Skin consists of epidermis and dermis. The epidermis is a layer of keratinized, stratified squamous epithelium (Fig. 18.2) that sends three appendages (hair follicles, sweat glands and sebaceous glands) into the underlying dermis. Because of their deep location, the appendages escape destruction in partial-thickness burns and are a source of new cells for reconstitution of the epidermis. The basal germinal layer of the epidermis generates keratin-producing cells (keratinocytes), which become increasingly keratinized and flattened as they migrate to the surface, where they are shed. The basal layer also contains pigment cells (melanocytes) that produce melanin, which is passed to the keratinocytes and protects the basal layer from ultraviolet light.

Fig. 18.2 Structure of skin.

The dermis is composed of collagen, elastic fibres and fat. It supports blood vessels, lymphatics, nerves and the epidermal appendages. The junction between the epidermis and the dermis is undulating where dermal papillae push up towards the epidermis.

The three types of epidermal appendage extend into the dermis and, in some places, into the subcutaneous tissues. Hair follicles produce hair, the colour of which is determined by melanocytes within the follicle. The sebaceous glands secrete sebum into the hair follicles, which lubricates the skin and hair. The sweat glands are coiled tubular glands lying within the dermis and are of two types; eccrine sweat glands secrete salt and water on to the entire skin surface, while apocrine glands secrete a musty-smelling fluid in the axilla, eyelids, ears, nipple and areola, genital areas and the perianal region. Hidradenitis suppurativa affects the latter.

The nails are flat, horny structures composed of keratin. They arise from a matrix of germinal cells, which can be seen as a white crescent (lunula) at the nail base. If a nail is avulsed, a new nail grows from this matrix. If the matrix is destroyed, nail regeneration is impossible, and the layer of epidermal cells covering the nailbed thickens to form a keratinized protective layer.

Wounds

A wound may be defined as disruption of the normal continuity of bodily structures due to trauma, which may be penetrating or non-penetrating. In both cases, inspection of the body surface may give little indication of the extent of underlying damage.

Types of wound

Wounds can be classified according to the mechanism of injury:

• Incised wounds. A sharp instrument causes these; if there is associated tearing of tissues, the wound is said to be lacerated

• Abrasions. These result from friction damage and are characterized by superficial bruising and loss of a varying thickness of skin and underlying tissue. Dirt and foreign bodies are frequently embedded in the tissues and can give rise to traumatic tattooing

• Crush injuries. These are due to severe pressure. Even though the skin may not be breached, there can be massive tissue destruction. Oedema can make wound closure impossible. Increasing pressure within fascial compartments can cause ischaemic necrosis of muscle and other structures (compartment syndrome)

• Degloving injuries. These result from shearing forces that cause parallel tissue planes to move against each other: for example, when a hand is caught between rollers or in moving machinery. Large areas of apparently intact skin may be deprived of their blood supply by rupture of feeding vessels

• Gunshot wounds. These may be low-velocity (e.g. shotguns) or high-velocity (e.g. military rifles). Bullets fired from high-velocity rifles cause massive tissue destruction after skin penetration

• Burns. These are caused not only by heat but also by electricity, irradiation and chemicals.

Principles of wound healing

The essential features of healing are common to wounds of almost all soft tissues, and result in the formation of a scar. Soft tissue healing can be subdivided into three phases (Table 18.1) according to the development of tensile strength (Fig. 18.3).

Table 18.1 Phases of wound healing

Lag phase (2–3 days)

• Inflammatory response

Incremental or proliferative phase (approximately 3 weeks)

• Fibroblast migration

• Capillary ingrowth (granulation tissue)

• Collagen synthesis with rapid gain in tensile strength

• Wound contraction

Plateau or maturation phase (approximately 6 months)

• Organization of scar

• Slow final gain in tensile strength (80% of original strength)

Fig. 18.3 Phases of wound healing.

Keloids

Epidermis

Epithelium heals by regeneration and not by scar formation. Epithelial cells at the edge of the wound lose their adhesion to each other and migrate across the wound until they meet cells from the other side. As they migrate, they are replaced by new cells formed by the division of basal cells near the wound edge. The cells that have migrated undergo mitosis and the new epithelium thickens, eventually forming normal epithelial cover for the scar produced by the dermis.

Primary and secondary intention

Wounds may heal by primary intention if the edges are closely approximated: for example, by accurate suturing. Epithelial cover is quickly achieved and healing produces a fine scar (Fig. 18.4). If the wound edges are not apposed, the defect fills with granulation tissue and the restoration of epidermal continuity takes much longer. The advance of epithelial cells across the denuded area may be hindered by infection. This is known as healing by secondary intention and usually results in delayed healing, excessive fibrosis and an ugly scar (Fig. 18.5). If a wound has begun to heal by secondary intention, it may still be possible to speed healing by excising the wound edges and bringing them into apposition, or by covering the defect with a skin graft.

Fig. 18.4 Wound healing.

A Healing by primary intention. B Healing by secondary intention, showing shrinkage of the wound.

Fig. 18.5 Healing by secondary intention.

Summary Box 18.1 Classification of wound healing

• Healing by first intention is the most efficient method and results when a clean incised surgical wound is meticulously apposed and heals with minimal scarring

• Healing by second intention occurs when wound edges are not apposed and the defect fills with granulation tissue. In the time taken to restore epithelial cover, infection supervenes, fibrosis is excessive and the resulting scar is unsightly

• The term ‘healing by third intention’ describes the situation where a wound healing by second intention (e.g. a neglected traumatic wound or a burn) is treated by excising its margins and then apposing them or covering the area with a skin graft. The final cosmetic result may be better than if the wound had been left to heal by second intention.

Factors influencing wound healing

Many of the factors influencing healing are interrelated: for example, the site of the wound, its blood supply, and the level of tissue oxygenation. Although some adverse factors, such as advanced age, cannot be influenced, others, such as surgical technique, nutritional status and the presence of intercurrent disease, can be modified or eliminated.

Blood supply

Wounds in ischaemic tissue heal slowly or not at all. They are prone to infection and frequently break down. When this occurs, the wound may not be able to sustain the metabolic demands of healing by second intention. Arterial oxygen tension (PaO₂) is a key determinant of the rate of collagen synthesis. Anaemia may not affect healing if the patient has a normal blood volume and arterial oxygen tension. Poor surgical technique, such as crushing tissue with forceps, approximating wound edges under tension and tying sutures too tightly, can make well vascularized tissue ischaemic and lead to wound breakdown.

Infection

The general risks of wound infection depend upon age, the presence of intercurrent infection, steroid administration, diabetes mellitus, disordered nutrition, and cardiovascular and respiratory disease. Local factors are also important. Bacterial contamination can be minimized by careful skin preparation and aseptic technique, but some wounds are more likely to be contaminated than others. Bacteria may enter wounds from the atmosphere, from internal foci of sepsis or from the lumen of transected organs. In some cases, contamination occurs in the postoperative period. Provided contamination is not gross and local blood supply is good, natural defences are usually able to prevent and contain overt infection. Devitalized tissues, haematomas and the presence of foreign material such as sutures and prostheses favour bacterial survival and growth. Common infecting organisms are staphylococci, streptococci, coliforms and anaerobes. Overcrowding of wards and excessive use of operating theatres increase the bacterial population of the atmosphere and hence the risk of wound infection. The failure of medical and nursing staff to wash their hands before and after touching and examining each patient is perhaps the greatest source of cross-contamination.

When wound contamination is anticipated, topical antibacterial chemicals or topical and systemic antibiotics can be used prophylactically. For example, a single dose of systemic antibiotic is normally used to reduce the risk of infection during gastrointestinal surgery and when prosthetic material (hip joint, cardiac valves, arterial bypass) is being inserted. In acute traumatic wounds, tetanus prophylaxis is routine, but antibiotics are not normally necessary provided prompt and thorough surgical treatment is undertaken. However, if there has been a delay in the treatment of such a wound, antibiotic prophylaxis may be necessary.

