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 fissuring-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 fissuring 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 modified 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 fissuring/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 influence the effect of incongruence and the pull of lever arms such as the biceps-brachialis complex and the flexor 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 significantly 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 difficult 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 difficult 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.
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 owner and clinician can under or overestimate lameness. This is a particular challenge when lameness is bilateral. With every stride each individual limb goes through a step cycle that comprises a stance (weight bearing) phase and a swing (non-weight bearing) phase. In the average dog, each thoracic limb is responsible for approximately 30% of weight bearing when standing and each pelvic limb approximately 20%.
It is important to observe over a distance in excess of approximately fifteen meters away from and toward the observer and also from both sides. Video allows one to build up a data-bank of typical gait patterns and also allows playback in slow motion which can be very helpful to examine for subtle lameness. We have demonstrated in a recent study that dogs affected by DED generally stand with front feet externally rotated and with a more upright elbow stance than normal.
With regard to clinical examination, in dogs affected by MCD and MCompD, flexion and supination generally produces pain. In dogs with humeral intercondylar fissure (HIF) pain can be evident on flexion and pronation or supination but is generally more evident on full extension of the elbow; the same is true of elbows affected by ununited anconeal process (UAP). Elbows affected by MCD and MCompD also generally manifest pain on deep pressure application to the medial aspect of the elbow over the insertion of the biceps brachialis complex on the medial aspect of the ulna. Pain may in fact radiate proximally to the shoulder along the biceps brachii and can be mistaken for shoulder pain.
Radiography remains the mainstay of diagnostic interrogation. Radiography of the elbow joint should involve pulling the elbow away from the thorax so there are no superimposed soft tissues and attainment of a fully flexed and fully extended medic-lateral projection is important. Cranio-caudal projections should be standardised such that the olecranon is always centralised relative to the humeral condyles. Oblique projections can occasionally be useful to skyline specific features such as the epicondyles of the edge margin of the medial coronoid process (MCP), but in reality, because most fissure-fragmentation of the MCP occurs in the region of the radial incisure, which is axial and next to the radial head, the standard or cranio-caudal oblique projections rarely demonstrate fragmentation and CT scan is required.
Exposure factors are important and radiographic contrast in some cases makes the difference between success and failure regarding accurate diagnosis. Subtrochlear sclerosis (STS), which is an increased opacification of the region of the ulna subjacent to the ulnar trochlear notch, is a really important early sentinel of DED and can sometimes be very difficult to detect in early MCD. STS is likely in major part attributed to stress remodelling of the subchondral bone and is frequently present before periarticular osteophytosis occurs. A properly positioned flexed or an extended medio-lateral radiographic projection of the elbow can make the difference between visibility or non-visibility of STS and of periarticular osteophytosis.
Elbow congruity is difficult to appreciate radiographically unless it is of significant magnitude, there can be subtle incongruity that may be dynamic and present only in different positions of flexion and extension, or there can be appreciable incongruity that may only be evident on CT scan or on arthroscopic interrogation. The anconeal process is best appreciated on full flexion of the elbow in medio-lateral projection and this is particularly pertinent for interrogation of new bone formation (periarticular osteophytosis) which is an early sentinel of degenerative joint disease sequel to DED and also for appreciation of UAP.
OCD is often evident radiographically on cranio-caudal projections as subchondral “scalloping” remodelling of the medial aspect of the humeral condyle. This can be confused with subchondral outline irregularity as a result of HUC that can be the consequence of the same supraphysiological overload precipitating MCD. This is generally termed MCompD. CT scan and arthroscopy are definitive for elucidation of a primary humeral defect secondary to OCD by comparison with a secondary humeral defect subsequent to HUC.
Humeral intercondylar fissure (HIF), which is the more correct terminology for what has hitherto been called incomplete ossification of the humeral condyle (IOHC), can involve a fissure line between the medial and lateral aspect of the humeral condyle that may be oblique and may not be apparent on direct cranio-caudal radiographic projections. In fact, the diagnosis may be missed when the HIF is subtle and early in the disease process. Later in the disease process, sclerosis of the margins of the fissure plane creates greater visibility of the lesion. Care must be taken to avoid overinterpretation of overlapping shadows of the cortical margins of the proximal olecranon (Mach Effect). CT interrogation is definitive.
