Chapter 7 Burns
Principles of Surgery Companion Handbook
|Pathology and Natural History|
|Hospital Admission and Burn Center Referral|
|Care at the Scene|
|Emergency Room Care|
|Escharotomy and Fasciotomy|
|Physiologic Response to Burn Injury|
|Metabolic Response to Burn Injury|
|Immune Response to Burn Injury|
|Special Considerations in Burn Shock Resuscitation|
|Electrical and Chemical Burns|
|Rehabilitation and Chronic Problems|
Thermal burns and related injuries are a major cause of death and disability in the United States. The introduction of burn centers in 1945 heralded a rapid improvement in survival and reduction in morbidity of burn patients and provided the basis for regional specialty treatment centers in other disciplines. The initial acute care of a burn is only a small part of the total treatment. Burn patients often require years of supervised rehabilitation, reconstruction, and psychosocial support.
In the United States, approximately 2 million individuals annually are burned seriously enough to seek health care. About 70,000 of these require hospitalization, and 5000 die. Burns are usually caused by carelessness or ignorance and are completely preventable; nearly half are smoking- or alcohol-related. More than 90 percent of all burns are preventable by taking ordinary precautions.
Advances in the care of burned patients during the past 20 years are among the most dramatic in medicine. The number of burn deaths in the United States has decreased from 15,000 in 1970 to 5000 in 1996. Over the same period, the size of burn associated with a 50 percent survival rate has increased from 30 percent of the total body surface area (TBSA) to over 80 percent TBSA in otherwise healthy young adults. Hospital stay has been cut in half. Ninety-six percent of patients admitted to burn centers survive, and 80 percent of them return to their preburn physical and social situation within a year of the injury.
The quality of burn care is not only measured by survival but also by long-term function and appearance. Although small burns are not usually life-threatening, they need the same attention as larger burns to achieve the best possible functional and cosmetic outcome. The interactive multidisciplinary burn team has proved to be the most efficient and least expensive method of treating serious burn injury. The goal for any burn is well-healed, durable skin with normal function and near-normal appearance. Scarring can be minimized by appropriate early surgical intervention and long-term scar management. These goals require individualized patient care plans based on burn characteristics and host factors. Omission of any step in the treatment regimen can result in less than optimal outcome.
Cutaneous burns are caused primarily by the application of heat to the skin resulting in coagulative necrosis of some or all of the epidermis and dermis. Cold, electricity, radiation, and caustic chemicals will result in similar pathologic damage. The thickness of skin varies with the age and sex of the individual and the area of the body. The thickness of the living epidermis is relatively constant, but keratinized (dead and cornified) epidermal cells may reach a height of 0.5 cm on the palms of hands and the soles of feet. The thickness of the dermis varies from less than 1 mm on eyelids and genitalia to more than 5 mm on the posterior trunk. The proportional thickness of skin in each body area in children is similar to that in adults, but infant skin thickness in each specific area may be less than half that of adult skin. The skin reaches adult thickness after puberty. In patients over 50 years of age, dermal atrophy begins, and the skin becomes thinner with age.
The depth of burn depends on the heat of the burn source, the thickness of the skin, the duration of contact, and the heat-dissipating capability of the skin (blood flow). A scald in an infant or elderly patient will be deeper than an identical scald in a young adult. Burns are classified according to increasing depth as first degree, second degree (superficial dermal and deep dermal), third degree (full thickness), and fourth degree. Because most deep burns are removed surgically and grafted, such a precise characterization is usually not necessary. A more pertinent classification might be shallow burns and deep burns.
Shallow Burns First-Degree Burns First-degree burns involve only the epidermis. They do not blister, but they are painful and become erythematous because of dermal vasodilation. In 23 days the erythema and the pain subside. By about day 4, the injured epithelium desquamates in the phenomenon of peeling, which is well known after sunburn.
Superficial Dermal Burns (Second Degree) Superficial dermal burns include the upper layers of dermis and characteristically form blisters at the interface of the epidermis and dermis. Blistering may not occur immediately, and burns originally appearing to be first degree may be diagnosed as superficial dermal burns after 1224 h. When blisters are removed, the wound is pink and wet, and currents of air passing over it cause pain. The wound is hypersensitive, and the burns blanch with pressure. If infection is prevented, superficial dermal burns heal spontaneously in less than 3 weeks and do so with no functional impairment. They rarely cause hypertrophic scarring, but the healed burn may never completely match the color of the surrounding normal skin.
Deep Burns Deep Dermal Burns (Second Degree) Deep dermal burns extend into the reticular layers of the dermis. Deep dermal burns also blister, but the wound surface is usually a mottled pink and white color immediately after the injury because of the varying blood supply to the dermis. The patient complains of discomfort rather than pain. When pressure is applied to the burn, capillary refill occurs slowly or may be absent. The wound is often less sensitive to pinprick than the surrounding normal skin. By the second day, the wound may be white and is usually fairly dry. If infection is prevented, these burns will heal in 39 weeks but do so with considerable scar formation. Unless active physical therapy is continued throughout the healing process, joint function can be impaired, and hypertrophic scarring is common.
Full-Thickness Burns (Third Degree) Full-thickness burns involve all layers of the dermis and can heal only by wound contracture, by epithelialization from the wound margin, or by skin grafting. Full-thickness burns appear white, cherry red, or black and may or may not have deep blisters. Full-thickness burns are leathery and firm and may be depressed when compared with adjoining normal skin. They are also insensitive to light touch or pinprick. The difference in depth between a deep dermal burn and a full-thickness burn may be less than a millimeter. The clinical appearance of full-thickness burns can resemble that of deep dermal burns. They may be mottled, they rarely blanch on pressure, and they may have a dry, white appearance. In some cases the burn is translucent, with clotted vessels visible in the depths. Some full-thickness burns, particularly immersion scalds, have a red appearance and may be confused with superficial dermal burns. However, they do not blanch with pressure. Full-thickness burns develop a classic burn eschar. If not debrided, the eschar separates from the underlying viable tissue over days or weeks.
Fourth-Degree Burns Fourth-degree burns involve not only all layers of the skin but also subcutaneous fat and deeper structures. These burns almost always have a charred appearance, and frequently only the cause of the burn gives a clue to the amount of underlying tissue destruction. Electrical burns, contact burns, some immersion burns, and burns sustained by patients who are unconscious at the time of burning are commonly fourth degree.
Scald Burns In civilian practice, scalds are the most common cause of burns, and the usual agent is water. Deliberate scalds are the most common form of reported child abuse and are responsible for about 5 percent of pediatric admissions to burn centers. At 140°F (60°C) (medium setting on a water heater), water results in a deep dermal or full-thickness burn in 3 s. At 156°F (69°C) (high), the same burn occurs in 1 s. Freshly brewed coffee from an automatic percolator generally is about 180°F (82°C). Hot cooking oil and grease may be in the range of 400°F, and scalds from these are usually deep dermal or full thickness. Factors that extend the duration of exposure also affect the depth of the burn. These include the viscosity of the hot liquid, clothing (which can retain heat), immersion, and the thickness of the skin burned.
Flame Burns Flame burns are the next most common and typically result in deep burns. Although the incidence of injuries caused by house fires has decreased with the use of smoke detectors, smoking-related fires, improper use of flammable liquids, automobile accidents, and ignition of clothing from stoves or space heaters still exact their toll. Patients whose bedding or clothes have been on fire rarely escape without some full-thickness burns.
Flash Burns Explosions of natural gas, propane, gasoline, and other flammable liquids cause intense heat for a very brief time. Unless it ignites, clothing is protective against flash burns. Flash burns generally have a distribution over all exposed skin, with the deepest areas facing the source of ignition. Flash burns are mostly dermal, but their depth depends on the amount and kind of fuel that explodes. These burns may cover a large skin area and be associated with significant thermal damage to the upper airway.
Contact Burns These burns result from contact with hot metals, plastic, glass, or hot coals. The area burned is usually limited in extent, but the injury is invariably very deep. Many industrial accidents involve contact with presses or other hot, heavy objects, resulting in associated crush injuries as well. Automobile accidents may leave victims in contact with hot engine parts. The exhaust pipes of motorcycles cause a characteristic burn of the medial leg that is small but usually requires excision and grafting. Contact burns are often fourth-degree burns, especially those in unconscious or postictal patients and those caused by molten materials.
Electrical and Chemical Burns Electricity and chemicals, most commonly acids and alkalis, also cause coagulative necrosis of tissue. These are discussed more fully later.
