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Green - Wound healing Flashcards

1
Q

What are the phases of healing?

A
  1. Inflammatory phase
  2. Proliferative phase
  3. Maturational phase
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2
Q

When does the inflammatory phase occur?

A

Days 0-7

  • Goals = stop bleeding, seal wound surface, remove necrotic tissues/FBs/bacteria
  • Therefore increased vascular permeability, cytokine secretion + GF secretion, chemotaxis
  • Neutrophils–>,macrophages + T cells –> IFN-y —> decrease collagen
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3
Q

When does the proliferative phase occur?

A

Day 3 to week 3

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4
Q

What does the proliferative phase consist of?

A
  • Angiogenesis
  • Fibroplasia: collagen synthesis “lag phase”
  • Epithelization
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5
Q

What stimulates angiogenesis in the proliferative phase?

A
  • FGF
  • TGF-alpha
  • TNF-alpha
  • VEGF
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6
Q

What type of cells proliferate and become dominant in the proliferative phase?

A

Fibroblasts

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7
Q

What stimulates collagen synthesis in the proliferative phase?

A
  • Ascorbic acid (Bit C)
  • TGF-beta
  • IGF-1
  • IGF-2

O2 + Vit c = important for collagen cross-linking by hydroxylation

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8
Q

How does collagen and wound strength correlate throughout the proliferative phase?

A

Collagen rapidly increases day 5 x 3 weeks then plateaus

  • First 3 weeks: correlate
  • After 3 weeks: Strength increases with no increase in collagen–>reflects scar remodelling
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9
Q

How does epithelization occur in the proliferative phase?

A
  • Partial thickness wounds: from remaining dermal appendages
  • Full thickness wounds: migrates in from the edges at a rate of 1-2 mm/day. Rate is dependent on vascularity of underlying granulation tissue

Begins 24h post=wound, @48h enlarge, prolific, migrate contact inhibition, d/c migration hen 2 edges meet

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10
Q

How does collagen synthesis work?

A

Procollagen gene–>translation–>preprocollagen–>hydroxylation (cross linking vit C)–>glycosylation–>disulphide bonding–>pro collagen–>packaging into lysosomes–>cleavage of peptides by peptidases–>collagen monomer

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11
Q

What are common types of collagen?

A
  • Type I: all connective tissue (bone) except cartilage and basement membranes
  • Type II: Articular cartilage, vitreous humour, and intervertebral disks
  • Type III: elastic tissues (blood vessels, uterus, skin), usually found with type I. Initial on in scars
  • Type IV: basement membranes
  • Type V, VI: widespread tissue distribution
  • Type VII: Fibrils that anchor epidermis to dermis
  • Type IX, XI: Hyaline cartilage
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12
Q

What are some known abnormalities of collagen?

A
  • Osteogenesis imperfecta: deletion of 1 pro collage alpha-1 allele
  • Ehlers-danlos syndrome: abnormal type III, deletion of part of type I collagen gene, abnormal copper utilization, deficiency of lysol hydroxylase
  • Epidermolysis bullosa: absence of type VII that is the main component of fibrils that anchor epidermis to dermis
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13
Q

What are elastic fibres?

A
  • Produced by smooth muscle cells and fibroblasts
  • Composed of: amorphous elastin, microfibrils
  • found in normal and hypertrophic scars
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14
Q

Where are elastic fibres most commonly found?

A
  • Thoracic aorta
  • Peripheral arterioles
  • Skin
  • Vocal cords
  • Sclera
  • Lungs
  • Pregnant uterus
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15
Q

What are stimulants of elastic production?

A
  • IGF-1

- TGF-beta

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16
Q

What are inhibitors of elastic production?

A
  • Glucocorticoids

- FGF

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17
Q

What cofactors/coenzymes are required for hydroxylation reaction in collagen synthesis?

A
  • Ferrous iron
  • alpha-ketoglutarate
  • ascorbic acid (vitamin c)
  • oxygen cofactors
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18
Q

What are stimulants of collagen synthesis?

A
  • Ascorbic acid
  • TGF-beta
  • IGF-1
  • IGF-2
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19
Q

What are inhibitors of collagen synthesis?

A
  • IFN-y

- Glucocorticoids

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20
Q

What is the best indicator of collagen breakdown?

A
  • Hydroxyproline in urine
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21
Q

What are GAGS?

A
  • Support cells
  • Provide tissue turgor
  • Facilitate cell-cell interaction
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22
Q

When does the maturational phase occur?

A

Week 3 to >1 year

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23
Q

What happens to collagen in the maturational phase?

A
  • Collagen synthesis/degradation equilibrates: change in predominant collagen III–>I
  • Cross linking of collagen occurs and random collagen fibrils are replaced with organized fibrils, therefore increased tensile wound strength
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24
Q

What happens to fibroblasts in the maturational phase?

