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FRCS Plastic Surgery > KEY NOTES CHAPTER 1: GENERAL PRINCIPLES - Wound healing and skin grafts > Flashcards

KEY NOTES CHAPTER 1: GENERAL PRINCIPLES - Wound healing and skin grafts Flashcards

0
Q

Tell me about haemostasis.

A

Haemostasis (immediate)

  • thromboxanes and PG from damaged cells cause vasoconstriction.
  • platelets bind to exposed collagen forming platelet plug
  • platelets degranulate and bind to fibrinogen.
  • membrane glycoprotein IIb/IIIa is modified (blocked by clopidogrel).
  • PAF, vWF and TXA2 stimulate conversion of fibrinogen to fibrin.

Thrombus propagates

  • initially white thrombus (platelets only).
  • red thrombus (red blood cells also trapped).
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1
Q

What are the phases of wound healing?

A
  1. Haemostasis
  2. Inflammation
  3. Proliferation
  4. Remodelling
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2
Q

Tell me about inflammation

A

Inflammation (2-3 days post-injury)

  • stimulated by physical injury, Ab-Ag reaction or infection.
  • Platelets release growth factors (PDGF) and pro-inflammatory factors e.g. serotonin, bradykinin, PG, TXA2, histamine which increase cell proliferation and migration.
  • endothelial cells swell, vasodilate and cause egress of PMNs and monocytes.

T lymphocytes

  • migrate into wound.
  • secrete cytokines e.g. epidermal growth factor and basic fibroblast growth factor (bFGF).
  • mediate cell immunity and antibody production.
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3
Q

Tell me about proliferation

A

Proliferation (from day 2-3 for 2-4wks)
- monocytes mature to macrophages, release PDGF & TGF-B, chemoattractant to fibroblast.
- fibroblasts enter wound,
secrete GAGs to produce ground substance .
- produce collagen (type III initially) and elastin.
- some fibroblasts become myofibroblasts and affect wound contraction.
- angiogenesis occurs.

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4
Q

Tell me about remodelling

A

Remodelling (From 2-4wks to 1+years).

  • Type III collagen is replaced by type I (stronger).
  • Haphazard collagen fibres are arranged in more organised manner.
  • tensile strength 50% at 3 months, 80% after remodelling.
  • scar initially red due to dense capillary network, apoptosis leads to a pale scar.
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5
Q

What is abnormal scarring?

A

Keloid and hypertrophic scarring

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6
Q

Tell me about keloid scarring hypertrophic scarring?

A
  • limited to original wound margins, commoner than keloids.
  • usually starts ~ 8wks.
  • rapid growth for ~6mths, then gradually regresses (may be years).
  • common around shoulders, neck, presternal area, knees, ankles.
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7
Q

Tell me about keloid scarring

A
  • extend beyond original wound margins
    dark skin more prone, family history
    may suddenly develop anytime after injury.
  • persist, don’t tend to regress.
  • can be painful, hypersensitive.
  • common on anterior chest, shoulders, earlobes, upper arms, cheek.
  • excision alone has high risk of recurrence.
  • microscopy: type I and III collagen bundles are poorly organised with few myofibroblasts.
  • expression of PCNA (proliferation cell nuclear antigen) and p53 upregulated.
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8
Q

How does epithelialisation occur?

A
  1. Mobilisation.
  2. Migration.
  3. Mitosis.
  4. Cellular differentiation.
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9
Q

What occurs during mobilisation?

A
  • Marginal epithelial cells elongate, flatten and form pseudopodia.
  • Cells detach from neighbour and basement membrane.
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10
Q

What occurs during migration?

A
  • decreased contact inhibition promotes cell migration.
  • meanwhile marginal epi cells proliferate to replace them.
  • when cells meet opposite migrating epi cells, contact inhibition is reinstituted and migration ceases.
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11
Q

What occurs during mitosis?

A

Epithelial cells

  • proliferate.
  • secrete proteins to form new BM.
  • desmosomes and hemidesmosomes re-establish themselves and anchor the cells to BM and each other.
  • becomes new stratum germinativum.
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12
Q

What occurs during cellular differentiation?

A
  • normal structure of stratified squamous epithelium is re-established.
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13
Q

Tell me about collagen.

