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the care of

wounds

A GUIDE FOR NURSES

FOURTH EDITION

Carol Dealey



The Care of Wounds

A Guide for Nurses

In memory of my husband

The Care of Wounds

A Guide for Nurses

FOURTH EDITION

Carol Dealey

PhD MA BSc (Hons) RGN RCNT
University Hospital Birmingham
NHS Foundation Trust and University of Birmingham, UK

This edition first published 2012 Ó 2012 by Carol Dealey

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Library of Congress Cataloging-in-Publication Data

Dealey, Carol.
The care of wounds : a guide for nurses / Carol Dealey. – 4th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN-13: 978-1-4051-9569-0 (pbk. : alk. paper)
ISBN-10: 1-4051-9569-X (pbk. : alk. paper)
I. Title.
[DNLM: 1. Wounds and Injuries–nursing. 2. Wound Healing–physiology. WY

154.2]
LC classification not assigned
617.1–dc23
2011032157

A catalogue record for this book is available from the British Library.

Set in 9.5/12.5pt Palatino by Thomson Digital, Noida, India

1 2012

Contents

Preface vii

1 The physiology of wound healing 1
Introduction 1
Definitions associated with wounds 1
The structure of the skin 2
Wound healing 3
Impaired wound healing 9
Conclusion 12

2 The management of patients with wounds 15
Introduction 15
Physical care 15
Psychological care 39
Spiritual care 45

3 General principles of wound management 61
Introduction 61
Wound assessment 61
Managing wounds 77
Documentation 85
Evaluating the dressing 86

4 Wound management products 93
Introduction 93
The development of dressings through the ages 93
Traditional techniques 100
The use of lotions 102
Clinically effective wound management products 108
Modern wound management products 110

5 The management of patients with chronic wounds 127
Introduction 127
The prevention and management of pressure ulcers 127
The management of leg ulcers 149
Diabetic foot ulcers 165
The management of fungating wounds 170

v

vi Contents 185
185
6 The management of patients with acute wounds 185
Introduction 199
The care of surgical wounds 205
Traumatic wounds 216
The burn injury
Radiation reactions 227
227
7 The organisation of wound management 227
Introduction 228
Managing wounds in the community 229
Nurse specialists in wound care 230
Multiprofessional wound care 230
Wound healing centres
Conclusions 233

Index

Preface

Since writing the previous edition of this book there have been many
developments in wound care, especially an increase in the number of
guidelines available to healthcare professionals. There is also increasing
recognition of the importance of multiprofessional working. The advances
in communication mean that we are much more aware of what is happening
around the world. I hope that I have reflected some of this in this new
edition of The Care of Wounds and that this book will be of use to those of you
providing care to patients with wounds.

Carol Dealey

vii



1 The Physiology of Wound
Healing

Introduction

Wound healing is a highly complex process. It is important that the nurse
has an understanding of the physiological processes involved for several
reasons:

l understanding the physiology of skin assists in understanding the
healing process;

l an understanding of the physiology of wound healing makes it possible
to recognise the abnormal;

l recognition of the stages of healing allows the selection of appropriate
dressings;

l understanding of the requirements of the healing process means
that appropriate nutrition can, as far as is possible, be given to the
patient.

Definitions associated with wounds

Any damage leading to a break in the continuity of the skin can be called a
wound. There are several causes of wounding:

l traumatic – mechanical, chemical, physical;
l intentional – surgery;
l ischaemia – e.g. arterial leg ulcer;
l pressure – e.g. pressure sore.

In both traumatic and intentional injury there is rupture of the blood
vessels, which results in bleeding followed by clot formation. In wounds
caused by ischaemia or pressure the blood supply is disrupted by local
occlusion of the microcirculation. Tissue necrosis follows and results in
ulcer formation, possibly with a necrotic eschar or scab.

The Care of Wounds: A Guide for Nurses, Fourth Edition. Carol Dealey.
Ó 2012 Carol Dealey. Published 2012 by John Wiley & Sons, Ltd.

1

2 Care of Wounds

Wounds in the skin, or deeper have been labelled in various ways. Some
of them can be described as follows.

(1) Partial- and full-thickness wounds
l A partial-thickness wound is one where some of the dermis
remains and there are shafts of hair follicles or sweat glands.
l In a full-thickness wound all the dermis is destroyed and deeper
layers may also be involved.

(2) Healing by first and second intention
l These definitions were first described by Hippocrates around
350 BC.
l Healing by first intention is when there is no tissue loss and the skin
edges are held in apposition to each other, such as a sutured
wound.
l Healing by second intention means a wound where there has been
tissue loss and the skin edges are far apart, such as a leg ulcer.

(3) Open and closed wounds
l These are the same as healing by second and first intention
respectively.

The structure of the skin

The skin is the largest and one of the most active organs of the body. It is
composed of two layers: the epidermis and dermis with the epidermis
forming the outer surface of the body and the dermis forming the deeper
layer of the skin. The main structures of the skin can be found in the dermis.
Figure 1.1 shows a cross-section of the skin.

Dermis

Dermis is composed of connective tissue, both collagen and elastic fibres,
which is both elastic and resilient and provides support for the structures in
the dermis. Blood vessels, lymph vessels, sensory nerve endings, sweat and
sebaceous glands and hair follicles can be found within the dermis. The
ducts of the glands and hair shafts pass through the epidermis to the skin
surface. Sweat glands have their own ducts opening on the skin surface, but
sebaceous glands open onto the hair follicles. The base or bulb of hair
follicles is sited deep into the dermis. They are lined with epithelial cells and
can play a role in the healing of partial-thickness wounds.

The surface of the dermis where it interlocks with the epidermis is
irregular with projections of cells called papillae. The base of the dermis is
less clearly defined as it blends into subcutaneous tissue, which contains
both connective tissue and adipose tissue and helps to anchor the skin to
muscle and bone.

The Physiology of Wound Healing 3

Dermal Epidermis
papillae Dermis

Sebaceous Pacinian
glands corpuscle
Hair root
Vein
Artery

Arrector Sweat
pili muscle gland

Figure 1.1 A cross-section of the skin

Epidermis

The epidermis comprises several layers of cells. The deepest layer is the
stratum basale and it is constantly producing new cells by cell division. These
cells are gradually pushed towards the skin surface taking about 7 weeks to
reach the surface. The stratum spinosum contains bundles of keratin fila-
ments, which hold the skin together. The top three layers of epidermis are
the stratum granulosum, which produces the precursor to keratin, the stratum
lucidum and the stratum corneum. As they move through the strata, the cells
gradually flatten and the protoplasm becomes replaced with keratin. The
cells in the stratum corneum are flat with no nucleus and are essentially dead
cells. They are constantly worn away and replaced by new cells moving to
the surface.

In addition the epidermis has cells called melanocytes, which contain
melanin that gives skin its colour. A high concentration of melanin pro-
duces a dark skin colour. Ultraviolet light increases melanin production.
This may occur naturally by sunlight resulting in a suntan or artificially
such as a treatment in dermatology.

Wound healing

The wound healing process consists of a series of highly complex interde-
pendent and overlapping stages. These stages have been given a variety of
names. They are described here as:

l inflammation;
l reconstruction;

4 Care of Wounds

l epithelialisation;
l maturation.

The stages last for variable lengths of time. Any stage may be prolonged
because of local factors such as ischaemia or lack of nutrients. The factors
that can delay healing are discussed in more detail in Chapter 2.

Inflammation

The inflammatory response is a non-specific local reaction to tissue damage
and/or bacterial invasion. It is an important part of the body’s defence
mechanisms and is an essential stage of the healing process. The signs of
inflammation were first described by Celsus, in the first century AD, as
redness, heat, pain and swelling. The factors causing them are shown in
Table 1.1.

When there is traumatic or intentional injury that causes damage to the
blood vessels, the first response is to stop the bleeding. This is achieved by a
combination of factors. First, by vasoconstriction that reduces the blood
flow and second by the release of a plasma protein called von Willebrand
factor from both endothelial cells and platelets, resulting in platelet aggre-
gation and formation of a platelet plug. The third factor is the initiation of
the clotting cascade and the development of a fibrin clot to reinforce the
platelet plug.

Hageman factor (factor XII in the clotting cascade) triggers both the
complement and kinin systems. The complement system consists of plasma
proteins, which are inactive precursors. When activated, there is a cascade
effect that leads to the release of histamine and serotonin from the mast cells
and results in vasodilation and increased capillary permeability. The
complement system also assists in attracting neutrophils to the wound.
The complement molecule, C3b, acts as an opsonin, that is, it assists in
binding neutrophils to bacteria. Five of the proteins activated during the
cascade process form the membrane attack complex, which has the ability
to directly destroy bacteria.

Table 1.1 The signs of inflammation

Signs and symptoms Physiological rationale

Redness Vasodilation results in large amount of blood in the area
Heat
Large amount of warm blood and heat energy produced by
Swelling metabolic reactions
Pain
Vasodilation and leakage of fluid into the wound area

May be caused by damage to nerve ends, activation of the
kinin system, pressure of fluid in the tissues or the pres-
ence of enzymes, such as prostaglandins, which cause
chemical irritation

The Physiology of Wound Healing 5

The effect of the complement system is enhanced by the kinin system,
which, through a series of steps, activates kininogen to bradykinin. Kinins
attract neutrophils to the wound, enhance phagocytosis and stimulate the
sensory nerve endings. The apparent delay in feeling pain after injury is
explained by the short time lag taken for the kinin system to be activated.

As the capillaries dilate and become more permeable, there is a flow of
fluid into the injured tissues. This fluid becomes the ‘inflammatory exudate’
and contains plasma proteins, antibodies, erythrocytes, leucocytes and
platelets. As well as being involved in clot formation, platelets also release
fibronectin and growth factors called platelet-derived growth factor
(PDGF) and transforming growth factor alpha and beta (TGFa and TGFb).
Their role is to promote cell migration and growth at the wound site.

Growth factors are a subclass of cytokines, proteins that are used for
cellular communication (Greenhalgh, 1996). The particular role of growth
factors is to stimulate cell proliferation. There are a number of growth
factors involved in the healing process, and they are listed in Table 1.2.
Some growth factors have been isolated and used as a treatment for chronic
wounds. This will be discussed in more detail in Chapter 4.

