Tag Archives: Joint Disease

Cartilage Loss, Pain and Surgery 1

This week has been a week of dealing with the end stage of incongruence: the loss of the pristine, almost friction free relationship between two opposing hyalinised joint surfaces. The coefficient of friction in a normal joint is so low that the articulation produces almost no extraneous energy; no heat, no noise like Teflon on Teflon. When this surface is absent, we as clinicians can feel this as grinding and crepitation, from the patient's perspective though they experience the pain initially from the contact between two sensitive structures (remember that cartilage is aneural- no nerve endings, like the enamel on your teeth). Ultimately though the body kills the surface by the process of eburnation so that the bone becomes like ebony, polished and dead on the surface. We can see this as sclerosis on radiographs. This strategy does not eliminate pain however it just delays it. The pain these patients experience is that which comes from heating. The heat is derived from friction and this heat can reach (in human hips) temperatures of 45 degrees Celsius. This heat causes bone pain and will “cook” the synovial membrane whose job it is to lubricate the joint. The joint becomes dry and the friction increases. As the friction increases so too does the speed of onset of discomfort.

A femoral head centrally denuded of cartilage.

The effects of friction though can be seen most clearly in the second image above which shows the complete loss of hemisphericity of the femoral head. This patient was felt to be doing fine on constant NSAID administration. Take it away and he was less happy, add Tramadol and he was happier than he was on NSAID alone. No Rehab or medical therapy will take the pain away entirely though and the mechanics of a flat head in a saucer like acetabulum will not be great. So he now has this:

No friction and a ball and socket for the first time for a long while.

This is one of the few procedures where we as surgeons can eliminate entirely the clinical effects of genetic inheritance and phenotypic expression and truly transform the entire life of our patients. No more pain in this hip and a proper and efficient mechanical relationship between femur and pelvis.

Over the weekend I will post another case where the effects of incongruence and subsequent cartilage loss has been replaced by a low friction comfortable articulation.

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Trochlear Prosthesis Part 4: A case example

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Before we go ahead with discussing the rationale and so forth regarding Trochlear Prosthesis I thought it might be helpful to discuss its application within a specific case.

Patient Details

Two year old Boston Terrier Female. History was of progressive hindlimb lameness towards the end of exercise sessions with intermittent skipping noted when moving at the walk and trot. The problem had progressed in the previous one month to complete non weight bearing lameness on return from even light exercise. The patient had shown depression, believed to be associated with discomfort on evenings after exercise. Current medical management was in the form of Meloxicam given once daily. The impact of the medication on the clinical problem had been minimal in terms of lameness or demeanour.

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Gait evaluation and Physical Findings

The patient showed a tendency to skip when moving at any speed above a slow walk. The foot was held in a non weight bearing position for three to four steps before being returned to the weigh bearing position. During load phase, the limb was under loaded.

On physical exam there was normal hip range of motion. There was apprehension on examination of the stifle and the patella was noted to spontaneously adopt a medial position and required manual pressure to relocate to the trochlea. Some discomfort was noted during this process. No cranial drawer nor postural thrust was noted on exam. The upper limb muscle mass was reduced compared to the contra lateral limb. No orthopaedic disease was noted in the structures distal to the stifle. Medial patellar luxation was also noted in the contralateral stifle although the patella would spontaneously return to the Trochlea in this stifle.

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Diagnosis

Grade 2 Medial Patellar Luxation with suspected retro patellar cartilage loss.

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Plan

Admit for radiographic assessment, palpation under anaesthesia and surgical management by Trochlear Prosthesis.

Radiography

Mediolateral projection showing patellar malalignment and mild effusion. Looking at the fact that the Tibial Tuberosity is clearly shown whilst the Talocrural joint is not in the mediolateral plane, proximal Tibial Torsion was present.

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Caudocranial Projection, showing the patella in the medial luxated position.

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Caudocranial Projection with lines drawn to indicate the Quadriceps Angle (Q-Angle) of 33 degrees.