Age

Wounds in the elderly may heal poorly because of impaired blood supply, poor nutritional status or intercurrent disease. However, as mentioned above, they tend to form ‘good’ scars.

Site of wound

Surgical incisions placed in the lines of least tissue tension are subject to minimal distraction and should heal promptly, leaving a fine scar. On the face, these lines run at right angles to the direction of underlying muscles and form the lines of facial expression.

Nutritional status

Malnutrition has to be severe before healing is affected. Protein availability is most important, and wound dehiscence and infection are common when the serum albumin is low. Healing problems should be anticipated if recent weight loss exceeds 20%. Vitamin C is essential for proline hydroxylation and collagen synthesis. The number of fibroblasts is not reduced in scorbutic states. Zinc is a co-factor for important enzymes involved in healing, and its deficiency retards healing. Supplements of ascorbic acid and zinc are effective in patients with known deficiencies, but do not improve healing in normal subjects.

Intercurrent disease

Healing may be affected by the disease itself or by its treatment. Cachectic patients with severe malnutrition (as seen in advanced cancer) have marked impairment of healing. Diabetes mellitus impairs healing by reducing tissue resistance to infection and by causing peripheral vascular insufficiency and neuropathy. Haemorrhagic diatheses increase the risk of haematoma formation and wound infection. Obstructive airway disease lowers arterial PO₂ and so affects healing. Abdominal wound dehiscence is more common in patients with respiratory disease because of the strain put on the wound during coughing. Corticosteroid therapy reduces the inflammatory response, impairs collagen synthesis and decreases resistance to infection. The effect of steroids on wound healing is most marked if they are given within 3 days of injury. Immunosuppressive therapy and chemotherapy impair healing by reducing resistance to infection. As radiotherapy greatly reduces the vascularity of the tissues, the healing of wounds in irradiated areas is often impaired.

Surgical technique

Where possible, skin incisions are placed in the line of least tissue tension. Aseptic technique, gentle handling and accurate apposition of wound edges favour healing by first intention. Dead spaces must be avoided, as the accumulation of blood and exudate encourage infection. Correct suturing of the deeper layers avoids dead space and often allows the skin edges to fall together without tension, so that superficial sutures or adhesive tape can achieve skin apposition. Drains should be used in contaminated wounds and those where exudate is expected. Drains may be connected to a suction apparatus or allowed to empty by gravity. The drain site is a potential portal of entry for infection and drains should be removed as soon as possible, especially when prosthetic material has been implanted.

Choice of suture and suture materials

Foreign material in the tissues predisposes to infection. The finest sutures that will hold the wound edges together should be used. Whereas 5/0 or 6/0 sutures are appropriate for the face, stronger ones (3/0 or 4/0) are needed for incisions near joints and still stronger ones for the abdominal wall. The suture should be strong enough to support the wound until tensile strength has recovered sufficiently to prevent breakdown. Absorbable materials are preferred for buried layers.

Wound infection

Classification

Surgical procedures can be classified according to the likelihood of contamination and wound infection as ‘clean’, ‘clean-contaminated’ and ‘contaminated’:

• Clean procedures are those in which wound contamination is not expected and should not occur. An incision for a clean elective procedure should not become infected. In clean operations, the wound infection rate should be less than 1%.

Summary Box 18.2 Factors affecting wound healing

The site of the wound and its orientation relative to tissue tension lines are major determinants of healing

Wounds with a good blood supply (e.g. head and neck wounds) heal well

Infection is a major adverse factor and the risk of infection is influenced by:

• general factors such as the patient’s age, presence of intercurrent infection, nutritional status and cardiorespiratory disease

• local factors including bacterial contamination, antibacterial prophylaxis, aseptic technique, degree of trauma, presence of devitalized tissue, haematoma and foreign bodies.

Intercurrent disease may impair healing. Important factors include:

• malnutrition

• diabetes mellitus

• haemorrhagic diatheses

• hypoxia (e.g. obstructive airways disease)

• corticosteroid therapy

• immunosuppression

• radiotherapy.

Surgical technical factors that have a major influence on wound healing include:

• gentle tissue handling

• avoidance of undue trauma

• accurate tissue apposition

• meticulous haemostasis

• appropriate choice of suture material.

• Clean-contaminated procedures are those in which no frank focus of infection is encountered but where a significant risk of infection is nevertheless present, perhaps because of the opening of a viscus, such as the colon. Infection rates in excess of 5% may suggest a breakdown in ward and operating theatre routine.

• Contaminated or ‘dirty’ wounds are those in which gross contamination is inevitable and the risk of wound infection is high; an example is emergency surgery for perforated diverticular disease, or drainage of a subphrenic abscess.

Antibiotic prophylaxis is appropriate for the latter two types of operation.

Clinical features

Wound infection usually becomes evident 3–4 days after surgery. The first signs are usually superficial cellulitis around the margins of the wound, or swelling of the wound with some serous discharge from between the sutures. Fluctuation is occasionally elicited when there is an abscess or liquefying haematoma. Crepitus may be present if gas-forming organisms are involved. In some cases of deep infection, there are no local signs, although the patient may have pyrexia and increased wound tenderness. Systemic upset is variable, usually amounting to only moderate pyrexia and leucocytosis. Toxaemia, bacteraemia and septicaemia can complicate serious wound infection, especially where there is an accumulation of pus. The differential diagnosis includes other causes of postoperative pyrexia, wound haematoma and wound dehiscence. Wound haematoma may result from reactive bleeding during the first 24–48 hours after an operation. It causes swelling and discomfort, but only minimal pyrexia and few systemic signs.

Prevention

The risk of wound infection is reduced by careful patient preparation, the prophylactic use of antibiotics in high-risk patients, and meticulous attention to good operating theatre techniques. Severely contaminated wounds are sometimes best closed by delayed primary suture; most gunshot wounds are treated in this way. Skin sutures may be inserted at this time but are not tied for several days, by which time it should be clear that infection has been avoided. Antibiotic therapy is essential for grossly contaminated wounds. The aim is to achieve high tissue concentrations as soon as possible. The choice of antibiotic is determined by the nature of the infection. Topical agents such as povidone-iodine may also be used to combat infection in contaminated wounds. Radical excision of the wound margins, thorough mechanical cleansing and delayed suture may also be required.

Management

A wound swab or specimen of pus is routinely sent for bacteriological culture and sensitivity determination. In urgent cases, a Gram stain may be useful. The state of immunity against tetanus is assessed and appropriate action taken. Trivial superficial cellulitis can be managed expectantly. The area of redness is ‘mapped out’ with an indelible pen so that its extent can be monitored. Spreading cellulitis is an indication for antibiotic therapy. Many infected wounds heal rapidly without further surgery, particularly if the original skin incision is placed in the line of least tissue tension. The problem is often to keep the wound open, rather than to achieve closure. If it appears that spontaneous wound closure will take a long time, secondary suture or skin grafting can be considered to speed healing, but only once it is clear that infection has been eradicated. The presence of clean healthy granulation tissue in the wound is usually a good indication that closure can be undertaken.

Involvement of other structures

All wounds must be inspected carefully in good light to assess the extent of devitalization and injury to other structures. However, it is important to appreciate that a small, apparently innocent wound may conceal extensive damage to deeper structures. Body cavities may have been penetrated, or tendons, nerves and blood vessels divided. Damage to muscles, tendons or nerves is assessed by checking relevant motor and sensory function. If the injury

Summary Box 18.3 Principles of management of contaminated traumatic wounds

• Contaminated wounds should be debrided under general anaesthesia

• The contaminated wound and its margins must be cleansed thoroughly, and grit, soil and foreign bodies/materials removed

• Devitalized tissue is formally excised until bleeding is encountered

• Primary closure is avoided if there has been gross contamination and when treatment has been delayed for more than 6 hours. Inappropriate attempts to achieve primary closure increase the risk of wound infection and expose the patient to the risks of anaerobic infection (tetanus and gas gangrene)

• Wounds left open may be suitable for delayed primary suture after 2–3 days, or for later excision and secondary suture (with or without skin grafting)

• Appropriate protection against tetanus must be afforded and the use of antibiotics should be considered.

involves a limb, the distal circulation must be checked. Where appropriate, X-rays will help to establish whether peritoneal, pericardial or pleural cavities have been entered, and whether there is underlying bony injury.

