PARTIAL AVULSION OF THE ORIGIN OF THE CRANIAL CRUCIATE LIGAMENT IN A 4 YEAR-OLD DOG

JAMIE WILLIAMS, MS, DVM, RANDALL B. FITCH, DVM, MS, ROSE J. LEMARI~, DVM

A four year-old intact male Dalmatian was referred to the veterinary teaching hospital at Louisiana State University for acute, non-weight-bearing left hindlimb lameness of three weeks duration. Infor- mation supplied by the referring veterinarian indicated the lameness was first diagnosed and treated seven months previously, but recurred three weeks ago. External rotation of the left stifle, mild dis- comfort upon stifle flexion, mild to moderate muscle atrophy and palpable joint effusion were noted during physical examination. Slight cranial drawer movement with a soft end-point was discovered during manipulation of the left stifle. A triangular bone fragment and thickened, confluent intracap- sular soft tissues were observed on radiographs of the stifle. Radiographically, moderate degenerative changes suggested chronicity. This report describes the clinical and radiographic findings of a rarely reported partial avulsion of the origin of the cranial cruciate ligament in a skeletally mature dog. Veterinary Radiology & Ultrasound, Vol. 38, No. 5, 1997, p p 380-383.

Key words: cranial cruciate ligament, partial avulsion, intra-articular stifle avulsion, canine stifle.

History

FOUR YEAR-OLD INTACT MALE Dalmatian was referred A to the veterinary teaching hospital at Louisiana State University for acute, non-weight bearing left hindlimb lameness of three weeks duration. The referring veterinarian diagnosed lameness in the left rear leg seven months prior to referral. The dog was initially treated with prednisone for 5 days. Lameness recurred in the limb 6.5 months after initial treatment (3 weeks prior to presentation at LSU). On radio- graphs made at that time, a bony fragment was seen in the left stifle. There was no history of trauma. Referral to the teaching hospital was suggested but the owner waited 2 weeks before bringing the dog to LSU. In the interim, the dog was treated with aspirin, which resulted in a small improvement in the lameness.

A weight-bearing left rear limb lameness was evident on physical examination. The dog held the left stifle in external rotation and was mildly painful during flexion of the stifle. The dog was mildly febrile (104.2 F), with mild to moderate muscle atrophy and palpable joint effusion in the affected limb. Slight cranial drawer movement with a soft end-point was elicited during manipulation of the left stifle. Maximum displacement was obtained with the stifle in flexion. No drawer movement was elicited in the right stifle. Physical

From the Department of Veterinary Clinical Sciences, School of Vet- erinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803.

Address correspondence and reprint requests to Dr. Jamie Williams. Received July 25, 1996; accepted for publication September 5 , 1996.

examination results were consistent with a chronic cranial cruciate ligament injury. Complete blood count, serum chemistry and electrocardiography were within normal lim- its.

A 6 x 4 mm triangular bone opacity superimposed over the intercondylar region of the left stifle was observed on lateral and caudocranial radiographs (Fig. la & b) made after hospital admission. The fragment was smooth and ap- peared remodeled. The intracapsular soft tissues immedi- ately caudal to the infrapatellar fat pad were thickened and appeared confluent with the bone fragment. Very slight ir- regular periosteal new bone proliferation was evident on the medial surface of the lateral femoral condyle on the slightly obliqued caudocranial view of the stifle. There was mild joint capsular thickening, especially in the caudal joint cap- sule, and moderate degenerative changes of the stifle. The size and appearance of the bone fragment, the osteophytes of the stifle and the thickened soft tissues suggested chro- nicity, Radiographic diagnosis was chronic avulsion of the origin of the cranial cruciate ligament, with moderate asso- ciated degenerative changes.

During arthrotomy for surgical stabilization of the left stifle, the triangular bone fragment was clearly identified and remained attached to the craniomedial band of the cra- nial cruciate ligament (Fig. 2). The caudolateral band of the cranial cruciate ligament was intact and not involved in the avulsion injury. The medial meniscus was torn and folded back on itself caudally. Periarticular osteophytes and articu- lar cartilage fibrillation were observed. The avulsed frag- ment was not large enough to allow reattachment, therefore

3 80

VOL. 38, No. 5

A

FEMORAL AVULSION OF THE CRANIAL CRUCIATE LIGAMENT

0

38 1

FIG. I . Caudocranial (a) and lateral (b) radiographs of the left stifle in a 4 year-old Dalinatian with partial avulsion of' the origin of the cranial cruciate ligament. Note the triangular bone fragment in the intercondylar region and the thickened "intra-articular" soft tissues.

it was removed with the cranial cruciate ligament and the medial meniscus. The stifle was stabilized with an extra- capsular suture technique. Recovery from anesthesia was uneventful. The dog was discharged 7 days later, with in- structions for strict cage rest for 6 weeks, followed by a gradual return to exercise. On follow-up examination 8

months postoperatively, the dog was doing well with no appreciable cranial drawer movement.

