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Equine ver. J . ( 1992) 24 ( 1) 46-5 1
Preliminary studies on the vascular anatomy of the equine superficial digital flexor tendon ANN E. KRAUS-HANSEN*, G. E. FACKELMAN*, C. BECKER*, R. M. WILLIAMS+ and F. S. PIPERS* Departments of *Surgery, tPathology and #Medicine, TuftsUniversity School of Veterinary Medicine, 200 Wesfboro Road, North Grafton, Massachusetts 0 1536, USA. Summary The vascular and microvascular anatomy of normal equine superficial digital flexor tendons was studied by dissection of vinyl-perfused specimens and by microangiography on high detail film. The presence of an extensive intratendinous vascular latticework was confirmed, and a 'nutrient artery' described closely associated with the accessory ligament of the superficial digital flexor tendon (proximal check ligament). Circumferential stripping of the paratenon from the tendon to eliminate afferent vessels was performed bilaterally in three horses and unilaterally in a fourth, followed by a treadmill training regimen. No resulting intratendinous lesions could be documented on gross post mortem and histological examination at three, 10, or 35 days post operatively. There was mild paratendinous proliferation in all instances. In one horse, four intratendinous ligatures were placed within the medial and lateral borders of the contralateral tendon to isolate further from its blood supply a 10 em segment. Gross lesions at 35 days post operatively included a marked paratendinous response involving the entire 10 cm segment, and a darkened, soft focus within the core of the tendon. Histopathology and electron microscopy demonstrated focal degeneration. It was concluded that the blood supply of the normal equine superficial digital flexor tendon is primarily intratendinous, rather than paratendinous as previously thought. The lesions in one horse similar to those in naturally occurring tendinitis supported a vascular aetiology of the disease, and set the groundwork for studies aimed at the development of a clinically relevant tendinitis model. Introduction EQUINE digital flexor tendinitis ('bow' of the superficial digital flexor tendon) is one of the most widespread and economically devastating athletic injuries affecting the performance horse. A number of aetiological factors have been implicated, including biomechanical forces (Webbon 1973; 1977; Evans and Barbenel 1975; Selway 1975; McCullagh, Goodship and Silver 1979; McIlwraith 1987), microtrauma (Selway 1975; Fackelman 1973), ischaemia (Stromberg 1971; Fackelman 1973; Stromberg and Tufvesson 1977), fatigue (McCullagh ef a/ 1979; McIlwraith 1987) and nutrition. The controversy created by defenders of the different theories is probably unfounded because equine tendinitis is most likely multi-aetiological, and embraces parts of all of the above. According to one theory, repetitive stretching of the tendon *Dr Kraus-Hansen's present address is: Department of Veterinary Physiology, Pharmacology and Toxicoiogy. School of Veterinary Medicine, Louisiana State University, Baton Rouge,Louisiana 70803. USA.
in the weight-bearing phase of the stride may cause microdamage to the collagen fibrils and delicate blood and lymphatic vasculature, thus setting the stage for mechanical failure (Fackelman 1973). The clinical course, which typically involves an early phase of mild heat, swelling and local pain prior to acute, partial tendon rupture, has been used by some authors to support a degenerative aetiology (Fackelman 1973) without any detailed description of a triggering mechanism. The predominant occurrence of lesions within the least vascularised mid-metacarpal region of the tendon (Fackelman 1973) and post mortem findings of intratendinous haemorrhage and focal intratendinous necrosis (Stromberg and Tufvesson 1969 Stromberg 1971; Stromberg and Tufvesson 1977; Webbon 1977) point toward an important vascular role in the early pathogenesis of the disease. In recent years, the topic of tendon nutrition (Manske and Lesker 1982; 1985) and blood supply (Brockis 1953; Bergljung 1968; Chaplin 1973; Lundborg 1979; Armenta and Lehrman 1980; Piaggi and Mingione 1981; Zbrodowski, Gajisin and Grodecki 1981; 1982; Azar, Culver and Fleegler 1983; Gajisin, Abrodowski and Grodecki 1983; Landi, Elves and Piaggi 1983; Hooper, Davies and Tothill 1984) has gained increased emphasis in the medical literature, in particular with regard to surgery and post operative care of the traumatised human digital flexor tendon. The basic principles of nutritional supply and anatomic design have been described in a number of animal models (Bergljung 1968; Chaplin 1973; Manske and Lesker 1982; Landi el al 1983; Kain et a1 1988). Because these' studies have concentrated on intrasynovial tendons, relatively little is known about the nutrition and blood supply of extrasynovial tendons. The equine superficial digital flexor tendon is unsheathed in the clinically affected region, and serves an important locomotor function, distinguishing it from its human counterpart. The need for species-specific research is apparent. A tendon receives its major arterial supply from its muscular attachment and periosteal insertions, and within a sheath is supplied by vessels carried within a connective tissue mesentery, or vinculum (Bergljung 1968). Peacock ( 1 959) demonstrated that the blood supply to the origins and insertions of a tendon provide perfusion only locally. He described the middle unsheathed region as supplied by the rich vascular network of the surrounding paratenon. The theory of tendon nutrition by diffusion was proposed by Peacock (1959) and substantiated by many recent works (Manske and Lesker 1982; 1985; Hooper et al 1984). I n vitro studies demonstrating the ability of tendon segments to survive in artificial media independent of vascular connections has placed a new emphasis on diffusional nutrition (Manske, Gelberman, Vande Berg, and Lesker 1984). The equine superficial digital flexor muscle arises from the distal humerus and its tendon is joined by its accessory ligament at the level of the distal radius, prior to coursing through the carpal canal (Sisson and Grossman 1953). The tendon is sheathed proximally and at the level of the metacarpophalangeal joint,
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where it encircles the deep flexor tendon and blends with the superficial transverse metacarpal (palmar annular) ligament prior to its bifurcation and insertion on the first and second phalanges (Sisson and Grossman 1953). The blood supply of the superficial digital flexor tendon is afforded: proximally through direct connections with the arterial supply of the superficial digital flexor muscle; by branches of the median artery carried within the carpal canal and subcarpal tendon sheath: and distally by vessels camed by the digital sheath (Webbon 1973). Branches coursing in the superficial transverse metacarpal ligament and periosteal insertions supply the distal extent of the tendon with a rich arteriolar network independent of the vasculature of the proximal and middle regions. The tendon is least well vascularised within its middle third, in the metacarpus (Fackelman 1973), and is reportedly dependent on its paratendinous covering in this region (Webbon 1973; McIlwraith 1987). The paratenon is richly supplied by many branches arising from the medial palmar artery. The intratendinous blood supply has been shown microangiographically; it is composed of an interlacing network, the architecture of which is noticeably disturbed in the instance of a naturally occumng injury (Norberg, Raker and Dodd 1967; Stromberg 1971; Stromberg and Tufvesson 1977). Longitudinally arranged vessels course between collagen bundles and anastomose with fine perpendicularly arranged intratendinous arterioles, some of which apparently arise from the surrounding paratenon. The present study was performed as part of a larger investigation aimed at developing a tendinitis model mimicking the aetiopathogenesis of the naturally occurring disease. Gross vascular and microvascular studies were performed to review relevant anatomy and, subsequently, selective surgical devascularisation procedures were performed on equine subjects.