I personally no longer operate on any elbow disease without CT scan because our experience is such that radiography regardless of positioning is not adequately specific for interrogation of MCD, MCompD, determination of the extent of OCD, or detecting ancillary pathologies.
The odds are very low of being able to find exactly comparable patterns of elbow disease using our scoring scheme to facilitate exact comparison of treatment options. The most logical route for comparison of techniques in different dogs, therefore, is to group diseased elbows. For example, those with coronoid disease only without affectation of the opposing medial surface of the humeral condyle would be grouped separately to those with coronoid and humeral lesions of varying degrees. Dogs affected by coronoid disease without affectation of the humeral condyle can be subgrouped into those affected by fissuring or fragmentation of the radial incisure regions or fissuring or fragmentation of the tip regions of the medial coronoid process.
Therefore, comparing medical management, FR, SCO, or various modifying osteotomies may be profoundly flawed since many affected elbows are not ostensibly fragmented, since the pattern of disease is different in individual clinical cases and since studies purporting to compare modalities have not clearly documented the category of disease treated in patient cohorts. If we address only the question, ‘how should we treat dogs with FCP,’ that would intrinsically preclude about 40% of all elbows affected by coronoid disease which are not actually fragmented, for example. At present the choice of medical or surgical management, the application of oral and intra-articular medications, or physiotherapy and the choice of various surgical procedures remain largely subjective. There is considerable variability due to surgeon experience and bias, owner experience and bias, finances, and many patient factors. How do we know if conservative or surgical management works if we do not first classify the disease process for an individual at that specific moment in time and track it throughout life with equally robust interrogation?
Both dog owners and dog breeders are given disparate advice from different sources, and whilst one individual may, for example, treat all juvenile DED medically because of perceived poor outcomes from FR or SCO, or the perception that surgical intervention may actually worsen the condition, there has been little acknowledgment of responsibility of the veterinary profession for the flaws inherent to such bias, since no two elbows are absolutely identical. Furthermore, even when elbows of individual dogs can broadly be categorised as similar - for example a radial incisure deep fissure with modified Outerbridge Grade 1 cartilage disease of the medial aspect of the coronoid process, but no visible humeral pathology, two different surgeons may treat this same condition differently. The same is true of late stage disease where the spectrum of options offered varies widely, where bias is a prominent feature of choices offered and where outcome measures are lacking. The same client may be offered for the same dog by different clinicians oral medication only, or steroid injection only, or stem cell/platelet rich plasma injections only, or physio modalities only, or an osteotomy only, or medial compartment replacement only, or total elbow replacement only, or any combination thereof for severe end-stage medial compartment disease.
There is a distinct paucity of documented case series comparing techniques and in no publication to date have groups of elbows been scored using CT and arthroscopy and then directly compared prospectively using different surgical or medical management protocols. Additionally, it can be difficult to ask the families of conservatively managed dogs to allow diagnostic arthroscopy and yet if the pathology is not graded appropriately, it may be significantly misleading to compare the treatment groups. This is even more apparent when comparing elbows which can broadly be categorised as end stage MCompD, where evidence is lacking for relative efficacy of procedures such as PAUL, SHO, CUE, or another technique which may be chosen based on intrinsic bias, finances, or available implants.
Paucity of evidence for or against any particular surgical technique is compounded by lack of validated comparable outcome measures. It is well documented that owner and veterinary assessment scales are flawed, but in clinical practice with significant case numbers, often that’s the best that can be achieved and it is superior to subjective clinical opinion of a single individual. Clearly kinetic and kinematic data are superior to both, but ideally clinician assessment, owner assessment, and force plate or motion capture assessment measures should be combined to optimise outcome measure accuracy.
The families of dogs expect results when they sustain financial outlay with the objective of reducing or removing pain and lameness with either conservative or surgical management. We need to elucidate by rigorous evidence-based medicine whether help or harm is being imbued by either managing developmental disease conservatively or surgically. It may be possible to harm a dog with surgery or to harm a dog by not intervening in a timely fashion. Conservative management does not work for all dogs and neither does surgery. The real question is how we advise the family of one specific dog and what is the evidence to justify any approach - medicine, rehab, arthroscopic debridement, or another more involved surgical procedure.
