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Equine Med & Surgery > Lameness > Flashcards

Lameness Flashcards

1
Q

Important aspects of the standing examination

A
  1. consistent complete; always performed and documented in same way
  2. NOT BIASED by Hx…..unless horse is non-weight bearing lame, follow routine
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2
Q

Hoof conformation/angle problems

A
  • sloping
  • stumpy
  • broken back
  • broken forward
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3
Q

areas of hoof palpation

A
  • frog
  • coronary band
  • heel bulbs
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4
Q

Lameness not perceptible under any circumstance

A

grade 0

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5
Q

Lameness is difficult to observe and is not consistently apparent, regardless of circumstances

A

grade 1

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6
Q

Lameness is difficult to observe at a walk or when trotting in a straight line but consistently apparent under certain circumstances

A

grade 2

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7
Q

Lameness is consistently observable at a trot under all circumstances

A

grade 3

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8
Q

Lameness is obvious at a walk

A

grade 4

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9
Q

Lameness produces minimal weight bearing in motion and/or at rest or a complete inability to move

A

grade 5

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10
Q

Flexion tests

A
  • help localize source of lameness
  • NOT factored into lameness score
  • should not “block” off positive flexion test lameness alone
  • perform and interpret consistently
  • evaluate limb flexed AND opposite limb for increased lameness after weight-bearing
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11
Q

Wedge test with heel elevated is done to evaluate ______________

A

suspensory ligament

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12
Q

Wedge test elevating the toe is done to evaluate __________

A
  • navicular structures
  • DDFT
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13
Q

A wedge test placed to elevate one side of the foot is evaluating __________

A

collateral ligaments

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14
Q

Examples of mechanical gait abnormalities

A
  • upward fixation of patella
  • fibrotic myopathy
  • stringhalt
  • shivers
  • ruptured peroneus tertius
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15
Q

Types of diagnostic analgesia

A
  1. Perineural = “nerve block”
  2. Intra-articular = “joint block”
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16
Q

Why are nuclear scintigraphy and thermography exceptions to the rule of performing blocks prior to imaging?

A

with these two modalities, any injection site will be “hot” regardless of pathology

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17
Q

What is the lowest nerve block?

A

Palmar/plantar digital (PD)

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18
Q

PD nerve block blocks:

A
  • L & M palmar/plantar digital nerves; back of pastern below level of dorsal branches

(so heel, more than toe)

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19
Q

Abaxial (basisesamoid) nerve block blocks:

A
  • L & M palmar/plantar digital nerves at level of sesamoid bones
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20
Q

Of the L&M artery, vein, and nerve, how do the structures go from lateral to medial?

A

L to M: VAN so nerves are most medial

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21
Q

Low 4 point - nerves blocked

A
  • L&M palmar/plantar metacarpal/tarsal nn
  • L&M palmar/plantar nn
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22
Q

Be cautious about what structure when doing low four point block?

A

digital flexor tendon sheath

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23
Q

Blocking the deep branch of the lateral plantar nerve is done for what purpose?

A

suspecting proximal suspensory disease

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24
Q

Local anesthetic considerations for blocks:

A
  • Lidocaine: rapid onset but shortest duration (~1.5h)
  • Mepivicaine: rapid onset and intermediate duration (~3h)
  • Bupivicaine: intermediate onset but longest duration (6-8h)
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25
Q

Preparation of joint/tendon sheath blocks and nerve blocks close to joints

A
  • sterile preparation (4-5 min contact)
  • sterile gloves and technique
  • new bottle of local anesthetic
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26
Q

Needle size for low blocks? What about higher blocks and joint blocks?

A

Low: 25g

Higher & joint: 20 or 21

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27
Q

Diagnostic imaging-anatomical only

A
  • Radiography
  • CT
  • MRI
  • Standard US
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28
Q

Anatomical and functional diagnostic imaging

A
  • Nuclear scintigraphy
  • MRI
  • Advanced US
  • Thermography
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29
Q

If you have a suspect stress fracture but normal rads, how long should you wait before re-imaging?

