MSK growth, injury and repair Flashcards
(47 cards)
1
Q
Decsribe cortical bone
A
○ Diaphysis ○ Resists - Bending - Torsion ○ Laid down circumferentially ○ Less biologically active
2
Q
Describe cancellous bone
A
○ Metaphysis ○ Resists/absorbs - compression ○ Site of longitudinal growth (physis) ○ Very biologically active
3
Q
What is a fracture?
A
○ Break in structural continuity of bone
○ May be a crack, break, split, crumpling, buckle
○ ( # = shorthand sign for a fracture )
4
Q
Why do bones fail?
A
○ High energy transfer in normal bones -Takes a lot ○ Repetitive stress in normal bones - Stress fracture ○ Low energy transfer in abnormal bones - Osteoporosis - Osteomalacia, metastatic tumour § Other bone disorders
5
Q
What haens in a fracture
A
○ Mechanical and structural failure of bone ○ Disruption of blood supply ○ Regenerative process - No scar - Four stages
6
Q
What is strain and how does it affect healing?
A
□ Degree of instability is best expressed as magnitude of strain (% change of initial dimension)
□ If strain is too low mechanical induction of tissue differentiation fails
□ Too high and healing process does not progress to bone formation
7
Q
What happens in stage 1 of bone healing?
A
- Begins immediately after fracture
- Hematoma and fibrin clot
- Platelets, PMN’s, Neutrophils, Monocytes, Macrophages
- Massive increase in blood supply in the first few days
- By products of cell death: lysosomal enzymes
- Starts off with muscle contraction for initial stability
- Fibroblasts come in to stabilise the bone
- Mesenchymal & Osteoprogenitor cells
□ Transformed endothelial cells from medullary canal and/or periosteum
□ Osteogenic induction of cells from muscle and soft tissues - Angiogenesis
□ Oxygen gradient required (low)
□ Macrophages: produce angiogenic factors under hypoxic conditions
8
Q
How might stage 1 be affetced?
A
□ NSAIDs ® Potential to slow down fracture repair □ Loss of haematoma ® Open fractures ® Surgery □ Extensive tissue damage ® Fewer live cells to grow back in again ® Poor blood supply
9
Q
What happens in stage 2 of bone healing?
A
- Begins when pain and swelling subside
- Lasts until bony fragments are united by cartilage or fibrous tissue
- Some stability of fracture
- Angulation can still occur
- Continued increase in vascularity
□ Falls off after 2 weeks
□ Less so than stage 1
10
Q
How might stage 2 be affected?
A
□ Replace cartilage ® DMB (Demineralised bone matrix) □ Jump straight to bone ® Bone graft ® Bone substitutes
11
Q
What happens in stage 3 of bone healing?
A
- Fibroblasts convert to osteocyte
- Conversion of cartilage to woven bone
- Typical long bone fracture
□ Endochondral bone formation
□ Membranous bone formation - Increasing rigidity
□ Secondary bone healing (natural healing)
□ Obvious callus - Primary bone healing is when you use surgery to insert a plate
12
Q
What happens in stage 4 of bone healing?
A
- Conversion of woven bone to lamellar bone
- Medullary canal is reconstituted
- Bone responds to loading characteristics Wolff’s Law
13
Q
What are Platelet concentrates?
A
○ “Buffy coat”
○ Platelet-derived growth factor (PDGF)
○ Transforming growth factor- beta (TGF-B)
○ Insulin like growth factor (IGF)
○ Vascular endothelial growth factor (VEGF)
○ Squirt it in in situations where patients have lost their own haematoma to encourage bone repair
14
Q
hat is autogenous cancellous bone grafts?
A
○ Gold standard
○ The patient’s own bone
○ Osteoconductive: bone regrows through it
○ Osteoinductive: stimulates bone growth
○ Best choice for the majority of bone graft needs
15
Q
What is allograft bone
A
○ From the bone bank ○ Cortical ○ Cancellous ○ Fresh ○ Prepared ○ Structural ○ Osteoconductive ○ Not osteoinductive ○ Creeping substitution - The osteoclasts work their way through eating the dead bone - The osteoblasts come in and replace the bone ○ Risk of Disease transmission
16
Q
What is delayed union of bone?
A
failure to heal in the expected time
17
Q
What might cause delayed union in bone healing?
A
○ high energy injury ○ distraction (increased osteogenic jumping!) ○ instability ○ infection ○ steroids ○ immune suppressants ○ Diabetics ○ Smoking (fracture will take 50% longer time to heal if they smoke when they are healing) ○ warfarin ○ NSAID ○ Ciprofloxacin
18
Q
What might cause non-union failure in bones?
A
○ failure calcification fibrocartilage ○ instability - excessive osteoclasts ○ abundant callus formation ○ pain + tenderness ○ persistent fracture line ○ sclerosis
19
Q
What should you do if there is delayed bone healing?
