Equine Lameness Flashcards
Brad
What is Lameness?
Abnormal stance or gait caused by structural or functional abnormality of the locomotor system
Lameness is a manifestation of pain, mechanical dysfunction, or neuromuscular deficit causing alteration of gait
How to grade lameness?
Grading:
0: Not detectably lame
1: Inconsistently lame at trot on circle
2: Inconsistent on straight line but consistent in circle
3: Consistent on straight line trot
4: Lame at walk
5: Non-weight bearing
How to pin point the site of lameness?
Method of Examination: *HEEL PHFNDT
1. History, breed, age, use of horse
- Examine from distance
- Reluctant to Flex Carpi:
Shift weight w/ sharp turns, trip on step, takes 1-2 short strides out of stable
- Obvious Abnormalities:
Conformation, Angular limbs, contracted hoof, pelvic symmetry, swollen joint, splints, m. atrophy - Examine gait in hand/lunge
Method:
- Walk in hand:
Foot landing & arc of flight of limbs: May indicate heel pain (Toe > Heel) or conformational (Varus)
- Trot: In hand towards & way from you to indicate which leg is lame
- Other Gaits: Not used as it is difficult to determine at higher speeds
- Lunging:
Indication: If lameness is not readily apparent
Method: From left to right (Vice-versa) from large (20m) to smaller (10m – exacerbates lameness)
Identification:
a) Lame Leg: Lameness more apparent when the lame leg is on the inside UNLESS the site of pain is on the medial aspect of the leg, e.g., proximal suspensory, medial hoof
b) Hindlimb lameness: Shortened cranial phase stride and ‘toe stabbing’ action with affected leg on inside of circle
- Lame leg Identification
Front leg: Head goes up when lame leg lands – observed with horse trotting towards you
Back leg: Hip hike – point of hip moves up/down more when lame lands – observed trotting away - Palpation of joints, tendons & ligaments
Feeling for: Heat (Hoof wall), pain, swelling, digital pulse (NVB at palmar/plantar abaxial border of proximal sesamoids), joint/tendon sheath effusion
Method: Ground up - Hoof testers & percussion
Tester
Method: Heels, quarters, toe, frog, repeat on other side
Percussion
Method: Use hammer and percuss around solar surface of hoof/shoe and allow trotting off
Indication: Deep pain, e.g., Navicular dz, pedal osteitis
- Flexion Tests
- Nerve & Joint Blocks
- Diagnostic Imaging
Describe flexion tests for detecting lameness
Method: Apply flexion to joints for 60 seconds to increase the intra-articular & subchondral bone pressure → exacerbates clinical/subclinical lameness
Static Flexion: Is flexing without trotting off afterwards
–> Screening test and assess joint range of motion
Dynamic Flexion: Involves trotting off post-flexion
Order of Flexion Tests:
- Distal Limb Flexion: Coffin, Pastern, Fetlock (contributes most in +ve flexion of a non-lame)
Flexes: Prox. Interphalangeal joint, DIJ, Metacarpophalangeal Joint & navicular apparatus
Cannon bone MUST perpendicular to avoid flexing
- Carpal Flexion: Carpus
Positive: Via lameness originating from carpus, MC3 or distal radius
Grab pastern and pull until hoof is lateral of elbow – pull up pastern & push radius down - Prox. Forelimb: Elbow, shoulder
Positive: Hard to isolate due to lacertus fibrosis - Spavin (Hock): Hock, stifle, hip
Positive: May also flex fetlock
Grasp fetlock and lift leg until cannon is parallel to ground
Describe nerve blocks for detecting lameness
Nerve/perineural Block
Method: 1.5-3ml of prilocaine/mepivacaine – 25G x 5/8” needle – alcohol wipe or aseptic scrub if by synovium → wait 10-15min & prick injection site
Joint Block
Method: 5ml fetlock, 35ml stifle → no shaving, but do aseptic prep – 21/20G x 1.5” needle w/ new bottle – does not result in loss of skin sensation
Forelimb:
- Distal Limb:
a) Palmar Digital NB (PDNB)
Location: Neurovascular bundle (NVB) proximal to collateral cartilages
Blocks: Caudal 1/3rd of foot – Heels, Navicular pone, P3, Varied amount of sole, DIP Joint
b) Abaxial Sesamoid NN (ABSNB)
Location: NVB at base of proximal sesamoids bones
Blocks: Mid pastern and entire distal foot including skin sensation
c) IA Coffin/DIP JB
Location: Dorsal or lateral approach to minimise P3 extensor process damage Blocks: DIP, sole & NBo
d) Navicular Bursa JB
Needle: 18G 3.5”
Location: Btwn heel bulbs at coronet level ~1cm distal with limb raised in partial flexion
Directed midway along circumference of hoof
- Fetlock
a) Low 4 Point
Location: Distal metacarpus near buttons of splints and btwn DDFT & suspensory
Blocks: Fetlock, sesamoid, SL br (Suspensory ligament?) & below
b) IA Fetlock JB (Intra-articular fetlock joint block)
Location: Through collateral lig. of sesamoid btwn palmar MC3 & suspensory lig
- Metacarpus:
a) High 2 Point - Carpus: 3 Joints
a) IA Middle Carpal JB & Radiocarpal JB: Middle carpal & carpometacarpal have communication, radiocarpal stands alone.
