Cranial cruciate ligament (CrCL) rupture is the most common cause of hindlimb lameness in dogs. Treatment of CrCL injury is an integral part of veterinary orthopedic practice, and represents a $1.23 billion/yr industry in the United States.
Cranial cruciate ligament (CrCL) rupture is the most common cause of hindlimb lameness in dogs. Treatment of CrCL injury is an integral part of veterinary orthopedic practice, and represents a $1.23 billion/yr industry in the United States. With training, diagnosis of CrCL rupture is often straightforward. However, the ideal treatment of CrCL injury is debated, and no single procedure has emerged as clearly superior for returning dogs to normal function.
The stifle is stabilized by four primary ligaments: medial collateral, lateral collateral, cranial cruciate, and caudal cruciate. The cranial cruciate ligament consists of two parts- the craniomedial band and the caudolateral part. Both parts originate from the caudomedial aspect of the lateral femoral condyle, and course diagonally across the intercondyloid fossa to the cranial intercondyloid area of the tibia, near the intermeniscal ligament. The craniomedial band is taut during all phases of the gait, while the caudolateral part is taut only in extension of the stifle. The caudal cruciate ligament originates on the lateral surface of the medial femoral condyle and runs caudodistally to the lateral edge of the popliteal notch of the tibia.
The function of the cranial cruciate ligament in stabilizing the stifle is threefold. It prevents cranial translocation of the tibia relative to the femur (also known as cranial drawer or cranial tibial thrust), limits internal rotation of the tibia, and prevents hyperextension of the stifle. Prevention of cranial tibial thrust is thought to be the most significant function of the CrCL, The caudal slope of the tibial plateau relative to its long axis causes the CrCL to be under strain during normal weightbearing. The absence of a CrCL results in cranial tibial thrust during the stance phase of the gait. Neutralization of cranial tibial thrust (or cranial drawer) is the primary goal of most surgical techniques.
Additional support to the stifle joint is provided by the medial and lateral menisci.The menisci are semilunar fibrocartilagenous discs that function in a hoop-stress mechanism to distribute force in the stifle joint. Cranially, the medial and lateral menisci are both anchored to the tibial plateau. Caudally, the lateral meniscus is attached to the caudal intercondylar fossa of the femur. In contrast, the medial meniscus is attached to the tibial plateau, just cranial to the tibial attachment of the caudal cruciate ligament. Understanding this difference is critical to understanding the etiology of meniscal tears associated with CrCL injury (see below).
Dogs with CrCL injury may present with acute onset lameness, however the injury is rarely of purely traumatic etiology. In most cases, the damage to the ligament appears to be chronic, and the damaged ligament frequently exhibits lymphoplasmacytic inflammation on biopsy. The injury is probably multifactorial, with causes including conformation, obesity, inactivity, aging, hormone imbalance, and repetitive trauma. A ligament that has been weakened by these insults may then proceed to rupture from normal or near-normal loads. Partial rupture is not uncommon, and in some cases a complete tear of only one portion (craniomedial or caudolateral) of the ligament may occur. Due to the degenerative nature of most CrCL ruptures, a significant proportion of dogs (20-40%) will proceed to injure the contralateral CrCL at some point during their life.
Pain and lameness with CrCL injury initially is due to instability of the stifle joint and stretching of the joint capsule. With time, this initiates a cascade of events, including synovitis, hyaline cartilage degradation, degenerative joint disease and periarticular fibrosis. In addition, tethering of the caudal pole of the medial meniscus to the tibia may cause this structure to become crushed under the medial femoral condyle, as it is drawn forward during cranial tibial thrust.
Cranial cruciate ligament rupture most commonly affects young to middle aged, large breed dogs. However, any breed dog may be affected, and CrCL injury should be suspected and ruled out in any case of hindlimb lameness. Affected dogs may have a variety of presentations, probably due to the multifactorial nature of the disease. They may be non-weightbearing, partially-weightbearing, or occasionally non-ambulatory.
Probably the most common presentation is a dog that has a history of acute onset hindlimb lamenes with improvement, then recent worsening of the lameness. These dogs may have had a partial tear that improved with rest, and then went on to rupture completely. In contrast, some animals will present with a chronic progressive lameness, with no inciting event. These dogs often are progressing due to worsening of osteoarthritis. They may also become acutely worse due to subsequent meniscal tear. Both of these presentations typically exhibit positive cranial drawer and varying amounts of osteoarthritis and joint effusion on radiographs.
Some dogs present with a mild, chronic lameness. These dogs may have no cranial drawer sign, but exhibit discomfort when tested for drawer or when the stifle is placed in hyperextension. They may have a partial CrCL rupture, with minimal effusion and no osteoarthritis visible on radiographs.
Less commonly, dogs may present acutely non-ambulatory, or with difficulty rising, or with shifting leg lameness. These dogs often have bilateral CrCL rupture, but may present with a variety of previous diagnoses, including spinal cord disease and hip dysplasia. When assisted to walk, they may have a very short-strided gait, mimicking dogs with lower motor neuron dysfunction due to lumbosacral spinal cord disease. A full neurologic exam, paying close attention to proprioception and spinal reflexes is needed to rule out neurologic disease. To make things more challenging, these patients sometimes DO have concurrent hip dysplasia/DJD and lumbosacral disease. Even with concurrent diseases, a good orthopedic exam can evaluate CrCL status with confidence.
