Suspensory Ligament Desmitis

TENDON AND LIGAMENT INJURIES: PART II

0749-0739/95 $0.00 + .20

SUSPENSORY LIGAMENT DESMITIS Sue J. Dyson, MA, VetMB, PhD, DEO, FRCVS, Rick M. Arthur, DVM, Scott E. Palmer, VMD, and Dean Richardson, DVM

The interosseous (medius) has been so much modified in the horse that it is termed the suspensory or superior sesamoidean ligament (SL). 28 It is predominantly a strong tendinous band containing variable amounts of muscular tissue. 28• 33 In the forelimb it originates from the palmar carpal ligament and the proximal palmar surface of the third metacarpal bone6 and descends between the second and fourth metacarpal bones. In the distal metacarpus it divides into two branches that insert on the proximal sesamoid bones. Extensor branches pass obliquely forward to join the common digital extensor tendon on the dorsoproximal aspect of the proximal phalanx. The suspensory apparatus is continued distally as the straight, oblique, cruciate, and short distal sesamoidean ligaments. In the hindlimb, the SL originates principally from the plantar proximal aspect of the third metatarsal bone. There is a close relationship between the joint capsule of the combined middle and carpometacarpal joints and the proximal SL in the forelimb, 12 and between the tarsometatarsal joint capsule and the proximal SL in the hindlimb. 10 The primary function of the SL is to prevent excessive extension of the metacarpophalangeal joint during weight bearing, 28 and by virtue of the extensor branches, it limits flexion of the interphalangeal joints

From the Equine Clinical Unit, Animal Health Trust (SJD), Suffolk, England; Arthur, Valla, and Associates (RMA), Sierra Madre, California; New Jersey Equine Clinic, PA (SEP), Clarksburg, New Jersey; and New Bolton Centre, University of Pennsylvania (DR), Kennett Square, Pennsylvania

VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 11 • NUMBER 2 • AUGUST 1995

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during certain phases of the stride. Mean maximal forelimb SL strain while standing (6%) and while walking (5.9%) are within the lower part of the linear range of the typical ligament stress strain-curve.15 Fetlock support wraps did not alter the mean maximal strain, standing or at the walk,15 although fetlock support did significantly reduce fetlock extension during weight bearing in horses exercised to fatigue.16 There is little information about the internal structure of the SL and any differences between the fore and hind limbs. It is claimed that the SL contains a variable amount of striated muscle tissue, especially centrally and in younger individuals. 28 A recent survey of forelimb SLs,33 however, found no such variations with age, although differences were noted between breeds (Thoroughbreds versus Standardbreds), sexes, and states of training. No relationship was found between the amount of muscular tissue and age or stage of training (Dyson S, Vatistas N, and Thorp B, in press), although the total content of muscle in the SL body ranged from 2.1% to 11%. The ligament contains muscle bundles that vary in number and size between individuals, but that are fairly consistent between the left and right forelimbs. The muscle bundles are scattered throughout the middle third of the body of the SL, but divide into two distinct bundles distally. In some horses there is very little muscle tissue proximally, whereas distally there are large muscle bundles. Sheets of loose connective tissue comprised mainly of fat cells run the length of the ligament and are often associated with blood vessels and nerves; the muscle bundles are usually adjacent or within the connective tissue. The quantity of loose connective tissue increases distally; there is often a sheet of loose connective tissue that continues proximally from the division of the ligament deep into its structure. The variable muscle content between horses may partly explain the variability between horses in ultrasonographic appearance of the SL. There is some evidence that training does increase the strength of the SL4; the mean absolute load to failure in a single load to failure compression test apparatus was significantly higher in horses that had been in racehorse training compared with those that had been confined to box rest or paddock exercise. In the trained group, failure in the suspensory apparatus was most likely to be by fracture of a proximal sesamoid bone, whereas in the untrained group, the SL failed. The margins of the proximal part of the SL cannot be palpated because it lies between the bases (heads) of the second and fourth metacarpal (metatarsal) bones. However, pressure can be applied over its palmar (plantar) aspect. The normal suspensory ligament is of fairly uniform thickness throughout its length. The medial and lateral margins of the ligament are sharp and well defined. The medial and lateral branches of the ligament are also of uniform and similar size.

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Information concerning the suspensory ligament and related structures can be obtained from palpation, and ultrasonographic, radiographic, and nuclear scintigraphic examinations. The body of the suspensory ligament is best examined ultrasonographically without a stand off from the palmar (plantar) aspect of the limb, whereas the branches are examined from the palmar (plantar) lateral and palmar (plantar) medial aspects, using a stand off. A 7.5-MHz transducer is ideal for the forelimb, but in the hindlimb of large (600 kilograms bodyweight) horses, the SL may be beyond the focal zone of the transducer. A 5-MHz transducer may be better, unless a 7.5-MHz transducer has a variable focal zone. There is considerable variation between normal horses in the ultrasonographic appearance of the body of the forelimb SL (Dyson S, Vatistas N, Thorp B, in press). The SLs of both forelimbs of 350 clinically normal horses and ponies were examined ultrasonographically; 22 horses were re-examined 3 to 8 months after initial examination. These horses were part of a random selection of those in which there was either a central ill- or well-defined hypoechoic area in the body of the SL or in which the accessory ligament of the deep digital flexor tendon was less echogenic than the SL and deep digital flexor tendon (DDFT). The forelimb SL is approximately rectangular in cross-section and may arise from two distinct heads, separated by a less echogenic band. Its palmar, medial, and lateral margins usually are well defined, but the dorsal border of the SL in the region 2 to 3 cm distal to the accessory carpal bone was defined poorly or was hypoechoic in 9% of limbs (Dyson S, Vatistas N, Thorp B, in press). There is no significant difference in size in the SL between left and right limbs of an individual at any level in the limb. The echogenicity of the SL usually is bilaterally symmetrical, but it varies considerably between horses. The SL may be of uniform echogenicity throughout its length, and of similar echogenicity to the DDFT. In the proximal third of the SL in 13% of limbs, a well- or poorly defined central hypoechoic area was identified, extending a variable distance proximodistally. The SL was of patchy echogenicity in 4% of limbs. The hindlimb SL is rounder in cross-section, but it seems to be of much more consistent echogenicity between horses compared with the forelimb.7a Assessment of the most proximal part of the ligament can be difficult because of shadowing artefacts and hyperechoic lines on the dorsal aspect of blood vessels. From a clinical point of view, injuries to the SL can be divided into three areas: 1. Lesions restricted to the proximal one third (proximal suspensory desmitis [PSD])

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2. Lesions in the middle one third, sometimes extending into the proximal third (body lesions) 3. Lesions in the medial and / or lateral branch (branch lesions). Because of the close relationship between the SL and the second, third, and fourth metacarpal bones and the proximal sesamoid bones, the ligament cannot be considered in isolation.

PROXIMAL SUSPENSORY DESMITIS

Proximal suspensory desmitis (PSD) occurs in both the forelimb 7• 73• and the hindlimb5 • 8 and is being recognized more frequently with better use of local analgesic techniques and with the advent of diagnostic ultrasonography8 • 9 • 34 and nuclear scintigraphy. 30 In acute cases, there may be localized heat in the proximal metacarpal (metatarsal) region and occasionally slight edematous swelling on the palmar (plantar) lateral, or less commonly, medial, aspect of the limb. 8• 9 It may be possible to elicit pain by firm palpation over the head of the SL; sometimes the margins of the SL are rounded slightly. In long-term cases, there frequently are no detectable palpable abnormalities. There may be a relationship between straight hock conformation, with or without hyperextension of the fetlock, with the incidence of hindlimb PSD (Fig. 1),9 Lameness may be acute or insidious in onset and varies from mild (0 = no lameness detectable; 1 = mild; 2 = moderate; 3 = severe; 4 = non-weight-bearing) to moderate, although it may be severe after fast work, Lameness in forelimbs usually improves rapidly with a few days rest but recurs when work is resumed, whereas hindlimb lameness is usually more persistent. (This may reflect the chronicity of the injury at the time of recognition of the lameness.) Flexion of the distal limb joints accentuated lameness in approximately 50% of forelimb or hindlimb cases of PSD,8• 9 whereas flexion of the hock accentuated lameness in approximately 85% of hindlimb cases. Forelimb lameness often is accentuated on a circle especially with the lame limb on the outside of the circle and may be worse on soft ground. Hindlimb lameness usually is most easily detected in straight lines or when the horse is ridden, Local analgesic techniques are usually necessary to (1) exclude a concurrent cause of lameness in horses with pain localised by palpation to the proximal metacarpal or metatarsal region and (2) identify the source(s) of pain in horses with no obvious clinical signs referrable to this area. Various analgesic techniques for localization of pain to the proximal metacarpaF· 12 and proximal metatarsal8• 10 regions have been described. It is important to be aware of the close relationship between the middle carpal and tarsometatarsal joint capsules and the proximal 19 • 23 • 27

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Figure 1. A, A 12-year-old dressage stallion. Note the straight hindlimb conformation and hyperextension (dorsiflexion) of the fetlocks. The horse had proximal suspensory desmitis of the left hindlimb. 8, Transverse ultrasonogram of the plantar metatarsal soft tissues, 3 and 5 cm distal to the tarsometatarsal joint. The SL is enlarged and diffusely hypoechoic.

