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Reconstructive plastic surgery, as opposed to cosmetic surgery, is concerned with the restoration of form and function following trauma, ablative surgery, necrotising infection or congenital anomaly. The various techniques by which this is achieved are applicable throughout the body, whether male or female, young or old, and the plastic surgeon must therefore have an excellent knowledge of applied anatomy and reconstructive techniques. The ‘reconstructive ladder’ stratifies these increasingly complex and demanding procedures and is useful conceptually, although in practice, it is often necessary to skip a step or even go directly to the top ( Fig. 19.1 ). The specialty is highly varied and includes the surgical management of skin and soft tissue malignancy; soft tissue trauma; breast, trunk and perineal reconstruction; burns; soft tissue infection; hand surgery, brachial plexus and nerve compression; facial reanimation; cleft lip and palate and craniofacial deformity; and cosmetic surgery.
The outermost layer, or epidermis, is composed of keratinised, stratified squamous epithelium through which three appendages (hair follicles, sweat glands and sebaceous glands) pass from the underlying dermis and subcutaneous tissue ( Fig. 19.2 ). These appendages can escape destruction in partial-thickness burns and are therefore a source of new epidermal cells for reconstitution of the epidermis. The basal layer of the epidermis generates keratin-producing cells (keratinocytes), which become flatter as they migrate towards the surface through substrata (spinosum, granulosum, lucidum and corneum), where they are shed. The basal layer also contains pigment cells (melanocytes) that produce melanin that is passed to the keratinocytes and protects the basal layer from ultraviolet light, as well as determining skin and hair colour.
The dermis, which is bound to the epidermis through a basement membrane, is composed of three cell types (fibroblasts, macrophages and adipocytes), collagen, elastic fibres and an extracellular gel-like matrix. It supports the blood vessels, lymphatics, nerves and the epidermal appendages as well as pressure and temperature receptors. At the junction between the epidermis and the superficial papillary dermis, vascularised papillae push upwards to nourish the epidermis. Beneath this, the reticular dermis provides the strength and elasticity of the skin.
Sebaceous glands within the dermis secrete sebum into the hair follicles to lubricate the hair and skin. The coiled tubular sweat glands are of two types: eccrine glands exist throughout the entire skin surface and secrete salt and water, primarily for thermoregulation, whereas the apocrine glands, which are largely confined to the axilla and genital skin, secrete a more fatty, odorous fluid that is a good medium for bacterial growth. Hidradenitis suppurativa is an infective process affecting the latter.
A wound may be defined as the disruption of normal tissue continuity and structure due to trauma or disease processes.
Wounds may be classified according to the mechanism of injury. Trauma caused by a sharp implement tends to produce ‘incised’ wounds, whereas blunt trauma is associated with lacerations, abrasions and crush and degloving injuries. Special consideration should be given to crush injuries, where the underlying tissue damage may exceed that apparent on the surface. Associated bleeding and oedema beneath the deep fascia can lead to compartment syndrome with ensuing ischaemic necrosis of involved tissues. Degloving injuries result from shear forces, for example, when a limb is compressed between rollers or beneath the wheel of a vehicle, which cause parallel tissue planes to separate. Due to the vascular anatomy in humans, such injuries can render large areas of intact skin ischaemic. Gunshot wound s caused by low- or high-velocity projectiles can produce massive internal destruction due to cavitation, despite relatively minor skin wounds. In contrast, burn wounds caused by flame, hot fluids (scalds), chemicals, irradiation and electricity may involve large areas of skin, with profound metabolic consequences. The management of burns is described in detail later. Natural disease processes such as neoplasia, vascular disorders and necrotising infections may also predispose to wounds.
The essential features of wound healing are common to almost all soft tissues and result in the formation of a scar. ‘Primary healing’ is achieved when the wound edges are approximated shortly after injury. Epithelial cover is quickly achieved, and healing usually produces a relatively fine scar. Delayed primary healing refers to sharp debridement and direct closure of an old wound, whereas secondary healing occurs when a wound is left to heal spontaneously, often resulting in excessive fibrosis and an unsightly scar ( Fig. 19.3 ). Conceptually, there are three phases of wound healing mediated by several growth factors, including fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF) and transforming growth factor beta (TGF-β) ( Table 19.1 ).
