Equine orthopaedics Flashcards
Hoof anatomy?
Wall - toe (dorsal third), quarters, heels, bars Sole Frog Periople Heel bulbs White line
What are the layers of the hoof wall?
External layer:
- periople = soft, pale ring of horn around coronary band
- stratum tectorial = thick outer layer shiny horn
Middle or stratum medium:
- bulk of horn (tubular)
Internal or stratum lamellatum
- non sensitive lamellae
Normal structure of lamellae?
Primary and secondary lamellae
Perfect strong interdigitation with tubular horn of hoof wall
How does the hoof grow?
Coronary groove contains dermis that grows hoof wall (horn)
P3 dermis (direct on bone) grows dermal/sensitive lamellae and epidermal/insensitive lamellae
Corium (dermis) contains blood vessels, nerves to supply epidermal cells with nutrients and oxygen etc
What is laminitis?
Inflammation of lamellae
Inflammation/degradation of attachments between hoof wall and coffin bone
Lamellar interdigitation fails
Significant loss of integrity -> sinking or rotation of P3 = ‘founder’
P3 stability compromised
Horse’s weight holding capacity is compromised
What are the 3 categories of causes of laminitis?
- Inflammatory laminitis: SIRS associated:
- retained afterbirth
- severe illness, especially GI disease
- black walnut shavings in USA
- feeding accidents e.g. grain overload - (non) Weight bearing laminitis (supporting laminitis)
- Endocrinopathic laminitis: (90% of cases)
- PPID
- Equine Metabolic Sundrome
- (Iatrogenic corticosteroid induced)
Why does inflammatory laminitis occur?
Pro-inflammatory signalling
Endothelial activation
Activation of degradation enzymes (ADAM-TS4, MMPs)
Early vasodilation
Arteriovenous shunts - produce clinical sign of bounding digital pulses
How does (non) weight bearing cause laminitis (supporting laminitis)?
Usually one single foot
Unilateral weight bearing for prolonged periods of time
Usually requires complete non weight bearing of contralateral limb
Presumed that immobile limb lacks adequate lamellar perfusion
Lamellar cell damage and inflammatory events
What causes endocrinopathic laminitis? Why?
Hyperinsulinaemia induces laminitis
Theory is via endothelial activation via altered intracellular signalling
Pro inflammatory mediators - lamellar damage
Clinical signs of laminitis? What to differentiate from?
Acute onset lameness, most obvious in forefeet Increased digital pulse and warmth in hooves Reluctant to move Limbs extended forward Caudal stride phase reduced Worse at the turn Worse on hard ground Painful to hoof testers Hoof rings Cap horn White line separation
Differentiate from:
- horse lying down, sweating, pawing (colic signs)
- reluctant to move, hard muscles (myopathy signs)
Obel grading system to categorise laminitis clinical signs?
Grade I:
- shifts weight from one foot to other or incessantly lift feet
- lameness not evident at walk but at trot has shortened stride
Grade II:
- moves willingly at walk and trot but noticeable shortened and stabbing stride
- foot can be lifted off the ground without difficulty
Grade III:
- moves reluctantly and resists attempts to life affected or contralateral feet
Grade IV:
- marked reluctance or absolute refusal to move
Changes to hoof seen in advanced laminitis cases?
Flattening-convexity of sole (P3 is moving)
Depression around coronary band (sinker)
Bruising, subdural abscessation
Why do laminitic horses get hoof rings? Significance?
Due to cell damage and lamellar elongation
Dorsal hoof wall growth is inhibited more than caudal so divergent rings (wider at heel than toe)
Indicates underlying disease/chronicity
Diagnosis of laminitis?
Clinical signs
Full history - determine cause/underlying cause
Radiography
What radiographic views are used for laminitis? What to look for?
Horizontal beam
Lateromedial:
- radio dense marker on dorsal hoof wall from coronary band distally
- may see rotation, sinking, modelling (ski jump), radiolucent line)
Dorsopalmar
- weight bearing
- assess P3 stability, mediolateral balance, lamellar separation
DPrPaDiO - solar margin P3 fractures (type VI)
What is measured on radiography for laminitis?
D = founder distance: - 2-8mm - >15mm poor R = angle of rotation - <5.5 degrees good - 6-11 degrees fair - >11 degrees poor S = solar depth - solar prolapse a poor sign
Venogram for laminitis? What for? How?