Hindlimb:
- Distal Limb:
a) PBDN
b) IA Coffin JB
c) Navicular Bursa JB
d) ABSNB:
Location: Inject medial nerve from contralateral side of horse +- Combine dorsal metatarsal n. at pastern either side of extensor - Fetlock
a) Low 6 Point
Location: Same as 4-point but inset two more cranial to the 3MC bone
b) IA Fetlock JB
- Metatarsus:
a) Lateral Plantar NB
Location: Elevate limb & hock partially flexed to displace ADFT medially → inject axial to prox. MT4
- Tarsus
Tibiotarsal & Proximal intertarsal ALWAYS communicate
Distal & tarsa-metatarsal sometimes communicate
a) Tarsometatarsal
Location: Head of splint & T4 at palpable notch – aim opposite to from fetlock
b) Distal intertarsal
Location: Medial 6-8mm proximal to tarsometatarsal at the distal calcaneon tendon
c) Tibiotarsal:
Location:
Dorsal pouch - either side of saphenous v. ~3cm below medial malleolus
Plantar pouch – Between lateral malleolus & Calcaenous
Explain how diagnostic imaging can be used to detect lameness
Radiography
Issues: Portability (minimalistic), delayed exposure, requires oblique views, mixed practice multi-application, less than ideal environment
Radiation Safety: Limit exposure, increase distance, body protection, limit personnel, safety badge
Definitions: Radio-lucency (the degree of ‘blackness’), Radio-opacity (the degree of ‘whiteness’)
Interpreting Hoof Radiographs:
* Forelimb
– “Craniocaudal” – proximal
to the radiocarpal joint
– “Dorsopalmar” – distal to the radiocarpal joint
- Hindlimb
– “Craniocaudal” – proximal
to the tibiotarsal joint
– “Dorsoplantar” – distal to the tibiotarsal joint
Musculoskeletal US
MOA: Ultrasound waves emitted from piezo-electric crystal
Method: Sedate, clip palmar/plantar region, mark 5cm intervals, alcohol clean, contact gel
Definition:
- Power: No. of sound waves
- Gain: No. sound waves receive by probe
- Higher freq: Poorer penetration, better resolution
- Lower freq: Better penetration, poor resolution
- Isoechoic: Uniform
- Hypoechoic: Less echogenic (Black)
- Anechoic: Absence of fluid/blood
- Hyperechoic: Increased echo (White)
- Fascicle Alignment: Parallel linear echoes
Defining Lesions:
a) CSA (Cross-Sectional Area): Most sensitive indicator of damage
- SDFT - <120mm,
DDFT <1.5mm, SL - <1.5mm
b) Lesion Type/Severity:
0: Isoechoic – normal
1: Slightly hypoechoic
2: 50% anechoic, 50% echoic
3: Mostly anechoic
4: Completely anechoic (Core lesion)
Hyperechoic – Cr. tendonitis:
1 – brighter cf. isoechoic = dense scar,
2 – Mineralisation
c) Fibre Alignment
Good predictor of outcome
0: >75% parallel
1: 50-75% parallel
2: 25-50%
3: <25%
d) Echogenicity
e) Location/length
Others:
- Scintigraphy (Technetium 99): Soft tissue and bone – uptake is increased at bone modelling
- MRI: Good for soft tissue but limited to distal limb
- CT: Good for bone & soft tissue, for distal limb & head
- Thermography: Subjective
What are some soft tissue causes of Distal Limb Lameness?
- Subsolar Abscess
- Septic Pedal Osteitis
- Seedy Toe AKA White Line Disease
- Corns
- Poor Hoof Quality
- Vertical Hoof Wall Crack
- Thrush
- Canker
- Navicular Disease AKA Caudal/Palmar Heel Pain
- P3 Fracture
- Sole Punctures
- Others
What is Subsolar Abscess?
Cause: Recent rain softens sole → easy to penetrate, shod recently & nail close to whiteline, subclinical seedy toe
CS: 4-5/5 lame, bounding digital pulse, hot hoof wall/coronet, +ve hoof tester +- coronet eruption
Ddx: Fracture, cellulitis, penetrating injury, septic synovitis – All 4-5/5 lameness
Tx:
- ABSNB sedation
- Find black holes/tracts in white line→ loop knife
- Drain (14G) → small loop knife to drain pus between sensitive sole corium and non-sensitive/cornified sole
- Sugar-iodine hoof poultice 7-10d or until drainage stops
What is Septic Pedal Osteitis?
Cause: Secondary to penetrating wound or unresolved hoof abscess
CS: Persistent lameness & discharging tract, under-run sole, concurrent cellulitis & coronet swelling
Dx:
- Radiography
Views: LM, High coronary
Path: Osteolysis, demineralisation, irregular margin +- Osseous sequestrum & involucrum
Tx:
- General anaesthesia, torniquet & ABSNB
- Pack defect w/ saline gauze q2-3d
- Ab: Systemic, topical, local
- Hospital plate: Bar shoe & solar plate
- Rx curettage of GT
- 3m rehabilitation
What is Seedy Toe/White Line Disease?
