The two skin layers are bound together by a complex mechanism that is essential for normal function. Epidermal appendages are distributed throughout the dermis layer, including the sweat glands, sebaceous glands, and hair follicles. The dermal layer is capable of producing new epithelial cells to replace those lost from the epidermis by burning or other injury to the skin because the shafts of these appendages are lined with epithelial cells.
Nerve endings occur throughout both skin layers, and the connective tissue of the dermis also provides a firm structural base for the skin. Burn injury is a very painful form of trauma because of the multitude of pain receptors and nerves that traverse the skin layers. Beneath the skin lie the subcutaneous tissues, muscle, and bone. Basic skin anatomy, showing the depth of injury for first-, second-, and third-degree burns. Adapted from reference with permission of the publisher.
The skin is one of the largest organs in the human body, in terms of both its overall size and weight. The average adult skin surface area is 1. The two skin layers together are up to several millimeters thick, but both epidermal and dermal thickness varies depending on the body site. The epidermis is the thinnest 0.
The dermis is thickest on the back. Males generally have thicker skin than females. General skin thickness peaks in midlife and gradually thins as part of the aging process , , , , Infants, young children, and elderly adults have a much thinner dermal layer to their skin, resulting in an increased propensity for deeper burn injury. Epidermal cells are constantly being shed and replaced every month through a process that continually pushes new cells to the surface. This natural process is designed to continually replenish and heal breaches in the outermost protective skin barrier, be it from the microtraumas sustained as part of daily living or from overt injury.
The epidermis therefore heals itself after superficial injury. Several important physiological functions of the skin are altered by thermal injury. Survival of the severely burned patient requires immediate access to a specialized burn care unit.
Modern emergency burn resuscitation and ongoing treatment are designed to alleviate the systemic changes that result from acute disruption of a large part of the skin barrier. Meticulous attention is given to the replacement and prevention of fluid loss, the maintenance of body temperature homeostasis within a constant normal range, the easing of severe pain, and the prevention of infection. In North America, burn injury is one of the main causes of injury deaths, particularly in children under the age of 14 years 7 , 68 - 70 , , , Although the age-adjusted death rate from burn injury in the United States has decreased substantially since , the United States still has one of the highest per capita burn death rates of any industrialized country , Between and , there were The highest fatality rates occur among children 4 years of age or younger and adults over the age of 55 years , , , Burn-related deaths in these two age groups account for more than two-thirds of all fire deaths.
Males are twice as likely to die of burn-related injury as females in all age groups. A significant proportion of adult burn patients also suffer from a high degree of mental illness Since legal action is taken in many of these cases, it is important to document the etiology and extent of the burn injury. Burn injuries incur a significant cost to the health care system in North America and worldwide. In the United States and Canada there are currently centers specializing in burn care, with over 2, beds Burn care centers in North America currently admit an average of more than patients per year, whereas other hospital units admit an average of fewer than five burn patients per year 7 , Overall, costs escalate for major burn cases because of repeated admissions for reconstruction and rehabilitation therapy.
The breached skin barrier is the hallmark of thermal injury. The body tries to maintain homeostasis by initiating a process of contraction, retraction, and coagulation of blood vessels immediately after a burn injury. Three distinct zones have been defined within the burn wound: Serious thermal injury causes total loss of the skin surface over large areas of the body. Because of the importance of the skin as a barrier to microbial host invasion, it is not surprising that the risk of subsequent burn wound infection and systemic infection correlates with the size of the burn injury , Zones of injury for superficial and deep second-degree burns.
Direct contact with flame, a hot surface or hot liquid scald , or a source of heat conduction, convection, or radiation causes a degree of cellular damage to the skin that varies with the temperature and duration of exposure 21 , , , , , , , As the temperature rises, increasing molecular collisions occur, resulting in altered molecular conformation and the disruption of intermolecular bonds. This process leads to cell membrane dysfunction as ion channels are disrupted, resulting in sodium and water intake.