Surgical Findings

A standard lateral para patellar incision extending proximal to the patella was performed. Both Cruciate ligaments were inspected and noted to be intact as were the menisci. The patellar surface was examined by applying Allis Tissue forceps proximal and distal to the patella and rolling the patella. This revealed central cartilage thinning with no clear full thickness lesion:

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The medial trochlear ridge was of reasonable height but there was clear femoral torsional deformity resulting in the Trochlea facing the lateral aspect of the femur. The medial trochlear ridge was also deficient proximally as can be seen in the second image below.

You can also see that there has been cartilage loss on the medial side of the medial trochlear ridge. The feeling then was that the patella was escaping proximally and following the straightest path for the quadriceps-patella-tibial alignment. This information would be used in considering where to position the prosthesis in the mediolateral and proximodostal plane. On this basis the measured size 2 prosthesis was considered too small to prevent proximomedial escape and thus the size 3 was chosen. The prosthesis would also need to be placed on the cut surface in a position that would mimic the preferred position of the luxated patella. The osteotomy plane would be used to correct the femoral torsion as can be seen below.

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This angle of cut gives the following appearance to the osteotomised Trochlea. The medial side is on the left. Removing the Trochlea at this angle resolves the torsional deformity of the distal femur and ensures that the prosthesis is correctly orientated in the Craniocaudal plane.

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The base plate of the Prosthesis is then placed as medial as possible based on the previous position of the luxated patella. The prosthesis will be press fit onto this base plate.

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The drill that you can see above is being used to clear bone from beneath the press fit points of the base plate. The prosthesis has three pegs that interdigitate with these holes, gentle hammering secures the prosthesis. We have found that clearing a little cancellous bone with a 1.5 mm drill allows the prosthesis to sit more flush with the base plate.

The patella is assessed for stability prior to closure of the capsule. It must be possible to maximally internally rotate the tibia in extension and full flexion and throughout range of motion without any tendency to luxate. I will never rely on capsular closure to provide stability.

Post Operative Radiographs

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You can see from the Craniocaudal projection how medial the prosthesis has been placed. On the radiograph below you can see that the Q-Angle is now around 6 degrees. This has been achieved without femoral osteotomy and without tibial tuberosity transposition. This tends to result in a far less complicated post operative process.

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I hope that this case report helps to highlight how a single procedure can resolve all of the aspects associated with even complex patellar luxation patients with various deformities present. With the groove it is possible to avoid these more complex procedures and achieve the mechanical and clinical goals of surgery.

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Trochlear Prosthesis Part 3: Standard Methods for MPL Management

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Introduction

For many years Patellar Luxation has been managed with a series of techniques that can broadly be divided into the following groups:

Femoral Techniques

Recession Sulcoplasties: Block and Wedge.

Femoral Wedge Osteotomies.

Rotational Trochleoplasty.

Fabello-Patellar Sling

Tibial Techniques

Tibial Tuberosity Transposition.

Femorotibial Sling

Tibial Wedge Osteotomies.

Soft Tissue Techniques

Lateral (or medial) Retinacular Imbrication.

Lateral or Medial Desmotomies.

Quadriceps Release.

Clearly not all of these techniques are used in every patient. The most commonly used techniques include Recession Sulcoplasty, Tibial Tuberosity Transposition and the imbrication and desmotomy techniques. The general rule is to apply techniques based on the observed pathology. For example many patients will not have a significantly shallow Trochlea and in these cases Trochleoplasty techniques would not be indicated. Despite this, many surgeons continue to perform these “out of habit”. In my view however Trochleoplasty techniques are not benign, especially if the medialising vector force has not been neutralised. The continued medial force will push the medial aspect of the patella against the exposed bony ridge that persists for a variable period following this technique on the medial and lateral aspects of the trochlear groove.

The most important technique in my view and one that is not performed as often as it should be in the standard management of Patellar Luxation is Tibial Tuberosity Transposition. As mentioned before, their technique is unique in the standard list in that it will alter the forces that are causing the patella to luxate. This is because this technique does not simply try to resist the forces that lead to patellar luxation but to neutralise the force by reducing the Q-Angle to within normal limits. Failure to achieve longterm patellofemoral stability can often be understood by either the failure to perform Tibial Tuberosity Transposition at all (relying on Trochleoplasty and/or Imbrication) or from failing to transpose the Tibial Tuberosity sufficiently to neutralise the luxating force.

