Brad lameness Flashcards

1
Q

Be able to recognise equine lameness (ie pick the lame leg / legs) ?

A

Picking the leg in lameness

The front
- head down on sound
- head up on lame leg (head goes up when the horse lands on the lame leg
- observe as the horse trots towards you

The hind limbs
- hip hike; point of hip moves up and down more when the lame leg lands
- best observed as the horse trots away from you

Other signs of lameness
- shortened cranial phase to stride (best observed side on).

Arc flight path of the hoof
- may indicate abnormal landing (eg landing toe first could indicate pain in the heel).
- could be conformational (eg fetlock varus tends to induce a paddling action where the distal limb wings outward.
- box hoof

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2
Q

Know the AAEP lameness grading system and its application ?

A

Describe the AAEP American Association of equine practitioners lameness grading.

Grade 0 = Not detectably lame
Grade 1 = Inconsistently lame at the trot on the circle
Grade two = Inconsistent lameness at the trot on a straight line, but consistently lame on the circle
Grade three = Consistently lame on the straight line at the trot
Grade 4 = lame at the walk
Grade 5 = non weight bearing lame.

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3
Q

Understand and describe how to perform an extensive lameness examination ?

A

Extensive lameness examination
Run your eyes over the horse in a systematic way to train yourself to do the same thing every time.

  1. Complete history (breed, age, use etc)
  2. examine from a distance
  3. Examine up close (conformation, pelvic symetry, swollen joint, contracted hoof)
  4. examine gait in hand / lunge
  5. Palpation of joints tendons and ligaments
  6. hoof testers
  7. percussion
  8. flexion tests - static / dynamic
  9. nerve and joint blocks
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4
Q

When carrying out a lameness examination describe how you would systematically assess the horses gaits ?

A

Systematic assessment of equine gaits / lameness examination.

Walk
1. Walk in hand - look at foot landing and arc flight of limbs

Trot - in hand
1. In hand towards and away from you
2. lunge on the circle to the left and right; begin with a large circle 20m, then make the circle smaller 10m
- inmost cases lamness will be more apparent when the lame leg is on the inside
- hind leg lameness will often present as a shortened stride / toe stabbingaction with the affected leg on the inside of the circle.

  • surface - even, regular hard surface best
  • other gaits - difficult for the human eye to detect lameness at speeds and gaits other then walk and trot.

Remember horses can be lame on more than one limb and these may or may not be related.

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5
Q

Define the terms bow legged and cow hocked ?

A

Definitions

Bow legged
- hocks out, with hind hooves angled inwards

Cow hocked
- hocks in with the hooves angled out

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6
Q

Describe how you would carry out a (dynamic, static) flexion test ?

A

Flexion test

Apply flexion to joints / jints for 60 seconds
- increasing intraarticular and subcondral bone pressure to exacerbate subclinical / clinical lameness.
- trot off
- pain on flexion
- reduced range of motion
- determine the level of significance eg is the horse affected for more than 3-6 strides
- mild, moderate or marked response

Static flexion = flexing the joint without trotting off.
Dynamic flexion - flex 60sec and trot off

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7
Q

Describe how you would carry out a Palmer digital nerve block (PDNB) ?

A

nerve block Palmer digital nerve block
(Perineural anaesthesia)
- can be carried out in the front and hind leg
- prilocaine / mepivacaine, small volume 2-1.5mls 25G needle
- wait 10-15 mins / assess through prick prod distal to injection site
- aseptic technique.

Technique
- neurovascular (VAN)
- just proximal to the collateral cartilages and medial and laterally

Blocks
Caudal 1/3rd of the hoof (heels including skin)
+ N bone + P3
+ variable amount of sole and DIP joint

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8
Q

Describe a abaxial sesamoid nerve block ?

A

Abaxial sesamoid nerve block
volume 3ml each site,medially and laterally
onset = 10-20 mins

Technique
The neurovascular bundle at the base of the proximal sesamoid bones.

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9
Q

Describe the characteristics of normal synovial fluid ?

