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Locomotor > Equine > Flashcards

Equine Flashcards

1
Q

What management changes can induce lameness?

A

Shoeing/ related changes Training/ performance intensity Stable/ working/ turn-out surface Housing Health and diet Current medication and response, response to rest

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2
Q

Name a lameness condition of older horses?

A

Chronic progressive osteoarthritis

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3
Q

What does palpation of the joint assess?

A

Distension Temp Pain ROM

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4
Q

What are the 2 principles limb movement is composed of?

A

Travel Action

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5
Q

What is the definition of travel?

A

Flight of a single hoof in relation to other limbs. Often viewed from the side or from behind.

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6
Q

What is the definition of action?

A

Overall description of gait characteristics. Takes into account joint, flexion, stride length, suspension and other qualities. Variation between different types and breeds

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7
Q

What are the phases of the stride?

A

Landing (+ gliding), loading, stance, brakeover (heel lift, toe pivot), swing

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8
Q

What are the features of the walk and how good is it at assessing lameness?

A

Even rhythmn 4 beat gait. Not v suitable for subtle lameness

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9
Q

What are the features of the pace and how good is it at assessing lameness?

A

Two beat lateral gait- ipsilateral fore- and hindlimb. Viable for STB racehorses and some others. Considered impure for most normal horses. Also not v easy to assess if subtle

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10
Q

What are the features of the canter and how good is it at assessing lameness?

A

3 beat gait with lead preference. Difficult to assess subtle lameness but useful for back/ rider/ saddle associated problems

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11
Q

What are the features of the trot and how good is it at assessing lameness?

A

2 beat diagonal gait. Steadiest and most rhythmic- preferred for lameness exam

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12
Q

What are the objectives of gait observation?

A

Is the animal lame- which legs? How lame?- appreciate difference w/ diagnostic analgesia? Localise the source of lameness in limb to allow for targeted diagnostic imaging and tx

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13
Q

How is a lameness recognised?

A

Fetlock drop- usually more on sound limb. Exception w/ tendon or SL damage Changes in limb flight- cranial and caudal phase of stride

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14
Q

What is the classic pattern of a forelimb lameness?

A

Head nod- when puts sound limb down

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15
Q

What is the classic pattern of a hindlimb lameness?

A

Pelvic hike

Elevation tuber calcis- higher on lame side

Drifting- moves away from lame limb, lame limb tracks under body (most often) or is posted out

Sound- harder landing on sound limb

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16
Q

What is the pelvic hike?

A

Hiking of pelvis when lame limb weight bearing Dropping of pelvis when sound limb is weight bearing Greater excursion of lame hindlimb- distance between top height and bottom height

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17
Q

How has the equine distal limb best adapted to locomotion?

A

Walking on one finger- stability over flexibility Reduced muscle mass- reduced swing time–> higher speed, tendons- efficient energy storage Straight- decreased joint forces/ moments

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18
Q

What are the features of the flexor tendon muscles?

A

Highly pennate. Muscle fibres ~1cm–> limited capacity for length change

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19
Q

What are the features of tendons?

A

Stores and releases energy. 7& lost as heat.

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20
Q

How have the bones in the distal limb been reduced?

A

Radius and ulna fused. Weight-bearing on the third MC/MT and digit. Lengthening of the limb, mass reduction. Increased energy storage (tendons). Lighter limb, shorter swing time, less mechanical energy.

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21
Q

What are the mechanical functions of the hoof?

A

Shock absorption, support and grip, propulsion.

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22
Q

What are the protective mechanisms of the hoof?

A

Shape of solar surface allows heel movement. Suspension of distal phalanx- forces transferred via distal border of hoof wall. Digital cushion- shock absorption and frog movement. Hoof sliding. Rotation and translation of DIP joint.

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23
Q

How does increased speed increase risk of injury?

A

Increased speed, decreased stance time. Force generated in less time, incr energetic cost. Incr peak limb force. Incr risk of injury

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24
Q

How are the phases of stance critical to injury?

