Jeannie Donnelly1, Alison Collins2 and Julie Santy-Tomlinson3
1 Queens University Belfast/Belfast Health and, Social Care Trust, Belfast, UK
2 Belfast City Hospital, Belfast, UK
3 University of Hull, Hull, UK
This chapter provides an outline of the knowledge and skills required by practitioners caring for patients with the main types of acute and chronic wounds in the field of trauma and orthopaedics. Recommendations for practice will often be pragmatic as empirical research is, in many instances, lacking. The chapter is divided into two sections. Section 1 focuses on the nursing management of wounds. This will include consideration of both surgical and traumatic wounds, an overview of the wound healing process and will discuss current thinking with regards to dressing techniques. Section 2 will consider issues relating to the prevention and management of pressure ulceration.
Whilst all wound types move through the three main stages of wound healing (inflammation, proliferation and contraction), speed and efficiency of healing is affected by a range of local and systemic factors. Key factors (according to wound type) will be highlighted. These must not, however, be viewed as mutually exclusive as all factors e.g. smoking and infection, will affect all wound types.
A simple surgical wound is a healthy and uncomplicated break in the continuity of the skin resulting from surgery. It is expected to follow a rapid and predictable pathway towards healing with minimal tissue loss, scarring and loss of function. Surgeons take great care to protect as much tissue as possible from injury, carefully considering the placement of the incision, managing blood loss (to prevent haemorrhage and haematoma) and considering the best way to bring each layer of tissue (muscle, fascia, subcutaneous tissue and skin) into approximation through wound closure (Coulthard et al., 2010). Approximation speeds time to healing, reduces scaring and helps prevent infection. The wound is said to heal by primary intention.
Traumatic wound care is an integral part of the care of the patient following musculoskeletal trauma as soft tissue wounds are often consistent with the rest of the pattern of injury. Such wounds present a number of additional challenges. A compound fracture wound with full thickness tissue loss, for example, requires careful assessment (as there may be damage to nerves, tendons or muscles) and debridement of devitalised tissue. Often the wound cannot be closed immediately due to the risk of or presence of infection or excessive oedema. Closing very oedematous tissue will result in a taut wound leading to stress which can cause tissue ischaemia (reduced blood flow), particularly at the wound edge, potentially leading to tissue death or wound dehiscence (gaping or bursting open). To prevent this from happening body cavities and deeper structures are sutured closed and the layers of the skin left open to allow for free drainage of foreign material or pus or whilst waiting for swelling to decrease. The patient will normally return to surgery after 3–4 days for a further wound assessment, followed by irrigation and debridement and wound closure if it is safe to do so. This is known as delayed primary closure. The wound is said to heal by tertiary intention (Lorenz and Longaker 2008).
Some wounds cannot be closed using surgical techniques due to one or more of the following reasons: (a) the patient is not well enough to undergo surgery, (b) the wound is small or superficial (c) the wound is heavily contaminated, infected or chronic or (d) the wound is deep with a ‘dead space’ and lack of subcutaneous tissue. If the skin is left open it is important to prevent the dead space filling with blood as haematoma is the perfect medium for bacteria to multiply and as it does not have a blood supply to initiate the immune system. Healing is by secondary intention.
The wound healing process
Wound healing is the process by which damaged tissue is replaced and function restored. The wound healing process is dynamic and can be divided into three overlapping phases: haemostasis/inflammation, proliferation and maturation (remodelling).
During haemostasis damaged blood vessels constrict and blood leaking from them begins to coagulate. Platelets in the vicinity are ‘activated’ by collagen fibres in the damaged vessels and clump together forming a relatively unstable plug. The activated platelets release vasoconstrictors and other chemicals which stimulate the clotting cascade and attract other platelets to the area. The end result is a clot (platelets intertwined with fibrin).
The goal of the inflammatory phase of wound healing is to limit the amount of tissue damage and prepare the wound for healing by removing unhealthy tissue and foreign matter such as bacteria. White blood cells (basophils, neutrophils and monocytes) play a major role. Basophils release heparin and histamine. Neutrophils and monocytes (converted to macrophages) migrate from the blood vessels and congregate at the site of injury, engulfing and destroying microorganisms. The inflammatory process is a necessary part of healing. Visible signs of the process are redness, heat, swelling, pain, loss of function and increased exudate.