A

Normal synovial fluid

Is an ultrafiltrate of plasma
- secreted by synoviocytes
- clear straw colour
- provides viscosity and lubrication to the joint
- hyaluronic acid (HA) non sulphated polysaccharide (glucuronic + glucosamine).

Normal synovial fluid characteristics in health
- Total protein <25g/L
- <0.3 *10^9 cells/L
- <10% neutrophils

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10
Q

Define OA ?

A

Osteoarthritis OA

Is progressive degradation of the articular cartilage
- failure of cartilage to withstand cyclical trauma of exercise and age.

OA is recognised by
- traumatic arthritis inflammation and damage to the structures of the diarthrodial joints (free moving with articular capsule)
- synovitis and capsulitis
- instability causing injury such as intraarticular and collateral ligament injury
- in articular fracture
- subchondral bone disease and meniscal injury (stifle)

The response to treatment often diminishes with time.

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11
Q

Terminology define osteoarthritis - osteochondral fragment, periarticular osteophyte and enthesiophyte ?

A

Terminology for osteoarthritis

Osteochondral fragment (OC)
- bone chip
- small seperated segment of bone and cartilage

Periarticular osteophyte
- bone spur on / around the joint

Enthesiophyte
- new bone formation within ligamentous insertions
- bone formation at the site of attachment of a muscle, tendon or ligament

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12
Q

Describe the underlying pathology of OA ?

A

Pathology (OA) osteoarthritis

All animals / humans develop OA as joint are used
Factors affecting OA development
- exercise intensity and frequency
- conformation
- level of fitness
- muscle fatique
- ground surface
- osteochondrosis

Pathology
Cartilage is the shock absorber
- with exercise the cartilage thins and transfers more weight to the underlying bone

  • pain, lameness and joint instability
  • soft tissue damage
  • Il-1, IL-6; proteoglycans and degradation of collagen
  • ultimately leading to chip fractures and spur formation
  • remodelling of microfractures / necrosis subchondral bond
  • inflammation of soft tissue (synovitis, capsulitis)
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13
Q

Compare the effect of osteoarthritis between the fetlock and hock joints of horses ?

A

Different joints respond differently to osteoarthritis

High motion joins
(eg fetlock and carpus)
- synovitis, capsultis
- osteophytosis
- OC fragmentation

High load, low motion joints
(eg hock, pastern, hip)
- joint space narrowing
- subchondral sclerosis, lysis
- osteophytosis

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14
Q

Define osteochondrosis (OC) ?

A

Osteochondrosis
Failure in endochondral ossification (OC)

Osteochondrosis (OC) in the horse is a disease characterised by the disturbance of the normal differentiatiation of chondrocytes in growing cartilage resulting in impaired endochondral ossification.

Histology
(centres of bone ossification in the epiphysis)
- persistent cartilage in the late hypertrophic zone
- failed BV ingrowth in late hypertrophic zone
- failed endochondrial ossification

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15
Q

Provide definitions for osteochondrosis, osteochondritis and osteochondritis dissecans (OCD) ?

A

Osteochondrosis terminology

Osteochondrosis - failure in endochondral ossification (OC)

Osteochondritis
- implies joint inflammation which occurs when a lesion reaches the joint surface.

Osteochondritis dissecans (OCD)
- refers to osteochondrosis cases in which a dissecting flap of cartilage / bone is present.

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16
Q

Identify this pathology ?

A

Osteochondrosis
Failure in endochondral ossification (OC)

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17
Q

Identify the main predisposing factors for osteochondrosis ?

A

Predisposing factors for osteochondrosis ?

1.Nutrition
- high carbohydrate diet = increase in blood glucose and insulin
- altered collagen in cartilage
2.Excess phosphorous
- acidifies cartilage and interfers with matrix formation
3.Deficient copper
- Cu is a requirement for collagen cross linking
4.Genetics
- young fast growing horses TB, WB, SB
- account for 30% variation in hock OC
5.Exercise
- trauma to weak cartilage, disruption to vascular supply, leads to granulation tissue formation and OC lesion.