Inflammatory phase (days 1–6) |
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Proliferative phase (days 3–21) |
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Remodelling or maturation phase (weeks 3–52+) |
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The initial phase begins with immediate vasoconstriction and coagulation, followed by vasodilation and increased vascular permeability that is mediated by histamine, nitric oxide (NO) and serotonin produced by platelets and endothelial cells. Neutrophils (1–2 days), macrophages (2–4 days) and lymphocytes (5–7 days) coordinate the inflammatory and growth factor response.
Fibroblasts, attracted to the wound by a process known as chemotaxis, arrive by day 3 and predominate by day 7. They produce the collagen necessary for scar formation and remodelling. Angiogenesis, the ingrowth of new blood vessels under the influence of VEGF and NO, occurs simultaneously, and wound tensile strength increases steadily ( Fig. 19.4 ).
During weeks 3 to 5, the rate of collagen breakdown approaches and then temporarily surpasses its synthesis. Subsequently, there is no net increase in collagen within the wound, although it becomes more organised and better cross-linked. The type III collagen that predominates initially is gradually replaced by type I collagen, eventually restoring the normal ratio of 4:1, although skin and fascia usually recover only 80% of their original tensile strength.
Clinically, wound healing is considered to be complete once the surface of the wound has been reepithelialised, although remodeling continues for 2 years or more. Epidermal cells from the wound edges and from within the skin appendages are mobilised to migrate across the wound surface, multiplying as they do so, until contact is made with the opposing wound edges. At this point, contact inhibition is reestablished, and the cells differentiate once more to form the normal epidermal layers. Concurrently, myofibroblasts scattered throughout the wound lead to wound contraction, especially in the absence of viable dermis.
Hypertrophic scarring occurs in up to 15% of wounds and is more common following healing by secondary intent, in areas of tension, on flexural surfaces or in the presence of infection. The appearance is of raised, red and often itchy scars whose borders are, by definition, confined to the original wound. Type III collagen and myofibroblasts predominate. Such scars tend to develop over the first 6 months and subsequently settle, although this may take 2 years or more. Resolution can be accelerated with regular massage, the application of topical silicone gel, steroid injections or pressure dressing. In some cases, surgical scar revision may be beneficial.
Keloid scars are similar to hypertrophic scars, except that they typically continue to enlarge beyond 6 months and expand outward with the original wound, appearing to invade the uninvolved adjacent skin. They most commonly occur across the upper chest, shoulders and earlobes. Black or dark-skinned individuals and those with a personal or family history of keloid formation or blood group A are particularly at risk. Such scars are difficult to treat, and surgical intervention is the last resort. In addition to the treatment options described for hypertrophic scarring, intralesional 5-fluorouracil, interferon, bleomycin and botulinum toxin have been used successfully, as have low-dose external beam radiation and cryotherapy.
Unstable scars are those that are prone to repeated cycles of ulceration and rehealing. They can develop where the dermis and subcutaneous tissue are thin, where the circulation is poor and pressure or shear forces are ever-present. Repeated cellular replication can lead to the accumulation of genetic errors and the formation of Marjolin ulcers, a form of squamous cell carcinoma. All chronic wounds and ulcers should therefore be biopsied to exclude such transformation.
Healing by primary intent is most efficient and rapid, resulting in minimal scarring. It is achieved through early debridement and direct closure of a wound.
Healing by secondary intent occurs when a wound is left open. Healing is delayed and often results in hypertrophic scarring and contracture.
Delayed primary healing occurs when an old wound is debrided and closed. The wound will heal more rapidly and with better scarring.
Many factors influence wound healing, and consideration should be given to optimising these where possible.
Any local or systemic condition that compromises the ability of blood to deliver oxygen and nutrients whilst removing waste products from the wound will adversely affect wound healing. This includes peripheral vascular disease, anaemia, cardiopulmonary disease, smoking and microvascular disease associated with diabetes, Raynaud disease and scleroderma. A poor surgical technique that damages or applies excessive tension to the wound edges can also render tissue ischaemic. Such wounds are more prone to infection and frequently break down because arterial oxygen tension (Pa o 2 ) is a key determinant of the rate of collagen synthesis. Similarly, wound healing in previously irradiated areas is often impaired due in part to compromise of the circulation.
