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UNIVERSITY OF PRETORIA
PLASTIC SURGERY
Wound and wound healing abnormalities number amongst the main causes of
patient morbidity and mortality. South Africa with an abnormally high incidence
of violence and road accidents, an ageing population and an epidemic of HIV/
AIDS and malnutrition is no exception. The allocation of resources towards more
dramatic diseases like cancer chemotherapy and organ transplantation is
worldwide disproportional.
One of the great challenges to health carers has always been the ability
to achieve wound closure by either operative or nonoperative methods.
Different methods included dressings, surgery, treatment of systemic disease
and control of infection and also the use of modalities like hyperbaric oxygen.
During the past 20 years more advances were made in wound care than
the previous 2000 years. This all came as a result of the rapid expansion
in knowledge of the intricate mechanisms of the healing process at
molecular level. Present wound-care methods have dramatically improved the
ability to heal wounds with fewer complications.
One of the most promising recent advents is the therapeutic use of growth
factors and local antibodies to generate new tissue. An even more
exciting technology creating new tissue, is that of tissue engineering.
Since 1987 this multi-disciplinary field combining biological science and
engineering technology, has developed rapidly to produce commercially
available live skin substitutes and cartilage. Research has created
live cultured cells fixed to an extracellular matric and eventually supported
by a three-dimensional vascular structure. We are on the brink of producing
through stem cell manipulation, live organs to replace alloplastic implantations
and donor transplantations.
II. GENERAL
As the clot dries it forms a scab, which protects the wound site from dehydration
and pathogen invasion. Concurrently vasodilatation ensues – ten to thirty
minutes after injury, mast cells in connective tissue release serotonin and
histamine causing vessels to dilate and increase their permeability. This
increased blood flow causes heat release and a temperature rise in the skin
around the wound. The increased permeability results from separation of
endothelial cells in the vessel walls induced by serotonin and histamine. Thus
plasma migrates into the interstitium, nourishing the wounded tissue and
leukocytes leak into the extracellular spaces surrounding the wound.
2. Tissue damage and the activation of clotting factors during the vascular phase
stimulate the release of inflammatory mediators - bioactive substances -
constituting the early aspect of wound healing known as the inflammatory phase.
This reaction, which begins within seconds of wounding, is the same whether the
cause is a surgical cut, or a wound invaded by pathogenic bacteria. The
qualitative nature and duration of this phase is critical in determining the eventual
outcome of wound healing, from the successful closure of the defect to the
quality of the resultant scar. The response occurs rapidly and can be detected by
the presence of localized heat, swelling, erythema, and discomfort, which usually
restricts function.
When it comes to the inflammatory process, permeability of the intravascular
space results in leakage of plasma, soluble components, and cellular
constituents arriving in the following sequence: first platelets, then neutrophils,
followed by monocytes and lymphocytes which differentiate into macrophages
as they enter the connective tissue.
The migration of epithelial cells then begins, resurfacing the injured tissue (Fig
1). The macrophage is the key player in the degradation of injured tissue debris
and in the reparative phase of wound healing, initiating the transition from initial
inflammation to the early repair phase of wound healing.
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INJURY
lymphocyte
HAEMORRHAGE complement
Interferon
bact\viral particles
oxygen Antigens
COAGULATION
THROMBOSIS INFLAMMATION
(PLATELETS) neutrophils prostaglandins helper T cells
monocytes lymphokines
cytokines cytokines
Epithelial Cell
cytokines MACROPHAGE
FIBROBLAST prostaglandins
REPAIR
In the adult, the normal repair of wounds occurs by the formation of granulation
tissue and its organization to a scar. Scar is a dynamic, metabolically active
tissue and tends to remain weaker than unwounded tissue. A scar tends to
contract abnormally, and overhealing may lead to a hypertrophic scar or keloid.
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The scar appears reddish at first but as the connective tissue grows tauter and
vascularisation slows, it gradually loses colour. Hair, sebaceous and sweat
glands are also absent, as is the ridged pattern of the epidermis. Thus the new
skin’s appearance is unusually smooth. The rate at which wounds gain tensile
strength is slow. For example, wounds have gained only about 20% of their final
strength by the third week. Wounded tissue fails to attain the same breaking
strength as uninjured skin. At maximum strength a scar is only 70% as strong as
intact skin.
c) WOUND ASSESSMENT
i) A full assessment of a problem wound is critical to successful management
and treatment and facilitates the choice of wound dressing required to
promote healing.
