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MSK2 > Equine MSK disease 5 > Flashcards

Equine MSK disease 5 Flashcards

1
Q

What may cause gas artefacts on a radiograph of the equine distal limb?

A

Nerve blocks prior to radiographs may introduce air into the soft tissues which may be seen on radiographs if taken soon after blocking

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2
Q

Which aspects of the equine limb are highlighted in the following radiographic views:

a: LM
b: DM
c: DLPMO
d: DMPLO

A

a: Dorsal and palmar aspects
b: Lateral and medial aspects
c: dorsomedial and palmarlateral
d: dorsolateral and palmarmedial

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3
Q

What is useful as a reference point when assessing radiographs of the equine hock?

A

The calcaneous is on the lateral aspect of the limb

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4
Q

What structures will be visible on the dorsal aspect of the equine hock on a DLPMO radiograph?

A
  • Medial trochlea of talus
  • Central tarsal bone
  • Third tarsal bone
  • Third metatarsal bone
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5
Q

What structures will be visible on the plantar aspect of the equine hock on a DLPMO radiograph?

A
  • Calcaneous
  • 4th tarsal bone
  • 4th metatarsal bone
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6
Q

What structures will be visible on the dorsal aspect of the equine hock on a DMPLO radiograph?

A
  • Lateral aspect of talus
  • Central tarsal bone
  • Third tarsal bone
  • Third metatarsal bone
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7
Q

What structures will be visible on the plantar aspect of the equine hock on a DMPLO radiograph?

A
  • Calcaneous (some superimposition)
  • 2nd tarsal bone
  • 2nd metatarsal bone
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8
Q

What structures will be visible on the dorsal aspect of the equine carpus on a DLPMO radiograph?

A
  • Radial carpal bone
  • 3rd carpal bone
  • 3rd metacarpal bone
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9
Q

What structures will be visible on the palmar aspect of the equine carpus on a DLPMO radiograph?

A
  • Accessory carpal bone
  • Ulnar carpal bone
  • 4th carpal bone
  • 4th metacarpal bone
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10
Q

What structures will be visible on the dorsal aspect of the equine carpus on a DMPLO radiograph?

A
  • Intermediate carpal bone
  • Third carpal bone
  • Third metacarpal bone
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11
Q

What structures will be visible on the palmar aspect of the equine carpus on a DMPLO radiograph?

A
  • Part of accessory carpal bone
  • Radial carpal bone
  • 2nd carpal bones
  • 2nd metacarpal bone
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12
Q

Which joints of the equine carpus always have an anatomic communication?

A

Carpometacarpal and the middle carpal

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13
Q

Discuss the importance of the rapid growth of young animals for the diagnosis and approach to lameness in young horses

A
  • Signs are the same, lameness evaluation is the same
  • Angular limb deformities may resolve, or worsen quickly
  • Cases need to be reviewed more frequently than in adults
  • Casts are quickly outgrown, need changing regularly
  • Need to treat quickly as adaptation of the bone and deformation of cartilage can occur quickly and affect adult conformation
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14
Q

Why can treatment of lameness be difficult in young horses?

A
  • Think skin → rapid development of pressure sores under bandages/casts
  • Small hooves with thin wall so shoes are difficult to attach
  • Manipulation/physical therapy may be resented
  • Inappropriate forces may initiate other/more pathology and reduce effectiveness of treatments
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15
Q

Discuss the key considerations when managing lameness in young horses

A
  • Contralateral limb - esp. in foals, lameness in one limb may lead to ALD due to abnormal forces
  • Other areas of same limb: e.g. carpal valgus may → fetlock varus
  • Need to alter mechanical forces on limbs using trimming, shoe extensions, valve casts
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16
Q

Give examples of juvenile ostrochondral conditions in the horse

A
  • Osteochondrosis/-itis dissecans
  • Subchondral cystic lesions
  • Physeal dysplasia
  • Cuboidal bone collapse
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17
Q

Give examples of developmental orthopaedic disease that may occur in young horses

A
  • Juvenile osteochondral conditions
  • Angular limb deformities
  • Flexural limb deformities
  • Cervical vertebral malformation
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18
Q

Explain the difference between angular and flexural limb deformities in horses

A
  • Angular: issue with angle of limb, related to growth of bone
  • Flexural: related to soft tissues, contracture of extensor/flexor tendons
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19
Q

Which breeds of horse are predisposed to developmental orthopaedic diseases?

