Surgery Wound Healing Part 1

AY 2018-2019 Lisa Marie C. Jayme, M.D.

2nd Bimonthly 11/09/2020

OUTLINE  Peak inflammatory phase because the neutrophils are the

I. PHASES OF WOUND HEALING primary producers of pro-inflammatory cytokines.
a. HEMOSTASIS AND INFLAMMATION  This is the time that you would expect the clinical
b. PROLIFERATION manifestation of inflammation: rubor, calor, dolor
c. MATRIX SYNTHESIS  48-96 hrs
d. MATURATION AND REMODELING  Predominant cells: Macrophages
II. HERITABLE DISEASES OF CONNECTIVE TISSUE  Neutrophils gradually decreases in number and replaced
III. HEALING IN SPECIFIC TISSUES by macrophages
IV. CLASSIFICATION OF WOUNDS  Function: phagocytosis, microbial stasis, activation
Note: For long outlines, use two columns to save space for main and recruitment of other cells, and regulate cell
content. For short outlines, just merge the two columns. proliferation, matrix synthesis & angiogenesis
 1 week
PHASES OF WOUND HEALING  Predominant cells: T-lymphocytes
 Main Function: Modulate the wound environment and
 Wounding downregulate collagen synthesis
 Disruption of tissue integrity
 Division of blood vessels II. PROLIFERATION
 Exposure of ECM (subendothelial collagen) initiates
everything that happens in the wound healing process  Days 4-12
 Wound Healing  Predominant cells:
 composed of 3 major phases that are overlapping.  Fibroblasts
 As the phases would come to an end, the succeeding phase  Deposits collagen fibers which is responsible for the
would also overlap with its beginning. structural strength of the skin
 There is a gray area, period of overlap  Most abundant in dermal layer of the skin
  Chemotactic factor: Platelet Derived Growth Factor
(PDGF)
 Regulator: lactate
 Matrix synthesis (collagen), lattice work arranged
haphazardly
 granulation of tissue
 Endothelial cells
 Responsible for angiogenesis
 Influenced by TNF-, TGF-, VEGF
 Clinically, you will observe granulation tissue formation and
I . HEMOSTASIS AND INFLAMMATION onset of angiogenesis
 As the proliferation phase goes by, wound bed would appear
Hemostasis finer in terms of granulation tissue and color would become
 Happens immediately after injury redder due to the development of more blood vessels.
 Response to minimize further blood loss
 Right after the destruction of the blood vessel, it tends to III. MATRIX SYNTHESIS
vasoconstrict, then the exposed subendothelial collagen attracts
the platelets  Involves the synthesis of Types I & 3 Collagen
 Platelet aggregation at the site of injury  degranulation  Functional integrity of wound
 release of mediators  activation of coagulation  Structural framework for the wound as it heals
 Platelets  Vitamin C
 Predominant cells in hemostasis  Electron donor in the hydroxylation and cross-linking or
 Initiates coagulation cascade procollagen
Inflammation  You would notice that surgical patients under severe
 Hours after hemostasis has begun, because of the release of stress are supplemented with high dose Vit C to promote
platelet granules containing platelet derived growth factors, proliferation/matrix synthesis to optimize wound healing
neutrophils are attracted to the site of injury.  Synthesis depend on: nutrients, cofactors, local wound
 Peak: 24-48 hrs post injury environment
 Predominant cells: neutrophils  Clinical significance: Smokers heal in a more prolonged
 Main function: phagocytosis of bacteria and tissue debris timeframe
 If prolonged, there will be a delay in epithelial closure  Effects of smoking usually cause vasoconstriction in the
distal organs. So there would be a suboptimal distribution

