Chapter 14: Burns & Other Thermal Injuries

A severe thermal injury is one of the most devastating physical and psychological injuries a person can suffer. Over 2 million injuries due to burns require medical attention each year in the United States, with 14,000 deaths resulting. Fires in the home are responsible for only 5% of burn injuries but for 50% of burn deaths—most due to smoke inhalation. About 75,000 patients require hospitalization every year, and 25,000 of those remain hospitalized for over 2 months—evidence of the severity of illness associated with this injury.

ANATOMY & PHYSIOLOGY OF THE SKIN

The skin is the largest organ of the body, ranging in area from 0.25 m² in the newborn to 1.8 m² in the adult. It consists of two layers: the epidermis and the dermis (corium). The outermost cells of the epidermis are dead cornified cells that act as a tough protective barrier against the environment, including bacterial invasion and chemical exposure. The inner cells of the epidermis are metabolically active, producing compounds like growth factor, which help the ongoing replication process every 2 weeks. The second, thicker layer, the dermis (0.06-0.12 mm), is composed chiefly of fibrous connective tissue. The dermis contains the blood vessels and nerves to the skin and the epithelial appendages of specialized function like sweat glands. The nerve endings that mediate pain are found in the dermis.

The dermis is a barrier that prevents loss of body fluids by evaporation and loss of excess body heat. Sweat glands help maintain body temperature by controlling the amount of water that evaporates. The dermis is also interlaced with sensory nerve endings that mediate the sensations of touch, pressure, pain, heat, and cold. This is a protective mechanism that allows an individual to adapt to changes in the physical environment.

The skin produces vitamin D, which is synthesized by the action of sunlight on certain intradermal cholesterol compounds.

DEPTH OF BURNS

The depth of the burn (Figure 14–1) significantly affects all subsequent clinical events. The depth may be difficult to determine and in some cases is not known until after spontaneous healing has occurred or when the eschar is surgically removed or separates, exposing the wound bed.

Traditionally, burns have been classified as first-, second-, and third-degree, but the current emphasis on burn healing has led to classification as partial-thickness burns, which can heal spontaneously, and full-thickness burns, which require skin grafting, although deep partial-thickness burns are usually excised and grafted as well.

A first-degree burn involves only the epidermis and is characterized by erythema and minor microscopic changes; tissue damage is minimal, protective functions of the skin are intact, skin edema is minimal, and systemic effects are rare. Pain, the chief symptom, usually resolves in 48-72 hours, and healing takes place uneventfully. In 5-10 days, the damaged epithelium peels off in small scales, leaving no residual scarring. The most common causes of first-degree burns are overexposure to sunlight and brief scalding.

Second-degree or partial-thickness burns are deeper, involving all of the epidermis and some of the corium or dermis. The systemic severity of the burn and the quality of subsequent healing are directly related to the amount of undamaged dermis. Superficial burns are often characterized by blister formation, while deeper partial-thickness burns have a reddish appearance or a layer of whitish, nonviable dermis firmly adherent to the remaining viable tissue. Blisters, when present, continue to increase in size in the postburn period as the osmotically active particles in the blister fluid attract water. Complications from superficial second-degree burns are mainly severe pain related. These burns usually heal with minimal scarring in 10-14 days unless they become infected.

Deep dermal burns heal over a period of 4-8 weeks with only a fragile epithelial covering developing that arises from the residual uninjured epithelium of the deep dermal sweat glands and hair follicles. Severe hypertrophic scarring occurs when such an injury heals; the resulting epithelial covering is prone to blistering and breakdown. Evaporative losses after healing remain high compared with losses in normal skin. Conversion of a partial thickness injury to a full-thickness burn by the actions of wound bacteria is common. Skin grafting of deep dermal burns, when feasible, improves the biologic quality and appearance of the skin cover.

Full-thickness (third-degree) burns have a characteristic white, dry, waxy appearance and may appear to the untrained eye as unburned skin. Burns caused by prolonged exposure to heat, with involvement of fat and underlying tissue, may be brown, dark red, or black. The diagnostic findings of full-thickness burns are lack of sensation in the burned skin, lack of capillary refill, and a leathery texture that is unlike normal skin. All dermal epithelial elements are destroyed, leaving no potential for reepithelialization.

DETERMINATION OF SEVERITY OF INJURY

Illness and death are related to the size (surface area) and depth of the burn, the age and prior state of health of the victim, the location of the burn wound, and the severity of associated injuries, particularly lung injuries caused by smoke inhalation.

The total body surface area involved in the burn is most accurately determined by using the age-related charts designed by Lund and Browder (Figure 14–2). A set of these charts should be filled out for every burn patient on admission and when resuscitation is begun.

