Wound Healing

Wound classifications and

Management
 Introduction
• Wound healing is a mechanism whereby the
body attempts to restore the integrity of the
injured part.
• This falls far short of tissue regeneration by
pluripotent cells, seen in some amphibians, and
is often detrimental, as seen in the problems
created by scarring, such as adhesions,
keloids, contractures and cirrhosis of the liver.
Several factors may influence healing.
 Factors influencing healing of a
wound
• Site of the wound, Structures involved and Loss of tissue
• Mechanism of wounding: Incision/Crush/Crush avulsion
• Contamination (foreign bodies/bacteria)
• Other local factors: Vascular insufficiency (arterial or venous)
/Previous radiation/Pressure
• Systemic factors: Malnutrition or vitamin and mineral deficiencies
• Disease (e.g. diabetes mellitus)
• Medications (e.g. steroids)
• Immune deficiencies (e.g. chemotherapy,AIDS)
• Smoking
 Types of Wound Healing

• Although various categories of wound healing have been

described, the ultimate outcome of any healing process
is repair of a tissue defect.
• Primary healing, delayed primary healing, and healing by
secondary intention are the 3 main categories of wound
healing. Even though different categories exist, the
interactions of cellular and extracellular constituents are
similar.
• A fourth category is healing that transpires with wounds
that are only partial skin thickness.
 NORMAL WOUND HEALING
• This is variously described as taking place in three or
four phases, the most commonly agreed being:
1 the inflammatory phase;
2 the proliferative phase;
3 the remodelling phase (maturing phase);
• Occasionally, a haemostatic phase is referred to as
occurring before the inflammatory phase, or a
destructive phase following inflammation consisting of
the cellular cleansing of the wound by macrophages
The inflammatory phase begins immediately after
wounding and lasts 2–3 days.
•Bleeding is followed by vasoconstriction and thrombus formation
to limit blood loss.
•Platelets stick to the damaged endothelial lining of vessels,
releasing ADP, which causes thrombocytic aggregates to fill the
wound.
•When bleeding stops, the platelets then release several
cytokines:PDGF, platelet factor IV and TGFβ.
•These attract inflammatory cells e.g, PMN and macrophages.
•Platelets and the local injured tissue release vasoactive amines,
such as histamine, serotonin and prostaglandins, which increase
vascular permeability, thereby aiding infiltration of these
inflammatory cells.
Macrophages remove devitalised tissue and microorganisms while regulating
fibroblast activity in the proliferative phase of healing. The initial framework for
structural support of cells is provided by fibrin produced by fibrinogen.
A more historical (Latin) description of this phase is described in four words:
rubor (redness), tumor (swelling), calor (heat) and dolor (pain).

•The proliferative phase lasts from the third day to the third
week, consisting mainly of fibroblast activity with the production of collagen
and ground substance (glycosaminoglycans and proteoglycans), the growth of
new blood vessels as capillary loops (angioneogenesis) and the re-
epithelialization of the wound surface.
•Fibroblasts require vitamin C to produce collagen. The wound tissue formed in
the early part of this phase is called granulation tissue. In the latter part of this
phase, there is an increase in the tensile strength of the wound due to
increased collagen, which is at first deposited in a random fashion and consists
of type III collagen.
•This proliferative phase with its increase of collagen deposition is associated
with wound contraction, which can considerably reduce the surface area of a
wound over the first 3 weeks of healing.
 Remodelling Phase
• The remodelling phase is characterised by maturation of
collagen (type I replacing type III until a ratio of 4:1 is
achieved).
• There is a realignment of collagen fibres along the lines
of tension, decreased wound vascularity, and wound
contraction due to fibroblast and myofibroblast activity.
• This maturation of collagen leads to increased tensile
strength in the wound which is maximal at the 12th week
post injury and represents approximately 80% of the
uninjured skin strength.
Hand abrasion

