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Partial rupture of the cranial cruciate ligament - in dogs H. Strem Department of Small Animal Diseases and Clinical Practice, The Royal Veterinary and Agricultural University, Copen- hagen. Biilowsvej 13 DK 1870 Frederiksberg C. Denmark Journal of Small Animal Practice (1990) 31, 137-140 ABSTRACT Four cases of partial rupture of the craniomedi- a1 part of the cranial cruciate ligament (CCL) are presented. Clinical examination revealed only subtle signs of CCL injury. The cranial drawer sign was present in two dogs and in flexion only. As the cranial drawer sign is not always evident a tentative diagnosis of partial CCL rupture should be based on history, joint tenderness and joint effusion. Arthrotomy and careful probing of the ligament is indicated. In these cases the lesion was treated immediately after diagnosis to prevent further degeneration and possible total rupture of the ligament. A fascial graft using the ‘over the top’ reconstruction technique was per- formed leaving the intact portion of the ligament in situ. Follow-up examination after four to six months revealed normal limb function in three dogs whereas slight and periodic lameness per- sisted in one dog. INTRODUCTION Instability of the stifle joint resulting from injury to the cranial cruciate ligament is one of the most frequent causes of hindlimb lameness in dogs [Pond and Campbell 1972, Arnoczky 1988). The cranial cruciate ligament (CCL) prevents cra- nial displacement of the tibia on the femur and the cranial drawer motion in a knee joint is considered pathognomonic for CCL-rupture (Arnoczky and Marshall 1977, Heffron and Campbell 1978, Henderson 1978). However, following experimental transection of the craniomedial or caudolateral component of the CCL the ‘cranial drawer’ sign is minimal making the clinical diagnosis of partial rupture of the cranial cruciate ligament difficult (Arnoczky and Marshall 1977, Heffron and Campbell 1978). Four cases of partial rupture of the CCL in dogs are presented; clinical features, surgical findings and treatment are discussed. CASE HISTORIES Case 2 A two-year-old female rottweiler of 35 kg was referred to the clinic for evaluation of left hindlimb lameness. Ten days earlier the dog was suddenly found lame after jumping. On admis- sion the dog showed a slight weightbearing lame- ness of the left hindlimb. The stifle joint was moderately distended with fluid but only mini- mal palpable pain on maximal extension of the joint was found on examination. Evaluation of cranial drawer motion was made through the joint range of motion. No instability was demon- strated even with the dog under general anaes- thesia. A partial cranial cruciate ligament rupture was suspected and an arthrotomy was performed; synovitis, joint effusion and an apparently nor- mal CCL were seen (Fig 1). During careful exami- nation of the ligament with a probe, some of the craniomedial fibres were found to be torn at their femoral attachment [Fig 2). No degenerative joint changes were seen. Treatment was accomplished by augmentation of the ligament by a fascial graft. The ligament tears were carefully trimmed and a slipknot of absorbable suture was made like a lasso or loop around the torn ligament (Fig 3). The fascia lata graft was prepared 1-5 cm in width extending from the middle of the femur to the tibia plateau where it was left attached. The free end of the graft was pulled through the lasso on the cranio- medial side of the patellar ligament and was then passed through the joint in the ‘over the top’ technique (Arnoczky and others 1979) along and 13’

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Page 1: Partial rupture of the cranial cruciate ligament in dogs

Partial rupture of the cranial cruciate ligament - in dogs H. Strem Department of Small Animal Diseases and Clinical Practice, The Royal Veterinary and Agricultural University, Copen- hagen. Biilowsvej 13 DK 1870 Frederiksberg C. Denmark

Journal of Small Animal Practice (1990) 31, 137-140

ABSTRACT Four cases of partial rupture of the craniomedi-

a1 part of the cranial cruciate ligament (CCL) are presented. Clinical examination revealed only subtle signs of CCL injury. The cranial drawer sign was present in two dogs and in flexion only. As the cranial drawer sign is not always evident a tentative diagnosis of partial CCL rupture should be based on history, joint tenderness and joint effusion. Arthrotomy and careful probing of the ligament is indicated. In these cases the lesion was treated immediately after diagnosis to prevent further degeneration and possible total rupture of the ligament. A fascial graft using the ‘over the top’ reconstruction technique was per- formed leaving the intact portion of the ligament in situ. Follow-up examination after four to six months revealed normal limb function in three dogs whereas slight and periodic lameness per- sisted in one dog.

