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Superficial Digital Flexor Tendon Injury
Superficial Digital Flexor Tendon Injury
C H A P T E R
190
TARALYN M. McCARREL
T
he superficial digital flexor tendon (SDFT) is at great risk for injury in the horse, and it is therefore not surprising that clinically relevant disease involving this structure is common in both racehorse and sport horse populations. Reasons for increased susceptibility to injury and sepsis are numerous and include the tendon’s superficial location, close association with synovial structures susceptible to penetrating injury, and inferior reparative response, plus the fact that the SDFT functions at its biomechanical limit in high-level performance horses. The following chapter will introduce the reader to the diagnosis and management of several different types of injury involving the SDFT and associated structures.
ANATOMY AND FUNCTION
The superficial digital flexor originates from the proximal aspect of the caudal surface of the humerus and inserts on the first and second phalanges. In addition, the accessory ligament of the SDFT (ALSDFT) originates at the level of the musculotendinous junction and has a fanlike insertion on the distal radius in close association with the carpal canal. The hind limb superficial digital flexor originates from the proximal aspect of the caudal surface of the femur and inserts on the phalanges, similar to the arrangement in the forelimb. The hind limb SDFT overlies the calcaneus, where it sends off medial and lateral attachments to this structure. The calcaneal bursa provides a gliding surface between the SDFT and the calcaneal tuber. The forelimb and hind limb SDFT are enveloped by the digital flexor tendon sheath (DFTS) from the distal half of the cannon bone to the pastern (Figure 190-1). The manica flexoria (MF) is an extension of the SDFT that encircles the deep digital flexor tendon (DDFT) within the DFTS. The superficial digital flexor muscle is composed of very little muscular tissue and thus has minimal role in flexion of the distal limb. Instead, the SDFT’s primary functions are stabilization and energy storage. Along with the suspensory ligament, the SDFT has a major role in supporting the fetlock joint. Furthermore, the muscle fibers are able to adapt to small vibrations that develop during locomotion, yielding a degree of shock absorption. Finally, the SDFT stores elastic energy when it is stretched during the stance phase of locomotion, and release of this energy allows the horse to propel its large mass with great efficiency.
TENDON REPAIR
Normal tendon is composed primarily of type I collagen arranged linearly in a hierarchical structure. Tenocytes, specialized tendon cells, produce the extracellular matrix, including collagen and noncollagenous molecules that assist in collagen fiber alignment. Blood supply is greatest at the periphery of the tendon, with relatively little vasculature supplying the tendon core.
Tendon repair proceeds through the classic stages of wound healing: inflammation, repair, and remodeling. The inflammatory phase begins at the onset of injury and lasts from a few days to weeks, depending on severity of the injury and antiinflammatory therapy instituted. The release of proteolytic enzymes results in expansion of the lesion, both in length and cross-sectional area, for several days. The repair phase overlaps with the inflammatory phase and is characterized by increased vascularity, cellularity, and production of disorganized small collagens. The remodeling phase is the longest of the tendon healing phases, lasting as long as 18 months. Remodeling overlaps with the repair phase and is characterized by increasing collagen organization and a greater proportion of collagen I. However, the resulting scar tissue is biomechanically inferior. Overall, the scarred area is stronger than normal tendon, but it is less elastic. The transition area between the inelastic repair tissue and the normal tendon is most susceptible to reinjury. A recent report suggested that the most crucial time for therapeutic intervention in the tendon healing process is the period from 12 to 16 weeks after injury.
TENDINOPATHY
Overstrain injuries of the SDFT are common in racehorses and top-level event horses. Although the clinical signs often manifest acutely, research into the pathophysiology of overstrain injury suggests that chronic degeneration leads to ultimate failure of the tendon. Despite considerable research effort and numerous proposed theories, the definitive cause or causes of SDFT tendinopathy remain elusive. Several risk factors have been identified for Thoroughbred racehorses, including fast work on hard surfaces, increased age at first race start, having a previous SDFT injury, fatigue, and heel elevation.
Diagnosis The horse with acute manifestation of classic midmetacarpal SDFT tendinopathy will have variable lameness, depending on lesion severity, and overt lameness may disappear rapidly. The horse should be observed for local swelling characteristic of a “bowed” tendon (Figure 190-2, A). The palmar structures of the metacarpus should be palpated both during weight bearing and with the limb unloaded. Horses with an active injury often resent palpation of the affected region, which may feel soft compared with normal tendon. More chronic lesions may be nonpainful and firm on palpation. A complete lameness examination is warranted because SDFT tendinopathy is often bilateral or may be a secondary overstrain injury arising secondary to lameness of a different cause in another limb. Diagnostic analgesia may be performed if confounding lameness exists, but information from the history, clinical signs, and ultrasound examination is often sufficient for diagnosis of tendinopathy.
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S
D
∗ L
Figure 190-1 Dissection of the distal part of the forelimb, viewed from the palmar-lateral aspect. The heel bulbs are at the bottom of the image. The superficial digital flexor tendon (S), deep digital flexor tendon (D), suspensory ligament (L) and distal end of the splint bone (*) are labeled for orientation. The end arrows indicate needles placed in the most proximal and distal extent of the normal DFTS. The central arrow points to a common location for centesis and injection of the DFTS, just distal to the base of the proximal sesamoids and palmar to the neurovascular bundle.