Cause:
- Chronic subclinical laminitis
- Inadequate hoof care
- Wet environment
- Impaction of white line: Separation of wall and white line resulting in foreign material impaction.
CS: Severe cases may have distal displacement of P3 via dorsal wall detachment caused by laminitis
Dx: Radiograph - Radiolucent area in hoof wall that extends to ground surface
Tx:
- Resect disease wall/laminae
- Bandage/iodine if sensitive laminae
- Wall strip disease wall contacts coronet
- Rx radiograph/farrier assessment
- Heart bar/Straight bar shoe with wall clips to stabilise wall +- support sole
What is Corns?
Cause: Ill-fitting shoe or prolonged shoeing interval
Deep bruising of sole often adject to the bar/heel region
Tx: Resection of bruised thickened sole,
Apply Sugar-iodine poultice until sole is firm enough to apply wide webbed seating out shoe with no sole pressure
What causes poor hoof quality?
Cause: Wet season
CS: 3-4/5 lame, worse on hard ground
Tx: Wide webbed deep-seated aluminium shoe. No sole sole pressure from shoe
Aluminium shoe attenuates force better, lighter shoe
What is vertical hoof wall crack?
Cause:
- Poor hoof care/farriery
- Previous coronary trauma
- Laminar damage
- Untreated hoof abscess
- Foreign body
- Seedy toe
- Laminitis
Type 1
NOT involving coronet Cause: Seeding toe, long toes, dermal lamellar cracks/bruises
Tx: Resection to normal, shoe w/ side clips (+-bar shoe), equilox patch/wall plates as temporary solution
Type 2
Involves coronet
Cause: Coronet trauma, progress from Type 1 crack
Tx: Same as above but may require complete hoof wall strip & bar shoe w/clips OR hoof cast
→ 9-12m to grow down
What is Thrush?
Thick black putrid discharge usually in frog sulci and heel bulbs
Cause: Poor hoof care, moisture
Treatment: Debridement, topical alcohol/iodine, dry environment, regular hoof care, open up sulci angles
What is Canker?
Cause: Environmental, Bacterial (Fusobacterium), ? Immune mediated, BPV
CS: Proliferative degeneration of frog, solar corium, digital cushion +- concurrent coronary dystrophy
Tx: Debridement under GA), pack w/ metronidazole paste, change enviro, improve hoof care
Px: HIGH recurrence rate
What is Navicular Disease?
Includes: Navicular bone (NB), Palmar DIP Joint, Suspensory L/Collateral L of NB, Navicular bursa, distal sesamoid lig., DDFT (Excl. tendonitis)
Cause: Degenerative process
Incidence: 30-50% of forelimb lameness
Onset: Insidious
Hosts: Usually 6-9yo (Some 3-4yo)
- QH & Western Performance Horses: Typically have small boxy upright hooves
- ASH
- Cleveland Bays
- TB: Usually low underslung heels & long toe conformation (>70% of clinically affected)
- WB: Often tall narrow hooves, inherited ↑ risk due to concave/undulating proximal dorsal articular border (Via chromosome 2 & 10 in Hanoverians)
CS:
- Bilateral lameness with a stiff gait that is worse in morning, on hard ground, ↓ w/ time
- Stand w/ pointed toes & elevated heels in bedding
- +- Lateral medial imbalance & mishappen hooves (Lamer is smaller/narrower w/ tall heels)
What is the treatment and diagnosis for navicular disease?
