WOUNDS - SURGERY.pptx very educative and learning purposes
1.
T O PIC : S U R GI C A L W O U N DS , W O U N D H E A L I N G
A N D S C A R S
B Y: K A S E N D WA A L L A N
FA C IL IT A T O R : D R O CE N WI L L IA M
LIRA UNIVERSITY
FACULTY OF MEDICINE
DEPARTMENT OF SURGERY
2.
SURGICAL WOUNDS,WOUND HEALING
ANDSCARS
Learning objectives
To understand normal healing and how it can be
affected
To know how to manage wounds of different
types ,of different structures and at different sites
To know aspects of disordered healing that lead to
chronic wounds
The variety of scars and their treatments
To differentiate between acute and chronic wounds
3.
WOUND HEALING
Woundhealing is a mechanism where by the body attempts
to restore the integrity of the injured part.
Several factors may influence healing :
Site of wound
Structures involved
Mechanism of wounding
Contamination
Loss of tissue
Local factors e.g. pressure and vascular insufficiency
Systemic factors e.g. malnutrition,diseases,steroids,smoking
etc.
4.
NORMAL WOUND HEALING
Normalwound healing occurs in three or four phases
The inflammatory phase
The proliferative phase
The remodeling phase(maturation)
The destructive phase may follow the inflammatory
phase consisting of cellular cleansing of the wound by
macrophages.
5.
Inflammatory phase
Inflammatoryphase begins 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 vessels, releasing ADP which
causes thrombolytic aggregates to fill the wound
When bleeding stops, platelets then release several cytokines from their alpha
granules.
These include platelet derived growth factor(PDGF), platelet factor IV and
transforming factor beta(TGFB), these attract polymorph nuclear leukocytes(PMN)
and macrophages.
Platelets and the local injured tissue release vasoactive amines such as histamines,
serotonin and prostaglandins which increase vascular permeability for infiltration of
PMN
Macrophages remove devitalized tissue and microorganisms.
Support of cells is provided by fibrin from fibrinogen.
Phase is described in four words- redness,swelling,pain and heat.
6.
Proliferative phase
Itlasts from third day to the third week, consisting mainly
of fibroblasts activity with the production of collagen and
ground substance.
Fibroblasts need vitamin C to produce collagen.
Growth of new blood vessels such as capillary loops.
The wound tissue formed earlier in this phase is called
granulation tissue.
Later in this phase, there is increase in tensile strength due
to increased collagen type III deposition hence the phase
is characterized by wound contraction reducing the surface
area of wound over the first three weeks of healing.
7.
Remodeling phase
Itis characterized by maturation of collagen .
There is re alignment of collagen fibers 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 twelfth
week post injury.
Normal wound healingat specific tissues
Bone: phases are as above but periosteal and endosteal
proliferation lead to formation of callus which consists of osteoid,
callus forming is minimal and primary healing occurs, if there is
gap then secondary healing occurs.
Nerve: distal to the wound , wallerian degeneration occurs,
proximally the nerve suffers traumatic degeneration as far as the
last node of Ranvier, regenerating nerve fibers are attracted to
there receptors by neurotropism followed by profuse growth of
new nerve fibers from the cut proximal end.
Tendon: here healing follows two mechanism, intrinsic consisting
of synovial diffusion and vincular blood flow and extrinsic which
depends on formation of fibrous adhesions between the tendon
and tendon sheath.
10.
Classification of woundclosure and healing
Primary intention:
Wound edges opposed
Normal healing
Minimal scar
Secondary intention:
Wound left open
Heals by granulation, contraction and epithelialization
Increased inflammation and proliferation
Poor scar
Tertiary intention:
Wound initially left open
Edges later opposed when healing conditions are favorable
11.
Types of wounds
There are two types of wounds i.e.
Tidy
Untidy
surgeons aim is to convert all untidy to tidy wounds by
removing all contaminated and devitalized tissue.
Appropriate tests for hepatitis viruses and
immunodeficiency virus are required.
differences
Tidy wounds;
Incised
Clean
Healthy tissues
Seldom tissue loss
Untidy wounds:
Crushed or avulsed
Contaminated
Devitalized tissues
Often tissue loss
15.
Managing acute wounds
Cleansing
Explorationand diagnosis
Debridement
Repair of structures
Replacement of lost tissue where indicated
Skin cover if required
Skin closure without tension
Some specific wounds
Bites :bites from small animals are common in children, these
wounds have high bacterial virulent counts hence prophylaxis is
required. Injuries to the ear, tip of nose and lower lip are most
common in victims of human bites.
Puncture wounds: wounds caused by sharp objects should be
explored to to the limit of tissue blood staining
Hematoma: it may require release by incision or aspiration,
untreated hematoma may also calcify and therefore require
surgical exploration if symptomatic.
Degloving : occurs when the skin and subcutaneous fat are stripped
by avulsion from the underlying fascia leaving the bone exposed. It
may be open or closed , an example is a ring avulsion injury with
loss of finger skin.
Chronic wounds
Canbe defined as a wound that fails to heal in
usually three weeks. Delays may occur in any phase
but usually the inflammatory phase.
Leg ulcers: most common, an ulcer is defined as a
break in the epithelial continuity. A prolonged
inflammatory phase leads to overgrowth of
granulation tissue which heals by scarring leaving a
fibrotic margin. Necrotic tissue at ulcer Centre is
called a slough.
22.
Pressure sores
Thesecan be defined as tissue necrosis with ulceration due
to prolonged pressure.
Pressure sore frequency in descending order : ischium,
greater trochanter,sacrum,heel,malleolus, occiput.
Stage 1; no breach in the epidermis
Stage 2: partial thickness skin loss involving epidermis
abnd dermis
Stage 3: full thickness skin loss extending into the
subcutaneous tissue but not through fascia
Stage 4: full thickness skin loss through fascia , extensive
tissue destruction involving muscle, bone, tendon or joint.
Necrotizing soft tissueinfections
These are commonly poly microbial infections with
gram positive aerobes and gram negative anaerobes
and beta hemolytic streptococcus.
There is usually a history of trauma or wound
contamination.
There are two types of necrotizing infections;
clostridial( gas gangrene) and non
clostridial(streptococcal gangrene and necrotizing
fascilitis)
Signs and symptomsof necrotizing infections
Unusual pain
Oedema
Crepitus
Skin blistering
Fever
Pink skin staining
Focal skin gangrene
Shock and multi organ failure
27.
SCARS
The maturationphase discussed earlier represents the formation of
scar.
The immature scar becomes mature over a period lasting a year or more
Scars are often described as being atrophic, hypertrophic and keloid.
Atrophic scar is pale , flat and stretched in appearance and easily
traumatized as epidermis and dermis is thin
Hypertrophic scar is an excessive scar tissue that doesn’t extend beyond
the boundary of the original wound. Its just due to prolonged
inflammatory phase.
A keloid is an excessive scar tissue that extends beyond the boundaries
of the original tissue due to elevated levels of growth factor
Treatment: excision, silicon gel, vitamin E etc.
CONTRACTURES
When scarscross joints or flexion creases, a tight
web may form restricting the range of movements at
the joint called contracture.
It may cause hyperextension or hyper flexion
deformity, in the head it affects head extension.
Treatment may be simple involving multiple Z-
plasties or more complex requiring the onset of
grafts or flaps.
Splintage and intensive physiotherapy are often
required post operatively.
REFRENCES
Bailey andlove textbook of short practice of surgery
27th
edition
Lippincott textbook of surgery 2004
An introduction to the use of vacuum assisted
closure .world wide wounds, 2001
END.