INTRODUCTION Instability of the stifle joint resulting from

injury to the cranial cruciate ligament is one of the most frequent causes of hindlimb lameness in dogs [Pond and Campbell 1972, Arnoczky 1988). The cranial cruciate ligament (CCL) prevents cra- nial displacement of the tibia on the femur and the cranial drawer motion in a knee joint is considered pathognomonic for CCL-rupture (Arnoczky and Marshall 1977, Heffron and Campbell 1978, Henderson 1978).

However, following experimental transection of the craniomedial or caudolateral component of the CCL the ‘cranial drawer’ sign is minimal making the clinical diagnosis of partial rupture of the cranial cruciate ligament difficult (Arnoczky and Marshall 1977, Heffron and Campbell 1978). Four cases of partial rupture of the CCL in dogs are presented; clinical features, surgical findings and treatment are discussed.

CASE HISTORIES Case 2

A two-year-old female rottweiler of 35 kg was referred to the clinic for evaluation of left hindlimb lameness. Ten days earlier the dog was suddenly found lame after jumping. On admis- sion the dog showed a slight weightbearing lame- ness of the left hindlimb. The stifle joint was moderately distended with fluid but only mini- mal palpable pain on maximal extension of the joint was found on examination. Evaluation of cranial drawer motion was made through the joint range of motion. No instability was demon- strated even with the dog under general anaes- thesia. A partial cranial cruciate ligament rupture was suspected and an arthrotomy was performed; synovitis, joint effusion and an apparently nor- mal CCL were seen (Fig 1). During careful exami- nation of the ligament with a probe, some of the craniomedial fibres were found to be torn at their femoral attachment [Fig 2). No degenerative joint changes were seen.

Treatment was accomplished by augmentation of the ligament by a fascial graft. The ligament tears were carefully trimmed and a slipknot of absorbable suture was made like a lasso or loop around the torn ligament (Fig 3). The fascia lata graft was prepared 1-5 cm in width extending from the middle of the femur to the tibia plateau where it was left attached. The free end of the graft was pulled through the lasso on the cranio- medial side of the patellar ligament and was then passed through the joint in the ‘over the top’ technique (Arnoczky and others 1979) along and

13’

Page 2: Partial rupture of the cranial cruciate ligament in dogs

H. STR0M

FIG 1. (Left) At arthrotomy an apparently normal cranial cruciate ligament was seen (case 11

FIG 2. (Right) Arthrotomy inspection alone is not sufficient to determine the status of the cranial cruciate ligament. During careful examination of the liga- ment with a probe, part of the craniome- dial fibres were found to be torn (case I)

medial to the torn cranial cruciate ligament. The graft was pulled tight over the lateral condyle and secured by suturing the free end to the femoro-fabellar ligament. The loop was tightened to hold the major bulk of the CCL around the graft as described by Johnson (1986). Exercise was restricted to walking on a leash for six weeks and then gradually increased. Recovery was uneventful and the lameness had resolved at the three months control visit.

