Equine orthopaedics Flashcards

1
Q

Hoof anatomy?

A
Wall - toe (dorsal third), quarters, heels, bars
Sole
Frog
Periople
Heel bulbs
White line
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2
Q

What are the layers of the hoof wall?

A

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

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3
Q

Normal structure of lamellae?

A

Primary and secondary lamellae

Perfect strong interdigitation with tubular horn of hoof wall

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4
Q

How does the hoof grow?

A

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

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5
Q

What is laminitis?

A

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

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6
Q

What are the 3 categories of causes of laminitis?

A
  1. Inflammatory laminitis: SIRS associated:
    - retained afterbirth
    - severe illness, especially GI disease
    - black walnut shavings in USA
    - feeding accidents e.g. grain overload
  2. (non) Weight bearing laminitis (supporting laminitis)
  3. Endocrinopathic laminitis: (90% of cases)
    - PPID
    - Equine Metabolic Sundrome
    - (Iatrogenic corticosteroid induced)
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7
Q

Why does inflammatory laminitis occur?

A

Pro-inflammatory signalling
Endothelial activation
Activation of degradation enzymes (ADAM-TS4, MMPs)
Early vasodilation
Arteriovenous shunts - produce clinical sign of bounding digital pulses

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8
Q

How does (non) weight bearing cause laminitis (supporting laminitis)?

A

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

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9
Q

What causes endocrinopathic laminitis? Why?

A

Hyperinsulinaemia induces laminitis
Theory is via endothelial activation via altered intracellular signalling
Pro inflammatory mediators - lamellar damage

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10
Q

Clinical signs of laminitis? What to differentiate from?

A
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)
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11
Q

Obel grading system to categorise laminitis clinical signs?

A

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

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12
Q

Changes to hoof seen in advanced laminitis cases?

A

Flattening-convexity of sole (P3 is moving)
Depression around coronary band (sinker)
Bruising, subdural abscessation

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13
Q

Why do laminitic horses get hoof rings? Significance?

A

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

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14
Q

Diagnosis of laminitis?

A

Clinical signs
Full history - determine cause/underlying cause
Radiography

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15
Q

What radiographic views are used for laminitis? What to look for?

A

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)

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16
Q

What is measured on radiography for laminitis?

A
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
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17
Q

Venogram for laminitis? What for? How?

A
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
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18
Q

Treatment for laminitis: principles? Drugs? Non drug treatment?

A
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
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19
Q

ACP for laminitis?

A

Doesn’t help the laminitis but calms horse down and lie down more

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20
Q

Shoeing/trimming plan for acute laminitis?

A

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

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21
Q

Prognosis for laminitis?

A
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
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22
Q

Chronic laminitis signs?

A
Altered hoof growth
Dishing dorsal hoof wall
Seedy toe
Dropped sole
Foot abscess common
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23
Q

Hoof care for chronic laminitis?

A

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

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24
Q

Indications for DDFT tenotomy for laminitis? When contraindicated?

A

Refractory cases
With rotation
Salvage procedure
For horses not intended for athletic purposes

Contraindicated in founders

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25
Q

What to check for on a front and lateral assessment of a horse’s limb conformation?

A

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

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26
Q

Foot balance from front view of hoof?

A

Medial and lateral hoof walls should be same angle and length
Assess coronary band in relation to the bearing surface

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27
Q

Foot balance from lateral view of hoof?

A

Hoof pastern axis
Coronary band from dorsal to palmar - level, undeviated
Dorsal hoof wall should be 2.5-3 x heel length

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28
Q

Foot balance from mediolateral view?

A

90 degrees to long axis
Assess symmetry
Evaluate heels for shunting/sheared heels

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29
Q

Foot balance from solar view of hoof?

A

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

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30
Q

How to correectivley shoe/trim a broken back hoof-pastern axis (HPA), long toe/low heel, underrun heels?

