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The Imposters By Barclay Slocum, DVM and Theresa Devine Slocum, MS Two major pathologic conditions of the hind limb are hip dysplasia and rupture of the cranial cruciate ligament. There are several conditions which mimic the clinical signs demonstrated by those two conditions, and are often misdiagnosed as a result. This paper presents some of the more common problems in diagnosis that are experienced clinically. Hip Dysplasia Imposters Hip Dysplasia creates soreness in the patient on extension of the hip, or abduction and extension of the hip. When the patient has extension of the hip joint, he also has extension of the spine, particularly the lower lumbar spine at L7-S1. The stand test is performed by the following instructions to the owner. "Have your dog come to a standing position. Now stand in front of your dog and pick up his legs as if you are going to dance with him." When the normal dog stands, he will relish this invitation, and he will stretch up to the owner and extend his back. Within the patient, the lower lumbar spine goes into lordosis as the hips are extended. For the normal dog, this presents no problem with compression of the cauda equina. If the dog is experiencing pain from cauda equina syndrome, then there is compression of the nerves which cross the disc space at L7-S1. This compression of nerves is responsible for pain upon extension of the hip joint. With a positive stand test, the compression of the nerve roots across the L7 disc space should be considered. This condition is called Cauda Equina Syndrome. In normal circumstances, the disc space is 1.5 times the size of all the other disc spaces when viewed on a lateral radiograph. In addition, the body of the seventh lumbar vertebra is shorter than the other lumbar vertebrae. This creates a highly mobile disc space which is designed to receive the forces created by the dog as he pushes off the ground and propels himself through the air. These forces cross the joints of the hind limb and are applied to the sacrum. The first disc space of the spine which receives the impact of these forces is L7-S1. Since this disc space is wide and the body of L7 is short, absorption of forces is quickly dissipated to the remainder of the spine. The anatomic construction of the L7-S1 disc space allows for the center of motion of flexion and extension to be located at the junction of the middle and dorsal one third of the L7-S1 disc space. In the early stages of trauma to this disc space, the disc has partial tears comparable to the sprain of a ligament. Since the disc is wide, it soon loses its integrity resulting in dorsal and ventral translation of the sacrum with respect to the L7 vertebra. This creates a stretching of the annulus which soon loses its tension ring capability. Consequently, the stretched annulus begins to collapse and the redundant portion of the annulus will project outward from the nucleus. Ventrally, this can cause a redundant annulus which is inflamed and stimulates a ventral spondylitic process. Dorsally, the redundant annulus projects into the spinal canal, and with lordosis, compresses the spinal nerves. The basis for diagnosis is a positive stand test in which the patient is reluctant to stand in the fully extended position because of pain at the L7-S1 juncture. This can be mistaken for hip dysplasia because the dysplastic patient experiences joint capsule pain and is reluctant to stand in the hip extended position. The dysplastic dog will demonstrate pain on the subluxation test as well as have radiographic evidence of hip dysplasia. The patient with a cauda equina syndrome will demonstrate pain by digital compression over the L7-S1 region. Localization of the problem at L7-S1 is performed by myelogram and epidurogram. The myelogram can show compression of the dural sac as it crosses the L7-S1 disc space. The dye will have good filling proximal and distal to the L7-S1 space. Unfortunately, there are many patients whose dural sac ends before the L7-S1 disc space. In these patient an epidurogram can be an adjunct procedure which will demonstrate bulging of the dorsal annulus in the extended position. When the patient is placed in a flexed position of the lower lumbar spine (DAR position), the dorsal annulus becomes flattened, the dural sac is decompressed and the dye usually obtains a normal profile. This radiographic study is conclusive evidence for a Cauda Equina Syndrome at L7-S1. In addition, a study showing these characteristics can accurately predict a successful outcome to the L7-S1 fixation fusion surgery. Often, the clinical signs are not so clearly delineated by a myelogram, as the dural sac ends prior to the L7-S1 disc space or the redundant annulus is lateral to the dural sac. Under these circumstances, the myelographic portion of this study is of no value, and the epidurogram is more diagnostic. Unfortunately, the epidurogram is difficult to read and misinterpretation may lead to an improper surgical strategy. A MRI is preferred if there are neurologic signs such as conscious proprioceptive deficits. As the clinical signs become more severe and involve the neurologic system in greater depth, the necessity to pinpoint the source of pathology is of greater importance. If the L7-S1 disc is herniated rather than protruding, a surgical decompression by laminectomy and possibly articular process removal plus a foramenotomy, may be indicated. A MRI can usually detect herniation of a disc around a nerve root or protrusion of a disc off the midline, and offer greater diagnostic insight as to the pathology to be treated by surgery. Since the cause of the projection into the spinal canal is the collapse of the disc space in the presence of a stretched annulus, the problem of the dorsally protruding annulus can be overcome by placing the patient in flexion which creates a flattening of the dorsal annulus and decompresses the cauda equina. In addition, the articular facets of L7 are fixed