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18
Q

Describe the four normal layers of cartilage ?

A
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19
Q

Describe how you could diagnose and prevent OC from occuring ?

A

Osteochondrosis OC

Diagnose through radiology
- osteochondritis dessicans (OC fragment) occurs in areas of shear force
- subchondral bone cyst in areas of compression

Prevention of the OC

  • genetics breeding
  • ensure appropriately balance nutrition (pregnant mare, yearling especially)
  • identify at risk foals
  • rapid growth 3-5months, risk of stifle OC
  • measure serum copper concentrations + consider Cu supplementation which is important for resolution of lesions
  • If OC lesions are left untreated, then the risk of OA is high.
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20
Q

Describe the five approaches to the treatment of OA

A

Treatment of OA Osteoarthritis (OA)

Possible corrective measures
1. Rest +/- anti - inflammatory drugs
2. joint / systemic medication (aimed at slowing / preventing / repairing joint damage)
3. corrective shoeing
4. arthroscopic surgery
5. joint fusion

Res and anti-inflammatory drugs
No radiographic changes
- synovitis/ capsulitis
- indicates 2-3 month spell
- hand walking to maintain cartilage integrity
- passive joint flexion, limit fibrosis of joint capsule

If significant cartilage / bone damage 6-9 month spell

Potential medical treatments
- NSAIDS
- Hyaluronic acid
- PSGAGS
- Oral glucosamines + chrondroitin
- Shock wave therapy
- Pentosan polysulphate
- Biophosphonates
- IRAP

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21
Q

Describe the MOA and dose of commonly used NSAIDS in the treatment of OA ?

A

Osteoarthritis

Commonly used NSAIDS
Flunixin meglumine 0.5-1.1 mg/kg PO/IV BID
Meloxicam (Metacam 0.6 mg/kg PO SID
Phenylbutazone

Mechanism of action
- inhibit PGE and TBX from arachhidonic acid by inhibiting the COX enzyme
- COX 1 - homeostatic Pglandins
- COX 2 - inflammatory Pglandins

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22
Q

Describe the MOA and common dose rate of corticosteroids in the treatment of OA ?

A

**OA osteoarthritis **

Commonly used corticosteroids / dose rate
- commonly used as intraarticular injections to suppress pain, heat and swelling
- high dose corts have negative effects on cartialge health, where as low dosages can be protective to cartilage health
- use lowest effective dose
- Triamcinalone $ Betamethasone

Corticosteroids / mechanism of action
- stabilise lysosomal membranes and enzyme release
- reduce vascular permeability

Inhibition
- white cell adherence to BV and diapedesis
- release of white cell superoxide synthesis
- platelet aggregation
- arachnidonic acid release and prostaglandin synthesis
- cytokine production and relaese

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23
Q

Describe the use of Hyaluronic acid in the treatment of osteoarthritis ?

A

Hyaluronic acid

Mechanism of action
- non sulphated glycosaminoglycan
- endogenous source synoviocytes
- provides hydrodynamic lubrication improves joint fluid viscosity
- anti- inflammatory effects decreasing Il-1, PGE2 and free radicals
- exogenous HA enhances endogenous HA production.

Treatment
- intravenous treatment weekly for three weeks
- intraarticular
- oral

Reccomend Corticosteroids in conjunction with HA
- there is a benefit of combination

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24
Q

Describe the mechanism of action and effects of pentosan polysulphate ?

A

Pentosan polysulphate

Mechanism of action - 3mg/kg weekly 4-7 weeks
- inhibits IL-1, MMp, PGE2
- enhances endogenous HA and proteoglycan synthesis (CHS) in cartilage
- improved lameness and reduced synovitis

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25
Q

Describe the mechanism of Extracoporeal shock wave therapy ?