A careful calculation of the percentage of total body burn is useful for several reasons. First, there is a general clinical tendency to both underestimate and overestimate the size of the burn and thus its severity. The American Burn Association has adopted a severity index for burn injury (Table 14–1). Second, prognosis is directly related to the extent of injury both size and depth. Third, the decision about who should be treated in a specialized burn facility or managed as an outpatient is based on the estimate of burn size and depth.

Patients under age 2 years and over age 60 years have a significantly higher death rate for any given extent of burn. The higher death rate in infants results from a number of factors. First, the body surface area in children relative to body weight is much greater than in adults. Therefore, a burn of comparable surface area has a greater physiologic impact on a child. Second, immature kidneys and liver do not allow for removal of a high solute load from injured tissue or the rapid restoration of adequate nutritional support. Third, the incompletely developed immune system increases susceptibility to infection. Associated conditions such as cardiac disease, diabetes, or chronic obstructive pulmonary disease significantly worsen the prognosis in elderly patients.

Burns involving the hands, face, feet, or perineum are at risk for severe complications if not properly treated. Patients with such burns should always be admitted to the hospital, preferably to a burn center. Chemical and electrical burns or those involving the respiratory tract are invariably far more extensive than is evident on initial inspection. Therefore, hospital admission is also necessary in these cases.

PATHOLOGY & PATHOPHYSIOLOGY OF THERMAL INJURIES

The microscopic pathologic feature of the burn wound is principally surface coagulation necrosis. Burned tissue has three distinct zones. The first is the zone of “coagulation,” or necrosis with irreversible cell death and no capillary blood flow. Surrounding this is a zone of injury or stasis, characterized by sluggish capillary blood flow and injured cells. Although damaged, the tissue is still viable. Further tissue injury can be caused by products of inflammation such as oxidants and vasoconstrictor mediators. Environmental insults such as hypoperfusion, desiccation, or infection can also cause the injured tissue to become necrotic. This process is called wound conversion. The third zone is that of “hyperemia,” which is the usual inflammatory response of healthy tissue to nonlethal injury. Vasodilatation and increased capillary permeability is typically present.

A rapid loss of intravascular fluid and protein occurs through the heat-injured capillaries. The volume loss is greatest in the first 6-8 hours, with capillary integrity returning toward normal by 36-48 hours. A transient increase in vascular permeability also occurs in nonburned tissues, probably as a result of the initial release of vasoactive mediators. However, the edema that develops in nonburned tissues during resuscitation appears to be due in large part to the marked hypoproteinemia caused by protein loss into the burn itself. A systemic inflammatory response occurs in response to a large body burn, resulting in the release of oxidants and other inflammatory mediators into unburned tissues. A generalized decrease in cell energy and membrane potential occurs as a result. This leads to a shift of extracellular sodium and water into the intracellular space. This process is also corrected as hemodynamic stability is restored but will return if the systemic inflammation is amplified. Smoke inhalation markedly increases the hemodynamic instability, fluid requirements, and mortality rates by adding another source of intense inflammation leading to local lung and systemic tissue damage.

METABOLIC RESPONSE TO BURNS & METABOLIC SUPPORT

The initial metabolic response appears to be activated by proinflammatory cytokines and in turn oxidants. The secretion of catecholamines, cortisol, glucagon, renin-angiotensin, antidiuretic hormone, and aldosterone is also increased. Early in the response, energy is supplied by the breakdown of stored glycogen and by the process of anaerobic glycolysis.

Profound hypermetabolism and catabolism occur in the postburn period, characterized by an increase in metabolic rate that approaches doubling of the basal rate in severe burns and a rapid loss of the components of lean body mass with muscle loss exceeding a pound a day. The degree of response is proportionate to the degree of injury, with a plateau occurring when the burn involves about 70% of the total body surface. The initiating and perpetuating factors are the mediators of inflammation, especially the cytokines and endotoxin. Added environmental stresses such as pain, cooling, and sepsis syndrome increase the obligatory hypermetabolism and catabolism.

During the first postburn week, the metabolic rate (or heat production) and oxygen consumption rise progressively from the normal level present during resuscitation and remain elevated until the wound is covered and no other sources of inflammation remain. The specific pathophysiologic mechanism remains undefined, but increased and persistent catecholamine and cortisol secretion are major factors, as is increased circulating endotoxin absorbed from wound or gut and proinflammatory cytokines.

The evaporative water loss from the wound may reach 300 mL/m²/h (normal is about 15 mL/m²/h). This produces a heat loss of about 580 kcal/L of water evaporated. Covering the burn with an impermeable membrane, such as skin substitute, reduces the heat loss. Similarly, placing the burn patient in a warm environment, where convection and radiant loss of heat are minimized, also modestly reduces the heat loss and the metabolic rate. The persistently elevated circulating levels of catecholamines and cortisol stimulate an exaggerated degree of gluconeogenesis and protein breakdown. Protein catabolism, glucose intolerance, and marked total body weight loss result.

