The skin is responsible for maintaining the body’s core temperature. It is controlled by the hypothalamus. The skin stabilizes heat generated by metabolism. This is done by heat conduction, convection and radiation from the skin surface. Heat loss is also influenced by vasodilation and constriction, varying the amount of blood flowing beneath the skin surface. This mechanism also prevents excessive heat loss in cold weather. Sweat production and evaporation have a cooling effect. The body is insulated from the environment by a layer of subcutaneous fatty adipose tissue

Vitamin D synthesis

Vitamin D is synthesized from ultraviolet light falling on the skin. Vitamin D is necessary for calcium absorption. Vitamin D can also be synthesized from dietary intake

Excretion and reserve

Some gaseous exchange takes place through skin. Sodium and urea are excreted via sweat. The skin provides a water reserve which is drawn into the circulating blood volume in cases of sudden fluid loss, such as haemorrhage or chronic dehydration. The fat layer can also be converted into energy

• protection

• sensation

• thermoregulation

• vitamin D synthesis

• excretion and reserve.

The skin is made up of two main parts, the epidermis and the dermis, which cover the subcutaneous fat layer and deep structures (Fig. 24.1) (Seidel et al. 2006).

Figure 24.1 Skin structure.

Wound healing

Terminology and the number of stages in the healing process vary between texts, however, the general consensus is that four phases of healing occur. They usually follow a set pattern (Clark 2002), but can occur concurrently, and different parts of the same wound can heal at different rates (Table 24.1). Wound healing can be complex and is affected by the mechanism of injury and the general health of the patient (Gantweker & Hom 2012).

Table 24.1

Phases of wound healing

Duration	Phase	Signs
First hour	Haemostasis	Initial vasoconstriction Coagulation of wound
10 minutes–5 days	Inflammatory	Vasodilation, pain, heat, swelling
3 days–1 month	Proliferation	Wound size diminishing
		Surrounding skin of normal colour
		Less pain
3 weeks–1 year	Maturation	Wound healed Scarring fades

The wound healing process occurs from the time of injury and may last days to years. The phases can be divided into haemostasis, inflammatory stage, the proliferative or maturation stage and the remodeling stage.

Haemostasis

The body’s initial response to a cut in the skin is bleeding. This extravasation initiates platelet activity and coagulation of blood. It also results in vasoconstriction and release of histamines and ATP, which also attract leucocytes. Platelets begin to aggregate and the coagulation cascade results in the development of a fibrin mesh and clot, or beginnings of a scab, which temporarily seals the wound. Once the clot is formed, fibrinolysis commences as part of the body’s defence mechanism. This ensures the clot does not extend and allows better migration of cells into the wound bed (Baranoski & Ayello 2008).

Inflammatory stage

As well as a haemostatic response, the body also responds to tissue trauma by releasing prostaglandins and activated proteins which initiate vasodilation in the area. This has two main functions:

• it increases blood supply to the area

• it increases capillary permeability.

This is to enable plasma to leak into tissues around the area of injury. This creates wound exudate. Neutrophils are the first leucocytes that usually arrive within 6–12 hours at the injury site (Lewis et al. 2011a), leak into the area of the wound and offer initial protection from infection by engulfing and digesting bacteria. Neutrophils have a short life span, and so are replaced by monocytes that are capable of phagocytosis. These promote new tissue formation and angiogenesis, and continue to engulf and destroy bacteria and debris from the wound, including old neutrophils (Baranoski & Ayello, 2008).

The signs of an inflammatory response are often confused with infection, so it is important to establish a clear history of the duration since injury. Inflammatory responses usually occur before infection has had time to develop. The signs of the inflammatory response include:

• redness – because of local vasodilatation

• heat – because of increased blood supply and metabolic activity

• oedema – because increased capillary permeability allows fluid to leak into the extracellular space

• pain – due to pressure of fluid in tissues and chemical irritation from enzymes such as prostaglandin.

This inflammation is vital to the natural healing. If it is suppressed by drugs or illness, healing will be delayed. Macrophages are essential for transition into the proliferation stage of healing, as they begin to produce transforming growth factor (TGF), which promotes angiogenesis and the formation of new tissues. Macrophages also produce fibroblast growth factor (FGF), which stimulates fibroblast production (Bale & Jones 2006).

Proliferation stage

This starts 3–5 days post-injury and can last up to three weeks (Lewis et al. 2011b). As its name suggests, this part of the healing process is about growth and reproduction of tissue to replace that lost in injury. By day five, the wound surface will only be 7 % of its pre-injury tensile strength (Waller & Tan 2009). In order to produce new tissue, the wound needs a good oxygen supply and essential nutrients such as vitamin C, protein and zinc (Kumar et al. 2005, Bishop 2008). As angiogenesis occurs in response to wound hypoxia and TGF, new capillary loops develop and the wound is oxygenated. Three distinct processes occur during the proliferation phase.