As the temperature rises further, protein denaturation occurs, oxygen radicals are liberated, and eventually cells die with the formation of the burn eschar Chemical interaction may also damage protein structures. A burn patient is a trauma patient. The initial assessment and resuscitation are therefore focused on the patient's airway, breathing, and circulation and an examination for other major injuries besides the burn itself.
Assessment of the burn injury should include a determination of the etiology of the burn as well as the extent of the burn injury. Although the assessment of the extent and depth of all types of burn injury is clinically difficult, chemical injuries are particularly challenging. The severity of injury is not only related to the areas and sites of skin injury, but also depends on the chemical agent and the duration of exposure.
In these cases, morbidity may be high even with small areas of injury, such as alkali injury to the eye, with inhalation of vapors such as anhydrous ammonia due to the systemic effects from absorption 9 , Subjective clinical methods have historically been used to determine the depth of burn injury. Areas of partial and full-thickness burn injury are described, noting areas of circumferential involvement and burn injury across joints.
However, the clinical methods outlined above may not provide sufficient accuracy of evaluation of burn depth to support crucial treatment decisions such as the extent of excision and grafting required. Laser Doppler imaging LDI has recently been shown to provide a more objective measurement on which to base the decision to operate 25 , , A recent prospective blinded trial compared the clinical outcome of using LDI versus clinical judgment to assess injury depth. A total of 23 burn patients and 41 wounds were analyzed by both methods.
LDI agreed with wound biopsy confirmation when the scan indicated a need for excision. LDI also enabled excision to proceed earlier even when the surgeon's clinical assessment agreed with the LDI scan results. LDI may therefore be used as an effective aid to clinical judgment in modern burn centers for deciding to excise burn wounds of indeterminate depth. Inhalation injury of the lung in adults is usually proportional to the depth and extent of body surface area burned , , , Children have a lower rate of inhalation injury because of the prominence of scald injury in this group , Hypoxia occurs when the carbon monoxide generated by combustion is inhaled and binds to hemoglobin.
Even a relatively low concentration of carbon monoxide in inhaled air can be significant because its affinity for hemoglobin is much greater than that of oxygen e. Hydrogen cyanide and other agents generated in smoke are potent toxins and exacerbate the acidosis that occurs as a result of burn injury 43 , The pathogenesis of pulmonary injury from smoke inhalation has been well described 99 - , , , Direct heat injury is restricted to the upper airway above the glottis and is manifested by rapid swelling with the threat of obstruction.
Steam inhalation is the only type of heat that damages the lower respiratory tract.
However, inhalation of smoke and products of combustion and destruction of the tracheobronchial respiratory epithelium cause chemical injury. Inhalation injury progresses during the first few days following a burn and results in edema and sloughing of the respiratory tract mucosa and impairment of the normal mucociliary clearance mechanism. Damage of the mucociliary lining of the respiratory tract decreases the clearance of invading microorganisms. Pulmonary edema results from direct microvascular injury and the release of oxygen free radicals and inflammatory mediators.
Cast formation due to aggregates of mucus and cellular debris causes obstruction of moderate-size airways when the mucosa sloughs. Disruption of endothelial and epithelial integrity results in exudation of protein-rich plasma into terminal airways, which, in combination with atelectasis, leads to bacterial growth and the subsequent development of pneumonia. Smoke inhalation also destroys type II pneumocytes, which results in impaired surfactant production 15 , , Advances in respiratory resuscitation support in trauma intensive care units have improved the prognosis for burn patients with inhalation injury 15 , , , The clinical effects of thermal inhalation injury typically become manifest within a few hours after injury, whereas chemical injury of the lower respiratory tract progresses more slowly e.
Stridor that develops immediately after heat injury associated with an increased respiratory rate, worsening hypoxemia, and trouble expectorating secretions are signs of worsening edema of the upper airway e. Similar signs of impending respiratory failure also develop in burn patients with a smoke inhalation injury and require immediate respiratory resuscitation.
