WOUND HEALING

Dr. Granada
September 10, 2013
Grupong WIT N WILD (WITWEEW)
Scope
1.
2.
3.
4.
5.
6.

Definition
Phases
Types of wound closures
Factors affecting wound healing
Abnormal healing/excess healing
Local care of wounds

Wound
- Any disruption of normal anatomical
relationship of tissues
- Result of injury
- Accidental ( stabbing, gun shot vehicular crash )
or intentional (self-inflicted or surgeons knife)

Consequences of wound:
Blood is lost
Defense of bacteria is broken
Tissues are destroyed and mechanical defects
may result
Role of surgeons:
Control bleeding
Prevent infection
Remove devitalized tissue
Correct any mechanical defects that develop

Wound Healing
- Response of a living organism
- Series of biochemical and cellular events
- Restore tissue integrity
Phases:
1. Hemostasis and inflammation
2. Proliferation
3. Maturation and remodeling

I Hemostasis and Inflammation

Injury results to disruption of blood vessels
Initial response: vasoconstriction (small blood
vessel retract spontaneously) due to release of
vasoactive amines
Exposure of extracellular matrix to platelets
Platelet aggregation,degranulation,activation of
coagulation cascade leading to fibrin clot (under
the influence of Platelet Deriged Growth
Factors)
o Fibrin clot forms the scaffold for
migrating cells (neutrophils and
monocytes)
Platelet granules secrete platelet-derived
growth factor(PDGF), transforming growth
factor (TGF-), platelet-activating factor (PAF)
fibronectin, serotonin
Vasodilatation (increased permeability for the
cells to migrate)
Polymorphonuclear cells (24-48 hrs)
o PMNs 1st to arrive and secrete
proteases
o Primary role is phagocytosis of bacteria
and tissue debris
o Good source of cytokines and other
growth factors
o Delays epithelial closure of wounds
Neutrophil migration stimulants:
increased vascular permeability
local prostaglandin release and
presence of chemotactic substances
(complement factors, interleukin1,tumor necrosis factor a,TNF-B,
platelet factor 4 or
bacterial products
Macrophages (peaks at 48 -96 hrs post
injury)
o remain present until wound healing is
complete
o

main role:attract fibroblasts

towards wound site

o
o

Derived from circulating monocytes

participate in wound debridement via
phagocytosis and microbial stasis via
oxygen radical and nitric oxide synthesis

Figure 1. Length of each phase

1

o
o

activates and recruites other cells via

cytokine and growth factors
regulates cell proliferation, matrix
synthesis and deposition, angiogenesis
or remodeling

Figure 3. Peak of cellular migration postinury

II Proliferative
spans 4-12 days post injury
Tissue continuity is reestablished

Figure 2. Macrophage activities during wound healing

EGF = epithelial growth factor; FGF = fibroblast growth
factor; IGF = insulin-like growth factor; IFN- =
interferon- ; IL =interleukin; PDGF = platelet-derived
growth factor; TGF = transforming growth factor beta;
TNF- = tumor necrosis factoralpha; VEGF = vascular
endothelial growth factor.
T lymphocytes (peaks 1wk post injury)
o role in wound healing is not fully
defined
o may inc. wound strength and collagen
content
o

o
o
o

Bridge the transition from the

inflammatory to the proliferative phase
of healing
modulates and maturates the wound
environment
selective depletion of CD8 T
lymphocytes enhances wound healing
down regulates fibroblast collagen
synthesis by cell assoc -interferon,
TNF-a and Il-1

Inflammatory phase depends on the number of

bacteria present. Heavily contaminated: prolong
inflammatory phase

Fibroblasts and endothelials are last to

infiltrate the healing wound
Fibroblasts appear (PDGF - strongest
chemotactic factor for fibroblasts) - synthesize
more collagen
proliferate and activate under the influence
of cytokine and growth factors from
macrophages
Lactate accumulates (~10mmol)-- a potent
regulator of collagen synthesis
Endothelial cells proliferate under the (TNF-a,
TGF-B, VEGF) would stimulate angiogenesis
Matrix synthesis
Biochemistry of Collagen
Collagen-most abundant protein in the body
Formation of extracellular matrix
Collagen 18 types, type I & III EC in skin
Glycine (third position), proline or lysine (second
position)
Protocollagen translated from mRNA
Release of protocollagen--chain hydroxylation
of prolinehydroxyproline and
lysinehydrooxylysine in endoplasmic
reticulum by specific hydroxylases
Prolyly hydroxylases requires oxygen and
iron as cofactors, a-ketoglutarate as cosubtrate
an vitamin C as electron donor
Protocollagen chain assumes a-helical
configuration after it is glycosylated by linking
of galactose and glucose at hydroxylysine
residues
3 alpha helical chains are formed called
procollagen
2

