SDFT: tendinitis in Horses (Equis) | Vetlexicon
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SDFT: tendinitis

ISSN 2398-2977


Synonym(s): Bowed tendon

Introduction

  • Cause: exercise at speed, fatigue.
  • Acute tendinitis is a medical emergency.
  • Signs: mild to severe lameness (forelimb > hindlimb) Musculoskeletal: gait evaluation; heat, palpable pain, swelling on palmar/plantar aspect of metacarpus or metatarsus (mid to lower third) Musculoskeletal: physical examination - adult.
  • Diagnosis: ultrasound Ultrasonography: flexor tendon.
  • Treatment: cold hosing, anti-inflammatories, rest and controlled exercise program, medical treatments, surgery.
  • Prognosis: guarded for return to same level of athletic performance.
Print off the factsheet on Tendon injuries to give to your clients.

Presenting signs

  • Forelimb lameness; hindlimb lameness is uncommon.
  • Soft tissue swelling palmar/plantar metacarpus/metatarsus.
  • SDFT tendinitis can occur proximal to the metacarpal region up to the level of the musculotendinous junction. The cases are uncommon and tend to occur in older horses (over 15 years old) that are showjumpers or dressage horses. They may occur post-midcarpal lesions or ALDDFT (check ligament) desmitis. They cause an overt lameness +/- enlargement of the affected tendon +/- carpal sheath tenosynovitis Carpus: sheath tenosynovitis. Diagnosis often requires localization to the region via regional and intrasynovial analgesia techniques, plus careful ultrasonographic examination. They have a poorer prognosis for return to soundness and may require surgical treatment.
  • SDFT tendinitis may also occur in the pastern region and involve one or both branches. These are uncommon but can present as acute onset lameness with swelling of the pastern +/- digital sheath tenosynovitis +/- other SDFT injuries. Diagnosis is following localization by an abaxial sesamoid regional nerve block and ultrasonographic changes in the branch. These carry a guarded prognosis.

Acute presentation

  • Variable lameness, sometimes severe, usually unilateral forelimb, and after exercise or competition.

Age predisposition

  • Older animals.

Breed/Species predisposition

  • Standardbred Standardbred pacers.
  • Thoroughbred Thoroughbred racehorses, both flat and particularly jumping.
  • Racing Arab Arab horses.
  • Racing Quarterhorses Quarterhorse.
  • High level eventers of any breed.
  • Fox or other hunters.

Cost considerations

  • Considerable costs incurred in treatment, extended periods in convalescence and retirement from athletic sport.

Special risks

  • Horses exercising at high speed, particularly over distances.

Pathogenesis

Etiology

  • Exercise.
  • Aging.
  • Direct trauma, eg kicking, interference injuries and blunt trauma.
  • Severe direct compression injuries from over-tight bandage or poultice.
  • Incorrect use of physiotherapy techniques, eg ultrasound.
  • Possible genetic factors as yet undetermined.

Predisposing factors

General
  • Prolonged and/or strenuous exercise at fast gaits over a period of time leads to exercise-induced weakening of extracellular collagen matrix and microtears within the tendon.
  • Mechanical triggers lead to increased stress on the tendon and subsequent tendinitis occurring either at normal or abnormal exercise levels.

Specific

  • Known factors include excessive heat generation within the tendon core during exercise, age-related degeneration of tendon substance, and inappropriate training intensity for the individual horse.
  • Postulated factors include variations in the vascular flow within parts of the tendon, hormone-related biochemical changes in the tendon matrix, and imbalance in the synthesis and degradation of extracellular tendon matrix proteins.
  • Specific trigger factors include:
    • The speed at which the horse exercises (much more common in fast gaited and galloping breeds).
    • Training methods.
    • Fatigue, particularly towards the end of exercise.
    • Loss of co-ordination of gait.
    • Ground surface conditions.
    • Jumping exercise.
    • Abnormal shoeing or foot shape, particularly dorsopalmar/plantar and mediolateral foot imbalance Foot: trimming and balancing.
    • Weight carriage, either of horse and/or rider.