A

Trim to reduce toe length, preserve heel
Shoe to raise heel
Caudal shoe support over frog to prevent back of foot descending

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31
Q

Corrective shoeing for medio-lateral imbalance with heel shunting?

A

Shoe with support at back over shorter side?

Float heel on that side so gap between heel and shoe - will come down over 48h

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32
Q

What is true P3 rotation?

A

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

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33
Q

What is a sinker?

A

P3 in normal alignement with P1 and P2
But pushing through sole
Clinical signs: coronary band depression, possible separation behind coronary band, serum exudate

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34
Q

Normal distance from coronary band to extensor process of P3 on radiography?

A

5-10mm

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35
Q

Dorsal wall resection technique for laminitis?

A
Trim hoof capsule
Apply heart bar shoe
Mark area to be removed
Dremmel or knife?
Sedation not nerve block
'Split' sole
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36
Q

Chronic laminitis: farriery?

A
Abnormal anatomy - lots of heel growth, corkscrew
Need regular farriery
Trim frog to margins
Remove excess sole
Lower heels
Rasp toe
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37
Q

Positives and negatives of glue on plastic shoes for laminitis?

A
Positives:
- less trauma
- easy fitting
- anti concussive
Negatives:
- expensive
- poor grip
- frog plate moveable
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38
Q

Intrinsic and extrinsic risk factors of orthopaedic problems in racehorses?

A
Intrinsic:
- age
- sex
- breed
- training regime
Extrinsic:
- racing surface
- exercise intensity
- time off before return to exercise following injury
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39
Q

What increases the risk of fatal condylar fractures of the third metacarpus/tarsus in UK racehorses?

A
No gallop work in training
First year of racing
Longer races
More runners
Amateur jockey races
Firm/hard going
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40
Q

Risk factors for palmar/plantar osteochondral disease in racehorses?

A

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

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41
Q

What increases the risk of superficial digital flexor tendinopathy in racehorses in hurdle starts?

A

Firm ground
Higher age at first race
Previous SDFT injury
Summer racing

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42
Q

What increases the risk of a horse falling in eventing?

A

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

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43
Q

Risk factors for lameness with dressage?

A
Age and height
Indoor arenas
Horse walkers
Lungeing
Back problems
Surface
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44
Q

Acceptable treatment for SDFT injuries? Evidence? What not to do?

A

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

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45
Q

Treatments with evidence basis for bone spavins (carpal chip)?

A

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

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46
Q

Acceptable treatments for osteoarthritis with evidence basis?

A

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

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47
Q

Hoof cracks - Which way do they run? Cause? Consequences of instability? Treatment?

A

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

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48
Q

Coronary band and hoof wall injuries - Aetiology? Clinical signs?

A

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)

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49
Q

Treatment of coronary band and hoof wall injuries?

A

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

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50
Q

Prognosis of puncture wounds of the foot?

A

Most are good and managed conservatively

But potential to involve deeper structures with life threatening complications

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51
Q

Foot penetration problems associated with shoeing?

A

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

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52
Q

Subsolar abscesses - Cause? Clinical signs? Treatment?

A
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
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53
Q

Foot penetrations involving synovial structures - What structures could be involved? Diagnosis?

A
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
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54
Q

Treatment of foot penetrations involving synovial structures? Prognosis?

A

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

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55
Q

Chronic hoof abscessation - Causes?

A

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

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56
Q

What is quittor? Cause? Clinical signs? Treatment?

A

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

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57
Q

Keratoma of foot - What is it? Clinical signs? Treatment?

A

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

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58
Q

Canker of the foot - What is it? Cause? Consequences? Treatment?

A

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

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59
Q

White line disease - What is it? Risk factors? Clinical signs? Treatment?

A

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

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60
Q

Which local anaesthetics are used for equine diagnostics? Onset and duration?

A

Mepivacaine: 1-2 min onset, 45-60 min duration
Bupivacaine: 4-5 min onset, 1-2hr duration

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61
Q

Contra-indications for diagnostic analgesia in the limb?