Discussion

Rotational and craniocaudal movement of osseous struc- tures of the stifle joint is limited via the action of the cranial and caudal cruciate ligaments, with additional contribu- tions from the patellar ligament and the menisci. Mediolat- era1 stability of the stifle is provided by the collateral liga- ments. The cranial cruciate ligament originates on the me- dial surface of the lateral femoral condyle, and extends in a craniomediodistal direction to insert on the cranial aspect of the intercondylar region of the tibia1 plateau. '22,495,73y The caudal cruciate ligament extends from the lateral surface of the medial femoral condyle in a caudodistal direction to the lateral edge of the popliteal notch of the The caudal cruciate ligament is longer and slightly heavier than the cranial cruciate ligament.4~9~.'0 The fibers of the cranial cruciate ligament spiral or rotate approximately 90" during the course of their traveL2 This rotation in fiber alignment aids the slight rotary movement of the distal femur during

mur relative to the proximal tibia occurs during flexion and

FIG. 2. Intraoperative photograph of the avulsion fragment (arrowhead) and the craniomedial band of the cranial cruciate ligament in the left stifle flexion' 'light craniocaudal repositioning Of the o l a 4 year-old Dalmatian.

382 WILLIAMS ET AL 1997

extension of the normal, intact stifle. The cranial cruciate ligament prevents cranial subluxation of the tibia relative to the femur (cranial drawer sign), hyperextension of the stifle and, along with the caudal cruciate ligament, excessive in- ternal rotation of the tibia on the femur.”‘ The caudal cru- ciate ligament acts to limit caudal displacement of the proxi- mal tibia during extension of the ~ t i f l e . ’ .~ .~~“ ’

The cranial cruciate ligament is composed of 2 sub- divisions, the craniomedial band and the caudolateral band. 12,5,6,8 Each functions independently during flexion and extension of the stifle joint. The caudolateral band com- prises the bulk of the cranial cruciate ligament; it is taut during extension, but loose during flexion of the stifle joint.”2 The smaller craniomedial band of the cranial cru- ciate ligament remains taut during both flexion and exten- sion of the stifle.1’2’6 The craniomedial band of the cranial cruciate ligament provides the primary check against cranial drawer motion within the This constant tension may predispose this portion of the cranial cruciate ligament to damage, leading to partial cranial cruciate ligament tears or partial avulsions as seen in this dog.

Ligamentous and meniscal injuries of the stifle are the most common causes of rear limb lameness in the adult

Instability secondary to cranial cruciate ligament injury is believed to be the most frequent cause of stifle instability in Concomitant medial meniscal dam- age, most often the caudal horn, is not uncommon with injury to the cranial cruciate ligament.4 Damage to the cra- nial cruciate ligament may occur secondary to trauma (acute cruciate rupture) or chronic degenerative changes in the ligament itself. ’,’,‘ Stifle hyperextension injury, or exces- sive internal rotation during partial flexion of the stifle are believed to be the most common causes of traumatic dam- age to the cranial cruciate ligament in dogs and hu-

Most authors agree that the majority of cranial cruciate ligament injuries occur secondary to chronic de- generative changes within the ligament itself, rather than from acute excessive t r a ~ m a . ~ ” , ~ ” ~ Degeneration of the ligament may occur for a number of reasons, including pre- vious “sublethal” injury or stress to the ligament,2 confor- mational variations of varus or valgus deformity,2 immune- mediated disease,’ as well as age-related changes within the fibers themselves.I2 The middle or central portion of the cranial cruciate ligament has been shown to have the poor- est blood supply.234 It has been reported that the interior and the midportion of the cranial cruciate ligament deteriorated earlier than either the surface of the cranial cruciate liga- ment or the areas close to its origin/insertion.I’ It is theo- rized that this poorly nourished portion is the most likely site of cruciate damage or rupture.

The cranial cruciate ligament is intra-articular but extra- capsular, residing within the osseous borders of the stifle joint, but being covered by the synovium of the joint cap-

mans. 1,3,6,l I

sule.426*9 The cranial cruciate ligament with its joint capsule covering accounts for the soft tissue opacity observed just cranial to the femoral condyles and caudal to the infrapa- tellar fat pad on a lateral radiograph.’‘ Mineralized opacities in the stifle most commonly result from trauma, and are usually avulsed fragments or ligamentous calcifications. Avulsed fragments from the intercondylar eminence of the proximal tibia occurring in conjunction with cruciate liga- ment i n j u r i e ~ , ~ , ~ , ’ I ,14317 or from the extensor fossa of the distal femur secondary to avulsion injury to the long digital extensor t e n d ~ n ~ , ~ ~ ” * account for the majority of these opacities. Avulsion of the cranial cruciate ligament is considered very rare:36,7,1 ‘,15,17319 It has been suggested that avulsion, rather than tearing, of the cranial cruciate ligament is a disease primarily of skeletally immature pa-

This is theorized to occur because the ligamentous attachments to bone via Sharpey’s fibers are stronger than the immature bone itself, allowing avulsion to occur under a force insufficient to cause actual rupture of the ligament. The avulsions described in the literature pri- marily occur at the insertion of the cranial cruciate liga- ment,798, I 5,17,19 with only an occasional reference to the pos- sibility of avulsion at the femoral a t t a~hmen t .~ ’~ , ’ ’ These theories, while valid, do not explain the avulsion of the origin of the cranial cruciate ligament in this four year-old dog.