Materials and methods Anatomic study
Eight anatomic specimens were prepared from horses destroyed at Tufts Large Animal Hospital for reasons unrelated to forelimb orthopaedic disease. Subjects were treated with 0.02 mg/kg body weight (bwt) intravenous (iv) acetylpromazine and 200 iukg bwt heparin sodium 10 mins prior to euthanasia. Euthanasia was performed with N-2-(methoxyphenyl)-2ethylbutyl-I-hydro-xybutyramide 4,4'-methylene biscyclohexyltrimethyl ammonium iodide and tetracaine hydrochloride (T-61; Hoechst Roussel Agrivet Co., Somerville, New Jersey, USA), administered iv. Immediately after death, the forelimbs were severed at midantebrachium. The median artery was cannulated with a 10 gauge catheter that was sutured in place, and the limbs placed in a water bath at approximately 37°C. In five specimens, the arterial tree was flushed with 4 litres of warm saline at a constant pressure of 100 mm Hg. A maximum amount of coloured vinyl (Red vinyl; Carolina Biological Supply Company, Burlington, North Carolina, USA) was then injected using a 60 ml syringe (approximately 100 to 200 ml). Three specimens were cannulated, placed in a water bath and perfused with 525 ml of a mixture of barium sulphate (Micropaque contrast; Picker International, Canton, Massachusetts, USA) in saline with 75 ml 10 per cent formalin added to the final 225 ml. Pressure was monitored by manometer and kept constant at 100 mm Hg. The procedure was deemed complete when infusion was almost imperceptible. Limbs were refrigerated for a minimum of 12 h to allow the barium sulphate perfusate to cure prior to anatomical dissection. Microangiographic protocol
Limbs perfused with barium suspension were radiographed prior to
anatomical dissection to document appropriate filling of the digital vasculature. A minimum of one dorsopalmar view was obtained. The superficial digital flexor tendons were then isolated and dissected free of paratenon for soft tissue radiography on high detail industrial film (Kodak Inductrex R-single coat 5 x 7 SR-5 film; E. M. Parker, Brookline, Massachusetts, USA). Cross-sectional views were then obtained of 5 mm segments. Radiography was performed with a Faxitron Cabinet (Faxitron Cabinet; Hewlett Packard, Oregon, USA) and films were processed manually (Kodak Rapid Fixer A and B Kodak Inductrex Manual developer and replenisher solutions A and B Kodak Indicator Stop Bath; Picker International, Canton, Massachusetts, USA). Tissue was subsequently placed in 10 per cent formalin for histopathological examination, or in 3 per cent glutaraldehyde for scanning electron microscopy. Surgical protocol
A perioperative course of penicillin was administered at 20,000 iu/kg bwt intramuscularly (im) bid, and phenylbutazone was used in one case at 4 mgkg bwt iv or PO bid. Paratendinous vascular disruption was performed bilaterally on four horses, according to the following protocol. Equine subjects were donated to Tufts University for reasons of mild unsoundness. The horses were geldings of performance breeds (Thoroughbred or Standardbred cross), aged 3 , 4 , 7 and 18 years, and were determined to be free of flexor tendon injury by clinical examination. A physical examination, lameness evaluation, and pre-operative serum chemistry screen and complete blood count were performed in each case. Horses were trained to exercise on a treadmill. Horses were pre-medicated with xylazine (0.4 m a g bwt). General anaesthesia was induced with an iv infusion of 10 per cent glyceryl guaiacolate administered (approximately 50 mgkg bwt) followed by an iv bolus of ketamine (2.2 mgkg bwt), and maintained with halothane and oxygen delivered by a semi-closed circuit. An alternative induction protocol employed a mixture of thiamylal sodium (5 mg/kg bwt) with 10 per cent glyceryl guaiacolate as an iv infusion. The horses were placed in left lateral recumbency and the distal forelimbs prepared routinely for aseptic surgery. Surgery was performed simultaneously on the limbs, which were approached by either a medial or lateral skin incision. A 10 cm longitudinal skin incision was made at the dorsal border of the superficial digital flexor tendon. The paratenon over the middle third of the tendon was incised and bluntly dissected free through the 360" circumference of the tendon, to sever all vascular connections throughout the surgical field (Fig 1). Judicious electrocoagulation of major vessels coursing over the tendon surface also was performed when deemed appropriate for more effective elimination of arterial routes. Having assured complete haemostasis, the paratenon was sutured closed in a continuous pattern, the subcutis with an interrupted horizontal mattress pattern, and the skin with simple interrupted sutures, using 2-0 polyglactin 9 10 (Vicryl; Ethicon Inc., Somerville, New Jersey, USA). A sterile wound dressing was applied. Post operatively, the horses were confined to a stall with the limbs bandaged. Handwalking was initiated on the first day post operatively, and treadmill exercise was instituted gradually, to a maximum rate of 500 m at 8 d s e c at three days post operatively, or to 3,000 m at 7 m/sec after 10 days. Ultrasonographic examination was performed on a weekly schedule with a two dimensional mechanical sector scanner (Ultramark 8; Advanced Technology Laboratories, Belleview, Washington, USA) using a 10 mHz transducer to evaluate the morphology of the flexor tendons and associated peritendinous reaction. 'Stand-off techniques were not deemed necessary because of the high frequency employed. Subjects were destroyed at three (two horses) or 10 days (one horse) post operatively, and the limbs prepared for microangiography according to the protocol described previously.