Aggressive nutritional support along with rapid wound closure and control of pain, stress, and sepsis will help control the hypermetabolic catabolic state. Controlled use of a beta-blocker has been shown to decrease catabolism. In addition, insulin, growth hormones, and testosterone analogues have been shown to both decrease catabolism and increase anabolism.

IMMUNOLOGIC FACTORS IN BURNS

A number of immunologic abnormalities in burn patients predispose to infection. Serum IgA, IgM, and IgG are frequently depressed, reflecting depressed B-cell function. Cell-mediated immunity or T-cell function is also impaired, as demonstrated by prolonged survival of homografts and xenografts.

Polymorphonuclear (PMN) chemotactic activity is suppressed. A decrease in chemotaxis predates evidence of clinical sepsis by several days. Decreased oxygen consumption and impaired bacterial killing have also been demonstrated in PMNs. Depressed killing is probably due to decreased production of hydrogen peroxide and superoxide; this has been demonstrated by decreased PMN chemiluminescent activity in burn patients.

ACUTE RESUSCITATION

The burn patient should be assessed and treated like any patient with major trauma. The first priority is to ensure an adequate airway. If there is a possibility that smoke inhalation has occurred—as suggested by exposure to a fire in an enclosed space or burns of the face, nares, or upper torso—arterial blood gases and arterial oxygen saturation of hemoglobin and carboxyhemoglobin CoHgb levels should be measured, and 100% oxygen should be administered. If CoHgb is elevated, 100% oxygen should be administered until levels return to normal.

Endotracheal intubation is indicated if the patient is semicomatose, has deep burns to the face and neck, or is otherwise critically injured. Intubation should be done early in all doubtful cases, because delayed intubation will be difficult to achieve in cases associated with facial and pharyngeal edema or upper airway injury, and an emergency tracheostomy may become necessary later under difficult circumstances. Respiratory support is necessary for severe smoke damage to the lower airways. If the burn exceeds 20% of body surface area, a urinary catheter should be inserted to monitor urine output. A large-bore intravenous catheter should be inserted, preferably into a large peripheral vein. There is a significant complication rate with the use of central lines in burn patients owing to the increased risk of infection.

Severe burns are characterized by large losses of intravascular fluid, which are greatest during the first 8-12 hours. Fluid loss occurs as a result of the altered capillary permeability, severe hypoproteinemia, and the shift of sodium into the cells. Both fluid shifts diminish significantly by 24 hours postburn. The lung appears to be reasonably well protected from the early edema process, and pulmonary edema is uncommon during the resuscitation period unless there is a superimposed inhalation injury. Increasing perfusion rather than infusion of bicarbonates is the appropriate approach.

Initially, an isotonic crystalloid salt solution is infused to counterbalance the loss of plasma volume into the extravascular space and the further loss of extracellular fluid into the intracellular space. Lactated Ringer solution is commonly used, the rate being dictated by urine output, pulse (character and rate), state of consciousness, and, to a lesser extent, blood pressure. Urine output should be maintained at 0.5 mL/kg/h and the pulse at 120 beats/min or slower. Base deficit has been shown to be an excellent marker, with an increasing deficit indicating inadequate perfusion.

Swan-Ganz catheters and central venous pressure lines are seldom needed except in the case of severe smoke inhalation injury or unless the patient has sufficient cardiopulmonary disease that accurate monitoring of volume status would be difficult without measurement of filling pressures or unless a persistent base deficit is present, indicating continued impaired perfusion. The amount of lactated Ringer necessary in the first 24 hours for adequate resuscitation is approximately 3-4 mL/kg of body weight per percent of body burn, which is the amount of fluid needed to restore the estimated sodium deficit. At least half of the fluid is given in the first 8 hours because of the greater initial volume loss. Dextrose-containing solutions are not used initially because of early stress-induced glucose intolerance.

Although the importance of restoring colloid osmotic pressure and plasma proteins is well recognized, the timing of colloid infusion remains somewhat varied. Plasma proteins are ordinarily not infused until after the initial plasma leak begins to decrease. This usually occurs about 4-8 hours postburn. The addition of a protein infusion to the treatment regimen after this period will decrease the fluid requirements and—in very young or elderly patients and in patients with massive burns (in excess of 50% of body surface)—will improve hemodynamic stability.

After intravenous fluids are started and vital signs stabilized, the wound should be debrided of all loose skin and dirt. To avoid severe hypothermia, debridement is best done by completing one body area before exposing a second. An alternative is to use an overhead radiant heater, which will decrease net heat loss. Cool water is a very good analgesic on a small superficial burn; however, it should not be used for larger burns because of the risk of hypothermia. Pain is best controlled with the use of intravenous rather than intramuscular narcotics. Tetanus toxoid, 0.5 mL, should be administered to patients with any significant burn injury.

