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

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…