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Anterior Cruciate Ligament Rupture
Anterior cruciate ligament injury in the dog has been recognised as a cause of lameness for many years. A large variety of methods of treatment have evolved and continue to do so. Probably no single method of treatment will result in success for each case. All have their advantages and disadvantages.
The classic history is of a sudden onset lameness following an injury at speed – usually in the nature of turning on a partially flexed knee, such as chasing a ball and overrunning it. The condition has generally been described as affecting adult dogs in middle age who tend to be overweight. Most of these cases are unilateral although occasional, simultaneous onset, bilateral cases occur which must not be confused with acute spinal problems.
More recently a phenomenon of cruciate ligament degeneration is being recognised. This affects younger dogs with a history of more insidious onset of lameness, often without a known specific injury or precise time of onset. Some breeds appear to be more commonly affected. These include many brachycephalic breeds such as Boxer, Rottweiler, Dogue de Bordeaux etc. as well as more conventional dog breeds such as Golden Retriever, Bernese Mountain Dog, Bull Terrier, West Highland White. The history may not be of a specific single leg lameness, but actually be consistent with bilateral lameness with such statements as the dog is ‘progressively slow or weak’ or being unable to get up readily on the hind legs –‘like an old dog’. The owner often fails to realise this is a bilateral leg problem. Stiffness after rest following exercise is a common early sign. (See video ‘Stiffness after rest’) These cases are often misdiagnosed as hip displasia (HD), other orthopaedic or neurological problems. Diagnostic problems are compounded when both legs are affected as there is no ‘normal joint’ available for comparison.
Video: Stifness after rest
Cruciate problems remain relatively rare in patients less than 1 year of age, and such a diagnosis should only be made after careful evaluation. Labradors seem more prone than other breeds and frequently have an osteochondral fragment attached to the cruciate ligament stump.
(A normal stifle joint in puppies always appears more ‘lax’ than in an adult, so that a ‘pseudo’ cranial draw might be suspected but the absence of any joint swelling or pain indicates this to be a false diagnosis.)
Acute traumatic cases are initially 10/10 lame or just toe touching. Swelling of the stifle joint may be visible in thin coated dogs. Lameness tends to improve after about 10 days and some weight bearing commences, although stride length is shorter and the toes touch but the main pad is non weight bearing. (See video ‘Toe touching, foot dabbing, shaking’) The leg is often lifted at paces faster than a slow walk.
Video: Toe touching, foot dabbing, shaking
Chronic cases have a similar but less marked lameness, with stiffness after rest becoming more obvious, which will reduce after some exercise. Even in dogs who use the leg, the stride length is reduced and some toe touching is noted. (See video ‘Toe touching, foot dabbing, shaking’) Muscle atrophy, especially of the thigh muscles becomes evident.
Initially, joint swelling resulting from joint effusion causing distension with excess synovial fluid is most readily found just caudal to the straight patellar ligament - so that the edges of the ligament become less clearly identified, and as a soft swelling around the apex of the patella.
More long standing cases have a variable degree of lameness, occasionally as bad as 10/10, toe touching when standing still or moving at speed. The joint swelling is more generalised and now a firm swelling over the region of the medial collateral ligament becomes evident. This swelling is often readily visible in shorter coated dogs such as Rottweilers.
Main confirmation of diagnosis is by joint manipulation. With experience this can be done in large conscious dogs, but sedation or general anaesthesia (GA) may be required. Manipulation can be painful, so care must be taken and possibly only one chance is available in the unsedated large dog!
Cranial draw test (See video ‘Cranial draw test’)
This tests the integrity of the cruciate ligaments by manipulation. The principle is to fix the femur with one hand while attempting to move the tibia cranially and caudally with the other, through a range of movement from full extension to flexion. The femur is stabilised by forefinger on the patella; and thumb behind on the lateral fabellum. Do not try and move both hands at the same time! Following a fresh injury the laxity is usually readily evident but in more long standing cases the excursion of the laxity may be less and have a more ‘spongy’ feel.
Video: Cranial draw test
Cranial thrust test (See video ‘Cranial tibial thrust’)
This mimics the effect occurring when weight bearing. The knee joint is stabilised with one hand attempting to keep the joint in an extended weight bearing type position. The limb is then flexed by pressing on the foot against the force of the other hand and then allowing the joint to gently flex. As the joint flexes the tibial tuberosity will tend to slip forwards if the anterior cruciate is ruptured and in many cases a click will also be palpated and/or heard as the medial meniscus slips forward.
Video: Cranial tibial thrust
If the medial meniscus has a displaced caudal horn as a result of meniscal folding, then loss of range of motion, diminished cranial draw and cranial thrust may be noted in these tests. In more chronic cases the tibia can adopt a permanently forwardly displaced position so that the cranial draw test may appear almost normal to the inexperienced.
