Joey A. Sapora Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA Canine Elbow Dysplasia (CED) is a commonly encountered orthopedic condition in veterinary general practice that causes lameness in juvenile, medium to large breed dogs. The use of the term dysplasia to explain the complex syndrome that leads to osteoarthritis and pain of the canine elbow may be an oversimplification, particularly to pet owners. The term Developmental Elbow Disease1 has been proposed to better capture the complexity of a condition where the relationship between genetics, biology, and biomechanics has not been fully elucidated. For clarity, the traditional term of CED will be applied in this chapter. Semantics aside, it is important to acknowledge the intricate and often frustrating condition of CED to optimize client education and patient care. This chapter will review the etiopathogenesis of CED, discuss common physical exam findings, diagnostic radiographic technique, and management strategies for various stages and components of the disease. Ununited anconeal process (UAP) in the dog was first recorded in the 1950’s,2,3 and medial coronoid disease, osteochondritis dissecans, and humeroradioulnar incongruity were first described in the 1970’s.4–6 The International Elbow Working Group (IEWG) defined Elbow Dysplasia almost 15 years later to consist of four entities: fragmented medial coronoid process (FCP), osteochondrosis (OC) of the medial humeral condyle, UAP, and elbow joint incongruity.6 The hereditary nature of CED is well‐established with multiple genes and environmental factors playing a role in the end‐stage manifestation of elbow osteoarthritis.7–11 The prevalence of cases of “elbow joint disease” presenting to primary care veterinary practices is around 0.56%,12 while the incidence of CED ranges from 0% to 55% depending upon the patient’s breed, the population evaluated, and the screening protocols applied.10 Some of the breed prevalence and odds ratios for UAP, medial coronoid disease, OC of the medial humeral condyle, and elbow joint incongruity currently published in the literature are listed in Figure 45.1. For example, a Gordon Setter has a CED prevalence of 0.126g, meaning 12.6% of the population is suspected to have CED (or 126 out of every 1,000). The odds ratio for Gordon Setters being diagnosed specifically with FCP is an OR of 19.8i, meaning that the odds of FCP occurring in this breed are 19.8 times more likely than other breeds. Figure 45.1 Published prevalence rates of Elbow Dysplasia based upon breed noted in the current small animal literature, in addition to prevalence and odds ratios for FCP, Elbow Incongruity, OCD, and UAP. Prevalence is the proportion of a population that has the condition over a set period of time and can be more easily interpreted as a percent. Odds ratio can be thought of as the odds the condition will occur in that breed compared to it not occurring. aBaers et al. (2019). bAlves‐Pimenta, S., Colaco, B., Silvestre, A.M., et al. (2013). Prevalence and breeding values of elbow dysplasia in the Estrela mountain dog. Veterinarni Medicina 58, 2013 (9): 484–490. cMorgan, J.,P., Wind A., Davidson A.P. (1999). Bone dysplasias in the labrador retriever: a radiographic study. Journal of the American Animal Hospital Association 35(4):332–340. dLavrijsen, I., Heuven, H., Voorhout, G., et al. (2012). Phenotypic and genetic evaluation of elbow dysplasia in Dutch Labrador Retrievers, Golden Retrievers, and Bernese Mountain dogs. The Veterinary Journal 193(2):486–492. eCoopman, F., Verhoeven, G., Saunders, J., et al. (2008). Prevalence of hip dysplasia, elbow dysplasia and humeral head osteochondrosis in dog breeds in Belgium. The Veterinary Record 163(22):654–658. fBeuing, R., Mues, C.H., Tellhelm, B., et al. (2000). Prevalence and inheritance of canine elbow dysplasia in German Rottweiler. Journal of Animal Breeding and Genetics 117(6):375–383. gOberbauer, A., Keller, G., Famula, T. (2017). Long‐term genetic selection reduced prevalence of hip and elbow dysplasia in 60 dog breeds. PloS one 12(2):e0172918. hLappalainen, A., Hyvärinen T., Junnila J., et al. (2016). Radiographic evaluation of elbow incongruity in Skye terriers. Journal of Small Animal Practice 57(2):96–99. iLaFond, E., Breur, G.J., Austin, C.C. (2002). Breed susceptibility for developmental orthopedic diseases in dogs. Journal of the American Animal Hospital Association 1;38(5):467–477. CED is not limited to medium and large breed dogs, with chondrodystrophic and toy breed dogs being affected as well.13,14 Male dogs, specifically male German Shepherd Dogs and Labrador Retrievers, may be at a higher risk of CED than female dogs.11,15 Identified environmental risk factors that may contribute to the disease include increased body weight, increased food intake, higher proportional intake of fat, and exercise involving chasing after balls and sticks thrown by the owner.16,17 It is also important to note that long‐term reduced food intake has been shown to decrease the severity of osteoarthritis over time, an expected sequela of CED.16 As there are no curative medical or surgical interventions available to treat CED, prevention of the disease through judicious breeding strategies is required. This starts with early identification and client education. Given the polygenic nature of the condition, the development of a single genetic test to screen for CED is unlikely for quite some