Diagnosis

Diagnosis of a complete cranial cruciate ligament tear of the left stifle for 
this case can be 
made based on clinical presentation, history, physical exam, and specialty exam 
results.

Clinical Presentation
Bonnie presented with a history of an acute onset of a partial weight-bearing 
lameness of 
the left hind limb, along with a concurrent history of an active lifestyle.  
This may imply 
that exercise induced trauma is the likely cause of injury. Two mechanisms can 
explain 
injury to the cranial cruciate ligament - ether violent internal rotation or 
hyperextension of 
the stifle.  With a violent internal rotation of the stifle, the cranial and 
caudal cruciate 
ligaments wind around themselves.  The cranial cruciate ligament undergoes 
damaging 
compressive forces as the caudomedial edge of the lateral femoral condyle 
rotates against 
the ligament.  The second mechanism involves hyperextension of the stifle, where 
upon 
hyperextension the roof of the intercondylar notch of the femur may transect the 
ligament. 
Age related degenerative changes within the stifle joint as well as the 
overweight status of 
our patient may have also played a role in further exacerbating the lameness 
associated with 
a cranial cruciate ligament rupture.

The presence of a 4-5 mm cranial drawer sign while under sedation is diagnostic 
for cranial 
cruciate ligament rupture. The initial absence of a cranial drawer sign was 
likely due to 
patient apprehension and muscle contraction. In this case, a complete tear of 
the ligament, 
as opposed to a partial tear, is more likely to result in a positive cranial 
drawer test. Only 
complete rupture involving both bands of the ligament would result in a cranial 
drawer sign 
that is apparent on both extension and flexion.


Specialty Exam Results

Radiographs were taken to rule out other possible causes of stifle joint 
lameness and 
confirm a diagnosis of cranial cruciate ligament rupture.  Evident radiographic 
changes 
included intracapsular joint effusion and a widening of the lateral joint space 
with 
concurrent diminished medial joint space. 
The effusion detected in the stifle joint radiographically is due to intra-
articular hemorrhage 
from the ligament tear as well as inflammatory vasodilation and neutrophil 
migration to the 
site of injury.  This mechanism is also supported by the joint fluid analysis, 
which is 
discussed in our specialty exam results.  The resultant trauma and instability 
induces an 
inflammatory response, including the release of cytokines from the chondrocytes, 
leading 
to destruction of the proteoglycan and collagen network of the articular 
cartilage by 
metalloproteinases. Exposed collagen from the torn ligament also elicits an 
autoimmune 
response, which increases the intra-articular inflammation. The swelling 
produces the 
distention of the joint capsule on either side of the patellar ligament present 
in this animal. 
Rupture of the cranial cruciate ligament produces a radiographically abnormal 
joint 
characterized by increased joint space laterally and diminished joint space 
medially. The 
cranial cruciate ligament holds the lateral femoral condyle tight against the 
medial tibial 
condle, providing support laterally.  Without this support, excessive 
compressive force is 
placed on the medial stifle resulting in decreased joint space medially.

Concurrent injury to other structures within the stifle joint is possible, 
particularly a 
meniscal tear, which can be a direct result of the instability produced by a 
cranial cruciate 
ligament rupture. Damage to the caudal body of the meniscus has been noted in 
fifty to 
seventy-five percent of patients with a torn cranial cruciate ligament.  This 
can be diagnosed 
through arthroscopy, where a tear can be noted and excised.

As this case was presented with an acute onset of lameness and acute rupture of 
the cranial 
cruciate ligament, chronic degenerative changes within the stifle were not 
apparent.  
Radiographic changes associated with a chronic cruciate ligament tear would 
include 
osteophyte formation along the trochlear ridge,