A
  • Irish TB (most common in England)

- Also WB and SB

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20
Q

Discuss the aetiology of developmental orthopaedic diseases in young horses

A
  • Poorly understood, multifactorial
  • Rapid growth leads to laxity, contraction, flexural limb deformities
  • Overnutritional (maternal and foetal)
  • Unbalanced nutrition
  • Genetic predisposition
  • Biomechanical forces (abnormal forces on normal tissue or normal forces on abnormal tissue)
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21
Q

Outline the pathophysiology of osteochondrosis

A
  • Failure of endochondral ossification as a result of cartilage necrosis associated with necrotic cartilage canal blood vessels
  • Does not ossify, leading to cartilage core in subchondral bone
  • May heal by specific ages varying by site, or progress to cause clinical signs (no cartilage covering bone leading to fragmentation)
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22
Q

By what age should osteochondrosis lesions of the following sites heal in order to not progress and cause clinical signs?

a: Lateral trochlear ridge of femur
b: Distal intermediate ridge of tibia

A

a: 8 months
b: 5 months

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23
Q

Discuss the role of exercise in the development of osteochondrosis in young horses

A

Increased risk with box rest and irregular exercise

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24
Q

Discuss the role of diet in the development of osteochondrosis in young horses

A
  • Excessive digestible energy
  • Excessive dietary phosphorous
  • Copper deficiency or low Cu:Zn ratio (lysyl oxidase)
  • Concentrate feeding during gestation
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25
Q

What are the 3 manifestations of osteochondrosis lesions in young horses?

A
  • Thickened cartilage
  • Intraarticular cartilage fragments (osteochondrosis dissecans)
  • Subchondral bone cysts
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26
Q

How might subchondral bone cysts develop in young horses?

A
  • As a result of ischaemic chondronecrosis lesions

- Can also be secondary to trauma

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27
Q

Describe the progression of osteochondrosis lesions in young horses

A
  • Thickened cartilage may progress to OCD lesions, or subchondral bone cyst
  • Either can occur but not at the same site i.e. a fragment will not develop into a cyst
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28
Q

What are the risk factors for the development of osteochondrosis in the young horse?

A
  • Hereditary and anatomic factors most important

- Also exercise and diet

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29
Q

Explain how cartilage vessel necrosis leading to focal ischaemia of the cartilage at the chondro-osseus junction may occur in the horse

A
  • Faulty joint conformation leading to increased mechanical stress to this area during the period where vessels are present
  • Trauma not thought to be major aetiological factor but cntributes to progression
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30
Q

What are the predilection sites for osteochondrosis in horses? Specify OCD or cystic where appropriate

A
  • Femoropatellar joint (medial and lateral (OCD) femoral trochlear ridges, lateral facet of patella), medial femoral condyle (cystic)
  • Tarsocrural/tibiotarsal joint (distal intermediate ridge of tibia, medial malleolus of tibia, lateral and medial trochlear ridges of talus)
  • Fetlock joint (midsagittal ridge of MC/MC III, condyles of MC/MT III)
  • Shoulder, elbow hip
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31
Q

Outline the clinical signs of osteochondrosis/itis/OCD in the horse

A
  • Joint effusion
  • Varying degrees of lameness
  • Onset may be associated with exercise
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32
Q

Compare the degrees of lameness seen in osteochondrosis/itis/OCD depending on site and lesion type in the horse

A
  • Overt lameness if subchondral bone involved +/- synovitis
  • Lame if OCD of stifle, less/not lame if in tarsus
  • Subtle lameness if subchondral bone cyst
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33
Q

Outline the radiographic signs of osteochondrosis/itis/OCD in the horse

A
  • If signs present, permanent lesion
  • Subchondral bone flatter, irregular contour, lucencies
  • +/- Intraarticular fragments
  • +/- subchondral bone cysts
  • NB may not see cartilage fragments that have not yet ossified
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34
Q

What factors influence the treatment of osteochondrosis/itis/OCD in the horse?