The first leucocyte to arrive at the wound is the neutrophil. Fibronectin
attracts neutrophils to the wound site, a process known as chemotaxis.
Neutrophils squeeze through the capillary walls into the tissues by dia-
pedesis, again this ability is enhanced by fibronectin. Within about an hour

Table 1.2 Growth factors involved in the healing process

Growth factor Abbreviation Action

Platelet-derived growth PDGF Chemotactic for neutrophils, fi-
factor broblasts and, possibly, mono-
cytes. Encourages proliferation
Transforming growth factor TGFa of fibroblasts
alpha TGFb
Stimulates angiogenesis
Transforming growth factor
beta Chemotactic for monocytes
(macrophages). Encourages
Fibroblast growth factor FGF angiogenesis. Regulates
Epidermal growth factor EGF inflammation
Insulin-like growth factors IGF-I, IGF-II
Stimulates fibroblast proliferation
Vascular endothelial growth VEGF and angiogenesis
factor
Stimulates the proliferation and
migration of epithelial cells

Promote protein synthesis and
fibroblast proliferation. Work in
combination with other growth
factors

Critical for angiogenesis and the
formation and growth of blood
vessels

6 Care of Wounds

of the inflammatory response being initiated, neutrophils can be found at
the wound site. They arrive in large numbers, their role being to phago-
cytose bacteria by engulfing and destroying them. Neutrophils decay
after phogocytosis as they are unable to regenerate the enzymes required
for this process. As the numbers of bacteria decline, so too, do the numbers
of neutrophils.

Transforming growth factor beta attracts monocytes to the wound where
they differentiate into macrophages. Fibronectin binds onto the surface
receptors on the cells promoting diapedesis and phagacytosis. Oxygen is
vital to this process and macrophages can be inactivated and their ability to
undertake phagocytosis reduced if the partial oxygen pressure falls below
30 mmHg (Cherry et al., 2000). Macrophages are larger than neutrophils and
so are able to phagocytose larger particles, such as necrotic debris, as well as
bacteria. The lifespan of the neutrophil can be a few hours or a few days.
When they die they are also phagocytosed by the macrophages.

T lymphocytes also migrate into the wound, although in smaller num-
bers than macrophages (Martin & Muir, 1990). They influence macrophage
phagocytic activity by the production of several macrophage-regulating
factors. They also produce colony-stimulating factors that encourage the
macrophage to produce a range of enzymes and cytokines. One such
substance is prostaglandins, which maintains vasodilation and capillary
permeability. It can be produced on demand to prolong the inflammatory
response if required. A study by Martin and Muir (1990) found that both
macrophages and lymphocytes are present in wounds from day 1, with
macrophages peaking between days 3 and 6 and lymphocytes between 8
and 14 days.

Mast cells play a supporting role in the healing process (Ng, 2010). They
produce a range of growth factors (PDGF and TGFb1), inflammatory
mediators interleukin 1 (IL-1), tumour necrosing factor alpha (TNFa)
and proteases (chymase and tryptase). Chymase and tryptase assist in
the breakdown of the extra-cellular matrix in anticipation of the phase
of reconstruction.

Inflammation lasts about 4–5 days. It requires both energy and nutri-
tional resources. In large wounds the requirements may be considerable. If
this stage is prolonged by irritation to the wound, such as infection, foreign
body or damage caused by the dressing, it can be debilitating to the patient
as well as delaying healing.

Reconstruction

The reconstruction phase is characterised by the development of granula-
tion tissue. It consists of a loose extracellular matrix of fibrin, fibrinectin,
collagen and hyaluronic acid and other glycosaminoglycans. Macrophages
and fibroblasts and the newly formed blood vessels can be found within this
matrix. Macrophages play a major role in this phase of healing. They

The Physiology of Wound Healing 7

produce PDGF and fibroblast growth factor (FGF), which are both chemo-
tactic to fibroblasts, attracting them to the wound and stimulating them to
divide and later to produce collagen fibres. Fibronectin has been shown to
play a role in enhancing fibroblast activity (Kwon et al., 2007). Collagen has
been seen in a new wound as early as the second day. Collagen fibres are
made up of chains of amino acids in a triple helix formation. There are a
number of different types of collagen characterised by different formations
of amino acids. Type III is present in the healing wound in greater
proportions than would normally be found in skin. Over time, this pro-
portion reduces in favour of higher levels of type I collagen.

Fibroblasts are key cells in this phase of healing (Harding et al., 2002). As
well as being responsible for the production of collagen, they also produce
the extracellular matrix, which is seen visually as granulation tissue.
Tryptase from the mast cells also supports deposition of collagen into the
extracellular matrix (Abe et al., 2002). As new extracellular matrix is
synthesised, the existing matrix is degraded by enzyme systems such as
matrix metalloproteinases (MMPs). There are a number of MMPs, in
particular MMP-1, MMP-2 and MMP-9, involved in the healing process,
although their role is imperfectly understood at present.

The activity of fibroblasts depends on the local oxygen supply. If the
tissues are poorly vascularised the wound will not heal well. The wound
surface has a relatively low oxygen tension, encouraging the macrophages
to produce TGFb and FGF, which instigates the process of angiogenesis, the
growth of new blood vessels. Undamaged capillaries beneath the wound
sprout buds, which grow towards the surface and loop over and back to the
capillary. The loops form a network within the wound supplying oxygen
and nutrients. Vascular endothelial growth factor (VEGF) produced within
the extracellular matrix is responsible for controlling blood vessel forma-
tion and growth (Schultz & Wysocki, 2009).

Some fibroblasts have a further role, they are involved in the process of
contraction. The exact process is not clearly understood and there are
currently two theories postulated: cell contraction and cell traction. The
theory of cell contraction is based on specialised fibroblasts known as
myofibroblasts and was proposed by Gabbiani et al. in 1973. Myofibroblasts
have a contractile apparatus, similar to that in smooth muscle cells. In in
vitro models, they have been shown to cause contraction of the wound.
Tomasek et al. (1989) found a higher level of contractile forces when a high
level of myofibroblasts was present. The concept of cell traction was put
forward by Stopak and Harris (1982), who demonstrated that fibroblasts
could contract collagen gels by a physical pull, resulting in a rearrangement
of the extracellular matrix. Dalton and Ehrlich (2008) reviewed the use of
fibroblast-populated collagen lattices to study the process of contraction. As
well as myofibroblasts and the concept of tractional forces they describe the
mechanism of cell elongation, which also can cause contraction provided
there is a high density of fibroblasts. In his review of the role of the mast cell,

8 Care of Wounds

Ng (2010) noted that mast cells also seem to be essential for wound
contraction. It must be noted that all these studies were undertaken in
vitro and there is no certainty that they could be repeated in vivo.

Whatever the actual process, contraction may start at around the fifth or
sixth day. It considerably reduces the surface area of open wounds. Irvin
(1987) suggests that contraction could be responsible for as much as 40–80%
of the closure. It is certainly of considerable importance in large cavity
wounds. However, in shallower wounds with a large surface area such as
burns, contraction may lead to contractures. Myofibroblasts disappear after
healing is completed.

In wounds healing by first intention, little can be seen of this stage of
healing. But in those healing by second intention, the granulation tissue can
be seen as it gradually fills the wound cavity. They are followed by capillary
buds growing towards the areas of low oxygen tension in the wound.

As the wound fills with new tissue and a capillary network is formed, the
numbers of macrophages and fibroblasts gradually reduce. This stage may
have started before the inflammation stage is completed and prolonged
inflammation can result in excessive granulation with hypertrophic scar-
ring. The length of time needed for reconstruction depends on the type and
size of wound, but may be about 24 days for wounds healing by first
intention.

Epithelialisation

This phase describes the phase whereby the wound is covered with
epithelial cells. Macrophages release epidermal growth factor (EGF), which
stimulates both the proliferation and migration of epithelial cells. Kerati-
nocytes at the wound margins and around hair follicle remnants synthesise
fibronectin, which forms a temporary matrix along which the cells migrate.
The cells move over the wound surface in a leapfrog fashion, the first cell
remaining on the wound surface and forming a new basement membrane.
When cells meet, either in the centre of the wound, forming islets of cells, or
at the margin, they stop. This is known as contact inhibition. Epithelial cells
only move over viable tissue and require a moist environment (Winter,
1962). In sutured wounds, epithelial cells also migrate along the suture
tracks. They are either pulled out with the sutures, or gradually disappear.

Once the cells stop moving on the wound surface, they start to recon-
stitute the basement membrane, which is essential in order for the
epidermis to ‘fix’ to the dermis. Until the basement membrane is fully
reconstituted it is easy for epithelial cells to be sheared off the wound
surface by mechanical forces (Cherry et al., 2000).

Epithelialisation commences as early as the second day in closed
wounds. However, in open wounds it is necessary for the wound cavity
to be filled with granulation tissue before it can commence. There is a very
variable time span for this stage.

The Physiology of Wound Healing 9

Maturation

During maturation the wound becomes less vascularised as there is a
reduction in the need to bring cells to the wound site. The collagen fibres
are reorganised so that, instead of being laid down in a random fashion,
they lie at right angles to the wound margins. During this process, collagen
is constantly degraded and new collagen synthesised. The highest level of
activity in this process occurs between days 14 and 21 (Cherry et al., 2000).
The scar tissue present is gradually remodelled and becomes comparable
with normal tissue after a long period of time. The scar gradually flattens to
a thin white line. This may take up to a year in closed wounds and very
much longer in open wounds.

Tensile strength gradually increases. This is a way of describing the
ability of the wound to resist rupture or dehiscence. Forester et al. (1969)
found that at 10 days an apparently well-healed surgical incision has little
strength. During maturation it increases so that by 3 months the tensile
strength is 50% that of normal tissue. Further work by Forester et al. (1970)
compared surgical incisions where the skin edges were held together by
tape with those where sutures were used. The findings showed that, when
tape was used, the wounds regained 90% strength of normal tissue,
whereas sutured wounds only regained 70% strength.

Impaired wound healing

Although the majority of wounds heal without problem, impaired healing
may sometimes occur. Some of the different types of impaired healing are
described here. Their management will be discussed elsewhere.

Hypertrophic scars

Hypertrophic scars are more common after traumatic injury, especially
large burns. They occur shortly after the injury or surgery and remain
limited to the area of the injury. They are raised scars with increases in
pigmentation, vascularity and pliability (Oliviera et al., 2009). However,
they will generally flatten out with time; about 1–2 years.

Van der Veer et al. (2009) suggest that an overabundant production of
extracellular matrix results in hypertrophic scars that can easily be recog-
nised by their stiffness and rough texture and their colour mismatch. They
reviewed all possible activity at the cellular and molecular level to identify
any potential causes of this type of scarring and concluded that a number of
factors were involved including an increase in the levels of fibronectin,
histamine, TGFb, PDGF, MMPs, IL-4 and IL-13. The impact of this is
increased proliferation of fibroblasts and extracellular matrix deposition
and reduced collagen breakdown. However, it must be noted that it is still

10 Care of Wounds

uncertain whether these changes are the cause or effect of scar formation
(Van der Veer et al., 2009).