Ultrasonography is the primary imaging modality for diagnosis and monitoring of tendon lesions. The palmar or plantar aspect of the distal part of the limb should be clipped, cleaned if necessary, and imaged with a 7.5- to 14-MHz linear probe with a standoff pad. The typical findings of acute tendinopathy include a hypoechoic core lesion with loss of linear fiber pattern, increased cross-sectional area of the tendon, and change in shape of the tendon (Figure 190-2, B). Lesions along the margins of the tendon are also possible. A tendon that is healing appropriately will have an increase in lesion echogenicity, improvement in linear fiber pattern, and decrease in tendon cross-sectional area. The timing of the first ultrasound evaluation and impact of lesion expansion on the ultrasonographic appearance of acute tendon lesions must always be considered. Initially, core lesions may not be evident but will appear several days later. Ultrasound examinations performed within the first week after injury should be repeated in 2 to 4 weeks to allow full assessment of lesion size and severity. Standardbreds may have SDFT tendinopathy as a part of the “curb” complex of plantar hock soft tissue injury. An atypical form of proximal SDFT tendinopathy was recently described. The lesions were detected in older horses performing lower-level work; horses had an acute onset of lameness, with prolonged lameness thereafter. Horses reacted positively to carpal flexion, and lameness was abated following ulnar nerve block. Diagnosis was confirmed by ultrasonography of the SDFT at the level of the carpal canal, and effusion within the carpal sheath was evident. Prognosis for return to previous use was poor.
Treatment The hallmarks of initial treatment for SDFT tendinopathy are aimed at reducing inflammation and limiting lesion expansion. Therapy should be instituted immediately and includes administration of nonsteroidal antiinflammatory drugs, cold
S S
D
L
A
B
D
L
LF SDFT 3A
Figure 190-2 Distal portion of a limb (A) of a horse with superficial digital flexor tendon (SDFT) tendinopathy. Notice the characteristic bowing of the tendon, indicated by the arrow. Transverse (left pane) and longitudinal (right pane) ultrasound images (B) showing a hypoechoic core lesion (arrowhead) in the SDFT. D, Deep digital flexor tendon; L, suspensory ligament; S, superficial digital flexor tendon. (Ultrasound images courtesy Dr. K. Garrett, Rood and Riddle Equine Hospital, Lexington, KY.)
CHAPTER
therapy (with cold hosing or use of a device such as Game Ready1) several times daily for no longer than 30 minutes per treatment, bandaging for support and to minimize swelling, and stall rest. A controlled, gradual return to exercise may be started after 2 weeks of stall rest in most cases. The length of time spent exercising is gradually increased, and each addition of a new gait (i.e., adding small amounts of trotting work in a horse that has been walking for 3 months) is preceded by reevaluation of the tendon with ultrasound. An increase in tendon cross-sectional area of 10% or greater is considered to indicate recurrence, and the exercise program must be adjusted. Numerous adjunct medical and surgical treatments have been investigated, most yielding modest results (see Suggested Readings for full review). The high reinjury rate (up to 56%) following SDFT injury has remained a consistent challenge. Therapeutic ultrasound has little supporting evidence for efficacy to date, with a recent publication reporting only an increase in temperature in treated normal tendon but no investigation of tendon ultrastructure. Growth factor therapy with intralesional injection of insulin-like growth factor-1 in naturally occurring lesions resulted in improved ultrasound characteristics, but no improvement in reinjury rate. Recent advancements are showing promise. Experimental studies have revealed a decrease in lesion expansion following cast application to distal limbs with acute lesions. Because prognosis is associated with lesion severity, applying a cast to limbs with acute SDFT lesions during the first 10 days after injury may result in improved outcome, but this effect has yet to be proven clinically. Intralesional injection of plateletrich plasma (PRP) in an SDFT tendinopathy model resulted in faster maturation and organization of repair tissue. Further, the importance of PRP composition has been emphasized recently with low–white blood cell (WBC) PRP stimulating superior gene expression patterns in normal tendons in vitro, compared with high-WBC PRP. Intralesional injection of bone marrow–derived mesenchymal stem cells into natu rally occurring lesions of flat and National Hunt racehorses resulted in a significant reduction in reinjury rate in National Hunt, but not flat, racehorses. These results are promising, and further research determining the best type of mesen chymal stem cells and PRP, dose, and treatment protocol may result in greater longevity for horses following SDFT tendinopathy. No recent advances in surgical therapy for SDFT tendinopathy have been reported, and surgeons have varying opinions regarding the value of the existing procedures. Surgical options include tendon splitting and desmotomy of the ALSDFT by open or tenoscopic approach. Tendon splitting is restricted to cases with clearly defined core lesions and allows drainage of the hematoma containing numerous proteolytic enzymes and may limit lesion size. Previous reports have indicated an increase in suspensory ligament injury following ALSDFT desmotomy. However, this was disputed in a paper investigating insulin-like growth factor-1 intralesional injection in which ALSDFT desmotomy was also performed.
INTRATHECAL TEARS
Definitive diagnosis of intrathecal tears of the SDFT presents a diagnostic challenge. Increased use of advanced imaging and surgical techniques has led to greater recognition of tears
1
Game Ready. Coolsystems, Inc, Concord, CA.
