Materials and Methods

Case selection—Medical records of all horses with ultrasonographic evidence of tendinitis involving the proximal portion of the SDFT admitted to Texas A&M University Veterinary Medical Center between February 2000 and June 2006 were retrospectively reviewed (group A horses). In addition, medical records of all horses with injury to the SDFT only in the midmetacarpal region of the forelimb (excluding horses with multiple tendon and ligament injuries) admitted during the same period were reviewed (group B horses).

On ultrasonographic evaluation, group A horses had a single SDFT injury in the forelimb within zone 0 and group B horses had a single SDFT injury in the forelimb within zone 1A to zone 3A. With the use of the base of the accessory carpal bone as a point of reference, zones 0 through 3A are defined as follows: zone 0 = the area approximately 5 cm long adjacent to the accessory carpal bone; zone 1A = area just distal (0.5 cm) to the accessory carpal bone extending approximately 4 cm; zone 1B = area extending approximately 4 to 7 cm distal to the accessory carpal bone; zone 2A = area extending approximately 7 to 10 cm distal to the accessory carpal bone; zone 2B = area extending approximately 10 to 14 cm distal to the accessory carpal bone; zone 3A = area extending approximately 14 to 18 cm distal to the accessory carpal bone.⁴

Medical records review—Information obtained from the medical records for group A horses included signalment, horse use, affected forelimb, severity and duration of lameness, diagnostic tests performed, ultrasonographic findings, and outcome of treatment. Information obtained from the medical records for group B horses included signalment, horse use, affected forelimb, ultrasonographic findings, and outcome.

Procedures—A lameness examination was performed on all group A horses to determine the affected forelimb, clinical signs, and severity of lameness. Diagnostic tests performed to locate the site of lameness consisted of perineural anesthesia with 2% mepivacaine hydrochloride and carpal flexion tests.

All group A and group B horses had an ultrasonographic evaluation of the affected forelimb and the opposite forelimb for comparison.^a Both transverse and longitudinal images were evaluated by use of a 7.5- to 13-MHz linear probe.^b All images were performed and reviewed by the same clinician (MKC). The MIZ was recorded for all horses. An ES and FAS were assigned to each horse as previously described.¹⁰ Briefly, the ES was determined on the basis of a scale of 0 to 4.¹⁰ An ES of 1 was defined as slightly less echogenic than normal; an ES of 2 was defined as 50% anechoic; an ES of 3 was defined as mostly anechoic; and an ES of 4 was defined as completely anechoic.¹⁰ The FAS was used to describe the alignment of tendon fibers.⁸ The FAS was scored on a scale of 0 to 3. An FAS of 0 indicated that 76% to 100% of fibers were parallel; an FAS of 1 indicated that 51% to 75% of fibers were parallel; an FAS of 2 indicated that 26% to 50% of fibers were parallel, and an FAS of 3 indicated that 0% to 25% of fibers were parallel.⁸ The CSA of the lesion was calculated as a percentage of the total area of the tendon for all horses. This percentage was calculated by measuring the CSA of the tendon at the location of the MIZ and the CSA of the lesion at the same location by use of ultrasonography. The CSA of the lesion was then divided by the CSA of the tendon and multiplied by 100 to produce a percentage value. The length of the lesion was estimated in centimeters by evaluating the longitudinal ultrasonographic images. The presence of carpal sheath effusion and peritendinous swelling was noted for each horse. The description of lesion location within the MIZ of the tendon was recorded for each horse (eg, palmar or diffuse).

Group A horses were rested in a stall with 15 minutes daily hand walking for 3 to 6 months (mean, 4.5 months; median, 3.5 months). Group A horses were reevaluated at approximately 2 months after injury before being allowed small paddock turnout for an additional 3 to 6 months (mean, 4.5 months; median, 2.5 months). Follow-up information was obtained a minimum of 10 months after the injury. Follow-up consisted of reexamination at the hospital or telephone communication with the owner or trainer. Outcome was considered successful if the horse returned to its previous performance level.

Statistical analysis—Age was compared between group A and group B horses by use of a Mann-Whitney U test. Use, limb affected, and whether horses returned to their original use were compared between group A and group B horses by use of a Fisher exact probability test. For all tests, a value of P < 0.05 was considered significant.

