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 brocken 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
- biphosphages (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
Which ligaments support P1/P2, PIPJ and MCPJ?
P1/P2 supported by collateral ligaments
PIPJ supported by distal sesamoidean ligaments and insertion of SDFT branches
MCPJ primarily supported by suspensory ligament (with contribution by SDFT)
Which nerve blocks may be positive for pastern/fetlock problems?
Perineurial: ASNB, L4/6NB
Intra-synovial: PIPJ, MCPJ
Which radiographic views are used to assess the pastern and fetlock region?
LM 10 degrees DP DMPLO DLPMO (Also flexed LM for fetlock)
Osteoarthritis of the pastern: Other name? What happens? Cause? Diagnosis and management?
Articular ringbone
Progressive destruction of articular cartilage with subchondral bone thickening and osteophyte production
Severe cases may have cystic formation/joint collapse
May be insidious or secondary to other problem e.g. trauma, sepsis, osteochondrosis
Diagnosis:
- lameness
- bony thickening over dorsal pastern
- perineurial or intra-articular diagnostic anaesthesia
- radiography (changes often dorsal)
Management:
- rest/light exercise, intra-articular medication, shoeing, NSAIDs
- arthrodesis
Osteochondrosis of pastern joint: How common? What happens? Prognosis? Management?
Uncommon (more often in tarsus and stifle)
Osseous cysts (P1 or P2) or palmar/plantar osteochondral fragmentation
Guarded prognosis
Management often palliative
(Arthrodesis)
Soft tissue injuries of the pastern area? Signs? Diagnosis? Management?
SDFT branch injury
Distal sesamoidean ligament injury
Usually acutely lame following traumatic injury
Moderate lameness and soft tissue swelling
Ultrasonography
Management: rest, NSAIDs, monitor healing by US
P1 fractures: Types? Which horses are more prone?
Sagittal, frontal, comminuted
Racehorses
Begin at sagittal groove at articular surface, extend distally (long >30mm, short <30mm)
Complete fractures exit lateral cortex or through PIPJ
Types of P2 fractures? Causes?
Palmar/plantar eminence, comminuted
Usually due to acute overload injury
Clinical findings, diagnosis and management of P1 or P2 fractures?
Clinical findings:
- usually acute onset severe lameness
- +/- instability
- +/- joint effusion
Diagnosis:
- radiography usually sufficient
First aid stabilisation: zone 1 external coaptation
Conservative treatment for short, incomplete fractures
Surgical - internal fixation in most cases
Euthanasia for comminuted, open, unstable fractures
Pastern subluxation: Aetiology? Clinical presentation? Diagnosis? Management?
Aetiology: - traumatic event e.g. cattle grid - fracture/subluxation common Clinical presentation: - acute lameness/instability - marked soft tissue swelling Diagnosis: - radiography +/- stress Management: - initially stabilise through external coaptation but often require pastern arthrodesis
Proximal sesamoid bone fractures of fetlock: Aetiology? Clinical signs? Diagnosis? Management?
Aetiology: - usually acute trauma - non adaptive modelling Clinical signs: - acute lameness with swelling and pain on palpation - +/- joint effusion Diagnosis: - radiography: may need additional oblique views - US important as may have concurrent SL injuries Conservative fractures for: - uniaxial PSB fractures in foals - non articular Surgical: - fragment removal - fracture repair Euthanasia if: - biaxial/comminuted fractures
Sesamoiditis of fetlock: What is it? Which horses is it seen in? Management?
Inflammation around the soft tissues of the palmar fetlock
Seen in young performance horses
May be indicator of SL branch/annular ligament injury - US
Management:
- rest/NSAIDs and local cold therapy
- shockwave therapy in refractory cases
Osteochondral fragmentation of P1: Cause? Clinical relevance? Diagnosis? Management?
Traumatic origin?
May nor be clinically relevant so need to prove significance e.g. diagnostic analgesia
Diagnosis: radiography (check contralateral limb)
Management:
- fragment removal arthroscopically
Osteochondrosis of the fetlock? What is seen? Which horses? Diagnosis? Management
Includes OCD of the sagittal ridge of Mc/MtIII and osseous cysts of distal McIII
OCD may be seen as flattening of the sagittal ridge to separate fragmentation
Usually seen in young horses (1-4 fetlocks involved) with joint effusions +/- lameness
Radiography
Management:
- surgical removal of fragments
- curettage of cyst
Fetlock osteoarthritis: What happens? Clinical findings? Management?
DJD resulting in joint effusion, cartilage loss, osteophyte production and loss of joint function
May be secondary to trauma, sepsis, osteochondrosis
Clinical findings:
- lameness exacerbated by fetlock flexion, reduced ROM
- positive i/a anaesthesia
Mild/early cases:
- intra-articular medication e.g. hyaluranon/corticosteroids
Moderate:
- NSAIDs, i/a corticosteroids
- autologous conditioned serum (IRAP)
- polyacrylamide gel
Severe:
- arthrodesis (salvage)
- euthanasia
Guarded prognosis for athletic use
Palmar/plantar osteochondral disease (POD): What is it? Cause? Clinical signs? Radiography? Management?
Degenerative condition of the distal condyles of young racehorses
Repetitive high strain on bone and articular tissues leading to wear lines and cartilage loss with eventual collapse of the articular surface
Associated with repeated corticosteroid use?
Clinical signs:
- mild/moderate lameness in 1 or more limbs localised to the fetlock
Radiography:
- minimal signs to focal increases in bone density (sclerosis) and change in contour of the subchondral bone
- advanced imaging include nuclear scintigraphy and MRI
Management:
- alteration in exercise schedule
Chronic proliferative synovitis: Aetiology? Clinical findings? Diagnosis? Management?
