Step 1. Prepare the environment

First, you need to create an environment that is suitable to conducting an assessment by ensuring:

Step 2. Gather relevant information

Second, you need to carefully explain what you are going to do and the purpose of assessing the skin. Typically, you obtain a history using a framework such as that shown in Table 30-3.

TABLE 30-3 SKIN ASSESSMENT

Step 3. Observe and feel the skin

The final step is to look at the skin (inspection) and feel (palpation) if there are any changes (Table 30-4). When conducting the physical assessment, proceed from head-to-toe and compare each body region for symmetry (i.e. right side with left side to differentiate structural from pathological changes). If lesions are identified, palpate them for density, induration (hardening or thickening of tissues) and tenderness.

TABLE 30-4 OBSERVATION OF THE SKIN

Now that you have a better understanding of how to assess the skin, you are ready to learn more about some strategies you can use to maintain skin integrity and prevent many skin problems from occurring. Review the suggested evidence-based strategies summarised in Table 30-5.

TABLE 30-5 PRESERVING SKIN INTEGRITY

Haemostasis

Immediately after injury, platelets initiate the wound-healing process by releasing a number of growth factors that rapidly disperse from the wound, drawing inflammatory cells to the area of injury. Haemostasis is comprised of three components:

1. vasoconstriction whereby bleeding is arrested by constriction of the arteries, arterioles and capillaries in or close to the wound

FIGURE 30-3 The four phases of wound healing.

Redrawn from Enoch S, Grey JE, Harding KG 2006 Recent advances and emerging treatments. Br Med J 332(7547):962–5.

2. formation of a platelet plug whereby the damaged endothelium of vessels exposes collagen fibres causing the platelets to stick to the collagen fibres in the wall of the vessels and to each other, resulting in a mechanical plug by the process of aggregation. The platelets release chemicals, including serotonin and prostaglandins, which enhance the vascular constriction and further reduce blood flow. Phospholipids and adenosine diphosphate (ADP) are also released and attract more platelets to the area, which increases the size of the platelet plug

3. a biochemical response is then activated, initiating the clotting cascade. This a complex process which sees the development of a clot, the retraction and compaction of the clot which causes the wound edges to come together and the breakdown of the clot by fibrinolysis.

Inflammation (0–3 days)

The inflammation phase of wound healing is a vascular and cellular response that removes microbes, foreign bodies and dying tissue in preparation for wound healing (Flanagan, 1997). The inflammatory phase is characterised by vasodilation, increased capillary permeability, complement activation and polymorphonuclear leucocytes (PMN) and macrophage migration to the wound (Flanagan, 1997; Traversa and Sussman, 2001). The increase in blood flow into the wounded area produces erythema, oedema, heat and discomfort such as a throbbing sensation.

Macrophages regulate the events in wound healing by attracting further macrophages and induce the proliferation of fibroblasts and endothelial cells. Macrophages release growth factors which stimulate endothelial cells lining the walls of capillaries to close the wounded area, and then divide and branch out to form new capillary loops (Flanagan, 1997). Fibroblasts migrate along fibrin threads and synthesise collagen and other extracellular matrix (ECM) molecules to support new cells and fragile capillary buds which appear during angiogenesis. This continues until newly formed granulation tissue joins up with intact blood vessels (arterioles) to form a network of vessels that fill the wound bed (Flanagan, 1997).

Proliferation (2–24 days)

The proliferation phase is characterised by extensive growth of epithelial cells, deposition by fibroblasts of collagen fibres in random patterns to form the ECM and ground substance and continued growth of blood vessels (Schulz and others, 2003). Fibroblasts and endothelial cells proliferate in response to growth factors, including platelet-derived growth factor (PDGF) and transforming growth factor B (TGF-B), and cytokines that are released from macrophages, platelets and mesenchymal cells or have been stored in the fibrin clot (Krishnamoorthy and others, 2001; Traversa and Sussman, 2001). Macrophage-released growth factors produce glycosaminoglycans (GAGs). These include hyaluronic acid, chondroitin-4-sulfate, dermatan sulfate and heparin sulfate, which cross-link to protein and are termed proteoglycans. These form an amorphous gel where collagen fibres deposit and aggregate (Traversa and Sussman, 2001). The ground substance secreted by fibroblasts determines the compliance, flexibility and integrity of the dermis. It provides compressive strength and support and density to tissue, reduces friction between collagen fibres during tissue stress or strain and protects tissue from invasion by microorganisms (McCulloch and others, 1995).

During the proliferation phase, new capillary development is seen as ruddy, bumpy granulation tissue in the base of a wound, and wound contraction occurs. Epithelial cell migration occurs over the granulated wound bed. Epithelial cells migrate from surrounding wound edges or from hair follicles, sweat or sebaceous glands in the wound and appear as thin, translucent film across the wound bed. At this stage, the epithelial tissue is very fragile and easily removed even by gentle cleansing. Migration of epithelial cells ceases when the wound is covered; then mitosis thickens the epithelium to the four to five layers needed to form the epidermis.

Maturation (24 days to 1 year)

The combination of fibronectin and collagen forms the ECM essential for the development of granulation tissue that eventually fills the wound. The endothelial buds increase in vascularity in response to the large metabolic demand of the repair tissue (Traversa and Sussman, 2001). The arrangement of collagen fibres in the wound is random and disorganised, and has a gel-like consistency that gradually matures to form cross-links which provide tensile strength to the wound (Flanagan, 1997).

The remodelling of collagen fibres is regulated by growth factors including TGF-B, PDGF and fibroblast growth factor (FGF), interleukin-1 (IL-1) and interferon-gamma (INF-γ). Depending on the type and severity of the wound, the maturation phase may take up to six months to a year (McCulloch and others, 1995). Collagen synthesis continues after wound closure, but undergoes continual lysis to form a more organised lattice structure that gradually increases tensile strength of scar tissue, fibroblast numbers decrease and blood vessels are restored to normal (Traversa and Sussman, 2001). The tensile strength of scar tissue is never more than 80% of that of non-scar tissue (Flanagan, 1997).