A

Suspect fracture
Cellulitis (acidic so less effective, iatrogenic sepsis if synovial block)
Uncooperative horse

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62
Q

Reasons for poor response to diagnostic analgesia in the limb?

A

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

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63
Q

Causes of severe lameness after nerve block?

A

Synovial sepsis

Or flare few hours later (reaction to local)

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64
Q

Palmar digital nerve block: Site? Technique Needle size? Volume? Structures desensitised?

A

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

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65
Q

Abaxial sesamoid nerve block: Site? Technique? Needle size? Volume? Structures desensitised?

A

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

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66
Q

Distal interphalangeal joint (DIP joint) block: Site? Technique? Needle size? Volume? Structures desensitised?

A
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)
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67
Q

Navicular bursa block: Site? Technique? Needle size? Volume?

A

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

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68
Q

Lateromedial X ray of the foot: technique? What can be assessed?

A

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

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69
Q

Horizontal dorsopalmar X Ray of the foot: Technique? What can be assessed?

A
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
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70
Q

What is side bone?

A

Mineralisation of collateral cartilages of foot

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71
Q

Dorsoproximal-palmardistal oblique-P3 X ray of foot: Versions? What can be assessed?

A

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

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72
Q

Dorsoproximal-palmardistal oblique-navicular bone X ray of foot: Versions? Technique? What can be assessed?

A
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
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73
Q

Palmaroproximal-palmarodistal oblique (“skyline”) X ray of the foot: Technique? What can be assessed?

A
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
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74
Q

Management of conditions of the DIPJ? Diagnosis?

A
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
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75
Q

Pedal bone fractures: Aetiology? Signs? Diagnosis?

A
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
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76
Q

Treatment of pedal bone fractures?

A

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

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77
Q

Pedal osteitis: What is it? Diagnosis?

A

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

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78
Q

Navicular bone fractures: Aetiology? Diagnosis? Treatment?

A
Uncommon
Traumatic aetiology
Diagnosis:
- moderate lameness
- diagnostic anaesthesia localised to foot
- radiography
Treatment:
- conservative healing by fibrous union
- surgical repair difficult
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79
Q

Navicular disease: Signs and history? Diagnosis?

A

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

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80
Q

Pathology associated with navicular disease?

A

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

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81
Q

Radiographic abnormalities of navicular disease in order of most important?

A

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

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82
Q

Treatment options for navicular disease?

A

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

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83
Q

Primary DDFT lesions in the foot: Diagnosis? Where commonly occur? Treatment?

A

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

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84
Q

Is the PIPJ or MCPJ high motion? Significance?

A

MCPJ
Hyperextension leads to dorsal contact and palmar loading
PIPJ is low motion - high loading esp dorsally

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85
Q

Which ligaments support P1/P2, PIPJ and MCPJ?

A

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)

86
Q

Which nerve blocks may be positive for pastern/fetlock problems?

A

Perineurial: ASNB, L4/6NB

Intra-synovial: PIPJ, MCPJ

87
Q

Which radiographic views are used to assess the pastern and fetlock region?

A
LM
10 degrees DP
DMPLO
DLPMO
(Also flexed LM for fetlock)
88
Q

Osteoarthritis of the pastern: Other name? What happens? Cause? Diagnosis and management?

A

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

89
Q

Osteochondrosis of pastern joint: How common? What happens? Prognosis? Management?

A

Uncommon (more often in tarsus and stifle)
Osseous cysts (P1 or P2) or palmar/plantar osteochondral fragmentation
Guarded prognosis
Management often palliative
(Arthrodesis)

90
Q

Soft tissue injuries of the pastern area? Signs? Diagnosis? Management?

A

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

91
Q

P1 fractures: Types? Which horses are more prone?

A

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

92
Q

Types of P2 fractures? Causes?

A

Palmar/plantar eminence, comminuted

Usually due to acute overload injury

93
Q

Clinical findings, diagnosis and management of P1 or P2 fractures?

