The skin is the largest organ of the body and performs many functions.

Healthy skin provides a

barrier against pressure, friction, chemicals, heat, cold, UV, radiation and micro organisms. In
addition, the skin is essential for maintaining the body's fluid balance and providing
thermoregulation, and communicates external stimuli to the body via touch, pressure,
temperature and pain receptors. In addition, we externalise our emotional state through the skin:
we blush, turn pale, our hair stands on end and we emit scents (pheromones).
The need to perform these numerous and diverse tasks accounts for the intricate structure of the
skin. The skin is made up of three layers of tissue:
the epidermis (outermost layer)
the dermis
the subcutaneous tissue.
Together, these layers form the body's outer covering.
Epidermis
The epidermis has an average thickness of only about 0.1 mm and it is normally composed of
four different layers (Figure 3):

horny layer (stratum corneum)

granular layer (stratum granulosum)
prickle-cell layer (stratum spinosum)
basal layer (stratum basale).

Where exposure to friction is greatest, such as in the palms of the hands and soles of the feet,
the epidermis has five layers. This extra layer is called the clear layer (straum lucidum), situated
between the horny layer and the granular layer.
Dermis
The dermis is the layer that gives the skin its tensile strength and elasticity. These characteristics
are derived from the high proportion of loosely interwoven connective tissue fibres (collagen and
elastin). Histologically, two layers are distinguished:

the papillary layer (stratum papillare)

the reticular layer (stratum reticulare).

The dermis is firmly intermeshed with the epidermis via the connective tissue papillae of the
papillary layer. These papillae are interspersed with fine capillary loops, which provide the
nutrient supply of the epidermis. The papillary layer also contains numerous free nerve endings
branching into the epidermis as well as heat, cold and touch receptors (Meissner's cells).
The free connective tissue cells comprise fibroblasts, macrophages, mast cells, lymphocytes,
plasma cells, eosinophils and monocytes. The free space between the cellular and fibrous
elements is filled with a gelatinous fluid in which the cells are able to move freely. The mobile
fibroblasts differentiate into fibrocytes, which link via elongated processes to form a threedimensional network. These fibrocytes synthesise components of the intercellular fluid (eg
hyaluronic acid) as well as collagen and elastin fibres, which are interspersed within the network
of cells. The other free cells of the connective tissue are components of the endogenous defence
system and play a major role in inflammation and in the immune regulation of the skin.
The reticular layer (stratum reticulare) contains fewer free cells than the papillary layer. The
collagen fibres within this layer form a dense network running parallel to the body surface.
Between this collagen mesh, the fibres of the elastin connective tissue branch out, giving the skin
its extensibility. The direction of maximum extensibility is indicated by Langer's lines. This is why
incisions made perpendicular to these lines cause gaping wounds. In surgical operations,
therefore, incisions should be made along these lines wherever possible to improve the cosmetic
result.
Special modifications of the skin, the hair follicles, sebaceous, sweat and scent glands, are
embedded in the dermis.

Subcutaneous tissue layer

The dermis merges into the subcutaneous tissue layer without a clear boundary. The loose
connective tissue of the subcutaneous layer is interspersed with many of the firm fibres of the
dermis, which anchor the skin to the underlying structures, eg the fascia or periosteum. If these
retaining bands are few in number the skin moves on its substrate to create a skinfold. For
example, on the soles of the feet or the scalp the skin is almost immovable since the fibrous
bands are highly developed and numerous.
The entire subcutaneous tissue layer contains pads of fat, which are either readily mobilisable fat
stores or non-mobilisable, structural fatty cushions providing insulation against heat loss, and
reducing pressure on underlying structures.
Below the subcutaneous tissue layer is the general fascia. Below that depending upon the part of
the body, there is muscle, fat, bone or cartilage (Figure 5).
Blood Composition
As well as supplying the organs and tissues with oxygen and nutrients and transporting
endogenous messenger substances and enzymes, the blood has two further important tasks
associated with wound healing; it contains cells of the defence system that recognise and remove
foreign particles which have invaded the body and, in addition, the blood contains components of
the coagulation system that seal leaks resulting from injury.
Dissolved components
Blood plasma is a slightly yellowish fluid containing 90% water. Dissolved in it are many proteins
(7-8%) such as albumins, which are responsible for maintaining the osmotic pressure in the
blood and act as transport proteins for water-insoluble materials and globulins that play a role as
antibodies (eg IgG, IgA, IgM) in humoral immunity. The plasma also contains:

nutrients (proteins, fats, sugars)

inorganic salts
metabolic waste products (especially urea)
enzymes
hormones

Fibrinogen is a component of plasma essential for blood coagulation. It is a 2-globulin that is

normally present at a concentration of 2-4 g/l.
Cellular components
Erythrocytes
Blood cells make up about 45% of the blood. Erythrocytes (red blood cells), which contain
haemoglobin, are the most numerous at 4-5 million/l. They take the form of a flat, biconcave
disk with a diameter of 7-8 m (1 m = 1/1000 mm), are non-nucleated and very flexible.
Red blood cells contain haemoglobin and are responsible for oxygen and CO2 transport. They are
produced in the bone marrow and are broken down in the spleen and liver. They have a lifetime
of about 120 days.
Leucocytes
Leucocytes (also known as white blood cells) are present in the blood in much smaller numbers,
4000 - 11000 /l. Their diameter is more than twice that of the erythrocytes. White blood cells
always have a nucleus and exhibit amoeboid movement. They are produced in the bone marrow
and mature in the different lymphatic organs (spleen, lymph nodes, tonsils, bone marrow,
thymus) into cells with a variety of functions and structural appearance.
Non-specific defence is provided by cells referred to as phagocytes. These cells can
recognise, engulf and digest foreign organisms such as fungi, bacteria and viruses. They include:

granulocytes
mononuclear phagocytes or monocytes.

Granulocytes (11-14 m) (also known as polymorphonuclear leucocytes) are the most numerous
phagocytic cell type. They circulate in the blood and derive their name from their granular cell
inclusion (granulae) easily recognisable under a light microscope. When foreign organisms invade
the body, granulocytes leave the blood capillaries, migrate into the affected area and eliminate
the invader by phagocytosis.
The mononuclear phagocytes are also involved in the general defence activities. Depending upon
their localisation, we distinguish between monocytes (in the blood) and macrophages (in the
tissue). Macrophages, as their name suggests, are the largest phagocytic cells with a diameter of
12-20 m. As well as destroying invading microorganisms they also remove degenerating
or ageing endogenous tissue.

A more specific and developed form of the general defence system (specific immunity) is
provided by the lymphocytes. These are specific defence cells since they possess on their cell
membrane, structures allowing them to recognise specific pathogens (antigens), which they
eliminate rapidly, and selectively, after contact.
Stem cells of the lymphocytes, like those of other leucocytes, are produced in the bone marrow.
During embryonic development they migrate into the lymphatic organs. Here they mature to
produce two different types of lymphocytes:

T-lymphocytes
B-lymphocytes

The maturation of the T-lymphocytes depends on the thymus gland (thus the name Tlymphocyte). Here they differentiate further into the following agents of cell-mediated defence:

killer cells, which release toxins, cytolytic enzymes or complement factors and thereby
selectively destroy invading pathogens
helper cells which, after contact with the antigen, assist the production of antibodies in the
B-lymphocytes and activate phagocytic cells by emitting chemotactic agents
supressor cells that inhibit the activity of other lymphocytes and thereby regulate the
immune response.

B-lymphocytes mature in the lymphatic tissue of the intestine and liver. In birds, this function is
performed by a rectal gland, the bursa of Fabricius, hence the name B-lymphocyte. Blymphocytes have specific antigen receptors on their cell surface and in the event of infection can
transform into memory cells (large plasma cells) after stimulation by the respective antigen.
These cells constitute the immunological memory since they "memorise" the antigen and, in the
event of a repeat infection, immediately trigger the appropriate immune response. Plasma
cells produce an antibody which is released into the blood. Here they bind to their target antigen
and either render it harmless directly or "mark" it for destruction by the phagocytic cells.
The platelets, (150,000 - 450,000 /l) are not cells in the true sense. The non-nucleated diskshaped platelets have a diameter of 2-3.5 m. They can clump together, ie aggregate, in
response to specific stimuli.
Once platelets have aggregated, platelet factors are released and these initiate blood coagulation.

Module 2
A wound is generally defined as a pathological state in which tissues are separated from each
other and/or destroyed. This event is associated with a loss of substance and impairment of
function.
Wounds can occur in all tissues of the body but most often affect the skin. The term "wound" is
most frequently used to describe damage of the body's outer covering, whereas the term injury
tends to be used more for damage to internal organs. Wounds heal by the same biochemical
mechanisms in all tissues. Wounds to the skin and their healing are described below as examples.

Regeneration versus repair

The body naturally attempts to close a wound and restore the functions of the damaged tissue as
quickly as possible. All tissues of the body are capable of wound healing with the sole exception
of the teeth. The original state can be restored by two different mechanisms: regeneration or
repair.
Physiology of wound healing
How does the body respond to a bleeding skin wound? Two main problems first have to be
solved: the invasion of infectious organisms must be halted and bleeding stopped. Once this has
been accomplished, foreign bodies and tissue detritus have to be broken down and new tissue
produced. In simplified terms, the processes involved can be divided into four phases:

vascular response
blood coagulation
inflammation
formation of new tissue.

These phases overlap and are to some extent interdependent.

Vascular response
A fresh wound usually bleeds rather profusely if cutaneous and deeper lying vessels are
damaged. The bleeding has the effect of cleansing the wound as the blood washes foreign bodies
and organisms away.
To prevent further blood loss, the affected vessels narrow within a few minutes of the injury
occurring. This vasoconstriction lasts for only a few minutes, however, long enough for the leaks
to be sealed by blood clots. The ends of the vessels also turn inwards.
Vasoconstriction is followed by widening of the vessels, reaching a maximum after about 10
minutes.
The vasodilation increases the blood circulation in the wound area. This causes an
increased production of heat and an associated rise in the temperature of the skin around the
wound. In this phase, the permeability of the capillary walls to components of the blood is
increased. As a result, blood constituents such as erythrocytes, leucocytes and platelets enter the
wound. Furthermore, the increased capillary pressure associated with vasodilation allows
increased amounts of blood plasma to escape into the interstitium.
Finally, vascular stasis (stoppage) occurs and persists for several hours. The oxygen deficiency in
the tissue causes the CO2 pressure to rise, and consequently the pH falls into the acidic range.
This acidosis causes a charge reversal of the chemical components in the connective tissue. As a
result, the collagen components depolymerise and lose their capacity to bind water. The
accumulation of fluid - especially the plasma - within the wound causes swelling of the collagen
fibres. The outcome of all these processes, ie the intensified blood flow, the increased leakage of
blood from the capillaries and the accumulation of fluid in the tissue, is wound oedema.
Obviously, these vascular responses do not take place in an uncoordinated manner. They are
controlled by a number of substances. Platelets adhering to the damaged vessels release
thromboxane A2, which causes vasoconstriction. The tissue hormones, histamine and serotonin
that are released by the mast cells present in the connective tissue and especially in the vicinity
of small vessels stimulate the dilation of the capillaries. They also cause the endothelial cells in
the vessels to move apart, thereby increasing their permeability to blood components.
Mast cells are in turn stimulated to release histamine and serotonin by other substances in the
wound area released from various cells and the blood plasma. These mediators include the
complement factors in the blood serum. Complement factors are made up of about 209 proteins,
which are involved in the defence against foreign bodies. Other mediators are the prostaglandins
(eg PGF2a); these hormone-like substances are particularly important for the inflammation
process.

Regeneration
This refers to the tissue-specific replacement of a lost part of the body or organ. The animal
kingdom contains many examples of this process, for example, the regeneration of a complete
earthworm from the anterior segments of its body or the complete replacement of a severed
extremity in the salamander. Among mammals, and especially in man, complete regeneration is
only possible in epithelial tissue (epidermis, mucous membranes of the gastrointestinal tract and
the female genitals) and is only possible to a limited degree in parenchymatous organs such as
the liver.
Thus, in man, tissue defects are remedied mainly by repair. In this process, lost or damaged
tissue is replaced by unspecific elements of connective and supportive tissue, which form a scar.
Only defects in supporting tissue, for example in bones, cartilage and tendons, are regenerated
with the typical structure of the tissue.

Wound healing can therefore be defined as the closure of a defect by scar-forming supporting
tissue associated with epithelial regeneration, ie epithelialisation. Its aim is to restore the form
and functions of the damaged tissue.
Blood coagulation
A fresh wound rapidly fills with blood, which coagulates and temporarily closes the defect (Figure
3). The scab formed protects the wound, reducing the risk of infection and dehydration.
Provisional wound closure by scab formation.
Damage to the skin results in the wound rapidly filling with blood. A process called coagulation
(clotting) then occurs which involves a large number of chemical reactions resulting in a 'scab'
(eschar), which provisionally closes the defect.
Underlying this process of blood coagulation are complicated biochemical reactions involving
various factors:

the blood vessel walls

the platelets
damaged connective tissue cells
the coagulation system.

Coagulation begins both in the opened vessels and in the wound gap. It starts when cells are
damaged, as these release certain substances (mediators) that activate the biochemical reactions
necessary for blood clot formation.
When a vessel wall is damaged, blood platelets - stimulated by mediators such as Von Willebrand
factor- immediately adhere to the exposed collagen of the vessel wall. In this activated state, the
platelets first change their form and change from flat, discs to spherical structures with long
extended processes known as pseudopods. These activated platelets also release a number of
substances that induce further reactions (the coagulation "cascade"). At first, even more platelets
from the blood adhere to those that are already adhering to form a clot.
This process is known as platelet aggregation (Figure 4). It is initiated by adenosine diphosphate
(ADP), thromboxane A2 and platelet activating factor (PAF) released from the activated platelets.
The clustered platelets partially coalesce with each other and release the platelet factors that
initiate the actual clotting process. During the clotting process a fine line network of fibrin forms
around the platelet plug and finally fills the entire wound gap. The purpose of this fibrin network
is to "catch" erythrocytes and other solid components of the blood, retain them and thereby form
a clot that provisionally seals the wound against the external environment and stops the
bleeding. Its surface rapidly dries in the air and a dense, protective scab forms.

Flowing blood understandably contains no solid fibrin, only its water-soluble precursor, fibrinogen.
Fibrinogen is only converted to fibrin at the wound surface, by the enzyme thrombin. This is also
present in the blood as an inactive precursor called prothrombin. Prothrombin and fibrinogen are
among the coagulation factors whose biochemical interaction ultimately leads to the formation of
the blood clot. The clotting factors are distinguished by Roman numerals; fibrinogen (I) and
prothrombin (II) are part of what is referred to as the coagulation cascade, a complex chain
reaction, which is set in motion by injury.
Coagulation is initiated firstly by the platelet factors released from the adhering platelets, and
secondly by substances liberated from damaged tissue cells. These thromboplastins activate the
conversion of prothrombin into thrombin with the involvement of various other coagulation
factors and calcium ions. Thrombin is now able to convert the water-soluble fibrinogen present in
the blood into fibrin monomers. These polymerise spontaneously to fibrin chains, which are finally
interlinked by coagulation factor XIII to form the stable fibrin mesh.
Fibrinogen, prothrombin and the other coagulation factors are formed in the liver. The synthesis
of prothrombin and three other factors is vitamin K dependant. This is why vitamin K deficiency
leads to disturbances of blood coagulation. On the other hand, this dependence can also be
utilised therapeutically eg for thrombosis or infarction prophylaxis: vitamin K antagonists (eg
coumarin derivatives) are administered to prolong the coagulation time, leading to a fall in
prothrombin level and delayed clot formation.
Inhibitors of the coagulation factors present in the blood ensure that coagulation is restricted to
the wound area in the event of injury. They inactivate the thrombin molecules entering the
circulation. The most important of these inhibitors is antithrombin III.
Inflammation
The substances released from the cell debris resulting from tissue destruction are responsible for
causing the characteristic inflammatory reactions. The vascular changes previously described also
contribute to this reaction. They create the preconditions for the body's inflammation:

redness (rubor)
heat (calor)
swelling (tumour)
pain (dolor)
functional disturbance (functio laesa).