190 Superficial Digital Flexor Tendon Injury
L
∗
815
D S
B
D
A
C
S
Figure 190-3 The same specimen as depicted in Figure 190-1 with the tendon sheath opened (A). The superficial digital flexor tendon (SDFT) is held by forceps, and the manica flexoria (MF) can be seen ensheathing the deep digital flexor tendon (DDFT). A pair of scissors has been placed between the DDFT and the MF and exits through the proximal reflection of the tendon sheath (black arrow), which is adhered to the proximal aspect of the MF. T2-weighted transverse magnetic resonance images demonstrating a torn manica (B, white arrow) and the normal continuous anatomy ensheathing the DDFT (C, white arrow). Notice the increased high-signal (bright white) synovial fluid in the tendon sheath. The distension highlights the normal mesotenon attachment to the SDFT (B, black arrow). D, DDFT; L, suspensory ligament; S, superficial digital flexor tendon; *, distal end of the splint bone. (Magnetic resonance images courtesy Drs. K. Garrett and S. Hopper, Rood and Riddle Equine Hospital, Lexington, KY.)
within the DFTS. The signalment of affected horses varies among studies, with MF tears reported to be more common in the hind limbs of cobs and ponies, whereas longitudinal SDFT tears accounted for 17% of tears in Warmblood show jumpers; in the latter, the forelimb was affected twice as often as the hind limb, and the MF represented only 4% of tears. Horses are presented with a history of tendon sheath distension and lameness. Nonseptic tenosynovitis may arise for a number of reasons, and determination of chronicity, presence of tendon tears, presence of intrathecal adhesions or masses, and contribution of palmar annular ligament thickening and constriction need to be considered for forming an accurate prognosis. Differentiating between tears of the DDFT and the MF is particularly important because prognosis for return to previous work following treatment of simple MF tears (80%) is twice as good as that for simple DDFT tears (40%). The intrasynovial structures of the DFTS are depicted (Figure 190-3, A). Several diagnostic modalities have been explored, and the tests used may reflect the equipment available and financial constraints of the owner. The accuracy of ultrasound for detection of tendon tears within the DFTS is only 49% to 76%. High synovial fluid cartilage oligomeric matrix protein concentration, compared with that in serum, in mature
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horses is highly indicative of tendon tears but does not identify the affected structure. This test is not clinically available at present but may be a useful screening tool in the future for horses with tenosynovitis that require further diagnostic evaluation and definitive therapy. Contrast radiography may aid in diagnosing MF tears. Ultimately, the most accurate diagnostic tools include magnetic resonance imaging and tenoscopy. Magnetic resonance imaging offers the advantage of enabling evaluation of all the structures within and surrounding the DFTS and permits surgical planning (Figure 190-3, B). However, there is added cost and the potential need for an additional anesthetic episode. Tenoscopy serves as both a diagnostic procedure and definitive therapy. Surgical debridement of tears is performed to remove damaging fibrillated material. At present, excision of the entire MF is recommended for treatment of partial and complete tears. Postoperative care includes bandaging and stall rest until 10 to 14 days after surgery. After this time, an exercise program starting with short bouts of daily hand walking and gradually increasing to full activity is recommended to reduce adhesion formation. Intrathecal injection of hyaluronic acid may also minimize adhesion formation. Prognosis for return to full activity is good in uncomplicated cases.
TENDON LACERATION
Lacerations of the SDFT occur in the forelimb and hind limb secondary to overreaching, kicking injuries, and wire cuts. The nature of the trauma will influence the degree of contamination, contusion, vascular compromise, and quality of tendon structure at the severed ends. The basic principles of first aid and wound care should be followed: keep the horse calm and comfortable, and minimize or eliminate the risk for further injury and contamination. The wound should be gently cleansed of obvious debris. When the SDFT is the only structure transected, there may not be a difference in fetlock angle if the horse stands squarely; however, if the opposite limb is lifted, the fetlock will drop. Transection of additional supporting structures causes obvious hyperextension of the distal part of the limb and significant distress for the horse. If there is any concern about the integrity of any structure, application of a heavy bandage and appropriate splint are warranted, and the horse should be transported to a clean environment for definitive treatment. A standard series of radiographs centered on the injured area is appropriate in determining whether there is bony involvement. Ultrasound examination of the soft tissues should be attempted before digital exploration of the wound, although the finding of air already in the wound may preclude imaging. Ultrasound may be repeated the following day after a period of bandaging. Sedation or regional anesthesia is usually necessary for complete evaluation. The wound should be thoroughly cleansed, a deep swab for bacterial culture performed, and the wound digitally explored. Any synovial structures that may be involved should be distended after collecting synovial fluid for cytology and culture if involvement is confirmed. In cases of confirmed tendon laceration, surgical wound management with the horse under general anesthesia is expected to result in the best possible outcome. When more than 50% of the tendon has been lacerated and the tendon ends are in good condition, the tendon ends are sutured. In cases with substantial trauma to the tendon ends, the tendon is left unsutured. The wound is closed, and the limb is placed in a cast or bandage cast for 6 to 8 weeks. Alternatively, a custom brace can be made that allows easier access to the limb for bandage changes and wound management. The horse is maintained
on stall rest for 2 to 3 months and during this time is transitioned to a bandage and splint, and then to only a heavy bandage as determined by ultrasonographic evidence of healing. Special shoeing may be indicated (see Chapter 189). Exercise is gradually increased, but the recovery process may take up to 1 year. The most common complications include permanent thickening of the injured region and persistent hyperextension of the fetlock. Tendon thickening does not appear to influence outcome. Persistent fetlock hyperextension (>6 months) is associated with complete tendon lacerations and decreased likelihood of return to prior level of performance. The number of lacerated structures is also a major prognostic indicator for future performance. Overall, the prognosis for survival is good (82%), but only 55% of horses will return to their previous level of activity.