Aetiology (usually forelimb): - chronic repetitive trauma to dorsal aspect of fetlock due to hyperextension leads to soft tissue inflammation - can lead to supracondylar bone lysis Clinical findings: - lameness - reduced range of motion - heat/pain Diagnsois: - radiography: crescent shaped bone loss distal McIII, soft tissue swelling - ultrasonography: thickening of dorsal synovial pad Management: - intra-articular medication - surgical resection
Fetlock subluxation: Aetiology? Diagnosis? Management?
Often due to trauma - disruption of the collateral ligaments +/- avulsion fracture
Diagnosis:
- acute, severe lameness +/- overt luxation
- radiography +/- stress
Management:
- closed reduction + cast: will fibrose but may end up with OA
- arthrodesis if unstable
Types of fractures of the third metacarpus/metatarsus? Cause? Clinical presentation?
Types: condylar, diaphysial, transverse, proximal articular
Cause:
- usually single overload injury or external trauma e.g. kick
- condylar fractures usually fail due to repetitive strain cycles
Clinical presentation:
- lame
- swelling, crepitus, pain on palpation/flexion
- +/- joint effusion
- displacement (diaphysial)
- open/closed
Diagnosis and management of metacarpus/metatarsus fractures?
Diagnosis: - radiography - nuclear scintigraphy, MRI First aid: - zone 2 external co-aptation - medial/lateral splints for lateral condylar fracture Conservative: - for non displaced, closed, transverse and some proximal articular fractures Surgical: - condylar and diaphysial fractures Euthanasia: - for displaced, open, comminuted
What is dorsal metacarpal disease also known as? Cause? Clinical presentation? Diagnosis? Management?
= “Sore shins” or “bucked shin complex” in young racehorses
Cause:
- excessive cyclic loading results in painful periostitis as 2yo
- some go on to develop dorsal cortical “stress” fractures as 3yo
Presentation:
- focal pain, swelling, reduced performance, mild lameness
Diagnosis by radiography/scintigraphy
Management:
- alterations in training regime
- some refractory cases undergo shockwave or osteostixis/screw placement
Fractures of the second/fourth metacarpal/metatarsal (splint) bones: Types? Cause? Diagnosis? Management?
Often lateral hind splint bone (MtIV)
Types: proximal, mid or distal, open/closed, proximal fracture may communicate with CMC/TMT (joint sepsis)
Cause: usually due to trauma (kick), distal fractures may be secondary to abnormal stress from fetlock hyperextension
Diagnosis: radiography
Conservative:
- rest, NSAIDs, ABs, remove small loose fragments, wound debridement
- watch out for sequestrum
Surgical:
- partial osteotomy
- internal fixation (proximal articular)
Exostosis of McII/MtIV (splints): Cause? Clinical signs? Diagnosis? Management?
Due to trauma resulting in periosteal bleed then bone formation
Often seen in horses that dish in front
Usually cosmetic but can cause lameness while forming or if interfere with SL
Clinical signs:
- acute phase: pain, heat, swelling
- chronic phase: bony swelling
Diagnosis:
- clinical exam
- radiography
Management:
- conservative: rest, cold therapy, NSAIDs, local c/s
- surgical: if recurrence or severe (otherwise avoid)
SDFT tendonitis: History? Clinical examination? Ultrasound? Treatment?
History: - acute lameness - age/discipline Clinical exam: - swelling, pain, loss of normal borders - fetlock sinking - (carpal sheath/DFTS effusion) Ultrasound: - change in cross sectional area, fibre echogenicity, margination - core lesion vs generalised changes
Treatment for SDFT tendonitis?
Acute (hours-days):
- limit inflammation with cold hosing/NSAIDs
- protect limb/reduce further damage with supportive dressing/box rest
Reparative/proliferative phase (days-weeks):
- promote angiogenesis: tendon splitting, stem cells, PRP, US
- minimise formation of excessive scar tissue: PRP, stem cells, US
- early exercise: positive effect of type III to type I collagen
Chronic modelling phase (weeks-months)
- controlled exercise programme
Monitor progress with repeat ultrasounds
What tendon/ligament injuries can there be in the distal limb of the horse, except SDFT tendonitis?
DDFT tendonitis: - less common cf SDFT/Sl - seen in DFTS or digit - also seen in carpal and tarsal sheath ALDDFT desmitis: - swelling in proximal palmar metacarpus deeper to SDFT Suspensory ligament desmitis: - can occur at origin, body or branch level
Palmar/plantar annular ligament (PAL) syndrome : Causes? Clinical signs? Diagnosis? Treatment?
Causes: - idiopathic - SDFT tear - DDFT tear - PAL desmitis - combination Clinical signs: - DFTS effusion (often marked) - notching of limb - PAL constriction - lameness (mild-moderate) - pain on flexion - +ve response to DFTS analgesia or perineural analgesia Diagnosis: - ultrasound: assess tendons/PAL thickness (1-2mm) Conservative: - cold hosing, rest, controlled exercise - systemic NSAIDs - local corticosteroids/HA into sheath Surgical (tenoscopy): - remove damaged portions of tendons - PAL desmotomy to relieve compression
Carpal osteoarthritis: What is it? Predispositions? Clinical signs? Diagnosis? Management?
