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Equine I > Orthopaedic disease > Flashcards

Orthopaedic disease Flashcards

1
Q

Indications for imaging of orthopaedic disease without blocking first

A

Heat, pain on palpation

Conformational changes

Joint effusions

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2
Q

Logical approach to lameness diagnosis

A

History

Clinical exam

Diagnostic anaesthesia

Imaging

Diagnosis and treatment

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3
Q

Foot radiography views

A

Lateromedial view

Dorsopalmar view

Dorsoproximal palmarodistal oblique (pedal) or ‘upright pedal’

Dorsoproxima palmarodistal oblique (navicular) or ‘upright navicular’

Palmaroproxmial palmarodistal oblique (navicular) or ‘skyline navicular’

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4
Q

Lateromedial view of equine foot

A

Good for: distal interphalangeal joint, foot balance, laminitis

Poor for: most navicular bone changes

Pay close attention to dorsal margins

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5
Q

Dorsopalmar view of equine foot

A

Good for: distal interphalangeal joint, foot balance, proximal interphalangeal joint, collateral cartilages

Poor for: navicular bone

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6
Q

Dorsoproximal palmarodistal oblique view (pedal) of equine foot

A

Pedal or Upright pedal view

Good for: pedal bone diseases – fracture, osteitis, keratoma

Poor for: navicular bone, distal interphalangeal joints

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7
Q

Dorsoproximal palmarodistal oblique view (navicular) of equine foot

A

Navicular or upright navicular view

Good for: navicular bone (especially distal border)

Poor for: everything else!

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8
Q

Palmaroproximal palmardistal oblique view of equine foot

A

Navicular or skyline navicular view

Good for: navicular bone

Poor for: everything else!

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9
Q

Radiographs to take after an abaxial sesamoid nerve block

A

A full foot series

Dorsopalmar view of the metacarpo/tarsophalangeal joint

+/- orthogonal views of the proximal interphalangeal joint

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10
Q

Standing low field MRI

A

Gold standard for distal limb imaging, can be used if nothing is showing on radiographs

Expensive (~£1300)

Soft tissue pathology

Prognostication

If not an option, then back to blocking!
§ Can return to block other more specific structures

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11
Q

Plan following a four point nerve block

A

Investigation of digital flexor tendon sheath (DFTS)
- U/S
- Contrast tenography
- MRI?
- Tenoscopy

Fetlock radiography, four orthogonal views
- lateromedial
- dorsopalmar
- Dorsomedial palmarolateral oblique
- Dorsolateral palmomedial oblique

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12
Q

Lameness localised with a deep branch of the lateral plantar nerve block

A

○ Limb is held flexed and rested on the vets knee​
○ The flexor tendons are pulled medially to open up injection site​
○ Needle is advanced along the axial surface of the lateral splint bone​
○ 3ml of local anaesthetic solution is injected (resistance should be low)​
○ The horse is re-examined after 10 minutes​

Then Proximal suspensory ultrasonography

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13
Q

Lameness localised with a lateral palmar nerve block

A

○ Horse is weightbearing
○ Needle is introduced on the medial side of the accessory carpal bone
○ Injection resistance is high – injecting into tight fascia. Worry if the resistance is low!
○ 3ml of local anaesthetic solution is injected
○ The horse is re-examined after 10 minutes​

then Proximal suspensory ultrasonography

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14
Q

Proximal suspensory ultrasonography

A

○ Longitudinal
○ Transverse
○ Weight-bearing
○ Non-weightbearing

Challenging – believe your blocks!

