Juvenile bone and joint diseases: large dogs front leg (Proceedings)

Ectrodactyly

Synonyms

Split-hand deformity, lobster claw.

Etiology

The deformity is inherited in cats, horses and people; probably inherited in dogs.

Pathogenesis

Agenesis and malformation of the phalanges, metacarpal and carpal bones in utero is the basic pathology, and is occasionally accompanied by subluxation of the elbow.

Signalment

The deformity is present at birth. It has been reported in 17 dogs, of which 15 were large dogs. Mixed and pure breed dogs have been afflicted, without breed predisposition. Two dogs had bilateral ectrodactyly.

History

The deformity is present at birth.

Clinical exam

Obvious deformity of the manus is present, but is not painful. Lameness is weight-bearing and mild. Two of the 17 reported cases had bilateral involvement.

Ancillary exam(s)

Radiography will demonstrate agenesis and malformation of the phalanges, metacarpus and carpus. Subluxation of the elbow is also a potential finding.

Treatment(s)

There is no known treatment.

Prognosis

Mild lameness without apparent pain is present that worsens with exercise. If elbow subluxation is present then progressive degenerative joint disease can be expected.

Carpal laxity syndrome

Synonyms

Dropped Carpus. Carpal hyperextension.

Etiology

Poor muscle tone and/or joint laxity.

Pathogenesis

Poor muscle tone allows hyperextension or hyperflexion of the carpus (carpii). The condition is self-limiting and permanent pathology rarely occurs.

Signalment

The condition has been reported in a puppies 2 - 5 months of age.

History

Owners note carpal hyperextension or hyperflexion, on one or both carpii.

Clinical exam

Carpal hyperextension or hyperflexion, unilaterally or bilaterally, with mild to moderate lameness. Pain and other deformity are absent.

Ancillary exam(s)

None. Radiographs do not image abnormalities.

Treatment(s)

Exercised puppies have been reported to spontaneously recover in 7-10 days, while confined puppies recover in about 6 weeks. The forelimbs should not be splinted or cast.

Prognosis/client education

Spontaneous recovery. Exercise should be encouraged.

Hypertrophic osteodystrophy (HOD)

Synonyms

Canine skeletal scurvy, idiopathic osteodystrophy, Barlow's disease, Moller-Barlow disease, metaphyseal osteopathy.

Etiology

Unknown. Previous theories of etiology that have been disproven include deficient dietary vitamin C, excessive dietary vitamin D, excessive dietary minerals and excessive calories. Since only primates and guinea pigs require dietary vitamin C, then a lack in the dogs diet is not a problem. Abnormal metabolism of vitamin C is a possibility. However, H.O.D. has as many differences from human scurvy as it does similarities. A history of overnutrition of vitamin D, minerals and/or calories is not present in the majority of cases and correction of nutrition (if needed) does not result in cure.

Pathogenesis

A band of metaphyseal bone immediately adjacent to the physis consist of disrupted trabeculae, hemorrhage, hemosiderin deposits, necrotic trabeculae and inflammatory cells. Large multiple foci of resorption of the metaphyseal trabeculae occurs and may be accompanied by neutrophil infiltration similar to that seen with osteomyelitis. This band corresponds to the pathognomonic radiolucent line (pseudophysis) seen radiographically. In some cases their may also be irregular widening of the physis (zone of hypertrophy - presumably due to disruption of metaphyseal blood supply), and subperiosteal hemorrhage. Later in the course of the disease dystrophic periosteal bone formation in the metaphyseal area frequently occurs that radiographically is similar to a fracture callus. Vascular supply does not cross the cartilaginous physis, and laminar flow dynamics cause the blood flow in the zone of necrosis to be stagnant. Slow blood flow reduces oxygen supply to these cells during a time of extremely rapid growth and high metabolism. This corresponds to HOD developing in giant breed dogs during their time of most rapid growth (3-5 months of age), especially if nutritionally stimulated to grow rapidly.

Signalment

Age is typically 3 - 5 months (range 2-8 months; occurs only in dogs with open physes), any large breed can be affected, and the sex ratio is 1:1.

History

History may range from a mild limp to peracute onset of refusal to stand, anorexia, malaise, depression and dehydration. Diarrhea and/or upper respiratory disease has been frequently reported in the literature prior to clinical signs of H.O.D.; the significance is unknown.

Clinical exam

A temperature of 104° F or above is a consistent finding. Deep palpation of the joints/metaphyseal region is moderately to extremely painful. Swelling and palpable warmth of the region may be found. Swelling may be soft in the peracute stage, or firm in more chronic cases. Pain is also elicited by placing the joint through a range of motion. The distal radius/ulna are most severely affected, followed by the distal tibia/fibula. In more severe cases all the appendicular joints can be affected as well as the temperomandibular joint.