DJD affecting one or more of the carpal joints Secondary to joint trauma, sepsis, fracture or soft-tissue injury (e.g. intercarpal ligament injury) Poor conformation may predispose to carpal OA Arabs predisposed to CMC OA Clinical signs: - lameness - joint effusion - fibrosis - reduced ROM - positive to carpal flexion - crepitus Diagnosis: - clinical signs - intra-articular anaesthesia - radiography Management: - intra-articular medication, NSAIDs - arthrodesis in advanced cases (drilling)
Osteochondral fragmentation of carpus: What happens? Diagnosis? Management?
= Carpal “chip fracture”
May be fragmentation of an osteophyte (in OA) or fragmentation of dorsal articular margin with training (racing breeds)
Sclerosis of subchondral bone may predispose pathology
Palmar fragmentation seen following recovery from GA (trauma)
DIagnosis:
- diagnostic anaesthesia
- radiography
Management usually involves arthroscopic removal of the fragment(s)
Carpal bone fractures: Types, cause ,diagnosis, management?
Types: slab, frontal and comminuted
Cause: often acute single overload but may result from stress maladaptation (e.g. sclerosis from repetitive loading)
Diagnosis:
- present as acute lameness and joint effusion with pain/crepitus on palpation
- radiography (inc. skyline views)
- nuclear scintigraphy
Management (slab and frontal):
- conservative for incomplete fractures
- surgical: usually internal fixation via arthroscopy, for incomplete or complete fractures
Accessory carpal bone fractures: Cause? Presentation? Diagnosis? Management?
Cause: trauma/single impact overload
Presentation:
- acute lameness with swelling/pain over the palmar carpus
- horse may stand with carpus semi-flexed
- radiocarpal joint effusion and/or carpal sheath effusion
Diagnosis: radiography
Conservative management: most cases heal by fibrosis
Surgical:
- repair difficult (shallow/curved bone)
- remove any fragments in joint
Carpal subluxation: Cause? Presentation? Diagnosis? Management?
Cause: usually trauma (e.g. high speed fall) - often have additional carpal bone fractures
Presnetion:
- severely lame with marked swelling, carpal instability and overt anatomical derangement
Diagnosis:
- radiograph to determine level of luxation and presence of fractures
Management:
- stabilise with full limb bandage plus splints (zone 3 external coaptation)
- euthanasia in many cases esp with fractures/carpal bone collapse
- surgical: partial or complete arthrodesis possible
Carpal hygroma: Cause? Presentation? Diagnosis? Management?
Cause: often secondary to repetitive trauma (e.g. hitting stable door)
Presentation:
- subcutaneous (fluid-filled) swelling over the dorsal carpus
- usually non-painful but can get infected/sore
Diagnosis:
- palpation
- radiography
- US
Conservative management:
- rest, NSAIDs, cold therapy, drainage, corticosteroid injection and bandaging
Surgical debridement often difficult with wound breakdown common
Carpal canal syndrome: What conditions does this include?
Conditions leading to restriction or pain in the carpal sheath:
- Idiopathic tenosynovitis: haemorrhage or secondary to other cause
- Septic tenosynovitis: may have a wound, seen secondary to elective tenoscopy
- Tendinitis of SDFT/DDFT (or muscle tears)
- AL-SDFT (SCL) desmitis
- Radial physeal exostosis: bony extension from caudal radius to impinge on DDF muscle belly
- Accessory carpal bone (ACB) fracture: ACB forms lateral boundary of carpal sheath through carpus
- Osteochondroma of distal radius: discrete separate centres of cartilage ossification
Clinical signs and diagnosis of carpal canal syndrome? Management?
Clinical signs:
- carpal sheath effusion
- lameness/pain: flexion often exacerbates lameness/pain
- puncture wound with sepsis
Diagnosis:
- diagnostic anaesthesia (median/ulnar nerve block or carpal sheath anaesthesia)
- synoviocentesis
- radiography
- ultrasonography
Treat underlying cause:
- tenoscopic lavage
- removal of exostosis/osteochondroma via tenoscopy
- debridement of damaged tendon/ligament
- local anti-inflammatories into carpal sheath
Radial fractures: Cause? Presentation? Management?
Cause: usually external trauma (e.g. kick) esp. distomedial radius
Presnetation: moderate swelling and lameness but can weight bear (incomplete fractures)
Open/complete fractures in adult horses usually euthanased
Conservative management:
- For most closed, incomplete fractures in adults
- full limb bandage plus caudal and lateral splint
- cross-tie but head down for feeding
- regular monitoring – can still displace!
Surgical: internal fixation in foals
Ulna fractures: Cause? Presentation? Diagnosis? Management?
Cause: trauma/kick leading to fracture of proximal ulna (olecranon)
Presentation:
- acute lameness
- +/- wound
- swelling/pain around elbow
- dropped elbow stance
(ddx radial nerve paralysis, triceps myopathy)
Diagnosis: radiography
First aid: splint carpus as lost stay apparatus
Conservative: often results in delayed or non-union in adults
Surgical:
- tension-band principal by converting distractive forces of triceps to compression
- plate fixation in adults generally do well (plate or wire/pins in foals)
Fractures of the humerus and scapula: Cause? Types? Presenting signs? Management?
Cause: usually acute trauma (kick, impact), also stress fracture in racehorses
Humeral types: diaphyseal (transverse/spiral), deltoid tuberosity, humeral tubercles
Scapula types: supraglenoid, body, spine
Presenting signs:
- moderate to severe lameness with loss of limb function with complete fracture
Diagnosis: radiography can be difficult in this region
Management
- complete humeral fractures = euthanasia
- conservative e.g. deltoid tuberosity, scapula spine
- sporadic reports of surgical repair but difficult!!!