Granulation

This is the formation of new tissue up from the base and in from the sides of a wound. It is dependent on the division of endothelial cells forming new capillary loops, until eventually they meet up with existing undamaged blood vessels. At the same time, fibroblasts begin to produce a network of collagen and ground substance that fills tissue spaces and begins to bind fibres together. Collagen synthesis depends on adequate nutrients, i.e., vitamin C, copper and iron (Kumar et al. 2005). These can usually be obtained from a healthy diet. Collagen forms in a haphazard and jelly-like structure, and with adequate vitamin C matures into a strong cross-linked structure which gives the tissue its tensile strength.

Contraction

This occurs at the same time as epithelialization. In wounds where tissue loss has occurred, once the wound bed has filled with healthy granulation tissue, myofibroblasts develop which contract and pull the wound edges together, therefore decreasing the overall size of the wound. Keratinocytes are responsible for the re-epithelialization from the wound edges (Naude 2010).

Epithelialization

This is the resurfacing of the wound by regeneration of epithelial cells. This will only occur where basal cells are in contact with the dermal layer, and therefore in deep wounds regeneration will only occur around wound margins until granulation has taken place. In wounds of varying depth, small islands of epithelialization will occur in superficial parts of the wound. This gradually migrates across wound surfaces until epithelialization is complete. The attachment of this layer to dermal connective tissue is fragile and easily displaced. Regeneration therefore continues until the epidermis has regained its usual thickness. Epithelial regeneration requires a warm, moist environment. If a wound surface has dry scabs or necrotic areas, these will form a barrier to migration of new cells. Cells eventually burrow under scabs.

As the wound cavity is filled with granulation tissue and the surface is regenerated with epithelial cells, the proliferation stops. If this does not happen, e.g., if overgranulation occurs due to continued hypoxic stimulation, perhaps as a result of local ischaemia, then excessive scar tissue is formed (Kumar et al. 2005).

Maturation or remodeling stage

This begins around three weeks after injury, and is a process of returning the area to its usual functional structure. The process is twofold.

Firstly, collagen is remodelled, sometimes over a period of years. The aim of this is to gradually replace newly formed type III collagen, laid down in the proliferation phase, with stronger, more organized collagen fibres. The amount of collagen does not change; its bundles become thicker and shorter and hold the wound together more tightly. Although the skin and wound scar become stronger, the area only usually regains about 80 % of the pre-injury tensile strength (Kumar et al. 2005). This takes a long time; at thee months post-injury 50 % of tensile strength is considered good healing (Baranoski & Ayello 2008).

The second part of the process is the rationalization of blood vessels bringing extra nutrients to the area. This process occurs gradually, and its progression can be monitored by the gradual fading of the scar. It will become paler and flatter as blood vessels diminish. Once maturation is achieved the scar will appear white; it is avascular, has no sebaceous glands and no hairs (Baranoski & Ayello 2008).

Scarring

Dermal damage results in an abnormal formation of connective tissue. This is permanent and manifests as a scar on the skin surface. Scarring follows three phases, although the time span increases with age, skin pigmentation and as a result of poor general health (Table 24.2). Certain areas of the body are notorious for poor scarring – the shoulder, knee, and sternal areas, which are areas under a lot of tension and motion (Bayat et al. 2003, Capellan & Hollander 2003).

Table 24.2

Scar formation

No. of weeks post-injury	Scar characteristics
0–4 weeks	Soft, weak scar line
4–12 weeks	Scar contracts, becomes harder and stronger
12–52 weeks	Scar line flattens and becomes soft and supple, moving easily with surrounding skin. Gradually whitens as vascularity decreases. Skin does not regain pre-injury elasticity

Keloid scarring is usually a genetic phenomenon where collagen type I is produced in a tumor-like fashion with uncontrolled growth of scar tissue (Widgerow 2011). Keloid scarring results from the formation of large amounts of scar tissue in the proliferation stage of healing. It results from an increase in collagen synthesis and lysis to an extent where tissue formation exceeds cell breakdown (Bryant & Nix 2006). Keloid scarring is also considered to be related to the melanocyte-stimulating hormone as it is much more common in people with heavily pigmented skin, predominantly those aged 10–30 years (Bayat et al. 2003, Mustoe 2004). Tissue growth is persistent, with scarring often being much larger than the original wound. Early effective wound management can reduce the risk of keloid scarring.