A
  • 30% of total body protein
  • amino acids lysine and proline are hydroxylated by enzymes (require Vit C)
  • procollogen (in cell)
  • tropocollagen (outside cell)
  • collagen - 3 polypetide chains wound in left handed helix, 2 chains wound in right handed coil to form basic tropocollagen unit
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14
Q

What inhibits collagen production?

A
  • colchicine, penicillamine, steroids and Vit C and iron deficiency inhibits collagen formation.
  • cortisol: stimulates collagen degradation
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15
Q

Name some common collagen types.

A
  • 28 types of collagen (diff cross-linkages and hydroxyproline and hydroxylysine).

Type I: mature skin, bone tendon (90% total body collagen).
Type II: hyaline cartilage and cornea.
Type III: healing tissue (esp fetal wounds).
Type IV: BM.
Type V: BM, hair and placenta.

Normal skin I:III = 5:1.

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16
Q

What is the function of a macrophage?

A
  • Derived from mononuclear leukocytes.
  • Debrides tissue, removes micro-organisms.
  • Co-ordinates angiogenesis and fibroblast activity by releasing growth factors: PDGF, FGF 1&2, TNF-a, TGF-b.
  • Orchestrator of wound healing
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17
Q

What is the function of myofibroblasts?

A
  • contains alpha-smooth muscle actin
  • responsible for wound contraction
  • increased numbers in fascia of Dupuytren’s disease
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18
Q

What secretes TGF-beta? What is it’s role in wound healing?

A
  • Macrophages, fibroblasts, platelets, keratinocytes, endothelial cells.
    Plays a central role in wound healing:
  • Chemoattractant for fibroblasts and macrophages.
  • Induction of angiogenesis.
  • Stimulation of extracellular matrix deposition.
  • Keratinocyte proliferation.

3 isoforms identified
1&2 - promote wound healing and scarring (unregulated in keloids).
3 - decreases wound healing and scarring (possible factor for deceased inflammation and improved scarring in fetal wound healing)

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19
Q

How are factors affecting healing classified?

A

Systemic

  • Congenital
  • Acquired

Local

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20
Q

Systemic factors: congenital

A 
Pseudoxanthoma elasticum
Ehler-Danlos syndrome
Cutis laxa
Progeria
Werner syndrome
Epidermolysis bullosa
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21
Q

Systemic factors: acquired

A

Nutrition - Vitamins A, C (collagen synthesis), Vitamin E, zinc, copper, selenium (cofactors for enzymes), hypoalbuminaemia.

Endocrine abnormalities - diabetes, hypothyroidism.

Pharmacological - steroids, NSAIDs, anti TNF-alpha drugs (RA), cytotoxics.

Age - mitosis rate decreases.

Smoking - nicotine (vasoconstriction), CO (decreased O2 carriage by Hb), hydrogen cyanide.

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22
Q

Local factors

A

Infection

Radiation - endothelial cell, capillary and arteriole, lymphatic damage. Fibroblasts secrete less collagen and ECM.

Blood supply - decreased by low pO2, low Hb, low O2 transfer from Hb, poor tissue perfusion. Decreased tissue O2 reduces collagen formation, ECM deposition, angiogenesis and epithelialisation.

Trauma - neoepidermis disrupted.

Neural supply - possibly related to levels of chemoattractant neuropeptides in wound.

23
Q

What do you know about fetal wound healing?

A

Foetus’ first 6 months - heals by regeneration, not repair, therefore no scarring.

  • Reduced inflammation.
  • Reduced platelet aggregation and degranulation.
  • Reduced angiogenesis.
  • More rapid epithelialisation.
  • No myofibroblasts, no wound contraction.
  • Type III > I collagen.
  • Wound contains more water and hyaluronic acid.
  • More TGF-B3 than 1&2
24
Q

Tell me about skin grafts

A

Full or split thickness (of epidermis and dermis).
Donor sites differ.
Primary contraction - immediate recoil after harvest.
Secondary contracture - after skin graft has taken, and is due to myofibroblasts.

25
Q

What are the reasons for graft failure?

A
  1. Haematoma.
  2. Infection (if >100,000 organisms / gram, less if Group A B-haemolytic Strep, as streptokinase and hyaluronidase prevent adhesion)
  3. Seroma.
  4. Shear.
  5. Inappropriate bed (cartilage, tendon, bone).
  6. Technical error.
26
Q

How do skin grafts take?