Osteochondrosis of elbow: What is seen? Management? Prognosis?
Osseous cyst-like lesions in proximal radius
Conservative (intra-articular medication) or surgical (extra-articular drilling)
Poor prognosis as often secondary joint disease present
Osteochondrosis of shoulder: What is seen? Prognosis?
Osseous cyst-like lesions in distal scapula (also proximal humerus)
OCD of glenoid cavity
Poor prognosis as often secondary joint disease present
Shoulder dysplasia and subluxation: Breeds affected? Presentation? Diagnosis? Management?
Seen in Shetland/Miniature breeds
Presentation:
- malalignment results in pain/instability
- subluxation can occur without dysplasia secondary to trauma
- moderate/severe lameness with pain on shoulder extension/abduction
Diagnosis: radiography - abnormal alignment of scapulohumeral joint, often secondary OA present
Management:
- reduction under GA possible but often recurs
- secondary OA managed conservatively
- shoulder arthrodesis a possibility but most cases euthanased
Shoulder OA: How common? Causes? Predispositions? Presentation? Diagnosis? Treatment? Prognosis?
Seen infrequently
Cause: secondary to trauma, intra-articular fracture, osteochondrosis, sepsis
Shetland ponies /Miniature breeds predisposed
May be related to shoulder dysplasia
Affected horses/ponies generally moderately to severely lame
Diagnostic anaesthesia of the shoulder
Radiography
Palliative treatment
Prognosis guarded
Elbow OA: How common? Cause? Diagnosis? Management? Prognosis?
Unusual to get OA in elbow of horses Secondary to trauma, sepsis, OCLL Can be difficult to diagnose: - diagnostic anaesthesia of the elbow joint difficult! - radiography - (nuclear scintigraphy) Management: - intra-articular medication, NSAIDs Guarded prognosis
Elbow hygroma (“capped elbow”): Presentation? Which horses? Treatment?
Non-painful swelling over point of elbow
Fluid-filled swelling secondary to repetitive trauma/inflammation
Can be painful if infected
Horses with a “high action” or ones that lie down regularly
Most cases cosmetic and not treated
Conservative management:
- NSAIDs, ABs, draining, correct underlying cause
High chance of wound breakdown with surgical debridement
Stifle OCD: Which horses affected? Which parts of the stifle usually? Presenting signs? Diagnosis? Treatment options?
Young horses - WBs>TBs - 6mo-4yo Lateral trochlear ridge > patella >>> medial trochlear ridge Presenting signs: - stifle effusion - (lameness) Diagnosis - radiography: subtle flattening, subchondral bone lysis, overt fragmentation - ultrasonography Conservative treatment: - <8-12mo - dietary advice, exercise restriction - monitor lameness Surgery - If >12mo +/- lameness - removal of osteochondral fragments - curettage to healthy subchondral bone Euthanasia of severe lesions
Osseous cyst-like lesion (OCLL): Other name? Where? Age? Presentation? Diagnosis? Treatment?
= Subchondral bone cyst
Usually medial femoral condyle (also proximal tibia)
Usually later than OCD (1-3yo+)
Also secondary to trauma
Presentation:
- lameness ++ (can be intermittent/severe)
- +/- MFT/FP joint effusion
Diagnosis:
- radiography
- (scintigraphy)
Treatment options:
- intra-articular corticosteroids
- inject cyst under GA with corticosteroids
- debride cyst: may worsen, pack with bone graft
- bone screw across cyst
Prognosis:
- better if <3yo
- 77% soundness with injecting cyst
- poor prognosis with caudal cysts in foals
Stifle soft tissue injuries?
Meniscal and mensicotibial ligament injuries:
- medial»>lateral
- range from cranial mensiscotibial tear to meniscal split
- about 50% return to soundness
- poorer if radiographic signs of OA
Cruciate ligament:
- difficult to assess
- uncommon but if involved usually poor prognosis
OA of stifle: Causes? Diagnosis? Treatment?
Causes: - trauma/soft tissue injury - secondary to fracture - sequelae to sepsis - OCD/OCLL Diagnosis: - moderate lameness - +ve response to diagnostic analgesia - radiography - (ultrasonography/ scintigraphy) Treatment: - palliative: see arthritides lecture - NSAIDs; intra-articular medication
What stifle fractures are there? Cause? Treatment?
Usually traumatic in origin - hitting fence/kick
Patella:
- surgical removal (<1/3) or fixation
Medial intercondylar eminence of the tibia:
- often associated with meniscal/cruciate damage
- remove/repair
Tibial tuberosity:
- kick injury +/- wound
- conservative management good outcome (can repair)
- care not to misdiagnose with growth plate!
Upward fixation of the patella: Aetiology? Clinical signs? Treatment?
Aetiology:
- medial pole of patellar hooks over medial trochlear ridge of femur (stay apparatus) - unlocked by quadriceps contraction
Clinical signs:
- poorly muscled/ rested/ muscle loss/ straight hind limb conformation
- limb locked in extension and dragged
- dorsal toe wear
- intermittent or persistent
Treatment:
- exercise/build up muscle
- look for concurrent problem!
- splitting/injecting medial patellar ligament
- medial patellar desmotomy – associated with secondary patella fragmentation
Treatment for upper hindlimb long bone fractures?
