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LIPHOOK EQUINE HOSPITAL Graduated Bristol University 2004 - PowerPoint PPT Presentation

Russell Parker BVSc MSc DipECVS MRCVS Liphook Equine Hospital LIPHOOK EQUINE HOSPITAL Graduated Bristol University 2004 Internship at Donnington Grove Equine Hospital 2007-8 Surgical residency then lectureship at Edinburgh University


  1. Russell Parker BVSc MSc DipECVS MRCVS Liphook Equine Hospital LIPHOOK EQUINE HOSPITAL

  2.  Graduated Bristol University 2004  Internship at Donnington Grove Equine Hospital 2007-8  Surgical residency then lectureship at Edinburgh University 2008-11  Awarded Msc. by Research with distinction 2011 “Investigating the effects of antibiotics on the gene expression of equine bone marrow derived mesenchymal stromal cells”  Awarded ECVS Diploma in Equine Surgery 2012  Currently one of 5 surgeons at Liphook Equine Hospital LIPHOOK EQUINE HOSPITAL

  3.  Equine referral hospital, ambulatory practice and commercial laboratory ◦ 5 ECVS surgeons ◦ 3 ECEIM medicine specialists  Radiography, ultrasonography, scintigraphy, MRI, CT unit currently being installed  Varied equine population LIPHOOK EQUINE HOSPITAL

  4.  Major cause of lameness, poor performance and lost training days  Economic impact  Welfare implications  Sites of injury often related to athletic discipline LIPHOOK EQUINE HOSPITAL

  5.  Racehorses ◦ 10% clinical incidence (Walsh et al. 2013) ◦ 1.8 joint injuries/100 horse months (Reed et al. 2012) ◦ 33% metacarpophalangeal OA (Neundorf et al. 2010) with incidence increasing with age on PME  General population ◦ 13.9% in the GB horse population (Ireland et al 2013) ◦ 97% in geriatric population >30 yo (Ireland et al 2012) as assessed by decreased range of motion LIPHOOK EQUINE HOSPITAL

  6.  Good Question!  “a group of disorders characterised by a common end stage: progressive deterioration of the articular cartilage accompanied by changes in the bone and soft tissues of the joint” (McIlwraith 2005) LIPHOOK EQUINE HOSPITAL

  7. LIPHOOK EQUINE HOSPITAL

  8. Same end stage, different pathways! LIPHOOK EQUINE HOSPITAL

  9. Abnormal stresses Normal stresses on on normal cartilage abnormal cartilage Morphologic breakdown of articular cartilage LIPHOOK EQUINE HOSPITAL

  10. Joint Cyclic athletic Loss of stability incongruity trauma Abnormal stresses Subchondral bone remodelling Direct damage Physical cell to collagen (chondrocyte) matrix damage Enzymatic degradation Matrix and decreased synthesis proteoglycan of PG and collagen loss Cartilage breakdown

  11. Athletic Osteochondrosis trauma Age Inflammation Abnormal (Synovitis and cartilage capsulitis) Enzymatic Decreased degradation of matrix proteoglycan synthesis and collagen Cartilage breakdown

  12. Trauma Synoviocytes Subchondral bone Il-1 TNFα Prostaglandin Free radicals Chondrocytes Matrix Proteinase Collagenase metalloproteinases Hyaluronan degradation Matrix degradation LIPHOOK EQUINE HOSPITAL

  13.  Synovitis  Subchondral bone remodelling  Intra-articular fracture  Osteochondral fragmentation  Periarticular soft tissue injury LIPHOOK EQUINE HOSPITAL

  14.  Increasingly implicated in the pathogenesis of OA (Sutton et al. 2009)  Inflamed synoviocytes are a rich source of inflammatory mediators ◦ Prostaglandins ◦ Cytokines ◦ Matrix metalloproteinases LIPHOOK EQUINE HOSPITAL

  15.  Subchondral bone is responsible for 30-50% of impact absorption (cartilage 1-2%) and maintenance of joint congruity (Radin et al. 1970)  During training the bones are subjected to repeated cyclical loading leading to increased bone density as per Wolff’s law  The point at which this physiological response becomes pathological is poorly understood (Boyde 2003) LIPHOOK EQUINE HOSPITAL

  16.  Histopathological changes ◦ Thickening of subchondral bone plate ◦ Trabecular thickening ◦ Microvascular necrosis ◦ Osteocyte death ◦ Microcrack formation ◦ Cartilage erosion and loss LIPHOOK EQUINE HOSPITAL

  17.  Significant cause of lameness ◦ Racehorses ◦ Sports horses  Unknown but suspected role in the pathogenesis of osteoarthritis (Kawcak et al. 2001, Cruz and Hurtig 2008)  Often difficult to diagnose ◦ Subtle lameness ◦ Minimal localising signs ◦ Variable response to joint blocks LIPHOOK EQUINE HOSPITAL

  18.  Clinical signs  Diagnostic analgesia  Radiography  Ultrasonography  Biomarkers  Scintigraphy  MRI/CT  Arthroscopy LIPHOOK EQUINE HOSPITAL