Collagen synthesis dependent on adequate O2,

sufficient amino, CHO, co-factors, local wound
environment

As scar collagen is deposited, proteoglycans

are incorporated in the collagen scaffolding
With scar maturation and collagen
remodelingproteoglcans diminishes

Epithelialization
- Migration &proliferation of epithelial cells
adjacent to the wound within 1 day of the injury
- Marginal cells (hair follicles, sweat
glands)migrate across surface of the provisional
matrix
-

Fixed basal zones undergo mitosis and

migrate by moving over one another in leapfrog
fashion until defect is covered
Once defect is bridged, epithelial cells lose their
flattened appearance and become more
columnar and inc. mitotic activity
Layering of epithelium is reestablished--keratinizes
Complete w/ in 48 hrs in incised wounds, longer
in larger wounds with significant
epidermal/dermal defect; water tight sealed
clean wounds may not be covered
If only epithelium and superficial dermis
(e.g split thickness skin graft/STSG) donor sites
or 2o burn)re-epithelialization with minimal or
no fibroplasia and granulation tissue formation
Process is mediated by
o combination of loss of contact
inhibition;
o exposure to constituents of extracellular
matrix (fibronectin);
o cytokines

Figure 4. The steps of collagen synthesis

Proteoglycan synthesis
- Glycosaminoglycans make up granulation tissue
- Couple with proteins they form
proteoglycans(glucoronic acid or iduronic acid &
hexosamine w/c is usually sulfated)
-

Heparin sulfate-10 disaccharide units;

hyaluronic acid-2000 units
Dermatan, chondroitin sulfate (major
glycosaminoglycans present in wounds) synthesized by fibroblasts during 1st 3 weeks of
healing
3

Metalloproteinases (MMPs) breaks down

collagen
o net wound collagen content result of
balance between collagenolysis &
collagen synthesis
if there is imbalance: more
collagen deposited, less degraded
keloid scars
o net shift toward collagen synthesis reestablishment extracellular matrix and
acellular collagen rich scar
Wound strength & mechanical integrity
depends on quality and quantity of newly
deposited collagen
Deposition of matrix at the wound site
follows pattern:
o First: Fibronectin and collagen type 3
o Second: Glycosaminoglycans and
proteoglycans
o Final: Collagen type

Figure 5. Healing by epithelialization of

superficial cutaneous wounds.
Wound contraction
- Process by w/c area of wound decreases in size
(actin and myofibroblasts)
- Myofibroblasts major cell responsible for
contraction;
o
o

o
o
o

differs from fibroblast by

possessing cytoskeletal structure
contain -smooth muscle actin in thick
bundles called stress fibers giving it
contractile ability
Undetectable until day 6
Increasingly expressed for the next 15
days
After 4 wks, process fades, cells
undergo apoptosis

Undifferentiated fibroblasts may

also contribute to wound contraction
Ex. Granulating wound (2ndary intention)

Figure 6: Matrix deposition postinjury

Several weeks postinjury, amount of

collagen reaches plateau but tensile strength
continues to increase for several months
Fibril formation and fibril cross-linking:
o decrease collagen solubility
o increase strength and
o increase resistance to enzymatic
degradation
Scar remodeling starts 6-12 months post injury,
mature, avascular scar
Mechanical strength of scar never achieves that
of normal tissues (
only about 70-80
strength of normal skin is achieved)

III Maturation & Remodeling

begins during the fibroblastic phase
Reorganization by collagen synthesis
4

Cardiovascular disease, metabolic diseases,

cancer, malnutrition (
must be corrected
first before surgery)
Delay of 1.9 days (epithelialization) in patients
older than 70 y.o.