Complete fracture femur/tibia:
- adult >250kg and/or comminuted/open = euthanasia
- foal or weanling possible to repair but need high expertise and high complication risk
Tibial stress fractures:
- common cause of acute HL lameness in TB flat racehorses
- often diagnosed by scintigraphy/radiography
- rest/alteration to exercise regime
Third trochanter of femur:
- uncommon, acute trauma
- conservative management
- good prognosis
What conditions fo the coxofemoral joint are there?
Dysplasia: - rare/bilateral - Norwegian Dole (inherited?) OA: - secondary to dysplasia, rupture of trees ligament, trauma - moderate-severe lameness - intra-articular medication poor results Subluxation: - miniature breeds overrepresented - reports of repair (toggle/pin)
What type of cartilage does the sacroiliac joint have?
Sacral surface = hyaline cartilage
Ilial surface = fibrocartilage
Pelvic fractures: Types? Aetiology? Clinical signs?
Types:
- tuber coxae
- ilial wing
- ilial shaft
- pubis/ischium
- acetabulum
Aetiology:
- trauma
- end stage bone fatigue in racehorses: ilial wing fractures in skeletally immature TBs
Clinical signs:
- pain, swelling, muscle spasm, asymmetry
- lameness (may resolve quickly if incomplete-care!)
- rectal exam: sharp discontinuity, sub-fascial haematoma, gentle rocking
- signs of shock: severance of iliac arteries with ilial shaft fractures - often die quickly
- nerve damage: muscle/anal tone
- muscle atrophy (chronic >2 weeks)
Diagnosis and treatment options for pelvic fractures? Outcome?
Ultrasound very useful for fractures of ilial wing, ilial shaft, tuber ischii and tuber coxae
Scintigraphy
Treatment options:
- NSAIDs
- box rest: cross tie for >1 month for major pelvic fractures, feed from floor several times daily, 2mo with daily walking out, 2mo field rest
Outcome:
- good for minimal/non displaced
- poor for acetabular/ilial shaft fractures
- foals do better than adults
Presenting complaints with sacroiliac disease? Diagnosis?
Large-framed horses with long backs and weak quarter: - associated with Warmblood breeds - dressage/showjumper activity Lameness: - variable: severe in acute - chronic, low grade, intermittent Poor performance: - lack of impulsion - resisting jumps Pelvic asymmetry: - not always a feature! - muscle atrophy Pain/swelling: - sacroiliac pain +/-thoracolumbar pain Diagnosis: - exclude other HL causes (e.g. tarsus) - diagnostic analgesia - scintigraphy - ultrasonography
Treatment for acute and chronic sacroiliac disease?
Acute: - 4-8 weeks box rest - NSAIDs - physiotherapy: massage/pain relief Chronic: - work and NSAIDs - aim to build up limb/pelvic muscles: pessoa, pole work, weighted shoes/boots, water treadmill - perilesional infection with corticosteroids - physiotherapy: stretches, TENS - shockwave for analgesia
Where are the calcaneal bursae in the tarsus?
Between gastrocnemius and SDFT, extending distally
Communicates with the gastrocnemius bursa which is deep between the gastrocnemius tendon and tuber calcis
What is an acquired superficial bursa of the tarsus?
Between SDFT and skin
“Capped hock”
OCD of tarsus: Distribution? Clinical signs? Treatment?
Distribution: - distal intermediate ridge of the tibia (“DIRT”) - lateral trochlear ridge - (medial malleolus) Clinical signs: - usually young horse (6mo-3yr) - effusion of the tarsocrural joint - (lameness) - check other limb/joints! Arthroscopy: - usually wait until 11mo+ - good success
Tarsal bone collapse: Cause? Treatment? Prognosis?
Incomplete ossification:
- dysmature/premature foal
- neonatal maladjustment
- cna present as angular limb deformities
Supportive therapy until matures
Poor prognosis especially if >30% collapse/fragmentation
OA of the small tarsal joints: Other name? Where? Which horses? Cause? Clinical presentation?
Common
“Bone spavin”
DIT and TMT mostly
Middle-aged to older horses
Cause: compression and rotation of small tarsal bones when stops/jumps?, Heritable - Icelandic
Clinical presentation:
- palpable exostoses: squared off toes or commonly NAD
- lameness (uni or bilateral), choppy, stabby gait, worse on inside/hard surface
- poor performance/”stiff”/”back pain”
- flexion test +ve (not specific)
- TC effusion esp with PIT OA
Diagnosis and treatment options for small tarsal bone OA? Outcome?
Diagnosis:
- diagnostic anaesthesia: intra-articular (TMT/DIT)
- radiography: poor correlation with clinical signs
- scintigraphy: increased uptake in small tarsal bones, normal physiological adaptation in performance horses
Treatment:
- NSAIDs, PSGAGs, HA, biphosphonates, nutraceuticals
- inta-articular corticosteroids +/- HA
- farriery: improve breakover, lateral width
- chemical arthrodesis: ethyl alcohol
- surgical arthrodesis
Outcome:
- 60-70% conservative
- 80-90% fusion with arthrodesis after 12mo
Tarsal fractures: Types and treatment?
Malleolar: can remove arthroscopically
Calcaneal: may be unstable so euthanasia
Small tarsal bones: conservative or internal fixation
Tarsal luxations: Which joints? Clinical signs? Diagnosis? Treatment?
Usually TMT or PIT - 4th tarsal bone prevents DIT subluxation
Clinical signs: severe lameness and swelling
Diagnosis: stress radiographs
Treatment:
- cast +/- internal fixation
- or euthanasia
What soft tissue injuries of the carpus are there?
Collateral ligament injuries
Tarsal sheath swelling
Calcaneal bursa/lateral lunation of SDFT
Signs and treatment of collateral ligament injuries of the tarsus? Prognosis?