Inflammation is not the same as infection

Redness and heat are consequences of the increased blood flow in the wound area, causing an
influx of immune defence cells into the site of injury (Figure 5).
Wound Oedema.
This photograph of oedema, after the skin has sustained a bleeding wound, displays the classic
signs of the inflammatory process ie redness (rubor), swelling (tumour) and functional
disturbance (functio laesa) with associated heat (calor) and pain (dolor).
The swelling or wound oedema results from collections of fluid in the soft tissue. These
accumulations of fluid in the tissue exert increased pressure on the small nerves, and nerve
endings, causing the wound to hurt. The pain, in turn, causes the inflamed part of the body to
assume a protective posture. This and the disturbed physiological processes account for the
functional disturbance of the injured organ.
The inflammatory reaction is induced independently of invasion by foreign organisms, and
therefore "sterile" inflammations can also develop in closed injuries, for example bruises in which
the skin remains intact. Open skin wounds are usually contaminated. Even in surgical wounds,
the invasion by millions of microorganisms cannot be prevented even under the strictest sterile
conditions. In such cases infection can develop initiating both the cellular and humoral immune
responses.
Non-specific immune defence

In the inflammatory phase, the number of white blood cells increases, manifested as leucocytosis
in the blood count. The defence cells migrate from the blood vessels that have become permeable
into the wound area. They are attracted by complement factors, which are part of the nonspecific
defence system. These are proteins present in the blood serum in an inactive form, which are
activated by invading pathogens. The presence of pathogens initiates what is known as the
complement cascade; complement factors become active and in turn activate other components
of the pathway finally resulting in a complement 'attack complex', which either destroys the
microorganisms directly or prepares them for destruction by other defence cells (opsonisation).
The activated complement factors also produce attractants (chemotaxins), which draw wandering
phagocytes into the injured area.
First to appear at the site of inflammation are a type of granulocyte called neutrophils. These
have the capacity to phagocytose (engulf and digest) foreign bodies. They also release enzymes
that break down degenerating connective tissue (collagenases, elastase). Soon afterwards,
monocytes arrive on the scene, attracted by chemoattractants released by aggregating platelets;
platelet derived growth factor (PDGF) and transforming growth factor- (TGF-). Both of these
growth factors stimulate the growth of new tissue. Monocytes are also capable of phagocytosis
and once they have ingested foreign bodies they transform into macrophages. Macrophages
produce a large number of substances, which act as mediators of other wound healing processes
and attract further phagocytic cells to the wound area for example:

growth factors TGF- a, TGF- (transforming growth factor alpha and beta), TNF-a (tumour
necrosis factor alpha) and FGF (fibroblast growth factor) that promote vascular and
connective tissue neogenesis
prostaglandins that sustain the inflammatory process and influence vascular dilation
complement factors C1-C5 responsible for non-specific defence
interleukin-1 which induces fever and attracts further neutrophil granulocytes.

Macrophages also release enzymes, which can destroy tissues. Necrotic tissue and dead
phagocytic cells filled with foreign bodies form 'pus', which surrounds the wound.
Specific immune defense
In addition to the nonspecific immune defence provided by the complement system and
phagocytes, the body is also capable of mounting a specific, targeted defence against a particular
pathogen. It does this by producing substances called antibodies. Antibodies are synthesised by
B-lymphocytes in response to a specific foreign bodies (antigen) and released into the blood.
Antibodies are proteins, which belong to a chemical class known as globulins and are therefore
referred to as immunoglobulins. They have the ability to bind specific antigens to form antigenantibody complexes, thereby rendering them harmless.
Immunoglobulins are divided into subgroups depending on their structure and size: IgG, IgA,
IgM, IgD and IgE. These different subgroups have different functions; for example IgM antibodies
are specifically directed against viruses while IgE antibodies are involved in allergic reactions.
Immunoglobulins circulate freely in the serum component of the blood. If they meet their
corresponding antigen, for example in a wound, they bind it and either inactivate it directly or
mark it for destruction by phagocytes.
B-lymphocytes continually produce antigen specific antibodies over a period of years and often
for a lifetime, resulting in the production of 'memory cells'. If the same microorganism enters the
body again at some later stage, the memory cells divide with great rapidity. The newly formed Blymphocytes transform into plasma cells and synthesise large amounts of this specific antibody to
eliminate the invaders rapidly and effectively. In this way, immunity against the respective
pathogen is created.
This mechanism is utilised in inoculation: by non-hazardous contact with attenuated or killed
pathogens the B-lymphocytes are stimulated to produce corresponding antibodies which protect
the inoculated person from an outbreak of the infectious disease on renewed contact.
Other immunocompetant cells involved in specific defence are the T-lymphocytes. These differ
from the B-lymphocytes in that they do not produce antibodies but, as 'killer cells', identify and
selectively destroy foreign cells. This is done through direct cell contact or by release of cell
toxins, complement factors or hydrolytic enzymes. As with the B-lymphocytes, certain killer cells
specialise in specific pathogens, which they are able to identify by their surface properties. Here

too there are memory cells that provide large numbers of specialised T-lymphocytes for defence
in the event of antigen contact.

T-lymphocytes, differentiated into helper cells assist the maturation of the B-lymphocytes into
plasma cells and promote their antibody production. A further T-lymphocyte subclass, the
suppressor cells, regulate the action of the T-helper cells and B-lymphocytes and thereby prevent
an excessive immune response.

To summarise, the inflammatory phase of wound healing is characterised by an influx of

granulocytes, macrophages and lymphocytes that absorb and enzymatically degrade foreign
matter and tissue detritus and thereby clean the wound. An inflammatory reaction is also induced
irrespective of whether an infection is present, for example in all closed injuries such as bruises
and contusions.
Whereas catabolic processes predominate in inflammation, the next phase of wound healing is
characterised mainly by repair ie anabolic reactions.
Formation of new tissue
The cleansed wound, provisionally sealed by a scab, can now be covered by new tissue. Various
preconditions for this have already been created:

mediators and growth factors released from different cells in the wound area (eg TNF-a
and TGF-a) activate the vascularisation ie the formation of new blood vessels
blood platelets and macrophages release growth factors (TGF- and PDGF) that stimulate
the production and influx of fibroblasts
the fibrin network acts as a guide structure for the cells moving into the wound area.

Vascularisation
The precondition for favourable wound healing is the presence of sufficient blood circulation. This
is why new blood vessels begin to grow into the wound only three days after an injury. The
vascular buds are formed by existing intact vessels. Stimulated by growth factors and other
substances released in the wound, the endothelial cells in the venules begin to produce enzymes
that break down the basal membrane in the area of the stimulus. Endothelial cells then migrate
through the resulting gap in the direction of the wound. They divide and form tubular structures
that connect with other buds. During the maturation process a new basal membrane develops
from the extracellular matrix components. The newly formed vascular loops then connect with
intact vessels and differentiate accordingly into arterioles or venules. Superfluous vessels are
broken down again.
Formation of new connective tissue
Parallel to vascularisation and also proceeding from the wound margins, new tissue is formed.
Fibroblasts, attracted chemotactically, migrate along the fibrin network and divide at a rapid rate.
They produce the connective tissue ground substance consisting of proteoglycans (protein
network with carbohydrate side chains) as well as the water-soluble collagen fibres essential for
tissue stability.

Collagen is a fibrous protein synthesised in several stages. Its precursors are assembled from
amino acids in the endoplasmic reticulum of the fibroblast.
These protocollagen chains are twisted together in threes, in helical formation and then
transferred to the Golgi complex. Here the chains are re-arranged slightly and interlinked more
closely. Golgi vesicles finally transport the molecules to the cell membrane where they are
released as soluble tropocollagen into the intercellular space. Here the tropocollagen molecules
accumulate to form protofibrils, which then polymerise into microfibrils. Several microfibrils unite
to form a collagen fibril, several of which, in turn, arrange themselves into bundles. In healthy
tissue the collagen fibres are aligned in certain patterns following the main contours of tension of

the skin. This organised structure is not achieved in wound healing, however, which is why the
collagen fibres in scar tissue have a disorganised appearance.
Collagen synthesis is dependent on the presence of vitamin C (ascorbic acid), which acts as a
coenzyme; further cofactors are iron and copper. If there is a deficiency of these substances,
satisfactory wound healing is not possible.
Granulation
New highly vascularised tissue grows in from the wound margins in the manner described.
Because of its granulated appearance it is known as granulation tissue and is visible to the naked
eye as pin-head-sized rounded nodules of tissue in the wound bed (Figure 7). The granulation
tissue is essential for permanent wound closure since it fills out defects and prepares the way for
epithelialisation.
Granulation tissue: pin-head sized, dark red fleshy nodules of tissue on the wound bed make
up the new, highly vascularised tissue that fills the defect and creates the preconditions for
epithelialisation.
The appearance of the granulation tissue gives an indication of how the wound will be healing.
Healthy granulations have a granular appearance, are moist and shiny, hyperaemic and have a
dark red colour. Poor healing can be expected however, if the granulation tissue is smooth,
covered with smeary fibrin deposits, soft, pale or shows a bluish discolouration.
Fibrinolysis
At the same rate as the fresh, highly vascularised connective tissue develops, the provisional
fibrin network is broken down and the closed vessels are recanalised. This breakdown process is
known as fibrinolysis and is caused by the enzyme plasmin. Plasmin is present in the blood in the
form of an inactive precursor, plasminogen. This, like prothrombin, is activated by a number of
substances released from damaged cells. The most important of these is tissue plasminogen
activator, t-PA.
The activators of fibrinolysis most widely used for therapeutic purposes are streptokinase and
urokinase, which are administered to dissolve life-threatening blood clots in the coronary arteries
of heart attack patients.
Contraction
With the formation of new fibres, the mitotic activity of the fibroblasts is concluded. They then
transform either into fibroblasts or myofibroblasts. Myofibroblasts, like the muscle cells, contain
contractile elements, which allow them to draw together (Figure 8). The collagen fibres become
taut and, as far as possible, aligned to the main contours of tension in the tissue. As a result, the
scar tissue shrinks and the functional cutaneous tissue at the wound margin contracts leaving
only a small defect.
This extensive wound after melanoma excision on the thigh cannot undergo primary closure by
surgical means because of its extent and depth. It heals by secondary intention and closes mainly
by formation of new tissue and contraction. Subsequent coverage by skin grafting was not
performed at the patient's request.
Epithelialisation
At the end of the wound healing process the surface of the wound is closed by epithelialisation.
The preconditions for this are an increased rate of cell division in the basal layer of the epidermis
and migration of the epithelial cells, which move towards each other from the wound margins
until the defect is covered by a fine skin. New epithelial cells are also formed by the appendages
of the skin ie the hair follicles, sebaceous glands and sweat glands.
The mechanisms underlying this cell migration are still largely unknown. Migration requires the
presence of a moist substrate, well perfused with blood, as is the case with granulation tissue. If
this migratory layer becomes dehydrated, the epithelial cells cannot travel. Recent experiments
suggest that the glycoproteins, fibronectin and vitronectin serve as a substrate across which the
cells are able to move. However, the way in which epithelial cells are stimulated to migrate in a

specific direction and how the reorganisation of the cell network necessary for this motion is
induced is still unknown.

Scar formation
Due to the repair and regeneration processes, the wound margins are bridged over by connective
tissue and a scar is formed. At first it is still elevated above the level of the skin and has a reddish
colour. With time, however, the connective tissue grows tauter and the vascularisation decreases.
As a result, the scar becomes slightly recessed and turns pale. Since the pigment producing cells,
the melanocytes, cannot be regenerated, the scar tissue does not turn brown but remains white.
Its surface is more or less smooth, since the ridged and tessellated pattern of the epidermis is
not restored. This tissue contains no hairs, sebaceous or sweat glands.
Remodelling
The process of remodeling is the reorganisation of the scar tissue and is the longest phase of
wound healing, and can continue for up to 20 years after an injury. It consists mainly of
restructuring of the collagen fibres, which are partially broken down again by enzymes contained
in the tissue (collagenases) or newly cross-linked.
Remodelling can be influenced to a certain extent by external factors. For example, the
application of compression bandages can reduce scar formation and so provide a better cosmetic
result.
Time Course of Wound Healing
As already mentioned, the individual processes of wound healing do not occur one after the other
but overlap to varying degrees:

the vascular response begins only seconds after the injury, reaches its peak after three to
seven days, and then slowly subsides
blood coagulation also begins immediately after the injury. The fibrin network is formed
within 24 hours
the peak of the inflammatory processes, initiated immediately after the injury, is reached
between the third and fifth day. These events are normally complete after 14 days
the formation of new connective tissue starts after only 10 to 12 hours, and reaches its
peak after 6 to 16 days. The mechanical strength of the scar ie its tearing resistance,
increases parallel to the collagen content. It reaches its maximum after 12 to 15 days.
However, only about 80% of the strength of normal healthy tissue is restored. The scar
may take several years to become fully differentiated.
epithelialisation of superficial wounds occurs within the first 24 hours and is generally
complete after 12 days. In the case of deeper, more extensive wounds however, it only
starts after new connective tissue has formed and takes correspondingly longer.

Module 3
Chronic wounds are often indicative of a serious long term condition in a patient. They have a
complex nature, and, unlike acute wounds, do not undergo the ordered molecular and cellular
processes of normal tissue repair (inflammation, proliferation, re-epithelialization and
remodelling.) Wounds may remain stuck in the inflammatory phase, for example, or specific cells
will become senescent, preventing healing.
Wound bed preparation, a new paradigm in wound care, is a concept that has developed current
practice for the treatment of chronic wounds by removing the barriers to healing. These barriers
have recently been defined as 4 clinical observations within the wound: Non viable tissue (T),
infection or inflammation (I), moisture imbalance (M), and a non advancing wound edge (E). The

goal of wound bed preparation is to accelerate endogenous healing and facilitate the effectiveness
of other therapeutic measures; in other words, to create a viable wound bed where healing can
take place.
Wound Bed Preparation was developed in 2000 by Drs Vincent Falanga and Gary Sibbald as a
means of preparing the chronic wound to accept advanced wound healing therapies.
Many nurses and other healthcare professionals have now adopted this concept and are using it
successfully to further develop their clinical practice. Wound bed preparation is still evolving, but
initial definitions are cited below.
Wound bed preparation is defined as the management of wounds to accelerate endogenous
healing or to facilitate the effectiveness of other therapeutic measures. Falanga V. Wound bed
preparation and the role of enzymes: a case for multiple actions of therapeutic agents. Wounds:
A Compendium of Clinical Research and Practice; 14(2);2002.
Dr. Gary Sibbald has also cited wound bed preparation as a changing paradigm that links
treatment of the cause and focuses on three components of local wound care: debridement,
wound-friendly moist interactive dressings and bacterial balance. Sibbald RG et al, Preparing the
wound bed debridement, bacterial balance and moisture balance Ostomy Wound Management;
46(11):2000.
This module begins with an overview of wound healing, explaining the processes involved in the
acute wound model and comparing these to the processes that take place in chronic wounds. The
components of wound bed preparation (represented by the acronym T.I.M.E, mentioned above)
are then explained, together with a discussion of cellular dysfunction and biochemical imbalance,
which contribute to the damaging microenvironment in the chronic wound bed.
A wound is only likely to heal when the right cellular and molecular mechanisms are in place to
promote the healing process. Chronic wounds are less likely to heal, even with sophisticated
wound management products, if the wound bed is not prepared properly.
The first step in wound management is to assess the patient as a whole, identify any underlying
causes (pathogenic abnormalities) and consider the patients overall physical condition.
Next, the wound must be carefully evaluated, before any treatment is undertaken, and regularly
thereafter, until healing is achieved. Constant attention to the appearance and condition of the
wound bed will prepare the wound for healing.
Proper wound bed preparation and evaluation are essential components of wound care. This is
especially true with chronic wounds, where signs of delayed healing or underlying infection may
be atypical and, therefore, easily overlooked.
In wound care it is important to identify all the potential barriers to wound closure. There are a
number of systemic factors that should be considered.

