SURGERY I

WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019

OUTLINE A. Hemostasis and Inflammation (Day 0-5)

I. Phases of Wound Healing
• Hemostasis - Precedes and initiates
A. Hemostasis and Inflammation
inflammation with the ensuing release of
B. Proliferation
chemotactic factors from the wound site
1. Matrix Synthesis
C. Maturation and Remodeling
Wounding
1. Epithelialization
II. Role of Growth Factor in Normal Healing Platelet ⍺ granules
A. Wound contraction Division of Blood vessels release wound-active
III. Heritable Diseases of Connective Tissue substance:

IV. Healing in Specific Tissues Exposure of subendothelial collagen

• PDGF
A. Gastrointestinal Tract to platelets
• TGF—β
B. Bone • PAF
C. Cartilage • Fibronectin
Platelet aggregation & degranulation
• Serotonin
D. Tendon and Ligament
E. Nerve
Activation of coagulation cascade
F. Fatal Wound Healing
V. Classification of Wounds
A. Timing and Wound Closure Fibrin clot formation serves as scaffolding for the
migration into the wound of inflammatory cells
B. Factors Affecting Wound Healing
C. Wound Contraction
• Inflammation
VI. Treatment of Wounds
o Cellular infiltration follows a
A. Wound Classification and Immunization Schedule
predetermined sequence
B. Antibiotic Prophylaxis
o Immediate response is
C. Classification and Infection Rates of Operative Wounds
vasoconstriction followed by
D. Methods of Wound Closure
vasodilation, allowing extravasation of
E. Dressing
fluid

• Polymorphonuclear Neutrophils (PMNs)

I. PHASES OF WOUND HEALING o First infiltrating cells
o Peaks at 24-48 hours
• Normal wound healing follows a predictable pattern o Neutrophil migration stimulated by:
• Hemostasis and Inflammation § Increased vascular permeability
• Proliferation § Local prostaglandin release
• Maturation and Remodeling § Chemotactic substances (e.g.
Complement factors, IL-1, TNF-
• These phases overlap each other and are defined
by their characteristic cellular populations and a, TGF-b, Platelet Factor 4,
biochemical activities bacterial products)
o Primary role: phagocytosis of bacteria
• All wounds need to progress through these phases
and tissue debris
to re-establish tissue integrity
o Other functions:
§ Major source of cytokines early
during inflammation
3
• NF-a influences
subsequent
angiogenesis and
collagen synthesis
§ Release proteases
• Collagenases
participate in matrix and
ground substance
degradation in the early
phase

