Horses 4 Flashcards

1
Q

What are the main areas of high load in the two main joints of the carpus

A
○ Midcarpal joint
§ Distal aspect Radial carpal bone - medial aspect 
§ Radial facet of third carpal bone
○ Antebrachiocarpal joint
§ Distal radius
§ Intermediate carpal bone
Radial carpal bone
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2
Q

How does carpal bone respond to high loads and what if fail to adapt

A
  • Modelling of subchondral bone in response to exercise (high loads)
    ○ Thickening of trabecular and subchondral bone
    § Sclerosis of third carpal bone
    § Chip fracture - common -> microdamage and front of bone chipped off
    § Slab fracture -> progress straight down
  • Failure of subchondral bone to adapt to increased stress
    ○ Subchondral bone necrosis
    ○ Chip fracture
    ○ Slab fracture
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3
Q

Carpal injury what swelling will you see dorsally and laterally

A
○ Dorsal
§ Antebrachiocarpal joint - lateral and medial aspect 
§ Midcarpal joint - linear swelling 
§ Extensor tendon sheaths
§ Subcutaneous - generalised swelling across front of carpus
○ Lateral
§ Carpal sheath - swell above sheath 
§ Antebrachiocarpal joint
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4
Q

Carpal injury flexion test results and lameness, what causes mild or marked lameness and diagnostic analgesia

A
Flexion test
○ Limited use
○ Pain on flexion useful
Lameness
○ Often bilateral - as cyclically loading both limbs 
○ Mild lameness
§ Chip fracture
§ OA
○ Marked lameness
§ Significant pathology
Diagnostic anaglesia
○ Regional blocks
§ Subcarpal block
§ Median and ulnar block - if block think in carpus 
○ Intra-articular blocks
§ Midcarpal joint
§ Antebrachiocarpal joint - proximal suspensory as well possible
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5
Q

What are the 4 main views for carpal lameness and why each important

A

1) flexed lateromedial - radial carpal bone sits lower than intermediate (able to see dital radial and proximal intermediate - where pathology occurs)
2) Dorsolateral palmaromedial oblique - able to see radial carpal bone and proximal of third carpal bone
3) Dorsomedial palmarolateral oblique - proximal intermediate and distal radial - common area of pathology - also second carpal bone is free projected
4) skyline of 3rd carpal bone - mandiotry on racehorse as common area of fracture

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6
Q

Carpal injury ultrasound what structures examining, sctintigraphy what looking for and arthroscopy

A
Ultrasound
§ Carpal sheath and flexor tendons
§ Proximal suspensory ligament
§ Extensor tendons and sheaths
Scintigraphy
§ Lameness localised to carpus but no radiographic changes
§ Subchondral bone injuries
§ Stress fractures
§ Proximal suspensory desmitis
Arthroscopy - often as diagnosis and treatment 
§ Midcarpal and antebrachiocarpal joints - GOOD FOR THIS 
§ Carpal sheath
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7
Q

What treatment would you do for mild subchondral bone injury on carpus or serious pathology found

A

Mild - rest for 3 months minimum

Serious - arthroscopy - debridement

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8
Q

Shoulder injury what seen on clinical examination and what diagnostic anaglesia generally postitive to

A
  1. Swelling not detectable
  2. Shortened cranial phase of stride - TYPICAL OF PROXIMAL LIMB LAMENESS
    ○ Brings forward shortened stride but let’s go all the way back
  3. Muscle atrophy - if chronic - which often they are as swelling cannot detect
    ○ Triceps atrophy
  4. Diagnostic analgesia
    ○ Intra-articular injection of shoulder joint
    ○ Intrathecal injection of bicipital bursa
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9
Q

Shoulder injury diagnostic imaging, what views and what structures for each

A
○ Radiography
§ Standing mediolateral
§ General anaesthesia
○ Scintigraphy
§ Lateral and cranial views
○ Ultrasound
§ Bicipital bursa - common to perform 
§ Biceps tendon - not common injuries here 
§ Lateral aspect of shoulder joint - cannot detect externally so useful 
○ Arthroscopy
§ Bicipital bursa
§ Shoulder joint
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10
Q

List the 4 main conditions of the shoulder and the 2 of the elbow

A
  1. Osteochondrosis
  2. Osteoarthritis
  3. Supraglenoid tubercle fracture
  4. Bicipetal bursitis
    Elbow
  5. Ulnar fractures common paddock injury
  6. Elbow joint problems rare
    ○ Subchondral cystic lesions
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11
Q

Conditions of the elbow localising signs, diagnostic anaglesia and diagnostic imaging views and diseases

A
1. Localising signs 
○ Elbow joint problems -> No localising signs
○ Ulnar fractures -> ‘Dropped elbow’
2. Diagnostic analgesia
○ Intra-articular
3. Diagnostic imaging 
a. Radiography
§ Mediolateral
§ Craniocaudal
b. Scintigraphy
§ Subchondral cystic lesions
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12
Q

Ulnar fractures how common, where generally occur and treatment

A
  • Common fracture
  • Generally intra-articular
  • Physeal fracture in foals
  • Non weightbearing bone - so can do internal fixation
    Treatment
  • Tension band plate - internal fixation
  • 70% return to athletic function
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13
Q

Tarsus how complex and the 3 main issues and what important about wounds in this area

A
  • Complex joint
    1. Prone to trauma
    2. Osteochondrosis
    3. Osteoarthritis
      Wound in tarsus often involve synovial structures - must assess with ultrasound
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14
Q