Age as we age the density of collagen decreases, fewer fibroblasts and mast cells are
produced and elastin fibres begin to fragment
Body build body size is important, and both obese and thin people are at risk of
pressure ulcer development and impaired healing
Stress psychological stress, pain and noise are major factors and the accepted
mechanism is thought to be stimulation of the sympathetic nervous system and the
outflow of vasoactive substances causing vasoconstriction
Nutrition impaired wound healing is usually associated with protein-calorie malnutrition
as opposed to a single depleted nutrient
Medication various medications have the potential to effect healing, but the ones most
noted are steroids. This is attributed to the anti-inflammatory action of steroids which may
interrupt the inflammatory phase of wound repair
Tissue oxygenation the deposition of collagen and phagocytic activity of white blood
cells is hindered if the oxygen levels in the tissue are inadequate
Concomitant Disease conditions such as diabetes, renal failure, peripheral vascular
disease and autoimmune disease can have a significant impact on the patients healing
process

Normal wound healing

Normal wound healing (which applies to acute wounds) starts as soon as an injury involving
blood vessel damage occurs. Essentially there are four main healing phases (outlined below),
when several molecular and cellular processes are initiated. There is significant overlap between
activities in these phases.
Hemostasis
In the minutes following acute injury, clot formation and platelet aggregation occurs. Once
aggregated, platelets degranulate releasing several growth factors; platelet-derived growth factor
(PDGF), insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and transforming
growth factor beta (TGF-).
Inflammation
In the first 2-3 days post-injury, inflammatory cells (neutrophils and macrophages) are drawn
into the injured area (chemotactic migration) where they engulf and destroy bacteria and debris
by phagocytosis. Neutrophils release proteases, which break down damaged extracellular matrix
(ECM) components in a process called proteolysis. Activated macrophages release growth factors,
which stimulate fibroblasts, epithelial cells and endothelial cells. In addition, macrophages release
a controlled amount of the pro-inflammatory cytokines tumour necrosis factor alpha (TNF-) and
interleukin-1 beta (IL-1), which stimulate endothelial cells to express cell adhesion molecules
(CAMs). CAMs are cell surface proteins which enable inflammatory cells to enter the tissues. IL-1
also draws fibroblasts into the wound and up-regulates matrix metalloproteinase (MMP) enzyme
levels. Importantly, there is a balance between levels of MMPs and tissue inhibitors of
metalloproteinases (TIMPs). TIMPs bind to MMPs and cause them to become inactive.
Proliferation
Platelets and macrophages release growth factors, such as TGF- and PDGF, which activate the
formation of new blood vessels (vascularisation or angiogenesis). In addition, the proinflammatory cytokines TNF- and IL-1 and growth factors released by activated macrophages
induce fibroblasts to produce collagen. In the healing wound bed there is a high level of mitogenic
activity. Blood vessel repair (angiogenesis) and granulation tissue formation occur over several
weeks.
Epithelialisation, scar formation and remodelling
New tissue formation is followed by epithelialisation; increased cell division in the basal layer of
the epidermis results in the wound being covered by a fine layer of skin. A scar is formed when
the wound margins are bridged over by connective tissue. The last phase in wound healing is
remodelling which involves scar tissue reorganisation by restructuring of collagen fibres. Collagen
fibres in the scar are reorganized to improve tensile strength. This final healing phase may take
several years. Wound healing occurs in a cascade of events.
The following model has been hypothesised to explain the key events that occur in chronic
wounds, although there is still much that is not fully understood. A chronic wound differs from an
acute normal-healing wound because it has a persistent pro-inflammatory stimulus, often caused
by one or several of the following factors (Mast BA and Schultz GS 1996):

repetitive trauma
local tissue ischaemia
necrotic tissue
heavy bacterial burden
tissue breakdown.

Inflammatory cells (neutrophils and macrophages) are drawn to the wound bed. In chronic
wounds the controlled stimulation of inflammatory cytokines is disrupted. This leads to an
elevated secretion of TNF- and IL-1, which causes an increase in MMP production and reduced
synthesis of TIMPs. Elevated levels of MMPs cause degradation of extracellular matrix, resulting in
impaired cell migration and connective tissue deposition. Furthermore, MMPs degrade growth
factors and their target cell receptors.
These processes prevent a wound from entering the proliferative phase of healing, and continue
the vicious cycle of the chronic wound.

Biochemical differences between healing wounds and chronic ulcers

Normal Acute

Chronic Wound

In healing wounds, there is a high level of mitogenic activity. Fluids collected from acute
mastectomy wounds were found to stimulate DNA synthesis when added to cell cultures (Schultz
GS and Mast B, 1998). Conversely, fluids collected from chronic venous leg ulcers did not
stimulate DNA.
Distinct differences in cytokine environments between wound types. In a healing wound
there is a balance of pro-inflammatory cytokines and their natural inhibitors. In chronic wounds,
the balance is disrupted and the levels of pro-inflammatory cytokines increase.
Pro-inflammatory cytokines influence MMP levels. In healing wounds MMPs and TIMPs are
in equilibrium, but MMP levels are significantly higher in chronic wounds. High MMP levels also
degrade various growth factors.

What is wound bed preparation?

Wound bed preparation has been defined as the process of removing the barriers to the healing.
Removal of these barriers is thought to allow the wound repair process to progress normally.
Wound bed preparation represents a combination of both scientific knowledge and practical skill;
its application can help correct abnormalities in chronic wounds and stimulate the healing process
(Schultz, Sibbald, Falanga et al 2003). Wound bed preparation addresses the following four
clinical observations listed below: and can be summarized by the acronym TIME which unite the
cellular and clinical components of wound healing.

Insert interactive box with links to appropriate sections.

Tissue, non-viable or deficient

Infection or inflammation
Moisture imbalance
Edge of wound non-advancing or undermined

The principles of TIME have been formulated to help clinicians gain a better understanding of the
pathogenesis of chronic wounds and can be used as a framework to guide clinical practice
(Schultz, Sibbald, Falanga et al 2003).
Tissue non viable or deficient
Tissue management is defined as the removal of non viable tissue and the encouragement of
viable, well vascularised tissue to grow. The removal of non viable tissue can be achieved by the
process of debridement. This involves the removal of dead or necrotic tissue and foreign material
from the wound and is an important step in wound bed preparation. Debridement enhances
wound assessment, decreases the likelihood of infection and removes necrotic tissue, which
otherwise would delay the formation of granulation and epithelial tissue.

Devitalized tissues (eschar and slough) in the wound bed reduce the clinicians ability to
assess the wounds depth, or the condition of tissue and surrounding structures
Necrotic tissue may mask signs of infection ( it supports significant bacterial growth and is
a physical barrier to healing
Devitalized tissue may also cause excessive amounts of proteases to be released, which
has an extremely detrimental effect on healing

A necrotic wound containing dead black tissue and yellow fibrinous slough
Debridement
Natural mechanisms facilitate debridement, but wounds heal more rapidly if this process is
accelerated. Methods of debridement: can be grouped into five categories: surgical, enzymatic,
autolytic, mechanical and biologic. In some cases, more than one method may be appropriate,
depending on the clinical circumstances.
Surgical (or sharp) debridement
Surgical or sharp debridement is the fastest way to remove debris and necrotic tissue from the
wound bed. Surgical debridement is sometimes performed where there is an extensive amount of
necrotic tissue in the wound. This is often the case when the depth of the wound cannot be
judged or if there is widespread infection requiring bone and infected material to be removed.
Other than being an efficient method, surgical debridement causes minimal damage to
surrounding tissue, and minor bleeding following the procedure can release inflammatory
mediators, such as cytokines, that can assist the wound repair process. Surgical debridement
does however, have limitations. It cannot be used for patients with bleeding disorders or who are
immunocompromised. The procedure may be painful, cause transient bacteraemia and damage to
nerve and tendons. Add hydrosurgical awaiting text
Enzymatic debridement
Enzymatic debridement is the most selective method of debridement employing the use of
manufactured proteolytic enzymes. When these are applied directly onto the wound surface, they
work together with naturally occurring enzymes to degrade necrotic tissue.
Some enzymatic debriding agents may cause minor transitory discomfort. Insert text on
agents
Autolytic debridement
Autolytic debridement is a process, which to some extent, occurs naturally in all wounds.
Phagocytic cells (such as macrophages) and proteolytic enzymes in the wound bed, liquefy and
separate necrotic tissue and eschar from healthy tissue. Wound dressings, which maintain a moist
wound bed, can provide an optimal environment for debridement, as they cleanse the wound by
allowing phogocytic cells to liquefy necrotic tissue thereby promoting granulation. Unsurprisingly,
the process of autolytic debridement can result in significant wound fluid, which should be
considered when selecting an appropriate dressing.
Autolytic debridement is easy to perform and does not damage healthy tissue surrounding the

wound. Furthermore, the pain experienced by the patient when using this method is minimal. As
autolytic debridement occurs naturally, the process requires limited technical skill.
Mechanical debridement
Mechanical debridement is a non-selective method that physically removes debris from the
wound. Examples of mechanical debridement include wet-to-dry dressings, wound irrigation and
whirlpool therapy. Wet-to-dry dressings are the simplest form of mechanical debridement. These
dressings cause mechanical separation of eschar from the wound bed once the dressing is
removed. This can, however, cause the patient significant discomfort and damage newly formed
tissue. Wound irrigation involves the use of a pressurised stream of water. High-pressure
irrigation removes bacteria and necrotic debris from the wounds but could drive bacteria into soft
tissue. Whirlpool therapy is another form of powered irrigation which loosens and removes
necrotic tissue, debris and wound exudate. This is suitable for use in inflammatory wounds but
not those with fragile granulation tissue.
Hydrosurgical Debridement
Hydrosurgical Debridement utilises a high-pressure jet of sterile saline that travels parallel to the
wound surface. This high-speed jet creates a Venturi effect that enables the surgeon to hold cut
and remove tissue, while irrigating and aspirating the wound, with a single instrument. This new
technology allows the surgeon to differentiate between tissue types through technique as well as
by varying power settings. Therefore sparing viable tissue while precisely targeting and removing
debris and damaged tissue. Rapid and effective hydrosurgical debridement can help to reduce
procedure times as well as potentially reducing the number of debridements each wound requires
compared to traditional modalities eg the use of scalpel and pulsed lavage. This modality is
suitable for surgical debridement of Chronic and Acute wounds in the Operating Room with the
patient undergoing General Anesthesia
Biologic (Larval) Therapy
Larval therapy using specially bred, sterile maggots offers an effective approach to wound
debridement and removing bacteria. These maggots break down and liquefy dead tissue using
powerful proteolytic enzymes. This treatment seems to have no adverse side effects. Although
initially viewed by clinicians as a treatment of last resort, reports of the success of larval therapy
has spread and its use is becoming more common.
Why a prolonged debridement is beneficial
It is unlikely that a single method of tissue debridement would be adequate to prepare the wound
bed of a chronic wound for the next stage or repair. In chronic wounds it is generally not possible
to remove the underlying pathogenic abnormalities, and consequently necrotic burden continues
to accumulate. Therefore, an important part of wound bed preparation is the recognition that
continual removal of necrotic burden is necessary throughout the lifespan of the wound, and
debridement should be viewed as an extended, ongoing process often referred to as maintenance
debridement. Autolytic and enzymatic methods of debridement, compared with other methods,
are more selective and may be less aaggressive therefore , generally less painful to the patient.
Within the context of maintenance debridement, autolytic and enzymatic agents that can be used
for extended periods of time can be extremely beneficial (Falanga V 2002)
Infection or inflammation
Wound bed preparation also identifies infection or inflammation as a barrier to healing .When
preparing the wound bed it is critical to assess the nature and extent of the infection or
inflammation component also referred to as bioburden so that these can be corrected or optimize
wound healing.
Bacteria present in the wound may prevent healing, even when there are no obvious signs of
infection. The clinician needs to identify when bioburden is acceptable, and when it reaches a
level where bacteria contribute to impaired healing.
Contamination
Bacteria are present on intact skin, but infection is rarely problematic because the following
mechanisms control the bioburden.

The hard outer layer of skin is a physical barrier to invasion

Skin has a slightly acidic pH, which is not conducive to bacterial growth

Skin normally secretes fatty acids and antibacterial polypeptides which inhibit bacterial
growth
Normal flora on the skin help to prevent potentially pathogenic bacteria from becoming
established

Although a wound creates a portal of entry for bacteria, an inadequate blood supply is one of the
most significant predisposing factors for wound infection (eg in pressure ulcers or ischaemic leg
ulcers).
Contamination-infection continuum
Chronic wounds exist along a bacterial continuum, ranging from contamination to infection (see
below figure). The challenge is to establish where the wound is positioned on this continuum, and
which clinical strategies are appropriate at that point. Bacteria present within a wound can be
divided into four distinct categories.

Contamination
Colonization
Critical colonization
Infection

Contamination: defined as the presence of non-replicating bacteria. This is a normal condition in

chronic wounds and does not contribute to impaired healing.
Colonization: defined as the presence of replicating bacteria without a host reaction. Replicating
bacteria colonise and contaminate all chronic wounds, but this does not mean that these wounds
are infected. Bacterial colonisation does not contribute to impaired healing.
Critically colonized wounds: defined as the presence of replicating microorganisms, which are
beginning to cause local tissue damage. There may be subtle local indications that a change in
the equilibrium, or increasing bioburden, could be contributing to delayed healing.
Infection: occurs when healing is impaired because bacteria have invaded tissue, are
multiplying, and are causing a host reaction.
When is bioburden a problem?
Bacterial bioburden can be defined as the metabolic load imposed by bacteria in the wound bed.
Bacteria compete with normal cells for oxygen and nutrients, and bacteria and their by-products
(eg endotoxins) can cause disturbances in all phases of wound healing. A high bacterial bioburden
can cause the following:

increased metabolic load

production of endotoxins and proteases
stimulation of a pro-inflammatory wound environment
delayed or impaired healing.

Chronic wounds are always contaminated and colonised with bacteria, so it can be difficult to
identify when bacterial loads reach levels where wound healing is impaired. Although there are no
firm guidelines on how to quantify bacterial levels within a wound, the clinician should consider
host resistance, wound characteristics and wound fluid (also known as exudate) when assessing
the bacterial burden.
Studies have shown (Robson MC 1997, Dow G 2001) there is a negative effect on wound healing
when the quantity of bacteria in a wound reach levels greater than 1 x 105 colony forming units
per gram of tissue. This effect has been seen in acute traumatic wounds, skin grafts, surgical
wounds and chronic wounds.
Wound infection
Acute wound infection, and often severe chronic wound infection, classically demonstrate the
following signs and symptoms:

purulence
advancing erythema

warmth
edema/periwound swelling
pain
fever
leukocytosis.