Most cases of CrCL rupture can be diagnosed by a complete physical exam. After obtaining a thorough history from the client, observe the dog at a walk and a trot in a straight line. Non-weightbearing lameness is not a challenging observation to make, but more subtle lameness can become apparent with gait analysis. Dogs with a CrCL injury and a subtle lameness may exhibit a shortened stride and a somewhat extended stifle. The normal limb will appear to land harder on the ground. Pay attention to how the dog sits. A dog with a CrCL injury often will not sit with its legs squarely beneath it, due to the stress placed on the CrCL in this position. Instead, the dog may sit with the leg extended and out to the side. Some clinicians refer to this as "the positive sit test".
Begin the physical exam with the dog standing and an assistant gently restraining the dog. This allows palpation and comparison of both hindlimbs, with the dog in a relatively relaxed position. Begin proximally, palpating the thigh muscles to assess atrophy. Continue distally, sliding the patella and patellar ligament between the thumb and index finger. The medial and lateral edges of the patellar ligament should palpate sharply. Indistinct margins indicate possible joint effusion distending the cranial joint capsule. Continue distally, palpating the medial aspect of the stifle for medial buttress, or periarticular fibrosis, a response to stifle instability. Medial buttress may be felt with or without concurrent cranial drawer.
After palpation, examine the dog in lateral recumbency on an exam table or the floor. Proceed to the good leg first, to allow the dog to relax and get an idea of what baseline responses are for the individual dog. The limb should be examined from the toes to the hip. When the stifle is reached, begin by flexing and extending the joint to assess range of motion, crepitus, or clicking noise. Patients may have diminished range of motion due to fibrosis, pain, or effusion. Crepitus can be consistent with degenerative joint disease (osteoarthritis). A palpable or audible click may indicate a meniscal tear.
Next, test cranial drawer by placing the thumb and index finger of one hand on the lateral fabella and patella, respectively. Place the other thumb and index finger on the fibular head and tibial tuberosity. Hold the patella/fabella firmly, while moving the tibia caudally and cranially. Except for puppies, which may have a small amount of motion, any amount of cranial drawer motion is abnormal. The cranial drawer test should be done with the leg in flexion and extension, to test both parts of the CrCL. If no drawer is palpated, but CrCL injury is still suspected, cranial drawer should be re-evaluated under sedation. Dogs with ACL injury may not exhibit cranial drawer either because they are resisting your palpation with their leg muscles, they have significant periarticular fibrosis which has stabilized the stifle, or they have a partial tear and the remaining intact ligament resists gross displacement. Remember that the craniomedial band is under tension both during flexion and extension. Thus a tear in the caudolateral part may not be appreciated with a drawer test. However, these dogs often are painful when cranial drawer is attempted, or on hyperextension of the stifle. They may also exhibit stifle effusion and buttress. In cases of suspected partial tears, an MRI, or arthroscopy/arthrotomy may be needed to confirm diagnosis of CrCL injury.
Even in cases where a clear diagnosis of CrCL rupture can be made in the exam room, radiographic examination of the joint is indicated. Radiographs are used to rule out concurrent diseases such as neoplasia and OCD. They are used to evaluate the degree of secondary signs of CrCL rupture, primarily: joint effusion with infrafatellar fat pad displacement, caudal joint capsule displacement, and degenerative joint disease (DJD) noted on the patella, trochlear ridges, and tibial plateau. The degree of DJD may be an indicator of prognosis, as dogs with minor degenerative changes probably have a better prognosis for long-term function than do those with advanced osteoarthritis. In cases without positive cranial drawer, these secondary signs give support to a diagnosis of CrCL rupture.
While very light dogs (<15lbs) may do well with medical management, heavier dogs have a significantly faster and more complete return to function with surgery. The goal of surgery is stabilization of the joint and thus minimization of DJD progression, as well as management of meniscal injury.
A variety of repair methods have been described for treatment of CrCL insufficiency. They can be divided into static repairs, which attempt to replace the function of the CrCL, and dynamic repairs, which alter joint biomechanics to absolve the need for a functioning CrCL. Static repairs include intracapsular grafting techniques, extracapsular lateral suture techniques and fibular head advancement. These techniques stabilize the joint through static neutralization of cranial drawer without alteration of stifle joint anatomy. Dynamic repairs include tibial plateau leveling osteotomy (TPLO) and tibial tuberosity advancement (TTA). These techniques provide dynamic stability to the stifle joint by altering tibial plateau angle and the insertion point of the patellar ligament. Neutralization of cranial tibial thrust by TPLO has been shown to provide stability to the CrCL deficient stifle by generation of caudal tibial thrust and increased stress on the caudal cruciate ligament during mid stance phase of the gait. The TTA neutralizes the contribution of the quadriceps muscle to cranial tibial thrust and also results in generation of caudal tibial thrust at certain points of the stance phase. Good results, often with maintenance of full range of motion and normal activity levels can be achieved with any of the above techniques. In a study comparing force plate analysis of dogs undergoing 3 different techniques for stabilization of CrCL deficient stifles, lateral suture technique and TPLO were found to result in similar clinical results.