A

Extracoporeal shock wave therapy

Meachanism of action
- high energy acoustic waves, focussed or unfocussed
- induce cytokines and shock wave proteins
- analgesia through nociceptor inhibition
- neovascularization

The analgesia effects can last for 2-4 days

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26
Q

Describe some medicinal treatments that could be implemented to improve osteoarthritis ?

A
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27
Q

Describe your systemic protocol for examination of the distal limb ?

A

Examination of the equine distal limb

  1. History - purpose use of the horse
  2. Identify the lame leg
  3. Start at hoof and work up, establish a protocol
  4. palpation
  5. Hoof testers / percussion
  6. Flexion tests
  7. Local anaesthesia
  8. Imaging

Careful palpation
- hoof capsule for asymetric heat
- palpate digital pulses
- Coronet - pain, swelling, discharge
- Collateral cartilages; pain + calcification
- Palmar pastern - SDFT, DDFT and distal sesamoid ligaments
- Coffin - joint effusion (dorsal just proximal to the coronet.

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28
Q

What clinical signs would indicate distal limb lameness ?

A

Distal limb lameness

  1. Increase or asymetric digital pulses
  2. Increased heat in the hoof capsule
  3. Pain on palpation of coronet
  4. Pain on hoof testers or hoof percussion
29
Q

Identify this pathology and describe its predisposing factors ?

A

Subsolar abscess
(Is an infection beneath the sole of the hoof)
Usually occur at the junction of the white line and wall.
- penetrating sole injury / foreign body
- septic synovitis
- fracture
- cellulitis

Predisposing factors for a subsolar abscess
- recent wet weather softens the sole making it more easily penetrated
- shod recently (nail bind - to close to the white line).
- subclinical seedy toe.

30
Q

What clinical signs would make you suspect a case of subsolar abscess ?

A

Subsolar abscess

Clinical signs
Grade 4-5 / 5 lame
- bounding digital pulse
- palpable heat hoof wall / coronet
- +ve hoof testers, useful to localise the most painful site

If a solar abscess is left untreated it may erupts at the coronet or between the heel bulbs
- this occurs if solar drainage is not established

31
Q

Describe how you could diagnose and treat a case of subsolar abscess ?

A

**Subsolar abscess

Diagnoses
- an infection below the sole of the hoof
- nerve block PDNB (palmer digital nerve block)
- inspect the white line 1st for black holes or tracts to follow

Treatment
- Drainage 14G needle
- small loop knife to drain pus from between sensitive sole corium and non sensitive cornified sole
- most importantly treatment must include adequate drainage to prevent solar corium from ‘plugging’ hole prematurely
- sugar iodine poultice
hoof poultice maintained for 7-10 days or until drainage stops and lameness has improved
- Tetanus prophylaxis
- Antibiotics - usually not indicated except of there is concurrent cellulitis

If eruption at the coronet / heel bulbs
- remove the wall below the site of eruption and bandage
- this wall defect will grow down with time and is often referred to as a ‘sand crack’

32
Q

Identify this pathology and demonstrate knowledge of its clinical signs and diagnoses ?

A

Septic osteitis
Usually a bacterial infection of the distal phalanx, often arising as a sequel to subsolar / lamina abscessation.

Clinical signs
- persistent lameness and discharging tract
- under run / seperated sole
- concurrent distal limb cellulitis (heat and painful to palpate) with swelling around the coronet

Diagnoses
If suspected osteitis osteitis diagnose through radiographs
- cranial palmer/plantar and lateral medial
- osseous sequestrum (lucent involucrum surrounding radio-opaque sequestrum.)
- P3 has no true periosteum
- irregular margin to P3
- osteolysis, demineralization

33
Q

Describe how you would go about treating a case of septic Osteitis ?

A

Treatment of septic osteitis is surgical
- general anaesthesia
- distal limb torniquet
- abaxial sesamoid nerve block + surgical curettage
- broad spectrum antibiotic therapy / systemic topical + regional IV

Pack the defect with saline gauze and double padded / gamgee bandage changing every 2-3 days.