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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019
o No role in collagen deposition or
acquisition of mechanical wound
strength
§ PMNs are implicated in delaying
epithelial closure of wounds
• Macrophages
o Second population of infiltrating cells
o Peaks at 48-96 hours and remain
o present until completion of wound
healing
o Primary role: phagocytosis of bacteria
and tissue debridement
o Other functions:
§ Synthesis of oxygen radical and
nitric oxide to contribute to
microbial stasis
§ MOST PIVOTAL FUNCTION:
Activation and recruitment of
other cells via mediators (eg.
Cytokines, Growth Factors) and
cell-cell interaction & o PDGF: strongest fibroblast chemotactic
intercellular adhesion molecules
(ICAM)
§ Release mediators to regulate
cell proliferation, matrix
synthesis, and angiogenesis
(e.g. TGF-b, VEGF, IGF, EGF,
Lactate)
th
Table 9-1 of Schwartz’s Principles of Surgery, 11 ed, p. 274
• T Lymphocytes
o Bridges transition from the inflammatory
to the proliferative phase
o Peaks about 1 week post-injury
o Plays an active role in modulation of the
wound environment
§ Depletion decreases wound
strength and collagen content
§ Selective depletion of CD8+
enhances wound healing
o Exerts a downregulating effect on
fibroblast collagen synthesis by cell-
associated IFN-g, TNF-a, and IL-1
B. Proliferation (Day 3-14)
• Tissue continuity is re-established
• Fibroblasts and endothelial cells are the last cell
populations to infiltrate
• Fibroblasts
factor
o Primary role: matrix synthesis and
remodeling
o Fibroplasia: formation of fibrous tissue
o Activated by cytokines and growth
factors released by wound macrophages
o Wound fibroblasts (vs. nonwound)
synthesize more collagen, proliferate
less, actively carry out matrix contraction
• Endothelial Cells
o Migrate from intact venules
o Participate in angiogenesis (formation of
new capillaries)
§ Revascularization proceeds in
parallel with fibroplasia
o Influenced by cytokines and growth
factors for migration, replication, and
angiogenesis
o TNF-a, TGF-b, VEGF
§ Major source: Macrophages
§ VEGF receptors are located on
endothelial cells
1. Matrix Synthesis
• Collagen
o Most abundant protein in the body
o Deposition, maturation, and remodeling
are essential to the functional integrity of
the wound
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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019
• Proteoglycan
o Glycosaminoglycans (GAGs) comprise a
large portion of the “ground substance”
that makes up granulation tissue
o GAGs couple with proteins to form
proteoglycans
o Major GAGs in wounds:
§ Dermatan sulfate
§ Chondroitin sulfate
Fibroblasts synthesize these compounds, increasing their
concentration during the first 3 weeks of healing.
C. Maturation and Remodeling
• Begins during the fibroplastic phase
• Characterized by reorganization of previously
synthesized collagen
o Collagen is broken down by matrix
metalloproteinases (MMPs)
o Net wound collagen content is the result
of a balance between collagenolysis and
collagen synthesis
o There is a net shift toward collagen
synthesis and eventually re-
establishment of ECM
• Deposition of matrix at the wound site follows a
characteristic pattern
• Fibril formation and fibril cross-linking result in
decreased collagen solubility, increased
strength, and increased resistance to enzymatic
degradation
o Scar remodeling occurs for 6-12 months
post-injury
o results to a mature, avascular, and
acellular scar
• mechanical strength of the scar never achieves
that of the uninjured tissue
• There is a constant turnover of collagen in the
ECM, both in healing wound and normal tissue
homeostasis
• Balance of collagen deposition and degradation
is the ultimate determinant of wound strength and
integrity
1. Epitheliazation
• Restoration of external barrier during healing
• Begins within 1 day of injury and is completed in
less than 48 hours in incised wound
• Proliferation and migration of epithelial adjacent
to the wound
o Marginal basal cells lose their
attachment to the dermis, enlarge, and
migrate across the surface
o Fixed basal cells undergo series of rapid
mitotic divisions and appear to migrate
by moving in a leapfrog fashion
o Once defect is bridged, cells become
more columnar in shape and increase
their mitotic activity
o Layering of epithelium is re-established
and surface layer keratinizes
II. ROLE OF GROWTH FACTORS IN NORMAL
HEALING
*see page 9*
A. Wound Contraction
• Inward movement of the wound edge
th
• Begins around 5 day and completed by 12-15
days
• Incised wounds without significant tissue loss
heal by primary intention
• Large wounds with significant tissue loss heal by
secondary intention
• Myofibroblasts
o Major cell responsible for a muscle-like
cell contraction in wound
o Possesses an a-smooth muscle actin in
thick bundles called stress fibers
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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019
o a-smooth muscle actin is undetectable
until day 6, and then increasingly
expressed for the next 15 days
III. HERITABLE DISEASES OF CONNECTIVE
TISSUE
• EHLERS-DANLOS SYNDROME
o Defect in collagen formation
o Most of the patients manifest genetic
defects encoding a chains of collagen