A

7-10 days (latent period)

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30
Q

How does MRI produce an image?

A

exciting hydrogen nuclei at a specific resonance frequency within magnetic fields then detecting the energy released as the nuclei relax

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31
Q

What is the only good way to image soft tissue structures within the hoof capsule?

A

MRI

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32
Q

Preferred modality for soft tissue imaging after lameness is localized to a specific region

A

MRI

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33
Q

What functional information does MRI give you?

A

fluid signal within tissues indicates edema & inflammation

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34
Q

Primary imaging modality for soft tissue structures outside of the hoof

A

ultrasound

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35
Q

Functional assessments-ultrasound

A
  • doppler-blood flow
  • elastography-tissue strain for tendons and ligaments; helps determine how functionally tendons are healing
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36
Q

What imaging modality may be indicated when you can’t effectively diagnose lameness from a block?

A

nuclear scintigraphy

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37
Q

mechanism-nuclear scintigraphy

A

99mTc - diphosphonate thought to bind to exposed hydroxyapatite crystals in areas of bone remodeling or in soft tissues undergoing mineralization

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38
Q

Pool phase-nuclear scintigraphy

A
  • less than 15 min
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39
Q

Thermography is touchy, but possible applications are:

A

detect inflammation or vascular damage in limbs

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40
Q

Origin of the majority of lameness in horses:

A

forelimb, within foot

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41
Q

Laminar corium

A

soft tissue attachment to the coffin bone

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42
Q

What structures are interdigitating in the hoof

A

epidermal lamina + laminar corium(dermal lamella)

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43
Q

abnormal foot angles predispose to:

A
  • coffin joint OA
  • navicular dz
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44
Q

With sheared heels, what side is generally longer?

A

medial longer than lateral

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45
Q

What abnormal hoof-pastern axis is most common?

A

broken back

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46
Q

angle of heels at least 5 degrees<toe>
</toe>

A

underrun heels

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47
Q

Breed disposition to underrun heels

A

TB

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48
Q

Consequences of underrun heels

A
  • subsolar abscesses
  • bruised heels
  • increased strain on DDFT
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49
Q

Underrun heels-corrective shoeing

A

heel support (wedge)

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50
Q

Etiology of contracted feet

A
  • secondary to lameness
  • induced through shoeing (too small)
  • hereditary
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51
Q

Tx for contracted foot

A
  • fix primary problem
  • keep barefoot
  • exercise-concussive forces encourage foot to grow
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52
Q

Single most common cause for sudden onset of severe unilateral limb lameness

A

subsolar foot abscess

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53
Q

Etiologies of subsolar abscess

A
  • sole trauma
  • laminitis
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54
Q

most important aspect of tx for subsolar abscess

A

debride to provide drainage

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55
Q

Dx for subsolar abscess

A

very reactive to hoof testers at the abscess site

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56
Q

Organism causing thrush

A

Fusobacterium necrophorum

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57
Q

Breeds with higher incidence of navicular than others

A

QH, TB, WB

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58
Q

Clinical signs of navicular syndrome

A
  • insidious onset
  • commonly bilateral & worse on hard surfaces and when circled
  • often short strided
  • may stumble/shuffle-trying to land on toe
  • often point the forelimb that is most painful
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59
Q

Predisposing factors-navicular syndrome

A
  • excessive weight
  • small or narrow feet (e.g. QH)
  • broken back conformation
  • medial-lateral hoof imbalances
  • work on hard surfaces
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60
Q

Structures involved in navicular syndrome

A
  • navicular bone
  • flexor surface of navicular bone
  • DIP (coffin) joint
  • DDFT
  • navicular suspensory ligaments
  • impar ligament
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61
Q

What is the origin of pain with navicular syndrome?

