CASE REPORT

Osteochondral lesion and cranial cruciate ligament rupture in an immature dog stifle

W

G. C. Macpherson* and G. S. Allan

Department of Veterinary Clinical Sciences, The University of Sydney, NSW 2006, Australia

Journal of Small Animal Practice (1993) 34, 350-353

ABSTRACT An osteochondral flap was present on the

medial femoral condyle of a stifle of a six-month- old female rottweiler in which there was also a ruptured cranial cruciate ligament. The lesion was probably osteochondritis dissecans, but the possibilities of it being secondary to joint in- stability or a subchondral fracture, as has been described in people with knee ligamentous injuries, are discussed.

* G. C. Macpherson’s current address is 31 Devonshire Street, Crows Nest NSW 2065, Australia

CASE HISTORY A six-month-old female rottweiler was present-

ed to the University of Sydney Veterinary Teach- ing Hospital for evaluation of intermittent left hindlimb lameness. The lameness was first noticed after the dog jumped from a vehicle two months previously. The lameness was more pro- nounced after exercise but resolved with rest. Clinical examination revealed moderate atrophy of the muscles of the left hip and hindleg, and a swollen crepitant left stifle. Palpation under gen- eral anaesthesia revealed cranial drawer in both extension and partial flexion that indicated cranial cruciate ligament rupture. Radiographs revealed significant distension of the stifle joint space, patchy osteolytic foci in the subchondral bone of the axial surface of the medial condyle of the left femur and an osseous fragment in the adjacent joint space (Figs 1 and 2). A tentative diagnosis of cranial cruciate ligament rupture and concurrent osteochondritis dissecans (OCD) was made. The possibility of rupture of a cranial cruciate ligament that had an aberrant origin on the femoral condyle was also considered (Due- land and others 1982).

FIG 1. Lateral radiograph of the affected stifle. There is con- siderable joint effusion. A small osseous fragment is present in the joint space (arrow)

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Osteochondral lesion and cranial cruciate ligament rupture in an immature dog stifle

FIG 2. Craniocaudal radiograph. There is a focal area of osteolysis on the axial surface of the medial femoral condyle (arrowhead). Adjacent to that area of osteolysis is a small osseous fragment

Surgical exploration and stabilisation of the stifle was recommended. A fair to guarded prog- nosis for limb function was given because of the likelihood of development of degenerative joint disease in the affected stifle. At surgery a strip of combined lateral retinaculum, lateral third of the patellar ligament and fascia lata was isolated. A lateral arthrotomy was then performed. The cranial cruciate ligament was inspected. Mid- ligament rupture was diagnosed. The respective ends appeared to have caps of granulation tissue on them. The proximal and distal remnants of the ligament were excised. The joint surfaces and meniscii were inspected. The meniscii were nor- mal. The presence of an osteochondral lesion on the axial aspect of the caudal articular surface of the medial femoral condyle was confirmed. The flap was excised and the site curetted. The joint was then irrigated with warm, sterile saline. The strip of combined fascia/partial patellar ligament was drawn under the cranial intermeniscal liga- ment and through the joint in the manner described by Shires and others (1984). With the joint at 130" to 140" the graft was pulled tight and then its proximal end was secured to the lat- eral metaphyseal region of the femur by a plastic spiked washer and a 3-5 mm cortical bone screw. The joint was irrigated with warmed, sterile

saline and the capsule closed with simple inter- rupted sutures of 3 metric polydioxanone (PDS; Ethicon). The lateral fabella was exposed and a suture of 5 metric polydioxanone was passed around the fabella, through a hole drilled in the proximal tibia1 crest, tightened and tied in a uni- lateral version of the technique of Flo (1975). The proximal fascia lata defect was sutured with 3.5 metric polydioxanone in a continuous simple pattern to the level of the patella and then sutured distally with a simple interrupted pat- tern of the same suture material. The subcuta- neous tissue and skin were sutured closed in separate layers.

The dog was discharged on the eighth postop- erative day and the owner instructed to restrict its exercise for eight to 10 weeks. At three months postoperatively, the owner reported, in a telephone conversation, that the dog had not walked on the leg initially hut had used the leg regularly when it was swimming. At this stage the dog was weightbearing evenly on all four limbs and led an active life. It had allegedly just won three major prizes in dog shows. The owner had moved the day after the dog was discharged from hospital and was unable to return it for re-examination.

DISCUSSION ~ ~

Cranial cruciate ligament injury and a concur- rent osteochondral lesion of femoral condyle have not been previously reported in an imma- ture dog. Cruciate ligament injuries are not com- mon in dogs under one year of age and are usually caused by acute trauma in this age group. In immature dogs they may be avulsion injuries which produce an intra-articular radiodensity (Arnoczky 1988). The radiodensity seen in the lateral radiograph of the present case was typical of changes seen with such an injury. However, the presence of subchondral osteolysis in the axial surface of the medial femoral condyle in the craniocaudal radiograph suggested the presence of an OCD or an OCD-like lesion.