POSTRESUSCITATION PERIOD

Treatment should aim to decrease excessive catecholamine stimulation and provide enough calories to offset the effects of the hypermetabolism. Hypothermia, pain, and anxiety all need to be aggressively controlled. Hypovolemia should be prevented by giving enough fluid to make up for the body losses.

Ongoing management of any smoke inhalation injury will be necessary using vigorous pulmonary toilet to avoid airway plugging and hypoxia. Nutritional support should begin as early as possible in the postburn period to maximize wound healing and minimize immune deficiency. Patients with moderate body burns may be able to meet nutritional needs by voluntary oral intake. Patients with large burns invariably require calorie and protein supplementation to reach a goal of 30 cal/kg body weight for calories and 1.5 g/kg body weight for protein. This can usually be accomplished by administering a formula diet through a small feeding tube. Parenteral nutrition is also occasionally required, but the intestinal route is preferred if needs can be met this way. Early restoration of gut function will also decrease gut bacterial translocation and endotoxin leak.

Vitamins A, E, and C and zinc should be given until the burn wound is closed. Low-dose heparin therapy may be beneficial, as with other immobilized patients with soft tissue injury.

CARE OF THE BURN WOUND

In the management of superficial partial or second-degree burns, one must provide as aseptic an environment as possible to prevent infection. However, superficial burns generally do not require the use of topical antibiotics. Occlusive dressings are used to minimize exposure to air, increase the rate of reepithelialization, and decrease pain. The exception is the face, which can be treated open with an antibacterial ointment. If there is no infection, burns will heal spontaneously.

The goals in managing deep partial-thickness or full-thickness (third-degree) burns are to prevent invasive infection (ie, burn wound sepsis), to remove dead tissue, and to cover the wound with skin or skin substitutes as soon as possible.

All topical antibiotics retard wound healing to some degree and therefore should be used only on deep second- or third-degree burns or wounds, which have a high risk of infection.

Topical Antibacterial Agents

Topical agents have definitely advanced the care of burn patients. Although burn wound sepsis is still a major problem, the incidence is lower and the death rate has been markedly reduced, particularly in burns of less than 50% of body surface area. A silver-containing product is the treatment of choice because silver has superior antimicrobial properties. Silver sulfadiazine is the most widely used preparation. Mafenide, silver nitrate, povidone-iodine, and gentamicin ointments are also used. Silver release dressings are now very popular. A secondary dressing is placed over the silver release dressing to retain heat and optimize the wound environment.

Silver sulfadiazine, a cream that is effective against a wide spectrum of gram-positive and gram-negative organisms, is only moderately effective in penetrating the burn eschar. A transient leukopenia secondary to bone marrow suppression often occurs with the use of silver sulfadiazine in large burns, but the process is usually self-limiting, and the agent does not have to be discontinued.

Silver release dressings are available in a slow-release form that release silver ions for several days, decreasing dressing changes and improving patient comfort.

Exposure Versus Closed Management

There are two methods of management of the burn wound with topical agents. In exposure therapy, no dressings are applied over the wound after application of the agent to the wound twice or three times daily. This approach is typically used on the face and head. Disadvantages are increased pain and heat loss as a result of the exposed wound and an increased risk of cross-contamination.

In the closed method, an occlusive dressing is applied over the agent and is usually changed twice daily. The disadvantage of this method is the potential increase in bacterial growth if the dressing is not changed twice daily, particularly when thick eschar is present. The advantages are less pain, less heat loss, and less cross-contamination. The closed method is generally preferred.

Temporary Skin Substitutes

Skin substitutes are another alternative to topical agents for the partial-thickness burn or the clean excised wound. A number of synthetic and biologically active temporary skin substitutes are in use. Reepithelialization is accelerated. Also, pain is better controlled. Homografts (human skin) work better for this purpose on large excised wounds but are difficult to obtain. Other alternatives include a number of tissue engineered skin substitutes, which contain bioactive matrix components.

Hydrotherapy

The use of immersion hydrotherapy for wound management has substantially decreased. A number of studies have shown that the infection rate is actually increased when patients are immersed in a tub because of the generalized inoculation of burn wounds with bacteria from what was previously a localized infection. Hydrotherapy, on a slant board, is a very useful approach once the wounds are in the process of being debrided and closed. Showering is also effective for wound cleansing in the more stable patient.