Tarsus what swelling can occur, when get pain on flexion and flexion test

A
  • Swelling
    ○ Tarsocrural joint - most common
    § Swelling noticed on the dorsal aspect -> medial and lateral to extensor tendons and palmar aspect -> between calcaneus and the tibia laterally and medially
    ○ Tarsal sheath
    ○ Calcaneal bursa
    ○ Extra-synovial
  • Pain on flexion
    ○ Only severe inflammatory disease (septic arthritis) or injury
  • Flexion test - get metacarpus parallel
    ○ Not specific because flexing all joints - hip, stifle, tarsus and fetlock
    ○ Fetlock and stifle problems often positive
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15
Q

Tarsus diagnostic anaglesia positive for regional and intra-articular blocks

A
○ Regional blocks
§ Subtarsal block
§ Tibial and peroneal - if positive to this but not above - then tarsus 
○ Intra-articular blocks
§ Tarsometatarsal joint
§ Centrodistal joint
§ Tarsocrural joint
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16
Q

Radiography for tarsus what are the 4 minimum views and the 3 special views

A

1) lateromedial
2) dorsoplantar
3) dorsomedial plantarolateral oblique
4) dorsolateral plantarmedial oblique
Special views
1) proximodistal alignment
2) skyline of calcaneus
3) flexed lateromedial

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17
Q

Ultrasound and scintigraphy what assessing with tarsus injuries

A
Ultrasound
- Assessment of tendons and ligaments
- Determining involvement of synovial structures
- Locating osteochondral fragments
Scintigraphy
- Must combine with local analgesic techniques
- Osteoarthritis of distal tarsal joints
- Subchondral bone injuries
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18
Q

Bone spavin in tarsus define, radiographic changes, what need to use for diagnosis and treatment

A
  • Osteoarthritis distal tarsal joints
  • Over diagnosed condition
  • Radiographic changes unreliable -> looks like osteophytes
  • Must use diagnostic analgesia - LOCALISE TO JOINT FIRST
  • Treatment
    § Phenylbutazone - generally not as good
    § Intra-articular corticosteroid - within the tarso-metatarsal joint
    § Arthrodesis - last resort
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19
Q

If have generalised tarsal sweling with lameness and open wound on medial aspect what would you do in terms of diagnosis

A
  1. take radiographs -> NADA -> assess the bony structures
  2. Ultrasound - to assess the soft tissue structures
    - Effusion in tarsocrural joint
    - Tarsal sheath synovial swelling
    § If wound going out the fluid will leave -> possible in this case
    - Calcaneal bursa structure normal
  3. Synovial fluid sample analysis
    - Collect fluid from tarsocrural joint
    § 60% neutrophils -> INFLAMMED BUT NOT INFECTED (if infected >90% neutrophils)
    - Cannot collect from tarsal sheath as not fluid
  4. Palpation/ surgical exploration
    - Need to clean it up, sterile glove
    - Feel where the open wound goes -> feel tendon
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20
Q

Stifle what structures are prone to trauma, possible swelling, where palpate and flexion test

A
Bony prominences 
- Prone to trauma 
1. Patellar 
2. Tibial crest 
Clinical examination
1. Examine for swelling
- Femoropatellar joint
- Medial femorotibial joint
2. Palpate patellar ligaments
- Assess for Medial patellar ligmanet resection - common surgery 
3. Flexion test 
- May be pain
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21
Q

Stifle diagnostic analgesia and what are the 3 main radiograpah views needed and why and the 2 special view

A

Diagnostic analgesia
- Intra-articular injection of ALL 3 compartments (communications vary)
Radiograph - if stifle swelling ALWAYS
1. lateromedial - patellar, two trochlea ridges, tibial plateu
2. flexed lateral media - condyle of the femur
3. caudocranial - condyles of femur, intracondyle eminencies of the tibia
Other view - flexed skyline view of patellar

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22
Q

Stifle injuries what looking for with ulrasound, scintigraphy and arthroscopy

A
Ultrasound 
§ Patellar ligaments
§ Abaxial aspects of menisci
§ Femortibial joints for effusion
Scintigraphy
§ Complex appearance - hard to interpret 
§ Poor access to medial aspect - often where trauma occurs 
Arthroscopy
§ Articular cartilage
§ Cruciate ligaments
§ Menisci and meniscal ligaments
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23
Q

Pelvis what are the 3 important aspects of the clinical exam and diagnostic anaglesia

A
  1. Palpate - bony prominences - tuber coxa, ischi
  2. Pelvic symmetry - tuber coxa how symmetrical, also muscle mass
  3. Rectal examination
    ○ Can palpate -> Iliac shaft, acetabulum, pelvis
    Diagnostic analgesia
    ○ Sacroiliac joint
    ○ Sacroiliac ligaments
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24
Q

Pelvis diagnostic imaging what important to assess and the 3 ones used

A

Radiography
§ General anaesthesia in adult horses
§ Harder to align the horse as needed
Ultrasound
§ Assessment of ligaments and muscles
§ Bony surface of pelvis -> tuber ischi, coxa etc.
□ Ilium and ischium easy but not acetabulum
Scintigraphy
§ Use when struggling to localise lameness
§ Pelvic fractures
§ Hip joints

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25
Q

Osteochondrosis define, and the 3 main presentations

A
- Osteochondral fragmentation of articular surface in young growing horses
Three presentations
1. Flap and fragment formation
2. Fragmentation alone
3. Subchondral bone cyst
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26
Q

In general with a young horse if swelling what disease and if lameness what disease

A

SWELLING -> osteochondrosis

LAMENESS -> subchondral cystic lesions

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27
Q

Flap and fragment formation and osteochondral fragmentation what apart of, what results from and where occurs

A

Osteochondrosis
Flap and fragment formation
- Retained cartilage -> with exercise may get fissures -> may then stay or move within joint (very bad if do this - inflammation and swelling -> Flap and fragment formation
- Occur at margin of weight bearing and non-weight bearing cartilage
○ Trochlear ridges femur, talus, sagittal ridge of MC/MT3, caudal humerus
Osteochondral Fragmentation
- Traumatic fractures at sites susceptible due to stage of growth
- Non weight bearing areas
○ Distal intermediate ridge of tibia
○ Proximal plantar P1 fragments