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 of nutrients and oxygen in the periphery, that’s why they Notes:
tend to heal suboptimally and in a more prolonged  As shown in the diagram, If you have a partial thickness
timeframe. wound, only a portion of the dermis is injured.
 Also involves proteoglycan  The precursors of epithelialization come from the keratinocytes
 GAG – glycosaminoglycans + protein found in the pilosebaceous units
 Glycosaminoglycans - ground substance of granulation  As long in the area of injury, there are still residual
tissue pilosebaceous units, it is capable of spontaneous re-
 Lattice for collagen assembly epithilialization
IV. MATURATION AND REMODELING  The keratinocytes lining the pilosebaceous units, it would tend
to migrate and re-establish continuity of epithelium.
 Longest phase and least understood phase  In the lowermost picture, we have here the re-establishment of
 May last up to 6-12 months post-injury according to Schwartz, epithelial integrity
but in other references, it could last up to 2 years especially
burns Role of Growth Factors in Normal Healing
 Reorganization of collagen into a more linear arrangement to  Stimulate cellular migration, proliferation and function
form a more rigid fibril  Autocrine
 The haphazardly arranged collagen will be broken to Matrix  Cell responsible for the production would affect itself
Metalloproteinases (MMPs)  Paracrine
 Balance between collagenolysis and collagen synthesis  Immediate surrounding tissues would be affected by the
 Excessive scar formation: If there is too much collagen growth factors
deposition  Endocrine
 Fibril formation and cross-linking of fibers so that it will end-up  Growth factor is released into the bloodstream and would
to become a more structurally strong lattice work. take effect on distant sites
 decrease solubility
 increase strength and resistance to enzymatic actions Wound Contraction
 At this time, when maturation has set in, tissue integrity has  Decrease in area of the wound
already been completed  Because of the presence of myofibroblasts
 By the end of maturation and remodeling, the maximal integral  Myofibroblast’s contractile capability
strength of the injured tissue is achieved.
 contains -smooth muscle actin in thick bundles called
 75-80% of the uninjured state
stress fibers
 2 processes: Epithelialization and contraction  appears at day 6 to 21
 after 4 weeks, contraction start to decline due to apoptosis
Epithelialization
 Clinical Significance:
 Final step in establishing tissue integrity  Even without suturing, naturally, the wound would contract in
 Characterized by proliferation and migration of epithelial cells the succeeding days
adjacent to the wound
 Complete in <48 hours in approximated incisions HERITABLE DISEASES OF CONNECTIVE TISSUE
 In a elective/clean surgical wound wherein you have an
incised wound and sutured primarily as its repair  Generalized, genetically determined, primary disorders of one of
 Clinical significance: after 48 hrs, it is already safe to wash the elements of connective tissue
the wound  Collagen
 Elastin
 Mucopolysaccharide
 5 major types:
 Ehlers-Danlos syndrome
 Marfan’s syndrome
 Osteogenesis imperfect
 Epidermolysis bullosa
 Acrodermatitis enteropathica

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 EHLERS-DANLOS SYNDROME MARFAN’S SYNDROME

 Defective fibrilin
 Group of 10 disorders present as a defect in collagen formation  Increase in TGF- signaling, particularly in the aortic wall
 Quantitatively/structurally defective in collagen type v  Classic phenotype
 “classic” EDS:  Tall stature
 Thin, fiable skin  Arachnodactyly
 Prominent veins  Lax ligaments
 Easy bruising  Myopia
 Poor wound healing  Scoliosis
 Atrophic scar  Pectus excavatum (cavity in the sternum)
 Onion skin in the area of scarring  Aneurysm of the ascending aorta
 Very much prone to be re-injured  Prone to hernias
 Recurrent hernias  Skin may be hyperextensible but shows no delay in healing
 Hyperextensible joint
 Ex. contortionist
 Considered in every child with recurrent hernias and
OSTEOGENESIS IMPERFECTA
coagulopathy
 Most of the EDS types are autosomal dominant. Only one gene
is required for the person to be affected.