The goal of the proliferation phase is to close the defect as quickly as possible. The wound fills with granulation tissue (unless it is very superficial in which case it will simply re-epithelialise), contracts down in size and epithelialises. Viable epidermal cells divide and migrate from the wound edges. Migration ceases when the epidermal cells come into contact with each other.
Granulation tissue is a network of collagen fibres, new blood vessels and white blood cells and peaks between five and nine days post-operatively, presenting as a ‘healing ridge’ along the margins of the wound (Doughty and Defriese 2007). New blood vessels form by the process of ‘angiogenesis’. New capillaries (containing oxygen-rich blood and micronutrients) give the tissue a bright red granular appearance. Oxygen is important for cellular activity and any condition that impedes oxygenation of the tissues (e.g. smoking, peripheral vascular disease) slows healing and can lead to wound breakdown (Knuutinen et al., 2002). Dark coloured granulation tissue, which bleeds easily, can be indicative of infection, poor perfusion or ischaemia.
Good nutrition (see Chapter 10) is central to successful wound healing. Malnutrition may involve a deficiency or excess (or imbalance) of energy, protein and other nutrients which can be a significant factor in wounds failing to heal or succumbing to infection.
Maturation occurs once the wound has re-epithelialised and strengthens the scar tissue. Weak Type III collagen fibres (produced by fibroblasts during granulation) are changed into or replaced by strong Type I collagen. As the wound has essentially healed there is a downturn in cellular activity and the need for extra oxygen and nutrients decreases.
In a simple surgical wound, the inflammatory phase is usually complete within 36–48 hours and the proliferative phase is complete in 28 days. Maturation can take around 100 days. A surgical wound is usually ‘sealed’ within 48 hours and will be dry (no bleeding or exudate) and can be exposed. The time frame is variable and may be extended depending on the complexity of the surgery, local wound conditions and the health of the patient. A patient whose wound continues to produce a high amount of exudate five days post-operatively, or who is complaining of increasing pain may have a surgical site infection (SSI). Wounds which are open or continue to ‘weep’ (exude) will need to be carefully monitored and dressed.
The phases of wound healing are dynamic; wounds may move forwards or backwards through each phase depending on the health of the patient. For example, a wound which was healing well (showing signs of granulation) but becomes infected, will move back into the inflammatory stage. A chronic wound is often described as a wound which is ‘stuck’ in the inflammatory or proliferative phase of wound healing.
Factors affecting wound healing
Factors affecting wound healing are often referred to as intrinsic (internal – specific to the individual) or extrinsic (external – applied to the individual). Any systemic condition which results in poor perfusion, a lack of essential micronutrients, the ability to fight infection or tissue wasting/destruction can delay wound healing (Table 12.1).
Table 12.1 Factors and conditions affecting wound healing
To aid wound healing, the general health and well-being of the patient must be optimised. This is achieved by creating a care plan which takes into account relevant health and psychosocial issues. Nurses, as ‘gatekeepers’ of care, have a responsibility to use their knowledge of the patient’s needs and refer to other practitioners when help is needed.
Extrinsic factors that affect healing can be mechanical (pressure, shear, friction), chemical (wound exudate, cleansing solutions etc.) or thermal (heat, cold, radiation). Some of these factors (such as a moist wound environment) can aid healing, whilst others can delay healing.
