Equine MSK disease 5 Flashcards
(100 cards)
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
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
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
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
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
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
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
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
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
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
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
12
Q
Which joints of the equine carpus always have an anatomic communication?
A
Carpometacarpal and the middle carpal
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
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
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
16
Q
Give examples of juvenile ostrochondral conditions in the horse
A
- Osteochondrosis/-itis dissecans
- Subchondral cystic lesions
- Physeal dysplasia
- Cuboidal bone collapse
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
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
19
Q
Which breeds of horse are predisposed to developmental orthopaedic diseases?
A
- Irish TB (most common in England)
- Also WB and SB
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)
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)
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
23
Q
Discuss the role of exercise in the development of osteochondrosis in young horses
A
Increased risk with box rest and irregular exercise
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
25
What are the 3 manifestations of osteochondrosis lesions in young horses?
- Thickened cartilage
- Intraarticular cartilage fragments (osteochondrosis dissecans)
- Subchondral bone cysts
26
How might subchondral bone cysts develop in young horses?
- As a result of ischaemic chondronecrosis lesions
| - Can also be secondary to trauma
27
Describe the progression of osteochondrosis lesions in young horses
- 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
28
What are the risk factors for the development of osteochondrosis in the young horse?
- Hereditary and anatomic factors most important
| - Also exercise and diet
29
Explain how cartilage vessel necrosis leading to focal ischaemia of the cartilage at the chondro-osseus junction may occur in the horse
- 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
30
What are the predilection sites for osteochondrosis in horses? Specify OCD or cystic where appropriate
- 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
31
Outline the clinical signs of osteochondrosis/itis/OCD in the horse
- Joint effusion
- Varying degrees of lameness
- Onset may be associated with exercise
32
Compare the degrees of lameness seen in osteochondrosis/itis/OCD depending on site and lesion type in the horse
- Overt lameness if subchondral bone involved +/- synovitis
- Lame if OCD of stifle, less/not lame if in tarsus
- Subtle lameness if subchondral bone cyst
33
Outline the radiographic signs of osteochondrosis/itis/OCD in the horse
- 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
34
What factors influence the treatment of osteochondrosis/itis/OCD in the horse?
- 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
35
Outline conservative management of osteochondrosis/itis/OCD in the foal
- Box/small paddock rest 6-90d
- Correct dietary imbalances
- reduce dietary energy intake
36
Outline the surgical management of osteochondrosis/itis/OCD in foals
- 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
37
Outline the treatment options for subchondral bone cysts in foals
- 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
38
Discuss the prognosis for osteochondrosis/itis/OCD in foals
- 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
39
Discuss the prevention of osteochondrosis/itis/OCD in foals
- 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
40
What is physeal dysplasia in young horses?
- Acquired developmental orthopaedic condition
| - Enlargement of physis +/- metaphysis during growth period
41
Which sites are predisposed to physeal dysplasia in the foal?
- Distal metacarpus/metatarsus
- Proximal first phalanx
- Distal radius
- Distal tibia
42
Discuss the pathogenesis of physeal dysplasia in the foal
- 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
Outline the clinical signs of physeal dysplasia in the foal
- Firm, warm, painful enlargement of physeal region
- Usually bi/quadrilateral
- +/- lameness/stilted gait
- Often associated with rapid growth and high plane of nutrition
44
Describe the radiographic signs of physeal dysplasia in the foal
- Focal widening of growth cartilage
- Sclerosis of metaphysis/loss of trabecular pattern
- Flaring of physis
- Periosteal new bone
45
How is physeal dysplasia diagnosed in the foal?
- Usually based on clinical signs
| - Radiography only taken if signs are persistent or severe
46
Outline the treatment of physeal dysplasia in the foal
```
- If mild and non-painful, monitor
Otherwise:
- Restrict exercise, NSAIDs if painful
- Balance diet and reduce energy intake
- Manage any associated ALD
```
47
Discuss the prognosis of physeal dysplasia in the foal
- 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
Explain how physeal dysplasia can be prevented
- 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
What are the 3 main sites for angular limb deformities to occur in foals?