  19.  Effusion  Heat  Soft tissue swelling  Reduced ROM  Pain on flexion  Lameness  None…. LIPHOOK EQUINE HOSPITAL

  20.  Essential for correct localisation of lameness as radiographic changes are often clinically insignificant  Lameness is usually reassessed 10 and 30 minutes post injection of mepivicaine  Volume of local anaesthetic varies depending on joint size ◦ Tarsometatarsal joint 2-4ml ◦ Fetlock/carpus 10ml ◦ Stifle 20-30ml each compartment LIPHOOK EQUINE HOSPITAL

  21.  Not an exact science!  A lower level of improvement may still be significant compared to perineural nerve blocks eg 50%  Some significant pathology may respond only partially to diagnostic analgesia eg subchondral bone pain, periarticular soft tissue injury  Response to diagnostic analgesia is no predictor of response to IA medication  Beware trying to block out a positive response to flexion LIPHOOK EQUINE HOSPITAL

  22.  Most commonly performed imaging modality for OA diagnosis  Uses ◦ Identification of osteochondral fragmentation ◦ Some indication of disease severity ◦ Allows monitoring of disease progression  Limitations ◦ Radiographic changes are no indicator of pain ◦ Provides limited information on soft tissues/subchondral bone ◦ Changes develop at a variable rate after injury ◦ Poor indicator of prognosis LIPHOOK EQUINE HOSPITAL

  23.  Periarticular osteophyte  Osteochondral fragmentation LIPHOOK EQUINE HOSPITAL

  24.  Subchondral bone sclerosis  Loss of joint space  Bone lysis  Ankylosis LIPHOOK EQUINE HOSPITAL

  25.  Under used in OA assessment  Safe and easily performed  Good for detection of soft tissue injury, osteochondral fragmentation, some cartilage injury  Limitations ◦ Requires operator experience ◦ Can only assess peripheral structures LIPHOOK EQUINE HOSPITAL

  26.  Synovial hypertrophy  Capsular thickening  Specific soft tissue injury  Osteochondral fragmentation  Cartilage defects LIPHOOK EQUINE HOSPITAL

  27.  Serum biomarkers could potentially identify the early stages of OA (Frisbie et al 2008) ◦ Osteocalcin ◦ GAG ◦ Collagen synthesis/degradation  Yet to be fully validated in clinical practice but show some promise in experimental studies LIPHOOK EQUINE HOSPITAL

  28.  IRU highly variable depending on bone involvement  Non specific indicator of bone injury  IRU poorly correlated with injury in some locations eg stifle LIPHOOK EQUINE HOSPITAL

  29.  MRI represents a significant advancement in our diagnosis and understanding of subchondral bone pathology  MRI: standing low field up to carpus/tarsus  Most comprehensive imaging modality available for fetlock pathology (Powell 2012) ◦ 131 horses. Mostly with inconclusive findings on radiography ◦ 35% had early fracture pathology ◦ 54% had palmar/plantar osteochondral disease LIPHOOK EQUINE HOSPITAL

  30. But, MRI still provides only limited assessment of articular cartilage, even with high field MRI LIPHOOK EQUINE HOSPITAL

  31.  Still remains the ’gold standard’ for evaluation of articular cartilage  Opportunity for lesion debridement  Indications ◦ Osteochondral fragmentation ◦ Articular fracture repair ◦ Periarticular soft tissue injury ◦ Poor response to IA medication LIPHOOK EQUINE HOSPITAL

  32.  Expensive compared with IA therapy  In most cases requires general anaesthesia  Does not allow access to some significant areas of pathology ◦ Subchondral bone ◦ Anatomical ‘blind spots’ LIPHOOK EQUINE HOSPITAL

  33.  Despite advances in our knowledge of the pathogenesis of OA, damage to articular cartilage is still irreversible LIPHOOK EQUINE HOSPITAL

  34.  Early identification of pathology  Treatment of underlying primary causes ◦ Osteochondral fragmentation ◦ OCD ◦ Soft tissue injury  Reduction of inflammatory mediators  Repair of cartilage damage  Modification of exercise LIPHOOK EQUINE HOSPITAL

  35.  What are the goals of therapy? 1 - Improve clinical signs (symptom modification) ◦ Reduce lameness ◦ Reduce effusion ◦ Improve range of motion 2 - Halt disease progression (disease modification) 3 - Allow ongoing athletic performance 4 - Avoid catastrophic fracture LIPHOOK EQUINE HOSPITAL

  36. Symptom modifying NSAIDS Corticosteroids drugs (SMOADS) ACS Gene therapy Hyaluronic acid Disease modifying drugs PSGAG’s (DMOADS) Green lipped mussel

  37.  Rest  Physiotherapy  Neutraceuticals  Systemic medication  Intra-articular medication  Surgery ◦ Arthroscopy ◦ Arthrodesis LIPHOOK EQUINE HOSPITAL

  38.  Allows targeted therapy at the site of pathology with reduced systemic side effects  Requires positive identification of affected joints  Beneficial effects persist after detection times  Repeatable  Low morbidity  Financially viable LIPHOOK EQUINE HOSPITAL

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