Canine hip dysplasia (Proceedings)

Etiology

CHD has been called inherited, a developmental disease, and most accurately in the author's opinion, a "moderately heritable disease". CHD is a multifactorial disease with part of its cause being from genetic influences (estimated at 25%-80%) and part from environmental influences. The specific gene(s) involved have not been identified, although karyotyping for dogs is actively progressing. Controlled breeding studies have shown that breeding phenotypically normal dogs will result in fewer offspring with clinical CHD than breeding an affected dog to a phenotypically normal dog, or by breeding two affected dogs. Despite controlled multi-generation breeding programs, selective breeding alone has not been able to eliminate CHD from any group of dogs. Less controlled breeding programs such as those promoted by Kennel Clubs of a specific breed have been somewhat effective. The percentage of affected dogs presented to the OFA for evaluation from 24 breeds for the time period 1972 to 1980 was compared to 1981 to 1988. Of the 24 breeds, 14 breeds had a reduction in the % of CHD ranging from 10% to 40.5%, and 5 breeds had a reduction ranging from 2.9% to 10%. Four breeds had an increase ranging from 1.1% to 9.7% and one breed had no change. Although the OFA is a good indicator, the % of dysplastic dogs reported by the OFA is an underestimation of dysplasia in the general population since radiographs from many dogs with obvious hip dysplasia are not sent to OFA for evaluation.

Body size and type, directly related to genes, are important risk factors for CHD. All breeds and size dogs have been reported to have hip dysplasia. Large and giant breeds of dogs are perceived by the lay public to be at greatest risk. The OFA indicates that many relatively small dogs (e.g. American Water Spaniel) have a very high incidence of CHD, while some large dogs (e.g. sight hounds) have very low incidences of CHD. Clinical signs of CHD and DJD are exacerbated in heavier dogs, which partially explains the public perception of CHD being a large breed disease. In addition to size, body type is important. Giant breeds with acromegally characteristics (e.g. Saint Bernard) are at greatest risk for CHD. Giant breeds at high risk for CHD are stocky, clumsy, have soft ill-defined muscles, and have 5% to 10% fat in the soft tissues of the hind quarters. Athletic dogs (e.g. Greyhound) have a lower prevalence of CHD and tend to be coordinated, have well defined and firm muscles, tightly adherent skin with 1% to 2% fat in the soft tissues of the hindquarters.

Environmental factors influencing the phenotypic expression of CHD include exercise and nutrition. A major factor in CHD is laxity between the femoral head and the acetabulum. In puppies that exercise heavily the laxity is exacerbated and the joint is traumatized by the abnormal motion and impact of repeated subluxations and reductions. This trauma is further exacerbated by increased body weight, causing the joint to withstand even more force. Therefore, clinically significant CHD is most prevalent in large and giant breed dogs, especially of non-atheletic breeds. Also, within a litter the fastest growing, most active dogs have a greater tendency toward CHD. In a study of 222 German Shephards, the 111 dogs that weighed more than the group mean at 2 months old had a 63% incidence of CHD at a year of age, compared to 37% of the dogs weighing less than the mean. The major nutritional factors promoting CHD are rapid weight gain (as promoted by excessive calories and ad libitum feeding) and excessive calcium supplementation. Slower rates of weight gain in puppies does not affect their adult size since the physes do not close until later in dogs with slower weight gain rates. Other factors have not been shown to have a significant influence on the development of CHD.