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28
Q

Subchondral cysts what apart of, results from and where occurs commonly

A

osteochondrosis
- Secondary change following injury to cartilage or subchondral bone
Most common in young growing horses at predictable sites
- Weight bearing areas
○ Medial condyle femur
○ Medial proximal radius
○ Glenoid of the shoulder
○ Proximal interphalangeal joint of the pastern

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29
Q

Osteochondrosis pathogensis and predisposing factors

A
- Weak cartilage and bone subjected to excessive forces
Multifactorial
1. Genetic
-- Large breeds predisposed
○ Thoroughbreds
○ Warmblood
- Standardbreds
○ Fragments
2. Dietary
- High CHO (carbohydrate) intake
- Mineral imbalances
○ Cu deficiency
○ Ca/P ratio
3. Exercise
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30
Q

Osteochondrosis what are the main affected sites in the tarsus, stifle, fetlock and shoulder

A
1. Tarsus (top to bottom most common)
○ Distal intermediate ridge
○ Lateral trochlear ridge
○ Medial malleolus
2. Stifle 
○ Lateral trochlear ridge 
○ Medial trochlear ridge 
○ Patellar 
3. Fetlock
○ Sagittal ridge MC3
○ Ununited palmar/plantar eminence
4. Shoulder
○ Humeral head
Glenoid cavity
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31
Q

Osteochondrosis swelling and lameness are they present if so what involved

A
Swelling
○ Most common presenting sign
○ Swelling not detectable in shoulder
○ Subchondralbone cysts
§ Swelling less obvious
§ Medial FT joint swelling
Lameness
○ Generally absent or mild
○ Exceptions
§ Shoulder - as swelling is not detectable 
§ Subchondral bone cysts
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32
Q

Osteochondrosis what is the best diagnostic imaging and what can examine

A

Radiographs
§ Diagnostic in most cases - good as young animals are generally hard to nerve block
§ Occasional lesion cartilage only
§ Subchondral cysts in areas of dense bone
§ Always radiograph contra lateral joint

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33
Q

Osteochondrosis treatment the two types and things within

A
- Conservative
○ Restrict exercise
○ Restrict diet
○ Monitor radiographically
- Surgical
○ Removal of osteochondral fragments
○ Debridement of subchondral cystic lesions
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34
Q

Stifle osteochondrosis what general present and what is diagnostic

A
  • Swelling in yearling
  • Occasionally present as older horse
    Radiographs - diagnostic
  • Caudolateral craniomedial view - best one to highlight lateral trochlear ridge where may see flattening or fragmentation
    ○ Lateral trochlear ridge sits in behind the medial trochlear ridge which is the larger one
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35
Q

Stifle osteochondrosis treatment options and prognosis

A
Treatment
1. Conservative
○ Lytic lesions
○ Minimal lameness
○ Younger horses
2. Arthroscopy
○ Fragmentation
○ Lameness
○ Older horses
Prognosis
- Dependant on size of lesion
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36
Q

tarsal osteochondrosis how common, swelling, lameness and diagnostic views

A
  • Most common site
  • Tarsocrural swelling - obvious
  • Minimal lameness
    Radiographs
  • Dorsomedial plantarolateral
    ○ DIR (distal intermediate ridge) tibia
    ○ Lateral trochlear ridge
  • Dorsoplantar
    Medial malleolus
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37
Q

Tarsal osteochondrosis treatment for the 2 main sites

A
1) DIRT (distal intermediate ridge of tibia) lesions
○ Arthroscopy
2) Lateral trochlear ridge lesions
○ Lytic lesions-conservative
○ Flaps or fragments-arthroscopy
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38
Q

Fetlock osteochondrosis clinical presentation, what age common and locations

A
  • Fetlock swelling young horse
  • Often bilateral, occasionally quadrilateral
  • Common incidental finding in yearling radiographs - generally resolve, only once fragment that we worry about them
  • Locations
    ○ Sagittal ridge lesions
    ○ Proximal P1 osteochondral fragments
    ○ Plantar P1 OC fragments
    ○ Ununited plantar eminence P1
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39
Q

Fetlock osteochondrosis radiographs and treatment

A
Radiograph
-  Flexed lateral
- Dorsopalmar/plantar
Treatment
- Conservative
○ Most cases
- Arthroscopy
○ If fragment present
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40
Q

Shoulder osteochondrosis how present generally and treatment and prognosis

A
  • Often presents in older horses (2yo)
  • Lameness
  • Muscle wastage
  • Upright foot - long heel, breaking of the heel - due to chronic osteochondrosis lesion
  • Significant degenerative changes present when diagnosed
    Treatment
  • Arthroscopy
    ○ Prognosis poor
    ○ 50% success rate - as generally advanced by the time you see them and secondary osteoarthritis
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41
Q

Subchondral bone cysts clinical signs and diagnosis

A
Clinical signs
- Lameness
- Swelling difficult to detect
Diagnosis
- Local analgesia
- Radiographs - diagnostic - HAVE TO BE GOOD QUALITY - CONTRAST IMPORTANT 
- Scintigraphy
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42
Q

Subchondral bone cysts treatment and prognosis

A
Treatment
1. Intra-articular corticosteroids - temporary response 
2. Intra-lesional corticosteroids
3. Surgical debridement
○ Intra-articular
○ Extra-articular
4. Arthrodesis
Prognosis
- Guarded
- Stifle cysts
65% athletic following surgery
43
Q

If had a yearling TB with no noticed lameness but observed swelling over front of stifle what would you do next and resulting things