The need for hospital admission and specialized care for burns and/or smoke inhalation is dictated by the severity of symptoms, the magnitude of associated burns, and the presence of associated injuries or medical problems. Otherwise healthy patients with no burns and only mild symptoms from smoke inhalation [only a few expiratory wheezes, minimal sputum production, carboxyhemoglobin (COHb) level < 10 percent, and normal blood gases] who have a place to go and someone to stay with them can be observed for an hour or two and then discharged. Any patient who is symptomatic with smoke inhalation and has more than trivial burns or preexisting cardiovascular or pulmonary disease should be admitted for observation. If the burns cover more than 15 percent TBSA, or if there are severe respiratory symptoms [air hunger, severe wheezing, copious (usually carbonaceous) sputum, COHb level > 10 percent], the patient should be referred immediately to a burn unit.
Burn Severity and Classification The severity of injury caused by burns is directly related to the size of the total burn, the depth of the burn, the age of the patient, and associated medical problems or injuries. Burns are classified as minor, moderate, and severe. Minor burns are superficial and involve less than 15 percent TBSA. Approximately 95 percent of all burns treated in the United States are minor, and they rarely require hospitalization, except for concomitant disease or high risk, pain control, or social reasons. The physician should have a low threshold for admission of elderly patients and infants. Any patient (child or adult) with suspicion of abuse must be admitted.
Moderate burns may be superficial and involve 1525 percent TBSA in adults or 1020 percent TBSA in children, or they may be full-thickness injuries involving less than 10 percent TBSA. These patients usually do require hospitalization at least briefly for stabilization and pain control. Newer techniques of wound care and closure have made burn care more complex, and an increasing number of patients with minor and moderate burns are being referred to specialized burn care facilities. Even if the total burn size is small, burns of the eyes, ears, face, hands, feet, or perineum require specialized care because of the cosmetic and functional risks associated with these injuries.
Burn Center Referral Criteria Patients with major burns should be referred to a specialized burn care facility or burn center. The currently accepted criteria defining major burns and identifying those patients who require triage to a burn center or referral after initial assessment and stabilization were promulgated by the American Burn Association (Table 7-1).
TABLE 7-1 BURN CENTER REFERRAL CRITERIA
Transport and Transfer Protocols Definitive care should begin at the initial hospital and continue without interruption during transport and at the burn center. Once a patent airway is ensured and resuscitation begun, burned patients are eminently suitable for transport. Resuscitation can continue en route because the patient usually will remain stable for some period of time. Transfer should be from physician to physician, and contact should be established as soon as the patient arrives in the emergency room of the initial hospital.
Before transport, special attention should be paid to airway and oxygenation. Supplemental oxygen can be given during transport, but if the patient's oxygenation is marginal or there is any question of upper airway edema, it may be best to intubate and ventilate the patient. Intubation is difficult en route, especially under urgent circumstances. Two large-bore intravenous lines are mandatory. Patients transported by air should have a nasogastric tube inserted and placed on dependent drainage. If there is danger of compromised circulation due to circumferential full-thickness burns, escharotomies (see below) should be considered at the referring hospital, especially if the total hospital-to-hospital time will be more than 2 h. Burned patients have difficulty maintaining body temperature, and they should be warmly wrapped prior to transport. Bulky dressings, a blanket, and a Mylar sheet (usually available from the flight team) can help maintain body temperature.
Airway Once flames are extinguished, initial attention must be directed to the airway. Immediate cardiopulmonary resuscitation is rarely necessary. Any patient rescued from a burning building or exposed to a smoky fire should be placed on 100% oxygen by tight-fitting mask because of the possibility of smoke inhalation. If the patient is unconscious, an endotracheal tube should be placed and attached to a source of 100% oxygen.
Other Injuries and Transport Once an airway is secured, the patient is assessed for other injuries and then transported to the nearest appropriate hospital per EMS protocol. If a burn center is within a 30-min drive and the burn is severe, the patient should be taken directly to that facility. If appropriately trained, the emergency medical technicians should place an intravenous line and begin fluid administration of crystalloid solution at a rate of approximately 1 L/h. For transport, the patient should be wrapped in a clean sheet and blanket. Sterility is not required. Before or during transport, constricting clothing and jewelry should be removed from burned parts because local swelling begins almost immediately and constricting objects will exacerbate the edema formation and possibly compromise distal circulation.
Cold Application Smaller burns, particularly scalds, are treated with immediate application of cool water. After several minutes have elapsed, further cooling does not alter the pathologic process. Iced water should never be used even on the smallest of burns. If ice is used on larger burns, systemic hypothermia may follow, and the associated cutaneous vasoconstriction can extend the thermal damage.
Initial Assessment Although a burn is a dramatic injury, following the ABCs of resuscitationairway, breathing, circulationand searching for other life-threatening injuries are the first priorities. Only after making an overall assessment of the patient's condition should attention be directed to the burns. The following sections address emergency department care of problems specifically encountered in the burn patient.
Assessment of Inhalation Injury The history is important. Inhalation injury should be suspected in anyone with a flame burn, especially if burned in an enclosed space. The rescuers are the most important historians and should be questioned before they leave the emergency facility. Hoarseness and expiratory wheezes are signs of potentially serious airway edema or smoke poisoning. The mouth and pharynx should be inspected for swelling, blisters, soot, or other signs of direct burn injury. Copious mucus production and carbonaceous sputum are sure signs of the inhalation of smoke and other products of combustion, but their absence does not rule out airway injury.
Arterial blood should be analyzed for blood gasses and carboxyhemoglobin (COHb) levels. A COHb level of greater than 10 percent or any symptoms of carbon monoxide poisoning are presumptive evidence of associated smoke inhalation. A decreased ratio of arterial PO2 to fraction of inspired oxygen (FIO2) is another early indicator of smoke inhalation. A ratio of less than 250 (e.g., PaO2 of 100 mmHg and an FIO2 of 0.4) is an indication for aggressive pulmonary support rather than for increasing the inspired oxygen concentration. Fiberoptic bronchoscopy is inexpensive, quickly performed in experienced hands, and useful for assessing and documenting edema of the hypopharynx, trachea, and major bronchi. It does not, however, materially influence the treatment of pulmonary injury.
Fluid Resuscitation Patients with burns of 20 percent or more TBSA typically develop burn shock. This is due in part to hypovolemia secondary to extravasation of fluid and protein. Thus fluid resuscitation should be instituted as soon as possible with lactated Ringer's solution at a rate of 1000 mL/h in adults and 20 mL/kg in children. Burn patients requiring intravenous resuscitation (those with burns over 20 percent TBSA) also should have a Foley catheter placed and urine output monitored hourly.
Patients with burns of less than 50 percent TBSA usually can be resuscitated with a single large-bore peripheral intravenous line. Because of the high incidence of septic thrombophlebitis, lower extremities should not be used as portals for intravenous lines. Upper extremities are preferable, even if the intravenous line must pass through burned skin. Patients with burns over 50 percent TBSA, those with associated medical problems, the very young or very old, or those who have concomitant smoke inhalation should be transferred as quickly as possible to an intensive care setting for cardiopulmonary monitoring and support.
Tetanus Burns are tetanus-prone wounds. The need for tetanus prophylaxis is determined by the patient's current immunization status. Previous immunization within 5 years requires no treatment, immunization within 10 years requires a tetanus toxoid booster, and unknown immunization status requires hyperimmune serum (Hyper-Tet).
Gastric Decompression Many burn centers begin tube feeding on admission. This protects the stomach from stress ulceration and may prevent the development of paralytic ileus, as well as providing nutrition. If the patient is to be transported, however, the safest course is usually to decompress the stomach with a nasogastric tube.
Pain Control During the shock phase of burn care, medications should be given intravenously. Subcutaneous and intramuscular injections are absorbed variably depending on perfusion and should be avoided. Pain control is best managed with small intravenous doses of morphine, usually 25 mg, given until pain control is adequate, without affecting blood pressure.
Psychosocial Care Psychosocial care should begin immediately. The patient and family must be comforted and given a realistic assessment regarding the prognosis of the burns. If the circumstances of a burn in a child are suspicious, physicians in all states are required by law to report the incident to local authorities as raising a concern about child abuse.
Care of the Burn Wound After all other assessments are complete, attention should be directed to the burn. If the patient is to be transferred during the first postburn day, which is almost always the case, the burn wounds do not require special dressings and can be left alone. However, the size of the burn should be calculated to establish the proper level of fluid resuscitation, and pulses distal to circumferential full-thickness burns should be monitored. The patient should be wrapped in a clean, dry sheet and kept warm until arriving at the definitive care center.
Coagulated, necrotic skin is called eschar. Unlike uninjured skin, it is rigid and unyielding. As fluid and protein extravasate into underlying tissues, the eschar cannot expand. Large, circumferential burns of the chest or extremities, therefore, can result in increased tissue pressure sufficient to interfere with breathing or limb perfusion. Incision of the eschar, escharotomy, may need to be performed early in a patient's course to restore normal function. Unless transport times are expected to be prolonged (>2 h), this procedure usually may be deferred until admission to the burn center.