In general terms a Figure of eight wire is not required as long as the distal periosteal attachment has been left intact at the time of transposition. The small A wires should protrude from the caudal aspect of the tibia and should be angled to avoid the joint. This is particularly important to remember in small breed dogs with high tibial slopes such as West Highland Terriers. Discomfort arising from the superficial presence of the pins is not uncommon and thus persistent lameness following Tibial Tuberosity Transposition will often necessitate removal of the wires following union (4-6 weeks post surgery). In general the Tibial Tuberosity should be slid along the osteotomy surface rather than placed lateral (or medial) to it. This prevents twisting the Straight Patellar Tendon which may cause post operative Sub Patellar pathology. Pierre Montavon has advised using an oblique osteotomy, such that when the Tibial Tuberosity is slid along the obliquity a small advancement is also created, reducing the retropatellar stress.

If the required transposition seems excessive, this is often an indication to perform Quadriceps release. This should reduce the required transposition. In cases of Medial Patellar luxation, the entire quadriceps mass is separated from the medial muscles using sharp and blunt dissection. The vast us medialis origin can often be palpated as a tight band and this can be freed using either sharp section with a scalpel blade or by blunt methods with a periosteal elevator. This technique will often align the patella more uniformly through range of motion assessment.

Sling Techniques should not be relied on in my view, in fact I have never used them. The patella should be stable without these by the application of other techniques. Reliance on a fabellopatellar sling to hold an unstable patella is not logical as the sling will ultimately (and in this case “ultimate” is not a long time) fail and the patella will become unstable again.

We should not leave theatre without having achieved complete stability throughout range of motion. This should be present before imbrication is performed. Any reliance on “tightening up the capsule” is doomed to failure in most if not all cases.

In the next article I will begin explaining the concept and physical properties of the Kyon Trochlear Prosthesis.

Trochlear Prosthesis Part 2: The Pathogenesis of Patellar Luxation

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As mentioned in the previous article in this series, Patellar Instability is broadly considered a purely mechanical condition. Intermittent or permanent patellar luxation induces temporary or persistent incompetence of the Quadriceps-Patella-Tibial (QPT) mechanism. The function of the QPT mechanism to maintain stifle extension in load phase of the stride by maintaining a matched antagonism to the hamstrings during stance phase. Failure of this mechanism therefore results in an inability to maintain stifle extension. In patients with intermittent patellar luxation the limb will adopt a flexed unloaded position (skip or hop) during the gait cycle whilst those with permanent luxation will often adopt a crouched stance. In this purely mechanical model of Patellar Luxation, resolution of the clinical impact is dependent on negating the factors that promote luxation. This leads to a “surgery by numbers” approach where specific procedures are applied in sequence until the patella is stable through flexion-extension and on internal/external tibial rotation. The “numbers” referred to above relates to the grading system used for patellar luxation. The image below shows the grading system for Medial Patellar Luxation:

The difference between Grades 1 and 2 above is the ease by which the patella returns to its normal position within the trochlea. The following image shows the factors that are generally accepted to be associated with medial patellar luxation:

Generally speaking these factors have been considered to promote or be Causal of medial patellar luxation and the degree to which they are present is felt to influence the grade of medial patellar luxation. Clearly not all factors will be present in all patients. The other way we could look at these factors is as effects of medial patellar luxation. For example lateral capsular stretch would result from recurrent Medial Patellar Luxation rather than being the causal pathology, the same could be said of the depth of the Trochlea and so forth. If this is the case, if the above described pathologies are effects of Medial Patellar Luxation, this would mean that there is a cause of these pathologies. One proposal (and one that has support) is that the chief risk factor for Medial Patellar Luxation is the Quadriceps Angle (Q-Angle). Relative shortening of one or more components of the Quadriceps Mechanism (Vastus Lateralis, Vastus Medialis, Vastus Intermedius and Rectus Femoris) leads to an alteration of the Q-Angle leading to an increased tendency to Patellar luxation. Human studies have shown that changes in the Q Angle are associated with increasing tendency for Patellar Luxation (http://jap.physiology.org/content/105/3/800.abstract , http://www.physther.net/content/80/10/956.short) and this mechanism has also been proposed in our patients (L’Eplattenier H, Montavon P. Patellar luxation in dogs and cats: Pathogenesis and diagnosis. Compend Contin Educ Pract Vet 2002; 24:234–239. ). The image below shows the components of the Q Angle:

This proposed mechanism suggests that the medial vector force on the patella is increased as the Q angle increases. The image below shows how this occurs in patients with femoral torsion for example:

This increased vector force then “drives” the patella medially or results in permanent medial positioning of the patella relative to the trochlea. The effects of this will depend upon the frequency of medialisation. If the patella is permanently or frequently absent from the developing Trochlea for example, this will lead to hypoplasia of the Trochlea, loss of the medial trochlear ridge and stretch of the lateral capsule for example.

From this is can be seen that the only surgical technique that is commonly applied in the surgical resolution of medial Patellar Luxation is that influences the Q-Angle directly is Tibial Tuberosity Transposition. Other techniques such as Recession Sulcoplasties and Retinacular Imbrications do not influence the Q-Angle and this may explain why these techniques when performed in isolation are rarely successful in resolving medial patellar luxation. We will see later in this series that we can influence the Q-Angle with the Trochlear Prosthesis.

In the next article we will look at traditional surgical techniques for managing Medial Patellar Luxation before moving on to discuss the Kyon Trochlear (Patellar) Groove Prosthesis in more detail.

Trochlear Prosthesis Part 1- Indications

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Trochlear Prosthesis for Patellofemoral Pathology: Introduction.

For the past eighteen months or so I have been using the Femoral Trochlear Prosthesis (Kyon) to manage patients with end stage patellofemoral pathology secondary to Patellar Luxation. So far I have performed this surgery in thirteen patients (one patient has had bilateral surgery) and I am very impressed with the results. The bilateral patient’s owners were so impressed with the outcome on the first stifle that they returned specifically for this procedure. Currently we are one of only about fifteen clinics that can offer this surgery. A post op radiograph of the bilateral patient is shown below:

For patients with chronic patellar luxation (in particular Bull type breeds) the repeated luxation of the patella imposes shear stressed across the subpatellar surface and the trochlear ridge. Over time these shear stresses may result in progressive loss of cartilage and exposure of sensitive subchondral bone. This process leads to low grade effusion and discomfort. Traditional techniques have addressed the patellofemoral instability, but have not been able to resolve the subpatellar pathology. With the Trochlear Prosthesis we can replace the pathological trochlea and ridges with a diamond coated, Titanium groove which has a coefficient of friction similar to that of pristine articular cartilage. The images below show some examples of trochlear and subpatellar pathology found at surgery:

Full thickness central "Ulcer" on subpatellar surface.

Severe cartilage erosion on the medial Trochlear Ridge

It may be argued that traditional techniques would adequately address these issues, however four of the patients that have had this surgery were revisions of failed standard surgeries. Three of these patients had persistent lameness associated with subpatellar pain rather than re luxation as the basis for their presentation. On this basis, I would argue that there are a number of patients that have been managed by traditional techniques and that whilst the mechanical incompetence may have been resolved, still experience pain and lameness. As such I would say that this is an important technique in the management of Patellofemoral instability.

I will discuss the approach to planning and surgical technique and post operative outcomes in future posts on this technique. In the meantime you can see a short YouTube video of a case below:

Diagnosing Cranial Cruciate Pathology-Part 4: Palpation

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So far in this series, we have established that there are no significant criteria in terms of radiographic appearance or synovial fluid aspirate findings that will permit a definitive diagnosis of Cranial Cruciate Ligament Rupture. All that we can say form these tests is that there is evidence of increased (non-inflammatory) synovial fluid production in a stifle displaying varying degrees of Degenerative Joint Disease.