Oliviera et al. (2009) compared the levels of types I and III collagen in
hypertrophic and normal scars of male children with burns of over 40% of
total body surface area. Scars on the thigh following deep burns were
studied at 12, 18 and 24 months. Wound biopsies were taken and the
collagen levels measured. They found that there was a higher level of
accumulation of type III collagen in the deep dermal layer of the skin in the
hypertrophic scars when compared with normal scars. There was no
difference in type I collagen.

Keloids

Keloids are similar to hypertrophic scars in that they are also the result of an
excessive fibrous response. Keloids take some time to form and may occur
years after the initial injury. They can range in size from small papules to
large pendulous growths (Munro, 1995). Keloids more commonly occur in
individuals aged between 10 and 30 years (Cosman et al., 1961) and in those
with a darker skin (Placik & Lewis, 1992). Unfortunately, unlike hypertro-
phic scars, keloids do not gradually flatten out.

Within keloids there are increased levels of collagen and glycosamino-
glycan deposition within the extracellular matrix with the collagen pre-
senting as thickened whorls of collagen bundles laid down in a very
haphazard manner (Robles et al., 2007). The precise pathogenesis is still
unknown, although overexpression of a number of growth factors such as
PDGF, TGFa and TGFb has been identified. In normal healing, there is a
negative feedback system to reduce fibroblast proliferation as healing
completes. It is proposed that this negative feedback mechanism is deficient
in keloidal fibroblasts, allowing scar formation to persist (Robles et al.,
2007). Ogawa (2008) has proposed an alternative theory that keloids
arise because of a mechanoreceptor or a mechanosensor disorder and
that mechanical force or stretching of the skin may be a major causative
factor.

Contractures

Wound contraction is part of the normal healing process, but occasionally
contraction will continue after re-epithelialisation has occurred resulting in
scar contraction (Tredget et al., 1997). Contractures can occur in any wound,
but they are more likely if there is delayed healing or in burns (Lee & Clark,
2003). There can be considerable restriction of movement if contractures
occur over a joint.

Hildebrand et al. (2008) used an animal model to study cellular changes
in the presence of contractures and found raised levels of myofibroblasts,
TGFb, MMP-1 and MMP-13 as well as reduced levels tissue inhibitor of

The Physiology of Wound Healing 11

metalloproteinases (TIMPs) and changes in collagen structure. The signif-
icance of these changes has yet to be ascertained.

Acute to chronic wounds

Chronic wounds may be called chronic because their underlying aetiology
makes healing a very long process. A good example is the venous leg ulcer.
However, some chronic wounds may have originally been acute wounds
that have failed to heal over a long period of time, perhaps years. The
original factor delaying healing may have been related to infection or local
irritation, perhaps caused by a suture. Once these problems have been
resolved the wound still fails to heal causing considerable misery to the
patient.

The differences between acute and chronic wounds are still imperfectly
understood. However, work by Phillips et al. (1998) did shed some light on
the problem. They used cultured fibroblasts from human neonatal foreskin
as a plated laboratory model and treated them with either chronic wound
fluid (CWF) or bovine serum albumen (the control). They found that CWF
inhibited the growth of the fibroblasts quite dramatically. The researchers
concluded that this study gave some indication of how the microenviron-
ment of a chronic wound has a negative effect on the healing wound. As
result of this work, other research groups have looked at wound exudate in
more detail.

Trengrove et al. (1999) used wound fluid from venous leg ulcers at both
non-healing and healing stages to measure MMP levels. They found
elevated levels of MMPs at the non-healing stage, which decreased signif-
icantly as the ulcers started to heal (p ¼ 0.01) The levels of MMPs in the
healing ulcers were similar to those in acute wounds, thus suggesting that
failure to heal may be linked to excessive matrix degradation. Ladwig et al.
(2002) collected wound fluid from 56 pressure ulcers and found lower levels
of MMP-9 in those ulcers that went on to heal well compared with those that
healed poorly.

Trengrove et al. (2000) undertook further studies of wound exudate from
non-healing and healing leg ulcers. They found significantly higher con-
centrations of a number of pro-inflammatory cytokines or growth factors in
the non-healing ulcers. They consider that wound healing is delayed in
chronic wounds because of an impairment of inflammatory mediators
rather than any deficit of growth factors.

Subramaniam et al. (2008) compared wound fluid from non-healing
venous leg ulcers, mastectomy wounds and donor sites to determine MMP
levels, TIMPs levels and fibroblast activity. They found a significantly
higher level of MMP-1 and MMP-3 production by dermal fibroblasts in
the chronic venous leg ulcer fluid compared with the acute wound fluid.
There was variation in TIMP-1 levels as the level was very low in both the
chronic leg ulcer fluid and the acute graft sites and high in the acute

12 Care of Wounds

mastectomy fluid. The authors concluded that this could be the result of
several variables including the types of wounds and the methods used to
collect the wound fluid. Further research s required to obtain greater
understanding.

Premature ageing of fibroblasts may also be a problem. Mendez et al.
(1998) investigated the characteristics of fibroblasts cultured from chronic
venous ulcers and found signs of accelerated ageing or senescence in these
cells. Senescent fibroblasts have reduced mobility, are less able to replicate,
have abnormal protein production and do not respond well to growth
factors. A small study of seven patients by Stanley and Osler (2001)
compared the senescence rates in fibroblasts taken from chronic venous
ulcers with fibroblasts taken from punch biopsies taken from the proximal
thigh of the same patient. They found a significantly higher senescence rate
in the fibroblasts from the leg ulcers (p ¼ 0.0001). Wall et al. (2008) found
that fibroblasts exposed to chronic wound fluid had a decreased ability to
withstand oxidative stress resulting in premature senescence. Telgenhoff
and Shroot (2005) suggest this is related to the chronic inflammation found
in chronic wounds.

Conclusion

This chapter has described ’normal’ physiology. However, not all wounds
heal without complication or delay and some of the differences between
acute and chronic wound healing have been discussed. But many factors
can affect the healing process and they will be considered in more detail in
Chapter 2.

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2 The Management of Patients
with Wounds

Introduction

This chapter looks at the assessment of the patient with a wound and how
appropriate care may be planned and evaluated. When caring for patients
with wounds of all types it is important to take a holistic approach to their
care, considering physical, psychological and spiritual care as they are
inextricably linked. There are many factors that can affect the healing
process but if they are taken into account when taking a history and
assessing the patient it may be possible to mitigate some of the effects.
Nursing interventions are not able to resolve every problem, for example,
age. Where nursing interventions can be effective, appropriate strategies
are suggested.

Physical care

Nutrition

The precise relationship between wound healing and nutrition remains
uncertain (Williams & Barbul, 2003). There is increasing evidence that
nutritional deficit impairs healing, such as the study by Legendre et al.
(2008) that compared 41 patients with leg ulcers with 43 controls (derma-
tology patients without leg ulcers). The research group found a significantly
higher incidence of protein deficiency in the leg ulcer group (27% compared
with 2% in controls). Protein deficiency was also independently associated
with increase in ulcer size at 12 weeks and the occurrence of wound
complications. A number of other studies have identified the impact of
malnutrition on the healing of surgical wounds, burns and pressure ulcers
(Haydock & Hill 1986; Andel et al., 2003; Mathus-Vliegen 2004). The
importance of nutrition in relation to pressure ulcer prevention and man-
agement is highlighted by the inclusion of the topic in the international
guidelines developed by the National Pressure Ulcer Advisory Panel and
the European Pressure Ulcer Advisory Panel (NPUAP/EPUAP, 2009).

The Care of Wounds: A Guide for Nurses, Fourth Edition. Carol Dealey.
Ó 2012 Carol Dealey. Published 2012 by John Wiley & Sons, Ltd.

15

16 Care of Wounds

Malnutrition is a pathological state that results from a relative or
absolute deficiency or excess of one or more essential nutrients. As protein
or carbohydrates are used in the largest quantities, they are usually the
deficient nutrients. This is referred to as protein–energy malnutrition or
PEM. In her Notes on Nursing, What it is and What it is Not, Florence
Nightingale said ‘Every careful observer of the sick will agree in this, that
thousands of patients are annually starved in the midst of plenty, from want
of attention to the ways which alone make it possible for them to take food’
(Nightingale, 1859/1974). A century and a half later this statement is still
true. A national nutrition screening survey was undertaken in the UK in
2007 in 175 hospitals, 173 care homes and 22 mental health units. A total of
9336 hospital patients were assessed and 28% were found to be malnour-
ished compared with care homes where 30% of the 1610 residents assessed
were malnourished and 19% of the 332 adults in mental health units
(Russell & Elia, 2007). A review of malnutrition surveys in hospitalised
children undertaken over a 10-year period in several different countries
(Germany, France, UK and USA) found a prevalence of malnutrition
ranging from 6.1 to 14% whereas in Turkey a prevalence of up to 32% was
found in two hospitals (Koen et al., 2008).

Overall, malnutrition is seldom recognised in hospital patients although
it has a major impact on morbidity and mortality (Pablo et al., 2003). Correia
and Waitzberg (2003) undertook multivariate analysis of the impact of
malnutrition on adult hospital patients and found mortality increased to
12.4% compared with 4.7% in the well nourished. Hospital costs increased
up to 308.9%. The EuroOOPS study monitored the clinical outcomes in 5051
patients across 26 hospitals in 12 countries in Europe and the Middle
East. They found that those identified as being at nutritional risk had
significantly higher complication rates, length of stay and mortality rates
(Sorensen et al., 2008). Older patients are at particular risk of malnutrition.
Guigoz et al. (2002) identified malnutrition in 20% of hospitalised patients
in a survey of more than 10,000 elderly Swiss people in the community,
nursing homes and hospitals. Similar results were found in a Spanish study
of hospital patients where 18.2% of patients had severe malnutrition
(Cereceda et al., 2003).

Nutritional status

The initial causes of malnutrition may be related to debilitating disease,
especially of the gastrointestinal tract, old age, poverty or ignorance. Once
admitted to hospital, other factors become relevant. An early study by
Hamilton Smith (1972) found that patients are starved for up to 12 hours
prior to surgery and for varying lengths of time afterwards. Chapman
(1996) showed little had changed in over 20 years. She found that patients
fasted for periods ranging from 4 to 29 hours. National guidelines in the UK
suggest that patients should have a 6-hour fasting period for food, but may

The Management of Patients with Wounds 17

have clear fluids up until 2 hours before their operation (Royal College of
Nursing (RCN), 2005). A survey of anaesthetists in five northern-European
countries found that the majority also followed this guidance (Hannemann
et al., 2006). However, its implementation may be far from perfect. A small
qualitative study of 15 nurses found that the ritualistic practice of fasting
from midnight was so deeply embedded into practice that it was difficult to
change it (Woodhouse, 2006). Although such a small study is not neces-
sarily generalisable to all areas, its findings may well resonate with others.

