STBS

WOUNDS, TISSUE
REPAIR AND SCARS
Wounds
Wound Definition
It refers to a breach in normal tissue continuity
resulting in a variety of cellular and molecular
sequelae.

Etiology
Wounds due to:
Accidents.
Wounds due to planned surgical intervention.

Classification
Acute wounds.
Chronic wounds:
Ulcers.
Pressure sores.

Wound Healing
It is a mechanism whereby body attempts to restore
the integrity of the injured part.

Normal Wound Healing

It takes place in three phases.
i. The inflammatory phase.
ii. The proliferating phase.
iii. The remodeling phase (maturation phase).
The Inflammatory Phase (Lag or Substrate or
Exudative Phase)
Duration immediately after wounding and lasts
for 2-3 days.
Bleeding is followed by vasoconstriction and
thrombus formation to limit blood loss.
Platelets stick to the damaged endothelial lining of

CHAPTER

01

the blood vessels releasing adenosine diphosphate

(ADP) causes thrombocytic aggregates to fill the
wound.
When bleeding stops platelets then release several
cytokines from the alpha granules, these are Platelet
derived growth factor (PDGF), platelet factor iv
+ transforming growth factor beta (TGF-)
PDGF and TGF- attract inflammatory cells (PMN
and macrophages).
Release of vasoactive amines by platelets
(histamine, serotonin) causes increased
permeability infiltration of inflammatory cells.
Macrophages remove the devitalized tissue and
microorganisms and regulate fibroblastic activity in
the proliferative phase.
This phase is described in Latin as:
Rubor redness.
Tumor swelling.
Calor heat.
Dolour pain.
Proliferative Phase (Collagen/Fibroblastic Phase)
It lasts from the 3rd day to the 3rd week.
It consists of mainly of fibroblastic activity with
production of collagen and ground substance
(glycosaminoglcans (GAG) and proteoglycans).
The wound tissue formed in the early part of this
phase is called as granulation tissue. Fibroblasts
require vitamin C to produce collagen.
In the later part of this phase there is increase inthe
tensile strength of the wound due to increased
collagen deposition.
80-90% of this final strength (in postoperative
wounds) is achieved in 30 days.
Remodeling Phase (Maturation Phase)
From 3rd week to 1 year.
It is characterized by the maturation of collagen
(type I replacing type III until a ratio of 4:1 is
achieved).

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There is a realignment of collagen fibres along the

lines of tension, decreased wound vascularity and
wound contraction due to fibroblast and
myofibroblast activity.

Stages of Wound Healing

Stage of inflammation
Stage of granulation tissue formation and
organization. Here due to fibroelastic activity
synthesization of collagen and ground substance
occurs.
Stage of epithelialization
Stage of scar formation and resorption
Stage of maturation.

Synovial diffusion.
Extrinsic
Depends upon the formation of fibrous adhesions
between the tendon and the tendon sheath.
The random nature of the initial collagen produced
means that tendon lacks tensile strength for the
first 3-6 weeks.
Active mobilization prevents adhesions limiting
range of motion, but the tendon must be protected
by splintage in order to avoid rupture of the repair.

Factors Influencing Healing Of A Wound

Local Factors

Normal Healing In Specific Tissues

Bones
The phases are as above but periosteal and endosteal
proliferation leads to callus formation which is
immature bone consisting of osteoid (mineralized by
hydroxyapatite and laid down by osteoblasts).
In the remodeling phase, cortical structure and the
medullary cavity are restored
If fracture ends are accurately opposed and rigidly
fixed, callus formation is minimal and primary healing
occurs
If a gap exists, then secondary healing may lead to
delayed union, nonunion or malunion.

Nerve
Distal to the wound Wallerian degeneration occurs
Proximally, the nerve suffers traumatic degeneration
as far as the last node of Ranvier.
Nerve regeneration is characterized by profuse
growth of nerve fibres which come from the cut
proximal end. Overgrowth of these, coupled with
poor approximation, may lead to neuroma formation.

Tendon
While following the normal pattern of wound healing,
there are two mechanisms where by nutrients, cells
and new vessels reach the severed tendon. These are:
Intrinsic
It consists of:
Vincular blood flow.

Site of the wound.

Structures involved.
Mechanism of the wounding:
Incision.
Crush.
Crush avulsion
Contamination (foreign bodies/ bacteria)
Loss of tissue.
Other local factors:
Vascular insufficiency (arterial or venous)
Previous radiation
Pressure
General (Systemic) Factors
Malnutrition or vitamin and mineral deficiencies.
Disease (e.g. diabetes mellitus).
Medications (e.g. steroids).
Immune deficiencies (e.g. chemotherapy, AIDS).
Smoking.

