Lecture 1 - finished Flashcards

1
Q

What is the healing timeline for fractures

A

Haematoma formation - first 2-3 days
Acute inflammation - first 3-5 days
Granulation tissue/ procallus formation - 3-7 days post fracture
Fibrocartilagenous callus formation - starts 1 week post fracture and lasts up to 3 weeks
Bony callus formation - starts 3-4 weeks post fracture and finishes about 2-3 months later
Remodelling - starts during bony callus formation and continues for several months

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2
Q

Fracture definition

A

A break in the continuity of bone

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3
Q

Clinical manifestations of OM in adults

A

Insidious onset of:

  • vague ssx
  • fever
  • malaise
  • anorexia
  • weight loss

Recent Hx of:

  • Infection
  • Instrumentation
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4
Q

Stages of fracture healing:

A

Stage 1: Fracture occurs

Stage 2: Haemorrhage and haematoma formation
- extravasated blood clots to form a haemotoma
- inflammation is initiated
- Activation of local inflammatory cells and migration of these cells into the region
- Activation and proliferation of local connective tissue cells
= Osteoblasts, osteogenic cells, fibroblasts, chondroblasts

Stage 3: Procallus formation/ organisation of the haematoma
- Haematoma is replaced by granulation tissue
- In this stage:
= Phagocytes remove debris
= Osteoblasts make woven bone (limited because of slow neovascularisation rate)
= Fibroblasts make collagen
= Chondroblasts make cartilage
= Blood vessels grow into the region

Stage 4: Fibrocartilagenous callus

  • All cells within the procallus makes massive amounts of cartilage and collagen
  • Woven bone is formed but still limited
  • As the cartilage and collagen amounts increase the granulation tissue gives way to fibrocartilagenous tissue.

Stage 5: Bony Callus formation
- In this stage we see:
= increased neovascularisation
= increasing mineralisation of osteiods
= destruction of fibrocartilagenous tissue by osteoclasts
= increased synthesis of woven bone
- This forms a bony callus which reunites the ends of fracture.

Stage 6: Remodelling

  • In this stage osteoclastic activity is greater than osteoblastic activity
  • Woven bone is destroyed and replaced with lamellar bone (which is laid down in concentric layers to form osteons)
  • Internal and external calluses are reabsorbed.
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5
Q

Diagnosis of osteomyelitis

A
Hx and clinical exam
Biopsy: needle aspiration
Blood tests: 
- cultures (+ve in 50% of cases)
- Increased WBC, CRP and ESR 

Imaging:

  • Radiography (bone infection not evident for 14-21 days)
  • MRI (good for early detection)
  • Radionuclide bone scanning
  • CT
  • US
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6
Q

Complications of #

A
Delayed union
Non union
Pseudarthrosis
Malunion
Bone necrosis
Compartment syndrome
Fat embolism
Infection
Shock
Local soft tissue injury
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7
Q

Local causes of delayed healing time

A
Malalignment
Excessive movement
Comminution
Bone disease
Severe soft tissue injury
Infection
Ischemia
Soft tissue interposition
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8
Q

What is the definition of a pathological fracture?

A

When a small/moderate force acts on a weakened of diseased bone causing a fracture

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9
Q

Clinical manifestation of vertebral OM

A

Back pain:

  • Intermittent or constant
  • worse with motion
  • throbbing at rest
  • -/+ radicular distribution

Spinal tenderness and rigidity
Hip contracture secondary to psoas irritation

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10
Q

Why is fracture classification important?

A
So we can assess: 
Occurrence (how it happened)
Seriousness
Type of treatment required
Prognosis
Complications
Stability of fracture
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11
Q

Osteomyelitis definition

A

Inflammation of bone caused by bacteria

occasionally caused by mycobacteria or fungi

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12
Q

Pathogenesis of osteomyelitis in children

A

Transient bacteremia

Bacteria reach the bone

Inflammation of bone
- inflammation spreads through haversian canals and causes compression of adjacent blood vessels.