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15
Q

Lameness localised to tarsus

A

Tarsal radiogrograhy
- Lateromedial (LM)
- Dorsopalmar (DP)
- Dorsomedial Palmarolateral oblique (DMPLO)
- Dorsolateral Palmaromedial oblique (DLPMO)

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16
Q

Lameness located to the carpus

A

Carpal radiography
- Lateromedial (LM)
- Dorsopalmar (DP)
- Dorsomedial Palmarolateral oblique (DMPLO)
- Dorsolateral Palmaromedial oblique (DLPMO)
- flexed lateromedial
- proximal and distal row (skyline)

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17
Q

Lameness localised to the stifle

A

(Can’t get orthogonal views)

Stifle radiography
- Lateromedial (LM)
- Caudolateral craniomedial oblique (CaLCrMO)
- Caudocranial (CaCr)
- Flexed lateromedial

Stifle ultrasonography
- patellar ligaments
- collateral ligaments
- medial and lateral menisci
- cartilage of the trochlear ridges
- meniscotibial ligaments

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18
Q

Common angular limb deformities (horses)

A

Carpal valgus
Fetlock varus
Tarsal valgus

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19
Q

Aetiology of angular limb deformities - congenital

A

Incomplete ossification of the cuboidal bones
□ Cuboidal bones ossify in late gestation
□ Carpus and tarsus

Diagnosis:
§ ALWAYS RADIOGRAPH PREMATURE FOALS

Treatment:
§ limiting weight bearing and activity
§ Strict stall rest 2 weeks; re-xray to monitor until able to do more activity
§ Depending on severity, casts

Prognosis: Guarded for athletic activity

Soft tissue laxity
§ Carpus most affected

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20
Q

Aetiology of angular limb deformities - developmental

A

Asynchronal growth
□ Dysplasia of the metaphysis or epiphysis
□ Common cause of ALD

Nutritional imbalance
□ Fast growth

Trauma/infection
□ Leads to early closure and asynchronal growth

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21
Q

Growth plate closure times in horses

A

Growth plates determine bone length

Closure time varies between breeds (lighter close earlier)

Most rapid growth 1st 10 weeks

Correct fetlock deformities within 70 days

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22
Q

Treatment of angular limb deformities in horses

A

Conservative
- most correct within 2 weeks
- restrict exercise
- Hoof correction
- Nutritional management

Surgical
- Periosteal transection and stripping
- Transphyseal bridging/implants
- corrective ostectomy

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23
Q

Periosteal Transection and Stripping

A

Growth Acceleration via inhibited growth with “release” of periosteum

Performed on short aspect of limb
- Varus: Performed medial
- Valgus: Performed lateral

good cosmetic result, no overcorrection possible

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24
Q

Transphyseal bridging/implants

A

Growth reduction via tension across the growth plate

Performed on mild-severe ALD

Performed on the long aspect of the limb
- Varus: Lateral
- Valgus: Medial

All techniques carry a risk of possible implant infection

Over correction can occur!

Foals monitored on a daily basis to ensure this doesn’t occur

Implants removed between 6-8 weeks (when the leg is straight)

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25
Q

Corrective ostectomy

A

Reconstruction

Foals with closed growth plates or severe diaphyseal deformities

Very rarely done

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26
Q

Flexural limb deformities

A

Abnormal angulation of the limb in the sagittal plane (flexed or extended)

Primarily soft tissue vs. ALD primarily bone

Forelimbs most often affected

Can be in one or more limbs

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27
Q

Contracture flexural limb deformities

A

Persistent hyperflexion

Can have tendon contracture as a result of scarring from tendon injury—seen in adults and rare in foals

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28
Q

Hyperextension flexural limb deformities

A

Elongation of tendinous unit in relation to bone

Congenital
· Birth up to 1 month
· Carpus or MCPJ most commonly
· Teratogenic
· Intrauterine positioning
· Genetics

Acquired
· 1-6 months
· DIPJ and MCPJ most commonly
· Nutrition
· Trauma
· Infections

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29
Q

Causes of contracture

A

Mostly multifactorial and difficult to explain

Intrauterine malpositioning with large foals

Diseases acquired by the mare in pregnancy:
□ Locoweed/hybrid sudan grass
□ Gene mutation in sire
□ Influenza
□ Defects in cross linking of elastin and collagen
□ Glycogen branching enzyme deficiency (QH foals)