It has become apparent that the classic signs and symptoms of the acute wound model may be
diminished or altered in a chronic wound, despite heavy bacterial burden. The precise
mechanisms of chronic wound infection remain unclear, and the clinical presentation and impact
of bacterial burden in chronic wounds remains a key focus for research. However, the following
secondary signs may alert a clinician to consider that a chronic wound has an increased bacterial
burden, which is delaying healing. This is sometimes referred to as critical colonisation. Some of
these secondary signs are listed below:

delayed healing
change in colour of granulation tissue
abnormal appearance of granulation tissue (ie it becomes friable). The tissue is sometimes
described as pocketing (where areas at the wound base fail to granulate) or as having a
cobblestone appearance
increased or abnormal wound odour increased serous drainage. (Sibbald, 2002)

Effects of infection in the chronic wound

Once a chronic wound becomes infected, progress towards healing is severely hindered because
infection can:
prolong the inflammatory phase of healing
disrupt normal clotting mechanisms
lead to disordered leukocyte function
lead to less efficient angiogenesis
alter the formation of granulation tissue (fibroblasts are reduced in number, have reduced
metabolic activity and form weak collagen in disorganised patterns in chronically infected
wounds).
It may be appropriate for the clinician to monitor blood values and undertake X-rays in a patient
with an infected chronic wound, to investigate whether there could be any underlying
osteomyelitis.
Bacterial balance: relationship between host resistance and bacterial quantity and
virulence
Bacteria are present in all chronic wounds but, for healing to occur, the balance between host
resistance and the quantity and virulence of bacteria must be maintained.

Host resistance: this is an important variable in determining the risk of infection in

chronic wounds, because local and systemic factors can impair healing. Perfusion is an
important factor that is associated with the pathophysiology of chronic wounds, and can
increase the risk of wound infection.
The following equation demonstrates that although bacterial quantity and virulence are
significant in assessing a wound for infection, host factors are of over-riding importance.
Bacterial dose x virulence
Risk of infection =
Host resistance
Other factors such as immunosuppression, diabetes and concomitant medications, can all
influence whether bacteria present will impair wound healing.
Bacterial quantity and virulence: The following factors listed below may tip the
equilibrium, thereby increasing bacterial burden.

o
o
o

Adhesins bacteria contain heterologous proteins on their cell surface, which

mediate cell adherence to and invasion of the host.
Cell capsules - these cell surface polysaccharides present on the surface of bacteria
confer protection against phagocytosis by host immune cells.
Biofilms - the importance of biofilms as an element of wound infection has recently
become apparent (Sibbald RG et al, 2000). When bacteria proliferate in wounds
they form microcolonies, which attach to the wound bed and secrete a glycocalyx

or biofilm that protects the organisms. These bacterial colonies undergo several
changes, which can then alter the organisms antimicrobial sensitivity. Organisms
may exist as clusters of individual bacterial types or as mixed bacterial colonies
such as Pseudomonas and Staphylococcus sp. The periodic release of motile
bacteria from these colonies may result in infection. Biofilms are protected foci of
infection and bacterial resistance within the wound, protecting bacteria from the
effects of antimicrobial agents such as antibiotics and antiseptics (Davey ME and
OToole GA, 2000).
Antibiotic resistance overuse use of antibiotics contributes to the development of
antimicrobial-resistant bacterial strains.

Moisture Imbalance
The management of moisture within the wound environment is the third consideration for wound
bed preparation. The goal is to identify factors which:

contribute to exudate
provide absorption
maintain a moist wound environment.

Why manage exudate?

Increased exudate in a chronic wound is often associated with other underlying complications in
the patient. For example, when bacterial burden increases, wound drainage also increases. Both
oedema (particularly in the lower extremities) and the breakdown of necrotic tissue can increase
the amount of exudate.
A comprehensive approach to exudate management should address underlying factors and
ensure that the wound environment remains moist. A moist wound environment is one where the
optimal level of moisture is maintained to allow for efficient cellular division and migration, while
ensuring the wound bed does not dry out or stay wet. In a moist wound environment, collagen
synthesis and granulation tissue formation improve; cell migration and epithelial resurfacing
occur faster; and scabs, crusts and eschar do not form.
Maintaining a moist wound environment has several additional benefits such as those listed
below.

Decreased healing time

Capacity for autolysis
Decreased infection rates
Reduced wound trauma
Decreased pain
Fewer dressing changes
More cost-effective (when defined as the total cost of care to achieve the desired outcome,
and not simply the cost of dressings).

Achieving moisture balance should begin with an assessment of factors that contribute to
increased levels, for example:

as bacterial burden increases, the amount of drainage may also increase, and intervention
should manage the microbial load in the wound environment
edema in the lower extremity can cause increased amounts of exudate and use of
compression therapy may be indicated
breakdown of necrotic tissue can increase the exudate produced, making debridement of
devitalized tissue essential.

This decision concerning choice of topical dressing should be based on several factors, including
the amount of moisture present in the wound.
Moisture level
Low

Topical dressings
Film dressings these semi-permeable polyurethane dressings that
are coated with an adhesive, are able to help manage bacterial

infection and absorb low amounts of exudate, while maintaining a

moist wound environment.
Hydrogel dressings these dressings gently re-hydrate dry necrotic
tissue, facilitating autolytic debridement, while being able to loosen
and absorb slough and exudate. Hydrogels are best used to treat
wounds with low exudate levels (Sibbald RG et al, 2000). They can
also be used to provide a moist wound management environment
during the later stages of wound closure.
LowModerate Hydrocolloid dressings contain absorbent material to absorb low levels of exudate
while maintaining a moist wound environment. Hydrocolloid dressings
are indicated for the management of partial thickness wounds, which
are mildly to moderately exuding.
Moderate-heavy Alginate

dressings highly absorbent dressings, which can be used to cover

moderate to heavily exuding wounds. The action of exudate on the
alginate fibres produces a gel, which creates a moist wound
environment.
Foam (hydrocellular) dressings provide thermal insulation, high
absorbency, a moist wound environment, and are gas permeable.
They are available as non-adherent or adherent and easy to shape to
the wound. Speciality absorbent dressings can be used as secondary
dressings.

Edge of wound non advancing or undermined

Epidermal edge migration is very much dependent on the overall environment of the wound.
Moisture balance, together with debridement and bacterial balance, are essential to achieving
wound closure. But there are also other factors which may be preventing the wound edges from
advancing. In chronic wounds the molecular and cellular processes are disrupted, leading to
significant differences in the microenvironment of the wound, both in terms of the cellular
components of the wound bed and the constituents of the exudate.
In chronic wounds, the specific cell populations and processes that prepare the wound for repair
are disrupted.

The epidermis fails to migrate across the wound tissue

Hyperproliferation of cells occurs at the wound edge and interferes with normal cellular
migration
As a result, apoptosis (programmed cell death) of fibroblasts and keratinocytes is inhibited
Fibroblast cells have an altered morphology and reduced proliferation rate
Reduced response of cells to growth factors such as PDGF- and TGF-
Fluid from chronic wounds is biochemically distinct from that of acute wounds. Chronic
wound fluid has a detrimental effect on healing, and can be attributed to the following:
o
o
o

increased levels of matrix metalloproteinases, which can degrade extracellular

matrix proteins and inhibit cell proliferation
greater levels of the proteins fibronectin and thrombospondin
macromolecules present in chronic wound fluid can bind growth factors making
them inactive.

Adequate debridement can remove non-viable tissue and cells that have accumulated and are no
longer responsive to signals required for closure of the wound (cellular sensescence)..
This in turn reduces the disruption to the extracellular matrix and releases growth factors, which
can then promote an angiogenic response leading to wound repair.
Epidermal edge migration lies at the heart of the concept of wound bed preparation, because if
there is no epidermal advancement the wound is not really healing. Advancement of the wound
edges means a reduction in wound area, the best visible predictor of healing.

The process of wound management cannot be fully understood unless the cellular and
biochemical factors are addressed alongside issues such as debridement, infection and exudate
management. Constant attention to the appearance and condition of the wound bed will prepare
the wound for healing. Wound bed preparation provides clinicians with a systematic approach to
achieve a stable wound with good granulation tissue that will progress assist with the efficient use
of advanced wound care products.
Wound bed preparation is not intended to be viewed in isolation. It is part of the process of
effective wound care, which includes close co-operation with the patient as to goal setting (and
pain management, if appropriate) before careful assessment and ongoing monitoring of a
comprehensive care regimen, using available resources.

Module 4
When assessing a patient with a wound it is tempting to focus on the wound. However it is vital
that general patient health issues, which affect healing, and the underlying pathology causing the
wound are addressed. Clear, logical, systematic assessment of the wound and the wound bed,
followed by communication and concise documentation using terminology that is accepted and
understood, ultimately optimise the patient's chances of wound closure.
Gathered information from wound assessments can be evaluated and a realistic and clearly
defined goal of care can be adopted. Furthermore, a wound management plan can be agreed
upon to achieve this goal in an effective manner.
Patient wound management must be constantly re-evaluated to ensure that therapeutic
interventions are both appropriate and effective. If this is not the case then changes can be made
and a more suitable treatment regime can be initiated.
Assessment is worth doing

Spending time accurately assessing a wound is not time wasted since the correct diagnosis
and an effective wound management plan will ultimately optimise patient care and reduce
healthcare costs (Khachemoune and Phillips, 2001).
Effective monitoring of wound progress is crucial since it can shorten the duration and
therefore the cost of inappropriate treatment for those that are not responding to current
treatment. In addition, wound assessment can reassure the clinician and patient that the
current treatment is working, which in turn can improve patient compliance.
Effective documentation of the progress of a wound allows the outcome of wound
management procedures to be monitored. It is important to note that assessment must be
documented for it to be communicated and acted upon if necessary.
Continual re-evaluation of the wound provides the clinician with important additional
information to monitor the effectiveness of therapeutic interventions.

Assessment is only worth doing if it is done well

The methodology employed in wound assessment must be consistent.

Data must be objective, precise and reproducible in order to draw any conclusions.
Interpretation should be objective (evidence-based) rather than subjective.

Assessment is only worth doing if it is acted upon

The information gathered should support the clinician in making decisions about the most
effective course of wound management and therapeutic interventions.
Patient assessment factors
Introduction
Different facilities and expertise are available to the patient depending upon where patient care is
being provided. For example, a hospital clinic may have access to more advanced measurement
techniques and to wound care experts with vascular and diabetes specialities.

There are many factors related to a patient's general health that may affect wound healing. If
these factors are not identified and resolved, where possible, wound healing is unlikely to be
optimised. There are two main areas that should be assessed related to a patient's general
health: associated conditions (see intrinsic factors) and the specific aetiology of the wound (see
aetiology).
Intrinsic factors
Intrinsic Factors refer to any factor, which may affect the healing of the patient's wound
regardless of its specific aetiology. These factors include those listed below.

Age - the skins capacity to regenerate decreases with increasing age. Since aged skin
contains less collagen and therefore has less elasticity, it is less able to withstand
mechanical stress making tissue damage more likely.
Infection - it is not just the number of bacteria but also their virulence and how these
bacteria interact with the patient's immune system that determines whether a wound
becomes infected. An infected wound may display classic signs of infection such as
advancing erythema, oedema, and foul odour. However, in some cases, wound infection
may be inapparent due to underlying pathogenesis such as diabetes, which reduces the
immune response.
Concomitant Diseases - many disease processes have a negative effect on wound
repair. For example, tissue repair requires oxygen and factors which decrease the
availability of oxygen to a wound such as cardiac disease, anaemia or chronic breathing
disorders, may result in a delay in healing. In addition, illness such as cerebrovascular
accidents and spinal or femoral fractures can result in a lack of sensation and/or
movement that increases the risk of pressure damage. Diseases such as rheumatoid
arthritis are associated with an increased risk of ulceration and an underlying disorder
such as this may complicate the healing process. The disease process of diabetes mellitus
is associated with peripheral neuropathy and arteriosclerosis, which can increase the risk
of ulceration. Diabetes can cause delayed wound healing due to reduced collagen levels,
defective granulocyte function and chemotaxis, and reduced angiogenesis (Silhi, 1998).
Drug therapies - steroids, non-steroid anti-inflammatory drugs, immunosuppressive
agents, anticoagulants and antiprostaglandins have all been shown to impair normal
wound healing.
Nutrition - Successful wound management depends on appropriate nutritional support.
Poor nutrition is recognised as one of the major causes of poor wound healing. Proteins,
carbohydrates, vitamins and minerals are all involved in the healing process and it is
possible that a higher than average daily intake of these components is needed for optimal
wound healing (Zagoren, 2001). Conversely, a reduced intake could interfere with healing.
There are a number of measurements that can be made to assess and monitor a patient's
nutritional status and indicate whether they are protein/calorie malnourished (PCM):
o body mass index - this is probably the easiest and most useful indicator of a poor
nutritional status and is calculated by dividing the patients weight in kilograms by
their height in metres squared. The normal range is 20-25
o serum albumin - 30-35g/litre is a possible indicator of PCM; <30g/litre is a possible
indicator of severe PCM
o lymphocyte count - <1.5x109/litre possible indicator of moderate PCM;
<1.0x109/litre is a possible indicator of severe PCM
o serum transferrin - 1.0g/litre-1.5g/litre is an indicator of moderate PCM;
<1.0g/litre is an indicator of severe PCM
o triceps skinfold thickness - <10mm in males and <13mm in females is an indicator
of PCM.

Pain
Pain is obviously a major patient concern that needs to be addressed and is also a useful tool in
wound assessment. Increasing pain could suggest further deterioration of the wound and possibly
infection.
Pain scales
Since pain can't be seen nor measured directly, clinicians need to have some way of judging
whether the patient is better or worse as treatment proceeds. The 'zero to ten scale' has become
a standard pain rating scale because it is a quantifiable measurement, although it is still an
individual measurement ie patients are not compared to each other only to their own pain level at
different times.

The two pain scales described above are only examples of numerous pain scales that are used by
clinicians. Developers of these scales tend to use different languages since each person views
their pain a little differently and can often describe the same pain in different ways.
Common questions that should be asked during assessment are:

is the wound painful?

if the wound is painful, does anything reduce the pain? (for example, in the case of an
arterial ulcer, lowering the limb can decrease the pain)
does anything make the pain worse?

Psycho/social concerns
A study by Felton et al (1976) has demonstrated that patients who were psychologically prepared
for surgery had better outcomes than those who were not. This study suggests that patients who
understand their care may heal better than those who do not. Therefore it is part of the
responsibility of the caregiver to ensure that the patient is sufficiently educated about the care
that they receive. Stress is another factor that has been implicated as a causative factor in
disease processes and may contribute to delayed wound healing. A study by Kiecolt-Glaser et al
(1995) demonstrated that punch biopsy wounds in women under stress took significantly longer
to heal than biopsy wounds in control patients. In addition, stress impairs bacterial clearance
during wound healing. As a result a significant increase in the incidence of opportunistic infection
has been demonstrated in patients under stress (Rogas et al 2002).