Dx:
- Palpation: Increased digital pulses, pain on palpation of distal DDFT, Coffin joint effusion
- Hoof Tester: Positive usually over central 1/3rd of frog & percussion & heel pain +- toe
- Flexion Tests: Distal limb/fetlock & DIPJ
- Toe Extension: Increasing force on navicular bone and tension in DDFT
- Local Anaesthesia:
o PDNB: Almost all with Navicuar Disease will block out within 10 minutes BUT is the least specific (PIP Joint)
o DIPJ: More specific but requires >5ml to block sole, 55% of NDz block to DIP in <10mins
o Nbursa: More specific as unlikely to block sole, heel, DIPJ
Results: +ve DIPJ & -ve Nbursa suggests DIPJ lameness
– both -ve unlikely navicular disease - Radiography: LM, High coronary, upright pedal, skyline/special navicular, oblique
Path:
o Enlarged/misshapen synovial fossae/invaginations/foramina
o Invagination of synovium from DIPJ
o Normal horses have 3-5 synovial fossae
o Contain small BV surrounded by synovium (Instead of ligamentous attachments)
o Significant changes - ↑ height/width, inverted Y shaped changed of fossae
Shape: Concave (1) NB are more associated with grade 3-4 & poor conformation
Grades:
0 – Navicular bones are symmetric with <6 distal foramina, good trabecular pattern & corticomedullary demarcation. Uniform flexor cortex
1 – Same as above but distal foramina are varied in shape/width
2 – <8 foramina. Mild enthesophyte formation, asymmetrical NB. Extension of flexor border, crescent lucent zone on sagittal ridge. Less corticomedullary demarcation
3 – Poor demarcation, thickening of cortices, poorly defined flexor cortex, >7 foramina. Larger enthesophyte formation & mineralisation on the collateral ligament
4 – Large cyst like lesion in medulla of NB, Lucent flexor cortex with new bone formation
- MRI: Useful for soft tissue, e.g., Distal DDFT, Impar lig., cartilage erosion, bone oedema
Ddx: Low DDF tendonitis, Digital cushion pain, distal digital annular lig. Desmitis, under-run heels
Tx:
1. Hoof-Therapeutic Farriery
Px: Better in Horses lame <10months, Less severe radiographic change, Good compliance
Time: Response expected in 3-4 shoeing intervals of rest(3-4m)
Method: Wide deep seated 30 raised heel shoe +- phenylbutazone therapy reduces lameness at 14d due to ↓ ground reaction force
Shoe Types: Egg-bar, Raised heel, Natural Balance +- Rolled toe shoe
- Intrathecal/Articular Medication (DIPJ, NBursa)
- Triamcinolone: Improves lameness but not biochemical parameters, no less than 10mg
- Methylprednisolone
- Hyaluronic acid (HA): Small efficacy when used alone +- breakdown NBursa adhesions
Location:
o 60-80% of horses that block to DIPJ respond to IA DIPJ medication
o Triamcinalone (TA) & Methylprednisalone acetate (MCP) diffuse readily from DIPJ to NBursa in therapeutic concentrations
o HA has no effect on TA diffusion o TA diffusion from DIPJ into navicular bursa is↓ as radiographic changes ↑
Px: NBursa Injections work better <6m lameness, success ~80% at 4-10m duration post injection
- Others
Chemical Neurectomy: Ethyl alcohol or formaldehyde into PD nerves, lasts for 4m
Bisphosphonates:
o Tiludronate: Improved lameness in 60% acute cases at 2-6m
o Clodronic Acid: 75% improved lameness grade (1) at 2m, 5% radiographic improvement
o Tiludronate 1 dose IV or IVRLP: No improvement with IVRLP, some benefit of single dose - Surgery (PD Neurectomy)
Px: 90% sound at 12m Complication: P3 Sepsis, DDFT rupture, NB fracture, neuroma
Role: 15% reduction in Peak NB force due to PDNB abolishing DDFT contraction
What is a P3 Fracture?
Hosts: SB > TB. Standard bred, thoroughbred
Cause: Trauma, high speed exercise or hoof imbalance
Dx:
- Hx: Racing/recent work
- Lameness: 4-5 Acute/2hrs post exercise
- Exam: ↑ Digital pulses, DIP Effusion via haemorrhage (If articular), +ve hoof tester
- Local: Blocks to PDNB or ABSNB depending on fracture type
Types:
- 1: Palmar process, non-articular
- 2: Edge of DIPJ → solar margin, articular: 2nd MC (most common), Oblique high coronary view best
- 3: Midsagittal, articular
- 4: Extensor Process:
- 5: Comminuted (>2 spots):
- 6: Solar margin fracture: most common, Rest 3m & bar-shoe + sole pad. Doesn’t heal radiographically: Fibrous union
- 7: Palmar fracture at solar margin
Tx: Bar shoe + side/quarter clips OR rim-shoe OR hoof slipper cast to stabilise wall for 3-6m
Px:
- Rx Radiography (Obliques): 3-4m; ↓ Px w/ articular involvement & DIPJ effusion
- Better Px: Horses <3yo (30-30% return to race)
- Not all develop bony union
- Recurrence: 90% risk w/o bar shoe
- Persisting lameness: Consider palmar digital Neurectomy (NOT in racing horses)
What are sole punctures?
Dx: Radiograph (2 Views) - Contrast (Omnipaque – proximity to TS, DDFT, NBursa, NB, DIPJ) or probe
Tx: Broad Ab, Iodine soaked bandage, tetanus prophylaxis, establish drainage, resect any under-running sole (Tx as subsolar abscess)
Consequence: Monitor for septic pedal osteitis 10-14d later
Synovial structures that may be affected with penetrating sole injuries:
Deep Digital tendon sheath, navicular bursa, DIP joint
Px: Suspicious of if foreign body enters frog (Esp. central/sulci), marked distal limb swelling, 5/5 lameness
Tx:
- ABSNB & DIPJ synovicentesis (Cytology & CS)
- Arthro/tenosynovostomy
- Needle lavage
- Artho/Tenoscopy/Buroscopy: Debride NB via sole wound, ↓ post-op $ & healing
- Street nail procedure:
Indication: Good for NBursa penetrating wounds
Incl: GA & Esmarch/torniquet, Window frog, digital cusion & DDFT into NBursa, hospital plate & prolonged post-op care
What is Synovial fluid?