Pathogenesis

CHD is a disease that develops between birth and 8 months of age, with the most influential time being up to 6 months of age. The canine hips are normal at birth by all test we currently have available. A relevant engineering principle is that when the height of a structure (e.g. leg length) doubles, then the bracing (e.g. muscle and supportive soft tissues) has to be tripled or the structure will collapse. CHD has been described as "a disparity between primary muscle mass and too rapid growth of the skeleton." In other words, the bone length grows at a faster rate than the muscle mass and ligament/tendon strength, thus making the hip unstable. Inability of muscle and other soft tissues (joint capsule, capital ligament) to hold the joint in a congruent position results in joint laxity. The soft cartilaginous skeleton is easily deformed by the abnormal forces of joint laxity or the excessive forces of a very active puppy. The greatest risk for deformation is in the neonate when the skeleton is primarily soft cartilage rather than bone. Excessive or abnormal forces deform the cartilaginous skeleton that results in joint incongruency and malformation or "dys" - "plasia". The earliest detectable changes occur at about a month of age. The teres ligament may be edematous, have petechial hemorrhage and have a few fibers torn. From 30 to 60 days of age the first radiographic signs may be detected and includes subluxation of the femoral head and delayed development of the craniodorsal acetabular rim. Grossly the joint capsule and teres ligament are stretched. Between 60 and 90 days old the previously described radiographic changes become more evident. Grossly the joint capsule is stretched and thickened, and the teres ligament is edematous and has significant rupturing of fibers. Osseous changes become evident such as rounding of the acetabular rim, medial bending of the greater trochanter and microfractures of the subchondral bone. Fibrillation of the articular cartilage is evident. As less and less area of femoral head contacts the acetabulum the forces transmitted across these areas are concentrated, thus accelerating the destruction of articular cartilage. Between 3 months and 9 months of age the acetabulum becomes shallow, the acetabular rim becomes rounded, the femoral head becomes flattened and the femoral neck thickens. In addition, the articular cartilage is destroyed, the teres ligament ruptures and the joint capsule becomes severely thickened. Pain associated with CHD comes from microfracture and collapse of subchondral bone, synovitis and tearing of the capsule and ligaments. Range of motion is decreased (especially extension) due to bone deformation and fibrosis of the joint capsule. The previously described pathogenesis is a worst case scenario. The severity of the disease varies with individuals.

History

History depends on the age of the dog. Dogs less than a year of age with joint laxity and minimal DJD will typically have mild clinical signs that include "bunny hopping" and short term stiffness after rest. Some young dogs have acute episodes of lameness, pain and reluctance to exercise. Rest and NSAID's will result in a temporary resolution of the lameness. There is often a period of minimal to no lameness between the initial development of hip dysplasia and clinical onset of lameness due to advanced DJD. The respite from clinical signs may last for months or years. Dogs with DJD (typically older dogs, but often occurs in dogs < a year of age) will have a history that reflects DJD secondary to hip dysplasia such as exercise intolerance, stiffness, difficulty in standing and lameness that are chronic.

Signalment

Virtually all breeds have been reported to have CHD. Giant and large breeds are at greatest risk for crippling clinical signs, especially those with acromegally body types. The onset of CHD and accompanying signs begins in the juvenile. DJD secondary to CHD usually develops in adults, but clinically significant DJD often occurs in dogs < 1 year of age. Dogs may be presented at any time after 5-6 months of age with lameness due to CHD and/or secondary DJD. There is not a gender predilection.

Clinical exam

Young dogs with CHD may have a normal or abnormal gait when first examined. Lameness is typically exacerbated with enough exercised. Muscle atrophy of young dogs is typically minimal. Older dogs will be lame with shortened length of stride, extension of the stifles and hocks to transfer weight to the front legs and will stand and walk with the rear legs abnormally close together. Older dogs will have muscle atrophy that may or may not be obvious. There may be a reluctance to stand and difficulty rising, especially on a slick floor.

With the dog in lateral recumbency the hip should be placed through a range of motion. Flexion will be near normal except in advanced cases of capsular fibrosis. Abduction will be near normal in mild cases but will be significantly less than 90° with chronic DJD/capsule fibrosis and may elicit a painful response. Pain with hip extension is the earliest and most consistent clinical sign of CHD; however, hip extension also extends the lumbosacral junction, and lateral radiographs of that region should be evaluated for pathology. Extension will be less than normal proportional to the amount of capsule fibrosis. Lameness should be evaluated again after manipulation of the hips. The amount of pain caused by extension and the severity of the lameness are good indicators of the clinical severity of the disease. The extent of muscle atrophy is a reliable indicator of chronicity of lameness.

Prior to sedation a neurologic examination (proprioception at least) and complete orthopaedic examination are important. Although lameness is a significant sign with CHD, it is also present with many other orthopaedic and neurological diseases such as cruciate ligament rupture, degenerative myelopathy of German Shepherds, patella luxation, cauda equina syndrome, etc..