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technique described earlier. The subject was destroyed 35 days post operatively and the limbs prepared according to the previously described protocol. During the course of the study, the horses showed minimal lameness, and administration of analgesics was not necessary. Post mortem examination The digital flexor tendons and surrounding paratendinous tissues were examined grossly prior to radiography. Cross-sections of the superficial digital flexor tendons were inspected for evidence of intratendinous injury. Histopathology Cross-sectional 6 pm microtome slices were stained with haematoxylin and eosin (H & E). Sections of gross lesions were prepared for scanning electron microscopy. Fig I : An intraoperative perspective of the paratendinous stripping procedure. The paratenon has been separated carefully for 360 around the tendon, severing all paratendinous vascular attachments
Results Anatomical study Anatomical findings concurred with earlier reports of the microvasculature of the superficial digital flexor tendon. An intensely anastomosing network of vessels was documented within the body of the flexor tendon with two major parallel vessels noted consistently in the medial and lateral borders of the tendon body, and small perpendicular anastomotic branches mimicking a ladder-like array. A previously undocumented branch of the median artery was found to course consistently through the distal one third of the accessory ligament of the superficial digital flexor tendon (proximal check ligament) to invade the substance of the tendon in a manner similar to that of a nutrient artery in bone (Fig 3). This nutrient artery arose as a first or second generation branch of the median artery, or of the medial palmar artery immediately following its bifurcation. It coursed along the palmar aspect of the accessory ligament and penetrated the palmar surface of the tendon just distal to the musculotendinous junction. Clinical response to elimination of paratendinous blood supply
Fig 2 : Prosection of a normal supeflcial digital flexor tendon illustrating the placement of four intratendinous ligatures as performed in Horse 4. This surgical site corresponds with the mid-metacarpal region of the tendon. The proximal muscular attachment and proximal check ligament are included
In one horse, the surgical procedure was modified on one forelimb to include intratendinous ligatures of 2-0 steel placed approximately 5 mm deep in the medial and lateral borders of the right tendon at the proximal and distal aspects of the surgical field (Fig 2). Surgery was performed on the contralateral limb using the
Subjects showed mild local swelling post operatively, and minimal lameness that resolved within days. Horses were willing to exercise on the treadmill. Ultrasonography demonstrated peritendinous oedema, but the intratendinous morphology remained intact. Gross post mortem examination revealed a mild paratendinous response that was most marked at the medial and lateral borders of the tendon, with adhesions to the skin at the surgical site. Paratendinous proliferation was least marked in the horses destroyed at three days, and was associated primarily with the surgical incisions in the horse destroyed at 10 days. Increased vascularity of the paratenon was apparent grossly and demonstrated microangiographically at 10 days. In the horse destroyed at 35 days, the paratenon had become diffusely thickened in the 10 cm middle region. No intratendinous lesions were documented on gross post mortem examination, microangiography or histopathology. Clinical response to elimination of intratendinous blood supply
In Horse 4, intratendinous ligatures were placed in an effort to occlude the intratendinous blood supply, as described earlier. Based on earlier microangiographic observations, this should have effectively devascularised a 10 cm middle segment. Post operatively, marked swelling developed, a typical 'bowed' appearance became apparent, and the tendon became palpably
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Fig 5: Section from the mid-region of the right fore superficial digital flexor tendon in Horse 4 . An increased number of round nuclei demonstrate ongoing tissue repair. Hdi E , X 300
thicker. Ultrasonographic evaluation performed one day prior to euthanasia revealed hypoechoic linear lesions coincident with the location of intratendinous sutures. Abnormality was not detected within the core of the tendon. At necropsy, a markedly increased amount of paratendinous proliferation was noted relative to the opposite limb. The mid-region of the tendon was palpably soft, corresponding with a rounded, darkened lesion seen on crosssection. A subtle, avascular focus was subsequently demonstrated by microangiography. An increased number of blood vessels was evident microangiographically in the medial and lateral borders of the tendon (Fig 4). Histopathology demonstrated tendon fibre degeneration and a decreased population of viable tenocytes within the central core of the tendon. Active repair was evidenced by an increased number of immature cells with rounded nuclei (Fig 5 ) , and a local vascular response, which was most prominent at the junction with degenerate tissue. Fibrillar damage was documented by scanning electron microscopy (Fig 6).
Discussion Fig 3: A microangiogram of the normal proximal segment of a superficial digital flexor tendon illustrating the arterial branch (arrnni carried in the check ligament, and the extensive intratendinous vascular I-..;,,"
lL4lllLC
Fig 4 : Cross-sectional microangiogram from the mid-region of the right fore superficial digital flexor tendon in Horse 4 , corresponding to a palpably soft region in the intact tendon. Note the vascular prolijeration in the medial and lateral borders nj'the tendon
At surgery, after the paratenon was stripped circumferentially from the tendon and the tendon isolated, no change in appearance to the tendinous tissue was noted. Vessels coursing on the surface of the tendon were momentarilv blanched bv digital Dressure and filled readilv when Dressure &as removed. Tiis was taken as evidence 0; failure' to eliminate the vascular supply by paratendinous stripping. Disruption of the paratendinous blood supply alone, at least in the relatively atraumatic manner employed here, was well tolerated in the early post operative course in horses placed in a light exercise programme. Intratendinous lesions did not develop and the peritendinous inflammatory response was minimal. It may be concluded that the middle portion of the normal superficial flexor tendon is mainly supplied and drained by intratendinous blood and lymphatic vessels. This is consistent with the definition of a vascular (extrasynovial) tendon (Chaplin 1973). The relative contributions of the paratendinous vasculature and other arterial routes to the intratendinous lattice could not be determined from this study. It is possible that the tendon is not heavily dependent on the paratenon, and was therefore not adversely affected by the surgical procedure, or that the blood supply was indeed disturbed but subsequently became re-established. Alternatively, the intact paratenon proximal and distal to the surgical site may have maintained an adequate local circulation. It is of interest that severence of paratendinous vascular
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The finding that disruption of the intratendinous blood supply results in a condition similar to that of acute tendinitis should be considered preliminary because only one tendon was so operated. If proven to be true in further studies, these findings could lend credence to a devascularisation aetiopathogenesis of acute tendinitis, whereby vascular damage sets the stage for intratendinous degeneration and subsequent paratendinous proliferation. As is often seen in the natural condition, the local wound healing process was much more dramatic, grossly, in the surrounding tissues than within the substance of the tendon because of the greater number of pluripotential cells in the fascia. The paratendinous angioblastic response produces, as an unfortunate byproduct, restrictive adhesions that can inhibit the gliding function of the tendon, thus predisposing it to chronic injury and recurrence of lameness in the natural situation (Fackelman 1973; Selway 1975). The structure of the intratendinous blood supply describes a 'watershed' zone in the mid-metacarpal region, at the terminations of vessels fed by the proximal 'nutrient artery' and of those reflexive from the distal tendon sheath. This supports previous reports of relative avascularity in this region and, therefore, of its predisposition to injury.
Conclusion
Fig 6: Scanning electron microscopir appearance of the mid-region of the right fore superficial digital flexor tendon in Horse 4 . Fihrillar disruption is apparent
connections has been performed as part of surgical treatment of tendinitis, and has been reported to be well tolerated (Proctor 1958; Potenza 1963; Fackelman 1971; 1973; Selway 1975). Peritendinectomy has been advocated for removal of motionlimiting adhesions (Selway 1975). The placement of a porous Teflon prosthesis (Selway 1975) or tendon transplant (Fackelman 1971; 1973) has been advocated, and implies disruption of paratendinous blood supply. The findings of the present study support the development of treatment methods aimed at enhancement of intrinsic tendon healing (Manske, Gelberman and Vande Berg 1984). and prevention of paratendinous fibrosis, which has been described as a sequella to a primarily intratendinous disease (Webbon 1973; 1977). Ligation of two major intratendinous vascular routes, as performed in Horse 4, apparently resulted in a significant insult to the blood supply. It was noted during surgery, as the final ligature was drawn tight, that the tendinous tissue took on a purplish hue, thought to indicate mainly venous embarrassment. The focal core lesion, associated disturbance in the microvascular pattern and fibrillar disruption were similar to those described in cases of naturally occurring tendinitis (Stromberg 1971; Webbon 1977; Stromberg and Tufvesson 1977; Silver et a/ 1983). The vascular response noted histologically presumably originated from the local, intratendinous blood supply and from vascular proliferation of peritendinous origin resembling that seen in clinical cases (Stromberg 1971; Fig 4).The more subtle nature of the experimentally created lesion likely explains the failure of ultrasonographic documentation. Tendon damage incited production of extratendinous granulation tissue, exhibited as a marked paratendinous response. This was in contrast to the mild paratendinous proliferation caused by paratendinous stripping alone, and illustrates a propensity for extrinsic healing. It is hypothesised that disruption of the intratendinous blood supply caused focal devitalisation of tendinous tissue and local haemorrhage, with resultant production of oedema, angiogenesis and subsequent fibroplasia.
