Trauma and Skeletal Injury Flashcards

1
Q

Describe the structure of a long bone (there are 4 regions)

A
Diaphysis
•	Shaft 
•	Hollow
•	Strength and lightness
•	Contains marrow
Epiphysis
•	Expanded ends of the bones
•	Proximally and distally
•	Covered in articular cartilage
•	Boundary defined by epiphyseal line
Medullary (Marrow cavity)
•	Marrow cavity
•	Red marrow and yellow marrow (fatty)
•	Site of haemopoiesis (blood cell production)
•	Stores fat
•	Makes bones lighter – but still strong
Periosteum
•	Connective tissue covering
•	Covers all bones
•	Fibrous layer
o	Sharpeys fibres
•	Inner 
o	Osteoblasts 
o	Osteoclasts 
Nutrient Foramen
•	External opening of the nutrient canal in a bone
•	Provides blood supply
•	Arteries and nerves
•	More prevalent towards epiphysis
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2
Q

What is the organic and inorganic parts of bone?

A
•	Organic
o	Collagen and other proteins
o	35% 
o	Flexibility
o	Tensile strength
•	Inorganic
o	Mineral salts 
o	65%
o	Compression strength 
o	Reason why it preserves so well
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3
Q

Describe the structure of bone

A

• Bone
o Compact
 Thicker
 Denser
 Comprised of osteons – basic units of compact bone
• Haversian canal
o Blood vessels
o Nerve fibres
• Lamellae
o Rings of collagen fibres around Haversian Canals
o Collagen fibres oppose each other diagonally
o Resists torsional strength
• Lacunae
o Tiny caverns between lamellae
o Residences of the osteocytes
• Osteocytes
o Living cells of bone tissue
o Maintains health of bone matrix
o If an osteocyte dies, the surrounding bone matrix is resorbed by osteoclasts.
• Canaliculi
o Tiny plasma membrane extensions of the osteocytes
o Allows communication between osteocytes
o Allows nutrient sharing between osteocyte
• Cancellous (Spongy)
o Trabeculae (struts) relay stress to the dense compact bone
o Houses marrow in between trabeculae.
o Blood Vessels
o Osteoblasts
o Fat Cells

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4
Q

What is the periosteum?

A
  • Fibrous Lining over the surface of the bone
  • Outer fibrous layer – ligaments and tendons attach
  • Inner layer – renew and form new bone, involved in healing
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5
Q

What is bone resorbed and layed down?

A
  • Resorption – destruction of old bone matter by Osteoclasts
  • Apposition – deposition of new bone matter by Osteoblast
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6
Q

What are the 6 types of fractures?

A

On image

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7
Q

What are the 4 stages of bone repair from a fracture?

A
  1. (1-3days) - Haematoma & Inflammation (Blood Clot + Fibrin Mesh)
  2. (1-3weeks) - Soft Callus (Deposition of Osteoid + Granulation Tissue + Fibroblasts)
  3. (1-2mths) - Hard Callus (Mineralisation of Osteoid)– NB: VISIBLE ON XRAY
  4. (>2mths) - Remodelling of Woven Bone with Lamellar Bone
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8
Q

Describe Haematoma & Inflammation (Blood Clot + Fibrin Mesh) stage of bone repair

A

• Bleeding starts the process of bone healing. Bleeding will then form a clot called a haematoma. You will also get the inflammation through inflammatory mediators from signalling cascades

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9
Q

Describe the formation of a soft callus

A

• A soft callus will then form (fibrocartilaginous callus formation). Since osteoblasts are very difficult to make, as they are very specialised and also require a huge amount of ATP to produce, fibroblasts are made instead (low ATP production requirement). Fibroblasts will deposit fibrocartilage between the broken edges of the bone to make sticky ends. This reduces the instability between the broken bone. You also have the deposition of osteoid and granulation tissue which will form the soft callus. New blood vessels will also form

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10
Q

Describe the formation of a hard bony callus

A

• A bony callus will then form (hard callus). The cartilaginous callus begins to undergo endochondral ossification. RANK-L is expressed, stimulating further differentiation of chondroblasts, chondroclasts, osteoblasts, and osteoclasts. As a result, the cartilaginous callus is resorbed and begins to calcify. Subperiosteally, woven bone continues to be laid down. The newly formed blood vessels continue to proliferate, allowing further migration of mesenchymal stem cells. At the end of this phase, a hard, calcified callus of immature bone forms.