A
  • intraosseous pressure
  • damaged supporting soft tissue structures
  • inflammation of bursa & coffin joint
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62
Q

Navicular syndrome-dx

A

CS, response to blocks, rads

  • PD - also blocks coffin joint and navicular bursa
  • rads: increase in #, size, shape of synovial invaginations. changes in navicular bone shape. flexor cortex (where DDFT glides over back of navicular bone) erosions, roughening. loss of corticomedullary distinction. medullary sclerosis. enthesopathy at collateral lig.
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63
Q

MRI findings - navicular syndrome

A
  • bone edema
  • adhesions
  • flexor cortex adhesions

can change prognosis, see things rads can miss

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64
Q

Corrective trimming/shoeing for navicular syndrome

A
  • enhance breakover w/ rocker or square toe
  • raise and support heel (2-3 degrees)

can vary with indiv. horses. have to see how they respond.

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65
Q

What does Tildren do?

A

inhibit bone resorption

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66
Q

Mainstay of surgical treatment of navicular syndrome

A

PD Neurectomy

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67
Q

Potential complications with PD neurectomy

A
  • neuroma
  • re-innervation
  • DDFT rupture-poor prognosis, maybe life ending
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68
Q

Laminitis CS

A
  • classic stance to take weight of front feet
  • reluctance to move/walk
  • increased recumbency
  • increased digital pulses
  • sinking at or separation of coronary band
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69
Q

Etiologies-laminits

A
  • mechanical-d/t overload from opposite leg lameness
  • endotoxemia-vascular microthrombosis
  • grain overload
  • metabolic derangements
  • black walnut shavings
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70
Q

A _______ can be done to stop P3 rotation

A

DDF tenotomy

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71
Q

Prognosis for a toe/quarter crack that starts at the bottom

A

good

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72
Q

Prognosis for coronary cracks

A

poor

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73
Q

Tx for toe cracks

A

patch, hoof resection, shoeing

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74
Q

chronic, hypertrophic, moist pododermatitis of the epidermal tissues of the foot

A

canker

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75
Q

Causes of canker

A
  • F. necrophorum
  • Bacteroides spp.
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76
Q

Main difference in canker vs. thrush

A

horn hypertorpy

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77
Q

Canker is most common in ____breeds

A

draft

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78
Q

Topical abx that would be suitable for canker

A

oxytetracycline, metronidazole

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79
Q

Treatment for a keratoma

A

remove affected hoof wall & debride all abnormal tissues

80
Q

Sterile medical maggots are sometimes used when?

A

after debridement of a keratoma; they eat the necrotic tissue

81
Q

White line disease can be caused by?

A

bacteria or fungi

82
Q

Sidebones are caused by:

A

calcification of collateral cartilages

83
Q

Necrosis of the collateral cartilages is called

84
Q

Quittor is most common in _____ breeds

85
Q

Chronic draining tracts above the coronary band is indicative of _______

86
Q

Etiology of pedal osteitis

A
  • concussion
  • thin soles
87
Q

Painting the soles of the hooves with iodine may be indicated in what condition?

A

pedal osteitis

88
Q

Structures at risk for sepsis when you have a sole puncture

A
  • navicular bursa
  • coffin joint
  • tendon sheath
89
Q

Foal recovery vs. adult recovery with septic OA

A

61% in foals vs. 88% in adults

90
Q

Normal synovial fluid

A

transluscent yellow/straw colored & highly viscous (string b/w fingers)

91
Q

What do the following values indicate (synovial fluid analysis)?

  • TP <2.5
  • WBC 500-20,000
  • 10-20% neutrophils
A
  • Inflammation
92
Q

What do the following values indicate (synovial fluid analysis)?