Case 2

A two-year-old female English bulldog of 24 kg with right hindlimb lameness was presented for examination. The lameness had shown a gradual increase in severity over two months. Initially the lameness responded well to treatment with non- steroidal anti-inflammatory drugs and rest but recurred after three weeks. The dog was referred to the clinic for further evaluation. On examina- tion the lameness was slight and the right stifle joint was moderately distended. The dog respond- ed to maximal extension of the joint. The cranial drawer sign was achieved under anaesthesia with the joint in 90" flexion. Radiography revealed joint effusion and periarticular osteophyte forma- tion. A tentative diagnosis of partial rupture of the cranial cruciate ligament was made and arthrotomy was performed. The ligament appeared intact. Probing, however, showed a fib- rillated and torn medial component involving one third of the ligaments total width. Additionally a thickened joint capsule, with an inflamed syn- ovial membrane and osteophytosis were found. A graft of fascia lata was prepared and placed as described in case 1. At clinical examination four months later slight lameness was noted.

Case 3

A four-year-old male weimeraner dog of 28 kg was presented with a six weeks history of lame- ness following play. The dog was obviously lame on the right hindlimb. Clinical examination revealed fluid distension and pain when the knee was extended. No instability was found even during anaesthesia. Radiography revealed joint

FIG 3. Partial cranial cruciate ligament repair with augmenta- tion with a fascia1 graft. Graft of fascia lata passed through a loop of suture around the torn ligamenta

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Page 3: Partial rupture of the cranial cruciate ligament in dogs

Partial rupture of the cranial cruciate ligament in dogs

effusion and slight osteophyte formation on the patella, tibial crest, femoral condyle and medial tibial condyle. A tentative diagnosis of partial rupture of the cranial cruciate ligament was made. The joint was explored and a partial rupture of the cranial cruciate ligament was seen. As in cases 1 and 2 the lateral component appeared normal. Further examination revealed capsule fibrosis, synovitis and osteophytosis. The CCL tear was augmented with a fascia lata graft as described in case 1. There was a gradual increase in limb func- tion with full recovery at five months.

Case 4

A nine-month-old male boxer of 28 kg was pre- sented with a recent history of trauma followed by marked hindlimb lameness. On examination the stifle joint showed synovial distension and mild pain on palpation was found. Under anaes- thesia a slight cranial drawer sign was evident in flexion only. Radiographs showed soft tissue changes with loss of infrapatellar fat pad shadow and distension of the joint capsule. A tentative diagnosis of partial rupture of the cranial cruciate ligament was made. Arthrotomy showed that the caudolateral portion of the ligament was normal but that most of the craniomedial fibres were torn at the femoral attachment. The CCL lesion was augmented with a fascia1 graft with the intact portion left in situ as in case 1. At six months the dog had regained normal limb function.

DISCUSSION Partial rupture or tear of the CCL is rare in dogs

(Tigari and Vaughan 1975). Tears may involve one or more of the ligament bundles. Two main functional components of CCL have been described; a caudolateral band (CLB) which is taut in extension and loose in flexion, and a cran- iomedial band (CMB) which is taut at all angles (Arnoczky and Marshall 1977). Damage exclu- sively to the CLB part of the CCL does not pro- duce the cranial drawer sign in either flexion or extension, while rupture of the CMB component is supposed to elicit the cranial drawer sign in flexion (Arnoczky and Marshall 1977). The par- tial ruptures in the cases presented here all involved the CMB part of the ligament. Bennett and others (1988) and Tarvin and Arnoczky (1985) have recently described this as the more common partial rupture of the ligament. This is contrary to the cases reported by Tigari (1977) who found a posterolateral involvement. The most common partial tear of the CCL in man is the CLB bundle tear (Johnson 1986). It has been questioned whether the minor instability follow- ing rupture of the CMB part of the ligament can be detected in clinical conditions (Heffron and

