58 Wounds

• Acute wound healing should progress through an orderly sequence of events to re-establish tissue integrity.

• A functional blood vessel network is fundamental for wound healing.

• Changes occur in the repaired tissue for up to 2 years with the scar tissue becoming stronger with time.

• A number of intrinsic and extrinsic factors can affect the healing process and include age, diabetes, infection, nutrition, smoking and drugs.

• Wounds are costly to treat and therefore accurate assessment of a patient and his/her wound is important.

• Assessment should be part of an ongoing process with opportunity for regular re-assessment.

• Acute wounds such as surgical incisions heal quickly with minimal complications; chronic wounds such as diabetic foot ulcers, leg ulcers and pressure ulcers take longer to heal.

• The management of patients with diabetic foot ulcers needs to include treatment of their diabetes as well as local wound management and off-loading techniques to reduce foot pressures.

• Venous leg ulcers are the most common cause of ulceration in the population and require the external application of compression bandages/hosiery to aid healing. These ulcers can be complicated by gravitational eczema; therefore, treatment of the surrounding skin is of equal importance.

• The majority of pressure ulcers are preventable. Management of patients requires a multi-disciplinary approach with the use of pressure-reducing/pressure-relieving support surfaces and repositioning as adjunctive measures to ensure appropriate care.

A wound can be thought of as any break in the integrity of the skin (Enoch and Leaper, 2005), although when this is due to minor trauma it might be termed a cut or an abrasion. Such wounds tend to heal fairly quickly by the process of regeneration of tissue and cells and generally do not pose any long-term problems. However, the time it takes for a wound to heal will depend on a number of factors related to the nature of the wound, the individual and environment. Many of these factors will be dealt with at different points throughout this chapter.

Structure of the skin

The skin is made up of the epidermis and dermis below which is the sub-cutis, muscle and bone. Within the epidermis, there are four layers:

Within the very thin structure of the epidermis, some of the key cells required for healing are present, in particular keratinocytes, dendritic cells and melanocytes.

The dermis is separated into the papillary and reticular dermis and is thicker than the epidermis. It is joined to the epidermis by structures known as rete ridges or ‘pegs’. In uninjured tissue, this arrangement helps the skin to maintain its normal function, something which can be affected when a wound occurs or as an individual’s skin changes with age. Like the epidermis, the dermis also contains many of the key cells/structures that are required for the normal healing response to occur; these include:

• Fibroblasts; for the production of collagen

• Endothelial cells; to stimulate blood vessel growth

• Leucocytes; such as lymphocytes, neutrophils and macrophages

• Smooth muscle cells

• Extracellular matrix.

The functions of the skin and factors that affect skin condition are listed in Table 58.1. How these roles link to wounds and wound healing will be explored in more detail later.

Table 58.1 Functions of the skin and factors affecting skin condition

Functions of the skin	Factors affecting skin condition
Protective covering	Dryness
Moisture retention	Age
Sensation	Environment
Regulation of body temperature	Nutrition
Release of waste	Hydration
Absorption of nutrients, that is Vitamin D

Wound healing

In adults, a scar is the normal end product of most injuries, with occasionally excessive scarring, that is hypertrophic or keloid complicating matters. However, wound healing can also be scarless, such as in fetal skin or the oral mucosa (Desai, 1997a; Wysocki, 2007). This type of healing presents an interesting concept and may offer some significant developments in the future. There are also many individuals for whom healing is delayed, and includes wounds often referred to as ‘chronic’ or ‘non-healing’. Other terminology is used in clinical practice to describe how wounds heal and includes:

• Primary intention

• Delayed primary closure

• Secondary intention.