As the key function of the Cranial Cruciate ligament is to limit cranial tibial displacement and internal tibial rotation, the presence of a palpable increase in either of these two components would (in most cases) be a definitive diagnostic finding. There are two main tests of femorotibial stability:

Anterior Drawer Test

In this test we place a thumb behind the fibular head with index finger on the tibial tuberosity with one hand and with the the other hand place a thumb behind the lateral fabella and index finger on the patella. We then push the tibial hand forward without moving the femoral hand. If the tibia slides forwards, this is indicative (in most cases) of cranial cruciate ligament degeneration. This test should be performed in both flexion and extension for the following reason:

The Cranial Cruciate comprises two main bands: The Craniomedial Band and the Caudolateral Band:

The Caudolateral band is shown in pink

The Craniomedial band is taut in both flexion and extension whilst the Caudolateral band is only taut in extension:

Both Bands are taut in extension

In Flexion, the Craniomedial Band is still taut but the Caudolateral Band is loose.

If the Anterior Drawer Test is performed only in extension, then partial ruptures (which are most common) may be missed. If the stifle is stable in extension but unstable in flexion, this indicates that partial rupture involving the Craniomedial Band is present as in flexion the Craniomedial Band should provide stability whilst the caudolateral band is loose. For this reason, this test should be performed in flexion and extension.

The test is best performed in anaesthetised patients as the pressure applied by the digits can cause pain and muscle tension can make it difficult to elicit a positive response even in a very unstable stifle. Care in interpreting the findings should be exercised in very young patients and in patients with effusions for other reasons. These patients may show a degree of Drawer, but there will be an abrupt stop to the Drawer motion in these patients which feels different from that felt in the Cruciate deficient stifle.

Tibial Compression Test

This test is often easier to perform in conscious patients but needs some practice to become confident that a negative response is a true finding rather than being due to error in technique. In patients that will bear weight on the affected limb it can often be tested by simply lifting the contralateral limb with a finger placed on the Tibial Tuberosity when the affected limb is loaded. In many patients you will easily appreciate the cranial tibial thrust as the limb is loaded. If the patient is non weight bearing, the procedure is to fix the stifle with one hand whilst upward pressure is applied to the paw of the same limb with the hock on a neutral standing position. This will elicit anterior displacement of the Tibia in most Cruciate Deficient stifles.

The problem with both of these tests is that they may give false negative results. As mentioned above, many patients will present in the partial rupture phase and it may be partial in the craniomedial band with intact caudolateral band. In these patients both of the above tests may prove negative. In Boxers in particular, there tends to be a marked fibrotic response from the joint capsule in the Cruciate Deficient stifle and this fibrosis may result in a degree of palpable stability that mimics the normal stifle. These are the “problem cases” and the clinician may fall back on history, breed, age and lack of contradictory findings to establish a strongly tentative diagnosis in these cases. If further certainty is needed, then arthroscopy or MRI may be used to visualise the cranial cruciate ligament pathology before proceeding to manage the patient with the appropriate surgical technique. In most cases however this is unnecessary as long as all of the tests indicated in this series have been followed and their results interpreted correctly.

Diagnosing CCL Rupture Part 3: Synovial Fluid Aspiration

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In this third part of diagnosing cranial Cruciate Ligament Rupture, we will look at Synovial Fluid aspiration and analysis. In general this is an under performed procedure and in my view should be part of the work up for any lameness that is suspected to be due to joint pathology. Synovial fluid reflects the current and (in some cases) historic environment of the joint. The chief role of synovial fluid aspiration and evaluation in respect to suspected Cranial Cruciate Ligament pathology is in confirming the absence of contradictory findings. As with any presenting patient, their history, clinical signs, physical findings and so forth form the basis for a differential diagnosis list. As most readers will know, this is a list of possible explanations for the clinical picture presented. This list is generally ordered in the clinician’s mind with some possible explanations being more likely than others. As we saw in the radiography post, the findings there simply reflect increased joint fluid production (effusion) with the possible addition (depending on duration of pathology) of findings consistent with Degenerative Joint Disease (DJD). These findings are not specific to CCL pathology. We still need to explain the presence of effusion. As mentioned in the previous post, effusion represents “active” joint pathology, the question remains: “What has activated the pathology?”.

