Wound Healing

Group 1
Content
• Phases of Wound Healing
• Heritable Diseases of Connective Tissue
• Healing in Specific Tissues
• Classification of Wounds
• Excess Healing
• Treatment of Wounds
PHASES OF WOUND HEALING
HEMOSTASIS and
INFLAMMATION

PROLIFERATION

MATURATION and
REMODELING
HEMOSTASIS and INFLAMMATION

Platelets - release a number of

wound-active substances:
• platelet-derived growth factor
(PDGF),
• transforming growth factor-β (TGF-β)
• platelet- activating factor (PAF)
• Fibronectin
• serotonin

Fibrin clot - scaffolding for the

migration into the wound of
inflammatory cells
Polymorphonuclear leukocytes
(PMNs)
- first infiltrating cells to enter the

wound site
- peak: 24 to 48 hours
- migration stimulated by:
• Increased vascular
permeability
• local prostaglandin
• chemotactic substances
(complement factors, IL-1,
TNF-α, TGF-β, platelet factor 4,
or bacterial products)
Polymorphonuclear leukocytes
(PMNs)
- Functions:
• phagocytosis of bacteria and
tissue debris
• major source of cytokines early
during inflammation (TNF-α) ->
angiogenesis and collagen
synthesis
• release proteases (collagenases) -
> participate in matrix and
ground sub- stance degradation
in the early phase of wound
healing
Macrophages
- second population of inflammatory
cells that invades the wound
- achieve significant numbers in the
wound by 48 to 96 hours postinjury
and remain present until wound
healing is complete
- significant role: regulating
angiogenesis and matrix
deposition and remodeling
Lymphocytes

- Less numerous than macrophages

- peak: 1 week postinjury

- play an active role in the modulation of

the wound environment

- bridge the transition from the

inflammatory to the proliferative phase of

healing
 PROLIFERATION

- Second phase of wound healing

- roughly spans days 4 through 12

- Fibroblasts and endothelial cells are

the last cell populations to infiltrate

the healing wound

PROLIFERATION

Fibroblasts
- strongest chemotactic factor: PDGF
- primary function: matrix synthesis
remodeling
- activation is mediated mainly by cytokines
and growth factors released from wound
macrophages

Endothelial cells
- proliferate extensively
- Function: participate in the formation
of new capillaries (angiogenesis)
- migrate from intact venules close to
the wound
Matrix Synthesis
• Collagen
• Most abundant protein
in the body
• Secreted by the
fibroblast
• Type I collagen
• Type III collagen
• During the fibroblastic phase:
• PDGF
• TGF
• EGF
• Type 3 is secreted in higher concentration
Collagen synthesis
• Systemic factor :
• Adequate oxygen supply
• Presence of sufficient nutrients
• Cofactors and local wound environment
PROTEOGLYCAN SYNTHESIS
• Glycosaminoglycans
• Comprises a large portion of the” ground substance” that
makes up granulation tissue
• Major glycosaminoglycans
•Fibronectin
•Matrix Metalloproteases
Maturation and Remodeling
• GOAL: scar contraction with
collagen cross-linking
shrinking and loss of edema
• Characterized :
reorganization of previously
synthesized collagen
ØMetalloproteinases breaks
down collagen
ØThe net wound collagen
content is the result of a
balance between collganolysis
and collagen synthesis
• Begins during the fibroplastic
phase
• Net shift toward collagen
synthesis
• Re-establishment of
extracellular matrix
Epithelialization
- Characterized primarily by proliferation and migration
of epithelial cells adjacent to the wound
- Fixed Basal cells in a zone near the cut edge undergo a
series of Rapid mitotic divisions, and these cells appear
to migrate by moving over one another in a leapfrog
fashion until the defect is covered
Epithelialization
- Once the defect is bridged, the migrating epithelial cells lose
their flattened appearance, become more columnar in shape,
and increase their mitotic activity.
- Layering of the epithelium is re-established, and the surface
layer eventually keratinizes
Epithelialization
Added info:
- The stimuli for re-epithelialization remain incompletely defined;
however, it appears that the process is mediated by a
combination of a loss of contact inhibition.
 Wound Contracture
- For wounds that do not have approximated edges (Non-
Surgical), the area of the wound will be decreased by this action
- Myofibroblast has been postulated as being the major cell
responsible for contraction, and it differs from the normal
fibroblast in that it possesses a cytoskeletal structure
- Contains α-smooth muscle actin in thick bundles called stress
fibers
 Wound Contracture
- For wounds that do not have approximated edges (Non-
Surgical), the area of the wound will be decreased by this action
- Myofibroblast has been postulated as being the major cell
responsible for contraction, and it differs from the normal
fibroblast in that it possesses a cytoskeletal structure
- Contains α-smooth muscle actin in thick bundles called stress
fibers
Heritable Diseases of
Connective Tissue
• Ehlers-Danlos Syndrome
• Marfan’s Syndrome
• Osteogenesis Imperfecta
• Epidermolysis Bullosa
• Acrodermatitis Enterohepatica
Ehlers-Danlos Syndrome
• 10 disorders that present as a defect in collagen formation
• Genetic defect encoding alpha chains of collagen type V
(quantitatively or structurally defective)
• Phenotypic findings:
ØThin, friable skin with prominent ØRecurrent hernia
veins ØHyperextensible joints
ØEasy bruising ØHiatal hernia
ØPoor wound healing ØIntestinal diverticulae
ØAtrophic scar formation ØRectal prolapse
Subtypes
Type Clinical Features Inheritance Defect