2.Hypoxia, anemia, hypoperfusion

Optimal collagen synth. req. O2 as cofactor for
hydroxylation
Factor affecting local O2 delivery: systemic (low
volume or cardiac failure) local (arterial
insufficiency, vasoconstriction, extensive
tension in tissues)
Low O2 tension-deleterious effect on wound
healing
Fibroblasts is impaired

Increased subcutaneose oxygen tension

levels and oygen delivery or increased FIO2
(fraction of inspired oxygen) results in enhanced
collagen deposition decreased wound infection
after elective surgery
Arterial insufficiency, Vasoconstriction
Mild to moderate anemia does not affect O2
tension unless hematocrit <15%

3.Steroids, chemotherapeutic drugs

Large doses of glucocorticoids decrease
collagen synthesis and wound strength
Inhibit inflammatory phase, release of
lysosomal enzymes,
Figure 7. Phases of wound healing viewed
histologically
A. The hemostatic/inflammatory phase. B. Latter
inflammatory phases reflecting infiltration by
mononuclear cells and lymphocytes. C. The proliferative
phase, with associated angiogenesis and
collagen synthesis.
FACTORS AFFECTING WOUND HEALING
1.Advancing age
delayed/impaired wound healing
direct correlation with older age and poor
wound healing such as dehiscence, incisional
hernias
Special measure done: Strong sutures,
reinforcement of repair

the stronger the anti-inflammatory effect of

the steroid, the greater the inhibitory effect on
wound healing
Steroids used after the 1st 3-4 days postinjury
do not affect wound healing as severely as
when they are used in immediate postoperative
period
If possible, their use should be delayed or
alternative forms with lesser anti-inflammatory
effects should be used
Inhibit epithelialization and wound
contractionincrease rate of wound infection
Reversed by topical application of Vit. A
Chemotherapy (CT) affects wound healing by
inhibiting early cell proliferation & wound DNA
& protein synthesis (delay for 2 wks)

Neoadjuvant patient given 2-4wks for recovery

before operation

4. Metabolic disorders
Diabetes Mellitus-- best known metabolic
disorder contributing to increased rate of wound
infection and impaired would healing
Dec. inflammation, angiogenesis, collagen
synthesis
Large & small blood vessel disease (hallmarkof
advanced DM) contribute to local hypoxemia
Defects in granulocyte function, capillary
ingrowth, fibroblast proliferation, lacking in
growth factors
insulin given during early phase of healing
restores collagen synthesis and granulation
tissue formation

Type I DM-decrease wound collagen

accumulation in the wound
Type II DM-no effect on collagen accretion
Improve wound healing by increasing inspired
O2 tension, judicious use of antibiotics and
correction of other coexisting metabolic
diseases
Uremia-decrease wound collagen synthesis and
breaking strength

5. Nutrition

Extremely rare to encounter pure protein or

energy malnutrition; majority exhibit combine
Malnutrition correlates with wound
complications and increased wound failure:
o Impaired healing response
o Decrease cell mediated immunity
o Decrease phagocytosis
o Decrease intracellular killing of bacteria by
macrophages and neutrophils
Brief preop illness or decrease nutrient intake
(correct first before subjecting to surgery)
results in impaired fibroplasias
Preop nutrition can reverse or prevent decrease
collagen deposition
In a malnourished patient with GIT
malignancy pre-op at least 7-10 days via
enteral: lessens bacteria; parenteral: expensive

o
o
o

Arginine:
o increases wound fibroplasias (30g for 14
days)
o No effect on epithelialization
Vit. C
o required for convertion of proline and lysine
to hydroxyproline and hydrozylysine;
o deficiency or scurvy results to:
failure of collagen synthesis & cross
linking
increase incidence of wound infection
due to decrease in neutrophil function,
complement activity and bacterial
walling-off
o Recommended Dietary Allowance (RDA) 60
mg/day
o 2 g/day in severely injured/extensively
burned
Vit. A
o inc inflammatory response:
increasing lability of lysosomal
membranes,
inc collagen production, EGF
receptors
o Reverse inhibitory effects of steroids,
diabetes, tumor formation,
cyclophosphamide & radiation
o Supplemental dose for severely injured:
25,000-100,000 IU/day
o Can reach toxic doses if taken in excess
Zinc
used in dermatologic conditions,
integral cofactor in many enzymes
deficiency results to:
dec fibroblast proliferation
dec collagen synthesis
impaired wound strength &
delayed epithelialization