Chest Escharotomy Early respiratory distress may be due to compromise of ventilatory function caused by a cuirass effect from a deep circumferential burn wound of the chest. Rapid, shallow breathing will develop, and if the patient is mechanically ventilated, peak inspiratory pressure and arterial PCO2 will rise. Inhalation injury, pneumothorax, or other causes also may result in respiratory distress.
When escharotomy is required in a patient with a circumferential chest wall burn, it is performed in the anterior axillary line bilaterally. If there is significant extension of the burn onto the adjacent abdominal wall, the escharotomy incisions should be extended to this area and should be connected by a transverse incision along the costal margin (Fig. 7-1).
FIGURE 7-1 Locations for escharotomy incisions. These incisions are placed along the midmedial and midlateral lines of the extremities. The skin is especially tight along major joints, and decompression at these sites must be complete. Chest and neck escharotomies are rarely necessary.
Escharotomy of Extremities Edema formation in the tissues under the tight, unyielding eschar of a circumferential burn of an extremity may produce significant vascular compromise that, if unrecognized and untreated, will lead to permanent, serious neurologic and vascular deficits. Skin color, sensation, capillary refill, and peripheral pulses must be assessed hourly in any extremity with a circumferential burn. The occurrence of any of the following signs or symptoms may indicate poor perfusion of the distal extremity: cyanosis, deep tissue pain, progressive paresthesia (loss of sensation), progressive decrease in or absence of pulse, or sensation of cold extremities. An ultrasonic flowmeter (Doppler) is a reliable means for assessing arterial blood flow. If the signal diminishes, this may indicate the need for escharotomy. Direct monitoring of intramuscular compartment pressure provides objective evidence for adequacy of deep circulation. While elevation and manipulation of the extremity may relieve minor deviations of pressure, escharotomy and, if ineffective, fasciotomy are necessary to decompress the tissues when pressures reach 30 mmHg or higher.
Both escharotomies and fasciotomies may be done as bedside procedures with a sterile field and scalpel. Local anesthesia is unnecessary because third-degree eschar is insensate. The incision should be placed along the midmedial or midlateral aspect of the extremity and should extend through the eschar down to the subcutaneous fat. The incision should be carried through the length of the constricting third-degree burn and across involved joints (see Fig. 7-1). When a single escharotomy incision in an extremity does not result in adequate distal perfusion, a second escharotomy incision on the contralateral aspect of the extremity should be performed. A finger escharotomy is seldom required.
Escharotomy and/or fasciotomy is rarely required within the first 6 h postburn. Because burn patients are at risk for developing a compartment syndrome up to 72 h postburn, any involved extremity should be reassessed continually for signs of dangerous elevation in compartment pressures that can occur even after initial decompression.
The severity of any burn injury is related to the size and depth of the burn and to the part of the body that has been burned. Burns are the only quantifiable form of trauma. Initial fluid resuscitation requirements, metabolic responses, nutritional requirements, need for specialized care, likelihood of complications, and mortality are all related to the size of the burn.
Burn Size A general idea of burn size can be made by using the Rule of Nines. Each upper extremity accounts for 9 percent of TBSA, each lower extremity accounts for 18 percent, the anterior and posterior trunk each account for 18 percent, the head and neck account for 9 percent, and the perineum accounts for 1 percent. Although the Rule of Nines is reasonably accurate for adults, a number of more precise charts have been developed. Most emergency rooms have a chart available comparable with the one shown in Figure 7-2. A diagram of the burn can be drawn on the chart, and a more precise estimation of burn size can be made.
FIGURE 7-2 Burn diagram for documenting extent and depth of burn. The most important concept for use of these diagrams is their provision for changing proportions of body surface area with increasing age. Clinical data for the burn diagrams are most accurately obtained immediately after initial burn debridement.
Even when using precise diagrams, individual observer variation may differ by as much as 20 percent. An observer's experience with burned patients rather than educational level appears to be the best predictor of accuracy of estimation. For small burns, an accurate assessment of burn size can be made by using the patient's hand. The palmar surface, including the fingers, accounts for 1 percent of the TBSA (see Fig. 7-2).
Burn Depth Along with burn extent and patient age, the depth of the burn is a determinant of mortality. It is also the primary determinant of the patient's long-term appearance and function. Burns not extending all the way through the dermis leave behind epithelium-lined skin appendages: sweat glands and hair follicles with attached sebaceous glands. When dead dermal tissue is removed, epithelial cells swarm from the surface of each appendage to meet swarming cells from neighboring appendages, forming a new, fragile epidermis on top of a thinned and scarred dermal bed. Skin appendages vary in depth, and the deeper the burn, the fewer the appendages that contribute to healing and the longer the burn takes to heal. The longer the burn takes to heal, the less dermis remains, the greater the inflammatory response, and the more severe the scarring.
Burns that heal within 3 weeks usually do so without hypertrophic scarring or functional impairment, although long-term pigmentary changes are common. Burns that take longer than 3 weeks to heal often produce unsightly hypertrophic scars, frequently lead to functional impairment, and provide only a thin, fragile epithelial cover for many weeks or months. Contemporary burn care, at least in patients with small to moderate-sized burns, involves early excision and grafting of all burns that will not heal within 3 weeks. Distinguishing between deep burns that are best treated by early excision and grafting and shallow burns that heal spontaneously is not always straightforward, however, and many burns have a mixture of clinical characteristics, making precise classification difficult.
Assessment of Burn Depth The standard technique for determining burn depth has been clinical observation of the wound. The difference in depth between a burn that heals in 3 weeks, a deep dermal burn that heals only after many weeks, and a full-thickness burn that will not heal at all may be only a matter of a few tenths of a millimeter. A burn appearing shallow on day 1 may appear considerably deeper by day 3. The kind of topical wound care used may dramatically change the appearance of the burn. Evaluation by an experienced surgeon as to whether an intermediate-depth dermal burn will heal in 3 weeks is about 50 percent accurate. Although there is considerable interest in technology that might be able to make an early, accurate assessment and prognosis of the wound, no technique to date has proven consistently superior to clinical assessment. In experienced hands, furthermore, early excision and grafting provide better results than nonoperative care for such indeterminate burns.
Burn shock is a complex process of circulatory and microcirculatory dysfunction not easily or fully repaired solely by fluid resuscitation. Hypovolemic shock and tissue trauma result in the formation and release of local and systemic mediators that produce an increase in vascular permeability and microvascular hydrostatic pressure. Most mediators act to increase permeability by altering venular membrane integrity. The early phase of burn edema, lasting from minutes to an hour, is attributed to mediators such as histamine, bradykinin, and vasoactive amines, products of platelet activation, the complement cascade, hormones, prostaglandins, and leukotrienes. Vasoactive amines also may act directly by increasing microvascular blood flow or vascular pressures, accentuating the burn edema.
The activation of the proteolytic cascades, including those of coagulation, fibrinolysis, the kinins, and the complement system, occurs immediately after burn injury. Kinins, specifically the bradykinins, increase vascular permeability. In addition to the loss of capillary integrity, thermal injury also causes changes at the cellular level. Baxter demonstrated a generalized decrease in cellular transmembrane potential involving uninjured and thermally injured cells. Platelet-activating factor is also released after burn injury and increases capillary permeability.
The reduction in cardiac output after burn injury is a result of hypovolemia; increased systemic vascular resistance due to sympathetic stimulation and the release of catecholamines, vasopressin, angiotensin II, and neuropeptide Y; and increasing viscosity. Decreased flow to the skin may result in ischemia of partially injured tissue, thus leading to additional coagulative necrosis and increasing the depth of burn. Decreased cardiac output may lead to cardiac depression with eventual cardiac failure in healthy patients or to myocardial infarction in patients with preexisting coronary artery disease. Reduced central nervous system (CNS) flow may manifest as restlessness followed by lethargy and finally by coma. If resuscitation is inadequate, burns of 30 percent or more TBSA frequently lead to acute renal failure, which almost invariably results in a fatal outcome. With successful resuscitation, however, cardiac output normalizes after 1824 h and then increases to supernormal levels during the wound-healing phase of burn management.
Hypermetabolism Resting energy expenditure (REE) increases after burn injury, usually in relation to burn size. It may be as much as 50100 percent above predictions based on standard tables for body size, age, and sex. Increased heat loss from the burn wound and increased beta-adrenergic stimulation are important factors. Radiant heat loss is increased from the burn wound secondary to high blood flow and loss of skin integrity.
Protein is broken down at an accelerated rate. The increased efflux of amino acids from muscle supports, in part, increased gluconeogenesis. In this process the amino acids lose their amino nitrogen as urea, making them unavailable for reincorporation into protein. Thus there is a progressive erosion of muscle mass, leading to weakness and debility. Plasma insulin levels that are usually normal are elevated in burn patients. Despite this, the basal rate of glucose production is elevated, reflecting hepatic insulin resistance. Fatty acids are released at a rate in excess of requirements of fatty acids and energy substrates. In burn patients, over 70 percent of released fatty acids are not oxidized but rather are reesterified into triglyceride, resulting in fat accumulation in the liver. This is unfortunate because use of fat for energy decreases dependence on proteolysis.