Skin: soft, hyperextensible, easy bruising, fragile,

I AD NK
atrophic scars; hypermobile joints; varicose veins

II Less severe than type I AD NK

Skin: soft, not hyperextensible, normal scars; small

III AD NK
and large join hypermobility

Skin: thin transluscent, visible veins, normal

IV scarring, no hyperextensibility, no joint AD Type III Collagen
hypermobility; arterial, bowel, and uterine rupture

V Similar to Type II XLR NK

Skin: hyperextensible, fragile, easy bruising; Lysyl hydroxylase

VI AR
hypermobile joints; hypotonia; kyphoscoliosis def.
Type Clinical Features Inheritance Defect

Skin: soft, mild hyperextensibility, no increased Type I Collagen

VII AD
fragility; extremely lax joints with dislocations Defect
Skin: soft, hyperextensible, easy bruising, abnormal
VIII scars with purple discoloration; hypermobile joints; AD NK
generalized periodontitis
Skin: soft, lax; bladder diverticula and rupture; Lysyl oxidase defect
IX limited pronation and supination; broad clavicle; XLR with abnormal
occipital horns copper use

X Similar to Type II with abnormal clotting studies AR Fibronectin defect

Absence of
TNx Hypermobile joints, skin fragility AR
tenascin X protein
Management
• Dermal wounds should be closed in two layers, approximated with
the sutures under tension
• Stitches should be left in place twice as long as usual
• External fixation with adhesive tape can help reinforce the scar and
prevent stretching
• Recurrent Hernia in Children:
o Avoid tearing the skin and fascia
o Adult-type repair with the use of mesh or felt may decrease incidence of
recurrence
Marfan’s Syndrome
• Features:
ØTall stature
ØArachnodactyly
ØLax ligaments
ØMyopia
ØScoliosis
ØPectus excavatum
ØAscending Aorta Aneurysm
ØHernia predisposition
• Genetic defect: FBN1 gene
§ Encodes for fibrillin
§ Intricate role in TGF-B signaling
§ Abnormal FBN1 gene function: may cause an increase in TGF-B signaling
Osteogenesis Imperfecta
• Features:
§ Brittle bones
§ Osteopenia
§ Low muscle mass
§ Hernias
§ Ligament and joint laxity
• Defect:
§ Type I collagen mutation
§ Prolidase mutation
Type Clinical Features Inheritance
I Mild bone fragility, blue sclera Dominant
“Prenatal lethal”; crumpled long bones, thin ribs,
II Dominant
dark blue sclera
Progressively deforming; multiple fractures; early Dominant/
III
loss of ambulation Recessive
Mild to moderate bone fragility; normal or gray
IV Dominant
sclera; mild short stature
Epidermolysis Bullosa
• Rare genetic disorder
• Recessive type
• Gene defect: COL7A1, type 7
collagen
• Impairment of tissue adhesion

• Management:
• Prevention of trauma and
decompression of blisters
• Surgical intervention:
• Esophageal dilatation
• Gastrostomy tube placement

Andrews Disease of the Skin 11th Ed pp. 547-550

Principles of Schwartz 10th Ed pp. 248-249
Acrodermatitis Enterohepatica
 • Autosomal- recessive, inherited
disorder
• Mutations in the SLC39A4 gene
– encodes for zinc transporter.
• Zinc deficiency is associated with
granulation tissue formation.
• Manifestation: impaired wound
healing
• Management:
• Oral supp. 100-400mg of zinc
sulfate
• 1-2 mg/kg/day (50mg elemental
zinc per 220 mg zinc tablet)

Andrews Disease of the Skin 11th Ed p. 473

Principles of Schwartz 10th Ed pp. 248-249
 HEALING IN
SPECIFIC TISSUES
GIT
Surgical or Mechanical reaposition of bowel
ends.

