Wound repair

In normal skin, the epidermis (outermost layer) and dermis (inner or deeper layer) exist in a
steady-state equilibrium and shield from the external environment.
2
NORMAL STRUCTURE OF SKIN

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Wound is defined as “ a disruption of normal anatomic structure and function”
It is an injury to the body (as from violence, accident, or surgery) that involves
breach in the contunuity of skin and usually damage to underlying tissues.
Structure of oral mucous membrane

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oropharynx etc
According to potential risk of infection in operative wounds, they have been classified
into 4 classes :
C
L
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I
F
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C
A
T
I
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N
N
:
1

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C
L
A
S
S
I
F
I
C
A
T
I
O
N
:
2

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Closed wound is an injury in which no blood escapes from
the body , although there may be some bleeding under the
skin. Continuity of skin is maintained.
Open wound is an injury that causes breach in the
continuity of skin or mucous membrane and there is escape
of blood from the body.
OPEN AND CLOSED WOUNDS

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INCISIONS– Incisions, commonly called cuts, are
wounds made by sharp cutting instruments such as
knives, razors. Incisions tend to bleed freely because
the blood vessels are cut cleanly and without ragged
edges. There is little damage to the surrounding
tissues. Of all classes of wounds, incisions are the
least likely to become infected, since the free flow of
blood washes out many of the microorganisms that
cause infection
LACERATION– They are open wounds having
ragged, irregular edges and masses of torn
tissue underneath.
Lacerations are frequently contaminated with
dirt, grease, or other material that is ground
into the tissue; therefore very likely to become
infected.
O
p
e
n
w
o
u
n
d
s

ABRASIONS–superficial wounds produced by
excoriation or removal of superficial layer of
mucous membrane. Rope burns, floorburns,
and skinned knees or elbows are common
examples of abrasions. This kind of wound can
become infected quite easily because dirt and
microbes are usually embedded in the tissues.
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PUNCTURES– Punctures are caused by objects
that penetrate into the tissues while leaving a
small surface opening. Wounds made by nails,
needles, wire, and bullets are usually
punctures. The possibility of infection is great
in all puncture wounds, especially if the
penetrating object has tetanus bacteria on it.
To prevent anaerobic infections, primary
closures are not made in the case of puncture
wounds.
O
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o
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Gunshot wounds: (Ballistic trauma)caused by a bullet or
similar projectile driving into or through the body. There
may be two wounds, one at the site of entry and one at the
site of exit, generally referred to as a "through-and-through.
Ballistic trauma is sometimes fatal for the recipient, or
causes long term negative consequences.
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Penetrating trauma is an injury that occurs
when an object pierces the skin and enters a
tissue of the body, creating an open wound.
Penetrating trauma can be serious because it
damages internal organs and presents a risk
of shock and infection.
O
p
e
n
w
o
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n
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Crush injury occurs because of pressure from a heavy object onto a body part. A crush
injury may also arise from squeezing of a body part between two objects. Depending
upon their severity, crush injuries can be complicated by bleeding, bruising, fractured
bones, poor circulation, or breakdown of muscle (rhabdomyolysis).
Compression of extremities or other parts of the body that causes muscle swelling and/or
neurological disturbances in the affected areas
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C
l
o
s
e
d
w
o
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n
d
s

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Contusions: more commonly known
as bruises, caused by a blunt force
trauma that damages tissue under the
skin i.e. the subcutaneous tissue is
injured but the continuity of skin is
maintained.
A hematoma a localized collection
of extravasated blood, in an organ,
space, or tissue & the mass
becomes palpable to the examiner .
C
l
o
s
e
d
w
o
u
n
d
s

