Cranial cruciate ligament disease in the dog (Proceedings)


The most common cause of lameness on dogs in North America is partial or complete rupture of the cranial cruciate ligament.

The most common cause of lameness on dogs in North America is partial or complete rupture of the CrCL. The annual economic impact of cranial cruciate ligament disease in dogs in the United States was estimated to be 1.2 billion dollars in 2003. Many surgical treatments have sought to restore stifle joint stability and minimize osteoarthritis through various techniques of replacing the ruptured ligament either inside the joint, or outside in an extracapsular method. The CrCL is composed of a craniomedial band (CrMB) and a larger caudolateral band (CLB). The CrMB is taut in flexion and extension, the CLB is taut in extension but lax in flexion. The CrCL functions to minimize internal rotation and hypertension of the stifle joint and prevent cranial translation of the tibial plateau relative to the femoral condyles.. Full extension of the stifle is limited by contact between the CrCL and the cranial intercondylar notch of the femur. Mechanisms of traumatic rupture of a normal CrCL include: internal rotation of the stifle in 20-50 degrees of flexion or forceful hyperextension. Tearing of the CLB alone (most likely from hyperextension) will not produce instability because the intact CMB is taut in both flexion and extension; no drawer motion will be present. Injuries caused by rotation or twisting are more likely to injure the CrMB, producing a small amount of drawer motion in flexion, but none in extension. Rupture occurs when the ultimate breaking strength of the ligament is exceeded which is estimated to be 4x the body weight of the dog.

There is no single cause of CrCL rupture in dogs. Acute trauma to a normal CrCL, which is the primary etiology of CrCL rupture in people, is a less common cause in dogs. Other factors that contribute to the degeneration and eventual rupture of the CrCL include anatomical factors, such as extreme tibial plateau angles (>35°), narrowing of the intercondylar notch, and an extended standing angle of the stifle joint; hormonal influences, shown to be important in athletic girls; immune mediated disease processes, such as the production of anti-collagen antibodies or deposition of immune complexes; and heredity in that some breeds appear to be predispose dogs to CrCL rupture. The genetic basis for hereditability of a predisposition for CrCL rupture has been shown in Newfoundlands. They have an autosomal recessive mode of inheritance with a recessive allele frequency of 0.65 and partial penetrance (59%). There may be certain phenotypic expressions that predispose dogs to developing CrCL rupture. Hyperextension of the stifle joint increases the standing TPA, which places increased stress on the CrCL. In addition, the stifle joint shifts medial to the longitudinal axis of vertical load in dogs with a "cow-hocked" stance, which also places greater stress on the CrCL.

The pathogenesis of CrCL rupture involves the ligamentous changes that occur with disuse, and progressing age that weaken the integrity of the structure. The degenerative changes progress as the animal ages, but may be less severe in animals less than 15 kilograms in body weight. Degenerative changes associated with aging may account for 20-40% of dogs that eventually develop bilateral CrCL rupture. It has been postulated that the sedentary lifestyle of the typical middle-aged dog, compounded by obesity, may lead to diminished mechanical strength of the CrCL.

CrCL rupture has been identified in all breeds of dogs, but with a higher incidence in obese dogs. Rottweilers, Labrador retrievers, Newfoundlands, bull mastiffs, and chow chows appear to be at particular risk. Recent studies indicate that younger, larger, more active dogs may be predisposed to CrCL rupture. There is not a sex predilection for CrCL rupture, but there may be a slightly higher incidence in female spayed dogs. Although the strength of a dog's CrCL deteriorates with age, loss of fiber bundle organization and metaplastic changes of cellular elements in the CrCL may be pronounced at a young age in certain large-breed dogs.

Patients may present for acute CrCL injury, in which there may be subtle to non-weight bearing lameness of unknown origin. The lameness often improves somewhat within weeks, but then plateaus especially in dogs over 15 kg. These larger dogs may never return to pre-injury levels of activity and develop a second, acute lameness after meniscal injury. The lameness often resolves completely within 1-5 months in dogs less than 15 kg, although these dogs may also develop meniscal damage later. Chronic, mild lameness is associated with the development of degenerative joint disease. The acute lameness improves as any hemarthrosis resolves and fibrous proliferation of the periarticular tissue stabilizes the joint, there is an acute exacerbation of lameness as a result of a meniscal tear or progression of degenerative joint disease. Partial CrCL tears may be difficult to diagnose and present as a mild weight-bearing lameness associated with exercise that resolves with rest until degenerative joint disease sets in. As the ligament continues to tear, the joint becomes less stable and degenerative changes exacerbate the lameness until it no longer resolves with rest.