A
  • Change into myofibroblasts that contract the wound

- Can be inhibited by colchicines and corticosteroids

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25
How does the wound strengthen during the maturational phase?
- Wound strength increases rapidly first 6 weeks | - Levels off at 70% of baseline in 6-8 weeks (why no lifting 6 weeks post-op)
26
Phases of healing
Phases 1) Inflammatory: 0-10 days 2) Proliferation: 4 days- 3 weeks 3) Remodeling: 3 weeks-1 year Vascular response 1) Vasoconstriction: initial injury 2) Vasodilation: after 1 days Cellular response 1) Neutrophils: initial-first few days 2) Macrophages: first few days- 4/5 days 3) Lymphocytes: Day 2-5/6 days 4) Fibroblasts: 4 days-1 year Major event 1) Clot formation and hemostasis 2) Growth factor and elaboration 3) Collagen deposition 4) Collagen cross linking: remodelling phase (3 weeks-1 year)
27
What are the short term effects of glucocorticoids on wound healing?
1. Suppress IL-2 production 2. Inhibit lymphocyte activation 3. Inhibit neutrophil migration to areas of inflammation 4. Inhibit monocyte migration to areas of inflammation 5. Inhibit histamine release and histamine-induced lysosomal degranulation by mast cells 6. Inhibit B cell activation and proliferation at high doses 7. Retards entry of free water into cells 8. Decreases capillary permeability to water 9. Weak mineralocorticoid effect 10. Stimulation of angiotensin release (maintains BP) 11. Inhibits PG12 (potent vasodilator)-->maintenance of BP 12. Impaired collagen mRNA transcription and fibroblast activity 13. Inhibit osteoclast activity 14. Promotes early closure of epiphyseal plates in kids
28
What are the long term effects of glucocorticoids on wound healing?
1. Catabolic state with negative N balance 2. Redistribution of body fat-->truncal obesity 3. Emotional and psychological disturbances 4. Cataracts 5. Corneal ulcers
29
What factors affect wound healing?
- Diabetes - Radiation - Advanced age - Hypoxia - Malnutrition - Infection - Drugs
30
How does infection affect wound healing?
Wound will not heal if: - Bacteria >10^5 organisms/gram - Beta-hemolytic strep Bacteria: prolong inflammatory phase, interfere with epithelization, collagen deposition, and contraction
31
How does wound hypoxia affect healing?
- Tissue oxygenation must be >35mmHg for healing | - Below this level: fibroblasts cannot replicate, collagen production impaired
32
How does diabetes affect wound healing?
- Impairs wound healing at all stages - Basement membrane thickened--> decreased perfusion - Lymphocyte and leukocyte function impaired - Increased collagen degradation - Decreased collagen deposition
33
How does radiation affect wound healing?
- Affects vascular endothelium - Causes endarteritis-->atrophy, fibrosis, delayed tissue repair - Arterial fibrosis-->impaired O2 delivery - Progressive obliteration of blood vessels - Intranuclear and cytoplasmic damage to fibroblasts (limits proliferative potential)
34
How does age affect wound healing?
- Healing slows as age progresses - Affects all stages of wound healing - Macrophages in particular are affected
35
How does malnutrition affect wound healing?
- Protein catabolism - Hypoalbuminemia - Essential FAs required for new cell synthesis - Zinc deficiency (RNA/DNA cofactors) - Vitamin C deficiency (needed for hydroxylation of proline and lysine)-->collagen - Vitamin B6 deficiency (collagen cross linking impaired) - Vitamin K wound hemostasis impaired - Thiamine deficiency - Riboflavin deficiency - Vitamin A deficiency (fibroplasia, collagen cross linking, epitheliazation)
36
What drugs affect wound healing?
- Doxorubicin - Beta-aminoproprionitrile - Bis-chlorethyl-nitrosourea - Cyclophosphamide - D-penicillamine - Glucocorticoids - Methotrexate - Nitrogen mustard - Tamoxifen
37
How does doxorubicin impair wound healing?
- Myelosuppression of platelets and inflammatory cells | - Direct inhibition of mitosis of local fibroblasts and keratinocytes
38
How does beta-aminoproprionitrile impair wound healing?
Inhibits collagen synthesis: inhibits cross-linking of collagen monomers by inhibition of lysol oxidase
39
How does bis-chloroethyl-nitrosourea (Carmustine-->chemo agent) impair wound healing?
- Myelosuppresion of platelets and inflammatory cells | - Decreases cellular proliferation
40
How does cyclophosphamide impair wound healing?
- Decreases cellular proliferation | - Myelosuppresion of platelets and inflammatory cells
41
How does D-penicillamine (treats wilsons disease) impair wound healing?
Binds to collagen substrate directly to prevent collagen cross-link formation
42
How do glucocorticoids impair wound healing?
- Impairs fibroblast proliferation - Impairs collagen synthesis: inhibits mRNA transcription - Decreases amount of granulation tissue form - Inhibits pro collagen secretion: stabilized the lysosomal membrane, can reverse with Vitamin A - Decrease in breaking strength - High dose with delay healing