Record of the vascular status of the foot: - coronary circulation - dorsal P3 circulation - terminal arch - bulbar circulation - circumflex vessels Tourniquet at fetlock Radiographs taken right away Can be performed over time Prognostic indicator
Treatment for laminitis: principles? Drugs? Non drug treatment?
Principles: - treat primary disease - pain relief - digital support Treat primary disease: - remove retained placenta - address SIRS/endocrine cause/increased weight bearing NSAIDs: - reduce inflammation and pain - flunixin or phenylbutazone Severe non responsive cases: - morphine - ketamine/lidocaine infusion - gabapentin (unlicensed) Digital support to reduce stress on damaged lamellae, weight transferred to frog: - deep soft bedding - frog support (lily pads) - styrofoam pads Box rest Cryotherapy: - continuous crushed ice up to proximal MC3/MT3 - reduces tissue metabolism - vasoconstriction - reduces severity of lamellar lesions - no detrimental effects on horses
ACP for laminitis?
Doesn’t help the laminitis but calms horse down and lie down more
Shoeing/trimming plan for acute laminitis?
If shoed, leave on
Provide frog pressure and hoof support - lily pads, styrofoam supports
Trim hoof carefully from quarters back
Fit heart bar shoe - frog plate on same plane as rest of shoe
If no shoes, foot trim with radiographic guidance, trim toe back to ease break-over and decrease DDFT tension, lower heels
Prognosis for laminitis?
Prognosis is proportional to severity and extent of lamellar pathology = P3 instability Poor if: - >15 degrees rotation - distal displacement of P3 - P3 prolapsing through sole - sinkers or founders
Chronic laminitis signs?
Altered hoof growth Dishing dorsal hoof wall Seedy toe Dropped sole Foot abscess common
Hoof care for chronic laminitis?
Aim = restore alignment of pedal bone to dorsal hoof wall and sole
Problems:
- diseases weak laminar growth
- tension by DDFT
- chronic pain
- chronic infections: seedy toe, abscesses
Reverse-shoes, heart bar shoes, imprint shoes glued on, EDSS
Remove abnormal horn/abscesses
Pain relief after trimming
Indications for DDFT tenotomy for laminitis? When contraindicated?
Refractory cases
With rotation
Salvage procedure
For horses not intended for athletic purposes
Contraindicated in founders
What to check for on a front and lateral assessment of a horse’s limb conformation?
Front - line should bisect limb all way through to middle of hoof
Lateral - point of shoulder bisecting through knee to heel of hoof, hoof-pastern axis (long axis) should be correct
Foot balance from front view of hoof?
Medial and lateral hoof walls should be same angle and length
Assess coronary band in relation to the bearing surface
Foot balance from lateral view of hoof?
Hoof pastern axis
Coronary band from dorsal to palmar - level, undeviated
Dorsal hoof wall should be 2.5-3 x heel length
Foot balance from mediolateral view?
90 degrees to long axis
Assess symmetry
Evaluate heels for shunting/sheared heels
Foot balance from solar view of hoof?
Bisect midline
Centre of foot just back from point of frog
White line reflects true shape of the foot
Length/shape of frog
Bar shape/angulation to hoof wall and heels
Concavity/convexity of sole
How to correectivley shoe/trim a broken back hoof-pastern axis (HPA), long toe/low heel, underrun heels?
Trim to reduce toe length, preserve heel
Shoe to raise heel
Caudal shoe support over frog to prevent back of foot descending
Corrective shoeing for medio-lateral imbalance with heel shunting?
Shoe with support at back over shorter side?
Float heel on that side so gap between heel and shoe - will come down over 48h
What is true P3 rotation?
Rotated in relation to P1 and P2
Can get ‘not true’ rotation where aligned with P1 and P2 but not aligned with dorsal hoof wall
What is a sinker?
P3 in normal alignement with P1 and P2
But pushing through sole
Clinical signs: coronary band depression, possible separation behind coronary band, serum exudate
Normal distance from coronary band to extensor process of P3 on radiography?
5-10mm
Dorsal wall resection technique for laminitis?
Trim hoof capsule Apply heart bar shoe Mark area to be removed Dremmel or knife? Sedation not nerve block 'Split' sole
Chronic laminitis: farriery?
Abnormal anatomy - lots of heel growth, corkscrew Need regular farriery Trim frog to margins Remove excess sole Lower heels Rasp toe
Positives and negatives of glue on plastic shoes for laminitis?
