Specialty Exam Results: consistent with Traumatic Cranial Cruciate Ligament Rupture

The specialty exam results confirm the presence of a cranial cruciate ligament rupture in 
the left stifle. The cranial cruciate ligament transverses the stifle from the cranial part of 
the intercondylar area of the tibia to the caudal part of the intercondylar fossa on the 
lateral femoral condyle. Complete rupture of the cranial cruciate ligament has produced 
an abnormal joint characterized by increased joint space laterally and diminished joint 
space medially. AP radiograph shows increased joint space between the lateral femoral 
condyle and the lateral condyle  of the tibia. The cranial cruciate ligament holds the 
lateral femoral condyle tight against the medial tibial condyle, and without this lateral 
support more stress is placed on the medial side of the stifle, decreasing the synovial fluid 
and joint space medially. Increased joint fluid is also seen on both AP and lateral views. 
Increased joint radioopacity and cranial displacement of the infrapatellar fat pad are 
indicative of intracapsular swelling, and are visualized on the lateral view.

The Clin Path results demonstrate a slight leukocytosis. This is most likely due to an 
acute inflammatory response in the stifle joint. Inflammatory mediators caused increased 
capillary permeability and attracted neutrophils and monocytes to the area. The increased 
demand for phagocytes dipped in to the storage pool of the bone marrow and produced 
the slight leukocytosis. These results are reinforced in the joint fluid analysis, where a 
modified transudate with a cell count of 3,500 / hpf was seen. The joint fluid was 
comprised of predominatly neutrophils and monocytes. The red color of the joint fluid is 
due to hemorrhage within the joint space, due to acute injury as well as increased local 
joint capillary permeability. This also accounts for the slight hypoalbuminemia, as 
albumin is a small serum protein of 69,000 Daltons and easily exits the fenestrated 
capillaries into the interstitium. Patients with hypoalbuminemia often show a concurent 
slight hypocalcemia, as this patient does. Forty percent of serum calcium is bound to 
albumin, but this bound calcium is not the biologically active ionized free calcium. The 
loss of calcium bound to albumin in the joint effusion would account for the lab test 
abnormality, however this is not associated with free ionized Ca2+  and no clinical signs 
associated with hypocalcemia would be seen.  There were no bacteria found in the joint 
fluid analysis, which rules out the possibility of infectious joint disease.