Chronic Lameness Flashcards

1
Q

What are some chronic lameness conditions in the horse?

A
  • Osteoarthritis (Join synovitis)
  • Navicular Dx
  • Chronic Laminits
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2
Q

What is the most common cause of lameness in horses?

A

Osteoarthritis

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3
Q

What factors to consider with OA?

A
  • Use of horse
  • OWner’s expectation
  • Age
  • Severity
  • N° of joint affected
  • Risk of lamainits
  • Other systemic dx
  • Owner’s financial situation
  • Associated soft tisue damage
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4
Q

Consequences of OA?

A
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5
Q

detail what steroids to use when?

A

INTRA-ARTICULAE ADMIN

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6
Q

Side effects of Corticosteroids?

A
  • Laminitis (BEWARE if suspicious of endocrine dx)
  • Iatrogenic Joint infection (low incidence)
  • Periarticular cellulitis (diffuse swelling, hot painful)
  • Joint flare - aseptic synovitis
  • Deleterious effects on cartilage (MPA)
  • SLows healing of joint injury
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7
Q

Describe the use of NSAId for OA ?

A
  • Analgesic - SMOAD
  • Improves joint mobility
  • Inhibition of COX (COX 2 esp inflammation)
  • Side effects due to COX 1 inhibition -> Gi ulceration, RDCn renal but Therapeutic effects due to COX 2
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8
Q

What do we HAVE to keep in mind abotu using NSAIDs?

A
  • Narrow safety margin
  • Not for competition animals
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9
Q

describe Phenylbut use?

A
  • Most commonly used
  • Cost effective –
    86p/sachet
  • Oral or IV
    administration
  • 2.2 mg/kg PO BID
  • NOT COX selective
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10
Q

What is the FEI Detection TIme for Phenylbut?

A

7 days

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11
Q

What other options for NSAIds?

A
  • > Suxibotazone (more palatable)

-> Firocoxib IV or PO
- 3mg/kg SID loading dose then 1 mg/kg SID maintenance
- COX 2 selective!
- FEI detection 14 days

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12
Q

What topical NSAID?

A

Diclofenac Cream - topical application BID
- licensed in UK not US
(equivalent in UK for humans is voltarol)

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13
Q

What other management considerations for OA?

A
  • Weight management → Diet
  • Recommendations: restrict forage to 1.5% bodyweight +
    balancer in feed
  • Housing and environment
  • Nutraceuticals
    -> Weak scientific evidence for in vivo efficacy
    -> Lots of anecdotal evidence
    -> Chondroitin sulphate and glucosamine
    -> Hyaluronic Acid
    -> Green lipped mussel
    -> Boswellia
    -> Devil’s claw – controlled substance under FEI
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14
Q

Biphosphonates - how do they work?

A
  • DMOAD
  • Osteoclast inhibitors – bind to osteoclasts which in turn
    decreases osteoblast activity and bone turnover
  • Reduce rate of bone resorption
  • Reduce bone pain
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15
Q

What evidence for use of Biphosphonates?

A
  • Bone spavin
  • Navicular dx
  • Thoracolumbar pain
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16
Q

Duration fo action for biphosphonates?

A

Approx 6 months

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17
Q

Risks associated with biphosphonates?

A

Colic and renal tox

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18
Q

give examples of biphosphonates

A
  • Tiludronate -> admin via saline infusion intravenously over 30 mins ; licensed for bone spavin
  • Clodronate -> Admin IM over 3 sites; licensed for navicular dx
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19
Q

Describe used of Sodium hyaluronate (HA)

A
  • Glycosaminoglycan
  • Component of articular cartilage and synovial fluid
  • Local anti-inflammatory effect and chondroprotective
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20
Q

How do we admin HA?

A
  • Intravenous(40mg) Repeated weekly for 3 treatments
  • SMOAD + DMOAD [Kawcak et al, 1997]or Intra-articular (20mg/joint)
  • Flare rate of 12%
  • Does not result in a substantial enough reduction in lameness when used alone
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21
Q

Best use of HA?

A

Acute/mild to moderate synovitis

22
Q

describe polysulfated glycosaminoglycans?

A

Increase HA synthesis, stimulate cartilage matrix synthesis, decrease matrix
degradation

23
Q

when are P O L Y S U L F A T E D G L Y C O S A M I N O G L Y C A N S used ?

A
  • Most commonly used intramuscularly →
  • Improves lameness and stride length [White et al, 1996]
  • 7 treatments(500mg) every 4 days for 28 days
  • Can be given intra-articularly
  • Associated with higher incidence of joint sepsis
24
Q

best use for polysulfated glycosaminoglycans?

25
Q

Pentosan Polysulfate used? (Cartrophen)

A

DMOAD
Stimulate synthesis of proteoglycans in extracellular matrix
→Healthier cartilage
→Stimulates increase production
of hyaluronic acid
→Lubricates and stabilises the
joint
→Anti-inflammatory

26
Q

What orthobiologics/regen medicine options?

A
  • Polycrylamide Hydrogel
  • Interleukin 1 receptor antagonist (IRAP)
  • Platelet Rich Plasma and alpha 2 macroglobulin
  • Stem Cells
27
Q

Describe Polyacrymide Hydrogel ?