Intubation and mechanical ventilation as well as intensive tracheobronchial care e. High-frequency ventilation may also be beneficial in the clearance of secretions and also stabilizes collapsed and diseased lung segments , Patients with inhalation injury have greater fluid requirements than those who have only sustained a cutaneous injury.
More fluid must be given in the immediate period following thermal injury in patients with inhalation injury , Various agents have been administered, including inhaled heparin along with bronchodilators or free-radical scavenging agents such as dimethyl sulfoxide or N -acetylcysteine, in the treatment of inhalation injury in order to decrease cast formation and small-airway obstruction 15 , 61 , , Nitric oxide is a potent vasodilator that has recently been administered as inhalation therapy to burn patients with acute respiratory distress syndrome due to lung injury in order to reduce ventilation-perfusion mismatch by dilating blood vessels perfusing lung alveoli 15 , Prior to the widespread use of early surgical excision of burn wounds, conservative management was practiced.
Colonization of the burn wound was permitted to break down the burn eschar so that it separated spontaneously. Daily cleansing and immersion hydrotherapy were used to debride necrotic surface eschar 49 , 73 , , , Skin grafting occurred only after the development of granulation tissue on the burn wound's surface. Although early surgical excision and grafting have been repeatedly attempted in the 20th century, the outcomes were initially poor , , , However, an improved understanding of the pathophysiology of burns allowed the advancement of multiple intra- and postoperative medical and surgical techniques that has resulted in gradual decreases in morbidity and mortality 66 , 87 , , , , , Medical support to maintain hemodynamic and respiratory function within the trauma intensive care unit and operating theater, the provision of early adequate nutrition, and the use of surgical techniques that minimize blood and heat loss allowed this approach to become the standard of care for large thermal injuries in modern burn centers.
Early burn wound excision now occurs within the first few days after burn injury and has resulted in improved survival 30 , , , , , , , , , Full-thickness and deep partial-thickness wounds are excised as soon after injury as possible once the patient has been hemodynamically stabilized. An appropriate burn care plan that includes a surgical timeline for wound closure must be developed based on the age of the patients and their clinical condition and extent of burn injury.
A more conservative surgical approach may be required for patients with severe inhalation lung injury on ventilator support, the elderly, and those with underlying medical conditions that increase the risk of operation , , The primary aims of early excision are removal of the dead tissue that stimulates an overwhelming systemic inflammatory response syndrome and prevention of infection by temporary or permanent closure of the burn wound.
Furthermore, shortening the period of wound inflammation, which in turn reduces the development of hypertrophic scarring, may optimize the outcome in terms of function and appearance 12 , 97 , This is achieved by early removal of necrotic tissue e.
Surgical excision of the burn wound may be carried out in a variety of ways, but the two most common methods are excision to fascia and tangential excision, whereby the eschar is removed in layers until viable tissue is reached , , , The extent of excision at any one operation is limited by factors such as blood loss and temperature control. The open wound is usually covered with autograft, fresh allograft, or frozen allograft, in descending order of preference , In otherwise healthy adults with burns, this process is repeated during several successive operative procedures until the entire burn wound has undergone debridement and secondary covering with new skin grafts.
However, skin substitutes may be used for resurfacing in burn patients who have limited skin graft donor sites because of the extent of the injury 52 , 53 , , , , , Biobrane, a bilaminar temporary skin substitute, has been used in burn treatment centers since the early s 28 , 98 , Application of Biobrane in the immediate e. However, older wounds and those with large areas of full-thickness injury may not be suitable for Biobrane treatment. More recently, these observations have been supported by the findings of prolonged allograft survival, anergy, and increased susceptibility to infection in burn patients 75 , , , , , Despite improvements in the early care of burn patients, systemic inflammatory response syndrome, severe sepsis, and multiple-organ dysfunction syndrome remain major causes of morbidity and mortality 47 , , As a result, further efforts in the development of immune modulators may hold some promise for the future pending ongoing research.