SL in the forelimb and hindlimb, respectively. Perineural analgesia of the palmar or plantar (mid cannon) and palmar metacarpal (plantar metatarsal) nerves occasionally produces slight improvement in lameness associated with PSD, probably the result of proximal diffusion of local anaesthetic. The possibility of another concurrent source of pain must always be considered. 8 Perineural analgesia of the palmar metacarpal nerves at subcarpal level does not always alleviate pain from the proximal suspensory ligament, and it may be necessary to perform an ulnar nerve block to alleviate lameness associated with forelimb PSD. 7a In the hindlimb, false-negative responses to perineural analgesia of the plantar metatarsal nerves at subtarsal level occasionally are obtained. 9• 10 Hindlimb lameness associated with PSD should be improved by perineural analgesia of the tibial nerve. Improvement in lameness associated with PSD is sometimes observed after intra-articular analgesia of the middle carpal or tarsometatarsal joint; the possibility of two concurrent sources of pain must always be considered. Ultrasonographic abnormalities associated with PSD in either the forelimb or the hindlimb include: l. Enlargement of the SL in the median and/ or transverse plane.

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2. Poor definition of one or more of the margins of the suspensory ligament, especially the dorsal margin (Fig. 2). 3. A well-circumscribed central hypoechoic area (Fig. 3). 4. One or more poorly defined hypoechoic areas, central or more peripheral (Fig. 4). 5. A larger area or areas of diffuse decrease in echogenicity, involving part (usually the dorsal part) or all of the cross-section of the ligament. 6. Small focal hyperechoic spots (usually only in long-term cases). 7. Irregularity in the palmar (plantar) contour of the third metacarpal (metatarsal) bone (see Fig. 2). 8. A combination of one or more of the above. Careful comparison with the contralateral limb is invaluable, because in the normal horse the SL is usually bilaterally symmetrical. Lesions will be overlooked if the gain controls are too high. A change in the ultrasonographic appearance of the ligament over a period of time also is considered to be substantive evidence of the significance of a lesion. A very recent injury may be extremely subtle, but it may become more obvious during the next 2 to 4 weeks. Alternatively, a lesion may start to

Figure 2. Transverse ultrasonogram of the palmar metacarpal soft tissues of an 8-year-old hunter, obtained 5 cm distal to the accessory carpal bone. The horse had lameness alleviated by perineural analgesia of the palmar metacarpal (subcarpal) nerves. Note the poor definition of the dorsal margin of the enlarged SL (arrows) and the irregular contour of the palmar cortex of the third metacarpal bone. The horse had recurrent lameness. Figure 3. Transverse ultrasonogram of the plantar metatarsal soft tissues of a 14-year-old ex-event horse, obtained 4 cm distal to the tarsometatarsal joint. The horse had lameness that was substantially improved by subtarsal analgesia. The SL is enlarged and has a central hypoechoic area. The horse has been persistently lame, despite various treatments, for more than 1 year.

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Figure 4. A, Transverse ultrasonogram of the palmar metacarpal soft tissues of a 6-yearold event horse, obtained 4 cm distal to the accessory carpal bone. The horse had left forelimb lameness alleviated by perineural analgesia of the palmar metacarpal (subcarpal) nerves. The SL is slightly enlarged, and there are several poorly defined hypoechoic areas. B, The same horse 5 weeks later. The SL is much more uniform in its echogenicity. The horse resumed work 5 weeks later, and there has been no recurrence of PSD.

"fill in." In horses with bilateral lameness, lesions usually are detectable bilaterally. Radiographic abnormalities of the proximal aspect of the third metacarpal (metatarsal) bone associated with PSD include: 1. Sclerosis of the trabecular pattern seen in a dorsopalmar (dor-

soplantar) projection. 2. Alteration of the trabecular pattern dorsal to the palmar (plantar) cortex, with or without sclerosis, seen in a lateromedial view. 3. Entheseophyte formation on the palmar (plantar) aspect of the bone in a lateromedial view. Radiographic abnormalities are seen more commonly in hindlimbs than in forelimbs. This may reflect the chronicity of the injury, perhaps subclinical, before the recognition of lameness or poor performance. The radiographic abnormalities are thought to reflect new bone around the insertion of the fibres of insertion of the suspensory ligament (Huskamp B, personal communication, 1990) and entheseophyte formation. Slight entheseophyte formation may be more easily detectable ultrasonographically.7a In forelimbs, the most common abnormality is sclerosis of the medial one half of the third metacarpal bone proximally, whereas in the hindlimb sclerosis more commonly occurs centrally or laterally. Incidental radiographic abnormalities are rarely seen in forelimbs, but they are sometimes seen in hindlimbs 7a; therefore, diagnosis should not be based on radiography alone. Radiographic examination is important to rule

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out an avulsion fracture of the palmar (plantar) cortex of the third metacarpal (metatarsal) bone, a palmar cortical stress fracture 7, 17, 26 or other bony pathology. Nuclear scintigraphy has been described as a sensitive, none invasive means of diagnosis of PSD,30, 34 using both soft tissue and bone phase scans, and could be used as a substitute to local analgesia and ultrasonography. Whether additional information not obtained from ultrasonography and radiography can be obtained, remains open to question. One author (SJD) has seen four horses in which pain was localized as definitively as possible to the proximal metacarpal region (one) or metatarsal region (three) in which no ultrasonographic or radiographic abnormalities were detected. Nuclear scintigraphic examination gave no additional information in these cases. Nonetheless, cases have been recognized in which there was increased radionucleotide uptake in the proximal palmar (plantar) metacarpus (metatarsus) in the absence of detectable radiographic or ultrasonographic abnormalities (Pilsworth R, personal communication, 1992). Whether this reflects PSD or primary bone pathology, also remains open to question. Many treatments have been tried, including box rest and controlled exercise, with or without local and / or systemic administration of a glycosaminoglycan polysulphate,8, 9 local injection of corticosteroids,23, 27 or an internal blister. 19 Since the advent of diagnostic ultrasound, there are limited references to the success of treatment of cases of PSD confirmed ultrasonographically8, 9 or by nuclear scintigraphy.30 Twenty-five of 29 horses (86%) with PSD unassociated with any concurrent cause of lameness resumed full work after box rest and a controlled exercise program for a minimum of 2 months (Tables 1 and 2).8 The majority of successfully treated horses had forelimb lameness. Progressive "filling in" of lesions was detected by serial ultrasonographic examinations in most horses (see Fig. 4). Most horses with forelimb PSD were rested (box rest and controlled exercise) for 3 to 6 months; the speed of resolution of the lesions and the total convalescence

Table 1. EXAMPLE OF CONTROLLED EXERCISE PROGRAM DURING CONVALESCENT PERIOD FOR FORELIMB PROXIMAL SUSPENSORY DESMITIS (NO UNCONTROLLED TURNOUT) Weeks 0- 4

4-8 8-12

Exercise 15 minutes walking, twice daily 20 minutes walking, twice daily 40-60 minutes walking and trotting

Re-examined after 12 weeks and if sound and lesion resolved ultrasonographically, gradually resumed normal work. If lesion still detectable ultrasonographically, horse maintained in controlled exercise with increased trotting. Re-assessed after further 6 to 12 weeks; if no further change in echogenicity, gradually resumed normal work thereafter.

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Table 2. EXAMPLE OF CONTROLLED EXERCISE PROGRAM DURING CONVALESCENT PERIOD FOR HINDLIMB PROXIMAL SUSPENSORY DESMITIS (NO UNCONTROLLED TURNOUT PERMITTED FOR AT LEAST 6 MONTHS) Weeks

Exercise

0-12

30 minutes walking , twice daily (ridden , in hand or on horse walker or horizontal treadmill) 30 minutes walking twice daily, with short periods of trot, if lameness substantially improved As above, with increased trotting if improving

12-24 24-36

Horses re-assessed at 3-month intervals.

time was proportional to the duration of lameness before instigation of treatment (Dyson S, unpublished data). Premature resumption of work resulted in recurrent lameness even if the lesion seemed to have been resolving satisfactorily on ultrasonography (Fig. 5). Some lesions persisted ultrasonographically; some increase in echogenicity and reduction of size was observed, but a hypoechoic area remained long term. The incidence of recurrence of forelimb PSD more than a year after a successful return to work is low, but warrants a guarded prognosis (Dyson S, unpublished data). Horses tend to remain lamer for longer and lesions are slow to resolve.

Figure 5. A, Transverse ultrasonogram of the palmar metacarpal soft tissue structures of a 12-year-old advanced event horse with mild right forelimb lameness of 2 days' duration , associated with slight heat in the proximal metacarpus and alleviated by perineural analgesia of the palmar metacarpal (subcarpal} nerves. There is a central hypoechoic area. B, The same limb as seen in Figure 5A, but 3 weeks later. The horse has been in a controlled exercise program, and the lesion has filled in , but it is still detectable. The horse resumed full work, but lameness recurred after the first event, which was 2 weeks later. C, The same limb as seen in Figures 5A and 58, 7 days after recurrence of lameness. The horse was rested for 2 months, and has competed successfully for 2 more years at champ ionship level.

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The prognosis for hindlimb PSD is much more guarded; only 6 of 35 (17%) horses had complete resolution of lameness and were able to resume full work, although two of the six had recurrent lameness due to a different cause.9 Twenty-nine of the 35 horses had been lame for 5 weeks or more. The four horses that were sound and have been in full work for more than 1 year had been lame for up to 5 weeks before diagnosis and treatment. The poor prognosis for hindlimb PSD may be the result of failure to recognize lameness in the early stages of injury, a tendency for lesions to be more diffuse when first diagnosed, and different biomechanical forces on the hindlimb SL compared with the forelimb . Local injection of corticosteroids usually results in temporary improvement or resolution of lameness, but it does not seem to be a long-term solution.7" Response to internal iodine blisters also has been poor. Some racehorses have been able to train and race horses while they are being medicated with phenylbutazone (where this is permitted), without marked deterioration in lameness. Forelimb PSD has often been seen either in association with poor foot balance or another concurrent cause of lameness. Treatment of both is considered important.