A long period of pre-operative starvation serves to compound the effects
of trauma and surgery, both of which cause marked catabolism. Demling
(2009) has described how a hypermetabolic–catabolic state can be seen after
injury and which, if left uncontrolled can lead to rapid loss of lean body
mass (LBM). A LBM loss of 20% will reduce the body’s ability to heal and the
wound will stop healing altogether with a loss of 30% or more (Demling,
2009). Miller and Btaiche (2009) describe how a negative nitrogen balance
results in poor wound healing and delayed patient recovery. Although
some patients will return to a normal diet fairly quickly and so redress the
balance, others will receive only intravenous fluids. A litre of dextrose 5%
contains approximately 150 calories and normal saline does not contain any
at all. These fluids obviously do not provide adequate calories to meet the
body’s requirements.

Burn patients are particularly vulnerable as they have been shown to
develop a higher metabolic rate than other critically ill or injured patients
(Lee et al., 2005). It may be exacerbated by pre-existing malnutrition. A
survey of 123 elderly burn patients found that 61% had pre-existing
malnutrition at the time of injury and, compared with well-nourished burn
patients in the same age group, they suffered slower healing, a significant
increase in infection and an increase in length of stay (Demling, 2005).
Adequate nutrition is therefore essential for burn patients, but there is
uncertainty as to the optimal time for commencing nutrition therapy. A
systematic review by Wasiak et al. (2007) compared early enteral support
(within 24 hours of injury) with late feeding (after 25 hours of injury). In the
five small studies included in the review there appeared to be some
promising results for early nutrition, but insufficient evidence to provide
clear guidance on the subject. Enhanced enteral nutrition has also been
used, for example in a study by Taylor (1999) of 106 burn patients who
received enhanced enteral nutrition (50% of energy and nitrogen require-
ments). There was a significantly greater incidence of infection and length
of hospital stay when there was a delay of 24 hours in commencing the
enhanced nutrition treatment.

It is the nurses’ responsibility to see that their patients have an adequate
diet and there has been much discussion of the topic in recent years (Patel &
Martin, 2008). Anecdotal evidence has described how patients have their
meal times disrupted by medical ward rounds or by being away from the
ward undergoing investigations as well as food being placed out of their

18 Care of Wounds

reach. However, several audits provide more specific information about the
causes of inadequate nutritional care. Kondrup et al. (2002) conducted a
study of 740 randomly selected patients in 3 hospitals in Denmark and
assessed their nutritional risk. A total 167 (23%) were found to be at risk and
their intake was monitored. Altogether 77 of these patients were in hospital
for more than a week and only 25% actually had a minimum of their
nutritional requirement met. Analysis of the reasons for this inadequate
feeding identified a lack of local guidelines and insufficient nursing knowl-
edge of nutrition. There were also problems with the suitability of the food
provided to patients many of whom suffered from loss of appetite. A
further study by the same research group questioned 4512 doctors and
nurses interested in nutrition from Denmark, Sweden and Norway about
their knowledge of nutritional practice (Mowe et al., 2008). The research
team found that the respondents lacked sufficient knowledge to be able to
adequately screen patients on admission, assess undernourished patients
or to be able to initiate nutritional support.

Hamilton et al. (2002) audited nutritional provision for elderly patients in
community hospitals in the UK. Analysis of the meals provided in a 14-day
cycle found they were inadequate for energy, fibre and vitamin D. The
portion sizes were small especially the protein element and many patients
did not receive the snacks they required. It should also be noted that the
patients were positive about many aspects of their meals and the assistance
they received from the nurses. Patel and Martin (2008) also addressed
the issues around nutrition in elderly patients and studied 100 elderly
patients in an inner-city teaching hospital. Altogether 425 assessments
were made of these patients and the authors identified that on 285 (67%)
occasions these patients were eating inadequately. They found that acute
illness, anorexia and oral problems were most common early in the hospital
stay. Other problems that they identified were confusion, mood/anxiety
disturbances, catering limitations and dysphagia. When compared with
well-nourished patients, it was found the malnourished individuals were
more likely to have oral problems and anorexia. The authors suggest that
detailed assessment of patients would allow nurses to more effectively
target the particularly vulnerable patients and ensure they have an im-
proved nutritional intake.

It is important to identify those who are malnourished in order that
appropriate steps can be taken to improve their nutritional status. A
number of screening tools have been developed and some have been
widely validated. One such is the Mini-Nutritional Assessment Tool
(MNA), which has been used to assess elderly patients with leg ulceration
(Wissing & Unosson, 2001). The first part of the MNA is a screening tool that
identifies those who require more detailed assessment. The second part
allows the assessor to identify those at risk of malnutrition and those who
are actually malnourished, allowing the healthcare professional to develop
an appropriate plan of care.

The Management of Patients with Wounds 19

The British Association for Parenteral and Enteral Nutrition (BAPEN)
launched the ‘MUST’ screening tool in 2003 (Elia & Stratton, 2004). It is a five-
step tool that has been validated to use with adults of all ages in both hospital
and community settings. It allows the assessor to determine if a patient is at
low, medium or high risk of malnutrition and provides appropriate man-
agement guidelines, depending on whether the patient is in hospital, a care
home or the community. The guidance also provides information on how to
calculate height for a patient who cannot be measured in the usual way.
Further information can be obtained from www.bapen.org.uk.

Hunt (1997) and her colleagues have devised a nutritional assessment
tool that considers various factors that can affect nutritional status. It was
devised with patients with wounds in mind. Patients are assessed accord-
ing to their mental condition, weight, appetite, ability to eat, gut function,
medical condition including chronic wounds and age. The tool provides a
score that indicates whether the patient is nutritionally at risk. Use of a
screening tool can be helpful in identifying those less obviously at risk of
poor nutritional status than those discussed above.

Nursing interventions

The nutritional needs for each individual varies according to their age,
gender, activity and the severity of any illness. If a patient has been assessed
as having a reduced nutritional status or falls into a high-risk category, then
his nutritional intake should be very carefully monitored. Each patient
requires sufficient nutrients to support his basal metabolic rate, his level of
activity and the metabolic response to trauma. Patients with heavily
exuding wounds, such as fistulae or leg ulcers, may lose large amounts
of protein without it being realised. Table 2.1 shows the nutrients required
for wound healing and their sources.

The dietician will be able to help in assessing individual needs, so that
very specific individualised goals can be set. If a patient is being cared for at
home, the carer must also be involved. Many patients will eat better at
home, where they can eat what they want, when they want to. Elderly
people may have special problems or needs. One problem may be devel-
oping disability. The occupational therapist can give guidance on adapting
cooking equipment. Another problem may be lack of education as to what
constitutes a ’good’ diet. Patel and Martin (2008) identified poor dentition or
mouth ulcers as common factors in poor nutritional intake. A new set of
teeth may be all that is needed to allow an elderly person to maintain an
adequate nutritional status.

There are a number of nutrition guidelines available to support clinical
practice, for example the European Society for Clinical Nutrition and
Metabolism (ESPEN) has produced guidance on managing the patient
journey through enteral nutritional care (Howard et al., 2006). Enteral
nutrition is the ideal route for nutritional provision and oral nutritional

20 Care of Wounds

Table 2.1 The nutrients required for healing

Nutrient RDAÃ Food source Contribution

Carbohydrates 1600–3350 kcals Wholemeal bread, wholegrain Energy for leucocyte,
cereals, potatoes, (refined macrophage and fibroblast
carbohydrates are seen function
as ‘empty’ calories)

Protein 42–84 g Meat, fish, eggs, cheese, Immune response,
pulses, wholegrain cereals phagocytosis, angiogenesis,
fibroblast proliferation, collagen
synthesis, wound remodelling

Fats 1–2% kcals Dairy products, vegetable oil, Provision of energy, formation of

oily fish, nuts new cells

Vitamin A 750 mg Carrots, spinach, broccoli, Collagen synthesis and cross-
apricots, melon linking, tensile strength of wound

B Complex 3 mg Meat (especially liver) dairy Immune response, collagen
products, fish cross-linking, tensile strength of
wound

Vitamin C 30 mg fruit and vegetables (but easily Collagen synthesis, wound
lost in cooking) tensile strength, neutrophil
function, macrophage migration,
immune response

Vitamin E Vegetable oils, cereals, eggs Appears to reduce tissue dam-
age from free radical formation

Copper Shellfish, liver, meat, bread Collagen synthesis, leucocyte
formation

Iron 10–12 mg Meat (especially offal), eggs, Collagen synthesis, oxygen

dried fruit delivery

Zinc 12–15 mg Oysters, meat, whole cereals, Enhances cell proliferation,

cheese increases epithelialisation,

improves collagen strength

ÃThese recommended daily amounts (RDAs) are the requirements in a healthy individual and may need
to be increased (see text).

supplements and tube feeding can be used to supplement patients’ diet
until such time that they are able to eat normally. The guidelines from the
National Institute for Health and Clinical Excellence (NICE) include par-
enteral as well as enteral nutrition (NICE, 2006). Parenteral nutrition may be
used for patients who are unable to tolerate an enteral intake for whatever
reason. Nutrients need to be prescribed on an individual basis and should
be introduced cautiously for those who are critically ill or seriously injured.
Burn patients need very specific management and Prelack et al. (2007) have
provided practical guidelines for nutritional management not just in the
initial stages of injury but also in the recovery phase.

Monitoring outcomes

Evaluation of outcomes may be achieved by regular weighing of the
patient and re-assessment using a nutritional screening tool, for example

The Management of Patients with Wounds 21

Gazzotti et al. (2003) used weighing and MNA to assess the outcome of a
randomised trial to determine the effectiveness of nutritional supplements
in preventing malnutrition.

Infection

Consideration of infection must include both systemic and localised wound
infection. There is limited knowledge about the precise impact of sepsis on
wound healing and what knowledge there is has been mostly gained from
animal studies. Rico et al. (2002) found that despite infected mice having
raised white blood cell and neutrophil counts peripherally, there were
significantly lower levels in their wounds. The study team also examined
the collagen levels re-epithelialisation rates and found them to be signif-
icantly lower in the experimental group compared with controls. Healing
may not take place until after the body has dealt with the infection. In
addition, systemic infection is frequently associated with pyrexia. Pyrexia
causes an increase in the metabolic rate, thus increasing catabolism or tissue
breakdown. Infection in a burn wound further increases the metabolic rate
and thereby increases the time with a negative nitrogen balance.

All wounds are contaminated with bacteria, especially open wounds.
This does not affect healing. However, clinical infection will certainly do so.
A review by White et al. (2006) suggests several ways in which bacterial
virulence factors can have an impact on wound healing:

l bacteria consume the nutrients and oxygen required for wound repair;
l virulent bacteria damage the extracellular matrix;
l anaerobic bacteria impair white cell function;
l oxygen-free radicals increase in numbers and disrupt the balance

between matrix metalloproteinases (MMPs) and tissue inhibitor of
metalloproteinases (TIMPs);
l the ability of fibroblasts to produce collagen is inhibited and any
collagen produced is disorganised.