Abnormal Healing
Healing By Primary Intention
Is also known as healing by first intention.
It occurs in a clean incised wound or surgical wound.
Wound edges are approximated with sutures.
It occurs with immediate closure of a wound
(primary suture) using sutures, clips, staples and
adhesive materials that favors healing with minimal
scarring.
There is more epithelial production than fibrosis.
Scar will be linear, smooth and supple (bending
easily).

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03

Healing By Secondary Intention

It occurs in wound with extensive soft tissue loss like
in major trauma, burns and wound with sepsis.
It occurs in the wound that is left open and allowed
to heal by granulation tissue, contraction and
epithelialization.

Healing By Third Intention

This is delayed closure of a wound after a variable
period of time for which it has been left open.
It is applied to wounds that are grossly contaminated
or present late, but do not have significant tissue
loss.

A Classification of Wound Closure and Healing

By primary intention
Wound edges are opposed. Normal healing. Minimal
scar.
By secondary intention
Wound left open. Heals by granulation, contraction
and epithelialization.
Increased inflammation and proliferation.
Poor scar.
By tertiary healing (delayed primary intention)
Wound initially left open.
Edges later opposed when healing conditions
favorable.

Types of wounds
Tidy

Untidy

Incised

Crushed or avulsed

Clean

Contaminated

Healthy tissue

Devitalized tissue

Seldom tissue loss

Often tissue loss

Fig. 1.1: Parts of an ulcer.

The surgeon aim is to convert untidy to tidy by

removing all contaminated and devitalized tissue.
Primary repair of all structures (e.g. bone, tendon,
vessel and nerve) may be possible in a tidy wound,
but a contaminated wound with dead tissue
requires debridement on one or several occasions
before definitive repair can be carried out ('second
look' surgery).

Managing the Acute Wound

The surgeon must remember to examine the whole
patient according to acute trauma life support (ATLS)
principles.

The wound itself should be examined, taking into

considerations the site and the possible structures
damaged.
It is essential to assess movement and sensation
while watching for pain and listening to the patient.
A bleeding wound should be elevated and a
pressure pad applied.
Clamps should not be put on vessels blindly as nerve
damage is likely and vascular anastomosis is
rendered impossible.
In order to facilitate examination adequate analgesia
and / or anesthesia is required.

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Remember
Wound Toilet
Is washing the wound thoroughly using normal saline.
Wound Debridement (French - Letting Loose)
Is allowing content to come out by release incisions or
faciotomies. But commonly debridement is used for
wound excision.
Wound Excision
Is actually correct terminology for excision of devitalized
tissues once or serially.
Radical Wound Excision (Is Pseudotumor Approach)
It mean excision of entire devitalized tissues leaving
tissues with visible bleeding from all layers.

Managing The Acute Wound

Cleansing.
Exploration and diagnosis.
Debridement.
Repair of structures.
Replacement of lost tissues where indicated.
Skin cover if required.
Skin closure without tension.
All of the above things are done with careful tissue
handling and meticulous technique.

Wound Classification
Simple Wounds
Only skin is involved.
Complex Wounds

Debridement
After assessment, a thorough assessment is essential.
Abrasions, 'road rash' and explosions all cause dirt
tattooing and require the use of scrubbing brush or
even excision under magnification.
A wound should be explored and debrided to the
limit of blood staining.
Devitalized tissue may be excised until bleeding
occurs with the obvious exception of nerves, vessels
and tendons. These may survive with adequate
revascularization subsequently.
The use of copious saline irrigation can be less
destructive than knife or scissors when debriding.
Muscle viability is judged by color, bleeding pattern
and contractility.
For Tidy Wound
Repair of all damaged structures may be attempted.
Skin cover by flap or graft may be required as skin
closure should always be required without tension
and should allow for the edema typically associated
with injury and the inflammatory phase of healing.
A flap brings in a new blood supply and can be used
to cover tendon, nerve, bone and other structures
that would not provide a suitable vascular base for a
skin graft.
A skin graft has no inherent blood supply and is
dependent on the recipient site for nutrition.

Vessels, nerves, tendons or bones are involved.