Results of this study underlie the importance of the intratendinous blood supply to the equine superficial digital flexor tendon. These findings support the use of treatments aimed at promoting intratendinous healing and decreasing adhesion formation, such as physical therapy in the form of early controlled mobilisation. The similarity of the lesion produced in Horse 4 to the naturally occurring condition further lends preliminary support to the vascular theory of tendinitis and to the potential development of a clinically relevant experimental model. The lesion(s) created appear to mimic closely those in the naturally occurring condition and may permit the testing of physical and other therapies aimed at restitution of the integrity of the intratendinous supply.
Acknowledgements This research was funded by a grant from the Massachusetts Thoroughbred Breeders' Association. The authors are grateful to R. Schenk for consultation, and to D. Willman and to Shelley E. Ebbett for medical photography. This paper was presented at the Scientific Meeting of the American College of Veterinary Surgeons in Tucson, Arizona, February 1988.
References Armenia, E. and Lehrman, A. (1980) The vincula to the flexor tendons of the hand. J. Hand Surg. 5 , 127-134. Azar, C. A.. Culver. 1. E. and Fleegler, E. J. (1983) Blood supply of the flexor pllicis longus tendon. J. Hand Surg. 8.471-475. Bergljung, L. (1968) Vascular reactions after tendon suture and tendon transplantation. A stereo-microangiographicstudy on the calcaneal tendon of the rabbit. Scand. J. Plast. Reconstr. Surg. Suppl. 4,7-63. Brockis, J. G. (1953) The blood supply of the flexor and extensor tendons of the fingers in man. J. Bone Joint Surg. 35-B, 131-138. Chaplin, D. M. (1973) The vascular anatomy within normal tendons, divided tendons, free tendons grafts and pedicle tendon grafts in rabbits. A rnicroangiographic study. J. Bone Joinr Surg. 55-B,369-389. Evans, J. H. and Barbenel, J. C. (1975) Structural and mechanical properties of tendons related to function. Equine vet. J. 7 , 1-8. Fackelman, G. E. (1971) Tendon transplantation: the technique and its histologic evaluation. Dissertation, Zurich. Fackelman, G . E. (1973) The nature of tendon damage and its repair. Equine wt. J. 5, 141-149. Gajisin. S.. Zbrodowski. A. and Grodecki. J. (1983) Vascularization of the extensor apparatus of the fingers. J. Anaf. 137,3 15-322. Hooper, G . . Davies. R. and Tothill, P.(1984) Blood flow and clearance in tendons -
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EQUINE VETERINARY JOURNAL studies with dogs. J . Bone Joinf Surg. 66-8.441-443. Kain, C. C., Russel, J. E.. Bum, R., Dunlap, J.. McCarthy, J. and Manske, P. R. (1988)the effect of vascularization on avian flexor tendon repair. A biochemical study. Clin.Orrhop. Rel. Res. 233,295-303. Landi. A,. Elves, M. and Piaggi, W. (1983)The blood flow of rabbits' tendons. Variation with age, activity and hypoxia. Acra Orrhop. Scand. 54,832-835. Lundborg, G . (1979)The vascularization of the human flexor pollicis longus tendon. The Hand lI,28-33. Manske. P. R. and Lesker, P. A. (1982)Nutrient pathways of flexor tendons in primates. J. Hand Surg. 7.436-444. Manske, I? R. and Lesker, I? A. (1985)Flexor tendon nubition. Handclinics 1, 13-24. Manske. P. R., Gelberman, R. H.. Vande Berg, J. S . and Lesker, P. A. (1984)Intrinsic flexor-tendon repair. A morphological study in vitro. J . Bone Joint Surg. 66-A,
385-396. McCullagh, K . G.,Goodship, A. E. and Silver, 1. A. (1979)Tendon injuries and their treatment in the horse. Ver. Rec. 105.54-57. Mcllwraith. C. W. (1987)Diseases of tendons, ligaments, and related structures. In: Adams' Lameness in Horses. 4th edn. Ed: T. S. Stashak. Lea and Febiger, Philadelphia, Pennsylvania, USA. pp 44740,463-468. Norberg, A. 1. Raker, C. W. and Dcdd, D. (1967)Equine tendinitis - an angiographic and histologic study. Proc. Am. Ass. Equine Pract. 13,243-254. Peacock. E. E. (1959)A study of the circulation in normal tendons and healing grafts. Ann. Surg. 149,415-428. Piaggi, V. and Mingione, A. (1981)A study of tendon blood flow using 133xenon. The Hand 13,48-50.
Potenza, A. D. (1963)Critical evaluation of flexor tendon healing and adhesion formation within artificial digital sheaths. J. Bone Joint Surg. 45-A.1217-1233. Proctor, D. L. (1958)Surgery for tendinitis. Proc. Am. Ass. Equine Pracr. 4,1 I I. Selway. S. (1975)Concepts of the pathogenesis of recurrence of tendinitis in the horse and a proposed surgical procedure to prevent such recurrence. Proc. Am. Ass. Equine Pracr. 21.53-66. Silver, 1. A,, Brown, P. N., Goodship, A. E., Lanyon, L. E., McCullagh. K. G., Perry, G. C. and Williams, 1. F. (1983)A clinical and experimental study of tendon injury, healing and treatment in the horse. Equine vef. J . Suppl. I, 5-22. Sisson, S. and Grossman, 1. D. (1953)The Anafomy of the Domesrir Animals. 4th edn. W. B. Saunders Co., Philadelphia, USA. Stromberg, B. (1971)The normal and diseased superficial flexor tendon in race horses. AcfaRadio/. Suppl. 305. Stromberg. B. and Tufvesson, G. (1969)Lesions of the superficial flexor tendon in race horses. A microangiographic and histopathologic study. Clin. Orrhop. Re/. Res. 62,113-123. Stromberg. B. and Tufvesson. G (1977)An experimental study of autologous digital tendon transplants in the horse. Equine vet. J. 9.231-237. Webbon. P. M. (1973)Equine tendon stress injuries. Equine vef. J. 5.58-64. Webbon, P. M. (1977)A post mortem study of equine digital flexor tendons. Equine vef.J . 9,61-67. Zbrodowski, A,, Gajisin, S., and Grodecki. J. (1981)Mesotendons of digital flexor muscles and their vasculature. The Hand 13,231-238.
Received for puhlicafion:30.3.90 Accepred: 22.7.91
Australian Veterinary Association
NATIONAL CONFERENCE Adelaide Convention Centre, Adelaide, South Australia
10th
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A maior multidisciplinary zoonosis symposium. Special plenary sessions on "the goanna track to success" - how veterinarians have created viable businesses all over Australia.