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Petechiae – small pinpoint hematomas less than 3 mm in diameter
Purpura – a bruise about 1 cm in diameter, generally round in shape
Ecchymosis – subcutaneous extravasation of blood in a thin layer under the skin,
i.e. bruising over 1 cm in diameter.
C
l
o
s
e
d
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Wound depth is another fundamental characteristics used to classify wounds. In our
assessment, wound depth is recorded as partial-thickness or full-thickness.
Partial-thickness
They normally heal very quickly because they involve only the epidermal layer of the skin or
extend through the epidermis into the dermis. The dermis remains at least partially intact to
generate the new epidermis needed to close the wound. They are also less susceptible to
infection because part of the body's first level of defense (the skin) is still intact.
Full-thickness They penetrate completely through the skin into underlying tissues. The
wound may expose adipose tissue, muscle, tendon, or bone.
These wounds heal by granulation and contraction, which require more body resources and
more time than the healing of partial-thickness wounds.
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C
L
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F
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C
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3

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Wound healing The healing wound is an overt expression of an intricate sequence of
cellular and biochemical responses directed toward restoring tissue integrity and
functional capacity following injury.
Day 1
Day 1-4
Day 4-21
Day 21- 2yrs

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Kane’s analogy to the repair of a damaged house provides a visual
understanding of and the connection to the basic physiology of wound
repair

Hemostasis
Once the source of damage to a house has been removed and before work
can start, utility workers must come in and cap damaged gas or water lines.
So too in wound healing damaged blood vessels must be sealed. In wound healing
the platelet is the cell which acts as the utility worker sealing off the damaged
blood vessels. The blood vessels themselves constrict in response to injury.
.
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Under normal conditions platelets are
discoid, with a diameter of 2-4 μm. Under
the influence of ADP (adenosine
diphosphate) leaking from damaged tissues
the platelets become spherical and extend
long pseudopodia which adhere to
subendothelium and other platelets. Upon
activation platelets granules discharge their
contents which encourages further platelet
aggregation and fibrin formation.

Platelets release platelet-derived growth factor (PDGF) and transforming
growth factor beta (TGF-b) from their alpha granules to attract
neutrophils and macrophages.
They also secrete factors which interact with and stimulate the intrinsic
clotting cascade through the production of thrombin, which in turn
initiates the formation of fibrin from fibrinogen.
The fibrin mesh strengthens the platelet aggregate into a stable
hemostatic plug.
Hemostasis occurs within minutes of the initial injury unless there are
underlying clotting disorders.
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Inflammation Phase
Clinically inflammation, the second stage of wound healing presents as erythema,
swelling and warmth often associated with pain, the classic “rubor , tumor, calor,
dolor”.
This stage usually lasts up to 4 days post injury.
In the wound healing analogy the first job to be done once the utilities are capped
is to clean up the debris. This is a job for non-skilled laborers. These non-skilled
laborers in a wound are the neutrophils or PMN’s (polymorphonucleocytes).
The inflammatory response causes the blood vessels to become leaky releasing
plasma and PMN’s into the surrounding tissue.
The neutrophils phagocytize debris and microorganisms and provide the first line
of defense against infection. They are aided by local mast cells.
As fibrin is broken down as part of this clean-up the degradation products attract
the next cell involved.
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The task of rebuilding a house is complex and requires someone to direct this
activity or a contractor. The cell which acts as “contractor” in wound healing is
the
macrophage.
Macrophages are able to phagocytize bacteria and provide a second line of
defense.
They also secrete a variety of chemotactic and growth factors such as fibroblast
growth factor (FGF), epidermal growth factor (EGF), transforming growth factor
beta (TGF) and interleukin-1 (IL-1) which appears to direct the next stage
21

Proliferative Phase ( Proliferation, Granulation and Contraction):
The granulation stage starts approximately four days after wounding and
usually lasts until day 21 in acute wounds depending on the size of the wound.
It is characterized clinically by the presence of pebbled red tissue in the wound base and
involves replacement of dermal tissues and sometimes subdermal tissues in deeper
wounds as well as contraction of the wound.
In the wound healing analogy once the site has been cleared of debris, under the direction
of the contractor, the framers move in to build the framework of the new house.
Sub-contractors can now install new plumbing and wiring on the framework and siders and
roofers can finish the exterior of the house.
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The “framer” cells are the fibroblasts which secrete the collagen framework on
which further dermal regeneration occurs. Specialized fibroblasts are responsible for
wound contraction.
The “plumber” cells are the pericytes which regenerate the outer layers of capillaries and
the endothelial cells which produce the lining.This process is called angiogenesis.
The “roofer” and “sider” cells are the keratinocytes which are responsible for
epithelialization.
In the final stage of epithelializtion, contracture occurs as the keratinocytes differentiate to
form the protective outer layer or stratum corneum.
.