Wound aetiology
It is essential that the cause of a wound, whether it be obvious or underlying, is identified as
quickly as possible during assessment, to ensure that the correct treatment is prescribed. For
example, in the case of venous leg ulcers, these wounds are unlikely to heal well without
adequate compression to correct the underlying venous hypertension. However, if compression
therapy were used to treat a patient with an arterial ulcer, the result is likely to be tissue damage
and further deterioration of the wound.
Location
Pressure ulcers A pressure ulcer, as defined by the European Pressure Ulcer Advisory Panel
(EPUAP), is a localised area of tissue necrosis that develops when soft tissue is compressed

between a bony prominence and an external surface for a prolonged period of time. They are
complex lesions of the skin and underlying structures that vary considerably in size and severity.
Pressure ulcers are caused by prolonged pressure in combination with a number of other
variables such as immobility; increased age; nutritional deficiencies; incontinence; and neurologic
disorders. Other variables that may increase the risk of pressure ulcer development are length of
hospital stay, a history of pressure ulcers and infectious complications and diabetes.
The main causative factor in pressure ulcer development is the application of local pressure to
an area of skin not adapted to the external force. This leads to direct occlusion of blood vessels
and subsequent cell death. In addition, in a clinical environment, the repetitive pressure that
patients are exposed to is complicated by friction and shearing forces. Friction is a mechanical
force exerted when skin is dragged across a surface whereas a shearing force is generated when
a skeleton moves beneath the skin. Shear is a combination of gravity (pushing down on the
body) and friction (resistance) between the patient and the surface. Both shearing and friction
cause tissue breakdown as a result of damage to arterioles and the microcirculation, causing
reduced perfusion.
Moisture, often as a result of incontinence, is another factor that may accelerate the
development of pressure ulcers. Research supports the concept that sustained skin wetness
increases vulnerability to pressure-induced blood flow reduction (Mayrovitz and Sims, 2001). This
effect appears to be mainly dependant upon wetness, although it is likely that the constituents of
urine exacerbate the effect. In addition, skin wetness is associated with a slightly lower skin
temperature and this reduced temperature may play a part in reducing skin durability. Therefore,
it is important that every effort is made to reduce skin exposure to wetness as part of a strategy
to reduce the risk of pressure ulcer formation.
Lower leg ulcers
Ulcers below the knee, with the exception of heel ulcers, usually involve a vascular component.
These lower leg ulcers can be subdivided into venous, arterial and diabetic ulcers.
Venous ulcers - Venous ulcers are frequently in the region of the medial malleolus but can occur
anywhere on the lower leg. Other clinical characteristics are the presence of lower limb pulses,
generalised oedema and ankle flare (distension of the small veins below the medial malleolus).
Arterial ulcers - Characteristics of arterial ulcers include absent or diminished pulses, localised
oedema and pain on elevation and/or at night.
Neuropathic foot ulcers - External pressure or trauma can cause ulceration on any part of the foot
in patient's with diabetic foot syndrome. However, a classic diabetic foot ulcer will develop on the
sole of the foot where the pressure is high when the patient walks. Usually, this prolonged
pressure results in the development of a callus. If the callus becomes very thick, the underlying
tissue will be injured and an ulcer is likely to develop.
Differential diagnosis of lower extremity ulcers
Venous Insufficiency

Arterial Insufficiency

Neuropathic

History

Previous DVT and/or

varicosities
Decreased mobility
Obesity
Traumatic injury
Family history
Previous venous ulcer
Pain when extremity is
dependent for prolonged
periods

Smoking
Diabetes
Hypertension
Aging
Hyperlipidemia
H/O arterial disease
Intermittent claudication
Pain with elevation,
improves with
dependency

Decreased pain and

swelling with elevation

Intermittent claudication

Location

Previous history of
ulceration
Loss of protective
sensation
Peripheral vascular
disease
Duration of diabetes
Poor glycaemic control
Impaired functional
abilities
Paresthesia - insensate

Gaiter area (lower calf

area and above the
ankle)
Most frequent is medial
aspect of lower leg
superior to malleolus

Generally at the ankle or

below
Over bony prominence or
area exposed to pressure

Interdigital spaces

Colour: wound base

pale, may see dry
necrotic tissue (eschar)
Size: tend to be small
round ulcers with smooth
wound edges "punched
out"
Drainage: minimal,
unless infected
Oedema: generally not
present unless co-morbid
CHF
Skin temperature:
decrease, cool and may
have dependent rubor
and pallor on elevation

Plantar or lateral aspect

of the foot
Metatarsal heads

Site of repetitive
pressure and/or friction

Colour: wound base

granular
Size: variable, usually
small, well defined
wound margins but may
be large.
Drainage: minimal,
unless infected
Oedema: generally not
present
Skin temperature: warm
Surrounding skin:
periwound has thick
callous, skin is dry often
with fissures

Appearance

Colour: wound base

fibrinous or granular
Size: shallow in depth,
small to large in surface
area, irregular margins
Drainage: moderate to
heavy
Oedema: frequently
present and often
associated with
dermatitis
Skin temperature:
normal
Surrounding skin: brown
staining called
haemosiderosis

Surrounding skin: shiny,

taut, thin, dry, scaly, no
hair on lower extremity,
thick brittle toe nails
Pulses diminished, may
only be audible with
Doppler or absent
ABI 0.7 or lower

May see structural

changes and bony
deformities

Palpable pulses
ABI may not be reliable
in diabetic patients

Capillary refill normal < 3

seconds

Pressure relief "off

loading" the plantar
surface of the foot with
appropriate footwear
Tight glucose control
Aggressive sharp
debridement of callous
No bathroom surgery
Aggressive treatment of
infection

Perfusion

Palpable pulses
ABI > 0.8

Capillary refill normal <

3 seconds

Capillary refill > 3

seconds

Vascular consult to
evaluate potential for
revascularisation
No smoking
Moisturise dry skin, do
not apply between toes
Avoid trauma
Appropriate footwear
Moist wound healing, if
adequate blood flow to
support healing, present

Treatment Considerations
Improve venous return
Compression therapy
Unna Boot
Multi-Layer
Compression Therapy
Tubular compression
dressing
Compression stockings
Compression pumps
Leg elevation
Must rule out arterial
disease before initiating
compression

Wound dimensions / Size

High risk for pressure

ulcers on heels

Routine professional foot

care

Measuring and recording the size of a wound are crucial to help clinicians make decisions about
how to manage the wound most effectively. For example, clinical studies of chronic wounds have
shown that the initial wound size affects the time taken to heal (Marks et al 1983). Ongoing
wound measurements quantify changes in wound size and give an indication of whether the
wound is healing.
Tape measurements and tracings are the most commonly used techniques for measuring wound
dimensions. Length and width measurements provide valuable information about the progress of
the wound, but multiplying these two-dimensional measurements will not provide an accurate
measurement of area. One wound measurement protocol is to record length as the longest
measurement of the wound and the width as the longest measurement perpendicular to the
length. An alternative measurement protocol is the 'clock' method using the analogy of a clock
face and visualising the patient's head at 12 o'clock. In this instance, the length is a
measurement of the wound from head to toe and width is a side-to-side measurement. A specific
disadvantage of length and width measurements are that they are unreliable for deeper wounds
such as stage III and IV pressure ulcers as they are highly dependant upon the position of the
patient at the time of measurement. Whichever method of wound measurement is employed, for
it to be useful, method consistency and accurate documentation of how the measurements were
obtained are of crucial importance.
Absolute area measurement, although key, is currently only available with computer software
such as computerised planimetry (area measurement on a plane). This calculates the area within
a tracing of the wound edge (either scanned from a grid or drawn with a mouse around a digital
image of the wound). Because of this, healthcare professionals have often been restricted to
approximations of wound area calculated by counting the number of full and half squares it takes
to cover the wound, from a grid placed over the top of the wound.
It is both intuitive and widely believed that wound closure, the migration of the wound edges
towards one another, is a useful parameter to monitor to help the clinician assess the progress of
wound healing. Published research now provides statistically significant evidence in favour of the
use of percentage area reduction for monitoring purposes. This can be done by either plotting
against time (Robson et al, 2000), or evaluation of this parameter as at a specific time period
(Arnold et al, 1994; Phillips 2000; van Rijswijk et al 2003). Either way there is now considerable
published evidence that percentage reduction in wound area is a useful measurement within the
first few weeks of treatment to help the clinician to differentiate between wounds that are
responding or are not responding to treatment. The consistent message from these papers is that
a percentage area reduction of less than 20-40 percent over the first two to four weeks is a
reasonable indicator that the wound is showing a low response to the treatment.
In summary, obtaining wound measurements has been found to provide clinically useful and valid
information provided that method consistency and documentation are rigidly adhered to.
Tunnelling / Undermining
Undermining refers to tissue destruction underlying intact skin along the margins of the wound.
This can often involve a significant proportion of the wound edge and in some cases may extend
entirely around the wound. Undermining usually involves subcutaneous fat necrosis, and
generally, there are greater quantities of aerobic and anaerobic bacteria present in these wounds
than in those without undermining.
Appearance of the wound base
It is very important to assess and document the appearance of the wound bed. For example, the
presence of healthy granulation tissue and epithelialisation in the wound bed is an indication of
wound healing.
It is also important to note the colour of the granulation bed. Terms often used to describe this
tissue include 'beefy red', 'pink', 'pale and/or 'dusky'.
Similarly, the presence of necrotic tissue, eschar and sloughy tissue in the wound base needs to
be documented. Necrotic tissue refers to tissue that changes to a brown or black/purple colour
as it becomes more dehydrated and lacks an effective blood supply. After some time this necrotic
tissue becomes thick, dry, black, and leathery in appearance, and at this point it is referred to as
eschar.
Slough, in contrast, is a moist, yellow, fibrinous tissue consisting of fibrin, proteinacous material
that can build up on the surface of a previously clean wound bed. Slough provides an ideal
culture medium for pathogenic organisms and may therefore predispose a wound to infection.
Many wounds contain a combination of granulation tissue and necrotic tissue. When trying to

document the effect of treatments, clinicians have quantified the percentage of tissue involved,
expressing it as a percentage of the total wound area (eg 75% of the wound bed contains
necrotic tissue, 25% contains granulation tissue). This type of assessment will facilitate the
documentation of changes in the wound related to debridement.
Wound edges
In addition to assessing the extent and depth of the wound, the condition of the wound edges
should be a part of regular wound assessment. The clinician should assess and document for
example, whether the wound edges are well defined and well supplied with blood or ragged,
swollen, crushed, and undermined with a poor blood supply. Other terms commonly used to
describe wound edges include: irregular, crater-like, punched-out, calloused, macerated and
desiccated.
Periwound skin The condition of the surrounding or periwound skin provides very important
information about the status of the wound and effects of treatment. Observation, assessment and
documentation should include evaluating colour, induration, any oedema, suppleness and/or
maceration. For example, redness of the periwound skin could indicate unrelieved pressure or
prolonged inflammation. Furthermore, redness, tenderness, warmth and swelling are the classic
signs of infection. Assessing the suppleness of the periwound skin is important since overly dry as
well as overly moist skin is more prone to injury. Signs of maceration (pale, grey or white tissue)
may be observed when surrounding skin has been exposed to moisture for a prolonged period of
time. Documentation of the condition of the periwound skin should include the location and
extent (measured in centimetres) of these characteristics.

Infection
There are several variables that are involved in determining whether a wound becomes infected.
These include the number of microorganisms present in the wound and bacterial virulence
although, what is of crucial importance is the way these bacteria interact with the host ie host
resistance factors. For example, immunosuppression, diabetes and medication, can lower a
patient's resistance to infection.
Studies have demonstrated that numbers of bacteria above 105 per gram of tissue can cause
infection (Dow, et al 1999). Conversely, some surgical studies have demonstrated that many
patient's with bacterial levels greater than 105 heal normally (Robsen, et al, 1973). Therefore it is
likely that the type of bacteria and their virulence increase the risk of infection rather than the
number of microorganisms alone.
The way in which these factors are related can be demonstrated by the following equation:
Risk of wound infection = number of bacteria x virulence
host resistance
The classic signs and symptoms of infection are:

advancing erythema
fever,
warmth,
oedema
pain
purulence.

However, not all infected wounds display these classic signs. For example, chronic wounds may
have a reduced immune response to invading microorganisms as a result of underlying
pathogenic abnormalities such as diabetes. In wounds of this nature, secondary signs and
symptoms could indicate that the chronic wound is infected. These include:

delayed wound healing

change in colour of the wound bed
friable granulation tissue
absent or abnormal granulation tissue

increased or abnormal odour

raised volumes of serous drainage
increased pain at the wound site.

Wound exudate
Wound exudate characteristics such as type and amount should be assessed because they
provide important information about the status of the wound and give an indication of what would
be the most appropriate treatment.
A moist wound environment has been shown to provide an optimal environment for wound
healing. However, if the wound becomes too wet as a result of excessive quantities of exudate
being produced, surrounding tissues become macerated and the wound may deteriorate further.
Different types of wound produce different amounts of exudate. For example, compared to acute
wounds venous leg ulcers are highly inflammatory wounds and produce large amounts of
exudate.

When describing exudate, it is important to document the amount, consistency, odour (if
applicable) and if there is a particular area of the wound bed in which the exudate produced is
more pronounced.
Terms used to describe the amounts of exudate are minimal (<5cc/24 hours), moderate (510cc/24 hours) or high (>10cc/24 hours) (Mulder, 1994).
Tissue involvement / Wound depth
Tissue involvement (or wound depth) can be sub divided into the categories below depending
upon which tissues are involved.

Superficial wounds - damage to the epidermis, exposing the underlying dermal layer
Partial thickness wounds - damage is limited to the epidermis and superficial dermis
Deep dermal wounds - damage extending through the epidermis and dermis up to the
junction with the subcutaneous fat layer
Full thickness wounds - injury involves loss of the dermis and extends into subcutaneous
fat, muscle and bone

Depth refers to the depth of the wound at its deepest point. However, wound depth is difficult to
ascertain, especially in irregular shaped wounds (Thomas and Wysocki, 1990; Harding 1994).
Pain
As well as being assessed on initial presentation, pain should also be monitored on an ongoing
basis. Increasing pain could suggest further deterioration of the wound and possibly infection.
Staging
Wound depth is a very important assessment variable because it has a direct impact on how long
wounds take to heal. For this reason descriptive wound assessment methods/systems are based
on wound depth. As a result of work by Shea (Shea, 1975) together with input from the
International Association of Enterostomal Therapy and the National Pressure Ulcer Advisory Panel
(NPUAP), pressure ulcer staging systems were devised, all based upon the level of tissue
involved.

The following definitions of staging for pressure ulcers are the latest put forward by the NPUAP:
Stage I - an observable pressure related alteration of intact skin with indicators, as compared to
an adjacent or opposite area on the body, which may include changes in one or more of the
following: skin temperature (warmth or coolness), tissue consistency (firm or slack), and/or
sensation (pain, itching). The ulcer appears as a defined area of persistent redness in lightly
pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or
purple hues.
Stage II - partial thickness skin loss involving the epidermis, dermis or both. The ulcer is
superficial and presents clinically as an abrasion, blister or shallow crater.

Stage III - full thickness skin loss involving damage to subcutaneous tissue that may extend
down to, but not through, the underlying fascia. A stage III ulcer presents clinically as a deep
crater with or without undermining of underlying tissue.
Stage IV - full thickness skin loss with extensive tissue destruction or damage to muscle, bone or
supporting structures such as tendons or joint capsules. Undermining and sinus tracts may also
be associated with Stage IV pressure ulcers.
An alternative classification system has been proposed by the European Pressure Ulcer Advisory
Panel (EPUAP). This is similar to that of the NPUAP but this system 'grades' rather than 'stages'
pressure ulcers as below:
Grade 1 - non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema,
induration or hardness may also be used as indicators, particularly on individuals with darker
skin.
Grade 2 - partial thickness skin loss involving epidermis, dermis or both. The ulcer is superficial
and presents clinically as an abrasion or blister.
Grade 3 - full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may
extend down to, but not through underlying fascia.
Grade 4 - extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting
structures with or without full thickness skin loss.
There are also more defined classification systems for diabetic foot ulcers such as the Wagner
scale and University of Texas diabetic wound classification system. Both systems are based upon
assessment of wound depth.
The classification of other wounds such as burns, is based upon depth and area. For example, in
terms of depth, partial thickness wounds are classified as superficial or as deep second degree
burns. The area of the wound is the total body area involved.
A limitation of all staging systems is that they rely on the clinician's ability to assess wound
depth. It is impossible to stage a wound that is covered with eschar because the depth cannot be
accurately determined. In some cases the outward appearance of the wound is just the tip of the
iceberg. It may extend deep into the underlying fascia, could involve bone and may be infected.
Another important point to note is that staging systems have not been designed to describe
changes that occur during the healing process. For example, if a pressure ulcer has been graded
as stage III on initial assessment, it should not subsequently be staged as stage II or stage I as
the healing process continues and the ulcer moves towards closure. The reason for this is that
clinical studies indicate that as ulcers heal, the lost muscle, fat and dermis are not replaced.
Instead, granulation tissue fills the defect before re-epithelialisation. Rather, the progress of the
ulcer should be charted by noting an improvement in characteristics ie size, depth, amount of
necrotic tissue, amount of exudate, etc.
Documentation
Documentation is obviously a crucial part of wound assessment and it is important that it is:

objective
thorough
accurate
consistent.