A plenary session on the future and opportunities in veterinary work over the next 1 O years. Special De Bono workshops. For further information contact Louise Stafford, GPO Box 498, Adelaide 500 1, South Australia. Tel: (08)232 08 7 3; Fax: (08) 232 09 18
EQUINE VETERINARY JOURNAL
Equine ver. J . ( 1992) 24 ( 1) 46-5 1
Preliminary studies on the vascular anatomy of the equine superficial digital flexor tendon ANN E. KRAUS-HANSEN*, G. E. FACKELMAN*, C. BECKER*, R. M. WILLIAMS+ and F. S. PIPERS* Departments of *Surgery, tPathology and #Medicine, TuftsUniversity School of Veterinary Medicine, 200 Wesfboro Road, North Grafton, Massachusetts 0 1536, USA. Summary The vascular and microvascular anatomy of normal equine superficial digital flexor tendons was studied by dissection of vinyl-perfused specimens and by microangiography on high detail film. The presence of an extensive intratendinous vascular latticework was confirmed, and a 'nutrient artery' described closely associated with the accessory ligament of the superficial digital flexor tendon (proximal check ligament). Circumferential stripping of the paratenon from the tendon to eliminate afferent vessels was performed bilaterally in three horses and unilaterally in a fourth, followed by a treadmill training regimen. No resulting intratendinous lesions could be documented on gross post mortem and histological examination at three, 10, or 35 days post operatively. There was mild paratendinous proliferation in all instances. In one horse, four intratendinous ligatures were placed within the medial and lateral borders of the contralateral tendon to isolate further from its blood supply a 10 em segment. Gross lesions at 35 days post operatively included a marked paratendinous response involving the entire 10 cm segment, and a darkened, soft focus within the core of the tendon. Histopathology and electron microscopy demonstrated focal degeneration. It was concluded that the blood supply of the normal equine superficial digital flexor tendon is primarily intratendinous, rather than paratendinous as previously thought. The lesions in one horse similar to those in naturally occurring tendinitis supported a vascular aetiology of the disease, and set the groundwork for studies aimed at the development of a clinically relevant tendinitis model. Introduction EQUINE digital flexor tendinitis ('bow' of the superficial digital flexor tendon) is one of the most widespread and economically devastating athletic injuries affecting the performance horse. A number of aetiological factors have been implicated, including biomechanical forces (Webbon 1973; 1977; Evans and Barbenel 1975; Selway 1975; McCullagh, Goodship and Silver 1979; McIlwraith 1987), microtrauma (Selway 1975; Fackelman 1973), ischaemia (Stromberg 1971; Fackelman 1973; Stromberg and Tufvesson 1977), fatigue (McCullagh ef a/ 1979; McIlwraith 1987) and nutrition. The controversy created by defenders of the different theories is probably unfounded because equine tendinitis is most likely multi-aetiological, and embraces parts of all of the above. According to one theory, repetitive stretching of the tendon *Dr Kraus-Hansen's present address is: Department of Veterinary Physiology, Pharmacology and Toxicoiogy. School of Veterinary Medicine, Louisiana State University, Baton Rouge,Louisiana 70803. USA.
in the weight-bearing phase of the stride may cause microdamage to the collagen fibrils and delicate blood and lymphatic vasculature, thus setting the stage for mechanical failure (Fackelman 1973). The clinical course, which typically involves an early phase of mild heat, swelling and local pain prior to acute, partial tendon rupture, has been used by some authors to support a degenerative aetiology (Fackelman 1973) without any detailed description of a triggering mechanism. The predominant occurrence of lesions within the least vascularised mid-metacarpal region of the tendon (Fackelman 1973) and post mortem findings of intratendinous haemorrhage and focal intratendinous necrosis (Stromberg and Tufvesson 1969 Stromberg 1971; Stromberg and Tufvesson 1977; Webbon 1977) point toward an important vascular role in the early pathogenesis of the disease. In recent years, the topic of tendon nutrition (Manske and Lesker 1982; 1985) and blood supply (Brockis 1953; Bergljung 1968; Chaplin 1973; Lundborg 1979; Armenta and Lehrman 1980; Piaggi and Mingione 1981; Zbrodowski, Gajisin and Grodecki 1981; 1982; Azar, Culver and Fleegler 1983; Gajisin, Abrodowski and Grodecki 1983; Landi, Elves and Piaggi 1983; Hooper, Davies and Tothill 1984) has gained increased emphasis in the medical literature, in particular with regard to surgery and post operative care of the traumatised human digital flexor tendon. The basic principles of nutritional supply and anatomic design have been described in a number of animal models (Bergljung 1968; Chaplin 1973; Manske and Lesker 1982; Landi el al 1983; Kain et a1 1988). Because these' studies have concentrated on intrasynovial tendons, relatively little is known about the nutrition and blood supply of extrasynovial tendons. The equine superficial digital flexor tendon is unsheathed in the clinically affected region, and serves an important locomotor function, distinguishing it from its human counterpart. The need for species-specific research is apparent. A tendon receives its major arterial supply from its muscular attachment and periosteal insertions, and within a sheath is supplied by vessels carried within a connective tissue mesentery, or vinculum (Bergljung 1968). Peacock ( 1 959) demonstrated that the blood supply to the origins and insertions of a tendon provide perfusion only locally. He described the middle unsheathed region as supplied by the rich vascular network of the surrounding paratenon. The theory of tendon nutrition by diffusion was proposed by Peacock (1959) and substantiated by many recent works (Manske and Lesker 1982; 1985; Hooper et al 1984). I n vitro studies demonstrating the ability of tendon segments to survive in artificial media independent of vascular connections has placed a new emphasis on diffusional nutrition (Manske, Gelberman, Vande Berg, and Lesker 1984). The equine superficial digital flexor muscle arises from the distal humerus and its tendon is joined by its accessory ligament at the level of the distal radius, prior to coursing through the carpal canal (Sisson and Grossman 1953). The tendon is sheathed proximally and at the level of the metacarpophalangeal joint,
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where it encircles the deep flexor tendon and blends with the superficial transverse metacarpal (palmar annular) ligament prior to its bifurcation and insertion on the first and second phalanges (Sisson and Grossman 1953). The blood supply of the superficial digital flexor tendon is afforded: proximally through direct connections with the arterial supply of the superficial digital flexor muscle; by branches of the median artery carried within the carpal canal and subcarpal tendon sheath: and distally by vessels camed by the digital sheath (Webbon 1973). Branches coursing in the superficial transverse metacarpal ligament and periosteal insertions supply the distal extent of the tendon with a rich arteriolar network independent of the vasculature of the proximal and middle regions. The tendon is least well vascularised within its middle third, in the metacarpus (Fackelman 1973), and is reportedly dependent on its paratendinous covering in this region (Webbon 1973; McIlwraith 1987). The paratenon is richly supplied by many branches arising from the medial palmar artery. The intratendinous blood supply has been shown microangiographically; it is composed of an interlacing network, the architecture of which is noticeably disturbed in the instance of a naturally occumng injury (Norberg, Raker and Dodd 1967; Stromberg 1971; Stromberg and Tufvesson 1977). Longitudinally arranged vessels course between collagen bundles and anastomose with fine perpendicularly arranged intratendinous arterioles, some of which apparently arise from the surrounding paratenon. The present study was performed as part of a larger investigation aimed at developing a tendinitis model mimicking the aetiopathogenesis of the naturally occurring disease. Gross vascular and microvascular studies were performed to review relevant anatomy and, subsequently, selective surgical devascularisation procedures were performed on equine subjects.