Remodeling or Maturation Phase:
Once the basic structure of the house is completed interior finishing may
begin.
So too in wound repair the healing process involves remodeling the dermal
tissues to produce greater tensile strength.
The principle cell involved in this process is the fibroblast. When the levels of
collagen production and degradation equalize, the maturation phase of tissue
repair is said to have begun] During maturation, type III collagen, which is
prevalent during proliferation, is replaced by type I collagen. Originally
disorganized collagen fibers are rearranged, cross-linked, and aligned along
tension lines.
Remodeling can take up to 2 years after wounding.

KANES ANALOGY TO WOUND REPAIR
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HEALING CAN BE DIVIDED INTO THREE
CATEGORIES:
HEALING BY PRIMARY INTENTION
HEALING BY SECONDARY INTENTION
HEALING BY TERTIARY INTENTION
WOUND HEALING CLASSIFICATION

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This type of healing occurs when there is essentially no contamination of the wound and the
edges of the wound are approximated thus closing the wound. The best example of this
situation is the surgical incision where contamination of the wound is minimized and the
wound is closed by suturing.
Once the wound is sutured, the incision space fills with blood, which contains fibrin and blood
cells and which subsequently clots. The surface of this clot becomes dehydrated and forms a
scab.
Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the
edges of the incision begins to proliferate. It migrates under the scab and forms a thin
continuous epithelial layer.
By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation
tissue starts to develop. Collagen fibers are present but do not bridge the incision site. The
epithelial cells continue to proliferate under the scab and the epidermal covering over the
incision becomes thicker.
By day 5, the incision space is filled with granulation tissue and collagen fibers begin to bridge
the incision. The epidermis returns to its normal thickness and keratinized architecture.
PRIMARY INTENTION

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Healing of a clean linear wound by primary intention

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Second intention healing differs from first intention healing in several ways.
First of all the greater injury invokes a more intense inflammatory response. If
conditions are less favorable, wound healing is more complicated and occurs through
a protracted filling of the tissue defect with granulation and connective tissue.
This process is called healing by second intention and is commonly associated with
avulsive injury, local infection, or inadequate closure of the wound.
Secondly, much more granulation tissue is formed. The wound is allowed to
granulate
Surgeon may pack the wound with a gauze or use a drainage system
And thirdly, wounds that are repaired by second intention healing undergo a
phenomenon known as "wound contraction" whereby specialized granulation tissue
fibroblasts called myofibroblasts contract and dramatically reduce the size of the
wound.

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Healing by secondary intention: there is more extensive of tissue that
has gradually to be filled in and replaced by new connective tisssue.