Essentially, healing by primary intention (Fig. 58.1) describes where the wound edges are opposed, that is brought together by sutures, staples or glue and wound healing occurs mainly by connective tissue formation. Delayed primary healing is used where there may be a risk of contamination or infection, that is if the patient has undergone emergency abdominal surgery. In this instance, some of the layers of tissue are stitched, and the sutures are placed in readiness for the remainder of the wound to be closed after 48 h when the risk of infection is less. In contrast, secondary healing (Fig. 58.2) describes a situation where the wound is left open to heal by the normal processes. This type of healing is relevant to many of the types of wounds that will be discussed later.

Fig. 58.1 Example of wound healing by primary intention.

Fig. 58.2 Example of wound healing by secondary intention. Wound bed shows healthy granulation tissue and epithelial tissue can be seen at the wound edges.

Any injury to the skin will result in a sequence of events aimed at repairing the defect. Figure 58.3 shows the process of wound healing and is divided into four phases:

• Haemostasis

• Inflammation

• Proliferation

• Remodelling or maturation.

Fig. 58.3 Phases of wound healing (from Enoch et al 2008).

An insult to the tissues causes a number of systemic processes to occur simultaneously. Platelets aggregate and adhere to the sub-endothelium; coagulation factors as well as growth factors are also released. Through changes in the platelet structure and function, thrombin and fibrin are released to aid clot formation and reduce excess blood loss. Once this has occurred, haemostasis is said to have been established. The initial fibrin matrix provides the scaffold for the subsequent structure. This process relies on the individual having a normal clotting response and may be affected by drugs or systemic disease.

Following haemostasis, the inflammatory phase extends from day 0 through to about day 10 in normal healing and involves neutrophils (early inflammation), and macrophages (late inflammation). Neutrophils phagocytose bacteria and kill foreign bodies by producing oxygen metabolites such as hydroxyl radicals, hydrogen peroxide and superoxide ion. In normal healing, the numbers of neutrophils decrease in number over time leading to an increase in the number of macrophages present. The key function of macrophage is to digest bacteria, dead tissue and old neutrophils. There is some evidence to suggest that in wounds which are not healing it may be the inflammatory phase and its related cells that are at fault. The classic signs of inflammation are well reported and include:

These signs are normal and should not be considered as indicating the presence of infection.

The proliferative phase begins approximately 1 day post-injury and should be resolving by about day 30. There are three main activities that occur during this time and include:

• Granulation tissue formation – requires new blood vessels and formation of collagen

• Contraction of the wound

• Epithelialisation.

The presence of a functional blood vessel network is fundamental for wound healing to progress. Angiogenesis, the formation of blood vessels, is required to supply oxygen to the wound environment and it is through the migration of capillaries through the provisional matrix that the vasculature is re-established. Endothelial cells migrate and proliferate to eventually join the existing blood supply to the injured area. Once this has occurred, granulation tissue can form to begin to repair the defect. The provisional tissue laid down (Fig. 58.2) is made up of fibrin, fibronectin, collagen and glycosaminoglycans. Through the action of fibroblasts, collagen is produced and the continued presence of macrophages ensures the wound is kept ‘clean’. Collagen production is essential for healing to progress and in particular Types I, III and IV are required.

In conjunction with the laying down of granulation tissue, the wound edges begin to contract at around day 8, and this process assists wound closure. The key cell involved is the myofibroblast which applies tension to the surrounding matrix to induce contraction. The normal process of contraction should not be confused with contracture, which is an abnormal feature of scarring.

Around the same time, it may also be possible to see signs of epithelialisation occurring (Fig. 58.2). Keratinocytes, the cell associated with this process, are initiated hours after injury; they migrate from the edge of a wound over the provisional matrix laid down or they dissect through it. Hair follicles can act as islands of regenerating epithelium in some areas. The wound bed can be easily damaged during the proliferative phase, with simple things like incorrect dressing choice causing significant damage. Moist wound healing (MWH) principles (Winter, 1962) are encouraged to support the normal physiological process of healing.

The final phase of the healing process is termed remodelling or maturation. During this time, the initial collagen that has been laid down is synthesised by enzymes ultimately leading to a more ordered network that increases in structure and strength over time. However, this repaired area is never as strong as normal tissue and is always at risk of breakdown should circumstances occur. These final changes can take place for up to a year or more after the initial insult.