A
  • Age (if in hock, may disappear up to 5months old, if in stifle may disappear up to 8-9 mo)
  • Site and severity of the lesion
  • Proposed/current career
  • Financial constraints
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35
Q

Outline conservative management of osteochondrosis/itis/OCD in the foal

A
  • Box/small paddock rest 6-90d
  • Correct dietary imbalances
  • reduce dietary energy intake
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36
Q

Outline the surgical management of osteochondrosis/itis/OCD in foals

A
  • Wait until 12-18mo before surgery except where there is a huge amount of effusion that will stretch joint capsule
  • Removal of fragments, debride abnormal tissue
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37
Q

Outline the treatment options for subchondral bone cysts in foals

A
  • Consservative: rest +/- NSAIDS or intraarticular corticosteroids
  • Intra-lesional corticosteroids
  • Arthroscopic debridement
  • Intralesional implantation with allogenic chondrocytes and IGF1
  • Screw in centre of condyle that goes through cyst to aid filling of cyst with bone
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38
Q

Discuss the prognosis for osteochondrosis/itis/OCD in foals

A
  • Depends on age, site, severity, treatment opted for, intensity of athletic career
  • Can be excellent (full athletic potential)to poor (persistent lameness/osteoarthritis)
  • Prognosis best for hock, ok for stifle
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39
Q

Discuss the prevention of osteochondrosis/itis/OCD in foals

A
  • Do not breed from affected animals, or those whose progeny show a high incidence
  • Balanced and adequate nutrition for pregnant mares, foals and weanlings
  • Keep foals on pasture during growing period
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40
Q

What is physeal dysplasia in young horses?

A
  • Acquired developmental orthopaedic condition

- Enlargement of physis +/- metaphysis during growth period

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41
Q

Which sites are predisposed to physeal dysplasia in the foal?

A
  • Distal metacarpus/metatarsus
  • Proximal first phalanx
  • Distal radius
  • Distal tibia
42
Q

Discuss the pathogenesis of physeal dysplasia in the foal

A
  • Mismatch between metaphyseal bone and applied load leading to osteochondral collapse
  • Normal load on bone: defective ossification/maturation (e.g. due to infection, nutritional deficiency/imbalance, rapid growth), under stimulation of bone forming process (e.g. exercise restriction)
  • Abnormal load on normal bone: trauma, poor conformation, abrupt increase in exercise
43
Q

Outline the clinical signs of physeal dysplasia in the foal

A
  • Firm, warm, painful enlargement of physeal region
  • Usually bi/quadrilateral
  • +/- lameness/stilted gait
  • Often associated with rapid growth and high plane of nutrition
44
Q

Describe the radiographic signs of physeal dysplasia in the foal

A
  • Focal widening of growth cartilage
  • Sclerosis of metaphysis/loss of trabecular pattern
  • Flaring of physis
  • Periosteal new bone
45
Q

How is physeal dysplasia diagnosed in the foal?

A
  • Usually based on clinical signs

- Radiography only taken if signs are persistent or severe

46
Q

Outline the treatment of physeal dysplasia in the foal

A 
- If mild and non-painful, monitor
Otherwise:
- Restrict exercise, NSAIDs if painful 
- Balance diet and reduce energy intake
- Manage any associated ALD
47
Q

Discuss the prognosis of physeal dysplasia in the foal

A
  • Excellent, usually resolves with appropriate management
  • May lead to ALD via bony bridging of physis on the affected side, flexural deformity secondary to lameness and reduced weight bearing
48
Q

Explain how physeal dysplasia can be prevented

A
  • Balance diet
  • Do not overfeed
  • Do not allow sudden or inappropriate increase in exercise
  • Treat any lameness or MSK deformity to avoid secondary physeal dysplasia
49
Q

What are the 3 main sites for angular limb deformities to occur in foals?

