The image shows the effects of increased joint fluid production on the soft tissues around the joint. These are non specific changes that do not definitively diagnose CCL pathology. We may also see evidence of Degenerative Joint Disease (DJD) and the extent of these changes will be influenced by chronicity and to some extent breed.
Radiograph showing reduction in Infrapatellar Fat pad and deviation of the caudal fascial plane secondary to increased Synovial fluid volume (effusion)
As with most orthopaedic radiography, positioning and correct exposure is essential to pick up these often subtle radiographic features. Over flexion of the stifle for example as in the image below will often reduce the appearance of the signs of effusion noted above. In the top case, the reduction in Infrapatellar shadow can be seen but the caudal fascial plane distortion is absent. Whilst the second radiograph obscures all meaningful information.
The 90 degrees of flexion seen here will often obscure the signs of effusion
This extreme flexion eliminates almost all meaningful information regarding synovial fluid volume.
This radiograph shows cranial tibial translation indicative of CCL rupture
The position of the stifle becomes even more critical in cases where TTA is planned. In general the current recommendation is that the stifle should be positioned in extension. This is not the often quoted 135 degrees but whatever represents the normal standing angle of the patient’s stifle. The third radiograph above whilst diagnostic of CCLR should not be used for templating for TTA as the tibia is already in a pathologically advanced position. This will reduce the accuracy of the required advancement for the procedure.
The craniocaudal view is less important in terms of diagnosing CCL pathology but is an essential view to rule out other pathologies that may result in effusion such as Femoral condylar osteochondrosis dissecans and neoplastic processes.
Essentially all effusion indicates is Active Joint Pathology. When this appearance is combined with appropriate history and patient age and breed, it may point in the direction of CCL pathology but is not Diagnostic.
I apologise in advance if this post is more of a “rant” than a post. I received my copy of Veterinary Comparative Orthopaedics and Traumatology the other day and saw this advert on the back page:
VCOT 5/2011 Back Page
This post should not be construed as being anti-Securos, but it goes to the heart of what is and what is not a TTA. The procedure was devised and improved by Kyon in association with Pierre Montavon, no patent was established for the technique and thus there is a flood of “me-too” products on the market. Very few Veterinary Orthopaedic Manufacturers do not now have a “TTA” system. The problem I have with this is that it confuses any consideration of complication rate associated with the procedure. It introduces a new variable and in my view, never has the variability been higher than it is in the manufacture, quality control and appearance of “TTA” implants.
The advert above states:
Faster and easier placement: How much easier and faster exactly? The TTA is a very forgiving procedure and I cannot see that there is any need for this procedure to be easier or any supporting evidence for this claim. The duration of surgery has an impact on Post Operative infection rate. But what is the claim here, that it halves the procedure, reduces it by 5 minutes, is faster for one specific surgeon or all surgeons?
No Fork: The benefit claimed here is that it offers greater versatility in contouring the plate. I have never felt constrained in my contouring by the fact that I am using a fork.
No Hammering: The benefit stated here is that you can separate the Tibial tuberosity and then apply the plate. This sounds fiddly and does not immediately suggest any great benefit over incomplete osteotomy and fork introduction. I would imagine that most surgeons using this system still perform a partial osteotomy, attach the plate and then complete the osteotomy.
More Flexibility: The benefit claimed here is that the plate can pivot around the top screw hole. The top hole is the key hole in the TTA and it is failure to plan for the position of this that causes most problems in aligning the plate. The ability to pivot the plate around an incorrectly positioned top hole does not immediately suggest benefit. The aim should be to plan carefully and execute precisely and no implant design will ever make this unnecessary. Strong Plan-Good Execution-Post Op check and learn. These are the keys to good TTA surgery.
Less Holes in Bone: Fewer stress risers is the claim here. The problem with screw placement as any Orthopaedic Surgeon knows is when the screw is tight and when it is not. The potential for fracture of the tibial tuberosity would be more highly associated with over tightening and misdirection of the screw than having a smaller number of holes in my opinion. A crack around the far side of the screw hole would be potentially more problematic than an increased number of holes. We have never seen (in over 700 cases) any issues associated with fork placement and subsequent failure.