Provided there is no deep damage, small, relatively uncontaminated wounds can be treated under local anaesthesia in the A&E department. The wound margins are cleaned with a mild antiseptic such as cetrimide and the wound is irrigated with sterile saline. Any devitalized tissue is removed, deep tissues are sutured with absorbable material and the skin margins are closed.

More extensive or severely contaminated wounds usually require inpatient treatment, with exploration and debridement under general anaesthesia. The wound and its margins are cleansed and all obvious foreign material picked out. Devitalized tissue is trimmed back until bleeding occurs. In areas of poor vascularity such as the leg, or if there is severe contamination, crushing or a fracture, the wound margins are formally excised (Fig. 18.6). Bleeding from the wound margin is not a certain indication of its ultimate survival, as impaired venous drainage can lead to progressive necrosis, particularly after a crushing or degloving injury. If there is any doubt, the wound should not be sutured and a ‘second-look’ dressing change should be undertaken under anaesthesia after 48 hours.

Fig. 18.6 Technique of wound debridement for a compound fracture.

A Excision of skin edges. B Excision of fascial layer. C Excision of traumatized muscle. D Removal of small bone fragments.

Primary closure should be avoided if there is significant delay in treating a grossly contaminated wound: that is, more than 6 hours without antibiotic cover. If primary closure is attempted, wound infection and breakdown are likely and there is a risk of anaerobic infection. It is also too late for formal excision but foreign bodies and dead tissue should be removed in the usual way. The wound is dressed and antibiotics are started. The dressing is changed daily, and if the wound is clean, delayed primary suture may be carried out after 48 hours. If closure is delayed, any granulation tissue is usually excised and secondary suture performed. If this is not possible, split-skin grafts (see below) can be applied to the granulations.

Provided that surgical treatment is carried out early, prophylactic antibiotics are only required for deeply penetrating wounds, especially those from dog and human bites or those caused by nails, where adequate debridement may be impossible. However, the early use of antibiotics in situations where a delay in surgical treatment is anticipated may allow primary suture of wounds after 8–12 hours, an interval that is normally considered safe.

Devitalized skin flaps

A common emergency problem is posed by the patient, usually an elderly woman, who falls and raises a triangular flap over the surface of the tibia (pretibial laceration). In some cases, the flap is blue-black in colour and obviously non-viable, but in most cases viability is uncertain. Similar injuries can occur elsewhere in the body. The wound must be cleansed and non-viable tissue excised. No attempt should be made to suture the flap back into place; because of the post-traumatic oedema this would only be possible under tension, and would lead to death of the flap. A small defect can be treated conservatively on an out-patient basis by wound dressing and an elastic supporting bandage providing the arterial circulation is normal; Ch. 21) and the patient is kept ambulant. The wound will normally take several weeks to heal. A larger defect may require a split-skin graft, either immediately or as a delayed primary procedure.

Wounds with skin loss

If skin has been lost as a direct result of trauma, or following the excision of a tumour or necrotic tissue, direct suture may not be possible. A small skin defect at a functionally or aesthetically unimportant site may be allowed to heal by secondary intention. However, it is often better to speed healing by importing skin to close the wound by means of a skin graft, which requires a vascular bed as it has no blood supply of its own, or a flap.

Skin grafts

These may be split-skin or full-thickness. Split-skin grafts are cut with a special guarded freehand knife or an electric dermatome. The donor site heals by re-epithelialization from epithelial appendages in the dermis within 2–3 weeks, depending on the thickness of the graft. To cover very large areas, the graft can be expanded by ‘meshing’. The thinner the graft, the more easily it will take on a bed of imperfect vascularity but the poorer the quality of skin will be and the more it will shrink. Split-skin grafts are used to cover wounds after acute trauma, granulating areas and burns, or when the defect is large. A full-thickness graft leaves a donor defect (which needs to be sutured or grafted) as large as the one to be filled and requires a well-vascularized bed to survive. However, such grafts are strong, do not shrink, and look better than a split-skin graft. They are rarely advisable after acute trauma but are commonly used in reconstructive surgery to close small defects where strength is needed (e.g. on the palm of the hand) or where a good functional and/or cosmetic result is important (e.g. on the lower eyelid). An area where there is skin to spare is chosen for the donor site (e.g. the groin for the former and the area behind the ear or upper eyelid for the latter).

Flaps

Whereas grafts require a vascular bed to survive, flaps bring their own blood supply to the new site. They can therefore be thicker and stronger than grafts and can be applied to avascular areas such as exposed bone, tendon or joints. They are used in acute trauma only if closure is not possible by direct suture or skin grafting, and are more usually reserved for the reconstruction of surgical defects and for secondary reconstruction after trauma. The simplest flaps use local skin and fat (local flaps), and are often a good alternative to grafting for small defects such as those left after the excision of facial tumours (Fig. 18.7). A flap may have to be brought from a distance (distant flap) and remain attached temporarily to its original blood supply until it has picked up a new one locally (Fig. 18.8). This usually takes 2–3 weeks, after which the pedicle can be divided. Advances in our knowledge of the blood supply to the skin and underlying muscles have led to the development of many large skin, muscle and composite flaps, which have revolutionized plastic and reconstructive surgery. One example is the use of the transverse rectus abdominis musculocutaneous (TRAM) flap for reconstruction of the breast. The ability to join small blood vessels under the operating microscope now allows the surgeon to close defects in a single stage, even when there is no local tissue available, by free tissue transfer (Fig. 18.9). Other tissues, such as bone, cartilage, nerve and tendon, can also be grafted to restore function and correct deformity after tissue damage or loss.

Fig. 18.7 Local skin flap used to repair a defect after the excision of a skin lesion.

A Before surgery. B After surgery.

Fig. 18.8 Example of a pedicled (cross finger) skin flap used to cover a defect on the tip of the index finger.

A Raised. B Inset. C Divided.

Fig. 18.9 Example of free tissue transfer based on inferior epigastric vessels.

A Rectus abdominis muscle transferred to shin and its vessels (inferior epigastric vessels) anastomosed to anterior tibial vessels. B Muscle covered by split-skin graft.

Crushing/degloving injuries and gunshot wounds

Wounds of this type should never be closed primarily due to the extensive tissue destruction. After thorough irrigation and the removal of any obviously dead tissue and foreign material, such wounds should be lightly packed and dressed. Dressings are removed 48 hours later under anaesthesia and further excision is carried out if necessary. The wound is closed by suture, skin grafting or flap cover, once it is clear that all dead tissue has been removed.

Burns

Mechanisms

Burn injuries range from the trivial to severe burns that pose a threat to life, involve a long hospital stay, and carry the risk of permanent disfigurement or impaired function. They may be caused by flames, hot solids, hot liquids or steam, irradiation, electricity or chemicals. Toddlers are particularly liable to scalding by hot liquids in kitchen accidents, and unguarded fires are a threat to all children. Burns sustained in house fires are often accompanied by smoke inhalation, with injury to the lungs. Alcohol is a common contributing factor in burn injury. In the elderly and infirm, impaired mobility, poor coordination and diminished awareness of pain increase the incidence of burns. Industrial accidents account for most physiocochemical burns, although the accidental or deliberate ingestion of caustic or corrosive chemicals is still an occasional cause of domestic burns.