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11
Q

Describe the final stage of bone repair: remodelling

A

• Bone remodelling will then occur. With the continued migration of osteoblasts and osteoclasts, the hard callus undergoes repeated remodelling - termed ‘coupled remodelling.’ This ‘coupled remodelling’ is a balance of resorption by osteoclasts and new bone formation by osteoblasts. The centre of the callus is ultimately replaced by compact bone, while the callus edges become replaced by lamellar bone. Substantial remodelling of the vasculature occurs alongside these changes. The process of bone remodelling lasts for many months, ultimately resulting in the regeneration of the normal bone structure. An important point to expand on is endochondral ossification, which is the name given for the process of conversion of cartilage to bone. As described above, this occurs during the formation of bony callus, in which the newly formed collagen-rich cartilaginous callus gets replaced by immature bone. This process is also the key to the formation of long bones in the foetus, in which the bony skeleton replaces the hyaline cartilage model. The second type of ossification also occurs in the foetus; this is intramembranous ossification; this is the process by which mesenchymal tissue (primitive connective tissue) is converted directly to the bone, which no cartilage intermediate. This process takes place in the flat bones of the skull

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12
Q

How long to heal?

A
  • Every bone is different
  • 6 weeks
  • Children are faster than older people
  • Blood supply to the bone affects healing process – slower for low blood supply
  • Takes longest for remodelling process….
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13
Q

What is primary healing?

A
•	Without callus
•	only achievable with surgery
•	suitable for 
o	simple fractures (jigsaw) 
o	articular fractures
•	slower
•	direct to remodelling 
•	cutting cones
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14
Q

What happens in a fracture?

What is the surrounding tissue to a fracture and what do they supply?

A
  • Energy is imparted to the limb
  • Energy is absorbed by the soft tissue and the bone
  • This forms direct tissue trauma and some is absorbed and stored by the bone
  • Energy stored in bone will cause the bone to fail – so deep capillaries are damaged that forms blistering particularly where there is a lack of muscle cover, the soft tissue is damaged, infection (secondary soft tissue damage)

The skin, muscles, subcutaneous fat, fascia, muscle, tendons, nerves, vessels are also all injured in a fracture. This is needed for fracture healing. It provides blood supply to bone, prevents infection, stability and are osteoprogenitor cell supplies.

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15
Q

What is an open and closed fracture?

What are the complications of an open fracture?

A
  • Open fracture (also called compound fracture): The bone pokes through the skin and can be seen, or a deep wound exposes the bone through the skin.
  • Closed fracture (also called simple fracture). The bone is broken, but the skin is intact.

Open fractures
• Hematoma lost, bone is stripped of soft tissues, so the bone does not heal properly
• soft tissue envelope damaged = infection risk / delayed healing
• higher complication

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16
Q

Describe the pathophysiology of an open fracture

Where can a open fracture occur?

What are the two types of open fractures?

Gives some examples…

A

A fracture is ‘open’ when there is a direct communication between the fracture site and the external environment. This is most often through the skin – however, pelvic fractures may be internally open, having penetrated in to the vagina or rectum.

Fracture may become open by either an “in-to-out” injury, whereby the sharp bone ends penetrate the skin from beneath, or an “out-to-in” injury, whereby a high energy injury (e.g. ballistic injury or a direct blow) penetrates the skin, traumatising the subtending soft tissues and bone.

Whilst any fracture can become open, the most common fractures are tibial, phalangeal, forearm, ankle, and metacarpal.

17
Q

What are the 4 outcomes of an open fracture?