Results

Signalment—Twelve horses that had a single SDFT injury in zone 0 fulfilled criteria for inclusion in the study as group A horses. There were 3 mares and 9 geldings. Mean age was 18 years (median, 17 years; range, 11 to 23 years). Nine horses were Quarter Horses, 1 was a pony, 1 was a Tennessee Walking Horse, and 1 was a American Paint Horse. Three horses were used for low-level English performance (dressage and jumping), 4 were used for trail riding, 4 were used for Western performance (roping and barrel racing), and 1 was used as a ranch horse.

Twenty-two horses that had a single SDFT injury in zone 1A to zone 3A fulfilled criteria for inclusion in the study as group B horses. There were 8 mares, 9 geldings, and 5 sexually intact males. Mean age was 6.3 years (median, 5 years; range, 2 to 11 years). Thirteen were Thoroughbreds, 5 were Quarter Horses, 2 were Arabians, 1 was a pony, and 1 was a warmblood. Eleven horses were used for flat racing, 7 horses were used for English performance, 2 were used for barrel racing, 1 was used for endurance riding, and 1 was used for team roping.

Group A horses were significantly (P = 0.001) older than group B horses. Group B horses were significantly (P = 0.005) more likely to be racehorses than group A horses (Table 1).

History—Duration of lameness prior to examination at the hospital for group A horses ranged from 1 to 10 weeks (mean, 3.8 weeks; median, 4 weeks). The right forelimb was involved in 5 group A horses, and the left forelimb was involved in 7 group A horses. The right forelimb was involved in 12 group B horses, and the left forelimb was involved in 10 group B horses. No significant (P = 0.721) difference in the affected forelimb (right vs left) existed between groups. Eleven of the 12 group A horses had become acutely lame while being ridden or while turned out in a field, whereas 1 group A horse had a history of intermittent lameness. Two group A horses became affected with a similar lesion in the SDFT of the opposite forelimb at 21 and 33 months, respectively, after the first injury.

Clinical findings of group A horses—One of the 12 group A horses had swelling of the proximopalmar aspect of the SDFT. Signs of pain were elicited by carpal flexion in 8 group A horses. At the time of hospital admission, 11 group A horses had a grade 3 of 5 lameness and 1 group A horse had a grade 4 of 5 lameness.⁴ In 11 group A horses, diagnostic anesthesia was used to locate the source of lameness. None of the horses improved after a palmar digital nerve block, abaxial sesamoid nerve block, or a low palmar nerve block. Two of the 12 group A horses improved substantially after perineural anesthesia of the lateral palmar nerve. The lameness resolved in 9 group A horses only after perineural anesthesia of the ulnar nerve was completed approximately 10 cm proximal to the accessory carpal bone.

Ultrasonographic findings of group A horses—Ultrasonographic findings were summarized (Table 2). The CSA of the SDFT in the affected limb was larger than the CSA of the SDFT in the unaffected limb in all group A horses. For group A horses, none of the lesions had a centralized (core lesion) location; all lesions affected the periphery of the tendon. The primary location of the lesion within the MIZ in the SDFT was diffuse in 5 of the 12 group A horses, palmar in 2 group A horses, palmarolateral in 2 group A horses, palmaromedial in 2 group A horses, and palmarolateral and palmaromedial in 1 group A horse. Of the 12 group A horses, 6 had peritendinous subcutaneous edema and 2 had carpal sheath effusion identified on ultrasonographic evaluation.

Ultrasonographic findings of group B horses—Ultrasonographic findings were summarized (Table 2). For group B horses, all lesions were centralized or core lesions.

Outcome—Follow-up information was obtained for group A horses by reexamination at our hospital at a minimum of 10 months after injury. One group A horse underwent desmotomy of the accessory ligament of the SDFT (proximal check ligament) and carpal fasciotomy 1 year after the injury because of continued lameness; these procedures were unsuccessful in resolving the lameness in this horse. Ten of the 12 group A horses remained lame; 8 of these horses were retired, and 2 were ridden occasionally at a lower level of activity than previously. Two of the 12 group A horses returned to their previous use; 1 was used for trail riding, and 1 was used for roping. Two horses sustained the same lesion on the opposite forelimb. One horse injured the opposite forelimb 3 years after the initial injury. The other horse injured the opposite forelimb 2 years after the initial injury, which was the same horse that had undergone desmotomy of the accessory ligament of the SDFT and carpal fasciotomy.