Campbell 1978). Whereas a cranial drawer sign in a clinical case with isolated rupture of the craniomedial fibres of the ligament has been reported by others (Tarvin and Arnoczky 1985). The instability was demonstrated with the stifle in goo of flexion; no cranial drawer sign was pre- sent with the joint in full extension. In the pre- sent study the partial ruptures all involved the CMB part of the ligament near the femoral attach- ment. This tear did not cause forward tibial dis- placement in two of the four dogs even though the test also was performed under general anaes- thesia with the tibia fixed in neutral, 90' flexion and full extension. During arthrotomy capsular fibrosis and effusion with capsular distension was seen. In cases of chronic CCL rupture, capsu- lar thickening and distension are present. This may hypothetically stabilise the joint making it difficult to produce a cranial drawer sign (Arnoczky 1988). Although the increased capsu- lar thickening and effusion may contribute to joint stability it seems unlikely that the joint cap- sule reaction is the only reason for the stability found in two cases. It is reasonable to assume that clinical instability demands a certain portion of the ligament to have ruptured, probably in addition to increased laxity of the intact portion. Thus arthrotomy and careful probing are essen- tial in the diagnosis of minor tears of the CCL.

Some authors question whether a relatively minor joint instability due to CCL insufficiency can result in lameness (Heffron and Campbell 1978, Bennett and others 1988). In this report CMB injury does cause lameness, pain and joint effusion even though no or only slight instability is demonstrated clinically.

Controversy exists as to the ability of partial ruptured CCL to regenerate and heal under vari- ous conditions. Experimental transection of half of the CCL followed by immediate joint immobil- isation in plaster resulted in a fibroblastic response extending throughout the length of the ligament (O'Donoghue and others 1966). The defect did not fill completely but collagen mate- rial was laid down and considerable strength gained. This experimental study is in contrast to clinical studies where untreated CCL rupture showed an ineffectual repair response with clini- cal disability and poor limb function (Vasseur 1984, Vasseur and others 1985). Case reports demonstrate that considerable time elapsed between detection of lameness and treatment. This may hamper an effective early repair response and cause additional strain and degen- eration of the injured ligament (Kappakas and others 1978, Bennett and others 1988). On this basis Tarvin and Arnoczky (1981) recommend total excision of the remaining ligament and graft replacement. In acute tears of the CCL in man however, healing of the CCL following suturing

139

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H. STROM

of the torn ends or fixation of the ligaments with staple implantation has been reported (Johnson 1986). Further, augmentation with tendon has been advocated in human cases of torn ligaments as studies have shown that tendon graft tissue contributes to ligament repair and preserves the CCL tissue incorporated in the graft (Lundborg and Rank 1980, Manske and Lesker 1982). The remaining CCL was preserved and a graft of fascia lata inserted with the ‘over the top tech- nique’ in all cases. Further clinical assessment including arthroscopy or arthrotomy and histolo- gy of the graft are necessary to evaluate the feasi- bility of this surgical procedure.

REFERENCES AKNOCZKY, S. P. & MARSHALL, J. L. (1977) The cruciate liga-

ments of the canine stifle: An anatomical and functional analysis. American Journal of Veterinary Research 11,

AKNOCZKY, S. P., TARVIN, G. B., MARSHALL, J. L. & SALTZMAN, B. (1979) The Over-the-Top procedure. A technique for anteri- or ligament substitution in the dog. ]ournal of the Ameri- can Animal Hospital Association 15, 283-290

ARNOCZKY, S. P. (1988) The cruciate ligaments: the enigma of the canine stifle. Journal of Small Animal Practice 29, 71-90

BENNETT, D., TENNANT, B. LEWIS, D. G., BAUGHAN, J., MAY, C. & CARTER, S. (1988) A reappraisal of anterior cruciate liga- ment disease in the dog. Journal of Small Animal Practice 29,275-297

HEFFRON, L. E. & CAMPBELL, J. R. (1978) Morphology, histology and functional anatomy of the canine cruciate ligament. Veterinary Record 102, 280-283

HENDERSON, R. A. (1978) The tibia1 compression mechanism: A diagnostic aid in stifle injuries. Journal of the American Animal Hospital Association 14,474-479

JOHNSON, L. L. (1986) Arthroscopic Surgery: principles & prac- tice Ed. L. L. Johnson and C. V. Mosby Company, town.

