Wound

healing ,wound
infection and
wound care
Section of Plastic Surgery
 Definition of wound

Any breach in the continuity

of skin
 Phases of wound healing

Haemostasis.

Inflammation.

Proliferation.

Remodelling.
 Sequence of events in
Haemostasis phase
The vessels constrict.

A platelet plug is formed.

The platelets degranulate and release PDGF and

thromboxanes.

First white thrombus then red thrombus.

 Sequence of events in
inflammation phase
Occurs in the first 2-3 days.
Its stimulus may be

1. Physical injury
2. Antigen- antibody reaction.
3. Infection.

. Endothelial cells swell causing egress of

polymorphs and mononuclear cells
 Sequence of events in
proliferation
Begins phase
form 2 or 3 day
nd following injury and lasts for 2-4
rd

weeks.
1 - Epithelialization ---- Migration of keratinocytes across a
partial thickness wound to restore epidermal
continuity
Macrophages release growth factors which are
chemoattractant to fibroblasts.
2 - Fibroplasia ------- fibroblast migrate along network of fibrin
into the wound.
Fibroblasts secrete GAGs and produce collagen and
elastin.
When GAGs hydrated , become ground substance.
3 - Angiogenesis
Sequence of events in
remodelling phase
Begins 2-4 weeks after injury.

State of collagen homeostasis.

Extensive capillary network begins to involute.

Collagen fibers become arranged in a more

organized manner.
Inflammatory cell cycles
Wound contraction
A process in which the surrounding skin is
pulled towards an open wound and thought
to be mediated by myofibroblast activity.

Contracture
A pathological manifestation of wound
contraction resulting in tissue shortening
that compromises joint mobility and function
(and potentially growth in children).
Fetal wound healing

Minimal to negligible scar

Shorter inflammatory phase.
Type III collagen.
Unique characteristics of fetal fibroblasts,
inflammatory cells, extra-cellular matrix, cytokine
profile, and developmental gene regulation may be
responsible for the scar-less phenotype of early
gestation fetal wounds.

Ground of recent research regarding fetal medicine

and wound healing.
Important cells in wound
healing
Macrophages.
Epithelial cells.
Collagen
Myofibroblast
 Macrophages
Derived from mononuclear leucocytes.
Debride tissue and remove micro-organism.
Essential for wound healing.
Co-ordinate the activity of fibroblasts by
releasing growth factors like
1. IL-1
2. TNF- alpha
3. TGF-beta
Epithelial cells
Epithelial repair by

1. Mobilization
2. Migration
3. Mitosis
4. Cellular differentiation.
Myofibroblast
First identified by
Gabbiani in 1971.
It resembles fibroblast
but also contain alpha-
actin smooth muscle.
This muscle fiber
responsible for wound
contraction.
Increased numbers of
myofibroblast are found
in abnormal
contracture.
Factors affecting wound
healing
Local factors
1. Blood supply.
2. Radiation.
3. Infection.
4. Trauma.
5. Nerve injury.
6. Foreign body.
7. Pressure.
8. Edema.
Factors affecting wound
healing
Systemic factors:
1. Nutrition.
2. Pharmacological -- steroids, chemotherapy.
3. Endocrine --- diabetes.
4. Medical --- jaundice, uraemia, cancer.
5. Age.
6. Smoking.
7. Toxins.
Factors affecting wound
healing
Congenital factors:
1. Ehlers Danlos.
2. Progeria.
3. Werners.
4. Epidermolysis bullosa.
5. Cutis laxa.
6. Pseudoxanthum elasticum
Ehlers Danlos
syndrome

Ehlers Danlos syndrome is

a group of inherited
abnormalities of the
connective tissues and is
characterized by easy
bruising, hyper elasticity
or laxity of the skin,
extremely loose joints or
hyper mobility of joints
and tissue weakness
Progeria

Nguyen Thi Ngoc, 13, reads

a book at home in Ho Chi
Minh City. Ngoc is Vietnam's
first known case of
Hutchinson-Gilford Progeria
Syndrome, a rare disease
which ages the body so
rapidly its victims die before
they have barely
experienced youth. Ngoc,
who lives in Ho Chi Minh
City, comes from a poverty-
stricken family and local
hospitals lack the means
and expertise to treat her.
Photo taken March 6
 Werners disease
Werner Syndrome (WS)
is an uncommon,
autosomal recessive
human genetic disease
that mimics premature
aging. Patients with WS
appear to age rapidly
following puberty, and
are at increased risk of
developing cancer and
cardiovascular disease.
Symptoms of WS include
premature graying and
loss of hair, bilateral
cataracts, osteoporosis,
atherosclerosis, diabetes
and scleroderma-like
changes and ulceration
of the skin.