Hospital plate = bar shoe
+ plate secured to solar surface for protection

Then apply a hospital plate shoe post surgery until site is granulated and cornified with new sole
- this may take upto 3 months

34
Q

Identify this pathology and its aetiology ?

A

Seedy toe / white line disease
( it is necrosis of the sensitive laminae, usually of the anterior wall of the hoof)

Seedy toe and its underlying aetiology
- Seperation of the wall and white line which often results in foreign material impaction, usually at the toe.
- underlying chronic subclinical laminitis
- wet environment
- inadequate hoof care

In severe cases the sole becomes dropped - distal displacement of P3 due to loss of the dorsal wall attachment due to underlying laminitis
(In these cases always reccomend hoof radiography).

35
Q

Describe how you could diagnose and treat a case of seedy toe ?

A

Seedy toe

Diagnoses
- clinical signs / history
- survey radiograpghs first to assess the position of P3 relative to the hoof capsule
- often have dropped sole

Treatment
- resection of the diseases wall and laminae with care
- if extends to coronet may require a complete wall strip
- heart bar / straight bar shoe with wall clips to stabilise wall plus or minus sole support
- bandage / iodine if it involves the senitive laminae
- follow up with regular radiographic assessment and farriery

The risk = progressive laminitis ie. pedal bone rotation or sinking

36
Q

Identify this pathology and discuss its possible aetiology ?

A

Corns
Deep bruising of the sole often adjacent to the bar/heel region.

Aetiology / cause
- ill fitting shoe
- prolonged shoeing interval (heels wear more when shod)
- shoe pressure on sole at heels
- excessive load bearing on the sole

37
Q

Describe your strategy for treating corns ?

A

Corns
Deep bruising of the sole often adjacent to the bar / heel region.

Treatment
- resection of the bruised thickened sole
- apply a sugar iodine poultice until the sole is firm enough to apply a wide webbed seated out shoe with no sole pressure.

38
Q

Describe the pathology you observe in this hoof and how you would attempt treatment ?

A

Poor quality hoof - thin sole
(horses are often 4/5 lame, and worse on hard ground)
- poor hoof conformation / generalised sole soreness / bruising.

Aetiology
- wet environmnet

Treatment
- generlised sole soreness and bruising
- use a wide web seated out aluminium shoe
- aluminium attentuates forces, lighter shoe
- deep seated out, relieves pressure on the sole from the shoe

39
Q

Identify common factors which could result in a vertical crack of the horses hoof ?

A

Vertical hoof wall crack

Aetiology
- previous coronary trauma
- laminar damage / excess laminar shear forces
- poor farriery, leading to uneven force on laminar / wall interface (eg unsupported heel)
- foreign body (stake wound at coronet)
- untreated hoof abscess
- seedy toe
- laminitis
- poor hoof care

40
Q

Describe type one wall crack vrs a type two wall crack and their respective aetiologies ?

A

Type one and two wall cracks

A type one wall crack dose not involve the coronet
- this can be due to inadequate trimming
- dermal lamellar cracks / tears / bruises
- seedy toe

A type two wall crack involves the coronet
Aetiology
- coronent trauma
- progress from solar surface as for type one

41
Q

Describe the potential strategies for treatment of a type one / two vertical wall crack ?

A

Vertical wall crack treatment

Type one / dose not involve coronet
- less severe
- resection to the normal laminae
- shoe with side clips / bar shoe
- equilox patch or wall plates as temporary solution.

Type two involves the coronet
- more severe
- treatment as for type one wall crack, but require complete hoof wall strip
- bar shoe with side clips / hoof cast
- severe will take 9-12 months to grow down

42
Q

Describe the aetiology, clinical signs, and treatment for equine thrush ?

A

Thrush in the equine hoof

Clinical signs
- thick black putrid discharge usually in frog sulci and heel bulbs

Aetiology
- poor hoof care
- moist environment

Treatment
- debridement
- topical alcohol / iodine
- dry environment
- regular hoof care, and open up frog sulci angles

43
Q

Identify this pathology and describe its aetiology and treatment ?