A

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

94
Q

Pastern subluxation: Aetiology? Clinical presentation? Diagnosis? Management?

A
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
95
Q

Proximal sesamoid bone fractures of fetlock: Aetiology? Clinical signs? Diagnosis? Management?

A
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
96
Q

Sesamoiditis of fetlock: What is it? Which horses is it seen in? Management?

A

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

97
Q

Osteochondral fragmentation of P1: Cause? Clinical relevance? Diagnosis? Management?

A

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

98
Q

Osteochondrosis of the fetlock? What is seen? Which horses? Diagnosis? Management

A

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

99
Q

Fetlock osteoarthritis: What happens? Clinical findings? Management?

A

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

100
Q

Palmar/plantar osteochondral disease (POD): What is it? Cause? Clinical signs? Radiography? Management?

A

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

101
Q

Chronic proliferative synovitis: Aetiology? Clinical findings? Diagnosis? Management?

A
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
102
Q

Fetlock subluxation: Aetiology? Diagnosis? Management?

A

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

103
Q

Types of fractures of the third metacarpus/metatarsus? Cause? Clinical presentation?

A

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

104
Q

Diagnosis and management of metacarpus/metatarsus fractures?

A
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
105
Q

What is dorsal metacarpal disease also known as? Cause? Clinical presentation? Diagnosis? Management?

A

= “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

106
Q

Fractures of the second/fourth metacarpal/metatarsal (splint) bones: Types? Cause? Diagnosis? Management?

A

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)

107
Q

Exostosis of McII/MtIV (splints): Cause? Clinical signs? Diagnosis? Management?

A

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)

108
Q

SDFT tendonitis: History? Clinical examination? Ultrasound? Treatment?

A
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
109
Q

Treatment for SDFT tendonitis?

A

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

110
Q

What tendon/ligament injuries can there be in the distal limb of the horse, except SDFT tendonitis?

A
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
111
Q

Palmar/plantar annular ligament (PAL) syndrome : Causes? Clinical signs? Diagnosis? Treatment?

A
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
112
Q

Carpal osteoarthritis: What is it? Predispositions? Clinical signs? Diagnosis? Management?

A
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)
113
Q

Osteochondral fragmentation of carpus: What happens? Diagnosis? Management?

A

= 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)

114
Q

Carpal bone fractures: Types, cause ,diagnosis, management?

A

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

115
Q

Accessory carpal bone fractures: Cause? Presentation? Diagnosis? Management?

A

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

116
Q

Carpal subluxation: Cause? Presentation? Diagnosis? Management?

A

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

117
Q

Carpal hygroma: Cause? Presentation? Diagnosis? Management?

A

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

118
Q

Carpal canal syndrome: What conditions does this include?

A

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
119
Q

Clinical signs and diagnosis of carpal canal syndrome? Management?

A

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

120
Q

Radial fractures: Cause? Presentation? Management?

A

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

121
Q

Ulna fractures: Cause? Presentation? Diagnosis? Management?

A

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)

122
Q

Fractures of the humerus and scapula: Cause? Types? Presenting signs? Management?

A

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!!!

123
Q

Osteochondrosis of elbow: What is seen? Management? Prognosis?

A

Osseous cyst-like lesions in proximal radius
Conservative (intra-articular medication) or surgical (extra-articular drilling)
Poor prognosis as often secondary joint disease present

124
Q

Osteochondrosis of shoulder: What is seen? Prognosis?

A

Osseous cyst-like lesions in distal scapula (also proximal humerus)
OCD of glenoid cavity
Poor prognosis as often secondary joint disease present

125
Q

Shoulder dysplasia and subluxation: Breeds affected? Presentation? Diagnosis? Management?

A

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

126
Q

Shoulder OA: How common? Causes? Predispositions? Presentation? Diagnosis? Treatment? Prognosis?

A

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

127
Q

Elbow OA: How common? Cause? Diagnosis? Management? Prognosis?