A
  • Skin – this can range from a very small wound to significant tissue loss, whereby coverage will not be achieved without the aid of plastics surgery (i.e. skin grafting or a local/free flap)
  • Soft tissues – this can also range from very little tissue devitalisation to significant muscle/tendon/ligament loss requiring reconstructive surgery
  • Neurovascular injury – nerves and vessels may be compressed due to limb deformity, go in to arteriospasm, develop and intimal dissection or be transected altogether
  • Infection – the rate of infection is very high following open fracture, due to direct contamination, reduced vascularity, systemic compromise (such as following major trauma) and need for insertion of metalwork for fracture stabilisation
18
Q

Describe the clinical features of an open fracture

A

Initial resuscitation and suitable management is essential, especially in cases of major trauma.
Patients will present with pain, swelling, and deformity, with an overlying wound or punctum (in severe cases, the bone end may be visible protruding from the wound).

On examination, ensure to check neurovascular status and overlying skin for any skin or tissue loss (Fig. 1).

Any evidence of contamination should be assessed for and documented – marine, agricultural, and sewage contamination is of the highest importance.

The need for plastic surgery input should be identified early, to allow both specialties to be present at the first operation and therefore avoid multiple procedures.

19
Q

What are the priorities in management of fractures?

A
•	patient survival
o	reusucitate etc
•	limb survival
o	vascularity, comp. syndrome
•	functional survival – can we get it to heal in a functional position
o	mt units, nerve
•	infection prevention
o	soft tissue coverage
20
Q

What are the initial stages of fracture management?

A
  1. control haemorrhage
  2. assess distal perfusion
  3. realign limb
  4. reduce dislocations
  5. assess nerve damage
  6. compartment pressure
21
Q

What is compartment syndrome?

A

Raised pressure in a closed fascial compartment that exceeds capillary perfusion pressure

Compartment syndrome is defined as a critical pressure increase within a confined compartmental space. Any fascial compartment can be affected. The most common sites affected are in the leg, thigh, forearm, foot, hand and buttock.

  1. Raised pressure in a closed fascial compartment that exceeds capillary perfusion pressure
  2. Fascia is membrane, inelastic, gives muscles there form, not permeable for fluid transfer.
  3. Pressure builds up in compartment, this affects blood supply (venous draining is high), this leads to necrosis. Acidosis occurs -> pain
22
Q

Describe the pathophysiology of compartment syndrome

causes

What happens to the veins and nerves?

Lastly to the arteries

A

Compartment syndrome typically occurs following high-energy trauma, crush injuries, or fractures that cause vascular injury. Other causes include iatrogenic vascular injury, tight casts or splints, deep vein thrombosis, and post-reperfusion swelling.

Fascial compartments are closed and cannot be distended; consequently, any fluid that is deposited therein will cause an increase in the intra-compartmental pressure.

As pressure increase, the veins will be compressed. This increases the hydrostatic pressure within them, causing fluid to move down its gradient and out of the veins in to the compartment. This increases the intra-compartmental pressure further.

Next, the traversing nerves are compressed. This causes a sensory +/- motor deficit in the distal distribution. Paraesthesia is therefore a common symptom.

Lastly, as the intra-compartmental pressure reaches the diastolic blood pressure, the arterial inflow will be compromised, leading to ischaemia (a cool, pale, pulseless and paralysed distal limb). This is a late sign of missed compartment syndrome

23
Q

How do we investigate compartment syndrome?

A

The diagnosis of compartment syndrome is essentially clinical, based on the symptoms and risk factors present. Clinicians should therefore have a high degree of clinical suspicion for compartment syndrome in post-operative patients.

The most reliable diagnostic test is siting an intra-compartmental pressure monitor, which may be utilised where there is clinical uncertainty, such as in atypical presentations or if the patient is unconscious / intubated. A creatine kinase (CK) level may aid diagnosis, if elevated (or trending upwards).

24
Q

What are the clinical features of compartment syndrome?

A
  • pain out of proportion to injury
  • Severe pain with passive stretch
  • Late signs: numbess/tingling
  • Paralysis: pallor and pulselessness
25
Q

How is compartment syndrome managed?

A

The most important part of the management is early recognition and immediate surgical treatment via urgent fasciotomies (Fig. 2).