Recently there has been research into the role of biofilms in wound
infection. Biofilms are complex structures that are created when bacteria
attach themselves to the wound surface and then surround themselves with
a protective polymeric matrix (Bjarnsholt et al., 2008). More than one type of
bacteria can be present in a biofilm, including anaerobic bacteria not found
by cultures from wound swabs (James et al., 2008). In their study of biofilms
in acute and chronic wounds James et al. (2008) found them to be present in
only 1/16 of acute wounds (6%) in comparison with 30/50 of chronic
wounds (60%). Clinical signs of a biofilm infection include an infection that
has lasted more than 30 days and seems to wax and wane. It may appear to
respond to antibiotics only to recur when the course is completed (Wolcott
et al., 2010b). Wound swabs are ineffective in identifying biofilms but

22 Care of Wounds

molecular diagnositics have been used successfully in specialised centres
(Wolcott et al., 2010a).

Some patients are more vulnerable than others to wound infection.
Research undertaken looking at surgical wounds has identified a number
of factors that increase the risk of developing a wound infection. These
studies have been reviewed and then summarised in the NICE Clinical
Guidelines on Surgical Site Infection (National Collaborating Centre (NCC) for
Women’s and Children’s Health, 2008). They are discussed below.

Age
A review of five studies found age to be a significant independent predictor
of the risk of surgical site infection (SSI). The reviewers also found a direct
linear trend of increasing risk with increasing age (NCC for Women’s and
Children’s Health, 2008).

Underlying illness
Severity of illness can be measured by using a classification developed by
the American Society of Anesthiologists (ASA) that gives a score of one for
those deemed normal healthy individuals moving through to a score of six
for those declared to be brain-dead whose organs are being removed for
donor purposes (ASA, 2002). The reviewers found for studies that indicated
that an ASA score of three or above was significantly associated with SSI
development (NCC for Women’s and Children’s Health, 2008). In addition,
diabetes has been found as an independent indicator for SSI in a number of
studies, for example Olsen et al. (2008) undertook a 5-year case–control
study of patients undergoing spinal surgery and, using multivariate anal-
ysis, they found that diabetes was an independent risk factor for SSI. (See
also section on Diabetes mellitus.)

Obesity
Obesity was found to be an independent risk factor (p ¼ 0.009) for super-
ficial SSI in a retrospective multivariate analysis of 3174 patients under-
going spinal surgery (Pull ter Gunne & Cohen, 2009). Similarly, a 5-year
surveillance programme of 2338 patients undergoing breast surgery for
cancer found obesity to be one of the risk factors for SSI (Vilar-Compte et al.,
2009). Other studies have found an increased risk of SSI in obese patients in
a wide range of surgical procedures including liver transplantation, cor-
onary artery bypass graft and breast reconstruction, (Schaeffer et al., 2009;
Russo & Spelman, 2002; Pinsolle et al., 2006).

Nutritional status
Poor nutrition increases the infection risk. A survey of 7035 patients with
SSI following general or vascular surgery found that pre-operative albumen
levels of 3.5 g/dl was an independent risk factor for SSI (Neumayer et al.,
2007). (See also section on Nutrition.)

The Management of Patients with Wounds 23

Smoking
Smoking has been shown to cause vasoconstriction (see also section on
smoking) and has been identified as an independent risk factor in the
review undertaken by for the NICE guidelines (NCC for Women’s and
Children’s Health, 2008). For example, Neumayer et al. (2007) in their study
of 7035 SSIs found smoking to be an independent risk factor.

Special risks
Irradiation, chemotherapy and steroids, cause greatly increased infection
rates and have been identified as independent risk factors by Pinsolle et al.
(2006), Neumayer et al. (2007) and Vilar-Compte et al. (2009).

Length of pre-operative stay
The longer anyone is in hospital the more chance there is that the patient’s
skin becomes colonised by bacteria against which the patient has no
resistance. A pre-operative stay over 4 days was found to be an independent
risk factor by de Boer et al. (1999), Herruzo-Cabrera et al. (2004) and Kaya
et al. (2006).

Shave
It is impossible to carry out a shave without causing injury to the skin.
Bacteria flourish and multiply rapidly in these minute cuts. Mishriki et al.
(1990) and Moro et al. (1996) found shaving to be a significant factor in the
development of infection. Mishriki et al. suggest that this is particularly so
when contaminated and dirty procedures are undertaken and bacteria are
shed on the skin. It is generally recommended that if a patient needs to be
shaved pre-operatively, it should be done just prior to surgery.

Type of surgery
Infection rates are much higher in some types of surgery than others. This is
discussed in more detail in Chapter 6. The appearance of infected wounds
will be discussed in Chapter 3.

Nursing interventions

The prevention of infection is the responsibility of all healthcare profes-
sionals. There are both general and specific measures that can be taken.
Most health authorities have infection control policies that provide guide-
lines both for the prevention of infection and to reduce the risk of cross-
infection. The infection control team, especially infection control nurses can
give advice and support.

Guidelines are a useful source of information. The Epic 2: National
Evidence-Based Guidelines for Preventing Healthcare-Associated Infections in
NHS Hospitals in England (Pratt et al., 2007) were commissioned by the UK

24 Care of Wounds

Department of Health. It is intended that these guidelines are incorporated
into local protocols. A major section of the guidelines covers hand hygiene.

The simplest and most effective measure to prevent infection is
good hand hygiene, especially as the spread of infection is mostly by
people from people. Cross-transmission has been found to be a major
factor in infection threats in hospitals (Pratt et al., 2001). Although the focus
is on hospitals, good hand hygiene is also required in the community as
many of the patients have complex care needs and are vulnerable to
infection (Nazarko, 2009).

Following a national prevalence survey of healthcare acquired infections
(HCAI) in Ireland, Creedon et al. (2008) undertook an observational study of
compliance with hand hygiene guidelines in four hospitals. They found
that the hospital with the poorest compliance with the guidelines also had a
higher prevalence of HCAI in the national survey than the other three.
Jenner et al. (2006) observed the hand hygiene of 71 healthcare professionals
on two medical and two surgical wards and then compared the findings
with those of a questionnaire assessing attitudes and self-reported behav-
iour of the same group of professionals. The results showed that despite
there being a high correlation between self-reported behaviour and inten-
tion in the questionnaires, the reality of practice was very different with
hand hygiene being undertaken on only 100 occasions of the 642 times when
it should have occurred. Education can improve compliance with guide-
lines as demonstrated by Creedon (2006) who found that a compliance rate
of 51% increased to 83% following an educational intervention. However, it
should be noted that the educational event was supported by the intro-
duction of alcohol hand rub by each patient’s bed.

The studies discussed above do not take into consideration the role of
the patient in cross-transmission. They also potentially touch hospital
equipment and share bathroom and toilet facilities with other patients.
Nurses have a responsibility to assist patients with their hand hygiene
when necessary. A survey by Burnett (2009) of clinical ward nurses in a
teaching hospital found that the majority (99.8% (n ¼ 442)) considered
patient hand hygiene to be important in preventing the transmission of
infection. Their self-reported behaviour did not always reflect this with 57%
(n ¼ 251) reporting that they ‘sometimes’ forgot to encourage patients to
wash their hands.

The national guidelines (Pratt et al., 2007) state that: ‘Hands must
be decontaminated immediately before each and every episode of
direct patient contact/care and after any activity or contact that potentially
results in hands becoming contaminated’. The systematic review under-
pinning the guidelines did not find good evidence to support the general
use of antiseptic hand washing agents over soap and they concluded
that choice of the method of decontamination should depend on assessment
of: what is appropriate for the episode of care; what is available and what
is practicable.

The Management of Patients with Wounds 25

l Hands that are obviously soiled or could be grossly contaminated must
be washed in soap and water.

l Hands should be decontaminated between patients or between differ-
ent care activities for the same patients. An alcohol-based handrub is
recommended.

l Hands should be washed with soap and water after several consecutive
applications of alcohol handrub.

In addition to hand hygiene, gloves and plastic aprons should be worn
when undertaking procedures involving non-intact skin such as wound
care (Pratt et al., 2007). Both items should be for single use and removed as
soon as the procedure is completed. Ideally hands should be washed with
soap and water after removal.

Smoking

There is increasing evidence that smoking has a deleterious effect on the
healing wound. One prospective study of 4855 patients undergoing gas-
trointestinal surgery found that smokers had a 64% higher risk of SSI and an
80% greater risk of wound dehiscence (Sorensen et al., 2005). The same
group studied the impact of abstinence from smoking on healing of
experimental incisional wounds in healthy individuals. They compared
never-smokers with smokers randomised to either continue smoking or
abstinence from smoking for a 4-week period. They found a significantly
higher incidence of wound infection in the smokers compared with the
never-smokers (12% v. 2%, p < 0.05). They also found there was a significant
reduction in infection in the abstinent smokers compared with continuous
smokers (Sorensen et al., 2003).

Manassa et al. (2003) undertook a retrospective study of 132 patients
undergoing abdominoplasty and compared outcomes for smokers and non-
smokers. They found a significantly higher incidence of wound complica-
tions for smokers including wound dehiscence (47.9% v. 14.8%, p < 0.01).
Increased infection and wound breakdown have also been identified in
other types of surgery such as cardiac surgery and breast construction and
reduction (Bartsch et al., 2007; Booi et al., 2007; Steingrimsson et al., 2009).

An in-vitro study by Ejaz et al. (2009) found cigarette smoke condensate
severely disrupted angiogenesis and there was deterioration of the extra-
cellular matrix. Sorensen et al. (2009) found a two-fold higher level of
MMP-8 in wound fluid of smokers compared with never smokers; MMP-8
is a neutrophil collagenase and contributes to increased collagen degrada-
tion. The research team also found delayed epidermal healing and an
altered inflammatory response.

A more recent study by Sorensen et al. (2010) used a similar methodology
for 78 healthy volunteers who received repeated punch biopsies at weeks 1,
4, 8 and 12 of a 13-week study. The researchers found that inflammation was

26 Care of Wounds

initially impaired among the smokers, but for the smokers who were
randomised to abstinence the level of inflammation rose to the same level
as the never-smokers after 4 weeks. However, abstinence did not reverse
the reduction in fibroblast activity and inhibition of collagen production.
They conclude that it is possible to reduce the incidence of wound infection
with pre-operative smoking cessation and their findings explain why
cessation does not reduce the incidence of wound dehiscence.

