References BekM,Smith W,LevyM.SullivanEandRubinG (1992)MedJAusi156:596 Bourhy H, Kiss1 B, Lafon M, Sacremento D and Tordo N (1992) J Clin

Committee of Inquiry on Rabies (1971) Report ofthe Commiriee of Inquiry

Faoagali JL., DeBuse P, Strutton GMand SamaratungaH (1988) Med JAusf

Feiden W, Kaiser E, Gerhard L, Dahme E, Gylstorff B ef a1 (1988) Zcntralbl

Geering WA and Forman kT (1981)Animol Health in Australia, Vol9,Exoiic

Gould AR (1987) Virus Res 7: 169 Gould AR and Pritchard LI (1990) Virus Res 1731 Gould AR and Pritchard LI (1991) Virus Res 21:l Grattan-Smith PI, O'Regan WJ, Ellis PSJ, O'Flaherty SJ, McIntyre PB and

King A and Crick J (1988) In Rabies, edited by Campbell JB and Charlton

MannenK,HiramatsuK,MifuneKandSakamotoS(199l)VirusGenes569

Microbiol302419

on Rabies: Final Repori, HMSO, London

149702

Veierinarmed (B) 35247

Diseases, Australian Government Publishing Service, Canberra

Barnes CJ (1992) Med JAusi 156651

KM, Kluwer, Boston, MA. p 177

Pullar EM and McIntosh KS (1954)Ausi VeiJ30326 Rudd RJ and Trimarchi CV (1989)J Clin Microbiol272522 SacrementoD,BadmneH, Bourhy Hand TordoN(1992)JGen ird73:1149 SangerF,NicklenS and Coulson AR (1977)ProcNailAcadSciUSA74:5463 SmirhTs andBaerGM(1988)InRubies,editedbyCampbellJB andcharlion

Smith JS and Seidel HD (1992) In Progress in Medical Virology, edited by

Smith JS, Fishbein DB. Rupprecht CE and Clark K (1991) N Engl J Med

Smith JS, Orciari LA, Yager PA, Seidel HD and Warner CK (1992)JIgect

Tordo N. Pcch 0, Ermine A, Keith G and Rougeon F (1986) Proc Nail Acad

Vellecs Wh4 and Forrester ET (1981) Lnborafory Methodsfor Detecting

Vieira J and Messing J (1982) Gene 19259 Webster WA and Casey GA (1988) In Rabies, edited by Campbell JB and

(Accepted for publication 4 December 1992)

KM, Kluwer. Boston, MA, p 267

Melnick JL, Karger, Basel (in press)

324205

D b 166296

SciUSA83:3914

Rabies, Centers for Disease Control, Atlanta, p 110

Charlton KM, Kluwer, Boston, MA, p 201

The incidence and severity of intercarpal ligament damage in the equine carpus

NJ KANNEGIETER and SA COLGAN

Department of Veterinary Clinical Sciences, University of Sydney, New South Wales 2006

SUMMARY: The arthroscopic findlngs in 104 intercarpal joints in 76 horses were reviewed to determine the incidence and severity of changes in the medial intercarpal ligament. Damage to the intercarpal ilgament was observed in 43 joints in 35 horses, ranging from mild fraying of the edges of the ligament to complete dlsruptlon of all flbres. This represented an incidence of 41% of joints being affected. In 9 joints examined arthro- scopicaily primarily as a further diagnostic procedure, ligament damage was evident in all cases. in horses undergoing arthroscopic surgery primarily for the treatment of osteochondral chip or slab fractures, there was some correlation between the severity of articular cartilage damage and the presence of ligament damage.

The prognosisfor horseswith severe damage to the medial intercarpal ligament appears to be poor. Aust Vet J70: 89 - 91

Introduction Lameness attributable to lesions within the carpus is frequently

encountered in the horse. Welldocumented causes of lameness arising in the midcarpal joint include intra-articular fractures, degenerative joint disease and capsulitis-synovitis (Bramlage et a1 1991). Intercarpal ligament damage has been less often diagnosed as a cause of lameness (Kannegieter 1990; Kannegieter and Burbidge 1990; Bramlage et ul 1991) but may play a si&icant role in the long term prognosis of horses with carpal lameness (McIlwraith 1992).

Two intercarpal ligaments within the palmar aspect of the midcarpal joint may be viewed arthroscopically. The lateral intercarpal ligament attaches between the intermediate and ulnar carpal bones and the lateral aspect of the third carpal bone. The second ligament is located medially and is found between the radial carpal bone and the second and third carpal bones (Hurtig and Fretz 1986; Kannegieter 1990). The medial ligament inserts on the fascia of the palmar aspect of the second and third carpal

bones, but variations of points of insertion exist within in- dividuals (McIlwraith 1992). Damage is most often observed in the medial palmar intercarpal ligament (Kannegieter 1990), which is larger than its lateral counterpart.