Evidence-based practice

Much of our understanding about how wounds heal is derived from examination of the wound-healing process in acute wounds. It is widely accepted that acute wounds heal through an orderly process of haemostasis, inflammation, proliferation and maturation. However, chronic wounds such as leg ulcers and diabetic foot ulcers do not follow this trajectory and are often characterised by prolonged inflammation and, even if they do heal, frequently recur even with the highest standard of care.

The concept of wound-bed preparation has emerged as an important paradigm in the management of chronic wounds in order to identify factors that influence wound healing and to provide a framework for clinicians to maximise the potential for wound for healing. There are four main principles underpinning wound bed preparation—TIME:

The TIME framework is a dynamic concept that can be translated into practical management of different wound types by utilising a standardised framework.

Wound cleansing

Wounds should be cleaned with a neutral, non-irritating, non-toxic solution such as clean tap-water or normal saline (Whitney and others, 2006). Cleaning should be undertaken with minimal chemical or mechanical trauma. The ultimate aim of wound cleansing is to remove both organic and inorganic debris while maintaining the optimum local environment to facilitate wound healing (Fernandez and Griffiths, 2012). Before performing wound cleansing, consider the purpose of wound cleansing and whether the advantages of cleansing outweigh the disadvantages; the most appropriate method of wound cleansing; whether the wound requires cleansing at each dressing change; and the type of wound-cleansing product that is most appropriate.

Common reasons for cleansing a wound are to help prevent wound infection and remove excess debris or foreign bodies from the wound; to rehydrate the wound to provide a moist environment; to make wound assessment easier so that the size and extent of the wound can be visualised; before applying a dressing, to minimise trauma when removing adherent dressings; and to promote patient comfort and psychological wellbeing.

The decision to cleanse a wound should be based on the shape, size and location of the wound; condition of the wound bed and stage of healing; availability and effectiveness of different methods of cleansing; availability and effectiveness of different cleansing agents; and the patient’s perceptions and needs.

Wound debridement

Wound debridement is an essential component of optimal wound management. Debridement describes any method that facilitates the removal of dead or devitalised tissue, metabolic waste, fibrin and foreign material from a wound (Gethin and others, 2010). Removal of necrotic and devitalised tissue can be undertaken through surgical, sharp, mechanical, autolytic, biological or enzymatic debridement techniques (Hopf and others, 2006; World Union of Wound Healing Societies, 2007). If dry gangrene or eschar (leathery brown or black necrotic tissue) is present, however, debridement should not be undertaken until arterial flow has been re-established (Whitney and others, 2006). There is insufficient evidence to conclude that any one debriding agent is more effective than another (Gethin and others, 2010; Williams and others, 2005).

When selecting an appropriate method of debridement a number of factors must be considered, including the patient’s individual wishes and concerns, medical history, factors affecting the wound-healing process, pain, wound characteristics, skill and knowledge of the clinician and available resources (Kirshen and others, 2006). Specific wound characteristics that influence debridement decisions include size, depth and amount of exudate, as well as the characteristics of wound tissue, potential for bleeding, and infection. Methods of debridement that are selective are generally preferred because they remove only necrotic tissue.

When selecting the most appropriate method of debridement, the indications and contraindications for the different types of debridement options must be considered. Evidence supports that debridement is an important step in preparing the wound bed for healing (Ayello and Cuddigan, 2004; Kirshen and others, 2006; Moffatt and others, 2008).

Provision of a moist wound environment

A moist wound environment is essential to promote wound healing because cells need moisture to be able to migrate across a wound bed. Extreme wetness or dryness may delay healing. Application of dressings to a wound may help to facilitate wound healing by providing the optimal wound environment. Wound dressings may also be applied to:

Before applying a dressing, it is essential that you know:

There are two different categories of wound dressings: primary dressings—those in direct contact with a wound; and secondary dressings—those not in contact with a wound but covering the primary dressing (Xue, 2008). When selecting a secondary dressing, it is important to ensure that it is compatible with the primary wound-contact layer.

Multiple factors inform the selection of a wound dressing: the type or aetiology of the wound, location or position of the wound, extent of tissue damage and size of the wound, phase of wound healing, presence of debris or infection, level of exudate, odour, pain, patient-centred concerns, cost-effectiveness, the indication/contraindication of the dressing, condition of the surrounding skin and desired patient outcomes (Xue, 2008).

Evidence suggests that dressings should:

Topical antimicrobial dressings may be beneficial when wounds are infected (Hopf and others, 2006).

Unfortunately there is no one dressing that is ideal for every wound. Dressings are classified according to their properties into generic groups. The main classes of wound dressing products and their properties are outlined in Table 30-11.

TABLE 30-11 WOUND DRESSINGS

Now that you have a better understanding of the principles of wound assessment, wound cleansing and wound dressings, you are ready to learn how to perform a simple wound dressing—see Skill 30-2.

SKILL 30-2 Performing a wound dressing

DELEGATION CONSIDERATIONS

A wound dressing can be undertaken by all healthcare professionals. Check organisational policies regarding which wound care interventions can be delegated to health workers. The assessment of a wound requires the problem-solving and knowledge-application skills of a registered nurse.