A
  1. Adherence (fibrin) - immediate.
  2. Serum imbibition (absorption of fluid and nutrients, graft swells) - D2-4.
  3. Revascularisation - D4.
    - Inosculation- direct anastomosis between vessels in graft and those in recipient tissue.
    - Revascularisation - new vessel ingrowth from recipient tissue along graft’s vascular channels.
    - Neovascularisation - new vessel ingrowth from recipient tissue along new channels in graft.
  4. Remodelling
    - histological architecture of graft returns to that of normal skin.
27
Q

Draw a cross-section of bone

A

Label
- Periosteum
- Cortical bone
+ Osteon: Haversian canal, lamellae, canaliculi.

  • Cancellous bone
    + Trabecullae
28
Q

Outline the structure of bone.

A
  • Outer cortical layer and inner cancellous layer.
  • Cancellous bone consists of loosely woven trabeculae of organic and inorganic bone.

• Cortical bone consists of:
- Multiple osteons (columnar bone units) and a central
Haversian canal that contains a central blood vessel.
- Transverse Volkmann nutrient canals connecting adjacent osteons.

  • Bone is laid down in concentric layers around each Haversian canal.
  • Osteocytes are scattered throughout osteons, each within its own space (lacuna).
29
Q

What is bone composed of and how does it develop embryologically?

A

• Derived from mesenchyme.
• Composed of organic matrix (osteoid), mineralised by hydroxyapatite (calcium
salt).
• Embryologically, bones form by:
1. Intramembranous ossification
∘ Deposition of bone within a vascularised membranous template.
∘ e.g. flat bones of face, calvarium and ribs.
2. Endochondral ossification
∘ Develops from a cartilage precursor, or anlage.
∘ e.g.: all long bones and iliac crest.

30
Q

What is the blood supply to bone?

A
  1. Periosteal vessels at muscle attachment.
  2. Apophyseal vessels at tendon and ligament attachment.
  3. Nutrient arteries supplying medullary cavity (endosteal supply).
  4. Epiphyseal vessels supplying growth plates.
31
Q

How do bones heal?

A
  1. Haematoma formation
  2. Inflammation
    - Fracture haematoma is gradually replaced by granulation tissue.
    - Osteoclasts remove necrotic bone.
  3. Cellular proliferation
    - Stem cell recruitment.
    - Periosteal proliferation occurs on outer aspect of cortex.
    - Endosteal proliferation occurs on inner aspect of cortex.
  4. Callus formation
    - Immature woven bone produced by osteoblasts and hyaline cartilage produced by chondroblasts.
    - This soft callus (osteoid) is mineralised with hydroxyapatite to form hard callus (mature woven bone).
  5. Remodelling
    - Woven bone slowly replaced by lamellar bone, until cortical structure and medullary cavity are restored.
    • Osteoblasts form new bone by producing osteoid.
    • Osteoclasts are responsible for bone resorption.
    • Osteocytes are osteoblasts that have become trapped within lacunae in bone matrix.
    • Osteoid is unmineralised, organic component of bone.
32
Q

What is primary bone healing?

A

• Healing without callus formation, when bone ends are directly fixed with absolute stability.
• Fracture haematoma is removed during surgery.
• Bone ‘tricked’ into thinking it was never fractured.
• Inflammatory and proliferative phases of healing do not occur.
• Rather, it is a process of osteonal bone remodelling:
∘ Osteoclasts ‘drill’ across fracture site from one cortex to other, blood vessels and osteoblasts cross fracture and new Haversian systems and bone architecture are established.

33
Q

What is secondary bone healing?

A
  • This is healing by callus formation.
  • Occurs if fragments are not rigidly fixed, or if a gap exists between bone ends.
  • It cannot occur if there is no fracture haematoma.
34
Q

What are the complications of fractures?

A
  • Delayed union
  • Non-union
  • Malunion - rotation, angulation, shortening.
  • Infection
  • Avascular necrosis (AVN)
  • Damage to adjacent structures.
35
Q

How can bone graft materials be classified?

A
  1. Biological
    - Autograft, allograft, xenograft
  2. Engineered biological
    - Growth factors, recombinant BMPs, stem cells, platelet-rich plasma concentrate (PRPC)
  3. Synthetic
    - Metals, ceramics, polymers.

• Gold standard is autologous.

36
Q

How do autologous bone grafts heal?

A

Incorporation
• Adherence of graft to host tissue.
• Maximised in immobilised, well-vascularised tissue.