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30
Q

Prognosis of contracture

A

Good prognosis if can straighten and no osseous changes—guarded if not

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31
Q

Treatment of contracture

A

Rads: helps rule out any bony abnormalities

Conservative:
□ Mild cases usually resolve with limited exercise
□ Need further treatment if don’t improve or unable to stand
® Splints/casts
® Toe extensions – be careful!
® Analgesics
® IV Oxytetracycline:
◊ Popular treatment to relax tendons (Possibly via Inhibition of collagen gel contraction by myofibroblasts)
◊ Very useful in mild to moderate cases—not as rewarding with severe cases

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32
Q

Digital hyperextension

A

Fetlock dropped and toe may rise; severe if plantar/palmar region on the ground

Can range from mild to severe

Caused by flaccid flexor muscles

Corrects often within a few weeks with increased muscle tone

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33
Q

Treatment of digital hyperextension

A

If needed

protect skin

place heel extensions

mild exercise

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34
Q

Acquired flexural limb deformities

A

DIPJ - distal interphalangeal joint
MC/MT - metacarpa/metatarsal

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35
Q

DIPJ flexural limb deformity

A

Due to DDFT

Stage 1: wall not passed vertical plane

Stage 2: wall passed vertical; worse prognosis

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36
Q

Treatment of DIPJ flexural limb deformity

A

Controlled exercise with Physiotherapy

Analgesics—address underlying cause of pain

Elevate heel to ease DDFT tension; Toe extension may be useful or cause more pain

Surgery:
□ ALDDFT desmotomy if unresponsive to medical treatment
□ DDFT tenotomy if very bad or doesn’t respond to all other treatments first

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37
Q

MC/MT flexural limb deformities

A

May be due to DDFT or SDFT (palpate which under tension—difficult)

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38
Q

Treatment of MC/MT flexural limb deformities

A

Controlled exercise with Physiotherapy

Analgesics—address underlying cause of pain

Elevate heel to ease DDFT tension; Toe extension may be useful or cause more pain

+/- splints with caution (can cause sores)

Surgery:
□ If no response to medical treatment or >180*
□ ALDDFT desmotomy and/or AL SDFT

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39
Q

Clinical signs of physitis

A

Enlarged physis

Usually painful on palpation

Variable lameness; may be reluctant to stand

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40
Q

Diagnosis of physitis

A

Clinical signs

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41
Q

Radiographs of physitis

A

Irreguar/wide growth plate; may see sclerosis

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42
Q

Treatment of physitis

A

Stall rest/restrict exercise

Nutritional balance/no gain

NSAIDs

43
Q

Developmental orthopaedic disease complex

A

A number of conditions often related that affect the immature skeleton

Includes:
○ OC/OCD, SCBC
○ ALD/FLD
○ Physitis
○ Cervical vertebral malformations

44
Q

Osteochondrosis (OC) and osteochondrosis dissicans (OCD)

A

Occurs at transition from weight bearing to non weight bearing

Causes clinical disease in 5-25% of cases

High incidence in TB, WB, SB

OCD (OC Dissicans occurs when cartilage and/or subchondral bone loose or detaches from joint)

45
Q

Subchondral bone cysts (SCBC)

A

Found underneath the cartilage in a weight bearing area of joint

Caused by in folding of weakened cartilage

46
Q

Pathology of osteochondrosis

A

Complex aetiology and not well understood

Essentially a disturbance of endochondral ossification

§ Causes cartilage in joints to form abnormally

§ Cartilage and subchondral bone become irregular in thickness and weak

§ May develop cartilage and bone flaps that may remain partially attached to the bone or break off and float around in the joint - OC to OCD

§ causes inflammation in the joint and over time may lead to the development of arthritis.

