The Care of Wounds E-Book

Carol Dealey

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 467

Veröffentlichungsjahr: 2012

Beschreibung

The Care of Wounds addresses all aspects of holistic wound management. The fourth edition of this successful clinical text continues to reflect current research and evidence-based practice, while incorporating the considerable developments which have occurred in wound care practice since the previous edition. It includes chapters on the physiology of wound healing, general principles of wound management, wound management products, and the management of patients with both acute and chronic wounds. The title is an essential read for all nurses and healthcare professionals working in the field of tissue viability and wound healing.

• Comprehensive and clinically-oriented
• Examines best practice in wound management
• Incorporates national and international clinical guidelines where applicable
• Superbly illustrated with full colour throughout

Leseprobe

Contents

Cover

Title Page

Copyright

Dedication

Preface

Chapter 1: The physiology of wound healing

Introduction

Definitions Associated with Wounds

The Structure of the Skin

Wound Healing

Impaired Wound Healing

Conclusion

Chapter 2: The management of patients with wounds

Introduction

Physical Care

Psychological Care

Spiritual Care

Chapter 3: General principles of wound management

Introduction

Wound Assessment

Managing Wounds

Documentation

Evaluating the Dressing

References

Chapter 4: Wound management products

Introduction

The Development of Dressings Through the Ages

Traditional Techniques

The Use of Lotions

Clinically Effective Wound Management Products

Modern Wound Management Products

Chapter 5: The management of patients with chronic wounds

Introduction

The Prevention and Management Of Pressure Ulcers

The Management of Leg Ulcers

Diabetic Foot Ulcers

The Management of Fungating Wounds

References

Chapter 6: The management of patients with acute wounds

Introduction

The Care of Surgical Wounds

Traumatic Wounds

The Burn Injury

Radiation Reactions

References

Chapter 7: The organisation of wound management

Introduction

Managing Wounds in the Community

Nurse Specialists in Wound Care

Multiprofessional Wound Care

Wound Healing Centres

Conclusions

Index

This edition first published 2012 © 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

In memory of my husband

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

Chapter 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:

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

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

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

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:

traumatic – mechanical, chemical, physical;

intentional – surgery;

ischaemia – e.g. arterial leg ulcer;

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.

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

(2)Healing by first and second intentionThese definitions were first described by Hippocrates around 350 BC.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.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 woundsThese 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.

Figure 1.1 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.

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 filaments, 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 produces 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 interdependent and overlapping stages. These stages have been given a variety of names. They are described here as:

inflammation;

reconstruction;

epithelialisation;

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.

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 metabolic reactions

Swelling

Vasodilation and leakage of fluid into the wound area

Pain

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

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 aggregation 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.

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 (TGFα and TGFβ). 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.

Table 1.2 Growth factors involved in the healing process

Growth factor

Abbreviation

Action

Platelet-derived growth factor

PDGF

Chemotactic for neutrophils, fibroblasts and, possibly, monocytes. Encourages proliferation of fibroblasts

Transforming growth factor alpha

TGFα

Stimulates angiogenesis

Transforming growth factor beta

TGFβ

Chemotactic for monocytes (macrophages). Encourages angiogenesis. Regulates inflammation

Fibroblast growth factor

FGF

Stimulates fibroblast proliferation and angiogenesis

Epidermal growth factor

EGF

Stimulates the proliferation and migration of epithelial cells

Insulin-like growth factors

IGF-I, IGF-II

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

Vascular endothelial growth factor

VEGF

Critical for angiogenesis and the formation and growth of blood vessels

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 diapedesis, again this ability is enhanced by fibronectin. Within about an hour of the inflammatory response being initiated, neutrophils can be found at the wound site. They arrive in large numbers, their role being to phagocytose 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 numbers 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 TGFβ1), inflammatory mediators interleukin 1 (IL-1), tumour necrosing factor alpha (TNFα) 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 nutritional 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 granulation 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 produce PDGF and fibroblast growth factor (FGF), which are both chemotactic 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 proportion 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 TGFβ 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 formation 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, 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 scarring. 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. Keratinocytes 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 reconstitute 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.

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 recognised 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, TGFβ, 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 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 hypertrophic scars, keloids do not gradually flatten out.

Within keloids there are increased levels of collagen and glycosaminoglycan deposition within the extracellular matrix with the collagen presenting 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, TGFα and TGFβ 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, TGFβ, MMP-1 and MMP-13 as well as reduced levels tissue inhibitor of metalloproteinases (TIMPs) and changes in collagen structure. The significance 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 microenvironment 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 significantly as the ulcers started to heal (p = 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 concentrations 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 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 = 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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Chapter 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 (dermatology 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 management 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).

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 malnourished 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 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 necessarily 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 requirements). 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 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 knowledge 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 improved 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 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 management 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 according 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.

Table 2.1 The nutrients required for healing

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 developing 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 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 parenteral 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 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 significantly 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:

bacteria consume the nutrients and oxygen required for wound repair;

virulent bacteria damage the extracellular matrix;

anaerobic bacteria impair white cell function;

oxygen-free radicals increase in numbers and disrupt the balance between matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs);

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 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 analysis, 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 = 0.009) for superficial SSI in a retrospective multivariate analysis of 3174 patients undergoing 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, coronary 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.)

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).

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