Ancillary exam(s)

Radiographs of the affected metaphyseal region will demonstrate a pseudophyseal line, which is pathognomonic for the disease. This is a radiolucent line immediately adjacent to the physis on the metaphyseal side. Soft tissue swelling is also observed. In more chronic cases periosteal dystrophic calcification may be present. The distal radius/ulna and distal tibia/fibula are most commonly affected. In severe cases radiographic changes may be observed throughout the appendicular skeleton, the mandible, maxilla, costochondral junction, scapula and anterior border of the ilium.

Synovial fluid analysis will indicate increased volume (1-3 ml) of transparent, straw colored fluid with normal stretch. Cytology will report increased numbers of neutrophils.

Treatment(s)

The disease will spontaneously resolve. However, pain relief should be provided. In mild cases a safe non-steroidal antiinflammatory such as aspirin can be given. Short term corticosteroids are very effective in all cases, and required for more severe cases. More severe cases will also require good nursing care such as fluid therapy, force feeding and avoidance of decubital ulcers. Supplementation with vitamin C and vitamin D are contraindicated since they both elevate serum calcium levels and may promote dystrophic calcification and decrease bone resorption. Mineral supplementation should likewise be avoided. Inappropriate nutrition, if any, should be corrected.

Prognosis/client education

In mildly affected cases the prognosis is good. More severely affected cases, and especially chronic cases, can result in permanent malformation of the affected metaphyses and mild to severe lameness. Death is rare, but is most often due to euthanasia subsequent to relapses of the condition. Episodes of relapse are fortunately rare.

Retained cartilagenous core (RCC)

Synonyms

None

Etiology

Retained cartilaginous core is a osteochondrosis that affects the distal ulnar physis.

Pathogenesis

Failure of the distal ulnar physis to undergo normal endochondral osteogenesis results in subclinical or mild shortening of the ulna.

Signalment

Great Danes. Any large or giant breed of dog is susceptible.

History

Mild lameness.

Clinical exam

Mild lameness and minimal or no deformity of the antebrachium.

Ancillary exam(s)

Radiographs show a pathognomonic "flame" appearance of the distal ulnar physis. The radiolucent ulnar physis extends 4-6 cm into the metaphysis and is surrounded by a sclerotic line of bone. Shortening and valgus deformity are minimal (10°) to absent.

Treatment(s)

Nutrition should be non-supplemented adult maintenance diet. Avoid growth diets (puppy chow) and supplementation with vitamins and/or minerals.

Prognosis/client education

Prognosis is good.

Asynchronous growth of the radius and ulna (AGRU)

Synonyms

Radius curvus. Radius curvus is an inaccurate term because there are forms of A.G.R.U. that do not cause curvature of the radius. Additionally, asynchronous growth of the tibia and fibula has been reported once in 6 month old Shetland Sheepdog. Shortening of the fibula caused fibular head dislocation (distal) and a valgus deformity.

Etiology

Partial or complete premature closure of the distal ulnar physis (most common), distal radial physis or proximal radial physis (uncommon) can cause A.G.R.U.. Premature closure of the physis is due to trauma to the physis (e.g. Salter-Harris fractures); however, the trauma may be minor enough to not be noticed or reported in the owner's history. Synostosis following fracture of the radius and ulna can also cause A.G.R.U.. If the fracture callus of the radius and the fracture callus of the ulna unite then sliding between the radius and ulna during growth is prevented. A history of trauma would be expected. Retained cartilaginous core of the distal ulna (discussed above) is another cause of A.G.R.U., and is probably a form of osteochondrosis.

Asynchronous growth not related to trauma may have a genetic influence and breed predisposition: achondroplasia in the bassett hound, chondrodysplasia in the Alaskan Malamute and Labrador retriever, and retained cartilage core in the Great Dane and other giant breeds.

Pathogenesis

The proximal radial physis contributes 40% of the length of the radius while the distal radial physis contributes 60%. In contrast, 100% of the ulna length distal to the elbow comes from the distal ulnar physis (85% of overall length). Therefore, as these bones grow in length the diaphysis of the ulna must "slide" distally relative to the radial diaphysis if the carpus and elbow are to remain parallel. In order for a.g.r.u. To occur the bones must be growing. The younger the dog the greater the potential deformity. The larger the breed (i.e. The longer the mature radius/ulna length) the greater the potential for deformity. The majority of bone length is obtained by 6 mo. Of age (approximately 90% depending on breed). A.g.r.u. Can not occur in dogs with closed physes.

Signalment

Dogs less than 6 months of age at the time A.G.R.U. occurs, presentation may be at older ages. Either sex since trauma is part of the etiology (except retained cartilage core). Any breed may be affected. Larger breeds (i.e. longer mature radius/ulna) have more potential for deformity. A.G.R.U. may be difficult to detect in chondrodystrophic breeds such as the bassett hound or dachshund.