Materials and methods Anatomic study
Eight anatomic specimens were prepared from horses destroyed at Tufts Large Animal Hospital for reasons unrelated to forelimb orthopaedic disease. Subjects were treated with 0.02 mg/kg body weight (bwt) intravenous (iv) acetylpromazine and 200 iukg bwt heparin sodium 10 mins prior to euthanasia. Euthanasia was performed with N-2-(methoxyphenyl)-2ethylbutyl-I-hydro-xybutyramide 4,4'-methylene biscyclohexyltrimethyl ammonium iodide and tetracaine hydrochloride (T-61; Hoechst Roussel Agrivet Co., Somerville, New Jersey, USA), administered iv. Immediately after death, the forelimbs were severed at midantebrachium. The median artery was cannulated with a 10 gauge catheter that was sutured in place, and the limbs placed in a water bath at approximately 37°C. In five specimens, the arterial tree was flushed with 4 litres of warm saline at a constant pressure of 100 mm Hg. A maximum amount of coloured vinyl (Red vinyl; Carolina Biological Supply Company, Burlington, North Carolina, USA) was then injected using a 60 ml syringe (approximately 100 to 200 ml). Three specimens were cannulated, placed in a water bath and perfused with 525 ml of a mixture of barium sulphate (Micropaque contrast; Picker International, Canton, Massachusetts, USA) in saline with 75 ml 10 per cent formalin added to the final 225 ml. Pressure was monitored by manometer and kept constant at 100 mm Hg. The procedure was deemed complete when infusion was almost imperceptible. Limbs were refrigerated for a minimum of 12 h to allow the barium sulphate perfusate to cure prior to anatomical dissection. Microangiographic protocol
Limbs perfused with barium suspension were radiographed prior to
anatomical dissection to document appropriate filling of the digital vasculature. A minimum of one dorsopalmar view was obtained. The superficial digital flexor tendons were then isolated and dissected free of paratenon for soft tissue radiography on high detail industrial film (Kodak Inductrex R-single coat 5 x 7 SR-5 film; E. M. Parker, Brookline, Massachusetts, USA). Cross-sectional views were then obtained of 5 mm segments. Radiography was performed with a Faxitron Cabinet (Faxitron Cabinet; Hewlett Packard, Oregon, USA) and films were processed manually (Kodak Rapid Fixer A and B Kodak Inductrex Manual developer and replenisher solutions A and B Kodak Indicator Stop Bath; Picker International, Canton, Massachusetts, USA). Tissue was subsequently placed in 10 per cent formalin for histopathological examination, or in 3 per cent glutaraldehyde for scanning electron microscopy. Surgical protocol
A perioperative course of penicillin was administered at 20,000 iu/kg bwt intramuscularly (im) bid, and phenylbutazone was used in one case at 4 mgkg bwt iv or PO bid. Paratendinous vascular disruption was performed bilaterally on four horses, according to the following protocol. Equine subjects were donated to Tufts University for reasons of mild unsoundness. The horses were geldings of performance breeds (Thoroughbred or Standardbred cross), aged 3 , 4 , 7 and 18 years, and were determined to be free of flexor tendon injury by clinical examination. A physical examination, lameness evaluation, and pre-operative serum chemistry screen and complete blood count were performed in each case. Horses were trained to exercise on a treadmill. Horses were pre-medicated with xylazine (0.4 m a g bwt). General anaesthesia was induced with an iv infusion of 10 per cent glyceryl guaiacolate administered (approximately 50 mgkg bwt) followed by an iv bolus of ketamine (2.2 mgkg bwt), and maintained with halothane and oxygen delivered by a semi-closed circuit. An alternative induction protocol employed a mixture of thiamylal sodium (5 mg/kg bwt) with 10 per cent glyceryl guaiacolate as an iv infusion. The horses were placed in left lateral recumbency and the distal forelimbs prepared routinely for aseptic surgery. Surgery was performed simultaneously on the limbs, which were approached by either a medial or lateral skin incision. A 10 cm longitudinal skin incision was made at the dorsal border of the superficial digital flexor tendon. The paratenon over the middle third of the tendon was incised and bluntly dissected free through the 360" circumference of the tendon, to sever all vascular connections throughout the surgical field (Fig 1). Judicious electrocoagulation of major vessels coursing over the tendon surface also was performed when deemed appropriate for more effective elimination of arterial routes. Having assured complete haemostasis, the paratenon was sutured closed in a continuous pattern, the subcutis with an interrupted horizontal mattress pattern, and the skin with simple interrupted sutures, using 2-0 polyglactin 9 10 (Vicryl; Ethicon Inc., Somerville, New Jersey, USA). A sterile wound dressing was applied. Post operatively, the horses were confined to a stall with the limbs bandaged. Handwalking was initiated on the first day post operatively, and treadmill exercise was instituted gradually, to a maximum rate of 500 m at 8 d s e c at three days post operatively, or to 3,000 m at 7 m/sec after 10 days. Ultrasonographic examination was performed on a weekly schedule with a two dimensional mechanical sector scanner (Ultramark 8; Advanced Technology Laboratories, Belleview, Washington, USA) using a 10 mHz transducer to evaluate the morphology of the flexor tendons and associated peritendinous reaction. 'Stand-off techniques were not deemed necessary because of the high frequency employed. Subjects were destroyed at three (two horses) or 10 days (one horse) post operatively, and the limbs prepared for microangiography according to the protocol described previously.