Dynamic lesions and change over time

47
Q

Biochemical factors that affect the outcome of OC lesions

A

Age: young

Genetics: Risk of OCD may be partially inherited

Rapid growth and large body size

Nutrition: Diets very high in energy or have an imbalance in trace minerals (low copper diets)

Metabolic activity/Hormonal imbalances: Insulin and thyroid hormones

Trauma and exercise: Trauma (including routine exercise) is often involved in the formation and loosening of the OCD flap

48
Q

Clinical signs of OC

A

Often have no clinical signs and found on screening radiographs incidentally

Persistent joint effusion in a young horse

May occur when very young or only when into work

Lameness, if present, varies with location and severity (usually sound at a walk)

49
Q

Diagnosis of OC

A

Clinical signs

Radiographs
§ Often bilateral (>50% of cases)
§ always radiograph the opposite limb
§ Various radiographic signs

Ultrasound
§ Some lesions may not be seen on radiographs if only cartilage is affected

50
Q

Predilection sites of OC

A

Tarsocrural joint

Femoropatellar joint

Fetlock

51
Q

OC of the tarsocrural joint

A
  1. Distal intermediate ridge of the tibia (DIRT)
  2. lateral trochlear ridge
  3. medial malleolus

More common in SB and WB
○ Can be ID arthroscopically without radiographic evidence

Treatment
○ Arthroscopic removal
○ Early better so not OA

Prognosis
○ Fair to good

52
Q

OC of the stifle

A

Femoropatellar joint:
1. Lateral trochlear ridge (best seen on lateral oblique view)
2. Medial trochlear ridge
3. Distal patella

More common in TB

Radiographs
○ Often, flattening of trochlear ridges

US
○ Can be useful for MTR lesions that cannot be seen radiographically

Treatment
○ Generally lesions monitored until >9 months and then possibly surgery - arthroscopic debridement

Prognosis
○ Better prognosis with lesions <2cm; worse with >4cm

53
Q

OC of the fetlock

A

Fetlock
1. Sagittal ridge of distal MC/MT III
2. Dorsoproximal P1 (considered traumatic in origin)
3. Palmar/plantar P1 (considered traumatic in origin)

HL and FL affected

Radiographs
○ Fragments and flattening

Prognosis depends on location - dorsal good, palmar/plantar poor

54
Q

Non-surgical treatment of osteochondrosis (OC)

A

Can only be expected to be successful in either very young animals or in very mild cases (Single small lesions without effusion or lameness)

Rest, controlled exercise, +/- NSAIDs, +/- IA corticosteroids

55
Q

Surgical treatment of osteochondrosis (OC)

A

Arthroscopic debridement
□ Horses >1 year ideally (to give some lesions a chance to heal; sooner may debride too much bone)

Surgery indicated if horse meets two of the following criteria
□ Joint effusion
□ Lameness localised to the joint
□ Radiographic evidence

56
Q

Pathology of subchondral bone cysts

A

Part of osteochondrosis complex

Found underneath the cartilage in a weight bearing area of joint vs. at transition zone for OC

Caused by in folding of weakened cartilage

57
Q

Common locations of subchondral bone cysts

A

Stifle (medial femoral condyle)

Phalanges

Can be found anywhere

58
Q

Breed signalment of subchondral bone cysts

A

TB : Mostly young at onset of training (1-3y)

WB: Often with OA—poorer prognosis

59
Q

Clinical signs of subchondral bone cysts

A

Often present with lameness with or without effusion

Size of lesion and amount of cartilage involved correlated with clinical signs and prognosis

60
Q

Diagnosis of subchondral bone cysts

A

Often block with IA anesthesia

Radiographs:
□ Radiolucent areas of bone often accompanied by thin sclerotic rim
□ Size of lesions vary from flattening, to slight indentation, to round lesions
□ Always radiograph both limbs or other joints that are effusive
□ Usually able to ID, but may need CT

61
Q

Medical treatment of subchondral bone cysts

A

Rest, NSAIDs

IA or Intralesional corticosteroids (under US or arthroscopic guidance)

62
Q

Surgical treatment of subchondral bone cysts

A

Moderate to severe cases

Newer techniques:

□ Trans cyst lag screw placement: Thought to compress and stimulate bone formation—recently much better success with improved technique using this method