Closed Wounds
Contusion
Abrasion
Hematoma
Open Wounds
Incised wounds
Lacerated wounds
Crush injuries
Penetrating wounds
Tidy wounds
Untidy wounds

Some Specific Wounds

Bites
Most bites involve either puncture wounds or
avulsions.
Small animal bites are common in childrens and
requires cleansing and treatment according to the
principles outlined in the table of managing the
acute wound.
Ear, tip of nose and lower lip injuries are most
usually seen in victims of human bites.
A boxing type injury of the metacarpo-phalangeal
joint may result from a perforating contact with the
teeth of a victim.
Anaerobic and aerobic organism prophylaxis is

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05

required as bite wounds typically have high virulent

bacterial counts.

Puncture Wounds
Wounds caused by sharp objects should be explored
to the limit of tissue blood staining.
Needle-stick injuries should be treated according to
the protocols because of hepatitis and human
immune deficiency virus (HIV) risks.
X-ray examination should be carried out in order to
rule out retained foreign bodies in the depth of the
wound.
Fig. 1.2: Degloving hand injury.

Hematoma
If large, painful or causing neural deficit a hematoma
may require release by incision or aspiration.
In the gluteal or thigh region there may be an
associated disruption of fat in the form of fat
fracture which results in an unsightly groove but
intact skin.
An untreated hematoma may also calcify and
therefore require surgical exploration if
symptomatic.

Degloving
It occurs when the skin and subcutaneous fat are
stripped by avulsion from its underlying fascia
leaving a neurovascular structures tendon or bone
exposed.
It may be open or closed.
Example of open degloving injury is a ring avulsion
injury with loss of finger skin.
A closed degloving may be a rollover injury, typically
caused by a motor vehicle over a limb. Such an
injury will extend far further than expected and
much of the limb skin may be non-viable.
Examination under anesthesia is required with a
radical excision of all non-bleeding skin as judged by
bleeding dermis.
Most surgeon rely upon skin serial excision until
punctate dermal bleeding is obvious.
Split skin grafts can be harvested from the degloved
non-viable skin and meshed to cover the raw areas
resulting from debridement.

Compartment Syndromes (Crush Injuries)

These syndromes typically occur in closed lower
limb injuries.
They are characterized by:
Severe pain.
Pain at passive movement of the affected
compartment muscles.
Distal sensory disturbances (paresthesia)
Absence of pulse distally (late sign).
Diffuse swelling.
Compartment pressures can be measured using a
pressure monitor and a catheter placed in the
muscle compartment.
Note:
Pain out of proportion to the condition - the most
reliable symptom. Affected muscle when passively
stretched worsens the pain - the most reliable sign.
Management
Fasciotomy
It is indicated when the pressure is constantly above
30mmHg or if the above clinical signs are present.
It involves incising the deep muscle fascia and is
best carried out via longitudinal incisions of skin, fat
and fascia.
In crush injuries that present several days after the
event a late fasciotomy can be dangerous as dead
(necrotic) muscle produces "myoglobin", which if
suddenly released into blood stream causes
myoglobinuria with glomerular blockage and renal
failure.
In the late treatment of lower limb injuries,
therefore, it may be safer to amputate the limb.

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Problems with the Compartment Syndrome

Infection, septicemia and abscess formation.
Renal failure.
Gangrene of the limb.
Chronic ischemic contracture.
Disabled limb.

Common Etiologies of Leg Ulcer

Venous disease leading to local venous HTN
(e.g. varicose vein).
Arterial disease, either large vessel
(atherosclerosis) or small vessels (diabetes mellitus).
Arthritis associated with autoimmune disease
(RA, SLE etc).
Trauma could be self inflicted.
Chronic infection (TB, syphilis)
Neoplastic (squamous or basal cell
carcinoma, sarcoma).

Biopsy of ulcer
Done when chronic ulcer is unresponsive to dressing
and simple treatment.
Is done to rule out neoplastic change or squamous
cell carcinoma known as Marjolin's ulcer
(commonest).
Fig. 1.3: Fasciotomy of the lower leg.

Chronic Wounds
Leg ulcers
Pressure sore

Leg Ulcers
In developed countries, the commonest chronic
wounds are leg ulcers.
An ulcer can be defined as a break in the epithelial
continuity.
A prolonged inflammatory phase leads to overgrowth
of granulation tissue, and attempts to heal by
scarring having a fibrotic margin.
Necrotic tissue often at the ulcer centre is called
slough.

