Cranial cruciate ligament (CrCL) injuries occur both as partial and as complete rupture. The ethiology of CrCL injures is traumatic and non traumatic. CrCL injuries of traumatic origin are caused by forced hyperextension and or internal torsion of the stifle; high impact trauma causes the complete rupture of the ligament, while less intense trauma causes partial rupture. Partial rupture usually evolves with time in complete rupture, because of the joint inflammation, of weakening of the ligament and of altered biomechanics imbalance that enhances the cranial tibial thrust. CrCL of non-traumatic origin are caused by a chronic biomechanics imbalance of the forces acting on the CrCL as it is seen in large breed dogs, in overweight dogs, in bowlegged dogs and in dogs with straight rear leg conformation and open knee angle in standing and walking. In these dogs the cranial tibial thrust caused by the forces acting on the slope of the tibial plateau continuously stresses the CrCL and causes its partial rupture progressing with time in complete rupture.
Clinical signs are different in intensity according to the degree and duration of CrCL partial rupture. In early CrCL partial rupture the dog runs normal, but in resting position the affected leg is held slightly off weight; during walking few steps limping and then normal. Sit test is normal with complete flexion of the stifle and the dog can jump normally. With the progression of the ligament sprain clinical signs become more evident with morning pain, incomplete weight bearing with central foot-pad lifted from the ground, lameness after exercise; when jumping over a surface (like a pick-up car) the affected leg is landed not simultaneously with the unaffected leg and when sitting the affected knee is not completely flexed, keeping the hock away from the ischiatic tuberosity. Because of the subtile signs, most often partial CrCL rupture is overlooked until it progress to complete rupture with more dramatic clinical signs.
In early partial rupture joint palpation is still normal and no swelling is felt on the caudomedial joint compartment were a separation between the femoral condyle and the tibial plateau is still well defined. The tibial compression test (TCT) is negative as it is the drawer sign. Early ligament sprains are suspected radiographically in the mediolateral view because of increased infrapatellar fat pad density without any sign of other diseases, like OCD of the lateral femoral condyle, avulsion of the extensor digitorum pedis longus tendon, immune-mediated joint disease. Arthroscopic observation shows fibrillation of ligament fibers, usually in the medial band, and synovitis. With the progression of the CrCL sprain, the palpation of the medial compartment of the knee shows a swelling between the femoral condyle and the tibial plateau that forms a buttress. TCT and drawer sign are slightly positive with the knee held in flexion. On medio-lateral radiograph the density of the infrapatellar fat pad is increased leaving a narrow space between the patellar tendon and the fat pad; the transparent lines of the popliteal fascia caudal to the joint is pushed backwards by a swollen joint capsule. The relationship between the femoral condyle and the intercondylar eminence of the tibial plateau shows a mismatch between the centre of the condyle and the tibial eminence, with cranial translation of the tibia; this cranial translation is proportional to the amount of CrCL rupture and its failure to keep the tibia in the anatomic position. In more chronic cases osteoarthritis (OA) signs become apparent, with osteophytes formation along the femoral condyle, the distal and proximal pole of the patella and on the tibial plateau. Arthroscopy shows a wide disruption of the medial band of the CrCL with increased synovitis and possibly meniscal tears.
Because of the constant evolution of partial CrCL rupture into a complete rupture in a time frame variable from weeks to months, and because of the OA progression following this condition, conservative treatment is not rewarding. Rest and non-steroidal-antiinflammatory-drugs (NSAID) reduce the clinical signs but do not avoid the progression of the CrCL sprain and rupture, neither the progression of OA. With the purpose to arrest the cranial tibial thrust and to stop the stress on the damaged CrCL, the tibial plateau leveling osteotomy (TPLO) is the treatment of choice because it eliminates the tibial slope producing the cranial tibial thrust. In early CrCL rupture the TPLO is performed as an extraarticular procedure, while in more advanced injures intra-articular treatment is required too to treat meniscal lesions and to perform a meniscal release. While meniscal release is not required in early partial CrCL injuries, this procedure is advisable in advanced partial rupture because the increased joint instability causes meniscal tear by the femoral condyle and joint pain. The medial meniscus is strongly connected to the medial collateral ligament and to the tibial plateau and its caudal horn could be crushed by the femoral condyle in stressed joint movements not halted by the failing CrCL. Through a caudal mini-approach, just caudal to the medial collateral ligament, the caudal pole of the medial meniscus is cut free to move caudally. TPLO in partial CrCL rupture restores joint stability during weight bearing and the OA progression is arrested; joint function is completely regained and the dog can progressively return to full activity.
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