A

Canker
Proliferative degeneration of the frog, solar corium and digital cushion.
Coronary band dystrophy may also occur concurrently.

Aetiology
- environment
- bacterial Fusobacterium spp

Treatment
- radical debridement under general anaesthesia
- packing with metronidazole paste
- change environmnet
- improve hoof care and hygiene
- high recurrence rate

44
Q

Interpreting radiographs; in a healthy horse describe the expected sole thickness, hoof-laminae thickness and founder distance ?

A

Interpreting radiograghs

In a health horse;
Sole thickness = approx 6mm TB and WB, 9mm QH
Hoof - lamellar zone (Dorsal hoof wall - Dorsal P3 thickness 18-20mm

The founder distance (FD)
This is the distance from the extensor process to the coronet (<10mm)

45
Q

Interpreting radiograpghs; provide a definition for the capsular angle, phalangeal rotation and solar angle ?

A

Interpreting radiograpghs

Capsular angle
The capsular angle is the angle of rotation between dorsal P# and dorsal hoof wall
- should be parallel (0 degrees)

Phalangeal rotation
The phalangeal rotation is the angle of rotation between dorsal P3, dorsal P2 and P1
- should be parallel (0 degrees)

Solar angle
The solar angle is between palmar P3 and the sole of the hoof should be atleast parallel to positive 4-5 degrees

46
Q

Interpreting radiograpghs; Describe the normal weight distribution over the hoof ?

A

Normal weight distribution in the hoof

Weight distribution between toe and heel
- To work this out find the centra of the DIP joint, and drop a vertical line to the sole
- measure distance from the toe to the vertical line and from the heel to vertical line to yeild a weight distribution

In a healthy horse should be

50/60 - 50/40 %

47
Q

Interpreting radiograpghs; Describe the breakover point ?

A

The breakover point

48
Q

What is navicular disease and describe its aetiology ?

A

Navicular disease (caudal/palmer heel pain).

Lameness / pain originating from navicular bone and associated structures.
- navicular bone
- palmer aspect of the DIP joint
- suspensory or collateral ligmament of N bone
- distal impar ligament
- DDFT

  • a degenerative process
  • accounts for 30-50% of forelimb lameness cases

Aetiology
- affected horses typically present approximately 6-9 years old (although some are 3-4 yr olds)
- usually bilateral and insidious, but sometimes acute onset
- traditionally greater prevalence in westernern performance horses

Horse conformation
- horses with navicular syndrome, have a small hoof, upright heels, tall heels
- small boxy uprght hoof conformation (Western)
- occassionally in Tb low underslung heel and long toe
- Wb often tall narrow hooves

49
Q

Describe how a horse with navicular disease would generally present ?

A

Navicular disease

Clinical signs
- stiff gait
- stumble / trip
- feel like the horse is rushing
- often presents worse in the mornings, and signs decrease as the horse warms up
- worse on hard ground
- lameness will become worse when lunged in tight circles on firm ground
- often will have lateral medial imbalance and misshapen hooves
- lamer hoof becomes smaller, narrower with a taller heel

The horse
- stand pointing toe / toes
- stand in an elevated heel position in stable bedding trying to unload caudal hoof

50
Q

Describe how you could go about assessing a case of navicular disease in your physical exam ?

A

Clinical examination findings

Palpation
- coffin joint effusion
- increased digital pulses (sometimes)
- pain on palpation of the distal DDFT
Hoof testers / percussion
- tradionally positive over central 1/3 of frog
- usually positive to percussion
- heel pain (although some have toe pain due to altered landing)

Flexion test
- distal limb / fetlock also felxing the DIP joint
Toe extension
- increasing tension in the DDFT and force on the navicular bone (NB)
Heel elevation
- compressing DDFT/NB

51
Q

Describe the location of the navicular bone and its associated structures ?