Moist wound healing
Surgical wound dressings are applied to stem bleeding, absorb exudate and provide protection but there is constant debate about which dressing product best achieves such functions. Dry dressings may adhere to the wound (as fibres integrate into the clot matrix) causing pain and trauma on removal. Woven dressings are commonly used with the objective of absorbing wound moisture. It is claimed, however, that moist wounds heal more quickly than those left to dry out under textile-based dressings because epithelialisation is retarded by the formation of a dry scab (Winter 1962). A dressing which facilitates an optimal level of wound moisture, on the other hand, promotes wound healing (Harle et al., 2005). Orthopaedic wound dressings should therefore have the attributes of the ideal dressing (Box 12.1) in addition to being absorbent and protective. The ability of a wound dressing to stretch with movement to avoid restricting limb movement and accommodate postoperative oedema is also important especially after hip and knee arthroplasty which requires a degree of force on behalf of the surgeon to position the prosthesis firmly, thereby resulting in postoperative bruising and swelling around the joint (Jester et al., 2000).
Permeability and transparency
The permeability of a dressing refers to its ability to permit gaseous exchange (including water vapour) between the wound and external environment. Transparent films allow wound exudate and peri-wound skin to be inspected without dressing removal, minimising the risk of accidental wound contamination and trauma. Exudate, however, can pool under film dressings and cause maceration of the wound and surrounding skin (Cutting and White 2002) and peri-wound blister formation (Harle et al., 2005). Absorbent central pad dressings with an adhesive border are quicker and easier to apply than traditional dressing pads, but offer no additional advantages in terms of permeability. Vapour-permeable film dressings transmit moisture away from the wound bed to varying degrees, but should not be applied as the primary dressing at sites of profuse drainage since absobency is limited. ‘Film plus fabric’ dressings combine transpiration and absorbency, helping to prevent accumulation of fluid (Aindow and Butcher 2005). The moist and relatively hypoxic environment produced by semi-occlusive and occlusive dressings accelerates angiogenesis and promotes tissue repair (Holm et al., 1998). See Box 12.2 for further discussion of wound moisture balance.
Ability to act as a bacterial barrier
Traditional absorbent dressings provide limited protection against microbial ingress and may shed fibres into the wound, causing a focal point for infection (Jones 2006). Microbes pass through the dressing rapidly when it is damp and are dispersed into the environment on dressing removal, increasing the risk of cross-infection (Cooper and Lawrence 1996). Vapour-permeable films, incorporated into a fabric-island dressing or used as a retention dressing, have the advantage of being impermeable to bacteria (Pudner 2001). Hydrocolloids protect the wound from exogenous bacteria and have the advantage of lowering the pH of wounds to slightly acidic, inhbiting the growth of microbes (Bryan 2004). Hydrofibre dressings protect the wound from bacterial invasion by absorbing and retaining large amounts of exudate (including microbes) (Clarke et al., 2009), reducing the need to change the dressing (Ravenscroft et al., 2006) and lessening dispersal of microbes on dressing removal (White 2001).
Bathing and showering
There is a strong correlation between patient satisfaction with the postoperative dressing and ability to perform their usual personal hygiene routine (Bhattacharyya et al., 2005). There is arguably no need to apply any dressing to a surgical wound after the early postoperative period since a natural bacteria-proof barrier (fibrin seal) is quickly re-established. Patient hygiene is facilitated and worry about the wound reduced by use of a vapour-permeable film until the wound is sealed with fibrin and drainage has ceased. Environmental moisture has a minimal effect on waterproof dressings providing it does not migrate under the surface. For this reason showering is preferable to bathing.
Ease of removal
Patients may experience pain where traditional gauze dressings adhere to the wound bed. Paraffin tulle gras also has a tendency to dry out and may result in postoperative wound trauma (Voegeli 2008). According to Gupta et al. (2002), spirit-soaked gauze lifts off the wound as it dries. However, spirit-soaked gauze is likely to cause pain on contact with broken skin due to the astringent properties of alcohol-based preparations. Alcohol solutions delay wound healing and usage should be restricted to prophylactic skin disinfection (Morgan 2004). Ravenscroft et al. (2006) found removal of hydrofibre and film combined to be less painful than an adhesive fabric dressing.
Wounds can exhibit a wide combination of different characteristics, e.g. deep tissues may be exposed or the wound may be malodourous with a high or low exudate. There is no one product which is ‘smart’ enough to manage all of these. Characteristics change as they move through the healing continum and practitioners must use their assessment to set realistic treatment objectives and make evidence based dressing choices.