AVULSION FRACTURES OF THE PROXIMAL SUSPENSORY LIGAMENT

A vulsion fractures of the proximal SL were first described in the forelimb of Standardbred trotters and pacers,2 but they also have been recognized in both the forelimb 7 and hindlimb of Thoroughbred racehorses.7a Lameness usually is acute in onset and moderate to severe. Pressure applied over the proximal aspect of the metacarpus or metatarsus generally elicits pain that is more severe than that associated with acute PSD. Diagnosis is based on radiographic and/ or ultrasonographic identification of the fracture. Diagnostic local analgesic techniques usually are not required for identification of discrete displaced fracture fragments, although they occasionally have been necessary for diagnosis of incomplete non-displaced fractures. Fractures usually are best identified on flexed lateromedial or dorsopalmar (dorsoplantar) radiographic views, although sometimes slightly oblique dorsopalmar (dorsoplantar) views can be helpful. A complete fracture usually is seen as a displaced bone fragment in either one or both of the lateromedial and dorsopalmar (dorsoplantar) views (Fig. 6). Incomplete fractures are seen as semicircular lucent lines in a dorsopalmar (dorsoplantar) projection. Complete fractures usually can also be diagnosed ultrasonographically (Fig. 7). Localized abnormalities of the suspensory ligament may be identified.

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Figure 6. Dorsopalmar radiograph of the left metacarpus of a 3-year-old Thoroughbred flat racehorse. with recurrent lameness of 6 weeks' duration. There were no detectable localizing clinical signs, but moderate lameness was alleviated by subcarpal analgesia. Note the crescent-shaped radiolucent zone co mpatible with an avulsion fracture .

Treatment by box rest, with monitoring of healing by serial radiographic examinations has produced good results in both forelimbs 2 and hindlimbs.7a Lameness often has been slow to resolve (2 to 3 months); total duration of convalescence has ranged from 3 to 6 months. Most horses have had an uneventful recovery, with return to full work without recurrent lameness. One horse with an avulsion fracture in a forelimb developed a sequestrum (Wright I, personal communication, 1991).

Figure 7. The same horse as seen in Figure 6. Longitudinal ultrasonogram of the metacarpus. Note the discontinuity of the palmar cortex of the third metacarpal bone, indicative of a fracture.

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PALMAR CORTICAL FATIGUE FRACTURES

The clinical, radiographic and nuclear scintigraphic features of palmar cortical fatigue fractures have been well documented,7, 17, 26 but the relationship between these injuries and proximal suspensory desmitis has been questioned, 7 Based on further experience accumulated since 1988/a it is considered unlikely that these are related problems, Twentyfive horses with unilateral or bilateral palmar cortical fatigue fractures have been examined clinically, radiographically, and ultrasonographically, All horses had radiographic evidence of a fracture, but no horse had abnormalities of the SL detectable ultrasonographically,

DESMITIS OF THE BODY OF THE SL

Desmitis of the body of the suspensory ligament usually is associated with the much more obvious clinical signs of localized heat, pain, and swelling compared with PSD, but lameness usually is much less obvious and may not be detectable. Standardbreds seem to be able to tolerate a much greater degree of SL damage than Thoroughbreds, without obvious lameness. If lameness is present, it usually improves rapidly with a few days rest Pain associated with the suspensory ligament should always be interpreted with care and related to the recent duration and intensity of work. Many event horses will have extremely sore forelimb SLs the day after an event, but this pain usually disappears rapidly. It does not seem to be associated with any detectable structural abnormality of the SL The absence of detectable pain associated with the SL does not preclude the presence of active desmitis, particularly in cases of long-term desmitis, The degree of swelling associated with SL desmitis is extremely variable; there may be only subtle enlargement of the ligament per se, or extensive periligamentous soft tissue swelling. SL desmitis (a body lesion) is a much more common occurrence in forelimbs than hindlimbs in all types of horses other than Standardbreds,20 In contrast to PSD and desmitis of the branches of the SL, body lesions are far more common in racehorses than other sport horses. Diagnosis usually can be based on clinical signs and local analgesic techniques are rarely required, Ultrasonographic examination, however, provides a more objective assessment of the degree of structural damage (Fig, 8) and can be invaluable in cases in which there is extensive periligamentous soft tissue swelling, which makes palpation of individual structures extremely difficult. Although ultrasonographic examina-

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Figure 8. Transverse ultrasonograms of the palmar metacarpal soft tissues of a 6-year-old Thoroughbred hurdler obtained 8 cm and 10 cm distal to the accessory carpal bone. The SL is enlarged and has a large acentric hypoechoic area. The lesion persisted ultrasonographically for more than 1 year. When the horse resumed training 15 months after the original injury, clinical signs recurred.

tion can also be useful for monitoring repair of the ligament, there are limitations. In many horses, fairly extensive hypoechoic areas persist for a long time despite resolution of clinical signs. Some horses may be able to return to full work without recurrent clinical signs despite persistence of these lesions. Nonetheless, there is a relatively high incidence of recurrent SL desmitis despite prolonged periods of rest (> 12 months); this may be related to incomplete healing of the ligament. The incidence of persistent ultrasonographic abnormalities of the SL is far higher than persistence of lesions in the superficial digital flexor tendon. Clinical appraisal should not be limited to the SL; foot balance and shoeing should be assessed carefully together with the horse's conformation. A tendency towards long pasterns or hyperextension of the fetlocks may predispose to SL injury. Management of SL desmitis depends on several factors including the breed of the horse, its occupation, the severity of the damage, whether the horse can compete while receiving medication, and the skill of the trainer. SL desmitis can be "managed" in some horses by aggressive physiotherapy treatment, i.e., whirlpool boots, massage, application of cooling lotions, or dimethyl sulfoxide (DMSO), and correction of foot imbalance, with lots of walking exercise combined with the regular trainin g program. If clinical signs deteriorate, however, alternative therapies should be tried; percutaneous ligament splitting can be useful for central core lesions. Intralesional treatment with hyaluronic acid, corticosteroids, or a glycosaminoglycan polysulphate has produced variable results. Pin firing apparently has been useful in some horses (see also the section on "Management of SL desmitis in Thoroughbred

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racehorses," page 197 and "Management of SL desmitis in Standardbred racehorses," page 199). Injuries to the body of the SL in event horses are less common than branch lesions; these carry a guarded prognosis for return to full athletic function without recurrent injury. Body lesions are relatively common injuries in horses that race over fences. Injuries often are accompanied by a fracture of the distal third of either the second or fourth metacarpal bone or both. Whenever there is diffuse soft tissue swelling associated with SL desmitis, radiographic examination of these bones is warranted. Fracture may be a consequence of hyperextension of the fetlock associated with excessive lengthening of the SL, resulting in increased tension in the fibrous bands, which connect the distal second and fourth metatarsal bones to the abaxial surfaces of the proximal sesamoid bones. 4 In horses with a history of enlarged SLs, there is frequently modelling of the distal aspect of the second and/ or fourth metacarpal bone with a change in its contour; this may predispose to fracture. 31 There may be periosteal new bone on the axial aspect of the diaphysis of either of these bones. Controversy persists concerning the sequence of events, i.e., whether periostitis is primary or secondary to SL desmitis. The authors have explored several cases with persistent lameness surgically. There was a variable amount of reactive fibrous tissue and adhesion formation between the enlarged SL and the splint bone. Occasionally, a primary "splint" impinges on the margin of the SL resulting in localized desmitis (Fig. 9). This can sometimes be difficult to assess clinically, by palpation, or radiographically, especially if the periosteal new bone is far axially. Ultrasonography is extremely useful for identification of localized desmitis. Surgical treatment may be required. Occasionally it is necessary to prove that a painful "splint" and associated SL desmitis are the sole sources of pain. Although pain associated with a painful "splint" usually is alleviated by local infiltration of anaesthetic solution or perineural analgesia of the ipsilateral palmar nerve proximally, these techniques may not remove pain from the SL. It may be necessary to perform perineural analgesia of the palmar metacarpal nerves proximal to the site of the lesions to produce significant improvement in lameness (Dyson S, unpublished data). Management of fractures of the distal third of the second or fourth metacarpal bone is also open to debate. Many fractures will heal satisfactorily if managed conservatively (box rest for 8 to 12 weeks). Callus formation may be quite large, but it usually progressively remodels. Healing is sometimes by fibrous union, but this seems to result in functional stability. 31 Displaced fractures may become stabilized by encapsulating fibrous tissue with a good functional outcome provided there is not impingement on the SL. There is usually an obvious firm

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Figure 9. A, Dorsomedial-palmarolateral oblique radiographic view of the metacarpus of an 11-year-old general purpose horse with mild lameness and pain on palpation of the second metacarpal bone and the adjacent SL. There is an active-appearing periosteal proliferative reaction on the diaphysis of the second metacarpal bone. B, Transverse ultrasonogram of the palmar metacarpal soft tissues obtained at the same level as the "splint." The medial margin of the SL is poorly defined and hypoechoic, which is indicative of secondary desmitis.

swelling that may be "proud" to the rest of the limb and, therefore, potentially at risk to external trauma. In the authors' opinions, surgical removal should always be considered, especially if the fracture fragment is d isplaced and impinging on the SL, or if there is callus formation irritating the SL. It must always be remembered that the degree of suspensory desmitis usually governs the prognosis. 1