Positives: - less trauma - easy fitting - anti concussive Negatives: - expensive - poor grip - frog plate moveable
Intrinsic and extrinsic risk factors of orthopaedic problems in racehorses?
Intrinsic: - age - sex - breed - training regime Extrinsic: - racing surface - exercise intensity - time off before return to exercise following injury
What increases the risk of fatal condylar fractures of the third metacarpus/tarsus in UK racehorses?
No gallop work in training First year of racing Longer races More runners Amateur jockey races Firm/hard going
Risk factors for palmar/plantar osteochondral disease in racehorses?
High number of lifetime races
High training gallops in previous season
High number of short between race intervals (less rest)
Raced more than one season
Not age at first race
No trainer effect
What increases the risk of superficial digital flexor tendinopathy in racehorses in hurdle starts?
Firm ground
Higher age at first race
Previous SDFT injury
Summer racing
What increases the risk of a horse falling in eventing?
Jumping into/out of water
Taking off from good-to-soft, soft or heavy ground
Non angled fences with spread >2m
Angled fences
Riders who knew they were in the lead at the start of the XC
Too fast/slow into the fence
No previous refusals at previous XC course
Rider has XC lessons
Risk factors for lameness with dressage?
Age and height Indoor arenas Horse walkers Lungeing Back problems Surface
Acceptable treatment for SDFT injuries? Evidence? What not to do?
Ice/hydrotherapy - no direct evidence for use
Corticosteroids - no evidence for use
NSAIDs - clinical improvement
Intralesional PRP - evidence
Intralesional mesenchymal stem cells - decreases re-injury rate, flat > jumping
Controlled exercise - evidence
NOT shock wave therapy or firing
Treatments with evidence basis for bone spavins (carpal chip)?
Tiludronate - improved by 1-2 grades of lameness but not sound
Triamcinoclone acetate (TCA) - decreases lameness, improves synovial fluid parameters, better histologic appearance of synovial and chondral tissue, so is chondroprotective and is preferred treatment
Autologous conditioned serum (ACS) - improved lameness, not sound, decreased synovial hyperplasia
Acceptable treatments for osteoarthritis with evidence basis?
NSAIDs - clinical improvement
Intra-articular corticosteroids - evidence for triamcinolone and methylprednisolone
PRP - evidence for soft tissue (not osteoarthritis)
IRAP - improved lameness grade and histological appearance
Oral poly-sulfated glycosaminoglycans - mostly anecdotal
Tiludronate - maybe, improved lameness grade but not sound)
Intra-articular ethanol
Hoof cracks - Which way do they run? Cause? Consequences of instability? Treatment?
Usually proximo-distal direction - poor foot balance/care, poor horn quality, environment, trauma
Occasionally transverse - coronary band injury
Instability -> shear forces, further separation, pain, infection
Treatment:
- don’t nerve block (need to determine sensitive/insensitive parts)
- farriery: decried/dremmel all necrotic tissue, filler to stabilise (plate, wire), trim foot, unload crack/bar shoe/quarter clips
- treat cause
- antibiotics
Coronary band and hoof wall injuries - Aetiology? Clinical signs?
Wire lacerations/foot trapped/overreach injuries
Clinical signs:
- avulsion/disruption to the hoof wall +/- coronary band
- lameness
- haemorrhage ++ (digital cushion highly vascularised)
- involvement of other structure (DIP/PIP/NB/DFTS, tendons/ligaments)
Treatment of coronary band and hoof wall injuries?
Primary or secondary intention healing - often heavily contaminated
Preserve coronary band if can - suture, stabilise hoof wall with wiring/cast/shoe
Antibiotics
NSAIDs
Bandaging initially to protect
Foot/distal limb cast to stabilise
Flush synovial structures - treat sepsis early and aggressively
Shoeing
Prognosis of puncture wounds of the foot?
Most are good and managed conservatively
But potential to involve deeper structures with life threatening complications
Foot penetration problems associated with shoeing?
Nail bind - nail close to sensitive structures, mild lameness, pain around nail
Shoeing prick - nail into sensitive structures, immediately painful/blood, may develop sub solar abscess if left
Subsolar abscesses - Cause? Clinical signs? Treatment?
