Diagnosis The patient has a complete tear of the cranial cruciate ligament of the left stifle. This rupture is likely due to a traumatic event while the dog was exercising. The cranial drawer movement, present in this patient, is diagnostic for cranial cruciate ligament injury. A normal stifle has craniocaudal movement of 0-2mm, a partial tear of the cranial cruciate ligament usually has only 2-3mm of instability, and a complete tear can have from 3-5mm of instability. The patient had 4-5mm of instability in the left stifle, which would indicate a complete rupture of the ligament. This should be compared with the 2mm of instability palpable in the normal right stifle, which is within the normal range. The joint tap and joint swelling indicate a slight acute inflammatory process in the left stifle due to the acute trauma to the joint with the ligament rupture. The trauma to the cranial cruciate ligament released inflammatory mediators, which increased the permeability of the vasculature. This would allow the influx of fluid, protein, and inflammatory cells. This would result in the non-septic exudate present in the patient causing the joint effusion. The lack of bacteria or neoplastic cell in the fluid would tend to rule out a neoplastic or infectious process causing the effusion. The cell numbers in the joint fluid were 3500 per high powered field. This is not consistent with secondary degenerative joint disease in which you would expect to see 6000-9000 cells. The hyaluronic acid has not been depolymerized by the inflammatory process and the integrity of the synovial fluid is intact due to the presence of a good mucin clot. On the lateral radiographs there is an increased fluid density in the joint with the patellar fat pad being pushed cranially away from the femoral condyles. The fluid density is consistent with an effusion in the joint causing the fat pad to be pushed away from the joint space. The anterior-posterior radiographs showed a slightly deceased joint space medially and a slightly increased joint space laterally. This is likely due to poor positioning/slightly oblique as the patella is not superimposed over the middle of the femur and femoral fabella are not symmetrical. There are no degenerative bony changes (lysis) visible on the radiograph which could be seen with later stage a neoplasm, especially synovial cell sarcoma. The general lack of radiographic changes is indicative of an acute tear versus a chronic ligament rupture instability. Radiographic findings associated with a chronic ligament tear would include osteophyte formation, fibrous thickening of the joint capsule, and subchondral sclerosis. The clinical pathology results showed a leukocytosis, slight hypocalcemia, and a hypoalbuminemia. The leukocytosis is likely due to the inflammatory response in the stifle due to the tissue damage from the ligament rupture. The inflammation would result increase the permeability of the vasculature and allow the influx of fluid, protein, and inflammatory cells. The loss of protein into the joint could lead to the hypoalbuminemia present in the patient. The hypoalbuminemia (2.4 g/dl) is only slightly below the reference interval (2.7-3.8 g/dl) and could be normal for the patient, as the reference interval only would be expected to include 95% of the population. The hypocalcemia is likely a result of the hypoalbuminemia. 40% of calcium is bound to albumin in the circulation. With a decrease in albumin, the biologically active/free calcium would increase. This is the portion of the plasma calcium that is regulated by PTH/calcitonin. An increase in free calcium would decrease PTH secretion, decreasing reabsorption of cacium in the kidney and resulting in calcium loss in the urine. This would lead to a decrease in the total calcium measured in the blood.