Initial management, prior to definitive intervention, includes:

Keep the limb at a neutral level with the patient (do not elevate or lower)

Improve oxygen delivery with high flow oxygen

Augment blood pressure with bolus of intravenous crystalloid fluids

This transiently improves perfusion of the affected limb)
Remove all dressings / splints / casts, down to the skin. No layers of any dressing must be left circumferentially.

Treat symptomatically with opioid analgesia (usually intravenous)

Once fasciotomies have been performed, the skin incisions are left open and a re-look is planned for 24-48 hours. This is to assess for any dead tissue, which will need to be debrided. Once happy that all remaining tissues are healthy, the wounds can be closed (the subtending fascia is often left open, however).
Monitor renal function closely, due to the potential effects of rhabdomyolysis or reperfusion injury.

26
Q

Where can a neck of femur fracture occur?

A

Neck of femur (NOF) fractures can occur anywhere from the subcapital region of the femoral head to 5cm distal to the lesser trochanter (Fig. 1).

27
Q

What are the 2 subdivisions of a neck of femur fracture?

A
  • Intra-capsular – from the subcapital region of the femoral head to basocervical region of the femoral neck, immediately proximal to the trochanters
  • Extra-capsular – outside the capsule, subdivided into:
  • Inter-trochanteric, which are between the greater trochanter and the lesser trochanter
  • Sub-tronchanteric, which are from the lesser trochanter to 5cm distal to this point
28
Q

Describe the blood supply to the neck of femur

A

The blood supply to the neck of the femur is retrograde*, passing from distal to proximal along the femoral neck to the femoral head. This is predominantly through the medial circumflex femoral artery, which lies directly on the intra-capsular femoral neck.

29
Q

What does a displaced intracapsular NOF fracture cause?

A

Consequently, displaced intra-capsular fractures disrupt the blood supply to the femoral head and, therefore, the femoral head will undergo avascular necrosis (even if the hip is fixed). Patients with a displaced intra-capsular fracture therefore require joint replacement (arthroplasty), rather than fixation.

30
Q

Where can the neck of femur fracture occur?

A
  • Sub-capital – directly underneath head
  • Transcervical
  • Basi – cervical
  • Inter-trochanteric
  • Sub- trochanteric
31
Q

What are the clinical features of a NOF fracture?

A

The leading symptom is trauma, often low-energy, which is followed by pain and an inability to weight bear. Pain is felt predominantly in the groin, thigh or, commonly in the elderly, referred to the knee.

On examination, the leg is characteristically shortened and externally rotated, due to the pull of the short external rotators (Fig. 2), with pain on pin-rolling the leg and axial loading.

Fortunately, distal neurovascular deficits are rare in isolated neck of femur fractures. However, a full neurovascular examination of the limb is essential, with any deficits urgently acted on.

It is essential that you remember to investigate the cause of their fall, especially if there is not a clear history of a trip or slip.

32
Q

How can fractures cause bone cancer?

A

Metastatic bone tumours make the most of the disease burden. Primary bone tumours are relatively rare, with an overall prevalence of less than 1% in the UK. In children & adolescents, bone cancer is more common, comprising around 5% of all cancers.
Metastatic Bone Cancer

Metastatic spread from other cancer types is the most common cause of bone cancer, the most common primary sites being renal, thyroid, lung, prostate, and breast. The most common site for a bony metastases is the spine.

Metastatic disease is rarely treated surgically, with the mainstay of disease management via systemic therapies and often are palliative. Prophylactic nailing of certain long bones can be performed in certain individuals at high risk of pathological fractures from metastatic disease, especially of the femur and humerus.

33
Q

What is non union?

What will patients experience?

causes?

A

Results from failure of the ends of a fractured bone to unite. The patient complains of persistent discomfort and abnormal movement at the fracture site. Factors contributing to union problems include infection at the fracture site, interposition of tissue between the bone ends, inadequate immobilization or manipulation that disrupts callus formation, excessive space between bone fragments (bone gap), limited bone contact, and impaired blood supply resulting in avascular necrosis.