Approximate days since injury

0 3 17 30
Approximate times of the different phases of wound healing, with
faded intervals marking substantial variation, depending mainly on
wound size and healing conditions, but image does not include
major impairments that cause chronic wounds.
There is considerable overlap among these phases.
 NORMAL HEALING IN SPECIFIC
TISSUES
BONE:
•The phases are as above, but periosteal and endosteal
proliferation leads to the formation of callus, which is
immature bone consisting of osteoid (mineralised by
hydroxyapatite and laid down by osteoblasts).
•In the remodelling 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, non-union or malunion.
 Nerve
• Distal to the wound, Wallerian degeneration occurs.
• Proximally,the nerve suffers traumatic degeneration as
far as the last node of Ranvier.
• The regenerating nerve fibres are attracted to their
receptors by neurotrophism, which is mediated by
growth factors, hormones and other extracellular matrix
trophins.
• Nerve regeneration is characterised by profuse growth of
new nerve fibres which sprout from the cut proximal end.
• Overgrowth of these, coupled with poor approximation,
may lead to neuroma formation.
 Tendon
• Although repair follows the normal pattern of wound healing, there
are two main mechanisms whereby nutrients, cells and new vessels
reach the severed tendon.
• These are intrinsic, which consists of vincular blood flow and
synovial diffusion, and extrinsic, which depends on the formation of
fibrous adhesions between the tendon and the tendon sheath.
• The random nature of the initial collagen produced means that the
tendon lacks tensile strength for the first 3–6 weeks.
• Active mobilisation prevents adhesions limiting range of motion, but
the tendon must be protected by splintage in order to avoid rupture
of the repair.
 Abnormal Healing
• Delayed healing may result in loss of function or poor cosmetic
outcome. The aim of treatment is to achieve healing by primary
intention (first intention). This occurs when there is apposition of the
wound edges and minimal surrounding tissue trauma that causes
least inflammation and leaves the best scar.
• Delayed primary intention healing occurs when the wound edges
are not apposed immediately, which may be necessary in
contaminated or untidy wounds. The inflammatory and proliferative
phases of healing are well established when delayed closure of the
wound is carried out. This is also called healing by tertiary intention
in some texts and will result in a less satisfactory scar than would
result after healing by primary intention.
• Secondary healing or healing by secondary intention occurs in
wounds that are left open and allowed to heal by granulation,
contraction and epithelialisation.
 Acute Wounds
• Acute Wound results from sudden loss of
anatomic structure in tissue following the
transfer of kinetic, chemical, or thermal
energy.
• They typically occurred in recently
uninjured and otherwise normal tissue.
• Healing is timely and reliable, completing
the entire process within 6-12 weeks.
• Most surgical wounds are ac.wounds.
 MANAGING THE ACUTE WOUND: The surgeon
must remember to examine the whole patient according to
acute trauma life support (ATLS) principles.

PRIMARY SURVEY

• Airway with Cervical spine protection

• Breathing and ventilation
• Circulation with hemorrhage control
• Disability: Neurologic status
• Exposure/ Environmental control
 RESUSCITATION
TREATMENT PRIORITY NECCESSARY PROCEDURE
Airway Jaw thrust/chin lift/
Suction/ Intubation
Cricothyroidotomy
( with protection of C-spine )

Breathing/Ventilation/ Chest needle decompression

oxygenation Tube thoracostomy
Supplemental oxygen
Seal open pneumothorax
Circulation/hemorrhage control IV line/ central line
Venous cutdown
Fluid resuscitation/Blood transfusion
Thorocostomy for massive hemothorax
Pericardiocentesis for cardiac tamponade
Disability Burr holes for trans-tentorial herniation
IV mannitol
Exposure/Environment Warmed crystalloid fluid
Temperature
 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 with careful tissue handling and
meticulous technique
 Classification of wound closure
and healing
• Primary intention
Wound edges opposed
Normal healing
Minimal scar
• Secondary intention
Wound left open
Heals by granulation, contraction and epithelialisation
Increased inflammation and proliferation
Poor scar
• Tertiary intention (also called delayed primary intention)
Wound initially left open
Edges later apposed when healing conditions favourable
 WHO Guidelines
CLASSIFICATION:
• Clean
• Clean contaminated: a wound involving normal but colonized tissue
• Contaminated: a wound containing foreign or infected material
• Infected: a wound with pus present.

