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An Urban Experience
E. Bogaerts1, J. Saunders1 1 Merelbeke, Belgium
With an estimated prevalence of 2.55% and an annual financial impact of well over a billion dollar, cranial cruciate ligament rupture (CCLR) is the most common cause of lameness in dogs. This disease also has an important impact on the performance of the population of working dogs (= assistance dogs and military working dogs). Aside from the acute inability to continue working and the long revalidation period, in the long term a daily medical treatment, supported by physiotherapy or even early retirement might be necessary.
The cranial cruciate ligament (CCL) is responsible for the stability in the stifle joint and controls the cranial drawer movement, hyperextension and internal rotation. A CCLR can be classified as complete or partial, based on anatomic definition. It results in lameness and surgery is nearly always required to alleviate symptoms. Often both stifles are affected as 22-54% of the unilateral ruptures become bilateral within 6 to 17 months.
Actually, there is no consensus about the aetiology of CCLR. In humans, the primary cause is non-contact trauma but in dogs a non-traumatic degeneration of the CCL is suggested as the primary cause for CCLR. Due to the degeneration of the CCL, rupture often occurs during normal daily activities. Several possible underlying mechanisms have been proposed: immune mediated joint inflammation, hypoxia of the central part of the ligament, abnormal tibial plateau angle and malformation of the hindlimbs, obesity and disturbed proprioception. Whereas the exact aetiology is unknown, breeds as Newfoundland, Rottweiler, Labrador Retriever, Golden Retriever and American Staffordshire Terrier are more susceptible to CCLR than others. As a result of this breed predisposition, a genetic basis is suspected. Further studies established a multifactorial mode of inheritance and major gene involvement could not be ruled out. As no screening methods exists to diagnose young dogs susceptible for CCLR, genetic screening might be a promising option to reduce the prevalence.
The diagnosis of a complete rupture of the CCL or
a partial rupture of the CCL with an instable joint
is made using a combination of clinical symptoms, orthopedic examination and radiographic images. Clinical symptoms include mild to non-weight bearing lameness and abduction of the affected limb during sitting to prevent flexion of the stifle joint. On an orthopedic examination, muscle mass asymmetry, joint effusion,
tissue warmth, painful flexion and extension of the stifle joint and decreased joint range of motion point towards knee involvement can be observed. A positive tibial compression test and cranial drawer test confirm CCLR. In general, radiographic images are used to visualize the instability of the stifle joint by tibial compression, to detect effusion and secondary osteoarthritic changes. The agreement for interpretation of stifle radiographs is high, using correct positioned radiographs taken by different technicians/radiologists. While there is a trend towards increased agreement for more experienced observers, overall the interpretation of stifle joint radiographs seems straightforward. This indicates that CCLR interpretation on radiographs should generally lead to the same conclusion, even between different veterinarians.
The most reliable radiographic method of diagnosing cruciate disease is through the use of tibial compression radiography. By taking a lateral radiograph of the stifle while performing the tibial compression test, cranial displacement of the tibia with respect to the femur
was demonstrated in 97% of subsequently confirmed ruptures of the CCL. Indeed, the sensitivity and specificity of this technique was superior to that of the cranial drawer test. A distal displacement of the popliteal sesamoid bone confirms the presence of a CCLR. A triangle of increased radiographic lucency caudal to
the patellar tendon on lateral projection of the stifle is associated with the infrapatellar fat pad, and it has been suggested as an indicator of cruciate disease. In the normal stifle, this area of lucency extends from the distal extent of the patella, proximally; to the tibial crest, distally; to the origins and insertions of the cruciate ligaments, caudally. Cruciate injury produces joint effusion and fibrous tissue that begins to obliterate this triangle, progressing from caudal to cranial as the fluid, fibrosis, or both, accumulate. However, detection of this change can be inconsistent, as it demands impeccable radiographic technique. Osteoarthritic changes are a nonspecific and an inconsistent finding in the cranial cruciate-deficient patient, and they are inevitably more severe when evaluated on exploratory arthrotomy than when observed on radiography. Once a diagnosis has been obtained, a therapeutic arthroscopy or arthrotomy can be performed. During this examination, the integrity of the meniscus will also be evaluated as the diagnosis of a injured meniscus is not reliable at clinical examination and the meniscus is not visible on radiography.
Ultrasonography is usually not performed for diagnosis of a CCLR but can be useful for evaluation of the meniscus. In acute cases, a synovitis/hematoma surrounding the area of ruptured ligament is always present although
the ruptured cruciate ligament itself is only seen in 20% of the cases. In chronic cases, irregular hyperechoic

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