6.Infection
Wound dehiscence, incisional hernia
Prolongs the inflammatory phase
Scar from infection is disfiguring, unsightly
delayed closures
Prevented by antibiotic prophylaxis
Staphylococcus, Streptococcus
Most surgical wound infections - apparent w/n
7 to 10d postoperatively
6

Wound infection - include all wounds draining pus,

whether or not the bacteriologic studies are positive;
wounds that are opened by the surgeon; and wounds
that the surgeon considers infected

Is of major concern when implants are used

Weakens an abdominal closure or hernia repair
leads to dehiscence or recurrent hernia
can be classified as superficial or suprafascial
and deep, involving fascia, muscle, or the
abdominal cavity
Deep wound infections arise immediately
adjacent to the fascia, either above or below it,
and often have an intra-abdominal component.
Most intra-abdominal infections do not,
however, communicate with the wound.
Deep infections present with fever and
leukocytosis
most dangerous of the deep infections is
necrotizing fasciitis. (high mortality, particularly
in the elderly).

Necrotizing Fascitis - an invasive process that involves

the fascia and leads to secondary skin necrosis.
Signs and symptoms:
hemorrhagic bullae
frank necrosis
edema
high fever
tachycardia
marked hypovolemia, which if uncorrected,
progresses to cardiovascular collapse
The mere presence of bacteria in an open wound, either
acute or chronic, does not constitute an infection,
because large numbers of bacteria can be present in the
normal situation
.
Antibiotic prophylaxis is most effective when:
o Adequate concentrations of
antiobiotics are present at time of
incision
o Adequate preoperative antibiotic
dosing and timing

Antibiotics after operative contamination has

occurred is clearly ineffective

Selection of antibiotics for use in prophylaxis

should be tailored to the:
- type of surgery to be performed
- operative contaminants
- profile of resistant organisms present
where the surgery is performed

The most common organisms responsible for wound

infections, in order of frequency:
1. Staphylococcus species,
2. Coagulase-negative Streptococcus,
3. enterococci
4. Escherichia coli.
The incidence of wound infection bears a direct
relationship to the degree of contamination that occurs
during the operation from the disease process itself:
class I - clean
class II - clean contaminated
class III - contaminated
class IV - dirty
Contamination - the presence of bacteria
without multiplication
Colonization - multiplication without host
response
Infection - the presence of host response in
reaction to deposition and multiplication of
bacteria
The host response that helps in diagnosing wound
infection comprises:
Cellulitis
abnormal discharge
delayed healing
change in pain
abnormal granulation tissue
bridging
abnormal color and odor
CLASSIFICATION OF WOUNDS
1.Acute

Ex. Incised wounds, lacerated wounds from

Vehicular Accidents
o Incised wounds - caused by a sharp
objects; edges are clean
o Lacerated wounds - from blunt objects;
edges are jagged
7

Acute wounds heal in a predictable manner

Few, if any complications
End result: well-healed wound

Wound Management
Primary intention
Secondary intention
Tertiary intention
2.Chronic wounds
Diabetic ulcers, venous stasis ulcers, pressure
sores
Difficult to manage, a challenge to surgeons

Failure to heal in 3 months after adequate

local care
Brought about by repeated trauma, poor
perfusion or oxygenation and excessive
inflammation
Biopsy is indicated to rule out Squamous cell
carcinoma

Chronic wounds: wounds that have failed to proceed

through the orderly process that produces satisfactory
anatomic and functional integrity or that have
proceeded through the repair process without
producing an adequate anatomic and functional result.

TYPES OF WOUND CLOSURE

1.Primary closure
Wound edges approximated w/ sutures or
staples
Healing by primary intention
Epithelialization occurs by 48-72 hrs
2.Secondary closure
Healing by secondary intention
Wound edges are left unopposed & open
Formation of granulation tissue
Margins allowed to heal by contraction
Ideal for Grossly contaminated wounds

Effective to some chronic wounds

3.Primary Delayed Closure

Healing by tertiary intention
Compromise between primary and secondary
closure
Approximation is delayed for several days
Wound is left open and observed for signs of
infection

Closure in 3-5 days if clean and without

signs of infection
Ex: ruptured AP in obese patients, close fascia,
skin SQ left open