Sedation is given to complete the physical examination and allow for proper positioning for radiographs.

The Ortolani sign, Barlow sign and Barden test should be performed with the patient sedated for reliable results. The Barlow and Ortolani signs are performed with the dog in dorsal recumbency (both legs at once) or in lateral recumbency (one leg at a time). One hand is placed on the croup and the other grasp the stifle, with the femur perpendicular in the saggital plane. Firm pressure is applied along the axis of the femur. If the hip luxates dorsally this is a positive Barlow sign, but it can be difficult to feel. Continuing dorsal pressure and ABduction of the femur(s) that reduces the hip luxation is a positive Ortolani sign. The Ortolani sign will often give a palpable and often audible "pop" as the hip reduces. The results of the Barlow and Ortolani test are independent of one another. Positive signs indicate hip luxation and reduction. Negative signs can be due to a normal hip, an excessively thick joint capsule, rounding of the dorsal acetabular rim and/or hip luxation prior to the manipulations, and do not rule-out CHD, especially in older dogs. The Barden sign is performed by palpating the greater trochanter with one hand and grasping the femoral diaphysis with the other. The femur is lifted or levered (adducted) laterally in an attempt to lift the femoral head out of the acetabulum. Lateral displacement of the greater trochanter of more than a quarter of an inch is a positive sign indicating joint laxity. One author has suggested that a positive Barden test in puppies is a reliable indicator of CHD, but is not widely accepted.

Ancillary exam(s)

Numerous radiographic views of the hips have been proposed, each with advantages and disadvantages. The standard position is ventrodorsal with the femurs extended and rotated internally. Symmetry is critical for accurate evaluation of the radiographs. The film should include the sacroiliac joint and the femoral condyles, and care taken that they are not underexposed. Abnormalities include less than 2/3 of the femoral head being in the acetabulum, non-parallel joint space from the craniodorsal aspect to the fovea capitis, sclerosis of the subchondral bone at the cranial margin of the acetabulum, rounding or osteophyte formation at the craniolateral margin of the acetabulum, thickening of the femoral neck or periarticular osteophytes. Based on these criteria the OFA grades hips as excellent, fair, good (these 3 receiving certification numbers), borderline (for dogs < 2 years old and ineligible for an OFA number), mild dysplasia, moderate dysplasia and severe dysplasia. OFA with only give a number for dogs ≥ 2 years old. An older grading system for dysplastic hips is grade one if the hip is 25% luxated, grade II for 50% luxation, grade III for 75% luxation and grade IV for 100% luxation. An additional measurement is the Norberg angle. A line is drawn from the center of one femoral head to the center of the other femoral head, and a line drawn from the center of the femoral head to the tip of the craniolateral margin of the acetabulum. An angle of < 105° indicates excessive laxity. Disadvantages of the standard position are that the positioning reduces the hips maximally and may be misleading as to the amount of laxity, and the dorsal acetabular rim and it's coverage of the femoral head are difficult to evaluate.

The Penn Hip is a stress radiograph that promotes luxation of the femoral head at the time of radiograph. The dog is placed in dorsal recumbency with the femurs perpendicular to the table. A bar is placed between the femoral diaphyses and the stifles are pressed together, levering the hips out. The distraction index (laxity) is calculated as the distance between the center of the acetabulum and the center of the femoral head divided by the radius of the femoral head. Dogs with a distraction index < 0.3 are unlikely to develop hip dysplasia compared to over 60% of dogs with a distraction index > 0.5 develop hip dysplasia.

Other stress radiographs techniques have also been described.

The dorsal acetabular rim (D.A.R.) view of the hip allows accurate evaluation of the amount of dorsal coverage provided for the femoral head. A craniodorsal projection is centered on and parallels the dorsal acetabular rim. The view is for triple pelvic osteotomy evaluation, but is not necessary for TPO.

Treatment(s)

CHD treatments include conservative, femoral head & neck excision (FHO), triple pelvic osteotomy(TPO), total hip arthroplasty (THA), juvenile pubic symphysiodesis (JPS), and others.