Follow-up for group B horses was obtained by an ultrasonographic and lameness examination at a minimum of 10 months after initial injury. Twelve of the 22 group B horses remained lame, which included 9 horses used for flat racing, 1 horse used for English performance, 1 horse used for barrel racing, and the 1 horse used for endurance riding. Ten of the 22 group B horses returned to their previous use, which included 6 horses used for English performance, 2 horses used for flat racing, 1 horse used for barrel racing, and 1 horse used for roping. The return to function for group B horses was greater when the racehorse population was removed from group B (ie, after the removal of racehorses, 8/11 group B horses returned to full function).

No significant (P = 0.140) difference existed in the ability to return to previous use between the 12 group A horses and 22 group B horses. However, group A horses were significantly (P = 0.012) less likely to return to previous use, compared with the 11 group B horses that were not used for flat racing.

Discussion

Results of our study indicated that injury of the SDFT at the level of the carpus (zone 0) appears to be an injury that occurs in older horses performing at lower-level activities, compared with tendinitis of the midmetacarpal region that tends to be more common in younger horses, specifically race horses. The pathogenesis of tendinitis of the proximal portion of the SDFT is likely different than that of lesions in the midmetacarpal region of the SDFT as a result of the signalment of the horse involved, location of injury, and type of lesion. Tendon injury may occur as a single event or as a cumulative fatigue failure that involves stretching of tendon fibers beyond their physiologic limit. Fatigue, poor conformation, lack of fitness, and incoordinate muscle activity can produce excessive biomechanical forces on the tendon. There also appears to be an age- and exercise-related tendon matrix deterioration that may contribute to tendon weakness.^4,11 Findings in a previous study¹² indicate that the SDFT matures at 2 years of age in horses, and tendon matrix degeneration, which includes matrix fibrillation, chondroid metaplasia, chondrone formation, neovascularization, and fibroplasias, becomes more evident in horses > 3 years of age. These changes induce tendon weakening and an increase in stiffness that is thought to be associated with the reduction of the tendon crimp angle, increased number of nonreducible cross-links, and decreasing fascicle size in older tendons.¹³ Results of another study¹⁴ indicate that there is a progressive increase in the ratio of type III to type I collagen within the tendon fibrils and that collagen fibril diameter decreases with age in the SDFT, which increases risk of injury. Because the median age of group A horses in our study was 17 years and 11 of 12 horses became acutely lame while being ridden, single event tendon injury may have been secondary to trauma- or age-related tendon degeneration.

Quarter Horses were overrepresented in group A (9/12 horses); Quarter Horses represent 49% of our hospital population. Because of the small number of group A horses, we cannot make any association between breed or sex and incidence of this injury; however, most of the horses (13/22; 60%) in group B were Thoroughbreds, which only make up 10% of our hospital population.

The diagnosis of an acute tendon injury is made on the basis of clinical signs of heat, pain, and swelling of the tendon and peritendinous tissues. Lameness is usually mild and transient.¹⁵ Diagnostic anesthesia is often not necessary but may assist the clinician in localization of the tendon injury if clinical signs are subtle or absent. Diagnostic anesthesia was performed in 11 group A horses because clinical signs alone failed to localize the source of lameness in the affected forelimb. This is uncommon for most horses sustaining a SDFT injury, especially when the lesion is located in the midmetacarpal region of the forelimb because clinical signs of tendon swelling and pain upon palpation are usually evident and diagnostic anesthesia is often not required.^2,4 The absence of overt clinical signs of SDFT injury in group A horses made the diagnosis difficult and necessitated diagnostic peripheral anesthesia.

Group A horses had a prolonged lameness, and 10 of the 12 horses never became sound. This may be at least partially the result of the location of injury being within the carpal sheath that runs from the lower third of the radius to the upper third of the metacarpus.¹⁶ The carpal sheath becomes narrower distal to the accessory carpal bone. Within the carpal sheath, the medial side of the SDFT is attached to the medial palmar artery and nerve. When the SDFT becomes injured, the horse may have some level of carpal canal syndrome, causing chronic inflammation and pain resulting from compression on the nerve. Because 8 of the 12 group A horses had a positive reaction to carpal flexion, it is likely that the flexion compresses the SDFT and the carpal sheath at this location, causing pain. The persistent lameness may be attributed to compression of the carpal sheath on the SDFT and medial palmar nerve rather than actually the result of tendon injury. With this mechanism of pain, transection of the accessory ligament of the SDFT and carpal fasciotomy would be expected to benefit these horses, as has been suggested, although in the only horse in this study that underwent these procedures, there was no improvement.⁴ In only 2 of 12 group A horses, the lameness improved following desensitization of the lateral palmar nerve. Anesthesia of the lateral palmar nerve was performed near the origin of the suspensory ligament, distal to the accessory carpal bone. If this nerve block had been performed as described by Castro et al,¹⁷ the lameness may have resolved as the result of more proximal placement of the anesthetic. The ulnar nerve block was proximal to all lesions, leading to a successful resolution of the lameness. Desensitizing the ulnar nerve does not explain why the horses became sound if the pain was caused by compression on the medial palmar nerve because desensitization of the ulnar nerve would not have an effect on the medial palmar nerve. This could, however, explain why the desmotomy and carpal fasciotomy were ineffective in the horse in which they were performed in our study.