There are several possible reasons for the development of the osteochondral flap on the medial femoral condyle. It may have been a true OCD lesion. Stifle OCD has not been previously reported in the rottweiler breed (Montgomery and others 1989), but that does not preclude the lesion in this dog being OCD. The breed is in the high risk category for OCD of other joint surfaces such as the humeral head (Rudd and others 1990), medial aspect of the humeral condyle (Mason and others 1980), and medial and lateral ridges of the trochlea of the talus (Breur and oth- ers 1989, Carlisle and others 1990, Wisner and others 1990). Histological examination of the

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excised flap was not performed which is unfortu- nate as it may have provided valuable informa- tion as to its aetiology. The opposite stifle was not radiographed but it did not show any clinical or palpable signs of OCD. The presence of a sim- ilar lesion in the opposite stifle would have pro- vided further evidence for the lesion discussed here being true OCD as stifle OCD often occurs bilaterally (Montgomery and others 1989).

If the flap was OCD it may have been a coin- cidence that it occurred concurrently with the cranial cruciate ligament rupture. However, an OCD lesion could have developed secondarily in the unstable, cruciate-deficient joint as a result of shearing forces generated by the motion of the caudal medial meniscus on the immature articu- lar cartilage of the medial femoral condyle. There is scientific evidence in other joints, such as the canine shoulder joint, that OCD lesions occur as a result of biomechanical forces generated at interfaces of contact and non-contact with oppos- ing articular surfaces (Lenehan and Van Sickle 1985, Olsson 1987). This explanation would account for the caudal articular surface of the medial femoral condyle being affected in this case. OCD lesions of the canine stifle rarely affect the medial femoral condyle; of 135 cases of canine stifle OCD reported before 1989 only 4 per cent affected the medial femoral condyle (Mont- gomery and others 1989). One can only speculate as to whether OCD could be initiated by these mechanisms, or whether osteochondrosis would have to pre-exist for an OCD lesion to develop (Olsson 1987).

The osteochondral lesion may also have been a traumatic osteochondral fracture that occurred at the time of the injury to the cranial cruciate liga- ment. Using magnetic resonance imaging, sub- chondral fractures have been documented in the femoral condyles of human patients with knee ligamentous injuries (Mink and Deutsch 1989, Vellet and, others 1991). A recent experiment showed that a single load delivered across the canine patellofemoral joint caused cracks and clefts in the zone of calcified cartilage and the subchondral bone in the absence of osteochon- drosis (Thompson and others 1991). Vellet and others (1991) suggested that the location of post traumatic subchondral fractures are related to the mechanism of injury. Mink and Deutsch (1989) noted that when osteochondral fractures were present over the anterior horn of the lateral meniscus there was often a concurrent tear of the anterior cruciate ligament. They associated this with compressive forces placed on the lateral side of the knee when external rotation of the femur occurred relative to a fixed tibia; one movement that commonly produces an anterior cruciate ligament tear. Similarly, the osteochon- dral lesion in the present case may have been ini-

tiated by compressive forces between the caudal horn of the medial meniscus and the medial femoral condyle at the time of the cranial cruci- ate ligament rupture.

If an occult subchondral fracture had occurred then joint instability may have had a role in its progression. Vellet and others (1991) suggested that there is a high prevalence of osteochondral sequelae to such fractures and the development of these sequelae is influenced by a number of factors such as the degree of force and its dura- tion and direction (eg, shearing); cartilage vol- ume involved and its elasticity; and the amount of blood supply to the basal cartilage in the region of the injury. The deep cracks and clefts produced by Thompson and others (1991) also progressed with time to involve the superficial cartilage layers.

One should also consider the possibility that the osteochondral flap developed first and the resultant intra-articular biochemical changes caused weakening of the cranial cruciate liga- ment which predisposed it to rupture. Synovitis would be initiated by proteoglycans of cartilage wear particles released from the damaged articu- lar cartilage. Proteases (such as collagenase), interleukin-1 and tumour necrosis factor are then released from the synovium. Interleukin-1 and tumour necrosis factor are cytokines that can activate chondrocytes to release latent metallo- proteinases. Intra-articular degradation becomes self-perpetuating.

The occurrence of mid-ligament rupture in this case contrasts with the consistent experimental finding in immature dogs of avulsion of the tibia1 attachment of cranial cruciate ligaments weak- ened by immobilisation (Klein and others 1982). The findings of that experiment suggested that despite ligament degeneration induced by im- mobilisation the bony attachment was still the weakest part of the immature bone-ligament- bone-unit. It further suggests that the ligament in the immature dog in this report was weaker than its bony attachment and therefore had undergone degeneration. However, if intra-articular bio- chemical changes subsequent to stifle osteochon- dral lesions such as OCD predisposed the cruciate ligaments to rupture one might expect this syndrome to have been previously recog- nised and reported. Histological evaluation of the remnants of the ligament should have been per- formed to determine if there was evidence of degenerative changes, although one would need to consider that degeneration may have occurred in the time from ligament rupture to sample col- lection.