Major trauma, burns, and sepsis have in common a rapid net catabolism of body protein, as well as a redistribution of the nitrogen pool within the body. Muscle protein breakdown is accelerated while acute phase proteins are produced at an increased rate in the liver. Wound repair requires amino acid protein synthesis and increased immunologic activity and may require accelerated protein synthesis. Protein intake over 1 g/kg/day has been recommended for thermally injured patients. If renal function is normal, the recommended protein intake is as much as 2 g/kg/day.
Neuroendocrine-Mediator Response Catecholamines appear to be the major endocrine mediators of the hypermetabolic response in thermally injured patients. Pharmacologic blockade of beta receptors diminishes the intensity of postburn hypermetabolism. Thyroid hormone serum concentrations are not elevated in patients with large burns. Total thyronine (T3) and thyroxine (T4) concentrations are reduced, and reverse T3 concentrations are elevated, while cellular concentrations are likely normal. Concentrations of free T3 and T4 fall markedly in the presence of sepsis in burned patients. Burn injury abolishes the normal diurnal variation in glucocorticoid concentrations. These hormones have a permissive role in catecholamine stimulation, and they are responsible for insulin resistance and, in part, for increased proteolysis. Glucagon concentrations are related directly to metabolic rate and cortisol concentrations and may modulate resting metabolism through anti-insulin effects.
The immune status of the burn patient has a profound impact on outcome in terms of survival, death, and major morbidity. The greatest difficulty in attempting to decipher the body's response to injury is the complex interaction of the cytokine cascade, the arachidonic acid cascade, and the neuroendocrine axis.
Cytokine Cascade Cytokines were considered originally to be regulatory chemicals secreted by cells of the immune system. Growth factors were seen as originating from inflammatory and reparative tissue. The distinction between growth factors and peptides, hormones, and cytokines, however, is no longer so distinct. The role of individual cytokines and other mediatory in the response to injury is discussed in Chapter 1.
Cell-Mediated Immunity Cell-mediated immunity is impaired after burn injury, including documented delays in allograft rejection, impairment in mitogenic and antigenic responsiveness of lymphocytes, burn-size-related suppression of graft-versus-host activity, suppression of delayed cutaneous sensitivity tests, and diminution of peripheral lymphocyte and thoracic duct lymphocyte concentrations. There is agreement that the functional capacity of thymus-dependent lymphocytes (T cells) to perform their normal physiologic response is impaired. Whether this failure is the result of overuse or indirectly the result of downregulation by cytokine cascades and other products of the inflammatory reaction is unclear.
Macrophages Macrophage function is impaired after thermal injury. Macrophage products suppress mitogenic responsiveness in normal lymphocytes. Proinflammatory cytokines are produced by macrophages in short bursts, probably inhibited by a feedback loop with decreased receptor expression. Activation includes pulmonary macrophages and may provide the background for the development of the adult respiratory distress syndrome seen in burn patients.
Neutrophils Neutrophil dysfunction after thermal injury is manifested by a decreased Fc receptor expression, depressed intracellular killing capacity, and decreased leukocyte chemotaxis that is accompanied by a brief increase in neutrophil respiratory burst. In addition, expression of CD16 (FcR, Fc, IgG receptors) and CD11 (adhesion molecules) on neutrophils is impaired, and this reduction seems to be related directly to the appearance of bacteremia and pneumonia. Baseline granulocyte oxidative activity in burn neutrophils is increased. Induction of neutrophil activation probably requires several different stimulants.
Humoral Immunity After thermal injury, there is a marked diminution in total serum immunoglobulin G (IgG) concentration and all subclasses. These levels return to normal between 10 and 14 days postburn. Extremely low levels of IgG on admission are predictive of a poor prognosis. These changes have been ascribed to a combination of leakage through the burn wound, protein catabolism, and a relative diminution in synthesis of IgG. IgM and IgA levels appear to be relatively unaffected.
The classical and alternative complement pathways are depleted, but the alternative pathway is more profoundly altered. Complement inactivation by heat appears to ameliorate cell-mediated immunosuppression, suggesting that some of the impairment of the cell-mediated immunosuppression postburn may be due to a complement-associated mechanism. The production of granulocyte colony-stimulating factor (GCSF) and of granulocyte-macrophage colony-stimulating factor (GM-CSF) is also impaired.
Proper fluid management is critical to survival in major thermal injury. In the 1940s, hypovolemic shock or shock-induced renal failure was the leading cause of death after burn injury. A vigorous approach to fluid therapy has led to reduced mortality rates in the first 48 h postburn, but 50 percent of the deaths occur within the first 10 days after burn injury from a multitude of causes. One of the most significant causes is inadequate fluid resuscitation therapy. Fluid management after burn shock resuscitation is also important.
Pathophysiology of Burn Shock Burn shock is hypovolemic and cellular in nature and is characterized by specific hemodynamic changes including decreased cardiac output, extracellular fluid, and plasma volume and oliguria. As with other forms of shock, the primary goal is to restore and preserve tissue perfusion. In burn shock, resuscitation is complicated by obligatory burn edema, and the voluminous transvascular fluid shifts that result from a major burn are unique to thermal trauma.
Maximal edema formation occurs between 8 and 12 h postinjury in smaller burns and between 12 and 24 h postinjury in major thermal injuries. The rate of progression of tissue edema depends on the adequacy of resuscitation.
In burns greater than 30 percent TBSA there is a systemic decrease in cell transmembrane potential. This decrease results from an increase in intracellular sodium concentration secondary to a decrease in sodium ATPase activity, which is responsible for maintaining the intracellular-extracellular ionic gradient. Resuscitation only partially restores the membrane potential and intracellular sodium concentrations to normal levels, demonstrating that hypovolemia, with its attendant ischemia, is not totally responsible for the cellular swelling seen in burn shock. Membrane potential may not return to normal for many days postburn despite adequate resuscitation. If resuscitation is inadequate, cell membrane potential progressively decreases, resulting ultimately in cell death.
Moyer, Baxter, and Shires established the role of crystalloid solutions in burn resuscitation and delineated the fluid volume changes in the early postburn period. Burn edema sequesters enormous amounts of fluid, resulting in the hypovolemia of burn shock, and the edema fluid is isotonic with respect to plasma and contains protein in the same proportions as that found in blood. Thus major burns result in complete disruption of the normal capillary barrier with free exchange between plasma and extravascular extracellular compartments. Animal and later clinical studies demonstrated that the extracellular fluid (ECF) volume could be effectively restored to within 10 percent of normal within 24 h using only crystalloid. This became the basis for the Baxter (Parkland) formula (4 mL/kg of body weight per percentage TBSA burned over the first 24 h) (Table 7-2). The associated mortality rate was comparable with that obtained with a colloid-containing resuscitation formula.
TABLE 7-2 FORMULAS FOR ESTIMATING TOTAL RESUSCITATION FLUID NEEDS IN ADULTS IN THE FIRST 24 h
Moncrief and Pruitt characterized the hemodynamic alterations in burn shock with and without fluid resuscitation. Their efforts culminated in the Brooke formula modification, which specified 2 mL/kg per percentage TBSA burned in the first 24 h (see Table 7-2). Fluid needs were estimated initially according to the modified Brooke formula, but the actual volume for resuscitation was based on clinical response. In their study, resuscitation permitted an average decrease of about 20 percent in both ECF and plasma volume, but no further loss accrued in the first 24 h. In the second 24 h postburn, plasma volume restoration occurred with the administration of colloid. Cardiac output, initially low, rose over the first 18 h postburn despite plasma volume and blood volume deficits. Peripheral vascular resistance rose during the initial 24 h but decreased as cardiac output improved. When plasma volume and blood volume loss ceased, cardiac output rose to supranormal levels, where it remained until healing or grafting occurred.
Resuscitation from Burn Shock The primary goal of fluid resuscitation is to replace fluid sequestered as a result of thermal injury. The critical concept in untreated burn shock is that massive fluid shifts can occur even though total body water remains unchanged. What actually changes is the volume of each fluid compartment, with intracellular and interstitial volumes increasing at the expense of plasma volume and blood volume. The edema formed is augmented by the resuscitation process. The National Institutes of Health consensus summary on fluid resuscitation in 1978 was not in agreement with regard to a specific formula, but there was consensus on two major issues: general guidelines to be used during the resuscitation process and type of fluid. The volume infused should be the least amount of fluid necessary to maintain adequate organ perfusion and should be titrated continually to avoid under-or overresuscitation. Replacement of the extracellular salt lost into the burned tissue and into the cells is essential for successful resuscitation.