The risk of wound infection is a reflection of patient age, the mechanism of wound formation, its location and environmental exposure, the presence of intercurrent infection, steroid administration or other immunosuppression states, smoking, diabetes mellitus, severe malnutrition and cardiovascular or respiratory disease. Microbial contamination can be minimised by careful skin preparation, aseptic technique and thorough wound debridement of devitalised tissue and foreign material. Poor hand hygiene before and after patient contact is perhaps the single greatest source of infection spread. The immune system provides natural defences against microbial invasion. Common infecting organisms include skin commensals as well as opportunistic organisms such as staphylococci, streptococci, coliforms and anaerobes. Pseudomonal infections are common in burns and chronic wounds.
When wound contamination is anticipated, or the consequences of infection would be severe, prophylactic antibacterial treatment may be used topically or systemically. In acute traumatic wounds, tetanus prophylaxis is considered routinely, but antibiotics are not normally necessary if prompt treatment is undertaken.
Protein, glucose and fatty acids are essential to wound healing, and in deficiency states, wound dehiscence and infection are common. Highly exudative wounds can contribute to total protein loss by up to 100 g each day. Healing problems should be anticipated if recent weight loss exceeds 20%.
Vitamin A is required for epithelial formation, cellular differentiation and normal functioning of the immune system, and supplements have been shown to mitigate the negative effects of steroids on wound healing. Vitamin C is essential for proline hydroxylation in collagen synthesis, and deficiency leads to reduced collagen production and tensile strength, immature fibroblast formation and capillary haemorrhage, all features of scurvy. Zinc is a cofactor for several important enzymes involved in healing. Other elements, including copper, iron and selenium, are also likely to be essential for promoting normal wound healing. Although supplements of trace elements and vitamins are effective in patients with known or suspected deficiencies, they do not appear to improve healing in normal subjects.
Healing may be affected by concurrent disease or its treatment. For example, cancer may be associated with severe malnutrition and marked impairment of healing. Diabetes mellitus impairs healing by promoting infection and by causing peripheral vascular insufficiency and neuropathy. Haemorrhagic diatheses increase the risk of haematoma formation and wound infection. Respiratory disease may lower arterial oxygen tension, and coughing can contribute to abdominal wound dehiscence. Corticosteroids, immunosuppressive therapy, chemotherapy and radiotherapy contribute to poor wound healing through various mechanisms, including impaired cellular function and inflammatory response, impaired collagen synthesis and decreased resistance to infection.
Tension-free primary wound closure and meticulous technique promote effective wound healing. Dead space should be avoided because the potential accumulation of blood and exudate encourages infection and increases tension on the wound. Drain placement can be helpful in the management of dead space, but drains should be removed as soon as possible and typically when the output falls below 40 mL/24 hours. Appropriate dressings are essential to protect the wound from infection, trauma and desiccation and to remove exudate whilst providing a favourable warm and moist environment.
All surgical procedures can be classified as ‘clean’, ‘clean–contaminated’ or ‘contaminated’, according to the likelihood of intraoperative contamination and subsequent wound infection. Clean procedures are those in which wound contamination is not expected and the wound infection rate is less than 1%.
Clean–contaminated procedures are those in which no frank focus of infection is encountered but where a significant risk of infection is present. Bowel surgery is a classic example. Infection rates of up to 5% may occur.
Contaminated procedures are those in which gross contamination is already present or inevitable and the risk of wound infection is high. Examples include bowel perforations, trauma and drainage of an abscess.
Antibiotic prophylaxis may be considered for the first two, whereas contaminated wounds are very likely to require therapeutic antibiotics (for further details on perioperative antibiotic prophylaxis, see Chapter 4 ) .
Wound location and cause
Presence of infection, contamination, foreign body or necrotic or devitalised tissue
Age
Family history
Genetic predisposition (progeria, cutis laxa, Ehlers–Danlos syndrome)
Smoking
Malnutrition
Diabetes mellitus
Haemorrhagic diatheses
Hypoxia states (e.g., cardiopulmonary and peripheral vascular disease)
Corticosteroid therapy
Immunosuppression
Chemoradiotherapy
Meticulous tissue handling and haemostasis
Minimal tension
Accurate tissue apposition
Appropriate suture materials and dressings
Wound infection typically becomes evident 3 to 4 days after surgery, although it can be delayed if prophylactic antibiotics have been used. Earlier infections suggest significant contamination of the wound at the time of surgery or initial injury.