Failure of Excessive
healing healing
Dehiscence
Stricture
Leaks
Stenosis
Fistulas
GIT : Gross anatomic features

CAN OCCUR WITHOUT SCARRING

ØThe ultimate peritoneal extension

ØSerosal healing à essential for quickly watertight seal from luminal side bowel
ØMesothelial (serosal) healing can occur without scaring
GIT
Collagen synthesis Collagen lysis

Fibroblast Collagenase

• Expressed post injury in all

segments of the GI tract
• colon>small bowel
•Derived from the;
Smooth muscle •Neutrophils
•Macrophages
•Intraluminal bacteria.
GIT
• Considerations specific o anastomotic healing:
• Ideal method for suturing two ends of bowel together has not yet
been identified
• Findings:
• stapled ileo-colic anastomoses® fewer leak
• hand-sutured everting anastomoses®­ risk for leak but ¯ incidence of
stenosis
BONE HEALING
Initial stage Bone
Soft tissues where ainbridge
bloodbetween
remodeling
formcallus accumulates
the
Hard stage
at the fracture sitebone segments
fractured

Liquefaction
Excessiveand degradation
callus is reabsorbedof
Softnonviable
tissues is deposited
products atinfracture
neovascularization
site
Mineralization of soft callus to
(preventing damage into the newly laid blood
bone
vessels) à fibrocartilaginous union
2-3 months à complete boney
Revascularization
union occurs in normal
boneMarrow
à newcavity
bloodisvessels
recanalized
growing
à fracture site (similar in the
External callus
formation of à soft callustissue
granulation in bonein shaft
soft tissue)
Remodeling allows;
Clinically, Strong
corrects
phase à allow weight
transmission
characterized ofofforces
end pain and
Sx: inflammation, swelling
bearingand
inflammatory sign erythema
restores the contours of bone
CARTILAGE

• Consist of chondrocytes surrounded by

extracellular matrix made up of;
• Proteoglycans
• Collagen fibers
• Water
CARTILAGE
• Hypervascular perichondrium contributes cartilage nutrients
• Healing response is dependent on depth on injury
• superficial: disruption of proteoglycan matrix and injury to the
chondrocytes à no inflammatory response, ­ synthesis of
proteoglycan and collagen dependent entirely on the chondrocyte
• slow to heal
• result in persistent structural defects
• deep: involve underlying bone and soft tissue à exposure of vascular
channels à formation of granulation tissue à fibroblast migrate
toward wounds à synthesize fibrous tissueà chondrificationà hyaline
cartilage is formed à restoration of structural & functional integrity
• hemorrhage® initiate inflammatory response®activation of cellular function
repair
TENDON
• Subjected into different injuries ;
• Laceration
• Rapture
• Contusions
TENDON
• Tendon vasculature effects

Hypovascular Tendon Hypervascular

Tendon
Heals with less motion More motion

More scar formation Less scar formation

NERVE
• 3 types of nerve injuries
• Neuropraxia

• Axonotmesis

• Neurotmesis
NERVE
3 Steps in nerve end progress in all types of injury

1. Survival of axonal cell bodies

2. Regeneration of axons that grow across the

transectednerve to reach the distal stump

3. Migration and connection of the regenerating nerve ends

tothe appropriate nerve ends or organ targets
FETAL WOUND HEALING
• Main characteristic is the lack of scar formation
• Transition wound
• occurs in third trimester, there is scarless healing

• Transforming growth factor-b (TGF- β, specifically, low levels of

TGF-β1 and TGF- β2 and high levels of TGF- β3—probably has a
central role in scar formation, and studies of its role are
ongoing.

• Low levels of platelet-derived growth factor (PDGF), a greater

amount of epidermal growth factor (a mitogen for
epithelialization), a faster rate of wound healing, and a greater
amount of hyaluronic acid in the extracellular matrix has been
documented and suggests a more efficient process of wound
healing in fetal models.
FETAL WOUND HEALING
• Characteristics that influence differences between
fetal and adult wounds;
• Wound n environment
• Inflammation
• Growth factors
• Wound matrix
Characteristics that influence differences between fetal and adult
wounds

• Fetus is bathed in a sterile temp-stable environment.