  • TP >4.0
  • WBC > 30,000
  • >80% neutrophils
93
Q

Systemic abx choice for septic joint

A

Penicillin combined with amikacin (foals) or gentamicin (adults)

94
Q

Mainstay of treatment for septic joints

A

IV regional limb perfusion

95
Q

Arthrotomy pro/con

A
  • eliminates infection more rapdily than arthroscopy
  • increased risk of ascending infection
96
Q

Arthroscopy pro/con

A
  • better exam; debridement if bony lesion
  • increased $
97
Q

Know adult vs. foal septic OA & study septic OA slides

98
Q

50% of equine lameness is due to _____

A

joint disease and injury

99
Q

Synovial fluid functions

A
  • nutrients
  • lubrication
100
Q

Synoviocytes that make synovial fluid

101
Q

Type A synoviocytes

A

macrophage like: cytokines, phagocytosis of bacteria

102
Q

Subchondral bone fxn

A

absorbs shock of forces acting on cartilage

103
Q

Is articular cartilage good at intrinsic repair?

104
Q

primary collagen type in cartilage

105
Q

Anabolic cytokines

A
  • IGF-1
  • BMP
  • TGF-B
106
Q

Catabolic cytokines

A
  • IL-1B
  • TNF-alpha
  • NO
107
Q

Abnormal cartilage with normal forces

108
Q

Normal cartilage with abnormal forces

A

poor conformation, articular fx

109
Q

Pain in OA is due to:

A
  • damaged subchondral bone
  • joint capsule; pressure from fluid distension, thickened capsule reducing joint mobility
110
Q

What are radiographic findings associated with OA?

A
  • periarticular osteophytosis
  • joint space narrowing
  • subchondral sclerosis
  • subchondral lysis
  • osteochondral bodies
  • ankylosis-distal hocks, pasterns
111
Q

The distal hock joints are a classic site of what?

112
Q

Failure of endochondral ossification and therefore abnormal cartilage and bone =

A

Osteochondrosis (OC)

113
Q

3 major scenarios for retained cartilage

A
  1. healing occurs
  2. break out and form flaps –> OCD
  3. necrosis and development of subchondral cystic lesions
114
Q

OC-heritable?

115
Q

Low copper, excess zinc or energy is linked to _______

116
Q

OC common locations

A
  • Stifle (femoropatellar joint)
    • trochlear redge of femur; L>M
    • patella
  • Hock (tarsocrural joint)
    • DIRT
    • trochlear ridges of talus; >M
    • medial malleolus - also a common site for fx
117
Q

Most common Tx of OCD lesions:

A
  • arthroscopic fragment removal and debridement
118
Q

When might an OCD lesion heal spontaneously?

A

LTR femur OCD in a very young horse

119
Q

Tx of MFC cysts

A
  • corticosteroid injections can be tried as first treatment
  • debridement +/- grafting
120
Q

Advantages of intra-articular corticosteroids

A
  • decrease MMPs, IL-1, TNF-alpha
  • decrease fibrin deposition
  • pain relief
  • economical
121
Q

Intra-articular corticosteroids

A
  • chondrocyte necrosis
  • decrease ECM production (up to 4 months)
  • laminitis
  • decreased resistance to infection
122
Q

Long acting intra-articular corticosteroid

A

methylprednisolone acetate

123
Q

Intermediate to long acting intraarticular corticosteroid

A

Triamcinolone

124
Q

short acting intraarticular corticosteroid

A

betamethasone

125
Q

What corticosteroid should be used in distal tarsal joints (“low motion”)

A

Methylprednisolone acetate

126
Q

Triamcinolone advantage?

A

has some protective properties

127
Q

HA-direct anti-inflammatory effects?

Y/N?

128
Q

Functional mechanisms directly of HA depends on?