type V
• MARFAN’S SYNDROME
o Mutation in the FBN1 gene, which
encodes for fibrillin
• OSTEOGENESIS IMPERFECTA
o Mutation in Type I collagen
• EPIDERMOLYSIS BULLOSA
o The recessively inherited dystrophic type
is characterized by defects in COL7A1
gene, encoding type 7 collagen
• ACRODERMATITIS ENTEROPATHICA
o Autosomal recessive disease of children
that causes inability to absorb sufficient
zinc from breast milk or food
o Genetic defect in SLC39A4 gene
IV. HEALING IN SPECIFIC TISSUES
A. Gastrointestinal Tract
• Failure to heal results in dehiscence, leaks, and
fistulas
• Excessive healing leads to stricture formation
and stenosis of the lumen
• Mesothelial (serosal) and mucosal healing can
occur without scarring
• Early integrity of anastomosis is dependent on:
o Formation of fibrin seal on the serosal
side (achieves watertightness)
o Suture-holding capacity of intestinal wall
(submucosal layer)
Submucosal layer imparts the greatest tensile strength supply for wound healing cells
and greatest suture-holding capacity •
• Collagenolysis
o Collagenase is expressed postinjury in
all segments, but more marked in the
colon
• Collagen synthesis
o Carried out by fibroblasts and smooth
muscle cells
o Colon fibroblasts produce greater
amounts of collagen than skin fibroblasts
o No evidence that a given technique has
any advantage over another
B. Bone
1. Soft Callus Stage
• 3-4 days following injury
• Soft tissue forms a bridge between fractured
bone segments
o Deposited where neovascularization
has taken place
o Serves as internal splint, preventing
damage to new blood vessels and
achieving fibrocartilaginous union
• Formed along bone shaft and internally
within the marrow cavity
• Characterized by end of pain and
inflammatory signs
2. Hard Callus Stage
• 2-3 months
• Mineralization of soft callus and conversion
to bone
• Leads to complete bony union
• Bone is strong enough and will appear
healed on radiographs
3. Remodeling Phase
• Allows for the correct transmission of forces
and restores contours of bone
• Excessive callus is reabsorbed
• Marrow cavity is recanalized
C. Cartilage
• Avascular and depends on diffusion for transmittal
of nutrients
o Hypervascular perichondrium contributes
substantially to the nutrition
• Injuries may be associated with permanent defects
due to meager and tenuous blood supply
o Leads to low amount of angiogenesis & less
Superficial Injury
o Disruption of proteoglycan matrix and injury
to chondrocytes
o No inflammatory response
o Increased synthesis of proteoglycan and
collagen are entirely dependent on the
chondrocyte
o End result:
§ Overall regeneration is incomplete
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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019
§ Slow to heal and result in persistent
structural defects
• Deep Injury
o Involve underlying bone and soft tissue
o Exposure of vascular channels of
surrounding tissue = help in formation of
granulation tissue
o Hemorrhage
§ Allows for initiation of inflammatory
response & mediator activation of
cellular function for repair
o Fibroblasts migrate and synthesize fibrous
tissue that undergoes chondrification
o End result:
§ Hyaline cartilage is formed
§ Restores structural and functional
integrity
D. Tendon and Ligament
• Tendon: muscle to bone
• Ligament: bone to bone
• Tendon vasculature has an effect on healing
o Hypovascular tendons tend to heal with less
motion and more scar
• Tenocytes
o Metabolically very active
o Retain a large regenerative potential, even in
the absence of vascularity
• Restoration of the mechanical integrity may never
be equal to that of the undamaged tendon
E. Nerve
• Types of injury
• Nerve ends progress through a predictable pattern
of changes:
o Survival of axonal cell bodies
o Regeneration of axons that grow across the
transected nerve to reach the distal stump
o Migration and connection of the regenerating
nerve ends to the appropriate nerve ends or
target organs
• Wallerian Degeneration
o Phagocytes remove the degenerating axons
and myelin sheath from the distal stump
F. Fetal Wound Healing
• Main characteristic that distinguishes it from adult
wounds is the lack of scar formation
o Healing also resembles tissue
regeneration
• Transition wound
o Phase during gestational life when a
more adult-like healing pattern emerges
rd
o Occurs at the beginning of 3 trimester
o There is scarless healing, but there is
loss of ability to regenerate skin
appendages
o Leads to a classic adult-patterned
healing with scar formation, but still faster
than in adults
Characteristics that influence differences between
fetal and adult wounds
1. Environment
• Fetus is bathed in a sterile, temperature-
stable fluid environment
2. Inflammation
• Inflammation reduced due to immature
fetal immune system
o Leads to decreased scar formation
• Fetus is also neutropenic and wounds
contain lower number of PMNs,
macrophages
3. Growth Factors
• Absent TGF-β (has a role in scarring)
o Blocking TGF-β1 or TGF-β2 via
neutralizing antibodies reduces scar
formation in adult wounds
o Exogenous application of TGF-β3
downregulates TGF-β1 and TGF-β2,
leading to scar reduction
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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019