History

Insidious onset of lameness and deformity, usually unilateral. Careful questioning may reveal minor trauma 3-4 weeks prior to presentation, i.e. lameness for a day or two after jumping off a porch. Major trauma (e.g. hit by car), Salter-Harris fracture of a radial physis or distal ulnar physis, or diaphyseal fractures of the radius and ulna are also possible histories.

Clinical exam

Lameness depends on the degree of deformity. Palpation of the area does not elicit a painful response. The deformity depends on the physis injured (or synostosis), the severity of the injury and the potential bone growth remaining at the time of injury.

Premature closure of the distal ulnar physis is the most common form of A.G.R.U.. The deformities include valgus deformity of the distal radius and carpus, cranial bowing of the distal radius, supination of the manus, humeroulnar subluxation with varus deformity and decreased length of the antebrachium. In chronic cases DJD of the carpus and elbow develop.

Partial closure of the lateral aspect of the distal radial physis results in deformity similar to those with premature closure of the distal ulnar physis, and is the second most common form of A.G.R.U.. Partial closure of the medial part of the distal radial physis is rare.

Cessation of growth from the entire distal radial physis results in decreased length of the antebrachium with the radius being shorter than the ulna. There is minimal angular deformity, widening and subluxation of the radiocarpal and humeroradial joints. DJD of the carpus and elbow develop.

Premature closure of the proximal radial physis results in widening and subluxation of the radiohumeral joint plus decreased length of the antebrachium. Angular deformity is uncommon.

The contralateral leg, if not affected with A.G.R.U., may show carpal hyperextension and spreading of the digits due to chronic excessive weight-bearing, and may be the reason for presentation (i.e. abnormality noticed by the owner).

Synostosis is secondary to fracture of the radius and ulna with the formation of a single callus incorporating both bones, or joining of these bones by a lag screw or other fixation device during fracture repair. Angular deformity of the antebrachium is the primary result. Shortening of the antebrachium and carpal involvement are usually not severe.

Ancillary exam(s)

Radiographs will confirm the angular and rotational deformity, joint malarticulation of the elbow and carpus, and the specific underlying etiology (the affected physis or synostosis). True craniocaudal and mediolateral projections are important if corrective osteotomies are considered.

Treatment(s)

Treatment depends on the age of the dog, the specific cause of A.G.R.U., and the surgeons experience/preference.

Ulnar osteotomy. This is by far the most effective treatment, but must occur before 5 months of age (i.e. while the dog is still actively growing). If malformation is mild to moderate and significant growth potential remains then an ulnar osteotomy is a reasonable consideration. A 1 cm or more section of the ulnar diaphysis is excised. Because this is a young dog with very good bone healing potential, union of the ulna becomes a problem. To avoid ulnar union at least a centimeter of ulnar diaphysis is removed, the periosteum is sutured over each end of the ulna and a fat graft is interposed at the osteotomy site to avoid bony union. Separation of the proximal and distal ulna obviates the need for the ulna and radius to "slide" relative to one another. Some degree of straightening of the radius will occur according to Wolff's law, and satisfactory results may be achieved if the deformity is not too severe.

Wedge osteotomy. If significant angular/rotational deformity exist, the ulna can be transacted and a wedge of bone from the greatest curvature of the radius removed. The wedge can be discarded and the radius realigned to correct rotation and curvature, resulting in a transverse fracture line. The size and orientation of the osteotomies of the radius are critical and are facilitated by true craniocaudal and mediolateral radiographs. Alternately, the wedge can be replaced in the osteotomy reversing it=s position, thus increasing the length of the radius. Fixation of the radius is then performed, usually with a bone plate.

Dome osteotomy. Dome osteotomy has been described which results in a "ball and socket" or dome osteotomy in the radial diaphysis. The concept is to allow easier rotational and axial alignment following the osteotomy. Unfortunately, a true dome is difficult to achieve, and technically difficult to the point of being impractical.

Periosteal stripping. This procedure is used primarily in large animals, and there is little experience with it in dogs. However, in cases of mild deformity periosteal stripping may be of some benefit.

Dynamic proximal ulnar osteotomy. This involves freeing the proximal ulna by ulnar osteotomy proximal to the interosseous ligament and loosing the soft tissue attachments between the radius and ulna. An intramedullary pin is then placed antegrade in the ulna that does not engage the ulnar cortex distal to the osteotomy. This allows the proximal ulnar articulation to move (dynamic) proximo-distally along the axis of the pin allowing the forces that act on the elbow to place the proximal ulna in the best position, hopefully correcting any incongruity if the trochlear notch is of normal size and shape. Limited experience suggest the procedure is of limited benefit but more clinical experience is needed.