A

molecular weight

129
Q

Polysulfated glycosaminoglycans MOA

A
  • inhibit MMPs
  • stimulate matrix synthesis
  • promote HA synthesis
  • anti-inflammatory: inhibit PGE2 & free-radicals
130
Q

Interleukin-1 receptor antagonist

131
Q

Used for facilitated ankylosis

A
  • IA corticosteroids
  • monoiodoacetic acid
  • ethanol
  • exercise
132
Q

“simple” fractures

A

not major long bone fractures

133
Q

examples of simple fractures

A
  • splint bone fractures
  • metacarpal stress fractrues
  • intra-articular fractures
  • proximal sesamoid bone fractures
  • condylar fractures
  • coffin bone fractures
134
Q

Splint bone fractures

A
  • more common in distal 1/3
  • forelimbs >>>>hindlimbs
135
Q

Surgical treatment if distal 1/3 of splint bones fractured

A

remove fragment

136
Q

Surgical treatment if splint bone fx in mid and proximal 1/3

A

secure fx to MC/MTII

137
Q

Which splint bone is substantially load-bearing?

138
Q

Prone to metacarpal stress fractures

A

young TB-race training

139
Q

What is the preferred tx for metacarpal stress fx?

A

Surgery: osteostixis + unicortical lag screw is optimal

140
Q

Sequelae to intra-articular fragments

A

recurrent synovitis & OA–>shortened athletic career

141
Q

“nutcracker” fractures are fractures of what?

A

palmar carpus; crush accessory carpal bone

142
Q

Locations of intra-articular fragments in race horses

A
  • Carpal OC or “chip” fx
  • proximal P1 chip fx
  • apical sesamoid fx
143
Q

What is the most commonly diagnosed IA fracture?

A

Carpal OC fx

144
Q

Hyperextension of the carpus is the underlying cause of_________

A

carpal OC fragments

145
Q

Most common sites of carpal OC fragments

A
  • radiocarpal bone
  • intermediate carpal bone
  • proximal 3rd carpal
146
Q

effusion and lameness after cooling out that subsides with rest and supportive care is consistent with ___________?

A

carpal OC fragments

147
Q

Hyperextension of fetlock joint is underlying etiology of _________ fractures

A

dorsal proximal P1

148
Q

What type of proximal sesamoid fracture is a catastrophic breakdown?

A

biaxial mid-body

149
Q

Type of tendons more affected by tendonitis

150
Q

Resolution of tendonitis?

A
  • slow to heal
  • healed tendon inferior in strength and elasticity
  • high incidence of recurrence
151
Q

which specific tendon is more commonly affected by tendonitis?

A

SDFT >DDFT

152
Q

Factors that predispose SDFT to tendonitis

A
  • smallest cross sectional area
  • most external=greatest strain, trauma
  • less vascular in metacarpal region where lesions occur
153
Q

Tendonitis phases

A

Sub-clinical

  • degradation of ECM
  • weakened tendon

Clinical

  • acute inflammation

Reparative (at 3 wks)

  • tenocyte migratoin
  • fibroplasia
  • angiogenesis
  • higher collagen III/I ratio

Remodeling (up to months post injury)

  • replace type III collagen with type I
  • formation of x-links
  • re-orientation of fibers with max tension
154
Q

When are tendonitis lesions usually the worst?

155
Q

Treatment of tendonitis-acute phase

A
  • stall confinement
  • control inflammation
    • NSAIDs
    • Ice boots, cold hosing, game ready
  • bandaging
156
Q

What is a critical treatment of tendonitis in repair phase?

A

controlled exercise

157
Q

Idea behind proximal check ligament desmotomy

A

increases elastic ligament of muscle tendon unit

158
Q

Do flexor or extensor tendons heal better?

159
Q

Hyperextension of fetlock is seen when _______is lacerated

160
Q

Laceration of DDFT=you see what?

161
Q

Loss of fetlock support occurs when what structures are lacerated?

A

SDFT, DDFT, suspensory ligament

162
Q

Other structures that can be affected with suspensory ligament desmitis?

A
  • splint bones
  • proximal sesamoid bones
163
Q

Suspensory ligament desmitis-can do neurectomy of _____

A

deep branch of lateral plantar n.