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DESMITIS OF THE MEDIAL OR LATERAL BRANCH OF THE SL

Desmitis of the medial or lateral branch of the SL occurs in both forelimbs and hindlimbs in all types of horses. The degree of lameness is extremely variable and can range from none detectable to moderate and occasionally is severe, depending on the extent of damage and its chronicity. There usually is palpable enlargement of the affected branch, with a variable degree of periligamentous soft tissue swelling and localized heat. Firm pressure over the branch, palpation of its margins, or pressure over the apex of the proximal sesamoid bone usually causes pain in acute cases. Accurate palpation of the SL branches can be difficult, if there is extensive enlargement of the digital flexor tendon sheath (windgall). One of the authors (SJD) has seen several dressage horses with hindlimb SL branch lesions that were extremely difficult to evaluate clinically for this reason. Passive flexion of the fetlock often induces pain, and lameness may be accentuated by distal limb flexion tests. This reaction to flexion usually diminishes within 7 to 14 days if the horse is rested. Acute forelimb SL branch injuries may be accompanied by distension of the metacarpophalangeal joint capsule and pain on passive flexion of the joint. If pain or joint capsule distension persist for more than 14 days, this may indicate a concurrent problem in the joint. Intraarticular analgesia of the metacarpophalangeal joint can be extremely helpful to identify concurrent problems. One of the authors (SJD) has seen a significant number of event horses that developed SL branch injuries and clinical signs related to the metacarpophalangeal joint simultaneously. The SL desmitis settled, but fetlock pain persisted; arthroscopic evaluation of the joint showed loose, soft, discolored cartilage easily removed from the subchondral bone of the medial condyle of the third metacarpal bone. Confirmation that lameness is associated with a long-term SL branch injury can sometimes be more difficult. This may be particularly important, if there is more than one potential cause of lameness. The ligament may be obviously enlarged, but palpation may not cause pain. Identification of structural abnormalities of the branch using ultrasonography is not necessarily confirmatory unless previous ultrasonograms are available for comparison. Frequently, SL branch lesions persist long term ultrasonographically. It may be necessary to use local analgesic techniques to establish the source of pain. In the author's experience, although a unilateral block may improve lameness associated with a branch lesion, it is rare that it will be fully alleviated. It may be necessary to perform perineural analgesia of the palmar (plantar) and palmar

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metacarpal (plantar metatarsal) nerves at subcarpal (subtarsal) level to alleviate the lameness fully. In view of the close relationship of the SL branches and the distal aspects of the second and fourth metacarpal (metatarsal) bones and the proximal sesamoid bones, radiographic examination should also be performed. Although clinical signs of SL branch desmitis may be acute in onset, radiographic abnormalities consistent with sesamoiditis may be pre-existing. Occasionally, small avulsion fractures of the abaxial or palmar surface of a proximal sesamoid occur. Dystrophic mineralization within the insertion of the ligament may develop and may be progressive. Most apical sesamoid fractures are associated with only slight concurrent SL branch desmitis. In the authors' experience the degree of SL branch desmitis and dystrophic mineralization (Fig. 10) are usually more important prognostically than radiographic evidence of sesamoiditis per se (Fig. 11). Ultrasonographic abnormalities associated with desmitis of a branch of the SL include: 1. Enlargement of the branch. 2. Poor definition of one or more margins, especially the axial margin. 3. Change in shape (more oval). (The imager should be aware that a change in the angle of the scan head can alter the apparent shape of a branch of the SL) (Fig. 12).

Figure 10. Transverse ultrasonogram of the lateral branch of the SL of a 12-year-old hunter with recurrent forelimb lameness associated with heat and enlargement of the branch. Note the enlargement of the branch, poor definition of its margins, central decrease in echogenicity, and focal hyperechoic areas indicative of fibrosis and/or dystrophic mineralization. There is also echodense material subcutaneously.

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Figure 11. A, Dorsolateral-palmaromedial oblique radiographic view of the right fore lateral proximal sesamoid bone of a 9-year-old advanced event horse. Note the irreg ular contour of the palmar aspect of the sesamoid bone and the broad lucent radiating lines, which are indicative of entheseophyte formation . The horse had pain and enlargement of the lateral branch of the SL. 8 , Transverse ultrasonograms of the lateral branch of the SL. The axial border is poorly defined. The horse has been unable to return to compete at championship three-day events without recurrent SL branch desmitis, but has competed successfully at one-day level for 2 years.

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4. 5. 6. 7.

Focal hypoechoic area(s) (see Figs. 10 and 11). A diffuse decrease in echogenicity. Focal hyperechoic spots. Periligamentous echodense material, especially between the branch and the skin (this often contributes significantly to the palpable enlargement of the branch) (see Figs. 10 and 12). 8. Occasionally echodense material between the medial and lateral branches (the author has only identified this in hindlimbs). 9. Irregularity in outline of the proximal sesamoid bone or an avulsion fracture. 10. Sometimes the lesion extends up to and includes the bifurcation and distal aspect of the body of the SL. Occasionally, a horse has palpable enlargement of or around a SL branch with associated soreness, but no detectable ultrasonographic abnormality of the internal structure of the ligament. One of the authors (SJD) has seen several dressage horses that preser-ted like this that were managed satisfactorily by correcting foot balance and shoeing with egg bar shoes. One of the authors (SJD) has seen two three-day event horses that presented similarly and successfully completed an event without marked exacerbation of clinical signs. Lameness was accentuated transitorily, but there was little change in swelling or the reaction to palpation, and no ultrasonographic abnormalities developed. This is in contrast to horses that have started a three-day event with active branch desmitis

Figure 12. Transverse ultrasonogram of the lateral branch of the SL of an 11-year-old hunter. The SL branch is shaped abnormally and is surrounded by considerable echodense material, especially subcutaneously.

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associated with internal structural abnormalities. These lesions have consistently gotten worse, and it has been difficult to present the horses for the final inspection. Treatment options are similar to those for desmitis of the body of the SL. Lameness usually resolves rapidly with rest unless considerable periligamentous adhesions develop. In the authors' experience, this occurs more frequently in hindlimbs compared with forelimbs and results in an extremely guarded prognosis. It was not prevented by daily exercise and passive manipulation of the distal limb joints. If there is a central hypoechoic region within the affected branch, the author considers that percutaneous splitting may be beneficial, but many horse have less well defined and/ or more diffuse lesions that generally are treated conservatively by box rest and controlled exercise, with or without concurrent treatment with a glycosaminoglycan polysulphate or sodium hyaluronate. Lesions often improve to some extent ultrasonographically during a 3- to 12-month period but frequently abnormalities persist long term (> 12 months). The prognosis for singlebranch lesions in fore- or hindlimbs of dressage and show jumping horses usually is fair. The total convalescent period depends on the severity of the original injury and varies from 3 to 12 months. Most event horse can be returned to competition, but there is a relatively high rate of recurrent injury especially in horses competing in three-day events as opposed to one-day events. (See also, "Management of SL desmitis in Thoroughbred racehorses," page 197 and "Management of SL desmitis in Standardbred racehorses," page 199.)

BREAKDOWN OF THE HINDLIMB SUSPENSORY APPARATUS

Progressive degenerative changes in hindlimb suspensory ligaments have been seen in horses with straight hock conformation, with or with out hyperextension of the fetlocks (see page 181). A similar condition has also been recognized in brood mares. There is progressive hyperextension of the hind fetlocks, which may result in abrasion of the plantar aspect of the fetlocks. Ultrasonographic examination of a small number of affected mares has shown a diffuse reduction in echogenicity throughout the length of the ligaments. The underlying cause is unknown. The incidence in brood mares seems to be higher than in breeding stallions of similar age, which suggests that there may be a hormonal influence. Some mares are helped by flat shoes with caudal extensions or egg bar shoes, which provide more support beneath the collapsed fetlocks .

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MANAGEMENT OF SL DESMITIS IN THOROUGHBRED RACEHORSES Rick M. Arthur

Suspensory ligament desmitis (SLD) remains a therapeutic challenge in Thoroughbred racehorses. Published clinical information for the management of SLD is largely anecdotal or empirical.8 • 18 • 27 Surgical splitting of the suspensory ligament branch (SLB) has never gained favor in the Thoroughbred racehorse despite the reports of reasonable results in the Standardbred. 21 The relatively recent introduction of diagnostic ultrasound has improved diagnostic capabilities for SLD greatly, but clinical studies evaluating therapeutic response have not been forthcoming. Clinical management strategies for the treatment of SLD in the Thoroughbred racehorse rely on the reduction or elimination of inflammation within the SL by the administration of anti-inflammatories, the application of cryotherapy, and the reduction or cessation of exercise. Systemic administration of steroidal and non-steroidal anti-inflammatories can be used effectively in combination. The maximum initial dosages for steroidal and non-steroidal anti-inflammatories respectively are 20 mg of dexamethasone once daily and 2 g of phenylbutazone twice a day. These dosages should be halved within 48 hours and all medication stopped within 5 days to allow for re-evaluation of the injury. A diureticsteroidal anti-inflammatory combination is particularly effective in reducing edema (Naquasone, 1 to 2 boluses initially followed by half to 1 bolus daily for a maximum of 3 days; Schering-Plough Animal Health, NJ). Local infiltration of steroidal anti-inflammatories at the site of injury has been advocated,23• 27 but systemic administration seems to be as clinically effective without the risk of tissue failure associated w ith local infiltration of steroidal anti-inflammatories. 24 Cryotherapy of the affected area with ice baths or ice packs is an effective means of reducing inflammation particularly in the more distal and accessible body and branches of the SL. Exercise must be limited to reduce or eliminate further aggravation of the injury. Less severe SLD often can be managed successfully with continued clinical evaluation and appropriate therapeutic adjustments. The clinical management of SLD is determined by the anatomic location of the desmitis and the severity of the clinical signs. SLD should be d ivided into three clinical entities based on the anatomic location of the desmitis within the SL. Each anatomic location has its own management implications and options. PSD offers the greatest latitude for therapeutic and clinical management. PSD rarely is associated with catastrophic breakdown of the