Prognosis/client education

The prognosis depends on the degree of deformity, the dogs age and the mature size (age & mature size equals potential bone length remaining). The more severe the deformity, the larger the breed, and if the dog has is over 5 months of age the poorer the prognosis for normal limb function. In addition to shortening of the front leg(s), progressive degenerative joint disease of the carpus and/or elbow can be significant problems throughout adulthood, which also formed abnormally during growth. If the dog is young, more than one corrective osteotomy may be required. For young and/or severely deformed dogs, results of surgery are satisfactory limb function at best; a normal limb is usually an unreasonable expectation. For nearly mature dogs (5-6 months or older) with minimal deformity conservative treatment may be satisfactory. Corrective osteotomies help cosmetics more than lameness, depending on the severity of joint disease.

Panosteitis

Synonyms

Eosinophilic panosteitis, enostosis.

Etiology

Unknown. The disease was originally reported to be a chronic eosinophic osteomyelitis.

Eosinophilia has since been a rare finding on histopathology or in systemic circulation. No evidence of bacterial infection has been shown by culture, histopathologic examination, nor response to antibiotics. Likewise, viral infection has been speculated but never proven. Initial reports of panosteitis in 1951 approximates the initial use of modified live distemper vaccination, which prompted recommendations of using killed, adenovirus, or recombinant DNA vaccines instead of MLV's. Koch's postulate has not been fulfilled for any microorganism. Because of the high percentage of German Shepherd dogs affected (86% in one study) a possible genetic influence has been proposed; however, a VMDB study reported 59 different breed diagnosed with panosteitis. Other proposed etiologies include transient vascular abnormalities, allergy, metabolic dysfunction, hyperestrinism, parasite migration and autoimmune disease. Stress has been proposed as a contributing factor.

Pathogenesis

Panosteitis affects the long bones of large and giant breed dogs. Death of the adipose tissue in the bone marrow is the initial histopathologic change of panosteitis. Osteoblastic and fibroblastic activity follows affecting the medullary canal, endosteum and periosteum. In its final stages osteoclastic activity becomes apparent histopathologically. Although the typical clinical course last ~ 1 week, the histopathological and radiographic course of the disease last approximately 90 days. Panosteitis rarely occurs twice in the same bone (1%). However, occurrence in multiple bones is the rule rather than the exception, and begins regardless of the stage of panosteitis in other bones. The total course (all episodes) of the disease may last from a week to over a year, and generally does not recur after 24 months of age.

Signalment

Any large or giant breed dog is at risk for panosteitis. One VMDB study reported 59 breeds with a diagnosis of panosteitis, with the most common being German Shepherds 39%; Labrador retrievers 11%; Bassett hounds, Golden retrievers and mixed breeds 8% each; Rottweilers 3%; and Great Danes and Doberman pinschers 2% each. Panosteitis has rarely been reported in small breed dogs (< 2 % in two separate studies). Typically, the initial episode of panosteitis occurs between 5 months and 18 months of age. However, dogs as young as 2 months and over 5 years old have been reported to have panosteitis. 57% of initial episodes occur at ≤ 12 months old, and 89% are ≤ 24 months old. Panosteitis affects males more than females, generally 4:1 (range 67% to 84% males). Females are very prone to have the initial panosteitis episode during their first estrus.

History

A sudden onset of weight-bearing lameness that may increases in severity over the first few days. Lameness due to panosteitis generally last 2 days to 2 weeks. A unique characteristic of panosteitis is that rest, exercise, and NSAID's have minimal effect on the severity of clinical signs. Panosteitis may affect more than one bone or leg, either sequentially or simultaneously. "Shifting" of the lameness to another leg every few weeks is a typical history. However, many dogs have one episode or few episodes of progressively less clinical severity. Panosteitis rarely occurs twice in the same bone but often recurs in the same leg. Owners may report listlessness, anorexia and reluctance to move.

Clinical exam

The lameness ranges from subtle to not bearing weight depending on the individual dog, severity of the disease, and the stage of the disease at the time of presentation. Most dogs have mild lameness. In the acute stage the dog will be most overtly lame, with some dogs appearing depressed and reluctant to walk. Body temperature is usually normal, but may be very slightly elevated. Deep palpation of the affected bone(s) will result in a very painful response for the amount of pressure applied, especially if palpation is near the nutrient foramen area (junction of the proximal third and distal two thirds of the bone). Care should be taken not to compress muscle or nerve during deep palpation thus giving a false response. Bones of the front leg are affected more often than bones of the rear legs. Reports do not agree which bones are most often effected (ulna, 42%; radius, 25%; humerus, 14%; femur, 11%; tibia, 8%) (humerus, 68%; femur, 68%; ulna, 54%; radius, 27%; tibia, 24%). The onset of disease in one bone is not affected by the presence or absence of disease in other bones, so more than one bone can be affected at a time with panosteitis or other orthopedic conditions.