Factors affecting wound healing

Generally, wound healing should progress as described above; however, a number of factors that affect healing have been identified (Grey and Harding, 2008). A summary of these is provided in Table 58.2, some of which include:

Table 58.2 Intrinsic and extrinsic factors affecting wound healing

Intrinsic factors systemic local		Extrinsic factors
Age	Blood supply	Nutrition
Uraemia	Changes in oxygen tension	Smoking
Jaundice	Vessel trauma	Radiotherapy
Diabetes	Abnormal scarring	Infection
Anaemia	Haematoma	Drugs
Hormones	Local infection	Iatrogenic influences
Malignant disease		Wound dressings

Age

Younger patients appear to have an increased rate of healing, and there are differences in fetal healing that mean the regeneration process is superior with little or no inflammation or scarring (Desai, 1997b). In comparison, wound repair in the elderly is slower (Ashcroft et al., 2002), and management may be more challenging because of concurrent disease processes. This is a particular problem in the proliferative and remodelling phases where tissue appears to be more friable and fragile. The overall effects of age on wound healing appear to be:

• Decreased inflammatory response

• Delayed angiogenesis

• Decreased collagen synthesis and degradation

• Slower epithelialisation.

Diabetes

Diabetes poses many problems for patients with wounds and management is often challenging because of concurrent peripheral neuropathy (PN), peripheral arterial disease (PAD), neuro-ischaemia and infection (Table 58.3).

Table 58.3 Complications of diabetes

Peripheral neuropathy	Causes damage to nerves that leads to a lack of the protective pain sensation, but the blood supply remains good. Very common and can lead to foot deformities and abnormal walking patterns. Neuropathy should be considered in terms of sensory, autonomic and motor changes. The foot is usually warm, numb and dry with palpable foot pulses
Peripheral arterial disease	Often develops as a result of atherosclerosis but develops at a faster rate in diabetic patients. Can affect the large (macro) and small (micro) vessels leading to decreased blood flow to the legs and feet, which can ultimately lead to minor or major amputations. The foot is often cool, clammy with absent or reduced foot pulses
Neuro-ischaemia	A combination of peripheral neuropathy and peripheral arterial disease
Infection	More common in diabetic patients, probably because they have an associated defective immunity. The neutrophil and lymphocyte response is slow (partly due to vascular problems); therefore, the inflammatory and subsequent phases are impaired. Hence, these patients have an increased tendency to develop infections

Infection

Bacterial invasion of wounds is very common. In fact, any break in the skin integrity places the wound at risk of local contamination or infection and if untreated can lead to systemic infection. The spectrum of infection from colonisation through to infection is demonstrated in Fig. 58.4. The difficulty may be in recognising when such circumstances are present. The normal inflammatory signs were discussed earlier, and these should be borne in mind when examining a patient’s wound. However, there are additional local signs that may be present in wounds healing by primary or secondary intention (Fig. 58.5) that suggest an infective process; these include:

• Increased pain

• Delayed wound healing

• Wound bleeds easily

• Friable, fragile tissue

• Pocketing/bridging of tissue

• Wound breakdown (dehiscence).

Fig. 58.4 Schematic representation for the outcome of bacterial invasion.

Fig. 58.5 Infection in a granulating wound.

Infection in a wound can often be diagnosed by clinical signs and symptoms alone and unless a systemic infection is suspected, that is the patient complains of flu-like symptoms, can be treated locally with topical antimicrobial dressings rather than oral antibiotics.

In recent years, there has been increased recognition that bacteria have the ability to build up colonies that present a challenge in terms of the management of bacterial load. Known as biofilms, they have the ability to resist removal and have been implicated in delayed healing of a number of wound types. The removal of dead and devitalised tissue from the wound bed seems to have some effect in preventing the growth of biofilms (Wolcott and Rhoads, 2008); however, this method is not suitable for all wounds; hence, other approaches are being sought.