The first part of a wound assessment is to take a history of all factors leading to the cause of the wound. This information will provide clues to the underlying aetiology, the amount and type of tissue damage as well as potential complications such as infection. The five questions listed in Table 12.2 will help in this process. The second part of the assessment is to carefully observe the wound and the surrounding tissues to guide care and the choice of dressing. Results of the assessment should be recorded on a wound observation chart.
Table 12.2 Wound history questions for wound assessment
|Why is it there?||
|Where is the wound?||
|When did it appear?||
|Who is looking after the patient/client and their wound?||
|What would the patient/client like to achieve?||
The length, width and depth of the wound should be recorded as accurately as possible using a sterile disposable tape measure (which must not touch the wound). The length and width of the wound should be measured using the body axes as a reference point (as opposed to the longest and shortest part of the wound). Dimensions can change rapidly and over time measurements can become confused. In a wound where depth is easily visualised, a sterile probe can used to measure the distance from the bottom of the wound to the surface of the skin. Some wounds consist of extensive cavities or extremely narrow sinuses and the skin can be undermined, leading to exposure of fragile structures (blood vessels, nerves, organs). Wounds should not be probed unnecessarily as these fragile structures can be easily damaged. A surgeon or a tissue viability nurse may be able to map out the wound to assess the direction/depth of cavities. The dimensions of a wound which contains necrosis or slough will increase as ‘dead’ tissue is autolysed.
The wound bed tends to be described by the colour of tissue observed (black/brown, yellow, red and pink) (Table 12.3), indicating underlying problems such as ischaemia or tendon exposure. For example, if hard black necrosis is noted on the heel (Figure 12.1) it would be wise to assess the blood supply to the lower limb before wound debridement. If there is no blood supply, tissue cannot regenerate or mount an effective host response to infection. Tendons on the other hand, need to be kept moist to prevent dessication and loss of function. If there is no blood supply the practitioner should keep the wound dry and seek specialist help. As wounds can contain a mixture of tissues it can be difficult to accurately quantify what can be seen. Clinical judgement can be used to make a subjective calculation of each tissue type. This is then expressed as a precentage, e.g. 20% black, 50% yellow, 30% red. During dressing changes the percentages are recalculated and compared to the previous assessment. Changes help to determine improvement or deterioration. Photographs can also be useful in charting the progress of extensive wounds.
Table 12.3 Wound bed assessment – tissue colour
|Black||Tissue is necrotic (dead). There is no blood supply. Hard black necrosis is called eschar.||Dressings and ointments which contain silver (Ag) can stain the tissues a black colour but staining is superficial and temporary|
|Yellow||This tissue is sloughy. Slough is made up of dead cells and wound debris.||Tendons, fascia, bone and fat can also appear yellow.|
|Red||This tissue is healthy. Granulating tissue is comprised of collagen fibres (Type III) and new blood vessels. The new capillaries give the tissue its bright red colour and slightly uneven ‘bumpy’ texture.
Dark red granulation tissue is a sign of poor perfusion or infection (Figure 12.2).
|Muscles, organs (such as bowel) and dermis will also be red.
Sometimes tissue can over-granulate; often referred to as ‘proud flesh’ as it sits above the level of the skin. It is often seen around trache and peg tube sites.
|Pink||This tissue is healthy and is re-epithelialising.||The skin surrounding a wound can become very wet and macerated due to excess exudate. This skin can appear pinkish/white in colour.|
The practitioner must have an understanding of the evidence-based rationale behind dressing selection to enable setting realistic wound management objectives. Dressing products range from those that actively donate moisture to a wound (hydrogels) to those that absorb or contain moisture. Some are impregnated with antimicrobial agents which should not be used unless there are clinical signs of infection or the patient is immunocompromised and there is a very high risk of infection. It is also important that general advice and support is given to the patient with respect to promoting healing and preventing infection.
