Lameness Flashcards
What is 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
Lameness scale - american association of equine practitioners
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
Identifying lameness
- 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
Foot lameness
- 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
Laminitis - what is it
= inflamation of sensitive laminae in foot
- thought to be a clinical syndrome resulting from several systemic diseases or concussion
Microscopy of laminae
- 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
High risk factors
- 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)
2 categories for risk factors
- 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
Changes that occur in foot with laminitis
- inflamation causes separation of sensitive laminae
- pedal bone can rotate and poke out through foot
Laminitis - vascular theory
- 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
Laminitis vascular theory - result of vasoconstriction of blood vessels in hoof
- 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
Laminitis - connective tissue theory
- 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
Laminitis - connective tissue theory - what triggers MMP activation
- 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
CT theory - Update on understanding
- 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
Laminitis - treatment
- 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)