A
  • Trot up horse and perform flexion test -> yearling may be hard to do
  • Radiograph stifle -> OCD until proven otherwise -> FIRST STEP GENERALLY
    1. Radiographs
  • Swelling of Femoropatellar joint
  • Doesn’t rule it out
    NOT ARTHROSCOPY -> only if have obvious fragment/flap -> quite invasive
    2. Ultrasound or wait and see (reassess 4-6 weeks later)
    ○ Mild -> management
    3. Restrict exercise
44
Q

Subchondral bone cyst what are 4 main treatment options and what do they provide, which is best

A

1) Not better with restricting exercise - conservative treatment
2) Intra-articular corticosteroid - short term benefit
3) Intralesional corticosteroid - first option
4) Arthroscopic debridement - last option but best - 65% success rate

45
Q

Osteochondrosis treatment when would you go for arthroscopic debridement

A

ONLY WHEN OBVIOUS FRAGMENT PRESENT in young horses - may get better by itself
cyst can do in older animal but last option

46
Q

Foal orthopaedics what is most common issues and types of deformities

A
  • Limb deformities
  • Septic arthritis/ osteomyelitis
    Limb deformities
    a. Angular limb deformities
    § Lateral (valgus) or medial (varus) deviation
    □ Knee -> Usually valgus
    □ Fetlock -> Usually varus
    b. Flexural deformities
    § Flexion of joint
    □ Foot - clubbed foot
    □ Pastern - proximal interphalangeal joint
    □ Fetlock
    □ Carpus
47
Q

With the two types of limb deformities what are congenital and acquired causes

A

1) Congenital
• Flexural deformity
○ Tendon laxity
○ Limb contracture - cannot straighten carpus
• Angular
○ Ligament laxity - collateral ligaments - lateromedial bending
○ Poor bone development - most common - bones haven’t ossified
2) Acquired
• Flexural deformity
○ Limb contracture - develop clubbed foot
○ Ruptured extensor tendons
• Angular
○ Growth plate abnormalities

48
Q

Limb deformities pathogensis for the two types

A

1) Angular limb deformity arising from physis
○ No one knows how occur -> self-propagating -> once limb deformity get asymmetric load sharing on growth plate -> more severe overtime
2) Flexural limb deformity
○ Any source of pain -> shoulder osteochondrosis
§ Reflex muscle contracture - If continues for length of time can become permanent

49
Q

Angular limb deformities congenital conditions what assess with what modalities

A

○ Can the limb be straightened - if so likely to be limb laxity and not developmental issue
§ Premature generally will straighten -> physio and exercise
○ Radiographs - look at the growth plate for abnormalities and assess ossification of the bones especially carpus and tarsus
○ Ultrasound - also to assess ossification

50
Q

Angular limb deformities acquired what need to assess and how and same for acquired flexural deformity

A

Angular
- Acquired
○ Age - how long before physis will close -> how long you have to correct
○ Radiographs - again to draw lines and assess ossification
Flexural deformity
- Acquired
○ Age - for prognosis
○ Joint involved - determine management
○ Radiographs - may helpful
○ Identifying inciting cause- difficult, required examination of whole limb

51
Q

Management of carpal or tarsal bone poor ossification

A
  • Only thing that will fix is TIME
  • Confine - need to prevent injury while waiting for ossification
  • Provide support -possible but can lead to complications due to management issues
    ○ Splints
    ○ Casts
52
Q

5 General management strategies for angular deformity from growth plate

A
  1. Confine - as self-propagating
  2. Maintain foot balance
  3. Lateral/medial extension
  4. Surgery - in more severe
    ○ Growth acceleration - concave side
    § Periosteal strip - common
    □ One off procedure
    ○ Growth retardation - convex side
    § Bridge growth plate with implant - lots of implants can be used but need to be STRONG
    □ Most common single screw but if really bad can go for plate and screw
    □ Have to then remove to ensure doesn’t over compensate - multiple procedures
  5. Foot extension band
    ○ Put on side that you want the limb to deviate to
53
Q

What are surgical indications for angular deforities from growth plates in the knee

A

□ Severe deformities
□ Not improving with confinement
□ Over three months of age
□ More specific - radiographic definitive
® 8-20° - periosteal strip
® >20° - physeal bridge
® Prognosis guarded if angle greater than 25°

54
Q

What are surgical indications for angular deforities from growth plates in the fetlock

A

□ Severe deformities
□ From 2 weeks of age - growth plate closes earlier □ Surgery required if >30 days - ASAP
□ More specific - radiogrpahic define
® 5-8° - periosteal strip
® >8° - physeal bridge
® Prognosis guarded if angle greater than 12°

55
Q

Treatment for flexural deformities with tendon laxity and congenital causes

A

Tendon laxity
- Confine
- Protect heels/fetlock - bandages to prevent ulceration
- Heel extension shoes
Congenital
- Most straighten if able to weight bear
- Tetracyclines
○ 3 gams IV, large dose - relaxation of tendons
○ Potential for side - diarrhoea, kidney disease
- Surgery if fail to respond

56
Q

Treatment for flexural deformities acquired cause and what involved in surgery

A

Acquired
- Treat cause
- Phenylbutazone
- Tetracyclines
○ 3 grams IV, large dose - relaxation of tendons
○ Potential for side effects - diarrhoea, kidney disease
- Surgery – required in most cases
Surgery
- Determine structures involved
○ DDFT – inferior check ligament desmotomy (cut)
○ SDFT – superior check ligament desmotomy (cut)
○ Must combine with aggressive reshaping of foot

57
Q

Management of carpal flexural derformities and pastern flexural deformity

A

Carpal flexural deformities
- Splinting
- Desmotomy
○ Flexor carpi ulnaris
○ Ulnaris lateralis
Pastern flexural deformity
- Often secondary to other cause of lameness
- Splinting - respond well to this generally
- Inferior check ligament desmotomy - last resort