Host defense against infection can be divided into innate and adaptive immune responses. The innate immune response acts immediately after the integument system is breached and relies on a phylogenetically ancient system for microbial recognition in which germ line-encoded receptors pattern recognition receptors recognize structural components of microorganisms and viruses pathogen-associated molecular patterns The adaptive immune response often takes longer, especially if it involves exposure to new antigens.
However, the adaptive immune response is a more efficient system for dealing with recurrent infections, relying on immune cell memory, antigen recognition, and clonal proliferation. The immunosuppression associated with burn injuries has effects on both of these systems. Many in vitro and in vivo studies have been conducted to characterize the immune responses and the relationships between various cell types and inflammatory mediators.
Several reviews have been written on the topic, discussing the findings of original works in more detail 82 , , , , This review is a synthesis of summarized data and original research that have contributed to our current understanding of the immune response following burn injury. Local inflammation following injury is essential for wound healing and host defense against infection. However, trauma or burns of sufficient magnitude can incite a systemic inflammatory response, along a continuum from systemic inflammatory response syndrome through septic shock, which has the ability to cause significant cellular and end-organ damage 46 , Initially, the immunologic response to severe burn injury is proinflammatory but later becomes predominately anti-inflammatory in an effort to maintain homeostasis and restore normal physiology.
Cytokines and cellular responses mediate both of these phases. Increased serum levels of proinflammatory cytokines characterize the systemic response to burns. Both of these cytokines contribute to the production of fever, acute-phase proteins, and an overall state of catabolism. They also up-regulate the production of prostaglandin E 2 PGE 2 , IL-6, and platelet-activating factor by endothelial cells and macrophages 80 , Levels of IL-6 are increased after injury through its production by a number of different cells 1 , Levels of IL-6 peak approximately 1 week after injury , and high levels have been associated with increased rates of morbidity and mortality, for which it is likely a marker of disease severity rather than an etiologic factor.
The anti-inflammatory response and the subsequent immunosuppression following burn injury are characterized by a set of opposing cell types and cytokines. Under these circumstances, macrophages produce increased amounts of PGE 2 and decreased amounts of IL, which have a cooperative effect on T-cell differentiation 82 , T helper cells begin to preferentially differentiate into Th-2 cells, which produce the anti-inflammatory cytokines IL-4 and IL , The exact sequence of events that result in immunosuppression after burn injury remains unknown; however, biochemical changes that may affect the immune system include those to the endocrine system, the arachidonic acid cascade, and the cytokine network.
Following severe burn injury, there is an increase in the levels of vasopressin, aldosterone, growth hormone, cortisol, glucagon, and catecholamines , Similarly, norepinephrine released early after injury inhibits Th-1 cell function, but not that of Th-2 cells Increased production of PGE 2 by inhibitory macrophages has been observed after severe injury Many of the changes in cytokine levels represent alterations of the adaptive immune system following burn injury, more specifically within the T-lymphocyte population.
Natural resistance to infection in traumatic wounds is predominantly a function of the innate immune system. Following thermal injury, the innate immune system responds immediately by stimulating localized and systemic inflammatory reactions. The innate immune response participates in activating the adaptive immune response; however, in so doing it has an adverse affect on the burn victim's ability to mount a vigorous immune response to invading microorganisms and, therefore, predisposes the burn victim to infectious complications.
The innate immune system itself is composed of natural barriers to microbial invasion as well as cellular leukocyte and humoral complement elements. Before a pathogen can establish invasive infection within the host it must break through the natural barriers of the skin or mucosa.
