TENDON AND LIGAMENT INJURIES: PART I
0749-0739/94 $0.00 + .20
TREATMENT OF SUPERFICIAL DIGITAL FLEXOR TENDINITIS Rick Henninger, DVM, MS
Exercise-induced tendinitis is an extremely frustrating disorder to treat because, despite treatment, tendon repair is prolonged in horses, and the composition, structure, and function of the mature repair tissue may never equal that of a normal, uninjured tendon. 32• 55 Even though the tendon eventually heals, the potential for reinjury and, often, loss of function, remains. There is no uniformly successful method for the treat ment of tendinitis and, consequently, a wide variety of treatments are being used to alter the suboptimal repair process and enhance the rate and quality of repair after an acute injury. The goals of therapy for acute tendinitis are to decrease inflamma . tion, minimize scar tissue formation, and promote restoration of normal · tendon structure and function. Knowledge of normal tendon anatomy and physiology, as well as an understanding of the mechanisms of injury and repair, are essential if these goals are to be achieved. This knowledge also allows the clinician to make rational decisions regarding the use of various drugs and treatment modalities presently advocated for the treatment of tendinitis. Because the severity of inflammation and pain does not always correlate with the extent of the injury to the intratendinous structures, treatment and prognosis for tendinitis are based most rationally on ultra sonographic evaluation of the tendon. This is especially true when eval uating a subacute tendon injury in which the acute inflammation has resolved but a tendon defect is still present. Acute tendinitis may be considered diffuse in nature, characterized by collagen fiber damage and inflammation without complete disruption of fibers, or described as tenFrom the Penn Paddock Equine Center, Annville, Pennsylvania VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 10 • NUMBER 2 • AUGUST 1994
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dinitis accompanied by core lesions. These differences in the ultrasono graphic appearance of the tendon often dictate the type and duration of treatment prescribed. The prognosis for future athletic performance also has been based on the ultrasonographic characteristics of core lesions.30• Structural lesions that involve a large portion of the cross-sectional area and length of the tendon often carry a poor prognosis for future athletic use regardless of the treatment used. Subsequent sequential sonograms allow monitoring of the healing process and guide the rehabilitation process. The duration of the injury, history of a previous injury, treat ments used, and the proposed use of the horse also are important consid erations in the initial evaluation and formulation of a treatment plan. 59
MEDICAL THERAPY DURING THE INFLAMMATORY STAGE OF HEALING
The initial therapy for acute tendinitis often is the same regardless of the type or severity of the injury and is directed at reducing the inflammation and edema. Although the inflammatory response is an important part of the repair process, attempts to reduce its magnitude decrease the deleterious effects of inflammation on the surrounding col lagen fibers and matrix. The reduction of acute inflammation is ac complished most effectively with a combination of local and systemic anti-inflammatory treatments. Cold-water hydrotherapy and ice help de crease fluid, protein, and inflammatory mediator loss from injured ves sels, which limits hematoma formation and reduces swelling. Cold ther apy should be performed for 20 to 30 minutes, several times a day, until the acute inflammation resolves. Short periods of cold therapy have been shown to have a sustained cooling effect.71 Prolonged application of cold should be avoided because it may result in reflex vasodilation. Bandag ing the lower limb with firm and even pressure also helps increase interstitial fluid pressure and counteract the Starling forces that promote fluid loss from the vessels. The persistence of hemorrhage and edema within the area of injury causes separation of surrounding collagen fiber bundles, prolongs the early phases of healing, and promotes the deposi tion of scar tissue. Various topical medications have been applied to tendons during the early stages of tendinitis. Dimethyl sulfoxide (DMSO) seems to have potential benefits in treatment for an acutely injured tendon. The phar macologic properties of DMSO are not completely known, but its solvent properties and ability to penetrate cellular membranes seem to be impor tant therapeutically. The anti-inflammatory properties of DMSO largely are the result of its ability to scavenge free radicals, produced by inflam matory cells and ischemic tissues, that may cause damage to surrounding uninjured structures.1• 11 The vasodilatory properties of DMSO also may be of benefit in ischemic conditions. Although DMSO is considered to be of low toxicity, one study in rats demonstrated that topical DMSO appli-