Synovial Fluids
Source: Ultrafiltrate of plasma secreted by synoviocytes
Components: Total protein <25g/L, <0.3x109 cells/L, <10% Neutrophils, clear/straw colour
Role: Viscosity & lubrication to joint via hyaluronic acid non-sulphated (Glucuronic & Glucosamine)
What is Osteoarthritis (OA)
PF: Exercise intensity/freq, conformation, level of fitness, muscle fatigue, ground, osteochondrosis
Causes:
- Traumatic Arthritis/Joint Instability: Damage to diarthrodial joints
o Synovitis & Capsulitis
o Osteoarthritis
o Instability → intra-articular & collateral lig. Injury, intra-articular fracture & subchondral bone dz, meniscal injury
- Progressive Degradation: Failure of cartilage to withstand exercise & cyclical age-based
Pathogenesis:
- Abnormal stress on cartilage → cell injury → activates IL1, 6, PGE2, Collagenases
- Enzymatic degradation + ↓ synthesis of proteoglycans & collagen
- Morphological cartilage breakdown, fibrillation & ulceration
Consequences:
- Soft tissue damage
- ↓ shock absorption of joint
- ↑ Wt. transfer onto underlying bone
- Pain, lameness, joint instability
- Chip fracture and spur formation
Response of Different Joints:
- High Motion, e.g., Fetlock, carpus: Synovitis, capsulitis, osteophytosis, OC (osteochondral) fragmentation
- Low, e.g., Distal hock, pastern: Joint narrowing, subchondral sclerosis/lysis, osteophytosis
Px: Response to injury decreases with time
Synovial Fluid: TP 25-30g/L, <5x109, Mainly mononuclear
How to treat Osteoarthritis
Tx:
- Corrective shoeing
- Arthroscopic Sx
- Joint fusion (Arthrodesis):
Indication: Distal hock, pastern, fetlock, shoulder, carpus (Middle & Carpometacarpal, pan carapal)
Fetlock Indication: SL/DSL failure, PDB Biaxial fracture, OA, Dropped fetlock - Joint Resurfacing:
Role: Re-establish cartilage tide mark
Methods: Cartilage autografts, Cultured chondrocytes, re-attachment of flaps (PDS pins) - Subchondral Micropricking:
Method: Microprick/fracture subchondral bone adj. to defect to access pluripotent cells - Rest +- Anti-inflams
Indication: Acute synovitis/capsulitis
o No Radiograph Change: 2-3m spelling o Significant Changes: 6-9m spell
o Hand-Walking: Maintain cartilage integrity o Passive Flexion: ↓ Fibrosis of capsule - Joint/Systemic Medication to slow joint damage
o NSAIDS: Phenylbutazone (PO/IV), Flunixin (PO/IV), Meloxicam, Firocoxib, Diclofenac (PO)
Role: Inhibit PGE & TBX from arachidonic acid by inhibiting COX enzyme
COX 1: Homeostatic PG (prostaglandins)
COX 2: Inflammatory PG
o Corticosteroids:
Admin: Intra-articular joint injection Indication: Pain, heat, swelling, effusion
Drugs: Triamcinolone & Betamethasone at low doses are chondroprotective
Contraindication: High doses (Methylprednisolone) → -ve on proteoglycan synth & collagen arrangement. Negative effects on cartiladge health
Role:
a) Stabilise lysosomal membranes & enzyme release
b) ↓ Vascular permeability
c) Inhibit: WBC adherence/diapedesis, platelet aggregation, cytokine production, release WBC superoxide synth, arachidonic acid release & PG synthesis
Side Effects: Systemic absorption, risk of laminitis (Triamcinolone), overuse arthropathy, sepsis
o Hyaluronic Acid:
Efficacy Depends on: Purity >2x103
a) Provides hydrodynamic lubrication & joint fluid viscosity
b) Anti-inflammatory effects: ↓ IL1, PGE2, free radicals
c) Exogenous HA enhances endogenous HA production (Chrondocytes/synoviocytes)
Admin:
IV: Weekly for 3wks, Time 1/2 45m, plasma cleared in 3hrs → ↓ lameness, PGE2, TP in carpal OC
Intra-articular Injection: T1/2 for hrs esp. in synovitis, Rx q7-14d
Oral: Evidence of reduced effusion/synovitis in horses post arthroscopy for tarsal OC
Adjunct: Combine HA + Corticosteroid, Csteroids decrease inflam thus decreases HA fragmentation thus enhance penetration for 24hrs
o Pentosan Polysulphate
a) Inhibits IL-1, MMP, PGE2
b) ↑ HA, HA molecular wt. & proteoglycan synth
c) ↓ lameness & synovitis
Admin: Weekly for 4-7wks, used only for 2-4wks due to cost
Dis: Prolonged clotting time, not allowed <48hrs of competition as ↑ EIPH
o Bisphosphonates
Role: Inhibit osteoclast activity
Tildren: Benefits early navicular disease & distal tarsal joint OA
Osphos: Improve lameness by 1 grade in 65-75% of horses w/ navicular dz +- Colic (10%)