Crystalloid Resuscitation Crystalloid, in particular lactated Ringer's solution with a sodium concentration of 130 mEq/L, is the most popular resuscitation fluid. Proponents of the use of crystalloid solution argue that other solutions, specifically colloids, are no better, and certainly more expensive, than crystalloid for maintaining intravascular volume after thermal injury. Even large proteins leak from the capillary after thermal injury, negating any theoretical advantage from colloid. Capillaries in nonburned tissues may maintain relatively normal protein permeability characteristics. The quantity of crystalloid needed depends on the parameters used to monitor resuscitation. If a urinary output of 0.5 mL/kg of body weight per hour indicates adequate perfusion, approximately 3 mL/kg per percentage TBSA burned will be needed in the first 24 h. If 1 mL/kg/h is optimal, considerably more fluid will be needed, and more edema will result. In major burns, severe hypoproteinemia usually develops with crystalloid resuscitation regimens. The hypoproteinemia and interstitial protein depletion may result in more edema formation.
Hypertonic Saline The resuscitation of burn patients with salt solution containing 240300 mEq/L of sodium rather than lactated Ringer's solution (130 mEq/L) guided by urine output as the indicator of adequate resuscitation may result in less edema and smaller total fluid requirements at least in the first 24 h. A shift of intracellular water into the extracellular space occurs as the result of the hyperosmolar solution. Extracellular edema increases as intracellular fluid decreases, giving the external appearance of less edema. Several studies have reported that this intracellular water depletion does not appear to be deleterious, but the issue is controversial. Gunn and associates, in a prospective, randomized study of patients with 20 percent TBSA burns, evaluated hypertonic sodium lactate versus lactated Ringer's solution and were not able to demonstrate decreased fluid requirements, improved nutritional tolerance, or decreased body weight gain percentage. If a hypertonic solution is used, hypernatremia (Na > 160 mEq/L) should be avoided.
Colloid Resuscitation Plasma proteins generate the inward oncotic force that counteracts the outward capillary hydrostatic force. Without plasma proteins under normal conditions, plasma volume could not be maintained. Thus protein replacement was an important component of early formulas for burn management. Because of the marked alteration in capillary permeability with acute burn injury, however, it is not clear how much oncotic force plasma proteins exert during resuscitation from burn shock. Demling demonstrated that restoration and maintenance of plasma protein content have no effect on plasma volume until at least 8 h postburn. Since nonburned tissues appear to regain normal permeability shortly after injury and hypoproteinemia may accentuate the edema, administering protein between 8 and 24 h postburn may offer some advantage to patients.
Albumin solutions are clearly the most oncotically active colloid solutions. Fresh frozen plasma contains all the protein fractions that exert oncotic and nononcotic functions. The optimal amount of protein is controversial. Demling uses between 0.5 and 1 mL/kg/percentage TBSA burned of fresh frozen plasma during the first 24 h, beginning at 810 h postburn. He argues that older patients, patients with burns and concomitant inhalation injury, and patients with burns in excess of 50 percent TBSA develop less edema and better maintain hemodynamic stability if fresh frozen plasma is used during resuscitation. In the young pediatric burn patient with major burn injury, colloid replacement is frequently administered because serum protein concentration decreases so rapidly.
Dextran Dextran is a colloid consisting of glucose molecules that have been polymerized into chains to form high-molecular-weight polysaccharides. This compound is available commercially in a number of molecular sizes. Dextran 40 (average molecular weight of 40,000 and called low-molecular-weight dextran) improves microcirculatory flow by decreasing red blood cell aggregation. Demling reported that the net fluid requirements for maintaining vascular pressure at the baseline levels with dextran 40 are about half those noted with lactated Ringer's alone during the first 24 h postburn.
Pediatric Patients Resuscitation must be more precise for children than for adults with a similar burn. Children have a limited physiologic reserve, and they require proportionately more fluid for burn shock resuscitation than adults with similar thermal injury. On average, fluid requirements for children approximate 5.8 mL/kg/percentage TBSA burned. Children with relatively small burns of 1020 percent TBSA also commonly require intravenous resuscitation. The Cincinnati Shriners Burns Institute begins with the Parkland formula and adds the estimated maintenance fluid requirement to calculate the expected total volume for the first 24 h (Table 7-3):
TABLE 7-3 FORMULAS FOR ESTIMATING TOTAL RESUSCITATION FLUID NEEDS IN CHILDREN IN THE FIRST 24 h
Inhalation Injury Inhalation injury accompanying thermal trauma increases the magnitude of total body injury and requires increased volumes of fluid and sodium to achieve resuscitation. Patients with documented inhalation injury require, on average, 5.7 mL/kg/percentage TBSA burned as compared with 3.98 mL/kg/ percentage TBSA burned in patients without inhalation injury.
Choice of Fluids and Rate of Administration All the solutions reviewed are effective in restoring tissue perfusion. Most patients with burns under 40 percent TBSA with no pulmonary injury can be resuscitated with isotonic crystalloid fluid alone. In patients with massive burns, young pediatric patients, and patients with burns complicated by severe inhalation injury, a combination of fluids can be used to achieve the desired goal of tissue perfusion while minimizing edema. Such a regimen starts with modified hypertonic saline solution (180 mEq/L lactated Ringer's + 50 mEq/L NaHCO3). After correction of the metabolic acidosis, which usually requires 8 h, lactated Ringer's is given for a second 8 h. In the last 8 h, 5% albumin in lactated Ringer's solution completes the resuscitation.
None of the resuscitation formulas can be more than a general guideline for burn shock resuscitation. In all cases the fluids should be adjusted as frequently as necessary based on the patient's response. The volume of infused fluid should maintain a urine output of 3050 mL/h or 0.5 mL/kg/h in adults and 1 mL/kg/h in children. In children weighing more than 50 kg, the urine volume should not exceed 3050 mL/h. Heart rate and blood pressure are not indicative of fluid volume status in the burn patient. If fluid volume status and adequacy of cardiac output are uncertain, they should be measured directly via thermodilution pulmonary artery catheterization, but a low measured filling pressure with evidence of adequate perfusion is common. Placement of a Swan-Ganz catheter to monitor burn shock resuscitation should be reserved for burn patients with limited cardiac reserve, such as the elderly or patients with significant concomitant disease, or burn patients who require large volumes.
Resuscitation is considered successful when there is no further accumulation of edema fluid, usually between 18 and 30 h postburn, and the volume of infused fluid needed to maintain adequate urine output approximates the maintenance fluid volume, which is the patient's normal maintenance volume plus evaporative water loss.
Fluid Replacement Following Burn Shock Resuscitation Heat-injured microvessels may manifest increased vascular permeability for several days, but burn edema at 24 h postburn is near maximal, and the interstitial space often may be saturated with sodium. Additional fluid requirements depend on the type of fluid used during the initial resuscitation. If a hyperosmolar state has been produced, additional free water may be required to restore the extracellular space to an iso-osmolar state. If the serum oncotic pressure is low because of intravascular protein depletion, protein repletion frequently is needed. Protein requirement varies with the resuscitation used. The Brooke formula proposes 0.30.5 mL/kg/percentage TBSA burned of 5% albumin during the second 24 h. The Parkland formula replaces the plasma volume deficit, which varies from 2060 percent of the circulating plasma volume, with colloid.
The total daily maintenance fluid requirement in the burn patient must account for the increased amount of evaporative water loss from the wound. In adults, the total fluid volume is estimated from the following formula:
This fluid may be given intravenously or via enteral feeding. The solution infused intravenously should be 0.5 normal saline with potassium supplements. Because of the loss of intracellular potassium during burn shock, the potassium requirement in adults is about 120 mEq/day.
After the initial 2448-h postburn period of resuscitation, urinary output is an unreliable guide to sufficient hydration. Adult patients with major thermal injuries require a urine output of 15002000 mL/24 h; children require 34 mL/kg/h. Indices of the state of hydration including body weight change, serum sodium concentration, serum and urine urea and glucose concentrations, the intake and output record, and clinical examination should be monitored closely. Other electrolytes, calcium, magnesium, and phosphate also should be monitored regularly and maintained within normal limits. For very large burns and in the pediatric burn patient, continuous colloid replacement may be required to maintain colloid oncotic pressure. Maintaining serum albumin levels above 2.0 g/dL is desirable.
Of the nearly 50,000 fire victims admitted to hospitals each year, smoke or thermal damage to the respiratory tree may occur in as many as 30 percent. Carbon monoxide poisoning, thermal injury, and smoke poisoning are three distinctly separate aspects of clinical inhalation injury, and although symptoms and treatment are distinct, they may coexist and require concomitant treatment.