Wound • But study show scarless healing can also occur outside of
environment amniotic fluid environment, and conversely scars can occur in
utero.

• Inflammatory response correlates directly the amount of scar

formation in all healing wounds
Inflammation • Immaturity of the fetal immune system à reduced inflammation
à lack of scarring observe.

Growth • Absence of TGFβ (significant role in scar formation) à lack of scar

factors formation
Characteristics that influence differences between fetal and adult wounds

• Fetal urine à stimulates hyaluronic acid à produces

HMW-gylcosaminoglycan à produce fibroblast.
Wound Matrix • Fetal fibroblast
• Produce more collagen
• Increase level of hyaluronc acid

• Collagen formation pattern of fetal wounds is reticular

Collagen in nature
CLASSIFICATION OF
WOUNDS
ACUTE WOUNDS
• Occurs in few (if any) complications
• End resultà well-healed wound
Surgical Wounds
• Primary Intention
• Secondary Intention
• Tertiary Intention or Delayed primary closure
• Constant and continual increase
that reaches a plateau at some
point post-injury.

• ↓ wound-breaking strength
• Same integrity and strength
• Nutritional deficiencies
• Infections
• Severe trauma

• Failure to achieve mechanical

strength equivalent to normally
healed wounds
• Diabetes
• Chronic steroid usage
• Tissues damaged
Factors Affecting Wound Healing
Advanced Age
§ Older age= poor wound healing
Hypoxia, Anemia, and Hypoperfusion
§ Low oxygen tension
§ Optimal Collagen Synthesis
§ ↑subcutaneous oxygen tension levels= ↑FIO2
§ Enhanced collagen deposition
§ Decreased rates of wound infection after elective surgery
Factors Affecting Wound Healing
Hypoxia, Anemia, and Hypoperfusion
§ Factors affecting local oxygen delivery
• Hypoperfusion
• systemic reasons (low volume or cardiac failure)
• local causes (arterial insufficiency, local vasoconstriction, or excessive tension on tissues)
• level of vasoconstriction of the subcutaneous capillary bed
• responsive to fluid status, temperature, and hyperactive sympathetic tone as is often
induced by postoperative pain.
Factors Affecting Wound Healing
Steroids and Chemotherapeutic Drugs
§ ↑glucocorticoids = ↓collagen synthesis and wound strength
§ ↑anti-inflammatory effect= ↑ inhibitory effect
§ X epithelialization and contraction
§ ↑ rates of wound infection
§ Chemotherapeutic antimetabolite drugs =X early cell proliferation and wound
DNA and protein synthesis
Factors Affecting Wound Healing
Metabolic Disorders
§ DM- ↑ rates of wound infection and failure
§ Uncontrolled diabetes- ↓inflammation, angiogenesis, and collagen synthesis.
§ Large- and small-vessel disease- HALLMARK of advanced diabetes
§ Local hypoxemia
§ Uremia- ↓wound collagen synthesis
 Factors Affecting Wound Healing
VITAMIN C VITAMIN A ZINC
Nutrition
Conversion of proline and lysine to Increases the inflammatory response in Most well-known element in wound
Lack
hydroxyproline§and of nutrients=
hydroxylysine, alters
woundwound
healing healing healing
respectively.
SCURVY OR VITAMIN C DEFICIENCY Reverse the inhibitory effects of Zinc deficiency
-Failure in collagen synthesis and corticosteroids on wound -↓fibroblast proliferation
cross-linking healing. -↓ collagen synthesis
-impaired overall wound strength
-delayed epithelialization
-Increased incidence of wound infection Restore wound healing impaired by diabetes,
tumor formation, cyclophosphamide, and
radiation.
-Impairment in neutrophil function, ↓ Vitamin A deficiency impairs wound healing
complement activity, and ↓ walling-off
of bacteria secondary to insufficient
collagen deposition.
Factors Affecting Wound Healing
Infections
§ Weaken an abdominal closure or hernia repair
§ Cosmetically- lead to disfiguring, unsightly or delayed closures.
§ Surgery-bacteria access to tissues and the bloodstream.
§ Significant hospital performance measure- adequate preoperative antibiotic
dosing and timing
• MOST COMMON ORGANISMS RESPONSIBLE FOR WOUND
INFECTIONS (IN ORDER OF FREQUENCY):
• Staphylococcus species
• Coagulase-negative Streptococcus
• Enterococci
• Escherichia coli
• Most surgical wound infections apparent within 7 to 10 days postoperatively
• WOUND INFECTION
• Wounds draining pus, wounds that are opened by the surgeon; and wounds
that the surgeon considers infected
• CLASSIFICATION
• Superficial Incisional
• Deep Incisional
• Organ/Space wound infections
• Fascia
• Muscle
• Abdominal Cavity
INSPECTION OF THE WOUND
• Most useful in detecting subtle edema around the suture or staple line
• Waxy appearance of the skin, characterizes the early phase of infection
DEEP WOUND INFECTIONS
• arise immediately adjacent to the fascia, either above or below it
• have an intra-abdominal component
• present with fever and leucocytosis
• wound dehiscence may occur
• Infections
• Necrotizing fasciitis is the most dangerous of the deep infections
• The skin demonstrates hemorrhagic bullae and subsequent frank necrosis
• The fascial necrosis is usually wider than the skin involvement or than the
surgeon estimates on clinical grounds
• Necrotizing fasciitis is the most dangerous of the deep infections
• The skin demonstrates hemorrhagic bullae and subsequent frank necrosis
• The fascial necrosis is usually wider than the skin involvement or than the
surgeon estimates on clinical grounds
• Infections
• The mere presence of bacteria in an open wound does not constitute an
infection
• Contamination is the presence of bacteria without multiplication
• Colonization is multiplication without host response
• Infection is the presence of host response in reaction to deposition and multiplication of
bacteria
• Infections
• The host response that helps in diagnosing wound infection
• Cellulitis
• Abnormal discharge
• Delayed healing Change in pain
• Abnormal granulation tissue
• Abnormal color and odor
• Infections
