LIPHOOK EQUINE HOSPITAL Graduated Bristol University 2004 - - PowerPoint PPT Presentation

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LIPHOOK EQUINE HOSPITAL Graduated Bristol University 2004 - - PowerPoint PPT Presentation

Oct 22, 2022 522 likes •1.03k views

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

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LIPHOOK

EQUINE HOSPITAL

Russell Parker BVSc MSc DipECVS MRCVS Liphook Equine Hospital

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 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

  • f equine bone marrow derived mesenchymal stromal cells”

 Awarded ECVS Diploma in Equine Surgery 2012  Currently one of 5 surgeons at Liphook Equine Hospital

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EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 Major cause of lameness, poor performance and lost

training days

 Economic impact  Welfare implications  Sites of injury often related to athletic discipline

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LIPHOOK

EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 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)

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EQUINE HOSPITAL

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EQUINE HOSPITAL

Same end stage, different pathways!

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EQUINE HOSPITAL

Abnormal stresses

  • n normal cartilage

Normal stresses on abnormal cartilage Morphologic breakdown of articular cartilage

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

  • f PG and collagen

Cartilage breakdown

Abnormal stresses

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

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EQUINE HOSPITAL

Trauma Synoviocytes Subchondral bone Prostaglandin Il-1 TNFα Chondrocytes Matrix degradation Free radicals Matrix metalloproteinases Hyaluronan degradation Collagenase Proteinase

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EQUINE HOSPITAL

 Synovitis  Subchondral bone remodelling  Intra-articular fracture  Osteochondral fragmentation  Periarticular soft tissue injury

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EQUINE HOSPITAL

 Increasingly implicated in the pathogenesis of OA

(Sutton et al. 2009)

 Inflamed synoviocytes are a rich source of

inflammatory mediators

  • Prostaglandins
  • Cytokines
  • Matrix metalloproteinases
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EQUINE HOSPITAL

 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)

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EQUINE HOSPITAL

 Histopathological changes

  • Thickening of subchondral bone plate
  • Trabecular thickening
  • Microvascular necrosis
  • Osteocyte death
  • Microcrack formation
  • Cartilage erosion and loss
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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

 Clinical signs  Diagnostic analgesia  Radiography  Ultrasonography  Biomarkers  Scintigraphy  MRI/CT  Arthroscopy

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EQUINE HOSPITAL

 Effusion  Heat  Soft tissue swelling  Reduced ROM  Pain on flexion  Lameness  None….

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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

 Periarticular

  • steophyte

 Osteochondral

fragmentation

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EQUINE HOSPITAL

 Subchondral bone sclerosis  Loss of joint space  Bone lysis  Ankylosis

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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

 Synovial hypertrophy  Capsular thickening  Specific soft tissue injury  Osteochondral fragmentation  Cartilage defects

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EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 IRU highly variable

depending on bone involvement

 Non specific indicator of

bone injury

 IRU poorly correlated with

injury in some locations eg stifle

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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

But, MRI still provides

  • nly limited assessment
  • f articular cartilage,

even with high field MRI

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EQUINE HOSPITAL

 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
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EQUINE HOSPITAL

 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’
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EQUINE HOSPITAL

 Despite advances in our knowledge of the pathogenesis of OA,

damage to articular cartilage is still irreversible

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EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 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

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Disease modifying drugs (DMOADS) Symptom modifying drugs (SMOADS)

NSAIDS Corticosteroids ACS Gene therapy Hyaluronic acid PSGAG’s Green lipped mussel

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EQUINE HOSPITAL

 Rest  Physiotherapy  Neutraceuticals  Systemic medication  Intra-articular medication  Surgery

  • Arthroscopy
  • Arthrodesis
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EQUINE HOSPITAL

 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

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EQUINE HOSPITAL

 Hard to assess in naturally occurring OA

  • Wide variation in disease progression and case management
  • Monitoring clinical signs only gives an indication of SMOAD properties

 Recent development of reproducible models of OA

has significantly aided quantitative assessment of therapy

  • Chemically induced synovitis eg LPS
  • Joint instability eg cruciate transection
  • Subchondral bone trauma
  • Osteochondral fragmentation model
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EQUINE HOSPITAL

 Pioneered by McIlwraith and colleagues at Colorado

State University

 An osteochondral fragment is created on the

radiocarpal bone, inducing OA in the post operative period

 This has allowed comparative

assessment f many different IA medications

 BUT – this model may not be

applicable to your case!