EQUIPMENT

• Examination gloves

• Apron

• Facemask and protective eyewear

• Sheet or towel for draping

• Normal saline

• Contaminated-waste bag

• Acetate grid for wound tracing

• Black fine-tip permanent marker

• Sterile wound probe

• Adhesive remover (optional)

• Wound dressing (choice is dependent on wound characteristics including level of exudate, condition of wound bed, location of wound, mobility, etc)

STEPS	RATIONALE
1. Assess size and location of wound.	Helps to plan for type and amount of supplies required.
2. Assess patient’s level of comfort.	Removal of dressing may cause pain and discomfort requiring pain medication.
3. Explain procedure to patient.	Decreases anxiety.
4. Close room or cubicle curtains and windows.	Provides privacy and reduces airborne microorganisms.
5. Position patient comfortably and drape with sheet or towel to expose only wound site.	Provides access to wound while minimising unnecessary exposure.
6. Place disposable contaminated-waste bag within reach of work area. Fold top of bag to make cuff.	Ensures easy disposal of soiled dressings.
7. Put on face mask and protective eyewear, if required, and wash hands thoroughly. Put on clean, disposable gloves.	Protects nurse from splashes and reduces risk of transfer of infection between patients.
8. Carefully remove dressing. If dressing is adhered, moisten to facilitate removal. Note the amount of exudate present on the dressing removed, any odour and condition of periwound skin. Remove gloves over contaminated dressing (see illustration) and discard gloves and dressing into prepared bag.	Moistening dressing upon removal decreases pain and trauma to tissue. Observing the dressing as it is being removed helps to determine the capacity of the current dressing to contain exudate, odour and its impact on the periwound skin. Removal of gloves over dressing reduces transmission of pathogens.
Step 8 Remove gloves over contaminated dressing
9. Cleanse wound with normal saline or potable tap water. The decision to cleanse the wound should be based on the following: • The shape, size and location of the wound • Condition of the wound bed and stage of healing • Availability and effectiveness of different methods of cleansing • The patient’s perceptions and needs.	The aim of wound cleansing is to remove both organic and inorganic debris from the wound and periwound skin to facilitate wound healing, and to make wound assessment easier so that the size and extent of the wound can be visualised.
10. Perform wound assessment. • Wound aetiology • Wound location • Wound dimensions and extent of tissue loss. Apply acetate grid to wound and trace the wound margin with the felt pen. If the wound is a cavity or there is undermining of the wound margins, gently insert a sterile wound probe to measure the depth of the wound. • Evaluate the clinical appearance of the wound bed by estimating the percentages of tissue type in the wound bed (yellow/sloughy, red/granulating, black/necrotic, pink/epithelialising, green/infected tissue). • Wound edge (sloping, punched-out, undermining, calloused, raised or rolled) • Exudate (type, amount, colour, consistency and odour) • Condition of surrounding skin (maceration, erythema, oedema, warmth, capillary refill time) • Pain (amount, character, quality, relieving or exacerbating factors).	Provides a combination of subjective and objective data to assess effectiveness of wound management plan and to plan appropriate interventions.
11. Put on clean gloves. Cover wound with appropriate dressing to provide a moist wound-healing environment. Dressing selection is based on the following factors: • Aetiology of the wound • Characteristics of the wound: — Location — Extent of tissue damage — Wound size — Phase of healing (epithelialising, granulating, sloughy, necrotic) — Level of exudate — Pain — Odour — Presence of infection • Factors affecting wound healing • Cost-effectiveness • Ease of application and removal • Dressing should cause minimum distress or disturbance to the patient • Awareness of the limitations/contraindications of dressings.	Provides a moist wound environment to facilitate wound healing, absorbs exudate, reduces risk of bacterial colonisation and pain.
12. Remove gloves by pulling them inside out. Dispose of in prepared bag.	Prevents contact of nurse’s hands with material on gloves.
13. Assist patient to a comfortable position.	Promotes patient comfort.
14. Document all relevant information in patient’s chart.	Provides relevant information about the patient and the wound, monitors healing process, guides wound management of the person as a whole, evaluates the success of management and fulfils legal requirement.

Drains

Drains may be inserted into a surgical wound if a large amount of drainage is expected and if keeping wound layers closed is especially important. Some drains are sutured in place. Caution should be exercised when changing the dressing over drains that are not sutured in place to prevent their being accidentally removed. A drain such as a Penrose drain may lie under a dressing, extend through a dressing or be connected to a drainage bag or a suction apparatus. The surgeon often places a pin or clip through the drain to prevent it from slipping further into a wound. It is usually a medical responsibility to pull or advance the drain as drainage decreases to permit healing deep within the drain site.

The nurse assesses the number of drains, drain placement, the character of drainage and the condition of collecting apparatus. The security of the drain and its location with respect to the wound are observed, and the character of the drainage noted. If there is a collecting device, the drainage volume is measured. Because a drainage system must be patent, drainage flow through the tubing as well as around the tubing should be looked for. A sudden decrease in drainage through the tubing may indicate a blocked drain, and the surgeon should be notified. When a drain is connected to suction, the system is assessed to ensure that the pressure ordered is being exerted. Evacuator units such as a Hemovac or Jackson-Pratt exert a constant low pressure as long as the suction device (bladder or bag) is fully compressed. These types of drainage devices are often referred to as self-suction. When the evacuator device is unable to maintain a vacuum on its own, the surgeon is notified, who can then order a secondary vacuum system (such as wall suction). If fluid is allowed to accumulate within the tissues, wound healing will not progress at an optimal rate, and the risk of infection is increased.

When drainage interferes with healing, drainage evacuation can be achieved by using either a drain alone or a drainage tube with continuous suction. Barrier preparations must be applied to protect the skin surrounding drain sites: drainage then flows on the barrier but not directly on the skin. Drainage evacuators are convenient, portable units that connect to tubular drains lying in a wound bed and exert a safe, constant, low-pressure vacuum to remove and collect drainage. The nurse ensures that suction is exerted and connection points between the evacuator and tubing are intact. The evacuator collects drainage, which is assessed for volume and character every shift and as needed. When the evacuator fills, the output is measured by emptying the contents into a graduated cylinder and immediately resetting the evacuator to apply suction.