• Chronic granulomatous disease (CGD) comprises a genetically heterogeneous
group of diseases in which the reduced nicotinamide adenine dinucleotide
phosphate - dependent oxide enzyme is deficient
• Impairs the intracellular killing of microorganisms, leaving the patient liable to
infection by bacteria and fungi
• When CGD patients require surgery, a preoperative pulmonary function test
should be considered
• Wound complications, mainly infection, are common
CHRONIC WOUND HEALING
• CHRONIC WOUNDS
• a wound that does not heal in an orderly set of stages and in a predictable
amount of time the way most wounds do
• Repeated trauma, poor perfusion or oxygenation, and excessive inflammation
may contribute to the chronicity of the wounds.
CHRONIC WOUND HEALING
• Skin Ulcers
• usually occurs in traumatized or vascularly compromised soft tissue
• Are chronic in nature
• Major component of chronic wounds
CHRONIC WOUND HEALING
• Ischemic Arterial Ulcers
• Venous Stasis Ulcers
• Diabetic Ulcers
• Decubitus or Pressure Ulcers
CHRONIC WOUND HEALING
• Ischemic Arterial Ulcers
• Occurs due to a lack of blood and are painful at presentation
• Common cause is PAD
• Mostly present in distal portion of extremities (interdigital cleft)
• Management is by revascularization and wound care
CHRONIC WOUND HEALING
• Venous Stasis Ulcers
• Occurs due to incompetence of either the superficial or deep venous systems
• Most common site is above the medial malleolus, over Cockett’s perforator
• Typical location combined with a history of venous incompetence and other
skin changes is diagnostic
• Wound is usually shallow with irregular margins and pigmented surrounding
skin
CHRONIC WOUND HEALING
• Venous Stasis Ulcers
• Treatment of venous ulcers is compression therapy
• Wound care focuses on maintaining a moist wound environment, which can
be achieved with hydrocolloids
CHRONIC WOUND HEALING
• Diabetic Wounds
• 60 to 70% are due to neuropathy
• 15 to 20% are due to ischemia
• 15 to 20% are due to a combination of both
CHRONIC WOUND HEALING
• Diabetic Wounds
• The neuropathy is both sensory and motor, and is secondary to persistently
elevated glucose
• The loss of sensory function allows unrecognized injury to occur from ill-
fitting shoes, foreign bodies, or other trauma
• The motor neuropathy or Charcot foot leads to collapse or dislocation of the
interphalangeal or metatarsophalangeal joints
• Diabetic Wounds
CHRONIC WOUND HEALING
• Diabetic Wounds
• Treatment involves local and systematic measures
CHRONIC WOUND HEALING
• Decubitus/Pressure Ulcers
• A localized area of tissue necrosis that develops when a soft tissue is
compressed between a bony prominence and an external surface
• Excessive pressure causes capillary collapse and impedes the delivery of
nutrients to body tissues
• Decubitus/Pressure Ulcers
CHRONIC WOUND HEALING
• Decubitus/Pressure Ulcers
• Four stages of pressure ulcer formation
• STAGE 1 – nonblanchable erythema of intact skin
• STAGE 2 – partial-thickness skin loss involving epidermis, dermis, or both
• STAGE 3 – full-thickness skin loss but not through the fascia
• STAGE 4 – full-thickness skin loss with involvement of muscle and bone
CHRONIC WOUND HEALING
• Decubitus/Pressure Ulcers
• Treatment of pressure ulcers
• Debridement of all necrotic tissues
• Maintenance of a favorable wound environment
• Relief of pressure
• Addressing host issues such as nutritional, metabolic, and circulatory status
Excess Healing
Excess Healing
• excess healing can be as significant as wound failure
• protein and differ in the skin (mutilating or debilitating scars, burn
contractions), tendons (frozen repairs), the GI tract (strictures or
stenoses), solid organs (cirrhosis, pulmonary fibrosis), or the
peritoneal cavity (adhesive disease).
Hypertrophic Scars
• rise above the skin level but stay within the
confines of the original wound and often
regress over time
• develop within 4 weeks after trauma
• initially erythematous and raised
• the collagen bundles are flatter, more
random, and the fibers are in a wavy pattern
Keloids
• rise above the skin level as well, but extend beyond the
border of the original wound and rarely regress
spontaneously more common in darker-pigmented
ethnicities
• autosomal dominant
• continuous production and synthesis of fibronectin-
promotes clot generation, granulation tissue formation,
re-epithelialization
• also increased levels of TGF-beta and insulin-like growth
factor
• result from surgery, burns, skin inflammation, acne,
chickenpox, zoster, folliculitis, lacerations,
abrasions,tattoos, vaccinations, injections, insect bites,
ear piercing, or may arise spontaneously.
• occur 3 months to years after the initial insult
Keloids
• rarely extend into underlying subcutaneous tissues
• Certain body sites have a higher incidence of keloid
formation, including the skin of the earlobe as well
as the deltoid, presternal, and upper back
• surgical intervention can lead to recurrence
• the collagen bundles are virtually nonexistent, and
the fibers are connected haphazardly in loose sheets
with a random orientation to the epithelium
• collagen fibers are larger and thicker, synthesize
collagen at a rate 20 times greater
Hypertrophic scar vs Keloids
 Peritoneal Scarring
• result of peritoneal injury: surgery or intra-
abdominal infection.
• due to surgery, thermal or ischemic injury,
inflammation, or foreign body reaction àdisrupts
the protective mesothelial cell layer lining the
peritoneal cavity and the underlying
• connective tissueàelicits an inflammatory
responseà
• transient fibrin depositionàinsufficient fibrinolytic
activity àpermanent fibrous adhesions will form by
collagen deposition
Treatment of Wounds
Mechanical Devices
• Augments and improves on certain functions of dressings, in
particular the absorption of exudates and control of odor.
Skin Replacement