Local effects of burn injury

The local effects result from destruction of the more superficial tissues and the inflammatory response of the deeper tissues (Table 18.2). Fluid is lost from the surface or trapped in blisters, the magnitude of loss depending on the extent of injury. Loss is greatly increased by leakage of fluid from the circulation (see below) where, instead of the normal insensible loss of 15 ml/m² body surface/hour, as much as 200 ml/m² may be lost during the first few hours. With deeper injuries, the epidermis and dermis are converted into a coagulum of dead tissue known as eschar. In its least severe form, the dermal inflammatory response consists of capillary dilatation, as in the erythema of sunburn. With deeper burns, the damaged capillaries become permeable to protein, and an exudate forms with an electrolytic and protein content only slightly less than that of plasma. Lymphatic drainage fails to keep pace with the rate of exudation and interstitial oedema leads to a reduction in circulating fluid volume. An increase of 2 cm in the diameter of the leg represents the accumulation of over 2 litres of excess interstitial fluid. Exudation is maximal in the first 12 hours, capillary permeability returning to normal within 48 hours.

Table 18.2 Effects of burn injury

Destruction of tissue

• (Depth depends on heat of causative agent and contact time)

• Loss of barrier to infection

• Fluid loss from surface

• Red cell destruction

Increased capillary permeability

• Oedema

• Loss of circulating fluid volume

• Hypovolaemic shock

Increased metabolic rate

Destruction of the epidermis removes the barrier to bacterial invasion and opens the door to infection. The burn surface may become contaminated at any time, and wound care must commence when the patient is first seen. Sepsis delays healing, increases energy needs, and may pose a new threat to life, just when the early dangers of hypovolaemia have been overcome.

General effects of burn injury

The general effects of a burn depend upon its size. Large burns lead to water, salt and protein loss, hypovolaemia and increased catabolism. Circulating plasma volume falls as oedema accumulates, and fluid leaks from the burned surface. With large burns, the effect is compounded by a generalized increase in capillary permeability, with widespread oedema. Some red cells are destroyed immediately by a full-thickness burn, but many more are damaged and die later. However, red cell loss is small compared to plasma loss in the early period, and haemoconcentration, reflected by a rising haematocrit, is the norm. The shifts in water and electrolytes are ultimately shared by all body tissues, and if circulatory volume is not restored, hypovolaemic shock ensues. Large burns increase metabolic rate as water losses from the burned surface cause expenditure of calories to provide the heat of evaporation. In severe burns, some 7000 kcal may be expended daily, and a daily weight loss of 0.5 kg is not unusual unless steps are taken to prevent it.

Summary Box 18.4 Consequences of burns

The morbidity and mortality of burns depend on the site, extent and depth of the burn and on the age and general condition of the patient

Early consequences

• hypovolaemia (loss of protein, fluid and electrolytes)

• metabolic derangements (hyponatraemia followed by risk of hypernatraemia, hyperkalaemia followed by hypokalaemia)

• sepsis, which may be both local and generalized

• haemolysis with anaemia and need for transfusion

• hypothermia.

Short-term consequences

• renal failure (acute tubular necrosis due to hypovolaemia, haemoglobinuria and myoglobinuria)

• respiratory failure (smoke inhalation, airway obstruction, acute respiratory distress syndrome)

• catabolism and nutritional depletion

• venous thrombosis

• Curling’s ulcer and erosive gastritis.

Long-term consequences

• permanent disfigurement

• prolonged hospitalization

• psychological problems

• impaired function.

Classification

Burns are classified according to depth as either partial- or full-thickness (Fig. 18.10).

Fig. 18.10 Depth of burn injury.

Superficial partial-thickness burns

Superficial partial-thickness burns involve only the epidermis and the superficial dermis. Pain, swelling and fluid loss can be marked. New epidermal cover is provided by undamaged cells originating from the epidermal appendages. The burn will usually heal in less than 3 weeks, with a perfect final cosmetic result.

Deep partial-thickness burns

In deep partial-thickness (also known as deep-dermal) burns, the epidermis and much of the dermis are destroyed. Restoration of the epidermis then depends on there being intact epithelial cells within the remaining appendages. Pain, swelling and fluid loss are again marked. The burn takes longer than 3 weeks to heal, as fewer epithelial elements survive, and often leaves an ugly hypertrophic scar. Infection often delays healing and can cause further tissue destruction, converting the injury to a full-thickness one.

Full-thickness burns

A full-thickness burn destroys the epidermis and underlying dermis, including the epidermal appendages. The destroyed tissues undergo coagulative necrosis and form an eschar that begins to lift after 2–3 weeks. Unless the raw area is grafted, epidermal cover can only occur through the inward movement and growth of cells from intact skin around the burn, and by contraction of its base. Fibrosis and ugly contracture are thus inevitable in all but small, ungrafted injuries.

Determination of burn depth

There is no infallible method for the early determination of burn depth; experienced plastic surgeons may not be able to make an accurate assessment for days or even weeks after injury.

Mechanisms

Burn depth is proportional to the temperature of the causal agent and to the length of contact time. Scalds from liquids below boiling point usually produce partial-thickness injury, whereas scalds from boiling water and burns due to prolonged contact with hot metal often produce full-thickness damage. Flame burns can be of mixed depth but nearly always include areas of full-thickness loss. Electrical burns are almost always full-thickness, and high-tension electricity can cause devastating necrosis of muscles and other deep tissues.

Appearance

Erythema means that epidermal damage is superficial, and blanching on pressure confirms that dermal capillaries are intact and that the injury is partial-thickness. Blisters are accumulations of fluid superficial to the basal layer of the epidermis and suggest partial-thickness injury. A dead-white appearance frequently indicates full-thickness injury, although at least some of these burns prove to be deep-dermal. A dry, leathery mahogany-coloured eschar with visible thrombosed veins denotes full-thickness destruction.

Sensation

Intact cutaneous sensation implies that the epidermal appendages have survived, as they lie at the same level as cutaneous nerve endings in the dermis. Superficial burns are thus very painful.

Prognosis

Age and general condition

Infants, the elderly, alcoholics and those with other co-morbidity fare less well than healthy young adults (see EBM 18.1).

18.1 Burns

‘Mortality is related to the size (% body surface area, BSA) and age of the patient.

Large burns > 15% in adults (> 10% in children) require intravenous resuscitation.’

This is a shorthand way of calculating actuarial survival based on Bull J P (1971) Revised analysis of mortality due to Burns. Lancet, 2, 1133-4.

Extent of the burn

The approximate extent of the burn can be quickly calculated in adults by using the ‘rule of nines’ (Fig. 18.11). Tables are available for more accurate estimations of burn area. The patient’s hand and fingers together constitute about 1% of body surface area (BSA). Hypovolaemic shock is anticipated if more than 15% of the surface is burned in adults, or more than 10% in a child. The ‘rule of nines’ cannot be used in children because of the relatively large head size (about 20% of body surface at birth) and the relatively small limbs (legs are about 13%).

Fig. 18.11 Rule of nines for calculating surface areas of a burn.

Depth of the burn

Superficial burns of whatever size should heal without scarring within 3 weeks if properly managed. Deep-dermal burns take longer and produce hypertrophic scarring. Full-thickness burns inevitably become infected unless excised early, and in the case of large burns infection may prove life-threatening.

Site of the burn

Burns involving the face, neck, hands, feet or perineum are particularly liable to threaten appearance or function. They require inpatient management.

Associated respiratory injury

This is now extremely common in house fires and usually results from the inhalation of smoke from burning plastic foam upholstery. It is frequently fatal.

Management

First aid

Prompt effective action prevents further damage and may save life or prevent months of suffering. The key principles are to arrest the burning process, ensure an adequate airway and avoid wound contamination (Table 18.3).

Table 18.3 First aid for burns

• Arrest the burning process

extinguish flames

remove clothing

cool with water

• Ensure adequacy of airway

• Avoid wound contamination

Clingfilm

Transfer for definitive treatment as soon as possible

Arrest the burning process

Burning clothing is extinguished by smothering the flames in a coat or carpet. The victim is laid flat to avoid flames rising to the head and neck, with inhalation of smoke and fumes. Heat within clothing can continue to cause damage for many seconds after flames have been extinguished or if soaked with scalding water; clothing must therefore be removed or doused with cold water. Cool water is an excellent analgesic and dissipates heat, but common sense must be applied; immersing a child in cold water or covering a patient with cold soaks can cause hypothermia. Cooling counteracts the heat of a burn only if applied immediately after injury. Chemical burns require copious irrigation particularly those involving the eyes. Electrical burning is arrested by switching off the current, not by pulling the patient free. If this is not feasible, the patient should be pushed free from the contact using a non-conductor such as a wooden chair.