Conservative management of CHD in the young dog is aimed at prevention of joint laxity and subsequent damage. Dogs kept in a cage will sit with their legs flexed and abducted reducing the hip joint maximally, and avoid the joint trauma associated with exercise. Research has demonstrated that pups kept in a cage until 6 months old will have stable hips and avoid CHD. Unfortunately, the lack of socialization made them unacceptable as pets or working dogs. However, applying this knowledge with common sense by combining socialization with cage confinement is a reasonable approach. Daily periods of exercise with socialization plus periods of cage confinement build muscle, socialize and allow stressed tissue time for healing. An additional factor in conservative management in young dogs is reducing the growth rates, shown by numerous studies to reduce the incidence of many JBJD's. In a study of 222 German Shepherds, the 111 dogs that weighed more than the group mean at 2 months old had a 63% incidence of CHD at a year of age, compared to 37% of the dogs weighing less than the mean. Feeding a good quality commercial diet at recommended levels, not ad libitum, and avoiding supplementation with vitamins and minerals is recommended by most veterinary nutritional experts. Maximizing growth rate of puppies does not result in larger adult dogs. One study followed dogs diagnosed with CHD at < a year old and managed conservatively. The mean follow up period was 4.5 years (range 18 months to 11 years). Although 89% had radiographic evidence of DJD, 76% of the owners reported that their dog had no or mild lameness and were acceptable as pets.

Conservative management of older dogs is aimed at relief of pain and maintaining function of hips that have irreversible DJD. Avoiding obesity is extremely important, but often overlooked. Keeping the dog in a warm environment decreases the activity of gamma fibers in the muscle spindle therefore decreasing muscle spasm. Exercise is necessary to maintain muscle mass and allow for cartilage nutrition, but dictated by common sense. Non-abusive activities such as swimming and leash walks should be encouraged. Abusive activities such as running and jumping stress the cartilage and joint capsule excessively and cause the release of inflammatory mediators that exacerbate the degenerative process and cause pain. Even after periods of non-abusive activity pain may be evident. If so, NSAID's are given for a day or two to allow return to exercise. Polysulfated glucosaminoglycans have been used with success in dogs to minimize the effects of DJD, and has very low incidence of reported adverse effects. Conservative therapy can result in an acceptable pet for years and delay or avoid the need for surgery. Pain that cannot be controlled by NSAID's, loss of function and readily appreciable muscle atrophy indicate failure of conservative therapy. Surgical treatment have better results if performed before muscle atrophy becomes significant.

Femoral head and neck excision (FHNE) (Gridlestone's procedure) was first described in 1929, has and is used extensively. The procedure is indicated for dogs with significant pain due to DJD secondary to CHD. The surgical procedure consist of a craniolateral approach and luxation of the hip. Visibility is improved with a modified Watson-Jones approach which is distal reflection of the vastus lateralis and intermedius m. origins to fully expose the neck shaft junction where the osteotomy begins. The osteotomy goes from the lesser trochanter to just medial to the greater trochanter, taking care to remove all of the femoral neck and leaving a smooth osteotomy. A modification of the procedure is transpositino of the deep gluteal tendon between the acetabulum and the femoral osteotomy site. Daily exercise should be encouraged a few days after surgery until normal use returns. Results are good to excellent in ~ 85% of the dogs. The percentage of good results decreases as the dogs weight increases. In addition, dogs with significant muscle atrophy consistently have poorer results. Use of deep gluteal transposition has been the author's standard for years with good results, but has not been formally evaluated.