58
Q

Septic arthritis how common, what occurs and how present

A
  • Most common cause of lameness in foals - ACUTE ONSET IN YOUNG ANIMAL THIS UNTIL PROVEN OTHERWISE
  • Haematogenous spread of bacteria
  • Sequelae in sick foals or may occur in healthy foals
  • Present with acute onset lameness
    ○ Common for owner to assume mare stood on foal - RARE
    ○ With or without obvious joint swelling
    ○ Often pyrexic initially
59
Q

Septic arthritis what are the 4 diagnosis options and what detect

A
1. Synovial fluid analysis - best 
○ Total WCC > 10x109/L
○ Protein >25g/L
○ Neutrophils >90%
2. Radiography
○ Often subchondral bone or physeal involvement - spread from here commonly 
○ If bone involved -> poor prognosis and would need to debride -> SO IMPORTANT TO KNOW 
3. Ultrasound
○ Detect swelling in deeper joints
○ Identify fibrin
4. CT
○ More accurate assessment of affected bone
○ Helps with surgical planning
60
Q

Septic arthritis treatment and prognosis

A
Treatment
- Treat FPT - failure of passive transfer -> if very young 
○ NEED TO FIX THIS 
- Broad spectrum antibiotics - penicillin or gentamicin 
- Lavage joint space
- Debride affected bone
Prognosis
- Guarded if bone involved
61
Q

What are the 3 main causes of back pain

A
  • Problem of the axial skeleton
  • Bilateral limb lameness
  • Rhabdomyolysis
62
Q

Palpable back pain what occurs and most common cause

A
  • Easy to focus
    ○ Common finding associated with lameness
    ○ Owners able to identify
    ○ Lameness difficult to observe
  • Most commonly muscle spasm - the muscles are very tight
    ○ Many treatments relieve muscle spasm
    ○ Attracts quackery - generally gets better on its own so “responds” to multiple treatment
63
Q

Important bones and ligaments of the axial skeleton

A
  • Spine
    ○ Vertebra
    § Cervical - 7 vertebrae
    § Thoracolumbar
    □ Thoracic - 18 vertebrae
    □ Lumbar - 6 vertebrae
    ○ Intervertebral discs - very thin so rarely a clinical problem
    ○ Intervertebral facet joints - where the problems generally arise
    ○ Ligaments
    § Supraspinous
  • Sacroiliac joint - limited but some movement within
    § Hyaline cartilage - sacrum
    § Fibrocartilage - ilium
    ○ Ligaments
    § Dorsal sacroiliac ligament - comes off tuber sacra
    § Interosseous - between pelvis and sacrum
    § Ventral
64
Q

Biomechanics of the axial skeleton where does flexion/extension, lateral bending occur and movement of sacroiliac joint

A
  • Flexion/extension - most at lumbosacral area
  • Lateral bending - mid thoracolumbar
  • Sacroiliac joint
    ○ Very little movement - oscillations in flexion and extension
    ○ Transfer of force from hindlimbs to axial skeleton
65
Q

Induced longissimus pain what is it and leads to and common post mortem findings in terms of back pain

A
- Induced longissimus pain 
○ Stiffness in thoracolumbar spine 
○ Inability to perform at fast paces 
○ DOES NOT LEAD TO LAMENESS 
- Post mortem finding in TB racehorses
○ 92% DSP impingement 
○ 97% articular facet DJD
○ 50% stress fractures spine or pelvis 
○ THEREFORE - all carry lots of pathology within spine - is it important?
66
Q

Clinical examination of back pain, what are the 4 important steps within

A
1. Observe 
○ Muscle mass and symmetry from Behind 
2. Palpate the muscles 
a. Dorsal spinous process 
b. Tubera sacrale 
3. Flexion and extension 
○ Variable in normal horses 
○ Pen down the back and go over rump - may react 
4. Examine limbs 
5. Gait 
○ Examine for lameness 
○ Lunge at canter 
§ Flexion and extension of spine 
○ Ridden
67
Q

Diagnostic analgesia for back pain where would you injection and how would you notice difference

A

○ Only objective means of assessing pain
○ Local injection
§ Dorsal spinous processes
§ Sacroiliac region
§ Dorsal SI (sacroiliac) ligament
□ But generally regional analgesia -> pass from contralateral side - periarticular injection
○ Ridden before and after -> to see improvement
§ Independent person not the owner is better

68
Q

Diagnostic imaging for back pain what modalities, views and what examining

A
1. Radiography 
§ Need 2 radiographs 
§ Need general anaesthesia 
§ Difficult exposures required 
□ DSP and facet joints 
§ Unable to assess 
□ Caudal lumbar spine 
□ Sacroiliac region 
2 Ultrasound 
§ Spinal ligaments 
§ Sacroiliac ligaments 
3. Scintigraphy 
§ Can image whole spine and sacroiliac region 
§ Interpretation difficult - all have pathology but is it important or not??
69
Q

Treatment for primary back problem what are 5 options and the most important

A
1. Increase muscle mass to support the spine 
○ Unridden exercise - BEST
2. Local injections 
○ Anti-inflammatories 
○ Counter irritants 
3. Manipulation 
4. Acupuncture 
5. Shockwave therapy
70
Q

Sacroiliac pain how common, diagnosis, treatment, what important to consider and two main areas of interest

A
- Human experience - similar to horses 
○ Common cause of lower back pain 
○ Diagnosis - periarticular joint block 
○ Treatment - corticosteroid injections 
- PM study of horses from racetrack 
○ 100% had degenerative changes in SI joint - IS IT CAUSING THE ISSUE?
Two major areas 
1. Dorsal sacroiliac ligaments and insertions 
2. Sacroiliac joints
71
Q

Sacroiliac pain what horses most common, what results from palpation, gait evaluation and other clinical signs