Debridement & Grafting

Burn wound inflammation, even in the absence of infection, can result in multiple organ dysfunction and perpetuation of the hypermetabolic catabolic state. Early wound closure would be expected to control this process more effectively. Surgical management of burn wounds has now become much more aggressive, with operative debridement beginning within the first several days postburn rather than after eschar has sloughed. More rapid closure of burn wounds clearly decreases the rate of sepsis and significantly decreases the death rate. The approach to operative debridement varies from an extensive burn excision and grafting within several days of injury to a more moderate approach of limiting debridements to less than 15% of the burned area. Excision can be carried down to fascia or to viable remaining dermis or fat. Excision to fascia is more commonly used when the burn extends well into the fat. A meshed skin graft can be covered with a biologic dressing to avoid desiccation of the uncovered wound. Excision to viable tissue, referred to as tangential excision, is advantageous because it provides a vascular base for grafting while preserving remaining viable tissue, especially dermis. Tourniquets can be used to decrease blood loss. Blood loss is substantial in view of the vascularity of the dermis.

A number of permanent skin substitutes could further facilitate wound closure, particularly in large burns with insufficient donor sites. Autologous cultures of epithelium have been applied with some success. Permanent skin substitutes composed of both dermis and epidermis have been designed to maintain coverage and improve skin function.

Maintenance of Function

The maintenance of functional motion during the evolution of the burn wound is necessary to avoid loss of motion at joints. Wound contraction, a normal event during healing, may result in extremity contracture. Immobilization will produce joint stiffness. Contracture of the scar, muscles, and tendons across a joint causes loss of motion, which can be diminished by traction and early motion.

The scar is a metabolically active tissue, continually undergoing reorganization. The extensive scarring that frequently occurs after burns can lead to disfiguring and disabling contractures, but it may be avoided by the use of splints and elevation to maintain a functional position. Following application of the skin graft, maintenance of proper positioning with splints is indicated along with active motion exercises.

If reinjury does not occur, the amount of collagen in the scar tends to decrease with time (usually over a year). Stiff collagen becomes softer, and on flat surfaces of the body, where reinjury and inflammation are prevented, remodeling may totally eliminate contracture. However, around joints or the neck, contractures can persist, and surgical reconstruction is necessary. The sooner the burn wound can be covered with skin grafts, the less likely is contracture formation.

MANAGEMENT OF COMPLICATIONS

Infection remains a critical problem in burns, though the incidence has been reduced by modern therapy with the combination of early excision and grafting along with topical antibacterial agents. An infection is present when a quantitative culture of the burn indicates a concentration of 10⁵ organisms; a semiquantitative swab culture is used more commonly. The cultures also show the sensitivity of the bacteria, and when the bacterial concentration passes 10⁵ organisms per gram, systemic administration of specific antibiotics should be instituted (Tables 14–2 and 14–3).

Sepsis syndrome occurs in all major burns. Fever, hypermetabolism, catabolism, and often leukocytosis are typical characteristics, the result of local burn and total body inflammation. Infection is often not present as this process can be attributed to an autodestructive response to inflammation. This intense inflammatory response can lead to death from multisystem organ failure and hemodynamic parameters comparable to sepsis shock.

Any significant infection can further perpetuate this response. Continued deterioration of a wound is likely due to invasive infection. A more common cause of infection today is a pulmonary complication—either a chemical or bacterial insult leading to pneumonia. Catheter sepsis is the third most common cause of infection. If infection is found, an aggressive antibiotics regime is indicated. Early excision and wound closure is the best way to avoid later development of burn wound sepsis.

Circumferential burns of an extremity or of the trunk pose special problems. Swelling beneath the unyielding eschar may act as a tourniquet to blood and lymph flow, and the distal extremity may become swollen and tense. More extensive swelling may compromise the arterial supply. Escharotomy, or excision of the eschar, may be required. To avoid permanent damage, escharotomy must be performed before arterial ischemia develops. Constriction involving the chest or abdomen may severely restrict ventilation and may require longitudinal escharotomies. Anesthetics are rarely required, and the procedure can usually be performed in the patient’s room.

Acute gastroduodenal (Curling) ulcers were at one time a frequent complication of severe burns, but the incidence is now extremely low, largely as a result of the early and routine institution of antacid and nutritional therapy and the decrease in the rate of sepsis.

A complication unique to children is seizures, which may result from electrolyte imbalance, hypoxemia, infection, or drugs; in one-third of cases, the cause is unknown. Hyponatremia is the most frequent cause. Systemic hypertension occurs in about 10% of cases in the postresuscitation period.

RESPIRATORY INJURY IN BURNS

Today the major cause of death after burns is respiratory failure or complications in the respiratory tract. The problems include inhalation injury, aspiration in unconscious patients, bacterial pneumonia, pulmonary edema, and posttraumatic pulmonary insufficiency. Smoke inhalation markedly increases mortality from burn injury.

Smoke inhalation injuries, caused by incomplete products of combustion and which predispose to other complications, are divided into three categories: carbon monoxide poisoning (Table 14–4), upper airways injury, and inhalation of noxious compounds in the lower airways (Table 14–5).