164
Q

Degenerative suspensory ligament disease

A
  • Peruvian Paso, arabian, saddlebreds
  • no treatment
  • painful
  • poor prognosis
165
Q

Muscles most common affected by fibrotic myopathy

A
  • semitendinosus
  • semimembranosus
  • also biceps femoris, gracilis
166
Q

CS of fibrotic myopathy

A

acquired non-painful “slapping” gait

167
Q

Australian dandelions can cause_________

A

stringhalt

168
Q

Fibrotic myopathy-treatment

A

possibly tenotomy or myotenectomy

best thing is prevention if muscle tear is recognized

169
Q

Lateral digital extensor myotenectomy is useful for treating _______

A

stringhalt

170
Q

Most common congenital flexural deformities

A

fetlock (SDFT, DDFT)

carpal (combination & carpal fascia)

171
Q

Congenital flexural deformities-Tx

A
  • increase exercise
  • oxytetracycline
  • NSAIDs
  • toe extension shoes
  • surgery (severe cases)
  • must assist to stand and nurse
  • splints-12h on 12h off
172
Q

Acquired flexural deformitis: most common joints affected

A

coffin or fetlock joints; unilateral or bilateral

173
Q

What tendon is affected if fetlock joint is affected by flexural deformity?

174
Q

Timeframe of development of acquired fetlock joint flexural deformity

A

9 months to 2 years

175
Q

Timeframe of development of acquired coffin joint flexural deformity

A

4 weeks to 4 months

176
Q

What complication of PD neurectomy (performed for navicular syndrome) is catastrophic?

A

DDFT rupture

177
Q

Do sidebones cause lameness?

178
Q

OC lesions are very often bilateral so you should ____________

A

always check/radiograph both limbs

179
Q

Arthrodesis is usually only performed in which joints?

A

distal hock joints, pastern joints

(low motion!)

180
Q

Carpal OC fragments are often bilateral so you need to____________

A

radiograph both carpi

181
Q

increasing evidence that the pathogenesis of tendon injury is what?

A

degenerative

182
Q

Valgus

A

lateral deviation of a limb below a joint

183
Q

Most common angular limb deformities

A

carpal valgus, fetlock varus

184
Q

Periostial transection

A

-to stimulate growth; perform on concave side, proximal to the physis

185
Q

Transphyseal bridging

A

performed to slow growth; on convex side of deformity. place screws proximal and distal to physis and figure of 8 wires around screws

186
Q

Inflammation and degradation of articular cartilage is initiated by _______ and propagate by ________

A

initiated: bacteria
propagated: synoviocytes, chondrocytes

187
Q

Septic OA in foals:

A

Hematogenous

  • patent urachus/umbilical infections often seen concurrently
  • common for multiple joints to be infected
  • common for larger joints to be infected
  • septic osteomyelitis & physitis common; may cause irreversible damage
  • complicaitons from septicemia & hematogenous spread: kidey, myocardial involvement. invection of vertebral bodies, scapula, etc.
188
Q

How long are the transphyseal vessels present?

A

7-10 days old

189
Q

With septic OA in foals, where do bacteria preferentially lodge?

A

synovial membrane, subchondral bone

190
Q

Classifications of septic OA in foals

A
  • Synovium
  • Epiphysis
  • Physis
  • Tarsal bones
191
Q

T-type septic OA in foals is most common in _______

A

premature foals

192
Q

Septic OA in adults is due to:

A
  1. wounds/penetrating injury to synovial structures
  2. intra-articular/intra-thecal injection or sx
193
Q

potential complications with IV regional limb perfusion

A
  • injection site morbidity
  • thrombosis
  • cellulitis
194
Q

Three components of drug therapy for septic OA

A

NSAIDs, sodium hyaluronate, doxycycline or minocycline

195
Q

Functions of sodium hyaluronate

A
  • decreases cell infiltration, granulation tissue, and total GAG loss
  • in tendon sheaths, it helps reduce adhesions

Equine Med & Surgery (11 decks)

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