A

Navicular bone

Located distal to P2 and caudal to the pedal bone P3

Deep digital flexor tendon
- wraps around the navicular bonebefore its insertion on the pedal bone
- digital cushion is below the navicular bone

Navicular collateral ligament
- attaches to the dorsal aspect of the navicular bone palmer and dorso medial / lateral P2

Impar ligament
- attaches distal border of navicular bone to palmer aspect of P3

52
Q

Describe potential nerve blocks which could be used to confirm a case of navicular disease ?

A

Local anaesthesia for distal limb to confirm navicular disease

  1. Palmer digital nerve block (PDNB)
  2. Distal interphalangeal (DIP) joint block
  3. Navicular bursa block (Nbursa)
53
Q

Describe how you would interpret the PDNB, DIP joint block and NB block in navicular disease ?

A

Interpretation of nerve blocks used to localise navicular disease

Interpreting PDNB local anaesthesia
- almost all horses with navicular disease will block out to PDNB
- least specific (toe, sole, heel, DIP joint and Nbursa)
- MINIMISE LOCAL VOLUME AND INTERPRET WITH TEN MINS (if not correctly administered Proximal interphalangeal joint may also be blocked.)

Interpreting DIP joint block
- more specific
- generally dosen’t block the sole
- 55% of ND horses block to DIP < 10mins

Interpreting anaesthesia of the N bursa
- more specific

Note if positive to DIP joint block and negative to Nbursa block suggests DIP joint disease rather than navicular
- if a negative response to N bursa and DIP unlikely to have navicular disease.

54
Q

Describe the modalities used when diagnosing a case of navicular disease ?

A

Diagnostics and navicular disease

  1. Radiography
    - lateromedial view
    - High coronary
    - upright pedal
    - skyline or special navicular view
  2. Magnetic resonance imaging MRI
    - useful for soft tissues DDFT, impar ligament and cartilage erosion
  3. Computed tomography
55
Q

Describe the changes seen on a radiograpgh which would suggest navicular disease ?

A

Radiograph Navicular disease

1 Synovial invaginations / fossae
- normal horses may have 3-5 small synovial fossae
- enlarged or misshapen synovial fossae, synovial invaginations
- clinically significant changes include; increased height + width, lollypop or inverted Y shapes

  1. Distal border fragments
  2. Osseous cyst like lesions
  3. enthesiophytes
  4. Navicular bone shape
    - has a role in pathogenesis / heritable
    - apparant shape predisposition to radiological changes
    - concave dorsal articular border is associated with a higher grade of disease eg warm bloods

Focal distal sesamoidean impar desmitis were identified as the most likely causes of pain and lameness.

56
Q

What are the three principles in the management of navicular disease ?

A

The three principles of managing navicular disease

  1. Address hoof - therapeutic farriery
  2. Intrathecal medication
    - (ie DIP joint and or navicular bursa
  3. Others
  4. Surgical options
    - ie PD neurectomy
57
Q

Describe the cases of navicular disease which would result in the best effects from therapeutic farriery ?

A

Therapeutic farrier and its effect on navicular disease

Affects on clinical signs of navicular disease
There is a better response
- in horses with a history of lameness < 10 months
- in horses with less severe radiograpghic changes
- in general any response will require 3-4 shoeing intervals
- there is a better response in cases with compliant clients

58
Q

Describe the process of therapeutic farriery in the correction of navicular disease ?

A

Therapeutic farriery and navicular disease

Egg bar shoe
- increases the contact surface area of the hoof
- dissipates the force evenly under the hoof and provides a caudal shift in the centre of pressure
- reduces pressure applied to the navicular bone

Raised heel
- reduces the strain on the DDFT and torque
- reduces the force upon the navicular bone
(prolonged use may predispose to crushed heels)

Natural balance
Heel first landing with selection of the optimal breakover point
- achieves correct phalangeal alignment
- reduces strain on DDFT
(dose no reduce navicular bone pressure).

Rolled toe shoe
- lowered peak hoof loading during breakover
- smoothed out breakover
- no reduced loading to navicular bone or DIP joint

59
Q

Describe the intrathecal medication available for the treatment of navicular disease ?