During the examination, a simple visual test is the sit test. Most normal dogs sit with the hock in sufficient flexion so the patient rests on its haunches. An affected dog may sit with the affected stifle in some degree of extension. Thickening around the joint or medial buttress, decreased range of motion, pain with stifle hyperextension or pressure over the caudomedial joint capsule can be found in dogs with partial or complete CrCL rupture. Significant atrophy of the quadriceps and hamstring muscles is a common finding in chronic cases. Dogs with angular malformations centered over the stifle, genu varum or valgum, have a higher incidence of CrCL rupture. An audible "clicking" may be heard when the stifle is taken through its range of motion when a meniscal tear is present. Positive cranial drawer and cranial tibial thrust during a tibial compression test are definitive tests for cruciate instability. To check for cranial drawer, the dog is placed in lateral recumbency with the affected limb up. The examiner places an index finger on the patella and the thumb of the same hand on the fabella, while the index finger of the opposite hand is placed on the tibial tubercle and the thumb on the head of the fibula. Cranial translation of the tibia relative to the femur is a positive drawer sign. This maneuver causes pain, and some dogs may require sedation before this test can be performed successfully. It is important to remember that dogs less than one year of age have slight laxity of 1-2 mm of normal drawer movement, and dogs with chronic rupture and joint thickening may have little or no drawer.

Other differential diagnoses that should be considered are caudal cruciate rupture, which is diagnosed by a caudal drawer sign or the tibial sag sign3, patella luxation that may accompany and/or cause CrCL rupture, osteochondrosis in young large breed dogs and neoplasia of the stifle that can both be diagnosed with radiography. Avulsion of the long digital extensor tendon, while uncommon, causes a firm swelling on the lateral aspect of the stifle, as well as a radiographic density in the craniolateral aspect of the joint. The extensor fossa may be more prominent, as a radiolucent defect on the lateral aspect of the femoral condyle. Lymphocytic plasmocytic synovitis syndrome may cause lameness mimicking CrCL rupture, and has been diagnosed in up to 10% of dogs having surgery for CrCL rupture. Less common conditions to consider are semimembranosus/gracilis contracture, patellar tendon rupture, other arthropathies, and neurological disease such as cauda equine syndrome.

Synovial fluid analysis may help differentiate partial CrCL rupture, immune-mediated arthropathies, joint sepsis, and acute trauma. Lateral and craniocaudal (or caudocranial) stifle radiographs are taken to assist in the diagnosis and to rule out other abnormalities. Radiographic findings (at least 32 have been defined) in dogs with chronic tears include osteophytes along the femoral trochlear ridges, caudal aspect of the tibial plateau, and pole of the patella; cranial displacement of the infrapatellar fat pad, and caudal joint capsule distension. Dogs with an acute or partial rupture may have joint effusion alone as a radiographic abnormality. Stifle exploration via arthroscopy or arthrotomy should confirm the diagnosis of CrCL rupture.

As mentioned earlier, nonsurgical, conservative or medical management is effective in 90% or more of dogs that weigh less than 15 kg. On average, it takes 3 to 4 months for these dogs to regain normal function as a pet. This treatment is less effective in dogs with a meniscal click that signifies meniscal injury. Medical management consists of a course of oral NSAID drugs, weight loss if necessary, and 2-weeks of activity restriction followed by daily leash walking and swimming is available.