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technique described earlier. The subject was destroyed 35 days post operatively and the limbs prepared according to the previously described protocol. During the course of the study, the horses showed minimal lameness, and administration of analgesics was not necessary. Post mortem examination The digital flexor tendons and surrounding paratendinous tissues were examined grossly prior to radiography. Cross-sections of the superficial digital flexor tendons were inspected for evidence of intratendinous injury. Histopathology Cross-sectional 6 pm microtome slices were stained with haematoxylin and eosin (H & E). Sections of gross lesions were prepared for scanning electron microscopy. Fig I : An intraoperative perspective of the paratendinous stripping procedure. The paratenon has been separated carefully for 360 around the tendon, severing all paratendinous vascular attachments
Results Anatomical study Anatomical findings concurred with earlier reports of the microvasculature of the superficial digital flexor tendon. An intensely anastomosing network of vessels was documented within the body of the flexor tendon with two major parallel vessels noted consistently in the medial and lateral borders of the tendon body, and small perpendicular anastomotic branches mimicking a ladder-like array. A previously undocumented branch of the median artery was found to course consistently through the distal one third of the accessory ligament of the superficial digital flexor tendon (proximal check ligament) to invade the substance of the tendon in a manner similar to that of a nutrient artery in bone (Fig 3). This nutrient artery arose as a first or second generation branch of the median artery, or of the medial palmar artery immediately following its bifurcation. It coursed along the palmar aspect of the accessory ligament and penetrated the palmar surface of the tendon just distal to the musculotendinous junction. Clinical response to elimination of paratendinous blood supply
Fig 2 : Prosection of a normal supeflcial digital flexor tendon illustrating the placement of four intratendinous ligatures as performed in Horse 4. This surgical site corresponds with the mid-metacarpal region of the tendon. The proximal muscular attachment and proximal check ligament are included
In one horse, the surgical procedure was modified on one forelimb to include intratendinous ligatures of 2-0 steel placed approximately 5 mm deep in the medial and lateral borders of the right tendon at the proximal and distal aspects of the surgical field (Fig 2). Surgery was performed on the contralateral limb using the
Subjects showed mild local swelling post operatively, and minimal lameness that resolved within days. Horses were willing to exercise on the treadmill. Ultrasonography demonstrated peritendinous oedema, but the intratendinous morphology remained intact. Gross post mortem examination revealed a mild paratendinous response that was most marked at the medial and lateral borders of the tendon, with adhesions to the skin at the surgical site. Paratendinous proliferation was least marked in the horses destroyed at three days, and was associated primarily with the surgical incisions in the horse destroyed at 10 days. Increased vascularity of the paratenon was apparent grossly and demonstrated microangiographically at 10 days. In the horse destroyed at 35 days, the paratenon had become diffusely thickened in the 10 cm middle region. No intratendinous lesions were documented on gross post mortem examination, microangiography or histopathology. Clinical response to elimination of intratendinous blood supply
In Horse 4, intratendinous ligatures were placed in an effort to occlude the intratendinous blood supply, as described earlier. Based on earlier microangiographic observations, this should have effectively devascularised a 10 cm middle segment. Post operatively, marked swelling developed, a typical 'bowed' appearance became apparent, and the tendon became palpably
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Fig 5: Section from the mid-region of the right fore superficial digital flexor tendon in Horse 4 . An increased number of round nuclei demonstrate ongoing tissue repair. Hdi E , X 300
thicker. Ultrasonographic evaluation performed one day prior to euthanasia revealed hypoechoic linear lesions coincident with the location of intratendinous sutures. Abnormality was not detected within the core of the tendon. At necropsy, a markedly increased amount of paratendinous proliferation was noted relative to the opposite limb. The mid-region of the tendon was palpably soft, corresponding with a rounded, darkened lesion seen on crosssection. A subtle, avascular focus was subsequently demonstrated by microangiography. An increased number of blood vessels was evident microangiographically in the medial and lateral borders of the tendon (Fig 4). Histopathology demonstrated tendon fibre degeneration and a decreased population of viable tenocytes within the central core of the tendon. Active repair was evidenced by an increased number of immature cells with rounded nuclei (Fig 5 ) , and a local vascular response, which was most prominent at the junction with degenerate tissue. Fibrillar damage was documented by scanning electron microscopy (Fig 6).
Discussion Fig 3: A microangiogram of the normal proximal segment of a superficial digital flexor tendon illustrating the arterial branch (arrnni carried in the check ligament, and the extensive intratendinous vascular I-..;,,"
lL4lllLC
Fig 4 : Cross-sectional microangiogram from the mid-region of the right fore superficial digital flexor tendon in Horse 4 , corresponding to a palpably soft region in the intact tendon. Note the vascular prolijeration in the medial and lateral borders nj'the tendon
At surgery, after the paratenon was stripped circumferentially from the tendon and the tendon isolated, no change in appearance to the tendinous tissue was noted. Vessels coursing on the surface of the tendon were momentarilv blanched bv digital Dressure and filled readilv when Dressure &as removed. Tiis was taken as evidence 0; failure' to eliminate the vascular supply by paratendinous stripping. Disruption of the paratendinous blood supply alone, at least in the relatively atraumatic manner employed here, was well tolerated in the early post operative course in horses placed in a light exercise programme. Intratendinous lesions did not develop and the peritendinous inflammatory response was minimal. It may be concluded that the middle portion of the normal superficial flexor tendon is mainly supplied and drained by intratendinous blood and lymphatic vessels. This is consistent with the definition of a vascular (extrasynovial) tendon (Chaplin 1973). The relative contributions of the paratendinous vasculature and other arterial routes to the intratendinous lattice could not be determined from this study. It is possible that the tendon is not heavily dependent on the paratenon, and was therefore not adversely affected by the surgical procedure, or that the blood supply was indeed disturbed but subsequently became re-established. Alternatively, the intact paratenon proximal and distal to the surgical site may have maintained an adequate local circulation. It is of interest that severence of paratendinous vascular
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The finding that disruption of the intratendinous blood supply results in a condition similar to that of acute tendinitis should be considered preliminary because only one tendon was so operated. If proven to be true in further studies, these findings could lend credence to a devascularisation aetiopathogenesis of acute tendinitis, whereby vascular damage sets the stage for intratendinous degeneration and subsequent paratendinous proliferation. As is often seen in the natural condition, the local wound healing process was much more dramatic, grossly, in the surrounding tissues than within the substance of the tendon because of the greater number of pluripotential cells in the fascia. The paratendinous angioblastic response produces, as an unfortunate byproduct, restrictive adhesions that can inhibit the gliding function of the tendon, thus predisposing it to chronic injury and recurrence of lameness in the natural situation (Fackelman 1973; Selway 1975). The structure of the intratendinous blood supply describes a 'watershed' zone in the mid-metacarpal region, at the terminations of vessels fed by the proximal 'nutrient artery' and of those reflexive from the distal tendon sheath. This supports previous reports of relative avascularity in this region and, therefore, of its predisposition to injury.
Conclusion
Fig 6: Scanning electron microscopir appearance of the mid-region of the right fore superficial digital flexor tendon in Horse 4 . Fihrillar disruption is apparent
connections has been performed as part of surgical treatment of tendinitis, and has been reported to be well tolerated (Proctor 1958; Potenza 1963; Fackelman 1971; 1973; Selway 1975). Peritendinectomy has been advocated for removal of motionlimiting adhesions (Selway 1975). The placement of a porous Teflon prosthesis (Selway 1975) or tendon transplant (Fackelman 1971; 1973) has been advocated, and implies disruption of paratendinous blood supply. The findings of the present study support the development of treatment methods aimed at enhancement of intrinsic tendon healing (Manske, Gelberman and Vande Berg 1984). and prevention of paratendinous fibrosis, which has been described as a sequella to a primarily intratendinous disease (Webbon 1973; 1977). Ligation of two major intratendinous vascular routes, as performed in Horse 4, apparently resulted in a significant insult to the blood supply. It was noted during surgery, as the final ligature was drawn tight, that the tendinous tissue took on a purplish hue, thought to indicate mainly venous embarrassment. The focal core lesion, associated disturbance in the microvascular pattern and fibrillar disruption were similar to those described in cases of naturally occurring tendinitis (Stromberg 1971; Webbon 1977; Stromberg and Tufvesson 1977; Silver et a/ 1983). The vascular response noted histologically presumably originated from the local, intratendinous blood supply and from vascular proliferation of peritendinous origin resembling that seen in clinical cases (Stromberg 1971; Fig 4).The more subtle nature of the experimentally created lesion likely explains the failure of ultrasonographic documentation. Tendon damage incited production of extratendinous granulation tissue, exhibited as a marked paratendinous response. This was in contrast to the mild paratendinous proliferation caused by paratendinous stripping alone, and illustrates a propensity for extrinsic healing. It is hypothesised that disruption of the intratendinous blood supply caused focal devitalisation of tendinous tissue and local haemorrhage, with resultant production of oedema, angiogenesis and subsequent fibroplasia.