4. Wound Matrix
• Excessive and extended hyaluronic acid
production
• Hyaluronic acid
o High molecular weight GAG produced by
fibroblasts
o Synthesis is sustained in fetal wounds
o Production can be stimulated by amniotic
fluid (fetal urine)
o Increased level may aid in the orderly
organization of collagen
o Used to topically enhance healing and
inhibit postoperative adhesion formation
• Fetal fibroblasts produce more collagen
than adult
o Fetal wounds: collagen pattern is
reticular in nature and resembles
surrounding tissue
o Adult: express large bundles of parallel
collagen fibrils oriented perpendicular
to the surface

IV. CLASSIFICATION OF WOUNDS

A. Timing of Wound Closure
th
• Primary Closure/First Intention Figure 9-6 of Schwartz’s Principles of Surgery, 11 ed, p. 282
o To close the wound at initial presentation
o Done when the tissue surface have been B. Factor Affecting Wound Healing
approximated (closed) • Local Factors
o Usually closed by sutures, staples, etc. o Infection
o Very minimal tissue loss, quick and easy o Foreign Bodies
healing
o Tissue Hypoxia
• Secondary Closure/Secondary Intention
o Allow the wound to heal on its own o Venous Insufficiency
o Done when there is a great deal of lost tissue o Local Toxins
or when the edges of the wound cannot be o Mechanical Trauma
brought together o Irradiation
§ Longer repair and healing o Cigarette Smoking
§ Greater chances of scarring • Systemic Factors
§ Greater infection chance
o Closed by re-epithelialization and contraction o Malnutrition
of wound o Cancer
o Dirty Wounds – Closed by secondary intention o Diabetes Mellitus
• Tertiary Intention/Delayed Primary Closure o Uremia
o Combination of the previous two methods o Jaundice
o Used when there is a need to delay closing o Old Age
wound, such as when there is poor circulation
o Corticosteroids
to the injured area or if there is presence of an
infection o Chemotherapeutic Agents
o Closed by primary closure after a period of o Alcoholism
secondary healing which allows drainage of
the wound C. Wound Contraction
• Regulation of wound contraction is still poorly defined

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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019

• Information regarding the effects of specific cytokines

on contraction is limited and often conflicting: Immunization Schedule & What to Give
o TGF-b has been found to promote contraction Patient Status Td+ TIG Td+ TIG
even in the absence of serum Unknown Td+ or
o PDGF has also been found to either increase Yes Yes Yes No
< 3 Doses
contraction or have no effect 3 or more Doses No‡ No No§ No
o FGF and EGF have been found by different
authors to either have no effect or cause
moderate enhancement of contraction Legend:

• (+): For Children <7 yr, Diphtheria, Tetanus

V. TREATMENT OF WOUNDS toxoids, and Pertussis vaccine adsorbed ( Or
diphtheria and Tetanus toxoids adsorbed, if
• Priorities are a careful, complete history and a Pertussis vaccine is contraindicated) is preferable
thorough physical examination to Tetanus toxoid alone.
• Most Cutaneous Wounds are obvious and easily • (‡): Yes, if more than 5 years since last dose
diagnosed, but are not life threatening • (§): Yes, if more than 10 years since last dose
• The wounded patient may also have less apparent • Td: Tetanus and Diphtheria Toxoids adsorbed (For
problems that are potentially lethal and demand adult use)
immediate attention. • TIG: Tetanus Immune Globin; Only given to
• The management of such potentially life- Tetanus prone patients
endangering problems take precedence over
wound management. B. Antibiotic Prophylaxis
• Patient’s tetanus immunization status should be
considered • Prophylactic antibiotics are not indicated for most
• Anti-Rabies treatment should be considered for wounds
patients who have been bitten by domestic by • Indicated for:
domestic and wild animals such as skunks, o Contaminated wounds in
raccoons, foxes, and bats. immunocompromised or diabetic patients
o Extensive injuries to the central area of the
face
A. Wound Classification and Immunization Schedule
o Patients with valvular disease
o Patients with prostheses
Wound Classification o Lymphedematous extremities
Tetanus Non-Tetanus o Stool-contaminated and human-bite
Prone Prone wounds
Wound Age >6 Hours ≤ 6 Hours o Dog-bite wounds
Stellate o Wounds with extensive amounts of
Wound, devitalized tissue
Configuration Linear Wound
Avulsion,
Abrasion C. Classification and Infection Rates of Operative
Depth >1 cm <1 cm Wounds
Missile,
Mechanism of Sharp Surface
Crush, Burn,
Injury (Knife or Glass)
Frostbite
*see page 10*
Signs of
Infection
D. Methods of Wound Closure
Devitalized
Tissue
Contaminants Present Present
• Direct Approximation
(Dirt, Feces,
o Sutures, Staples, Tapes, and Tissue Adhesives
Soil, Saliva)
• Skin graft (Autograft)
• Local Flap