Signs: - swelling ++ - TC effusion Treatment: - Rest - NSAIDs, cold hosing, bandaging - physiotherapy - intra-articular medication? - monitor with US Poor prognosis if OA of joint develops
Tarsal sheath synoviocoele (“thoroughpin”): signs? Diagnosis? Management?
Signs:
- mild or no lameness
- large unilateral swelling in caudodistal crus: tear in synovial wall, valve effect
- usually no osseous pathology
Diagnosis:
- ultrasonography: effusion+++ with fibrinous deposits, usually no DDFT lesion
Conservative management:
- drainage and corticosteroids
- tends to recur
Surgical management: enlarge communication tenoscopically
Calcaneal bursa/lateral lunation of SDFT: What usually happens? Signs? Diagnosis? Treatment?
Tend to tear medial attachment leading to lateral luxation Signs: - often lots of swelling - bursal effusion ++ - horse agitated ++ - may see SDFT “sliding off” point of hock as walks Ultrasound may visualise tear Rest, NSAIDs Surgery (debride tear)
Horse cervical spine anatomy:
- How many cervixal vertebrae?
- Which have specific characteristics that enable radiographic recognition?
- What do the other cervical vertebrae look like?
7 cervical vertebrae
First two and last two have specific characteristics (1st, 2nd, 6th, 7th)
C3-C5 have a long body, ventral surface has a medial ventral crest, dorsal surface has a flat central area (attachment of he dorsal longitudinal ligament)
Characteristics of C1?
= Atlas
No body or articular processes
Radiolucent line seen between the two halves on VD view in foals before ossifies
Characteristics of C2?
= Axis
Separate centres of ossification for dens, head, body and caudal epiphysis
Dens fuses with head at apron 7mo
Cranial borders of the arches have lateral vertebral foramina - incomplete in young horses and appear as a notch which may ossify with age or remain incomplete
Occasionally a small bony spur is seen on dorsal aspect of caudal epiphysis
Characteristics of C6 and C7?
C6 is shorter than C5 and C7 is shorter than C6
C6 has transverse process split into cranial, caudal and ventral parts
The extra ventral lamina may sometimes be unilaterally or bilaterally transposed onto the ventral surface of C7 or even more rarely onto C5
Ventral processes of C6 may have small centres of ossification at the caudal limits
C7 has small dorsal spinous process which may be fairly prominent
T1 recognised by large dorsal spinous process
Presenting signs of neck pain (cervical spine)?
Neck stiffness/pain/”locking”
Acute trauma
Poor performance or problems performing specific manoeuvres e.g. correct outline, reluctance to work on the bit
Ataxia - usually low grade (I-II)
Examination for neck pain? What to rule out?
Lowered head carriage/extended neck with pain Position of limbs/gait Palpation: - symmetry/presence of atrophy - pain on palpation - fasciculations/spasm ROM: - lateral flexion and extension in the axial plane Neurological examination Walk/trot/lunge/ridden Rule out: - lameness - back problems - tack - dentistry
Common conditions of the neck?
Developmental - crvical vertebral malformation (“wobblers”)
Degenerative - OA
Trauma - fractures
Cervical vertebral malformation: Also known as? What is it? Predispositions? Clinical presentation?
“Wobblers”
Developmental orthopaedic disease -> malformation of bones
WB and TB predisposed
If changes are marked, often identified as young as 1-4yo
If mild can sometimes manage for many years - OA, ataxia, pain can develop later in life
Osteoarthritis/arthropathy of the neck/dorsal articular facet arthropathy: Aetiology? What is seen? Treatment? Negative prognostic indicators?
Aetiology: age, CVM, previous trauma Cartilage erosion and subchondral bone sclerosis Periarticular osteophytosis Synovial cysts/soft tissue hypertrophy Nerve root impingement - forelimb lameness at 6th and/or 7th cervical nerves Diagnosis: confirm with diagnostic analgesia Treatment: - NSAIDs - Intra-articular corticosteroids/HA - Physiotherapy: stretching, massage - Exercise: loose rein schooling, working Often palliative treatment only Negative prognostic indicators: - severity of signs/radiographs - young horse - ataxia
Prognosis of cervical spine fractures?
Depends on location, configuration, open or closed, single or polyostotic
Many not treatable
Conservative treatment only realistic chance
Presenting signs of back pain (thoracolumbar spine)
Poor performance Behaviour changes Uncomfortable when ridden/"doesn't feel right" Stiffness in back back spasms Difficulty being tacked up Bucking/rearing
Physical examination for back pain (thoracolumbar spine)?
Conformation and body condition
Check for lordosis, kyphosis, scoliosis
Obvious swellings - fractured withers, acute supraspinous desmitis, muscle haematoma, poor fitting saddle
Presence of white hairs - poss poor saddle fit esp behind saddle
Palpation - abnormal reactions:
- ears back, teeth grinding, biting, kicking, tail swishing
- muscle fasciculations
- guarding or splinting of back in anticipation
- bucking/rearing
Flexion of back:
- use blunt object
- thoracolumbar extension then flecion
- lateroflexion away from stimulus
Lungeing:
- muscle fasciculations, spasms, guarding, splinting
- breaking into canter
- head held forward, neck extended
- lack of hindlimb impulsion
Under saddle/ridden - careful
Cause, treatment and secondary complications of withers fractures?
Trauma e.g. horse falling over backwards Treatment: - rest (2-3mo box rest) - NSAIDs - long term fair/good outcome for fibrous union Secondary complications: - pain - FL lameness - discharging tract - resentment of saddling
Saddle induced trauma: Identifying? Treatment?