The clinical signs of infection include bright erythema radiating from the wound associated with swelling, discomfort or pain and discharge that is often malodorous. On palpation, there may be fluctuance indicative of an abscess, an infected haematoma or a seroma, whilst crepitus may be felt in the presence of gas-forming organisms. In deep-seated infection, there may be no signs on the skin surface, although the patient may have wound tenderness, pyrexia and other signs of sepsis. Toxaemia, bacteraemia and septicaemia can complicate any wound infection, especially where there is a collection of pus.
Careful preoperative planning and preparation; meticulous aseptic technique, tissue handling and debridement; and the prophylactic use of antibiotics in high-risk patients all help reduce the risk of wound infection. Severely contaminated wounds may be left open for subsequent inspection and closed days later; most blast and gunshot wounds are treated in this way.
In the event of infection, a wound swab or specimen of pus is sent routinely for bacteriologic culture and sensitivity determination. In urgent cases, Gram staining may be useful to indicate the class of bacteria involved. The area of erythema is ‘mapped out’ with an indelible marker so that progression can be monitored. Whilst minor superficial cellulitis can be managed expectantly, spreading cellulitis is an indication for intravenous antibiotic therapy, with drainage of an abscess or debridement of necrotic tissue as required. Antibiotic therapy is usually initiated on an empirical basis and refined later, depending on culture and antibiotic sensitivities .
Contaminated wounds should be debrided under general anaesthesia: the margins must be cleansed or sharply excised, and grit, soil and foreign bodies removed. Devitalised tissue is formally excised until viable bleeding tissue is encountered.
Primary closure is best avoided if there has been gross contamination or when treatment has been delayed for many hours. In such circumstances, attempts at primary closure increase the risk of wound infection, especially with anaerobes.
Wounds may be suitable for delayed primary closure after 24 to 48 hours or later.
Appropriate protection against tetanus and the use of antibiotic prophylaxis should be considered.
All wounds must be examined carefully to assess the skin viability and injury to deeper structures. Even small, apparently innocent wounds may conceal extensive damage to underlying muscle, bone, tendons, nerves and blood vessels. Damage to most of these structures should be evident on examination of distal motor and sensory function and the circulation. In some cases, appropriate radiologic imaging may help establish the extent of soft tissue and bony injuries.
Extensive injury or severe contamination usually necessitates inpatient exploration and repair under general anaesthesia. The wound and its margins are cleansed and all foreign material removed. Devitalised tissue is excised to a healthy bleeding wound edge ( Fig. 19.5 ). Bleeding from the wound margin does not guarantee its ultimate survival because 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 closed primarily, and a ‘second-look’ procedure should be undertaken after 48 hours. When closure is delayed, any granulation tissue is usually excised, and secondary closure performed if possible. If not, skin grafts (see later discussion) can be applied to the wound bed.
The frequency of subsequent dressing changes depends on the risk of wound healing problems. If there is a high risk of infection or skin necrosis, or excessive exudate, a wound inspection should be carried out daily. If there is little concern, however, dressing changes can be carried out on alternate days or even less frequently.
When a traumatic injury causes the skin to be undermined, this usually occurs at the level between the subcutaneous fat and underlying deep fascia and may seriously compromise the circulation to the elevated flap. This occurs commonly in pretibial lacerations in the elderly. Skin of dubious viability will often appear pale initially, becoming purple in colour before finally changing to a more distinctive dark purple-black with impending necrosis. In many cases where the viability is initially uncertain, staged reassessment should be considered after patient resuscitation. Closing such a wound under tension risks exacerbating the ischaemia as ensuing tissue inflammation and oedema compromise the circulation further.
Regardless of the cause, direct closure will not be possible if significant amounts of skin and subcutaneous tissue have been lost. Small defects in less functionally or aesthetically important areas may be allowed to heal by secondary intention, especially in patients who are not fit for reconstructive surgery or where the necessary skills and resources are unavailable. For the initial management of larger wounds, a vacuum-assisted closure (VAC) device can be employed to encourage granulation tissue formation and shrink the wound whilst providing protection and removing exudate. The device is contraindicated in the presence of infection, necrosis and neoplasia but is often used to render a wound more ‘graftable’ or to ‘buy time’ whilst complex reconstruction is planned. Nonetheless, it is often preferable to accelerate wound healing and reduce complications or scarring by ‘importing’ skin and other tissues from elsewhere in the body. This is done with either a ‘graft’, which, by definition, has no intrinsic circulation and therefore requires a vascularised recipient bed, or a ‘flap’, which, by contrast, incorporates its own vascular supply.