Flow sheets are useful and convenient when documenting daily observations and treatments. A
narrative summary, however, is necessary on admission and with any significant changes in the
wound characteristics or management plan.
Once the information has been systematically documented it can be reviewed, analysed and
compared to other reported outcomes in the literature to develop and modify wound care
management procedures and individual patient care plans.

Summary and Conclusion

Comprehensive, initial assessment enables the clinician to make an informed diagnosis of a
patient and their wound. Routine monitoring of the wound's progress/status enables the clinician
to make informed clinical decisions about whether an individual patient should continue with their
current treatment or whether the treatment should be reassessed.
As we have seen, wound assessment incorporates measurement of wound size and depth, the
condition of the wound edges and the surrounding skin. The presence of necrotic and granulation
tissue, eschar and slough in the wound bed are also important criteria for assessment, as are
qualitative and quantitative measurements of wound exudate.
Communication among healthcare professionals is a crucial part in achieving clearly defined and
realistic goals of care and the only way to achieve this is through objective, accurate and
consistent documentation.

Module 5
Accurate assessment is the key to effective leg ulcer management.Chronic venous insufficiency,
diabetic complications and arterial insufficiency are responsible for over 90% of leg ulcers.
Of all lower leg ulcers the venous ulcer is a common medical problem that affects 1 to 2% of the
population
The cost of management of leg ulcers has been estimated to be:
Scandinavia - $25 million (1985 U.S. dollars)
United Kingdom - $200 Million (1989 U.S. dollars)
United States - Projected $1 Billion
The impact on quality of life is immeasurable but includes pain, decreased mobility, negative selfimage, and feelings of anger, fear, isolation and depression.1,2
An initial assessment of the patient with an ulcer of the lower extremity must include a detailed
patient history, which will provide clues as to the differential diagnosis. Careful physical
examination is necessary to evaluate the size and characteristics of the wound and should
highlight any associated medical conditions. This should also include evaluation of the patient's
social circumstances as these may impact on both care and healing.3
A Recommended Management Pathway for Leg Ulcers
The International Leg Ulcer Advisory Board comprises some of the most eminent clinicians and
researchers in the field from Europe, North America and Australia. The panel designed a
recommended management algorithm based on a review of the available literature and expert
consensus and also looked at relevant conferences and existing guidelines when making their
decision about the algorithm. The International Leg Ulcer Advisory Board Published their review in
the Journal of the European Wound Management Association, May 2002.4
In order to ensure ease of use and effectiveness, the algorithm has been kept as simple and
straightforward as possible. The algorithm can be broken down into four stages: Assessment,
Diagnosis, Recommendations for Treatment and Outcomes.
This algorithm will serve as the organising framework for this educational module and can be
found as a printable file.

Assessment

Patient Assessment
The assessment of a patient with a wound begins with a thorough patient history and physical
exam.
The clinician must begin by identifying:

Previous history of deep vein thrombosis or venous ulcer

History of leg oedema
Cause of the wound such as trauma or pressure
Treatment history of the wound to date
Wound duration: acute (< 6 weeks) or chronic (> 6 weeks)
Identification of systemic factors that affect wound healing (medications, acute and
chronic illnesses, age etc)
Nutritional status
History of travel or known exposure to fungal or parasitic causes

Investigating and obtaining a thorough patient history will help in identifying the correct cause
and facilitate management.
Wound Assessment
A complete wound assessment consists of a careful evaluation of the wound and surrounding
tissue. Components of the wound assessment include:

Location of the wound

Physical characteristics of the wound including size and depth of injury
Presence of undermining, tunneling, sinus tracts, foreign bodies and exposed bone
Appearance of the wound bed
Skin color and condition
Skin temperature
Amount and characteristics of exudate
Presence of local or general oedema
Presence and nature of pain

The following table will guide the clinician in identifying classic signs and symptoms of venous
disease and an accurate differential diagnosis of a lower extremity ulceration. This table is also
available in a printable format for easy reference.
Venous Insufficiency

Arterial Insufficiency

Neuropathic

History

Previous DVT and/or

varicosities
Decreased mobility
Obesity
Traumatic injury
Family history
Previous venous ulcer
Pain when extremity is
dependent for prolonged
periods

Smoking
Diabetes
Hypertension
Aging
Hyperlipidemia
H/O arterial disease
Intermittent claudication
Pain with elevation,
improves with
dependency

Decreased pain and

swelling with elevation

Intermittent claudication

Paresthesia - insensate

Generally at the ankle or

below
Over bony prominence or
area exposed to pressure

Plantar or lateral aspect

of the foot
Metatarsal heads

Previous history of
ulceration
Loss of protective
sensation
Peripheral vascular
disease
Duration of diabetes
Poor glycaemic control
Impaired functional
abilities

Location

Gaiter area (lower calf

area and above the
ankle)
Most frequent is medial
aspect of lower leg
superior to malleolus

Interdigital spaces

Site of repetitive
pressure and/or friction

Appearance

Colour: wound base

fibrinous or granular
Size: shallow in depth,
small to large in surface
area, irregular margins
Drainage: moderate to
heavy
Oedema: frequently
present and often
associated with
dermatitis
Skin temperature:
normal
Surrounding skin: brown
staining called
haemosiderosis

Colour: wound base

pale, may see dry
necrotic tissue (eschar)
Size: tend to be small
round ulcers with smooth
wound edges "punched
out"
Drainage: minimal,
unless infected
Oedema: generally not
present unless co-morbid
CHF
Skin temperature:
decrease, cool and may
have dependent rubor
and pallor on elevation

Surrounding skin: shiny,

taut, thin, dry, scaly, no
hair on lower extremity,
thick brittle toe nails
Pulses diminished, may
only be audible with
Doppler or absent
ABI 0.7 or lower

Colour: wound base

granular
Size: variable, usually
small, well defined
wound margins but may
be large.
Drainage: minimal,
unless infected
Oedema: generally not
present
Skin temperature: warm
Surrounding skin:
periwound has thick
callous, skin is dry often
with fissures

May see structural

changes and bony
deformities

Palpable pulses
ABI may not be reliable
in diabetic patients

Capillary refill normal < 3

seconds

Pressure relief "off

loading" the plantar
surface of the foot with
appropriate footwear
Tight glucose control
Aggressive sharp
debridement of callous
No bathroom surgery
Aggressive treatment of
infection

Perfusion

Palpable pulses
ABI > 0.8

Capillary refill normal <

3 seconds

Capillary refill > 3

seconds

Vascular consult to
evaluate potential for
revascularisation
No smoking
Moisturise dry skin, do
not apply between toes
Avoid trauma
Appropriate footwear
Moist wound healing, if
adequate blood flow to
support healing, present

Treatment Considerations
Improve venous return
Compression therapy
Unna Boot
Multi-Layer
Compression Therapy
Tubular compression
dressing
Compression stockings
Compression pumps
Leg elevation
Must rule out arterial
disease before initiating
compression

High risk for pressure

ulcers on heels

Routine professional foot

care

Pathophysiology of Chronic Venous Insufficiency

Normal Venous Return
Normal venous return is the result of two mechanisms. First the calf pump during ambulation:
the calf muscle contracts and compresses the venous compartment, which propels blood in the
veins up towards the heart.
The one way valves open when the calf muscle contracts and close when the calf muscle relaxes
and this prevents the reflux of blood and distention of the veins.

Pathogenesis of Venous Ulcers

Definition: The basic physiologic abnormality underlying the manifestations of "Chronic Venous
Insufficiency" is an elevation of ambulatory venous pressure.

The pathogenesis of venous ulcers is the focus of much research. It is generally agreed that
venous hypertension is the fundamental problem. There are several hypotheses that have
emerged to explain the formation of venous ulcers.

Venous hypertension is often the result of valvular incompetence secondary to Deep Vein
Thrombosis. As a DVT forms, the thrombus adheres to the endothelium, contracts and scarring
destroys the valves. Recanalisation of the vessel leaves high resistance incompetent channels.

It has been suggested that venous hypertension leads to the distention of vessels causing an
increased permeability of the vessel wall resulting in the leakage of large molecules or blood
components into the skin. It is the presence of these components that interferes with the
diffusion of oxygen and the delivery of nutrients to the skin.

One hypothesis suggests that it is the presence of fibrin, which forms pericapillary fibrin cuffs,
which impedes the diffusion of oxygen and nutrients between the blood vessel and the dermis.
This results in anoxia leading to ulceration. While this hypothesis has some merit, a number of
flaws have been identified.

Another hypothesis suggests that white blood cells can become entrapped in areas of reduced
venous flow adhering to endothelium, causing occlusion of the capillaries and damage to dermal
vasculature releasing fluid and inflammatory mediators into the tissue leading to chronic
inflammation.

The following animation will assist the learner in understanding venous blood flow and the
pathogenesis of ulceration.
Regardless of the exact pathogenesis, clinically one observes that the ulcers fail to reepithelialise
often in the presence of a granulated wound bed.
Non-Invasive Vascular Assessment
An accurate vascular assessment of the extremity is necessary to ensure that the correct
aetiology of the ulceration has been identified and to exclude those patients with arterial disease
for whom compression is dangerous. There are a number of non-invasive methods used to
confirm venous disease when a patient presents with suspected venous ulceration. Methods of
assessment include:
Examination of:

Skin color and temperature

Areas of dryness and cracking skin
Capillary refill time;- this is a simple test that provides information about the extent of
ischaemic disease, normally colour should return in 3-4 seconds.
Palpation of peripheral pulses;- there can be significant discrepancies with documentation
of pulses when the 1+, 2+, 3+ etc technique is used. It is more reproducible to document
palpable or absent.
The following system for grading palpable pulses is often used.
0 - Absent

3+ - Normal

1+ - Barely palpable 4+ - Bounding

2+ - Palpable but diminished
Doppler Assessment and Ankle Brachial Index
The Doppler is a vital tool of assessment when trying to determine the underlying aetiology of leg
ulcers and determine a course of treatment that will maximise wound healing potential.
Predominantly leg ulceration is of venous origin and requires sustained compression to facilitate
venous return from the lower extremities. However, before any type of compression management
can be considered, a Doppler test should be performed to determine whether there is arterial
involvement or whether the ulcer is the direct cause of arterial compromise. The significance of
assessing for adequate arterial flow in the affected extremity is of utmost importance as the
application of compression to an ulcer of arterial or mixed aetiology could further compromise
blood flow and result in ischaemia.
Ankle Brachial Index Procedure
Recording Ankle Brachial Index (ABI) also known as Ankle Brachial Pressure Index (ABPI) or
Resting Pressure Index (RPI)

Checks should be made that the patient has rested for the appropriate amount of time
(15-20 minutes)
Prepare the patient's arms and legs for access
The brachial pressure is first measured in both arms using the Doppler. The Doppler probe
should be held at a 45- 60-degree angle to the limb. The electrode gel assists the
transmission of the pulse to the probe.
Identify the sound of the arterial flow. The artery has a high-pitched sound. If the sound
you hear is a gale-like whoosh with ill-defined beats you are listening to venous return and
need to change the probe position.
For the purpose of this test, systolic pressure only is required.
To measure the ankle pressure the correct position of the cuff should be located
approximately 5cm above the malleolus. Any wounds which have had their dressings
removed need to be covered by a sterile shield to prevent contamination of the wound bed
and also to prevent cross contamination of the cuff.
Prior to inflating the cuff, the pedal pulses have to be located using the Doppler. There are
two main pulses (the dorsalis pedis and the posterior tibial) to identify, from which an
arterial sound may be heard. It is quite common in arterial compromise to find foot pulses

absent or diminished. The posterior tibial pulse is more reliable than the dorsalis pedis
that is congenitally absent in 10% of people: in a further 10% the dorsalis pedis is
impalpable.
The systolic measurements should be taken on each ankle using different pulse points for
greater accuracy. When all the measurements have been taken and recorded the Ankle
Brachial Index can be calculated using the highest brachial systolic Doppler recordings and
readings from each of the ankles.
Note ABI isn't always reliable in patients with diabetes due to arterial calcification that
can lead to falsely high ABI's.

ABI Calculation
ABI = Ankle Systolic Pressure / Brachial Systolic Pressure
Example
Ankle systolic pressure = 80 mm Hg
Brachial Systolic Pressure = 100 mmHg
80 / 100 = 0.8
ABI Clinical Significance
0.9 - 1.1 normal range for ABI
0.7 - 0.8 mild disease and the patient may begin to experience intermittent claudication or pain
with ambulation.
0.4 - 0.6 moderate to severe disease and at this point there is likely to be impaired healing.
< 0.4 severe occlusive disease.
1.2 may represent a falsely elevated ABI, which can result in patients with sclerotic vessels for
example patients with Diabetes or Renal Failure. The blood vessels become stiff and ridged and
are not readily compressible leading to falsely elevated reading. These patients may require
further vascular testing to determine adequacy of perfusion.
It is important to periodically repeat the ABI to monitor progression of disease. A decrease of
more than 0.2 is consistent with a decrease in perfusion and progression of disease.
Segmental Pressure Recordings
In this examination, systolic pressures are measured sequentially up the leg from ankle to thigh.
A pressure difference of greater than 25 mmHg between levels indicates occlusive disease.

Duplex Ultrasonography measures blood flow velocity through a vessel and is the primary
method of identifying venous obstruction or abnormal venous reflux
A number of plethysmographic methods, including air and photo plethysmography, may be used
to assess venous function. Other investigations may also take place to exclude disorders such as
rheumatoid arthritis, diabetes, renal failure, anaemia, tumours and auto-immune disorders.
A comprehensive physical exam can provide important information for the differential diagnosis of
venous disease. It is essential to determine the adequacy of arterial perfusion because
compression therapy is the gold standard of treatment for venous ulcers and high level
compression is contraindicated in the presence of arterial disease with an ABI of less than 0.8.
Reduced levels of compression are recommended in the case of mixed aetiology ulceration with
an ABI 0.6 - 0.8 mm Hg.
Clinical Features
There are a number of clinical signs that are associated with chronic venous insufficiency (CVI)
and are helpful in making a differential diagnosis. It is helpful to remember that the clinical
presentation is in part the result of the blood components leaking into the interstitial space.
Hyperpigmentation CVI leads to distension of the
blood capillaries and damage to the endothelium,
leading to leakage of red blood cells. The breakdown
products of haemoglobin cause dark staining of the
skin or hemosiderosis.

Lipodermatosclerosis may be described

as "woody" induration of the tissues with
fat replaced by fibrosis. The leg often
assumes an inverted champagne bottle
shape.