time. Screening based on Estimated Breeding Values (EBV) is recommended and has been shown to be superior to screening based on phenotype. EBVs have been used for decades in livestock populations and involve tracking and measuring heritable traits using statistical models. This industry‐tested process is superior to phenotypic selection and provides faster genetic progression when attempting to decrease the prevalence of CED in various canine populations.8,9,18–20 These tools are already being employed by certain universities and the Orthopedic Foundation for Animals (OFA) to combat hip and elbow dysplasia. The medial coronoid process forms the most distomedial aspect of the trochlear notch and increases the contact area of the ulna with the humerus21 (Figure 45.2). The medial coronoid process is cartilaginous at birth, and complete ossification, occurring from base to apex, has been shown to occur in small dogs by 16 weeks of age and in larger dogs by 20 weeks of age.22 Changes to the medial coronoid process can include fissuring, fragmentation, and subchondral bone fatigue that commonly involve either the coronoid apex or base.23 Studies have demonstrated that histologic changes to the coronoid originate in deeper layers of the articular cartilage, mainly in the calcifying zone, prior to any changes at the level of the articular surface. Retained hyaline cartilage and excessive amounts of Type X collagen have been identified in affected coronoids.24–26 FCP is the most common form of CED (>96%), and the disturbance in ossification is thought to also give rise to cleft formation as a result of either normal physiologic or abnormal biomechanical forces.10,24 These biomechanical forces are the premise behind elbow joint incongruity and its contribution to FCP development. For example, a patient with a “short radius” leading to an “elevated” medial coronoid at the level of the elbow joint may have an increased load placed over the medial coronoid, leading to fragmentation. Approximately 24% of FCP cases have computed tomographic (CT) signs of joint incongruity. FCP can occur as a single entity or in conjunction with OC or, less commonly, with UAP.27 Figure 45.2 Anatomic specimens of the canine ulna showing the medial coronoid process (yellow arrow) from a medial (top left) and cranial (top right) view of the proximal ulna. Bottom images are similar views with the addition of the radius. Note the size of the medial coronoid and its intimate association with the radial head. Source: Image courtesy of Joey Sapora. With computed tomography and arthroscopy now commonplace in small animal specialty hospitals, we are better able to characterize FCP pathology and its relationship with arthroscopic cartilage change. These cartilage changes mainly affect the humeroulnar articulation along the medial aspect of the joint with the degree of joint incongruity and the presence of an FCP correlating with the degree of cartilage injury present.28 The descriptive term Medial Compartment Disease (MCD) is now preferred over “medial coronoid disease,” to describe the severe and sometimes widespread cartilage wear that may be present with or without the presence of coronoid pathology or joint incongruity.29,30 These changes include chondromalacia, full‐thickness cartilage erosions, and “kissing lesions” believed to be secondary to humeroulnar conflict. Although there is currently controversy about which terms should be used with inconclusive verbiage used in the published texts, that debate is beyond the scope of this chapter. While asynchronous bone growth can lead to humeroulnar conflict, a musculotendinous contribution from the biceps brachii and brachialis muscle complex has also been proposed.31 The biceps brachii and brachialis muscle complex inserts along the radial tuberosity in addition to the ulna along the medial aspect of the joint, and contraction causes both flexion of the elbow in addition to supination. This leads to rotation of the radial head along the radial incisure of the ulna, essentially squeezing the medial coronoid into the radial head.31,32 This focal pressure over time is theorized to contribute to FCP and is the rationale for the Biceps Ulnar Release Procedure (BURP). OC refers to the failure of the normal process of endochondral ossification, in which hyaline cartilage is replaced with bone.33 This normal endochondral ossification is required for the developing medial coronoid, anconeal process, and humeral condyle. In 1976, Olsson was one of the first to consider that all three of these conditions (FCP, UAP, OCD) could, in fact, be manifestations of OC,33 and it is still proposed that FCP, UAP, and asynchronous growth between the radius and ulna may be clinical manifestations of this disease.34 The underlying etiology of OC of the medial humeral condyle is believed to be a combination of genetic and environmental factors, including nutritional imbalance, rapid growth, physical activity, and microtrauma.23 The role that elbow incongruity plays in the development of elbow OC is unclear. Diets high in calcium and phosphorus, as well as excessive vitamin D intake, have been associated with the development of OC.35–37 It is reported more commonly in males than females.23 The anconeal process of the ulna does not have a separate center of ossification in small breed dogs,2,38 but the failure of appropriate fusion of this process is well‐documented in many large and