(TERTIARY INTENTION OR DELAYED PRIMARY CLOSURE)
For more complex wounds, the surgeon may attempt healing by third intention through a
staged procedure that combines secondary healing with delayed primary closure.
The avulsive or contaminated wound is débrided and allowed to granulate
and heal by second intention for 5 to 7 days.
Once adequate granulation tissue has formed and the risk of infection appears minimal, the
wound is sutured .
The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.
The wound is purposely left open.
If the wound edges are not reapproximated immediately, delayed primary wound healing
transpires. This type of healing may be desired in the case of contaminated wounds.
By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes
of epithelization, collagen deposition, and maturation are occurring.
Foreign materials are walled off by macrophages that may metamorphose into epithelioid
cells, which are encircled by mononuclear leukocytes, forming granulomas.
Usually the wound is closed surgically at this juncture, and if the "cleansing" of the wound
is incomplete, chronic inflammation can ensue, resulting in prominent scarring.
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Difference between 'repair' and ‘regeneration’.
When restitution occurs by means of tissue that is structurally and functionally
indistinguishable from native tissue, regeneration has taken place. However, if tissue
integrity is reestablished primarily through the formation of fibrotic scar tissue then
repair has occurred.
Repair predominates when injuries occur in tissues formed largely of permanent cells
or when the injury results in extensive damage to stromal framework and supporting
connective tissues. In these situations, the injured tissue is replaced by fibroblastic
cells, usually in the form of granulation tissue, which eventually results in the
formation of a scar.
True tissue regeneration or complete regeneration, refers to the replacement of
lost/damaged tissue with an ‘exact’ copy, such that both morphology and functionality
are completely restored.
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Based on their regenerative capabilities, the cells of the body are divided into three
groups: labile cells, stable cells, and permanent cells.
Labile cells proliferate normally throughout life replacing cells that are continually
being destroyed. In this group are such cells as surface epithelia and the
hematopoietic cells of the spleen, lymphoid organs and bone marrow.
Stable cells replicate at very low levels under normal circumstances, but can be
stimulated to divide rapidly in response to various stimuli. Cells in this group include
the parenchymal cells of most glandular organs, vascular endothelial cells, and
mesenchymal cells such as fibroblasts, smooth muscle cells, osteoblasts, and
chondroblasts.
Permanent cells are cells that either do not replicate in postnatal life or do so to an
insignificant extent. This group includes nerve cells, skeletal muscle cells, and cardiac
muscle cells.

Factors Affecting Wound Healing
Holistic assessment of the patient is an important part of the wound care process. A
number of local and systemic factors can delay or impair wound healing. These may
include:
Reduced Blood supply (oxygenation) - Cardiovascular disorders and Ischaemia.
Oxygen is important for cell metabolism, especially energy production by means of
ATP, and is critical for nearly all wound-healing processes. It prevents wounds from
infection, induces angiogenesis, increases keratinocyte differentiation, migration, and
re-epithelialization, enhances fibroblast proliferation and collagen synthesis, and
promotes wound contraction .
Chronic wounds are notably hypoxic; tissue oxygen tensions have been measured
transcutaneously in chronic wounds from 5 to 20 mm Hg, in contrast to control tissue
values of 30 to 50 mm Hg .
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Drugs- Non-steroidal anti inflammatory drugs and Corticosteroids. Systemic glucocorticoids
(GC), which are frequently used as anti-inflammatory agents, are well-known to inhibit wound
repair via global anti-inflammatory effects and suppression of cellular wound responses,
including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal
with incomplete granulation tissue and reduced wound contraction .
Non-steroidal anti-inflammatory drugs (NSAIDs) There are few data to suggest that short-term
NSAIDs have a negative impact on healing. However, the question of whether long-term NSAIDs
interfere with wound healing remains open.
Most chemotherapeutic drugs are designed to inhibit cellular metabolism, rapid cell division,
and angiogenesis and thus inhibit many of the pathways that are critical to appropriate wound
repair. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased
fibroplasia and neovascularization of wounds .

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Obesity - decreases tissue perfusion. Obese individuals frequently face wound complications,
including skin wound infection, dehiscence, hematoma and seroma formation, pressure ulcers,
and venous ulcers. Many of these complications may be a result of a relative hypoperfusion and
ischemia that occurs in subcutaneous adipose tissue. This situation may be caused by a
decreased delivery of antibiotics as well.
Underlying Disease - Diabetes Mellitis and Autoimmune disorders:Several dysregulated cellular
functions are involved in diabetic wounds, such as defective T-cell immunity, defects in
leukocyte chemotaxis, phagocytosis, and bactericidal capacity, and dysfunctions of fibroblasts
and epidermal cells. These defects are responsible for inadequate bacterial clearance and
delayed or impaired repair in individuals with diabetes.