For example, there is a loss of barrier function of the gastrointestinal epithelium in burn patients, which may be induced by up-regulation of the nitric oxide synthetase gene and the overproduction of nitric oxide ; postoperative changes, such as decreased intestinal motility and mucus secretion; and increased exposure to endotoxin 4. The development of multiple-organ dysfunction syndrome in critically ill patients has also been associated with a derangement in intestinal permeability As a result, higher rates of bacterial translocation and endotoxin absorption through the gastrointestinal mucosa may contribute to the inflammatory response seen in burn patients.
The cellular elements of the innate immune system have important roles in antimicrobial killing and in coordinating the immune response. The function of NK cells is diminished following significant injury Neutrophil dysfunction after significant thermal injuries has also been reported 44 , , , Endothelial adherence of neutrophils is initially decreased after injury and then increases ; however, the site of endothelial adhesion may not be at the point of injury, and this misguided neutrophil adhesion and activation contribute to neutrophil-mediated endothelial injury, which may play a significant role in the pathogenesis of systemic inflammatory response syndrome and multiple-organ dysfunction syndrome.
Neutrophil chemotaxis and intracellular killing are impaired following major burns 1 , , Diminished cytotoxic activity follows from a surge of degranulation early after injury and a subsequent inability to replenish intralysosomal enzymes and defensins , Macrophages also demonstrate diminished phagocytic capacity following severe injury 5 , Lower levels of major histocompatibility complex class II expression and antigen presentation disrupt their roles in coordination of the immune response , They also produce larger quantities of PGE 2 , resulting in the suppression of B- and T-cell reactivity The complement cascade represents an important humoral component of the innate immune system.
Following significant burn injuries, the alternative pathway of the complement cascade is primarily depressed, while there is little effect on the classical pathway Complement levels fall in proportion to injury severity and then rise to supranormal levels Activation of the complement cascade by thermal injury 39 increases levels of C3a and C5a, which may result in changes in blood pressure, vascular permeability, and leukocyte function , Small amounts of C5a have been shown to stimulate leukocyte function; however, large amounts lead to suppression of activity Membrane attack complexes may target normal cells near the site of injury, contributing to reactive cell lysis, which may induce end-organ damage Lastly, increased levels of C3b may be directly immunosuppressive, as they have been shown to decrease phagocytosis and contribute to lymphocyte dysfunction 4.
These alterations to the innate immune system have the combined effect of increasing the burn patient's exposure to pathogens and decreasing the natural defenses that are responsible for counteracting them. Exposure to pathogens occurs via the burn wound, invasive monitoring devices, and the gastrointestinal tract, which loses some of its capacity to act as an effective barrier to bacterial translocation. The effects of an anti-inflammatory cytokine milieu on NK cells, neutrophils, and macrophages impair the eradication of these pathogens by the innate immune system.
Furthermore, the activation of complement following burn injury may be directly immunosuppressive. As a result of these phenomena and subsequent alterations to the adaptive immune system, burn patients are more susceptible to wound infections, severe sepsis, and multiple organ failure.
Following significant injury, several changes in the T-lymphocyte population have been observed. Total numbers of T lymphocytes fall in proportion to injury severity during the first week after injury , and there is a decrease in T-cell-dependent immune functions 75 , , , , The production of immunoglobulin G IgG in response to T-cell-dependent antigens is also impaired after serious injury; however, no impairment of antibody formation to T-cell-independent antigens has been observed Concomitantly, Th-2 lymphocytes are present in increased numbers along with higher levels of the anti-inflammatory cytokines IL-4 and IL, which may inhibit Th-1 cell activation by suppressing antigen presentation A correlation between increased levels of IL and septic events has been reported , It remains uncertain whether the relative predominance of Th-2 cells over Th-1 cells represents a phenotypic change or an increase in the rate of apoptosis of Th-1 cells Alterations in the balance between T suppressor lymphocytes and T helper lymphocytes and the ratio of Th-1 to Th-2 cells appear to be important etiologic factors in the suppression of the adaptive immune response.