Bone necrosis and abscess formation

Sequestrum
- dead bone separates from living bone

Reactive bone growth:

  • inflammatory exudate may extend to the surface of the cortical bone; abscesses and oedema form and cause elevation of the periosteum.
  • periosteal elevation disrupts the blood supply to the bone in that area and deprives underlying bone of blood supply
  • lifting of the periosteum also stimulates intense osteoblastic activity which results in the formation of new bone (involucrum) which may surround the affected bone.

Sinus formation:

  • pus and necrotic tissue from the infection focus may drain towards the surface of the skin.
  • superficial drainage site is called the cloaca.
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13
Q

Local ssx of #

A
  • Deformity
  • Oedema
  • Pallor
  • Bruising/erythema
  • Loss of function
  • Palpation will reveal - pulselessness, tenderness, paresthesia
  • Movement will reveal - crepitation, muscle spasm, abnormal movement
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14
Q

OM on plain film x-ray

A

First manifestation:
- soft tissue oedema 3-5 days post infection
Bony changes:
- initial periosteal elevation
- subperiosteal bone formation (involucrum)
- cortical and medullary radiolucencies as bone is destroyed

(** remember that bone loss has to be 40-50% for it to be evident on x-rays)

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15
Q

Causes of Physiological Fractures

A

Fatigue
Accident
Unusually strong muscle contractions
Prolonged/repetitive physical stress

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16
Q

Signs of fat embolism

A
Hypoemia
Tachypnoea
Fever of unknown origin
Chest pain
Altered mental status
Possibly petechiae
17
Q

Classification types for fracture

A

According to aetiology

  • physiological
  • pathological

According to the site of force on the bone

  • direct
  • indirect
According to visual characteristics
- spiral
- transverse
- oblique
- chip
etc
According to the extent of the fracture
- greenstick
- comminuted (many pieces)
- complete (2 pieces)
etc

According to whether the overlying skins is broken

  • simple
  • compound (broken overlying skin)

According to joint involvement

  • intracapsular
  • extracapsular

Common fractures:
Colles - distal radius
Potts - eversions sprain causing avulsion of med mal and fracture of lat mal

18
Q

Define cloaca:

A

Superficial drainage site for the focus of infection in the underlying bone in OM

19
Q

Systemic causes of delayed healing time

A
Mineral deficiency
Vitamin deficiency
Comminution
Systemic infections
Bone disease
Ischemia (atherosclerosis)
Endocrine disease
Medications
Poor general health
Advanced age
20
Q

Clinical manifestations of OM in children

A

Sudden onset of high fever, chills and nausea
Progressively increasing local pain
Local muscular spasm
Local oedema and warmth of the soft tissues

21
Q

General ssx of #

A

Shock
Ssx secondary to other organs damaged eg viscera, CNS
Ssx due to underlying pathology

22
Q

6 signs of compartment syndrome

A
Pain
Pulselessness
Perishingly cold
Paraesthesia
Paralysis
Pallor
(Pressure increase)
23
Q

What are the differences in bone usually affected by OM between children and adults?

A

Adults: usually spine, pelvis or small bones
Children: usually the metaphysis of long bones

24
Q

Fracture epidemiology

A
Young people - 15-24
- tibia
- clavicle
- lower humerus
Usually secondary to trauma
Old people - 65+
- Upper femur
- upper humerus
- vertebrae
- pelvis 
Usually secondary to osteoporisis
25
What affects bone healing times
Age Type of # Bone #'d Health of patient
26
What is the most common scenario for osteomyelitis?
Haematogenous spread of staphylcoccus aureus from an unknown primary site
27
Pathogenesis of osteomyelitis in adults
Transient bacteremia Bacteria reach the bone Inflammation of bone - inflammation spreads through haversian canals and causes compression of adjacent blood vessels. Bone necrosis and abscess formation Sequestrum - dead bone separates from living bone
28
What are the main forms of spread of bacteria into bone?
Contiguous - dental - cutaneous - sinus - aural Traumatic Haematogenous
29
Causes of Pathological fractures
Focal bone disease Metabolic disorders Disuse
30
Do adults get the reactive bone growth and sinus formation stages of OM?
No, because the periosteum is firmly attached to the bone cortex in adulthood and resists displacement
31
What is the definition of a physiological fracture?
When a strong external force acting on a normal bone exceeds the mechanical strength of the bone