The purpose of this study was to determine the incidence of lesions in the medial intercarpal ligament and to correlate this with the severity of other changes in the joint. It was found that 41% of joints examined had some changes in the intercarpal ligament, and that the degree of tearing was greater in those joints with more severe osteochondral lesions.

Materials and Methods Consecutive case records were reviewed of 76 horses that had

arthroscopic surgery performed on one or more midcarpal joints between January 1991 and July 1992. On admission, all horses underwent a standard lameness examination, which included intra-articular anaesthesia where appropriate, to localise the

Australian Veierinary Jownal Vol. 70, No. 3, March 1993 89

lameness to the intercarpal joint. A standardised radiographic examination of both carpi involving 5 views was performed. These views include a flexed lateromedial, 45” dorsomedial- palmarolateral oblique, 45O dorsolateral-palmaromedial oblique, dorsopalmar views and a dorsoproximal-dorsodistal view (skyline) of the distal row of carpal bones.

Arthroscopic examination of the joints was carried out in a routine manner (McIlwraith et ul1987). In order to examine the intercarpal ligament thoroughly the degree of flexion was greatly increased totheextent that, ifrequired. the foot was ahnostresting on the elbow. This position was important in allowing good visualisation of, and instrument access to, the palmar ligaments.

Changes in the medial palmar ligament were graded from 1 to 4. Grade 1 represented mild damage, with rupture, fraying or stretching of a small number of fibres from the edge, usually the lateral edge, of the ligament. Grade 2 changes constituted damage to up to one-third of the ligament. Grade 3 included those liga- ments that had damage involving one- to two-thirds of the liga- ment. Grade 4 was complete rupture of the ligament.

The severity of ligament damage was then correlated with the severity of osteochondral changes observed during surgery. Severity of cartilage lesions was assessed arthroscopically and graded from 1 (mild) to 3 (severe) as previously described (Kan- negieter and Ryan 1991).

Results A total of 76 horses had arthroscopic surgery of the midcarpal

joint, with 28 operated on bilaterally, resulting in a total of 104 joints being examined. Of the 76 horses, 35 had some damage to the intercarpal ligament, including 8 with bilateral changes, making a total of 43 (41%) of the 104 joints affected. The most common reason for arthroscopic examination was the presence of one or more osteochondral chip or slab fractures in the mid- carpal joint, which occurred in 95 joints. The site of the main lesion was on the distal aspect of the radial carpal bone in 61 joints, the third carpal bone in 3Ojoints (18 chip fractures, 7 slab fractures and 5 sagittal fractures) and the intermediatecarpal bone in 4 joints. The left carpus was affected in 53 horses, the right in 42 horses.

In 7 horses (9 joints) arthroscopic examination was performed as a further diagnostic procedure after lameness had been localised to the midcarpal joint by diagnostic intra-articular anaesthesia. In such horses lameness had been chronic, and had recurred after rest periods of between 3 and 6 months. Clinical examination did not reveal pain on joint flexion or joint effusion in any case. One horse was found to have persistent haemarthrosis in the midcarpal joint. No other abnormalities could be found in the carpus or proximal suspensory region on clinical examination, and radiographic findings were normal. During arthroscopic ex- amination of these joints the primary abnormality was considered to be intercarpal ligament damage. It was observed that in the joint that had persistent haemanhrosis, the lateral intercarpal ligament had severe lesions in addition to the grade 4 tearing in the medial ligament. In 7 of these 9johts no or negligible articular cartilage damage was evident. In the remaining 2 joints small areas of fibrillated cartilage were present on the radial and third carpal bones.

Of the 28 horses that had bilateral arthroscopy, 8 were found to have bilateral ligament lesions and 4 had unilateral lesions. The average severity of bilateral ligament damage was 3.2 out of 4 in each joint, compared with an average grading of 1.7 out of 4 in unilaterally affected joints.

Grade 4 ligament damage occurred in 10 joints. Three horses had bilateral grade 4 ligament lesions (6 joints). Of the remaining horses with grade 4 ligament lesions, one had grade 3 damage in the contra-lateral limb, whereas only one joint was examined

TABLE 1 Relatlonshlp between the Incidence and severlty of intercarpol

ligament lesions and joint lesions

Joint Number of joints showing Total lesions grade of ligament damage joints

0 1 2 3 4

Diagnostic 0 0 2 4 3 9

Moderate(grade2) 35 5 2 3 4 49

Mild (grade 1) 1 6 0 4 3 0 23

Severe (grade 3) 8 3 3 6 3 23

Total joints 59 8 11 16 10 104

arthroscopically in the remaining 3 horses that had a ruptured ligament.

