The epidermis is the most superficial layer and is connected to the dermis. It is avascular, receiving nutrients from the dermis below, and is composed of keratinized stratified squamous epithelial cells. Four principal types of cells are found in this layer: keratinocytes, melanocytes, Langerhans cells and Merkel cells. The epithelial cells are produced in the basal layer and gradually migrate upwards over a period of 40–56 days.

The epidermis is made up of four to five layers of cells, depending on the location in the body. The first layer, next to the dermis, is the stratum basale. Cell division occurs here, with the cells dipping down into the dermis to surround sweat glands and hair follicles. Keratin is manufactured by the keratinocytes found in this layer. Keratin is an insoluble protein that is resistant to changes in temperature and pH, and helps waterproof and protect the skin. Also found in this layer are Merkel cells, which are in contact with the flattened end of sensory neurons, and are involved in the sensation of touch. The second layer is the stratum spinosum, which contains prickle cells and Langerhans cells (Tortora and Derrickson, 2006). The prickle cells prevent cell separation by their intercellular bridges. Langerhans cells participate in immune responses and are thought to have a role in allergic or immunological skin disorders (Bennett and Moody, 1995).

The third layer is the stratum granulosum, where the keratinocytes flatten and accumulate lamellar granules. Secretions from the lamellar granules slow the loss of body fluids and entry of foreign materials (Tortora and Derrickson, 2006). The fourth layer is the stratum lucidum, which is only found in the thick skin on the palms of the hands and soles of the feet, i.e. areas of excessive wear and tear. The cells in this layer start to undergo nuclear degeneration and contain large amounts of keratin. The fifth and final layer is the stratum corneum, consisting of many layers of dead cells that are completely filled with keratin. These cells are constantly shed from the body surface, i.e. desquamation, as a result of friction and washing. They also have the ability to soak up extra moisture (Hinchliff et al, 1996).

The dermis lies beneath the epidermis and forms the main part of the skin, providing the skin with its strength and elasticity. It is formed of connective tissue containing collagen and elastic fibres, and contains blood and lymph vessels, sensory nerve endings, hair follicles, and sweat and sebaceous glands. In the dermo–epidermal junction, melanin is produced by melanocytes, under the influence of sunlight. Melanin gives colour to various body structures, e.g. hair, iris and skin, but the main function of melanin is to protect the body from ultraviolet light (Tortora and Derrickson, 2006).

The upper region of the dermis is the papillary region, which consists of a series of undulations called dermal papillae. This cellular arrangement prevents the epidermis shearing off from the dermis when shearing forces are applied to the skin. The reticular layer is the remaining portion of the dermis, and consists of dense, irregularly arranged connective tissue containing interlacing bundles of collagenous, reticular and coarse elastic fibres. It is within the spaces between these fibres that hair follicles, sensory nerves and sweat glands are located (Hinchliff et al, 1996).

The dermis is constructed of ground substance or matrix, various fibres and cells. Ground substance is an amorphous matrix, resembling a gel, which provides connective tissue with its bulk. It is permeated by strands of collagen, elastin and fibronectin and other cells. The gelatinous material is composed of water, electrolytes, glycoproteins and proteoglycans, and is synthesized by fibroblasts (Hinchliff et al, 1996).

Collagen, reticular fibres and elastin fibres are all produced by mesodermal fibroblasts, situated in the dermis. Collagen is a family of connective tissue proteins with immense tensile strength, due to their rigid and durable structure. The fibres come together to form thick bundles in which numerous cross-links form, so increasing the strength of the fibres. Collagens are important as a structural support, but also control many cellular functions, including cell shape and differentiation. Ascorbic acid is necessary for the formation of collagen. There are many types of collagen which have been identified, with Types I and III being found to be important in wound healing (Fletcher, 2000). Type I is usually physically allied with Type III collagen, whereby Type III collagen synthesis is dominant in the early stage of wound healing, but with Type I synthesis being more predominant in the later stages of healing. The reticular fibres form a loose framework in the dermis and envelop the collagen bundles. The elastin fibres (elastin) are branching yellow fibres which provide elasticity and resilience to the skin (Hopkinson, 1992).