Skin grafts

Ideally, wounds heal by primary intention. However, large, surgically created wounds and traumatic and chronic wounds can cause extensive tissue destruction, making primary intention healing impossible. Skin grafts may then be necessary to protect underlying structures or to reconstruct areas for cosmetic or functional purposes. Survival of skin grafts relies on revascularisation of the grafted skin (Beldon, 2007).

Skin-graft take is the process by which the donor site is incorporated into a recipient or host bed. Successful graft take requires an unhindered process of restoration of vascular perfusion to the donor skin. A graft will take better if the donor site, the area from where the skin is harvested, is highly vascularised.

For a skin graft to take, it must be closely applied to the recipient bed. Any accumulation of oedema, haematoma or seroma between the skin graft and the recipient bed will prevent the skin graft taking. Movement between the graft and the recipient bed damages the in-growth of capillaries and prevents revascularisation. When skin grafts are applied to movable body parts, splinting is used to immobilise adjacent joints. Bed rest and positioning of the patient to prevent distortion or tension and shearing forces between the graft and the wound bed is essential. Tie-over dressings that immobilise skin grafts, particularly on the face, may be sufficient to immobilise problematic areas.

Several methods are used to fixate the graft, including the open method, the closed method and topical negative pressure wound therapy. The open method is where the graft is laid onto the recipient site and left open to the air. Initially the graft is pricked every hour with a sterile needle to express any seroma or haematoma that has built up under the graft. As the wound exudate decreases, the procedure is reduced to every few hours. The closed method of skin grafting is where a pressure dressing is applied over the skin to keep it well approximated to the recipient bed (Terrill, 2003). There are many different techniques to achieve this; most involve using a non-adherent dressing on the surface of the graft, such as tulle gras or paraffin-impregnated gauze, and a stack of cotton gauze cut to fit within the defect or a foam sutured/stapled onto the wound margins or a flexible polyamide net coated with soft silicone against the graft with a secondary absorbent dressing secured with sutures or staples (Terrill, 2003; Young and Fowler, 1998). Sutures or staples are not used if the skin graft is applied in the operating theatre. The fibrin that forms between the skin graft and the recipient bed binds the two surfaces together.

Topical negative-pressure wound therapy is utilised for skin grafts in complex anatomical areas where the base is irregular (Banwell and Teot, 2003). A topical negative-pressure dressing achieves good apposition of the skin graft to the recipient site, absorbs exudate, reduces oedema, stimulates granulation-tissue formation and decreases bacterial colonisation (Banwell and Teot, 2003). Excellent graft take (>95%) has been reported in the literature with this technique for graft fixation (Banwell and Teot, 2003).

With the closed or topical negative-pressure wound therapy techniques, the skin grafts are usually reviewed after 5 days and assessed for graft take. A graft that has taken has a purple-pink hue and has adhered to the wound bed. The graft usually needs protection for at least 2 weeks or 3 months if located on the lower limbs. Any graft that has not taken is dressed using normal moist wound-healing principles. After 4–6 weeks the graft is usually pale pink and the skin depression should be filling in. Further cosmetic improvement can continue with graft maturation over 6–12 months. Cosmesis can be improved using pressure therapy and silicone gel sheeting to soften scars and reduce erythema.

Skin flaps have their own blood supply, and the ability to monitor the status of the flap perfusion or its viability is essential in the prevention, recognition and treatment of complications. A healthy skin flap is similar in colour and texture to the donor site. The colour, temperature, capillary refill time, tissue turgor, dermal bleeding and quantity of exudate are techniques used to assess tissue flap viability.

Donor sites are frequently painful. Factors that affect the healing rate of donor sites are the site, size and depth of tissue excised (Beldon, 2007). Healing of donor sites is primarily through re-epithelialisation of the exposed dermis. The sites tend to produce moderate amounts of exudate, and epithelial cells in the hair follicles, sebaceous and sweat glands migrate across the wound bed to form a new layer of epithelium. This process takes approximately 10–21 days. The ideal donor-site dressing should be easy to apply, reduce pain, minimise leakage of exudate, promote rapid wound healing and be inexpensive and acceptable to the patient (Beldon, 2007).

Skin tears

A skin tear is a traumatic injury to the skin that occurs as a result of friction alone, or shearing and friction. It separates the epidermis from the dermis (known as a partial-thickness wound) or separates both the epidermis and the dermis from the underlying structures (known as a full-thickness wound). Most skin tears occur on the arms and hands. Other common sites are the lower legs, feet or the head, although they can occur anywhere on the body. Skin tears are the most common type of wound in older people, so it is important to understand why this is so and to be able to identify those most at risk. Most skin tears occur when the person accidentally bumps into an object such as a wheelchair or furniture, when being transferred, or following a fall.

There are many risk factors for skin tears. These are explained in Table 30-12.

TABLE 30-12 RISK FACTORS FOR SKIN TEARS

CLASSIFICATION OF SKIN TEARS

Skin tears vary in size, location and the amount of tissue loss. It is important that you know how to classify the type of skin tear so that you can determine the appropriate management options.

The STAR Skin Tear Classification System (see Figure 30-19) was developed by the Silver Chain Nursing Association and the Curtin University of Technology (2007) to provide an evidence-based consensus on skin tear classification. This means that if you use this system, you are more likely to be able to identify the type of skin tear and be able to select the correct treatment and prevention strategies. Skill 30-3 explains the assessment and management of a skin tear.

FIGURE 30-19 STAR (Skin Tear Audit Research) skin tear classification system.

Source: Silver Chain Nursing Association and Curtin University of Technology (School of Nursing and Midwifery) 2007 (revised 2010). Online. Available at www.silverchain.org.au/assets/GROUP/research/STAR-Skin-Tear-tool-04022010.pdf 20 Apr 2011.

SKILL 30-3 Assessment, management and prevention of skin tears

DELEGATION CONSIDERATIONS

The management and prevention of skin tears can be undertaken by all healthcare professionals. Check organisational policies regarding which wound care interventions can be delegated to health workers. The assessment of a person with or at risk of skin tears requires the problem-solving and knowledge-application skills of a registered nurse.