Surgical site infection
Healthcare-associated infections (HAIs) collectively affect approximately one in ten hospital patients every year (DoH 2006). Such infections are costly complications of heath care that cause pain and discomfort, complicated and delayed recovery and sometimes death (Srinivasaiah 2007). Surgical site infection alone has been reported by NICE (2008) to be responsible for over one-third of perioperative deaths, increased healthcare costs and a significant impact on patient quality of life. Surveillance and prevention of infection are a major focus of health care and are seen as a care quality indicator.
Any infection is the outcome of complex interactions between a host, a pathogen and the environment (EWMA 2005) and is defined as:
(The deposition of organisms in tissues and their subsequent growth and multiplication along with an associated tissue reaction.)
(Ayliffe et al., 2001)
Bacteria cannot penetrate intact skin, but can enter easily if the skin is damaged or an incision is made such as in the case of a surgical or traumatic wound. Infection is a painful and distressing complication that impairs the process of wound healing and is instrumental in delayed recovery. If it is allowed to progress it can lead to death through the spread of infection, septicaemia and organ failure.
The colonisation of any wound with microorganisms is unavoidable. The human body is host to a large number of bacteria and fungi that are part of the normal homeostatic mechanisms and are essential to many physiological processes. Harmful pathogenic organisms, however, are ever-present on the human body, in the atmosphere and in the environment. Ordinarily, the human immune system prevents these potential pathogens from entering the human body and causing harm. Organisms that are normally relatively harmless can become problematic when conventional preventive mechanisms fail.
In the orthopaedic patient the major risk from the spread of infection is osteomyelitis (infection of bone tissue) which is extremely difficult to eradicate. Osteomyelitis is also associated with biofilms attached to implanted devices or haematogenous seeding (spread of bacteria from the blood stream to implant sites) (Trampuz and Zimmerli 2006) and is a much feared complication of bone injury and surgery as the condition often becomes chronic and prevents bone from healing, leading to long-term pain and disability. The prevention of infections, including surgical site infection which may lead to osteomyelitis, is particularly central to the care of all orthopaedic patients.
Surgical site infection (SSI) is defined as:
(Infection occurring up to 30 days after surgery (or up to one year after surgery in patients receiving implants and affecting the incision or deep tissue at the operation site.)
(Owens et al., 2008)
An estimated average of 2–5% of surgical patients develop SSI during their recovery and up to a year following orthopaedic implant surgery (NICE 2008). Most SSIs are caused by skin-derived bacteria, primarily staphylococcus aureus (Dohmen, 2008). Studies of SSI in orthopaedic patients report the incidence of serious deep infections associated with SSIs and highlight consequential increases in the length of hospital stay (Coello et al., 2005). For example, deep wound infection occurs in up to 3% of patients following hip fracture repair. Surveillance data focus on high volume orthopaedic procedures such as arthroplasty and internal fixation of fractures (Morgan et al., 2005). Although rates are dropping each year, SSIs in this group remain a significant problem. In many countries surveillance of SSI rates following orthopaedic surgery for total hip replacement, total knee replacement, hemiarthroplasty and open reduction of long bone fracture is mandatory. Many patients are now discharged from hospital before the surgical wound has healed, so it is likely that the symptoms of SSI may not appear until after discharge from hospital. Following orthopaedic implant surgery, deep surgical site infections may take up to one year to manifest (Health Protection Agency 2008).
Preventing surgical site infection
The use of the most recent evidence-based guidelines for preventing HAIs is central to the prevention of surgical site infection. This should focus on local and national guidance (Chapter 9). Specific measures for the prevention of surgical site infection include:
- Evidence-based preoperative preparation and perioperative care including skin preparation and antibiotic prophylaxis.
- Strict aseptic technique when dressing or handing wounds and wound drains.
- Wound drains should be removed as soon as possible, preferably within 24 hours of surgery.
- Keeping wounds covered in the hospital environment and until the proliferation phase of healing is complete (Box 12.3) and tampering with the wound/dressing as little as possible.
- Ensuring the patient’s general health status and tissue perfusion is optimised through good nutrition and hydration.
- Close postoperative assessment and surveillance of the wound for signs of infection until recovery is complete and immediate medical referral if infection is suspected.