A
  • MCP and MTP (fetlock joints)
  • Carpus
  • Tarsus
50
Q

Compare valgus and varus deformities

A
  • Valgus: limb deviates laterally distal to the side of deformity (more common)
  • Varus: limb deviates medially distal to the site of deformity
51
Q

List the 4 pathogenic mechanisms that may underlie congenital angular limb deformities

A
  • Periarticular laxity
  • INcomplete ossification of carpal/tarsal bones
  • Epiphyseal dysplasia
  • Abnormal intra-uterine positioning
52
Q

Explain how periarticular laxity may lead to angular limb deformities in foals

A

Soft tissue around joints loose, unable to hold limb in the position it should be held

53
Q

Explain how incomplete ossification of carpal/tarsal bones may lead to ALD in foals

A
  • Can develop in premature/dysmature/twins

- If left untreated may lead to carpal/tarsal valgus or tarsal collapse

54
Q

Explain what is meant by “windswept” foals

A

All legs bent to the side as though being blown from the side - congenital ALD as a result of abnormal intra-uterine positioning

55
Q

Explain how acquired angular limb deformities may develop

A
  • Abnormal pressure on certain aspects of the limb
  • Physeal trauma/fracture
  • Unbalanced nutrition
  • Osteochondrosis
56
Q

Explain how abnormal pressures on the limb may lead to acquired ALD in foals

A
  • Increased pressure within physiological range = increased growth rate, if pathological leads to decreased growth rate
  • Excessive compression may be caused by: contralateral limb lameness, poor conformation, excessive BWT/exercise
57
Q

Outline the assessment of ALD in a foal

A
  • Stand directly in front of affected limb
  • Manipulate limb to differentiate between periarticular or ossification causes
  • Assess in motion
  • Radiography (at least DP view at least, ideally also LM)
  • Angle of deviation and point of intersection
58
Q

Outline what should be assessed on radiography in a case of ALD in the foal

A
  • Degree of ossification of cuboidal bones
  • Shape of all skeletal components
  • Angle of deviation
  • Pivot point
59
Q

Explain what the “pivot point” is used for in the radiographic assessment of ALD and how this is calculated

A
  • Identifies the primary site of deformity
  • Draw line down the middle of the proximal and the distal bones
  • Where these lines meet is the origin of the ALD
  • Can measure the angle of deviation which allows objective estimate of severity and allows comparison with follow up radiographs
60
Q

How can ALD of skeletal origin vs. periarticular laxity be distinguished on radiography?

A

If skeletal components are all normal, assume periarticular laxity

61
Q

Give the degrees of deviation for mild, moderate and severe ALD in foals

A
  • Mild: <5˚
  • Moderate: 5-10˚
  • Severe: 10-15˚
62
Q

When should radiographs of the carpus and tarsus always be taken in foals?

A
  • <310 days gestation
  • Dysmature foal (silky coat, floppy ears, domed forehead)
  • Congenital ALD
63
Q

Outline the treatment and prognosis for ALD as a result of periarticular laxity and normal ossification in the foal

A
  • Box rest and controlled exercise (10-20min/day)
  • Monitor closely
  • Increase exercise gradually once angulation normalised
  • Prognosis good if managed well and early
64
Q

Discuss the use of external coaptation for the treatment of congenital angular limb deformities in the foal

A
  • Generally contraindicated unless severe or incomplete ossification, definitely not for soft tissue laxity
  • If use tube casts leave foot out
  • Intermittent splinting will minimise laxity
  • Major risk of tissue necrosis, need to change bandages q3-4d, casts q10-14d
65
Q

Outline the management and prognosis of ALD in the foal resulting from incomplete ossification

A
  • Strict box rest
  • Maintain axial alignment using bandage, tube cast, splint
  • Monitor radiographically every 2 weeks
  • Remove support once sufficient ossification evident
  • Good prognosis if manage well and early
66
Q

Outline the conservative management of acquired ALD in the foal

A
  • Correct inciting factors e.g. lameness, diet
  • Restrictive exercise
  • Corrective trimming/shoeing
67
Q

What are the surgical techniques that can be used for the management of acquired ALD in the foal/

A
  • Periosteal stripping
  • Transphyseal bridging
  • Osteotomy/ectomy (no longer recommended)
  • Combination of surgical techniques
68
Q

