Cranial cruciate ligament (CCL) injuries are among the most common reasons for pain, discomfort, and lameness of the stifle joint of the dog. While this may be true, the testament to our inability to decide on the most appropriate treatment regime is evidenced by the myriad number of techniques commended to repair a cruciate deficient stifle. The recognition and appropriate treatment of these lesions play an important role in the successful management of a small animal veterinary practice. It is the purpose of this as well as subsequent articles to address the causes, effects, and surgical options most suited to reconstruction of a clinically stable and fully functional stifle joint.
The CCL plays a vital role in the maintenance of stability of the stifle joint. It prevents cranial displacement of the tibia on the femur (which often leads to impingement of the caudal horn of the medial meniscus), prevents hyperextension of the stifle, and limits internal rotation of the tibia on the femur. These functions are directly related to the anatomic location and orientation of the CCL within the stifle joint and has lead to the belief that the technique for repairing the CCL should duplicate the ligament’s normal anatomy and function as well as maintain normal joint function.
The cruciate ligaments are dynamic structures and the mechanism of cruciate ligament injury is directly related to the function of the cruciate ligaments as constraints of joint motion. The most common mechanism of cruciate ligament rupture is excessive internal rotation of the tibia when the joint is partially flexed. In this position, the CCL is wound very tightly and is easily subject to trauma to the lateral side. In full extension, the CCL is quite tight, such that in hyperextension injuries, the CCL is the first structure subject to injury. Obviously, direct trauma can also induce CCL as well as other structural injury to the stifle joint. While excessive forces during the extremes of the aforementioned motions will result in acute CCL injury, chronic degenerative CCL lesions may also eventually result in rupture. Conformational deformities of the stifle (i.e. patella luxation) contribute to repeated excessive stress on the CCL, and in the obese animal, these stresses are increased. It has also been shown that ligament strength and stiffness decrease with age because of disuse, inactivity, and disease states. As the degeneration gradually progresses, the tensile strength of the CCL is reduced, making it even more susceptible to acute rupture. These changes are also associated with the normal aging process and may explain the increased incidence of ligament injury in dogs over 5 years of age. In addition, immune mediated processes may play a role in weakening and eventual failure of the CCL.
While acute complete rupture of the CCL is the more common scenario, partial CCL rupture is by no means uncommon. Because known trauma is lacking in the majority of dogs with a partial CCL tear, degenerative or immune mediated processes may be playing a more significant role in these cases. With complete ligament rupture, dogs typically develop a sudden severe lameness classically detected with cranial drawer sign or positive tibial compression test. With partial tears, mild to moderate lameness of acute onset is more likely, and a cranial drawer sign is elicited in only about 50% of the cases. The severity of the lameness will wax and wane over time and may respond to rest and analgesic therapy, but the condition gradually worsens over the course of several weeks to months. Accurate diagnosis of CCL injury is hampered by the fact that there is tremendous variability in eliciting cranial drawer motion, as it is based upon subjective evaluation and may vary from case to case depending on the type of lesion present and the length of time it has existed.
In dogs with acute complete rupture of the CCL, there is usually pain upon manipulation of the stifle, and a cranial drawer sign is elicited with the stifle flexed or extended. Excessive internal rotation of the tibia on the femur is detected and the stifle joint may be placed in a more full extension than is normally possible. Dogs that are apprehensive or tense may resist manipulation of the limb such that accurate evaluation of the amount of instability is impossible without resorting to sedation or anesthesia. In addition, over time, periarticular soft tissue fibroplasias may prevent manual detection of a cranial drawer sign, even under sedation. The radiographic presence of periarticular osteoarthritis at this stage, however, should support the diagnosis of a chronic CCL rupture. In dogs with partial CCL tears, the variability of the cranial drawer test results are due to the fact that the CCL is composed of a large caudolateral band and a smaller craniomedial band. The craniomedial band is taut throughout flexion and extension, while the caudolateral band is taut in extension only. Therefore, a solitary caudolateral band tear should not result in a cranial drawer sign at all, while a tear of the craniomedial band should result in a cranial drawer sign when the joint is in flexion only. In my experience, increased internal rotation is also evidenced with a craniomedial band tear as well. If rupture of the CCL is suspected and a positive cranial drawer sign cannot be elicited with the stifle in flexion or extension, or with the dog conscious or sedated, and the radiographs do not support a diagnosis, the next option includes and MRI, arthroscopy, or exploratory surgery.
It is an established fact that rupture of the cruciate ligament results in progressive degenerative changes within and around the joint and predisposes the contralateral joint to similar injury. It is for these reasons that the majority of veterinary surgeons agree that surgical correction of CCL rupture is preferable to conservative medical therapy and enforced rest alone. While some studies have indicated that dogs weighing less than 15kg can achieve at least good function without surgical intervention, these same studies conclude that if restoration of limb function and a normal activity level is desired, then surgical intervention is still warranted even in these smaller patients. With regard to partial rupture of the CCL, spontaneous healing of the torn fragment and/or restoration of full stability does not seem to occur, given the protracted clinical course seen in the majority of cases. If partial rupture is due to ongoing immune mediated mechanisms or other degenerative changes rather than trauma, it would seem reasonable to assume that the remaining intact portion is similarly affected and would eventually fail. In fact, most of the dogs suspected of having partial ligament tears initially eventually undergo surgical intervention within a few weeks or months when the ligament completely ruptures in spite of appropriate medical therapy and rest.
Surgical repair of the CCL has been and continues to be the topic of considerable interest, and the multitude of techniques and material used suggested for the surgical reconstruction can leave anyone confused. Basically, the procedures can be divided into the intraarticular versus extra-articular techniques and arthroscopy versus standard arthrotomy. These considerations will be discussed in the next article concerning surgical management of cruciate ligament injuries.
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