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cation decreased the tensile strength of normal tail tendons, with a max imum decrease in strength of 20% after 7 days of use.1 Antiphlogistic poultices also have been used successfully to limit edema and inflam mation. Systemic administration of nonsteroidal anti-inflammatory medica tions (NSAIDs) helps combat the formation of prostaglandins and throm boxane from injured tissues. Phenylbutazone (4.4 mg/kg twice a day) seems to be the most popular anti-inflammatory for initial therapy and does not appear to affect the repair process adversely. Various other NSAIDs also have been found to be of benefit. These medications should be used only for as long as is needed to control inflammation and not to alleviate lameness because the prolonged use of these drugs has the potential to induce gastrointestinal ulceration and renal injury. Corticosteroids are the most potent anti-inflammatory drugs avail able and have been used both locally and systemically to decrease in flammation, edema, and adhesion formation. Although these properties of corticosteroids are of potential benefit in acute tendinitis, several stud ies have shown steroids to be detrimental to tendon repair. Corticoste roids inhibit fibroplasia as well as collagen and glycosaminoglycan syn thesis, both of which are important to the repair process.8 Injection of corticosteroids into normal tendons has been shown to cause collagen fiber necrosis, fibrocyte death, and dystrophic calcification that results in a decrease in tendon strength for up to 1 year after injection.5• 3 • 5 • 2 Long-acting steroids seemingly would prolong these deleterious effects. Although the initial use of corticosteroids may be of benefit, prolonged use probably should be avoided because of the adverse effects on the tendon repair process as well as surrounding normal collagen. Race plates or shoes with grabs should be removed and the hoof should be trimmed and balanced to reduce any abnormal forces on the limb. An excessively long toe or high heel should be corrected to decrease tendon stress. Raising the heel was advocated to decrease stress on the superfi cial flexor tendon, but this theory has been refuted.12• 6
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MEDICAL THERAPY DURING THE REPAIR STAGE OF HEALING
Hyaluronate has a structural as well as a regulatory role in connec tive tissues. Hyaluronate has been shown to have an effect on the prolif eration, migration, and differentiation of cells during wound repair.2• · 31· 62• 68 During the first 5 to 7 days of healing, high-molecular-weight hya luronate appears in high concentrations within the wound. The increased levels are associated with the processes of proliferation and migration of undifferentiated mesenchymal cells into the area of injury. It is thought that hyaluronate hydrates the extracellular matrix, which promotes cel lular migration. Additional evidence indicates that hyaluronate may have a direct stimulatory effect on migrating repair cells.31• 42• 9 Following the initial increase in concentration and molecular weight, hyaluronate is 7
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degraded by hyaluronidase into low-molecular-weight disaccharides. This process seems to promote differentiation of mesenchymal cells into collagen-producing fibroblasts and to stimulate angiogenesis.22, 3 s, 74 Ex perimental studies have demonstrated that the addition of high-molecu lar-weight hyaluronic acid to a wound results in more rapid healing, a decrease in fibrosis, and enhancement of repair tissue maturation.3, 34, 61, 75 Several studies have revealed that fetal tissues, which heal without a scar, have higher wound concentrations of hyaluronate than do adult tissues.39, 4o, 63 Hyaluronate has been used in the treatment of tendinitis in horses to enhance repair and prevent adhesions. In a collagenase-induced ten dinitis model, peritendinous hyaluronic acid resulted in greater improve ment in tendon lesion grade compared with untreated tendons. 65 Instil lation of hyaluronic acid within the tendon sheath surrounding a collagenase-injured tendon improved the histologic appearance and mat uration of the repair tissue at 8 weeks after injury compared with con trols.28 Although hyaluronic acid has been advocated to decrease adhe sion formation and improve gliding function in flexor tendon injuries in people, the importance of gliding function in the unsheathed portion of the superficial digital flexor tendon in horses is unknown and adhesions potentially serve as a source of additional blood supply to the relatively avascular central core of the tendon. It also is hard to explain how the peritendinous injection of hyaluronic acid has an effect on the intraten dinous repair process. A more recent study casts doubts on the benefit of peritendinous hyaluronic acid as a treatment for tendinitis involving the unsheathed portion of the tendon. Hyaluronic acid did not improve the ultrasonographic characteristics, histologic appearance, or biome chanical properties of the repair tissue when compared with controls in this collagenase-induced tendinitis model.23 Based on existing evidence, it appears that hyaluronic acid may be of benefit in the reduction of adhesions involving the tendon sheath but further investigation of its effects on the repair process following injury is warranted. Commercially available polysulfated glycosaminoglycans have been used in the treatment of tendinitis. These products have been shown to inhibit