MANAGEMENT:

• Close clean wounds immediately to allow healing by primary

intention
• Do not close contaminated and infected wounds, but leave them
open to heal by secondary intention
• In treating clean contaminated wounds and clean wounds that are
more than six hours old, manage with surgical toilet, leave open and
then close 48 hours later. This is delayed primary closure.
 Surgical Wound Classification (CDC)
United States Centers for Disease Control and
Prevention

Class I/Clean:
An uninfected operative wound in which no inflammation is encountered and the
respiratory, alimentary, genital, or uninfected urinary tract is not entered. In addition,
clean wounds are primarily closed and, if necessary, drained with closed drainage.
Operative incisional wounds that follow nonpenetrating (blunt) trauma should be
included in this category if they meet the criteria.
• I. Clean: Uninfected, no inflammation
- Resp, GI, GU tracts not entered
- Closed primarily
Examples: Ex lap, mastectomy, neck dissection, thyroid, vascular, hernia, splenectomy

Class II/Clean-Contaminated:
An operative wound in which the respiratory, alimentary, genital, or urinary tracts are entered
under controlled conditions and without unusual contamination. Specifically, operations involving
the biliary tract, appendix, vagina, and oropharynx are included in this category, provided no
evidence of infection or major break in technique is encountered.
• II. Clean-contaminated:
- Resp, GI, GU tracts entered, controlled
- No unusual contamination
Examples: Chole, SBR, Whipple, liver txp, gastric surgery, bronch, colon surgery
 Surgical Wound Classification
(CDC)
Class III/Contaminated:
Open, fresh, accidental wounds. In addition, operations with major
breaks in sterile technique (e.g., open cardiac massage) or gross
spillage from the gastrointestinal tract, and incisions in which acute,
nonpurulent inflammation is encountered are included in this
category. Examples: Inflamed appy, bile spillage in chole,
diverticulitis, Rectal surgery, penetrating wounds.
Class IV/Dirty-Infected
Old traumatic wounds with retained devitalized tissue and those that
involve existing clinical infection or perforated
viscera. This definition suggests that the organisms causing
postoperative infection were present in the operative field before the
operation. Examples: Abscess I&D, perforated bowel, peritonitis,
wound debridement, positive cultures pre-op
 Some Specific Wounds
• BITES: Most bites involve either puncture wounds or avulsions. Bites from
small animals are common in children.Injuries to the ear, tip of nose and
lower lip are most usually seen in victims of human bites. Anaerobic and
aerobic organism prophylaxis is required as bite wounds typically have high
virulent bacterial counts.
• PUNCTURE Wounds: Wounds caused by sharp objects should be explored
to thelimit of tissue blood staining. Needle-stick injuries should be treated
according to the well-published protocols because of hepatitis and HIV risks.
X-ray examination should be carried out in order to rule out retained foreign
bodies in the depth of the wound.
• HAEMATOMA: If large, painful or causing neural deficit, a haematoma 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 a fat fracture, which
results in an unsightly groove but intact skin. An untreated haematoma may
also calcify and therefore require surgical exploration if symptomatic.
 Degloving Wounds
• Degloving occurs when the skin and subcutaneous fat are stripped by
avulsion from the underlying fascia, leaving neurovascular structures,
tendon or bone exposed. A degloving injury may be open or closed. An
obvious example of an open degloving is a ring avulsion injury with loss of
fingerskin. 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.
HAND BUTTOCK
• Examination under anaesthetic is required with a radical excision of all non-
bleeding skin, as judged by bleeding dermis.
• Fluoroscein can be administered intravenously while the patient is
anaesthetised. Under UV light, viable (perfused) skin will show up as a
fluorescent yellowish green colour, and the non-viable skin for excision is
clearly mapped out but possible anaphylaxis hinders its routine use.
• Most surgeons therefore rely upon 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. Meshed split-skin graft
 Compartment Syndrome
• Typically occurs in closed lower limb injuries.
• Severe pain, pain on passive movement of muscle, distal
sensory disturbance, and finally absent pulse (late).
• Compartment pressure measured using a pressure
monitor and a catheter placed in the muscle comp.
• If pressure constantly >30 mmHg or above signs are
present- fasciotomy should be performed.
• Two incisions, each being lateral to the subcutaneous
border of tibia via longitudinal incisions of skin, fat and
fascia which give access to the two postr. comparts. and