Ancillary exam(s)

The radiographic phases tend to lag behind the clinical stages by 1-2 weeks. There appears to be no relationship between the severity of clinical signs and radiographic appearance. Radiographic findings can be divided into early, middle and late phases of the disease. The sum of these phases is typically 90 days, but can last twice that long. The initial radiographic change is increased radiolucency of the medullary canal in the region of the nutrient foramen that is so mild that it is usually not appreciated, or at best leads to a presumptive diagnosis. In what is recognized as the early phase there is increased opacity of the medullary canal at the metaphyseal-diaphyseal junction (area of the nutrient foramen). The opacity is initially mild and progresses to obvious. This corresponds to the osteoblastic and fibroblastic activity observed histologically. There is a loss of normal trabecular pattern or a granular appearance. As the opacity increases there may be difficulty distinguishing the cortex from the metaphysis. In the middle phase the radiodensities become patchy rather than completely filling the medullary canal. The endosteal surface becomes thick and rough. The fine trabeculae of normal bone is usually replaced with fewer, courser trabeculae. Smooth periosteal new bone may be observed in some cases. In the late phase the opacity of the medullary canal regresses but the course trabecular pattern remains. The roughened endosteal surface and periosteal new bone return toward normal. The epiphysis is never affected radiographically or histopathologically. Clinical pathology is not enlightening; despite the synonym "eosinophilic panosteitis", eosinophilia is a rare finding with panosteitis.

Treatment(s)

Panosteitis is a self-limiting inflammatory disease of the medullary cavity of long bones. Therefore, treatment is either unnecessary or limited to good nursing care and anti-inflammatory drugs (aspirin, corticosteroids) as needed for patient comfort.

Prognosis/client education

Repeated clinical episodes are common, although not a certainty. Subsequent episodes tend to have progressively less severe clinical signs. Episodes typically have clinical signs that last a week or less, with long time periods free of clinical signs. The clinical signs, including all recurrences, may last from a week to over a year. Recurrence after 24 months of age is unusual (11% of cases). The vast majority of dogs can be satisfactorily treated with aspirin or short acting corticosteroids.

Elbow dysplasia

Synonyms

The Elbow Registry (formed by the OFA Jan. 1, 1990) defines elbow dysplasia as "developmental degenerative joint disease" characterized by "smooth periosteal reaction on the proximal anconeal process and/or joint incongruity." The literature defines joint incongruity as proximal placement of the trochlear notch creating a step deformity between the coronoid process and the proximal radial articulation (with the medial coronoid up to 3 mm more proximal than the radius), increased or uneven humeroulnar and humeroradial joint spaces, and cranial displacement of the humerus from the trochlear notch. Older literature used elbow dysplasia and ununited anconeal process synonymously.

Etiology

Etiology is unclear. The length, size and shape of the proximal ulna and trochlear notch are determined primarily by the cartilage model, with minimal contribution from the olecranon apophysis and articular cartilage growth plate. The elbow cartilage models of he radius and ulna are not complete until 16 weeks of age. Growth in length of the proximal ulna is minimal after 16 weeks and complete by 24 weeks of age. After 24 weeks minor growth of the trochlear notch comes from the articular cartilage growth plate. Incongruity of the elbow joint has been the primary focus of etiology. However, the possibility of normal elbow bone formation with excessive forces from the biceps and brachialis muscles has been proposed.

Pathogenesis

The size and shape of the trochlear notch being achieved by 24 weeks of age means that heavier breed dogs must achieve their larger trochlear notch size in the same 24 week period as smaller and finer boned breeds. Failing to do so results in too small a trochlear notch (arc of curvature) to encompass the humeral trochlea. The result is a widened joint space between the center of the trochlear notch and the humeral trochlea, abnormally tight contact between the anconeal process and the humerus, and abnormally tight fit between the medial cornoid process and humerus. These are the breeds and locations that most commonly develop OCD, FCP and UAP. The possibility of excessive tension by the biceps muscle and/or the brachialis muscle causes compression of the joint in the presence of normal bone shape of the elbow has also been proposed.

Signalment

The OFA list breeds with elbow dysplasia on their web site (www.offa.org/stats_ed.html), which should be viewed for the most current information available. Initial onset of lameness due to elbow dysplasia is in young dogs, primarily of large breeds. As of December 2010, the breed with the highest percentage of elbow dysplasia was the Pug (45.7% normal / 105 evaluations). Rankings 2- 40 are large breed dogs. The next small breed dog is the Havanese ranked 41st (92.7% normal). There does not appear to be a sex predisposition.

History

Dogs may be presented because of a subtle front leg lameness or because breeders/owners want to apply for an OFA Elbow Registry certification number.