Ensure an adequate airway

The patient must be moved as quickly as possible into a smoke-free atmosphere. Smoke and fumes can cause asphyxia, often contain poisons and can precipitate respiratory arrest. Mouth-to-mouth ventilation is commenced, if necessary. If cardiac arrest follows electrocution, resuscitation is instituted.

Avoid wound contamination

The burn should be covered with a clean sheet or clingfilm. Traditional household remedies must be avoided. At best they are messy and interfere with subsequent care; at worst they are destructive, converting a partial injury to a full-thickness one.

Transfer to hospital

The patient should be transferred to hospital as quickly as possible, unless the burn is obviously trivial. Severe burns are best treated in a specialized burns unit from the outset. Hypovolaemia takes time to become manifest and it is easy to misjudge the severity of injury, thereby missing the opportunity for uncomplicated early transfer. Patients embarking on a journey expected to take more than 30 minutes should be accompanied by a trained person. An intravenous infusion should be commenced if the burn is extensive. Transfer of patients with large burns between hospitals should be avoided between 8 and 24 hours after injury.

Full-thickness burns are often relatively painless. Partial-thickness injuries can be excruciating and opiates are usually needed. Analgesics must be given intravenously and the dose and route of administration noted.

Adequate ventilation

On arrival at hospital, the maintenance of an adequate airway remains the first priority. Lack of respiratory symptoms on admission is no guarantee that the patient will remain free from airway problems. Every patient who has been exposed to smoke in a closed room should be admitted for observation. Respiratory tract injury is suggested by dyspnoea, cough, hoarseness, cyanosis, coarse crepitations on auscultation, and the presence of soot particles around the nostrils, in the mouth or in the sputum. Endotracheal intubation is advisable if there is anxiety about airway patency, and assisted ventilation may be needed. Tracheostomy is never undertaken lightly in view of the danger of infection of burned tissues around the stoma.

Initial assessment and management

Once airway patency is assured, the time of injury, the type of burn, its previous treatment, and its extent and depth are established (Fig. 18.12). If the burn is over 15% in extent (10% in children), establishing an intravenous infusion takes priority over a detailed history and physical examination. Intravenous therapy may be needed for many days, but there may be few veins available and they must be treated with great respect. It is best to start with the most peripheral vein available in the upper limb, but in shocked patients with vasoconstriction, cannulation of the internal jugular or subclavian vein may be needed. Blood is withdrawn for cross-matching and for determination of haematocrit and urea and electrolyte concentrations. Arterial blood gas analyses are performed and carboxyhaemoglobin levels measured if there is concern about the airway and smoke inhalation. Once an infusion has been established, the pulse rate, blood pressure and core/peripheral temperature difference are monitored. In patients with burns of more than 20%, a catheter is inserted to measure hourly urine output. Severe pain is relieved by intravenous opiates. Tetanus can complicate burns, and tetanus toxoid is given if the patient has not received it recently. In general, patients with burns involving more than 5% of body surface should be admitted to hospital, as should all those with significant full-thickness injury or burns in sites likely to pose particular management problems.

Fig. 18.12 An extensive mixed-depth burn of back with full thickness burn evident centrally.

Prevention and treatment of burn shock

The aim of management is to prevent hypovolaemic shock by prompt and adequate fluid replacement (Table 18.4). Opinions vary as to the relative amounts of colloid and crystalloid that should be used. Various formulae are available to help calculate replacement needs, but all are merely guides and the amounts of fluid given must be adjusted in the light of the patient’s response to resuscitation.

Table 18.4 Hypovolaemic shock and burns

• Anticipate if burn more extensive than 15% (10% in children)

• Prevent by early intravenous resuscitation

• Control pain by adequate intravenous administration of opiates

• Fluid requirements assessed from patient’s response

‘Formulae’ for fluid replacement provide rough guides only

The Parkland formula, which uses crystalloids, is now widely used in the United Kingdom. The fluid volume in millilitres over the first 24 hours is:

Half of that volume is given in the first 8 hours, the remainder over the next 16 hours. There is debate about introducing colloid, as purified protein solution (PPS) in the second 24 hours. The need for fluid is greatest in the early hours, but excessive losses may persist for 36–48 hours.

Despite renal retention of sodium after injury, there is a tendency to hyponatraemia in the first 2–3 days owing to the secretion of antidiuretic hormone and the sequestration of sodium in oedema. As inflammatory oedema is reabsorbed, the serum sodium concentration returns to normal, and unless water intake is maintained, there is now a danger of hypernatraemia. Tissue destruction releases large amounts of potassium into the extracellular fluid (ECF), but hyperkalaemia is largely prevented by increased renal excretion as part of the metabolic response to injury. Once the first few days have passed, continuing potassium losses can produce hypokalaemia in a patient unable to eat and drink normally.

Water replacement

Daily water losses are replaced using 5% dextrose solution, taking care to avoid water intoxication, especially in young children, in the first few days following injury. Excessive evaporation continues until the burn has re-epithelialized, and a high water intake must be maintained. Although most patients are thirsty, paralytic ileus may occur during the first 48 hours in those with very large burns, so that giving oral fluids too soon can cause gastric distension, vomiting and aspiration. Most patients are able to drink normally after 48 hours and should be encouraged to do so.

Blood transfusion

Blood should not be given in the first 24 hours but may be needed thereafter in patients with large full-thickness burns. Continuing red cell destruction in deep burns with bone marrow suppression can necessitate repeated transfusion. Haemoglobin concentration and haematocrit should be monitored regularly.

Organ failure and burn shock

Organ failure and shock are discussed in detail in Chapter 1.

Respiratory complications

Inhalation of smoke and fumes can cause direct heat damage, carbon monoxide poisoning and damage from other chemicals, all of which predispose to infection. Patients with head and neck burns are best nursed sitting up to encourage the dispersal of oedema. Continued observation is mandatory and physiotherapy is essential to clear bronchial secretions. Chest X-rays and blood gas analyses are repeated regularly in patients with ventilation problems. Arterial hypoxaemia and carbon monoxide poisoning require oxygen therapy, and may necessitate early endotracheal intubation and assisted ventilation. Antibiotics should be prescribed. Tracheostomy is occasionally unavoidable despite the problems associated with its management. Encircling eschar impairing chest or abdominal expansion must be incised (escharotomy) or excised.

Renal failure

Acute tubular necrosis may complicate extensive burns, especially in the elderly, those with pre-existing renal disease and those who develop haemoglobinaemia or myoglobinuria. These pigments appear in the urine after massive red cell destruction or extensive muscle damage (particularly after electrical injury), and can damage the tubules and obstruct urine flow by forming casts. Hourly urine output should be maintained at 30–50 ml in adults. Falling output reflects inadequate resuscitation or impending renal failure (acute tubular necrosis). Measurement of urine osmolality and the response to a test infusion will distinguish between them. Diuretics are used only if oliguria persists despite adequate fluid replacement, when 20% mannitol (1 g/kg) may be infused over 30 minutes.

Nutritional management

The increased energy expenditure following a severe burn can be reduced by nursing in an environmental temperature of 30–32°C. A high-calorie intake is impractical during the period of hypovolaemic shock, but is encouraged as soon as the patient can drink. The daily caloric intake in adults can be calculated as 20 kcal/kg body weight plus 70 kcal/per cent burn. It is particularly important to provide sufficient protein intake (1 g/kg body weight plus 3 g/% burn). In large burns oral intake can usually be supplemented at 48 hours by enteral feeding using a fine-bore nasogastric tube and weight loss can be limited. Vitamin supplements and iron must also be provided. It is considered undesirable to use parenteral nutrition in burned patients.