to the peroneal and antr.compart. of leg.
 Fasciotomy
• Fasciotomy involves incising the deep muscle fascia
and is best carried out via longitudinal incisions of
skin, fat and fascia. The muscle will be then seen
bulging out through the fasciotomy opening.
• In crush injuries that present several days after the
event, late fasciotomy can be dangerous as dead
muscle produces myoglobin which, if suddenly
released into the bloodstream, 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 once viable and
non-viable tissues have demarcated.
 Chronic Wounds
• A chronic wound may be defined as one that fails to heal in the
expected time for a wound of that type, which is usually less than 3
weeks. Delays in healing can occur at any phase but most often
occur in the inflammatory phase.
• Deregulation of one of the phases (prolonged inflammatory phase)
of normal acute wound healing.
• Tissue and wound hypoxia, failed epithelization due to repeat
trauma or desiccation may also result in a chronic partial thickness
wound.
• Surgeons may sharply convert a chronic wound into an acute
wound.
 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 leave a fibrotic margin. Necrotic tissue, often at the ulcer
centre, is called slough. A chronic ulcer, unresponsive to dressings and
simple treatments, should be biopsied to rule out neoplastic change, a SCC
known as a Marjolin’s ulcer being the most common. Effective treatment of
any leg ulcer depends on treating the underlying cause, and diagnosis is
therefore vital. Causes are:
• Venous disease leading to local venous hypertension (e.g.varicose veins)
• Arterial disease, either large vessel (atherosclerosis) or small vessel (DM)
• Arteritis associated with autoimmune disease (RA, Lupus etc.)
• Trauma – could be self-inflicted
• Chronic infection – tuberculosis/syphilis
• Neoplastic – squamous or basal cell carcinoma, sarcoma
 Leg Ulcers: Arterial insufficiency
ulcers
• It tend to occur distally on the tips of the toes or near
the lateral malleolus. The surrounding skin is thin,
shiny, and hairless.
• Patients frequently complain of claudication or rest
pain; however, some patients may have sufficient
neuropathy that they lack any pain symptoms even in
critical limb ischemia.
• Peripheral pulses are diminished or absent.
• When arterial ulcers are suspected, a vascular
evaluation should be obtained, including a peripheral
and central pulse examination and segmental Doppler
limb pressures and flow waveforms with calculation of
ABP.
An ischemic (arterial) leg ulcer
with deep 'punched out' appearance
 Venous stasis ulcers
• Venous stasis ulcers are among the most
common types of leg ulcers and typically
occur on the medial leg in the supramedial
malleolar location.
• A patient with a venous stasis ulcer
usually has a history of ulceration and
associated leg swelling or of deep venous
thrombosis.
Venous leg ulcer. Wounds are generally irregular and
shallow
 Pressure Ulcers:
Pathophysiology.
• Prolonged pressure applied to soft tissue over bony prominences,
usually caused by paralysis or the immobility associated with severe
illness, predictably leads to ischemic ulceration and tissue
breakdown.
• Muscle tissue seems to be the most susceptible. The prevalence of
pressure ulcers is 10% of all hospitalized patients, 28% of nursing
home patients, and 39% of spinal cord injury patients.
• Pressure ulcers increase in-hospital mortality rates more than
twofold as well as increase the risk of hospital readmissions. The
particular area of breakdown depends on the patient's position of
immobility, with ulcers most frequently developing in recumbent
patients over the occiput, sacrum, greater trochanter, and heels.
• In immobile patients who sit for prolonged periods on improper
surfaces without pressure relief, ulcers often develop under the
ischial tuberosities.
 Pressure ulcers: stages
• 1 Non-blanchable erythema without a breach
in the epidermis
• 2 Partial-thickness skin loss involving the
epidermis and dermis
• 3 Full-thickness skin loss extending into the
subcutaneous tissue but not through
underlying fascia
• 4 Full-thickness skin loss through fascia with
extensive tissue destruction, maybe involving
muscle, bone, tendon or joint
I Nonblanchable erythema of intact skin; wounds
generally reversible at this stage with intervention
II Partial-thickness skin loss involving epidermis or dermis;
may present as an abrasion, blister, or shallow crater
III Full-thickness skin loss involving damage or necrosis of
subcutaneous tissue but not extending through
underlying structures or fascia
IV Full-thickness skin loss with damage to underlying
support structures (i.e., fascia, tendon, or joint
capsule)
Unstageable Full-thickness tissue loss with actual depth of ulcer
unknown due to slough and/or eschar in wound bed