No Forks: Less inventory. That is certainly true.
Less Complications: This is the big claim here and I suppose the main reason for my rant. This is apparently being “researched at the moment”. If it is still being researched, how can any conclusion be drawn? Complications associated with TTA are generally due to surgeon error (as long as the implants used are of sufficiently high quality), so the view that the XGen plate is associated with fewer complications seems spurious and I would like to see statistical data before this claim can realistically be made in an advert. I would also like to see a reference to peer reviewed article cited as a reference for this claim. Surely the statement “Less complications” when referring to a product or procedure should be followed by “…than XYZ”, the statement then is rather “empty” as it doesn’t reference the object against which it is being compared.
So when is a TTA a TTA? When it is a Kyon TTA! I think that any future papers on TTA should indicate the source of their implants in order that like to like comparisons of outcome and complications can be made.
So a food manufacturer involved with dog food production has decided to target our dogs with their most recent advert. Admittedly it is a German advert (dubbed over) but it will probably be coming to a TV set near you soon. The Ad uses high pitched sounds audible only to our pets to stimulate their interest and encourage us to buy it on this basis.
You can se the Ad here
What do you think? Making the advert stimulate our pet surely has nothing to do with the merit or otherwise of the product surely. Then again I suppose that’s what adverts always do!
Just to let you all know that the iPhone App “Torrington Orthopaedics” has now been updated and the update is now available on the App store. It permits background activity so that it will update posts better. You can also pull down on the home page to load new posts.
I ma currently working on my next post which is how to diagnose Cranial Cruciate Ligament Rupture. I am drawing on the data from 650 of our cases and using video and animation to help make the subject more interesting, enjoyable and relevant. If I get a move on I may get this up by the end of the day.
If you have been using the App and enjoy it, why not take the time to rate it on the App store.
Cranial Cruciate Ligament (CCL) pathology is the commonest cause of hindlimb lameness in medium and large breed dogs. Whilst Cranial Cruciate Ligament Rupture in man is primarily the result of an injury (sports), in our patients it is generally the result of progressive mechanical failure of the ligament. As an Orthopaedic Referral Service, we probably only see two acute ruptures each year compared with over 150 patients presenting as a result of progressive failure of the ligament. This often insidious onset can lead to a delay in owners contacting their primary veterinarian and can often “stay the hand” of the primary vet. As a result there is almost always evidence of chronicity in most patients presenting with Cranial Cruciate Ligament Deficiency (CCLD). Another aspect of this disease that can delay presentation is that it is generally bilateral (both knees affected simultaneously). This can result in a delay on the owners part to recognize the problem. That may seem contradictory, but often lameness is only seen when it is present relative to a normal limb. The asymmetry is perceived easily by most owners and attention is sought. In cases with bilaterally symmetric pathology (whether this be due to CCL pathology, Elbow Dysplasia or Hip Dysplasia) often passes unnoticed until one limb displays more overt lameness than the other. An analogy that I often use to explain this is the following:
If someone lets some air out of both front car tyres we will likely drive around oblivious to the problem. If more is let out of one than the other, the asymmetry will be experienced by us immediately and we will pull over to inspect the tyre with least inflation.
The purpose of this article is to define the disease and outline its progression in order to assist in it’s early diagnosis and intervention. Given that we have techniques such as Tibial Tuberosity Advancement (TTA) available there is no reason why these patients cannot make a full recovery and restore their desired lifestyle speedily. Whilst there is no direct indication that delayed intervention adversely affects long term outcome, it is not difficult to imagine that chronic progressive instability is likely to give rise to a less benign joint long term than a joint that has been stabilized using a procedure that normalizes Intra articular contact pressures (Kim and Pozzi) which is a uniquely derivable outcome for the CCL deficient stifle post TTA.