SEPTIC TENOSYNOVITIS
Sepsis of the synovial structures associated with the SDFT can result in adhesions to the tendon as well as direct tendon damage resulting in persistent lameness, which may warrant euthanasia. Sepsis of the DFTS is the focus of this section, but the same general principles apply to the calcaneal bursa and carpal canal. Sepsis may develop secondary to penetrating injury, joint injection, or hematogenous spread (particularly in foals). The source of the infection should guide selection of antimicrobials, which should be started before culture and sensitivity results (see Chapter 186). Recognition of the potential involvement of a synovial structure and immediate aggressive therapy is paramount for achieving the best possible outcome. Horses with a closed synovial sheath are often markedly lame, whereas minimal to no lameness may be evident if the sheath is draining. Systemic evidence of sepsis (e.g., fever, complete blood count changes) may or may not be apparent. Diagnostic evaluation should include radiography for bony injuries in cases of laceration or when there is evidence of osteomyelitis in chronic cases or in cases in which infection was of apparent hematogenous origin. Ultrasonography should also be performed to evaluate the soft tissues, quantity and character of the synovial fluid, and presence or absence of fibrin within the sheath. A synovial fluid sample should be obtained (see Figure 190-1) before administration of antimicrobials and submitted for cytologic evaluation, total protein determination, and culture and sensitivity testing. If only a small volume of fluid is present, a broad tourniquet can be wrapped from the level of midmetacarpus to the base of the proximal sesamoids and fluid collected from the distal aspect of the DFTS. Treatment includes lavage of the DFTS and administration of antimicrobials (by one or more of these routes: systemic, intrasynovial, or regional perfusion) and systemic antiinflammatories. Tenoscopy may offer the advantage of more thorough lavage and the ability to remove foreign debris and fibrin. Unless needed in the case of concurrent tendon laceration, cast application is avoided. Hand walking is initiated as soon as possible to minimize adhesion formation. After the infection has resolved, hyaluronic acid may be injected on a biweekly basis to further limit adhesion formation in horses with chronic infection. Although there is evidence in the literature to the contrary, many clinicians are of the opinion that early treatment and resolution of contamination before the tendon sheath becomes infected is associated with improved outcome, whereas the prognosis for horses with chronically infected DFTS is guarded. Concurrent infection of the tendons or osteomyelitis also decreases prognosis.
SEPTIC CORE LESIONS
CHAPTER
Primary infection of the SDFT is exceedingly rare, but a small series of cases has been reported. Sepsis of the SDFT may arise secondary to penetrating injury, joint injection, or hematogenous spread. Affected horses show marked lameness, cellulitis, and pain on palpation. Presence of fever and changes on complete blood count are variable. Ultrasound examination reveals a lesion similar to a core lesion, with edema of the tendon and localized cellulitis. Surgical excision of affected DDFT and the accessory ligament of the DDFT have been reported. When the extent of sepsis does not permit excision, surgical drainage, debridement, and lavage should be performed to minimize the bacterial load and remove proteolytic enzymes. Systemically and locally administered antimicrobials should be given, chosen on the basis of culture and sensitivity results of infected material. Antiinflammatory treatment is indicated to control pain and minimize local inflammation. In one series of three cases, only one horse survived, although surgical drainage of the lesions was not performed. All horses presented after 1 to 2 weeks of lameness. Bacteria isolated included Staphylococcus spp in two horses (both euthanized) and a mixed infection in the survivor.
Suggested Readings Arensburg L, Wilderjans H, Simon O, et al. Nonseptic tenosynovitis of the digital flexor tendon sheath caused by longitudinal tears in the digital flexor tendons: a
190 Superficial Digital Flexor Tendon Injury
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retrospective study of 135 tenoscopic procedures. Equine Vet J 2011;43:660-668. Avella CS, Smith RKW. Diagnosis and management of tendon and ligament disorders. In: Auer JA, Stick JA, eds. Equine Surgery. 4th ed. St. Louis: Saunders Elsevier, 2012: 1157-1179. Chesen AB, Dabareiner RM, Chaffin MK, et al. Tendinitis of the proximal aspect of the superficial digital flexor tendon in horses: 12 cases (2000-2006). J Am Vet Med Assoc 2009;234: 1432-1436. Dahlgren LA. Management of tendon injuries. In: Robinson NE, Sprayberry KA, eds. Current Therapy in Equine Medicine. 6th ed. St. Louis: Saunders Elsevier, 2009:518-523. David F, Caddy J, Bosch G, et al. Short-term cast immobilization is effective in reducing lesion propagation in a surgical model of equine superficial digital flexor tendon injury. Equine Vet J 2012;44:570-575. Jordana M, Wilderjans H, Boswell J, et al. Outcome after laceration of the superficial and deep digital flexor tendons, suspensory ligament and/or distal sesamoidean ligaments in 106 horses. Vet Surg 2011;40:277-283. Kidd JA, Dyson SJ, Barr ARS. Septic flexor tendon core lesions in five horses. Equine Vet J 2002;34:213-216. Ross MW, Dyson SJ. Diagnosis and Management of Lameness in the Horse. 2nd ed. St. Louis: Saunders Elsevier, 2011. Witte TH, Yeager AE, Nixon AJ. Intralesional injection of insulin-like growth factor-1 for treatment of superficial digital flexor tendinitis in Thoroughbred racehorses: 40 cases (2000-2004). J Am Vet Med Assoc 2011;239: 992-997.
