Introduction. Soft tissue injury Common occurrence in performance horses Mild sprains Severe damage and tearing, rupture 10/23/2012

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1 Indiana Association of Equine Practitioners November 2012 Duncan Peters DVM, MS Equine Lameness and Sports Medicine Michigan State University College of Veterinary Medicine East Lansing, Michigan Introduction Tissue Structure Pathogenesis of soft tissue injury Diagnosis i of soft tissue injuries i Targeted therapy for tissue repair Case presentations Soft tissue injury Common occurrence in performance horses Mild sprains Severe damage and tearing, rupture Variable microdamage to tissue breakdown Variable swelling, heat, pain and clinical signs 1

2 Tissue structure Normal tendon and ligaments Small proportion of tenocytes Mostly extracellular matrix 60 70% water Dry matter mostly type 1 collagen arranged as 1, 2 and 3 fiber bundles crimp, elastic, electrostatic cross linking Some type 2 collagen specific function, rigidity (scutum) Non collagenous proteins Tissue structure Non collagenous proteins 20% of dry matter Organization of collagen fibrils Tendon matrix ti remodeling dli Potential markers of tendon injury Cartilage Oligomeric Matrix Protein (COMP) Glycoprotein Weight bearing tendons (SDFT) high levels Positional tendons (CDET) low levels Possibly influence the quality of matrix Correlation of mechanical strength and COMP levels Tissue structure Tenocytes Role not fully known Cells change with age Interact with other cells to act as organ fibripositors secreting and organizing collagen fibrils fibripositors secreting and organizing collagen fibrils Blood supply Intratendinous from attachments to muscle/bone Extratendinous (paratendinous) mesotenon Relatively high similar to resting muscle Variable response to exercise same to 3X Definite increase with injury 2

3 Pathogenesis of injury Intrinsic (strain) or extrinsic (lacerations) damage Over strain injury severe overload of tissue Overload following a phase of tendon degeneration Young horses loading has stimulatory effect on matrix Older horses stimulatory effect not present Fibril crimp angle reduced Collagen fibril diameter variation occurs Reduced new collagen formation by tenocytes Loss of glycosaminoglycans and COMP Half life of collagen decades Half life of non collagenous proteins months Means a loss of compounds to maintain matrix integrity Pathogenesis of injury Results in overall poor ability of tendons/ligaments to adapt to exercise loading after skeletal maturity Microdamage degeneration that can not be adequately repaired non collagenous protein matrix loss Compounded by age and exercise load Minimal signs (molecular inflammation) without inflammation or the stimulation of a reparative process Reduced growth factors (TGF β), synthetic ability and cellular communication Mechanism? vascular (reperfusion injury), mechanical (hyperthermia), cytokine (proteolytic enzyme release) Pathogenesis of injury Clinical disease initiation Load exceeds the capacity of the degenerative tendon Fibrillar slippage Individual fiber rupture Fascicle rupture Parting of the tendon usually paratenon is intact Initiates reparative process Scar formation forms less elastic tissue Adjacent tissue susceptible (transition zones) 3

4 Diagnosis of clinical injury Can be straightforward or complex Thorough examination and accurate diagnosis are essential for targeted treatment Many diagnostic tools available Diagnosis of injury Digital palpation Can be extremely effective at localization Systematic Enlargement, surface temperature, retraction response May need repeat palpations (DSL) or contralateral controls Axial skeletal injury more difficult to localize Diagnosis of injury Movement evaluation Stride phase (DDFTcaudal, SDFT stance) Asymmetric loading with lunging or sloped ground (SL, distal DDFT, collateral lig) Flexion tests tension or reloading neural effect? 4

5 Diagnosis of injury Regional anesthesiaverify painful locale Radiology Soft tissue swelling DR/CR capsulitis, enlargement, effusion Avulsion fragments Sclerosis Osteolysis Diagnosis of injury Ultrasonography Tool of choice for soft tissue concerns Insensitive for predicting injury Evaluate anatomy, size, shape, fiber pattern, fiber damage, fluids, tissue type, bone/soft tissue interface Diagnosis of injury Ultrasonography Dependent on expertise of operator Useful for following progression of injury or healing Axial skeletal injurysupraspinous, sacroiliac Constantly improving technology and education Thermography useful applications, variable 5

6 Diagnosis of injury Nuclear scintigraphy Targets physiologic activity Poor anatomic definition Soft tissue phase distal DDFT, SL Bone phase attachment concerns sacroiliac, proximal SL, dorsal spinous processes Diagnosis of injury MRI Both anatomic and metabolic evaluation Help determine clinical significance of a variant Help to age an injury Contrast sequences for enhancement Assist veterinarian with treatment modality decisions (PRP acute?, EWST more chronic?) Therapy of soft tissue injury Wide range available rest to hyperbaric therapy Relatively short window to affect the functional healing Repairing i tissue can be reinjured with excessive loading anytime Current research does not provide a cookbook for repair and rehabilitation Therapeutic modality promises 6