The WS associated gene

Epidermolysis
bullosa

Epidermolysis bullosa (ep-

ih-dur-MOL-uh-sis buhl-LO-
sah) is a group of skin
conditions whose hallmark
is blistering in response to
minor injury, heat, or
friction from rubbing,
scratching or adhesive
tape. Four main types of
epidermolysis bullosa
exist, with numerous
subtypes. Most are
inherited
Cutis laxa
Cutis laxa is a disorder of
connective tissue, which is the
tissue that forms the body's
supportive framework.
Connective tissue provides
structure and strength to the
muscles, joints, organs, and
skin

Since that in 2002 researchers

started working on Cutis Laxa
7 gene mutations have been
identified:
Elastin (ELN) (2 mutations)
Fibulin5 (FBLN5)
Fibulin4 (FBLN4)
ATP6V0A2
SCYL1BP1 (Groderma
Osteodysplastica)
PYCR1
LTBP4
Pseudoxanthum
elasticum
Pseudoxanthoma
elasticum (PXE), also
known as Grnblad
Strandberg syndrome,
is a genetic disease that
causes fragmentation and
mineralization of elastic
fibers in some tissues. The
most common problems
arise in the skin and eyes,
and later in blood vessels
in the form of premature
atherosclerosis PXE is
caused by
autosomal recessive mutat
ions
in the ABCC6 gene on the
short arm of
chromosome 16 (16p13.1
Types of wound healing
according to management
Primary intention.

Delayed primary closure.

Secondary intention.
Types of wounds

Abrasion / Friction.

Laceration.

Contusion.

Burns.

Punctured wound/ bite wound.

Laceration
and
punctured
wound
Laceration
Trim wound edges
which are ragged and
contused and suture.

Punctured wound
Evaluate underlying
damage
Explore wound for
foreign body
Debride and leave open
or close depend on time
since bite and anatomic
location
Friction/abrasi
on

Cleanse to remove
foreign material
Consider scrub
brush/dermabrasion
to prevent traumatic
tattoos , should be
within 24 hours of
injury
 Contusion
Consider need to
evacuate hematoma if
collection is present

Early : minimize by
cooling
with ice(24-48hrs)

Later : warmth to speed

the absorption of

blood
Burns wound

Manage according to
trauma protocol
Life threatening injuries
must give priorities
Major burns needs
admission and IV fluids
resuscitation
Full thickness
circumferential burns
around chest and arms
needs escharotomy
Wound on face
Important to use careful technique.

Facial laceration are secondary importance than

airway problems, hemorrhage or intracranial bleeding.

Beware of overaggressive debridement.

Isolate cavity form each other.

Use anatomic landmarks.

Special wounds

Amputated wounds :
Transfer of amputated part in proper way and in time.

Cheek injury:
Parotid duct and facial nerve injury.

Eyelids injury :
Align grey line and repair in layers

Ear injuries :
Cauliflower

Human and animal bites :

 Wound management

Goal
Obtain a closed wound as soon as possible to
prevent infection,
fibrosis and secondary
deformity
Management of clean wound
General principles :
1. Immunization.

2. Pre-anaesthsia.

3. Local anesthesia.

4. Tourniquet.

5. Cleansing of surrounding skin.

6. Debridement.

7. Closure.

8. Dressing.
Contaminated wound
Difference between
contamination and wound
infection

All wound have a high tendency of

contamination but not all
wounds become infected
Infected wound

If post debridement, the tissue culture shows no

of bacteria 102 of gram positive streptococcus
and 105 of any other bacteria.
Management of contaminated
acute wound
Majority of can be closed primarily after adequate
debridement

Exceptions
1. Heavy bacterial contamination(human bite)
2. Long time lapse since wounding(relative).
3. Crush or ischemic tissue
4. Sustained high level of steroid ingestion

Antibiotics
Wound closure
5. Buried sutures
6. Monofilament skin sutures
7. Porous tape

Followup
.If doubt exists, it is always safer to delay the closure.
 Classification of wound according
to associated risk of infection

Type Class Infection risk

%
Clean Class I <2%
Clean contaminated Class II < 10 %
Contaminated Class III < 20 %
Dirty Class IV < Approximately 40%
Chronic wound

Any wound more than 3 months suppose to

be called chronic wound
Patho-physiology of chronic
wound
Healing is trapped into phase of inflammation.

MMPs (matrix-metalloproteinases) are the

hallmark of chronic wounds.

Inhibitors of MMPs suppose to be a mainstay of

chronic wound management
Types of chronic wounds
Pressure ulcer / wound.

Diabetic ulcer / wound.

Neuropathic ulcer / wound.

Radiation ulcer/ wound.

Factitious ulcer / wound.

Management of contaminated
chronic wound
Debridement :
1. Excision.
2. Frequent dressing.
3. Enzymatic.

Systemic antibiotics : (of little use)

Topical antibiotics creams :

4. Silver sulfadiazine(flemazine).
5. Mafenide acetate (sulfamylon).

Biological dressings :
Final closure :
6. With flap or skin graft
7. Convert the chronic contaminated wound bacteriologically to an acute clean
wound by debridement
Ideal characteristics of dressing
Available, absorptive.

Barrier (protective).

Cost effective, comfortable, conformable.

Dead or necrotic material removal.

Epithelialization encouraged.

Flexible.

Healing promoted, hydration.

Non irritant.
Thank you