Skin grafts may be split- or full-thickness grafts. The former includes the epidermis and a thin layer of dermis and is harvested freehand using a specialised guarded blade (Watson knife) or by means of a powered dermatome. Split-thickness grafts can be harvested from any region of the body, although the thighs are commonly used for ease of access and their acceptable donor site morbidity. The donor site heals by secondary intent with rapid reepithelialisation from epithelial appendages within the remaining dermis. After just 2 to 3 weeks, the donor site can be reharvested once more if required. When it becomes necessary to cover very large wounds with a limited availability of donor sites (in major burns, for example), the graft can be ‘meshed’, permitting expansion of 1.5 to 6 times its original size.
Full-thickness skin grafts include the epidermis and all of the dermis, leaving a donor defect that must be closed directly or grafted. The graft size and donor sites are therefore limited; the neck, inner arm and groin are commonly used. The advantages of full-thickness grafts are that they exhibit less secondary contraction and generally produce a more aesthetic and robust scar; hence, they are commonly used in reconstructive surgery of small defects of the face and hands.
All grafts require close contact with a well-vascularised wound for nourishment and survival. They will not ‘take’ on bone, cartilage or tendon denuded of periosteum, perichondrium or paratenon. In such cases, fresh tissue with an intrinsic blood supply must be brought into the wound.
Flaps, by definition, have an intrinsic vasculature and can be categorised by their components (skin, fascia, fat, muscle, bone or viscera such as bowel or omentum), their circulatory supply or ‘pedicle’ (random or named vessels, perforator vessels) and their congruity (local, distant or free). Thanks to the large variety of flap designs, they can be used to fill defects of any size, as well as to replace missing bone, muscle, tendon and nerve as required. The simplest flaps employ local skin, fat and fascia in various configurations (designs and methods of transfer) and are good alternatives to grafting for smaller defects, such as those resulting from the excision of facial tumours ( Fig. 19.6 ). Where no local option is suitable, a ‘distant’ flap may be brought to a wound whilst remaining attached temporarily to its original blood supply ( Fig. 19.7 ). After 2 to 3 weeks, the flap will have picked up a local blood supply, and the original pedicle can be safely divided.
When local or distant flaps are not available or appropriate, the pedicle of almost any flap can be divided and anastomosed to a donor artery and vein adjacent to the wound ( Fig. 19.8 ). These so-called ‘free’ flaps have almost completely replaced the need for the complex staged reconstructions that were commonly used before the introduction of microsurgical techniques in the developed world ( Fig. 19.9 ).
Major advances in our knowledge of the blood supply to the skin and underlying tissues have led to an explosion of new flap designs and compositions, which have revolutionised plastic and reconstructive surgery. One example is the use of the deep inferior epigastric artery perforator (DIEP) flap for reconstruction of the breast following mastectomy. Another is the masseter muscle transfer used to restore the ability to smile for patients with facial paralysis. The ability to join small blood vessels and nerves under the operating microscope allows the surgeon to close defects and restore both form and function in a single operation (see also Chapter 26 ).
Burns range from trivial to life-threatening injuries that require extensive, multidisciplinary treatment and rehabilitation, with the prospect of permanent disfigurement and impaired function. The aetiologies include flame or contact burns, scalds from hot liquids or gasses, irradiation and electrical or chemical insults. Individuals at the extremes of age and those with impaired mental or physical abilities are particularly vulnerable. Whilst health and safety legislation has led to dramatic reductions in the number and severity of burns, most cases are still considered to be preventable. Industrial accidents account for the majority of electrical and chemical burns, whilst alcohol and smoking are common contributing factors in many domestic burn injuries. House fires are often accompanied by smoke inhalation that injures the lung parenchyma and impairs tissue oxygenation. In every case, it is important to diagnose and treat concurrent preexisting comorbidities as well as other injuries that may have occurred at the time of the accident.
