Juvenile bone and joint diseases: large dogs, rear legs; and small dogs (Proceedings)
OCD of the hock occurred bilaterally in 42% of the reported cases. The lateral trochlear ridge is involved in 25% of the cases and the medial trochlear ridge in 75% of the cases.
JBJD's of large dogs, rear legs
Osteochondritis Dissecans (OCD) Hock
OCD of the hock occurred bilaterally in 42% of the reported cases. The lateral trochlear ridge is involved in 25% of the cases and the medial trochlear ridge in 75% of the cases. Lesions tend to be very large and most commonly are located at the proximal or central aspects of the medial trochlear ridge. Multiple OCD lesions per joint has been reported in 3 dogs. In addition, subchondral bone cyst similar to those reported in man and horses has been reported in one dog. OCD of the hock accounts for 9% of all canine OCD reported to the VMDB.
Age at presentation ranges from 4 months to 4 years, with less than year old being most common. Rottweiler's have accounted for 41% of the reported cases. Males account for 50% of the reported cases.
Lameness is often subtle with an insidious onset. Several months between initial lameness and presentation to a veterinarian is common.
Marked hyperextension of the tarsus is common. Swelling of the periarticular tissues and distention of the joint is common, unlike OCD of other joints. Additional findings may include decreased range of flexion, valgus deformity of the tarsus and pain at full flexion and/or extension.
Imaging of the OCD lesion of a tarsus can be difficult, and requires excellent technique and "skyling" of the lesion. In addition, lateral trochlear ridge lesions might be missed due to superimposition of the calcaneous in dorsoplantar radiographs. Therefore, several radiographic projections are recommended to visualize the OCD lesion(s). A D45° L-P1MO projection skylines the medial trochlear ridge while the D45° M-P1LO projection skylines the lateral trochlear ridge. Flexion of the tarsal joint to an angle 10° -15° from the X-ray beam removes the superimposition of the calcaneous to better visualize the central portion of the lateral trochlear ridge, but not the proximal part of the lateral trochlear ridge. Widening of the medial tibiotarsal joint space due to flattening of the medial trochlear ridge is an early and progressive radiographic sign. Additional radiographic changes suggestive of OCD of the tarsus include osteophyte formation, and soft tissue swelling. Lameness might be minimal despite severe DJD changes radiographically.
The benefit of surgery over conservative treatment of OCD of the tarsus is debatable. In one report of 11 dogs (17 joints), with a follow up time of 16-79 months, the authors reported no difference between operated and un-operated joints based on clinical examination by two veterinarians (one blinded to treatment method) and radiographs. In contrast, a different study stated that surgery is usually successful if it is performed prior to the onset of debilitating osteoarthritis, reporting good to fair results 10 months after surgery, but poor results with conservative therapy. Numerous other authors state surgery is preferred over conservative treatment. OCD lesions of the tarsus tend to be quite large and their removal produces a significant defect and instability of the joint. Maintaining the OCD cartilage flap in situ is preferable to removal of the flap IF it can be stabilized and healing promoted. Attachment of an OCD flap with autogenous bone plugs, lag screw or Kirschner wires has been reported, but the lack of significant subchondral bone with the flap often makes this difficult or impossible. Drilling of an attached flap to create vascular access channels is common in man. The use of N-Butyl 2-Cyanoacrylate for stabilization of tarsal OCD lesions has been reported in 3 dogs that resulted in a 30-40° loss of range of motion but no progression of DJD radiographically and no lameness at 9, 13 and 16 months after surgery. The author has used forage to create vascular access points of fixation with fair to good results, dependant on existing DJD. Surgical technique is probably important to the outcome. Approaches include transaction of the collateral ligament, malleolar osteotomy or combined approaches dorsal and plantar to the collateral ligament without transaction of a collateral ligament or osteotomy. Most lesions can be adequately exposed without osteotomy or desmotomy thus avoiding the additional morbidity of these procedures. Surgery of an asymptomatic joint is questionable.
Prognosis of OCD of the tarsus is guarded, but depends on many factors. Minimal curettage is important to minimize joint instability. Additional factors that affect prognosis include unilateral versus bilateral joint involvement, size of the OCD lesion, surgical approach and the duration between onset of clinical signs and treatment (severity of DJD at the time of treatment). Postoperative lameness might be minimal despite progressive and or severe DJD radiographically.
