Diagnosis:

Our diagnosis is right cranial cruciate ligament rupture and a possible meniscal tear due to trauma at play.  Our findings on bloodwork indicate that there is a mild inflammatory process associated with a hydroarthrosis of the joint space caused by the ligamentous tear.  The radiographic findings indicate a generalized opacity of the joint due to effusion with a loss of dimension of the infrapatellar fat pad, which is associated with an effusion of the joint.  There was no finding of osteosarcoma, an avulsion fracture or definite OCD lesions on radiographs. There is also no history of a past major traumatic event, which could cause a fracture.   The clinical findings of a 4-5mm cranial drawer sign and acute onset of partial weight bearing lameness further support cranial cruciate ligament rupture.  The increase in severity of the lameness leads us to believe that there is also a medial meniscal tear, but this will be explored further during surgical repair of the cruciate tear.

We presume that this injury occurred while Bonnie was at play, running and abruptly fixed her tibia, possibly by stepping in a hole, while the rest of her body continued forward. This caused hyperextension of the stifle or rotation of the tibia.  The stifle was flexed 20-50 degrees as the tibia was forcibly rotated internally and as Bonnie rotated her body externally, the stifle was twisted and the cranial cruciate ligament ruptured. Bonnie presented with effusion of the left stifle joint with distension of the joint capsule.  The pathophysiology of this effusion is that the torn cruciate and trauma to surrounding tissues would lead to disruption of the vascular supply, which causes plasma exudation and leads to acute edema.  Then inflammatory cells migrate into this exudate and release inflammatory mediators, which cause vasodilation and further exacerbate the edema.  Both the inflammatory mediators and the joint capsule distension will cause the clinical sign of lameness.  The inflammatory mediators increase nociceptor response.  The distension of the joint capsule causes lameness by increasing pressure on the fibrous joint capsule, where the nociceptors are abundant.  This increased pressure causes mechanical stimulation and thus the clinical lameness.  Another mechanism of lameness associated with a rupture of the cranial cruciate ligament is a pathological rolling and sliding of the femur in the stifle joint, which causes partial weight bearing lameness of the left hindlimb.  Also, up to 80% of cranial cruciate ligament tears result in tears or detachment of the medial meniscus.  This occurs because the meniscus cannot follow the pathological motion of the femur due to its attachments to the tibial plateau and thus the meniscus tears.  Cranial cruciate ligament rupture causes only mild lameness with the animal avoiding full extension of its stifle during motion.  If the medial meniscus is also injured there is resulting moderate to severe lameness, which is what is being seen in Bonnie's case.  A definitive diagnosis will be made by evaluation of the stifle during the surgical correction of the cranial cruciate tear.

We believe this to be an acute event, rather than a chronic condition due to the lack of degenerative changes noted on the radiographs, as well as the lack of macrophages in the joint fluid.  The presence of a mucin clot is indicative of a non-septic effusion; the lack of bacteria and degenerate neutrophils also lead us to this conclusion.