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suspensory apparatus as found with suspensory branch desmitis (SBD). There have been no deaths or euthanasias associated with PSD in 630 Thoroughbred racehorses necropsied for musculoskeletal injuries in California between February 1990 and June 1992, whereas suspensory branch failure has been the primary diagnosis for 20 of these horses, with nine of the suspensory branch failures occurring immediately proximal to the sesamoid bone (Johnson W, personal communication, 1993). PSD can present as a lameness with or without other clinically apparent signs. The diagnosis is made by the use of diagnostic nerve blocks and confirmed by diagnostic ultrasound as previously described. When performing diagnostic nerve blocks, special attention must be made not to confuse proximal suspensory lameness with third carpal bone pain, another common source of clinically quiet lameness in Thoroughbred racehorses. Two clinical factors relative to PSD are worth noting. Even though the lameness may present unilaterally, PSD can occur bilaterally. First, this is especially true in young horses early in their training, in which case the lameness can switch to the opposite limb when performing diagnostic nerve blocks. Second, PSD can develop into a stable condition in which the unsoundness shows little change over time. The unsoundness may increase after a hard work or racing, but it can return to its previous level after a few days of rest or in response to therapy. Nonresponsive PSD will require relatively extended periods of rest. Although the rest period is arbitrary, 4 to 6 months should be considered the minimum of time required for recuperation for SLD. There is evidence that suggests that low levels of controlled exercise may be beneficial during rehabilitation by maintaining the intrinsic strength of the SL. 4 Desmitis of the body of the SL in Thoroughbreds is less common than PSD and SBD. Clinical management is similar to PSD but with a few important clinical considerations. Desmitis of the body of the SL can descend distally into one or both branches of the SL thereby limiting the therapeutic options. Lameness associated with desmitis of the body of the SL seldom stabilizes as can occur with PSD, and the prognosis for the return to racing must be considered less favorable than with PSD. SBD is a serious, high-risk injury to Thoroughbred racehorses that is associated with catastrophic breakdown of the suspensory apparatus. Injury to the SLB, therefore, must be managed with caution and careful evaluation. Clinical lameness is a particularly dangerous sign that cannot be ignored, under estimated, or masked without significant risk to the patient. SBD can be evaluated easily for pain and inflammation. Localized areas of heat, pain, or softness should be eliminated before returning to training. Cryotherapy is particularly effective in SBD. Systemic steroidal and non-steroidal anti-inflammatories can be used to reduce inflamma-

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tion, but care should be taken to avoid masking any underlying structural weakness. The use of leg sweats with or without DMSO can be beneficial. Direct application of DMSO over the site of injury can be accomplished with desmitis of the body or branches of the SL. The second (MCII) and fourth (MCIV) metacarpal bones significantly complicate SBD in the Thoroughbred. While the underlying SBD is the ultimate prognosticating factor, a fracture or thickened and flared distal MCII/IV seems to aggravate the SBD. Fractures of the distal MCII/IV, therefore, are routinely removed by the authors. Additionally, the removal of nonfractured, flared, or thickened distal MCII/IV is advocated by the authors when SBD is nonresponsive and evidence of irritation exists in the MCII/IV. SLD of the hindlimb is relatively infrequent in Thoroughbred racehorses. Only 2 of 127 diagnostic ultrasound examination of the SL involve the hindlimb in one of the authors' (RMA) practices during the last 30 months. Limited experience with hindlimb SLD in Thoroughbreds suggests that the long-term prognosis for return ·to racing is poor, which is consistent with published findings. 8 SLD is a more serious injury for Thoroughbreds than for other breeds. Although successful return to racing has been reported in Standardbreds for avulsion fractures of the proximal palmar surface of the MCIIF and surgical splitting of the SLB,21 the same has not been reported in Thoroughbreds. Safe and effective management of SLD, particularly SBD, is complicated by the real risk of SL failure and subsequent catastrophic breakdown during racing. Identification of SLD in the early stages of the disease process allows for the best opportunity for successful clinical management. The use of some therapies may be prohibited or limited by local racing jurisdictions.

MANAGEMENT OF SLD IN STANDARDBRED RACEHORSES Scott E. Palmer

SLD is a common injury of the Standardbred racehorse that impacts on the racing career of individual horses to varying degrees. Devastating breakdown-type injuries of the SL are rare in this breed, and many Standardbreds are able to compete successfully with a degree of fiber disruption, albeit at a reduced level of competition. SLD in the Standardbred may be seen as a primary pathologic event involving either the main body or branch segments, or it may also be associated with periostitis or fractures of the distal portion of the small metacarpal/ metatarsal bones or proximal sesamoid bones. Desmitis of the proximal

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portion of the SL with or without an avulsion fracture of the palmar surface of the third metacarpal bone is occasionally seen in the Standardbred as well. Clinical signs of acute SLD include localized heat, swelling, and pain on palpation of the affected area of the ligament. Unless the injury is severe or a fracture is present, the degree of lameness is quite variable and may not be evident during slow jogging. Pacers may get on one line or lean on the shaft of the sulky, whereas trotters may have a tendency to break gait. In more severe cases or if the horses are worked at speed, a typical head nod or hiking of the affected hindlimb may be evident. In cases of acute mild injury, some trainers may choose to treat the inflammation symptomatically and continue to train the horse until progressive fiber disruption occurs, creating an obvious lameness with gross enlargement of the SL. Clinical signs of long-term SLD include thickening of the body and branch segments of the ligament with varying degrees of lameness and pain. Long-term desmitis is more commonly associated with periostitis or fractures of the small metacarpal/metatarsal bones, sesamoiditis and fractures of the sesamoid bones, fibrosis of the fetlock joint capsule, and, occasionally, dystrophic mineralization of the SL. These secondary soft tissue changes lead to a decreased range of motion of the fetlock joint. Bilateral desmitis of the SL is common in Standardbreds with one limb acutely injured in an attempt to take weight off of a contralateral longterm injury. Diagnosis of SLD is confirmed by ultrasonographic examination. In the authors' experience, fiber disruption of the body of the SL usually is seen as irregular longitudinal tearing with separation of the fibers, whereas discrete core lesions are more commonly seen in the distal branches of the ligament (Figs. 13 and 14). Because periostitis and fractures of associated small metacarpal/metatarsal bones and sesamoiditis and fractures of the sesamoid bones are commonly observed in association with SLD, a complete radiographic examination of the metacarpus/ metacarpus and fetlock also is indicated. Desmitis of the proximal portion of the SL may be differentiated from middle carpal joint disease or desmitis of the ALDDFT by careful use of digital palpation, local anaesthesia, ultrasonography, radiography, and/ or scintigraphy. Treatment of acute SLD includes systemic, topical, and physical therapy. Systemic non-steroidal anti-inflammatory drugs are helpful to reduce swelling and local inflammation of the damaged tissues. Hydrotherapy is also useful to reduce swelling. The application of a gelatin-impregnated bandage (Gelocast, Beiersdorf, Inc, Norwalk, CT) helps to prevent the development of local edema and supports injured tissues. This bandage can be applied immediately after a cold water

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Figure 13. Transverse ultrasonogram of severe fiber disruption of the body of the SL of a Standardbred . This 4-year-old pacer presented with hyperextension of the metacarpophalangeal joint.

Figure 14. Transverse ultrasonogram demonstrating a core lesion of the lateral branch of the SL in the same horse imaged in Figure 13.

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hydrotherapy session and left in place for 48 hours. Cold water hosing or hydrotherapy can be performed on the following day with the bandage in place. The bandage should be replaced at 48-hour intervals, and the daily hydrotherapy should be continued until the acute inflammation is resolved, usually within 48 to 72 hours. Injured SLs of Standardbred racehorses have been injected with a wide assortment of corticosteroids; mixtures of corticosteroids, ammonium salts, and alcohol; iodine compounds; sodium hyaluronate; and glycosaminoglycan preparations in an effort to reduce inflammation, relieve pain, and promote a more rapid return to racing. In acute cases in which fiber disruption is minimal and local anti-inflammatory treatment is indicated, one of the authors (SEP) prefers perilesional injection of low doses of corticosteroid (5-10 mg methylprednisolone acetate) in conjunction with 2 to 3 weeks of limited exercise (walking and swimming). It is important to emphasise to the trainer that, in some cases, the soft tissues appear grossly normal after this treatment, even though there may be significant fiber disruption of the ligament. This apparent discrepancy between clinical signs and the findings of the diagnostic ultrasound examination needs to be addressed so that the horse is not subjected to premature exercise loads that will worsen the condition. Most long-term SL injuries of harness horses are accompanied by some degree of acute inflammation as a result of remodeling of the ligament with exercise and associated fiber disruption. Long-term injuries, therefore, also benefit from systemic or local anti-inflammatory medication. As in the case of management of acute lesions, it is important to recognize that although aggressive anti-inflammatory treatment helps to restore the limb to a more stable condition, it will not restore normal fiber architecture if fiber disruption is present. Cryotherapy with liquid nitrogen is used by some clinicians to provide pain relief in the management of long-term suspensory desmitis. Great caution is indicated, however, when considering such treatment, because any therapy that diminishes or modulates protective pain reflexes (e.g., cryotherapy and ammonium sulfate "blocks or radiation therapy") can put the damaged tissues at increased risk because of overuse if horses are kept working. Pin firing and blistering are used to tighten-up or "set" long-term SL injuries. Although scientific information to support use of thermocautery is lacking, one of the author's (SEP) anecdotal experience supports the use of pin firing and blistering as a useful treatment of moderate-tosevere suspensory body injuries when combined with a commitment from the trainer to extended rest and careful, sonographically monitored rehabilitation. This author also believes that most Standardbreds benefit from the application of mild iodine-based leg paints during the con-

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Figure 15. A controlled exercise program for rehabilitation of a SL injury may be initiated after healing of the lesion has been confirmed by ultrasonographic examination. Beginning with 5 miles per week, jogging is increased gradually during a 4-week period, with the mileage reduced to the previous week's level at the start of the subsequent period of increased mileage. This mileage plan is followed as long as soundness is maintained and ultrasound evaluations confirm good remodelling of damaged tissues until the horse is able to jog 4 or 5 miles each day.