Sepsis

Septicaemia is a constant threat until skin cover has been fully restored, as resistance to infection is low. The wound provides a reservoir of infecting organisms. Catheters, cannulae and tracheostomy wounds are all potential sources of infection. The incidence of septicaemia has been reduced by topical antibacterial agents and early excision and grafting. However, in large burns the risk remains high. Regular monitoring by means of blood cultures is advisable. Systemic antibiotics are not prescribed routinely for fear of producing superinfection with resistant organisms. Their use is reserved for invasive infection and for patients with positive blood cultures.

Curling’s ulcer and gastric erosions

Acute duodenal ulceration (Curling’s ulcer) and multiple gastric erosions may follow major burns. Early resumption of feeding reduces their incidence, and H₂-receptor antagonists such as ranitidine are prescribed prophylactically.

Local management of burns

Care of the burn wound commences at the time of injury and continues until epithelial cover has been restored. Infection poses the main threat to life once the first 48 hours have passed.

Initial cleansing and debridement

The wound is cleaned with a mild detergent containing antiseptic and saline in an operating theatre or clean dressing room using aseptic technique. Adherent clothing and loose devitalized tissues are removed. Blisters are punctured and serum expressed. Broken blisters are completely deroofed. General anaesthesia may be necessary, but in most cases pain can be relieved by intravenous opiates. In shocked patients, the wound is covered with a sterile drape and further local care is postponed until the circulatory state has stabilized.

Prevention of contamination

In full-thickness injury, thrombosis of cutaneous vessels impairs the normal response to infection. In large burns, cellular and humoral immune mechanisms are depressed. Organisms readily colonize the burn wound and will multiply and invade surrounding tissues if dead tissue is present. Staphylococci remain the most common infecting organism. Pseudomonas aeruginosa remains troublesome in most burn units. Haemolytic streptococci are feared because they can convert superficial into deep burns, and can cause a severe systemic illness.

Once contaminating organisms have been cleared, further contamination can be prevented in a number of way as dictated by the patient’s needs.

Exposure

After cleansing and debridement, burns to a single surface such as to the face and neck, may be exposed to the air. Evaporation of the protein-rich exudate leaves a dry, adherent crust that is an effective barrier to bacteria as long as it remains intact.

Evaporative dressings

These dressings prevent contamination, allow exudate to evaporate and provide comfortable support. After initial cleansing, the wound is covered by a layer of sterile non-adherent dressing, e.g. paraffin gauze or Mepotil, a layer of cotton gauze swabs, a bulky layer of cotton wool or Gamgee, and an outer retaining crepe bandage. The dressing is reviewed daily but left in place for 8–10 days, unless exudate soaks through to the outside.

Semi-occlusive and occlusive dressings

Clingfilm is useful in first aid, but leaks and is too messy for use as a definitive dressing. OpSite is an adhesive film that is effective for small burns; it may also leak initially, and should be covered with a well-padded dressing for 48 hours, after which time it can be patched or replaced as necessary. Hydrogel and hydrocolloid dressings absorb exudates but offer no particular advantages in acute management. Commercial polythene bags are cheap, sterile when taken from the roll, and useful for treating superficial hand burns. The hands are smeared with liquid paraffin for the first 24–48 hours until a decision as to depth is made. If the decision is made to continue with a conservative regimen, then silver sulfadiazine cream (Flamazine) is applied. The bags are kept in place with a bandage at the wrist. They must be changed at least daily after washing the hand and reapplying the antibacterial cream. Such ‘hand bags’ allow the patient to continue to use the hand and so prevent stiffness.

Topical antibacterial agents

Silver sulfadiazine cream and povidone-iodine (Betadine) are valuable local antibacterial agents for large burns if reapplied daily. They are not necessary or cost-effective for minor burns.

‘Biological’ dressings

Freeze-dried xenografts such as porcine skin can be reconstituted for use as temporary occlusive ‘biological’ dressings, but are expensive. Amnion or stored homograft skin is used rarely because of the danger of infection with human immunodeficiency virus (HIV). Sheets of keratinocytes grown in tissue culture are fragile and easily destroyed by infection – limitations which may be overcome in the future by growing the cells on sheets of collagen or synthetic ‘dermis’.

Relief of constriction (escharotomy)

The danger of progressive respiratory embarrassment from encircling eschar has been mentioned. Increasing oedema beneath encircling eschar in the limbs may also imperil the circulation. Relieving incisions (escharotomy), which run from the top to the bottom of circumferential deep burns, may be needed in the first few hours after injury. As these wounds can bleed profusely, it is important to have available methods for controlling haemorrhage.

Restoration of epidermal cover

Full-thickness and deep-dermal burns of less than 10% are suitable for primary excision of eschar and grafting under general anaesthesia within 48–72 hours of injury. Tangential excision is used for deep-dermal burns. The dead outer layers of skin are shaved away down to the deep-dermal layer and a split-skin graft is applied immediately. More extensive burns can be partially excised and grafted soon after injury, and the remaining areas of skin destruction treated by delayed grafting. After some 2 weeks, eschar begins to separate spontaneously but is accelerated by infection and delayed by topical antibacterial agents. As the slough separates, healthy granulation tissue should be revealed, and when all the slough has gone or has been excised, the burn should be ready for grafting. Haemolytic streptococci are a troublesome cause of graft loss, and when such infection is present, grafting must be deferred until the patient has been treated with intravenous penicillin and barrier nursed until three successive wound swabs are negative.

Only split-skin grafts are used to cover acute burns and medium-thickness grafts are most commonly used. The donor site forms a new epidermis from residual islands of epithelium, and more skin can be harvested after 14 days. Excess skin can be stored at 4°C for up to 3 weeks.

Full-thickness grafts are used for secondary reconstruction in cosmetically important areas where contraction has to be avoided, or in areas such as the palm of the hands that are subject to repeated trauma.

Functional and cosmetic result

With energetic treatment, it is usually possible to restore skin cover to even the most extensive injury within 3 months, but wound closure is not the end-point. Skin grafts and donor sites must be kept soft and supple by applying moisturizing cream several times a day for many months. Splints may be needed to prevent contractures, and physiotherapy is essential to mobilize joints. Elastic pressure garments help to prevent the build-up of hypertrophic scars. In spite of all this care, reconstructive procedures may be required for many years to correct contractures or rebuild missing or distorted features. Severely burned patients often have difficulty coming to terms with their disfigurement and limitations to their way of life. Long-term support, with counseling from surgeon and supporting staff, is invaluable.

Skin and soft tissue lesions

Diagnosis of skin swellings

In addition to describing the site and size of the lesion, it is necessary to determine whether it arises from the skin or is deep to it. Surface changes indicate an epidermal origin, whereas the surface is stretched over dermal lesions but remains normal. Ulceration may occur as a result of pressure necrosis. The colour of a skin lesion is also an important feature in its diagnosis.

Summary Box 18.5 Key questions when examining skin swellings

• Is the swelling located in the skin or in the subcutaneous tissues, i.e. can the overlying skin be pinched up and moved independently of the swelling?

• Is the swelling epidermal or dermal? Epithelial swellings create irregularity of skin surface, whereas dermal swellings do not

• Is the swelling pigmented? Pigmentation most often (although not always) indicates melanocytic activity.

Cysts

Sebaceous cysts

Sebaceous (or epidermoid) cysts are dermal swellings covered by epidermis (Fig. 18.13). They have a thin wall of flattened epidermal cells and contain cheesy white epithelial debris and sebum. They form soft smooth hemispherical swellings over which the skin cannot be moved. A small surface punctum is often visible. If infection supervenes, the cyst becomes hot, red and painful. Infected cysts are incised to allow the infected material to escape. Excision is deferred until the inflammation has settled. In some cases, the inflammation destroys the cyst lining so that excision is not necessary.

Fig 18.13 Types of cyst.

A Sebaceous (epidermoid). B Dermoid.