A
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
128
Q

Elbow hygroma (“capped elbow”): Presentation? Which horses? Treatment?

A

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

129
Q

Stifle OCD: Which horses affected? Which parts of the stifle usually? Presenting signs? Diagnosis? Treatment options?

A
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
130
Q

Osseous cyst-like lesion (OCLL): Other name? Where? Age? Presentation? Diagnosis? Treatment?

A

= 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

131
Q

Stifle soft tissue injuries?

A

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

132
Q

OA of stifle: Causes? Diagnosis? Treatment?

A
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
133
Q

What stifle fractures are there? Cause? Treatment?

A

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!

134
Q

Upward fixation of the patella: Aetiology? Clinical signs? Treatment?

A

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

135
Q

Treatment for upper hindlimb long bone fractures?

A

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

136
Q

What conditions fo the coxofemoral joint are there?

A
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)
137
Q

What type of cartilage does the sacroiliac joint have?

A

Sacral surface = hyaline cartilage

Ilial surface = fibrocartilage

138
Q

Pelvic fractures: Types? Aetiology? Clinical signs?

A

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)

139
Q

Diagnosis and treatment options for pelvic fractures? Outcome?

A

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

140
Q

Presenting complaints with sacroiliac disease? Diagnosis?

A
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
141
Q

Treatment for acute and chronic sacroiliac disease?

A
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
142
Q

Where are the calcaneal bursae in the tarsus?

A

Between gastrocnemius and SDFT, extending distally

Communicates with the gastrocnemius bursa which is deep between the gastrocnemius tendon and tuber calcis

143
Q

What is an acquired superficial bursa of the tarsus?

A

Between SDFT and skin

“Capped hock”

144
Q

OCD of tarsus: Distribution? Clinical signs? Treatment?

A
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
145
Q

Tarsal bone collapse: Cause? Treatment? Prognosis?

A

Incomplete ossification:
- dysmature/premature foal
- neonatal maladjustment
- cna present as angular limb deformities
Supportive therapy until matures
Poor prognosis especially if >30% collapse/fragmentation

146
Q

OA of the small tarsal joints: Other name? Where? Which horses? Cause? Clinical presentation?

A

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

147
Q

Diagnosis and treatment options for small tarsal bone OA? Outcome?

A

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

148
Q

Tarsal fractures: Types and treatment?

A

Malleolar: can remove arthroscopically
Calcaneal: may be unstable so euthanasia
Small tarsal bones: conservative or internal fixation

149
Q

Tarsal luxations: Which joints? Clinical signs? Diagnosis? Treatment?

A

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

150
Q

What soft tissue injuries of the carpus are there?

A

Collateral ligament injuries
Tarsal sheath swelling
Calcaneal bursa/lateral lunation of SDFT

151
Q

Signs and treatment of collateral ligament injuries of the tarsus? Prognosis?

A
Signs: 
- swelling ++
- TC effusion
Treatment:
- Rest
- NSAIDs, cold hosing, bandaging
- physiotherapy
- intra-articular medication?
- monitor with US
Poor prognosis if OA of joint develops
152
Q

Tarsal sheath synoviocoele (“thoroughpin”): signs? Diagnosis? Management?

A

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

153
Q

Calcaneal bursa/lateral lunation of SDFT: What usually happens? Signs? Diagnosis? Treatment?

A
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)
154
Q

Horse cervical spine anatomy:

  • How many cervixal vertebrae?
  • Which have specific characteristics that enable radiographic recognition?
  • What do the other cervical vertebrae look like?
A

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)

155
Q

Characteristics of C1?

A

= Atlas
No body or articular processes
Radiolucent line seen between the two halves on VD view in foals before ossifies

156
Q

Characteristics of C2?

A

= 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

157
Q

Characteristics of C6 and C7?

A

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

158
Q

Presenting signs of neck pain (cervical spine)?

A

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)

159
Q

Examination for neck pain? What to rule out?

A
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
160
Q

Common conditions of the neck?