Pathophysiology

  • Multifactorial:
    • Cyclical fatigue.
    • Previous injury.
  • Cumulative cyclical fatigue microdamage of tendon matrix and failure of intrinsic repair mechanisms   →   accumulation of damage and fatigue of the tendon. Tendinitis is initiated by maximal loading either during a normal period of exercise or where sudden supramaximal loading occurs due to specific trigger factors.
  • In addition to the tendon matrix alterations, the longitudinally-arranged Type 1 collagen fibers which are normally present in tendons is increasingly replaced by Type 3 which are poorly aligned. These latter fibers have a decreased elasticity and resistance to cyclic strain. Mechanical stretching of the tendon, either at normal or abnormal levels, can then lead to straining or even rupture of collagen fibers.
  • Local direct trauma usually → localized lesions with paratendinitis extending to tendinitis in more severe cases.
  • Inflammation is initiated after platelets are released and degranulate within the hemorrhage that occurs from the endotendon capillaries:
    • Cellular invasion (neutrophils, macrophages, monocytes).
    • Increased blood flow → edema.
    • Release of proteolytic degradative enzymes → removes damaged tissue but also destroys surrounding normal tendon.
    • Pain, heat and swelling.
Intratendinous degenerative changes may occur in horses with little or no evidence of inflammation and tendinitis.
  • Repair phase:
    • Strong angiogenesis response.
    • Fibroblast accumulation (local tenocytes and migratory cells) begins around 4 days after injury, peaks at 3 weeks → synthesis of Type III collagen and small diameter disorganized fibrils.
    • Degree of fibroplasia depends on severity of injury and exacerbation of injury by premature exercise.
    • Fibroplasia at periphery of tendon can → adhesion formation either with the paratendon tissues or tendon sheath wall → reduced function.
    • Resultant 'scar' is weaker and less elastic than original tendon.
  • Remodeling phase:
    • Begins several months after injury and can last for up to 18 months.
    • Collagen transforms from Type III to Type I although fibrils still not arranged in functional longitudinal pattern.
    • Functional loading is required to encourage haphazard scar tissue to mature into Type I collagen with stable cross-links, and therefore controlled exercise should be introduced at an early stage following as short a period of initial rest as the severity of the injury dictates.
    • Some Type III persists and the healed tendon is strong but has reduced elasticity and resistance to cyclic tensile strains.
    • Poorer blood supply in the tendon sheath areas of the tendon may lead to poorer healing in these regions.