A

A promising alternative with a long duration of action
- Integrates into joint capsule and tissue via vessel in growth
- Creates a cushion like effect in the joint
- Preservation of joint cartilage and aid regeneration

28
Q

Describe use of IL-1 Receptor antagonist PRotein (IRAP) ?

A
  • Aim: block action of pro-inflammatory cytokine IL-1
  • used in humans for many years to manage OA
29
Q

Protocol for use of IL-1 IRAP

A
  • Protocol: 3 injections 7-10 days apart
  • Used most often in chronic progressive OA
30
Q

Describe Platelet RIch lasma use?

A
  • Autologous biological product prepared from whole blood
  • Enrichment of platelets and degranulation to release
    growth factors
  • Evidence to support use in younger patients for joint
    tissue healing
    → acute traumatic injuryD
31
Q

Describe use of Alpha 2 Macroglobulin -

A
  • Alpha2EQ
  • Naturally occurring protein in blood
  • Anti-inflammatory with multimodal mechanism of action
  • Can be used with other treatments/pre-treatment
32
Q

stem Cells - two types?

A
  • Bone marrow derived Mesenchymal Stem cells
  • Chondrogenic induced Mesenchymal stem cells
33
Q

Describe Bone marrow derived MEsenchymal Stem clels?

A

Bone marrow aspirated from sternum
Cultured over several weeks
Promote repair and regeneration
May participate in repair of cartilage
May be beneficial in cases with intra-articular
soft tissue injuries to promote healing

34
Q

Describe Chondrogenic induced mesenchymal stem cells?

A

Derived from equine allogenic peripheral blood
No need to wait for cultures – comes ready to use
Cost – timing/storage

35
Q

If all else fails what surgical options for OA?

A
  • arthrodesis
  • Neurectomy
36
Q

What different conditions encompass Navicular syndrome ?

A

o Navicular Bone Pathology
o Navicular Bursitis
o Navicular suspensory desmitis ( collateral sesamoidean ligament)
o Distal Sesamoidean Impar Desmitis
o DDFT injury/tear or adhesions of the DDFT

37
Q

What are the mainstays of Navicular syndrome?

A
  1. Rest
  2. Anti-inflammatories
  3. Bone metabolism medications
38
Q

Describe the ‘Rest stage’

A
  • Dependant on degree of soft tissue damage
  • Box rest with hand walking
  • If DDFT affected: more prolonged → up to 12 months
39
Q

describe the use of Anti-inflammatories ?

A
  • Most common long term, palliative medical treatment
  • Intra-articular: Distal interphalangeal joint-> Corticosteroids (TA and MPA)
  • Intra thecal: Navicular bursa-> More effective clinically?; Corticosteroid +/- hyaluronic acid
40
Q

What can be used for aspect 3 of treatment -> bone metabolism medications?

A
  • Bisphosphonates
  • Treat bone pain
  • Inhibit osteoclast activity and bone resorption

IM injection OR?→Intravenous regional limb perfusion :
no scientific to support this currently

41
Q

How can we use remedial farriery for navicular syndrome

A
  • Dependant on confirmation of the foot
  • Optimise foot balance
  • Often have long toe and low, underrun heels, contracted heels
42
Q

Step 1 of Remedial farriery?

A
  1. Correct and maintain dorsopalmar and mediolateral balance
    * Correct hoof pastern axis
    * Elevate heel with wedge (2° - 4°)
43
Q

Step 2 of Remedial farriery?

A
  1. Ease of breakover achieved by shortening and/or rolling the toe
    * Decreases the work of moving the foot
44
Q

Step 3 of Remedial farriery?

A
  1. Maintenance of foot and especially heel mass
45
Q

Step 4 of Remedial Farriery?

A
  1. Protect palmar aspect of foot from concussion
    Types of shoes → aim to move weight bearing axis
    * Egg bar shoe
    * Heart bar shoe – central support shoe
    * Natural balance
    * Leverage Reduction Shoe
    * Frog support
    * Remove shoes??
46
Q

Other medications for navicular syndrome?

A
  • Isoxuprine
  • Warfarin
  • Botulinum Toxins
47
Q

Detail use of Isoxuprine?

A

Peripheral vasodilator, dec blood viscosity and platelet aggregatiion
-> Inc in distal limb circulation

48
Q

Use fo warfarin?

A

dec blood viscosity HOWEVER ischaemic pathogenesis largery disproved therefore NO LONGER COMMONLY USED

49
Q

detail Botulinum toxins

A

-> interference with pain pathway reducing lameness
- Prelim studies suggest improvement in lameness intra-thecal injection)
- More ivestigation required to evaluate dosage and long term efficacy

50
Q

Navicular bursoscopy?

A
  • Fibrillation or tearing of DDFT visible on MRI
    →Assess and debride lesions → reduce inflammation
51
Q

Palmar digital neurectomy?

A
  • Effective but potential for complications
  • Horse cannot compete under FEI rules
  • British Dressage - pre-2023 couldn’t compete
  • 2024/25 can be signed competition legal by vet