A

1st impact- large accelerations, low forces, incr bruising 2nd impact- low acceleration, high forces, natural breaking Large vertical force- excessive dorsiflexion of fetlock Breakover/ propulsion- tensile strength

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25
Q

Which tendons are high strain and which are low strain?

A

SDFT+SL- high strain DDFT+DAL- low strain % length change w/ force

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26
Q

What adaptations to horses joints decrease the metabolic cost?

A

Reduction of phalanges and fusion of bones–> movement in saggital plane only. Interlocking configuration (ridges/ grooves) and collateral ligaments–> restriction of movement w/out muscular control, decrease in metabolic cost

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27
Q

How does a heel wedge affect loading of tendons?

A

Moves PZM towards heels thus reducing DIP momentt arm- unloads DDFT and NB

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28
Q

How does hoof trimming help improve strength?

A

Horn arranged in tubules- ideal to withstand high compressive forces. This diminishes w/ length. *collapsed/ underrun heels- tubules start bending when grown distal to the distal phalanx, impairment of natural hoof deformation and BF, application of carbon fibre patches benificial

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29
Q

What is laminitis?

A

Failure of attachment of the epidermal cells of the epidermal (insensitive) laminae to the underlying BM of the dermal (sensitive) laminae

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30
Q

What are some of the risk factors for laminitis?

A

Diseases characterised by sepsis and systemic inflamm Endocrine disorders- PPID, EMS Mechanical overload Access to pasture Metabolic disorders Retained placental membranes

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31
Q

What are some predisposing factors for pasture-associated laminitis?

A

Pony Season (spring/ summer) Gender (F) Incr age Obesity Insulin resistance

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32
Q

What are the 3 stages in the pathogenesis of laminitis?

A

Developmental (contact w/ trigger, lasts up to 72h) Acute laminitis Resolution or chronic laminitis

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33
Q

What is the role of the ECM in the laminae?

A

Responsible for maintenance of structural support, movement, growth, remodelling and healing, along w/ modulation of cytokines, inflamm, healing and cell migration

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34
Q

Why can laminar separation occur following and insult?

A

Failure of epithelial adhesion molecules (hemidesmosomes) which attach the epidermal cells to the BM

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35
Q

What types of insults can cause laminar separation?

A

Inflammatory and/or hypoxic cellular injury

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36
Q

What are two endocrinological disorders that may play a role in the predisposition to laminitis in certain horses?

A

Excess glucocorticoids- PPID Insulin resistance- EMS

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37
Q

What will exacerbate insulin resistance in horses?

A

Increased CHO consumption

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38
Q

What vascular events occur in the early stages of laminitis?

A

Digital venoconstriction and consequent laminar oedema

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39
Q

What are the aims when approaching a suspected case of laminitis?

A

Make a definitive dx Determine underlying cause Determine if likely to recover to expected level of soundness

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40
Q

How is a diagnosis of laminitis reached?

A

Clinical signs, +/- radiography and endocrine tests

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41
Q

Name the clinical signs of laminitis

A

-Lameness affecting 2/more limbs. -Characteristic chance -Bounding digital pulses -Incr hoof wall temp -Pain on hoof tester pressure at the region of the point of the frog -Palpable depression at the coronary band

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42
Q

What are some radiographic signs of laminitis?

A

-Pedal bone rotation -Founder distance -Angle between line of P3 and wall of hoof (should be parallel) -Decreased sole thickness

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43
Q

What endocrine tests may be appropriate for dx of laminitis?

A

PPID: CS, basal ACTH, Dex suppression (not autumn), TRH stim test EMS: hx, CS, demonstration of IR

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44
Q

What are three that can be done to medically treat laminitis?

A

Analgesia Vasodilation/ vasoconstriction Foot support- essential, incr bedding, frog/ sole support

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45
Q

What can be used for analgesia in laminitic horses?