A
  • Most common in older larger warmblood horses
  • Pain on palpation of tuber sacrale
    ○ Dorsal sacroiliac ligament injury
    ○ Ilial stress fracture
    ○ NOT SACROILIAC JOINT
  • Gait evaluation
    ○ Restricted hindlimb impulsion, most obvious when ridden
    § Not lame
  • Poor thoracolumbar muscle development
  • hind quarter asymmetry
  • Straight hindlimb flight
  • Restricted thoracolumbar flexibility (35%)
  • Pain on pressure over tuber sacrale (16%)
  • Reluctant to stand on one hindlimb for prolonged period (19%)
  • Tuber sacrale asymmetry
    ○ Very common - no association with sacroiliac pain
    ○ Thought to be due to bending of ilium
72
Q

What are 4 main differential diagnosis for sacroiliac pain

A
  1. Bilateral hindlimb lameness
  2. Thoracolumbar spine pain
  3. Pelvic fracture
  4. Exertional rhabdomyolysis
73
Q

Sacroiliac pain what diagnosis techniques are needed

A

1) Orthopaedic examination - rule out lameness
2) Diagnostic analgesia
○ Block structures separately
§ Dorsal sacroiliac ligaments
§ Sacroiliac articulation
3) Diagnostic imaging
a. Radiography
b. ultrasound
c. scintigraphy
COMBINATION

74
Q

Diagnostic imaging for sacroiliac pain what are the 3 modalities used, how useful and views

A
1. Radiography 
§ General anaesthesia 
§ Overlying GIT -> need high power radiograph and often still not enough 
2. Ultrasound 
§ Dorsal sacroiliac ligaments - can see asymmetry 
§ Easy to asses but Hard to interpret 
3. Scintigraphy 
§ Able to image joint 
§ Attenuation of radiation by muscle 
§ Artefacts 
□ Motion 
□ Positioning 
□ Bladder - biggest issue 
§ Views 
□ Dorsal 
□ Oblique 
§ 99% of horses with positive SI regional block had sctinigraphic changes associated with SI joint
75
Q

Sacroiliac pain treatment for acute and chronic case

A
- Acute case 
○ Rest 
○ Controlled exercise 
○ Anti-inflammatories 
- Chronic case 
○ Periarticular infection of corticosteroids 
○ Phenylbutazone 
○ Unridden exercise 
○ Shockwave therapy 
DIFFICULT TO MANAGE
76
Q

Overriding dorsal spinous processes significance, clinical findings and diagnostics

A
  • Common finding
  • Significance can ONLY BE DETERMINED VIA NERVE BLOCKS
    Clinical findings
  • Poor performance
  • Reduced muscle mass
  • Reduced flexion and extension of spine
    Treatment
  • Rest
  • Local corticosteroid injection
  • Surgical resection if the DSP or intraspinous ligament
77
Q

Diagnosis processes 3 used for overriding dorsal spinous processes

A
Diagnostic 
1. Poor alignment of DSP -> palpation can feel or imaging 
2. Diagnostic analgesia
○ Horse ridden before and after local infusion  
3. Diagnostic imaging 
○ Radiography 
§ Overriding, sclerosis, focal lysis 
§ Easier to see than other parts 
○ Scintigraphy 
§ Increased uptake 
§ Common finding
78
Q

Exam questions - A trainer asks you to examine a 3 year old thoroughbred race horse that is performing poorly and is reported to have a shuffling forelimb gait. On examination you observe moderate swelling over the dorsal aspect of the left and right carpi and moderate pain on flexion of both capri. When trotted there is no gait asymmetry is observed, however the horse is observed step short in both forelimbs
Describe in detail how you would further investigate this case

A
  • Already taken history, done clinical exam - NOT WHAT HAVE ALREADY DONE
  • NOW
    1. Nerve blocks -> distal to proximal nerve blocks - NEED TO JUSTIFY
    ○ Not sure exactly where lame so start at foot and work up
    ○ What order of nerve blocks - list
    ○ IF BLOCK - do imaging - describe the imaging techniques
    ○ IF DON’T BLOCK - sctingraphy?
    2. Radiography
    ○ Which part of body and views
    ○ IF SEE -> fracture or obvious pathology then have diagnosis
    ○ IF DON’T SEE OBIVOUS THINGS -> then more advanced imaging
    3. Sctingraphy -describe why - RACEHORSE SO WOULD DO THIS NEXT
79
Q

When wouldn’t you nerve block a horse

A

1) obvious swelling and pain around tendon

2) IF NOT LAME

80
Q

Excercise physiology why does blood flow increase to muscle during exercise and how is this achieved

A
  • During moderate-intensity exercise, blood flow to the muscles increases by 30- to 80-fold:
    1. Increased delivery of nutrients and O2 to contracting musculature
    2. Removal of waste products of metabolism (including heat)
  • This increase in blood flow is achieved by:
    1. Increased heart rate (and stroke volume)
    2. Redistribution of blood
    3. Fluid shifts from reservoirs
81
Q

Thermoregulation of horses during exercise how occurs and cardiovascular problem during excercise

A
  • Horses rely of evaporation of sweat to dissipate the heat generated during exercise:
    1. Heat from muscle contraction is transferred to the skin by the cardiovascular system
    2. Heavily exercising horses may lose 10-15L sweat/hour
    3. Equine sweat contains high concentrations of electrolytes (Na+, K+, Cl− etc)
    Cardiovascular system faces a dual challenge:
    1. Must pump blood to the working musculature to meet their high metabolic demand
    2. Must pump blood from the core to periphery (skin) to dissipate heat generated by exercise
82
Q

Define rhabdomyloysis and the 2 main types

A

Rhabdomyolysis: The breakdown or destruction of muscle with the release of myoglobin (nephrotoxic) into the bloodstream