Smoking may also act as an appetite depressant. Smokers have been
found to be deficient in vitamins B1, B6, B12 and C. Smoking reduces
subcutaneous oxygen tension significantly for up to 30–45 minutes after
each cigarette. However, most studies in this area have been undertaken
looking at surgical wounds and there is little information regarding smok-
ing and chronic wound healing (Sorensen, 2003).

Nursing interventions

Nurses can play a significant role in both educating patients in the harmful
effects of smoking on a healing wound and encouraging them to abstain
over the peri-operative period. Prescription of nicotine patches may also be
helpful for some patients. Additional support from help-lines and other
agencies may also be beneficial.

Diabetes mellitus

Both type 1 and type 2 diabetes have been shown to be associated with
delayed healing and also a higher level of infection compared with the
general population (Patel, 2008). King (2001) suggested infection occurs
because high glucose levels encourage proliferation of bacteria. There are,
however, a number of other problems that may be encountered in people
with diabetes with deep wounds such as surgical incisions. They may be
encountered through each stage of the healing process.

l Signs of inflammation may be limited because of a thickened basement
membrane causes a rigidity that prevents vasodilation (Renwick et al.,
1998).

l In addition, high glucose levels make erythrocytes, platelets and leu-
cocytes more adhesive and they tend to stick together filling the vascular
lumen (Alberti & Press, 1992).

l There is decreased phagocytosis and poor chemotactic response in
neutrophils that Ochoa et al. (2007) suggest is because of alterations in
the chemokine system.

l Chbinou and Frenette (2004) found reduced levels of neutrophils,
macrophages and angiogenesis in a diabetic animal model

l Several studies have demonstrated that diabetics have abnormal fibro-
blasts with reduced capacity for proliferation and collagen synthesis.

The Management of Patients with Wounds 27

This results in abnormal cross-linking of collagen and reduced wound
contraction, further prolonging the healing process (Loughlin & Arlett,
2009).
l An in vitro study found that MMP-2 and MMP-9 were both down-
regulated in hyperglycaemic conditions, which the research team
believed to be linked to reduced keratinocyte activity resulting in
reduced migration and proliferation and inadequate re-epithelialisation
(Lan et al., 2008).
l Also, people with diabetes deal with the stress of wounding (trauma or
surgery) by producing increased levels of glucagons, cortisol and
growth hormone leading to raised levels of blood glucose and an
increased need for insulin. If this situation is not corrected the patient
can become catabolic. Left untreated, the body will start to break down
proteins and fats, ultimately resulting in a state of negative nitrogen
balance (Rosenberg, 1990).

Nursing interventions

In planned procedures it is possible to ensure that the patient is adequately
prepared and the diabetes well controlled. Obviously this is not possible
when a patient suffers traumatic injury. In either event during any period of
fasting the greatest risk is from hypoglycaemia and it may be necessary
to commence a dextrose intravenous infusion. In the immediate post-
operative or post-injury period the patient is at considerable risk of
hyperglycaemia as a result of the stress of the event. Perkins (2004)
discussed this problem in relation to critically ill patients, in particular the
danger of intensive insulin therapy resulting in hypoglycaemia. She pro-
posed that effective interventions could only be achieved by effective
multiprofessional teamwork and agreement of planned actions or protocols.
Such an agreement would need to consider the frequency of monitoring for
blood glucose and the level at which insulin therapy would be commenced.
Perkins describes the regime that was set for the critically ill trauma patient:
2-hourly monitoring with insulin therapy set to commence if blood glucose
levels rose above 7 mmol/l. Insulin was to be administered according to a
sliding scale in order to ensure titration. American guidelines suggest the
use of an insulin intravenous infusion is in order to provide tight glucose
control (Patel, 2008). Obviously, this level of intervention is not necessary
or appropriate for every patient, but the principle of team working and
developing agreed planned action can be applied to any situation where
diabetic control is challenged because of stress.

The physical effects of stress

Stress has a physiological effect. Stimulated by the release of adrenalin,
a primary biochemical change in stress is an increased secretion of

28 Care of Wounds

adrenocorticotrophic hormone (ACTH), which stimulates production of
adrenal cortex hormones. In particular, ACTH regulates production of
glucocorticoids, cortisol and hydrocortisone. Glucocorticoids cause the
breakdown of body stores to glucose, raising blood sugar. They cause a
reduction in the mobility of granulocytes and macrophages, impeding their
migration to the wound. In effect this suppresses the immune system and
reduces the inflammatory response. Glucocorticoids also increase protein
breakdown and nitrogen excretion, which inhibits the regeneration of
endothelial cells and delays collagen synthesis.

Kiecolt-Glaser and colleagues (2005) studied 42 healthy married couples
who were given suction blister wounds and then assessed for healing
following either a social interaction or a discussion resulting in conflict.
They found that the wounds healed more slowly after the conflict discus-
sions that the social interaction. The researchers also found that there were
higher levels of the pro-inflammatory cytokines interleukin-6 (IL-6) and
tumour necrosing factor alpha (TNFa) in the wound fluid following conflict
suggesting that stress prolongs inflammation (Kiecolt-Glaser et al., 2005).
There also seems to be an increased risk of wound infection in a stressed
patient (Kiecolt-Glaser et al., 2002). An animal model study found a
significantly higher incidence of opportunistic infection compared with
the control group as well a 30% rate of delayed healing (Rojas et al., 2002).
Jones et al. (2006) assessed 190 patients with chronic venous leg ulcers for
anxiety and depression and found that high scores for anxiety or depression
were most commonly associated with pain and malodour. A great number
of factors can cause stress and they will be discussed throughout the rest of
this chapter.

Pain

Pain and stress are closely related because pain can increase stress and
stress increase pain (Augustin & Maier, 2003). Fear of pain can cause much
anxiety to patients. Pracek et al. (1995) found that procedural pain expe-
rienced by burn patients in the early stages of their admission could be a
causal factor in their ability to adjust after discharge. The greater the pain
levels, the poorer the adjustment. Soon and Acton (2006) suggested that
persistent wound pain is not only distressing but will ultimately result in
psychological problems.

Vuolo (2009) described three types of wound pain: nociceptive, neuro-
pathic and emotional. Nociceptive pain occurs as a result of tissue damage
and it can be persistent and may be described as gnawing or aching with
tenderness (Coutts et al., 2008). Neuropathic pain is caused by nerve injury
and patients may use words such as stabbing, burning, stinging or shooting
sensation to describe it (Coutts et al., 2008). Emotional pain may occur
because of the psychological impact of the wound maybe because of the

The Management of Patients with Wounds 29

impact on body image or physical problems because of odour or leaking
exudate (Vuolo, 2009).

There has been increasing recognition of the effect of pain on patients
with chronic wounds. Gu€nes (2008) studied 47 patients with pressure
ulcers and found that 44 (94.6%) had pain from their ulcer. Those with
more severe pressure ulcers described their pain as ‘horrible’.
Basic activities such as walking, standing or climbing stairs can increase
chronic wound pain (Woo & Sibbald, 2008). A large international survey of
2018 patients with chronic wounds was undertaken across 15 countries
and found that 31.1% had pain ‘quite often’ and 36.6% had pain ‘most’ or
‘all of the time’ (Price et al., 2008). The survey also addressed pain intensity
and found that patients with leg ulcers or burns had the greatest
pain intensity. The authors found that 64% of the patients surveyed
were taking medication for their pain and of these, 82% found it effective,
which they noted to be higher than that found in previous studies
(Price et al., 2008).

A small study of women undergoing gastric bypass surgery found
evidence of an association between pain and delayed wound healing.
Seventeen women were studied for 5 weeks for post-operative pain inten-
sity and subsequent healing of a punch biopsy wound. The researchers
found a significant association between greater wound pain and delayed
healing of the punch biopsy (McGuire et al., 2006).

Procedural pain such as pain caused by dressing change can be
very stressful for patients. Apart from the actual pain caused by the
procedure, they may become stressed and anxious anticipating the
pain (Woo & Sibbald, 2008). In the survey by Price et al. (2008) 40.3%
said that pain at dressing changes was the worst part of living with
an ulcer.

There is a wealth of evidence that lack of adequate pain control is
common. A recent paper by Macpherson and Aarons (2009) examined
barriers to effective pain relief in the Caribbean and concluded that they
were similar to those found elsewhere in the world namely:

l patient and family attitudes;
l inadequate knowledge or care provision by healthcare professionals;
l organisational factors.

Patient and family attitudes

Many older patients see pain as something that happens as they get older
and that they should just live with it. There is also a fear among all age
groups of becoming addicted to analgesia (Bell & Duffy, 2009). In addition,
many patients may be passive recipients of pain relief, in other words they
wait to be asked if they have pain. Manias et al. (2006) observed patients’

30 Care of Wounds

decision-making strategies for managing their post-operative pain and
found that this passive approach included waiting to be asked, refusing
analgesia even when in pain and postponing analgesia until later. It was
the most frequent strategy employed by patients and was more than twice
as common as problem-solving with the nurse to plan pain control. The
least common strategy was active negotiation by the patient to ask for pain
relief and to select one of the solutions proposed by the nurse.

Inadequate knowledge or care provision by
healthcare professionals

Macpherson and Aarons (2009) suggest that nurses and other healthcare
professionals have inadequate education about pain management.
Although this may be true to a varying extent in different countries, nurses’
attitudes also need to be taken into consideration. In their review, Bell and
Duffy (2009) identified several barriers to effective pain relief raised by
nurses: they were too busy; too concerned with the task in hand; they
believed that patients should expect pain and often underestimated the
level of pain. Dihle et al. (2006) undertook observations in surgical wards
and conducted in-depth interviews with some of the nurses and found
considerable discrepancy between what the nurses said they did and what
they actually did. They found that the nurses had theoretical knowledge,
but did not always seem to translate it into the clinical setting. Both Dihle
et al. (2006) and Manias et al. (2006) found there was limited use of pain
scales despite the considerable amount of research that has been under-
taken demonstrating their usefulness. Dihle et al. (2006) also noted that very
little re-assessment of patients took place following analgesia to determine
its effectiveness. This finding is supported by an observational study by
Bucknall et al. (2007) that set out to determine when and how nurses re-
assessed post-operative pain after analgesia. They concluded that there was
an extraordinary lack of re-assessment undertaken by nurses.

Organisation factors

Bell and Duffy (2009) suggest that time management is a major barrier to
effective pain management. Nurses are constantly interrupted by telephone
calls, assisting doctors, dealing with patient admissions and discharges and
searching for equipment (Manias et al., 2006). Even when nurses were acting
to manage pain effectively, there could be delays because medication
needed to be prescribed by a doctor or obtained from the pharmacy.

Parsons (1992) gave an overview of studies of cultural aspects of pain and
concluded that definitions of pain by both the sufferer and carer are shaped
by cultural beliefs. In some cultures free expression of feelings of pain is
expected whereas in others it is unacceptable. There needs to be recognition
of these cultural differences in order to manage pain successfully.