A

NSAIDs (PBZ, flunixin, carprofen etc. IV/oral) Opiates (morphine, pethadine, fentanyl etc)

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46
Q

What is the main tx for PPID?

A

Pergolide

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47
Q

What is the main tx for EMS?

A

Weight loss, exercise, may/ may not use pharmacological agents

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48
Q

What is NSC and when does it increase/ decrease?

A

Energy for growth of plants. Incr when plant photosynthesising. Decr when plant growing. Aim is to minimise NSC content

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49
Q

What can be done to high quality hay to decrease NSC content?

A

Soak hay in water for at least 20 mins, not reliable however.

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50
Q

If a laminitic horse needs extra energy, what can be added to the diet to provide it?

A

Oil, unmollassed beet pulp

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51
Q

What are some mineral supplements that can be added to the diet to help with insulin levels?

A

Cinnamon Magnesium Chromiun

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52
Q

What are the indications for imaging of the equine foot?

A

Lameness is localised to the foot. Penetrating wounds. Prepurchase. Farriery management

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53
Q

What are the routine views for imaging of the equine foot?

A

Lateromedial Dorso-60’-proximal palmarodistal oblique (collimated for navicular bone/ distal phalanx) Dorso-45’-proximal palmarodistal oblique (collimated for navicular bone) Palmaro-45’-proximal palmarodistal oblique

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54
Q

How are XRay views named?

A

Point of entrance of XRay beam to point of exit

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55
Q

What variation occurs in normal radiographic anatomy of the collateral cartilages?

A

Variation in ossification. Separate centres of ossification may resemble fractures.

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56
Q

How is the dorso-60°-proximal palmarodistal oblique view of the equine foot taken?

A
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57
Q

How is the palmaro-45°-proximal palmarodistal
oblique taken?

A

Flexor view

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58
Q

What variations in normal radiographic anatomy of the equine foot can be misleading?

A
  • Collateral cartilages- variation in ossification, separate centres may resemble fractures
  • Variable shape of the extensor process
  • Wolfs law- bone responds to loading, e.g. attachement of collateral ligaments of DIP joint
  • Crena
  • W/ Pa45’PrPaDiO view- flexor cortex can appear falsely thick, medulla incr in opacity resembling sclerosis
59
Q

What is the step-by-step approach for radiographic appraisal of the equine foot?

A

Assess diagnostic quality. Identify a lesion. Describe the lesion by its Rontgen signs (opacity, size, margination, no, shape, location). Radiographic dx. Recommend further investigations

60
Q

What are the radiographic signs of laminitis in the equine foot?

A

Angle dorsal hoof wall and dorsal wall distal phalanx >15’- poor px

Founder distance >13mm indicates sinking

Dorsal hoof wall thickness >3cm in horses, 2cm in ponies indicator of chronic laminitis

Lucent line in dorsal hoof wall- separation of lamina

Horizontal lucent lines at coronet- sinking

Remodelling and fracture of solar margin- chronic

61
Q

What is the radiographic sign of osteoarthritis?

A

Osteophyte formation

62
Q

Why do entheseophytes form?

A

Aka spurs. Proximal border build-up. Attachment of collateral ligaments

63
Q

What are the radiographic changes of navicular disease?

A

Loss of corticomedullary junction. Lucency. Abnormal distal border synovial fossae

Pathognomonic sign- flexor cortex erosions (often mistaken for central cysts)

64
Q

What is a keratoma of the equine foot?

A

Abnormal horny tissue present at white line. Splitting and deviation of white line around abnormal horn. Loss of bone from distal phalanx. Well defined margins.

Aetiology- mechanical irritation, hoof abscess

65
Q

How does a pedal bone osteitis appear radiographically

A

Moth-eaten appearance.

66
Q

What are the layers of the hoof between the sole and the hoof wall?

A

Sole

White Line

Stratum Lamellum

Stratum Internum

Stratum Medium Hoof Wall

67
Q

What are the features identified on a physical exam of laminitis?