A

Intrathecal medication (injection of the navicular bursa) - Navicular disease treatment

Return to function rates range 74-80%

Triamcinalone (TA)
- diffuses readily into navicular bursa and DIPJ
- not less the 10mg

Methylprednisalone

Hyaluronic acid

60
Q

If a horse suffering from navicular disease is unresponse to madication and therapeutic farriery we may consider surgical opetions;
what are these ?

A

Surgical options for the treatment of navicular disease.

Chemical neurectomy
- Formaldehyde 1-3ml into PD nerves
- indused analgesia lasting approximately 4 months
- 88% sound at three months

Not very effective as it dose not treat the underlying cause
- eg horse continues to progress in CS

61
Q

Provide a summary of care for a horse with navicular disease ?

A
62
Q

Describe the aetiology and clinical signs of a coffin bone fracture ?

A

Coffin bone fractures

Clinical signs
* Hx racing or in recent work
* 4-5 grade lameness
* acute onset or 1-2 hours post exercise
* increased digital pulses
* positive on hoof tester
response depends upon fracture type
* DIP effusion - haemorrhage in articular fracture

Aetiology
* Most common in standard breds followed by thoroughbreds
* trauma high speed excercise
* hoof imbalance are contributing factors

63
Q

Describe a type six and type two fracture of the coffin bone ?
Describe how you could go about treating a pedal bone fracture ?

A

Coffin bone fractures

Type two Oblique wing
- second most common
- articular - oblique wing fracture running from coffin joint to solar margin
- image high coronary rad

Type six - solar margin / chip fracture
- the most common fracture type
- non articular lower grade lameness
- positive digital pulses / percussion and hoof testers

64
Q

Describe how you could go about treating a pedal bone fracture ?

A

Treatment of a pedal bone fracture

Start by stabilizing the hoof capsule and limit hoof capsule expansion with weight bearing
Bar shoe
Side / quarter clips or a rim shoe or hoof slipper cast
maintain shoe for a minimum of atleast 3-6 months.

P3 fracture outcomes + prognosis
Should repeat radiograpghs at 3-4 months
- evaluate articular margin
- DIP joint involvment + articular involvement = poor prognosis
- maintain the bar shoe when the horse is in work
- I/A medication of the DIP joint

65
Q

Describe sheared heels, their aetiology and treatment ?

A

Sheared heels
This is uneven heel growth and loading due to poor confirmation and poor hoof care.

Pathology
- one heel becomes loaded more than the other leading to disruption of the digital cushion so heels move independantly

Treatment
- Bar shoe or heart bar shoe with the longer / higher heel
- ‘floated’ or unloaded so it is non-weight bearing allowing the heels to realign
- adrress improper hoof care

66
Q

Identify this pathology, describe its aetiology and treatment ?

A

Side bone
Progressive ossification / calcification of the collateral cartilage - more commonly lateral cartilage affected.

Pathology
- normal collateral cartilage assist with concussion dampening and with soft tissue attachments
- if palpated proximal to heel bulbs in helath they should have some flex/give
- Become ossified due to concussive force and uneven hoof loading, address shoeing

Clinical signs
- varaible lameness and often in conjunction with other underlying lameness
- may have seperate centres of ossification
- in some cases the ossified centre can fracture causing severe lameness

67
Q

Identify this pathology ?

A
68
Q

Write a differential list for distal limb lameness in the horse ?

A

Differentiallist for distal limb lameness in the horse

-Osteoarthritis
- Ostechondrosis
- Subsolar hoof abscess
- Septic osteitis of the pedal bone
- Seedy toe / white line disease
- Corns
- Thin sole - poor quality hoof
- Vertical hoof wall crack
- Thrush
- Canker
- Navicular disease
- Coffin bone fractures
- Shared heels
- Side bone
- Navicular fractures
- Sole punctures
- Quittor
- Keratome
- SDFT tendonitis, collateral ligament desmitis

69
Q
A