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Infection –(prolong inflammatory phase, use vital nutrients, impair epithelialisation and
release toxins). prolonged inflammation also leads to an increased level of matrix
metalloproteases (MMPs), a family of proteases that can degrade the ECM. P aeruginosa and
Staphylococcus appear to play an important role in bacterial infection in wounds. Many chronic
ulcers probably do not heal because of the presence of biofilms containing P. aeruginosa, thus
shielding the bacteria from the phagocytic activity of invading polymorphonuclear neutrophils
(PMNs). This mechanism may explain the failure of antibiotics as a remedy for chronic wounds .

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Age
Delayed wound healing in the aged is associated with an altered inflammatory response,
such as delayed T-cell infiltration into the wound area with alterations in chemokine
production and reduced macrophage phagocytic capacity.review of the age-related changes
in healing capacity demonstrates that every phase of healing undergoes characteristic age-
related changes, including enhanced platelet aggregation, increased secretion of
inflammatory mediators, delayed infiltration of macrophages and lymphocytes, impaired
macrophage function, decreased secretion of growth factors, delayed re-epithelialization,
delayed angiogenesis and collagen deposition, reduced collagen turnover and remodeling,
and decreased wound strength.
Stress
The pathophysiology of stress results in the deregulation of the immune system, mediated
primarily through the hypothalamic-pituitary-adrenal (HPA) and sympathetic nervous system
. Stress up-regulates glucocorticoids (GCs) and reduces the levels of the pro-inflammatory
cytokines IL-1β, IL-6, and TNF-α at the wound site. Stress also reduces the expression of IL-1α
and IL-8 at wound sites—both chemoattractants that are necessary for the initial
inflammatory phase of wound healing

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Malnutrition- inadequate supply of protein, carbohydrates, fatty acids, and trace elements
essential for all phases of wound healing
Substance abuse including alcohol and cigarette smoke: Alcohol abuse and smoking cause a
disruption in healing time. Proper nutrition and an adequate amount of oxygen in the blood
contribute to a successful recovery time. Alcohol blocks the absorption of many important
nutrients in the body, and it keeps the body from using needed nutrients during healing
time.
Smoking may adversely affect wound healing. Nicotine causes vasoconstriction,therefore
reduces blood supply to the skin and periphery.
This reduces the perfusion of wounds. Smoke also contains carbon monoxide which increases
the proportion of carboxyhaemoglobin in the blood. Another problem is that smokers lose more
vitamin C than non-smokers. Smoke causes the breakdown and increased excretion of vitamin C
from the body, resulting in a chronic shortage. As vitamin C is essential for collagen formation
wound healing will be correspondingly inhibited.

Factors that impair wound healing, ( in an otherwise healthy individual)
Foreign material
Necrotic tissue
Ischemia
Tension
Foreign material is evrything that the hosts organisms immune system views as “non
self”,
Including bacteria, dirt, suture material etc
Necrotic tissue: its presence serves as a barrier to ingrowth of reparative cells,the
inflammatory stage is then prolonged .
Also, necrotic tissue serves as niche for bacteria. It frequently includes blood that
collects in a wound (hematoma), where it can serve as an excellent source of bacteria.
41

Ischemia: decreased blood supply to a wound interferes in wound
repair in several ways;
It can lead to further tissue necrosis and lessen the delivery to a
wound of antibodies, wbc’s, and antibiotics which thereby increase the
chances of wound infection.
Wound ischemia decreses the delivery of oxygen & nutrients
necessary for proper healing.
Ischemia can be caused by several things, including– tight &
incorrectly placed sutures, improperly designed flaps, excessive
external pressure on a wound, systemic hypotension, peripheral
vascular disease and anemia.
42

Tension: tension on a wound is the final factor that can impede
wound healing. Anything tending to hold wound edges apart.
If sutures are used to overcome excessive wound tension, the tissue
encompassed by sutures will be strangulated, producing ischemia.
If sutures are removed too early in the healing process, the wound
under tension will probably reopen and then heal with excessive
scar formation and wound contraction.
If sutures are left in too long, in an attempt to overcome wound
tension, the wound will still tend to spread open during the
remodelling stage of healing, and
the tract into the epithelium through which the sutures ran will
epithelialize and leave a permanent disfiguring mark.
43