7 Therapy and Repair Acute (inflammatory) phase days First 7 14 days post injury Reduce inflammation, minimize mechanical stress, remove cellular byproducts, initiate reparative processes Subacute (fibroblastic) phase weeks 3 10 weeks post injury Stimulate repair and optimize functional healing Chronic (tissue maturation) phase months 12 weeks to > 12 months Improve quality and strength of repair Acute phase Cold +/ compression Bandages support and +/ medication Topical osmotics Topical NSAID (Surpass) Systemic meds NSAIDs, corticosteroids < 24 hrs Minimal loading exercise Surgery?, injections? (Adequan) Subacute (fibroblastic) Encourage fibroplasia, organize scar optimally Regenerative therapies PRP growth factors, scaffold matrix ACP growth factors BMA scaffold, growth factors, cells Stem cells cellular factors 7

8 Subacute Hydrotherapy programs Therapeutic US Cold laser Electromagnetic Hyperbaric therapy Novel injectable collagen cross linking substance Subacute Surgery? splitting, tenotomy, fasciotomy Shock wave therapy Graduated exercise load art of healingtreadmill, pools, vibration plates Farriery reduce mechanical load on tissues DDFT vs. SL vs. collateral ligament Chronic (tissue maturation) Optimize function of the scar tissue Prevent re injury Li k d t f tti t il D Linked to performance expectations trail vs3day Graduated exercise program of non damaging, increased loading of tissue 8

9 Chronic Treatments focused at continued remodeling, vascularization, cellular proliferation, cross linking, fiber alignment Shockwave, LITUS, electromagnetic, electrostatic bandages, hydrotherapy, acupuncture incremental benefits? Chronic Exercise load program has to accompany the tissue maturation for the specific athletic endeavor Varied shoe types to diminish mechanical stress on tissues Overall Selection of treatment modalities and the timeframe of an increasing exercise load program is at the discretion of the veterinarian Based on a multitude of factors Based on a multitude of factors Art of practice as it translates to treatment and rehabilitation No single, optimal treatment or rehabilitation program 9

10 10 yr old Dressage Horse On and Off lame in circle to left when ridden over last 3 weeks Rested for few days fine Lame (2/5) RF circle to left RF lower leg flexion + (3/5) Blocks to low palmar 10 yr old Dressage Horse 10 yr old Dressage Horse Suspensory branch insertional desmopathy Treated with BMA/PRP 2X, Shockwave, rest, therapeutic US, electromagnetic wraps, treated joint 1X, support shoe, nutraceuticals 8 months back to very light riding 17 months back to regular riding exercise 10

11 7yr old Jumper Fluid swelling of distal tendon sheath following schooling on new arena footing, possible stumble, horse bucking Lame (2+/5) with lower leg flex + (3+/5) Sound with anesthesia of tendon sheath 7yr old Jumper 7yr old Jumper Tenosynovitis with mild enlarged lobe of tendon Treated with IRAP within sheath 4X at weekly intervals, walking, Surpass, hydrotherapy, bandages 6 weeks post injury started light riding 12 weeks post injury started jumping 11

12 9yr old TB Event Horse Seen running in field 3 days before Mild lame (1+/5) LF in circle to right Moderate increased fetlock joint effusion LF lower leg flexion + (3/5) IA fetlock block sound Rads NSF 9yr old TB Event Horse 9yr old TB Event Horse Traumatic capsulitis and synovitis Injected fetlock joint HA/triamcinalone Aggressive cold hydrotherapy for 48 hrs, bandages, poultice li Rest and hand walk 10 days, NSAIDs, joint supplements Back to regular flat work in 2 ½ weeks Jumping at 4 weeks Cartilage problem? 12

13 6yr old Reining Horse RF tendon injury as 3yr old, chronic swellingfluid and tissue, Sx to transect annular ligament 10 months ago Acute lame RF (3/5) after training, Flexion + (3+/5) Tendon sheath anesthesia 75% improved 6yr old Reining Horse 6yr old Reining Horse Adhesion tissue disruption? SDF tendinitis/tendonopathy Cold hypertonic hydrotherapy x 12 weeks Poultice/sweat bandages for 4 weeks then ceramic bandages for 4 months Therapeutic US 6 months Ride at walk start 2 weeks post injury Training hard 8 months 13

14 Summary Soft tissue injuries are a common occurrence in performance horses Most are result of ongoing degenerative processes within the tissue prior to excess overload Variety of treatments targeted at various phases of tendon / ligament repair Goal is for optimal functional healing through treatment and controlled exercise loading More basic and clinical research needed to assess factors of injury and treatment / rehabilitation Questions? 14