Osseoconduction
• Bone graft acts as a scaffold along which vessels and osteoprogenitor cells travel.
• Creeping substitution - old bone is resorbed as new is deposited.

Osseoinduction
• Differentiation of mesenchymal cells within recipient local tissue into osteocytes. (Osteoclasts, osteoblasts and osteocytes within bone graft are not capable of mitosis).
• Controlled by BMPs.

Osteogenesis
• Formation of new bone by surviving cells within bone graft.
• Vascularised bone grafts incorporate rapidly this way, without creeping substitution.
• Minimal osteogenesis in non-vascularised bone grafts.

37
Q

What factors influence the survival of bone grafts?

A
  1. Systemic factors
  2. Intrinsic graft factors
  3. Graft placement.
Systemic factors
• Age
• Nutrition
• Immunosuppression
• Drugs
• Diabetes
• Smoking
• Obesity.

Intrinsic graft factors
• Grafts with periosteum included undergo less resorption.
• Membranous bone undergoes less resorption than endochondral bone.
• Cancellous grafts revascularise easier than cortical grafts.

Graft placement factors
(a) Ortho / Heterotopic
• Orthotopic - graft placed into a position normally occupied by bone (less resorption).
• Heterotopic - graft in a position not normally occupied by bone.

(b) Quality of recipient bed
• Radiotherapy, scarring and infection adversely affect graft survival.

(c) Graft fixation
• Rigid fixation survive better than mobile.

(d) Site of graft placement
• Better survival in areas where bone is normally laid down (depository sites) e.g. zygoma and mandible in children.

38
Q

What is the structure of cartilage?

A

• Derived from condensed mesenchyme.
• Differentiates into chondroblasts that secrete ECM.
• Chondroblasts trapped in lacunae within matrix become chondrocytes.
• Matrix contains type II collagen, elastin and ground substance (GAGs).
• Cartilage is classified according to relative proportions of these 3 components into:
1. Hyaline cartilage
2. Fibrocartilage
3. Elastic cartilage.

Cartilage has no blood, nerve or lymph supply, and has little reparative ability.

39
Q

Where is cartilage harvested from?

A

∘ Ear conchal bowl
∘ Nasal septum (via lateral rhinotomy incision)
∘ Costal cartilage.

40
Q

Describe the anatomy of a nerve.

A
  • Nerve cells (neurons) consist of a cell body.
  • Outgoing impulses are carried axons.
  • Impulses are received either on cell body or dendrites.
Layers (inside to out)
• Axon (nerve fibre)
• Endoneurium
• Fascicles
• Perineurium.
• Intraneural epineurium (+blood vessels).
• Outer epineurium 
• Peripheral nerve.
41
Q

What is the function of a nerve?

A
  • Schwann cells produce multilaminated myelin sheath of myelinated nerves.
  • Unmyelinated nerves are ensheathed by a Schwann cell-derived double basement membrane.
  • Schwann cells of myelinated nerves abut at nodes of Ranvier.
  • Nerve conduction involves passage of an action potential along a nerve.
  • Saltatory conduction: impulse in myelinated nerves jumps between adjacent nodes of Ranvier.
42
Q

How are nerve fibres classified based on their diameter?

A

Group A - Myelinated, large-diameter, high-conduction velocity nerves.

  • Group A-α fibres: motor and proprioception.
  • Group A-β fibres: pressure and proprioception.
  • Group A-γ fibres: motor to muscle spindles.
  • Group A-δ fibres: pain, touch, temperature.

Group B - Myelinated, small-diameter, low-velocity fibres.
• Preganglionic autonomic nerves.

Group C
• Unmyelinated, small-diameter, low-velocity fibres
• Postganglionic autonomic nerves
• Dorsal root nerves for pain, temperature, touch, pressure and itch.

43
Q

How is nerve function classified?

A

MRC grading of nerve function.

44
Q

What happens after a nerve is injured?

A

• Degeneration proximally → nearest node of Ranvier.
• Distally → axons and myelin undergo Wallerian degeneration (phagocytosis by macrophages and Schwann cells).
∘ Remaining basement membranes form endoneurial tubes which guide regenerating axons to their targets.

• Neurotropism = selective, directional growth of fibres towards end organs, mediated by nerve growth factors and cell-cell interactions:

  1. Proximal axon sprouts many new daughter axons, forming a growth cone.
  2. Fibres growing in inappropriate direction atrophy.
  3. Those growing in correct direction survive.