Results of this study underlie the importance of the intratendinous blood supply to the equine superficial digital flexor tendon. These findings support the use of treatments aimed at promoting intratendinous healing and decreasing adhesion formation, such as physical therapy in the form of early controlled mobilisation. The similarity of the lesion produced in Horse 4 to the naturally occurring condition further lends preliminary support to the vascular theory of tendinitis and to the potential development of a clinically relevant experimental model. The lesion(s) created appear to mimic closely those in the naturally occurring condition and may permit the testing of physical and other therapies aimed at restitution of the integrity of the intratendinous supply.
Acknowledgements This research was funded by a grant from the Massachusetts Thoroughbred Breeders' Association. The authors are grateful to R. Schenk for consultation, and to D. Willman and to Shelley E. Ebbett for medical photography. This paper was presented at the Scientific Meeting of the American College of Veterinary Surgeons in Tucson, Arizona, February 1988.
References Armenia, E. and Lehrman, A. (1980) The vincula to the flexor tendons of the hand. J. Hand Surg. 5 , 127-134. Azar, C. A.. Culver. 1. E. and Fleegler, E. J. (1983) Blood supply of the flexor pllicis longus tendon. J. Hand Surg. 8.471-475. Bergljung, L. (1968) Vascular reactions after tendon suture and tendon transplantation. A stereo-microangiographicstudy on the calcaneal tendon of the rabbit. Scand. J. Plast. Reconstr. Surg. Suppl. 4,7-63. Brockis, J. G. (1953) The blood supply of the flexor and extensor tendons of the fingers in man. J. Bone Joint Surg. 35-B, 131-138. Chaplin, D. M. (1973) The vascular anatomy within normal tendons, divided tendons, free tendons grafts and pedicle tendon grafts in rabbits. A rnicroangiographic study. J. Bone Joinr Surg. 55-B,369-389. Evans, J. H. and Barbenel, J. C. (1975) Structural and mechanical properties of tendons related to function. Equine vet. J. 7 , 1-8. Fackelman, G. E. (1971) Tendon transplantation: the technique and its histologic evaluation. Dissertation, Zurich. Fackelman, G . E. (1973) The nature of tendon damage and its repair. Equine wt. J. 5, 141-149. Gajisin. S.. Zbrodowski. A. and Grodecki. J. (1983) Vascularization of the extensor apparatus of the fingers. J. Anaf. 137,3 15-322. Hooper, G . . Davies. R. and Tothill, P.(1984) Blood flow and clearance in tendons -
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EQUINE VETERINARY JOURNAL studies with dogs. J . Bone Joinf Surg. 66-8.441-443. Kain, C. C., Russel, J. E.. Bum, R., Dunlap, J.. McCarthy, J. and Manske, P. R. (1988)the effect of vascularization on avian flexor tendon repair. A biochemical study. Clin.Orrhop. Rel. Res. 233,295-303. Landi. A,. Elves, M. and Piaggi, W. (1983)The blood flow of rabbits' tendons. Variation with age, activity and hypoxia. Acra Orrhop. Scand. 54,832-835. Lundborg, G . (1979)The vascularization of the human flexor pollicis longus tendon. The Hand lI,28-33. Manske. P. R. and Lesker, P. A. (1982)Nutrient pathways of flexor tendons in primates. J. Hand Surg. 7.436-444. Manske, I? R. and Lesker, I? A. (1985)Flexor tendon nubition. Handclinics 1, 13-24. Manske. P. R., Gelberman, R. H.. Vande Berg, J. S . and Lesker, P. A. (1984)Intrinsic flexor-tendon repair. A morphological study in vitro. J . Bone Joint Surg. 66-A,
385-396. McCullagh, K . G.,Goodship, A. E. and Silver, 1. A. (1979)Tendon injuries and their treatment in the horse. Ver. Rec. 105.54-57. Mcllwraith. C. W. (1987)Diseases of tendons, ligaments, and related structures. In: Adams' Lameness in Horses. 4th edn. Ed: T. S. Stashak. Lea and Febiger, Philadelphia, Pennsylvania, USA. pp 44740,463-468. Norberg, A. 1. Raker, C. W. and Dcdd, D. (1967)Equine tendinitis - an angiographic and histologic study. Proc. Am. Ass. Equine Pract. 13,243-254. Peacock. E. E. (1959)A study of the circulation in normal tendons and healing grafts. Ann. Surg. 149,415-428. Piaggi, V. and Mingione, A. (1981)A study of tendon blood flow using 133xenon. The Hand 13,48-50.
Potenza, A. D. (1963)Critical evaluation of flexor tendon healing and adhesion formation within artificial digital sheaths. J. Bone Joint Surg. 45-A.1217-1233. Proctor, D. L. (1958)Surgery for tendinitis. Proc. Am. Ass. Equine Pracr. 4,1 I I. Selway. S. (1975)Concepts of the pathogenesis of recurrence of tendinitis in the horse and a proposed surgical procedure to prevent such recurrence. Proc. Am. Ass. Equine Pracr. 21.53-66. Silver, 1. A,, Brown, P. N., Goodship, A. E., Lanyon, L. E., McCullagh. K. G., Perry, G. C. and Williams, 1. F. (1983)A clinical and experimental study of tendon injury, healing and treatment in the horse. Equine vef. J . Suppl. I, 5-22. Sisson, S. and Grossman, 1. D. (1953)The Anafomy of the Domesrir Animals. 4th edn. W. B. Saunders Co., Philadelphia, USA. Stromberg, B. (1971)The normal and diseased superficial flexor tendon in race horses. AcfaRadio/. Suppl. 305. Stromberg. B. and Tufvesson, G. (1969)Lesions of the superficial flexor tendon in race horses. A microangiographic and histopathologic study. Clin. Orrhop. Re/. Res. 62,113-123. Stromberg. B. and Tufvesson. G (1977)An experimental study of autologous digital tendon transplants in the horse. Equine vet. J. 9.231-237. Webbon. P. M. (1973)Equine tendon stress injuries. Equine vef. J. 5.58-64. Webbon, P. M. (1977)A post mortem study of equine digital flexor tendons. Equine vef.J . 9,61-67. Zbrodowski, A,, Gajisin, S., and Grodecki. J. (1981)Mesotendons of digital flexor muscles and their vasculature. The Hand 13,231-238.
Received for puhlicafion:30.3.90 Accepred: 22.7.91
Australian Veterinary Association
NATIONAL CONFERENCE Adelaide Convention Centre, Adelaide, South Australia
10th
- 15th May, 1992
The programme will include:
A maior multidisciplinary zoonosis symposium. Special plenary sessions on "the goanna track to success" - how veterinarians have created viable businesses all over Australia.
A plenary session on the future and opportunities in veterinary work over the next 1 O years. Special De Bono workshops. For further information contact Louise Stafford, GPO Box 498, Adelaide 500 1, South Australia. Tel: (08)232 08 7 3; Fax: (08) 232 09 18