Clinical exam

Pain may be elicited with full extension and flexion. Lameness is exacerbated with exercise and/or full extension and flexion of the elbow. A stance with elbows abducted and "winging out" while gaiting is sometimes observed.

Ancillary exam(s)

Elbow incongruity may be diagnosed radiographically or may require CT imaging. A flexed lateral radiograph should be performed to rule out UAP. Elbow incongruity has an abnormally tight fit between the humerus and the anconeal process, an abnormally tight fit between the humerus and coronoid processes, increased joint space between the trochlea and the center of the trochlear notch and/or a step deformity up to 3 mm with the coronoid processes being more proximal than the radial head. The OFA Elbow Registry grades elbow dysplasia as Grade I: minimal bone change on the anconeal process of ulna (< 3 mm); Grade II: additional bone proliferation along anconeal process (3-5 mm) and subchondral bone changes (trochlear notch sclerosis); and Grade III: well developed degenerative joint disease with bone proliferation along anconeal process being > 5 mm. Synovial fluid analysis would reflect D.J.D. in advanced cases.

Treatment(s)

Elbow incongruity (without FCP, OCD or UAP) is not currently treatable surgically. Treatment is limited to treatment for degenerative joint disease.

Prognosis

Dogs with elbow incongruity are at risk for DJD, OCD, FCP and UAP. Prognosis is unpredictable because the severity of clinical signs from DJD that will develop in unpredictable on an individual basis. Elbow disease with crippling DJD may be treated with artificial elbow replacement or arthrocentesis.

Fragmented coronoid process (FCP)

Synonyms

Ununited medial coronoid process, elbow dysplasia

Pathophysiology

The etiology of FCP is unclear. The medial coronoid process does not develop from a separate ossification center, thus the term "ununited" is not appropriate. In addition, pathology has resulted from fissures or cartilage erosion of the process without complete bone separation from the rest of the ulna. FCP with concurrent OCD of the medial humeral condyle has been reported, and has been described as a "kissing lesion". The author's experience is that FCP and OCD in the same joint is rare; most humeral condyle lesions are cartilage abrasions from the FCP's sharp edge. Cartilage erosion due to the FCP edge scraping the opposing humeral condyle's cartilage is not OCD. Abnormal articulation of the elbow joints (see elbow dysplasia) has been postulated as a cause of FCP. Normal articulation but with excessive pressure from biceps muscle and/or brachialis muscle contraction; or repetitive excessive compressive impacts have also been speculated to cause FCP.

History & signalment

A sex predisposition does not exist. Onset of lameness may be acute or chronic and usually occurs between 6 months and a year of age.

Clinical exam

Pain may be elicited with full extension and flexion, and with deep palpation of the medial coronoid process, taking care not to compress the ulnar nerve or pronator muscle. Lameness is exacerbated with exercise and/or full extension and flexion of the eblow. A stance with elbows abducted and "winging out" while gaiting is typical.

Ancillary exam(s)

Radiographs with craniocaudal, flexed mediolateral (to rule out UAP), and oblique views are infrequently diagnostic. Most often non-specific radiographic signs of DJD will be seen. Initial signs of DJD are along the olecranon (caution not to mistake the normal craniomedial and craniolateral tubercles of the olecranon as osteophytes), and later signs include subchondral bone sclerosis, narrowing of joint space, multiple periarticular osteophytes, etc. Linear tomography, CT or MR may be required to visualize the FCP with imaging equipment. CT is the author's preferred method of imaging a FCP. Exploratory arthroscopy is a justified and economical method of diagnosis. Radiographs will occasionally identify OCD of the medial humeral condyle. Synovial fluid analysis is helpful to confirm elbow pathology of some type in early or subtle cases. Injection of the joint with local anesthetics does not decrease lameness appreciably.

Treatment(s)

Excision of the FCP via arthroscopy, and treatment of the OCD if present, is indicated if DJD is not advanced. If radiographs are not diagnostic, some have suggested repeating radiographs in 4-8 weeks. If clinical exam and synovial fluid analysis indicate pathology of the elbow, exploratory arthroscopy is probably a better option to slow the progression of DJD as soon as possible. UAP should be ruled out with radiographs, and elbow incongruity may identifiable on radiograph, leaving FCP and OCD as the remaining non-traumatic diseases, both of which are treated arthroscopically. In cases of advanced DJD medical therapy alone is indicated.

Prognosis

Prognosis is guarded, and becomes worse with concurrent OCD or significant DJD. The elbow is the most congruent joint in the dog's body, and unforgiving of insult. Postoperative recovery has been reported to be 3-4 months, although many dogs show immediate improvement after surgery.

Ununited anconeal process (UAP)

Synonyms

Patella cubiti, elbow dysplasia

Etiology

Failure of the physis of the anconeal process to close for unknown reason(s). Potential etiologies include osteochondrosis, or elbow dysplasia that results in excessive pressure on the anconeal process by the humeral condyle.