- MCP and MTP (fetlock joints)
- Carpus
- Tarsus
50
Compare valgus and varus deformities
- Valgus: limb deviates laterally distal to the side of deformity (more common)
- Varus: limb deviates medially distal to the site of deformity
51
List the 4 pathogenic mechanisms that may underlie congenital angular limb deformities
- Periarticular laxity
- INcomplete ossification of carpal/tarsal bones
- Epiphyseal dysplasia
- Abnormal intra-uterine positioning
52
Explain how periarticular laxity may lead to angular limb deformities in foals
Soft tissue around joints loose, unable to hold limb in the position it should be held
53
Explain how incomplete ossification of carpal/tarsal bones may lead to ALD in foals
- Can develop in premature/dysmature/twins
| - If left untreated may lead to carpal/tarsal valgus or tarsal collapse
54
Explain what is meant by "windswept" foals
All legs bent to the side as though being blown from the side - congenital ALD as a result of abnormal intra-uterine positioning
55
Explain how acquired angular limb deformities may develop
- Abnormal pressure on certain aspects of the limb
- Physeal trauma/fracture
- Unbalanced nutrition
- Osteochondrosis
56
Explain how abnormal pressures on the limb may lead to acquired ALD in foals
- 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
Outline the assessment of ALD in a foal
- 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
Outline what should be assessed on radiography in a case of ALD in the foal
- Degree of ossification of cuboidal bones
- Shape of all skeletal components
- Angle of deviation
- Pivot point
59
Explain what the "pivot point" is used for in the radiographic assessment of ALD and how this is calculated
- 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
How can ALD of skeletal origin vs. periarticular laxity be distinguished on radiography?
If skeletal components are all normal, assume periarticular laxity
61
Give the degrees of deviation for mild, moderate and severe ALD in foals
- Mild: <5˚
- Moderate: 5-10˚
- Severe: 10-15˚
62
When should radiographs of the carpus and tarsus always be taken in foals?
- <310 days gestation
- Dysmature foal (silky coat, floppy ears, domed forehead)
- Congenital ALD
63
Outline the treatment and prognosis for ALD as a result of periarticular laxity and normal ossification in the foal
- Box rest and controlled exercise (10-20min/day)
- Monitor closely
- Increase exercise gradually once angulation normalised
- Prognosis good if managed well and early
64
Discuss the use of external coaptation for the treatment of congenital angular limb deformities in the foal
- 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
Outline the management and prognosis of ALD in the foal resulting from incomplete ossification
- 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
Outline the conservative management of acquired ALD in the foal
- Correct inciting factors e.g. lameness, diet
- Restrictive exercise
- Corrective trimming/shoeing
67
What are the surgical techniques that can be used for the management of acquired ALD in the foal/
- Periosteal stripping
- Transphyseal bridging
- Osteotomy/ectomy (no longer recommended)
- Combination of surgical techniques
68
Discuss periosteal stripping for the treatment of acquired ALD in the foal
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
Discuss transphyseal bridging for the treatment of acquired ALD in the foal
- 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
List the indications for surgical intervention in ALD in the foal
- 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
What is the result of flexural limb deformities in foals?
Unable to fully extend limb
72
Which sites are predisposed to congenital flexural limb deformities in the foal?
- Carpus and MCP most common
| - Tarsus, MTP, PIP and dip less common
73
Which sites are predisposed to acquired flexural limb deformities in the foal?