Suspected Localized area of discolored skin or blood-filled blister due

to
Deep Tissue damage of underlying tissue
Injury

National Pressure Ulcer Advisory Panel Classification

Scheme
 Prevention
• Skin care. Skin should be kept well moisturized
but protected from excessive contact with
extraneous fluids. Barrier products may reduce the
risk of pressure ulcers by protecting skin against
excessive moisture. Skin should also be cleaned
promptly following episodes of incontinence.
• Frequent repositioning. High-risk patients should
be repositioned at a minimum every 2 hours,
either while seated or in bed.
• Appropriate support surfaces. Adequate support
surfaces redistribute pressure from the bony
prominences that cause pressure ulcers.
 Prevention
• Static support surfaces. Foam, air, gel, and water-
overlay support surfaces are appropriate for low-
risk patients.
• Dynamic support surfaces. These are support
modalities that are powered and actively
edistribute pressure. These include alternating
and low air-loss mattresses. These surfaces are
appropriate for highrisk patients.
• Nutrition. High-risk patients should also undergo
nutritional screening to ensure that caloric and
protein goals are met.
 Treatment
• Debridement. Eschar and necrotic tissue should be debrided
unless contraindicated.
• Wound cleansing. The base of uninfected ulcers should be
cleaned with saline irrigation or a commercially available
wound cleanser at each dressing change.
• Dressing. Dressings should be selected to ensure the wound
base remains moist while keeping the surrounding skin dry.
• Control of infection and bacterial colonization.
• Nutrition. Successful treatment of pressure ulcers requires
adequate nutrition.
• Surgical management may include simple closure, split-
thickness skin grafting, or creation of a musculocutaneous
flap;
 Vacuum-assisted closure
• This is now more correctly known as negative pressure wound closure.
Applying intermittent negative pressure of approximately −125 mmHg
appears to hasten debridement and the formation of granulation tissue in
chronic wounds and ulcers. A foam dressing is cut to size to fit the wound. A
perforated wound drain is placed over the foam, and the wound is sealed
with a transparent adhesive film. A vacuum is then applied to the drain.
Negative pressure may act by decreasing oedema, by removing interstitial
fluid and by increasing blood flow. As a result, bacterial counts decrease
and cell proliferation increases, thereby creating a suitable bed for graft or
flap cover.
 Wound debridement
Gentle handling of tissues minimizes bleeding. Control
residual bleeding with compression, ligation or
cautery.Dead or devitalized muscle is dark in color, soft,
easily damaged and does not contract when pinched.
During debridement, excise only a very thin margin of
skin from the wound edge

1. Systematically perform wound toilet and surgical

debridement, initially to the superficial layers of tissues
and subsequently to the deeper layers.
2. After scrubbing the skin with soap and irrigating the
wound with saline, prep the skin with antiseptic..
3. Do not use antiseptics within the wound.
 Dedridement (contd)
4. Debride the wound meticulously to remove any loose foreign
material such as dirt, grass, wood, glass or clothing.
5. With a scalpel or dissecting scissors, remove all adherent foreign
material along with a thin margin of underlying tissue and then
irrigate the wound again.
6. Continue the cycle of surgical debridement and saline irrigation until
the wound is completely clean.
7. Leave the wound open after debridement to allow healing by
secondary intention.
8. Pack it lightly with damp saline gauze and cover the packed wound
with a dry dressing.
9. Change the packing and dressing daily or more often if the outer
dressing becomes damp with blood or other body fluids.
10.Large defects will require closure with flaps or skin grafts but may
be initially managed with saline packing
Diabetic Foot Ulcers: Evaluation
•The quality of the peripheral circulation, the extent of the wound,
and the degree of sensory loss should be recorded.
•Web spaces and nails should be examined for evidence of
mycotic infection, which may lead to fissuring of the skin and
subsequent infection.
•Neuropathic, arthropathic, and vasculopathic ulcers occur on
the plantar surface of the metatarsals and extend to the
metatarsal head, leaving exposed cartilage.
•Evaluation of diabetic foot ulcers should include plain x-rays of
the foot to evaluate for osteomyelitis, ankle brachial index(ABI)
measurements for vascular insufficiency, and the Semmes
Weinstein monofilament test for neuropathy.
Wagner Classification of Diabetic
Foot Ulcers
• Grade 0: No ulcer in a high risk foot.
• Grade 1: Superficial ulcer involving the full skin
thickness but not underlying tissues.
• Grade 2: Deep ulcer, penetrating down to
ligaments and muscle, but no bone involvement or
abscess formation.
• Grade 3: Deep ulcer with cellulitis or abscess
formation, often with osteomyelitis.
• Grade 4: Localized gangrene.
• Grade 5: Extensive gangrene involving the whole
foot
Diabetic Foot
University of Texas Wound Classification
System of Diabetic Foot Ulcers