WOUND ASSESSMENT
Considerations for assessment Wound Bed
Granulating: healthy red tissue which is deposited during the repair process,
presents as pinkish/red coloured moist tissue and comprises of newly formed
collagen, elastin and capillary networks. The tissue is well vascularised and
bleeds easily.
Epithelializing: process by which the wound surface is covered by new
epithelium, this begins when the wound has filled with granulation tissue. The
tissue is pink, almost white, and only occurs on top of healthy granulation tissue
44

Sloughy: A layer or mass of dead tissue separated from surrounding
living tissue. ( devitalized yellowish tissue). Is formed by an accumulation
of dead cells. Must not be confused with, pus.
Necrotic: wound containing dead tissue. It may appear hard dry and
black. Dead connective tissue may appear grey. The presence of dead
tissue in a wound prevents healing
Hypergranulating; granulation tissue grows above the wound margin.
This occurs when the proliferative phase of healing is prolonged usually
as a result of bacterial imbalance or irritant forces
45

Red
If the wound is red (the colour of healthy granulation tissue) the wound is healthy and
normal healing is under way. When a wound begins to heal, a layer of pale pink
granulation tissue covers the wound bed. As this layer thickens, it becomes beefy red.
(The Royal College of Surgeons of Edinburgh [RCSE], 2005)
The Red-Yellow-Black is a simple classification, which identifies what healing
phase a wound is in. (Cuzzell) 1988
RYB CLASSIFICATION
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If the would is yellow, beware!
A yellow color in the wound bed may be a film of fibrin on the tissue. Fibrin is a
sticky substance that normally acts as a glue in tissue rebuilding. However, if the
wound is unhealthy or too dry, fibrin builds up into a layer that can't be rinsed off and
may require debridement. Dead tissue due to ischemia or infection also may be yellow
and must be debrided.
47
Yellow

the wound bed is black, be alarmed.
A black wound bed signals necrosis (tissue death). Eschar (dead, avascular tissue)
covers the wound, slowing the healing process and providing microorganisms with a
site in which to proliferate. When eschar covers a wound, accurate wound depth is
difficult and should be defered until eschar is removed.
Black
48

Wound Edges
Healthy wound edges present as advancing pink epithelium growing
over mature granulated tissue.
Colour - pink edges indicate growth of new tissue; dusky edges indicate hypoxia;
and erythema indicates physiological inflammatory response or cellulitis
Raised - wound edges (where the wound margin is elevated above the surrounding
tissue) may indicate pressure, trauma or malignant changes
Rolled -wound edges (rolled down towards the wound bed) may indicate wound
stagnation or wound chronicity
Contraction - wound edges are coming together, signs of healing
49

Exudate
An exudate is any fluid that filters from the circulatory system into lesions or
areas of inflammation.
Is produced by all acute and chronic wounds (to a greater or lesser extent) as
part of the natural healing process. It plays an essential part in the healing
process in that it:
Contains nutrients, energy and growth factors for metabolising cells
Contains high quantities of white blood cells
Cleanses the wound
Maintains a moist environment
Promotes epithelialisation
It is important to asses and document the type, amount and odour of exudate to
identify any changes.
Too much exudate leads to maceration and degradation of skin while too little
can result in the wound bed drying out. It may become more viscous and
odorous in infected wounds.
50

Type Colour Consistency Significance
Serous Clear, straw coloured Thin, watery Normal. An increase may
be indicative of infection
Haemoserous Clear, pink Thin, watery Normal
Sanguinous Red Thin, watery Trauma to blood vessels
Purulent Yellow, grey, green Thick Infection. Contains
pyogenic organisms and
other inflammatory cells
51