Four types of cell are found in the dermis: fibroblasts, tissue macrophages, tissue mast cells and white blood cells. The fibroblasts lie between the collagen bundles and are concerned with collagen and elastin synthesis. The tissue macrophages or histiocytes are wandering phagocytic cells. Tissue mast cells produce histamine and heparin, and are found near blood vessels and hair follicles. Neutrophils, lymphocytes and monocytes are transient cells, and are constantly moving between blood vessels (Hinchliff et al, 1996).

The cutaneous blood vessels lie entirely within the dermis and have a rich sympathetic nerve supply, so allowing vasoconstriction or vasodilatation, depending on the local environment. The lymphatic vessels are found throughout the dermis and are responsible for draining excess tissue fluid and plasma proteins which may have leaked into the tissues. The dermis contains sensory nerves which have three types of nerve ending, each responding to a specific stimulus. The hair follicles lie in the dermis, each surrounded by its own blood and nerve supply. The basal layer of the epidermis dips down to surround the hair follicle, so the process of epithelialization can occur from this area. The sweat glands – eccrine and apocrine – are formed as coiled tubular downgrowths from the epidermis. The sebaceous glands are formed as outgrowths of the developing hair follicles, producing sebum which waterproofs the skin and has some action against fungal and bacterial infections (Hinchliff et al, 1996).

Adipose tissue lies beneath the dermis and is a valuable store of triglycerides, which provide a potential source of energy. The adipose tissue insulates the body, so preventing heat loss, and acts as a shock absorber, so preventing trauma to the underlying structures. It has very little ground substance, and the tissue is divided into lobes by septa which carry blood vessels and nerves. The cells which make up adipose tissue consist of a flat nucleus surrounded by a large single fat globule.

The early inflammatory phase occurs from the time of injury to approximately 3 days. The body’s immediate response to wounding is to stop bleeding and prevent the entry of microorganisms. Vasoconstriction occurs in the immediate area, due to the release of serotonin and other chemical mediators from the platelets, which helps to reduce the flow of blood to the wound. Damage to the blood vessels in the wound causes the platelets to become sticky and clump together to form a platelet thrombus, so further reducing blood loss. The clotting cascade is also initiated following injury to the vascular endothelium, resulting in the formation of a fibrin thrombus in the wound (Silver, 1994).

Inflammation is a natural response to trauma. A number of mediators (chemical substances), including prostaglandins, are released into the wound, resulting in vasodilatation, increased capillary permeability and the stimulation of pain fibres. The effect of increased capillary permeability is that mediators, plasma proteins, antibodies, neutrophils and monocytes migrate into the wound and surrounding tissue. The neutrophils and macrophages phagocytose any microorganisms or dead tissue present in the wound space. The wound and surrounding area will therefore appear red, swollen, hot and painful, with possible loss of function.

The late inflammatory phase occurs approximately 2–5 days after injury. The polymorphonuclear leucocytes (polymorphs) and macrophages continue the process of phagocytosis, so cleaning the wound of any debris or microorganisms. The tissue macrophages also control wound healing through the production of a variety of growth factors, e.g. platelet-derived growth factor (PDGF), transforming growth factor (TGF), interleukin (IL) and tumour necrosis factor (TNF) (Schultz, 2007). These growth factors stimulate the production of various cells, e.g. PDGF stimulates the growth of blood vessels (angiogenesis). This process demands substantial resources and energy, and considerable amounts of heat and fluid can be lost, especially in an open wound.

Following the initial inflammatory response, the phase of tissue repair takes place. This occurs from approximately 4–28 days, but may be longer in some wounds. The macrophages continue phagocytosis of cell debris and microorganisms. Through monocyte-derived growth factor (MDGF), the macrophages attract fibroblasts to the area. The fibroblasts, in the presence of vitamin C, ferrous iron, nutrients, oxygen and a slightly acidic environment, produce collagen fibrils, which are laid down in a haphazard fashion. Vitamin C is vital in this phase of healing, as it is involved in the hydroxylation of proline in collagen to hydroxyproline, which aids the cross-linkage of the collagen fibres. Endothelial cells respond to the secretion of various growth factors and form new capillaries, which grow into the wound. This process is known as angiogenesis and is stimulated by the hypoxic environment. The matrix of the collagen fibres forms scaffolding for the new capillaries, while the new capillaries provide nutrients and oxygen for continued growth (Doughty and Sparks-Defriese, 2007). This process is often called granulation because in a wound healing by secondary intention the wound bed appears red and granular. As the wound defect is filled with the newly formed tissue, the numbers of macrophages and fibroblasts diminish.