A
○ Consider alternative management
- Different fixation
- Dynamisation
- Bone grafting
20
Q
Describe the anatomy of tendons
A
- longitudinal arrangement of cells (mostly tenocytes) and fibres (collagen type 1 - triple helix)
- fascicles of long narrow spiralling collagen bundles
□ COLLAGEN BUNDLES covered by endotenon,
□ FASCICLES covered by paratenon,
□ TENDON covered by epitenon - tendon sheath - e.g. flexor tendons in distal palm and fingers
□ tendons connected to sheath by vincula
□ synovial lining + fluid (gliding lubrication and nutrition)
□ thickenings which form strong annular pulleys
21
Q
What is the function of tendons?
A
- flexible and very strong in tension
- movement is life; immobility reduces water content & glycosaminoglycan concentration and strength
22
Q
Why might a tendon degenerate?
A
- Due to aging □ Repetitive injuries □ Poor blood supplies □ Occurs from 30s onwards - e.g. Achilles tendon □ intrasubstance mucoid degeneration □ may be swollen, painful, tender; may be asymptomatic □ May precursor to rupture - (rheumatoid arthritis considered elsewhere)
23
Q
Why might a tendon be inflammed?
A
- Inflammation of the synovial lining
- Can be caused by an inflammatory condition or could be caused by repetitive use
- e.g. de Quervain’s stenosing tenovaginitis
□ tendons of EPB + APL passing through common tendon sheath at radial aspect of wrist
□ swollen, tender, hot, red
□ positive Finklestein’s test
24
Q
What is enthesioathy?
A
§ Repetitive use injury § Inflammation at insertion to bone -Muscle/Tendon □ Usually at muscle origin rather than tendon insertion - e.g. lateral humeral epicondylitis (tennis elbow) - common extensor origin - Ligament □ Plantar Fasciitis
25
What is traction apophysitis and give an examle?
- Apophysis is the growing end of a tendon
- e.g. Osgood Schlatter's disease
□ insertion of patellar tendon into anterior tibial tuberosity
□ adolescent active boys
□ Recurrent load
□ Inflammation
□ No treatment- it is annoying and discomforting you have to decide whether you want to carry on with the activity or not
26
What is avulsion +/- bone fragment?
- Failure at insertion
- Load exceeding failure strength while muscle contracting
- Mallet finger
□ insertion of extensor tendon into dorsum of base of distal phalanx of finger
□ forced flexion of extended finger
-Treatment
□ Conservative (tends to be just in finger)
® Limited application
® Retraction tendon
□ Operative (majority)
® Reattachment tendon
◊ Through bone
®Fixation bone fragmen
27
What is intrasubstance (rupture) tear?
- tear - intrasubstance - e.g. Achilles tendon
- Load exceeds failure strength
- Mechanism
□ pushing off with weight bearing forefoot whilst extending knee joint (53%) e.g. sprint starts or jumping movements
□ unexpected dorsiflexion of ankle (17%) e.g. slipping into hole
□ violent dorsiflexion of plantar flexed foot (10%) e.g. fall from height
- Achilles tendon rupture
□ “positive” Simmond’s (squeeze) test
□ palpable tender gap
28
Give an example of a musculotendendinous junction tear
- e.g. medial head of gastrocnemius at musculotendinous junction with Achilles tendon
□ “plantaris syndrome” (mis-called)
□ often partial
29
What is the treatment for tendon rupture?
```
○ Conservative
- Where ends can be opposed
□ Mobilise (partial rupture) e.g. med lig knee
□ Splint/cast
- Where healing will occur
□ Not intraarticular
○ Operative
- High risk rupture
- High Activity
- Ends cannot be opposed
```
30
What are ligaments?
○ Dense bands of collagenous tissue (condensations capsule)
○ Span a joint
○ Anchored to the bone at either end
○ Joint stability through range motion
○ Different portions ligament tensioned at different joint positions
○ Multiple
31
Describe ligament structure
```
○ Collagen fibres (type 1)
○ Fibroblasts (communicate)
○ Sensory fibres
- Proprioception
- Stretch
- Sensory
○ Vessels (surface)
○ Crimping (allow stretch)
```
32
Compare ligaments and tendons
```
○ Composition
- Compared to tendons, ligaments have
□ Lower percentage of collagen
□ Higher percentage of proteoglycans and water
□ Less organised collagen fibers
□ Rounder fibroblasts
```
33
What happens in ligament rupture?
```
○ Forces exceed strength ligament
- Expected
- Unexpected (position/muscle)
- Rate load
○ Complete vs incomplete
○ Stability joint?
○ Proprioception loss?
```
34
How do tendons heal?