The Management of Patients with Wounds 31

Effective pain management

Coutts et al. (2008) described the ABCD guide for the management of
wound pain:

A ¼ assess the pain;
B ¼ be aware of the cause;
C ¼ consider local treatment;
D ¼ do we need systemic treatment?

A: assess the pain
Pain is very personal and the only person who truly understands it is the
patient. Woo et al. (2008) suggest that it is best to assume that all patients
with chronic wounds have pain unless they indicate otherwise. Coutts et al.
(2008) suggested it is useful to ask the patient how much the pain has an
impact on everyday life such as its impact on sleep, mobility or appetite. It is
also useful to know how long the pain has been present and if it is present
continuously and, if not, when it starts. The Royal College of Physicians has
provided a useful algorithm on assessment in their guidance on assessing
pain in older people including those with cognitive impairment (Royal
College of Physicians, 2007).

Other information that is needed as part of the pain assessment is to
understand the level of pain intensity and what words the patient uses
to describe the pain. A number of scales have been developed to assess
pain intensity. Most of them involve a numerical rating where the
highest score is the worst pain imaginable and the lowest (usually zero)
is no pain. Figure 2.1 shows a pain scale that also includes a list of words
to assist patients in selecting the best descriptor for their pain. Where
patients are unable to communicate with staff about their pain other
methods of assessment are required. This might include observing
facial expressions and body movements (Royal College of Physicians,
2007). Li et al. (2008) reviewed assessment tools available to patients in
critical care. They concluded that the Behavioural Pain Scale and the
Critical-Care Pain Observation Tool showed validity and reliability
but there was a need for a more rigorous evaluation to determine
their robustness.

In the Wound Pain Management Model (Price et al., 2007) the authors
have produced a guide for wound pain assessment and management that
has four levels: wound assessment, local wound management, wound pain
assessment and wound pain management. The first two will be considered
in Chapter 3 and their proposed wound pain assessment is summarised
in Figure 2.2.

Good record keeping of the assessment is essential as a starting
point to enable a treatment plan to be developed and to monitor
its effectiveness.

32 Care of Wounds

Numbers corresponding Words to describe pain
to severity of pain
Match the word(s) that apply to your
Excrutiating pain 10 pain with a number in the ruler which
(no control) 9 corresponds to the severity of your
8 pain.
Extreme Pain Draw an arrow from the word to the
(disabling) number, or tell the nurse.
prevents you doing
your usual activities tender
crushing
7 squeezing
stabbing
Moderate pain 6 sharp
5 burning
feels like an electric shock
throbbing
cramping
dull
sore
aching
gnawing
feels like a weight pressure
a discomfort

4

3

2

Slight pain 1
No pain 0

Figure 2.1 A pain chart (from Bourbonnais, 1981, reproduced with permission)

B: be aware of the cause
Most wounds cause pain to a greater or lesser extent and treatment of the
underlying aetiology and promotion of healing will assist in alleviating
pain. In addition, wound infection or skin problems associated with the
wound will cause increased pain. Identifying such problems is essential
both to promote healing and reduce pain. These issues are discussed in
greater detail in later chapters of this book.

The Management of Patients with Wounds 33

Wound Pain
Assessment

Location Duration Intensity Description QoL/daily
activities
Within or
around Days/weeks/ Use pain Nociceptive Sleep
wound months assessment or disturbance
tools e.g. VAS, neuropathic
Referred Persistent or descriptive Mood/anxiety/
pain temporary questionnaire depression
Check
functional Mobility
limitation
Appetite

Figure 2.2 Wound pain assessment (adapted from Wound Pain Management
Model (Price et al., 2007); reproduced with permission). QoL, quality of life; VAS,
Visual analogue scale

C: consider local treatment
Local treatment for pain may be more appropriate than systemic treatments
as they reduce the risk of side-effects (Coutts et al., 2008). A number of
different strategies can be employed including the use of moist wound
dressings, dressings that contain analgesia and topical analgesics. They will
be discussed in detail in Chapter 4.

D: do we need systemic treatment?
Systemic treatment will be needed for large traumatic wounds, burn injury
and surgical wounds. It will also be needed for patients with chronic
wounds for whom local treatment has been found to be ineffective.
Specific pain management protocols may be in place for some wound
types. The World Health Organization pain relief ladder was originally
developed for cancer pain, but is widely used for all types of pain. It uses
three steps that move from non-opioids through weak opioids and on to
strong opioids and uses adjuvant therapies such as muscle relaxants or
steroids to enhance the effect of the analgesia (http://www.who.int/
cancer/palliative/painladder/en/). Price et al. (2007) also suggest that
tricyclic antidepressants or anticonvulsants may be more appropriate for
neuropathic pain.

Effective pain management will only be achieved by careful initial
assessment and ongoing re-evaluation of the effectiveness of the plan
of care.

34 Care of Wounds

Sleeping

Most people consider sleep to be important as it provides a sense of
refreshment and well-being. In recent years there has been considerable
research on sleep and its effects. Sleep deprivation causes people to become
increasingly irritable and irrational (Carter, 1985). They may complain of
lassitude and loss of feelings of well-being. The sleep–activity cycle is part
of the circadian rhythms. During wakefulness the body is in a state of
catabolism. Hormones such as catecholamine and cortisol are released.
They encourage tissue degradation to provide energy for activity, in
particular, protein degradation occurs in muscle.

Growth hormone is secreted from the anterior pituitary during sleep and
stimulates protein synthesis and the proliferation of a variety of cells
including fibroblasts and endothelial cells (Lee & Stotts, 1990). Rose et al.
(2001) reviewed the impact of burn injury on the sleep patterns of children
and the need to aggressively treat growth hormone insufficiency. They
speculate that improved sleep would improve growth hormone levels.
However, Brandenberger et al. (2000) argue that the body is able to
compensate during the day and the levels of growth hormone secreted
over 24 hours remain much the same, regardless of any sleep deprivation.

There has been some reliance on animal studies to determine the impact
of sleep deprivation and the surrogate measure, noise, on wound healing.
Wysocki (1996) measured the impact of noise on wound healing and found
that wounds healed more slowly compared with the controls. Two studies
of wound healing seem to have contradictory results: Gu€mu€stekin et al.
(2004) found that sleep deprivation may delay wound healing; whereas
Mostaghimi et al. (2005) found the reverse, that sleep deprivation appeared
to make no difference to healing rates. It should be noted that these studies
were undertaken on basically healthy animals and the findings may not be
transferable to sick humans. Further studies, especially clinical studies, are
needed to clarify the matter.

There is considerable evidence that sleep patterns are disturbed in
hospital. A study exploring the experiences of older men in hospital found
that patients were expected to fit in with the nurses work schedule rather
than being able to follow their usual sleep routines (Lee et al., 2007). Also,
many patients are disturbed during the night, especially in the critical care
unit. A review by Patel et al. (2008) noted that ventilated patients have been
found to have up to 74 arousals and awakenings per hour. Friese et al. (2007)
monitored the sleep patterns of 16 patients in a surgical critical care unit.
They found that the patients had a mean of 8.2 hours sleep (standard
deviation (s.d.) ¼ 6.53) but that it was highly fragmented. Measurement of
the stages of sleep showed that approximately 96% of sleep time was in
superficial sleep and very little was actually the deep sleep of rapid eye
movement (REM) sleep. Freedman et al. (1999) surveyed 203 patients
immediately after discharge from different types of intensive care units

The Management of Patients with Wounds 35

and found that poor sleep quality was common to all intensive care units.
They also found that sleep disruption was caused by human interventions,
diagnostic testing and environmental noise. A further study from the same
research centre investigated the impact of environmental noise on sleep.
The sleep patterns of 22 medical patients in an intensive care unit were
monitored for 24–48 hours continuously. Patients were found to sleep for
short periods throughout a 24-hour time period with a mean number of
sleep periods of 41 Æ 28 and the mean length of a sleep nap was 15 Æ 9
minutes. Overall, environmental noise was responsible for only 17% of
sleep disturbances (Freedman et al., 2001).

Other factors may also disturb sleep as shown in a survey by Southwell
and Wistow (1995) of 454 patients and 129 nurses across a variety of wards
in three hospitals. Half the patients had difficulty in sleeping through the
nights and did not get as much sleep as they wished. Many of the patients
complained that the ward was too hot and the mattresses were uncom-
fortable and they disliked having plastic covers on both mattresses and
pillows. Pain and worry were also likely to make sleeping more difficult. A
variety of factors were found to disturb sleep including: other patients
making a noise, nurses attending other patients, telephones ringing, lights
in the ward, nurses talking to each other or to patients, having treatment
including medication, toilets flushing or commodes being used, nurses
shoes making a noise. Christensen (2005) measured noise on a surgical
ward and found that it did dip to reasonable levels at night time, but that
25% of the human noise came from the nurses’ station. Nurses appeared to
be unaware of the level of noise they made and the impact it had on the
patients’ psychological and physiological well-being.

Sleep-Enhancing interventions

Richardson et al. (2009) introduced a sleep promotion guideline on three
wards in a teaching hospital. It included strategies such as turning tele-
phone volume down or to vibrate at night and encouraging patients to use
ear plugs or eye masks. After introduction of the guideline and a relevant
education programme they found a significant reduction in peak noise
levels although not in average noise levels.

Hospital routines can disrupt normal sleep patterns. The lights of a ward
may go off late, around 23.00 hours and come on again at 06.00 hours
(Southwell & Wistow, 1995). Patients are woken for their drugs and a drink.
It seems not unreasonable for more flexibility be introduced with a reduc-
tion of the 06.00-hour drug round to a minimum and an arrangement not to
wake those who would prefer to sleep later. Jarman et al. (2002) experi-
mented with flexible morning and evening medication times and found
that patients were able to sleep for longer. It should be possible, with careful
planning, to provide an environment that is conducive to sleep and a
patient who is comfortable and able to benefit from it.

36 Care of Wounds

Some people find their sleep disrupted because of pain. This may be
acute pain following trauma or surgery or a more chronic pain relating to a
long-standing illness or condition. Adequate pain control is essential. Pain
is a resolvable problem (see also section on Pain). The position of patients
may affect their comfort. It is helpful to ensure that the patient is in a
comfortable position, with a bell close to hand.

During the night, many fears that are suppressed during the day come to
the surface. Sleep may be disturbed because of a particular anxiety. Night-
time is a quieter time on the ward. It may provide an opportunity for the
nurse to sit and listen and allow patients to express their fears and anxieties.
Once this has happened, the patient may be able to return to normal
sleep patterns.

Hypothermia

Anaesthesia for major surgery can result in hypothermia as a result of
decreased metabolic rate and impaired thermoregulation (Sellden, 2002).
There is increased understanding of the impact even mild levels of intra-
operative hypothermia can have on post-operative recovery.