□ Absorbable Implants: Very promising success with improved soundness

63
Q

Major causes of OA

A

Joint instability
○ soft tissue injury

Intra articular fracture

Synovitis/capsulitis

Synovial sepsis

Subchondral bone disease

Previous OCD/Bony cysts

64
Q

Pathogenesis of osteoarthritis

A

Disorder of movable joints

Characterised mainly by articular cartilage degeneration and loss
○ With or without changes to the synovium or subchondral bone
○ Result of complex biological and mechanical processes

Abnormal mechanical load, inflammation and metabolic tissue failure (anabolic repair overwhelmed by catabolic process)

65
Q

General clinical signs of OA

A

Low grade, chronic, often bilateral lameness

Lameness may improve with work

Joint effusion typically present (not the TMTJ)

+/- decreased range of motion

+/- positive to flexion

66
Q

Radiographic signs of osteoarthritis

A

Periarticular enthesophytes and osteophytes
○ Enthesophytes - at the attachment of a tendon or ligament
○ Osteophyte - at the joint margin

Narrow joint space

Subchondral bone sclerosis or lysis

May see osteochondral fragments along with osteoarthritic changes if fragments are potentially chronic/diagnosed late

67
Q

Common sites of osteoarthritis

A

Distal interphalangeal joint (DIPJ-coffin joint)

Metacarpophalangeal joint (MC/MTPJ-fetlock joint)

Proximal interphalangeal joint (PIPJ-pastern joint)

Carpus

Tarsus

Stifle

68
Q

Aetiology of osteoarthritis of DIPJ (coffin joint)

A

Relatively common cause of forelimb lameness

May be due to extensor process fracture of P3, septic arthritis

69
Q

Clinical signs of osteoarthritis of DIPJ (coffin joint)

A

Often bilateral, mildly positive to distal limb flexion

Worst on the inside of a hard circle

Effusion at coronary band

Mature sports horses and leisure horses

Common FL

Improve to a PDNB, sound after ASNB

70
Q

Diagnosis of osteoarthritis of DIPJ (coffin joint)

A

Often block to a PD but sometimes blocked out with Abaxial

Most specific diagnosis blocking to the DIPJ

Radiographs often display subtle changes to extensor process

71
Q

Osteoarthritis of PIPJ (Pastern joint)

A

“High ringbone”

Moderately common cause of forelimb lameness (can also occur in hind limb)

Young horses may have induced by OC

Sport horses, heavy breeds, hunters

72
Q

Clinical signs of Osteoarthritis of PIPJ (Pastern joint)

A

Often palpable enlargement of PIPJ

Insidious onset unless secondary to fracture; usually gets worse with work

Less commonly bilateral

Worst on the inside of a hard circle

Positive to distal limb flexion

Firm bony enlargement of pastern (not effusion)

73
Q

Diagnosis of Osteoarthritis of PIPJ (Pastern joint)

A

Often blocks to abaxial sesamoid

Radiographs display OA changes often

Usually negative PDNB, positive ASNB

PIPJ block most diagnostic

74
Q

Aetiology of osteoarthritis of MCPJ (fetlock joint)

A

Common in athletic horses; often race horses

Can be caused by OC, fragmentation from OCD or SCBL
§ Dorsoproximal P1
§ Dorsal sagittal ridge

Can be caused by traumatic fracture
§ Palmar/plantar

General wear and tear

75
Q

Clinical signs of osteoarthritis of MCPJ (fetlock joint)

A

Usually forelimb, usually effusion usually palpable

Can lead to moderate-severe unrelenting lameness

Often bilateral

76
Q

Diagnosis of osteoarthritis of MCPJ (fetlock joint)

A

Blocks usually to fetlock IA

Rads: Can cause development of periarticular osteophytes, enthesophytes and joint space collapse (usually medially)

Consider developmental diseases too!