Factors include:
• the history of the wound
• the location of the wound
• the condition of the surrounding skin and the wound margins
• the extent and depth of the wound and the condition of the wound bed.
ii). Physiological assessment is also essential. This includes:
• general health status
• associated systemic disease
• associated vascular disease
• Neurosensory and neuromuscular status
• wound severity and tissue type involved
• factors affecting treatment option selection
• presence of foreign material
iii) Acute and chronic wounds. Acute wounds usually occur without an
underlying cause, usually trauma related. They are of short duration,
eliciting a normal inflammatory response, usually followed by healing
without subsequent breakdown.
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Wound care has developed into a distinct scientific field. There is no single
dressing that is ideal for all wound types. Many variables in patient factors,
product factors and the different stages of wound healing necessitate a wide
choice of dressings for different situations. The wound dressing function is to
provide the environment that will maximize the body’s potential to do this. Ideally
we need the dressing to provide mechanical protection, thermal insulation,
gaseous exchange, protection against infection and absorption of excess
exudates. We would also like as little sensitization potential as possible –
adhesive constituents may cause contact dermatitis. Provision of a moist
environment has been a prerequisite for healing in most wounds and with few
exceptions, the basis of wound management now involves the provision of this
high humidity at the wound dressing interface.
Additionally, occlusive dressings have been shown to decrease pain and
inflammation, to decrease wound infection in most wounds and to improve scar
formation.
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Essentially, the more difficult the wound is to heal, the more sophisticated the
dressing choice needs to be. Depending on their structure and composition,
dressings may be used to absorb exudate, combat infection or odour, relieve
pain, promote debridement, provide and maintain a moist environment
encouraging granulation tissue production and promoting epithelialisation. The
choice of dressings is made according to these different requirements unique to
each wound.
Dressing Categories
Transparent Film Dressings (examples Tegaderm, Op-Site)
Transparent films are semi-permeable membranes made of polyurethane. Most
are adhesive, although non-adhesive varieties do exist. The adhesives may have
the potential for sensitization. The film dressing serves as a non-absorptive
barrier. They provide moist healing, allow visualization of wounds and can serve
as a secondary dressing holding the primary dressings in place. They are also
excellent in protecting intact skin or in situations of superficial epidermal injury
such as burns and abrasions. They are contraindicated in deep, infected wounds,
or those with a macerated margin. Disadvantages include the fact that excessive
exudate may accumulate and adhesive trauma is possible.
Hydrogel Dressings (examples Intrasite, Granugel, Nugel)
Hydrogel dressings are available as a gel or as sheets. They are predominantly
composed of water, and thus are able to donate moisture to the wound.
Hydrogels can be packed into wounds to fill dead space - they provide a moist
protected environment, offer pain relief, encourage granulation and autolytic
debridement. They can be used on infected wounds.
The gels’ ability to donate moisture may be altered by combination with a
secondary dressing – thus combining with gauze will increase water loss,
combining with a film dressing will decrease water loss.
Hydrocolloid Dressing (examples Granuflex, Comfeel, Combiderm)
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Very often the individual cost of newer dressings is higher, but when compared
with the number of dressings that need to be done and the effective time taken to
full healing, patient comfort and out patient treatment, these dressings are
usually found to be more cost effective.
Pathophysiologic Treatment
factors option
ouou
Description of wound
according to assessment outcome
Improving Deteriorating
Fluctuating Static
a. ACUTE WOUNDS
Wounds may firstly be classified according to the mechanism of injury
and secondly to the amount of contamination (American Association
of Trauma Surgeons).
ii) Abrasions
v) Burns
vi) Bites
AATS classification
b. CHRONIC WOUNDS
3. Metabolic
- diabetes
- gout
- calcinosis
- Gaucher’s disease
4. Inflammatory disorders
- pyoderma gangrenosum
- vasculitis – polyartheritis nodosa, granulomatoses
- panniculitis – necrobiosis lipoidica diabeticorum
5. Infections
- bacterial – TB, osteomyelitis
- other – fungal, treponemal, viral, protozoal
7. Hematologic
- rbc (sickle cell anemia, thallassemia, spherocytosis, polycythemia
vera)
- wbc (leukemia)
- platelet (thrombocytosis, hypercoagulable states)
- dysproteinemia (amyloidosis, cryoglobulinemia)
8. Neoplastic
- marjolin’s ulcer
- primary and metastatic skin tumours
- lymphomas, sarcomas (kaposi)
- haemangiomas, vascular-, lymphatic malformations
9. Miscellaneous
- drugs (Coumadin – protein C deficiency)
- fictitious (malingering)
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ii) Pathophysiology (From Nwomeh et al: Clin in Plast Surg. Vol 25, no.