EQUIPMENT

• Examination gloves

• Apron

• Facemask and protective eyewear (optional)

• Normal saline

• Sterile cotton tip

• Contaminated-waste bag

• Black fine-tip permanent marker

• Limb protector

• Wound dressing (choice is dependent on wound characteristics including level of exudate, condition of wound bed, location and size of wound, condition of periwound skin, mobility, etc)

STEPS		RATIONALE
1. Explain procedure to patient.		Decreases anxiety.
2. Assess size and location of wound.		Helps to plan for type and amount of supplies required.
3. Position patient comfortably.
4. Place disposable contaminated-waste bag within reach of work area. Fold top of bag to make cuff.		Ensures easy disposal of soiled dressings.
5. Put on face mask and protective eyewear, if required, and wash hands thoroughly.		Protects nurse from splashes and reduces risk of transfer of infection between patients.
6. Control bleeding and clean the wound:		The aim of wound cleansing is to remove both organic and inorganic debris from the wound and periwound skin to facilitate wound healing, and to make wound assessment easier so that the size and extent of the wound can be visualised.
	a. Stop bleeding by applying firm pressure. Elevate the limb, if applicable, above heart level. b. Clean the wound by gently irrigating with warm normal saline. Carefully clean under the skin flap to remove foreign debris or blood clots. c. Pat dry the surrounding skin.
7. Realign (if possible) any skin or flap.
	a. Carefully realign by rolling the skin flap with a moist, sterile cotton bud. The use of a moistened cotton bud assists with approximation of the flap edge. b. Do not stretch the skin to ‘make it fit’. Otherwise, the skin flap will shrink back on itself or it may tear off completely. c. If the skin flap cannot be realigned, apply moist wound-dressing principles to promote wound healing.
8. Assess the degree of tissue loss and skin or flap colour:		Provides a combination of subjective and objective data to assess effectiveness of wound management plan and to plan appropriate interventions.
	a. Using the STAR Skin Tear Classification System (see Figure 30-19), select the skin tear category that best describes the type of skin tear you are treating. b. Note the colour of the skin flap. If the skin or flap colour is pale, dusky or darkened when compared with the person’s normal surrounding skin, this may indicate reduced blood flow (ischaemia) or the presence of a blood clot (haematoma), which may affect the skin or flap viability. c. If the skin or flap colour is pale, dusky or darkened, reassess in 24-48 hours or during the first dressing change.
9. Assess the surrounding skin condition for fragility, swelling, discolouration or bruising. This information will assist you when selecting an appropriate dressing.
10. Assess the person, their wound and their healing environment.		A person’s overall medical condition may affect how quickly the wound is likely to heal. This will guide the management and preventive strategies you decide to use.
11. Apply a dressing. Regardless of what type of dressing you select, you should follow these principles:
	• Ensure the dressing extends over the wound edge by at least 1.5–2 cm. • Before applying the dressing, draw arrows on top of the dressing with a felt pen to indicate the direction of the skin flap and write the due date for removal. When removing the dressing, ensure that you remove it in the direction of the arrow to avoid pulling back the skin flap. • Leave in place for 5–7 days. Change earlier only if there is 75% leakage on the dressing. • Reapply a new dressing if healing is not established and leave the dressing intact for 5–7 days. • If the wound is healed, leave it open and moisturise twice daily with a pH-neutral emollient.	Reduces the risk of trauma on removal of the dressing and increases the ability of the dressing to absorb any leakage from the wound.
12. Protect limbs: Apply a limb protector or tubular retention bandage to prevent further damage or to hold any dressing in situ.
13. Document the skin tear:		Provides relevant information about the patient and the wound, monitors healing process, guides wound management of the person as a whole, evaluates the success of management and fulfils legal requirements.
	a. Document the skin tear category and location in the patient’s record and wound-care assessment chart.
	b. Submit an incident report as required.
14. Monitor the healing of the wound:
	a. Check the dressing and surrounding skin regularly for signs of complications or infection, but leave the dressing intact unless an inspection is clinically indicated. b. Educate the patient about the signs and symptoms of complications or infection. Advise them to report problems, especially any increase in pain, warmth, odour, redness, purulent exudate or fever.
15. Implement skin-tear prevention strategies, including the following:
	• Assess and recognise risk. • Use extreme caution and a gentle touch. • Avoid direct contact with the skin: use slide sheets where possible to reduce the risk of friction or shearing forces on the skin, especially when transferring someone. • Protect fragile skin: if a person has fragile skin or has had repeated skin tears, encourage them to wear long sleeves and long trousers to protect their skin. • Apply a pH-neutral moisturiser and/or barrier cream at least twice daily. This will help to prevent dry skin. • Use soap-free alternatives; avoid using soaps and perfumed lotions as these can dry the skin. Instead, use a pH-neutral cleanser or moisturiser. • Avoid using adhesives. Adhesives may increase the risk of tearing the skin when they are removed. It is advisable to use a limb protector instead. • Use protective padding on furniture and equipment: pad bed rails, wheelchair arms and leg supports to reduce the risk of skin injuries. • Ensure adequate lighting. A well-lit environment helps to reduce risk of people bumping into furniture, doors or equipment.	People with fragile, thin, bruised or discoloured skin are at a high risk for further skin tears. Many skin tears occur when performing normal daily activities such as bathing, dressing and transferring individuals at risk. Avoid wearing jewellery or a watch.
16. Provide continuing education: Help other staff members, patients and their family members understand the importance of identifying those at risk for skin tears, appropriate treatment and prevention strategies.
17. Document all relevant information in patient’s chart.		Provides relevant information about the patient and the wound, monitors healing process, guides wound management of the person as a whole, evaluates the success of management and fulfils legal requirement.