o Oral Glucosamines & Chondroitin
Absorption: CHS (Chrondroitin sulfate) degraded by colonic bacteria, GLN (Glucosamine) absorbed in SI → better together
Role: Prevent PG degradation in cartilage, ↑ HA viscosity, ↑ PG dynth, ↑ synovial CHS
o PSGAGs
Role: ↓ IL1, MMP, PGE2, ↑
endogenous HA & proteoglycan
Time: q3-5d 5x
Route: IM & IA
Dis: IA causes sepsis → combine with Ab to inhibit complement
o 4-Cyte:
Role: Modulate IL-1 effect on chondrocytes, ↓ PGE2 in synovial fluids
Combines: Glucosamine, Chondroitin, Keratin, Dermaten and Heparin
o Extracoporeal Shock Wave Therapy
Role: Induce cytokines (TGFb), analgesia via nociceptor inhibition (2-4d), neovascularisation
Indication: Navicular disease, shin soreness, SL desmitis +- soft tissue/bone effects
o IRAP Arthrex (IL Receptor Antagonist Protein)
Indication: In OA joint IL-Ra < IL-1, normally they are in balanced concentrations
Role: Improves lameness scores in caprus for 5wks
Contains: Horse blood incubated 24hrs → monocytes bind to beads
o Platelet Rich Plasma Injection (PRP)
Method: Blood collected in citrate → concentrated via centrifuge → injection into joint
Role: Activated platelets contain a-granules (GF) → VEGF, FBGF, IGF-1, GF causing +ve effects on collagen, angiogenesis, anti-inflammatory
o Stem Cells:
Methods: Adipose derived; autologous (Adicell) & Allogenic (Cryoshot)
Role: Inhibition of cytokines after 6wks Dis: Risk of post injection flare-up
- Growth Factors:
IGF-1:
From fibrin, chondrocytes or mesenchymal cells
Indication: Distal femoral bone cyst
Px: Type 2 collagen content only 40-60% of normal cartilage
Gene Therapy:
o Adenovirus vectors, IGF1, bone morphogenic protein
o Culture chondrocytes infected with adenovirus gene encoding IGF-1/BMP-7
What is Osteochondrosis?
Failure in endochondral ossification
Pathogenesis:
- Disturbance of chondrocyte differentiation in growing cartilage → impaired endochondral ossification
- (Horses & Pigs): Disruption of blood vessels in cartilage canals supplying hypertrophic zone of growth
Causes:
1. Nutrition:
o Excess Diet Energy: ↑ blood glucose & insulin → Altered collagen in cartilage
o Excess Phosphorous: Acidifies cartilage & interferes with matrix formation
o Deficient Cu: Required for collagen cross-linking
- Genetics: Young fast-growing Horses; TB, WB, SB, account for 30% variation in hock OC
- Exercise: Trauma to weak cartilage disrupts the vascular supply → granulation tissue formation → OC lesion
Histopathology:
- Persistent cartilage in later hypertrophic zone
- Failed BV ingrowth & osteogenesis
- Failed endochondral ossification
Prevention:
- Genetics
- Ensure Nutrition: Mares during preg, weanling-yearlings
- Identify at-risk foals: Rapid 3-5m growth (Stifle), Measure serum Cu & supplement
Consequences: Osteoarthritis if untreated
What is Laminitis?
Is an inflammatory disturbance to the lamina/lamellar attachments between the P3 & Hoof wall
RF: Ponies, mares, older horses, obesity, endotoxaemia, spring/summer
Describe hoof anatomy in relation to laminitis
- Lamellae: 600 primary epidermal lamellae & 150 secondary epidermal lamellae
- Hoof-Lamellar Interface: Balances downward wt. bearing force, upward ground reaction force & caudal/proximal pull of the deep digital flexor tendon
- Basement Membrane:
Location: Lies between 2nd epidermal lamellae (SEL) & 2nd Dermal Lamellae (SDL)
Role: Influences GF & nutrient exchange, regulates keratinocyte migration, structural role
Connection: Basal cells are anchored to the BM by hemidesmosomes; attach SEL to P3 SDL
Normal Growth: Degradation by MMP’s & resynth by basal cells in a normal balance
Components: Collagen IV & VII Is coated w/ glycoproteins (Laminin) which has receptors for GF, cytokines & adhesion molecules - Vasculature:
P3 Centre: Digital A./V. anastomose in a terminal arch w/ osseous foramen to allow small vessels to enter the sub-lamellar dermis bed.
Dorsal Laminae & Solar Plexus: Last to be perfused; ↑ susceptibility due to hypovascularity in dorsal laminae
& solar laminae compressed by P3 rotation/sinking
Solar P3: No perforating vascular canal (No BV penetrate solar surface of P3); sole is perfused from circumflex & bulbar a.