• Neurotrophism = non-selective, non-directional growth of nerve fibres.
• Neurotrophic factors are almost all produced by Schwann cells:
e.g. Growth factors: Nerve growth factor, ciliary neurotrophic factor, insulin-like growth factor.
e.g. Extracellular matrix components: Fibronectin, laminin, neural cell adhesion molecule, N-cadherin.

45
Q

What is Seddon’s classification of nerve injury?

A 
Seddon classification:
1 Neurapraxia (1st)
2 Axonotmesis (2nd-4th)
3 Neurotmesis (5th)
46
Q

What is Sunderland’s classification of nerve injury?

A

1st-degree injury
• Axon in continuity but conduction is impaired.
• Recovery should be complete.

2nd-degree injury
• Axonal injury, Wallerian degeneration distally.
• Endoneurium and connective tissue layers intact, recovery is good.

3rd-degree injury
• Axon and endoneurium divided.
• Perineurium and epineurium intact.
• Recovery reasonable.

4th-degree injury
• Complete division of all intraneural structures.
• Epineurium intact.
• Recovery of some function is expected.
• May result in neuroma-in-continuity.

5th-degree injury
• Nerve trunk completely divided.
• Early surgical repair.

47
Q

Quick summary of Sunderland’s classification!

A 
1st - axon squashed
2nd - axon divided, endo intact
3rd - endo divided
4th - peri divided
5th - epi divided
48
Q

What are the principles of nerve repair?

A

Tensionless repair, trim nerve, magnification, 9/0 S&T epieneural repair.

Fascicular identification by:

  • Matching of anatomical structures
  • Electrical stimulation (motor nerves only respond for 72hrs post injury)
  • Knowledge of internal nerve topography
49
Q

Tell me about nerve grafts.

A

Sural: behind lat malleolus
Lateral antebrachial cutaneous nerve: adjacent to cephalic vein alongside ulnar border of brachioradialis.
Medial antebrachial cutaneous nerve (20cm): in groove between triceps and biceps, alongside basilic vein
Terminal branch of PIN: base of 4th ext compartment.

50
Q

What are the principles of nerve grafting?

A

Nerves can be mobilised prox and dist, or transposed to reduce tension on repair.
Can be vascularised / healthy wound bed.
If cable graft, stagger levels of repairs.
Other sources: allograft (give immunosuppression (tacrolimus) until Tinel’s sign is in distal nerve.

51
Q

.

A

• Tendons are composed of dense, metabolically active connective tissue.

∘ Collagen is predominantly type I, with small amounts of types III and IV.

∘ Tenocytes
∘ Synovial cells
∘ Fibroblasts.

52
Q

What layers surround a tendon?

A
  • Endotendon encloses tendon bundles. Continuous perimysium and periosteum.
  • Epitenon = outer layer of synovial tendons.
  • Paratenon is a loose adventitial layer that surrounds extra-synovial tendons.
53
Q

Where do tendons receive their blood supply?

A

1 Musculotendinous junction
2 Bony insertion
3 Mesenteric vincular vessels.

54
Q

What are the mechanisms of tendon healing?

A

Extrinsic healing
• Dependent on fibrous attachments forming between tendon sheath and tendon.

Intrinsic healing
• Dependent on:
∘ Blood flow through long and short vinculae.
∘ Diffusion of nutrients from synovial fluid.

55
Q

What research suggests intrinsic healing takes place, making EAM possible?

A

• Lunborg showed tendons heal when wrapped in a semipermeable membrane (permits passage of nutrients, but not cells) and placed in knee joint of a rabbit.

56
Q

What are the phases of tendon healing?

A

Inflammation
• Inflammatory cells infiltrate the wound.
• Secrete growth factors that attract fibroblasts.

Proliferation
• Fibroblasts are responsible for tissue proliferation.
• They secrete type III collagen and GAGs.
• Collagen is initially arranged randomly; consequently, the tendon lacks strength.

Remodelling ~ 3 weeks
• Type III collagen is replaced by type I.
• The tendon remodels into an organised structure.
• Early motion limits fibrous attachments between tendon and sheath and promotes intrinsic healing over extrinsic.
∘ Mobilised tendons are stronger than immobilised tendons.

FRCS Plastic Surgery (63 decks)

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