Sinus

A sinus is a cavity or a track that extends from the skin surface to underlying tissue. A sinus may be the result of an infection, ulceration or necrosis of the dermis and underlying tissue, or a surgical wound dehiscence. The goal of management is to gently pack the sinus from the base upwards to eliminate dead space in the wound, prevent abscess formation and facilitate granulation tissue formation (Joanna Briggs Institute, 2011).

Fistula

A fistula is an abnormal passage between two or more structures or spaces. This can involve a communication tract from one body cavity or organ to another organ or to the skin. The goal of management is closure of the fistula, either spontaneously or surgically. Fistulae may be internal or external and are often associated with inflammatory diseases or a postoperative complication. External fistulae may be the result of trauma, infection, malignancy, obstruction, surgery or radiation damage. Management of patient with a fistula requires complex, multidisciplinary care.

Burns

The initial assessment of a burn injury informs the plan of care. Burn injury assessment is notoriously difficult, and therefore access to specialist services for guidance to appropriate assessment, definition/classification and treatment is essential. Types of burn injury include damage to the skin caused by heat (thermal), chemical, electrical or radiation sources. Thermal burns are the most frequent type of burn; severity is related to temperature and duration of contact. Chemical burns are more likely to be full-thickness in depth and it may take several days for the severity of burn injury to develop or ‘declare’ the extent of tissue injury. The severity depends on the manner and duration of contact, the amount of skin and area of body involved, the concentration of the chemical and how the incidence occurred. Electrical burn injury is most commonly caused by alternating current; severity is due to the voltage (force) and amperage (strength). Tissue injury occurs when electrical energy is converted to heat. Electrical burns have a point of entrance and exit, and the depth of injury can be difficult to determine.

Burn injury is classified according to the mechanism of injury, depth of injury and extent of total body surface area involved (see Table 30-13 and Figure 30-20).

TABLE 30-13 CLASSIFICATION OF BURN INJURY

Adapted from Carville K 2007 Wound care manual, ed 5. Osborne Park, WA, Silver Chain Foundation; NSW Severe Burn Injury Service 2009 Clinical Practice Guidelines: Burn Wound Management, NSW Health, p. 51.

FIGURE 30-20 Recognising burn depths.

From New South Wales Agency for Clinical Innovation (ACI) n.d. Recognising burns depths. Sydney, ACI. Online. Available at www.aci.health.nsw.gov.au/__data/assets/pdf_file/0006/162636/Recognising_Burn_Depths_Chart_A3_11_10_28.pdf 7 Jun 2012.

There are several techniques for assessing the amount of tissue damage in relation to total body surface area (TBSA), which is important for clinical management (Joanna Briggs Institute, 2010). Wallace’s ‘rule of nines’ tool divides the body surface of adults into areas of 9% (or multiples of 9%), with the exception that the perineum is estimated at 1% (Figure 30-21). This allows the extent of the burn to be estimated with reproducible accuracy. Children have different body surface area (BSA) proportions, and the paediatric rule of nines is adjusted for age by taking 1% BSA from the head and adding 0.5% BSA to each leg for each year of life after 1 year of age, until age 10 years where adult proportions are reached.

FIGURE 30-21 Wallace’s rule of nines tool. A, Adult; B, Child.

From Elliot D, Aitken L, Chaboyer W, editors 2006 ACCCN’s Critical care nursing. Sydney, Elsevier.

Age-dependent burn graphs such as the Lund and Browder chart is the preferred method to estimate BSA burn, especially in children and neonates (Figure 30-22) (Joanna Briggs Institute, 2010).

FIGURE 30-22 Lund and Browder chart for estimating and documenting the severity and extent of burn wounds in adults and children (revised Feb 2008)

From Therapeutic Guidelines Limited 2012 (Jul) eTG complete. www.tg.org.au

Small burns may be estimated using the area of the palmar surface (fingers and palm) of the patient’s hand, which approximates to 1% BSA.

Pressure injuries

Pressure ulcer, pressure sore, decubitus ulcer and bed sore are terms commonly used to describe pressure injuries. A pressure injury is an injury to the skin and/or underlying tissue, usually over a bony prominence. It occurs as a result of pressure alone, or pressure in combination with shear and/or friction.

Shearing forces usually occur as a result of sliding or dragging the skin across a support surface such as a mattress. Friction is the abrasion of the epithelial surface of the skin by rubbing against an abrasive or resistant surface. Friction may occur if the patient repeatedly rubs their heels on their mattress or on wheelchair foot plates. The presence of constant moisture from perspiration, urinary and/or faecal incontinence or wound leakage affects the ability of the skin to resist this type of damage.

Pressure injuries can occur in any location, but are most commonly found on the sacrum or coccyx and heels. They may also occur on other bony prominences, including the ischium, toes, elbows, ears, ankles, nose or other areas of the body. All patients are at risk of developing a pressure injury. Table 30-14 reviews some key risk factors for the development of pressure injuries.

TABLE 30-14 RISK FACTORS FOR PRESSURE INJURIES

Pressure is the major cause of tissue injury and is related to the intensity and duration of pressure and the ability of the tissue to tolerate pressure. Sustained pressure on a localised area of tissue results in occlusion of blood flow to the vascular and lymph vessels that supply oxygen and nutrients to the tissues. This results in tissue ischaemia and reperfusion injury, leading to cell destruction and tissue death (Queensland Health, 2009).

The likelihood of developing a pressure injury is dependent on a number of factors which affect tissue tolerance (see Table 30-12). The intensity and duration of pressure in combination with other risk factors determine a patient’s capacity to tolerate pressure (Queensland Health, 2009).

Pressure injuries are staged to help determine how severe the damage to the skin and underlying tissue structures might be. The Pan Pacific clinical practice guidelines for the prevention and management of pressure injury (Australian Wound Management Association, 2012) have recently been released and recommend the use of a pressure injury classification system to provide a consistent and accurate means by which the severity of a pressure injury can be communicated and documented. Presently there are four stages of pressure damage. The higher the stage, the deeper the tissue involvement.