lysosomal enzymes and curtail the inflammatory process.77 There also is evidence to show that the glycosaminoglycan composition of the extracellular matrix changes during tendon repair and may be important in collagen regulation.2, 16' 26' 42' 68 As such, there may be a place for these products in treating tendon injury, but their clinical efficacy remains to be proved. Clinical evaluation of a small number of performance horses with injuries to the superficial digital flexor tendon indicated that treat ment with polysulfated glycosaminoglycans was more successful in al lowing horses to return to work than conservative or laser therapy, but fewer than 50% of the horses were able to race and there was a higher injury recurrence rate with polysulfated glycosaminoglycans.41 Heparin potentiates the anticoagulant activity of antithrombin III and has been used successfully to decrease abdominal adhesion forma tion in horses; it also has enjoyed anecdotal success in the treatment of tendinitis. Heparin also plays a regulatory role in angiogenesis and,
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although it has been shown to stimulate endothelial cell proliferation under certain conditions, other studies indicate that heparin actually inhibits angiogenesis.13' is, 24 No studies indicate that heparin has a bene ficial effect in treating acute tendinitis. The distinguishing characteristic of the tendon repair process follow ing injury is the formation and deposition of collagen. Collagen fibrils are deposited initially in random fashion and, as maturation proceeds, subsequently are organized into a more normal longitudinal alignment.49 The initial crosslinking of collagen is essential for the stabilization of the newly synthesized collagen. These crosslinks are termed reducible be cause they are soluble and easily denatured by heat. As collagen matures, the reducible links are converted to stable crosslinks that impart the tensile strength and other mechanical properties characteristic of mature repair tissue.76 The enzyme lysyl oxidase is required for the normal formation of reducible crosslinks. 13-Aminoproprionitrile (BAPN) is a lathyrogen that acts by irreversibly binding to lysyl oxidase which, in turn, inhibits the covalent crosslinking of connective tissue proteins, elas tin, and collagen.49 BAPN has been shown to decrease scar tissue forma tion and has been used in the prevention and treatment of wound con tracture, fibrotic diseases, and adhesions in people.53• 54• 64 Systemic administration has resulted in toxicity in people but local administration has not. A recent clinical study in horses with tendinitis indicates that intrale sional injection of BAPN results in more rapid improvement in the ultra sonographic appearance of an injured tendon than other methods of therapy.29 In this study, affected tendons were injected every other day for 10 days and ultrasonographically evaluated during a 19-week period. The sonograms were evaluated by assigning a severity rating to the tendon lesions, which consisted of a quantitative assessment of lesion grade and size. At all time periods, the BAPN-treated tendons had a greater reduction in severity score than tendons treated by various other methods. It is hypothesized that BAPN treatment diminishes the number of immature collagen crosslinks in the repair tissue, which promotes a more rapid longitudinal organization of the collagen fibers within the tendon. Although this treatment presents a unique and interesting ap proach to the management of equine tendon injuries, several issues need to be addressed to establish its long-term efficacy. Following the initial period of rapid collagen deposition in wound healing there arises a balance between collagen deposition and enzymatic degradation that is essential for the functional maturation of repair tissue.49 The early BAPN induced reduction in collagen crosslinking seemingly would render wound collagen more susceptible to enzymatic degradation and poten tially favor the removal of collagen. A reduction in collagen content in the wound certainly would decrease the rate of gain of strength of the repair tissue and possibly slow the overall healing process. Stable cross link formation depends on the prior formation of reducible crosslinks.48 The effect that BAPN may have on the formation of stable crosslinks and on the strength of the healed tendon therefore obviously is an important issue, especially in performance horses. The wound recovery period after
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withdrawal of BAPN therapy should be investigated. Other considera tions relate to an effective dose and method of delivery of BAPN to the injury site and its effects, if any, on collagen type in the wound. The reduction of scar tissue formation in an injured tendon is a worthy goal, but ideally should be accomplished without prolonging the healing process or adversely affecting the ultimate mechanical properties of the healed tendon. Clinical studies evaluating return to performance and reinjury rate would help establish the efficacy of BAPN therapy. THERAPEUTIC LASERS