Discuss periosteal stripping for the treatment of acquired ALD in the foal

A

aka Periosteal transection and elevation

  • Speeds growth of that section
  • For valgus, operate on lateral side of physis, for varus operate on medial side
  • ~80% success rate
  • Effect time limited to ~1-2 months, limited ability to correct at a later time
69
Q

Discuss transphyseal bridging for the treatment of acquired ALD in the foal

A
  • Slows growth
  • Valgus: medial aspect, varus: lateral aspect
  • Use screws and wire/bone plate
  • Transphyseal screw placement possible (quicker), or old fashioned method is using staples
  • Aggressive treatment
  • Requires secondary surgery
  • Risk of over correction
  • Indicated at later time points than periosteal stripping
70
Q

List the indications for surgical intervention in ALD in the foal

A
  • ALD too severe to spontaneously correct before physeal closure
  • Self correction not occurring or too slow to achieve correct conformation before physeal closure
  • ALD leading to, or likely to lead to, secondary deformity
  • Likely not indicated unless ALD is severe or future growth potential is limited
71
Q

What is the result of flexural limb deformities in foals?

A

Unable to fully extend limb

72
Q

Which sites are predisposed to congenital flexural limb deformities in the foal?

A
  • Carpus and MCP most common

- Tarsus, MTP, PIP and dip less common

73
Q

Which sites are predisposed to acquired flexural limb deformities in the foal?

A
  • DIP and MCP most common

- MTP and PIP less common

74
Q

Describe the typical scenario seen with flexural limb deformities in the foal

A
  • Previously straight limb, then growth spurt

- Now suddenly knuckling over - bone grew but soft tissue did not, leading to LD

75
Q

Discuss the pathogenesis of congenital FLD in the foal

A
  • Usually unknown
  • Intrauterine malpositioning (usually bilateral)
  • Disparity in mare to foal size
  • Teratogens
76
Q

Discuss the pathogenesis of acquired FLD in the foal

A
  • Pain in affected limb
  • Over-nutrition and rapid growth
  • Genetic predisposition
77
Q

Describe the clinical signs of congenital FLD in the foal

A
  • Usually bilateral
  • May cause dystocia
  • If severe may be unable to stand, ambulate, suckle
  • +/- common digital extensor tendon rupture
78
Q

Describe the clinical signs of acquired FLD in the foal (consider site)

A
  • Uni or bilateral
  • DIP: mainly foals and weanling, “club” foot, concave dorsal wall +/- remodelling of P3
  • MCP: mainly yearlings, upright fetlocks, hoof normal
79
Q

Describe how you would assess FLD in the foal

A
  • Observe stance and ambulation
  • Manipulate limb and determine degree of correction possible
  • Palpate limb, determine structures involved
  • Determine stage
80
Q

Describe the staging for FLD in foals

A
  • Stage I: dorsal hoof wall not yet vertical
  • Stage II: dorsal hoof wall is beyond vertical (when vertical, fetlock will knuckle over, physically unable to push fetlock back)
81
Q

Outline the management that can be used in the management of congenital FLD

A
  • If mild and able to ambulate, resolve spontaneously
  • Physiotherapy, controlled exercise possible
  • Heavy bandage/splint/brace/cast for short periods
  • IV tetracycline daily or EOD 3-4x
  • Consider NSAIDs +/- gastroprotectants
  • Farriery
  • Ensure foal can nurse
  • Protect toe/dorsal fetlock
  • Consider transection of lig/tendon involved
  • Euthanasia in severe cases
  • CDE tendon rupture, box rest +/- splint, repair necessary
82
Q

What are the possible complications associated with using tetracycline for the treatment of FLD in foals?