In cases of partial tear, cranial draw and thrust may be so limited as to make the diagnosis uncertain particularly in bilateral cases and other diagnostic features may be needed to ensure the diagnosis.
Can be helpful but the physical exam is often more useful! X-rays should be made under sedation or GA.
Use normal screen film – no grid required.
Views – medio lateral; and cranio caudal or caudo cranial centred on the joint space.
To make measurements of bones or tibial plateau angle a full length view of the tibia is required.
Stressed views may be helpful but are usually unnecessary.
Acute case – may be little to see initially – later some swelling of the joint capsule. This is seen as displacement of the infrapatellar fat pad and an increased soft tissue density around the joint margins with caudal displacement of the tissue planes behind the stifle joint.
More chronic case – joint capsule swelling still visible. A few cases have a slight cranial displacement of the tibia related to the femoral condyles but this not a reliable sign. Degenerative joint disease (DJD) signs now commence with new bone forming along the margins of the femoral trochlea, at poles of the patella, on the tibial plateau.
Later with more established DJD there are wider regions of new bone formation as above and on a cranio caudal projection, osteophyte formation on the lateral side of the intercondylar space is pathognomic. New bone develops on the joint margins of tibia medially and laterally. There may be elevation and separation of popliteal sesamoid from its normal position at the caudal tibial plateau.
NB. cranial draw may often be identified on physical exam but may not be identified radiographically and cannot be used as a diagnostic sign. The tibia may finally become displaced cranially in long standing cases as a result of maturation of scar tissue in the soft tissue parts of the joint.
There is a tendency for a damaged joint to become more stable as the result of the inflammatory process which follows anterior cruciate rupture. The initial swelling of the joint is synovial effusion and possibly haemorrhage, but later there is thickening of the joint capsule by oedema and developing fibrous tissue which will provide some stabilisation. In some dogs the gradually increasing function may be adequate, particularly in smaller breeds or old dogs with a low demand exercise tolerance.
Treatment with medication relies mostly on anti-inflammatory drugs. These will reduce joint effusion as well as reduce the signs of discomfort. However it could be argued that Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) may reduce the formation of scar tissue in the joint capsule, the presence of which, paradoxically, is probably what aids returning function. For medical management to have the best chance of success, it is important for muscle tone and mass to be retained so NSAIDs may allow the patient to use the limb and thus retain and regain function. Cartilage sparing drugs may be helpful, but corticosteroids will inhibit fibrous scar formation and if injected intra-articularly will often result in a worsening of the instability and are contraindicated.
Medication alone will not be sufficient. It is most important that the patient is allowed to move enough to develop the soft tissue support and muscle tone which is going to be required. Therefore excessive rest and confinement are counterproductive beyond the period around the initial injury, when the signs are most severe. Once the initial period of about 2 to 3 weeks has passed, a gradually increasing programme of controlled exercise mainly on the lead, as well as possible physiotherapy or hydrotherapy should be instituted to minimise muscle atrophy. The author increases exercise periods by 5 minutes per walk per week.
A wide range of surgical options have been used and include:
• Debridement of the joint to remove torn ligament and damaged meniscus.
• Intra-articular injection of blood or other drugs.
• Injection of extra articular sclerosing agents.
• Restabilisation by replacing the torn ligament with some form of intra-articular natural graft or synthetic material.
• Restabilisation using some form of extra-articular support to mimic the function of the original ligament1.
More recently, operations to alter the mechanics of the joint by osteotomy of the proximal tibia so that anterior cruciate function is less necessary have gained favour. These include tibial plateau levelling (TPLO)2, cranial wedge osteotomy (CWO)3, tibial tuberosity advancement (TTA ), tibial tuberosity osteotomy (TTO). These procedures are more specialised and require special equipment and training and involve the insertion of special implants to fix the osteotomy. The tibial plateau angle is altered so as to eliminate the effect of cranial tibial thrust. Normally this will aim to be a plateau angle of about 6 degrees. Generally return of function is more rapid than following ligament repair methods and the need to restrain what may be a very active young dog for a significant period is reduced. Overall results tend to be better than with previous methods. However complications such as tibial tuberosity fracture, osteotomy non union, implant issues and meniscal lesions which may require further treatment can still develop and the owner should be appraised of these before surgery. However the overall incidence of complications is low with experienced surgeons.
In all cases a programme of rehabilitation of the patient is required and this may include hot/cold packs, massage, passive exercises, active exercises, hydrotherapy. NSAIDs are useful to enable the rehabilitation process by providing analgesia and limiting unnecessary inflammatory reaction.
This article was kindly provided by Merial, makers of Previcox:
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GENERAL TEXTS with variety of surgical techniques
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