Bilateral lesions occurred in 72% of the 135 reported in the literature. A single lesion on the lateral femoral condyle (medial aspect or the weight-bearing surface) occurred in 95% of the cases. Lesions on the medial condyle occurred in 4% of cases and multiple lesions per stifle occurred in 2 dogs. OCD of the stifle accounts for 4% of all OCD cases reported to the VMDB.
Males were affected in 76% of the 135 reported cases of OCD of the stifle reported in the literature. The most common breeds are German Shepherds (56% of reported cases) and Great Danes (24% of reported cases). Age at onset was 3-4 months old in 17% of the reported cases, 5-9 months old in 59% of reported cases and > 9 months old in 24% of reported cases.
A familial association has been reported in two cases.
Discomfort and a decreased range of motion (especially extension) are found with manipulation of the stifle. An audible click has been reported during joint manipulations. Concurrent pathologies (e.g. patella luxation, hip dysplasia) is common with OCD of the stifle.
The most common radiographic lesion is flattening of the lateral femoral condyle or a punctate radiolucent area of the lateral femoral condyle. Oblique views that skyline the lateral femoral condyle should be performed in suspected cases (lateral projection with slight external rotation of the tibia). A single lesion on the medial or weight-bearing aspect of the lateral femoral condyle has been reported in 95% of the cases. Lesions occur on the medial femoral condyle in approximately 4% of cases. OCD lesions on the trochlear ridge, patella and multiple lesions per stifle have also been reported. Joint mice, osteophytes and varying degrees of DJD may be seen.
Removal of the OCD flap or joint mouse, beveling the edge of the OCD bed and forage of the bed are recommended. With extremely large flaps the lesion has been reattached using small K-wires, and in humans with bone pegs.
A limited numbers of dogs have been followed for a sufficient postoperative period to make definitive statements. However, as with OCD elsewhere the amount of DJD and the size of the lesion are important considerations. Our impression is that the stifle is less tolerant of OCD than the shoulder but more so than the hock, and a fair to guarded prognosis can be given if the lesion is of moderate size, the lesion is not on a weight bearing articular surface, and DJD is minimal.
Panosteitis and HOD See front leg Juvenile Bone and Joint Diseases.
Hip Dysplasia (CHD)
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.
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 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.
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.
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, 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.
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.
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 affects 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 can not 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 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.
Congenital Patella Luxation (MPL; LPL)
Medial patella luxation (MPL), Lateral patella luxation (LPL)
Coxa vara (bowleg), and excessive retroversion of the femoral head causes of MPL. Coxa valga (knock-kneed) cause LPL. Traumatic patella luxation is not discussed here.
The patella is a type A (primary function is articulation) sesamoid bone located in the tendon of insertion of the quadraceps muscles. The origins of the quadriceps muscles are the proximal femur and immediately cranial to the acetabulurn (rectus femoris m.). The quadriceps m. follows a straight line, by necessity, to its insertion at the tibial crest. If the quadriceps muscles are displaced medial, then the patella must also be displaced medially. Coxa vara, and to some extent excessive retroversion, displace the origin of the quadriceps m. medially. In the 6 week old dog, altered quadriceps muscle pull causes permanent bone changes in 2-4 weeks. The resulting deformities are bowing and torsion of the distal femur, bowing and torsion of the proximal tibia due to compression from the medially located quadriceps. The trochlear groove is shallow because pressure from the patella on the articular-epiphyseal growth plate is necessary to retard bone growth locally and form a trochlear groove. Absence of the patella due to luxation results in failure of the trochlear groove to achieve a normal depth. Rotational instability of the stifle occurs because of stretching of the lateral joint capsule and other lateral supporting structures. The severity of MPL is progressive until about 6 months of age. Grade II - IV MPL in a juvenile dog can be expected to progress and surgical correction should not be delayed. The grade of MPL is stable after 6 months of age. However, DJD will be progressive and there is a report of 15% increased risk of cranial cruciate ligament rupture in dogs with MPL.
MPL is a very common juvenile joint disease which necessarily develops in dogs less than 6 months of age. MPL and LPL are developmental diseases, not "congenital" and the conventional name indicates. However, dogs may not be presented until months or years later when DJD or cruciate rupture become clinical. Predominantly small breeds of dogs are affected, although it does occur in large dogs. Lateral patella luxation is a less common occurrence and typically occurs with coxa valga associated with hip dysplasia in large breeds of dogs. Feline patella luxation is rare and occurs in association with bilateral congenital hip luxation. There is no sex predisposition. A review of 124 cases of patella luxation reported that in small breeds 98% are medial and 2% are lateral; in medium breeds 90% are medial and 10% lateral; large breeds have 80% medial and 20% lateral; giant breeds 66% medial and 33% lateral.