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 SURGERY I
WOUND HEALING
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o Random (Unnamed Blood Supply) or

Axial (Named Blood Supply)
• Distant Flap
o Requires microvascular anastomose

E. Dressing

• The purpose of a dressing must be carefully

considered before the dressing is applied.

1. Warm, Moist Environment

• Biologic dressings (e.g., Allograft, Amnion, or
Xenograft)
• Synthetic Biologic Dressings (e.g., Biobrane)
• Hydrogel Dressings
• Dressings of Semipermeable or Non-Permeable
Membranes (e.g., Op-Site or Duoderm)

2. Wounds containing Necrotic Tissue, Foreign

Bodies, or other Debris
• Wet-to-Dry Dressings
• Wet-to-Wet Dressings
• Enzymatic Agents (e.g., Travase, Santyl, and
Accuzyme)
3. Lower the bacterial count in infected wounds
• Silver Sulfadiazine

4. To prevent bacterial contamination

• Xeroflo, a fine-meshed gauze impregnated with
a hydrophilic substance
• N-terface, a synthetic fine-meshed gauze

Transcribed by: Aira Cayago & Juan Dalmacio

Edited by: Haidee Cosilet & Paolo Cunan
Checked by: Nick Cajano

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 SURGERY I
WOUND HEALING
Nilo De Los Santos, MD || Aug. 14, 2019