Treatment
Effective treatment of many leg ulcers depends on
treating the cause and diagnosis is therefore vital.
Arterial and venous circulation should be assessed,
as should sensation throughout lower limb.
Surgical Treatment
Is only indicated if non-operative treatment has
failed or if the patient suffers from intractable pain.
Meshed skin grafts are more successful than sheet
grafts and have an advantage of allowing mobilization
as any time exudate can escape through the mesh.
Recurrence rate is high in venous ulceration.
Patient compliance with a regime of hygiene,
elevation and elastic compression is essential.

Pressure Sores
These can be defined as the tissue necrosis with
ulceration due to prolonged pressure.
Less preferable terms are bed sores, pressure ulcers
and decubitus ulcers.
They should be regarded as preventable but occur in
approximately 5% of all hospitalized patients.
There is high incidence in paraplegic patients, in the
elderly and in the severely ill patients.
Pressure Sore Frequency in Descending Order
Ischium
Greater tronchanter

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WOUNDS, TISSUE REPAIR AND SCARS

Heel
Malleolus (lateral then medial)
Occiput

American National Pressure Advising Panel

Staging of Pressure Sores
Stage 1 Non-blanchable erythema without a
breach in the epidermis.
Stage 2 Partial thickness skin loss involving the
epidermis and dermis.
Stage 3 Full thickness skin loss extending into
the subcutaneous tissue but not through
underlying fascia.
Stage 4 Full thickness skin loss through fascia with
extensive tissue destruction, may be
involving muscle, bone, tendon or joint.

If the external pressure exceeds the capillary occlusive

pressure (over 30mmHg) blood flow ceases leading
to the tissue anoxia, necrosis and ulcers.

Prevention
Good skin care.
Special pressure dispersion cushions or foams.
Use of low air loss and air fluidized beds
Urinary or fecal diversion in selected cases.
Pressure sore awareness is vital.
Bed bound patient should be turned atleast
every 2 hours with the wheel chair bound patient
being taught to lift themselves off their seat for
10 seconds every 10 minutes.

Treatment
Prevention is the best treatment.
Surgical management of pressure sore follows the
same principles involved in acute wound
management.
Pre-operative management of pressure sore involves:
Adequate debridement.
Use of vacuum assisted closure.
Vacuum-Assisted Closure (VAC)
It provides suitable wound for surgical closure.
Applying intermittent negative pressure of
approximately -125 mmHg appears to hasten
debridement and the formation of granulation
tissue in chronic wound and ulcers.
A foam dressing is cut to size to fit the wound.
A perforated wound drain placed over the foam and

07

the wound is sealed with a transparent adhesive

film.
A vacuum is then applied to the drain.
Negative pressure may act by decreasing edema,
by removing interstitial fluid and by increasing
blood flow as a result bacterial count decreases
and cell proliferation increases, there by creating a
suitable bed for graft or flap cover.
A vacuum is then applied to the drain.
Negative pressure may act by decreasing edema,
by removing interstitial fluid and by increasing
blood flow as a result bacterial count decreases
and cell proliferation increases, there by creating a
suitable bed for graft or flap cover.

Necrotizing Soft Tissue Infections

They are rare but often fatal.

Common Microorganism Involved

i. G+ve
aerobes
(staphylococcus
aureus,
staphylococcus pyogens).
ii. G-ve aerobes (E.coli, Pseudomonas, Clostridium,
bacteroides).
iii.-hemolytic Streptococcus.
There is usually a history of trauma or surgery with
hematoma.
Sometimes, the patient's own defense mechanism
may be deficient.
These infections are characterized by sudden
presentation and rapid progression.
The fact that deeper tissues involved often leads to
a late or missed diagnosis.

Signs of Necrotizing Infection

Edema beyond the area of erythema
Crepitus.
Skin blistering.
Fever (often absent).
Greenish drainage ('dish water pus').
Pink / orange skin staining.
Focal skin gangrene (late sign).
Final shock, coagulopathy and multiorgan failure.

Types
i. Clostridial infection (gas gangrene)
ii.Non clostridial infection (streptococcal gangrene
and necrotizing fascitis)

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The variant of necrotizing fascitis with toxic shock

syndrome results from streptococcal pyogens and is
often called the "flesh-eating bug".

Types
i. Atrophic.
ii. Hypertrophic.
iii. Keloid.

Atrophic Scar (Linear Scar)

Fig. 1.4: Necrotizing fascitis with extensive skin

involvement.

Treatment
Surgical excision with tissue biopsies sent for culture
and diagnosis.
Wide raw areas require skin grafting.

Scars
"Scar result as maturation phase of wound healing".