Pathogenesis

The anconeal process forms from a separate ossification center in large breeds of dogs, bassets and dachshunds; the breeds affected with UAP. In smaller dogs a separate ossification center does not develop and therefore UAP cannot occur. Closure of the physis between the anconeal process and the ulna occurs between 20 & 24 weeks of age. Failure to close results in UAP.

History & signalment

Subtle onset of intermittent lameness between 6 months and a year of age that is exacerbated by exercise. Males are affected twice as often as females. The German shepherd is the most common breed affected, although other large breeds, bassets and dachshunds are also affected.

Clinical exam

Unilateral pathology occurs in 70% of cases, in bilateral cases the lameness may shift from one leg to the other. Flexion of the elbow and application of pressure over the anconeal process may cause pain, as will full flexion and extension. The elbows are often abducted when standing and during gaiting ("winging out"). Some dogs will be asymptomatic until DJD is advanced.

Ancillary exam(s)

A fully flexed lateral radiograph, to avoid superimposition of the anconeal process with the humeral condyles, is diagnostic in dogs over 24 weeks of age. Prior to 24 weeks of age, clinical signs consistent with UAP, irregular margin of anconeal physis radiographically, ± abnormal joint fluid is enough to justify a diagnosis of UAP. DJD is often present by the onset of clinical signs. Synovial fluid analysis will document DJD in chronic cases.

Treatment(s)

The anconeal process may be removed or fixed with a lag screw. Fixation does not give better clinical results and does not always result in union.

Prognosis

Results of surgery are usually good if performed prior to significant DJD. Some degree of DJD is always present, and prognosis should be based on the degree of DJD, the stoic or wimpy nature of the dog, and cognizance that the elbow is a very unforgiving joint.

ODC elbow

Etiology

OCD of the medial humeral condyle is occasionally associated with a concurrent fragmented medial coronoid process (FCP). A "kissing lesion" (abrasion of the humeral condyle cartilage by an FCP) is often incorrectly called an OCD lesion. OCD of the elbow requires systemic osteochondrosis, and will have a subchondral bone defect and a cartilage flap.

Pathogenesis

Elbow OCD accounts for 11% of all OCD reported to the VMDB annually. Osteochondrosis is a failure of normal endochondral osteogenesis, the process by which bone is made from a cartilage model in the growing animal. The disease osteochondrosis is systemic, affecting all articular cartilages (articular-epiphyseal complex ) and physis, but is manifested clinically only at certain locations (osteochondritis dissecans, UAP, RCC). See OCD of the shoulder for more detail.

Signalment

Dogs are usually 4-6 months of age at the onset of lameness. All giant and large breeds are at risk.

History

Lameness may become persistent after a few months (6-8 months of age). Radiographic evidence may not be detected until 6 months of age, despite the lesions presence for weeks to month earlier.

Clinical exam

Pain is usually elicited with full extension, and sometimes full flexion. Lameness is exacerbated with exercise and/or full extension and flexion of the elbow. A stance with elbows abducted and "winging out" while gaiting may be observed.

Ancillary exam(s)

Radiographic diagnosis is more difficult in the elbow than other joints. The earliest radiographic change is often the development of osteophytes at the proximal olecranon. The normal craniomedial and craniolateral tubercles of the olecranon should not be mistaken for osteophytes. Linear tomography, CT or MRI can be useful. Synovial fluid analysis will indicate DJD in chronic cases. Exploratory arthroscopy is justified if clinical signs and synovial fluid analysis strongly suggest FCP and/or OCD of the elbow, and UAP has been ruled out by flexed lateral radiographs.

Prognosis/client education

Since the elbow is the most congruent joint in the dog, the prognosis is guarded for return to normal activity (especially working dogs) and poor for avoidance of DJD. Concomitant lesions of FCP and/or UAP worsens the prognosis, although these combinations are rare. Advanced DJD substantially worsens the prognosis. Postoperative care is similar to OCD for other joints.

Bicepital tenosynovitis

Synonyms

None.

Etiology and pathogenesis

Bicepetal tenosynovitis is ostensibly a repetitive motion injury.

Signalment & history

The most typical signalment and history in the author's experience is a pair of large breed dogs between 6 months and 24 months of age spend hours every days in continuous, high impact activity. Dogs may be more lame later in the day after long periods of exercise. Older dogs, and single dogs, have a greater tendency to rest periodically.

Clinical exam

Lameness is typically mild, but occasionally moderate. Full flexion of the shoulder with extension of the elbow (i.e. pull front legs straight caudally along side of the body) ± direct digital pressure just medial to the greater tubercle may or may not elicit pain.