43
How does methotrexate impair wound healing?
- Myelosuppresion of platelets and inflammatory cells | - Decreases cellular proliferation
44
How does nitrogen mustard impair wound healing?
Inhibits fibroblast proliferation
45
How does tamoxifen impair wound healing?
Decreases cellular proliferation
46
What are risk factors for wound dehiscence?
- Inadequate closure - Increased stress/pressure/tension on closure - Increased age - Comorbidities - Malnutrition - Drugs - Wound events (bleeding, hematoma, contamination, ischemia, radiation)
47
What are risk factors for hematoma?
- Myeloproliferative disorders - Polycythemia vera - Hyperthrombocytosis - Hepatic insufficiency - Coagulopathy - Inadequate hemostasis
48
What are patient risk factors for non-healing wounds and infection?
- Increased age - Malnutrition - DM - Smoking - Obesity - Co-existant infection - Wound colonization - Altered immune system - Chemotherapy - Radiation - Length of post-op stay - Poor tissue perfusion - Malignancy
49
What are operative risk factors for non-healing wounds and infection?
- Length of scrub - Skin antisepsis - Pre-op sharing - Pre-op skin prep - Duration of surgery - Antimicrobial PPV - OR ventilation - Equipment sterilization - Foreign material in surgical site - Drains - Poor hemostasis - Failure to obliterate dead space - Tissue trauma - Type of surgery (clean vs contaminated)
50
What is the management of wound dehiscence
- Urgent exploration | - Reclosure of fascia: mesh, retention sutures
51
What is the management of a hematoma?
- Found immediately post-op: exploration, evacuation | - Small, found late: heat, immobilize, support
52
What is the management of a serum?
- Aspiration | - Pressure dressing or closed suction drain
53
What are keloids?
- Abnormal wound healing - Occur several months after injury - Over abundance of collagen without increased fibroblasts
54
How can you improve a keloid?
Some improvement seen with excision and - Intralesional steroid injection - Short course radiotherapy - Triamcinolone
55
What is a hypertrophic scar?
- Similar to keloid by respects boundaries of scar | - Develop within first month
56
How can you improve a hypertrophic scar?
- Prevent by decreased tension on wound closure | - Treatment: pressure garments, topical silicone sheeting, excision + reclosure
57
What are the most common pathogens in wound infections?
- S. auerus - S. epi (coga negative staph) - Enterococcus - E. coli - Pseudomonas aeruginosa - Enterobacter
58
What is the most likely cause of superficial wound infection?
- Head/Neck/Trunk: S. aureus, streptococci - Axillary: gram negatives - Below waist: mixed aerobes and anaerobes
59
What is a necrotizing soft tissue infection?
- Marked by absence of clear local boundaries | - Layer of necrotic tissue not walled off by surrounding layer of inflammatory reaction
60
What are the 2 types of necrotizing soft tissue infection?
- Clostridial: typically involve underlying layer of muscle-->clostridial myonecrosis or gas gangrene - Non-clostridial: speed in SC layer between skin and muscle-->necrotizing fasciitis
61
What do soft tissue infections with underlying gas layer indicate?
- Most bacteria produce an insoluble gas when forced to use anaerobic metabolism - Human tissues can't survive anaerobic conditions = yea tissue = surgical infection
62
What are early signs of a necrotizing infection?
- Marked hemodynamic response - Failure of response to conservative measures - Rapid progression - Apparent cellulitis with bull, any dermal gangrene, extensive edema, or crepitus
63
What are the most common clostridial organisms?
- C. perfringens - C. novyi - C. septicum
64
What is the most common non-clostridial organism?
- Beta-hemolytic S. Pyogenes: no trauma, no surgery | - Polymicrobial: trauma, surgery
65
What is the classification of wounds and their infection rates?
- Clean (1.5-2.9%) - Clean contaminated (2.8-7.7%) - Contaminated (6.4-15.2%) - Dirty/infected (organisms present before operation)
66
What is considered a clean wound?
- Non-traumatic - No break in technique - No tract entered
67
What is considered a clean contaminated wound?
- Gi or respiratory tract entered without significant spillage - Oropharynx, vagina, or non-infected GU/biliary tract entered - Minor break in technique
68
What is considered a contaminated wound?
- Major break in technqiue - Fresh traumatic wound - Gross spillage from GI tract - Entrance in GU/biliary tree in presence of infection
69
What is considered a dirty/infected wound?
- Pus encountered - Trauma wound with retained devitalized tissue - Foreign bodies - Fecal contamination - Delayed treatment - From a dirty source

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