trolled exercise period of rehabilitation, because this topical therapy seems to minimize local inflammation. In uncomplicated conditions in which the suspensory apparatus is sound structurally (as indicated by a normal fetlock joint angle and normal alignment of the pastern bone) and provided that the horse is not lame at the walk, a controlled exercise program may begin as soon as the acute inflammation is resolved (Fig. 15). Horses may be walked in h and for 4 weeks, at which time a second ultrasonographic examination should be performed. As long as the injury shows some improvement and provided that the horse is not lame when jogged in hand, the horse may then be harnessed and walked in the bike for 4 more weeks. This introduces a draft load, but does not subject the SL to the additional load of jogging. "Pressure bikes" with clamps on the axle that can be adjusted to increase the draft load without the introduction of speed work can be used to increase the work gradually during this phase of controlled exercise. A third ultrasonographic examination is performed 8 weeks after the injury, and if the injury seems to be healing well with additional filling-in of defects by well-aligned fibrous tissue, limited jogging may be resumed. Initially, the jogging periods should be limited to 1 mile at a very easy pace, with the distance increased to 3 miles during an 8-week period. The temperament of the individual patient is

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an important consideration during the controlled exercise period, because it is critical to prevent uncontrolled or premature stress to the injured ligament. Those horses that will not willingly walk in harness should be towed alongside another horse or behind a vehicle. Horses that will not jog easily also may be towed in a similar manner. After 8 weeks of jogging, a final ultrasonographic examination is performed before normal jogging is resumed (4 or 5 miles per day) and speed work is initiated. Before speed work, the lesion should be healed with uniform echogenicity and a linear arrangement of fibers. If sonolucent lesions persist in a clinically sound horse, limited jogging is continued for another 4 weeks, at which time another ultrasonographic examination is performed. If clinical signs of lameness are shown, or if the lesions worsen ultrasonographically, the exercise level is reduced until these conditions are resolved. Swimming is a popular form of non-weightbearing exercise for injured Standardbreds and can play an important role in rehabilitating SL injuries. It is important to realize, however, that although this form of therapy can help to reduce inflammation initially, and it can be used to provide or maintain a degree of cardiovascular fitness, its benefits are limited when used without some degree of racetrack exercise. The ligament needs to be "trained" by gradually increasing the load in such a way that remodelling takes place and progressive or catastrophic injury is avoided. This is best accomplished by "periodizing" the stress load with alternation of hard and easy days and by gradually increasing the weekly mileage during a 4-week period, then reducing the load during the subsequent week before moving on to the next increment of training (see Fig. 16). Horses that are "swum" back to training without regular track work are vulnerable to re-injury as soon as speed work is resumed. Surgical procedures for treatment of SL injury are directed partly at treatment of associated bony injury of the "suspensory apparatus." Fractures of the distal segments of the small metacarpal/metatarsal bones should be removed surgically before rehabilitation with a controlled exercise program as previously mentioned. The surgeon should use methods for removal of these fragments that insure minimal disruption of the SL. Fractures of the proximal portion of the small metacarpal/ metatarsal bones may be treated with internal fixation or stall rest with heavy bandaging until the fracture seems to be healed radiographically. In some cases of long-term SL injury, the small metacarpal/metatarsal bones will develop a marked periostitis with bony enlargement of the distal segments. It is in the authors' opinion that if the longitudinal axis of the bone is normal and if no fracture is present, " prophylactic" surgical removal of the distal segments of these thickened small metacarpal/ metatarsal bones is not indicated. On the other hand, surgical removal of the distal segments of small metacarpal/metatarsal bones that

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are displaced laterally at an acute angle from the third metacarpal/ metatarsal bone in conjunction with long-term SL thickening may have merit, because these bones are likely to fracture and generally do not return to their normal alignment with conservative treatment. Horses that have had small metacarpal/metatarsal bone fragments removed should be confined to a stall for at least 2 weeks postoperatively before beginning the walking period. Controlled exercise is then initiated as previously outlined for uncomplicated desmitis of the SL. Fractures of the proximal sesamoid bones commonly are observed in conjunction with some degree of SL injury. Selected apical, abaxial, and small base fractures are managed best by arthroscopic surgical removal of the fragments. Nondisplaced transverse fractures may be managed by internal fixation with screws or wires or by external fixation w ith a cast or a rigid splint and extended rest. Displaced transverse fractures of the proximal sesamoid bones are best managed with open reduction and internal fixation. Horses undergoing arthroscopic surgery for removal of sesamoid chip fracture fragments shou.ld be confined to a stall for 4 weeks postoperatively, followed by 30 to 60 days of walking and limited turnout before beginning the controlled exercise program. Transverse fractures of the sesamoid may require 6 to 12 months to achieve bony union, which must be accomplished before a controlled exercise program is begun. Horses with avulsion fractures at the origin of the SL on the proximal and palmar surface of the third metacarpal bone should be confined to a stall until radiographic evidence of fracture healing is evident (usually within 6-9 months), at which time the controlled exercise program may begin. Percutaneous longitudinal splitting of damaged portions of the SL is not performed in standards by one of the authors (SEP), but is reported to be of value in the treatment of selected cases of SLD (coretype lesions with normal tissue at the periphery). The success of percutaneous splitting of the SL is reported to be superior to that for splitting injured tendons because the development of periligamentous adhesions is less critical than is the development of adhesions in association with similar tendon surgery. Therapeutic shoeing also plays an important role in the management of SLD in the Standardbred racehorse. The goal of shoeing these horses is to minimize nonphysiologic loading of the ligament during exercise. In pacers, the use of half round/half wedge shoes or shoes with trailers and heel caulks should be avoided as these shoes tend to place a torque on the limb when the foot comes into contact with the ground. Flat shoes are ideal, but if traction is a concern, use of flat shoes with a toe crease or full-wedge shoes should be considered. In both trotters and pacers, the length of toe should be minimized to avoid

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excessive strain during breakover. For the same reason, excessive trimming of the heels should be avoided. Conscientious daily bandaging and massaging of injured SLs with emollient oils, leg tighteners with or without DMSO, and sweats has a time-honored place in the successful management of SL injury. Topical application of these compounds and local massage seems to stimulate circulation, reduce local inflammation, and provide a degree of analgesia. As in the management of tendinitis, protective bandaging and leather boots can be useful equipment to protect the affected limb when speed work is resumed, particularly if the horse is prone to interference. The prognosis for racing after SL injury is, of course, a function of the degree of injury, temperament of the patient, presence of associated bone injury, and the level of commitment on the part of the trainer and owner. Generally, pacers have a better prognosis for racing than trotters with similar injuries. Uncomplicated cases with minimal disruption of the ligament can recover to resume competition at the pre-injury level. Horses with more extensive lesions, or lesions that do not fill-in or remodel as indicated by sonographic examination, however, have a reduced prognosis. Patients with associated fractures of the splint bone can still have a good prognosis for racing, provided that the degree of SL injury is not severe. Published reports of Standardbreds with splint bone fractures and concurrent SL disruption that returned to their previous level of performance ranged from 25% to 50%. 1• 14 In the author's experience, harness horses with associated fracture of the proximal sesamoid bone also can have a good prognosis for racing, provided that the damage to the sesamoid bone is not extensive, and sesamoiditis is not present to an advanced degree. The prognosis for horses with transverse fractures of the proximal sesamoid bone is guarded, because these fractures often recur when speed work is resumed, especially if sesamoiditis is present.

TRAUMATIC DISRUPTION OF THE SUSPENSORY APPARATUS Dean Richardson

Traumatic disruption of the suspensory apparatus (TDSA) is almost exclusively an injury occurring in the forelimbs of Thoroughbred racehorses, although it may be suffered by any horse running at high speed. This includes young foals that are chasing their dams in the pasture. Speed alone does not account for the injury, and it is likely that fatigue

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of the flexor muscles supporting the fetlock and digit leads to higher stresses in each component of the suspensory apparatus. There also may be a history of the horse being "bumped" or making a misstep. The history and clinical presentation of TDSA in adult horses are straightforward, because the horses are either breezing or racing and come up acutely and severely lame. The major physical finding is a dropping of the fetlock joint as the horse attempts to bear weight. Many horses become anxious or even frantic as they attempt to control the injured limb. There is obvious swelling and pain over the site of the injury. In foals, the diagnosis is often not made as quickly. 11 The typical history of a foal with TDSA (or lesser injuries of the suspensory apparatus) is of being turned out in a large field with its dam and other mares and foals shortly after birth or shortly after being confined to a box stall for an extended period of time. As the mare runs with the other horses, the foal attempts to keep up, running at speed and to the point of exhaustion. This results in the same combination of speed and fatigue that leads to injury in the racehorse. The clinical ·signs of complete disruption of the suspensory apparatus are similar but less dramatic than in adult horses. The same clinical signs of fetlock "drop" and severe lameness will be seen with complete disruption of any portion of the suspensory apparatus. The most common injury in both adults and foals is fracture of both proximal sesamoid bones. In most cases, the fractures are comminuted, especially their basilar portions. The second most common type of TDSA is complete avulsion of the distal sesamoidean ligaments. This is recognized easily on radiographs by the proximal displacement of the intact sesamoid bones. The least frequently recognized type of TDSA is a complete tear of the suspensory ligament body or both branches. With any TDSA, the excessive dorsal flexion of the fetlock may result in stretching or even tearing of the digital vessels. Either can result in avascularity or hypovascularity of the digit. Simultaneous damage to the superficial and deep digital flexor tendons is also common and should be assessed ultrasonographically. Although sesamoid fractures and suspensory injuries are both common hindlimb injuries, the severe "breakdown" type injuries tend to be only a forelimb problem. TDSA is virtually always a career-ending injury. The only exceptions are simple displaced mid-body fractures of both sesamoids that can be repaired individually and suspensory body / branch injuries in some Standardbreds. It is important to recognize the severity of the injury so that an informed decision can be made concerning treatment. Most horses can be saved as pasture sound or breeding animals, but treatment is often prolonged and expensive, regardless of the therapeutic approach selected.