The following data are derived from Torrington Orthopaedics’ database of the most recent 650 cases.
The graph below shows the breeds that were over represented in the group. Labradors are the commonest breed with CCL in this group with Retrievers and Rottweilers second. As you can see, Springer Spaniels are another common breed with CCL pathology and in my view as a breed are experiencing increasing frequency of CCL problems.
Age at Presentation
Whilst we always feel that this is a juvenile condition (presenting sub 18 months of age), this is not borne out by the figures in this dataset. The average Labrador is sub 4 years of age whilst Springer Spaniels, Rottweilers and West Highland White Terriers are on average over five years of age.
The following Chart is probably more interesting from a diagnostic standpoint. It shows the incidence at different ages for the five top presenting breeds in this group:
The chart shows a couple of interesting points:
Labradors have two peaks of presentation the first at under four years and the second at over six year.
Springer Spaniels and West Highland Terriers present at over two years and then progressively more frequently as they grow older.
Rottweilers present most common under four years of age and don’t have the double peak incidence seen in Labradors.
Retrievers may present as juveniles but become increasingly likely to present with CCL pathology as they age.
From a diagnostic point of view:
Westies and Springer Spaniels under two years presenting with Hindlimb lameness are unlikely (based on this group) to have Cranial Cruciate Ligament Pathology and thus we should probably look elsewhere for the cause in this Breed-Age demographic. The presentation of a four or five year old Labrador with hindlimb lameness is less likely to indicate CCL pathology, whilst for Retrievers it becomes increasingly likely that they have CCL pathology.
Clearly the breed and age of a patient is going to assist in the diagnosis of any condition, but this should never be used as a sole diagnostic criterion, simply a method whereby we can shuffle the Differential Diagnosis list based on this understanding.
Clinical Signs of Cranial Cruciate Ligament Pathology
Clearly the chief sign of this condition is hindlimb lameness. As mentioned above however in bilateral patients it may be a “poverty of hindlimb function” rather than overt lameness that would be recognised by a casual observer. The video below shows a patient with Cranial Cruciate failure. Motion tracking overlay may help with visualisation of reduced stifle flexion:
Other signs that we may observe are:
Classical Sitting Posture for CCL Disease
This patient is sitting off to the side with the stifle held in only partial flexion. The reasons for this sitting posture are likely to include the following:
The presence of effusion (increased joint fluid) results in increased intra articular pressure. On flexion there is distension of the synovial membrane and joint capsule, the stretch receptors then fire early, inhibiting normal flexion.
Patients with CCL pathology may experience cranial tibial translation with hock and stifle flexion. This posture reduces stifle and hock flexion and may reduce this experience.
History (derived from patient histories of Torrington Orthopaedics)
The history is generally one of progressive hindlimb lameness, stiffness after rest and difficulty rising. The latter sign is more likely in patients with bilateral Cranial Cruciate Ligament problems. There may be peaks of lameness which settle down to periods of soundness or more likely periods of relative improvement. Long-lasting spikes may represent medial meniscal injury and spikes derived from this are unlikely to resolve to a lameness of less than 3/10. In many cases it is the meniscal pathology that prompts attention to the chronic undulating lameness of the patient experiencing progressive Cranial Cruciate degeneration.
Exercise intolerance would be common in patients with bilateral pathology as their shift of limb load distribution shifts from the normal 60:40 (forelimbs:hindlimb) to 70:30 or 80:20. The strain of forequarter loading without hindquarter propulsion leads to fatigue and difficulty in maintaining active mobility for extended periods.
Difficulty rising would also be common especially in the bilateral patient, but is also seen in the unilateral patient. Periods of reduced weight bearing after rest in the latter group may be of 10 minutes or more. Evening difficulty is common and often this is described as the patient’s worst phase of the day.
Vocalisation in pain is rare and is often restricted to those dogs with medial meniscal pathology.
Next Part: Further Diagnostic Techniques coming soon…