Carbon Monoxide Poisoning As many as 6070 percent of deaths from house fires can be attributed to carbon monoxide poisoning. Carbon monoxide (CO) is a colorless, odorless, tasteless gas that has a high affinity for iron-containing proteins. When inhaled and absorbed, carbon monoxide binds to hemoglobin, myoglobin, and other iron-containing proteins. CO interferes with oxygen delivery to tissues by at least four mechanisms. First, when bound to hemoglobin (COHb), it prevents reversible displacement of oxygen. Second, COHb shifts the oxygen-hemoglobin dissociation curve to the left, thereby decreasing oxygen unloading from normal hemoglobin at the tissue level. Third, CO inhibits the cytochrome oxidase a3 complex, resulting in less effective intracellular respiration. Fourth, CO may bind to cardiac and skeletal muscle, causing direct toxicity and interfering with function. In addition, CO affects the CNS in a poorly understood fashion, causing demyelination and associated neurologic symptoms. Although levels of carboxyhemoglobin can be measured easily, the degree of enzymatic and/or muscle impairment may not directly correlate with these values. COHb levels less than 10 percent usually do not cause symptoms, except in some patients with limited cardiac reserves.
Carbon monoxide is reversibly bound to the heme pigments and enzymes and, despite its intense affinity, readily dissociates according to the laws of mass action. The half-life of COHb, when breathing room air, is between 4 and 5 h. On 100% oxygen, the half-life is reduced to 4560 min. Patients burned in an enclosed space or having any suggestion of neurologic symptoms should be placed on 100% oxygen while awaiting measured carboxyhemoglobin levels.
Thermal Airway Injury The term pulmonary burn is a misnomer. True thermal damage to the lower respiratory tract and lung parenchyma is extremely rare, unless live steam or exploding gases are inhaled. Air has such poor heat-carrying capacity that most of the heat is dissipated in the nasopharynx and upper airway. Mucosal burns of the mouth, nasopharynx, and larynx result in edema formation and may lead to upper airway obstruction at any time during the first 24 h postburn. Patients with the greatest risk of upper airway obstruction are those injured in an explosion (gasoline vapor, propane, butane, or natural gas) with burns of the face and upper torso and those who have been unconscious in a fire. Any patient with burns of the face should have a careful visual inspection of the mouth and pharynx, and if these are abnormal, the larynx should be visualized immediately. Red or dry mucosa or small mucosal blisters raise the possibility of airway obstruction; in patients from a closed-space fire, significant smoke poisoning may be present. The presence of significant intraoral and pharyngeal burns is a clear indication for early endotracheal intubation, since progressive edema can make later intubation extremely hazardous, if not impossible. Mucosal burns are rarely full thickness and can be managed successfully with good oral hygiene. Once the patient is intubated, the tube should remain in place for 35 days, until the edema subsides.
Smoke Inhalation A vast number of toxic products are released during combustion (flaming) or pyrolysis (smoldering), depending on the type of fuel that is burned, whether burning occurs in a high-or low-oxygen environment, and the actual heat of combustion. Some 280 toxic products have been identified in wood smoke. Petrochemical science has produced a wealth of plastic materials in homes and automobiles that, when burned, produce nearly all these and many other products not yet characterized. Prominent by-products of incomplete combustion are oxides of sulfur, nitrogen, and many aldehydes.
Smoke inhalation can cause direct epithelial damage at all levels of the respiratory tract from the oropharynx to the alveolus. The anatomic level at which the damage occurs depends on the ventilatory pattern, the smoke constituents (e.g., particulate concentration, particulate size, and chemical components), and the anatomic distribution of particulate deposition. Although the chemical mechanisms of injury may be different with different toxic products, the overall end-organ response is reasonably well defined. There is an immediate loss of bronchial epithelial cilia and decreased alveolar surfactant. Microatelectasis, and sometimes macroatelectasis, results and is compounded by mucosal edema in small airways, with immediate development of atelectasis that is only slowly reversible by normal ventilation. The regional hypoventilation results in significant alveolar atelectasis, intrapulmonary shunt, and subsequent hypoxemia. Chemical irritation of the respiratory tract, particularly the upper and lower airways, causes an acute inflammatory response.
Wheezing and air hunger are common early symptoms of smoke inhalation. In a few hours, tracheal and bronchial epithelium begins to slough, and a hemorrhagic tracheobronchitis develops. The pulmonary parenchymal injury appears to be dose-dependent. In very severe cases, the hemorrhagic tracheobronchitis and small airway plugging result in severe ventilatory difficulty during the first 48 h, and patients succumb to a severe respiratory acidosis because of their inability to clear CO2. In moderately severe cases with associated extensive burns, interstitial edema becomes prominent, resulting in adult respiratory distress syndrome (ARDS), with difficulty in oxygenation.
Concomitant cutaneous burn injury aggravates pulmonary injury independent of smoke inhalation. Mediators such as thromboxane A2 released from burned tissue may induce a variety of changes in the lung, including pulmonary hypertension, reduced dynamic compliance, and increased lipid peroxidation. Oxidants generated as a consequence of neutrophil activation and increases in xanthine oxidase also contribute to lung injury. Decreased plasma oncotic pressure from the loss of plasma protein through increasingly permeable vessels in both burned and unburned tissue creates an abnormal oncotic pressure gradient in the lung that, when combined with pulmonary hypertension, results in transient hydrostatic pulmonary edema. These changes help explain the degree of comorbidity in cases of combined inhalation and burn injuries. Much of the variability in pulmonary response appears to be related more to the severity of the associated cutaneous burn than to the degree of smoke inhalation. Without associated cutaneous burns, the mortality from smoke inhalation is very low, the process rarely progresses to ARDS, and symptomatic treatment usually leads to complete resolution of symptoms in a few days. In the presence of burns, smoke poisoning approximately doubles the mortality from burns of any size. Pulmonary symptoms are usually present on admission, but they may be delayed for 1224 h. The earlier the onset, the more severe is the disease.
Diagnosis Anyone with a flame burn and anyone burned in an enclosed space should be assumed to have smoke poisoning until proved otherwise. The assessment of the patient should proceed as discussed above (Emergency Room Care). In obtaining a history, emphasis should be placed on data specific to the smoke exposure and to the type of therapy instituted prior to hospitalization. Signs of smoke inhalation should be sought in the examination of the head and neck: edema, stridor, or soot impaction suggesting smoke inhalation; wheezing or rhonchi suggesting injury to lower airways; and decreased level of consciousness due to hypoxemia, CO poisoning, or cyanide poisoning. Hoarseness and expiratory wheezes are signs of potentially serious airway edema or smoke poisoning. Copious mucus production and carbonaceous sputum are also signs of injury but are not always present. Elevated COHb levels or any symptoms of CO poisoning are presumptive evidence of associated smoke poisoning. An inappropriately low arterial PO2 indicates the need for vigorous respiratory support. Because of the limitations of fiberoptic bronchoscopy, it is recommended that the history, clinical examination, and laboratory studies be used to make the diagnosis of inhalation injury and that the use of fiberoptic bronchoscopy be reserved for exceptional cases (e.g., expansion of lobar atelectasis or removal of obstructing intrabronchial secretions).
Treatment Upper Airway In the presence of increasing laryngeal edema, nasotracheal or orotracheal intubation is indicated. A tracheostomy is never an emergency procedure and should not be used as the initial step in airway management in patients with burns to the face and neck. Oropharyngeal edema often subsides sufficiently by 72 h to permit extubation. Adult patients should be able to breathe around the tube with the cuff deflated before it is removed. This assessment is difficult in children due to their smaller anatomy, the use of uncuffed endotracheal tubes, the increased incidence of postextubation stridor, and the frequent need for reintubation. The incidence of postextubation stridor in burn victims is as high as 47 percent, compared with 4 percent in elective surgical patients. The treatment of postextubation stridor includes the administration of racemic epinephrine and helium-oxygen (Heliox) mixtures.
Lower Airway Tracheobronchitis, commonly seen in smoke and toxic gas inhalation victims, produces wheezing, coughing, and retained secretions. The ventilation-perfusion mismatch present in these patients can result in mild to moderate hypoxemia, depending on the degree of underlying lung disease. High-flow supplemental oxygen should be administered routinely to supplement oxygenation and to reduce carboxyhemoglobin in cases of carbon monoxide inhalation. Further treatment for smoke poisoning is supportive, with the goal of maintaining adequate ventilation and oxygenation until the lung heals itself. Mild cases of smoke poisoning are treated with highly humidified air, vigorous pulmonary toilet, and bronchodilators as needed. More severe cases may require mechanical ventilation. For patients requiring prolonged endotracheal intubation, tracheostomy should be performed between 3 and 30 days after intubation. Patients with anterior neck burns who require tracheostomy should undergo excision and grafting of the area 57 days prior to creation of the tracheostomy. This minimizes pulmonary and burn wound infectious complications associated with the tracheostomy.