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First Aid

The most important first aid is to apply an appropriate splint that aligns the metacarpus and phalanges in a column so that bending of the fetlock and loading of the suspensory apparatus is prevented. Although homemade splints can be fashioned to accomplish the same objective, commercially available splints (Kimzey Lifesaver Splint, Kimzey Welding Works, Woodland, CA, and Monkey Splint, Primary Structures, Huntingdon, England) are quick and easy to apply and very effective for temporary immobilization. Most horses are less anxious and able to move comfortably immediately after the splint is applied. If a prefabricated splint is not available, a lightly padded bandage with a splint applied to the dorsal aspect of the metacarpus, phalanges, and hoof will serve the same purpose if the heel is kept elevated. This can be done by taping the heel and a heel wedge with nonelastic tape (e.g., duct tape) to the dorsal splint. Excessive padding should be avoided because it will allow dorsal flexion within the bandage and shifting of the splint. Other first aid measures include the administration of phenylbutazone, intravenous fluids to replace water and electrolytes lost through sweating, and broad-spectrum antibiotics. Antibiotics should be given even if the fracture is closed ostensibly. High concentrations of antibiotics in the fracture haematoma are desirable because skin abrasions and lacerations over hypovascular tissue are common. The vascularity of the foot should be assessed by palpation of the digital vessels and assessment of hoof temperature. Horses that are extremely anxious and difficult to calm should be given xylazine and/ or butorphanol as needed for restraint and to prevent the horse from further injuring itself. Nonsurgical management involves long-term splinting of the injury in an attempt to achieve enough fibrosis of the injured tissues that satisfactory support of the fetlock returns. The primary advantage of this approach is that the obvious surgical risks are associated with operating in a hypovascular and possibly contaminated site are avoided. The surgical and technical expertise and equipment required are modest and the expense of initial treatment is relatively small. There are some disadvantages of nonsurgical management. One is that the fibrosis that develops may not be adequate to support the fetlock over an extended period of time with the horse receiving exercise at pasture. This is more of a problem with distal sesamoidean ligament avulsions than fractured sesamoid bones. The other major disadvantage of splinting as definitive treatment is that many horses are still far from comfortable on the splinted limb and are also unable to use it normally because of the abnormal posture it requires. Complications of supporting limb breakdown and laminitis, therefore, are constant worries. Long-term splinting also demands meticulous daily bandage changes if rub sores at the

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proximal dorsal metacarpus and suppurative dermatitis of the palmar pastern and heel bulbs are to be avoided. The technique of successful long-term splinting of TDSA cases primarily involves meticulous nursing care. Most clinicians use a prefabricated splint because of the ease of its removal and application. The Kimzey splint can be improved for long-term use by welding a heel extension on it to increase its bearing surface area. This helps minimize the tendency to develop rub sores at the proximal dorsal edge of the splint. The prefabricated splints are not perfectly fitted for every horse so some modifications in padding may be required to avoid excessive pressure on the proximal dorsal metacarpus. An alternative is the "board splint" described by Wheat and Pascoe,32 in which a rigid splint is secured to the bottom of the hoof with wire. A padded bandage is placed up to the carpus, and the caudally extended board is folded upward and fixed to the bandage with nonelastic tape. This results in essentially the same limb posture as the manufactured splints. Regardless of which splint is used, the leg should be checked daily for developing sores or dermatitis. If the leg is washed, it should be dried before applying the bandage. When a skin infection develops, it can be difficult to manage. Both systemic and local antibiotics usually are necessary. The most critical decisions to be made when managing a TDSA with splints concern removal of the splints and gradually allowing a return to more normal fetlock and digit joint angles. Most horses are kept splinted upright for approximately 6 weeks, but many, particularly those with distal sesamoidean ligament avulsions, may require much longer. The process of dropping the fetlock should be gradual and can either be done by splinting at decreasing angles or by using a fetlock support shoe incorporating an adjustable sling. Horses should be kept confined to a stall for a prolonged period of time (4-6 months) because a single mis-step could lead to tearing of the still maturing scar tissue. The results of conservative management appear to vary greatly with some clinicians reporting excellent results 29 and others having considerable complications. The primary advantage of a nonsurgical approach is that the surgeon cannot be blamed for specifically causing a horse's demise unlike surgical repair where infection or mechanical failure can be fatal complications. Surgical management of TDSA nearly always involves fetlock arthrodesis although repair of simple displaced midbody sesamoid fractures can be performed to save joint function. The major advantage of an arthrodesis is that the procedure usually affords the horse immediate comfortable use of the limb and avoids the complications of prolonged overuse of the contralateral limb. Because the fixation is usually stable, postoperative immobilization is minimal, and the various complications of casts and splints can be avoided. The primary disadvantage of surgi-

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cal arthrodesis is the increased risk of infection. An additional consideration is that successful arthrodesis requires both surgical expertise and investment in equipment and facilities. The most widely used technique for fetlock arthrodesis is that of a dorsal plate with creation of a tension band on the palmar aspect. 3 Dorsal plating without a tension band on the palmar aspect of the fetlock is ill advised because the plate will be cycled in bending on the joint's dorsal surface and will fatigue and eventually break. The specific technique used to create the tension band depends on the type of TDSA, but both involve the same surgical approach. An incision should be made between the common and lateral digital extensor tendons leaving enough on either side of the incision to allow closure. The incision should then extend without lateral dissection through the periosteum to the surface of the bone. The incision extends from the proximal metacarpus to the distal aspect of the proximal phalanx. A sharp periosteal elevator and/ or scalpel is used to expose a 5-cm strip of the dorsal surface of the proximal phalanx. As the fetlock joint is crossed, the capsule is elevated medially and laterally, and the lateral collateral ligament is transected. The joint should be luxated so that all the articular cartilage also can be removed with a curette from both joint surfaces. If the sesamoids are intact, the cartilage should be removed. Multiple 3.2-mm holes are then made through the dense subchondral bone on all joint surfaces. A 3.2-mm hole is drilled transversely through the distal metacarpus 2 cm proximal to the physeal scar. Another hole is made transversely through the mid-diaphysis of the proximal phalanx. Two 1.2- or 1.5-mm wires are passed through the proximal drill hole in a lateral to medial direction. The wires are then passed palmarly to the distal palmar margin of the metacarpus. A bent 8- or 10-gauge bleeding trocar is directed adjacent to the proximal phalanx proximally and palmarly so that its tip exits the soft tissue immediately palmar to the mid-sagittal groove of the proximal phalanx. The wires are passed through the needle and then through the proximal phalanx. The procedure is repeated to make a figure eight tension band. Final tightening of the wire is done so that the wire is very tight when the fetlock is in complete extension (180 degrees). A 14-hole broad dynamic compression plate (Synthes USA, Paoli, PA) is prebent to a fetlock angle of approximately 150 to 160 degrees. The distal four screws in the plate are inserted through the plate into the proximal phalanx using the neutral drill guide. As the prebent plate is held against the bone, the tension band wire should be bow string tight. If it is not, the fetlock should be flexed palmarly slightly, and the wire should be tightened a bit more. The plate tension device is used to compress the joint surfaces together. Except for the two screws on either side of the joint, the remaining holes in the plate are filled with screws using a neutral drill guide. The two

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screws next to the joint are placed in lag fashion, crossing the joint (Fig. 16). A small cancellous bone graft should be placed at the joint level under and adjacent to the plate. Although the technique can certainly be successful with 4.5-mm screws, 5.5-mm screws are stronger and should be used throughout except for the two screws angled across the joint through the plate. It is difficult to sharply angle 5.5-mm screws through the plate holes without damaging the screw threads. If the distal sesamoidean ligaments are intact and the basilar sesamoid fragments are large enough, the te1,1sion band wiring can be avoided. Instead, the fetlock is positioned approximately 5 degrees of palmar flexion, and a 5.5-mm lag screw is placed through the metacarpus into each sesamoid. When the prebent plate is placed, the distal sesamoidean ligaments serve as the tension band that will prevent the plate from bending and eventual fatigue failure. This is the preferred surgical technique in the less common cases involving disruption of the SL body or both branches. The incision is easy to close because the s~tures can be placed through the edges of the extensor tendon. Usually simple interrupted

Figure 16. Dorsopalmar and lateromedial postoperative radiographs of an MCP arthrodesis performed in a horse with a complete disruption of the distal sesamoidean ligaments. Note the placement of the tension band wire, use of 5.5-mm screws, and crossing of lag screws at the joint surface. Care must be taken not to hit the wire(s) with the drill, tap, or screws.