  • Myoglobin is the oxygen carrying protein found in muscle
    1. Non-Exertional Rhabdomyolysis: Associated with a range of inciting causes other than exercise
    2. Exertional Rhabdomyolysis: Associated with exercise
83
Q

What are the 2 main types of rhabdomylosis and the types within

A

1) non-exertional - inflammatory or infectious cause
2) extertional - excercise
a. sporadic exertional - no intrinsic muscle abnormality
b. chronic - intrinsic muscle abnormality
i. recurrent externtional - recurrent episodes
ii. polysaccharide storage myopathy - mild episodes

84
Q

Non-exertional rhabdomyolysis what are the 6 main causes

A
1. Bacterial
○ Clostridium spp. (wound infection)
○ Streptococcus equi (immune mediated secondary to strangles) 
○ Salmonella (haematogenous?)
2. Viral (?)
○ Equine influenza virus - exotic in Australia 
○ Equine herpesvirus 1
3. Parasitic
4. Nutritional
○ Vitamin E and/or Se deficiencies
5. Toxicities
○ Ionophores - molecules that bind up cations, used as antibiotics to change microflora of rumen in cattle -> increase growth rates, horses highly sensitive to this 
6. Traumatic
85
Q

Atypical myopathy where occur, what reslated to, what occurs

A
  • Atypical Myoglobinuria
    ○ Large outbreaks reported sporadically in Europe
    ○ Increasing frequency(?) -> can affect several hundred horses
    ○ Related to Sporadic Pasture Myopathy described in North America
    ○ Has been described in Australia and New Zealand
  • Highly fatal (75% mortality), non-exertional rhabdomyolysis - always affects cardiac -> cardiomyopathy as well
    ○ Metabolic derangement secondary to ingestion of hypogylcin A from Acer spp.
86
Q

Extertional rhabdomyolysis what is important about it and the 2 main types within

A
  • Complex syndrome with a similar clinical appearance:
    ○ Numerous, poorly defined causes
    ○ Environmental/managerial “trigger” factors important
    ○ Genetic pre-disposition
  • Exertional rhabdomyolysis has been divided into:
    a. Sporadic Exertional Rhabdomyolysis: one or two episodes of exertional rhabdomyolysis - Normal muscle function
    b. Chronic Exertional Rhabdomyolysis: repeated episodes of exertional rhabdomyolysis - Underlying abnormality in muscle function
87
Q

Sporadic exertional rhabdomyolysis what occurs and list the 7 main predisposing factors

A
- Many horses have 1-2 episodes of ER which do not significantly impact future performance
○ No intrinsic muscle abnormality
1. over-exertion 
2) excessive dietary soluble carbohydrates 
3) temperament 
4) cocurrent illness
5) electrolyte imbalances 
6) hormonal imbalances 
7) vitamin E and selenium deficiency
88
Q

Overexertion and excessive dietary soluble carbohydrates what predisposes to and why

A

Sporadic and chronic externtional rhabdomyolysis
a. Over-exertion
§ Common cause of ER in horses (and humans!)
□ Exercise that exceeds the underlying level of training or fitness
□ Excessive intensity (speed)
□ Excessive duration of moderate intensity exercise
b. Excessive dietary soluble carbohydrates
§ Animals on high grain diets are more like experience ER (exertional rhabdomyolysis) □ Effects on insulin and glucose metabolism???
□ Psychogenic effects -> horse temperament -> tend to be more nervous

89
Q

Temperament, co-current illness and hormonal imbalance what predisposes to and why

A

Sporadic and chronic externtional rhabdomyolysis
c. Temperament
§ ‘Nervous’ animals are more like experience ER
d. Concurrent illness
§ Incidence of ER appears to increase with outbreaks of (viral) respiratory disease - can target for management!!
□ Equine Herpesvirus 1
□ Equine Influenza virus A2
f. Hormonal imbalances
§ Incidence of ER is higher in females
§ Episodes of rhabdomyolysis occur most frequently during oestrus in some fillies/mares
§ Some animals benefit from oestrus suppression (regumate)
§ A connection between disease and hormone concentrations has been difficult to prove

90
Q

Electrolyte imbalance what predipose to, why and how to measure

A

Sporadic and chronic externtional rhabdomyolysis
§ Insufficient sodium, potassium, magnesium, and calcium -> needed for mitochondrial reticulum
§ Inappropriate calcium:phosphorus ratios
§ Excessive sweat losses (high volumes of K and Na) with prolonged exercise
§ Incidence of ER has decreased when deficit corrected in some cases
§ Usually difficult to diagnose with simple blood tests
□ total calcium doesn’t give whole story (ionised calcium important)
□ Majority of electrolytes live within cells and other structures NOT plasma and blood
§ Measure urinary concentrations of electrolytes -> fractional excretion to determine the whole body level
□ If fractional excretion of K is low then possible K electrolyte deficiency

91
Q

Vitamin E and Selenium deficiency what predisposes to, why and treatments

A

Sporadic and chronic externtional rhabdomyolysis
§ Exercise associated with the production of free radicals
□ Damage cell membranes and impair enzyme function →“oxidative stress”
§ Vitamin E and selenium are components of the body’s anti-oxidant mechanisms →free radical scavengers
§ Little evidence of vitamin E or selenium deficiency in most cases of ER
§ Benefits of supplementation are unproven
§ Administration of vitamin E is very safe -
§ Excessive selenium administration causes severe toxicities → Only supplement in areas of proven deficiency

92
Q

Chronic exertional rhabdomyolysis whatoccurs and predisposing factors

A
  • Repeated episodes of ER which often significantly impact athletic performance
    ○ Intrinsic muscle abnormality
  • Inciting or pre-disposing factors shared with the sporadic form of disease - SAME TRIGGER FACTORS AS ABOVE
    a. Excessive dietary soluble carbohydrates
    b. Temperament
    c. Electrolyte imbalances
    d. Hormonal imbalances
    e. Vitamin E and selenium deficiency
93
Q