Grade 1 and 2 MPL are often an incidental finding on orthopedic examination. History often reveals the dog carries his leg for a few steps then returns to weight-bearing, without evidence of pain. Onset is insidious. Dogs with grades 3 and 4 patella luxation have more severe and consistent lameness and deformity of the leg(s).
Observation of a dog with MPL from the rear will demonstrate a bowlegged stance with the point of the hocks (calcaneal tuber) pointed laterally. Walking the dog may or may not carry the leg for a few steps then return to weight-bearing. MPL occurs bilaterally in most cases. With grade 4 MPL the dog is unable to extend the affected leg to the floor. Palpation and manipulation of the stifle is not painful. Medial patella luxation is graded during physical examination by extending the stifle and determining the location and ability to reduce the patella.
• Grade 1: The patella is located in the trochlear groove. It can be manually luxated, but reduces itself as soon as manual pressure is released.
• Grade 2: The patella may be found either in or out of the trochlear groove, and is easily manipulated to the other location, where the patella remains when manual pressure is stopped.
• Grade 3: The patella is located out of the trochlear groove. It can be manually reduced, but reluxates as soon as manual pressure is released.
• Grade 4: The patella is out of the trochlear groove and cannot be reduced. As the grade of medial patella luxation gets worse, so does the degree of bowing of the femur and tibia, rotation of the tibia and shallowness of the trochlear groove.
"Sloppy" patella is when the patella can be luxated both medially and laterally. It is important to evaluate for this condition during examination so appropriate surgical correction for the lateral luxation (imbrication of the medial joint capsule) can be performed.
When evaluating patella luxation, the amount of internal rotation of the tibia is important. A straight tibia helps reduce the patella, while internal rotation (which can be extreme in some dogs) pulls the patella medially.
Radiography is only useful in documenting the severity of DJD, and assessing the amount of osseous deformity if osteotomies are required for treatment of grade 3 & 4 MPL. Synovial fluid analysis also documents DJD.
Goals of surgery are to straighten the quadriceps mechanism (quadriceps-patella/trochlear groove-tibial crest), achieve adequate depth of the trochlear groove and to effect minimal postoperative pain (both acute and chronic) so the patella will stay in the trochlear groove and the dog will use the leg. Some authors state a set list of procedures for a given grade of MPL. Others advocate use of prosthetic sutures to pull the patella and/or tibial crest laterally rather than straighten the quadriceps mechanism. It is our belief that each case is unique and any combination of the procedures described below should be used as needed to achieve the surgical goals.
• Abrasion trochleoplasty is deepening the trochlear groove with a file, threaded Steinmann pin, or burr. The groove should be deepened until 50% - 100% of the patella's cranial to caudal depth will sit in the groove (as with the other techniques of deepening the trochlear groove). Excessive deepening will hold the patella in place but will cause chronic pain and prevent the dog from using the leg. This technique destroys the hyaline cartilage, which is replaced with fibrocartilage. The technique is simple, but tends to cause more postoperative morbidity in large dogs.
• Wedge resection of the trochlear groove deepens the trochlear groove by removing the trochlear groove, deepening the bone bed from which it came, then replacing the trochlear groove. A fine toothed "hobby saw" is used to make a cut from the lateral trochlear ridge that is directed caudally to the midline of the bone (approximately the origin of the caudal cruciate ligament) with the saw blade placed lengthwise from proximal to distal. A similar cut is started at the medial trochlear ridge and meets the first cut caudo-centrally. The trochlear groove with its subchondral bone is lifted out and the cut in the femur is deepened with a second cut or a flat file. The wedge is then replaced, resulting in a deeper trochlear groove. Pins or other fixation devices are not needed to hold the wedge in place. The advantage of this technique is that it preserves normal hyaline cartilage. Although it is technically simple in larger dogs (> 15 lbs), it becomes technically more difficult as the dog becomes smaller.
• Block resection of the trochlear groove is similar to the wedge resection. Rather than a pie shaped wedge, a brick shaped block is made by parallel craniocaudal cuts at each trochlear ridge with a "hobby" saw which are joined by a distal to proximal osteotome cut in the coronal plane. Wedge vs block resections are selected based on width to depth ratios and surgeon preference.
