VOL: 97, ISSUE: 03, PAGE NO: 3
Pauline Beldon, RGN, DipPsych. Couns, is a tissue viability nurse, Epsom and St Helier NHS Trust, Surrey
The inflammatory phase is a vital stage in the wound-healing process, without which healing will not progress.
Inflammation is apparent in all wounds at some point. However, its presence may also signal the onset of infection, an allergic reaction or dermatitis (Lawton and Rich, 1999).
With the advent of resistant organisms, such as methicillin-resistant bacteria, it has become increasingly important that nurses recognise and differentiate between inflammation as a normal process of healing and as a response to infection.
Failure to recognise a normal inflammatory process can result in pointless wound-swabbing and an unnecessary course of antibiotics. Alternatively, if an infection goes unrecognised this will prolong patient discomfort and the wound-healing process.
A break in the integrity of the skin provides an opportunity for bacteria to enter a wound and multiply. Whether or not this will result in an infection depends on the ability of the individual to resist infection (Cutting, 1998).
A wound will become contaminated within a few minutes of coming into being. In some instances this will lead to colonisation of the wound and in others it will result in infection (Cutting, 1998). It is important to be able to distinguish between the two.
Assessing for infection
Some groups of people will not produce the classical symptoms associated with wound infection (Table 1), particularly older people with a diminished immune response, people with neutropenia and those receiving long-term steroids or non-steroidal anti-inflammatory drug therapy. A person with diabetes may also fail to produce the classical symptoms of infection owing to reduced neutrophil activity (Mulder et al, 1998). In this instance additional signs should be looked for.
Inflammation due to injury
The inflammatory phase acts as a precursor to the remaining phases of wound-healing. Following a traumatic injury the body’s immediate physiological response aims to halt bleeding. The severed ends of the blood vessels contract and platelet aggregation accelerates coagulation (Iocono et al, 1998). Insoluble fibrin acts as a weak biological glue, and the wound edges are pulled together to make a temporary seal. Inflammatory mediators, including histamine and serotonin, are released which cause vasodilation and increased cell permeability around the injured area. This results in redness, swelling, heat and pain.
The predominant aim of the inflammatory phase is to slow the circulation in and around the damaged region. This allows the migration of phagocytic white cells into the wound area. Once present, they perform multiple complex functions mainly aimed at clearing debris and bacteria from the wound site and initiating the subsequent phases of wound-healing.
Other causes of inflammation
Apart from the normal physiological response to injury, the skin can become inflamed for a number of reasons.
Inflammation due to dermatitis
Acute eczema, for example, will frequently present with symptoms such as redness, swelling, oozing, pain, heat and possibly blistering (Mackie, 1997). This can be mistaken for inflammation due to infection, especially if the patient has a pre-existing wound.
Contact dermatitis has very similar clinical symptoms and can also be mistaken for infection. Allergic contact dermatitis is caused by sensitisation due to exposure to an allergen. Irritant dermatitis is caused by exposure to a substance that damages the normal barrier function of the skin. Application of new wound management products without patch-testing may produce this reaction in a sensitive individual. Such products might include moisturisers, soaps, adhesive dressings or antiseptics (English, 1997).
In addition to inflammation, other symptoms can also be confused with infection in certain circumstances. In both acute eczema and contact dermatitis, erythema due to dilated blood vessels and blistering due to oedema between epidermal cells and within them result in excess production of keratin and thickening of the epidermis. Both these effects are commonly seen in patients with venous insufficiency.
Varicose eczema may also cause confusion. This is endogenous, secondary to venous stasis and is associated with increased capillary pressure due to venous hypertension. An individual with varicose eczema will report severe irritation, swelling, heat, pain and, possibly, exudate.
Prolonged inflammation due to autolysis
If an area of the body sustains damage the healing process is initiated. However, if the damage to the tissue is too great the non-viable tissue is separated from the body. This gradually demarcates precisely to outline the area of non-viable, necrotic tissue. This process is known as autolysis.
Normally the inflammatory phase lasts between three and seven days. However, the presence of large amounts of necrotic tissue, such as may be present in a large pressure sore, will lead to a prolonged period of inflammation (Thomson, 1998).
It is important to be aware that in this instance the inflammation may not be due to infection and autolysis should be facilitated by using an appropriate method of debridement. This will prevent the prolongation of inflammation (Flanagan, 1997).
Debridement of necrotic tissue results in neovascularisation (Iocono et al, 1998). Improved circulation may help reduce infection by delivering naturally occurring antimicrobial agents and cells to the wound site (Thomson, 1998).
Necrotic tissue and infection
Necrotic tissue may predispose towards infection as it acts as a source of food for bacterial growth, and the resultant anaerobic environment decreases leukocyte activity (Moorehead and Whiteside, 1999). The malodour produced results from volatile fatty acids produced by anaerobic bacteria, but malodour is not in itself indicative of infection (Flanagan, 1997).
The value of wound swabs
The general consensus is that wound swabs are of limited value (Trengrove et al, 1996). In the absence of symptoms of clinical infection the results from a wound swab may even be deceptive, producing a culture of surface organisms, while missing a potential pathogen. Furthermore, there is no consensus on how best to take a wound swab, and this increases the possibility of obtaining unreliable results (Gilchrist, 1996).
It is imperative that nurses should be able to differentiate between a patient undergoing an allergic reaction, one with a dermatology problem, a wound in the early stages of healing and one that is infected.
The indiscriminate and unnecessary prescribing of antibiotics for possible wound infections based solely on the results of a laboratory report may well have contributed to the growth of resistant organisms. Nurses need to take action through education and observation to limit their further misuse.