Chronic exertional rhabdomyolysis why chronic and the two reasons

A
  • Condition recurs despite implementation of management/environmental changes
  • Often occurs in fit horses at the beginning of light or slow exercise
    ○ i.e., not always associated with intense exercise
  • Abnormal muscle function that is thought to have an inheritable basis in many cases:
    i. Recurrent Exertional Rhabdomyolysis (RER): Exact mechanism of disease unknown – might be related to calcium handling
    ii. Polysaccharide Storage Myopathy (PSSM): Abnormal accumulation of glycogen in the muscle
94
Q

Recurrent exertional rhabdomyolysis what occurs, what most common in and why occurs

A
  • Recurrent episodes of muscle stiffness, sweating, and reluctance to move
  • Occurs most commonly in young THB, STB, and Arabian racing fillies as they begin race training - same genetic background
  • Intrinsic muscle abnormality → defect in muscle contraction
    ○ Speculated that calcium handling by muscle cell SR (sarcoplasmic reticulum) is abnormal
    Muscle in RER have an increased sensitivity to caffeine, halothane, and potassium
95
Q

Polysaccharide storage myopathy how generally occurs, most common type and pathogenesis

A
  • Generally mid episodes with light training
    ○ Accumulation of abnormal glycogen in muscle
  • Most common in QH and QH-types (6-12%)
  • Also been reported in several other breeds:
    ○ Draft and Warmblood breeds (high prevalence)
    ○ Thoroughbreds and Arabian (low prevalence)
  • Pathogenesis - know
    ○ Glycogen accumulation is a result of increased production → Rather than impaired glycogen breakdown
    ○ Glycogen in affected animals is slightly different from that found in normal animals → Less branched
    cause - unknown
96
Q

What are the 5 main diagnostic techniques for equine rhabdomyolysis

A
  1. Physical Examination
  2. Serum/Plasma biochemistry
    ○ AST, CK, LDH (lactate dehydronase) - muscle function - first two most important
    § AST - muscle and liver, CK (normal 0-400, rhabdomyolysis 10,000-100,000) - muscle specific
    □ If single episode of muscle injury CK will start going down after 24 hours
    ○ Sporadic types -> as far as would go
  3. Exercise Challenge - if present for poor performance
  4. Urinary Fractional Excretions - electrolytes adequate?
  5. Muscle Biopsy
97
Q

Sporadic Exertional Rhabdomyolysis typical clinical signs, differentials and diagnosis

A
  • Typical clinical signs - may lay down, painful and scared, stiff gait
    ○ Differentials - colic, pelvic fracture, laminitis, neurologic disease
  • Serum/Plasma biochemistry (AST, CK, LDH)
    ○ Increase in CK and AST proportional to the extent of muscle necrosis
  • Myoglobinuria (→ guide for fluid therapy)
    ○ Positive “blood” test on urine dipstick even in the absence of obvious discoloration
  • ± Muscle biopsies - not necessary
98
Q

Polysaccharide Storage Myopathy diagnosis

A
  1. Serum/Plasma biochemistry (AST, CK, LDH)
  2. Test for genetic mutation in GYS1 gene
    ○ Hair (root) or blood sample
    ○ Second mutation (MH) in some QH - make worse
  3. Muscle biopsies: - not always done - Increased PAS-positive staining for muscle glycogen
99
Q

Recurrent exertional rhabdomyolysis typical clinical signs and diagnosis

A
  • Frustrating to diagnose
  • Typical clinical signs and history
    ○ Repeated episodes of rhabdomylosis in fit horses with light exercise
  • Serum/plasma biochemistry (AST, CK, LDH)
  • Muscle biopsies
  • Urinary Fractional Excretions
  • Muscle bundle stimulation
    ○ Increased sensitivity to caffeine, halothane, and potassium
100
Q

General treatment and management and prognosis of equine rhabdomyolysis

A
  • Most horses with ER recover
    ○ Severely affected horses may die
  • Muscle has a tremendous ability to regenerate
    ○ Prognosis depends on form of ER
    ○ Sporadic ER has an excellent prognosis
    ○ Chronic ER often limits athletic performance
  • Prompt and appropriate therapy required
    ○ Continued exercise may lead to permanent muscle damage or acute renal failure
101
Q

What can equine rhabdomyolsis lead to and what may excerbate this injury

A

Acute renal failure
- Myoglobin is released into the blood with muscle injury/destruction
○ Iron containing protein that transports O2 within muscle cells
○ Excreted by the kidneys into the urine
○ Toxic to the kidneys →acute kidney failure
- Renal injury might be exacerbated by:
○ Dehydration
○ Non-Steroidal Anti-Inflammatory Drugs (Flunixin, phenylbutazone) - need to be careful while managing

102
Q

Treatment for severe acute rhabdomyolysis

A
  • Intravenous fluids
    ○ Correct dehydration
    ○ Provide diuresis and limit pigment nephropathy
  • Manage pain
    ○ Be alert for GI stasis and colic
    ○ May have to find alternatives to NSAIDs -> due to renal injury
  • IMPORTANT - no exercise until better
103
Q

management of chronic rhabdomyolysis

A
  • Manage/eliminate trigger factors
    ○ Reduce “stress” (sedation, routine)
    ○ Address electrolyte imbalances
    ○ Oestrus control (synthetic progesterone)
    ○ Free radical scavengers(?)
    1. Diet – reduce carbohydrate content
    ○ Provide additional calories with fat - high fat diets
    ○ Psychogenic benefits
    2. Daily exercise programs and turnout
    ○ Train “out of a pasture” -> don’t put in stalls
    ○ Exercise every day in a set routine