Of the horses with mild or moderate articular cartilage damage 70% (16/23) and 71% (35/49), respectively, had normal inter- carpal ligaments. Of the horses with severe articular cartilage lesions only 35% (8/23) had normal ligaments. The correlation between the incidence and severity of ligament damage and joint lesions is shown in Table 1. The diagnostic group in Table 1 represents those joints that were examined arthroscopically be- cause of chronic lameness, which was localised to the mid-carpal joint by local anaesthesia, and in which no radiographic abnor- malities were evident.

Discussion The incidence of intercarpal ligament damage was much higher

in this than in previous studies. In a study of 150 joints Kan- negieter and Burbidge (1990) recognised 3 joints in 3 horses with intercarpal ligament lesions, an incidence of 2%. No mention of ligament damage was made in earlier reports by McIlwraith et ul (1987), but it was later stated (McIlwraith 1992) that 3 horses had been identified in the initial series, representing an incidence of 0.3%. McIlwraith (1992) found some tom ligaments in 8.7% of joints. The incidence in the present study, 41%, was therefore far higher than was previously suspected. The lack of recognition of intercarpal ligament lesions in initial reports is attributable to three factors. Firstly, the absence of radiological evidence of ligamentous damage, secondly the relative difficulty in viewing the ligament arthroscopically using normal positioning and tech- niques, and finally the fact that before arthroscopic surgery radiographically normal joints were very rarely surgically examined (Kannegieter 1990; Kannegieter and Burbidge 1990). The true incidence of intercarpal ligament damage may be as- sessed accurately only when all horses with chronic carpal lame- ness undergo arthroscopic examination (Mcllwraith 1992). The incidence of intercarpal ligament damage in horses that do not exhibit lameness is unknown at this time, but should be inves- tigated further.

The importance of the intercarpal ligaments in joint function has not been defined fully, but they would appear to play an important function in both decreasing the force placed on the articular surface and maintaining joint stability. One of the prin- cipal means of stress neutralisation in a joint is the dissipation of forces from the joint surfaces to the interosseu ligaments (Bram- lage et d 1991). In addition, during axial weight bearing the intercarpal ligaments absorb some of the load created by medial- to-lateral displacement of the carpal bones, which results in considerable force dissipstion (Bramlage et a1 199 1). The mechanism by which damage to the ligaments causes lameness is not clear. It is most likely that instability occurs in the joint because of ligament damage, particularly if complete rupture

90 Australian Veterinary Journal Vol. 70, No. 3. March 1993

occurs, and that this predisposes to abnormal weight bearing and stresses on the joint, which can result in pain It has been sug- gested by Bramlage et al(l991) that much of the carpal lameness in young horses during initial training occurs because of pain arising from inflammation of the intercarpal ligaments.

Although the medial ligament is most often affected, the lateral ligament may also be damaged (Kannegieter 1990), as was recognised in at least four horses in this present study. McIlwraith (1992) did not detect any cases of lateral ligament damage in his series. The severity of damage in the lateral ligament appears to be less than in the medial ligament, and minor tearing may go undetected unless the lateral ligament is examined closely. It was not routinely examined in all horses in this series.

A major difficulty in determining whether a horse has ligament damage is the apparent lack of clinical signs that directly impli- cate the carpus as the source of lameness, unless concomitant osteochondral lesions are present. This was a consistent feature of this series and of earlier reports (Kannegieter 1990). However, the clinical signs present in horses with ligament damage only is not made clear by McIlwraith (1992). who indicated that the presenting clinical signs were of lameness and/or carpal joint effusion in all horses presented, which would be in contrast to the findings in this study. Haemarthrosis was evident in only one joint in this series, in a horse that was found to have severe damage to the medial and lateral intercarpal ligaments. Haemarthrosis has been observed in other studies in association with ligament damage (Kannegieter 1990; McIlwraith 1992), as well as in one case in which the source of the haemorrhage was unknown (Dyson 1986). In the report of Kannegieter (1990) persistent haemorrhage was found to be the cause of severe lameness in an eventing horse, and which was only slightly improved by intra- articular anaesthesia. Arthroscopic examinationof the mid-carpal joint revealed haemorrhage to be occuning from the tom ends of the medial intercarpal ligament, which would have been clas- sified as a grade 4 ligament lesion.