Mahoney and Odom (1999) reviewed the outcome costs for mildly
hypothermic patients compared with normothermic patients undergoing
a range of operations. They were able to pool the findings of the studies and
undertake a meta-analysis. They found that mildly hypothermic patients
were more likely to require blood transfusions and to develop wound
infections and the cost of these adverse outcomes ranged between $2500
and $7000. Flores-Maldonado et al. (2001) studied a prospective cohort of
290 surgical patients and found that mild peri-operative hypothermia was
significantly associated with SSI. Similar results were found by Walz et al.
(2006) in a study of 1446 patients following bowel surgery.

Qadan et al. (2009) studied the evidence relating to the impact of
hypothermia on the wound and noted that hypothermia causes vasocon-
striction in the skin in order to reduce heat loss, but also has the side-effect of
causing wound hypoxia. In addition, hypothermia inhibits T-cell mediated
antibody production and neutrophil activity thus reducing the ability to
counter the bacterial challenge posed by the surgery. Using an in vitro
model, the research team found that hypothermia significantly depressed
monocyte activity, delayed clearance of TNFa and increased the release
of IL-10. Again this has the result of reducing the ability to respond to
bacterial invasion.

Plattner et al. (2000) tested an experimental warming bandage system
and compared it with conventional gauze with elastic adhesive in
40 normothermic patients following elective abdominal surgery. The ex-
perimental bandage consisted of an adhesive shell and a foam frame
surrounding a clear window. A heated card was inserted into the frame
approximately 1 cm above the wound surface and left in situ for 2 hours at a

The Management of Patients with Wounds 37

time. Oxygen tension was measured via a probe inserted 2–3 cm laterally to
the incision. Their results were unexpected. They found that the oxygen
tension was considerably lower in those receiving conventional dressings
because of the pressure exerted by the elastic strapping. The warming
device did not appear to benefit normothermic patients particularly,
although it had potential for use for hypothermic patients.

Peri-operative hypothermia is associated with a higher incidence of
wound infection. This is of particular relevance in surgery where there is
already a high risk of infection such as abdominal surgery. It is less likely to
be important in surgery with a low risk of infection, such as neurosurgery.
There are also occasions when cooling the patient is appropriate during
surgery such as during craniotomy.

Steroids

Glucocorticoids or corticosteroids are widely used in the treatment of
inflammatory diseases. Although they produce effective anti-inflammatory
outcomes, this can have a serious impact on wound healing. A review by
Anstead (1998) has highlighted the fact that glucocorticoids affect every
stage of the healing process. This includes overall effects such as the
increased risk of infection and dehiscence in surgical wounds, although
this is probably dose dependent. Grunbine et al. (1998) studied 73 patients
who had had a steroid injection following surgery to the foot or ankle and
compared the outcome with those who did not. The use of a single dose of
steroids made no difference to healing rates.

Anstead (1998) summarised the effects of glucocorticoids on wound
healing as follows.

l Inflammation is suppressed because of a reduction in the numbers of
neutrophils and macrophages and an impaired ability to digest phago-
cytosed material.

l Wound contracture is poor as a result of inhibition of fibroblast
proliferation.

l There is reduced wound strength as collagen structure and cross-
linking are affected.

l Epithelialisation is delayed and the cells are thin, producing a weak
wound covering.

A study by Stojadinovic et al. (2007) explored the genomic effects of
glucocorticoids on cultured human keratinocytes in an in vitro study. They
found that glucocorticoids inhibited cell motility and also the expression of
pro-angiogenic factor and vascular endothelial growth factor. They also
found glucocorticoids suppressed production of transforming growth
factor beta (TGFb1 and 2) and MMP-1, -2, -9 and -10 and encouraged
production of TIMP-2.

38 Care of Wounds

There has been some interest in the potential of vitamin A to counteract
the unwanted side-effects of glucosteroids. Vitamin A has been found to
restore a normal inflammatory response (Ehrlich et al., 1972) and also
epithelial regeneration, fibroblast proliferation and collagen content (Talas
et al., 2003). A more recent study suggests that androstenediol, an immune-
regulating hormone, can reverse the effects of glucocorticoids in wound
healing (Feeser et al., 2009). However, both of these products have only been
tested using animal models and clinical trials are needed to confirm
the findings.

Radiotherapy

Radiation effectively destroys cancer cells as they are more radio-sensitive
than normal cells. A dose high enough to kill cancer cells does not affect the
surrounding cells. Using radiotherapy as an adjuvant treatment to surgery
has been shown to have beneficial outcomes in tumour downstaging
(Marks et al., 2009). Radiotherapy is sometimes given before surgery to
shrink the tumour and make it easier to remove and sometimes after
surgery to eradicate all traces of cancer cells. However, an unwelcome
side-effect is the impact on the healing surgical wound. For example,
Bullard et al. (2005) found that there was a significantly higher incidence
of wound complications for patients with rectal cancer who were treated
with radiotherapy as well as undergoing surgery.

The timing of radiotherapy in relation to surgery seems to be a
factor in the incidence of wound healing complications. Lin et al. (2001)
found a history of radiotherapy was a factor in wound healing complica-
tions of breast reconstruction. Similar results were found by Wang et al.
(2003) and O’Sullivan et al., (2002), when comparing pre- and post-
operative radiotherapy. Both studies found a significantly higher rate
of wound healing complications when radiotherapy was given
pre-operatively.

Akudugu et al. (2006) studied 46 cancer patients undergoing surgery. A
total of 28 patients received pre-operative radiotherapy and the remaining
18 patients acted as the control group. Wound complications were found in
8 (29%) of the radiotherapy group compared with none in the control group.
A larger study of a cohort of 216 head and neck cancer patients was
undertaken by Halle at al (2009). They found those having pre-operative
radiotherapy had a significantly higher incidence of total and partial flap
failures compared with those who did not. They also found that there was a
significant linear trend to increasing numbers of flap failures when there
was a gap of more than 6 weeks between the last dose of radiotherapy and
surgery. Marks et al. (2009) also found similar results in a group of 62
patients with rectal cancer. They found a wound complication rate of 25.6%
(11 patients) in the radiotherapy group compared with 0% in the non-
radiotherapy group.

The Management of Patients with Wounds 39

The conclusions of these research groups were that the timing of
radiotherapy must be based on the best course of action for treating the
tumour. If it was appropriate, then post-operative radiotherapy was pref-
erable. However, the wound healing problems are not considered an
insuperable problem (Marks et al., 2009) and Halle et al. (2009) suggest
surgery should be timed to be within 6 weeks of the last radiotherapy
treatment to allow optimum result.

Radiation may affect the healing of an existing wound or it may cause
changes to the skin so that any later wound will heal slowly. The skin may
show signs of damage from the radiation during treatment. This is known
as a radiation reaction and will be discussed in Chapter 6.

Psychological care

Nurses have always excelled at the physical care of patients. It is only
recently that the emotional needs of patients have been considered. Many
situations may cause psychological distress. This may be described as
stress. The physiological effects of stress and its effect on wound healing
have already been described above. Factors causing psychological distress
may be defined as stressors. Those that may be particularly associated with
wounded patients will be discussed in this section. It should be noted that
other factors, not addressed here, can also act as stressors.

Anxiety

Anxiety has been defined as ‘a diffuse, unpleasant, vague sense of ap-
prehension’ (Sadock & Sadock, 2008). Anxiety is experienced by everyone
at one time or another, especially when the future is uncertain, such as
health problems or because of experiences such as admission to hospital.
Much research has been undertaken into pre-operative anxiety and the
following dimensions have been identified: fear of the unknown, fear of
feeling ill and fear for life (Rosen et al., 2008). Anxious patients have more
severe pain and their blood pressure and cortisol levels have been shown to
be higher (Augustin & Maier, 2003). Levandoski et al. (2008) monitored
patients undergoing total abdominal hysterectomy that had been rando-
mised to either diazepam 10 mg orally or placebo pre-operatively. They
found a surgical site infection (SSI) rate of 25.8% (16/62) in the placebo
group compared with 6.6% (4/61) in the diazepam group.

Assessment

Zigmond & Snaith (1983) have designed a simple questionnaire, known at
the Hospital Anxiety and Depression Score (HAD) Score, that can identify
the degree of stress being suffered and can be completed by patients. The

40 Care of Wounds

questionnaire comprises a series of questions on topics such as whether
an individual is worried or able to relax and enjoy watching television.
There is a choice of four answers to each question such as ‘most of the time’
or ‘seldom’. Most patients found it simple to use and were enthusiastic
about the concept. Cole-King and Harding (2001) used the HAD score to
identify stress in 53 patients with leg ulcers and found it to be useful
research tool.

A more general assessment tool is the State Trait Anxiety Inventory
(STAI-State) that has been used in a wide variety of situations (Spielberger,
1966). It is able to differentiate between the transient condition of ‘state
anxiety’, where an individual finds a situation stressful and becomes
anxious and the more general and long-standing quality of ‘trait anxiety’,
where an individual has a predisposition to become anxious. The STAI-
State has been widely used in studies to assess pre- and post-operative
anxiety (for example: Ciccozzi et al., 2007; Hermes et al., 2007; Detroyer et al.,
2008; Bringman et al., 2009; Badura-Brzoza et al., 2009)

Nursing interventions

Much of the work addressing patient anxiety in relation to wounds has been
undertaken in relation to elective surgery and the provision of effective pre-
operative information. The UK Department of Health has produced a
reference document that makes it clear that all patients have the right to
understand their treatment and the risks involved (Department of Health,
2009). The role of the nurse is to ensure that each patient receives appro-
priate pre-operative information about the surgery and about what to
expect in the post-operative period. Ideally, individual patients should be
assessed for their level of anxiety so that relevant strategies can be deter-
mined. However, with many patients being admitted on the day of surgery,
this may be difficult to achieve.

A number of studies have looked at the provision of written information
prior to a surgical intervention and found it effective in reducing anxiety.
Van Zuuren et al. (2006) suggest that the use of simple brochures could
easily be implemented into practice. Eberhardt et al. (2006) suggest that it is
the clarity of information that is important rather than the volume.

Multimedia approaches have also been used. Doering et al. (2000)
assessed the impact of providing a videotape of a patient undergoing a
hip replacement from time of admission to discharge, purely from a
patient’s perspective. One hundred patients were randomly allocated to
either preparation group (shown the videotape) or a control group. They
were assessed for levels of anxiety and pain for 4 days post surgery. The
researchers found significantly lower levels of anxiety in the preparation
group as well as a lower intake of analgesia, although there were no
differences in the amount of pain. Similar results were found by Jlala
et al. (2010) in a study of patients undergoing upper or lower limb surgery.