Refer to table 9-3 in the appendix for the Clinical, genetic, and
biochemical aspects of Ehlers-Danlos subtypes

Clinical Significance
 Inguinal hernias in children
 Best managed with mesh/felt repair
 Because it is not only caused by patent processus vaginalis
but are also caused by structural defect in terms of collagen,
thus having weak inguinal floors.
 Wound repair
 Closed in 2 layers
 Deep dermal suture  Mutation in type I collagen
 Outer skin suture  Presentation
 Done under tension  Brittle bones
 Stitches left twice as long  Osteopenia
 External fixation with adhesive tape called skin tapes or steri-  Low muscle mass
tapes, which reinforces the repair and provides the stability of  Hernias
the surrounding tissue as epithelialization occur in wound  Ligament and joint laxity
areas.  Dermal thinning & increased bruisability
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 Scarring is normal  Surgical interventions
 Skin is not hyperextensible  Esophageal dilatation
 Bones fracture easily even under minimal stress  Gastrotomy tube placement
 Surgery can be successful but difficult  Dermal incisions meticulously placed
 To avoid further skin trauma
 Skin requires nonadhesive pads covered by a “bulky”
dressing

ACRODERMATITIS ENTEROPATHICA

Note: All of them could be autosomal dominant; there is a strong family

history of OI.

EPIDERMOLYSIS BULLOSA

 Inability to absorb sufficient zinc from breast milk/food leading

to inhibition of cell proliferation and impaired granulation tissue
formation
 Diagnostic: blood zinc level <100 mg/dL
 Impaired wound healing and erythematous pustular dermatitis
(extremities and orifices)
 Treatment:
 Zinc sulfate 100-400 mg/day, orally
 curative for impaired healing

HEALING IN SPECIFIC TISSUES

 Defective type 7 collagen
 Responsible for connecting the epidermis to dermis GASTROINTESTINAL TRACT
 4 major subtypes
 EB simplex  Full thickness injury
 Junctional EB  repair by surgical or mechanical reapposition (sutures and
 Dystrophic EB staples)
 Kindler’s Syndrome  In ileocolic anastomoses, staplers have lower incidence of
 Involves all skin layers of the dermis anastomotic leak.
 Impared tissue adhesion within the epidermis, basement  Submucosa layer
membrane or dermis leading to tissue separation and  Greatest tensil strength and suture-holding capacity
blistering with minimal trauma  Layer that one should be able to get in its bites during suture
 A very gentle pinch on the patient would mean separation of to afford a seal off of the defect
the epidermal layer from the dermis like partial thickness  Failure of healing
burn  Dehiscence of the repair, therefore there will be
 Often times present with oral erosions and esophageal anastomotic leaks, which leads to spillage of intestinal
obstruction which compromise nutrition
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 contents into the abdominal cavity sometimes leading to NERVE
formation of fistulas
 Excessive healing  3 types of nerve injuries
 lumen stricture & stenosis eventually making a form of  Neuropraxia: focal demyelination
obstruction  Axonotmesis: interruption of axonal continuity but
 Mesothelial (serosal) and mucosal healing can occur without preservation of Schwann cell basal lamina
scarring  Neurotmesis: complete transection
 Ex. Facial fractures from motor vehicular crashes  Heal in 3 Crucial steps:
 Survival of axonal cell bodies
Technical Consideration  Regeneration of axons
 For an anastomosis to heal without complications it must be:  To reach the distal stump
 Tension free  Migration and connection of the regenerating nerve ends
 Have an adequate blood supply to the appropriate nerve ends/organ targets
 Adequate nutrition
 Free of sepsis  Note: in cases where there is one step missing, there would be
no regeneration of the nerve. Thus, there will be a permanent
 Overzealous fluid administration will lead to fluid third spacing,
tissue edema and increased intraabdominal pressure. deficit
 Distal blood flow to the edges of the bowel segments being
FETAL WOUND HEALING
anastomosed and repaired will be compromised therefore
there will be interference of the GI healing.  Early gestation
 If left unrecognized, it will lead to dehiscence and  Lack of scar formation
anastomotic leak and etc.  Resembles tissue regeneration
 Third trimester: “transition wound”
Refer to Appendix for Comparison of Wound Healing in the GI tract  Scarless healing
and skin  Loss of skin appendage regeneration
 Eventually follows adult pattern but faster.
BONES  Theories on its Etiology
 Wound environment
 Phases of healing resemble those observed in dermal healing  Bathed in a sterile, temperature-stable fluid environment
 Fracture site hematoma  liquefaction and degradation  Inflammation
(inflammatory symptoms)  revascularization  Reduced due to immaturity of fetal immune system
 3-4 days  Lesser inflammation, lesser scar formation
 Soft callus stage (cessation of pain)  Growth factorts
 2-3 months  Absence of TGF- (significant role in scarring)
 Hard callus stage  Wound Matrix
 Maximum strength of bone is achieved  Excessive and extended hyaluronic acid production
 Remodeling  Collagen pattern is reticular in nature  resembles
 Balance the deposition of new bone and the breakdown surrounding tissue
 In aesthetics, Hyaluronic acids are being used to
CARTILAGE restore lost volume on the face in elderly individuals
and also used to augment certain areas such as lips.
 Avascular (pouty lips)
 Only depends on diffusion for nutrients and oxygen supply in
the surrounding tissues CLASSIFICATION OF WOUNDS
 Superficial injury
 Healing power often inadequate  Acute
 Regeneration is incomplete  Heal in a predictable manner and time frame
 Slow healing with persistent structural defect  Slightest complication that could potentially work
 Deeper injury  Chronic
 Exposure of vascular channels of underlying bone/soft tissue  Healing not achieved after 4 weeks of treatment
 hemorrhage  inflammation  activation of cellular repair  Evolution of the wound has deviated.
 Either one of the three phases has been prolonged
TENDON  Healing is not achieved after 4 weeks
 Most common cause is the presence of infection
 Healing progresses in similar fashion as in other areas of the
body REFERENCES
 Hypovascular tendons
 Heal with less motion and more scar formation Dr. Jayme’s Lecture
Scwartz’s Principles of Surgery