in that position, so that the position can be maintained. A strip bone graft from the wing of the ilium is placed over the dorsum of L7 and the sacrum. This corticocancellous graft consists of multiple strips and cancellous bone which rapidly produces a fusion between L7 and the sacrum. The adolescent patient may be presented for hip dysplasia with definite signs of hip pain. The history of the dog is slipping on a slick surface and going into involuntary abduction. Hip pain may be demonstrated on the stand test, abduction external rotation test, subluxation test, and external hip rotation test. Upon radiographic evaluation, the ventrodorsal view will show a normal pelvis and apparently normal hip joint. The lateral view appears normal. The distraction view may demonstrate hip laxity or be normal. The compression view is normal. The DAR view and tomogram are normal. The frog view with the dog in abduction only is normal. The frog view with the hip in abduction and flexion allows visualization of the capital femoral physis which may be widened at the least and displaced if more severe. This is the clinical picture of a nondisplaced capital physeal fracture. If there is minimal displacement of the capital epiphysis, then immediate surgery is indicated and reduction by forced internal rotation will replace the capital femoral physis to its normal position. A singular intramedullary pin from the third trochanter through the femoral neck and seated into the capital epiphysis is sufficient to maintain reduction during healing. A growing patient may have the capital epiphysis grow away from the pin. If there is no displacement of the capital physis, then the patient can be placed in hobbles and restricted to good footing for one month and reradiographed to confirm healing. Often the young patient may be presented with the history of chronic lameness which is thought to be hip dysplasia. On the above examination, a slipped capital epiphysis may be in evidence. If this is slightly displaced, a pin will help in the healing. If the patient has a displaced capital epiphysis, it is usually displaced caudally and ventrally. If there is only a mild amount of displacement, then the capital epiphysis can be maintained in position by open reduction and internal fixation. Care must be taken to remove the exposed cranial calcar which will abrade the articular cartilage of the acetabulum if left intact. This occurs with internal rotation of the hip. This type of repair results in a retroverted femoral head with a short femoral neck. The only cases in which this will be successful are those cases with near perfect orientation of the acetabulum with good depth. Healing time is two months. The patient presented for hip pain may show minimal or no radiographic signs of hip dysplasia. External rotation of the hip may be normal as well as abduction. Although the hips may seem normal, the dog is sensitive to the stand test, yet is normal on the lordosis test. Upon detailed examination of the hip, pain can be established upon extension or internal rotation of the hip. Once this source of pain is established, direct palpation of the iliopsoas muscle will demonstrate pain. A diagnosis of iliopsoas myositis is warranted, and the treatment is conservative. Small dogs presented with severe hip pain are often diagnosed as unilateral hip dysplasia. Close observation of the radiographs will often show the patient to have a thin, but normal appearing femoral neck. If the femoral head is roughened and collapsed dorsally and intact medially, a diagnosis of Legge Calve Perthes disease is warranted. In this condition blood supply to the capital epiphysis is disrupted, and the patient will fracture the subchondral bone of the dorsal femoral head from activities of normal living. Rather than spontaneously repair from such a minor insult, the bone remains unchanged and waits for additional trauma. The cause of this nonresponsive behavior to the femoral head is loss of blood supply which allows the dog to repair even minor damage to the femoral head. Once the vast necrosis has occurred to the femoral head, the destruction to the head is imminent. Since these patients are quite small, recommendation for an excision arthroplasty is warranted. Cranial Cruciate Ligament Rupture Imposters The cranial drawer sign is pathognomonic for rupture of cranial cruciate ligament, or so it seems. Laxity and drawer motion can occur in young dogs with painful stifle joints. In these patients there is an cranial drawer motion and a diagnosis of a rupture of the cranial cruciate ligament often accompanies the patient. On close examination of these patients there is radiographic evidence of a subchondral defect on the lateral condyle. This is an OCD of the lateral femoral condyle. You will often notice a joint mouse in the suprapatellar pouch or the caudal limit of the intercondylar notch. The key elements for diagnosis are the young patient with a drawer sign, pain and a positive sit test. Radiographs confirm the defect on the lateral femoral condyle and inflammation around the cranial horn of the meniscus, rather than around the caudal horn of the medial meniscus. The laxity is created by a loss of bone substance rather than a loss of ligamentous integrity. The loss of bone substance simply makes the ligament too long for the stifle. OCD can also occur in the medial femoral condyle. Although OCD of the lateral condyle is a typical picture for a dog such as a 6 month old Labrador retriever, we can have additional limb alignment pathology associated with the longer limbed dogs or dogs with more severe pathology. The Great Dane puppy who has developed OCD of the lateral condyle may create a genu valgus secondary to the loss of the cartilage surface. Following the creation of genu valgus, a craniomedially rotary instability will occur at the stifle. This excessive pressure at the stifle will stretch the anteromedial joint capsule just cranial to the medial horn of the meniscus along the medial