A

Developmental - crvical vertebral malformation (“wobblers”)
Degenerative - OA
Trauma - fractures

161
Q

Cervical vertebral malformation (CVM): Also known as? What is it? Predispositions? Clinical presentation?

A

“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

162
Q

Osteoarthritis/arthropathy of the neck/dorsal articular facet arthropathy: Aetiology? What is seen? Treatment? Negative prognostic indicators?

A
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
163
Q

Prognosis of cervical spine fractures?

A

Depends on location, configuration, open or closed, single or polyostotic
Many not treatable
Conservative treatment only realistic chance

164
Q

Presenting signs of back pain (thoracolumbar spine)

A
Poor performance
Behaviour changes
Uncomfortable when ridden/"doesn't feel right"
Stiffness in back
back spasms
Difficulty being tacked up
Bucking/rearing
165
Q

Physical examination for back pain (thoracolumbar spine)?

A

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

166
Q

Cause, treatment and secondary complications of withers fractures?

A
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
167
Q

Saddle induced trauma: Identifying? Treatment?

A
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
168
Q

Back ligament damage: Which ligament usually? Signs? Diagnosis? Treatment?

A
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?
169
Q

Impingement of dorsal spinous processes: Cause? Diagnosis? Treatment?

A
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
170
Q

What is the aim of GF administration to tendon injuries? Is it proven?

A

Produce true tendon rather than scar tissue
Reduce amount of scar tissue

No not proven - dosage, treatment intervals and best administration time all unknown

171
Q

IGF-1 for tendon injuries: findings from study?

A

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?

172
Q

TGF-beta for tendon injuries: What is it? Findings from study?

A

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

173
Q

Platelet rich plasma for tendon/ligament injuries: What is it? How does it work? Which injuries may it be beneficial for?

A

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

174
Q

Where are stem cells taken from for regenerative therapy?

A

Bone marrow of tuber coxae of sternum

175
Q

What are valgus and varus angular limb deformities?

A
Valgus = lateral deviation
Varus = medial deviation
176
Q

Where do most foal congenital angular limb deformities arise from? Where else can they arise from?

A
Most common = metaphysical growth plate
Epiphysis
Cuboidal bones - carpus, tarsus
Diaphysis (rare)
Soft tissue laxity
177
Q

Problems with premature foals and angular limb deformities?

A

Incomplete mineralisation of bones
High risk of crushing injury to cuboidal bones of carpus/tarsus
Tarsal bones often collapse dorsally as delayed dorsal ossification

178
Q

What does it mean if a foal’s congenital angular limb deformity can be straightened manually?

A

Premature - incomplete ossification

Or peri-articular laxity

179
Q

Management of a foal with a congenital angular limb deformity with positive manipulation due to incomplete mineralisation of carpal bones?

A

Restrict exercise
Bandage with splint - light, digit outside
Repeat radiographs every 2 weeks
Balanced nutrition
Usually improves unless systemic involvement

180
Q

Management of a foal with a congenital angular limb deformity with positive manipulation due to peri-articular laxity?

A

Controlled exercise to strengthen peri-articular soft tissues
Careful with bandaging
Usually resolves unless other systemic problems

181
Q

Causes of acquired angular limb deformities?

A

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

182
Q

Prognosis of angular limb deformities?

A
Good if:
- early treatment
- physis or epiphysis
Fair to poor:
- metaphysical or diaphyseal
- crushed cuboidal bones
- severe angulation
- secondary DJD
183
Q

Treatment angular limb deformities with negative manipulation?

A

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)

184
Q

How long do the fetlock, carpus and tarsus joints have fast growth as a foal before closure?

A

Fetlock: <6-8 weeks
Carpus: <5 months
Tarsus: <7 months

185
Q

What is the technique of growth acceleration for angular limb deformities of foals?

A
Concave side
Just proximal to physis
Periosteal elevation
Does not over-correct
Also restrict diet and aways combine with hoof balancing
186
Q

What is the technique of growth retardation for angular limb deformities of foals?