Skin ulcers are the major component of chronic

wound
Unresponsiveness to normal regulatory signals
also has been implicated as a predictive factor
of chronic wounds.
Characterized by failure of growth factor
synthesis and decreased fibroblast proliferative
potential
Malignant transformation of chronic ulcers can
occur in any long-standing wound (Marjolin
ulcer).
Any wound that does not heal for a prolonged
period of time is prone to malignant
transformation.
Malignant wounds are differentiated clinically
from nonmalignant wounds by the presence of
overturned wound edges. Do biopsy
Figure 8: Types of wound closure

Venous stasis ulcers

most common being above the medial

malleolus, over Cockett's perforator.
wound usually is shallow, with irregular margins
and pigmented surrounding skin upon physical
examination
Wound care in these patients focuses on
maintaining a moist wound environment, which
can be achieved with hydrocolloids.
Other approaches:
o use of vasoactive substances
o growth factor application
o skin substitutes.
Most venous ulcers can be healed with
perseverance and by addressing the venous
hypertension

Ischemic Arterial ulcers

Occur due to Lack of blood supply, painful at
presentation
From emboli, a mobile thrombus
Associated with Intermittent claudication, rest
pain, night pain, color changes
Distal portion of the extremities, absent pulses
with decreased ankle-brachial index and poor
formation of granulation tissue
Usually shallow w/ smooth margins, pale
surrounding skin
Tx: revascularization and wound care

Lipodermatosclerosis - brownish pigmentation

of skin combined with the loss of subcutaneous
fat
Tx compression therapy ZnO2 boots, elevate
affected extremity
Venous stasis occurs due to the
incompetence of either the superficial or deep
venous systems.
Chronic venous ulcers usually are due to the
incompetence of the deep venous system and
are commonly painless.
Stasis ulcers occur at the sites of incompetent
perforators

5 Ps in ischemia :
o Pain,
o Pallor
o paresthesia (sensation of pin and
needles)
o paralysis
o pulselessness
Prevention:
- Removal of restrictive stockings (in
patients with critical ischemia)
- frequent repositioning
- surveillance

Diabetic Wounds
10-15% risk to develop ulcers
There are approximately 50,000 to 60,000
amputations performed in diabetic patients
each year in the United States
9

Major contributors : Neuropathy( 60-70%), foot

deformity, ischemia (15-20%)
Neuropathy+ischemia: 15-20%
Both Motor and sensory secondary to
persistently elevated blood glucose levels
Loss of sensory function injury (ill-fitted shoes,
foreign bodies )
Tx: wound debridement, antibiotics, control of
blood sugar

Contributory factors:
o Immobility
o Altered activity levels
o Altered mental status
o Chronic conditions
o Altered nutritional status

Pressure ulcer formation is accelerated in the

presence of:
o Friction
o Shear forces
o Moisture

Diabetic wound

The four stages of pressure ulcer formation are as

follows:
Stage I - nonblanchable erythema of intact skin
Stage II - partial-thickness skin loss involving
epidermis or dermis, or both
Stage III - full-thickness skin loss, but not
through the fascia
Stage IV- full-thickness skin loss with extensive
involvement ofmuscle and bone.

Additional treatment modalities:

Topical application of PDGF and granulocytemacrophage colony-stimulating factor
Application of engineered skin allograft
substitutes (expensive)
Prevention: foot care play an important role in
the management of diabetics.
Decubitus Ulcer (pressure sores)
A localized area of tissue necrosis develops
when a soft tissue is compressed between a
bony prominence & external surface
Constant Pressure capillary collapse impede
delivery of nutrition
Risk factors: Immobility, altered mental status,
nutritional status
Treatment: multidisciplinary: internist,
surgeons, nutritionist

Additional management:
Care of the Ulcer :
comprises dbridement of all necrotic tissuedone surgically
maintenance of a favorable moist wound
environment that will facilitate healing - by
employing dressings that absorb secretions but
do not desiccate the wound
relief of pressure
addressing host issues such as nutritional,
metabolic, and circulatory status.
Operative repair, usually involving flap rotation, has
been found to be useful in obtaining closure
Heritable Diseases
1. Marfans Syndrome
Tall stature, arachnodactyly, lax ligaments ,
myopia
Scoliosis, pectus excavatum
Aneurysm of ascending aorta
Defect in fibrillin (extracellular protein,
associated with elastic fibers)