Carbon monoxide poisoning must be considered in every patient suspected of having inhalation injury on the basis of having been burned in a closed space and physical evidence of inhalation. Arterial blood gases and carboxyhemoglobin levels must be determined. Levels of carboxyhemoglobin above 5% in nonsmokers and above 10% in smokers indicate carbon monoxide poisoning. Carbon monoxide has an affinity for hemoglobin 200 times that of oxygen, displaces oxygen, and produces a leftward shift in the oxyhemoglobin dissociation curve (P₅₀, the oxygen tension at which half the hemoglobin is saturated with oxygen, is lowered). Calculations of oxyhemoglobin saturation may be misleading because the hemoglobin combined with carbon monoxide is not detected and the percentage saturation of oxyhemoglobin may appear normal.

Mild carbon monoxide poisoning (< 20% carboxyhemoglobin) is manifested by headache, slight dyspnea, mild confusion, and diminished visual acuity. Moderate poisoning (20%-40% carboxyhemoglobin) leads to irritability, impairment of judgment, dim vision, nausea, and fatigability. Severe poisoning (40%-60% carboxyhemoglobin) produces hallucinations, confusion, ataxia, collapse, and coma. Levels in excess of 60% carboxyhemoglobin are usually fatal.

Various toxic chemicals in inspired smoke produce tracheobronchial respiratory injuries. Inhalation of kerosene smoke, for example, is relatively innocuous. Smoke from a wood fire is extremely irritating because it contains aldehyde gases, particularly acrolein. Direct inhalation of acrolein, even in low concentrations, irritates mucous membranes and causes severe airway damage. Smoke from some plastic compounds, such as polyurethane, is the most serious kind of toxic irritant, and some plastics give off poisonous gases such as chlorine, sulfuric acid, and cyanides. Cyanide absorption can be lethal. Oxidants are released after all smoke exposures, causing mucosal and alveolar injury.

Inhalation injury causes severe mucosal edema followed soon by sloughing of the mucosa. The destroyed mucosa in the larger airways is replaced by a mucopurulent membrane. The edema fluid enters the airway and, when mixed with the pus in the lumen, may form casts and plugs in the smaller bronchioles. Terminal bronchioles and alveoli contain carbonaceous material. Acute bronchiolitis and bronchopneumonia commonly develop within a few days. Sputum smears should be examined daily to detect early bacterial tracheobronchial infection.

When inhalation injury is suspected, early endoscopic examination of the airway with fiberoptic bronchoscopy is helpful in determining the area of injury (ie, the extent of upper and lower airway involvement). Unfortunately, the severity of the injury cannot be accurately quantified by bronchoscopy—it can only be shown that an injury is present. Direct laryngoscopy probably gives as much information.

After several days, small bronchi become obstructed by inflammation and mucin plugs, leading to severe atelectasis and resulting hypoxia. This process is typically confined to the airways; in severe cases, alveolar edema will be present.

The most common cause of respiratory failure is a chemical tracheobronchitis due to the inhalation injury. Airway clearance is impeded due to ciliary damage and denuded airways. Alteration of oropharyngeal normal flora with colonization by pathogens then leads to bronchopneumonia.

Pulmonary insufficiency is associated with systemic sepsis. Differentiating acute respiratory distress syndrome (ARDS) from bacterial pneumonia may be difficult in severe cases of inhalation of sepsis. There is damage to the pulmonary capillaries and leakage of fluid and protein into the interstitial spaces of the lung, resulting in loss of compliance and difficulty in oxygenation of the blood. Modern methods of ventilatory support and vigorous pulmonary toilet have significantly reduced the death rate from pulmonary insufficiency.

Treatment

Management of a burn patient should include frequent evaluation of the lungs throughout the hospital course. All patients who initially have evidence of smoke inhalation should receive humidified oxygen in high concentrations. If carbon monoxide poisoning has occurred, 100% oxygen should be given until the carboxyhemoglobin content returns to normal levels and symptoms of carbon monoxide toxicity resolve. With severe exposures, carbon monoxide may still be bound to the cytochrome enzymes, leading to cell hypoxia even after carboxyhemoglobin levels have returned to near normal. Continued oxygen administration will also reverse this process. Hyperbaric oxygen is often used in these cases.

The use of corticosteroids for inhalation injuries is no longer controversial and is clearly contraindicated with the exception of chronic bronchiolitis obliterans. The exception is the patient with a relative steroid insufficiency.

Bronchodilators by aerosol or aminophylline given intravenously may help if wheezing is due to the reflex bronchospasm typically present. Chest physical therapy is also required.

When endotracheal intubation is used without mechanical ventilation (eg, for upper airway obstruction), mist and continuous positive pressure ventilatory assistance should be included. The humidity will help loosen the secretions and prevent drying of the airway; the continuous positive pressure will help prevent atelectasis and closure of lung units distal to the swollen airways. Tracheostomy is indicated in the first several days for patients who are expected to require ventilatory support for a few weeks or more. If the neck is burned, excision and grafting followed by tracheostomy is indicated in order to improve pulmonary toilet.