• Chondroplasty is a groove deepening technique that is possible only in young dogs (i.e. < 5 months). The hyaline cartilage is cut with a scalpel and the cartilage elevated from the subchondral bone with a periosteal elevator, a procedure that is not possible in older dogs without tearing the cartilage. Subchondral bone is removed to the desired depth with rongeurs or other instruments, and the cartilage laid back in place. This procedure also preserves hyaline cartilage and is possible in any size stifle. If the cartilage is damaged during elevation then trochleoplasty is performed.
• Lateral imbrication of the joint capsule and retinaculum pulls the patella laterally. The amount of tightening is based on judgment to make the patella track in the center or slightly lateral in the trochlear groove. The most important sutures are from the center of the patella distally toward the tibial crest, and should be placed first to evaluate effectiveness. It is important to imbricate the joint capsule since tightening the retinaculum alone will not prevent luxation.
• Medial desmotomy releases the medial pull of the joint capsule and retinaculum. This should not be done unless the patella can not be reduced otherwise. Equal tension from the medial and lateral joint capsules pulls the patella caudally into the trochee groove. Medial desmotomy allows the patella to displace cranially and makes it easier to luxate, perhaps laterally.
• Tibial crest transposition realigns the quadriceps mechanism by moving the tibial crest laterally (for medial patella luxation). An osteotome is used in the medial to lateral plane. The tibial crest is left attached distally by a small amount of bone and periosteum to minimize the risk of avulsion of the transposed crest by pull of the quadriceps. A new bed is created for the tibial crest laterally and the crest is "broken" (breaking the distal attachment without breaking the periosteum) over to its new position. A K-wire or 2 are used to fix the tibial crest in place.
• Derotational suture is placed laterally from the lateral femorofabellar ligament through the tibial crest, as a lateral suture for cranial cruciate ligament rupture. The tibial crest is held in external rotation while the derotational suture is tied. Unlike, the tibial crest transposition, a derotational suture constantly holds the patella tendon insertion laterally, and does not have the risk of avulsion of the patella tendon insertion.
• Osteotomy of the distal femur and/or proximal tibia may be required in grade 3 and will be required in grade 4 MPL to straighten the leg. Fixation is typically with bone plates.
Prognosis varies from excellent with grade 1 to terrible with grade 4. The second most important predictor is whether surgery is performed unilaterally or bilaterally; if patella luxation exist bilaterally then surgery should be performed bilaterally to promote self induced physical therapy on both rear legs. Grade 2 patella luxation will usually respond well to surgical correction if DJD and/or cranial cruciate rupture are not present. If CCL rupture is present, surgery to stabilize the CCL takes precedence, and surgery for patella luxation (other than joint capsule imbrication) should be delayed as the postoperative treatments for these two surgeries are diametrically opposed. If the leg carrying lameness is chronic then difficulty may be encountered in getting the dog to bear weight on the leg despite an excellent surgery. These dogs are light weight and can get along very well on three legs, plus the habit of carrying the leg. Any pain in the stifle after surgery will also cause the dog not to use the leg. If the dog is < 6 months old the grade of MPL may worsen and surgery should not be delayed. Dogs > 6 months old are not urgent.
Small Dogs, Rear Legs
Legg-Calves'-Perthes Disease (LCP)
Avascular necrosis of the femoral neck, coxa plana, osteochondritis deformans juveniles.
LCP disease has been shown to be highly heritable in Manchester Terriers.
The exact pathogenesis is unclear. Vascular supply to the femoral head and neck is apparently a component, although experimental creation of avascularity does not mimic the syndrome seen clinically. Estrogen and/or testosterone have been implicated due to the 4:1 male to female ratio seen in humans, however, there is no sex predisposition in dogs.
Dogs are presented between 3 and 13 months of age. Breeds less than 20 pounds are affected. There is no sex predisposition.
Lameness is unilateral in approximately 85% of the cases, and insidious in onset. History of trauma is usually absent.
A weight-bearing lameness is usually present, although leg carrying will occasionally be seen. Mild to moderate pain will be elicited with extension and/or internal rotation of the hip. Muscle atrophy and shortening of the affected leg may also be appreciated.
The earliest radiographic changes are a widened joint space and a mottled appearance to the femoral neck (focal areas of radiodensity mixed with focal areas of radiolucency). An "apple core" appearance of the femoral neck occurs as the disease progresses and is often followed by collapse of the femoral head and/or neck.
