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Equine > Orthopaedic disease > Flashcards

Orthopaedic disease Flashcards

1
Q

what is physitis
and where does it commonly occur

A

inflammation of the physis (growth plate) at the end of long bones

often around carpus and fetlock (pain, heat, lameness)

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2
Q

when do the growth phases end for
- distal metacaprus
- distal radius
- distal tibia

A
  • distal metacaprus = 4 months
  • distal radius = 18-20 months
  • distal tibia = 18-20 months

limited time to fix angular limb deformities

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3
Q

causes of physitis (4)

A

sudden increase in feed intake (or energy)
abrupt increase in exercise
direct trauma to the physics
yearling physitis

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4
Q

dx and tx of physitis

A

Radiographs

Tx: Exercise restriction
Pain relief
correct underlying cause (like angular limb deformities)

Potential sepsis!!

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5
Q

what are the salter Harris grades for articular fractures

A
  • S = straight across growth plate
  • A = above and comes down into growth plate. Most common
  • L = lower and comes up into growth plate
  • TE = Through everything (inc epiphysis)
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6
Q

what foals are at risk of incomplete ossification

A

dysmature or preamture foals

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7
Q

what bones do you see incomplete ossification in

A

carpus and tarsus

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8
Q

what are the two main angular limb deformaties

A

Varus = ()
Valgus = )(
can have both )) = windswept foal

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9
Q

causes of angular limb deformities

A
  • incomplete ossification (dysmature or premature foal, placentitis, colic during gestation, or heavy parasite burden, abnormal uterine positioning),
  • or peri-articular laxity

Can also be acquired

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10
Q

4 steps to evaluate angular limb deformities

A

Static examination:
- Stand perpendicular to the frontal plane of the limb

Manipulate:
- for peri-articular laxity

Dynamic:
- Assess how foal uses limb

radiograph
- Both limbs, orthogonal views
- DP view and LM
- Need long plates to include middle radius and middle metacarpus

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11
Q

conservative tx for angular limb deformities

A

If entire limb facing one way:
- Box rest and controlled exercise (hand walking)
- Box rest only if incomplete ossification
- Can trim feet (Carpal valgus = trim lateral hoof
Fetlock varus = trim medial hoof wall)
- Glue on shoes (Carpal valgus = medial shoe, fetlock varus = lateral shoe)

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12
Q

what joints do you usually see congenital hyper-extension in

A

fetlock and PIP, DIP joints

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13
Q

signs of congenital hyperextension

A

Toe elevated
fetlock sunken

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14
Q

signs of congenital hyperflexion

A
  • May prevent foal from standing
  • Occurs at DIP, PIP, fetlock, carpal or tarsal joints.
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15
Q

unique treatment for congenital hyperflexion

A
  • Oxytet (3g) in 500ml saline slow IV within a few days of birth.
    → inhibits tractional structuring of collagen fibrils → tendons & ligaments more susceptible to elongation during normal weight bearing.
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16
Q

what drug should be given alongside NSAIDs in neonates

A

Omeprazole as a gastroprotectant

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17
Q

extensions for congenital hyper flexion Vs extension

A

Flexion = toe extensions and heel reduction
Extension = heel extensions

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18
Q

two forms of acquired hyperflexion

A

coffin (DDFT) and fetlock (DDFT, SDFT or suspensory)

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19
Q

age and stage of coffin joint contracture

A
  • 1-4 months old
  • Metacarpal / tarsal bones growing rapidly = Functional shortening of DDFT
  • Stage 1: dorsal hoof wall is not past vertical - good prognosis
  • Stage 2: dorsal hoof wall is past vertical – guarded prognosis
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20
Q

age and stage of fetlock joint contracture

A
  • 10-18 months old
  • Radius / tibia growing rapidly = Functional shortening of SDFT and suspensory ligament.
  • Stage 1: Fetlock is behind vertical
  • Stage 2: Fetlock in front of vertical, but can move behind vertical during weight bearing.
  • Stage 3: Fetlock in front of vertical always.
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21
Q

general treatment principles for acquired hyper-flexion (Surgical and medical)

A

Medical management:
- Toe extension (and heel reduction to stretch DDFT in coffin)
- NSAIDs (and omeprazole).
- Reduce growth rate by reducing nutrition
- Suitable for stage 1 only

surgery:
- in combo with medical
- desmotomy
= coffin = ddft
= fetlock = identify under GA culprit and snip

22
Q

signs of juvenile osteochondritis

A

often not lame
varying degrees of joint effusion

23
Q

causes of JOCC

A

Multifactorial
Focal failure of endochondral ossification (Epiphyseal or metaphyseal growth cartilage)
Polygenetic heritable disease

24
Q

most common sites of OCD

A

FL: shoulder and fetlock
HL; stifle, hock and fetlock

25
Q

common site for OCD on the fetlock

A

sagittal ridge of the distal metacarpus

On DP: middle bit, bottom of bone, along mi-point of the sesamoids

26
Q

what two other conditions lead to fragmentation on the fetlock? and where?

A

o Plantar/palmar P1: Avulsion fragmentation (due to sesamoidan ligaments)
o Dorsal proximal P1: (racehorse hyperextension)

27
Q

views to take for fetlock OCD

A

Take: DP, LM (+/- Flex lateral), DMPLO, DLPMO

28
Q

sites of OCD lesions on the hock/tarsus

A
  • 1 = distal intermediate ridge of the tibia (DM PL oblique)
  • 2 = Lateral trochlea ridge of the talus (DM PL oblique)
  • 3 = medial malleolus of the tibia (DP)
29
Q

views to take for tarsus OCD

A
  • Take: DP, LM, DMPLO, DLPMO
30
Q

sites of different stifle joint OCD lesions

A

Femoral patella joint = Lateral trochlea ridge (lateral medial)

Medial femoral tibial joint = on medial femoral condyle (CC view)

31
Q

views to take for all stifle joints

A
  • Take: LM, cranio-caudal, caudolateral-craniomedial oblique
    o Cranio-caudal highlights femoral condyles
    o Oblique highlights femoral condyles and lateral trochlea ridges
32
Q

treatment for fetlock, then tarsus and stifle lesions

A

Fetlock
§ OCD: Remove fragment
§ Dorsal P1: Remove fragment
§ Palmar/plantar P1: Evidence says only remove if high speed

tarsus / stifle
§ Can leave fragments but removal reduces risk of development of OA in the future

33
Q

at what age can stifle and tarsal lesions dissapear

A

femoral patella = 8 months
tarsocrural = 4 months

34
Q

what two conditions can lead to subchondral cysts developing?

A
  • OC: failure of blood supply to growth cartilage = ischemic chondronecrosis of bone
  • OA: Weight bearing + trauma to articular cartilage = cyst

Sites: Medial femoral condyle, phalanges, metaC/T and radius common

35
Q

low motion v high motion joints

A

o High: DIP, fetlock, tarsocrural, stifle. Can be significantly affected by mild disease
o Low: PIP, distal tarsal joints. Can tolerate significant changes, but unpredictable.

36
Q

threshold for improvement after a JOINT block that indicates success

A

50%

37
Q

most common area for osteoarthritis in the hock

A

distal tarsal joint

38
Q

views to take when investigating DIP OA

A
  • Dorsal palmar
  • Lateral medial
  • Dorsal proximal palmar distal 60 oblique - pedal
  • Dorsal proximal palmar distal 60 oblique - nav
  • Palmar proximal palmar distal 45 oblique
39
Q

views to take when investigating tarsal OA

A
  • Dorsal plantar
  • Lateral medial
  • Dorsal lateral plantar medial oblique
  • Plantar lateral Dorsal medial oblique
40
Q

common radiographic signs of hock OA

A

bone remodelling (third and central tarsal bones)
lysis and sclerosis (Distal inter tarsal joint)
loss of joint space

41
Q

high motion treatment options for OA

A
  • NSAIDs (bute or flunixin (or Suxibuzone))
  • Intra-articular steroids, DMSO, hyaluronic acid, PRP, mesenchymal cells
  • Controlled exercise
  • Weight loss diet
42
Q

low motion treatment options for OA

A
  • No radiographic changes = Steroids or other IA meds to calm down inflammation
  • If not, arthrodesis = minimal effect on performance.
  • Method: Pain relief and work to naturally arthrodesis, or Surgical arthrodesis
43
Q

methods of arthrodesis

A
  • Intra-articular steroids (lasts 1-3 months so need repeated injections)
  • Systemic NSAIDs (long term use and toxicity)
  • Neurectomy (disease continues, consequences of loss of sensation, nerve often regrows)
  • Chemical arthrodesis: Distal tarsal joints only. (Proximal joint communicates with high motion tarso-crural). Success with MIA or ethanol1,2

Surgical arthrodesis
- Tarsal joints – drill cartilage. Requires up to 12 months
- PIP and carpometaphalanegal joint – fixation with plate and screws

Fetlock can be.. But is high motion joint so effects horses function (salvage procedure)

44
Q

what is associated with an increased risk of SAPO in foals

A

Omphalophlebitis

45
Q

clinical signs of septic arthritis in foals

A
  • lameness, effusion of the fetlock joint, reluctance to stand, rectal temperature 37.6oC
46
Q

joint fluid signs of sepsis

A

turbid to opaque
high WBC
high protein (over 25)

47
Q

what is SAPO

A

SAPO = septic arthritis, physitis + osteomyelitis
* Predominantly E.coli, Actinobacillus, Klebsiella, Staph, Strep, Rhodoccus equi.
* Inflammation in 1 or more joints as a result of bacterial infection.
* Haematogenous or wound.
* Common in neonates secondary to sepsis.

48
Q

4 forms of SAPO

A
  • 4 different forms:
    Type S = via haematogenous inoculation of the synovial membrane,
    Type E = in epiphysis,
    Type P= in physis,
    Type T = trauma with direct external incoulation.

Bacteria normally enter via lungs, GI or umbilicul.

49
Q

tx of SAPO

A

Antibiotics + surgical removal of infectious and inflammatory material
NSAIDs (+ omeprazole)

50
Q

treatment example for septic physitis

A
  • Penicillin + gentamycin IV
    • Flunixin IV
      Clinical reassessment of lameness after 5 days of therapy.

Equine (11 decks)

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