Lamellae: Multiple connecting complex vascular networks
Describe the pathogenesis and clinical signs of laminitis
Pathogenesis:
- Anabolic < Catabolic processes (MMP 2 & 9 via inflam cells) & glucose deprivation (In-vitro)
- Degradation of laminin & Collagen IV
- BM detachment and separation from epidermal lamellae → Laminitis
*Breakdown of the lamellar basement membrane is a KEY feature of acute laminitis - Laminin (glycoprotein) and collagen IV are degraded – BM progressively loses its attachment to the basal cells and strips away from the epidermal lamellae resulting in failure of the hoof-lamellar
Key Alterations of Hoof- P3 Lamellar Interface:
- Inflam cell infiltration in ass. w/ disrupted Basement membrane
- Lengthening & narrowing of Primary & Secondary epidermal lamellae
- Alteration in epidermal & basal cells
- ↓ Mechanical properties by 40-60%
CS:
- Stance: Characteristic sawhorse, rocking back on heels, shifting weight
- Lameness/Gait: Debilitating bilateral forelimb lameness, stiff gait or lame on turns
- Exam: Flat/convex sole, ↑ digital pulses & heat, reluctant to lift limbs, +ve hoof test at toe
- Other: Elevated HR/RR, Sx of endotoxaemia, endocrinology diseases, severe pain, etc.
What are the types of laminitis?
- Septic Laminitis:
Causes: Grain overload, metritis, retained foetal membranes, Nutri (Se, Oxalates), Toxic (Avo, Walnut), pleuro-pneumonia, Anterior enteritis, LC volvulus, colitis
Endotoxic
Cause: Gram -ve LPS Stimulate: IL1, IL8, TNF, TBA2, PGF2, PGE2, iNOS, COX2, PMN, MMP
Path: Vasoconstriction, vascular leakage, coagulation, hypotension, hypoperfusion
Exotoxic
Cause: Gram +ve streptococcus faecalis spp.
Stimulate: MMP2 & 9, Thermolysin, Strep. Pyrogenic exotoxin B
- Endocrinopathic Laminitis:
Cause:
o PPID (pars pituitary intermedia dysfunction)
o EMS (Equine Metabolic Syndrome)
o Euglycemic hyperinsulinemia: Laminitis <48hrs
o Hyperglycaemia (CHO induced): Separation of lamellar dermal/epidermal interface
o Hyperinsulinemia: Elongated lamellae & ↓ density of basement membrane hemidesmosomes
Associated Drugs:
o Corticosteroids: cause BV constriction, inhibit NO synthase, alteres insulin, influences terminal cornification of laminae
o Triamcinolone: Causes Prolongerd period (3-4d) of hyperglycemia/insulinaemia/triglyceridaemia.
o Dexamethasone
Prevention: Avoid use in risky horses with above conditions, under 18-20mg Triamcinolone!!
- Concussive/Mechanical Overload Laminitis
Cause: Contralateral limb overload, over-exercise
Timing: Sometimes takes months or days PF: Weak laminar attachment
Path: Pain-mediated stress ↑ cortisol/inflam → BM (basement membrane) damage → Exacerbated by MMP release
What are the stages of laminitis?
Stages:
- Developmental (24-60hrs): Prior to lameness
- Acute (24-72hrs): Onset of lameness
- Subacute: No radiographic sins of digital collapse
- Chronic: Radiographic/Physical Sx of rotation/collapse
How would you grade laminitic horses?
- Lameness:
1: Shifting lameness, lifts hooves, lame on trot
2: Stiff gait on walk, lifts hooves
3: Reluctant to move/lift hooves
4: Requires force to move/recumbent - Radiology
HLZ: Hoof Lamellar Zone
P3: Angle of Rotation
Sole Thickness/Sole Depth
FD: Founder distance: Distance from extensor process to coronet
1: H-L zone - <20mm, FD - <10-14mm, P3 angle – 5-90, Sole depth – Normal
2: H-L zone – 20-25mm, FD – 15-16mm, P3 angle – 10-140, Sole depth – Decreased
3: H-L zone – 25-30mm, FD – >16mm, P3 angle – >150, Sole depth – Greatly Decreased
4: H-L zone – >30mm, FD – >16mm, P3 angle – >15-2-0, Sole depth – P3 penetrates sole
- Chronic Cases
o Abnormal growth rings
o Closer at toe cf. heel o Excess heel & thick sole
o Phalangeal rotation
Consequences:
- P3 sinking: All lamellae fail simultaneously
- P3 (Capsular) Rotation: Dorsal lamellae failure
- Digital Ischaemia:
Occurs: 8-12hrs in the developmental phase just prior to lameness/acute phase
Cause: Blood flow varies, ↑ via AV-shunts but ↓ digital perfusion
- Sole Penetration by P3
Tx: Egg-bar shoe, topical management, Tx of septic pedal osteitis, Ab, DDFT tenotomy
How to treat laminitis
- Treat or Remove Underlying Cause
- Analgesia
Types: NSAIDS (PBZ, Flunixin), A2 agents, Gabapentin, Opiods, Ketamine, Epidural, NB
Sources of Pain: Inflam mediators, ↑ submural hoof pressure, ↑ intraoessous P3 pressure, Ischaemic/reperfusion episode, laminar/vascular/neural tearing - Hoof Support (Farriery, Surgery, Medical)
a) Pharmacological:
Acetylpromazine (ACP): Sedative, vasodilator, ↑ blood flow to digit but not dorsal laminae