C H A P T E R
190
TARALYN M. McCARREL
T
he superficial digital flexor tendon (SDFT) is at great risk for injury in the horse, and it is therefore not surprising that clinically relevant disease involving this structure is common in both racehorse and sport horse populations. Reasons for increased susceptibility to injury and sepsis are numerous and include the tendon’s superficial location, close association with synovial structures susceptible to penetrating injury, and inferior reparative response, plus the fact that the SDFT functions at its biomechanical limit in high-level performance horses. The following chapter will introduce the reader to the diagnosis and management of several different types of injury involving the SDFT and associated structures.
ANATOMY AND FUNCTION
The superficial digital flexor originates from the proximal aspect of the caudal surface of the humerus and inserts on the first and second phalanges. In addition, the accessory ligament of the SDFT (ALSDFT) originates at the level of the musculotendinous junction and has a fanlike insertion on the distal radius in close association with the carpal canal. The hind limb superficial digital flexor originates from the proximal aspect of the caudal surface of the femur and inserts on the phalanges, similar to the arrangement in the forelimb. The hind limb SDFT overlies the calcaneus, where it sends off medial and lateral attachments to this structure. The calcaneal bursa provides a gliding surface between the SDFT and the calcaneal tuber. The forelimb and hind limb SDFT are enveloped by the digital flexor tendon sheath (DFTS) from the distal half of the cannon bone to the pastern (Figure 190-1). The manica flexoria (MF) is an extension of the SDFT that encircles the deep digital flexor tendon (DDFT) within the DFTS. The superficial digital flexor muscle is composed of very little muscular tissue and thus has minimal role in flexion of the distal limb. Instead, the SDFT’s primary functions are stabilization and energy storage. Along with the suspensory ligament, the SDFT has a major role in supporting the fetlock joint. Furthermore, the muscle fibers are able to adapt to small vibrations that develop during locomotion, yielding a degree of shock absorption. Finally, the SDFT stores elastic energy when it is stretched during the stance phase of locomotion, and release of this energy allows the horse to propel its large mass with great efficiency.
TENDON REPAIR
Normal tendon is composed primarily of type I collagen arranged linearly in a hierarchical structure. Tenocytes, specialized tendon cells, produce the extracellular matrix, including collagen and noncollagenous molecules that assist in collagen fiber alignment. Blood supply is greatest at the periphery of the tendon, with relatively little vasculature supplying the tendon core.
Tendon repair proceeds through the classic stages of wound healing: inflammation, repair, and remodeling. The inflammatory phase begins at the onset of injury and lasts from a few days to weeks, depending on severity of the injury and antiinflammatory therapy instituted. The release of proteolytic enzymes results in expansion of the lesion, both in length and cross-sectional area, for several days. The repair phase overlaps with the inflammatory phase and is characterized by increased vascularity, cellularity, and production of disorganized small collagens. The remodeling phase is the longest of the tendon healing phases, lasting as long as 18 months. Remodeling overlaps with the repair phase and is characterized by increasing collagen organization and a greater proportion of collagen I. However, the resulting scar tissue is biomechanically inferior. Overall, the scarred area is stronger than normal tendon, but it is less elastic. The transition area between the inelastic repair tissue and the normal tendon is most susceptible to reinjury. A recent report suggested that the most crucial time for therapeutic intervention in the tendon healing process is the period from 12 to 16 weeks after injury.
TENDINOPATHY
Overstrain injuries of the SDFT are common in racehorses and top-level event horses. Although the clinical signs often manifest acutely, research into the pathophysiology of overstrain injury suggests that chronic degeneration leads to ultimate failure of the tendon. Despite considerable research effort and numerous proposed theories, the definitive cause or causes of SDFT tendinopathy remain elusive. Several risk factors have been identified for Thoroughbred racehorses, including fast work on hard surfaces, increased age at first race start, having a previous SDFT injury, fatigue, and heel elevation.
