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Wound healing seminar 24 sept 2019 [autosaved]
1. Basic sciences of Wound healing
1This Photo by Unknown Author is licensed under CC BY
Presenter Dr. Shashank
Dr. Saurabh
Moderator Dr Shreesha
2. The ancient Egyptians were the first civilization to have
trained clinicians to treat physical aliments. Medical papyri,
such as the Edwin Smith papyrus (circa 1600 BCE) and the
Ebers papyrus (circa 1534 BCE), provided detailed
information of management of disease, including wound
management with the application of various potions and
grease to assist healing. [1, 2]
History of Wound Management
2
3. Contents:
3
• Wound definition
• Classification of wounds
• Healing
• Types of wound healing
• Stages of wound healing
• Phases of wound healing
• Factors affecting wound healing
• Complication
4. Definition of wound
• A wound is a break in the integrity of
the skin or tissues often which may be associated
disruption of the structure and function
4
5. • Tidy wound – Primary closure of all structures (bone, tendon,
vessel and nerve) may be possible
• Contaminated wound – Require debridement before definitive
repair
5
Rank and Wakefield classification
6. Types of Wounds
Tidy wounds Untidy wounds
Incised Crushed or avulsed
Clean Contaminated
Healthy tissues Devitalized tissues
Seldom tissue loss Often tissue loss
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7. Normal Wound Healing
• Three phases
• Inflammatory phase
• Begins immediately after wounding, lasts 2-3 days
• Vasoconstriction, thrombus formation
• Platelet aggregation
• Infiltration of inflammatory cells
• Removal of devitalized tissue and microorganisms by macrophages
7
8. Normal Wound Healing
• Proliferative phase
• 3rd day to 3rd week
• Fibroblast activity, with production of collagen and ground substance
• Angioneogenesis
• Reepithelialisation of wound surface
• Remodelling / Maturation phase
• Maturation of collagen
• Type III replaced by type I (1:4)
8
10. The Reconstructive Ladder
• A heirachy of options available for closing a wound
• Systematic, modern and safe approach to reconstruction
▫ Choose least aggressive method initially
▫ Rise-up rungs of the ladder as necessary
▫ More problematic wounds may require higher rungs
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11. Step 1: Dressings
• Adjunct applied to a wound to promote healing and
prevent further harm
• Allow the wound to heal by secondary intention
• Aim – maintain a moist environment without excess
exudate
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12. Low Adherence Dressing
Maintain a moist wound bed
• Allow exudate to pass through into a secondary dressing e.g gauze
Semi Permiable Film
Transparent polyurethane sheet coated with hypoallergenic adhesive • Permeable to air and water vapour; impermeable to
fluids and microorganisms • Example - Tegaderm
Foam Dressing
Highly absorbent with a hydrophobic backing to prevent strikethrough
Hydrocolloids
Virtually impermeable
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13. Alginate
Very absorbent – used only on wound with high exudate
Antimicrobial dressing
Reduce microbial load in colonised or infected wounds • Silver =
most common active ingredient; Iodine also effective
Vaccum Assisted Closure
• Draws excess exudate away from the wound
• Promotes angiogenesis and granulation
• Continuous or intermittent suction
• ▫ 50-70mmHg – chronic wounds/skin grafts
• ▫ ~120mmHg – acute wounds
13
14. Step 2: Primary (or delayed) closure
• Primary closure – appose + secure incised wound edges
• Traumatic/dirty wounds – may require debridement
delayed closure
Step 3: Skin grafting
• Block of tissue transferred without blood supply
• Classified according to tissue of origin:
▫ Autograft ▫ Allograft ▫ Xenograft
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15. Step 4: Tissue expansion
• Increases surface area of locally available skin
• Expander implant into subcutaneous pocket
serial injection with saline via port over weeks/months
• Expander removed skin advanced
Step 5: Flaps
Flap = “a unit of tissue which maintains its
own blood vessels whilst being transferred
from a donor site to a recipient site”
• 3 broad types –
random pattern, pedicled and free
15
16. Managing The Acute Wound
• Cleansing
• Exploration and diagnosis
• Debridement
• Repair of structures
• Replacement of lost tissues where indicated
• Skin cover if required
• Skin closure without tension
16
17. Factors Influencing Wound Healing
• Site of wound
• Structures involved
• Mechanism of wounding – Incision / Crush / Crush avulsion
• Contamination (Foreign bodies / bacteria)
• Loss of tissue
• Other local factors
• Vascular insufficiency
• Previous radiation
• Pressure
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18. •Systemic factors
• Malnutrition or vitamin and mineral deficiencies
• Disease (Diabetes)
• Medications (Steroids)
• Immune deficiencies (Chemotherapy, AIDS)
• Smoking
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19. •Contraction
• Spontaneous closure of full thickness skin wounds or contraction of tubular organs
such as common bile duct or oesophagus after injury
• Active biologic process that decreases the dimension of involved connective tissue
• May be useful for healing of large open full thickness wounds
• May lead to severe functional and asthetically deforming contractures
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20. •Connective tissue matrix deposition
• Fibroblasts are recruited at site of injury and produse new connective tissue matrix
• Important process in primary wound closure
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21. Types of Wound Closure
• Primary closure / Healing by first intention
• Immediate closure of wound using sutures, clips, staples and adhesive materials
• Minimal scarring
• Delayed primary closure
• Approximation delayed until several days to prevent infection
• Wounds with significant bacterial contamination, foreign bodies or extensive
tissue trauma
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22. Types of Wound Closure
• Spontaneous / Secondary wound healing
• Wound left open
• Heals by granulation, contraction and epithelialisation
• Poor scar
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23. Difference between 1˚ & 2˚ union of
wound
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FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT
29. Type of scar
• Normal scar
: normal wound healing process
• Abnormal scar
: Multiple disturbance in wound healing process
: Excessive collagen production
: Reduce collagen degradation
29
30. What is a Keloid?
• Non-cancerous fibrous proliferations that occur in the dermis after
trauma or injury to the skin
• Keloids grow beyond the boundaries of the original wound site (vs.
hypertrophic scar)
• Etiological factors that determine how a scar becomes a keloid
remain unknown
30
31. Who and Why?
• Individuals with darker-pigmented skin or who freckle are more
predisposed
• Seen largely in Africans, African-Americans, Hispanics, and Asians
• Can be a familial/genetic predisposition
• Can be due to immunological causes
• Bottom line… No one knows!
31
32. How? (Pathophysiology)
• A result of an overactive inflammatory response and fibroblast
proliferation
• A result of an abnormal collagen deposition in healing skin wounds
• Skin wound tension is a contributing factor in keloid formation
• Individuals with an inflammatory or infectious element are at a
predisposition for keloids
32
39. Hypertrophic scar
• Linear, red, raised firm scar
• Confined to the original injury site
• Pruritic, but not pain or hyperesthesia
• Common affect under constant pressure and stretching area
• Usually arise within 1 month of injury
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42. Hypertrophic Scar / Keloid
42
Hypertrophic scar Keloid
Can regress Does not regress
Oriented collagen Random eosinophilic
collagen
Confined to wound Not confined
Scant mucin Mucinous stroma
No myofibroblasts Myofibroblasts
43. • In this stage alkaline phosphatase plays an important
role in mineralization.
• Several growth factors identified as a key components in
the production of osseous tissue are:
a. TGF- ß
b. BMP
c. PDGF
d. FGF
e. IGF
43
44. Growth Factors
• Growth Factors and Biologic Wound Products
• • Biologic wound products aims to accelerate healing by
augmenting or modulating inflammatory mediators
• • Prostaglandin E1
• • Cytokines-Chemokines , lymphokines, monokines, interleukins,
colony-stimulating factors, and interferons.
•
• • Becaplermin(Regranex)rhPDGF & EGF-FDAapproved products
in the growth factor family
44
45. COMPLICATION:
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1. Deficient scar formation:
a) Wound dehiscence
b) Ulceration
2. Excessive formation of the repair components:
a) Aberrations of growth: -hypertrophic scar
-keloid
b) Excessive amount of granulation tissue
formation
46. c) Exuberant proliferation of fibroblasts and other
connective tissue elements: Desmoids or Aggressive
fibromatoses
46
3. Formation of contractures
48. 48
Silver Sulfadiazine and Nitrate
• Higher rate of resistance
Nanocrystalline Silver Dressing
• Impaired reepithelialization
• Pseudoeschar formation
• Bone marrow toxicity from the propylene glycol
• High enough initial concentration (3176mg/L and 3025mg/L, resp. but have little to no
residual activity
49. 49
•Nanocrystalline Silver Dressing
Two layers of high-density polyethylene net sandwiching a layer of
rayon/polyester gauze
• Outer layer is coated with a nanocrystalline (<20nm), noncharged
form of silver (Ag0), and the inner layer helps maintain a moist
environment for wound healing
![The ancient Egyptians were the first civilization to have
trained clinicians to treat physical aliments. Medical papyri,
such as the Edwin Smith papyrus (circa 1600 BCE) and the
Ebers papyrus (circa 1534 BCE), provided detailed
information of management of disease, including wound
management with the application of various potions and
grease to assist healing. [1, 2]
History of Wound Management
2](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)