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EQUINE HOSPITAL

 OA is not treatable or reversible; early intervention is

essential for successful outcomes

 In advanced end stage disease IA medication is

unlikely to have a prolonged beneficial effect

 Further options?

  • Retirement
  • Euthanasia
  • Arthrodesis

 Surgical  Chemical

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EQUINE HOSPITAL

Distal tarsus Pastern Fetlock Carpus Shoulder Coffin joint

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EQUINE HOSPITAL

 Isolated reports  Stolk et al 1996; metacarpophalangeal joint  Unlikely to withstand the cyclical loading required for

normal equine life

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EQUINE HOSPITAL

 Enhanced disease detection

  • Imaging
  • biomarkers

 Improved intra-articular therapy

  • DMOAD development
  • Gene therapy (IL-1)

 Surgical cartilage augmentation

  • Chondrocyte grafts
  • Full thickness grafts
  • BMAC
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EQUINE HOSPITAL

 The horse as a model of naturally occurring

  • steoarthritis by McIlwraith et al (2012); review

article

 “Diagnosis and management of lameness in the

horse” 2nd Ed by Ross and Dyson, Published by Elsevier

 “Joint disease in he horse” by McIlwraith and Trotter,

Published by Saunders

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EQUINE HOSPITAL

 Boyde, A. (2003) The real response of bone to exercise. J. Anat. 203,173-89.  Cruz, A.M., Hurtig, M.B., (2008) Multiple pathways to osteoarthritis and articular fractures: is

subchondral bone the culprit? Vet. Clin. North. Am. Equine Prac. 24, 101-16

 Frisbie DD1, Al-Sobayil F, Billinghurst RC, Kawcak CE, McIlwraith CW. (2008) Changes in

synovial fluid and serum biomarkers with exercise and early osteoarthritis in horses. Osteoarthritis Cartilage. 16(10):1196-204.

 Ireland JL1, Wylie CE, Collins SN, Verheyen KL, Newton JR. (2013) Preventive health care and

  • wner-reported disease prevalence of horses and ponies in Great Britain. Res Vet

Sci.95(2):418-24

 Ireland JL1, McGowan CM, Clegg PD, Chandler KJ, Pinchbeck GL (2012) A survey of health care

and disease in geriatric horses aged 30 years or older. Vet J. 192(1):57-64

 Kawcak, C.E. (2001) The role of subchondral bone in joint disease: a review. Equine Vet. J. 33,

120-6

 McIlwraith CW. Frank Milne Lecture: From arthroscopy to gene therapy: 30 years of  looking in joints. Am Assoc Equine Pract 2005;51:65–113.  McIlwraith CW, Frisbie DD, Kawcak CE.(2012) The horse as a model of naturally occurring

  • steoarthritis. Bone Joint Res. 1(11):297-309.
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 Neundorf RH1, Lowerison MB, Cruz AM, Thomason JJ, McEwen BJ, Hurtig MB(2010)

Determination of the prevalence and severity of metacarpophalangeal joint osteoarthritis in Thoroughbred racehorses via quantitative macroscopic evaluation. Am J Vet Res. 71(11):1284-93.

 Powell SE1 (2012) Low-field standing magnetic resonance imaging findings of the

metacarpo/metatarsophalangeal joint of racing Thoroughbreds with lameness localised to the region: a retrospective study of 131 horses. Equine Vet J.;44(2):169-77.

 Reed SR1, Jackson BF, Mc Ilwraith CW, Wright IM, Pilsworth R, Knapp S, Wood JL, Price JS,

Verheyen KL. (2012) Descriptive epidemiology of joint injuries in Thoroughbred racehorses in training. Equine Vet J. 2012 Jan;44(1):13-9.

Stolk PW1, de Waal Malefijt MC, Buma P, Barneveld A (1996) Total replacement of the metatarsophalangeal joint in the horse. A single pilot study. Vet Q. 18 Suppl 2:S90-3.

 Sutton S1, Clutterbuck A, Harris P, Gent T, Freeman S, Foster N, Barrett-Jolley R, Mobasheri A

(2009) The contribution of the synovium, synovial derived inflammatory cytokines and neuropeptides to the pathogenesis of osteoarthritis. Vet J. 179(1):10-24.

 Welsh CE1, Lewis TW, Blott SC, Mellor DJ, Lam KH, Stewart BD, Parkin TD (2013) Preliminary

genetic analyses of important musculoskeletal conditions of Thoroughbred racehorses in Hong

  • Kong. Vet J. 198(3):611-5