Very common Causes: - tracking of bacteria along nail placed near to laminae - nail puncture or other object - sole bruise (blood acting as media) Abscess puts pressure on sensitive hoof lamina Clinical signs: - usually severe acute lameness - increased digital pulse - increased hoof temperature - sensitive to hoof testers Treatment: - key = drainage - remove shoe/nail if present - pare foot - follow tracts and remove all necrotic/underrun horn - poultice/tub 1-2x daily, MgSo4 - bandage to protect - (NSAIDs/antibiotics) mostly not needed - tetanus prophylaxis - re-shoe once dry/hardened - hospital plate in severe cases
Foot penetrations involving synovial structures - What structures could be involved? Diagnosis?
Usually involve middle third of frog: - navicular bone/bursa - DDFT - distal sesmoidean impar ligament - DIP joint - DFTS Diagnosis: - moderate-severe lameness - presence of nail/foreign body in foot - puncture wound - distal limb swelling/DIP effusion/DFTS effusion - increased digital pulse - sensitive to hoof testers over tract (can be difficult in painful horse) - radiography +/- probe, contrast study - synoviocentesis (NB/DIP/DFTS): increased turbidity, cells, protein, dark/red if infection - MRI
Treatment of foot penetrations involving synovial structures? Prognosis?
GA:
- debridement of infected tissue
- flush affected synovial structures: navicular bursoscopy/DIP arthroscopy/DFTS tenoscopy
- resection of damaged tissue
- systemic ABs/IVRA/intrasynovial medication/PMMA beads in tract
Bandaging then hospital plate and raised heel
NSAIDs
Fair success:
- 56% survival to discharge
- return to athletic function is guarded
Chronic hoof abscessation - Causes?
May be masked by antibiotics or persist from poor drainage/insufficient removal of necrotic tissue
Underlying causes:
- immunocompromised e.g. cushings
- keratoma
- sequel to laminitis
- bone sequestrum/collateral cartilage infection
- infective (pedal) osteitis
What is quittor? Cause? Clinical signs? Treatment?
Infection of the collateral cartilages of the foot
Cause: trauma/wound
Clinical signs: swelling/chronci discharge from coronary band
Treatment: surgical debridement of infected tissues
Be careful of DIPJ
Keratoma of foot - What is it? Clinical signs? Treatment?
Benign tumour of hoof/solar horn
Signs:
- intermittent lameness/discharge
- characteristic circular area of abnormal keratinisation with discharging tract
- radiography may show smooth radiolucent defect in P3
Treatment: surgical resection under GA
Canker of the foot - What is it? Cause? Consequences? Treatment?
Often heavily feathered breeds
Chronic condition associated with hypertrophy of the germinal layer of the foot epithelium - may affect frog, bars, heels and sole
Often linked with Fusobacterium/Bacterioides
Infection leads to dyskeratosis
Results in abnormal hyperkeratotic horn with keratosis and fronds of unconnected interlobular horn
Treatment of early/mild cases:
- improve environment
- decried abnormal areas
- metronidazole bandages +/- systemic ABs
- astringents: picric acid and benzoyl peroxide
- dilute formalin
Treatment of advanced/severe cases:
- aggressive surgical debridement
- bandaging/shoeing
Recurrence common
White line disease - What is it? Risk factors? Clinical signs? Treatment?
Progressive, crumbling, poor quality hoof wall with separation at the white line
Risk factors:
- warm, wet weather
- biotin/methionine/zinc/selenium deficiency
- bacterial infection common
Clinical signs:
- +/- lameness
- separation of hoof wall esp at toes/quarters
- grey/black crumbly horn
Treatment:
- remove abnormal horn
- support remaining horn: bar shoe and clips, hoof acrylic
- prevent progression: environment, topical povidine/iodine, feed supplementation
Which local anaesthetics are used for equine diagnostics? Onset and duration?
Mepivacaine: 1-2 min onset, 45-60 min duration
Bupivacaine: 4-5 min onset, 1-2hr duration
Contra-indications for diagnostic analgesia in the limb?
Suspect fracture
Cellulitis (acidic so less effective, iatrogenic sepsis if synovial block)
Uncooperative horse
Reasons for poor response to diagnostic analgesia in the limb?
Severe pain e.g. P3 fractures and sub solar abscessation
Poor technique/inadequate volume
Nerve variation - aberrant nerve roots/anatomical variations
Subchondral bone pain - bone pain modelling may not be desensitised by intra-articular anaesthesia
Previous neurectomy - check for suspicious thickenings/scar
Pain originating more proximal e.g. neck pain
Neurological/mechanical
Causes of severe lameness after nerve block?