STAGE 1 pressure injuries present as areas of persistent, non-blanchable redness when compared with the surrounding skin. The skin around the wound may be painful or itchy, firm or boggy, and warmer or cooler to the touch when compared with the surrounding skin.

Stage 1 pressure injury may be difficult to detect in individuals with dark skin tones. In lighter skin-toned individuals, if you press on the skin for a few seconds, normal skin typically goes white in colour (blanching) and then returns to a normal pink colour when the pressure is released. However, patients with more darkly pigmented skin may not have visible blanching and skin colour may differ from the surrounding area. This means that when you press on the skin, changes in skin colour are difficult to detect.

STAGE 2 pressure injuries represent partial-thickness loss of the dermis, and present as shallow open ulcers with a red or pink wound bed; they may also present as an intact or open/ruptured fluid-filled blister. If a blister is found with clear fluid present and the epidermis is clearly separated from the dermis, this is recorded as a Stage 2 pressure injury.

Stage 2 pressure injuries present as shiny or dry shallow ulcers without any bruising present, since bruising represents suspected deep-tissue damage.

STAGE 3 pressure injuries represent full-thickness skin loss. Subcutaneous fat may be visible but bone, tendons or muscle are not exposed. Thick yellow tissue (slough) may be present but this does not obscure the depth of tissue loss. There may be undermining and tunnelling of the wound (i.e. the wound is deeper than it appears on the surface of the skin).

The depth of a Stage 3 pressure injury varies depending on where it is located anatomically. A pressure injury on the bridge of the nose, ear, scalp and ankle does not have subcutaneous tissue and Stage 3 pressure injuries can be shallow. In contrast, areas of significant adiposity or fatty tissue can develop extremely deep Stage 3 pressure injuries, although bone and/or tendon is not visible or directly palpable.

STAGE 4 pressure injuries are the most severe, and represent full-thickness tissue loss with exposed bone, tendon or muscle. Thick yellow tissue (slough) or black necrotic tissue may be present on some parts of the wound bed. Often there is undermining and tunnelling of the adjacent tissue.

The depth of a Stage 4 pressure injury varies by anatomical location. The bridge of the nose, ear, scalp and ankles do not have subcutaneous tissue, so ulcers in these locations can be shallow. Stage 4 pressure injuries can extend into muscle and/or supporting structures (e.g. fascia, tendon or joint capsule), making osteomyelitis (infection in the bone) possible. Exposed bone/tendon is visible or directly palpable.

FIGURE 30-23 Stage 1 pressure injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

FIGURE 30-24 Stage 2 pressure injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

In addition to the above stages of pressure injuries there are two other categories of tissue damage. Suspected deep tissue injury presents as purple or maroon discoloured intact skin or a blood-filled blister due to damage of the underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, or warmer or cooler as compared with adjacent tissue.

Deep-tissue injury may be difficult to detect in individuals with dark skin tones. The tissue injury may develop into a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Changes may develop rapidly, exposing additional layers of tissue, even with optimal treatment.

Unstageable pressure injuries present as full-thickness tissue loss in which the base of the wound is covered by thick yellow, tan, grey, green or brown tissue and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (i.e. dry, adherent, intact without erythema/redness) eschar on the heels serves as ‘the body’s natural (biological) cover’ and should not be removed.

There are limitations to the staging system for pressure injuries, including the following:

• Reactive hyperaemia may be mistaken for a Stage 1 pressure injury. The presence of non-blanching erythema requires the patient to be repositioned off the area of redness and reassessed in 30 minutes before diagnosing a Stage 1 pressure injury (Queensland Health, 2009).

FIGURE 30-25 Stage 3 pressure injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

FIGURE 30-26 Stage 4 pressure injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

• Stage 1 pressure injury can be difficult to identify in patients with dark-coloured skin (see Figure 30-29).

• Necrotic tissue (eschar or slough) can conceal the extent of tissue injury, so should be debrided where possible to correctly stage the degree of pressure injury and then be reclassified once debridement has occurred.

• Reverse staging of a healing injury is not generally acceptable.

• The progress of pressure-injury healing should be documented using objective parameters such as size, depth, amount of necrotic tissue, amount of exudate and presence of granulation and epithelial tissue.

• The staging system depends on visual observation of tissue involvement. Factors such as location, wound dimensions, description of wound bed, edge of the wound, condition of periwound skin, pain and other factors which may delay wound healing should also be assessed (Australian Wound Management Association, 2012).

FIGURE 30-29 Comparison of stage I pressure sores in patients with lightly and darkly pigmented skin.

Courtesy ConvaTec. Modified from Gaskin FC 1986 Detection of cyanosis in the person with dark skin. J Nat Black Nurses Assoc 1:52; Henderson CT and others 1997 Draft definition of stage I pressure ulcers: inclusion of persons with darkly pigmented skin. Adv Wound Care 10(5):16.

FIGURE 30-27 Suspected deep-tissue injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

FIGURE 30-28 Unstageable pressure injury.

Diagram used with permission of the National Pressure Ulcer Advisory Panel, Washington DC, 10/07/12. Image courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

SITES OF PRESSURE INJURIES

All parts of the body are at risk of pressure injury. The most common sites are those over bony prominences, as shown in Figure 30-30.

FIGURE 30-30 Bony prominences most frequently underlying pressure ulcer.

From Grey J, Enoch S 2006 Pressure ulcers. Br Med J 332(7539):472–75.