A
  • Diarrhoea
  • Excessive laxity of previously normal joints
  • Renal failure
83
Q

Outline the treatment options for acquired FLD in the foal

A
  • Treat any primary lameness
  • Reduce and balance nutrition
  • Farriery
  • moderate exercise
  • Anlgesics +/- gastric protectants
  • Cast incorporating foot
  • Oxytetracycline
  • Surgical
84
Q

Outline surgical treatment of FLD originating in the distal interphalangeal joint

A
  • If stage II or no improvement within 4-8 weeks
  • ALDDFT desmotomy to allow lengthening of DDFT
  • +/- DDFT tenotomy
  • Combine with correct farriery
85
Q

Outline surgical treatment of FLD originating in the metacarpophalanageal joint in the foal

A
  • Transect ALSDFT +/- ADDFT (can be done if ALSDFT ineffective, or simultaneously)
  • Can be done under standing sedation
  • Salvage: SDFT tenotomy, suspensory lig desmotomy
86
Q

Discuss the prognosis for congenital FLD in the foal

A
  • Good if improve within first 7-14d, (prognosis decreases with time past 14 days)
  • Depends on extent of correction achieved
  • Transection of ligs/tendons likely to compromise future athletic potential
87
Q

Discuss the prognosis for acquired FDL of the DIP in the foal

A
  • Good if mild and responds to treatment
  • ALDDFT desmotomy reasonable for athetic potential
  • DDFT tenotomy: salvage procedure
88
Q

Discuss the prognosis of FDL of the MCP in the foal

A
  • Worse prognosis than in DIP

- Depends on response to treatment and aggressiveness of surgical intervention

89
Q

Describe the clinical signs of digital hyperextension in the foal

A
  • Common in neonates, usually mild
  • Toe off ground in first few days after birth
  • Hyperextension of MCP/MTP joints
90
Q

Outline the pathogenesis of digital hyperextension in the foal

A

Flaccid/weak flexor muscles in newborn foal

91
Q

Discuss the treatment and prognosis of digital hyperextension in foals

A
  • Good prognosis if avoid secondary trauma
  • Usually self-corrects within a few days
  • Box rest, thick bed to prevent heel bulb damage, bandage heel bulbs to allow hand walking
  • If severe, risk of trauma to palmar/plantar aspect of phalanges so restrict exercise and protect (without heavy bandaging)
  • Heel extensions can be placed if not self correction, or if very severe
92
Q

Explain why the superficial digital flexor tendon is prone to injury

A
  • Operates at close to functional limit, esp. in racehorses (function is to support MCP joint)
93
Q

Which horses are most commonly affected by superficial digital flexor tendonitis?

A

TB racehorses most common, also event horses and showjumpers

94
Q

Describe your approach to the diagnosis of superficial digital flexor tendonitis

A
  • Observe a characteristic palmar bow at level of the cannon bone
  • Assess both limbs
  • Assess for pain on palpation, suppleness of tendons, size of tendon, peritendinous oedema
  • Ultrasonography
95
Q

Outline the staging of tendon damage

A
  • Stage I: tendon matrix degradation, cumulative ageing, impossible to detect ultrasonographically
  • Stage II: fibrillar slippage, breakage of cross links
  • Stage III: fibril rupture, may be seen ultrasonographically
  • Stage IV: complete rupture, seen ultrasonographically
96
Q

When does tendon ageing begin to occur in the horse? Briefly outline these changes

A

> 2 years of age

  • Cumulative fatigue damage
  • Loss of tendon matrix
  • Little or no ability to repair microdamage or adapt to load
  • Loss of crimp, so loss of ability to stretch before fibres are under strain, fibres now under strain earlier
97
Q

Describe the alterations in physicochemical environment that occur in the equine tendon as a result of exercise

A
  • Energy loss through hysteresis
  • → rise in tendon core temp to 45˚C
  • Increased cytokine production as a result of high temp
98
Q

Describe the alterations in physicochemical environment that occur in the equine tendon as a result of cellular effects/molecular inflammation

A
  • Loss of ultimate tensile strength induced by cyclical loading depends on presence of live cells
  • Get elevation in active and proMMP2 which facilitates loss of ultimate tensile strength
99
Q

What ultrastructural changes occur within the equine tendons as a result of exercise and age

A
  • Changes in interfascicular matrix

- Higher proportion of small diameter fibres rather than thick fibres

100
Q

Describe the morphological changes that occur within the equine tendon as a result of exercise and age

A
  • Reduced crimp angle and length

- Central region more affected than peripheral by loss of crimp, hence more central lesions

MSK2 (29 decks)

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