Prophylactic antibiotics are not valuable in burn-related chemical pneumonitis, and subsequent burn management and treatment of eventual bacterial pneumonia can be made more difficult if the early use of antibiotics leads to the selection of resistant organisms. Although steroids are commonly used in patients with severe asthma for their spasmolytic and anti-inflammatory action, there has been no study to date demonstrating a net benefit in smoke inhalation. One prospective study, in fact, demonstrated that mortality and infectious complications were higher in patients treated with steroids.
The burn wound is typically treated with once- or twice-daily washing, removal of loose, dead tissue, and topical application of an antimicrobial agent. Three preparations have demonstrated effectiveness in controlling bacterial proliferation on the burn wound: mafenide acetate, silver sulfadiazine, and silver nitrate. All are equally effective in controlling burn wound infection if applied before heavy colonization is established. Mafenide acetate is the only agent able to penetrate eschar and suppress dense bacterial proliferation. It is especially effective against clostridia. The main disadvantage of mafenide acetate is its strong carbonic anhydrase inhibition, which results in bicarbonate wasting, retained chloride, and metabolic acidosis.
Excision and Grafting For many years no attempt was made to cover burns with skin grafts until the eschar had sloughed and granulation tissue was well developed, a process that could take up to 8 weeks. Several technical advances, including safer blood, better monitoring equipment and methods, and a better understanding of the altered physiology and increased metabolic demands of burn patients, have made it possible to stabilize the patient within a few days of the injury. Now, rather than waiting for spontaneous separation, the eschar is removed surgically and the wound is closed before invasive infection occurs. An aggressive surgical approach to large and small burns has produced a number of advantages. Early wound closure shortens hospital stay and duration of illness. Although studies at first did not demonstrate dramatic differences in cosmetic and functional results, as surgeons have become more experienced, both improved function and appearance have resulted. This is particularly true with burns of the face, hands, and feet.
More burn centers are practicing early excision and grafting, and thus it is becoming the treatment of choice for all deep dermal and full-thickness burns. The procedure is still limited by difficulty in diagnosing burn depth, by limited donor sites, and by the difficulties involved in excision of three-dimensional areas, such as the perineum, ears, and nose. Evidence supports the following conclusions:
Technical Considerations Excisional procedures should be performed as early as possible after the patient is stabilized. This allows the wound to be closed before infection occurs and, in extensive burns, allows donor sites to be recropped as soon as possible. Cosmetic results are better if the wound can be excised and grafted before the intense inflammatory response associated with burns becomes well established. Any burn projected to take longer than 3 weeks to heal is a candidate for excision within the first postburn week. Wound excision is adaptable to all age groups, but infants, small children, and elderly patients require close perioperative monitoring.
Wound Excision Excision can be performed to include the burn and subcutaneous fat to the level of the investing fascia (fascial excision) or by sequentially removing thin slices of burned tissue until a viable bed remains (sequential excision). Fascial excision ensures a viable bed for grafting but takes longer, sacrifices potentially viable fat and lymphatics, and leaves a permanent cosmetic defect. Sequential (or tangential) excision can create massive blood loss and risks grafting on a bed of uncertain viability. It sacrifices minimal living tissue, however, and leads to a far superior cosmetic result than fascial excision. Current practice reserves fascial excision for patients with fourth-degree burns and patients with such massive burns that they can afford no graft loss.
Donor Sites For years donor sites have been treated superficially. They are covered with either dry, fine-mesh gauze or gauze impregnated with a dye or other antimicrobial agent. Over the next 23 weeks, they desiccate. The gauze usually separates from the wound spontaneously, but it can remove substantial areas of new epithelium. Now, with aggressive programs of early excision and grafting, donor sites are a priority. Early wound closure may spare the patient the painful daily debridement of the burn, but with burn pain diminished, patients now concentrate on donor-site pain.
There are hundreds of dressings available for donor-site and after-grafting wound care. Unfortunately, there appears to be no optimal donor dressing. All dressingsincluding the traditional gauze dressingsseem to work, and differences in healing times are only 12 days. Comfort levels and ease of care are the most significant factors in choosing a dressing.
Healed donor sites are not free of complications. In addition to hypertrophic scarring and changed pigmentation, patients may be troubled by blistering for several weeks. Blisters are self-limiting and are usually treated with bandages or ointments until they reepithelialize. Infections occur in about 5 percent of patients. Infection is treated with systemic antibiotics and continuously moist dressings or silver sulfadiazine.
Skin Substitutes The next major step in burn care is likely to be an artificial skin that will be readily available, perform barrier function (epidermis), and provide the structural durability and flexibility of the dermis. It must be permanent, affordable, not susceptible to hypertrophic scarring, provide normal pigmentation, and grow with developing children. Progress toward this goal has been substantial over the past decade. Cultured epidermal autograft (CEA) consists of a thin sheet of keratinocytes grown from a biopsy of a patient's unburned skin. It can only provide a barrier function, so at best it may be a temporary measure that might permit survival in a patient with massive burns. More promising is a dermal substitute consisting of collagen that is covered with a thin epidermal graft at the time of placement on the wound. It provides a matrix for the ingrowth of native fibroblasts, epidermal cells, and macrophages, resulting in a pseudodermis. At least two products are available commercially.
The hypermetabolic responses in patients with burns can be among the most intense in clinical medicine. All burn patients have increased resting energy expenditure and accelerated rates of protein (primarily skeletal muscle) breakdown that are related to the severity of the injury, i.e., to the size of the burn. The goals of nutrition support are to provide sufficient calories to match energy expenditure and protein to minimize the draft on muscle protein. Patients with burns involving 50 percent TBSA or more may require 1½ to 2 times their normal (preburn) caloric needs, with 25 percent of those calories provided as protein. For a more complete discussion of nutritional support assessment and techniques, see Chapter 1 and Chapter 2.
Enteral nutrition is much the preferred modality. Patients with small burns (<20 percent TBSA) often can meet their nutritional needs with a high-protein, high-calorie diet, provided that they can feed themselves and that they have effective pain control. Those with larger burns, those unable or unwilling to eat, or those with preexisting malnutrition often require exogenous nutritional support. This is best provided via small-bore nasal feeding tubes passed into the duodenum or jejunum, since small bowel motility is usually preserved, even in large burns. In many burn centers, enteral nutrition is begun during resuscitation. If the airway is protected, this often may be done through the nasogastric tube and the feeding tube placed later. The techniques, benefits, and difficulties of enteral nutrition are discussed elsewhere. Intravenous nutrition is provided only when the patient's needs cannot be met via the enteral route.
Energy expenditure can be minimized by blunting stressful stimuli. Because of the apparent change in the hypothalamic set point of thermal neutrality, burn patients require higher ambient temperatures for comfort. In an ambient environment that is comfortable for uninjured patients, the burn patient feels cold, and this will increase the energy expenditure to generate heat. The temperature of comfort is approximately 30.5°C (87°F), 5 degrees higher than that of normal subjects. Keeping burn patients warm decreases their metabolic rate and corresponding energy requirements, even if they have fever. Thermal blankets, radiation reflectors, and heat lamps may be required to maintain the patient's comfort. Pain and anxiety that accompany wound manipulation and other patient care procedures accentuate metabolic expenditure. Administration of narcotics or other analgesics and sedatives reduces the metabolic rate.
Human growth hormone increases nitrogen retention when administered with adequate calories and nitrogen. In patients with large burns, it has improved survival and reduced hospital stay by accelerating the rate of donor-site healing, reducing the time between sequential skin-grafting operations. Other anabolic agents (e.g., oxandrolone) also may be of benefit. Lack of activity also promotes muscle wasting and atrophy. Vigorous physical therapy promotes preservation of muscle bulk and must be provided on a daily basis to all patients requiring prolonged hospitalization. Patients in skeletal traction or air-fluidized beds are relatively immobile and lose lean body mass as a result. Simple isometric exercises, however, usually can be done and will reduce the rate of disuse atrophy. Wound care and expeditious wound closure are the most effective measures for limiting the injury and its metabolic sequelae.
Considerable morbidity and mortality in burned patients are related to infection. Thermal injury causes severe immunosuppression that is directly related to the size of the burn.
Wound Infection All burn wounds become contaminated soon after injury with the patient's endogenous flora or with resident organisms in the treatment facilities. Microbial species colonize the surface of the wound and may penetrate the avascular eschar. This event is without clinical significance. Bacterial proliferation may occur beneath the eschar at the viable tissuenonviable tissue interface, leading to subeschar separation. In a few patients, microorganisms may breach this barrier and invade the underlying viable tissue, producing systemic sepsis. Burn wound infection can be focal, multifocal, or generalized. The likelihood of septicemia increases in proportion to the size of the burn wound. With the use of currently available topical antimicrobial agents and an early and aggressive surgical approach to the burn wound, burn wound sepsis is much less common.