Identify early Any dry spots under saddle after riding: - indicates excessive pressure - often see hair loss, swelling, increased sensitivity Treatment: - rest/ice - US therapy - low powered laser for indolent wounds - correct inciting cause
Back ligament damage: Which ligament usually? Signs? Diagnosis? Treatment?
Usually supraspinous ligament Signs: - rigid gait, head elevated, reduced stride - heat, pain, swelling (acute) - thickening (chronic) Diagnosis: US Treatment: - acute: cold compress, NSAIDs, rest - chronic: physiotherapy, shockwave?
Impingement of dorsal spinous processes: Cause? Diagnosis? Treatment?
Common Probable conformational as well as degenerative underlying aetiology Diagnosis: - confirm significance - intra-lesional LA - exclude other causes of pain first Medical/conservative treatment: - PBZ - shockwave, physiotherapy Surgical: remove affected DSPs
What is the aim of GF administration to tendon injuries? Is it proven?
Produce true tendon rather than scar tissue
Reduce amount of scar tissue
No not proven - dosage, treatment intervals and best administration time all unknown
IGF-1 for tendon injuries: findings from study?
Reduced swelling
Lesion smaller at 3 and 4 weeks but not afterwards
Cell proliferation and collagen content increased
Increased stiffness
But poss just increasing scar tissue?
TGF-beta for tendon injuries: What is it? Findings from study?
Major anabolic GF, associated with cartilage formation
Rapid resolution of core lesion
Enlargement of tendon - often persists
But just more cartilage like tissue - not ideal for tendon
Platelet rich plasma for tendon/ligament injuries: What is it? How does it work? Which injuries may it be beneficial for?
Concentration of platelets (by centrifugation or filtration) from autogenous blood and then GFs released for treatment
GFs released by freeze thawing, calcium or thrombin prior to administration
Where are stem cells taken from for regenerative therapy?
Bone marrow of tuber coxae of sternum
What are valgus and varus angular limb deformities?
Valgus = lateral deviation Varus = medial deviation
Where do most foal congenital angular limb deformities arise from? Where else can they arise from?
Most common = metaphysical growth plate Epiphysis Cuboidal bones - carpus, tarsus Diaphysis (rare) Soft tissue laxity
Problems with premature foals and angular limb deformities?
Incomplete mineralisation of bones
High risk of crushing injury to cuboidal bones of carpus/tarsus
Tarsal bones often collapse dorsally as delayed dorsal ossification
What does it mean if a foal’s congenital angular limb deformity can be straightened manually?
Premature - incomplete ossification
Or peri-articular laxity
Management of a foal with a congenital angular limb deformity with positive manipulation due to incomplete mineralisation of carpal bones?
Restrict exercise
Bandage with splint - light, digit outside
Repeat radiographs every 2 weeks
Balanced nutrition
Usually improves unless systemic involvement
Management of a foal with a congenital angular limb deformity with positive manipulation due to peri-articular laxity?
Controlled exercise to strengthen peri-articular soft tissues
Careful with bandaging
Usually resolves unless other systemic problems
Causes of acquired angular limb deformities?
Imbalanced nutrition - excessive E (concentrates), mineral imbalance (lack of Cu, excessive Zn)
Genetics (rapid growth)
Trauma:
- damage to growth cartilage -> abnormal/asymmetric growth
- overload opposite limb
Prognosis of angular limb deformities?
Good if: - early treatment - physis or epiphysis Fair to poor: - metaphysical or diaphyseal - crushed cuboidal bones - severe angulation - secondary DJD
Treatment angular limb deformities with negative manipulation?
Depends on age, joints involved, severity
Limited exercise
Bandages, splints
Corrective hoof trimming
- mediolateral foot balance: lightly rasp to lower lateral side for valgus, lower medial side for varus
- glue on shoes: medial extension for valgus, lateral extension for varus
- only treatment for mild cases, combine with surgery if moderate-severe
- avoid drastic changes -> joint problems
Limit mare and foal nutrition
Surgery:
- growth acceleration of concave side (elevate periosteum)
- growth retardation of convex side (bridge the physis)
- (osteotomy)
How long do the fetlock, carpus and tarsus joints have fast growth as a foal before closure?
Fetlock: <6-8 weeks
Carpus: <5 months
Tarsus: <7 months
What is the technique of growth acceleration for angular limb deformities of foals?
Concave side Just proximal to physis Periosteal elevation Does not over-correct Also restrict diet and aways combine with hoof balancing
What is the technique of growth retardation for angular limb deformities of foals?
For moderate and severe cases
Bridge the physis on convex side
Risk of over-correction - remove implants once straightened (essential)
Also restrict diet and always combine with hoof balancing
Close monitoring aftercare:
- skin pressure sore over metallic implants
- box rest until improved
- limit exercise until straight
What are the origins and insertions of the SDFT? Function?
Origin: - distal humerus - proximal radius Insertion: - proximal P2 - distal P1 Function: - flexion of MCP/MTP joint
Accessory ligament - disto-palmar radius (AL-SDFT)
What are the origins and insertions of the DDFT?
Origin: - humeral epicondyle - medial olecranon - proximal radius Insertion: - ventral-palmar P3 Function: - flexion of DIP joint
Accessory ligament - palmar carpus (AL-DDFT)
Digital hyperextension in foals: Cause? Management?
