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Diagnosing Cranial Cruciate Pathology-Part 4: Palpation

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

Diagnosing Cranial Cruciate Ligament Rupture Part 1

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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.

Patient Profile

Breed Distribution

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:

Sitting Posture

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…