3, July 1998)
Tissue injury
Chronic Inflammation
Activiation of Neutrophil
Macrophages Infiltration
Inflammatory Reactive
Cytokines Oxygen Species
Protease Inhibitors
Chronic Wound
Although the association between cigarette smoking and delayed wound healing
is accepted in clinical practice, no controlled clinical studies have proved this
relationship (Burns).
Venous stasis ulcers make up 70% of vascular ulcers. They result from
chronic venous insufficiency. It is critical to differentiate venous from
arterial ulcers as the compression therapy used for venous ulceration
could have dire consequences if used in a patient with an arterial ulcer.
Venous malfunction initiates a series of events that result in increased
hydrostatic pressure, venous hypertension and, ultimately skin
ulceration.
Clinical Presentation
Venous ulcers are also characterized by irregular wound margins; they are
non-tender, associated with eczema, covered with exudate and usually
located on the medial aspect of the lower leg or ankles. (Arterial ulcers occur
on toes, feet and unusual locations, are tender, gray and may contain necrotic
tissue) Palpation of peripheral pulses and temperature assessment
of lower limbs and hands is essential. Cold skin with diminished pulses suggest
arterial disease.
v. Arterial Ulcers
Peripheral ischaemia and reduced skin blood flow may lead to arterial
ulcers. Arterial insufficiency and occlusive disease is usually caused by
atherosclerosis of the extremities. The incidence of arterial insufficiency
and ulceration increases with age – the sixth and seventh decade
accounts for the highest incidence. Risk factors are also increased in
patients who are male, and those who have diabetes mellitus, hyper-
tension, Raynaud’s Disease, sickle cell anaemia, hypercholesterolaemia,
lead a sedentary lifestyle, suffer from obesity and smoke.
Arterial ulcers occur in patients with the risk factors mentioned above and are
usually located on the lower leg over the toes, between the toes or on the
tips, on the heels or bony prominences of the foot and rarely over the
medial malleolus. They have deep pale wound beds with even wound
margins. The surrounding atrophic skin changes described previously are
present as well as the symptoms and signs of arterial insufficiency.
A history of intermittent claudication, coldness, numbness in the toes and
feet is typical. Resting pain in the lower limbs which improves when the
limb is dependent, is a sign of advanced atherosclerotic vascular
disease.
Diabetic ulcers of the lower leg often present innocently but may progress rapidly
to fulminating infection and amputation. It has the highest lower limb
amputation rate of any chronic leg wound. Ulceration mainly affects the feet.
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1. Ischemia
2. Neuropathy
a. Loss of pain protection and protective reflexes. The foot muscles loose
their motor feedback causing the arch of the foot to collapse resulting in
deformed metatarsals and clawing of the toes. Painless repetitive
injuries from minor wounds like trimming of toe nails lead to chronic
ulceration and ill fitting shoes to pressure necrosis on the plantar
surface and tips of the toes. Protective calluses increase the chance of
pressure.
3. Uremia
Silent or overt renal failure causes loss of protein and edema but also
independantly alters wound healing.
4. Suppressed immunity
Management
5. Meticulous protection and wound care will heal superficial shallow ulcers.
“Total contact” casts will “off-load” pressure and restricted activity should heal
moderately deep ulcers.
The effects of surgery are permanent – the effects of radiation are permanent,
continuous and progressive.
Pathophysiology
Management
Basic management principles are used eg nutritional support, elimination of
causative agents, control of infection, debridement, pressure irrigation,
occlusive dressings and eventual reconstructive procedures. Promising
options for the future remain the therapeutic use of growth factors and
cytokines (transforming GF-beta, platelet derived GF, interleukin–3 and
granulocyte-macrophage GF).
When operating in irradiated tissue, some basic principles should be adhered to:
Pathophysiology:
1. Hypoxia
These wounds are hypoxic due to vascular damage, clotting, vaso-
constriction and increased cellular oxygen consumption.
A low O2 supply and increased oxygen demand causes
acidosis and the elevated lactate stimulates vascular growth factors.
2. Hypovascularity
Normal angiogenic capillary ingrowth occurs across a steep gradient
of high-O2- lactate towards low-O2- high- lactate levels (Niinikoski).
Severe hypoxia suppresses angiogenic and vascular endothelial
growth factor production (Gimbel).