Wound dehiscence is a surgical complication in which a wound ruptures
along surgical suture. Risk factors are age, diabetes, obesity, poor knotting or grabbing of
stitches, and trauma to the wound after surgery.
Wound dehiscence can be caused by inadequate undermining (cutting the skin away
from the underlying tissues) of the wound during surgery, excessive tension on the
wound edges caused by lifting or straining, or the wound being located on a highly
mobile or high tension area.
Individuals with Ehlers–Danlos syndrome also commonly experience wound
dehiscence. Risk factors can include any of the above as well as obesity, smoking,
previous scarring, surgical error, cancer and chronic use of corticosteroids
53

Dehiscence can be prevented through adequate undermining to reduce stress on the wound
edges, avoiding heavy lifting and hematomas and speeding healing through adequate nutrition,
controlled diabetes.
Sterile strips may also be used to cover the sutures for up to a week.
Once wound dehiscence occurs, it can be treated by allowing granulation, revising and
suturing the edges and providing prophylactic antibiotics.
Exposure to the air, debridement and if indicated, frequent dressing changes may also help.
HOW TO PREVENT DEHISCENCE
54

They often contain nerves and blood vessels. They
generally develop after thermal or traumatic injury that
involves the deep layers of the dermis .
When a normal wound heals, the body produces new
collagen fibers at a rate which balances the breakdown
of old collagen. Hypertrophic scars are red and thick
and may be itchy or painful.
They do not extend beyond the boundary of the
original wound, but may continue to thicken for up to
six months. They usually improve over the one or two
years, but may cause distress due to their appearance
or the intensity of the itching; they can also restrict
movement if they are located close to a joint.
A hypertrophic scar is a cutaneous condition characterized by deposits of excessive amounts
of collagen which gives rise to a raised scar, but not to the degree observed with keloids.
55
SCARS: are areas of fibrous tissue that replace normal skin after injury. A scar
results from the biological process of wound repair in the skin and other tissues
of the body. Thus, scarring is a natural part of the healing process.

Langer's lines, also called cleavage lines, is a term used to define the direction
within the human skin along which the skin has the least flexibility.
These lines correspond to the alignment of collagen fibers within the dermis. They
were first given detailed attention in 1861 by Austrian anatomist Karl Langer
(1819-1887)
CONCEPT OF LANGERS LINES
56
Usually, a surgical cut is carried out in the
direction of Langer's lines, and incisions made
parallel to Langer's lines generally heal better
and produce less scarring, while
perpendicular injuries will gape because they
are pulled by tension. This can have important
implications for surgery, particularly in
cosmetic procedures where the goal may be
to minimize the appearance of scarring.

A keloid is the formation that a type of scar which, depending on its maturity, is composed
mainly of either type III (early) or type I (late) collagen. It is a result of an overgrowth of
granulation tissue (collagen type 3) at the site of a healed skin injury which is then slowly
replaced by collagen type 1. Keloids are firm, rubbery lesions or shiny, fibrous nodules, and can
vary from pink to flesh-coloured or red to dark brown in colour.
A keloid scar is benign and not contagious, but sometimes accompanied by severe itchiness,
pain, and changes in texture. In severe cases, it can affect movement of skin.
Keloids should not be confused with hypertrophic scars, which are raised scars that do not grow
beyond the boundaries of the original wound.
Keloids expand in claw-like growths over normal skin.
57

Injuries such as burns that involve damage to the dermis rarely heal without
formation of a scar. Scar tissue is not identical to the tissue that it replaces and is
usually more fibrous and of inferior functional quality.
The scar shows an increase in the thickness of the new epithelial layer but the
attachment of epidermis is poor making the surface vulnerable to further injury.
Restrictive contractures due to serious burn injuries can result in long term aesthetic
and physical consequences.
Skin contractures bridging or located proximal to a joint lead to joint deformities that
severely restrict range of motion of the effected joint.
Skin contractures are also often accompanied by debilitating levels of chronic pain
requiring a high dependency on pain medication.
SCAR CONTRACTURES
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Wound repair

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