Pathological fractures profoma Flashcards

1
Q

Define fracture

A

loss of continuity of the cortex of a bone.

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2
Q

Define pathological fracture

A

a fracture through bone weakened by a pre-existing pathological process.

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3
Q

Epidemiology of pathological fractures

A

Occurs in 8% to 30% of patients w/ bone metastases

80% occur in breast (50%), prostate, kidney, lung, or thyroid cancer.

Proximal long bones are more commonly involved than distal bones.
- 50% of pathologic fractures occur in femur
- 15% occur in humerus

Femoral neck & head - most common location for pathological fracture due to tendency for metastases to involve proximal bones & because of the stress of weight placed on this part of the femur.

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4
Q

Aetiology (causes) of pathological fractures

A
  • Bone tumours- benign or malignant.
  • Paget’s disease of bone
  • Lymphoma or multiple myeloma (MM can cause lytic lesions & osteoporosis).
  • Osteoporosis
  • Osteomalacia or rickets
  • Hyperparathyroidism
  • Hyperthyroidism
  • Rheumatoid Arthritis
  • Osteomyelitis
  • Osteogenesis imperfecta

NOTE: Too much thyroxine speeds up the rate of bone resorbtion, leading to osteoporosis.

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5
Q

Pathophysiology of pathological fractures

A

Fractures occur in patients w/ decreased bone strength & those who experience an injury.
- Factors that determine bone strength= age, bone mass, bone quality.

Tumour= uncontrollable cell division
- if it remains stationery= benign
- if it invades other tissues & metastasizes= malignant

Primary malignancies arise from bone cells, secondary malignancies develop elsewhere e.g. breast, prostate, thyroid and kidneys.

Bone are made from:
- Osteoblasts → build new bone
- Osteoclasts → breakdown bone (resorption)
- Mesenchymal stem cells + neuroectodermal cells which can differentiate into other cell types

Proto-oncogenes stimulate normal cell growth
- These can mutate & become oncogenes which overstimulate cell growth.

Tumour suppressor genes promote apoptosis
- mutated tumour suppressor genes = cause growth of tumours.

E.g. of bone tumours:
- osteochondroma
- giant cell tumour
- osteoblastoma
- osteoid sarcoma

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6
Q

Presentation of pathological fractures

A

Deformity- angulation or shortness. e.g. Neck of femur fractures are shortened, externally rotated & abducted.

Affected limb will be swollen & bruised

Significant tenderness to palpation.

Mild or severe pain near affected joint

Numbness & tingling

Skin - open or closed fractured.

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7
Q

Investigation for pathological fractures

A
  1. Neurovascular examination
  2. Blood tests:
    - Serum calcium
    - PTH
    - ALP
    - Vitamin D
    - Myeloma screen
    - Thyroxine screen
    - Phosphate
    - FBC
  3. Evaluation of possible primary sites - breast, prostate, lung, thyroid, kidney.
  4. X-ray - taken in 2 planes (anteroposterior (AP) & lateral), 90° degrees to each other, of injured bones. Surrounding bones should also be examined- above & below
  5. N-telopeptide & C-telopeptide-
    markers of bone collagen breakdown measured in urine & serum
    - confirm increased destruction caused by bone metastasis & measure the overall extent of bone involvement.
  6. Biopsy- confirm diagnosis in suspected primary malignant tumour - for patients over 40 w/ lesions of unknown cause. - However, can cause seeding of cancer cells.
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8
Q

Initial management of pathological fractures

A
  • Analgesia
  • Control any external bleeding by direct pressure.
  • For open fractures, cover wounds w/ sterile dressings & give IV antibiotics
  • Immobilise the fractured bone - plaster, splint, brace, sling.
  • Arrange imaging & further investigations.
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9
Q

Definitive management for pathological fractures

A
  1. Reduction of any deformities (displacement, angulation, rotation)
    - Closed reduction- performed by manipulating the fracture into position - can be done under sedation or a general anaesthetic.
    - Open reduction - involves surgical procedure to open fracture site & reduce the bones accurately - usually accompanied by operative stabilisation.
    - Intra-articular fractures are treated w/ open reduction so that joint can be accurately reduced, minimizing the risk of secondary osteoarthritis.
  2. Stabilisation (maintain reduction until healing occurs).
    - Allows for early mobilisation.
    - Achieved by external splinte.g. plaster cast, without an operation.
    - Intra-operative fixation can be w/ percutaneous pinning w/ wires, plates & screws, intra-medullary nail for long-bone fractures or external frame fixation

NOTE- View notes for diagrams!

3.Rehabilitation (rehabilitate the limb & patient).
- Range-of-movement exercises.
- Physiotherapist
- Following hip fracture, elderly patients require input from physiotherapy, occupational therapy & social workers to become self-caring & safe prior to discharge

  1. Prevention of further fractures
    - Bisphosphonates - stops bone resorbtion.
    - Adcal
    - Denosumab - RANK-ligand inhibitor - stops osteoclast differentiation.

NOTE: Bisphosphonates can cause osteonecrosis of jaw

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10
Q

Prognosis for pathological fractures

A

Prognosis extremely poor

Pathological fractures are frequently a marker of end-stage cancer & the end of functional independence.

Surgery successfully reduces local pain & allows early mobilisation - low complication rate too.

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