A

Local heat

Digital pulses

DIP joint effusion

Pastern oedema

68
Q

What is a nail prick vs nail bind?

A

Farriery-related problems:

Nail prick- nail driven through sensitive laminae

Nail bind- nail driven too close to sensitive laminae

69
Q

What is the treatment for septic pedal osteitis?

A

Curettage

Wound care

70
Q

What are hoof cracks and what is their aetiology?

A

Disruption of hoof wall parallel to horn tubules and lamellae. Can extend into sensitive laminae

Poor horn quality, thin hoof wall, abnormal hoof angles

71
Q

What are hoof wall avulsions?

A

Damage to coronary band. Permanently disturbed growth

72
Q

What is hoof capsule thrush?

A

Infection leading to necrotic processes in frog area. Usually limited to lateral and medial sulci of the frog

73
Q

What is canker?

A

Mixed bacterial infection in deeper tissue layers of the entire frog and heel leads to disintegration intertubular horn. Warm, humid environment. Cheesy white pus, pungent odour, tendency to bleed

74
Q

What is the recommended treatment diseases of the hoof capsule?

A

Debridement of all necrotic and diseased horn

Disinfect area

Sensitive lamina- protective bandage

Sulci- hardening solutions- formalin, alternatives

75
Q

What is quittor?

A

Infection of the lower leg characterised by inflammation of the collateral cartilage

76
Q

What are bipartite navicular bones?

A

A congenital anomal. Important ddx to fractures (usually lamer). Can result in chronic lameness and DIP joint OA

77
Q

What is navicular syndrome?

A

Non-specific syndrome causing palmar heel pain. Multiple structures involved- navicular bone/ bursa, DDFT, DIP joint, collateral ligaments DIP joint etc. Accoutns for 1/3 of chronic TL lameness. 6-12YO. Usually bilateral, insidiuous onset. Occasionally toe first gait. Hoof testers usually -ve. +ve response to PDNB (navicular bursa and DIP joint analgesia)

78
Q

What are the approaches to nerve block of the DIP joint?

A

Dorsal midline approach

Lateral/ medial to extensor tendon

Palmar/ Plantar approach

79
Q

How is the navicular bursa block performed?

A

Midline- navicular position horizontal approach

Midline- navicular position 30’ oblique approach

Lateral palmar/ plantar approach

80
Q

What conditions affect the distal phalanx?

A

Osseous cyst-like lesions- P3 near collateral ligament, verify significance using blocks. Tx variable- arthroscopy, drilling, midication DIP joint

Fractures- acute severe lameness, exercise, kicking out

81
Q

What are the 6 different types of fractures of the distal phalanx?

A

Type I: wing, non-articular

Type II: wing, articular

Type III: sagittal

Type IV: extensor process

Type V: comminuted

Type VI: solar margin

82
Q

What are the treatment options for a wing fracture of the distal phalanx and what complications can occur?

A

Bar shoe, foot/ hoof cast, lag screw.

Complications- OA DIP joint (type II), fibrous union

83
Q

What are the treatment options for a midsaggital fracture of the distal phalanx and what complications can occur?

A

Lag screw, bar shoe

Complications- OA DIP joint

84
Q

What are the treatment options for a small extensor process fracture of the distal phalanx?

A

Arthroscopy, arthrotomy

85
Q

What are the treatment options for a large extensor process fracture of the distal phalanx and what complications can occur?

A

Removal- arthrotomy, lag screw

Complications= OA DIP joint

86
Q

What are the treatment options for a comminuted fracture of the distal phalanx and what complications can occur?

A

Transfixation cast, euthanasia

Complications- OA DIP joint, laminitis

87
Q

What are the treatment options for a solar margin fracture of the distal phalanx?

A

Bar shoe?

88
Q

What is the recommended treatment for a DIP joint osteoarthritis?