Characteristics
The immature scar becomes mature over a period
lasting a year or more but is at first:
Pink ( vascularity)
Hard (due to edema)
Raised
Itchy (often)
The disorganized collagen fibres become aligned
along stress lines with their strength being in their
weave rather in their amount.
As the collagen matures and becomes denser, the
scar becomes almost acellular as the fibroblasts
and blood vessels reduce.
Then the scar external appearance becomes
(mature scar):
Pale
Softer
Flattens
Itchiness diminishes
Most of the above changes occur over the first 3
months but a scar will continue to mature for
1-2 years.
Tensile strength will continue to increase but will
never reach that of normal skin.

Pale.
Flat.
Stretched in appearance.
Appears on the back and areas of tension.
Early traumatized as the epidermis and dermis are
thinned.
Excision and resuturing may only rarely improve
such a scar.

Hypertrophic Scar
It is defined as excessive scar tissue that does not
extend beyond the boundary of original incision or
wound.
It results from a prolonged inflammatory phase of
wound healing and from unfavorable scar siting
(i.e. across the lines of skin tension)

Keloid ('Like a Claw') Scar

It is defined as excessive scar tissue that extends
beyond the boundaries of the original incision or
wound.
There is defect in maturation and stabilization of
collagen fibers.
Etiology
Exactly unknown.
Common in blacks.
It is associated with elevated levels of growth
factors, deeply pigmented skin.
An inherited tendency.
When keloid occurs following an unnoticed trauma
without scar formation is called as 'spontaneous
keloid'.
Keloid continues to grow even after 6 months, may
be for many years.
May be associated with Ehlers-Danlos syndrome.
Pathologically keloid contains proliferating immature
fibroblasts, proliferating immature blood vessels and
type III collagen.
Occurs on certain areas of body.
Triangles where points are the xiphisternum, each
shoulder tip.

STBS
WOUNDS, TISSUE REPAIR AND SCARS

Other sites are:

Upper arm
Chest wall
Lower neck in front

09

Epidermis Linear scar in

clean wound
Dermis
Scar (linear)

Subcutaneous tissue

Hypertrophic scar
in infected wound
limits to scar
Scar (hypertrophic)

Keloid in genetically
predisposed extends
to normal skin

Scar (keloid)

Fig. 1.6: Diagrammatic representation of linear,

hypertrophic and keloid scar.

Contractures
Fig. 1.5: Keloid in the upper part of the scar. It is
the previous parotidectomy scar.

Treatment of Hypertrophic And Keloid Scar

Pressure local moulds or elasticated garments.
Silicone gel sheeting (mechanism unknown).
Intralesional steroid injection (triamcinolone).
Excision and steroid injection.
Excision and postoperative radiation (external beam
or brachytherapy).
Intralesional excision (keloid only).
Laser to reduce redness (which may resolve in any
event).
Vitamin E or palm oil massage (unproven).
Hypertrophic scar improves spontaneously
with time, while keloids do not.

"When scar crosses joints or flexion creases, a tight

web may form restricting the range of movements at
the joint, this is called as contracture
Contracture can cause hyperextension or
hyperflexion deformity".
In the neck it may interfere with head extension.

Treatment
Multiple Z-plasties.
Complex contracture requires inset of flap or grafts.
Splintage and intensive physiotherapy are often
required postoperatively.

Fig. 1.7: Multiple Z-plasty release of finger contracture.

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WOUNDS, TISSUE REPAIR AND SCARS

Difference
between
Hypertrophic Scar

Keloid

and

Keloid

Hypertrophic
Scar

Genetic
Composition

Yes

No

Site Of
Occurrence

Chest wall,

Anywhere in

upper arm,
lower neck, ear

the body

Common in
flexor surfaces

Growth

Continues to
grow without
time limit

Extent

Extends to
normal skin

Treatment

Poor response

Growth limits
for 6 months

Limited to scar
only

Good response
to steroids

Recurrence

Very high

Is uncommon

Collagen
Synthesis

20 times more

Is 6 times more

Relation of
Size of
Injury And
Lesion

No relation.

Age

Adolescents,

than normal skin

(Type III thick )

Small healed
scar can form
large keloid

than normal skin

(Type III fine
collagen)

Related to the
size of injury and
duration of
healing

Children

middle age
Sex

Common in

Equal in both

females
Race

More in blacks

No racial relation

(15 times)
Structure

Thick collagen
with increased
epidermal
hyaluronic acid

Fine collagen with

increased alpha
acting