margin of the tibial plateau. This deformation creates greater pressure on the lateral portion of the physis and a proximal tibial valgus or distal femoral valgus may result. In addition a lateral patellar luxation or a lateral placement of the tibial tubercle may be a response to the abnormal forces created by this valgus growing limb. The treatment for this patient is directed towards limb alignment by means of a distal femoral osteotomy and/or a proximal tibial varus osteotomy. In addition, this correction will usually resolve the patellar luxation problem and cast the weight bearing on the medial femoral condyle, assume a lateral femoral condylar OCD lesion is not found. The tibial tubercle may have to be medially transposed in order to align the tibial tubercle in the sagittal plane. Occasionally the trochlear sulcus may need to be deepened to help retain the patella. If the depth of the OCD lesion is excessive, then the cranial horn of the lateral meniscus will become impinged during weight bearing and the cranial horn of the lateral meniscus may be necessary to be removed. Once normal limb alignment has been achieved, a Tibial Plateau Leveling Osteotomy and a slight amount (five degrees) of internal tibial torsion will place the weight bearing on the better cartilage surface of the medial condyle. In cases when a drawer motion is detected, a cranial cruciate ligament rupture is usually diagnosed. On closer examination the radiographs show inflammation at the cranial horn of the meniscus and fat pad, with minimal changes around the caudal horn of the medial meniscus. In addition, the caudal margin of the tibial plateau may be projected caudal to the femoral condyle. Correct position for the lateral radiograph may be difficult as internal rotation of the stifle occurs. On physical examination under anesthesia, a crisp endpoint to the cranial tibial thrust or anterior drawer motion, and a sluggish endpoint of the posterior drawer motion with no defined end point, may be experienced. Excessive internal rotation is noted, and the caudomedial corner of the tibial plateau will move caudally and laterally rather than the caudolateral aspect of the tibial plateau moving cranially and medially. Correct diagnosis is rupture of the posterior cruciate ligament. The damage to the joint may be seen at arthrotomy. The occurrence is one out of 150 cases. Secondary is damage to the caudomedial joint capsule. Surgical correction is a patella to caudomedial tibial plateau suture and a tibial tubercle recession. This has been highly effective due to enhancing the effects of the cranial tibial thrust which are protective of the posterior cruciate ligament deficient knee. A positive sit test is highly suggestive of a rupture of the cranial cruciate ligament because the caudal horn of the medial meniscus is impinged secondary to rupture of the cranial cruciate ligament. Patients are reluctant to bear weight after exercising if there is a partial rupture of the cranial cruciate ligament. These two characteristics are also present if a patient has a fractured or fragmented fabella. This fabella lies within the gastrocnemius muscle and is stressed by weight bearing, yet is basically extra-articular. Attempts to repair fractured fabella have been unsuccessful in my hands. Conservative treatment has been fruitful, but it requires a long period of time for healing to occur. The sit test may also be positive in Rottweilers that have a long tibia with respect to the Achilles mechanism. These patients cannot flex their hocks when sitting, and as a result, they are forced to sit on their tuber ischii. This is the appearance of a positive sit test. These patients will also have a straight hock during normal standing. Normal flexion of the stifle and hock will demonstrate the stifle hock angle to be significantly greater than normal. Surgical treatment is to remove a segment of tibia which will allow the dog to return to a normal standing angle. The osteotomy site should be bone grafted as the bone is slow to healing otherwise. The sit test is usually positive in the presence of hock pathology. Dogs with an OCD lesion of the hock will be unable to completely flex the joint and will therefore give a positive sit test. Direct observation of the patient usually reveals an enlargement of the caudomedial aspect of the joint capsule. Lateral, caudocranial and sunrise view (parallel to the metatarsus) radiographs are used to demonstrate the OCD lesion. If fragmentation is not seen over the caudal or dorsal portions of the medial trochlear ridge, the fragment may be located on the lateral trochlear ridge or the fragmented portion may be displaced into the caudal joint capsule or synovial sheath of the deep digital flexor tendon. Later stages of the disease will cause the talus to become oval in shape and the caudal malleolus will elongate. Additional fragmentation most often occurs with torsional activities and is least likely with straight ahead linear activities. Removal of fragments alleviates pain caused by interposing the fragment between the talus and the articular surface, but additional fragmentation can occur. The medial portion of the joint from which the fragment came has a tendency to collapse on that side and compound the excessive weight bearing on the pathologic portion of the joint. An external torsion osteotomy of the tibia will transfer the weight bearing to the lateral trochlear ridge of the talus and provide some relief, but the joint is still susceptible to trauma from twisting of the patient. Swelling of the caudomedial joint capsule and radiographic evidence of fragmentation on the medial side of the origin of the medial collateral ligament are indicative of a sprain of the medial collateral ligament. These patients have no evidence of fragmentation of the medial trochlear ridge of the talus or deformation of the truncated cone appearance. Conservative treatment is usually successful.
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