A

Intraarticular mediaction: sodium hyaluronate, corticosteroids, (polysulphated GAGs), IL-1 R antagonist protein

Prolonged use of NSAIDs

Corrective farriery

89
Q

What is pedal osteitis?

A

Radiographic finding of demineralisation of the solar margin of the distal phalanx commonly associated w/ widening of vascular channels near solar margin. Repetitive concussion leads to chronic inflammation of the laminae–> bone resorption

90
Q

Name the different types of tendon injuries seen in the horses

A

Percutaneous- laceration, penetration

Subcutaneous- strain, displacement

91
Q

Name some causes of overstrain injury

A

Sudden over extension (DDFT)

Preceding tendon degeneration w/ superimposed sudden over-extension (SDFT, SL)

92
Q

How is a diagnosis made of a tendon injury?

A

Hx: usually preceding intense period of exercise and signs can be delayed

PE: lameness (can be temp or persistent for some tendon/ ligament injuries)

93
Q

When is metacarpophalangeal joint extension decreased?

A

Reduced weight-bearing (pain)

Fibrosed (stiff) tendon

94
Q

What injury is an elevated toe pathognomonic for?

A

DDFT rupture- we know this because inserts more distally than other support tendon

95
Q

When is MCP joint extension increased?

A

With severe SDFT or SL injuries

96
Q

What areas are most difficult to assess when palpating the limb?

A

Proximal SL in the HL

Pastern

97
Q

What is the most common tendon injury seen in horses and what are the clinical signs?

A

Superficial digital flexor tendinopathy

Initial lameness (variable), palmar metacarpal swelling w/ pain on palpation

Core lesion on US

98
Q

What are some clinical signs for proximal suspensory desmitis?

A

Conformation (esp HL)- straight hock and overextending MTP joint

Lameness- will often be lamer w/ the limb on the outside of the circle (cf for most injuries which are worse when affected leg is on inside as is taking the weight), pain on palpation

Proximal MC/ MT swelling

99
Q

What is seen on ulstrasonography with suspensory body and branch desmitis?

A

Focal/ generalised lesions on medial and lateral aspects of body/ branches

Enlargement

Periligamentar fibrosis

Bilateral involvement v common

100
Q

What is ususally associated with a suspensory body and branch demitis?

A

Concurrent bony abnormalities visisble on radiographs. Fracture of the distal part of splint bone can occur

101
Q

What are some clinical signs associated wtih desmitis of the accessory ligament of the DDFT?

A

Lateral swelling in the proximal metacarpal region dorsal to SDFT

Lameness variable (often absent)

102
Q

What is the least common tendon/ ligament injury seen in horses?

A

DDFT tendinopathy

103
Q

What are the most common sites of injury in the DDFT?

A

Usually within the digital sheath or navicular bursa, never in the metacarpal region (tends to only get injured within a synovial cavity)

104
Q

Where are intra-thecal DDF tendon tears usually seen?

A

Lateral border. Forelimbs

105
Q

What is the manica flexoria and where does it usually tear?

A

Just proximal to the metacarpophalangeal joint, the SDFT forms a ring-like structure which wraps around the DDFT. This structure is known as the manica flexoria. Usually tears in the HL

106
Q

What are the ddx for tenosynovitis of the digital sheath?

A

Idiopathic distension

Non-septic inflamm- 1ry, most 2ry

Penetrating injuries- sepsis

107
Q

What clinical signs are seen with annular ligament syndrome?

A

Mild to mod lameness minimally response to rest w/ occasionally irregular gliding of tendons

Distended digital sheath

Notch at level of PAL

108
Q

What thickness of the annular ligament on ultrasound is indicative of ALS?

A

>2mm thickeness

109
Q

What are some general principles for tx of tendonitis?

A

V few evidence based tx choices available

Rational tx based on tendon pathology and phases of tendon healing

Never returns to normal- remains fibrotic

110
Q

What clinical signs occur during the acute inflammatory phase of tendon injury?