Mechanical ventilation should be instituted early if a significant pulmonary injury is anticipated. A large body burn with chest wall involvement will result in decreased chest wall compliance, increased work of breathing, and subsequent atelectasis. Tracheobronchial injury from inhaled chemicals is accentuated by the presence of a body burn, with a resultant increase in the potential for atelectasis and infection. Controlled ventilation along with sedation will diminish the degree of injury and also conserve energy expenditure. Early excision of the deep chest wall burn will help remove the constricting component. Wound closure in turn will decrease the excessive CO₂ production caused by the hypermetabolic state.

REHABILITATION OF THE BURNED PATIENT

Plastic surgical revisions of scars are often necessary after the initial grafting, particularly to release contractures over joints and for cosmetic reasons. The physician must be realistic in defining an acceptable result, and the patient should be told that it may take years to achieve. Burn scars are often unsightly, and—although hope should be extended that improvement can be made—total resolution is not possible in many cases.

Skin expansion techniques utilizing a subdermal Silastic bag that is gradually expanded have greatly improved scar revision management. The ability to enlarge the available skin to be used for replacement of scar improves both cosmetic appearance and function. Advances in microvascular flap surgery have also resulted in substantial improvements in outcome.

The patient must take special care of the skin of the burn scar. Prolonged exposure to sunlight should be avoided, and when the wound involves areas such as the face and hands, which are frequently exposed to the sun, ultraviolet screening agents should be used. Hypertrophic scars and keloids are particularly bothersome and can be diminished with the use of pressure garments, which must be worn until the scar matures—approximately 12 months. Since the skin appendages are often destroyed by full-thickness burns, creams and lotions are required to prevent drying and cracking and to reduce itching. Substances such as lanolin, vitamin A and D ointment, and Eucerin cream are all effective.

ELECTRICAL INJURY

There are three kinds of electrical injuries: electrical current injury, electrothermal burns from arcing current, and flame burns caused by ignition of clothing. Occasionally, all three are present in the same victim.

Electrical current injury, or “hidden injury,” results from the passage of electrical current through the body. Flash or arc burns are thermal injuries to the skin caused by a high-tension electrical current creating local heat and damaging skin. The thermal injury to the skin is intense and deep, because the electrical arc has a temperature of about 2500°C (high enough to melt bone). Flame burns from ignited clothing are often the most serious part of the injury. Treatment is the same as for any thermal injury.

Once current enters the body, its pathway depends on the resistances it encounters in the various organs. The following are listed in descending order of resistance: bone, fat, tendon, skin, muscle, blood, and nerve. The pathway of the current determines immediate survival; for example, if the current passes through the heart or the brain stem, death may be immediate from ventricular fibrillation or apnea. Current passing through muscles may cause spasms severe enough to produce long-bone fractures or dislocations.

The type of current is also related to the severity of injury with low-voltage (150 V) current. The usual 60-cycle alternating current that causes most injuries in the home is particularly severe. Alternating current causes tetanic contractions, and the victim may become “locked” to the contact. Cardiac arrest is common from contact with low-voltage house current.

High-voltage electrical current injuries are more than just burns. Focal deep burns occur at the points of entrance and exit through the skin. These burns often extend through local muscle, resulting in fourth-degree burn. Once inside the body, the current travels through muscles, causing an injury more like a crush than a thermal burn. This leads to blood and fluid extravasation, increasing interstitial pressure in the muscle compartments. A fasciotomy is often necessary, opening all the muscle compartments involved. Early action is necessary to avoid severe vascular insufficiency or nerve damage. Thrombosis frequently occurs in vessels deep in an extremity, causing a greater depth of tissue necrosis than is evident at the initial examination. The greatest muscle injury is usually closest to the bone, where the highest heat of resistance is generated. The treatment of electrical injuries depends on the extent of deep muscle and nerve destruction more than on any other factor.

Severe myoglobinuria may develop with the risk of acute tubular necrosis as the muscle pigment is released from muscle and precipitates in renal tubules. The urine output must be kept two to three times normal with intravenous fluids. Alkalinization of the urine and osmotic diuretics may be indicated if myoglobinuria is present to more rapidly clear the pigment.

A rapid drop in hematocrit sometimes follows as sudden destruction of red blood cells by the electrical energy occurs. Bleeding into deep tissues may occur as a result of disruption of blood vessels and tissue planes. In some cases, thrombosed vessels disintegrate later and cause massive interstitial hemorrhage. Increased fluid infusion is required for initial resuscitation compared to extent of external thermal burns alone.