Flexor tendon laxity
Can be congenital or acquired later (fast growth)
Mild-moderate: laxity reduces with exercise, corrects in 1-2 weeks
Severe: protect heel bulbs
Usually not associated with bone/tendon pathology
Exercise to strengthen muscle-tendon unit
Palmar/plantar extensions if moderate-severe
Avoid bandages if possible - just to protect heel bulbs in severe cases
No splints!
Treatment of foal flexural limb deformities of foals?
Conservative:
- physiotherapy with restricted exercise
- force-extend affected joint: splints (casts), cause pain
- analgesia v important: NSAIDs (risks of GIT ulcers, kidney toxicity - give GIT protectants, hydration)
- if DIP joint: farriery to lower heel, extended toe shoe, decrease nutrition
Medical:
- oxytetracycline (congenital only) - important to hydrate as nephrotoxic
Surgical
Surgery for foal flexural limb deformity of the DIPJ? Prognosis?
Desmotomy of AL-DDFT (distal check ligament)
Combine with conservative treatment
Good-excellent for grade 1
Fair-guarded for grade 2
Surgery for foal flexural limb deformity of fetlock?
Palpate which tendon/s most affected when extension is forced
If SDFT -> proximal check ligament desmotomy
If DDFT -> distal check ligament desmotomy +/- proximal check ligament desmotomy
Both proximal and distal check ligament for severe cases
Septic arthritis in foals: Route of bacteria access? Aetiology? Clinical signs?
Usually haematogenous in foals (also traumatic, iatrogenic) Aetiology: - FPT - impaired defences - sub-infective dose of bacteria - systemic disease - gram negative bacteria most common Clinical signs: - may be reluctant to stand - joint effusion(s) - peri-articular swelling - lameness: often increasing - filling of mare's udder
Diagnosis of septic arthritis/physitis/synovitis in foals?
Full history v important - FPT? Check all joints and umbilicus Radiography: - bone involvement (fracture, osteomyelitis) - lag behind pathological changes in bone - irregular/widened physis with radiolucency if septic physitis Ultrasonography: - umbilicus and affected joint Blood culture: - septicaemia Synoviocentesis: - EDTA for nucleated cell count - plain/with culture media for c+s - total protein - check if communication with wound
Reference ranges from synoviocentesis to diagnose septic synovitis in foals?
Turbid, serosanginous, reduced viscosity
>20x10^9 cells/L
>80% neutrophils
Total protein >30-35g/L
But not always
Prognosis of septic arthritis/physitis/synovitis in foals?
Fair-good: - rapid treatment - single joint - no bone involvement - systemically well Guarded-grave: - long time between diagnosis and treatment - >1 joint involved - bone involvement - concurrent systemic illness e.g. FPT, neonatal hypoxia, immune deficiency
What to check a physiotherapist is registered with?
ACPAT
RAMP
Only ‘physiotherapist’ is protected, not ‘animal/veterinary physiotherapist’
What are kVP, mA and S for radiography?
kVp = speed of electrons mA = number of electrons released S = time
What are the 6 points to consider when assessing radiograph quality?
Positioning Collimation Contrast Exposure Labeling Artefacts
Define sclerosis and osteolysis? Causes?
Sclerosis = increased bone density: - local increase in bone mass - result of stress - wall off infection - protect a weakened area Osteolysis = decreased bone density: - decrease in bone mass - result of infection or pressure - result of bone damage (blunt trauma, fracture line)
How do active and inactive bone lesions appear differently on radiography?
Active: - irregular - sharp edges - poorly demarcated - destructive or productive Inactive: - smooth - rounded edge - well defined
What are osteophytes?
Periarticular focal new bone production
Active: sharp, irregular
Aged: smooth, uniform
What are enthesiphytes?
Focal new bone production at origin or insertion of soft tissue (due to stress at attachment)
E.g. at joint capsule, tendon, ligament
How does gamma scintigraphy work?
Intravenous injection of radioisotope: technetium 99 MDP (binds actively remodelling bone)
Gamma ray emission
Gamma rays detected by gamma camera (giant Geiger counter)
Increased binding in areas of:
- inflammation
- bone repair/remodelling
- osteomyelitis
- neoplasia
Semi quantitative:
- more intense colour = more gamma rays detected
What are the phases of bone scanning by gamma scintigraphy?
Phase I - blood pool: - rarely used in equine - immediate Phase II - soft tissue: - 2-15 mins - diffusion to ECF Phase III - bone: - 2-3 hours - bound to hydroxyapatite crystals
When might nuclear scintigraphy be indicated?
- Isolated lameness but no abnormalities on imaging
- Lameness not isolated
- Lameness proximal to stifle
- Suspect stress or non-displaced fracture
- Spinal problems (thoracic, lumbar and pelvic)
- Horse not amenable to blocks
How does US work?
Sound wave produced by piezoelectric crystal
Reflected, absorbed or scattered from tissue interface
Degree of reflection determined by tissue density
Stifle joint compartments? Which ones communicate?
Femoropatella Medial femorotibial Lateral ferotibial FP and MFT communicate (60-85%) FP and LFT sometimes communicate (5-17%)
Differentiating between acute and chronic muscle conditions?
Acute: swelling/pain Chronic: - stiffness - cramping - pain - fasciculations - weakness - atrophy - fibrosis/calcification
Presentation of forelimb proximal suspensory desmitis?
More noticeable when leg on outside of circle on soft ground
Improves with rest but returns when work increases again
May be pain on palpation of proximal third palmar metacarpus
Physitis: What is it? Signs?
Enlargement of physis - inflammation and disruption of endochondral ossicication
Self limiting
Signs:
- lameness and/or stiffness