77
Q

Palmar osteochondral disease (POD)

A

Specific osteoarthritic/subchondral bone disease of the fetlock

Results from accumulated stress and sclerosis during racing

Sclerosis in palmar region of condyle

Moderate to severe lameness

Predisposes to condylar fracture

78
Q

Diagnosis of Palmar Osteochondral disease (POD)

A

Radiographs:
· Sclerosis of some kind present within the palmar aspect of the condyle
· Can see intense sclerosis of the palmar region of the condyle, potentially deep to a lytic lesion
· can appear as variously shaped palmar defects with or without secondary arthritis changes present

Scintigraphy
· Sensitive for detecting early stress fracture and bony deposition forming the sclerotic zone within the palmar region of the condyle
· Early recognition helpful to reduce sclerosis and allow remodeling vs. progression into condylar fracture

CT and MRI
· More sensitive means vs. rads for detection early

79
Q

Treatment of palmar osteochondral disease (POD)

A

Rest with controlled exercise

Corticosteroids IA

80
Q

Oesteoarthritis of carpus

A

Very common in currently racing or previously raced TB, more rare in other breeds (older typically)

Radiocarpal (RC) and middle carpal (MC) joints most commonly
- Less commonly CMC
- Affects the two high motion joints of the carpus

81
Q

Clinical signs of Oesteoarthritis of carpus

A

Usually chronically thickened joint capsule and decreased ROM

Moderate to severe lameness

82
Q

Osteochondral fragments in carpus osteoarthritis

A

Often very performance limiting as progress to chronic OA quickly

Can be acute trauma related, but often due to chronic stress and adaptive remodeling

Dorsal distal radiocarpal bone most common

May find palmar fragments (more often due to overt trauma)

83
Q

Subchondral lucency of C3 in capus osteoarthritis

A

Osteoarthritic process

Due to chronic stress and adaptive remodeling

Sclerosis of the radial facet of C3

Often progresses to slab fracture, which leads to chronic OA

Usually can diagnose on CS and radiographs, but sometimes NS or CT assists for earlier diagnosis and prevention of further injury

84
Q

Diagnosis of carpus OA

A

Easily localised with intra-articular blocks

85
Q

OA of tarsus

A

OA of the distal hock joints in the most common cause of hindlimb lameness in the horse

Distal intertarsal joint (DIT) and tarsometatarsal (TMT) joint most common = “Bone Spavin”

Less common PIT (if occurs, typically associated with trauma/fractures/previous sepsis)

86
Q

Distal hock OA

A

Sport horses, western performance and standardbreds most prone

Poor conformation a contributing factor (Often sickle hocked) - causes abnormal loading of small tarsal bones

Foals can be predisposed due to incomplete ossification of tarsal bones poorly managed

87
Q

Clinical signs of distal hock OA

A

May present as a back problem or poor performance

Mild-severe lameness
□ Most lame on the inside of a hard circle
□ Sometimes undetectable because bilateral
□ Sometimes history undetectable lameness but deterioration of attitude

Toe dragging/reluctant to flex tarsus

Short cranial phase of stride

Pain on back palpation

May appreciate new bone formation, but hard to appreciate any joint distension

May warm out of it

May be positive to flexion

88
Q

Diagnosis of distal hock OA

A

Clinical signs

Blocks: TMT joint local anesthetic has been shown to diffuse into the DIT joint, therefore some clinicians only block and treat this joint
□ Complete resolution may not occur with blocking and a 50% improvement is considered significant

Radiographs:
□ Commonly bilateral so radiograph both
□ Lameness can exist with little to no radiographic changes
□ Also there can be extensive changes with no lameness
□ May see osteophytosis or sclerosis and/or lysis
□ Poor sensitivity, so believe the blocks

NS: correlates well with MRI lesions

MRI: very useful for tarsus as rads often have a low sensitivity

89
Q

Stifle OA

A

All breeds and types

Occurs typically secondary to trauma or injury

90
Q

Diagnosis of stifle OA

A

Very positive to proximal limb flexion

Most lame on outside of a soft circle

IA blocks
§ Should block all three compartments (MFT, LFT, FP)