All attempts at establishing an algorithm for treatment of the various manifestations of DED, including that presented here, are intrinsically flawed by lack of an evidence-base on which decisions can be made. As a result, this presentation will be offered as subjective clinical opinion based on arthroscopic evaluation of in excess of 3000 dogs affected by DED, in conjunction with available evidence to date for each technique in each individual circumstance. The limitations are acknowledged, i.e., that the scoring system and the judgments deriving thereof are subject to a constant process of re-evaluation and evolution as more evidence becomes available.
The objectives of this presentation are to enable appropriate clinical examination and judicious interrogation of diagnostic imaging and to encourage open-minded unbiased evidence-based adjudication of outcomes of any physiotherapeutic, medical, or surgical management protocol based on comparison of objectively scored elbow disease. This may help provide a starting framework upon which future developments can be structured. The algorithm should not be taken out of context and is no more than compartmentalisation of thought, opinion, and experience combined with the techniques available to try to give families and clinicians some basis on which to make a decision regarding intervention for an individual dog affected by DED. The goal is to alleviate pain and optimise function for the longest possible period in clinically affected patients.
The algorithm balances the perceived influence of mechanical, biological, and clinical factors for a specific dog being treated by the author. Due consideration is given to the age of the patient, practical and financial circumstance of the family, dietary and medical management, intra-articular injections (both pharmaceutical and biological), and modalities of physical therapy, but the main focus of the algorithm is classification of disease groups and apportionment of potential surgical intervention based on current availability of the technique, evidence for clinical application, and author experience. In all cases, dogs affected by DED and operated on by the author have kinetic assessment, clinical evaluation, anamnesis derived from consultation with the owner, radiography, CT scan, and arthroscopic evaluation as pre-requisites for surgical intervention and decision making.
Surgical procedures commonly employed by the author:
a. Low grade coronoid disease +/- RI or RIT fissuring, none or very limited disease of the medial aspect of the humeral condyle, no static incongruity and no significant osteophytosis, usually young.
b. In elbows affected by synovitis and low grade superficial coronoid disease contralateral to overt coronoid pathology requiring focal arthroscopic treatment, with a view to amelioration of disease progression.
c. Ancillary to SCO or FR in cases of RI or RIT fissure/fragmentation to attempt amelioration of ongoing HUC.
Less than 1-year-old with low grade coronoid disease of any kind +/- static or dynamic incongruity and without disease of the medial aspect of the humeral condyle.
Rare in isolation. Only with T fragmentation pattern and minimal cartilage disease caudal to the fragment or on opposing medial aspect of humeral condyle.
4. SCO alone.
Coronoid disease with fissuring or fragmentation of any pattern but none or very limited disease of the medial aspect of the humeral condyle and no measured incongruity. SCO for all RI and RIT fragmentation patterns because abaxial aspect of MCP is also diseased.
5. BURP+ SCO.
Diffuse medial coronoid disease grade 1–3 with focal. Grade 1 or 2 disease of the medial aspect of the humeral condyle.
6. BODPUO +/- FR or SCO.
Coronoid disease with or without fragmentation plus up to grade 3 focal cartilage erosion of the coronoid or humerus with or without static or dynamic incongruity.
7. BODPUO + anconeal headless compression screw.
Detached but not remodeled UAP.
8. BODPUO alone.
HUI, HRI, RUI without coronoid fragmentation or UAP which is still fibrous-attached.
9. Transcondylar 4.5 mm Ti screw, or shaft screw +/ reinforcing epicondylar plate or F2T2 screw.
Partial or complete thickness HIF.
10. OATS or SOR + BODPUO.
Focal grade 4 lesion of humerus constituting OCD.
+/- SCO for MCD.
Diffuse grade 3 or focal grade 4 lesions of humerus opposing MCD.
12. SHO and cSHO.
Diffuse grade 4 lesions of humerus opposing MCD in a young to middle-aged without aggressive periarticular osteophytosis or HRI. Radial head intact.
13. CUE and cMCR.
Diffuse grade 4 or 5 lesions humerus and coronoid +/- limited erosion of medial edge of radial head due to medial compartment collapse.
14. TER and cTER.
Global elbow arthrosis with pervasive grade 5 lesions of medial compartment and across humeral isthmus, obvious disease extension onto the radial head and/or aggressive periarticular osteophytosis impairing range of motion.
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