Dermoid cysts

Dermoid cysts arise from nests of epidermal cells that have been sequestered in the dermis during development or implanted as a result of trauma. Congenital dermoid cysts are found at sites of embryonic fusion, notably on the face, the base of the nose, the forehead and the occiput. External angular dermoid is the most common congenital dermoid cyst and lies at the junction of the outer and upper margins of the orbit, in the line of fusion of the maxilla and frontal bones. Implantation dermoid cysts are found at sites of injury, notably the palmar surfaces of the hands and fingers. They are lined by squamous epithelium and contain sebum, degenerate cells and, in some cases, hair. A soft rubbery swelling forms deep to the skin. The cyst may be fixed deeply, particularly when situated on the face. Implantation dermoids can be removed under local anaesthesia. Congenital dermoids usually require formal dissection under general anaesthesia, as they may extend deeply.

Tumours of the skin

Epidermal tumours are common and can arise from basal germinal cells or melanocytes, whereas dermal tumours arising from connective tissue elements are rare (Table 18.5).

Table 18.5 Classification of skin tumours

Epidermal neoplasms (common)
From basal germinal cells:	From melanocytes:
Papilloma	Benign pigmented mole
Infective wart	Common mole
Senile wart	Giant hairy mole
Pedunculated papilloma	Blue naevus
Keratoacanthoma	Halo naevus
Premalignant keratosis	Malignant melanoma
Carcinoma in situ	Melanotic freckle (lentigo maligna)
Epidermoid cancer	Superficial spreading melanoma
Basal cell cancer (rodent ulcer)	Nodular melanoma
Squamous cell cancer	Other forms of melanoma

Dermal neoplasms (rare)
Fibroma Lipoma Neurofibroma

Epidermal neoplasms arising from basal germinal cells

Papillomas

Papillomas (or warts) are common benign skin neoplasms.

Infective warts

These are caused by viral infection. and are found most commonly on the hands and fingers of young children and adults. They spread by direct inoculation and are often multiple. They form greyish-brown, round or oval elevated lesions with a filiform surface and keratinized projections (Fig. 18.14), and may be studded with spots of blood. They often regress spontaneously but can be removed by caustics (acetic acid) or freezing (liquid nitrogen or CO₂ snow). Plantar warts (verruca plantaris) are particularly troublesome infective warts acquired in swimming pools and showers. They are found under the heel and metatarsal heads. They are flush with the surface (Fig. 18.15) and may be intensely painful. If persistent, they are treated by curettage or freezing. Infective warts in the perineum and on the penis may be of venereal origin and are associated with gonorrhoea, syphilis, HIV infection and lymphogranuloma. Infective warts are also common in immunosuppressed patients.

Fig. 18.14 Verruca vulgaris.

Infective warts affecting the hands.

Fig. 18.15 Verruca plantaris (plantar warts).

A plaque of closely grouped warts on the sole of the foot.

Senile warts

These are basal cell papillomas and are common in the elderly (Fig. 18.16). They form a yellowish-brown or black greasy plaque (synonym: seborrhoeic keratosis) with a cracked surface that falls off in pieces. Senile warts are often multiple, commonly affect the upper back and trunk, and are best treated by curettage.

Fig. 18.16 Senile wart or seborrhoeic keratosis.

Pedunculated papillomas

These simple non-infective papillomas form a flesh-coloured spherical warty mass on a stalk of normal epithelium. If small, they can be dealt with by grasping with fine forceps, pulling out from the skin surface and cutting off with scissors; a stitch is rarely required. If they are large, the papilloma and its pedicle are removed formally with an ellipse of normal skin.

Keratoacanthoma (molluscum sebaceum)

This lesion can be confused with squamous cancer because of its clinical appearance. It grows rapidly over 4–6 weeks and then involutes. Histologically, it has a well-defined ‘shoulder’, but even under the microscope it may resemble a squamous carcinoma. The distinction between the two is the history. Keratoacanthoma occurs most commonly on the face as a hemispherical nodule with a friable red centre crusted with keratin (Fig. 18.17). It is found mainly in those over 50 years of age. It heals after shedding its central core, but can also be eradicated by curettage.

Fig. 18.17 Keratoacanthoma affecting the temple of an elderly man.

Actinic (solar) keratosis

This is a premalignant keratosis and is characterized by small, single or multiple, firm warty spots on the face, back of the neck and hands (Fig. 18.18). Such keratoses are particularly common in older, fair-skinned people who have been exposed to excessive sunlight. The scaly lesions drop off periodically to leave a shallow premalignant ulcer. The keratoses should be biopsied to exclude frank malignancy, and then treated by freezing.

Fig. 18.18 Actinic keratosis.

Intraepidermal cancer (carcinoma in situ)

This non-invasive form of skin cancer forms a discrete, often solitary, raised brown or red fissured plaque which is keratinized. Histologically, the plaques are composed of hyperplastic atypical epithelial cells, but there is no evidence of invasion through the basement membrane. Intraepidermal skin cancer is also known as Bowen’s disease and, when it affects the penis or vulva, as erythroplasia of de Queyrat.

Cancer of the epidermis

Epidermal cancer occurs primarily on exposed areas and in those with poor natural protection against sunlight. Albinos and patients with xeroderma pigmentosa (a congenital defect leading to undue sensitivity to sunlight) are at particularly high risk, whereas skin cancer is rare in black-, brown- and yellow-skinned races. Chronic skin irritation by chemicals (e.g. arsenic, tar and soot), chronic ulceration (e.g. old burns or varicose ulcers) and exposure to other forms of radiation are also established causes. Epidermoid cancer is particularly common in those over 50 years of age. There are two distinct pathological forms.

Basal cell carcinoma (rodent ulcer)

Rodent ulcers are slow-growing, locally invasive and never metastasize. They commonly arise in the skin of the middle third of the face, typically on the nose, inner canthus of the eye, forehead and eyelids (Fig. 18.19). The earliest lesion is a hard pearly nodule, dimpled in its centre and covered by thin telangiectatic skin. Cystic degeneration may make the lesion raised and translucent. Clinical types are described as cystic, nodular, sclerosing, morphoeic, centrally healing and ‘field fire’. Over a period of years, the rodent ulcer repeatedly scales over and breaks down. Growth is extremely slow. Occasionally, the tumour is highly invasive and can burrow deeply, despite little apparent surface activity. All suspicious lesions must be biopsied. Surgical excision or radiotherapy can be used for definitive treatment, but the latter is contraindicated if the lesion is close to the eye or overlies cartilage. Complex reconstructive surgery may be needed to restore structure and function in patients who present late.

Fig. 18.19 Basal cell carcinoma (rodent ulcer).

Note the raised pearly edge.

Squamous cell carcinoma

This tumour may affect any area (Fig. 18.20) but is particularly common on exposed parts such as the ear, cheeks, lower lips and backs of the hands. It commonly develops in an area of epithelial hyperplasia or keratosis. In mucosa, such as the lips, the analogous change is leucoplakia. The lesion starts as a hard erythematous nodule, which proliferates to form a cauliflower-like excrescence or ulcerates to form a malignant ulcer with a raised fixed hard edge. The cancer grows more quickly than a rodent ulcer but more slowly than a keratoacanthoma. The regional nodes can be involved early. The choice of treatment (surgery or radiotherapy) depends on the tumour’s size, site and aggressiveness. Palpable lymph nodes require regional lymphadenectomy by block dissection. Adjuvant radiotherapy may be required if histology shows extracapsular spread.

Fig. 18.20 Squamous cell carcinoma.

A warty nodule with induration of the adjacent skin.

Epidermal neoplasms arising from melanocytes

Benign pigmented moles

The number of melanocytes is relatively fixed (approximately 2000 million), regardless of the colour of the individual, but the amount of pigment produced varies greatly. As a developmental abnormality, conglomerates of melanocytes may migrate to the dermis or epidermis to form a melanocytic naevus or mole. The naevus cells can cause a variety of pigmented spots and swellings (naevi) according to their site and activity (Fig. 18.21). Moles showing melanocyte activity at the junction of epidermis and dermis (junctional change) are common in childhood; all moles on the soles and palms are of this type. Migration of sheets of naevus cells to the dermis produces a dermal naevus; migration to both dermis and epidermis produces a compound naevus.

