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
Corrective ostectomy
Reconstruction Foals with closed growth plates or severe diaphyseal deformities Very rarely done
26
Flexural limb deformities
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
27
Contracture flexural limb deformities
Persistent hyperflexion Can have tendon contracture as a result of scarring from tendon injury—seen in adults and rare in foals
28
Hyperextension flexural limb deformities
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
29
Causes of contracture
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)
30
Prognosis of contracture
Good prognosis if can straighten and no osseous changes—guarded if not
31
Treatment of contracture
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
32
Digital hyperextension
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
33
Treatment of digital hyperextension
If needed protect skin place heel extensions mild exercise
34
Acquired flexural limb deformities
DIPJ - distal interphalangeal joint MC/MT - metacarpa/metatarsal
35
DIPJ flexural limb deformity
Due to DDFT Stage 1: wall not passed vertical plane Stage 2: wall passed vertical; worse prognosis
36
Treatment of DIPJ flexural limb deformity
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
37
MC/MT flexural limb deformities
May be due to DDFT or SDFT (palpate which under tension—difficult)
38
Treatment of MC/MT flexural limb deformities
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
39
Clinical signs of physitis
Enlarged physis Usually painful on palpation Variable lameness; may be reluctant to stand
40
Diagnosis of physitis
Clinical signs
41
Radiographs of physitis
Irreguar/wide growth plate; may see sclerosis
42
Treatment of physitis
Stall rest/restrict exercise Nutritional balance/no gain NSAIDs
43
Developmental orthopaedic disease complex
A number of conditions often related that affect the immature skeleton Includes: ○ OC/OCD, SCBC ○ ALD/FLD ○ Physitis ○ Cervical vertebral malformations
44
Osteochondrosis (OC) and osteochondrosis dissicans (OCD)
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
Subchondral bone cysts (SCBC)
Found underneath the cartilage in a weight bearing area of joint Caused by in folding of weakened cartilage
46
Pathology of osteochondrosis
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
Biochemical factors that affect the outcome of OC lesions
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
Clinical signs of OC
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
Diagnosis of OC
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
Predilection sites of OC
Tarsocrural joint Femoropatellar joint Fetlock
51
OC of the tarsocrural joint
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
OC of the stifle
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
OC of the fetlock
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
Non-surgical treatment of osteochondrosis (OC)
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
Surgical treatment of osteochondrosis (OC)
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
Pathology of subchondral bone cysts
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
Common locations of subchondral bone cysts
Stifle (medial femoral condyle) Phalanges Can be found anywhere
58
Breed signalment of subchondral bone cysts
TB : Mostly young at onset of training (1-3y) WB: Often with OA—poorer prognosis
59
Clinical signs of subchondral bone cysts
Often present with lameness with or without effusion Size of lesion and amount of cartilage involved correlated with clinical signs and prognosis
60
Diagnosis of subchondral bone cysts
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
Medical treatment of subchondral bone cysts
Rest, NSAIDs IA or Intralesional corticosteroids (under US or arthroscopic guidance)
62
Surgical treatment of subchondral bone cysts
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
Major causes of OA
Joint instability ○ soft tissue injury Intra articular fracture Synovitis/capsulitis Synovial sepsis Subchondral bone disease Previous OCD/Bony cysts
64
Pathogenesis of osteoarthritis
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
General clinical signs of OA
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
Radiographic signs of osteoarthritis
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
Common sites of osteoarthritis
Distal interphalangeal joint (DIPJ-coffin joint) Metacarpophalangeal joint (MC/MTPJ-fetlock joint) Proximal interphalangeal joint (PIPJ-pastern joint) Carpus Tarsus Stifle
68
Aetiology of osteoarthritis of DIPJ (coffin joint)
Relatively common cause of forelimb lameness May be due to extensor process fracture of P3, septic arthritis
69
Clinical signs of osteoarthritis of DIPJ (coffin joint)
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
Diagnosis of osteoarthritis of DIPJ (coffin joint)
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
Osteoarthritis of PIPJ (Pastern joint)
“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
Clinical signs of Osteoarthritis of PIPJ (Pastern joint)
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
Diagnosis of Osteoarthritis of PIPJ (Pastern joint)
Often blocks to abaxial sesamoid Radiographs display OA changes often Usually negative PDNB, positive ASNB PIPJ block most diagnostic
74
Aetiology of osteoarthritis of MCPJ (fetlock joint)
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
Clinical signs of osteoarthritis of MCPJ (fetlock joint)
Usually forelimb, usually effusion usually palpable Can lead to moderate-severe unrelenting lameness Often bilateral
76
Diagnosis of osteoarthritis of MCPJ (fetlock joint)
Blocks usually to fetlock IA Rads: Can cause development of periarticular osteophytes, enthesophytes and joint space collapse (usually medially) Consider developmental diseases too!
77
Palmar osteochondral disease (POD)
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
Diagnosis of Palmar Osteochondral disease (POD)
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
Treatment of palmar osteochondral disease (POD)
Rest with controlled exercise Corticosteroids IA
80
Oesteoarthritis of carpus
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
Clinical signs of Oesteoarthritis of carpus
Usually chronically thickened joint capsule and decreased ROM Moderate to severe lameness
82
Osteochondral fragments in carpus osteoarthritis
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
Subchondral lucency of C3 in capus osteoarthritis
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
Diagnosis of carpus OA
Easily localised with intra-articular blocks
85
OA of tarsus
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
Distal hock OA
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
Clinical signs of distal hock OA
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
Diagnosis of distal hock OA
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
Stifle OA
All breeds and types Occurs typically secondary to trauma or injury
90
Diagnosis of stifle OA
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
Medical treatment of OA
NSAIDs IA corticosteroids Weak anti-inflammatories Autologous biologics/'regenerative' medicine
92
NSAIDs in OA treatment
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
IA corticosteroids in OA treatment
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
Weak anti-inflammatories in OA treatment
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
Biologics in OA treatment
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
Surgical treatment of OA
Diagnostic arthroscopy Surgical arthroscopy Abrasian arthroplasty Microfracture Ankyloisis/atrodesis
97
Diagnostic arthroscopy for OA treatment
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
Surgical arthroscopy for OA treatment
Removal of OC fragments if present Articular cartilage debridement Reconstruction of IA fractures Joint resurfacing
99
Abrasion arthorplasty for OA treatment
Stimulates endogenous repair Debridement of SCB plate disease tissue to allow for healing Replaced with fibrocartilage
100
Ankylosis
Fusion of the joint
101
Ankylosis for OA treatment
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
Fascilitated ankylosis for OA treatment
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
Arthrodesis in OA treatment
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