When complete rupture occurred in one ligament, it was often accompanied by rupture in the contralateral limb. In addition, when bilateral changes were present, they were more severe than the changes seen in unilaterally affected joints. This may suggest that predisposing factors, such as conformation, gait, or increased stress on the ligament, may be involved in ligament tearing.

The relationship between the presence and severity of ligament damage and the severity of cartilage damage is uncertain. It is clear that damage to the ligament is unlikely to result in severe articular cartilage damage. This is evident by the finding that in the 8 joints in this study that underwent diagnostic arthroscopy and that had grade 4/4 damage, little cartilage damage was evident, as well as the experimental work of C Little and B Hilbert (Murdoch University 1991 unpublished). In this latter report the medial palmar intercarpal ligament was severed during arthro- scopic examination of the joint. The experimental horses then underwent a treadmill exercise programme, and despite the development of varying degrees of lameness and osteophyte production, minimal change to the articular cartilage occurred. In addition McIlwraith (1992) could find no correlation between the degree of articular cartilage damage and the degree of ligamen- tous tearing. Despite this, it was evident in this present series that those horses with the most severe articular cartilage damage also had a higher incidence of ligament lesions, and the severity of these lesions was also slightly greater. It is suggested that while ligament damage will not induce cartilage lesions, the presence of ligament damage may predispose the joint to more severe articular damage, if an osteochondral lesion occurs, or converse- ly, severe articular cartilage lesions may predispose to ligament lesions.

The prognosis of horses with severe medial palmar intercarpal ligament damage appears to be poor (Kannegieter and Ryan 1991; McIlwraith 1992). Later evaluation of some horses with grade 4 ligament damage in this series (unpublished data) indi- cated that long periods of rest, up to 12months in one horse, were usually ineffective in resolving the lameness, which recurred when fast work resumed. The most consistently effective resolu- tion of lameness was obtained when high doses, usually 180 to 200 mg per joint, of methylprednisolone acetate was injected intraarticularly, although it was often only effective for 8 to 10 weeks. Further to this, McIlwraith (1992) suggested that the prognosis in joints with intercarpal ligament damage and severe cartilage damage is most dependent on the extent of ligament damage. It is not known what proportion of tom ligaments will repair, or to what extent. The intercarpal ligament does have some capacity for repair, as was found in one horse in this series (unpublished data). This horse had been diagnosed as having a grade 4 medial intercarpal ligament tear and an osteochondral chip fracture of the distal aspect of the radial carpal bone. Eighteen months after surgery, having been in training for 12 months and winning one race, it sustained slab fractures of the third and radial carpal bones, and was euthanased. Necropsy revealed the ligament to be intact but with an obvious thinning and loss of the characteristic fibre alignment that is normally clearly evident arthroscopically. Ligaments with a similar ap- pearance have been seen by us in horses undergoing arthroscopy for chip fracture removal, but which were classified at the time as having no tearing. These findings suggest the intercarpal ligament does have some ability to heal. The effectiveness of this repair is uncertain, but the poor prognosis associated with com- plete tearing would suggest the ligament is unable to return to normal function.

Damage to the intercarpal ligaments should be suspected as a cause of lameness in any horse that has a chronic lameness referable to the midcarpal joint, that fails to improve with rest, and in which no or minimal radiographic changes are present, or in which the degree of lameness is much worse than radiographic examination suggests. At least 41% of horses with midcarpal lameness have some degree of ligament tearing, which is more severe in horses with extensive osteochondral damage. The aetiology of the tearing, and the mechanism by which it may cause lameness is not fully understood, and warrants further investigation. The prognosis for horses with severe damage to the medial intercarpal ligament appears to be poor.

Acknowledgments We would like to thank those veterinarians who referred cases

included in this study, and Dr C Little for providing details of his unpublished wprk.

References Bramlage LR. Schneider RK and Gabel AA (1991)Proc 13th Bain-Fallon

Lectures, Aust Equine Vet Assoc. Australian Veterinary Association. Sydney, p 167

Dyson SD (1986) Equine Vet J 18224 Hurtig RDand FretzPB (1986) J A m Vet MedAssoc 18g1314 Kannegieter NJ (1990) Proc 12th Bin-Fullon Lectures, Aust Equine Vet

Assoc. Australian Veterinary Association, Sydney, p 175 Kannegieter NJ and Burbidge HM (1990)Awt VetJ 67132 KannegieterNJandRyanN(1991)Awt VetJ68.258 Mcnwraith CW, Yovich JV and Martin GS (1987) J Am Vet Med Assoc

McIlwraith CW (1992)Eqlcine Vet J24367 191531

{Accepted for publication 4 December 1992)

Austruliun Veterinary Journal Vol. 70, No. 3, March 1993 91