Timecourse

  • From injury to repair: 6-24 months.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Estrada R J, van Weeren P R, van de Lest C H et al (2014) Comparison of healing in forelimb and hindlimb surgically induced core lesions of the equine superficial digital flexor tendon. Vet Comp Orthop Traumatol 27 (5), 358-365 PubMed.
  • Hu A J & Bramlage LR (2014) Racing performance of Thoroughbreds with superficial digital flexor tendonitis treated with desmotomy of the accessory ligament of the superficial digital flexor tendon: 332 cases (1989-2003). JAVMA 244 (12), 1441-1448 PubMed.
  • Welsh C E, Lewis T W, Blott S C et al (2014) Estimates of genetic parameters of distal limb fracture and superficial digital flexor tendon injury in UK Thoroughbred racehorses. Vet J 200 (2), 253-256.
  • Tipton T E, Ray C S & Hand D R (2013) Superficial digital flexor tendonitis in cutting horses: 19 cases (2007-2011). Am Vet Med Assoc 243 (8), 1162-1165 PubMed.
  • Smith R K, Werling N J, Dakin S G et al (2013) Beneficial effects of autologous bone marrow-derived mesenchymal stem cells in naturally occurring tendinopathy. PLoS One 25 (8), 9.
  • Tully L J, Murphy A M, Smith R K et al (2014) Polymorphisms in TNC and COL5A1 genes are associated with risk of superficial digital flexor tendinopathy in National Hunt Thoroughbred racehorses. Equine Vet J 46 (3), 289-293.
  • Carvalho Ade M et al (2013) Equine tendonitis therapy using mesenchymal stem cells and platelet concentrates: a randomized controlled trial. Stem Cell Res Ther 22;4(4), 85 PubMed.
  • Montgomery L, Elliott S B & Adair H S (2013) Muscle and tendon heating rates with therapeutic ultrasound in horses. Vet Surg 42 (3): 243-249 PubMed.
  • Marr C M & Bowen I M (2012) Does firing have a valid place in the treatment of superficial digital flexor tendon injury in the 21st century? Equine Vet J 44 (5), 509-510 PubMed.
  • Reardon R J et al (2012) Risk factors for superficial digital flexor tendinopathy in Thoroughbred racehorses in hurdle starts in the UK (2001-2009). Equine Vet J 44 (5), 564-569.
  • Caniglia C J, Schramme M C & Smith R K (2012) The effect of intralesional injection of bone marrow derived mesenchymal stem cells and bone marrow supernatant on collagen fibril size in a surgical model of equine superficial digital flexor tendonitis. Equine Vet J 44 (5), 587-593 PubMed.
  • Witte T H, Yeager A E & Nixon A J (2011) Intralesional injection of insulin-like growth factor-I for treatment of superficial digital flexor tendonitis in Thoroughbred racehorses: 40 cases (2000-2004). JAVMA 239 (7), 992-997 PubMed.
  • Whitlock D, Garcia T C, Vallance S A & Stover S M (2012) Possible role of carpal hyperextension in superficial digital flexor tendinopathy. Equine Vet J 44 (5), 59-63 PubMed.
  • Godwin E E, Young N J, Dudhia J et al (2012) Implantation of bone marrow-derived mesenchymal stem cells demonstrates improved outcome in horses with overstrain injury of the superficial digital flexor tendon. Equine Vet J 44 (1), 25-32 PubMed.
  • O'Meara B, Bladon B, Parkin T D et al (2010) An investigation of the relationship between race performance and superficial digital flexor tendonitis in the Thoroughbred racehorse. Equine Vet J 42 (4), 322-326 PubMed.
  • Thorpe C T, Clegg P D & Birch H L (2010) A review of tendon injury: why is the equine superficial digital flexor tendon most at risk? Equine Vet J 42 (2), 174-180 PubMed.
  • Bosch G, van Schie H T, de Groot M W et al (2010) Effects of platelet-rich plasma on the quality of repair of mechanically induced core lesions in equine superficial digital flexor tendons: A placebo-controlled experimental study. J Orthop Res 28 (2), 211-217 PubMed.
  • Moraes J R, Facco G G, Moraes F R et al (2009) Effects of glycosaminoglycan polysulphate on the organisation of collagen fibres in experimentally induced tendonitis in horses. Vet Rec. 15;165(7), 203-205 PubMed.
  • Chesen A B, Dabareiner R M, Chaffin M K &Carter G K (2009) Tendinitis of the proximal aspect of the superficial digital flexor tendon in horses: 12 cases (2000-2006). JAVMA 234 (11), 1432-1436 PubMed.
  • Patterson-Kane J C & Firth E C (2009) The pathobiology of exercise-induced superficial digital flexor tendon injury in Thoroughbred racehorses. Vet J 181 (2), 79-89 PubMed.
  • Dyson S (2007) Superficial digital flexor tendon injuries in teenage and older horses. Equine Vet Educ 19 (4), 187-188.
  • Pickersgill C H, Marr C M & Reid S W J (2001) Repeatability of diagnostic ultrasonography on the assessment of the equine superficial digital flexor tendon. Equine Vet J 33 (1), 33-37 PubMed.
  • Hogan P M & Bramlage L R (1995) Transection of the accessory ligament of the superficial digital flexor tendon for treatment of tendinitis - long term results in 61 Standardbred racehorses (1985-1992). Equine Vet J 27, 221-226 PubMed.

Other sources of information

  • Ross M W et al (2011) Superficial Digital Flexor Tendonitis. In: Diagnosis & Management of Lameness in the Horse. Eds: Ross M W & Dyson S J. Saunders, Missouri. pp 706-726.