A

Lameness

Pain on palpation

Heat

Swelling

111
Q

What pathology occurs during the acute inflammatory phase of tendon injury?

A

Haemorrhage

Inflammation (neutrophils, macrophages+ monocytes, incr BF, oedema, proteolytic enzymes)

112
Q

What is the rational treatment option for the acute inflamm phase of treatement?

A

Minimise inflammation

113
Q

What can be done to treat an acute tendon injury?

A

Physical therapy (ice, compression, MCP joint support, rest)

Medication- short acting steroids (only within 24/48hr, beware of laminitis and interference w/ healing), NSAIDs (analgesia)

114
Q

What clinical signs occur during the subacute/ reparative phase of tendon injury?

A

Reduction or absence of lameness. Resolution of signs of inflamm. Still palpably enlarged and soft. Signs of re-injury if exercised too early

115
Q

What pathology is seen during the subacute/ reparative phase of tendon injury?

A

Angiogenesis

Fibroplasia (lots of fibroblasts, formation of coll III, small collagen fibrils formed)

116
Q

What is the rational treatment for the subacute/reparative phase of tendon injury?

A

Promote fibroplasia and optimize organization of the scar.

117
Q

What can be done to treat a tendon injury during the subacute phase?

A

Early and progressive mobilization (trotting after 3m), and regular ultrasonographic monitoring every 2-3 months.

118
Q

What can be used to attempt to induce regeneration rather than repair in a tendon injury?

A
  • Scaffolds (ACell; lyophilized pig bladder submucosa)
  • Growth factors (platelet rich plasma)
  • Cell therapy (mesenchymal stem cells)
119
Q

What clinical signs occur during the chronic remodelling phase of tendon injury?

A

Tendon size decreases

Tendon less pliable

Reduced fetlock extension

(Contractures)

120
Q

What pathology is seen during the chronic remodelling phase of tendon injury?

A

Collagen transformation from III to I

Cross linking occurs

Thicker collagen fibrils form

121
Q

What treatment is done during the chronic phase of a tendon injury?

A

Controlled ascending exercise

Continued ultrasonographic monitoring

Surgery if needed; desmotomy of the accessory ligament of the superficial digital flexor tendon

122
Q

What surgical options are available for proximal suspensory desmitis?

A

Fasciotomy and neurectomy; used in hindlimb PSD which has failed to improve after first 2 treatments with extracorporeal shock wave therapy.

123
Q

What surgical options are available for intra-thecal tendon/ ligament lesions?

A

Tenoscopy

Arthroscopy

124
Q

What are the causes of flexural limb deformities and what are the treatment principles?

A

Congenital- uterine malpositioning, CDET rupture

Acquired- part of developmental orthopaedic dz, pain (OCD, physitis)

Treatment principles- conservative (exercise, shoeing, splints), surgical release

125
Q

What is a type I DIP joint flexural deformity and how is it treated?

A

Dorsal hoof wall less than vertical. Exercise and physiotherapy, toe extension shoe, sx (desmotomy of ALDDFT)

126
Q

What is a type II DIP joint flexural deformity and how is it treated?

A

Dorsal hoof wall past vertical. Usually sx neccessary. Desmotomy of ALDDFT

127
Q

What can a MCP joint flexural deformity occur 2ry to and what is the recommended tx?

A

Can occur 2ry to chronic SDFT tendinopathy in adults.

Tx- exercise/ physio, toe extension and raised heel shoe, splints/ braces. Sx- desmotomy of the ALDDFT/ ALSDFT, SDFT tenotomy

128
Q

What conditions can be seen in fast growing, high performance horses?

A

Osteochondritis dessicans

Subchondral bone cysts

129
Q

Name some corticosteroids that used for intra-articular use in horses?

A

Betamethasone

Triamcinolone acetonide

Flumethasone

Isoflupredone acetate

Methylprednisolone acetate

130
Q

What is the mechanism of polysulphated GAGs in the tx of DJD?