A

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

187
Q

What are the origins and insertions of the SDFT? Function?

A
Origin:
- distal humerus
- proximal radius
Insertion:
- proximal P2
- distal P1
Function:
- flexion of MCP/MTP joint

Accessory ligament - disto-palmar radius (AL-SDFT)

188
Q

What are the origins and insertions of the DDFT?

A
Origin:
- humeral epicondyle
- medial olecranon
- proximal radius
Insertion:
- ventral-palmar P3
Function:
- flexion of DIP joint

Accessory ligament - palmar carpus (AL-DDFT)

189
Q

Digital hyperextension in foals: Cause? Management?

A

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!

190
Q

Treatment of foal flexural limb deformities of foals?

A

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

191
Q

Surgery for foal flexural limb deformity of the DIPJ? Prognosis?

A

Desmotomy of AL-DDFT (distal check ligament)
Combine with conservative treatment
Good-excellent for grade 1
Fair-guarded for grade 2

192
Q

Surgery for foal flexural limb deformity of fetlock?

A

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

193
Q

Septic arthritis in foals: Route of bacteria access? Aetiology? Clinical signs?

A
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
194
Q

Diagnosis of septic arthritis/physitis/synovitis in foals?

A
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
195
Q

Reference ranges from synoviocentesis to diagnose septic synovitis in foals?

A

Turbid, serosanginous, reduced viscosity
>20x10^9 cells/L
>80% neutrophils
Total protein >30-35g/L

But not always

196
Q

Prognosis of septic arthritis/physitis/synovitis in foals?

A
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
197
Q

What to check a physiotherapist is registered with?

A

ACPAT
RAMP
Only ‘physiotherapist’ is protected, not ‘animal/veterinary physiotherapist’

198
Q

What are kVP, mA and S for radiography?

A
kVp = speed of electrons
mA = number of electrons released
S = time
199
Q

What are the 6 points to consider when assessing radiograph quality?

A
Positioning
Collimation
Contrast
Exposure
Labeling
Artefacts
200
Q

Define sclerosis and osteolysis? Causes?

A
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)
201
Q

How do active and inactive bone lesions appear differently on radiography?

A
Active:
- irregular
- sharp edges
- poorly demarcated
- destructive or productive
Inactive:
- smooth
- rounded edge
- well defined
202
Q

What are osteophytes?

A

Periarticular focal new bone production
Active: sharp, irregular
Aged: smooth, uniform

203
Q

What are enthesiphytes?

A

Focal new bone production at origin or insertion of soft tissue (due to stress at attachment)
E.g. at joint capsule, tendon, ligament

204
Q

How does gamma scintigraphy work?

A

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

205
Q

What are the phases of bone scanning by gamma scintigraphy?

A
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
206
Q

When might nuclear scintigraphy be indicated?

A
  1. Isolated lameness but no abnormalities on imaging
  2. Lameness not isolated
  3. Lameness proximal to stifle
  4. Suspect stress or non-displaced fracture
  5. Spinal problems (thoracic, lumbar and pelvic)
  6. Horse not amenable to blocks
207
Q

How does US work?

A

Sound wave produced by piezoelectric crystal
Reflected, absorbed or scattered from tissue interface
Degree of reflection determined by tissue density

208
Q

Stifle joint compartments? Which ones communicate?

A
Femoropatella
Medial femorotibial
Lateral femorotibial
FP and MFT communicate (60-85%)
FP and LFT sometimes communicate (5-17%)
209
Q

Differentiating between acute and chronic muscle conditions?

A
Acute: swelling/pain
Chronic:
- stiffness
- cramping
- pain
- fasciculations
- weakness
- atrophy
- fibrosis/calcification
210
Q

Presentation of forelimb proximal suspensory desmitis?

A

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

211
Q

Physitis: What is it? Signs?

A

Enlargement of physis - inflammation and disruption of endochondral ossicication
Self limiting
Signs:
- lameness and/or stiffness