• Grade I-A: non-infected, non-ischemic superficial ulceration

• Grade I-B: infected, non-ischemic superficial ulceration
• Grade I-C: ischemic, non-infected superficial ulceration
• Grade I-D: ischemic and infected superficial ulceration
•  
• Grade II-A: non-infected, non-ischemic ulcer that penetrates to capsule or bone
• Grade II-B: infected, non-ischemic ulcer that penetrates to capsule or bone
• Grade II-C: ischemic, non-infected ulcer that penetrates to capsule or bone
• Grade II-D: ischemic and infected ulcer that penetrates to capsule or bone
•  
• Grade III-A: non-infected, non-ischemic ulcer that penetrates to bone or a deep abscess
• Grade III-B: infected, non-ischemic ulcer that penetrates to bone or a deep abscess
• Grade III-C: ischemic, non-infected ulcer that penetrates to bone or a deep abscess
• Grade III-D: ischemic and infected ulcer that penetrates to bone or a deep abscess
 Diabetic Foot- management
• Prevention: Meticulous attention to hygiene and daily inspection for
signs of tissue trauma prevent the progression of injury. Podiatric
appliances or custom-made shoes are helpful in relieving pressure
on weight bearing areas and should be prescribed for any patient
who has had neuropathic ulceration. Critical to treatment of any
diabetic foot wound is complete offloading of the ulcer with an
appropriate diabetic shoe or other orthotic device.
• Antibiotic therapy. For infected wounds, initial antibiotic therapy
should be broad spectrum directed at both Gram +/- organisms. In
the acute phase I.V. is indicated. Wound cultures should be
obtained prior to initiation of antibiotics. Duration of antibiotics
depends on severity of infection. Mild soft tissue infections :1-2 wks
of therapy is sufficient, whereas moderate or severe infections
require 2 -4 wks of total antibiotic therapy. For OM involving viable
bone, 4-6 wks of IV therapy may be indicated.
 Dry/ Wet Gangrene
• Neglected chronic arterial insufficiency can result in
dry or wet gangrene. Wet gangrene can lead to an
ascending necrotizing infection while dry gangrene
can convert to wet at any time.
• Critical to treatment of these wounds is restoration of
arterial inflow. After optimization of arterial inflow,
devitalized tissue can be resected to facilitate healing.
• Arterial insufficiency wounds and dry gangrene must
be carefully assessed for signs of infection. If infection
is suspected, obtain wound cultures, debride infected
tissue, and institute appropriate antibiotics.
Dry gangrene Wet gangrene of the foot
affecting the toes as
a result of 
peripheral artery dise
ase
 NECROTISING SOFT-TISSUE
INFECTIONS
• They are most commonly polymicrobial infections with Gm+
aerobes (Staphs), Gm- anaerobes (E coli,Pseudomonas,
Clostridium, Bacteroides) and -haemolytic Strepto.
• There is usually a history of trauma or surgery with wound
contamination.
• There are two main types of necrotising infections: clostridial
(gas gangrene) and non-clostridial (streptococcal gangrene
and necrotising fasciitis).
• The variant of necrotising fasciitis with toxic shock syndrome
results from Streptococcus pyogenes and is often called the
‘flesh-eating bug’ in this situation.
• Treatment is surgical excision with tissue biopsies being sent
for culture and diagnosis. Wide raw areas requiring skin
grafting often result toxic shock syndrome
Signs and symptoms of necrotising
infections
• Unusual pain
• Oedema beyond area of erythema
• Crepitus
• Skin blistering
• Fever (often absent)
• Greyish drainage (‘dishwater pus’)
• Pink/orange skin staining
• Focal skin gangrene (late sign)
• Shock, coagulopathy and multiorgan failure
Necrotising fasciitis of the anterior abdominal wall.
 Hypertrophic Scar & Keloid
• A hypertrophic scar is defined as excessive scar
tissue that does not extend beyond the boundary
of the original incision or wound. It results from a
prolonged inflammatory phase of wound healing
and from unfavourable scar siting (i.e. across the
lines of skin tension).
• A keloid scar is defined as excessive scar tissue
that extends beyond the boundaries of the original
incision or wound. Its aetiology is unknown, but it is
associated with elevated levels of growth factor,
deeply pigmented skin, an inherited tendency and
certain areas of the body (e.g. a triangle whose
points are the xiphisternum and each shoulder tip).
 Treatment of hypertrophic and keloid scars
(The histology of both hypertrophic and keloid scars shows excess collagen with
hypervascularity, but this is more marked in keloids where there is more type III collagen)