The local effects of a burn result from destruction of the tissues and the inflammatory response of the adjacent areas ( Table 19.2 ). In its least severe form, the dermal inflammatory response consists of capillary dilation, as seen with the erythema of sunburn. With deeper burns, however, the damaged capillaries become permeable to protein, and an exudate forms with an electrolytic and protein content only slightly less than that of plasma. Increased capillary permeability can raise the typical insensible fluid loss of 15 mL/m 2 body surface/hour to as much as 200 mL/m 2 within the first few hours, resulting in blistering, hypovolaemia and oedema as lymphatic drainage fails to keep pace. Exudation peaks in the first 12 hours, and capillary permeability returns to normal within 48 hours.
Destruction of tissue |
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Increased capillary permeability |
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Increased metabolic rate |
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Destruction of the epidermis also impairs the physical and immunologic barrier to infection. Sepsis delays healing, increases energy demands, and poses a threat to life, making early wound care and protection essential. With deeper burns, the epidermis and dermis are converted into a coagulum of necrotic tissue known as eschar, which contracts and can compromise limb circulation, chest expansion and ventilation.
With the exception of superficial burns, the systemic effects of a burn depend more upon its size than its depth. 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 wound surface. With large burns, the effect is compounded by a systemic increase in capillary permeability with widespread oedema. Red cell loss is small compared with plasma loss in the early period, and haemoconcentration, reflected by a rising haematocrit, is normally evident. If circulatory volume is not restored, hypovolaemic shock ensues. The metabolic rate increases such that in severe burns, some 7000 kcal may be expended daily, and consequent weight loss of 0.5 kg each day is not unusual unless steps are taken to prevent it.
Burns are classified according to the aetiology, the surface area affected and the burn depth.
The approximate extent of any burn can be quickly calculated using a combination of three methods. The Wallace ‘rule of nines’ divides the body into areas that each represent approximately 9% of the total body surface area (TBSA) of an adult ( Fig. 19.10 ). However, this technique is less useful in children because of the relatively large head size (about 20% of body surface at birth) and small limbs (legs are about 13%). Burn injuries rarely conform to such neat patterns. Another commonly employed technique is based on the assumption that the surface area of the patient’s palm and closed fingers together constitute about 1% of their TBSA. Perhaps the most accurate and widely employed method is the Lund and Browder charts that provide a physical documentation of burn size and compensate for age ( Fig. 19.11 ). The charts also act as a visual medical record that can be helpful once the wounds are covered with dressings. Simple erythema usually subsides in a few hours and should not be included in calculations of overall burn size. Hypovolaemic shock is more likely with 15% (10% in children) surface burns, prompting the need for resuscitation fluids.
The accurate assessment of burn depth is critical because it indicates the likelihood of spontaneous healing and therefore the need for grafting. Superficial burns, like sunburn, are typically more painful, may present with blistering and blanch on pressure, whereas the deeper burns may be dry, waxy and painless, with no evidence of dermal circulation. Burn depth is classically subdivided into three groups, superficial, partial and full thickness. In North America and elsewhere, these are described as first, second and third degree, respectively. In practice, many burns are of mixed depth ( Fig. 19.12 ).
Superficial and superficial partial-thickness burns affect the epidermis alone or the epidermis and the superficial dermis, respectively. Reepithelialisation occurs from cells originating within the deeper epidermal appendages, such as sweat glands and hair follicles. Such wounds are therefore anticipated to heal spontaneously within 2 to 3 weeks and usually with excellent cosmetic outcomes. However, pain, swelling and fluid loss can be marked.
In deeper partial-thickness (also known as deep-dermal ) burns, the epidermis and much of the dermis are destroyed. Restoration of the epidermis then depends on relatively few intact epithelial cells within the remaining appendages and those at the wound edges. Pain, swelling and fluid losses are again marked, but the burn takes longer than 3 weeks to heal and often leaves unsightly hypertrophic scars and contractures. Superimposed infection may delay healing further and can cause additional tissue destruction, effectively converting the injury to a full-thickness burn.
Full-thickness burns destroy the epidermis and underlying dermis, including the epidermal appendages, and therefore drastically limit the healing potential. The tissues undergo coagulative necrosis to form an eschar that, if not debrided, begins to lift after 2 to 3 weeks. Without skin grafting, epidermal cover can only proceed from the inward migration of uninjured cells at the periphery of the burn and by contraction of its base. Fibrosis, contracture and poor scars are inevitable in all but the smallest ungrafted wounds .
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.
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