Radiographic changes typically seen later in the disease
§ First sign often osteophyte formation of the medial tibial plateau and intercondylar eminence
§ Narrowing of joint space interpreted with caution due to positioning of radiograph

May need diagnostic arthroscopy to make a diagnosis
§ Blocks to IA anesthesia or scintigraphy positive, but rad/US negative good candidates

Evaluate for possible initiating cause
§ ie. Meniscal tears
§ may need US or diagnostic arthroscopy

91
Q

Medical treatment of OA

A

NSAIDs

IA corticosteroids

Weak anti-inflammatories

Autologous biologics/’regenerative’ medicine

92
Q

NSAIDs in OA treatment

A

Phenylbutazone, firocoxib

Risks of toxicity -> right dorsal colitis

Only palliative and should be limited to acute phase; firocoxib likely more safe for long term use

93
Q

IA corticosteroids in OA treatment

A

Justifiable and clinically effective form of joint medication

Can have detrimental effects on normal cartilage (suppress chondrocyte activity)

Not the case in inflamed or abnormal joints (chondroprotective in low doses)

Methylprednisolone acetate (Depo-Medrone) - used least

Triamcinolone acetonide (Adcortyl) - used most

Often expect about 3-6 months of pain relief or longer ideally—not uncommon for horses to be injected twice yearly

Caution
§ Iatrogenic sepsis:
§ Corticosteroid induced laminitis

Dosing recommendations:
□ Triamcinolone
- 18mg
- 2000 cases treated with 20-45mg of triamcinalone = 0.15% cases of laminitis (all but 1 were ponies)
□ Methylprednisalone
- 200mg

94
Q

Weak anti-inflammatories in OA treatment

A

IA hyaluronic acid (HA)
- notmal component of joint fluid
- never given on its own

PSGAGs
- IM/SQ
- Chondroitin sulfate

Pentosan (Pentosan or cartrophen)
- beechwood hemicellulose

95
Q

Biologics in OA treatment

A

Evidence is poor
Unlikely to work if corticosteroids didn’t
Consider for laminitis risk horses

IRAP (interleukin receptor antagonist protein)

PRP (platelet rich plasma)

Stem cells (allogenic or autogenic)

96
Q

Surgical treatment of OA

A

Diagnostic arthroscopy

Surgical arthroscopy

Abrasian arthroplasty

Microfracture

Ankyloisis/atrodesis

97
Q

Diagnostic arthroscopy for OA treatment

A

Used commonly for the stifle as other diagnostics can be limiting

Allows for the simultaneous diagnosis and treatment of some pathology (i.e. cartilage fibrillation, meniscal tears)

Only an option for high motion joints

98
Q

Surgical arthroscopy for OA treatment

A

Removal of OC fragments if present

Articular cartilage debridement

Reconstruction of IA fractures

Joint resurfacing

99
Q

Abrasion arthorplasty for OA treatment

A

Stimulates endogenous repair

Debridement of SCB plate disease tissue to allow for healing

Replaced with fibrocartilage

100
Q

Ankylosis

A

Fusion of the joint

101
Q

Ankylosis for OA treatment

A

Rids the bone of diseased and unstable articular cartilage in order to fuse the bones together—this alleviated instability and pain

Salvage procedures

Warranted in horses with OA that are no longer responsive to medical management or have overt damage or pain that may be alleviated with fusion intervention.

102
Q

Fascilitated ankylosis for OA treatment

A

Destroying articular cartilage to encourage self fusion

Low motion joints typically (i.e. distal hock joints»PIPJ)

Goal = athletic performance

Types: – Chemical: Ethyl alcohol
- Trans-articular surgical drilling/curettage of cartilage

103
Q

Arthrodesis in OA treatment

A

Destroying articular cartilage and surgical stabilization to aid in fusion

Can perform in low or high motion joints

Much more expensive than ankylosis

Complication rates much higher

Reasons to perform:
- Performed with OA in some cases (PIPJ common)
- Performed with soft tissue injury, septic arthritis, fractures

Types:
- Transarticular screws alone
screw/plate

Equine I (21 decks)

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