Synovial sepsis
Or flare few hours later (reaction to local)
Palmar digital nerve block: Site? Technique Needle size? Volume? Structures desensitised?
Site: just proximal to collateral cartilage, abaxial to edge of DDFT
Technique: limb non weight bearing, palpate neuromuscular bundle with thumb, place needle angled distal and over bundle, do on both sides, check heel bulb sensation after 5 mins with blunt object e.g. pen/key
Needle: 23/25G, 5/8”
Volume: 1.5-2ml
Navicular bone and bursa, collateral suspensory ligaments, distal sesamoidean impar ligament, distal DDFT and tendon sheath, insertion of SDFT, digital cushion, palmar third of lamellar corium and corium of sole, palmar processes of the pedal bone, collateral cartilages, +/- collateral ligaments of DIP joint, palmar pouch of DIP joint
+/- PIP joint analgesia
Abaxial sesamoid nerve block: Site? Technique? Needle size? Volume? Structures desensitised?
Site: immediately palmar to neuromuscular bundle at the abaxial surface of the base of the PSB
Technique: limb non weight bearing, palpate neuromuscular bundle with thumb, insert needle distal and parallel to bundle
Needle: 23/25G, 5/8”
Volume: 2ml
As for PDNB but rest of digit
Rest of P3/P2 and palmar P1
Collateral ligaments of the DIP and PIP joints
DIP and PIP joints
Distal sesamoidean ligaments
Lamellar corium and coronary band
Distal digital extensor tendons
Dorsal extension branch of the suspensory ligament)
May partially desensitise fetlock joint if too high
Distal interphalangeal joint (DIP joint) block: Site? Technique? Needle size? Volume? Structures desensitised?
Site: dorsal approach Technique: weight bearing, midline, palpate depression just proximal to coronary band (1-2cm) on dorsal pastern, insert needle vertically through skin and extensor tendon Needle: 20G, 1.5" Volume: 6ml DIP joint \+/– Collateral ligaments of DIP joint Navicular bone/bursa Toe region of sole (not heel)
Navicular bursa block: Site? Technique? Needle size? Volume?
Site: palmar approach between heel bulbs, horizontal, midline through DDFT
Technique: weight bearing or in a navicular Hickmans block, skin bleb (use radiographic control
Needle: 18G spinal
Volume: 2-4ml
Lateromedial X ray of the foot: technique? What can be assessed?
Technique:
- horizontal beam
- foot on edge of block/weight bearing (otherwise will miss sole)
- centre 1-2cm below coronary band, halfway between dorsal hoof walls and heels
- markers on dorsal hoof wall/frog
Assess:
- phalangeal/solar angle
- relationship to dorsal hoof wall and sole/shoe
- P3/P2/NB?DIPJ
- P3 extensor process
- navicular bone
Horizontal dorsopalmar X Ray of the foot: Technique? What can be assessed?
Technique: - stood on blocks - important that stood straight - horizontal beam centred 2cm below coronary band and perpendicular to limb Assess: - P3 margins: relationship to hoof wall (lateromedial balance with markers), sidetone - DIPJ and PIP joint space - PIPJ joint margins - navicular bone margins
What is side bone?
Mineralisation of collateral cartilages of foot
Dorsoproximal-palmardistal oblique-P3 X ray of foot: Versions? What can be assessed?
Versions:
- upright pedal: ‘truer’ image as beam perpendicular to plate, horses toe in a Hickman block
- high coronary: easier to perform with horse standing on tunnel containing a cassette, angle down about 65 degrees through coronary band, slight elongation of foot
Assess:
- P3 body, solar margin and wings: arena versus lysis, vascular channels versus fracture
Dorsoproximal-palmardistal oblique-navicular bone X ray of foot: Versions? Technique? What can be assessed?
Versions: upright pedal or high coronary view Technique: - collimate well - centre 1-2cm above coronary band Assess navicular bone: - proximal and distal borders - lateral and medial wings - DIPJ margins
Palmaroproximal-palmarodistal oblique (“skyline”) X ray of the foot: Technique? What can be assessed?
Technique: - foot on cassette tunnel - leg back/fetlock extended - tube head under horse - vulnerable! - centre between heel bulbs, 45 degrees - look at LM view or foot conformation Assess: - navicular bone - flexor cortex and surface
Management of conditions of the DIPJ? Diagnosis?