- DIP and MCP most common
| - MTP and PIP less common
74
Describe the typical scenario seen with flexural limb deformities in the foal
- Previously straight limb, then growth spurt
| - Now suddenly knuckling over - bone grew but soft tissue did not, leading to LD
75
Discuss the pathogenesis of congenital FLD in the foal
- Usually unknown
- Intrauterine malpositioning (usually bilateral)
- Disparity in mare to foal size
- Teratogens
76
Discuss the pathogenesis of acquired FLD in the foal
- Pain in affected limb
- Over-nutrition and rapid growth
- Genetic predisposition
77
Describe the clinical signs of congenital FLD in the foal
- Usually bilateral
- May cause dystocia
- If severe may be unable to stand, ambulate, suckle
- +/- common digital extensor tendon rupture
78
Describe the clinical signs of acquired FLD in the foal (consider site)
- Uni or bilateral
- DIP: mainly foals and weanling, "club" foot, concave dorsal wall +/- remodelling of P3
- MCP: mainly yearlings, upright fetlocks, hoof normal
79
Describe how you would assess FLD in the foal
- Observe stance and ambulation
- Manipulate limb and determine degree of correction possible
- Palpate limb, determine structures involved
- Determine stage
80
Describe the staging for FLD in foals
- 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
Outline the management that can be used in the management of congenital FLD
- 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
What are the possible complications associated with using tetracycline for the treatment of FLD in foals?
- Diarrhoea
- Excessive laxity of previously normal joints
- Renal failure
83
Outline the treatment options for acquired FLD in the foal
- Treat any primary lameness
- Reduce and balance nutrition
- Farriery
- moderate exercise
- Anlgesics +/- gastric protectants
- Cast incorporating foot
- Oxytetracycline
- Surgical
84
Outline surgical treatment of FLD originating in the distal interphalangeal joint
- If stage II or no improvement within 4-8 weeks
- ALDDFT desmotomy to allow lengthening of DDFT
- +/- DDFT tenotomy
- Combine with correct farriery
85
Outline surgical treatment of FLD originating in the metacarpophalanageal joint in the foal
- Transect ALSDFT +/- ADDFT (can be done if ALSDFT ineffective, or simultaneously)
- Can be done under standing sedation
- Salvage: SDFT tenotomy, suspensory lig desmotomy
86
Discuss the prognosis for congenital FLD in the foal
- 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
Discuss the prognosis for acquired FDL of the DIP in the foal
- Good if mild and responds to treatment
- ALDDFT desmotomy reasonable for athetic potential
- DDFT tenotomy: salvage procedure
88
Discuss the prognosis of FDL of the MCP in the foal
- Worse prognosis than in DIP
| - Depends on response to treatment and aggressiveness of surgical intervention
89
Describe the clinical signs of digital hyperextension in the foal
- Common in neonates, usually mild
- Toe off ground in first few days after birth
- Hyperextension of MCP/MTP joints
90
Outline the pathogenesis of digital hyperextension in the foal
Flaccid/weak flexor muscles in newborn foal
91
Discuss the treatment and prognosis of digital hyperextension in foals
- 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
Explain why the superficial digital flexor tendon is prone to injury
- Operates at close to functional limit, esp. in racehorses (function is to support MCP joint)
93
Which horses are most commonly affected by superficial digital flexor tendonitis?
TB racehorses most common, also event horses and showjumpers
94
Describe your approach to the diagnosis of superficial digital flexor tendonitis
- 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
Outline the staging of tendon damage
- 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
When does tendon ageing begin to occur in the horse? Briefly outline these changes
>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
Describe the alterations in physicochemical environment that occur in the equine tendon as a result of exercise
- Energy loss through hysteresis
- → rise in tendon core temp to 45˚C
- Increased cytokine production as a result of high temp
98
Describe the alterations in physicochemical environment that occur in the equine tendon as a result of cellular effects/molecular inflammation
- 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
What ultrastructural changes occur within the equine tendons as a result of exercise and age
- Changes in interfascicular matrix
| - Higher proportion of small diameter fibres rather than thick fibres
100
Describe the morphological changes that occur within the equine tendon as a result of exercise and age
- Reduced crimp angle and length
| - Central region more affected than peripheral by loss of crimp, hence more central lesions