Low-level laser therapy-also called soft or cold laser therapy-has been used in the treatment of various soft tissue and skeletal disorders in the horse.58 This treatment modality uses light emissions in a specific energy range to induce certain biologic effects in tissues. The beam of coherent light penetrates tissues and directly stimulates cellular metabo lism and the release of pharmacologically active substances from various cells that, in turn, indirectly enhance the inflammatory and repair phases of the healing process. The full extent of low-level lasers' therapeutic effects are not known but are believed to include enhancement of protein synthesis, augmentation of blood flow, promotion of lymphatic regener ation, and pain relief.19• 58 Other proposed beneficial effects include the enhancement of cellular phagocytic activity, fibroblast proliferation, and collagen production.27 The extent of these biologic effects depends on the characteristics of the laser light (frequency, wavelength, and energy), tissue type, and the duration and frequency of application. The most popular clinical use of the therapeutic laser is the treat ment of superficial wounds. Experimental studies conducted in labora tory animals indicate that laser stimulation of wounds results in a more rapid healing process. Histologic and biochemical evaluations point to ward more rapid fibroblast proliferation and enhanced collagen synthe sis as the reasons for more rapid repair.21• 44 Although clinical experience indicates that laser therapy is of benefit in wound healing in horses, experimental studies have not substantiated these claims. Kaneps et al35 found no benefit from laser irradiation of skin and tendon wounds in horses. These apparent contradictory results may be related to the differ ences in wound healing between horses and other species and to the various treatment parameters used in the different studies. Laser therapy for superficial digital flexor tendinitis resulted in a 50% return to training, 30% return to racing, and 20% injury recurrence rate in a group of National Hunt racehorses.41 Although the differences were not statistically significant, these results were not as favorable as those in a group of horses treated conservatively. Another clinical study found that 66% of Standardbred racehorses were able to return to racing following laser treatment of tendinitis.43 Unfortunately, neither of these studies controlled for severity or duration of injury which, obviously, will affect outcome and recurrence rate, regardless of the treatment used.
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Many factors must be considered to use lasers in the treatment of tendinitis rationally. The effectiveness of this treatment will remain spec ulative until the biologic effects of lasers on tissues are better understood and the many therapeutic issues are resolved. THERAPEUTIC ULTRASONOGRAPHV Therapeutic ultrasonography has been used for many years in treat ing a wide variety of soft tissue injuries in people and, to a lesser extent, in animals. 52 Although there is substantial clinical support for the efficacy of this treatment modality, few experimental studies have investigated its use. The specific biologic effects of ultrasound waves on tissues have not been fully elucidated. Soundwave energy produced by an ultrasound unit is absorbed readily by soft tissue and is transformed mainly into thermal energy.14 Nonthermal effects such as acoustical streaming and cavitation also are thought to occur in isonated tissues. 18 The variety of biologic effects produced and their extent depend on the frequency, intensity, and mode of the wave produced by the unit. Alterations in blood flow, protein metabolism, collagen extensibility, and membrane permeability have been observed when tissues are exposed to ultrasound waves in the therapeutic range. 14• 17• 46 Other evidence suggests that therapeutic ultra sonography facilitates fibroplasia and collagen production. 33 Improved healing of surgical wounds, pressure sores, and other types of soft tissue injuries have been reported in people. 18• 52 Scar tissue reduction has been observed clinically in people with traumatic wounds and contracture. 52 Exposure to low-intensity ultrasound induced an increase in tensile strength in tenotomized rabbit tendons within 10 days of the initiation of treatment.20• 21 This indicated that ultrasound may hasten the healing process when applied early in the course of the injury, but the increase in strength may have been related only to an increase in tendon size because there was no difference in tensile stress and strain among ten dons. In contrast, others have not demonstrated any benefit with the use of low-intensity ultrasound in tendon repair.60• 70 High-intensity ultra sonographic therapy seems to have the potential to retard healing by causing blood flow stasis, endothelial damage, and decreases in collagen synthesis.17• 70 The contradictory results reported in the various studies easily could be explained by the differences in timing and duration of treatment as well as differences in the soundwave parameters used. One study in horses45 did find improved healing in surgically split tendons that underwent ultrasonographic therapy compared with tendons not treated with therapeutic ultrasound. Therapeutic ultrasonography appears to have the potential to en hance healing of soft tissue injuries, but many questions remain regard ing the treatment parameters that would be most beneficial, and the potential for thermal damage exists. It would seem that the most benefit would come from its use during the repair stages of healing because