Synovitis/OA/OC fragment: - intra-articular medication e.g. hyaluranon/corticosteroids, IRAP - NSAIDs - remove fragment Joint trauma/subchondral bone pain: - rest - NSAIDs Collateral ligament desmitis: - rest - farriery/shoeing (rolled shoe) - shockwave, intra-articular medication OCLL: - intra-articular medication
Diagnosis:
- uni or bilateral lameness
- DIPJ effusion
- lameness localised to foot by diagnostic anaesthesia
- radiography
- US often unrewarding
- MRI - collateral ligament desmitis
Pedal bone fractures: Aetiology? Signs? Diagnosis?
Aetiology: - kicking wall, blunt trauma - penetrating injury/hoof wall trauma Signs: - acute foot pain - increased digital pulse - hoof tester +ve, percussion +ve (may not be specific) - +/- DIPJ effusion Diagnosis: - clinical signs - local anaesthesia: usually improves but may not fully block out - radiography: evaluate wings of P3 - occasionally need MRI/CT etc
Treatment of pedal bone fractures?
Conservative management:
- immobilisation and rest with bar shoe or hoof/foot cast
- fracture heals by fibrous union
- most foal P3 fractures heal without casting/shoeing (can lead to foot contraction)
- prognosis reduced if articular involvement
Surgical:
- removal of fragment(s) e.g. extensor process fragments
- internal fixation e.g. sagittal articular fractures
- PD neurectomy for non healing wine fracture
Pedal osteitis: What is it? Diagnosis?
Vague term - radiographic changes in pedal bone in horses with chronic foot soreness
Often associated with foot imbalance
Diagnosis:
- lameness localised to foot
- variable radiographic changes: demineralisation/widening of vascular channels
Treatment:
- correct foot imbalance/reduce abnormal stresses through foot
Navicular bone fractures: Aetiology? Diagnosis? Treatment?
Uncommon Traumatic aetiology Diagnosis: - moderate lameness - diagnostic anaesthesia localised to foot - radiography Treatment: - conservative healing by fibrous union - surgical repair difficult
Navicular disease: Signs and history? Diagnosis?
Signs/history:
- intermittent chronic bilateral forelimb lameness
- may stumble, be unwilling to go forward, refuse jumps etc
- associated with low heel/long toe conformation
Diagnosis:
- history, signalment, age
- foot conformation
- hoof tester +ve over frog not consistent finding
- land toe first
- lameness worse on hard and circle
- local anaesthesia: PD+ve, DIP+ve, NB+ve
- may switch lameness or worsen lameness on other limb
- radiography
Pathology associated with navicular disease?
Age related - thinning of fibrocartilage and roughening of DDFT
Defects in palmar surface fibrocartilage - palmar cortex erosion and medullary lysis
DDFT damage - surface fibrillation, core lesions, adhesions
Defects in palmar cortical bone - replacement of normal medullary tissue with highly vascularised connective tissue
New bone formation along collateral sesamoidean ligament
Degenerative changes around DIP/NB articulation
Radiographic abnormalities of navicular disease in order of most important?
Medullary cyst
Flexor cortex erosion/irregularities
Loss of corticomedullary definition - endosteal sclerosis
Distal border fragmentation
Entheseophytes on lateral (or medial) border
Enlarged or increased number of synovial fossae
Treatment options for navicular disease?
Farriery very important:
- balance foot
- reduce breaker by rolling toe/reducing leverage/improving centre of rotation of DIPJ
- engage frog with ground/shoe and improve heel support
Medical treatment:
- NSAIDs
- intra-articular or intra-bursal medication e.g. hyaluranon/corticosteroids
- bisphosphonates (tiludronate, clodronate licenced) significantly improve lameness but don’t resolve
Surgical management:
- neurectomy
Primary DDFT lesions in the foot: Diagnosis? Where commonly occur? Treatment?
Diagnosis:
- midl-severe acute onset unilateral lameness
- clinical exam often unrewarding
- diagnostic analgesia: most +ve to PDNB and NB
- radiography often NAS
- MRI best
Commonly occur just proximal to navicular bone
Conservative treatment - rest, shoeing
Surgical treatment - debridement via navicular bursa
Is the PIPJ or MCPJ high motion? Significance?
MCPJ
Hyperextension leads to dorsal contact and palmar loading
PIPJ is low motion - high loading esp dorsally