RISK ASSESSMENT

In order to identify patients at risk of pressure injury, patients must all be screened for risk using an acceptable pressure ulcer risk assessment tool, on admission and regularly throughout their episode of care (Queensland Health, 2009). Pressure ulcer risk assessment tools have been developed to assist in the identification and assessment of patients at risk for pressure injury. Examples of risk assessment tools include the Waterlow, Braden and Norton tools (copies of each of these tools are available from the Australian Wound Management Association guidelines; see Online resources). Risk assessment tools commonly use a rating scale to weight the severity of risk as no risk, low, medium or high risk (Queensland Health, 2009). Risk assessment tools also commonly address risk factors such as mobility, nutritional status, sensory impairment, level of consciousness, neurological status and incontinence (Queensland Health, 2009). The presence of any condition that limits mobility to the point where a patient is unable to move independently or change position to relieve pressure means that the patient is automatically ‘at risk’.

Skill 30-4 demonstrates how to perform an assessment to identify patients at risk of pressure injury; this risk assessment is part of the admission process and ongoing preventative management for each patient (Australian Wound Management Association, 2012). An assessment to determine risk for pressure injury should be performed (Queensland Health, 2009):

SKILL 30-4 Assessment for risk of pressure injury

DELEGATION CONSIDERATIONS

The management and prevention of pressure injuries can be undertaken by all healthcare professionals. Check organisational policies regarding which wound care interventions can be delegated to health workers. The assessment of a person with or at risk for or with a pressure injury requires the problem-solving and knowledge-application skills of a registered nurse.

EQUIPMENT

• Pressure injury risk assessment tool

All patients identified at risk of developing a pressure injury should have a comprehensive preventative management plan in place which aims to maintain tissue tolerance to pressure and protect the individual against the forces of pressure, shear and friction.

PREVENTION STRATEGIES

The Australian Wound Management Association (AWMA, 2012) has recently released clinical guidelines to guide clinicians in identifying patients at risk and in selecting appropriate preventive interventions (see Figure 30-31). These guidelines are freely available online (see Online resources).

FIGURE 30-31 Flow chart for the prevention and management of pressure injury.

From Australian Wound Management Association 2012 Pan Pacific clinical practice guideline for the prevention and management of pressure injury. Osborne Park, WA, Cambridge Media, p. 12. Online. Available at www.awma.com.au/publications/2012_AWMA_Pan_Pacific_Guidelines.pdf 4 Jul 2012. Reproduced with the permission of the AWMA. All rights reserved.

There are many strategies that can be implemented to prevent pressure injuries.

BOX 30-2 THE BRADEN SCALE FOR PREDICTING PRESSURE SORE RISK

Working as part of a team is important to ensure that appropriate pressure ulcer-prevention strategies are implemented. Your team includes the patient, family members, general practitioner, nurses, care staff and allied health professionals. Education of the patient, family members and other healthcare professionals is essential so that they understand the causes of skin damage.

SUPPORT SURFACES

The optimal support surface is one that relieves pressure, shear and friction and maintains a stable skin temperature (AWMA, 2012). Support surfaces should distribute bodyweight over a large surface area or totally remove pressure from the body surface, thereby reducing point pressure and tissue damage. Support surfaces alone do not eliminate the risk of pressure injury, as pressure-injury prevention requires comprehensive clinical care, regular repositioning and ongoing assessment.

There are many support surfaces available such as mattresses, overlays or chair cushions made up of a variety of different fabrics including foam, gel or air. Comfort equipment includes overlays, pads, cushions and sheepskins; these are mostly used for comfort and in combination with existing mattresses or chairs that a patient is using. They may provide a degree of pressure reduction and reduce shearing and friction because of their low-resistance or non-abrasive properties. Comfort devices are suitable for low-risk patients who are relatively mobile and require minimal intervention.

Constant low-pressure devices conform to body contours and aim to redistribute weight over a wider area, thereby reducing tissue interface pressure (AWMA, 2012). These devices include foam- or fibre-filled mattresses and overlays, water beds, gel pads, air overlays and mattresses with both static/constant air and low-air-loss devices (AWMA, 2012). These devices may be powered, mechanical devices or non-powered, non-mechanical devices. Constant low-pressure devices may be appropriate for medium-risk patients who are able to reposition themselves or who receive frequent repositioning.

Alternating-pressure devices generate alternating high and low pressure between the body and the support surface by periodically deflating air cells under the body and redistributing the pressure on the tissue, which encourages reperfusion of previously supported areas (Queensland Health, 2009). These devices are available as overlays or single or multi-layered mattress replacements. They are suitable for high-risk patients who are immobile or obese.

Specialty beds combine a bed and sleeping surface and are designed for patients at very high risk for pressure injury.

Pressure injury prevention and management requires a collaborative approach. The patient’s risk status and risk factors provide the basis for the formation of an individualised prevention and management plan. The management plan should provide specific details of what care is required, who is responsible for that care, frequency of turning, equipment required, referrals and expected outcomes (AWMA, 2012). Clinical interventions must be regularly monitored and documented and communicated to staff, patients, families and carers.

FIGURE 30-32 Mr Bukowski’s leg ulcer.

Courtesy Wound Healing Community Outreach Service, Queensland University of Technology.

Mr Bukowski re-presents 6 months after the skin tear on his left arm with a new wound located on his left lateral leg (gaiter region). The wound is failing to heal despite using the strategies that were recommended to treat his skin tears. Mr Bukowski states that the wound has been present for approximately 4 months and started as a minor skin tear. The wound has gradually been increasing in size and it has been leaking a lot. He says that sometimes he has to change the dressings every day because it leaks that much. Mr Bukowski has noticed that his skin is very dry and scaly and that his skin looks like it is going rusty. He reports that the wound is sometimes painful, particularly after he has been standing for a while, and that the pain is worse when he first gets out of bed in the morning and by late in the afternoon. He has also noticed that his ankles become quite swollen and finds that elevating his legs can help to reduce his pain and swelling. Mr Bukowski reports feeling a bit ‘out of sorts’; he can’t go out like he used to because he is worried that others can smell his wound, he is fearful that the leakage will ruin his good clothes and his wound might get worse. He hasn’t told his daughter about his wound because he doesn’t want to worry her.