Repair difficult : soft connective tissue fails

to hold sutures
10

Prone to hernia
Skin may be hyperextensible, but shows no
delay in wound healing

Diseases of connective tissue:

1.Ehlers Danlos Syndrome (plastic man)
A group of 10 disorders
Present as a defect in collagen formation
Thin, friable skin, with prominent veins, easy
bruising
Poor wound healing, abnormal scar formation
Recurrent hernias, hyperextensible joints,
coagulopathy
Hyperelasticity of skin, hyperflexibility of joints

Large vessels may develop aneurysms,

varicosities, arteriovenous fistulas that may
spontaneously rupture
Great care should be taken to avoid tearing the
skin and fascia.
The transversalis fascia is thin, and the internal
ring is greatly dilated
An adult-type repair with the use of mesh or
felt may result in a lower incidence of
recurrence

2.Acrodermatitis enteropathica
Autosomal recessive in children
Poor wound healing
Inability to absorb zinc from breast milk or food
Mutation affects zinc uptake in the intestine by
preventing zinc from binding to the cell surface
and its translocation into the cell
Associated with impaired granulation tissue
As zinc is a necessary cofactor for DNA
polymerase and reverse transcriptase, and its
deficiency may impair healing due to inhibition
of cell proliferation
Erythematous pustular dermatitis involving the
extremities and the areas around the bodily
surfaces
Dec. zinc level (>100 ug/dl), yes according to
Schwartz)
Tx: 100-400 mg zinc SO4/ day

If with infected pustular dermatitis may

need to do debridement

3.Keloids & Hypertrophic scars

Represent as overabundance of fibroplasia in
dermal healing process
Trauma to skin, mechanism is unknown
Immune system is involved
As evidenced by Inc. deposition of IgG, IgA, IgM
Antinuclear antibodies vs fibroblast, epithelial
cells
Keloids
Hypertrophic scars
-Scar extends beyond
-w/ in the boundaries
-Does not regress
-regress with time
-excision results in higher -less recurrence
recurrence
-3 months after trauma
-4weeks after trauma
Acne, injections, piercings
Treatment:
Relief of symptoms(pruritus), restoration of
function,(especially in fingers) prevent
recurrence
Excision alone, recurrence rate 45-100%
Excision+ corticosteroid injection, application of
pressure, radiation --- lower recurrence
Pressure utilizes silicone garment to be worn 24
hrs for 3 months; hydrates, decrease
inflammation, decrease collagen depostitin
Intralesional Inj w/ corticosteroids, the 1st line
of treatment for keloids;( by eschemia,
decrease collagenase, for early scars not after
12 months)
Effective scar for young scars, soften, flatten
Radiation has variable results 10-100% RR
Topical retinoids for keloids, Hts, response 50100%

Additionals:

Keloids result from surgery, burns, skin

inflammation, acne, chickenpox, zoster,
folliculitis, laceration, tattoos
Pedunculated lesions with a soft to rubbery or
hard consistency.
Keloids also have increased deposition of
immunoglobulin G (IgG), IgA, and IgM, and their
formation correlates with serum levels of IgE.
11

Antinuclear antibodies against fibroblasts,

epithelial cells, and endothelial cells are found
in keloids, but not HTSs.
HTSs have higher T-lymphocyte and Langerhans
cell contents.
In HTSs, the collagen bundles are flatter, more
random, and the fibers are in a wavy pattern.
In keloids, the collagen bundles are virtually
nonexistent, and the fibers are connected
haphazardly in loose sheets with a random
orientation to the epithelium
Body sites with higher incidence of keloid
formation, including
the skin of the earlobe as well as the deltoid,
presternal, and upper back regions

4.Peritoneal Scarring/ adhesions

Fibrous band of tissues formed between organs
& internal body wall
Sec to peritoneal injury by a prior surgical
procedure or intraabdominal infection
67% of pts had surgery
35% had intraabdominal infection
Most common cause of SBO
Increase incidence in lower abdominal surgery
Cause of sec infertility in women

Intraabdominal infection are the most

common cause of small bowel obstruction (6575%)