○ Haemorrhage
- Blood clot
- resorbed
- Replaced with a heavy cellular infiltrate.
- hypertrophic vascular response
○ Proliferative phase
- production of "scar tissue“
- disorganised collagenous connective tissue
○ Remodelling.
- Matrix becomes more ligament like
- Major differences in composition, architecture and function persist.
○ Will never be completely normal again
- There will always be a scar
35
How is a tendon injury treated?
```
○ Conservative
- Partial
- No instability
- Poor candidate surgery
○ Operative
- Instability
- Expectation (sportsmen)
- Compulsory (multiple)
- Repair
□ Direct
□ Augmentation
□ Replacement
```
36
What happens in compression (give examples)
```
○ Entrapment
○ Classical conditions
- Carpal tunnel syndrome
□ Median nerve at wrist
○ Sciatica
- Spinal root by intervertebral disc
○ Morton’s neuroma
- (digital nerve in 2nd or 3rd web space of forefoot)
```
37
What is neuropraxia?
- Caused by trauma
- nerve in continuity
- stretched (8% will damage microcirculation) or bruised
- reversible conduction block - local ischaemia and demyelination
- Nerve fibers are still intact so there is only temporary ischaemia and demyelination
- prognosis good (weeks or months)
38
What is axonotmesis?
- Caused by trauma
- endoneurium intact (tube in continuity), but disruption of axons; more severe injury
- Still a potential for the axon to re-grow
- stretched ++ (15% elongation disrupts axons) or crushed or direct blow
- Wallerian degeneration follows
□ The axon dies back a bit before it starts to recover by re-growing down the tube
- prognosis fair
□ Sensory recovery often better than motor - often not normal but enough to recognise pain, hot & cold, sharp & blunt
39
What is neurotmesis?
- Caused by trauma
- complete nerve division
-□ Two ends that are separated
-□ Try to regrow but cannot find the end point as they are blind
- laceration or avulsion
- no recovery unless repaired (by direct suturing or grafting)
- endoneural tubes disrupted so high chance of “miswiring” during regeneration
- prognosis poor
□ Very poor without repair
□ With repair it is by no means certain
40
What are closed nerve injuries and give examples?
```
○ Associated with nerve injuries in continuity
- neuropraxis
- axonotmesis
○ spontaneous recovery is possible
○ surgery indicated after 3 months
- if no recovery is identified
□ Clinical
□ Electromyography
- Measure growth using Tinel's test
□ Tap the end of the nerve and you get a shooting pain up the limb until the nerve ends
○ axonal growth rate (1–3 mm/day)
○ Examples
- Typically stretching of nerve
□ brachial plexus injuries
□ Radial Nerve humeral fracture
```
41
What happens in open nerve injuries?
○ Frequently related to nerve division
- neurotmetic injuries
- E.g. knives /glass
○ Treated with early surgery
○ Distal portion of the nerve undergoes Wallerian degeneration
- Occurs up 2 to 3 weeks after the injury
42
What are the clinical features of a nerve injury?
○ Sensory
- dysesthesia (disordered sensation)
□ anaesthetic (numb), hypo- & hyper-aesthetic, paraesthetic (pins & needles)
○ Motor:
- paresis (weakness) or paralysis ± wasting
- dry skin
□ loss of tactile adherence since sudomotor nerve fibres not stimulating sweat glands in skin
○ Reflexes:
- diminished or absent
43
Describe nerve injury healing
○ very slow!!
○ starts with initial death of axons distal to site of injury
- Wallerian degeneration
- Then degradation myelin sheath
○ proximal axonal budding occurs after about 4 days
○ regeneration proceeds at rate of about 1 mm/day (or 1 inch/month) - poss. 3-5 mm/day in children
- pain is first modality to return
44
What does the prognosis for nerve injury recovery depend on?
- whether nerve is
□ “pure”
® Only sensory or only motor
® Quicker recovery
□ “mixed”
® Both sensory and motor within same nerve
- how distal the lesion is (proximal worse)
45
How can nerve injuries be monitered?
○ Tinel’s sign can monitor recovery
- (tap over site of nerve and paraesthesia will be felt as far distally as regeneration has progressed)
○ Injury can be assessed, and recovery monitored
- by electrophysiological Nerve Conduction Studies
46
How can the nerve be repaired?
```
○ Direct Repair
- Laceration
- No loss nerve tissue
- Microscope/Loupes
- Bundle repair
- Growth factors
○ Nerve Grafting
- Nerve loss
- Late repair
□ (retraction)
□ Sural nerve
```
47
What is the surgical timing for different traumatic peripheral nerve injuries?
○ Immediate surgery within 3 days for clean and sharp injuries
○ Early surgery within 3 weeks for blunt/contusion injuries
○ Delayed surgery, performed 3 months after injury, for closed injuries