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 APPENDIX

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 Surgery Wound Healing Part 2
AY 2020-2020 Lisa Marie C. Jayme, M.D.
2nd Bimonthly 11/09/2020

OUTLINE Acute Wounds

Wound Healing  Acute wounds or non infected wounds or Regular wound
Acute Wounds Excess Healing  Maximal wound strength reached after 6 weeks of healing
Factors Keloid (75% to 80% of a normal tissue)
Chronic Wounds Hyperthropic Scar
Ischemic Arterial Dressing
Factors affecting Wound Healing
Ulcers Primary
1. Nutriotional deficiencies (Vit A, Vit C and Antioxidant)
Venous Stasis Secondary 2. Infection
Ulcers Classification of 3. Severe trauma
Diabetic Ulcer Dressing 4. Immunocompromised host
Decubitus or Skin Grafting
Pressure Ulcers

Wound Healing
Primary Intention
 Repair of the direct opposiotion od the two wound edges,
either by suturing or application of staple devices or
adhesives ( skin tapes)

Secondary Intention
 Healing by secondary intention is there is a chunk of tissue
that is missing
 Allow reestablishment of tissue continuity by allowing collagen
deposition or healing by scar formation
 No surgical closure
 Just let granulation tissue to fill in the gap and eventually turn
into scar tissue

Tertiary Intention
 Delayed primary closure
 Combination of primary and secondary intention
 True to infected wounds, where it is not allow to have direct
closure, for pus to drain out.

Age
 Elderly
o Delayed healing
o Prone to Dehiscence, Incisional hernia)

Hypoxia, Anemia and Hypoperfusion

 Anemia with 15% less hematocrit
 When the patient id too anemic, blood transfusion is given
preoperatively
 Preoperative CBC, to prepare if the patient needs blood
transfusion

Steriod and Chemotherapeutic Drugs

 Inhibit inflammation phase
 Inhibit epitheliation and contraction
 Delay steroid useafter 3-4days postoperative
o Administer Vit A to reverse the systemic effects of
steroids
 Delay chemo use after 2 weeks