A

They inhibit MMP, stimulates HA production and stimulates matrix synthesis. 500mg IM q4d for 28d

131
Q

What is the mechanism of pentosan polysulphate (GAG) in tx of DJD?

A

Stimulates cartilage matrix synthesis, stimulates HA synthesis, MMP inhibitions, inhibits inflamm mediators, mobilizes thrombi and fibrin in synovium, mobilizes lipids and cholesterol in vessels, inhibits platelet aggregation and clotting, increases plasma lipase levels.

132
Q

What is the anti-inflammatory function of sodium hyaluronate in tx of DJD?

A

Steric hindrance

Chemotactic response

Commonly used in combo with corticosteroids

133
Q

What is the recommended tx for septic arthritis?

A

Acute infection= emergency. Eliminate organisms from joint, eliminate enzymes and mediators that cause cartilage destruction. Abx/ lavage and artrotomy. Intra articular abx, IV abx (penicillin and gentamicin). Resample joint fluid q48hr. Oral abx

134
Q

What are the layers used in external coaptation of a fracture?

A

Wound dressing (non adherent) covered with orthopaedic padding (as w/ SAs). Apply padding (large rectangle), conform to limb with gauze. Apply cohesive bandaging tape. Seal top and bottom w/ adhesive bandage and white tape

135
Q

When is transixation casting indicated?

A

Repaired or conservatively treated distal limb fracture that is unstable under axial loading. Fetlock breakdown injuries

136
Q

What chemical restraint can be used to approach the fracture patient?

A

a2 agonist: xylazine IV, detomidine IV, romifidine IV

a2 agonist/ narcotic combo: detomidine IV, butorphanol IV (never use narcotic alone- excitement)

Avoid phenothiazine tranquilizers e.g. ACP as hypotensive effects in presence of circulating catecholamines

137
Q

How is a fracture classified?

A

Incomplete/ complete

Simple/ comminuted

Closed/ open

Articular/ non-articular

Tendon/ ligament

Status surrounding soft tissues

138
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the coronary band to distal metacarpus division of the fore- and hindlimb?

A

Suspensory apparatus and flexor tendons cause bending focus over fracture site- need to counteract these and achieve axial alignment of dorsal cortices.

Padded bandage/ cast bandage w/ dorsal splint to immobilise in flexion. Some clinicians argue that flexion is counterproductive and would recommend rigid external coaptation w/ limb weight bearing.

139
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the distal metacarpus to distal radius division of the forelimb cf hindlimb?

A

Use bones proximal and distal to attach splints bridging fracture site. RJ bandage w/ rigid splints up to elbow- lateral and caudal. Splints difficult to apply due to angulation of tarsus- RJB up to tuber calcaenus (lateral and plantar), usually less voluminous than TL

140
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the distal radius to elbow division of the forelimb?

A

Digital extensors and flexors act as abductors of the limb- need to prevent this and prevent soft tissue damage on medial aspect of limb.

RJB w/ extended lateral splint

141
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the delbow to scapula division of the forelimb?

A

Elbow can’t be fixed for weight bearing. Humerus, ulna and scapula well protected by soft tissues- don’t require direct protection

Splint carpus in extended position to allow for weight-bearing and balance

142
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the proximal metatarsus to stifle division of the hindlimb?

A

Overriding at fracture site instead of hock flexion. Stifle joint can’t be immobilised. Muscles laterally over tibia act as abductors

RJB w/ extended lateral splint up to coxofemoral joint- angulation at tarsus and stifle prevents application of cranial or caudal splint

143
Q

What are the goals of immobilisation and the technique used for external coaptation of a fracture in the stifle to coxofermoral division of the pelvic limb?

A

Remains controllable due to more distal muscl insertions. Impossible to stabalise by external means. Non-weight-bearing lameness. Poor px

144
Q

How do the functional divisions of the equine limbs differ in their external coaptation technique for fracture repair?

A

Locomotor (4 decks)

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