Lameness

• clinical presentation of impaired locomotion • disruption to normal gait • mechanical = result of conformation or old injury where animal has constnt disruption to normal gait but actual lameness doesnt cause pain anymore • health and welfare problem • acute = start suddenly severe • chronic = long term and milder

0 - no lameness uder any circumstances 1 - lameness difficult to observe and not consistently apparent 2 - lameness is dificult to observe when trotting in a straight line but is consistantly apparent under certain circumstances 3 - lameness observable at the trot in a straight line 4 - lameness is obious at the walk 5 - lameness produces minimal weight-bearing or an inability to move 1-10 sometimes used in uk • hard to agree low on scale as hard to see slight lameness • need to do other surfaces and flexion tests to identify grde confidently

• sensor based system of motion analysis for detection and quantification of lameness in horses • sensors on animal at different points • identify subtle move changes (e.g. move head when one limb up) • RVC equine refferal = offer quantitative gait analysis

• things that can affect bones (cancer, fracture) • joints (arthritis, infection) • soft tissues, tendons and ligaments (torn, stretched, overheat, lesions, infected • nav bone • digital cussion • laminae ~ fractures - P3, extensor process ~ penetrating wound - stand on nail ~ white line infection, thrush ~ solar bruises, corns ~ toe cracks, heel cracks ~ keratoma ~ shoeing problems - nail prick and bind ~ navicular syndrome ~ pedal osteitis ~ sub-chondral bone cysts ~ laminitis

= inflamation of sensitive laminae in foot - thought to be a clinical syndrome resulting from several systemic diseases or concussion

• dermal epidermal layer of hooves • primary epidermal and primary dermal inter link one after the other • laminitis ~ elongation of dermal and epidermal layers = odema ~ weaker structures, layers come apart, adherence of pedal bone being suspened within hoof capsule starts to drop down and rotate as no longer being adhered

• obesity • overeating carbohydrate rich foods or rapidly fermentable fibres • toxamia = blood poisoning by toxins from a local bacteial infecion (metritis, retaied foetal membrane) • mechanical damage (working on hard surfaces = excesive concussion or injury on one foot so baring all weight on other leg which gets laminitis) • metabolic stress (overheating, separate from herd, vaccination) • ingestion of black walnut shavings and butternut shavings • hormaone changes (cushings, hypothiroid) • drug induced (steroids, wormers)

• systemic inflamatory response syndrome • endocrinopathies -EMS and or PPID (pituitary pars intermedia dysfunction) most common diseases behind laminitis • EMS (equine metabolic syndrome) - obesity, insulin resistance/dysregulation • PPID - causes hyperinsulinaemia • differences in pathology than from toxaemia and concussion

• inflamation causes separation of sensitive laminae - pedal bone can rotate and poke out through foot

• equine digital vessels very sensitive to vasoconstriction induced by endogenous substnces e.g. serotonin, prostaglandin, norepinepherine, amines, interleukin • result of inflamation, flight or flight, immune response wbc • endogenous substances produced during: ~ toxaemia ~ systemic illness ~ CHO overload ~ in response to other stimuli

• ischaemia = reduced blood flow to tissues = cause tissues to die • increased hydrostatic pressuer in vessles (increased digital pulse BUT decreased perfusion of cappilary beds in sensitive laminae • AV shunts - take blood quickly from an artery to vein without going to cappilary beds • odema surround tissue - lack of oxygen to tissue, lead to inflamation, fluid come out into tissues but in a hoof capsule = stops it being able to expand a lot • re-perfusion injury = after area of body has ischaemia, if reintroduce blood to area = cause inflamation due to tissues starting to die, cells are being damaged, inflamation help heel (lead to more odema, swelling and oxidative damage) • laminal bonds tear and pedal bone rotates and drops

• degeneration of connective tissue of basement membranes • mediated by activation of matrix metalloproteinases = enzymes and when activated, degrade extracellular matrix on basement membrane components and anything else touching the cells • blood vessels deliver factors to epidermal laminae and MMPs are activated ~ 2x increase in MMP-2 seen in horses with laminitis • MMPs disrupt laminar basement membranes • leads to dissaperance of anchoring filaments and structual failure of hoof laminae • laminar separation along dermo-epidermal junction

• some bacterial proteins = MMP-2 and 9 • reduction in glucose utilisation can trigger MMP activation • result of ~insulin failure ~ obesity ~ cuschings ~ EMS ~ metabolic response to sepsis ~ CHO overload increases blood cortisol resulting in glucose sparing ~ high levels of oligofructoses grass) can decrease hemidesmosome numbers in laminae (attaching epidermal layers down on basement membrane

• primary role of CT theory is debateable for both endocrinopothies and other assosiated factors • but does play a role on how laminitis develops (may not be intial starting point of laminitis) • laminar lesions seen in early stages • early intervention may prevent laminar stretching = lesions, swelling and separation early, owner may not see visible lameness/symptoms but performance may be off/footy or slight increase in digital pulse • once laminae stretched = very difficult to heal and animal more prone as so much damage • paradigm shifts in understanding equine laminitis 2018 • ex vivo effetcs of insulin on the structula integrity of equine digital laminae 2018

• diet • enviro - bedding, surface working on • ACP/vasodilators (take away odema and prevent ischaemia) ~ foot pads = increase load through frog and caudal foot to provide relief ~ remidial shoeing ~ NSAIDs bute, meloxicam ~ nerve blocks around palmer digital nerves for short term relief (3-8 hours depending on drug used) - opiods - buprenorphine (short term 8 hours)