Diagnosis The horse with acute manifestation of classic midmetacarpal SDFT tendinopathy will have variable lameness, depending on lesion severity, and overt lameness may disappear rapidly. The horse should be observed for local swelling characteristic of a “bowed” tendon (Figure 190-2, A). The palmar structures of the metacarpus should be palpated both during weight bearing and with the limb unloaded. Horses with an active injury often resent palpation of the affected region, which may feel soft compared with normal tendon. More chronic lesions may be nonpainful and firm on palpation. A complete lameness examination is warranted because SDFT tendinopathy is often bilateral or may be a secondary overstrain injury arising secondary to lameness of a different cause in another limb. Diagnostic analgesia may be performed if confounding lameness exists, but information from the history, clinical signs, and ultrasound examination is often sufficient for diagnosis of tendinopathy.
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S
D
∗ L
Figure 190-1 Dissection of the distal part of the forelimb, viewed from the palmar-lateral aspect. The heel bulbs are at the bottom of the image. The superficial digital flexor tendon (S), deep digital flexor tendon (D), suspensory ligament (L) and distal end of the splint bone (*) are labeled for orientation. The end arrows indicate needles placed in the most proximal and distal extent of the normal DFTS. The central arrow points to a common location for centesis and injection of the DFTS, just distal to the base of the proximal sesamoids and palmar to the neurovascular bundle.
Ultrasonography is the primary imaging modality for diagnosis and monitoring of tendon lesions. The palmar or plantar aspect of the distal part of the limb should be clipped, cleaned if necessary, and imaged with a 7.5- to 14-MHz linear probe with a standoff pad. The typical findings of acute tendinopathy include a hypoechoic core lesion with loss of linear fiber pattern, increased cross-sectional area of the tendon, and change in shape of the tendon (Figure 190-2, B). Lesions along the margins of the tendon are also possible. A tendon that is healing appropriately will have an increase in lesion echogenicity, improvement in linear fiber pattern, and decrease in tendon cross-sectional area. The timing of the first ultrasound evaluation and impact of lesion expansion on the ultrasonographic appearance of acute tendon lesions must always be considered. Initially, core lesions may not be evident but will appear several days later. Ultrasound examinations performed within the first week after injury should be repeated in 2 to 4 weeks to allow full assessment of lesion size and severity. Standardbreds may have SDFT tendinopathy as a part of the “curb” complex of plantar hock soft tissue injury. An atypical form of proximal SDFT tendinopathy was recently described. The lesions were detected in older horses performing lower-level work; horses had an acute onset of lameness, with prolonged lameness thereafter. Horses reacted positively to carpal flexion, and lameness was abated following ulnar nerve block. Diagnosis was confirmed by ultrasonography of the SDFT at the level of the carpal canal, and effusion within the carpal sheath was evident. Prognosis for return to previous use was poor.
Treatment The hallmarks of initial treatment for SDFT tendinopathy are aimed at reducing inflammation and limiting lesion expansion. Therapy should be instituted immediately and includes administration of nonsteroidal antiinflammatory drugs, cold
S S
D
L
A
B
D
L
LF SDFT 3A
Figure 190-2 Distal portion of a limb (A) of a horse with superficial digital flexor tendon (SDFT) tendinopathy. Notice the characteristic bowing of the tendon, indicated by the arrow. Transverse (left pane) and longitudinal (right pane) ultrasound images (B) showing a hypoechoic core lesion (arrowhead) in the SDFT. D, Deep digital flexor tendon; L, suspensory ligament; S, superficial digital flexor tendon. (Ultrasound images courtesy Dr. K. Garrett, Rood and Riddle Equine Hospital, Lexington, KY.)
CHAPTER
therapy (with cold hosing or use of a device such as Game Ready1) several times daily for no longer than 30 minutes per treatment, bandaging for support and to minimize swelling, and stall rest. A controlled, gradual return to exercise may be started after 2 weeks of stall rest in most cases. The length of time spent exercising is gradually increased, and each addition of a new gait (i.e., adding small amounts of trotting work in a horse that has been walking for 3 months) is preceded by reevaluation of the tendon with ultrasound. An increase in tendon cross-sectional area of 10% or greater is considered to indicate recurrence, and the exercise program must be adjusted. Numerous adjunct medical and surgical treatments have been investigated, most yielding modest results (see Suggested Readings for full review). The high reinjury rate (up to 56%) following SDFT injury has remained a consistent challenge. Therapeutic ultrasound has little supporting evidence for efficacy to date, with a recent publication reporting only an increase in temperature in treated normal tendon but no investigation of tendon ultrastructure. Growth factor therapy with intralesional injection of insulin-like growth factor-1 in naturally occurring lesions resulted in improved ultrasound characteristics, but no improvement in reinjury rate. Recent advancements are showing promise. Experimental studies have revealed a decrease in lesion expansion following cast application to distal limbs with acute lesions. Because prognosis is associated with lesion severity, applying a cast to limbs with acute SDFT lesions during the first 10 days after injury may result in improved outcome, but this effect has yet to be proven clinically. Intralesional injection of plateletrich plasma (PRP) in an SDFT tendinopathy model resulted in faster maturation and organization of repair tissue. Further, the importance of PRP composition has been emphasized recently with low–white blood cell (WBC) PRP stimulating superior gene expression patterns in normal tendons in vitro, compared with high-WBC PRP. Intralesional injection of bone marrow–derived mesenchymal stem cells into natu rally occurring lesions of flat and National Hunt racehorses resulted in a significant reduction in reinjury rate in National Hunt, but not flat, racehorses. These results are promising, and further research determining the best type of mesen chymal stem cells and PRP, dose, and treatment protocol may result in greater longevity for horses following SDFT tendinopathy. No recent advances in surgical therapy for SDFT tendinopathy have been reported, and surgeons have varying opinions regarding the value of the existing procedures. Surgical options include tendon splitting and desmotomy of the ALSDFT by open or tenoscopic approach. Tendon splitting is restricted to cases with clearly defined core lesions and allows drainage of the hematoma containing numerous proteolytic enzymes and may limit lesion size. Previous reports have indicated an increase in suspensory ligament injury following ALSDFT desmotomy. However, this was disputed in a paper investigating insulin-like growth factor-1 intralesional injection in which ALSDFT desmotomy was also performed.