Hypertrophic scarring forms in a similar fashion to tissue growth, but follows the line of incision. This type of scarring is more common in the young and in fair-skinned people and typically occurs after burn injury on the trunk and extremities. In these scars, there is an imbalance in collagen synthesis versus collagen degradation. The resulting wounds are red and raised and can be itchy. In the majority of cases, this is temporary and resolves without treatment although it may take a year or more.

Tattoo scarring results from gravel or foreign bodies being left in a wound. It forms unsightly purple or blue blotches in the scar and is difficult to remedy after initial wound healing. Generally, scars that lie parallel to the body’s natural tension lines have a better cosmetic prognosis.

Factors affecting wound healing

Although patients with sudden traumatic wounds do not have the same physiological and educational preparation as patients undergoing surgery, many of the influences on wound healing can be optimized by effective education and empowerment during their initial visit for wound management. Clinical factors affecting healing potential can also be identified at this early stage, and the patient’s care can be designed to accommodate them. The main influences on wound healing are listed in Box 24.2.

Box 24.2 Factors affecting wound healing

Age

With age, all metabolic processes slow down and collagen production is lower; therefore wounds heal more slowly and have less tensile strength

Tissue perfusion

Many diseases cause hypoxia and reduced tissue perfusion. Those with a significant effect on wound healing include:

• Anaemia

• Peripheral vascular disease

• Respiratory disease

• Arteriosclerosis

• Dehydration

The result of this is reduced fibroblast activity and collagen synthesis, reduced epithelial regeneration and greater susceptibility to infection because of decreased leucocyte activity

Other diseases

These include diabetes, immune disorders and cancer, because of dampened inflammatory response and susceptibility to infection. Also, inflammatory conditions, liver failure and uraemia

Psychological factors and body image

Stress and anxiety suppress the immune system and are linked with sleep disturbance. This has been shown to delay healing. Anabolic healing is enhanced by sleep. Altered body image can occur from seemingly minor wounds and this can adversely affect healing in terms of stress and compliance with wound care strategies

Poor wound care

Inadequate wound cleansing or inappropriate wound dressing is an avoidable factor in healing

Nutrition

Protein, vitamins and trace elements are vital for prompt, adequate wound healing. These include:

Vitamins B, E and K also influence healing, and adequate protein and calorie intake is also necessary

Hydration

To maintain metabolism, between 2 and 2.5 L of fluid in 24 hours is needed. Less than this will result in fluid being drawn from interstitial spaces. Patients who are already clinically dehydrated will have delayed healing

Smoking

Both carbon monoxide and nicotine, as end-products of smoking, have an adverse effect on peripheral tissue perfusion, therefore increasing hypoxia risk. There is also an increased risk of thrombus formation in smokers

Drug therapy

Anti-inflammatory agents, immunosuppressive drugs, cytotoxic agents and corticosteroids all impinge on the healing process

Nutrition

Nutrition deserves more elaborate exploration, as it is fundamental to adequate healing and is often overlooked both in discharge information and in promoting well-being in hospital inpatients. Malnutrition affects healing in several ways:

• poor healing with reduced tensile strength and an increased risk of wound dehiscence (Scholl & Langkamp-Henken 2001)

• an increased likelihood of infection (Lansdown 2004)

• poor-quality scarring.

Protein and calorie intake need to be above normal recommended levels to support additional collagen synthesis and metabolic activity (Table 24.3).

Table 24.3

Calorie and protein intake in wound healing

	Energy (kcal)	Protein (g)
Men	2150–2510	54–63
Women	1680–2150	42–45

Vitamin deficiency

Vitamin C is essential for the synthesis of collagen; a deficiency reduces wound tensile strength, increases the fragility of capillaries and impairs angiogenesis. Vitamin A supplement improves healing in patients on corticosteroids (Scholl & Langkamp-Henken 2001). It can help to restore inflammatory response and reduces the risk of wound infection. Similarly, a vitamin A deficiency increases infection risk. Vitamin B complex is necessary for wound strength as it contributes to cross-linking of collagen fibres. Vitamin K is essential for the clotting process in early wound healing (Lansdown 2004).

Trace element deficiency

Iron deficiency has two significant impacts on wound healing: first, in patients with anaemia, oxygen transportation is reduced and therefore tissue perfusion is inhibited; and second, iron is a necessary co-factor in collagen synthesis. Copper deficiency is rare but where it occurs, enzyme activity is restricted and collagen cross-linkage is impaired. Zinc deficiency delays wound healing because it slows collagen synthesis, reduces wound strength and decreases speed of epithelialization (Baranoski & Ayello, 2008). The use of a dietician may be of benefit to patients with nutritional issues.