3. Hypocellularity
Oxygen is essential for the normal collagen synthesis and maturation
from fibroblasts. Spontaneous wound break down may occur due to
an imbalance between cell death (collagen lysis) and cell replacement
(collagen formation). A non-healing wound thus results from metabolic
demands for healing and homeostasis that exceeds the vascular and
oxygen supply (Marx).
4. Infection
Neutrophils and macrophages normally kill micro-organisms via
O 2-dependant and O2-independant systems forming oxygen and
superoxide radicals that damage bacterial cell membranes. In hypoxic
cells the O2-dependant pathway is severely incapacitated, causing a
higher incidence of infection (Jonsson).
HBO therapy
The principles of managing problem wounds include correction of perfusion and
oxygenation insufficiencies, debridement, control of infection, wound care
and surgical reconstruction. If a patient suffers from deficient tissue
oxygenation due to nonreconstructable vascular disease, HBO as an adjunctive
therapy may be indicated. The best tool available to evaluate tissue hypoxia is
transcutaneous oxygen tension (TcPO2). A value greater than 50mm Hg
indicates spontaneous healing, whereas between 30-50mm is marginal and
below 30mm Hg requires HBO therapy. HBO therapy delivers 100% oxygen to
the patient at greater than two times the normal atmospheric pressure at sea
level.
Different options should follow the reconstructive ladder from simple to complex,
but often it will be necessary to travel by lift bypassing simpler options and
electing the best but complicated one:
The pre-requisite for choosing a non-surgical option is the belief that the wounds
will heal with conservative treatment in a reasonable time. Allowing
full-thickness skin defects to heal by secondary intention leaves a poor
quality scar and should only happen if the patient’s general condition dictate.
Skin grafting requires an adequate bed for the graft to take. Five common
reasons why skin grafts fail are:
IV. KELOIDS:
Clinical:
A keloid is descriptive of an uncontrollable growth of scar tissue. Keloids must be
differentiated from hypertrophic scars. A hypertrophic scar is confined to the area
of injury or incision and usually flattens with time.A keloid grows beyond the
boundaries of injury and does not usually improve with time. Keloids are
unpredictable in their behaviour. Despite all other things being equal, they
sometimes occur only in certain wounds and not in others in the same individual.
With multiple ear piercing in vogue at present, another intriguing phenomenon
has become apparent. One can get keloid formation at the second piercing and
not at the time of primary piercing. There is also the phenomenon of
spontaneous keloids. These are keloids that are usually multiple and occur on
most parts of the body. These patients do not give a preceding history of injury.
Animals do not form keloids and cannot be used as research models.
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Aetiology:
The precise aetiopathogenesis of keloids is unknown. Several associated
factors have been observed.
Genetic: Although there have been sporadic reports of keloids in families,
the majority of patients with keloids do not have a positive family history.
No gene markers have yet been identified.
Race: Keloids are more common in the Negroid and Asian population groups
and less common in people of Caucasian descent.
Melanocytes or melanin pigment may play a role in the aetiopathogenesis of
keloids because none have been reported in albinos.
Anatomical sites: There are certain areas of the body that have a
predilection for keloids. These include the ears, back, presternal, arms
and shoulder regions. It is rarely found in the upper eyelids, palms,
soles and genitalia.
Wound Factors: Factors in wound closure influencing the likelihood of
keloid formation.
· Tension
· Suppurative wounds or those that heal by secondary intention.
· Growth factors and cytokines. The ones most studied are the three
isoforms of transforming growth factor beta.
Immune theory: Some have likened the occurrence of a keloid to that of a
secondary immune response. The progression of initial keloid may be slow
(primary response), the recurrence is more florid (secondary response).
Biochemistry:
· Collagen type in normal skin - the dermis has approximately 85% of
collagen type I and 15% collagen type III. In keloids the collagen type
III is increased.
· Increased chrondoitin-4-sulphate.
· Collagenase activity normal or increased.
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· Increased alpha-2-macroglobulin.
· Increased alpha-1-antitrypsin.
Treatment
No single mode of therapy is effective for keloids. Because of the high
occurrence rates, a multimode therapy approach is recommended.
Pharmaceutical:
· Steroids. Intralesional injection of steroid can be used preoperatively
to soften the keloid and postoperatively to prevent, or treat early
recurrences. Injections are reapeated every 2 to 6 weeks.
· Bleomycin has been used intralesionally.
· Several other agents such as colchicine, D-penicillinamine and beta amino
propionitile.
Lasers
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