The large number of surgical treatment options for dogs with CrCL rupture is a testament that an ideal surgical repair has not been identified. Surgical treatment for CrCL rupture ideally includes stifle exploration, removal of the remnants of the ligament, inspection of the menisci with removal of any damaged portions, and stabilization of the joint followed by an appropriate course of physical therapy. Stabilization techniques are usually categorized as intracapsular or extracapsular. Among the many intracapsular techniques are the Paatsama and the Under-and-Over that use a fascia lata strip to replace the cruciate ligament and the Over-the-Top developed by Arnoczky that uses a graft of patellar tendon, patella and quadriceps tendon. These procedures thread the graft in various ways through the joint to replace the CrCL. There are many methods of extracapsular stabilization using a variety of graft materials. The capsular imbrication technique, retinacular technique first described by DeAngelis and Lau, the modified DeAngelis technique and the Three-in-One technique all describe using non-absorbable suture threaded outside the joint capsule to mimic the function of the CrCL. The Four-in-One Over-the-Top is a combination of intra- and extracapsular methods to stabilize the stifle. The fibular head transposition described by Smith and Torg uses cranial advancement of the lateral collateral ligament to minimize cranial drawer and internal rotation of the tibia. The tibial plateau leveling osteotomy (TPLO) was first described as a treatment for dogs with CrCL rupture in 1993 by Slocum. TPLO "levels" the tibial plateau angle (TPA) by a predetermined number of degrees as determined from preoperative radiographs, to a point where the tibial plateau is perpendicular to the functional axis of the tibia (or Achilles' tendon)This leveling is thought to enhance the effectiveness of the active forces of the flexors of the thigh, resulting in a stable stifle with a TPA of approximately 6 degrees and neutralization of the tibiofemoral shear forces. Although that a higher TPA increases stress on the CrCL there is no difference in the TPA in Labradors with or without CrCL tears or between Labrador retrievers with CrCL rupture and Greyhounds that rarely have CrCL rupture.

If the entire meniscus is not damaged, only a partial meniscectomy should be performed. The axial portion of a bucket handle tear should be removed or the entire caudal pole is removed when that is damaged. When the entire meniscus is damaged, a complete meniscectomy is performed. Complete meniscectomy should only be performed when necessary because bone-on-bone contact is increased by ~300% following this procedure. To remove the entire meniscus, cut the cranial tibiomeniscal and intermeniscal ligaments, grasp the cranial pole of the meniscus and apply traction toward the midline. An Oschner-Kocher forceps works well for grasping the meniscus. The abaxial attachments are cut taking care not to transect the medial collateral ligament. A #11 or Beaver blade or meniscal knife can be used to cut this attachment. The entire meniscus can be removed when the caudal tibiomeniscal ligament is transected taking care not to also cut the caudal cruciate ligament. There is a great amount of debate about whether it is necessary or advisable to perform a release of the medial meniscus. Since leveling the tibial plateau does not prevent cranial tibial translation during all activities, some of the dogs (1-5%) that have a TPLO develop medial meniscal damage following the procedure. Therefore it was proposed that the medial meniscus be "released" to allow the caudal horn of the medial meniscus to move away from the medial femoral condyle during cranial translation of the tibia. It is not known whether the meniscal tears occurred after the TPLO or if they were present but missed at the time of the TPLO surgery. It is important to realize that a meniscal release, whether the caudal tibiomeniscal ligament is cut or a radial mid-body transection is performed, obliterates most of the function of the meniscus and results in more articular cartilage damage. Because of this, some surgeons are no longer releasing the meniscus and others are only releasing the meniscus if there is a complete, not partial, rupture of the CrCL. There is some evidence during "second look" arthroscopies that a partially torn CrCL heals following a TPLO. It has been postulated that the ligament heals because there is less stress on the ligament after the plateau has been leveled. Release of the medial meniscus can be achieved by cutting the caudal tibiomeniscal ligament or by radial mid-body transection of the meniscus. The meniscus can only be released through an arthrotomy if the CrCL has been completely debrided. Extreme care must be taken that the caudal cruciate ligament is not cut when attempting to release the meniscus. The caudal cruciate ligament attaches to the tibial plateau just caudal to the caudal tibiomeniscal ligament of the medial meniscus. The caudal pole of the meniscus should move cranially when the tibia plateau is forced into cranial translation if the caudal tibiomeniscal ligament has been completely cut. Radial mid-body transection to release the meniscus can be performed through a cranial arthrotomy or through a caudomedial mini-arthrotomy. A short incision is made through the joint capsule just caudal to the medial collateral ligament in the caudomedial miniarthrotomy. A small Gelpi self-retaining retractor is used to retract the joint capsule. The abaxial border and the proximal surface of the medial meniscus should be visible. If these structures are not seen, the caudal pole is flipped cranially or there is some other damage to the meniscus. A #11 scalpel blade should be directed from the caudal border of the medial collateral ligament and Gerdy's tubercle on the craniolateral aspect of the tibia plateau for the mid-body transection. The cranial and caudal poles of the medial meniscus should separate completely after the radial cut. Care should be taken to prevent damaging the articular cartilage of the tibial plateau during the release. The joint should be thoroughly flushed prior to closing the arthrotomy.


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