Despite our increasingly detailed understanding of the immunological suppression that follows thermal injuries, no attempts at directly modulating the immune response at a specific site have been shown to be clinically effective. It is becoming increasingly clear that any therapies directed at addressing this immunodeficiency in burn patients will likely have to target multiple points in the inflammatory response and the neuroendocrine axis. Immune function in burn patients can only be restored through intensive resuscitation and support.
Early excision of burn eschar and prompt wound coverage remove a significant inflammatory stimulus and restore the barrier function of the skin. Providing adequate analgesia and maintaining adequate tissue perfusion, ambient temperature, and blood volume help optimize the oxidative killing capacity of neutrophils Early and adequate nutritional support is also important in restoring protein synthesis and normal immune function.
Research efforts have focused on the topic of immune-modifying diets, such as glutamine-enriched diets, and their clinical benefits However, there is insufficient evidence to support the use of such diets in burn patients at this time. Burn wound infections are one of the most important and potentially serious complications that occur in the acute period following injury 10 , 11 , 38 , , , The most important patient characteristics that influence morbidity and mortality from burn wound infection and sepsis are outlined below. In addition, the impact of early excision on reducing burn wound infections is discussed.
Other factors that have played a significant role in decreasing the overall fatality rates from burn wound infection and sepsis include the use of topical and prophylactic antibiotics and advances in infection control measures in modern burn units see Prevention of Burn Wound Infections, below. Very young children and the elderly have an increased risk of being burned and worse clinical outcomes than patients in other age groups 68 - 70 , 72 , , , Individuals with deliberate self-inflected burn injuries and the disabled have been shown to have more severe injuries and longer hospital stays than those with accidental injuries 18 , , Obese adults and those who have an underlying medical condition such as diabetes have also been shown to have higher morbidity and mortality , , AIDS patients appear to have more complications due to infection, delayed wound healing, and increased mortality, although reported outcome data for human immunodeficiency virus-infected and AIDS patients are limited , , , It is expected that burn patients with other types of severe immunosuppression would have similar problems, particularly increased problems with wound infection and sepsis and a higher mortality, although this group has not been studied.
Burns in the elderly constitute more severe injuries than in the general population and result in a higher number of fatalities. Approximately one-third of the elderly patients in this study also sustained smoke inhalation injury. A recent study also assessed the factors affecting burn mortality in the elderly and analyzed changes that occurred over the past three decades The study included patients 75 years of age of older that had been admitted to a university-based burn center between and Almost half of these patients died 95, or Due to improved burn care, however, the elderly are much less likely to die from burns now than in the s unless they have an inhalation injury.
Mortality increased significantly with inhalation injury despite advances in intensive respiratory support. Children have a much higher risk of being burned than adults In the United States in to , an estimated 92, children aged 14 years and under required emergency care for burn-related injuries, and approximately of these children died Male children have a higher risk of burn injury and burn-related death than females, and obese boys represented a disproportionate number of the patients admitted to a pediatric burn center from to Children who show failure to thrive e. Much of the steady decline in burn wound infections, subsequent tissue invasion and sepsis, and associated mortality that has been realized in the past 50 years has been attributed to the substantial advances that have occurred in burn wound care, particularly early excision 15 , 79 , , , , , , , There was a substantial reduction in one burn center in in the incidence of both burn wound infection and sepsis after the advent of early excision therapy However, there are only two randomized, controlled trials of early excision versus conservative exposure therapy, and neither of these studies demonstrated a significant reduction in burn wound infections in patients with a major thermal injury e.
Limited data have been published that provide a clear picture of the epidemiology of different types of burn wound infections according to the recently published classification system see Classification of Burn Wound Infections, below. Most of our understanding of the epidemiology of burn wound infections has been gleaned from studies carried out in the s through during the preexcision era of burn care It is not surprising that the overall morbidity and mortality of burn wound infections, tissue invasion, and secondary sepsis were extremely high during this time period because the growth of bacteria on the burn wound surface was controlled but not eradicated.
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