• Pressure – local moulds or elasticated garments

• Silicone gel sheeting (mechanism unknown)
• Intralesional steroid injection (triamcinolone)
• Excision and steroid injectionsa
• Excision and postoperative radiation (external
beam or brachytherapy)
• Intralesional excision (keloids only)
• Laser – to reduce redness (which may resolve in
any event)
• Vitamin E or palm oil massage (unproven)
**All excisions have high rates of recurrence.
 Future and Controversies

• Future advances in wound healing will focus on affecting the agents

that influence the processes involved in the repair of damaged
tissue.
• Laser techniques, nonlaser techniques, and other modalities are
being explored to enhance the proliferation of cells, the migration of
cells, and the acceleration of the healing of wounds.
• Human cell–conditioned media developed in embryologic like
conditions has been shown to improve healing times in post laser
facial skin. Fetal tissue can heal scarless due to the unique
characteristics of fetal epithelial and mesenchymal cells and the
functioning of the fetal immune system.
• The inclusion of transforming growth factor (TGF)–β3 during the
healing of wounds in adults can be beneficial. TGFs -β1, -β2, and -
β3 all have significant roles in wound healing, and the simple
addition, subtraction, or ratio of these growth factors may not be
fully explanatory for scarless healing.
• Hyperbaric oxygen has also been used to promote healing.
• Agents such as platelet-rich plasma (PRP) and erythropoietin (EPO)
are modulators that have a positive effect on tissue regeneration
and have been used successfully to enhance the healing of wounds.
Although peptide growth factors are considered essential to the
wound-healing properties of PRP, the lipid fraction of PRP also
plays an important role in this, by aiding in the proliferation and
migration of primary adult human dermal fibroblasts and overcoming
the suppression of fibroblast proliferation by chronic wound fluid.
• Nutritional aspects are also critical for proper wound healing.
Improvement in the nutritional status of adults correlates with
enhanced wound healing.
• Honey was been shown to be less beneficial, despite its use since
early times, and has even caused delayed healing in certain types
of wounds. Treatment with honey causes partial-thickness burns to
heal more quickly than they would with conventional management
and that infected postoperative wounds may heal more quickly with
honey than with antiseptics and gauze, but the investigators
determined evidence for honey’s effects on other wounds to be of
low or very low quality.
• Reparative strategies involving engineered tissue matrices, either
exogenous or endogenous, have also been used.
 Stem Cells
• Stem cells continue to be a new frontier of research in the
armamentarium of wound healing strategies. There still exists
controversies with the use of fetal stem cells.
• Stem cells, in particular adipose-derived stem cells, have been
shown to ameliorate wound healing, and continued research in these
areas appears promising.
• Exogenous mesenchymal–derived stem cells, commonly obtained
from bone marrow, but available from other sources, are being used
in the setting of nonhealing inflammatory wounds.
• Third trimester human fetal placental chorionic stem cells did not
compare favorably with first semester ones in promoting wound
healing. However, first-,and more recently mid-trimester amniotic
stem cells, when treated using valproic acid, obtained
pluripotentialism.