Page 598 - ONLINE PROCEEDING BOOK WSAVA 2017
P. 598

An Urban Experience
WSVA7-0587
ORTHOPAEDIC SURGERY
DEVELOPMENTAL ELBOW DISEASE – HOW I TREAT?
N. Fitzpatrick1
1Fitzpatrick Referrals, Eashing, Surrey, UK
Background:
A triad of pathologies has been historically-grouped under the generic term of ED: MCD, OC or OCD
and UAP. EI may have a key underlying role in most manifestations and may also be associated with other conditions of the juvenile elbow, such as HIF. While several diseases may coexist within the same joint, it is apparent from histomorphometric, biomechanical and heritability data that there is considerable independence in development of these multifactorial disease processes. This is further complicated by the spectrum of clinical signs and macroscopic pathology associated with any single disease process, which has important implications for treatment and prognosis. For example, MCD may predicate and be part of a disease continuum with lesions associated with the medial aspect of the humeral condyle, becoming MCompD, and potentially warranting an entirely different interventional approach.
Since these disease processes may or may not be aetiopathogenically related from a biologic and/or biomechanical perspective, the term ED isn’t particularly helpful with respect to explaining the pathology to dog owners or with regard to treatment. DED may be a more appropriate umbrella for these disparate but inter-related conditions. These diseases are the result of complex inter-related biomechanical and biological phenomena. We have recently demonstrated three distinct patterns of  ssuring-fragmentation of the medial coronoid process (tip, radial incisure and radial incisure-tip), and we have developed a grading scheme for lesions of the medial compartment. This system evaluates and grades position and type of  ssuring or fragmentation of the medial coronoid process as well as grade of cartilage erosion and whether it is locally or diffusely affecting the medial coronoid process or the opposing aspect of the medial surface of the humeral condyle. Cartilage erosion is graded according to the modi ed Outerbridge score, 0 being normal and 5 being fully eroded and eburnated.
Pathologic changes initially affect subchondral bone with formation of microcracks, characteristic of local fatigue failure. Although the precise nature of this fatigue phenomenon remains elusive, several biomechanical hypotheses encompass the disparate range of recognised pathologic changes, all of which may be attributable to HUC, with radial incisure or coronoid tip  ssuring/fragmentation potentially arising from varying
ectopic focal overload phenomena. Physiologic overload may be the result or anomalous interaction between the radius, ulna and humerus in the sagittal or transverse planes and in axial or torsional loading patterns. HRI, HUI, RUI and HCD are all possible forms of EI and could contribute to varying patterns of disease. Intrinsic or secondary conformational variations may in uence the effect of incongruence and the pull of lever arms such
as the biceps-brachialis complex and the  exor tendons originating on the medial epicondyle may be relevant with regard to how disease manifests.
In our study which interrogated the medial coronoid process using micro-CT, coronoid processes affected
by radial incisure fragmentation showed signi cantly altered subchondral trabecular architecture compared with normal controls, whereas tip fragmentation did not. This intimates that variable patterns of biomechanical overload (regional mechanical variance) or variable biologic response within zones of the medial coronoid process (regional biologic variance) may result in
differing patterns of disease. For example, the radial incisure pattern of disease closely mirrors an earthquake phenomenon whilst the tip pattern is more akin to an avalanche, using geophysics as an analogy. The inciting forces and patterns of incongruity giving rise to these variances are not fully understood at this time, nor is the fact that disease progression varies enormously between affected dogs with ostensibly similar disease patterns
ab initio. Clinical signs associated with these processes may also vary widely, and this may be attributable at least in part to variability of patient response to pain, patient accommodation to the disease process, or bilateral concomitance of disease rendering ostensible lameness dif cult to discern.
There is a growing body of evidence that disease occurs in the very early stages of skeletal development, but may not be clinically evident until later and that subtle early changes can be dif cult to elucidate on conventional imaging. Conversely clinical signs with profound disease may be present in some patients from a few months of age. Conformational differences have been demonstrated by our group between normal Labrador Retrievers
and those affected by medial coronoid disease, but whether anomalous conformation predicates abnormal biomechanics or vice-versa remains to be determined.
Work-Up:
A thorough clinical history is key to the assessment
of any lameness, including duration and intensity of lameness and the owner’s actual perception of the problem. A clinician’s perception of lameness is very subjective and it has been well established that force plate data diverges from this perception and that both
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42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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