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earlier treatment would contribute to the inflammatory process and worsen edema and hematoma formation, although some studies contra dict that theory. ELECTROMAGNETIC THERAPY
Evidence is increasing that the application of electrical energy can influence the piezoelectric potential of tissues as well as enhance cellular metabolism. Early electrical stimulation used implantable devices and direct current, whereas transcutaneous pulsating electromagnetic stimu lation is more popular today. It has been proposed that electricity me diates its effects through induction of changes in the cellular environ ment, which influences cellular function and differentiation.4 The biologic effects attributed to electrical stimulation include pain reduction, increased circulation, dissipation of edema, and enhancement of cellular migration.4• 57 These effects vary depending on the properties of the cur rent, treatment protocol, and tissue type involved. Most interest in electrical stimulation has been in the area of fracture nonunion, but benefits have been found in the healing of soft tissues as well. 8 Experimental studies show that a variety of cells and tissues are capable of response to electrical stimulation. Direct current stimulation of tendon in vitro induced increases in praline and hydroxyproline levels compared with nonstimulated controls, indicating enhancement of cel lular activity and collagen synthesis.68 Low-level direct current also has been shown to promote longitudinal cellular, fibrin, and collagen orientation. 6• Electromagnetic stimulation increased histologic maturity, tensile strength, and collagen content in cut and repaired collateral liga ments in rabbits. 25 Greater breaking strengths were found in tenotomized rat tendons that underwent pulsed galvanic current therapy. 51 Studies relating to electrical stimulation of equine soft tissues are limited. Low-level direct-current stimulation did not improve the histo logic appearance of experimentally-created equine skin wounds.66 Wat kins et aF found that daily electromagnetic therapy did increase the vascularity of surgically created superficial digital flexor tendon defects but repair tissue maturation and collagen type transformation actually were delayed by the treatment in samples collected at 8 and 12 weeks after surgery. One study using direct current5° also found no therapeutic benefits on tendon healing. Many of the proposed physiologic effects of electrical stimulation on tissues would seem to be of benefit to tendon repair but evidence is insufficient to support its use in tendon injuries. Further investigation into the type of stimulation used and the timing of therapy in relation to the onset of injury may reveal a place for its use in the treatment of tendinitis in horses. 37
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SURGICAL TREATMENT OF TENDINITIS
The superficial digital flexor tendon inserts on the palmer aspect of the second phalanx and is joined to the distal medial aspect of the radius
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through the superior check ligament. This bone-tendon-bone segment sustains the majority of the load that the entire musculotendinous unit experiences. Bramlage9 proposed that transection of the superior check ligament will allow the superficial digital flexor muscle belly to assume a greater portion of the load and create a more extensible musculotendi nous unit, which would serve to protect the repaired superficial digital flexor tendon. In a retrospective study on the use of a superior check ligament desmotomy in the treatment of tendinitis in 62 Thoroughbred racehorses, Bramlage found that 92% of the horses were able to train and race after surgery and 66% started at least five races after the surgery. Forty-seven percent of the horses that raced maintained or increased their average earnings per start and 86% maintained their race class. 10 Only 19% reinjured the tendon, which appears to be significant consid ering that the majority of the horses in this study were experiencing at least their second episode of tendinitis at the time of the surgery. These results compare favorably with results from conservative management of tendinitis published by Reef et al,59" who found that approximately 50% of the horses were able to return to their previous type of competi tion but most competed in a lower class or were not performing as well in the same class. It appears from these data that a superior check liga ment desmotomy increases a horse's chances of returning to its previous level of competition and decreases the incidence of reinjury compared with other methods of therapy. A superior check ligament desmotomy is performed under general anesthesia and complete transection of the ligament appears to be essen tial for optimal results. The check ligament's function is re-established to some extent because it heals with fibrous tissue over time, but complete division of the ligament most likely will allow maximal lengthening and greater involvement of the muscle in the musculotendinous unit's func tioning. Typical aftercare consists of 2 to 3 weeks of stall rest, 6 weeks of hand walking, and 8 weeks of light jogging or pasture exercise. The tendon is re-evaluated ultrasonographically at the end of 4 months. The horse then is allowed to begin training if the lesions have improved in echogenicity to at least a grade 2 and the fiber pattern shows evidence of longitudinal organization. Training should progress slowly and the ten don should be closely evaluated for evidence of inflammation because each subsequent injury results in further tendon fibrosis. Tendon splitting originally was used to promote vascularization of the tendon in cases of chronic tendinitis. 