INTRATHECAL TEARS
Definitive diagnosis of intrathecal tears of the SDFT presents a diagnostic challenge. Increased use of advanced imaging and surgical techniques has led to greater recognition of tears
1
Game Ready. Coolsystems, Inc, Concord, CA.
190 Superficial Digital Flexor Tendon Injury
L
∗
815
D S
B
D
A
C
S
Figure 190-3 The same specimen as depicted in Figure 190-1 with the tendon sheath opened (A). The superficial digital flexor tendon (SDFT) is held by forceps, and the manica flexoria (MF) can be seen ensheathing the deep digital flexor tendon (DDFT). A pair of scissors has been placed between the DDFT and the MF and exits through the proximal reflection of the tendon sheath (black arrow), which is adhered to the proximal aspect of the MF. T2-weighted transverse magnetic resonance images demonstrating a torn manica (B, white arrow) and the normal continuous anatomy ensheathing the DDFT (C, white arrow). Notice the increased high-signal (bright white) synovial fluid in the tendon sheath. The distension highlights the normal mesotenon attachment to the SDFT (B, black arrow). D, DDFT; L, suspensory ligament; S, superficial digital flexor tendon; *, distal end of the splint bone. (Magnetic resonance images courtesy Drs. K. Garrett and S. Hopper, Rood and Riddle Equine Hospital, Lexington, KY.)
within the DFTS. The signalment of affected horses varies among studies, with MF tears reported to be more common in the hind limbs of cobs and ponies, whereas longitudinal SDFT tears accounted for 17% of tears in Warmblood show jumpers; in the latter, the forelimb was affected twice as often as the hind limb, and the MF represented only 4% of tears. Horses are presented with a history of tendon sheath distension and lameness. Nonseptic tenosynovitis may arise for a number of reasons, and determination of chronicity, presence of tendon tears, presence of intrathecal adhesions or masses, and contribution of palmar annular ligament thickening and constriction need to be considered for forming an accurate prognosis. Differentiating between tears of the DDFT and the MF is particularly important because prognosis for return to previous work following treatment of simple MF tears (80%) is twice as good as that for simple DDFT tears (40%). The intrasynovial structures of the DFTS are depicted (Figure 190-3, A). Several diagnostic modalities have been explored, and the tests used may reflect the equipment available and financial constraints of the owner. The accuracy of ultrasound for detection of tendon tears within the DFTS is only 49% to 76%. High synovial fluid cartilage oligomeric matrix protein concentration, compared with that in serum, in mature
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horses is highly indicative of tendon tears but does not identify the affected structure. This test is not clinically available at present but may be a useful screening tool in the future for horses with tenosynovitis that require further diagnostic evaluation and definitive therapy. Contrast radiography may aid in diagnosing MF tears. Ultimately, the most accurate diagnostic tools include magnetic resonance imaging and tenoscopy. Magnetic resonance imaging offers the advantage of enabling evaluation of all the structures within and surrounding the DFTS and permits surgical planning (Figure 190-3, B). However, there is added cost and the potential need for an additional anesthetic episode. Tenoscopy serves as both a diagnostic procedure and definitive therapy. Surgical debridement of tears is performed to remove damaging fibrillated material. At present, excision of the entire MF is recommended for treatment of partial and complete tears. Postoperative care includes bandaging and stall rest until 10 to 14 days after surgery. After this time, an exercise program starting with short bouts of daily hand walking and gradually increasing to full activity is recommended to reduce adhesion formation. Intrathecal injection of hyaluronic acid may also minimize adhesion formation. Prognosis for return to full activity is good in uncomplicated cases.