Most SDFT injuries occur in the forelimbs with the exception of Standardbred racehorses, which tend to be injured in the hind limb at the level of the tibiotarsal joint.⁴ Initial injuries (group A and group B horses) in this study were unilateral; however, 2 group A horses later sustained injuries of the proximal portion of the SDFT on the opposite forelimb (1 horse 2 years later and the other 3 years later). With SDFT injuries in the midmetacarpal region, it is common to have subclinical damage in the tendon of the opposite limb, even though lameness and clinical signs are apparent in only 1 limb.¹⁵ The horse with intermittent lameness at time of admission may have sustained a previous acute injury that was undetected by the owner. This horse was used for trail riding but was not used routinely and was kept in a large pasture.

The SDFT and deep digital flexor tendon both flex the equine foot; however, they have different mechanical roles in locomotion. The SDFT is loaded early in the stance phase and acts as an elastic energy supply that undergoes high stress and strain during high-speed locomotion. The deep digital flexor tendon is loaded later and under less strain and thus has less energy storage.¹⁸ It has been suggested that the midmetacarpal area of the SDFT is weak because it has a smaller CSA and poorer blood supply, compared with other regions of the limb.¹ However, Birch et al¹ demonstrated that although the CSA was smaller in the midmetacarpal region of the SDFT, it was not significantly weaker than other regions. The CSA decreases from the proximal part of the tendon to the midmetacarpal region, then increases in the distal region of the SDFT. On the basis of the amount of collagen present, Birch et al¹ concluded that the metacarpophalangeal and phalangeal regions of the SDFT were the strongest part of the tendon. Findings of our study may lend support to the fact that the proximal aspect of the SDFT is weaker than other distal regions of the tendon and that this weakness may increase with age.

It is important when evaluating the proximal region of the SDFT by use of ultrasonography to remember that there are muscle fibers present; therefore, the tendon normally appears more echogenic, compared with the more distal portion of the SDFT. To help identify lesions versus normal anatomic structures, all group A horses had both the affected forelimb and unaffected forelimb examined via ultrasonography. The CSA of the tendon involved in the MIZ was 50% to 100% in most horses in our study, which indicates that most of the tendon was involved. An increase in tendon CSA is reportedly the most sensitive indicator of fiber damage,² which would be considered severe in horses in our study. By performing desmotomy of the accessory ligament of the SDFT and a carpal retinacular release and fasciotomy, the SDFT may be able to glide easier through the sheath.⁴ Without the effusion and lack of ultrasonographic evidence of carpal tenosynovitis, the surgical procedure may have questionable results. The 2 horses in this study with carpal sheath effusion had acute lameness when examined (< 1 week of lameness), but neither had signs of resentment to carpal flexion.

In this study, only 2 of 12 group A horses were able to return to their previous use, which was trail riding or roping. In comparison, 10 of 22 group B horses returned to previous use, which was primarily flat racing or English performance (dressage and jumping). The return to function for group B horses was even greater when the racehorse population was removed from group B (ie, after the removal of racehorses, 8/11 group B horses returned to full function). By removing the racehorse population from group B, the lesion, not the use of the horse, is able to be more critically compared with group A. The poor prognosis for successful return to athletic performance for SDFT lesions of zone 0 may be the result of the location and severity of the lesion or secondary to the advanced age of horses in our study. The reported⁴ success of desmotomy of the accessory ligament of the SDFT and carpal fasciotomy as treatment for horses with injury to the proximal portion of the SDFT should not be discounted on the basis of the horse in this study that did not respond to the procedure.

In conclusion, injuries of the proximal portion of the SDFT are a cause of prolonged lameness in older horses. Prognosis for return to function is guarded to poor. Further investigation into the surgical treatment options may prove to be beneficial for these horses.