3a Although the procedure ap peared to be of clinical benefit, controlled experimental studies estab lished that tendon splitting was detrimental to the tendon during the later phases of the repair process. 63a With the advent of ultrasonographic evaluation of tendons, it was recognized that many cases of acute tendi nitis were accompanied by core lesions and that the lesions often per sisted for several months. It was theorized that tendon splitting during the early phases of tendinitis would decrease the size of the core lesions and promote more rapid revascularization and subsequent repair of the injured area of the tendon. Creation of vascular access channels in the meniscus enhanced re-
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generation following partial meniscectomy in dogs. It was believed that the channels improved healing by allowing repair cells and vessels to penetrate the injured tissue more easily. 34c A clinical study34b demon strated that the surgical splitting of acutely to subacutely injured tendons that contained core lesions led to a significant reduction in lesion size, tendon diameter, and lesion grade within 8 to 12 days after surgery. Long-term follow-up in many of these cases revealed that this early reduction in lesion area was followed by an ultimate decrease in tendon diameter and, therefore, most likely a reduction in fibrous tissue deposi tion. A recent ultrasonographic and clinical study2a found a similar re duction in lesion size of 44% and mean decrease in lesion grade of 0.9 by day 10 following ultrasonographically guided tendon splitting. Eighty one percent of the horses were able to return to performance and 68% competed at the same level following surgery. These results are impres sive considering that the tendinitis was accompanied by grade 3 or 4 lesions that involved up to 80% of the cross-sectional area of the tendon. These clinical findings were substantiated by a controlled experimental study using a collagenase-induced tendinitis model.34a In addition to the significant improvement in the ultrasonographic characteristics of lesions in tendons that underwent splitting, there was an earlier revasculariza tion of the lesions and superior-quality repair tissue at 4 and 8 weeks after surgery. It is hypothesized that splitting creates a communication between the tendon core and the surrounding peritendinous tissues that promotes more rapid resolution of inflammatory edema and expedites revascular ization and collagen production within the area of injury. It would ap pear that tendon splitting during the early phases of tendinitis has bene ficial effects on the early repair process, but its effects on the mechanical properties of the mature collagenous repair tissue remain to be deter mined. COUNTERIRRITATION
The primary purpose of counterirritation is to transform a chronic condition into an acute form by inducing inflammation in the tissues. This is believed to promote increased blood supply and increase inflam matory cell influx to an area in order to expedite the healing process. Counterirritation, mainly in the form of thermocautery (pin-firing) and blistering, has been used most commonly in the treatment of injuries that are slow to heal and have a propensity to reoccur, such as tendinitis and bucked shins. Counterirritation as therapy for tendinitis potentially would increase blood flow, but the inflammation created would only serve to increase fibrous tissue deposition in and around the tendon. The additional scar tissue may give strength to the tendon by increasing its functional cross-sectional area but would adversely affect the vital vis coelastic properties of the tendon, which ultimately would decrease func tion. Silver et al63a found that pin-firing during the chronic stages of
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tendinitis prolongs healing of the tendon and results in further damage to the tendon. There therefore appears to be no place for counterirritation in the treatment of tendinitis, especially if athletic function is a goal of treatment. THERAPY DURING THE MATURATION STAGE OF HEALING