Ancillary exam(s)

Joint fluid will be normal to very mild indications of synovitis. Radiographs are normal in early cases. Chronic cases may show calcification (enthesiophytes) in the biceps and/or supraspinatous tendon(s); a "groove shot", i.e. radiographic beam directed parallel to and centered in the bicepital groove, is necessary to separate shoulder radio densities from superimpositions from other areas.

Treatment(s)

Numerous treatments have been described. Most cases are adequately treated by forcing a few hours of rest every day until the dog(s) are 2 + years old, thus interfering with the etiology. Lancing the calcification(s), which are typically semi-solid cyst of gritty mucoid matrix, can also be effective; although this is best done with intra-operative radiology. Transection of the biceps tendon, ± reattachment of the tendons origin on the proximal humerus, can also be effective.

Prognosis

Long term prognosis is good, although lameness may persist for prolong time periods if not treated.

OCD shoulder

Etiology

OCD lesions of the humeral head are located on the caudal portion. Lesions may be caudolateral, caudomedial but most often caudocentral. This is the area of greatest weight-bearing, the area of thickest cartilage and the last area in which primary spongiosa is converted to subchondral bone. Rapid growth and excessive activity, i.e. trauma, are thought to be a major inciting causes of OCD.

Pathogenesis

OCD of the shoulder accounts for 74% of the OCD cases reported to the VMDB. Osteochondrosis is a failure of normal endochondral osteogenesis, the process by which bone is made from a cartilage model in the growing animal. The disease osteochondrosis is systemic, affecting all articular cartilages (articular-epiphyseal complex ) and physis, but is manifested clinically only at certain locations (osteochondritis dissecans, UAP, RCC). Physes (including A-E complexes) with osteochondrosis are thickened and have histologically disorganized rows of chondorcytes in the zone of proliferation rather than the normal straight columns of cells. As the physis nears the metaphysis (zone of degeneration), the transverse septa (of the empty chondrocyte lacunae) should break, allowing capillaries to enter and bone matrix to be deposited on the cartilage template (called primary spicules). The major disease causing abnormality is failure of the transverse septa of the cartilage matrix to break down, thus preventing infiltration of capillaries and the conversion of the cartilage template into bone. Therefore, as the germinal layer and zone of hypertrophy continue to produce more cartilage, the cartilage becomes thicker and thicker. Eventually, the cartilage becomes so thick that diffusion from the synovial fluid can no longer supply it's nutrition (cartilage has no blood vessels) resulting in areas of necrosis at the cartilage-subchondral bone junction. Fissure fractures develop in necrotic areas that eventually extend to the articular surface. Lameness is caused by both mechanical irritation (cartilage flap), and chemical synovitis caused by lysosomal enzymes released from the necrotic areas of cartilage when the cartilage fissure communicates with the joint. Long term lameness is caused by development of DJD.

Signalment

Onset is usually between 5 and 10 months of age. Males are affected more often than females. OCD of the shoulder is common in all large and giant breeds, and has been reported in smaller breeds such as the cocker spaniel, whippet, border collie, beagle and miniature poodle.

Clinical exam

Pain is elicited when the joint fully extended. Pain comes from stretching of the joint capsule, specifically from stretching the irritated nerve endings in the joint capsule.

Ancillary exam(s)

The shoulder may need to be internally or externally rotated to "skyline" the lesions located medially or laterally. Radiographs ± joint taps should be performed bilateral even if the lameness is unilateral.

Treatment(s)

Antiquity treated canine OCD of the shoulder conservatively. The results were an abnormal stance but return to no lameness after exercise in 9-12 months for unilaterally affected dog, and 1-2 years in bilaterally affected dogs. As the dogs got older advanced DJD developed with occasional periods of pain and lameness. Dogs with minimal lesions occasionally return to soundness in 2-3 months and had minimal DJD later in life. Reasonable outcomes with conservative treatment is probably due to reattachment of articular cartilage to subchondral bone or a small flap breaking off and the bed healing with minimal deformity; this ostensibly occurs in only ~ 10% of cases.

Surgery significantly decreases the onset and severity of DJD. One study reported 90% good to excellent results after surgery for OCD of the shoulder, versus only 10% good to excellent results with conservative therapy. Surgery is indicated for dogs with shoulder OCD and less than moderate DJD. Failure of conservative therapy is usually not an indication for surgery as DJD is advanced enough to cause persistent lameness despite removal of the OCD flap and forage of the OCD bed. The goals of surgery are to remove the joint mouse/flap, remove unattached cartilage from the edge of the lesion and promote granulation tissue in the bed, if it is not already present, via forage.

Prognosis/client education

Seroma is the most common postoperative complication, but can usually be avoided by surgical approaches that avoid tenotomy, or arthroscopic surgery. Dogs treated surgically typically begin weight-bearing in a few days to 2 weeks. Although surgery minimizes development of DJD, some degree of DJD will develop with time that may or may not result in lameness.