APPENDIX 1. ROLE OF GROWTH FACTORS IN NORMAL HEALING

Growth Factor Wound Cell Origin Cellular & Biologic Effects
• Chemotaxis (Fibroblasts, smooth muscle, monocytes,
neutrophils)
Platelets (a granules), macrophages, • Mitogenesis (Fibroblasts, smooth muscle cells)
PDGF monocytes, smooth muscle cells, • Stimulation of angiogenesis and collagen synthesis
endothelial cells • Activates TGF-b
• Enhance re-epithelization
• Modulate tissue remodeling
• Stimulation of angiogenesis
Fibroblasts, endothelial cells, • Involved in endothelial cell proliferation, collagen and
FGF keratinocytes, smooth muscle cells, matrix synthesis, wound contraction, epithelialization
chondrocytes • Produce Keratinocyte Growth Factor
• Mitogenesis: mesoderm and neuroectoderm
• Stimulates fibroblasts, keratinocytes, chondrocytes,
myoblasts
HGF Fibroblasts
• Suppresses inflammation, granulation tissue formation,
angiogenesis, re-epithelialization
Keratinocyte • Significant homology with FGF
Keratinocytes, fibroblasts
Growth Factor • Stimulates keratinocytes
• Stimulates proliferation and migration of all epithelial
Platelets, macrophages, monocytes (also
cell types
EGF identified in salivary glands, duodenal
• Stimulate re-epithelialization, angiogenesis, and
glands, kidney, & lacrimal glands)
collagenase activity
• Homology with EGF; Binds to EGF receptor
TGF-a Keratinocytes, platelets, macrophages • Mitogenic and chemotactic for epidermal and
endothelial cells
• Stimulates angiogenesis
Platelets, T lymphocytes, macrophages, • Stimulates leukocyte chemotaxis
TGF-b
monocytes, neutrophils, fibroblasts, • TGF-b1 stimulates wound matrix production (fibronectin,
( 1, b2, b3)
b keratinocytes collagen GAGs); regulation of inflammation
• TGF-b3 inhibits scar formation
Insulin-like Platelets (IGF-1 in high concentrations in
• Promote protein/ECM synthesis
Growth Factor liver; IGF-2 high in fetal growth); likely the
• Increase membrane glucose transport
(IGF-1, IGF-2) effector of GH action
Vascular • Mitogen for endothelial cells (not fibroblasts)
Macrophages, fibroblasts, endothelial
Endothelial • Stimulates angiogenesis
cells, keratinocytes
Growth Factor • Proinflammatory
Macrophages, leukocytes, keratinocytes, • Proinflammatory
IL-1
fibroblasts • Stimulates angiogenesis, re-epithelialization, tissue
IL-4 Leukocytes remodeling
Fibroblasts, endothelial cells • Enhances collagen synthesis
IL-6 • Stimulates inflammation, angiogenesis, re-
macrophages, keratinocytes
epithelialization, collagen deposition, tissue remodeling
Activin Keratinocytes, fibroblasts • Stimulates granulation tissue formation, keratinocyte
Angiopoitein-1/- differentiation, re-epithelialization
Endothelial cells
2 • Stimulates angiogenesis
CX3CL1 Macrophages, endothelial cells • Stimulates inflammation, angiogenesis, collagen
deposition
Macrophage/monocytes, endothelial
GM-CSF • Stimulates macrophage differentiation/proliferation
cells, fibroblasts

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 SURGERY I
WOUND HEALING
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APPENDIX 2. CLASSIFICATION AND INFECTION RATES OF OPERATIVE WOUNDS

Infection
Class Description Example
rate (%)
• No infection or Inflammation present
• Skin microflora may potentially contaminate the • Elective Surgery
wound • Thyroidectomy
• No hollow Viscus (GIT/GUT/RT Organs) that • Breast
Clean (Class 1) 1.5 – 5.1 Surgery/Mastectomy
contain microbes is entered
• No opening of GIT/GUT/RT (Excision, Lumpectomy,
• Atraumatic MRM)
• Generally, no need to give antibiotic prophylaxis
• Elective Surgery
• Entails opening of the GIT/GUT/RT (has • Cholecystectomy
indigenous bacterial flora) • Gastrectomy
Clean-
Contaminated 7.7 – 10.8 • Under controlled circumstances without • Colon Resection
(Class II) significant spillage of contents • Inguinal Hernias
• Minor breaks in sterile technique • Given antibiotic
prophylaxis

• Shows signs of infection or inflammation but • Emergency

absent purulent or fecal material cholecystectomy for
• Extensive introduction of bacteria into a normally acute cholecystitis
sterile area • Emergency Surgery for
o Major breaks in the sterile technique Small Bowel Perforation
Contaminated
15.2 – 16.3 o Gross spillage of viscus contents due to trauma
(Class III)
o Incision through inflamed (Non-purulent) • Open accidental
tissue wounds encountered
• Entry into infected tissue, bone, urine, or bile early after injury
• Emergency surgeries without proper preparation • Open Cardiac Massage
• Given antibiotic prophylaxis
• Emergency surgery for
generalized peritonitis
• Presence of fecal purulent material in the wound • Surgery for ruptured
• Traumatic wounds in which a significant delay in appendicitis
treatment occurred (Necrotic Tissue) • Diverticulitis
• Wounds created in the presence of purulent • Perforated peptic ulcer
material o Presence of E. coli
Dirty (Class IV) 28 – 40 in the peritoneal
• Wounds created to access a perforated viscus
(GIT/GUT/RT) accompanied by a high degree of cavity
contamination • Trauma surgery with
• Given antibiotic prophylaxis Colon Perforation
• Tertiary Closure • Drainage of Abscess
• Debridement of Soft
Tissue Infection

10
AM CAYAGO, JS DALMACIO, H COSILET, JP CUNAN ,