The choice of topical treatment for the management of local wound infection will be dealt with in a later section.

Nutrition

The nutritional requirements for wound healing have been the subject of debate with limited evidence as to the exact dietary components for individual wound types. In general, if the patient has a balanced diet, this should be sufficient for the normal processes to take place. However, a diet that is lacking in vital nutrients can lead to delayed wound healing and wound breakdown. In the extreme, the patient can become malnourished with surgical patients most at risk of protein energy malnutrition (PEM). Box 58.1 outlines the nutritional factors that should be considered in the assessment of individuals, many of which have been incorporated in nutritional risk assessment tools. Individuals at most risk of nutritional deficiencies are those affected by:

• Ill-health in old age

• Cancer

• Chronic neurological disease

• Chronic inflammatory bowel disease

• Surgery (pre- and post-operatively)

• Stroke

• Acute and chronic pain

• Immuno-deficiency disease such as HIV and AIDS.

Smoking

Smoking is known to be detrimental to health generally, and in addition the effect of nicotine and carbon monoxide on skin and muscles is well documented (Møller et al., 2002). These substances reduce the oxygen levels in the tissues and can lead to the formation of thrombi. A good blood supply and adequate vascularisation is important for normal wound healing. There has been debate about the period of time patients should abstain from smoking to reduce relevant, potential complications. This has been suggested to vary from 4 (Sorensen et al., 2003) to 8 weeks (Møller et al., 2002). However, the role of nicotine replacement interventions in further reducing complications is less clear.

Drugs

There are certain drugs that are suggested to have an effect on the healing process. These include NSAIDs, corticosteroids and immunosuppressive agents (Grey and Harding, 2008), which affect the inflammatory response, collagen synthesis and mitosis, respectively. Whilst drugs do not generally cause wounds, there have been recent reports that nicorandil, used for the treatment of angina, may cause peri-anal wounds that resolve on cessation of the medication (Baker et al., 2007).

Wound assessment

Wounds are costly to treat; therefore, it is important to appreciate the various considerations that need to be taken into account when assessing a patient. Assessment should not be viewed as a one-off occurrence but instead should be undertaken as part of an ongoing process with the emphasis on the patient, not just their wound.

A structured approach to the assessment of a patient with a wound is required. The six key elements of the original wound healing matrix are listed here and the key concepts depicted in Fig. 58.6:

• Phase of wound healing

• Aetiology

– Acute, that is surgical, trauma, burns

– Chronic, that is leg ulcers, diabetic foot ulcers, pressure ulcers

• Clinical manifestation

– Size

– Shape

– Characteristics, that is exudate, odour, tissue type

• Environment and care

– Primary care

– Secondary care

• Healthcare system and resources

• Site of the wound.

Fig. 58.6 Assessment of a patient with a wound.

Diabetic foot ulcers

Epidemiology

It was estimated that there were 1.4 million people diagnosed as diabetic in 2002 with these figures expected to double by 2010 (Cradock and Shaw, 2002). The cost of treating individuals with diabetes accounts for at least 9% of the acute healthcare costs in the UK. These costs, however, do not take into account the personal cost to the individual, such as a reduction in the ability to work and time they may need to take off work (Waters and Holloway, 2009). Diabetic foot problems are the most common cause for admission, and patients admitted to hospital for in-patient care are often hospitalised for 4–6 weeks, which obviously increases the financial costs considerably.

One of the major risks to patients with diabetic foot disease is that of amputation, which could be minor, that is mid-foot to toe; or major, that is mid-foot and above. National Service Frameworks for diabetes (Department of Health, 2001) have emerged to address this and, in turn, have been built upon (Department of Health, 2007a,b). Of concern is that up to 85% of amputations are preceded by foot ulcers. Therefore, if the incidence of foot ulcers can be reduced, this might lead to a reduction in amputations.