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  Longer time to reach the maximal wound strength (more than
Metabolic Disorders a year)
o Classic example: Extensive burns
 Diabetes Mellitus
o Moderate control of blood glucose  Other causative mechanisms
o From 120 to 180 mg/dl o Unresponsive to normal regulatory signals
o Fibroblasts have decreased proliferative potential
 Uremia
o Malignant transformation
o Tissue deposition of calcium phosphate
 Non healing wound: Marjolin’s Ulcer
o Uremic Gangrene Syndrome (Calciphylaxis)
 Squamous or basal cell carcinoma
Nutrition
Ischemic Arterial Ulcers
 Nutrients and essential elements tend to as cofactors in
Pathophysiology
deposition and synthesis of collagen fibers which is needed
for wound healing  Lack of blood supply
 Typically extremely painful
Infection  Usually associated with other Peripheral Vascular Diseases
(PVD)
 Infections is different from contaminitaion
 Mostly associated with other PVD’s
o Contamination
 Presence of microorganism, multiply but  Mostly affect distal portions of extremities
no presentation of symptoms
o Infection Physical Examination
 Minimum number of organism, Organism >  Diminished/ absent pulses (Decrease ABI)
10^5/gm of tissue  Poor granulation tissue formation
 Threat to wound healing o Due to hypoxic environment
 With signs and symptoms (fever,  Wound: Shallow, Smooth margin, pale base
leukocytosis, and incisional pain)  Signs of ischemia
 Most common microoorganisim o Dry skin
o Staph sp. o Hair loss
o Coaagulase (-) Strep o Scaling
o Enterococci o Pallor
o E. coli
 Develops in 5-10% of post-op patient
o Differs to classes of wounds

Classified as
1. Superficial Incisional
o Skin and SQ only
o 75% of cases
o With mild leukocytosis and low grade fever and pain
in incisional site
o Evident between 7-10days post operatively
o Management
 Release the skin sutures and apply cotton
down to SQ tissue to allow drainage
accumulation

2. Deep Incisional
o Immediately adjacent to fascia layer, above or below
o Most dangerous type: Necrotizing fasciitis
o When it occurs in the perineum area
 Fournier Gangrene
 Present with hemmoragic bullae formation
with purplish discoloration
 Management
 Surgical debridement Management
 Systemic antibiotics, IV Penicillin
1. Revascularization
(20-40units per day)
2. Wound care
 Obtain culture sensitivity in the
wound bed, shift to targeted
antimicrobial therapy
Venous Stasis Ulcers
3. Organ/Space wound infections Pathophysiology
o Deepest wound. Deeper than the fascia  Venous stasis + Increased venous pressure
o Involving fascia, muscle or the abdominal cavity or
o Fibrinogen leak from capillary  perivascular
thoracic cavity
cuffing  impedence of oxygen blood flow
o Capillary endothelial plugging  diminished blood
Chronic Wounds flow
 Wounds that does not heal in 3 months or does not heal in 4  Capillary damage  extravasation of Hgb 
weeks despite treatment Lipodermatosclerosis (brownish pigmentation of skin
 Skin ulcers in traumatized or vascular compromised soft combined with the loss of SQ fat)
tissue

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Physical Examination Stages
 Ulcer that fails to reepithelize despite the presence of 1. Stage I
adequate granulation tissue  No blancing erythema of intact skin
 Skin color changes (pigmented) 2. Stage II
 Painless  Partial-Thickness ski loss involvinf epidermi/dermis
 Most common site or both
o Above the medial malleolus (Cockett’s perforator) 3. Stage III
 Full-thickness skin loss, but not through the fascia
4. Stage IV
 Full-thickness skin loss + muscle and bone

Management
 Multidisciplinary wound care team (physicians, nurses,
dietitians, physical therapist, and nutritionist)
 Do nursing care, to off load the pressure, proper turning
schedule every 2 hours
 Wound care + proper timely closure of the wound

Excess Healing

Keliod Vs. Hypertrophic Scar

Management
1. Compression therapy
 Mainstay of treatment, prmote venoous return
to the heart, addressing venous stasis
 Most common
o Zinc oxide-impregnated, nonelastic
bandage
2. Wound care
 Hydrocolloids

Diabetic Ulcers
 25% of diabetic patient
 Major contributors
o Neuropathy (60-70%)
o Foot deformity
o Ischemia