Oedema Venous pressures and increased

capillary permeability can lead to increased
interstitial fluid. Venous disease can also be
complicated by poor lymphatic drainage.
Characteristically oedema associated with CVI
may involve the lower leg and foot, is
considered pitting oedema and will occur in
one or both legs depending on the extent of
the venous disease.

Venous dermatitis and eczematous changes These are often associated with CVI and can be
aggravated by wound care products through irritation and allergy. Persistent scratching may
cause secondary infections.

Ankle flare refers to the collection of small

venular channels inferior to the medial
malleolous and extending onto the medial
surface of the foot. This sign is indicative of
CVI.

Venous Ulcer Characteristics

Location
Size
Wound bed
Drainage
Skin
Pain

Gaiter area - most frequently above the medial malleolus but can occur anywhere
on the leg
Can be small to circumferential, shallow, with irregular wound margins
Ruddy color, granulation or fibrinous tissue
Frequently moderate to large
Scaling, pruritis, weeping, staining
Varies greatly - painless to painful

Recommendations for Treatment

There are fundamental principles for developing a comprehensive management plan for the
patient with CVI and /or venous ulcers.
Compression therapy is the gold standard for treatment of venous ulcers. It is extremely
difficult for venous ulcers to heal in absence of compression. There are a variety of interventions
for providing compression, however not all have the same level of effectiveness.
Sustained compression provides the mainstay of treatment in venous leg ulcers. This should be
supported with adjunctive medical and surgical therapy, appropriate dressings and patient
education. Sustained compression is provided by multi-layer elastic or inelastic bandage systems.
There is now considerable evidence to show that this form of sustained high compression
improves ulcer healing and provides quality of life and cost benefits. Multi-layer high compression
bandaging improves healing of venous leg ulcers when compared with single layer, low
compression bandaging although there is little reliable evidence to date of large randomised
controlled trials which directly compare 4-layer compression to 3-layer or 2-layer bandaging.
Multi-layer bandage systems are complemented by reduced compression systems (15-25 mmHg)
for those patients who cannot tolerate high compression systems, and compression stockings.
Intermittent pneumatic compression (IPC) is a useful adjunct to multi-layer compression and has
been shown to improve ulcer-healing rates when used with multi-layer compression.
Compression
The degree of compression produced by any bandage system over time is determined by complex
interactions between four principle factors - the physical structure of the elastomeric properties of

the bandage, the size and shape of the limb to which it is applied, the skill and technique of the
bandager and the nature of any physical activity undertaken by the patient.

Laplace's Law (Determining Sub-Bandage Pressure) - The pressure generated by a

bandage immediately following application is determined principally by the tension of the fabric,
the number of layers applied, and the degree of curvature of the limb. P=T/R
P pressure
T tension
R radius
Applied pressure is directly proportional to the tension in a bandage (P increases with T) but
inversely proportional (P decreases as R increases) to the radius of the curvature of the limb to
which it is applied.

Methods of Compression
Elastic compression (long-stretch) bandages exert high compression during rest and
exercise whereas
Inelastic (short-stretch) bandages produce passive compression mainly when the calf
muscle contracts, increases in volume and creates pressure against the bandage. At rest,
inelastic compression bandages exert pressure dependent on the tension used during
application.

Sustained compression - Any bandaging system providing sustained compression for at

least one week (More frequent dressing changes may be needed if the wound is large
and/or heavily exuding)
Multi-layered (elastic) compression - Currently presented as 4-layer high compression
bandaging providing sustained, graduated compression (including bandages >50%
extension and exerting pressure at rest). (N.B. There are substantial differences in
systems depending on bandage characteristics).
Multi-layered (inelastic) compression - Multi-layer inelastic bandaging (<50%
extension and exerting pressure at rest dependent on the tension used during application)
Reduced compression - Compression of 15-25 mm Hg using a 1- or 2-bandage layer
system. Reduced compression stockings are a valuable alternative.
Compression stockings - Ideally, compression hosiery that provides compression of 3545 mm Hg, but if not tolerated 25-35 mm Hg. There remains no international consensus
on definition of the different classes of compression hosiery.
Intermittent pneumatic compression - one of a number of devices which surround the
leg and can be inflated to provide short-term pressures up to a maximum of 100 mm Hg.

Recommendations for treatment

A number of adjunctive medical therapies, including pentoxifylline, are currently in use without
unequivocal support in the literature. There is also increasing realisation that chronic wounds,
such as venous ulcers, benefit from an overall approach aimed at optimising the wound bed. This
approach, termed wound bed preparation, includes a number of aspects critical to wound care,
such as elimination of excessive exudate and bacterial burden, debridement [debridement
includes elimination of necrotic tissue], angiogenesis and the formation of a wound matrix that
promotes re-epithelialisation.
There is emerging evidence that skin substitutes may be beneficial in the treatment of hard to
heal venous leg ulcers (especially in those with duration >1 year) when used in conjunction with
multi-layer compression bandaging.11,12 Other biological agents, such as growth factors and
protease inhibitors are currently being evaluated for their efficacy in the management of venous
leg ulcers. Many patients with leg ulcers suffer pain that can adversely affect quality of life and
may influence speed of healing. Reduced compression should be used until pain and oedema
resolves and then high compression bandaging can be introduced. In most cases, appropriate
dressings or oral analgesics can effectively manage pain although skin grafting may be required
in cases of intractable pain.
Appropriate Dressing Selection and Education

Patients with leg ulcers are prone to contact sensitivity particularly from wool alcohols, topical
neomycin, framycetin, cetylstearyl alcohols and rubber mixes which are present in many
dressings, ointments and creams. Emphasis should be placed on allergen avoidance to allow
optimal wound healing. However this remains a difficult management issue in individual patients.
Education
Factors that encourage ulcer healing, such as improved nutritional status, diabetic control,
appropriate bandage use and mobility, are dependent on patient involvement. Education to
improve patient understanding of the condition will aid compliance to therapy.4

Treatment of mobile and immobile patients

Reduced mobility and reduced ankle function, as well as other factors such as ulcer size and
duration, have been shown to independently affect healing rates. As inelastic bandages lose
pressure when leg oedema is reduced, multi-layer elastic compression is recommended as firstline therapy for immobile patients with venous leg ulcers. The incidence of venous leg ulcers
increases with age, rising to 6% among the population aged over 80 years old: a high proportion
of this age group suffer from some degree of immobility.

Addition of intermittent pneumatic compression is recommended as second-line therapy in these

patients. Multi-layer compression (elastic or inelastic) is recommended as first-line therapy in
mobile patients. Elastic stockings can be used as second-line therapy in mobile patients,
particularly those that are young and working or who are unable or unwilling to tolerate multilayered compression.4
Outcomes
The International Leg Ulcer Advisory Board recommend a definition of failure to heal as no
reduction in ulcer size in 1 month. Patients with ulcers <10 cm2 who have failed to achieve
complete healing in 3 months should be referred to a specialist for re-evaluation including
diagnosis and re-assessment and evaluation for surgical correction of any venous abnormality.
Patients with ulcers >10 cm2 are likely to take a long time to heal and skin grafting may be
required. Following healing of the ulcer, steps must be taken to minimise the risk of recurrence by
using compression hosiery and maintaining education and support to the patient. Control of
oedema by elevation and use of compression hosiery for life may be required. Compression
hosiery should be applied at the highest level of pressure subject to patient compliance and
dexterity.4
Conclusions
The International Leg Ulcer Advisory Board's recommended guidelines based on a comprehensive
review of the literature and expert consensus, confirm the role of sustained compression (elastic
and inelastic) as first-line therapy for venous leg ulcers. Reduced compression and compression
hosiery are useful alternatives in those patients with additional arterial disease or who cannot
tolerate multi-layer bandaging. Intermittent pneumatic compression is a valuable adjunctive
therapy in the treatment of venous leg ulcers although there is a need for further evidence-based
findings on these techniques. In addition there is a need for further randomised, controlled trials
on the other medical and surgical therapies to be used in conjunction with compression therapy.
It is hoped that the algorithm provides a useful working tool for primary care physicians and
nurse practitioners to provide appropriate care based on the latest findings in the literature.

Sustained multi-layer compression is confirmed as first-line therapy for venous leg ulcers
Reduced compression and compression hosiery are useful alternatives
IPC is a valuable adjunctive therapy
A need for further RCTs on the other adjunctive therapies.4

Stacey M et al. The use of compression therapy in the treatment of venous leg ulcers: a
recommended management pathway. EWMA Journal 2002.

Module 6
Pressure Ulcers; The Problem
Pressure ulcers pose a significant public health problem, with the incidence ranging from <1% to
38% in hospitals and from 2.2% to 23.9% in the long-term care setting. 1 In the acute care
setting, the average length of hospital stay can increase by 4 to 17 days among patients with
pressure ulcers and related complications.2
For patients, pressure ulcers cause great pain and suffering, decreasing quality of life. Infections,
secondary to pressure ulcers, are associated with increased morbidity - and even mortality - in

bed-bound individuals. Pressure ulcers can be demoralizing to both patients and staff. Pressure
ulcers are costly in terms of money, morbidity, mortality, and quality of life.
It has been suggested that 95% of pressure ulcers can be prevented.3 Other literature suggests
that good preventive care can result in less skin breakdown and fewer pressure ulcers and leads
to emotional benefits for patients, families, and caregivers. Good skin care can have a positive
impact on the patient's overall health, including morale, self-esteem, and susceptibility to pain
and infection. Families are reassured when quality care is evident and gain confidence in the staff
and facility. Caregivers are motivated when they see the difference they can make. And a
motivated staff can lead to increased employee satisfaction and improved patient outcomes.
To help clinicians and care providers develop quality skin care and pressure ulcer prevention
programs, a number of national and international guidelines for the prevention of pressure ulcers
have been developed. Two examples are the European and American Guidelines.4,5 The goals are
to enhance the quality, appropriateness and effectiveness of health care services provided. The
clinical practice guideline, Pressure Ulcers in Adults: Prediction and Prevention was made
available 1992. The European Pressure Ulcer Advisory Panel adopted these guidelines for practice
for European countries in 1998. The following module is based on these Guidelines and will assist
the learner in the comprehensive assessment of intact skin, determining risk factors for skin
breakdown as well as the implementation of prevention strategies.
Classification
Pressure damage is common in many healthcare settings, affecting all age groups, and is costly
both in terms of human suffering and use of resources. With an ageing population, and changes
in patterns of illness, this problem will increase unless action is taken. In all care settings the risk
of pressure damage should be highlighted. Most pressure damage could be prevented and it is
important to have prevention and educational strategies in place. These should be based on the
best available evidence. All interventions and outcomes should be monitored and documented. 6
Prior to designing a comprehensive skin care prevention program, it is appropriate to determine
what skin/wound problems exist in the facility. Tracking prevalence and incidence rates are one
way to monitor clinical outcomes. Often the terms incidence and prevalence are used
interchangeably. This data should not be interchanged because prevalence relates to the number
of facility acquired ulcers, whereas incidence refers to the number new ulcers that developed over
a period of time.
Definitions:
Incidence refers to new cases of ulceration occurring over a given time period for a particular
patient population.
Prevalence includes new and old cases and is usually assessed on a cross-sectional basis.
Prevalence may be divided into:
Point Prevalence - data are collected on one day, providing a snapshot in time
Period Prevalence - data are collected over a specific period of time.7
Pressure Ulcer - A pressure ulcer is an area of localized damage to the skin and underlying
tissue caused by pressure, shear, friction and or a combination of these.
Pressure Ulcers Grades and/or Stages

Grade 1:
EPUAP Definition - Non-blanching erythema of
intact skin4
AHRQ Definition - Non-blanchable erythema
of intact skin

Discoloration of the skin, warmth, edema, induration or hardness may also be used as indicators,
particularly on individuals with darker skin.4

Grade 2: partial thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial
and presents clinically as an abrasion or blister.
Grade 3: full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may
extend down to, but not through underlying fascia.
Grade 4: extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting
structures with or without full thickness skin loss.5
Recognising Risk Factors for Skin Breakdown
Healthy intact skin provides a barrier against microorganisms and is crucial to patient welfare.
Preventing skin breakdown begins with identifying patients at risk and recognizing the warning
signs that can lead to breakdown.

The risk for development of

skin breakdown is based on
the presence of intrinsic and
extrinsic risk factors.
Understanding and
recognizing these factors
proactively, helps staff
members to provide optimal
care for patients at higher
risk.

Extrinsic and Intrinsic

Factors
Intrinsic factors are related to the patient's overall health status and include:
Age - Skin changes considerably through the ageing process, making it more vulnerable to
breakdown. Skin cell turnover slows.
Dry Skin affects 59% to 85% of individuals over the age of 64 years.
Dry skin is also at risk for breakdown. As we age, many changes occur that diminish the body's
natural ability to retain moisture. These changes, associated with aging, are manifested as dry
skin. The proliferation of epidermal cells decreases. The slower regeneration time and slower
desquamation results in a thinned layer of corneocytes, thus increasing the surface area for fluid
loss.
Collagen and elastin decrease - makes the skin less pliable, thus increasing the risk for traumatic
injury.
Decreased vascularity at the dermal/epidermal junction results in reduced homeostasis.
While it was once thought that sebum production decreased with aging, newer information
suggests that the sebum composition changes. These changes in sebum composition results in
less water coming to the skin surface.8

Nutrition - Improper nutrition, especially insufficient amounts of protein, fats, vitamins,

minerals, and water, can impede the skin's ability to repair itself. Wounds pose additional
challenges to a patient's nutritional status. Wounds can create a stress response within the
patient, resulting in catabolism, hypermetabolism, and decreased immune function. This
increased stress response requires increased nutritional requirements.
Medication - Prescription drugs may have detrimental effects on the skin. Steroids may be
associated with thinning of the skin. Several classes of medication, including antihypertensives,
tricyclic antidepressants, antihistamines and others, can increase the skin's sensitivity to sunlight.
Sensory perception - Poor sensory perception, such as that caused by diabetic neuropathy,
increases the risk of pressure ulcer development. Patients may not feel the discomfort that
signals the onset of tissue ischemia and the onset of skin breakdown and, thus, fail to reposition
themselves to reduce pressure.
Cognitive function - As mental status changes (due to medication or functional decline)
patients become unable to communicate their need for repositioning, toileting, or pain
management.
Mobility - Limited movement predisposes patients to pressure ulcers development, as they are
unable to reposition themselves to maintain adequate blood flow to the skin and underlying
structures.
Health status - Patients with diabetes or cardiovascular disease are more likely to develop
pressure ulcers. This can be due to decreased sensations and limited feelings of pain in the
extremities, or by vascular complications that do not permit sufficient blood flow to oxygenate
tissues.
Extrinsic Factors
Extrinsic factors refer to stresses placed on the skin by the patient's immediate surroundings and
may be altered by care providers of the patient themselves. These extrinsic factors include:
Pressure - Body weight or the weight of the skeleton on a pressure surface can reduce the
lumen of blood vessels between the resting surface and the bony prominence. This interrupts the
flow of blood, which delivers oxygen and other nutrients to the skin and leads to tissue hypoxia,
ischemia and breakdown.
Friction - Friction occurs when the patient's body - usually the elbows or heels - rub against a
rough surface, such as the sheet. This frequent rubbing causes sloughing of epidermal cells and
decrease in tissue strength.
Shear - Shear occurs when the head of the bed is raised. Although the skin and tissue remain
stationary, the body's skeleton is forced downward by gravity. This can twist and compress blood
vessels, depriving the skin of oxygen and nutrients leading to tissue ischemia and cell death.
In the bed bound patient, the combined forces of pressure,
friction and shear can lead to large areas of skin breakdown
especially in the sacral, ischeal and gluteal areas. The
following picture demonstrates this problem.