Most pathologies can be categorised using the DAMNIT mnemonic:

Differential Diagnosis using DAMNIT mnemonic

With regards to stifle effusion we would generally consider that there are conditions within each of these groups that may explain the clinical and radiographic findings. Only synovial fluid aspiration and analysis will permit us to narrow this list. The expected characteristics of Synovial fluid aspirated from the Cruciate deficient stifle would be an increased volume of cytologically normal synovial fluid. We would not expect to see evidence of increased White cell populations or the presence of neoplastic cells. An example of some of the different appearances of synovial fluid can be seen in the next image:

Some of the pathological processes that may be seen in Synovial Fluid

The gross physical and cytological characteristics of synovial fluid aspirated from joints with different pathologies can be seen in the table below:

Table showing the gross and cytological aspects of Synovial Fluid associated with different pathologies.

In terms of Diagnosing CCL pathology we want to exclude the presence of significant inflammatory disease or neoplastic processes. We may therefore see fluid that is consistent with DJD and we may see evidence of erythrophagocytosis indicative of recurrent historic bleeds into the joint.

As indicated, we will not find evidence of CCL pathology, we are simply ruling out other conditions that may present with a similar history and have broadly similar radiographic changes. In my view this is a mandatory component of the investigation of the suspected CCL deficient stifle. Failure to perform this simple test may lead to inappropriate treatment or raise the risk of post operative sepsis if a low grade septic arthritis has been overlooked by failing to perform this simple test.

Synovial Fluid aspiration should be performed with Aseptic Technique and should be practiced in order to reduce iatrogenic injury to the structures of the joint. In general I recommend using a spinal needle as this reduces the risk of taking a skin core into the joint and the rounded end is less traumatic. I routinely use a 5 ml syringe for collection of fluid. The needle can be introduced lateral to the Straight Patellar Tendon and directed into the femorotibial joint or angled (in the slightly flexed stifle) upwards to a point below the patella. If the fluid appears turbid or if there is cytological evidence of inflammation, a small amount of the fluid should be injected into a “Bloodgrow” bottle to improve the likelihood of a positive bacterial culture in cases where Septic Arthritis is suspected. In this way Bacteriology and Sensitivity can be determined and the antibiotic regime directed by these findings which is best practice for managing any infection and reduces the risk of encouraging bacterial resistance.

Diagnosing CCL Rupture Part 2: Radiography

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Further Diagnostic Techniques 1

Radiography

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.

Radiograph showing cranial tibial translation

This radiograph shows cranial tibial translation indicative of CCL rupture

Recommendation

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.

Conclusion

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.

Coming next… Synovial Aspiration and Palpation.

Test Post: Hindlimb Anatomy (Patellofemoral)

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Press Play to see a video of Hindlimb anatomy relating to Patellofemoral Joint function and Structure. I am testing whether I can use this method to embed multimedia in the iPhone App. If it doesn’t work for you please let me know. If it does, let me know that too! So far it doesn’t work in the App but you can press the view Video button below to see the video.

Okay I think I have it now:

What no Post?

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This is an apologetic post for the lack of new content this week. I have been preparing for tomorrow’s CPD on Elbow Dysplasia. I have a tendency to get carried away with 3D modelling for these things and have taken it a stage further with pretty complex animated models showing the pathogenesis of Elbow Dysplasia and the rationale behind the newer “geometry modifying” procedures for this debilitating disease. An example of the new approach to Elbow Dysplasia is the Stepped Ulnar Osteotomy using a modified Kyon Alps Plate to shift the ulna and offload the medial compartment of the elbow.

The concept behind this procedure is not easy to understand and so I have used a 3D model animated to show how the intra operative change translates to reduced medial compartment load in the Dysplastic Elbow.

If you can’t make the seminar, I will I am sure upload some of the content as we move forward.

In other news, for all of you iPhone App users, there is an update on the way with better iOS4 compatibility like background activity and a pull to refresh function that was sadly absent in the first version. I think you will like the changes. If you don’t have the App yet, why not follow the link in the previous post or simply search for Torrington Orthopaedics in the App store.