Management
 Glycemic control
 Debridement of necrotic tissue
 Infection control

Decubitus or Pressure Ulcers

 Aka Bed sores
 Localized area of tissue necrosis whe soft tissue is
compressed between a bony prominence and an external
surface
 If the position is maintained in 2 hours, the weight of area of
prominence will exucute form of pressure in soft tissue 
increase in inteavenous pressue  hypoxia  ischemia 
necrosis

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 Hypertropic Scarring from Electrical Burn
Treament:
Intralesionalsteroids injection
Maintenance of yearly injection of steroids, after treatment

Treatment of Wound

Acute Wounds

Management

Chronic Wounds
 TIME Concept
o A framework for a structured approach to wound
bed preparation
o Plastic surgery concept to help assess the wounds
in preparation of skin fgrafting
o Guide for both assessment and management of
chronic wunds

1. Tissue Management
2. Inflammation and Infection control
3. Moisture balance
4. Epithelial (Edge) advancement

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 Dressing
The main purpose of wound dressings is to provide the ideal
environment for wound healing. The dressing should facilitate the
major changes taking place during healing to produce an optimally
healed wound. Although the ideal dressing still is not a
clinical reality, technological advances are promising
Alginates
 Alginates are derived from brown algae and contain long
chains of polysaccharides containing mannuronic and
glucuronic acid.
 The ratios of these sugars vary with the species of algae
used, as well as the season of harvest.
 Processed as the calcium forms, alginates turn into soluble
sodium alginate through ion exchange in the presence of
wound exudates.

Absorbable Materials
 Absorbable materials are mainly used within wounds as
hemostats and include collagen, gelatin, oxidized cellulose,
and oxidized regenerated cellulose.

Medicated Dressings
 Medicated dressings have long been used as a drug-delivery
system.
 Agents delivered in the dressings include benzoyl peroxide,
zinc oxide, neomycin, and bacitracin-zinc.
 These agents have been shown to increase epithelialization
by 28%.

Primary Dressing Classified- Exudates

Placed directly on the wound and may provide absorption of fluids Less Exudate
and prevent desiccation, infection, and adhesion of a secondary
dressing Hydrogels
Films
Secondary Dressing Composite
One that is placed on the primary dressing for further protection,
absorption, compression, and occlusion

Classes of Dressing
Absorbent Dressings.
 This type of dressing helps control exudate without soaking
through the dressing, which can increase infection potential.

Nonadherent Dressings.
 Nonadherent dressings are impregnated with paraffin,
petroleum jelly, or water-soluble jelly for use as nonadherent More Exudate
coverage. Hydrocolloids
 A secondary dressing must be placed on top to seal the
edges and prevent desiccation and infection.

Occlusive and Semiocclusive Dressings

 Occlusive and semiocclusive dressings provide a good
environment for clean, minimally exudative wounds.
 These film dressings are waterproof and impervious to
microbes but permeable to water vapor and oxygen.

Hydrophilic and Hydrophobic Dressings

 These dressings are components of a composite dressing.
 Hydrophilic dressing aids in absorption, whereas a
hydrophobic dressing is waterproof and prevents absorption.

Hydrocolloid and Hydrogel Dressing

 Hydrocolloid and hydrogel dressings attempt to combine the
benefits of occlusion and absorbency.
 Hydrocolloids and hydrogels form complex structures with
water, and fluid absorption occurs with particle swelling, which
aids in atraumatic removal of the dressing.
 Absorption of exudates by the hydrocolloid dressing leaves a
yellowish-brown gelatinous mass after dressing removal that
can be washed off.

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 REFERENCES
Heavy Exudate
Aliginates Dr. Jayme’s Lecture
Foams Scwartz’s Principles of Surgery
Negative Pressure Wound Therapy (NPWT)

Skin Grafting
 For definitive closure for skin grafting
 Fine granulation tissue
 Beefy red in color, grown enough number of blood vessel
required to accept the graft
 No more exudates present
 Surrounfing skin is no longer swollen clinically free from
infection

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