giant breeds,39 with the German Shepherd Dog overrepresented.27 Mineralization of the process begins by around 10–16 weeks of age with complete fusion occurring at approximately 20 weeks.40,41 The process is termed “ununited” if ossification is not completed by 20 weeks of age, and it was the first described component of CED initially reported in the 1950’s.2,3 The currently accepted pathogenesis for UAP involves asynchronous growth of the radial head relative to the ulna, leading to a “longer radius” generating increased pressure across the anconeal process.23 This likely occurs in the early phase of radial growth (ages four to five months). As some patients can have both UAP and FCP concomitantly with a short radius, a subsequent stunted radial growth phase (five to six months of age) has also been proposed.23,27 The role of elbow incongruity in the proposed manifestations of FCP and UAP has been well‐established42–44 with up to 60% of dogs with FCP having underlying joint incongruity.45 Three forms of elbow incongruity are proposed and these include radioulnar incongruity (RUI), humeroulnar incongruity, and radial incisure incongruity.29 RUI is further broken down into positive RUI (short radius) and negative RUI (short ulna). A “short radius” is suspected to place supra‐physiologic loads on the medial coronoid leading to FCP, while a “short ulna” is suspected to place supra‐physiologic loads on the anconeal process leading to UAP.46 Humeroulnar incongruity has more recently been investigated47–49 and refers to the congruency of the trochlear notch with the humeral articulation. Some patients may have an abnormal “C‐shape” to their trochlear notch, appearing to have a more shallow, or in other cases, a more acute curve to the notch, which is suspected to alter the biomechanics of the joint.46,50 Assessment of radial incisure and humeroulnar incongruity is complex and requires advanced diagnostic imaging, and its role in the progression of disease is yet to be fully understood. When considering elbow incongruity in general practice, a routine radiographic elbow series will aid in the detection of severe RUI (step ≥3 mm). More subtle RUI, in addition to a detailed assessment of humeroulnar and radial incisure incongruity, is better evaluated with a CT scan, however, the estimation of incongruity can be affected by patient positioning. In models of experimentally induced RUI, arthroscopic assessment has been shown to be a more sensitive and reproducible technique when compared to radiographic and CT analysis.51 Characteristic gait changes in patients with CED include lifting up of the head as the painful limb strikes the ground during the stance phase (i.e., “head bob”) and decreased stride length during the swing phase of the gait cycle. In bilaterally affected patients, weight is often shifted caudally onto the pelvic limbs. At a stand, patients with medial compartment disease may shift their weight to the lateral compartment and tend to stand with slight external rotation of the distal extremity (pseudovalgus, Figure 45.3) or may have a bow‐legged stance (elbow abduction) when more severely affected.23 Palpation of joint effusion during the standing exam can improve the detection of subtle effusion as the joint is loaded. The effusion may or may not be present and is most commonly identified along the lateral aspect of the joint between the lateral epicondyle and olecranon, underneath the anconeus muscle (Figure 45.4). With chronicity, remodeling of the joint occurs, and normal bone prominences become less identifiable, particularly along the lateral compartment. Discomfort may be elicited when placing the joint through a range of motion depending upon the degree of effusion and capsulitis present. The diagnosis of medial compartment disease based on a pain response is challenging, and patients can be asymptomatic. It is also important to note that the degree of synovial inflammation is directly related to exposure to subchondral bone, which may be present in varying degrees based on the stage of OC or medial compartment disease.23 Figure 45.3 A one‐year‐old spayed female mixed breed dog with elbow dysplasia characterized by medial coronoid process fragmentation and 3 mm of positive RUI (left > right). Note the external rotation of the left forepaw, a conformational change thought to improve comfort related to medial compartment pain. Source: Image courtesy of Joey Sapora. Various maneuvers that should be performed include a complete range of motion assessment, full elbow flexion, pronated flexion, elbow hyperextension, and the “Campbell’s test.” Subjective assessment for the normal range of motion of the canine elbow includes full elbow extension to approximately 180°, and flexion of the elbow with the dorsal aspect of the carpus reaching the level of the shoulder (Figure 45.4). This degree of normal elbow flexion may not be normal for well‐muscled breeds (i.e., French Bulldogs, English Bulldogs, Pit Bulls, etc.).
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Canine Elbow Dysplasia
Introduction
Etiopathogenesis of Canine Elbow Dysplasia
Components of Canine Elbow Dysplasia
Fragmented Medial Coronoid Process (FCP) and Medial Compartment Disease (MCD)
Osteochondrosis of the Medial Humeral Condyle
Ununited Anconeal Process
Joint Incongruity
Physical Exam Findings
Elbow Range of Motion
Elbow Flexion
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