TENDON LACERATION
Lacerations of the SDFT occur in the forelimb and hind limb secondary to overreaching, kicking injuries, and wire cuts. The nature of the trauma will influence the degree of contamination, contusion, vascular compromise, and quality of tendon structure at the severed ends. The basic principles of first aid and wound care should be followed: keep the horse calm and comfortable, and minimize or eliminate the risk for further injury and contamination. The wound should be gently cleansed of obvious debris. When the SDFT is the only structure transected, there may not be a difference in fetlock angle if the horse stands squarely; however, if the opposite limb is lifted, the fetlock will drop. Transection of additional supporting structures causes obvious hyperextension of the distal part of the limb and significant distress for the horse. If there is any concern about the integrity of any structure, application of a heavy bandage and appropriate splint are warranted, and the horse should be transported to a clean environment for definitive treatment. A standard series of radiographs centered on the injured area is appropriate in determining whether there is bony involvement. Ultrasound examination of the soft tissues should be attempted before digital exploration of the wound, although the finding of air already in the wound may preclude imaging. Ultrasound may be repeated the following day after a period of bandaging. Sedation or regional anesthesia is usually necessary for complete evaluation. The wound should be thoroughly cleansed, a deep swab for bacterial culture performed, and the wound digitally explored. Any synovial structures that may be involved should be distended after collecting synovial fluid for cytology and culture if involvement is confirmed. In cases of confirmed tendon laceration, surgical wound management with the horse under general anesthesia is expected to result in the best possible outcome. When more than 50% of the tendon has been lacerated and the tendon ends are in good condition, the tendon ends are sutured. In cases with substantial trauma to the tendon ends, the tendon is left unsutured. The wound is closed, and the limb is placed in a cast or bandage cast for 6 to 8 weeks. Alternatively, a custom brace can be made that allows easier access to the limb for bandage changes and wound management. The horse is maintained
on stall rest for 2 to 3 months and during this time is transitioned to a bandage and splint, and then to only a heavy bandage as determined by ultrasonographic evidence of healing. Special shoeing may be indicated (see Chapter 189). Exercise is gradually increased, but the recovery process may take up to 1 year. The most common complications include permanent thickening of the injured region and persistent hyperextension of the fetlock. Tendon thickening does not appear to influence outcome. Persistent fetlock hyperextension (>6 months) is associated with complete tendon lacerations and decreased likelihood of return to prior level of performance. The number of lacerated structures is also a major prognostic indicator for future performance. Overall, the prognosis for survival is good (82%), but only 55% of horses will return to their previous level of activity.
SEPTIC TENOSYNOVITIS
Sepsis of the synovial structures associated with the SDFT can result in adhesions to the tendon as well as direct tendon damage resulting in persistent lameness, which may warrant euthanasia. Sepsis of the DFTS is the focus of this section, but the same general principles apply to the calcaneal bursa and carpal canal. Sepsis may develop secondary to penetrating injury, joint injection, or hematogenous spread (particularly in foals). The source of the infection should guide selection of antimicrobials, which should be started before culture and sensitivity results (see Chapter 186). Recognition of the potential involvement of a synovial structure and immediate aggressive therapy is paramount for achieving the best possible outcome. Horses with a closed synovial sheath are often markedly lame, whereas minimal to no lameness may be evident if the sheath is draining. Systemic evidence of sepsis (e.g., fever, complete blood count changes) may or may not be apparent. Diagnostic evaluation should include radiography for bony injuries in cases of laceration or when there is evidence of osteomyelitis in chronic cases or in cases in which infection was of apparent hematogenous origin. Ultrasonography should also be performed to evaluate the soft tissues, quantity and character of the synovial fluid, and presence or absence of fibrin within the sheath. A synovial fluid sample should be obtained (see Figure 190-1) before administration of antimicrobials and submitted for cytologic evaluation, total protein determination, and culture and sensitivity testing. If only a small volume of fluid is present, a broad tourniquet can be wrapped from the level of midmetacarpus to the base of the proximal sesamoids and fluid collected from the distal aspect of the DFTS. Treatment includes lavage of the DFTS and administration of antimicrobials (by one or more of these routes: systemic, intrasynovial, or regional perfusion) and systemic antiinflammatories. Tenoscopy may offer the advantage of more thorough lavage and the ability to remove foreign debris and fibrin. Unless needed in the case of concurrent tendon laceration, cast application is avoided. Hand walking is initiated as soon as possible to minimize adhesion formation. After the infection has resolved, hyaluronic acid may be injected on a biweekly basis to further limit adhesion formation in horses with chronic infection. Although there is evidence in the literature to the contrary, many clinicians are of the opinion that early treatment and resolution of contamination before the tendon sheath becomes infected is associated with improved outcome, whereas the prognosis for horses with chronically infected DFTS is guarded. Concurrent infection of the tendons or osteomyelitis also decreases prognosis.
SEPTIC CORE LESIONS
CHAPTER
Primary infection of the SDFT is exceedingly rare, but a small series of cases has been reported. Sepsis of the SDFT may arise secondary to penetrating injury, joint injection, or hematogenous spread. Affected horses show marked lameness, cellulitis, and pain on palpation. Presence of fever and changes on complete blood count are variable. Ultrasound examination reveals a lesion similar to a core lesion, with edema of the tendon and localized cellulitis. Surgical excision of affected DDFT and the accessory ligament of the DDFT have been reported. When the extent of sepsis does not permit excision, surgical drainage, debridement, and lavage should be performed to minimize the bacterial load and remove proteolytic enzymes. Systemically and locally administered antimicrobials should be given, chosen on the basis of culture and sensitivity results of infected material. Antiinflammatory treatment is indicated to control pain and minimize local inflammation. In one series of three cases, only one horse survived, although surgical drainage of the lesions was not performed. All horses presented after 1 to 2 weeks of lameness. Bacteria isolated included Staphylococcus spp in two horses (both euthanized) and a mixed infection in the survivor.
Suggested Readings Arensburg L, Wilderjans H, Simon O, et al. Nonseptic tenosynovitis of the digital flexor tendon sheath caused by longitudinal tears in the digital flexor tendons: a
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