In humans, OCD lesions of the classical site on the medial femoral condyle appear to be less prone to the development of osteoarthritis than lesions of the lateral condyle (Twyman and

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Osteochondral lesion and cranial cruciate ligament rupture in an immature dog stifle

others 1991). Whether stifles of dogs with OCD of the medial femoral condyle generally develop milder osteoarthritis than those with lesions of the lateral condyle remains to be determined. Long term follow-up on this case would be very interesting but unfortunately has not been pos- sible.

ACKNOWLEDGEMENTS ~~

We thank R. Ratcliffe for referring this case and R. B. Parker, College of Veterinary Medicine, University of Florida and D. J. Francis, formerly of the Faculty of Veterinary Science, Melbourne University, for contributing to the discussion.

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BREUK, G., SPAULDING, K. & BRADEN, T. (1989) Osteochondritis dissecans of the medial trochlear ridge of the talus in the dog. Veterinary and Comparative Orthopaedics and Trau- matology 2, 168-176

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DUELAND, R., SISSON, M. & EVANS, H. (1982) Aberrant origin of the cranial cruciate ligament mimicking an osteochondral lesion radiographically: a case history report. Veterinary Radiology 23, 175-177

FLU, G. (1975) Modification of the lateral retinacular imbrica- tion technique for stabilizing cruciate ligament injuries. Journal of the American Animal Hospital Association 11,

KLEIN, L., PLAYER, J., HEIPLE, K., BAHNIUK, E. & GOLDBERG, V. (1982) Isotopic evidence for resorption of soft tissues and bone in immobilized dogs. Journal of Bone and Joint Surgery 64A, 225-230

LENEHAN, T. M. & VAN SICKLE, D. C. (1985) Canine osteochon- drosis. In: Textbook of Small Animal Orthopaedics. J. B. Lippincott, Philadelphia. p 985

MASON, T., LAVELLE, R., SKIPPER, S. & WRIGLEY, W. (1980) Osteochondrosis of the elbow joint in young dogs. Journal of Small Animal Practice 21, 641-656

MINK, J. & DEUTSCH, A. (1989) Occult cartilage and bone injuries of the knee: detection, classification, and assess- ment with MR imaging. Radiology 170, 823-829

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OLSSON, S.-E. (1987) General and aetiological factors in canine osteochondrosis. Veterinary Quarterly 9, 268-278

agement of osteochondritis dissecans of the humeral head in dogs: 44 cases (1982 to 1987). Journal of the American Animal Hospital Association 26, 173-178

SHIRES, P. K., HULSE, D. A. & LIIJ, W. (1984) The under-and- over fascia1 replacement technique for anterior cruciate lig- ament rupture in dogs: a retrospective study. Journal of the American Animal Hospital Association 20, 69-77

THOMPSON, R., OEGEMA, T., LEWIS, J. & WALLACE, L. (1991) Osteochondrotic changes after acute transarticular load.

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RUDD, R., WHITEHAIR, J. & MARGOLIS, J. (1990) Results O f man-

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dissecans of the knee. A long-term study. Journal of Bone and Joint Surgery 73B, 461-464

VELLET, A,, MARKS, P., FOWLER, P. & MUNRO, T. (1991) Occult posttraumatic osteochondral lesions of the knee: preva- lence, classification, and short-term sequelae evaluated with MR imaging. Radiology 178, 271-276

WISNER, E., BERRY, C., MORGAN, J., POOL, R., WIND, A. & VASSEUR, P. (1990) Osteochondrosis of the lateral trochlear ridge of the talus in seven rottweiler dogs. Veterinary Surgery19,435-439

ABSTRACTS

Enteral feeding of dogs and cats: 51 cases (1989 to 1991)

TWENTY-five dogs and 26 cats were given nutri- tional support via nasogastric tube. Four com- mercial liquid diets and one protein supplement devised for humans were used. In addition, cats were given supplementary arginine. Return to eating, maintenance of bodyweight, and compli- cations associated with the diet were used to assess the efficacy and safety of the nutritional support. Resumption of voluntary food intake began before the animals left the hospital in most cases. Weight was maintained in 61 per cent of the animals. Complications included vomiting, diarrhoea and tube removal. Most problems resolved by changing the diet or strict observance of the feeding protocol. Enteral feeding begun before the animal becomes nutrient-depleted is more likely to succeed and avoids serious com- plications. Choice of diet depended on the dura- tion of anorexia and compromised organ function. No complications were associated with the placement of the nasogastric tube. Six dogs and two cats removed their nasogastric tube by sneezing, coughing or vomiting. Thirty-six (71 per cent) of the animals survived.

ABOOD, S. K. & BOPINGTON, C. A. T. (1992) Journal of the American Veterinary Medical Association 201, 619-622

Internal cardiac compression

INTERNAL cardiac compression is more effective than closed thorax compression in cardiopul- monary resuscitation, providing it is undertaken by properly trained personnel using correct equipment. It maximises artificial circulation of the blood and especially improves myocardial perfusion. It should be performed after 10 min- utes if a continuous spontaneous rhythm has not been attained. The chance of successful resusci- tation decreases markedly after 15 minutes.

HASKINS, S. C. (1992) Journal of the American Veterinary Medical Association 200, 1943-1946

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