Moisture - Moisture softens skin and weakens its integrity,

causing it to break more easily. Effective management of
moisture, whether it is due to wound exudate, ostomy
fluids, perspiration or incontinence episodes, is essential to keep patients from developing
moisture related skin problems like maceration. Faecal incontinence also contributes to skin
breakdown due to enzymes present in feces, which alter the skin and are further stimulated by
the presences of urine. Moisture increases the skin's permeability to irritants and its susceptibility
to microorganisms, reduces the strength of the skin and increases damage due to friction and
abrasion, increasing the risk of forming an ulcer and can lead to denuded skin, maceration and/or
fungal infections.

Soap and water - Traditionally, soap & water have been used for incontinence care. The effects
of soap and water can put the skin at risk for further breakdown. Soap is alkaline and is not
easily rinsed, so a film residue may remain on the skin. The pH of the skin is acidic (4.5-5.5) and
the acid mantle helps deter the growth of unwanted bacteria.
Soap and other cleansers are made with surfactants, which remove dirt or debris from the skin.
Surfactants are either natural or synthetic. Soap is a natural surfactant and natural surfactants
remove the body's natural lipid layer, reducing the barrier function of the epidermis. 8,9
Prevention Guidelines and Recommendations
A program for the prevention of skin breakdown must be developed consistent with best-evidence
keeping in mind the unique needs of the patients, caregivers and care setting. The European and
American Guidelines have been developed to address the following considerations of patient care:

1.
2.
3.
4.

Risk assessment tools and risk factors

Tissue tolerance
Mechanical loading and support surfaces
Education

Risk assessment tools and risk factors

The goal for prevention of skin breakdown is to identify 'at risk' individuals needing prevention
and the specific factors placing them at risk.
Much has been written of the importance of assessing patients for their risk of developing
pressure ulcers. A number of tools have been developed, and undergone varying degrees of
testing and validation. The following is a partial list of available "Risk Assessment Tools":
Norton Scale
Knoll Scale
Waterlow Scale
Douglas Scale
Gosnell Scale
Braden Scale
The Braden Scale is an example of a tool that has been tested extensively in various care
settings. This scale is made up of six subscales that reflect sensory perception, skin moisture,
physical activity, nutritional intake, friction and shear, and the ability to change and control body
position. Each subscale is rated on a low to high scale.
Risk assessment tools are used to trigger timely and appropriate interventions to reduce the
incidence of tissue damage.5
Select and use a method of risk assessment. Whether you use pen and paper or a computer tool,
it is important that the tool is easy to use. Assess risk on admission and at regularly prescribed
intervals, according to acuity and practice setting. The primary caregivers should be familiar with
the signs of tissue damage as well as developing pressure ulcers. The following changes are
examples of tissue damage that should be addressed immediately.

Reddened or discolored (bluish or purplish) skin Such discolorations may represent a stage 1 pressure ulcer,
especially if accompanied by temperature change (warm or cool) or
changes in skin tone (firm or boggy).

Blistered heel - A blister on the

heel is evidence of tissue damage. If
the blister is a result of pressure, it
may be defined as a stage II
pressure ulcer.

Black heel - Keep all black heels off of the bed surface. A hard, black
covering or eschar, usually represents deep tissue damage. Black heels
must be assessed daily. Dry, intact eschar on the heel may be left in
place and monitored. Intervention is required if the eschar is fluctuant
(boggy) if exudate is present or advancing erythema. Arterial status
should be evaluated on any patient with evidence of tissue damage to
the lower extremities.

Skin tears - Excessive dryness

can contribute to skin tears, which provide an entry point
for microorganisms. Moisturizing the skin regularly to
replenish lost moisture may reduce the occurrence of skin
tears. When moving or repositioning patients, handle the
skin gently and use caution to avoid skin tears.7

Rashes - Rashes should be assessed for the presence of

fungal infection. All rashes should be evaluated and treated
appropriately.
Intervention
Assess and document skin condition on admission and at
regular intervals.
A head to toe skin assessment should be completed daily and
findings and interventions documented.
Maintaining Tissue Integrity

The goal is to maintain and improve tissue tolerance to pressure in order to prevent injury.
Assess and treat incontinence
One of the most significant threats to skin integrity is incontinence. Urinary incontinence is not a
normal age related change. Incontinence is frequently caused by reversible conditions such as a
urinary tract infection, fecal impaction and medications.
The AHRQ guideline recommends using tepid, not hot, water & mild cleansing agents that
maintain the acid mantle. Pat, do not rub the skin dry.
Non-detergent (or synthetic detergent) cleansers are milder than detergent soap. These products
contain synthetic surfactants, which decrease the complications associated with soap.
Non-Ionic Surfactant - While there are several types of surfactants, a non-ionic surfactant has low
toxicity potential and results in fewer skin irritations.
pH balanced, rather than alkaline products are desirable
Anti-microbial agents decrease odor-causing bacteria
Moisturisers help to condition the skin5
Prevent Dryness and Moisturize Dry Skin

Urine and fecal exposure is a primary contributor to dry skin which in turn, contributes to skin
breakdown and skin tears. Establishing a routine practice of moisturizing the skin, especially of
older adults, is a critical skin saving intervention.
No Vigorous Massage

Evidence suggests that this action may lead to underlying tissue damage.

Protect Skin from Moisture and Maceration

Excessively moist skin is more vulnerable to friction and shear injuries. The goal is to protect the
skin from excessive moisture. If the moisture is a result of perspiration, check often to make sure
that the patient is clean and dry. Ostomy effluent can be kept off the skin with an appropriate
pouching system. Wound exudate can be managed with an appropriate dressing. However, for
added protection, a protective ointment or paste may be beneficial on intact peri-wound skin to
prevent maceration. Finally, to protect the patient's skin from exposure to urine and/or feces,
select a protective cream, ointment or paste.
Microorganisms flourish in a warm moist environment. For this reason, fungal infections are
frequently seen surrounding the perineum, the perineal areas, and areas such as under the
breast and inguinal skin folds. The use of antibiotics, which alter normal skin flora, may
predispose patients to fungal infections. Other health problems such as diabetes or those that
leave the patient immunocompromised, can also increase patients' susceptibility to fungal
infections. The irritation caused by these infections leads to rapid skin breakdown.

Unprotected skin exposed to prolonged episodes

of moisture is at high risk for fungal infections.
Fungal infections are commonly caused by tinea
corporis, tinea cruris, and tinea pedis or candida
albicans (yeast). These superficial infections pose
a serious threat to skin integrity and can cause
burning and itching. Fungal infections, which
usually appear as red, irritated patches
accompanied by satellite lesions (lesions outside
the primary margin of the rash) and / or raised
vesicular pustules, should be treated promptly.

Skin care is an essential part of a preventive care plan.10 Knowing which ingredients are
important for good quality skin care products allows you to make the right decision when
choosing products. Also ask about available safety data on the products that you use. Most
importantly, establish a preventive skin care regimen, targeting patients at risk for skin
breakdown.
Nutritional Assessment
Nutritional status is a risk factor for the prevention and treatment of pressure ulcers. Those at
risk should have a comprehensive nutritional assessment, which may include a history and
physical exam, lab values, routine weights and an assessment of nutritional intake.
Lab Data
Common lab values for assessing protein stores are Albumin and Pre-Albumin levels. Albumin has
a half-life of 20 days or more and therefore may not reflect recent protein status. Remember, too,
that if the patient is dehydrated, Albumin values may be falsely elevated. Transferrin levels rely
on iron stores and may not be accurate if the patient is anaemic. Pre-Albumin, with a half-life of 3
to 5 days, may be the most reliable lab value for recent nutritional status. Other lab values may
include total protein or total lymphocyte count.
Nutritional Support
The goal of nutritional support is to restore and/or maintain lean body mass and to provide
enough energy and protein to meet the patient's needs. Identifying the need for nutritional
intervention early is crucial. It is more difficult to change the cascade of events with malnutrition
than to prevent it's occurrence.
Following assessment, nutritionally compromised individuals should have a plan of appropriate
support and/or supplementation that meets individual needs and is consistent with overall goals
of therapy.
All interventions and outcomes should be monitored and documented.

Mechanical Loading and Support Surfaces

The goal is to reduce the incidence of pressure ulcers through the use of a turning schedule and
support surfaces.
Mechanical forces that contribute to skin breakdown include pressure, friction and shear. Pressure
is one of the most common causes for skin breakdown. Pressure occurs when a localized area of
soft tissue is compressed between a bony prominence and an external surface, like the bed or
chair, diminishing or occluding blood flow to the area.
The amount of tissue damage is influenced by three factors:
1. Intensity of pressure - pressure may cause tissue damage in a short period of time.
2. Duration of pressure - Low pressure can cause tissue damage if applied over a longer time
period.
3. Tissue tolerance (the ability of the tissue to endure pressure).
Pressure Intensity Duration Curve
The period of time necessary for a pressure ulcer to develop will vary according to many intrinsic
and extrinsic factors. In this slide, the photograph of the skeleton, on the left, clearly illustrates
how much of our weight it supported by the ischial tuberosities when seated. You can also see the
prominence of the posterior trochanters. The photograph is a dramatic example of tissue damage
created over the ischial tuberosities and posterior trochanters.

Mechanical Forces: Friction and Shear

Friction is another significant factor in pressure ulcer development. Friction occurs as a result of
skin surfaces sliding against the surface on which the individual is resting (bed, chair, etc.) or
from skin sliding against skin causing damage to the epidermal and upper dermal layers. Shear
results from a combination of gravity (pushing down on the body) and friction (resistance)
between the patient and the surface. Shear exerts force parallel to the skin. For example, when a
supine patient is positioned with the head of the bed elevated, the body is pulled toward the foot
of the bed by gravity. Meanwhile the resistance of the bed surface attempts to hold the skin in
place. The result is shear.
Shear also occurs when a patient is pulled up in bed without a proper lifting technique.
Interventions to Reduce Pressure, Friction and Shear
Implement a Turning/Positioning Schedule
Turning is one intervention for reducing pressure. It is important to remember that even small
changes in position can help to redistribute pressure over bony prominences.
Turning is still important, even when the patient is on a special bed or mattress. The support
surface only reduces the intensity of the pressure. Turning reduces the amount of time spent on
that site. Turning is the only way to totally relieve a site of pressure. Changing position is also
important when the patient is in a chair.

Positioning To avoid high pressure on the hip area when positioning a patient on their side, the
patient should be positioned by arranging pillows below the scapula but above the sacrum. An
additional pillow is placed between the knees. This position simultaneously relieves pressure on
the trochanter and the sacrum and is the position of choice if the patient is lying for an extended
period of time.
A little more time may be required to position some patients . . . especially the first few times.
But taking the time is important.
Suspend ("Float") the Heels!
Suspend or "Float" the heels. If heels cannot touch the bed, they cannot develop pressure ulcers.
Pillows under the lower legs may work well. If patients will not keep their legs on the pillows, the
physical therapist, occupational therapist or the wound, ostomy, continence nurse may be able to
recommend special air- or gel-filled boots or splints. Remember that any products used on or
under the legs should be removed periodically as pressure on the calves can lead to venous stasis
and thrombosis. And make sure that you are instructed on the use of special boots or splints to
avoid creating pressure by incorrect use.
To Reduce Friction and Shear
1. Keep Head of Bed 30 degrees or less if not contraindicated by medical condition.
2. Lifting devices - use lift or draw sheets, allow patients to help lift (with trapeze, for example)
when possible. Do not encourage patient to "push with your heels" while lifting!
3. Use support surfaces that help to redistribute pressure.
Prevent Bottoming
Support surfaces must prevent bottoming. Bottoming occurs when the patient sinks into the
support surface until he/she rests on the standard mattress (for overlays) or on the bed frame
(for mattress replacements).
A simple hand check may be performed to assess for bottoming. Place your hand under the
support surface at bony prominence sites, (sacrum, coccyx, scapulae, trocanter, etc.). If you are
unable to slide your hand under the patient at these points, the patient has bottomed and the
support surface is not reducing/relieving pressure at that site.
Considerations for Seating
Postural alignment and weight distribution are important considerations for seating. Choose
chairs that fit the patient. Physical therapists may be helpful for wheelchair selection. The foot
rests should be low enough to allow the users thighs to help support the weight.
Balance and stability may be accomplished with special cushions. Pressure relief and reduction
products should be based on the patient's need.
Look for products that evenly distribute the patient's weight. Some examples include a foam
cushion, indicated for those at risk or low risk for pressure ulcer development.
Position patients and teach patients to position themselves so that parts of the chair (arm rests,
etc.) do not create pressure. Patients should be positioned so that they do not "bottom-out" on
air-filled cushions.
Teach wheelchair users to reposition themselves every 15 minutes. Those who are able should
lean side to side or push themselves up to relieve pressure. For patients who are unable to
reposition, caregivers must assist patients with repositioning.
Quadriplegic individuals may have someone tilt their chair back every hour to redistribute
pressure.
Education
The goal is to reduce the incidence of pressure ulcers through education.
The last section of the guideline focuses on education. To reduce the incidence of pressure ulcers,
everyone, including the one with the wound and their significant carers, need to be involved in
pressure ulcer prevention.

Sources of Educational Support

Journals
Seminars & Conferences
Internet
EPUAP Guideline
Others

Educational programs for the prevention of pressure damage should be structured, organized and
comprehensive, and made available at all levels of health care providers, patients and family or
caregivers.
The educational program for prevention of pressure damage should include information on the
following items:

Pathophysiology and risk factors for pressure damage.

Risk assessment tools and their application.
Skin assessment.
Selection and instruction in the use of pressure redistributing and other devices.
Development and implementation of individualized programs of care.
Principles of positioning to decrease risk of pressure damage.
Documentation of processes and patient outcome data.
Clarification of responsibilities for all concerned with this problem.
Health promotion.
Development and implementation of guidelines.

The educational program should be updated on a regular basis based on the best available
evidence. The content of the program should be modified according to the audience.
Improving Clinical Outcomes through "Early Intervention"
Prevention protocols have been shown to decrease the incidence of pressure ulcers in long-term
care facilities as well as acute care.
Reductions in the occurrence of skin breakdown were demonstrated in a 125-bed nursing home
that adopted a formalized preventive care program. The program was modelled after the
previously discussed guidelines and was implemented along with staff education. The residents
were assessed according to the Braden Scale at baseline and at 2-month increments throughout
the 8-month study. The occurrence of pressure ulcers fell 87% in the first 2 months of the
program's implementation and was 96% lower 8 months after program implementation than at
baseline.11
Pressure ulcers are often associated with high mortality rates because they can occur more
frequently in the frail, sick, and otherwise compromised patients. In the hospital setting,
mortality rates are significantly higher in patients who develop pressure ulcers. Compared with an
at-risk population, one study correlated the presence of pressure ulcers with a twofold increase in
mortality and the presence of a nonhealing ulcer with a three-fold increase in mortality.7
The association between pressure ulcers and mortality rates demonstrates the importance of a
preventive care program to overall patient health. Implementing a program may help to reduce
the incidence of pressure ulcers and associated mortality rates.
Summary
The implementation of a successful pressure ulcer prevention programme focuses on the role of
each caregiver and his or her ability to make a difference and improve patient care. Knowledge,
consistent education, and skin care products are vital tools that can help to motivate caregivers
to become involved and take ownership for patient care.
Quality of life benefits extend to patients and their families. Prevention of skin breakdown and
fewer pressure ulcers represent the core of prevention programs and equate to higher levels of
patient dignity and comfort. Prevention can also enhance family confidence about the caregivers
and facility.

The development and implementation of a comprehensive pressure ulcer prevention program is a

viable strategy to minimize the occurrence of pressure ulcers, and, as a result, reduce treatment
costs and improve the quality of life for residents and staff.