KMPAKAS, G. S., BROWN, T. D. & GOODMAN, M. A. (1978) Delayed surgical repair of ruptured ligaments: a compara- tive biomechanical and histological study. Clinical Ortho- pedics and Related Research 135, 281-186

LUNDHOKG. G. & RANK, F. (1980) Experimental studies on cellu- lar mechanisms involved in healing of animal and human flexor tendon in synovial environment. The Hand 12, 3-8

MANSKE, P. R. & LESKER, P. A. (1982) Nutrient pathways of flex- or tendons in primates. lournal of Hand Surgery 7, 436-439

O’DONOGHLE, D. H., ROCKWOOD, C. A., FRANK, G. R., JACK, S. C. & KENYON, R. (1966) Repair of the anterior cruciate ligaments in dogs. Journal of Bone and Joint Surgery48a, 503-519

POND, M. J. & CAMPBELL, 7. R. (1972) The canine stifle joint. Rupture of the anterior cruciate ligament. Journal of Small Animal Practice 13, 1-10

TARVIN, G. B. & ARNOCZKY, S. P. (1985) Incomplete rupture of the cranial cruciate ligament in a dog. Veterinary Surgery 10,94-95

TIGARI. M. & VAUGHAN, L. C. (1975) Arthritis of the canine sti- fle joint. Veterinary Record 96, 394-399

TICARI, M. (1977) Changes in the canine stifle joint following rupture of the anterior cruciate ligament. Journal of Small Animal Practice 19, 17-26

VASSEIJR, P. B. (1984) Clinical results following nonoperative management for rupture of the cranial cruciate ligament in dogs. Veterinary Surgery 13, 243-246

1807-1814

VASSEUR, P. B., POOL, R. R., ARNOCZKY, S. P. & LACJ, R. E. (1985) A correlative biomechanical and histological study of the cranial cruciate ligament in dogs. American Journal of Veterinary Research 46, 1842-1854

ABSTRACT

Congenital defects in cocker spaniel litter mates CONCOMITANT pericardial, diaphragmatic, caudosternal and cranioventral abdominal wall defects were found in five cocker spaniel litter mates. Three of the pups also had ventral septa1 defects (VSD’s). A sixth pup, with cranioventral abdominal wall defect died aged four days. The abdominal wall and diaphragmatic wall defects were corrected surgically in each case, at between 10 and 12 weeks old. The VSD’s were not corrected. Radiography, at six months of age, revealed moderately enlarged hearts in two of the pups with VSD. All pups were well one year postoperatively.

BELLLAH, J. R. SPENCER, C. P. BROWN, D. J. & WHITTY, D. L. (1989) Journal of the American Veterinary Medical Associa- tion 194, 1741

Hepatic lipidosis in cats ELEVEN cats with idiopathic hepatic lipidosis (confirmed by biopsy) were treated by the feed- ing of balanced nutrients through gastrotomy tubes. The gastrotomy tubes were inserted at the same time as liver biopsy was performed, Feed- ing was begun the day after surgery. Food con- sisted of canned prescription diet watered down to a suspension, supplemented with liquid vita- mins, minerals and powdered L-carnitine. Any additional fluid to meet daily requirements was given intramuscularly or subcutaneously initial- ly. Initially four to six feeds a day were necessary. By seven to 10 days after surgery all nutrient and fluid requirements were being met via the gastro- tomy tube. This enabled feeding to be continued at home by the owner. As appetite improved the cats were offered food per 0s and the amount given via the tube was reduced in volume and frequency. When sufficient food was taken by mouth the gastrotomy tube was removed. The mean duration of tube feeding was 48 days. The most frequent complications were vomiting, associated with feeding and localised cellulitis at the gastrotomy site. Four of the 11 cats died. Death was due to either peritronitis or hepatic encephalopathy or pneumonia or cardiopul- monary arrest. The surviving seven animals made a good recovery.

JACOBS, G., CORNELILIS, L., ALLEN, S. & GREENE, C. (1989) Jour- nal of the American Veterinary Medical Association 195, 635

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