Pneumonia With improved resuscitation and modern patient support techniques, severely burned patients are surviving longer in critical care units, and the respiratory tract has become the most common locus of infection. A diagnosis of pneumonia is confirmed by the presence of characteristic chest radiograph patterns and the presence of offending organisms and inflammatory cells in the sputum. After inhalation injury, early infiltrates usually represent chemical pneumonitis and not infectious pneumonia, but the damaged lung tissue commonly becomes infected. Prophylaxis with antibiotics should not be used, however, because it does not reduce the incidence of pneumonia and selects resistant organisms. Colonization of the upper airway of patients requiring intubation and mechanical ventilation should not be confused with a respiratory tract infection. For the diagnosis of bronchopneumonia, analysis of sputum samples may be adequate. If there is concern about the identity of the organism, bronchoscopy should be used.
Suppurative Thrombophlebitis Suppurative thrombophlebitis occurs in up to 5 percent of patients with major burns. It is associated with the use of intravenous catheters, especially if the catheters have been inserted by cut-down techniques. The incidence increases with the duration of vein cannulation. This complication can be reduced or eliminated by the placement of catheters in high-flow veins, such as the femoral, subclavian, or internal jugular veins, and by changing insertion sites every 4872 h.
Electrical burns are thermal burns from very high intensity heat and from electrical disruption of cell membranes. As electric current meets the resistance of body tissues, it is converted to heat in direct proportion to the amperage of the current and the electrical resistance of the body parts through which it passes. The smaller the size of the body part, the more intense is the heat and the less the heat is dissipated. Fingers, hands, forearms, feet, and lower legs are frequently totally destroyed. Areas of larger volume, like the trunk, usually dissipate enough current to prevent extensive damage to viscera unless the entrance or exit wound is directly on the abdomen or chest. High-voltage (>1000 V) injuries are often deep and destructive. While cutaneous manifestations of electrical burns may appear limited, massive underlying tissue destruction may be present.
Disruption of muscle cells releases cell fragments and myoglobin into the circulation to be filtered by the kidney. Myoglobinuria is evident by the ruddy or brown color of the urine. If this condition is untreated, the pigments may precipitate in the renal tubules and lead to permanent kidney failure. Cardiac damage, such as myocardial contusion or infarction, may be present, or the conduction system may be deranged. Even with injuries resulting from high-voltage currents, however, normal cardiac function on admission generally means that subsequent cardiac dysrhythmia is unlikely.
The nervous system is particularly sensitive to electricity. The most severe brain damage occurs when current passes through the head, but spinal cord damage is possible whenever current has passed from one side of the body to the other. Myelin-producing cells are susceptible, and delayed transverse myelitis can occur days or weeks after injury. Conduction remains normal through existing myelin, but as the old myelin wears out, it is not replaced, and conduction stops. Damage to peripheral nerves is common and may cause permanent functional impairment.
Acute Care Resuscitation needs are usually far in excess of what would be expected on the basis of the cutaneous burn size, and associated flame and/or flash burns often compound the problem. The infusion rate of resuscitation fluid should be adjusted based on the patient's response. If myoglobinuria is present, the infusion rate should be increased to promote a urine flow twice that of the usual target, i.e., 60100 mL/h in adults, in an attempt to flush the pigments through the kidney. If the urine does not appear to become less pigmented, mannitol may be administered, and bicarbonate should be administered to try to alkalinize the urine. This increases the solubility of the pigments.
Every patient with an electrical injury must have a thorough neurologic examination as part of the initial assessment. Persistent neurologic symptoms may lead to chronic pain syndromes, and so-called posttraumatic stress disorders are much more frequent after electrical burns than after thermal burns. Cataracts are a well-recognized complication of electrical contact burns. They occur in 57 percent of patients followed, they are frequently bilateral, and they can occur even in the absence of contact points on the head. They often occur within a year or two of injury. Electrically burned patients should undergo a thorough ophthalmologic examination during the admissions phase of acute care.
Wound Management There are two situations in which early surgical treatment is indicated for patients with electrical burns. Massive deep tissue necrosis may lead to acidosis or myoglobinuria that does not improve with standard resuscitation techniques. In this case, major debridement and/or amputation may be necessary on an emergency basis. More commonly, the deep tissues swell, and a compartment syndrome develops. Careful monitoring, including measurement of compartment pressures, is mandatory, and escharotomies and fasciotomies should be performed at the slightest suggestion of progression.
Chemical burns are most commonly caused by strong acids or alkalis. In contrast to thermal burns, chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue or diluted by flushing with water. Individual circumstances vary, but acid burns may be more self-limiting than alkali burns because alkalis combine with cutaneous lipids to create soap and thereby continue dissolving the skin until they are neutralized. Chemical burns should be considered deep dermal or full-thickness burns until proved otherwise. A full-thickness chemical burn may appear deceptively superficial at first, causing only a mild brownish discoloration of the skin. The skin may appear to remain intact during the first few days postburn and only then begin to slough spontaneously.
Acute Care Any involved clothing should be removed immediately, and the burns should be flushed thoroughly with copious amounts of water, beginning at the scene of the accident. Chemicals will continue to burn until removed, and washing for at least 15 min under a running stream of water may limit the overall severity of the burn. No thought should be given to searching for a specific neutralizing agent. Delay deepens the burns, and neutralizing agents may cause burns themselves, since they frequently generate heat while neutralizing the offending agent. Powdered chemicals should be brushed off skin and clothing. Unless the characteristics of the chemical are well known, the treating physician is advised to call the local poison control bureau for specifics in treatment, in case there is a possibility of toxicity.
Inpatient Therapy Maintaining function and preventing the complications of prolonged immobility are the specific goals of the rehabilitative treatment of burn patients. Daily assessment of the patient's range of motion, ambulation, and functional status is necessary to determine the effectiveness of ongoing treatment plans and to make modifications as needed. In most burns of extremities, the position of maximal comfort promotes the formation of scar contractures. Compliance is a major factor in a successful rehabilitation program, so the burn therapist and the entire burn team must gain the patient's trust, understanding, and confidence. Burn teams should include physical and occupational therapists and a play therapist who can engage children in physical activities.
Occupational and physical therapy begin on the day of admission. Burned extremities are elevated and actively exercised to minimize edema and reduce the need for escharotomy. Stable patients are initially placed in chairs. Ambulation begins when it can be tolerated. Excessive use of analgesics and antianxiety drugs impedes a successful mobilization program. Active exercises maintain muscle mass and strength. Passive exercises are used most often in debilitated patients and patients whose state of awareness is clouded. Passive exercises must be planned carefully, because overzealous activity may lead to tendon disruption, muscle tears, heterotopic ossification, and traumatic release of scar contractures.
All second- and third-degree burns produce permanent scarring. Some scars in healed second-degree burns are barely noticeable, whereas deeper burns, even when grafted, may develop bulky hypertrophic scar tissue. Scar hypertrophy can be retarded by pressure applied to the developing scar. In the burn center, pressure is usually applied with elastic bandages or a generic tubular elastic stocking.
Outpatient Therapy Many functional deficits persist after burn patients have been discharged. Outpatient therapy and long-term follow-up should be continuous. For many patients, the burn center outpatient facility provides their only access to primary care. Some patients may require complex physical training devices and special attention to retain or restore range of motion, strength, and stamina. After the surface of the burn scar stabilizes, the patients may be fitted for custom-made compression garments. These require regular refitting. Adults may wear these garments for 6 months or more, whereas small children may require up to 4 years of compression therapy before scar maturation is complete. Patients may develop follicular infection in the burn wound several months after injury. These plugged follicles usually disappear once hair erupts through the overlying epithelium. Severe itching and vague but intense neuritic pain are long-lasting and are poorly responsive to antipruritic medications and analgesics.
Psychosocial Support Burned patients display a variety of psychological responses to their injury, including anxiety, depression, denial, withdrawal, and regression. Withdrawal and regression are especially common in children, who may refuse to participate in treatment regimens. Nearly half of older children and adults develop posttraumatic stress disorder after thermal injury, which is characterized by recurrent and intrusive recollections of the initial injury, avoidance of circumstances that invoke memories of the event, loss of interest in daily activities, feelings of isolation, hyperalertness, memory impairment, and sleep disturbances. Noncompliance with burn therapy is a serious outward manifestation of a patient's attempt to avoid recollections of the traumatic event. Even though burn patients rarely seek treatment for psychological problems, psychosocial support is critical for optimal recovery and should be provided for the duration of the course of treatment and follow-up. Initially this is provided by the burn team and the patient's family. Later, patients should have the opportunity to participate in a burn support group composed of other burn survivors. Even long after their physical wounds have healed, these courageous patients continue to help and support each other and new burn victims and their families. They have learned that burn injuries are never completely cured or forgotten.
For a more detailed discussion, see Warden GD, Heimbach DM: Burns, chap.7 in Principles of Surgery, 7th ed.
Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook