Fracture Healing and Avascular Necrosis Flashcards

1
Q

Describe the blood supply to the bone.

A

Endosteal (inner 2/3)

Periosteal (outer 1/3)

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2
Q

What is Young’s modulus?

What is it like in:

a) Cortical bone?
b) Trabecular bone?

A

Measure of a bone’s resistance to torsion/bending

In cortical bone: high
In trabecular bone: low

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3
Q

What are the 2 types of bone healing?

A

Indirect/secondary - physiological

Direct/primary/artificial - via medical intervention

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4
Q

What are the 3 main stages in secondary/indirect fracture healing?

A

Inflammation
Repair
Remodelling

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5
Q

Describe the process of inflammation during secondary/indirect fracture healing. (3)

A
  1. Haematoma formation (6-8 hours after injury)
    a. Blood from broken vessels in the bone forms a clot
  2. Swelling occurs at fracture site
  3. Inflammation occurs around dead bone cells at the fracture site
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6
Q

Describe the processes of repair in secondary/indirect fracture healing. (5)

A
  1. Fibrocartilage (soft) callous formation
    a. New capillaries grow and organise the haematoma into granulation tissue (pro-callous)
    b. Fibroblasts and osteoblasts invade the pro-callus
    c. This leads to collagen production (soft callous)
    d. Chondrocytes produce fibrocartilage
  2. Bony (hard) callous formation
    a. Osteoblasts produce woven bone
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7
Q

Describe the process of remodelling during secondary/indirect fracture healing. (1)

A
  1. Osteoclasts remodel woven bone into compact and trabecular bone
    a. This does NOT leave a scar
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8
Q

How long does each stage of secondary/indirect fracture healing take?

A

Inflammation: 6-8 hours

Soft callous: 3 weeks

Hard callous: 3-4 months

Remodelling: years

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9
Q

Describe the process of direct/primary/artificial bone healing. (2)

What is the main difference to secondary bone healing?

A
  1. Bones are realigned/compressed by medical intervention
  2. Direct formation of bone occurs via osteoclast resorption and osteoblast formation
    a. This forms cutting cones across the fracture sites
    b. Therefore new bone is laid down directly across the fracture

MAIN DIFFERENCE: no callous formation

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10
Q

List 8 factors which might inhibit normal fracture healing.

A

Patient factors, e.g.

  • Malnutrition
  • Peripheral vascular disease
  • Hypothyroidism
  • Smoking
  • Alcohol

Drugs, e.g.

  • NSAIDs
  • Steroids
  • Bisphosphonates
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11
Q

Define avascular necrosis.

A

Bone infarction, i.e. tissue death due to loss of blood supply to the bone

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12
Q

List 4 causes of avascular necrosis.

A
Sickle cell anaemia (NOTE: rigid RBCs block blood vessels, preventing blood supply)
Vascular damage (e.g. due to fractures)
Increased intraosseous pressure
Mechanical stress
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13
Q

List 4 types of fracture which commonly have compromised blood supply.

A

Proximal pole of scaphoid
Talar neck fractures
Intracapsular hip fractures
Surgical neck of humerus fractures

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14
Q

Describe the clinical features of avascular necrosis. (4)

Describe specific features found in:

a) Surgical neck of femur fractures (4)
b) Lunate fracture (3)

A

Asymptomatic
Rest pain
Night pain
Bilateral pain

SURGICAL NECK OF FEMUR:
Groin pain
Limp
Tenderness around joint
Restricted motion (esp. internal rotation, abduction)

LUNATE FRACTURE:
Weak grip strength
Wrist stiffness
Pain

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15
Q

What is Kienbock’s disease?

A

Avascular necrosis resulting from a fracture of the lunate bone (wrist)

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16
Q

List the 3 main complications of AVN.

A

Subchondral erosion
Joint surface collapse
End stage arthritis

17
Q

Describe the pathophysiology of avascular necrosis. (5)

A
  1. Bone marrow lesions formed, involving:
    a. Oedema
    b. Haemorrhage
    c. Fibrilloreticulosis
    d. Hypocellularity
  2. Necrosis of medullary bone forms empty lacunae
    a. Surrounding adipocytes undergo necrosis and release fatty acids
    b. FAs bind to calcium to form insoluble calcium salts
  3. Fracture healing occurs via creeping substitution
  4. If creeping substitution not fast enough, there are too many empty lacunae
    a. Structural weakness
    b. Bone collapse
  5. This causes osteoarthritis
    a. Subchondral bone collapse forms incongruent joint surfaces
    b. This causes osteoarthritis
18
Q

List 4 major risk factors for avascular necrosis.

A

History of trauma (esp. dislocation)
Steroid use/Cushing’s syndrome
Alcohol abuse
Sickle cell anaemia/haemoglobinopathies

19
Q

Which 2 investigations would you do for AVN?

A

X-ray

MRI

20
Q

What features of AVN can be seen on an x-ray? (6)

A
No change
Mild density change
Sclerosis
Cysts
Crescent sign
Osteoarthritis signs
21
Q

What features of AVN can be seen on MRI? (2)

A

Oedema in bone

Inflammation

22
Q

How would you treat AVN? (4)

Consider how treatment differs before/after joint collapse.

A

Reduce risk of AVN, e.g.
-Patient education

Before joint collapse:

  • Reperfusion
  • Core decompression (with/without bone graft)

After joint collapse:
-Total hip arthroplasty