Canine hip dysplasia is most commonly diagnosed in head osteophyte) and the femoral neck (caudolateral
medium‐ and large‐breed dogs (see Table 174.1). Male curvilinear osteophyte = Morgan’s line). Osteophytes
and female dogs are equally affected. Patients younger may also be seen on the cranial and caudal acetabular
than 1 year of age are usually presented because of pain margins, and sclerosis of the craniodorsal acetabulum
and lameness caused by synovitis following hip laxity. As may be noted. Later stages of the disease are character-
a result of progressive joint capsule fibrosis, older, mature ized by varying degrees of remodeling of the femoral
patients usually have minimal laxity but suffer from sub- head (flattening) and acetabulum (shallowing) and thick-
sequent hip OA. ening of the femoral neck.
Radiography is also used as a screening tool to identify
History and Clinical Signs dogs suffering from CHD and at risk for OA, to predict
Young patients with hip dysplasia (hip laxity) usually progression of the disease, and to assist in identifying
present with uni‐ or bilateral lameness, bunny hopping, suitable breeding animals. Several techniques are in use.
difficulty rising, reluctance to walk, trot, jump, or climb In the USA, the Orthopedic Foundation for Animals