Breaking strength of the cranial cruciate ligament, the force necessary to cause acute ligamentous rupture, has been suggested to be approximately equal to four times the body weight of the dog.5 Avulsion of the origin of the cranial cruciate ligament has been described as 1*20

In one report which included 95 canine stifles with injury to the cranial cruciate ligament, only six had avulsed frag- ments associated with the cruciate ligaments.20 All six dogs were less than 2 years of age, and all avulsed the tibia1 insertion, with no avulsions of the femoral origin of the cranial cruciate ligament.20 This is supported by other stud- ies which concluded that avulsion fragments attached to the cranial cruciate ligament most commonly arise from the tibia.7,s,15,17319 No previous reports of partial avulsion of the origin of the cranial cruciate ligaments have been found in the veterinary literature.

The partial avulsion of the origin of the cranial cruciate ligament presented herein is inconsistent with previous re- ports describing appearance, and the site and age of onset of avulsion fractures associated with cranial cruciate ligament injury. Based on clinical history, this avulsion fracture in this skeletally mature, four year-old dog could be no more than 7 months old. Radiographic changes support the clini- cal history in that the degenerative changes present were consistent with stifle instability of several months, but cer- tainly not several years, duration.

tiellts .‘,I I 3 1s. 19

VOL. 38, No. 5 FEMORAL AVULSION OF THE CRANIAL CRUCIATE LIGAMENT 3 83

REFERENCES

1. Moore KW, Read RA. Rupture of the cranial cruciate ligament in dogs-Part 1. Comp on Cont Ed 1996;18(3):223-233.

2. Arnoczky Sp, Marshall JL. Pathomechanics of cruciate and menis- cal injuries. In: Bojrab MJ. Pathophysiology in small animal surgery. Phila- delphia: WB Saunders, I98 1 .

3. Arnoczky SP. Cranial cruciate repair. In: Bojrab MJ. Current tech- niques in small animal surgery, 3rd ed. Philadelphia: Lea & Febiger, 1990.

4. Hohn RB, Newton CD. Surgical repair of ligamentous structures of the stifle joint. In: Bojrab MJ. Current techniques in small animal surgery, 1st ed. Philadelphia: Lea & Febiger, 1975.

5. Johnson JM, Johnson AL. Cranial cruciate ligament rupture. Vet Clin North Am Small Anim Pract. 1993;23(4):7 17-733.

6. Kirby BM. Decision-making in cranial cruciate ligament ruptures. Vet Clin North Am Small Anim Pract. 1993;23(4):797-819.

7. Rich FR, Glisson RR. In vitro mechanical properties and failure mode of the equine (pony) cranial cruciate ligament. Vet Surg. 1994;23(4): 257-265.

8. Prades M, Grant BD, Turner TA, Nixon AJ, Brown MP. Injuries to the cranial cruciate ligament and associated structures: summary of clini- cal, radiographic, arthroscopic and pathological findings from 10 horses. Equine Vet J. 1989;21(5):354-357.

9. Evans HE. Arthrology. In: Evans HE. Miller’s anatomy of the dog, 3rd ed. Philadelphia: WB Saunders, 1993.

10. Harari J. Caudal cruciate ligament injury. Vet Clin North Am Small Anim Pract 1993;23(4):821-829.

11. Wdsilewski SA, Frank1 U. Osteochondral avulsion fracture of femo-

ral insertion of anterior cruciate ligament. Case report and review of lit- erature. Am J Sports Med. 1992;20(2):224-226.

12. Vasseur PB, Pool RR, Arnoczky SP, Lau RE. Correlative biome- chanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985;46(9): 1842-1854.

13. Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc 1993;203(7): 1016- 1019.

14. Park RD. Radiographic evaluation of the canine stifle joint. Comp on Cont Ed 1979;1(11):833-841.

15. Brinker WO, Piermattei DL, Flo GL. Diagnosis and treatment of orthopedic conditions of the hindlimbs. In: Brinker WO, Piermattei DL, Flo GL. Handbook of Small Animal Orthopedics and Fracturc Treatment, 2nd ed. Philadelphia: WB Saunders, 1990.

16. Huss BT, Lattimer JC. What is your diagnosis? lntra-articular avul- sion fracture of the left tibia at the insertion of the cranial cruciate ligament. J Am Vet Med Assoc 1994;204(7): 1017-1018.

17. Innes JF, Butterworth SJ, Barr ARS, Dieppe PA. Bilateral, chronic cranial cruciate ligament avulsion in a six-year-old dog. Vet Comp Orthop Traum 1996;9:84-87.

18. Salmeri KR. Radiographic Diagnosis (Avulsion of the long digital extensor tendon). Vet Radio1 1990;31(3): 132-1 33.

19. Gupta BN, Brinker WO, Subramanian KN. Breaking strength of cruciate ligaments in the dog. J Am Vet Med Assoc 1969;155:1586-1588.

20. Reiiike JD. Cruciate ligament avulsion injury in the dog. J Am Anim Hosp Assoc 1982;18:257-264,