Nitric oxide (NO): NOS & Arginine → vascular smooth mm. → digital vasodilation but unknown laminae flow
Polymixin B: Binds to LPS of endotoxin
Pentoxyphylline (Rheologic): ↓ TNFa & ↑ RBC deformability, no effect on blood flow
Heparin (Anticoagulant): Binds to ATIII to ↓ severity/incidence of laminitis +- haemorrhage
Flunixin: Analgesia, ameliorates CS of endotoxaemia
Aspirin: Bind platelets & ↓ thrombosis
Corticosteroids: ↓ COX & NO & Epidermal cell metabolism is contraindicated
Dimethylsulphoxide (DMSO): Free radical scavenger with unknown efficacy
MMP Inhibitors: Batimastat, in-vitro efficacy only
Local Anaesthetics: ↓ neurogenic vasoconstriction, contribute to mechanical failure → lignocaine may delay CS
b) Digital Support
Role: Distribute weight evenly between sole + wall & ↓DDFT tension
Method: Cut foam pad and achieve a solar angle of 25o taped to sole with Elastoplast
Includes: Closed cell foam rubber, Styrofoam, sand bedding (Unloads dorsal laminae)
c) Farriery
Shoe Type: Heart bar shoe
Subacute & Chronic: Grow more heel cf toe and sole thickness
o Remove excess heel to re-align P3 with hoof capsule
o +- PBZ post trim
o Unload dorsal hoof wall via removing excess toe & rolling toe
o Improve digital stability with heart bar (Wide webbed +- 3-5o) shoe + sole support
- Radiographic Assessment
Views: Min LM & DP
Assess: H-L zone, P3 rotation (Capsular, phalangeal), Sole thickness, Bony modelling, Air/radiolucent lines, P3 sinking relative to coronet
Normal H-L Zone: 18-20mm (TB/QH); may be normal in acute laminitis, compare limbs
Signs that Laminitis has Stabilised: Increasing sole thickness
Gas Line: Type 1 – Acute <24hrs (Coronet separation), Type 2 – Mummified laminae
Important: Angles are estimates subject to 1-2o variation each measurement - Cryotherapy
Indication: Only if caught early (Prior to CS) or if at risk
Method: Submerge hooves in 1 degree C 100kg ice/water bath for >48-72hrs till hoof temp <10o
Role: ↓ Clinical & histopathology severity, ↓ MMP & blood flow to 10-15% non-iced hooves
Pathogenesis: Vasoconstriction ↓ delivery of trigger factors & ↓ laminae cell metabolism
Dis: Hard in clinic, risk of reflex vasodilation if not done continuously, ice changed q2hr
AVOID: Use of dry ice packs, monitor for thermal skin injury
Px:
- Determine by: Degree of improvement, rapid stabilisation of P3 rotation, ↑ sole thickness
- Return to race, RTR: 25%
- Pasture sound: 50%
- E&D: 25%
How to stabilise a horse with musculoskeletal trauma?
- Sedation
Role: Improve safety for personnel & horse
Dose: Enough to reduce stress w/o ataxia
Drugs:
- Xylazine: Low dose, short acting
- Detomidine: Longer acting
- ACP: Longer +- hypotension, ↓ sedation
- Opioids: Butorphanol & Morphine
- Analgesia
Dose: Not much as makes diagnosis harder
Drugs: PBZ, Flunixin - Restraint: Sit on horses head if recumbent, nose twitch
- Limb Immobilisation
- Immobilise joint proximal and distal to the limb
Role: ↓ mechanical force on limb but horse must still be ambulatory
Materials: Cotton wool, gauze bandage, Elastoplast, duct tape, ½ PVC pipe, timber heel elevation
Robert Jones RJB Method: Place Elastoplast stirrups medially & laterally from proximal to distal point → place x3 layers of cotton wool → fold stirrups in and apply Elastoplast over entire bandage → tape splint externally ensuring it goes to ground surface at a size of 2-3x diameter of leg
Splint devices: Kimzey splint, comppression/ski boot
How to do a distal limb/distal cannon injury splint?
- Distal limb/Distal Cannon
Aim: Align dorsal cortices of the phalanges with the cannon bone
Methods: Raised heel with dorsal splint, kimzey splint, compression boot
Includes: Phalangeal fractures, Suspensory rupture, biaxial sesamoid fracture, distal sesamoidean ligament rupture, Distal condylar fracture, SDFT/DDFT laceration
How to resolve P1/P2 and distal MC/MT3 fractures (third metacarpal/metatarsal bones)
P1/P2 & Distal MC/MT3 Fractures
Method: Dorsal splint w/ raised heels
Aim: Align dorsal cortices of P2/P1/MC3
How to resolve Sagittal P1 fractures? And metacarpus and carpal fractures
Sagittal P1 Fracture
Origin: At the mid-sagittal groove
Dx: lateromedial (LM) views, multiple obliques if non-displaced
- Metacarpus
Method: RJB, Lateral & palmar splint, dorsal splint, dorsal Kimzey splint
Method (Spiral): Lag plate & full limb cast/Kimzey splint
- Carpal Fx
Complications: May be comminuted, joint instability or collapse
Method: Immobilise from proximal radius distally