In early cases with minimal radiographic changes conservative therapy with strict cage confinement for 6-8 months has been suggested. However, most veterinary surgeons advocate femoral head and neck excision as the treatment of choice. Excellent clinical results after surgery have been obtained, partly due to the low weight of affected animals.
Normal or near normal gait can be expected. Affected animals should not be bred.
Hip Dysplasia and Patella Luxations See discussion under JBJD, Large Dogs, Rear Legs.
Small Dogs, Front Legs
Congenital Shoulder Luxation (CSL)
All cases of congenital shoulder luxation reported in the literature have been medial, indicating a defect in the medial collateral ligament and medial joint capsule. The role of osseous and muscle abnormalities is uncertain.
Age at presentation usually ranges from 3 - 8 months of age, although older and younger can occur. The most common reported breed are mixed breeds and toy poodles, but it has also been reported in the Chihuahua, Pomeranian, griffon, miniature pinscher, wire-haired fox terrier, pug, King Charles spaniel, Lhasa apso, Pekingese, dachshund, Shetland sheepdog, collie, and Norwegian elkhound. There is no apparent sex predisposition.
A weight-bearing lameness of insidious onset is the typical history. The dog may occasionally carry the leg(s) for brief periods of time.
Palpation will indicate the medial position of the humeral head, or the ability to easily luxate the humeral head medially. Mild discomfort may be present. There may also be loss of extension. Congenital shoulder luxation can be unilateral or bilateral. Muscle atrophy may be noted, especially in unilateral cases.
Radiographs will indicate the medial luxation of the shoulder, although stress may need to be applied to luxate the shoulders. Careful evaluation of the depth of the glenoid and medial rim of the glenoid are needed to evaluate the chance of successful surgical repair. In addition, the humeral head may be flattened.
Surgical reduction is difficult to maintain even if the glenoid depth and medial glenoid rim are not too malformed. Methods of reduction include biceps tendon transfer, transposition of a portion of the supraspinatous muscle, synthetic suture patterns, autogenous skin or fascia grafts and transarticular pinning. In many cases reduction is impossible to maintain. If the dog is satisfactory clinically, conservative therapy may be preferrable. Shoulder arthrodesis may also an option.
Surgical correction can be attempted with an understanding with the client that chances for success are poor. Arthrodesis can be recommended for cases where lameness is severe. Affected animal should not be bred.
Congenital Elbow Luxation (CEL)
Several etiologies have been suggested, but none proven. Hypoplasia or aplasia of the ligaments (especially the medial collateral ligament) has been suggested, however, our dissection of affected joints has found these structures normal in appearance. Congenital elbow dislocation has also been associated with polyarthrodysplasia and ectrodactyly. Elbow dislocation associated with asynchronous growth of the radius/ulna is discussed in that section.
Unknown. The olecranon is displaced laterally making contraction of the triceps muscle ineffective in extending the elbow. One case of medial congenital elbow luxation has been reported with the same results.
The condition is present at birth and is generally recognized at 6 - 8 weeks old when puppies begin to walk. Any toy breed can be affected. There is no recognized sex predilection.
The dog is unable to extend the elbow and does not bear weight on the affected leg(s). There is obvious deformity of the elbow. Bilaterally affected dogs crawl on their front legs or stand on their rear legs only and have a "praying Mantiss" appearance.
There is limited or no ability to extend the elbow. Obvious deformity of the elbow is due to lateral displacement of the olecranon and medial displacement of the humeral condyles. The forearm is pronated. Palpation is not painful.
Craniocaudal radiographs image lateral displacement of the olecranon; the olecranon will appear as if it were a mediolalateral radiograph. The radial head may or may not be displaced. In addition, there will be severe malformation of the joint's osseous structures.
The goal of surgical treatment is to achieve a functional joint, not reconstruct the joint so it appears normal radiographically. Surgical reduction and maintenance in young dogs (6-12 wks old) is closed. The joint is manually reduced and held in reduction with a pin from the olecranon to the distal humeral metaphysis (avoiding the joint), or dynamic pinning where a pin is placed mediolaterally in the olecranon and mediolaterally across the humeral epicondyles. A rubber band is placed from the lateral point of the olecranon pin to the medial point of the humeral pin to maintain reduction (opposite for medial dislocation). An external bandage may be added and reduction is maintained for 7-10 days. In older dogs where the joint cannot be reduced, transposition of the olecranon to the caudal aspect of the joint has been used successfully.
Despite the severity of the deformity, surgical treatment has usually returned normal function to the joints if treated while the joint can still be manually reduced. Affected dogs should not be breed.