Following rectal surgery, left colectomy, or

total colectomy, there is an 11% chance of
developing SBO within 1 year, and this rate
increases to 30% by 10 years.
Peritoneal injury --- damage to mesothelial cells and
underlying connective tissue --- inflammatory response
--- coagulation complement cascade --- fibrin deposition
--- not degraded by fibrinolysis (*degraded by proteases
of the fibrinolytic system) collagen deposition --adhesive bands
*according to schwartz
Prevention or reduction
Careful handling of tissues, avoid dessication
and ischemia, spare use of cautery, laparoscopy
Use of barrier membrane & gels (oxidized reg.
cellulose hyaluronic acid)

Separate and create barriers between

damaged surfaces, allowing for adhesionfree healing
Oxidized
regenerated
cellulose
and
hyaluronic acid membranes or solutions have
been shown to reduce adhesions in gynecologic
patients and are being investigated for use in
general surgical patients.
-

Local Treatment of Wounds

History and PE
Infiltration of local anesthesia lidocaine w/ or
w/o epinephrine
Debridement (3 Cs of tissue viability: color is
pink/red, contractility, and circulation)
Irrigation high pressure w/NSS avoid using
povidone iodine, H2O2 (povidone iodine is used
for closed wounds only)

Epinephrine should not be used in wounds of

the fingers, toes, ears, nose, and penis, due to
the risk of tissue necrosis secondary to terminal
arteriole vasospasm

Iodine, povidone-iodine, hydrogen peroxide,

and organically based antibacterial preparations
have all been shown to impair wound healing
due to injury to wound neutrophils and
macrophages
Closure of wound
Primarily w/ sutures, smallest, nonabsorbable,
or slowly absorbable monofilament sutures
Drain (rubber drains if indicated)
Tissue loss, use flaps, grafts for coverage
Cyanoacrylate tissue glues (ex. Bulldog)

Additional layers of suture closure are

associated with increased risk of wound
infection, especially when placed in fat
Antibiotics
Only as prophylaxis, treat when infected
Based on suspected organisms, and overall
immune status

Signs of infection to look for include

erythema, cellulitis, swelling, and purulent
discharge
Tetanus prophylaxis
Active and passive immunization
Tetanus Toxoid and Tetanus Immunoglobulin
12

2. Hydrocolloid
Gel agents, pectin or gelatin
Complex structures w/ h2O
Yellowish gelatinous mass
Minimal to moderate exudates

Figure 8. Algorithm for management of acute wounds

Dressings Objectives:
To protect from bacterial invasion
To absorb fluid
To provide psychologic benefit
To produce rapid, cosmetically acceptable
healing
To remove & contain odor
To reduce pain
To apply pressure if hematoma formation is
likely

Dressings can be classified as primary or

secondary. A primary dressing is placed directly
on the wound. The secondary dressing is placed
on the primary dressing
Types of wound dressings
1. Absorbent
Absorbs fluid, avoid maceration & bacterial
growth
Wool, cotton gauze, sponge
2. Nonadherent
Paraffin, petroleum jelly, or water-soluble jelly
Requires a secondary dressing to prevent
drying, seal the edges, and prevent dessication
and infection
Dressings
1. Occlusive/ semiocclusive dressings
For minimally exudating wounds
Waterproof, impervious to microbes
Permeable to water vapor & O2
Not ideal for infected wounds

3. Hydrogels
Sheets, gauze or gel
Soothing & cooling effect
Moist environment for healing
Applied directly to wound & covered w/
secondary dressing
Burns
4. Alginates
Brown algae, polysaccharides, manuronic acid,
glucoronic acid
Calcium--- sodium alginatesswells & absorbs
fluid
Skin loss, open surgery. Wounds w/ exudates,
full thickness chronic wounds
Wound healing Treatment
Skin Replacement
1. Conventional skin grafts
- Acute & chronic wounds
- Split or full thickness
- Wound bed adequately prepared
Autografts, allografts/homografts,
xenografts/heterografts
2. Skin substitutes
- Manufactured by tissue engineering
Adv:
readily available
not requiring painful harvest
applied freely or with surgical suturing
Disadv:
limited survival
high cost
need for multiple applications
Source: Schwartzs Principles of Surgery, Jaxs notes, lecture audio
Time heals all wounds. And if it doesn't, you name them something other
than wounds and agree to let them stay. Emma Forrest, Your Voice in My
Head
Made by: Lumancas FP, Basmayor RR, Mandawe, AJ
Edited by: Mandawe AJ

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