Body type

Body type may also affect wound healing. An obese patient, for example, may experience a compromise in wound healing due to poor blood supply to adipose tissue. In addition, some obese patients have protein malnutrition, which further impedes the healing. Conversely, when a patient is emaciated, the lack of oxygen and nutritional stores may interfere with wound healing (Thomas Hess 2011).

Wound assessment

It is essential that an accurate history is elicited from the patient to ensure systematic assessment and appropriate management of the wound. As with all patients attending the ED, the immediate history of events leading up to ED attendance is imperative. Assessment should consider when, where and how the injury occurred. The mechanism of injury gives important clues to the type of wound being dealt with as well as any materials involved in the injury, such as wood splinters, glass, metal, etc. (Flarity & Hoyt 2010). Table 24.4 relates the mechanism of injury to wound type. The type of skin damage of injury is usually related to the mechanism of injury (Fig. 24.2).

Table 24.4

Mechanism of injury: wound classifications

Figure 24.2 Mechanism of injury and skin damage.

The size, shape, wound depth and anatomical site of the wound should be assessed and documented. Diagrams in the patient’s notes, or a photograph with a measurement scale, are useful if the wound is likely to need follow-up care.

Table 24.5 demonstrates the essential principles of wound assessment.

Table 24.5

Wound assessment

Assessment question	Rationale
How did the wound occur?	To establish mechanism of injury and classification of wound To exclude serious or other injuries To assess potential contamination risk (Clark 2004)
When did the injury occur?	To ensure it is appropriate for primary closure To assess for infection risk (wounds >6 hours old are more prone to infection)
Size, site and depth of wound	To ascertain the most appropriate method of wound closure (e.g., wounds over joints or requiring high tensile strength usually require sutures) (Autio & Olson 2002) To ensure base of wound can be visualized
Past medical history	To detect pathology that may delay or influence healing
Medication history	To detect medication that may delay or influence healing To avoid prescribing contraindicated medications as part of wound management
Allergies	To avoid allergic reactions during the wound management process and during subsequent treatment
Tetanus status	To ensure the patient has tetanus immunity
Occupation and dominant hand	To assess the effect of the injury on the patient’s lifestyle To ensure treatment is appropriate for the patient’s lifestyle

Wound examination

Extensive wounds may often distract the novice emergency clinician, however it is paramount that the clinician completes the primary survey to rule out life-threatening problems. Please refer to previous chapters for a review of primary survey.

Effective wound examination should reveal the extent of tissue damage, the degree of contamination and specifically the integrity of the nerves, tendons and vascular supply (Autio & Olson 2002, Clark 2004). It should also exclude the presence of foreign bodies (FBs). All findings should be documented, including the normal ones.

Most traumatic wounds occur in unsterile conditions, and therefore all carry a risk of infection. A number of factors affect infection potential, such as mechanism of injury, degree of tissue loss, age of the wound prior to cleansing and anatomical location. All traumatic wounds should be considered contaminated; some of these will appear clean on initial examination, while others will be obviously contaminated. Potential for infection due to all the above reasons may assist with the method of wound closure, i.e., primary or delayed primary closure.

Excessive bleeding and macerated or badly damaged tissue can detract from a thorough examination. Bleeding should be controlled to allow an accurate examination to be carried out (Clark 2004). Assessment of vascular integrity should include the patient’s estimation of blood loss, together with objective evidence of haemorrhage. The wound should be carefully inspected for continuous oozing of blood (suggestive of venous bleeding), spurting of bright-red blood (indicative of arterial injury) and haematoma formation, which could pose a risk to healing in the form of potential infection. Haemostasis is usually achieved through direct pressure and elevation of the injured area. Where bleeding cannot be controlled specialist input should be sought. Vascular integrity distal to the wound can be assessed by observing skin colour distally to the wound, feeling skin temperature, and checking distal pulses and the speed of capillary refill (McKenna 2006).

Nerves have both a sensory and a motor function and therefore both can be checked to eliminate injury. This assessment should occur before local anaesthetic is used. Sensory function distal to the wound should be assessed either by use of a cotton wool wisp to detect the absence or presence of sensation, or by gentle pinprick tests to assess sharp and dull sensation. Motor function should be assessed, particularly in hand or wrist injuries, and this can be done by assessing a variety of movements of the patient’s hand and wrist (McKenna 2006).

Tendon injury should also be identified and eliminated as part of the examination stage of wound management. Tendons can often be partially severed and still retain their function, so elimination of this type of injury should be done in two ways. An initial systematic examination of the patient’s function in the affected limb may demonstrate reduced power or function. This should be followed by direct visualization of the wound to discover any structural damage (Waller & Tan 2009

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