Triple pelvic osteotomy (T.P.O.) prevents hip subluxation by rotating the dorsal rim of the acetabulum laterally to provide more coverage of the femoral head. TPO is indicated for CHD in dogs with minimal degenerative changes radiographically. Ideally the patient should be 6 to 7 months old with deep acetabuli and no radiographic evidence of DJD. However, dogs up to a year of age and mild DJD frequently yield good results. Controversy exist over dogs > 1 year of age with mild radiographic DJD, but good results are often achieved in these dogs as well. Contraindications for TPO are a more than mild DJD: shallow acetabulum, loss of the dorsal acetabular rim, femoral neck osteophytes, etc. Triple pelvic osteotomy includes osteotomy of the pubis, ischium and ilium resulting in a freely moveable acetabulum. A plate is then applied to the ilium that rotates the dorsal rim of the acetabulum laterally. Plates are available in 30°, and 40° of rotation (other angles from other manufacturers). A 30° plate is applied and the Ortolani test performed; if + then the 30° plate is replaced with a 40° plate. Adjunctive procedures include arthrocentesis to remove excessive joint fluid, imbrication of the joint capsule and/or distal transposition of the greater trochanter (used with the Gorman approach) and are very effective in tightening the joint. The procedure can be done bilaterally at the same time. If two surgeries are used the time between surgeries should be minimal (less than 3-4 weeks). Immediate postoperative joint radiographs may show improvement but persistent subluxation due to filling of the acetabulum with the edematous round ligament and excessive joint fluid. Radiographs a month after surgery will demonstrated improved joint congruity. Postoperatively the dog should be cage confined until the ilial osteotomy heals. Prognosis varies directly with the amount of DJD at the time of surgery. Excellent results are common for dogs operated before the onset of DJD.

Juvenile pubic symphysiodesis, like TPO, is intended to stop hip luxation/subluxation (which leads to DJD) by altering the dorsal acetabular coverage of the femoral head. Candidates for JPS are 3-4 months old (although reports of up to 6 months of age with poorer results has been reported). Electrocautery is used to kill the physis at the ventral midline, or pelvic symphysis. Electrocautery units with indicate dose (joules or other) of electricity used is necessary to reliably kill the physis with out additional damage to adjacent tissues (e.g. urethra). Caution must be taken to protect the urethra which is immediately dorsal to the pelvic symphysis. When the pelvis symphyseal physis stops growing and the other pelvic physes continue to grow the result is lateralization of the dorsal acetabular rim. Obviously, JPS must occur while the pubis is still actively growing (not just radiographically open physes), and 90% of bone growth is complete by 6 months of age in all but giant breed dogs according to Headhammer. JPS candidates is based on Penn Hip index scores, Ortolani signs, and lack of or minimal DJD in dogs 3-4 months of age.

Total hip arthroplasty (THA) involves replacement of the femoral head and acetabulum with artifical components. THA is indicated in dogs over 40 pounds (i.e. large enough to accept the implants) with pain and lameness due to CHD and irreparable femoral head/neck or acetabular fractures (after the acetabular fractures have healed). Other reported indications that the author disagrees with are irreducible chronic hip luxations, failed femoral head and neck excision, and revisions of failed THA's. Contraindications include lack of pain or lameness regardless of radiographic appearance, infection anywhere in the body (e.g. cystitis, bacterial dermatitis, gingivitis), neurologic disease affecting the rear legs, concurrent orthopedic problems (e.g. cruciate rupture) or dogs with an open trochanteric physis. Surgical technique depends on the type of implant used. Implants can be held in place with bone cement or press fits (cementless). Cementless implants have been developed due to the problems of cement disease (bone lysis due to reaction with the bone cement) and infection. Postoperative care includes cage confinement for 3-4 weeks followed by an additional month of avoiding excessive activity (i.e. running, jumping). Complications include cement disease, luxations, fissure fractures, infection, neurapraxia, and bone resorption and occur in about 10% of the cases. However, many of the complications are potentially correctable.

Prognosis/client education

Prognosis for CHD depends on the severity of the disease, the treatment used, and the dog's use and pain tolerance. Triple pelvic osteotomy and juvenile pubis symphysiodesis are theoretically best (if the dogs is a candidate) because they preserve a normal hip. Selecting candidates for JPS or TPO should only include dogs with minimal to no DJD if good outcomes are desired. This depends on client education when the dog is a puppy for breeds at high risk so CHD can be radiographically detected by 4 months of age for JPS and by 6 months of age for TPO. Once DJD has developed, conservative therapy is reasonable but will eventually fail in many dogs. Clients using conservative therapy should be cautioned that poorer results are to be expected with surgical procedures if muscle atrophy is allowed to become severe. Total hip arthroplasty, when complications do not occur, gives excellent results and maintains a ball and socket mechanics for the hip joint. Femoral head and neck excision is a reasonable and less expensive alternative with a lower rate of significant complications that THA. FHO has been routinely successful for the author in all size dogs for many years.