Fig. 18.21 Histopathological types of benign mole.

Common moles

The common mole is a flat or slightly raised brown-black lesion covered by normal epidermis. It has a period of active growth during childhood as a result of junctional activity, but usually becomes quiescent at puberty and may later atrophy. If naevus cells migrate to the dermis, the lesion becomes firm and raised, and there is often aberrant hair growth. The epidermis remains smooth if it remains uninvolved, but can become soft and roughened in a compound naevus. As only 1 in 100 000 moles becomes malignant, they need not normally be removed. Active growth in childhood need not cause concern, but growth after puberty demands removal. An increase in pigmentation, scaliness, itching and bleeding may also give rise to anxiety about malignancy and indicate the need for excision biopsy. Any mole that develops these characteristics should be removed. Further treatment depends on the histological appearances (see below).

Giant hairy naevus

Unlike the common mole, this lesion is present at birth. It can cover a large area, which may correspond to a dermatome. Typical sites are the bathing-trunk area and face. The risk of malignant change is small but such moles should be kept under observation, and in some cases there may be cosmetic indications for excision.

Blue naevus

This intradermal naevus can appear blue because the melanin-containing cells are deep in the dermis. It can develop at any time from birth to middle age.

Halo naevus

This pigmented naevus is surrounded by a white circle of depigmentation associated with lymphocytic infiltration.

Summary Box 18.6 Epidermal neoplasms arising from melanocytes

• A mole is due to a conglomeration of melanocytes

• Melanocyte activity at the junction of epidermis and dermis (i.e. junctional activity) is common in childhood

• Migration of melanocytes into the dermis produces a dermal naevus, while migration to both dermis and epidermis produces a compound naevus

• Only 1 in 100 000 moles becomes malignant, so that the presence of a mole is not in itself an indication for removal. Active growth in childhood need not cause concern, but growth thereafter should

• Excision is indicated if a mole shows an increase in pigmentation, scaliness, itching or bleeding. A 3 mm excision margin is adequate in the first instance.

Malignant melanoma

Malignant melanomas predominantly affect fair-skinned people. They are rare in blacks but can occasionally affect the depigmented areas such as the palms, soles and mucosa. Exposure to sunlight is the major precipitating factor. In Scotland, the incidence is 8 per 100 000 individuals per year, compared to 40 per 100 000 in Queensland, Australia. The incidence has increased world-wide, and in Scotland there has been a 100% increase over the last 10 years. Malignant melanomas are more common in females, with a higher incidence on the legs, presumably because of greater exposure. About half of all malignant melanomas are thought to arise in pre-existing naevi. The average individual has 14 melanocytic naevi and the risk of any one of them becoming malignant is very small. However, the greater the number of moles, the greater the risk, particularly in those with a family history of malignant melanoma. The essential feature of malignant melanoma is invasion of the dermis by proliferating melanocytes with large nuclei, prominent nucleoli and frequent mitoses. Three distinct clinicopathological types of malignant melanoma are described.

Hutchison’s melanotic freckle (lentigo maligna)

One in 10 malignant melanomas arises in a melanotic or senile freckle. They occur most commonly on the face of elderly women (Fig. 18.22), beginning as a brown-red patch that grows slowly, advancing and receding over the years. The edge of the lesion appears serrated but its margin with normal skin remains abrupt. Kaleidoscopic pigmentation of the surface is typical. This premalignant phase may last for 10–15 years. The first sign of malignancy is a brownish-red papule that develops eccentrically within the freckle and indicates vertical extension of melanocytes into the dermis in the form of a lentigo maligna melanoma.

Fig. 18.22 Melanotic freckle on the face of an elderly man.

Superficial spreading melanoma

This is the most common type of malignant melanoma (Fig. 18.23). It occurs on the trunk and exposed parts, and is most common in middle age. During a pre-invasive phase, which lasts for at most 1 or 2 years, malignant cells spread outwards (horizontal growth phase) in the epidermis in all directions. The surface is slightly raised, the outline is indistinct, pigmentation is patchy and there may be a wide range of colours. Invasion of the dermis (vertical growth phase) occurs while the lesion is still relatively small and produces an indurated nodule, which soon ulcerates or bleeds.

Fig. 18.23 Superficial spreading melanoma.

Nodular melanoma

This elevated, deeply pigmented melanoma can occur at any site and at any age. Nodular melanomas are particularly common in females on the leg. They may occur at the site of a pre-existing benign naevus. Nodular melanomas are vertically invasive from the start and there is no initial intra-epidermal spread and therefore no surrounding pigmented macule. The nodule enlarges steadily, both centrifugally and on the surface. Surface spread is detected by the destruction of normal skin lines. The lesion darkens progressively and the surface over the area of active growth becomes jet black and glossy. Bleeding may follow trivial injury and is noted as spots of blood on clothes. Crusting, scab formation, itching, irritation and ulceration are typical. Satellite nodules may form around neglected lesions.

Other types of malignant melanoma

Amelanotic melanomas are rare, pale pink lesions that can grow rapidly. Careful histological examination will demonstrate pigment in virtually every case. Acral lentiginous melanoma is seen on the soles and palms (Fig. 18.24). It resembles superficial spreading melanoma in its behaviour, although the thick skin of the affected regions may mask some of the features and cause late presentation, with nodularity and ulceration. Subungual melanomas typically affect the thumb or great toe of the middle-aged and elderly, causing chronic inflammation beneath the nail. Pigmentation is not usually visible in the early stages and the lesion is often misdiagnosed as a paronychia or ingrowing toenail.

Fig. 18.24 Acral lentiginous melanoma arising on the sole of the foot.

Spread of malignant melanoma

Malignant melanomas spread readily via the lymphatics and bloodstream. In transit metastases may develop in the subcutaneous or intracutaneous lymphatics, and form painless discoloured nodules in the line of the lymphatics between the primary and the regional nodes. Lymph node metastases often present as firm enlargement of a node. The disease then spreads to adjacent regional and central nodes. Blood-borne metastases can occur at any site but are common in the brain, liver, lungs, skin and subcutaneous tissues. In about 5% of cases, metastases are present in the absence of a recognizable primary site.

Summary Box 18.7 Malignant melanoma

• Malignant melanoma is predominantly, but not exclusively, a disease of fair-skinned individuals

• Exposure to sunlight is the key aetiological factor

• The lesion is more common in females, reflecting the higher incidence of malignant melanomas of the lower leg

• 50% of all malignant melanomas arise in a pre-existing naevus

• The essential feature of malignancy is invasion of the dermis by proliferating melanocytes (which show large nuclei, prominent nucleoli and frequent mitoses)

• Malignant melanoma spreads rapidly by the lymphatic system and the bloodstream. ‘In transit’ metastases may develop in the lymphatics of the skin and subcutaneous tissues.

Clinical and pathological staging

Three clinical stages are recognized and staging has major prognostic implications (Table 18.6). For lesions in clinical stage I, the most reliable prognostic indicator is the depth of the lesion (Fig. 18.25); the more superficial the lesion, the better the prognosis. Depth can be measured by reference to the normal layers of skin (Clark) or by a micrometer gauge (Breslow). As the skin layers may be distorted by the tumour, the Breslow system is usually preferred. Mitotic activity also influences prognosis, and tumours can be graded according to the number of mitotic figures in each field. Lymphocytic response and features of regression can also influence prognosis. Melanotic freckles and superficial spreading melanomas tend to remain superficial and so have a better prognosis than nodular melanomas.

Table 18.6 Prognosis in relation to the stage and depth of malignant melanoma

Clinical stage	5-year survival rate (%)
I Primary lesion only
Breslow depth (mm)	70
< 1.5	93
1.5–3.5	60
> 3.5	48
II Primary lesion + regional lymph node or satellite deposit	30
III Metastatic disease	0