Ultrasonographic evaluation of the healing process and controlled rehabilitation of the injured tendon are important considerations in the management of tendinitis regardless of the initial treatment used. Each horse's exercise program should be adjusted individually in accordance with periodic clinical and ultrasonographic assessment. Walking and mild exercise are helpful in promoting blood and lymph flow to the lower limb and usually are begun several weeks after the inflammation has resolved. A gradual increase in stress on the tendon promotes matu ration and longitudinal organization of the collagen fibers, but the stress should be kept below the yield strength of the repair tissue to prevent reinjury. Fibrous repair tissue reportably reaches 50% of its ultimate strength by approximately 2 months, which indicates that strenuous exercise should not be allowed during that period. Pasture exercise may be allowed at that point, but controlled exercise in the form of jogging is a better alternative. The tendon is evaluated ultrasonographically be tween 3 to 4 months, and a gradual return to training is allowed if satisfactory healing has occurred. The hooves should be trimmed regu larly to maintain a normal axis and hoof balance and work should be avoided when surface conditions are poor. Exercise should be curtailed or restricted if inflammation or swelling of the tendon arises. A more prolonged recovery period should be considered if recurrent inflamma tion or ultrasonographic evidence of reinjury arises. Support bandaging of the lower limbs is a common practice in performance horses. They aid in protecting the limb against trauma and are believed to augment the soft tissue support structures of the lower limb. The angle of the fetlock angle decreases (hyperextension or dorsi flexion) during the support phase of the stride. This results in extension of the superficial flexor tendon and an increase in tendon strain. The magnitude of these changes depends on several factors such as the gait and velocity, but the strains approach and often may exceed the elastic limit of the tendon in performance horses. 67 It therefore is apparent that any method of bandaging that supports the fetlock and decreases the magnitude of hyperextension during exercise would serve to protect a normal or injured tendon by decreasing the strain experienced by the tendon. Kobluk et al37b reported that lower limb bandaging resulted in a reduction in fetlock hyperextension during exercise, although there was some variation among horses. A more recent study37a used three different types of elastic bandages in an attempt to aid in the support the lower limb. They found no difference in suspensory ligament strain, between
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bandaged and unbandaged limbs, while the horses were standing or walking. This signified that, under the conditions of the study, bandag ing alone did not appear to support the fetlock. The bandages in this study were not applied as heavily as those used by Kobluk et al, and it is possible that a bandage stretches sufficiently to support the fetlock and thereby limit tendon strain only during exercise. It appears that support bandaging may be of benefit in protecting both the normal tendon against damage and the healed tendon against reinjury. Certainly, the type and bulk of the bandage as well as the technique of application play important roles in the degree of protection afforded by bandaging. It also is possible that a bandage substantial enough to reduce tendon strain during exercise would adversely affect the horse's gait and performance. FUTURE DIRECTIONS
There is no doubt that additional clinical and experimental investi gation is needed in the areas of tendon injury and repair if full athletic function is going to be restored following a stress-induced injury. Further study of tendons' response to exercise and the mechanisms of injury ideally would help reduce the incidence of tendinitis. Improved training methods and track surfaces also would contribute to this goal. Unfortu nately, these injuries are going to occur even under the most optimal conditions, and better methods of therapy therefore are needed. Tech niques to enhance revascularization of central lesions seemingly would provide a more suitable environment in which repair would be opti mized. Because mechanically inferior scar tissue formation is the inevi table consequence of tendon repair, new means to modulate this process should be pursued. The use of BAPN or similar drugs may provide insight into the problems of promoting functional maturation of the collagen repair tissue. Finally, new and improved methods of monitoring intratendinous repair would allow better direction of rehabilitation and provide a more accurate indication of when a horse can return to work. References 1. Albrechtsen SJ, Harvey JS: Dimethyl sulfoxide: Biomechanical effects on tendons. Am J Sports Med 10:177-179, 1982 2. Alexander SA, Donoff RB: The glycosaminoglycans of open wounds. J Surg Res 29:422429, 1980 2a. Allen AK: Experience with ultrasound-guided tendon puncture or splitting. In Pro ceedings of the 38th Annual Meeting of the American Association of Equine Practition ers, Orlando, FL, 1992, pp. 273-277 3. Amie! D, Ishizue K, Billings E: Hyaluronan in flexor tendon repair. J Hand Surg 14A:837-843, 1989 3a. Asheim A: Surgical treatment of tendon injuries in the horse. J Am Vet Med Assoc 145(5):447-451, 1964 4. Auer JA, Burch GE, Hall P: Review of pulsing electromagnetic field therapy and its possible application in horses. Equine Vet J 15:354-360, 1983
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