Contraction of the wound can also occur in wounds healing by secondary intention during this phase of healing, and is thought to be due to the presence of myofibroblasts within the wound. Myofibroblasts are cells containing the features of a fibroblast and a smooth muscle cell, which appear to have contractile qualities, so reducing the surface area of the wound (Monaco and Lawrence, 2003).

Epithelialization is the last stage in this phase of wound healing. Epithelial cells at the wound edges divide and migrate across the surface of the wound until they meet other epithelial cells. When this occurs, migration ceases, a process called contact inhibition. If the remnants of hair follicles are still present in the wound bed, epithelial cells will migrate from these areas and traverse the wound bed until they meet other epithelial cells. The rate of epithelialization is enhanced by maintaining a moist environment, as it allows the epithelial cells to migrate across the surface of the wound more easily (Winter, 1962) (Fig. 5.1). However, in surgical wounds it is important that the incisional wound is not allowed to become too wet as maceration can occur, so affecting the cosmetic result of the scar.

This is the final phase of wound healing and occurs from 15 days to 365 days approximately. The original Type III collagen laid down in the wound bed is converted to Type I collagen, which is laid down following the tension lines within the wound, and is also cross-linked so as to give strength to the scar tissue. As the remodelling process continues, cellular activity reduces and there is a gradual closure of the nutrient blood vessels in the wound. The scar should become paler and flatter in appearance. However, for some people this process may lead to hypertrophic scars (thickened appearance of the scar), whereas keloid scarring is due to a local disturbance during the healing process where the scar tissue extends outside the wound margins (Doughty and Sparks-Defriese, 2007).

Sutures are used to promote healing by eliminating dead space in a wound, realigning tissue planes and holding the skin edges in apposition until healing has taken place and the wound no longer needs the support of the suture material. They can be used to aid haemostasis, but if applied too tightly can cause necrosis of the surrounding tissue. The type of suturing technique, technique of knot tying and the width of the tissue bites all affect wound strength and healing.

Suture materials are chosen for their strength, handling characteristics and absorptive properties. Different types of suture material are required in a variety of circumstances, and for different types of tissue and parts in the body. The choice of suture material depends on the rate at which the tissue is likely to heal, the amount of strain or stress to which the wound site will be subjected, the likely growth of the wound and whether the suture is to give temporary or permanent support to the wound (Ethicon, 2005). The surgeon will select a suture material which loses its strength relative to the gain of strength in the wound itself as it heals.

The use of staples for skin closure is often preferred if the cosmetic appearance of the scar is a concern, as well as for their time-saving nature in application and painless removal. As the stapler is squeezed, the open staple is forced against an anvil located in the nose of the stapler. This action bends the staple legs, causing them to penetrate the everted skin edges, and results in the staple’s final rectangular shape (Fig. 5.4). They will also allow haemostasis without causing necrosis to the tissue.

Removal of staples is achieved by inserting the lower jaw of the staple remover under the staple and closing together the two edges of the staple remover. The staple needs to be placed in the V-shaped retaining slot situated in the bottom jaw of the staple remover, in order to ensure it is removed correctly. Squeezing the handles of the staple remover reforms the staple, so that it can be lifted from the skin.

Adhesive skin tapes are used for some types of skin closure, especially if the cosmetic appearance of the scar is a concern of the patient. Westaby (1985) states that the lax skin of the face and abdomen makes them amenable sites for wound closure by tapes, whereas the skin over joints is subjected to frequent movement, and so limits the adherence of the tapes and success of wound closure. Westaby (1985) also claims that the use of adhesive skin tapes keeps inflammation at the skin edges to a minimum, and results in a good cosmetic outcome with only minimal scarring.