• Conventional Skin Grafts

• Full-thickness grafts
• Autologous grafts (autografts)
• Allogeneic grafts (allografts, homografts)
• Xenogeneic grafts (heterografts)
Desired Features of Skin Substitutes
• Skin Substitutes
1. Rapid reestablishment of functional skin
(epidermis/dermis)
2. Receptive to body’s own cells
3. Graftable by a single, simple procedure
4. Graftable on chronic of acute wounds
5. Engrafment w/o use of extraordinary clinical
inervention
Antibiotics

• Signs of infection:
Erythema
Cellulitis
Swelling
Purulent discharge
Dressings
• Primary dressing
• Secondary dressing

Desired characteristics of wound dressings:

• Promote wound healing

• Conformability
• Pain and odor control
• Non-allergenic and non-irritating
• Permeability to gas
• Safety
• Non-traumatic removal
• Cost-effectiveness
• Convenience
Types of dressings:

1. Absorbent Dressings
2. Nonadherent Dressings
3. Occlusive and Semiocclusive Dressings
4. Hydrophilic and Hydrophobic Dressings
5. Hydrocolloid and Hydrogel Dressings
6. Alginates
7. Absorbable Materials
8. Medicated Dressings
Growth Factor Therapy

• Inadequate growth factors in wound environment would lead to non-

healing wounds

• flood wound with single or multiple growth factors = jump start

healing and epithelialization
Thank you!