Group 11 - Diagnosis: Acute Left Cranial Cruciate Rupture due to Trauma

Orthopedic Exam:
	On observation, Bonnie presented with an acute partial weight bearing left hind limb lameness. Rupture of the cranial cruciate ligament due to acute trauma will cause joint instability. The significant cranial drawer, 4-5mm, elicited on orthopedic manipulation of the left stifle supports the diagnosis of complete cranial cruciate ligament rupture.  In cases of partial tears, the cranial drawer sign is typically either absent or slight. Orthopedic exam revealed several findings that refute the presence of a chronic primary degenerative process in the stifle. Mechanical limitations imposed by a fibrotic joint capsule typically do not allow for the significant tibial displacement elicited in this case. As the joint was manipulated through its full range of motion, no crepitation or clicking could be felt.  These are usually considered to be signs of osteophyte formation and/or articular cartilage (i.e. meniscal) wear.  Although meniscal injury can occur in acute situations, and often does, the absence of supportive signs helps to rule out chronic disease. This is attributed to the fact that early DJD is characterized by cartilage damage. In primary degenerative joint disease, joint effusion tends not to be as marked or as readily detectable as it was in Bonnie's case. Furthermore, the patient showed a significant pain response on joint palpation that also suggests an acute traumatic or infectious situation.	


Radiographs:
Radiographs, although not diagnostic for cranial cruciate tears, were taken to rule out intra-articular disease.  The radiographs support the diagnosis of injury due to acute trauma.  Intracapsular joint effusion is indicated radiographically by capsular distention and infrapatellar fat pad compression.  These changes are seen on the lateral AP view of the stifle.  No indication of chronic degenerative changes to the bony joint is present.  The articular surfaces appear normal with no evidence of osteophytic change.  Normally in cases of DJD, osteophytes would be found at junctions between articular cartilage and synovial membrane.  Examples of such sites would be the trochlear ridge, the caudal surface of the tibial plateau and the inferior pole of the patella.  Medial enlargements due to the presence of osteophytes were not found on physical exam of the stifle further supporting acute injury.  Another characteristic sign of DJD is subchondral bone sclerosis and/or cyst formation.  Over time as cartilage wears down, subchondral bone will become exposed through tears, or fibrillations, of the cartilage.  Increased pressure loads are placed on these sites causing hemorrhage and bone necrosis.  Subsequently osteochondral repair takes place in these areas and the bone becomes sclerotic. Radiographically, this would be seen as areas of increased radio-opacity with respect to surrounding normal bone.  Cysts may develop beneath these areas due to loss of trabeculae and fibromyoid degeneration of the marrow.  These are seen as rounded radiolucent figures deep to the subchondral bone on radiographs.  Neither of these changes were present on Bonnie's radiographs.

Clinical Pathology - Joint Tap:
The hypothesis of infectious arthritis is not supported by the bloodwork or joint tap results.  Although a slight leukocytosis is present, it is not supported by a left shift, monocytosis, or clinical signs.  The combination of which would indicate a significant inflammatory response.  The joint fluid was reddish-clear, moderately cellular, and without evidence of bacterial infiltration.  It also displayed a good mucin clot that further refutes degenerative joint disease and septic arthritis. 

Pathophysiology of Cranial Cruciate Rupture:
 
	The cranial cruciate ligament is attached to a fossa on the caudal aspect of the medial side of the lateral femoral condyle.  It courses medially and distally across the intercondylar fossa and attaches to the cranial intercondyloid area of the tibia.  The cruciate ligaments function as constraints on the stifle joint.  Specifically, the cranial cruciate acts to prevent cranial displacement of the tibia on the femur, limit extensive internal rotation of the tibia on the femur, and to prevent hyperextension of the joint.  The mechanisms of injury to the cranial cruciate ligament can be related directly to its normal functions.  
	The most common traumatic injury to the cranial cruciate ligament occurs due to sudden rotation of the stifle with the joint in 20 - 50 degrees of flexion.   The cruciate ligaments begin to twist on each other and themselves to limit the rotation of the tibia on the femur.   With excessive internal rotation of the tibia the cranial cruciate ligament becomes wound very tightly and is subject to injury from the lateral femoral condyle as it rotates against it.  This may cause the ligament to rupture in its mid portion or to avulse a portion of its bony attachment.  The latter is more common in younger animals and was not supported radiographically by the presence of a bony fragment in this case.  A dog can cause rotational injury to the cranial cruciate if it is running and quickly changes direction while the paw is planted.  Another mechanism of injury to the cranial cruciate ligament is hyperextension.  The cranial cruciate ligament is the primary check ligament against hyperextension of the stifle joint.  Therefore, if the joint is hyperextended the cranial cruciate is the first structure subject to injury. Hyperextension of the stifle can occur when a dog is running and abruptly fixes the hind limb but the body continues to move forward, an example being stepping in a hole while running.  While out exercising with her owner, either of these scenarios could have easily caused Bonnie's injury.
     Bonnie's cranial cruciate ligament may have been chronically weakened as a result of several underlying factors inherent to her case.  This degenerative process would predispose her to a ligament rupture from minimal trauma.  Her history does not indicate a significant traumatic event that the owner associated with the onset of lameness.  Thus, these factors should be considered as potentially contributing to the pathophysiology of Bonnie's injury. 
Bonnie is a spayed female 6 year old Labrador Retriever that would be considered overweight. 	Bonnie's obesity either applies excessive strain on the stifle primarily or exacerbates any pre-existing abnormal forces from other causes secondarily.  Furthermore, long term hypoestrogenism from ovariohysterectomy has been implicated in ligament breakdown due to increased collagenase activity.	Based on Bonnie's age, in general her body has begun to go through changes associated with aging. Orthopedically, these may result in a progressive instability of the stifle that subsequently places abnormal stresses on intra-articular supportive structures, such as the cranial cruciate ligament. If this ligament is overloaded chronically as the joint goes through its normal range of motion, logically it will begin to weaken.  Alterations in microstructure occur including a loss of fiber-bundle organization and hyalinization of collagen fibrils.  Overall, there is a loss of tensile strength and stiffness, predisposing the ligament to damage from even minimal trauma.
Inadequate musculature whether due to aging, sporadic exercise, or body condition also subjects intra-articular joint structures, such as the cranial cruciate ligament, to increased loading.
Structurally incorrect conformation may also be contributing to Bonnie's lameness.  Some large breed dogs inherently stand with their femurs at a greater angle in respect to their tibias.  This decreases the space within the intracondylar notch that the cruciate ligaments can pass through.  Ultimately, these breeds are predisposed to partial or complete tears of the craniomedial band of the CrCL as it runs past the roof of the notch.  A second anatomical problem that may be a possibility involves abnormal tibial conformation.  Secondary to this, within the dog's normal gait, small degrees of excessive internal tibial rotation or hyperextension may be occurring.  Eventually, these repeated minor stresses would wear down the ligament and decrease its functional effectiveness through aforementioned degenerative processes.  Valgus or varus deformities may incur the same results.  Overall, these structural abnormalities may or may not be sufficient to cause bony degenerative changes in association with the ligament degradation.
	Acute cranial cruciate ligament rupture due to trauma is supported by history, physical/orthopedic exam, and specialty diagnostics.