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synthetic absorbable sutures are followed by a subcuticular suture line and skin staples. A fiberglass cast is placed for anesthetic recovery. The cast can be left in place for 2 weeks or longer if the horse wears it comfortably. If there is obvious discomfort in the cast, it should be removed immediately because cast sores can be a serious problem, and the fixation is secure enough that the cast is unnecessary. Radiographs should be obtained at regular intervals. If healing is routine, most horses have a solid fusion by 3 months after surgery and can begin some limited turnout in a small paddock. The major complication of bone plating for fetlock arthrodesis is infection. This repair is very strong and stable if performed properly; however, healing can take place even in the face of infection. The combination of instability and infection rarely succeeds and re-operation of unstable, infected sites usually is necessary to achieve fusion. Implant failure is also a concern, but proper technique and the use of 5.5-mm screws will mitigate the problem. Additional strength and fatigue life can be obtained by luting the plate, although this usually is not necessary. A common long-term complication associated with TDSA is degenerative joint disease of the proximal and/ or distal interphalangeal joints. The joints are stressed more by the fusion of the fetlock and often by the presence of serious injury to the flexor tendons that insert on the phalanges. Every effort should be made to remove the cast on the distal limb as quickly as possible because the concomitant muscle and tendon weakness quickly exacerbates the pastern and coffin joint instability. Many horses with TDSA suffer open contaminated fractures or such extensive soft tissue damage that internal fixation may carry an unacceptable risk of infection. An alternative means of managing such injuries is with external skeletal fixation. 25 An external fixator offers the advantages of excellent immobilization of the injured site, minimal surgical trauma at the injured site, and the ability to observe and to treat the open wound(s). The primary disadvantage of an external fixator is that comfort in the device tends to diminish over time as the pins loosen, and the horse is at risk of fracturing MC3 through a pin hole. Application of an external fixator has been described. 22, 25 Briefly, three large (~9 mm) threaded pins are placed transversely through the cannon bone. The hoof is attached by nails or an adhesive to a foot plate connected to vertical side bars. The transfixation pins are then attached to the side bars by enclosing them in flexible rubber tubing in which a fast setting cement is poured. After the fixator is secure, a 5-cm straight incision is made over the dorsal surface of the joint. A large drill bit (9-12 mm) is used to make a hole across the joint destroying both articular surfaces, The hole is then packed with a cancellous bone graft, and the incision closed routinely. The horse should be recovered from

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general anesthesia using any available special recovery system such as deep mats, slings, or swimming pool. The fixator is bandaged loosely to keep bedding away from the incision and the pin tracts are cleaned daily. The fixator is left in place as long as the horse remains comfortable (generally, approximately 7-10 weeks). The fixator is removed with the horse standing simply by cutting the transfixation pins with a hacksaw and unthreading them. A fiberglass cast is then placed and remains until the fusion is radiographically solid.

Prognosis and Complications

The prognosis for any horse with traumatic disruption of the suspensory apparatus depends on the specific nature and severity of the injury. Distal sesamoidean ligament avulsions have a poorer prognosis than displaced sesamoid fractures because the latter tend to form fibrous scar tissue more quickly. The relatively uncommon suspensory body or bilateral branch tears probably have the best prognosis because they seem to heal more quickly and usually cause less fetlock instability. At least 65% to 75% of horses with closed disruptions of the suspensory apparatus and an intact blood supply should be saved with proper treatment. Open injuries obviously have a much poorer prognosis regardless of the therapy chosen and open injuries with vascular compromise have a very poor prognosis. Complications of TDSA regardless of treatment include laminitis or breakdown of the contralateral limb. The primary complications of longterm splinting are rub sores and inadequate fibrosis leading to instability and chronic pain. Surgical arthrodesis has the advantage of affording comfort more quickly, but the risks of infection are much greater. Incorrect surgical technique also can lead to mechanical failure of the internal fixation.

References 1. Bowman K, Evans L, Herring M: Evaluation of surgical removal of fractured distal

splint bones in the horse. Vet Surg 11:116- 124, 1982 2. Bramlage L, Gabel A, Hackett R: Avulsion fractures of the origin of the suspensory ligament in the horse. J Am Vet Med Assoc 176:1004-1010, 1980 3. Bramlage L: An initial report on a surgical technique for arthrodesis of the metacarpophalangeal joint in the horse. In Proceedings of the 27th Annual Con vention of the American Association of Equine Practitioners, New Orleans, LA, 1981, pp. 257-261 4. Bramlage L, Bukowiecki C, Cabe! A: The effect of training on the suspensory apparatus of the horse. In Proceedings of the 35th Annual Convention of the American Association of Equine Practitioners, Boston, MA, 1989, pp. 245-247

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5. Dik K, Gunsser I: Atlas of Diagnostic Radiology of the Horse, Part 2. Diseases of the Hindlimb. London, Wolfe Publishing, 1989, pp. 74-75 6. Dyce K, Sack W, Wensing C: The Forelimb of the Horse. In Dyce K, Sack W, Wensing C (eds): Textbook of Veterinary Anatomy. Philadelphia, WB Saunders, 1978, pp. 561-562 7. Dyson S: Some observations on lameness associated with the proximal metacarpal region. Equine Vet J 6(suppl):43-52, 1988 7a. Dyson S: Problems encountered in equine lameness diagnosis with special reference to local analgesic techniques, radiology and ultrasonography. Newmarket, UK, R & W Publishers, 1995, pp. 33-41, 47-54 8. Dyson S: Proximal suspensory desmitis: Clinical, ultrasonographic and radiographic features. Equine Vet J 23:25- 31, 1991 9. Dyson S: Proximal suspensory desmitis of the hind limb. Proceedings of the Bain Fallon Memorial Lectures 15:55-62, 1993 10. Dyson S, Romero J: An investigation of injection techniques for local analgesia of the distal tarsus and proximal metatarsus. Equine Vet J 25:30-35, 1993 11. Ellis D: Fractures of the proximal sesamoid bones in Thoroughbred foals. Equine Vet J 11:48-52, 1979 12. Ford T, Ross M, Orsini P: A comparison of methods for proximal palmar metacarpal anaesthesia in horses. Vet Surg 18:146-150, 1988 13. Genovese R, Rantanen N, Hauser M, et al: Diagnostic ultrasonography of equine limbs. Vet Clin North Am Large Anim Pract 2:171-177, 1986 14. Jones R, Fessler J: Observations on small metacarpal and metatarsal fractures with or without associated suspensory desmitis in Standardbred horses. Can Vet J 18:29-32, 1977 15. Keegan K, Baker G, Boero M, et al: Evaluation of support bandaging during measurement of proximal sesamoidean ligament strain in horses by use of a mercury strain gauge. Am J Vet Res 53:1203-1208, 1992 16. Kobluk C, Martinez del Campo L, Harvey-Fulton K: A kinetic investigation of the effect of a cohesive elastic bandage on the gait of an exercising Thoroughbred racehorse. In Proceedings of the 37th Annual Convention of the American Association of Equine Practitioners, San Diego, CA, 1988, pp. 135-148 17. Lloyd K, Koblik P, Ragle C, et al: Incomplete palmar fractures of the proxima l extremity of the third metacarpal bone in horses: Ten cases (1981-1986). J Am Vet Med Assoc 192:798-803, 1988 18. McI!wraith CW: Desmitis of the Suspensory Ligament. In Stashak T (ed): Adams' Lameness in Horses, ed 4. Philadelphia, Lea & Febiger, 1987, pp. 469-470 19. Marks D, Mackay-Smith M, Leslie A, et al: Lameness resulting from high suspensory disease (HSD) in the horse. In Proceedings of the 27th Annual Convention of the American Association of Equine Practitioners, New Orleans, LA, 1981, pp. 493-497 20. Martin B, Reef V, Molesworth L: Ultrasonic evaluation of hind limb suspensory desmitis in Standardbred Racehorses. In Proceedings of the 35th Annual Convention of the American Association of Equine Practitioners, Boston, MA, 1989, p . 275 21. Nilsson G, Bjorck C: Surgical treatment of chronic tendonitis in the horse. J Am Vet Med Assoc 155:920-926, 1969 22. Nunamaker D, Richardson D, Butterwick D: A new external skeletal fixation device that allows immediate full weightbearing: Application in the horse. Vet Surg 15:345355, 1986 23. Personnett L, McAllister E, Mansmann R: Proximal suspensory desmitis. Mod Vet Pract 64:541-545, 1983 24. Pool R, Wheat J, Ferraro G: Corticosteroid therapy in common joint and tendon injur.ies of the horse. Part II. Effects on tendons. In Proceedings of the 27th Annua l Convention of the American Association of Equine Practitioners, New Orleans, LA, 1981, pp. 407410 25. Richardson D, Nunamaker D, Sigafous R: Use of an external skeletal fixation device and bone graft for arthrodesis of the metacarpophalangeal joint in horses. J Am Vet Med Assoc 191:316-322, 1987 26. Ross M, Ford T, Orsini P: Incomplete longitudinal fracture of the proximal palmar cortex of the third metacarpal bone in horses. Vet Surg 17:82-86, 1988

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27. Selway S: Suspensory desmitis. In Mansmann R, McAllister E (eds): Equine Medicine and Surgery, ed 3. Santa Barbara, CA, American Veterinary Publications, 1982, pp. 1085-1086 28. Sisson S: Equine syndesmology. In Getty R (ed): Sisson and Grossman's The Anatomy of Domestic Animals, vol 1, ed 5. Philadelphia, WB Saunders, 1975, pp. 349-375 29. Snyder J, Wheat J, Bleifer D: Conservative management of metacarpophalangeal joint instability. In Proceedings of the 32nd Annual Convention of the American Association of Equine Practitioners, Nashville, TN, 1986, pp. 357- 364 30. Ueltschi G: Diagnosis of proximal suspensory desmitis. Pferdheilkunde 5:65-69, 1989 31. Verschooten F, Gasthuys F, De Moor A: Distal splint bone fractures in the horse: An experimental and clinical study. Equine Vet J 16:532-536, 1984 32. Wheat J, Pascoe J: A technique for managing traumatic rupture of the equine suspensory apparatus. J Am Vet Med Assoc 176:205- 210, 1984 33. Wilson D, Baker G, Pijanowski G, et al: Composition and morphologic features of the interosseous muscle in Standardbreds and Thoroughbreds. Am J Vet Res 52:133-139, 1991 34. Young R, O'Brien T, Craychee T: Examination procedures for the diagnosis of suspensory desmitis in the horse. In Proceedings of the 35th Annual Convention of the American Association of Equine Practitioners, Boston, MA, 1989, pp. 233-241

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J.

Dyson, MA, VetMB, PhD, DEO, FRCVS Equine Clinical Unit Animal Health Trust Snailwell Road Newmarket Suffolk CBS 7DW England