The skin burn at the entrance and exit sites is usually a depressed gray or yellow area of full-thickness destruction surrounded by a sharply defined zone of hyperemia. Charring may be present. The lesion should be debrided to underlying healthy tissue. Frequently, there is deep destruction not initially evident, especially to muscles beneath the skin surface. This dead and devitalized tissue must also be excised as soon as possible. Amputation rate for extremity involved is still high but decreasing. A second debridement is usually indicated 24-48 hours after the injury, because the necrosis is found to be more extensive than originally thought. The strategy of obtaining skin covering for these burns can tax ingenuity because of the extent and depth of the wounds. Microvascular flaps are now used routinely to replace large tissue losses.

In general, the treatment of electrical injuries is complex at every step, and these patients are referred to specialized centers. There are no formulas for determining severity and outcome of high-voltage electrical injuries.

HEAT STROKE & RELATED INJURIES

Heat stroke occurs when core body temperature exceeds 40°C and produces severe central nervous system dysfunction. Two related syndromes induced by exposure to heat are heat cramps and heat exhaustion.

In humans, heat is dissipated from the skin by radiation, conduction, convection, and evaporation. When the ambient temperature rises, heat loss by the first three is impaired; loss by evaporation is hindered by a high relative humidity. Predisposing factors to heat accumulation are dermatitis; use of phenothiazines, beta-blockers, diuretics, or anticholinergics; intercurrent fever from other disease; obesity; alcoholism; and heavy clothing. Cocaine and amphetamines may increase metabolic heat production.

Heat cramps—muscle pain after exertion in a hot environment—are usually attributed to salt deficit. It is probable, however, that many cases are really examples of exertional rhabdomyolysis. This condition, which may also be a complicating factor in heat stroke, involves acute muscle injury due to severe exertional efforts beyond the limits for which the individual has trained. It often produces myoglobinuria, which rarely affects kidney function except when it occurs in patients also suffering from heat stroke. Complete recovery is the rule after uncomplicated heat cramps.

Heat exhaustion consists of fatigue, muscular weakness, tachycardia, postural syncope, nausea, vomiting, and an urge to defecate caused by dehydration and hypovolemia from heat stress. Temperature usually exceeds 39°C. Although body temperature is normal in heat exhaustion, there is a continuum between this syndrome and heat stroke.

Heat stroke, a result of imbalance between heat production and heat dissipation, kills about 4000 persons yearly in the United States. Exercise-induced heat stroke most often affects young people (eg, athletes, military recruits, laborers) who are exercising strenuously in a hot environment, usually without adequate training. Heat production exceeds the ability to dissipate the heat; core temperature then rises and hypovolemia is evident. Sedentary heat stroke is a disease of elderly or infirm people whose cardiovascular systems are unable to adapt to the stress of a hot environment and release sufficient heat such that body temperature rises. Epidemics of heat stroke in elderly people can be predicted when the ambient temperature surpasses 32.2°C and the relative humidity reaches 50%-76%.

The mechanism of injury is direct damage by heat to the parenchyma and vasculature of the organs. In addition, there is a marked cytokine-induced activation of inflammation similar to sepsis, leading to inflammation-induced organ damage. The central nervous system is particularly vulnerable, and cellular necrosis is found in the brains of those who die of heat stroke. Hepatocellular and renal tubular damage are apparent in severe cases. Subendocardial damage and occasionally transmural infarcts are discovered in fatal cases even in young persons without previous cardiac disease. Disseminated intravascular coagulation may develop, aggravating injury in all organ systems and predisposing to bleeding complications.

Clinical Findings

A. Symptoms and Signs

Heat stroke should be suspected in anyone who develops sudden neurological changes in a hot environment. If the patient’s temperature is above 40°C (range: 40-43°C), the diagnosis of heat stroke is definitive. Measurements of body temperature must be made rectally. A prodrome including dizziness, headache, nausea, chills, and goose-flesh of the chest and arms is seen occasionally but is not common. In most cases, the patient recalls having experienced no warning symptoms except weakness, tiredness, or dizziness. Confusion, belligerent behavior, or stupor may precede coma. Convulsions may occur.

The skin is pink or ashen and sometimes, paradoxically, dry and hot; dry skin in the presence of hyperpyrexia is virtually pathognomonic of heat stroke. Profuse sweating is usually present in runners and other athletes who have heat stroke. The heart rate ranges from 140 beats/min to 170 beats/min; central venous or pulmonary wedge pressure is high; and in some cases the blood pressure is low. Hyperventilation may reach 60 breaths/min and may give rise to respiratory alkalosis. Pulmonary edema and bloody sputum may develop in severe cases. Jaundice is frequent within the first few days after onset of symptoms.

Dehydration, which may produce the same central nervous system symptoms as heat stroke, is an aggravating factor in about 50% of cases.

B. Laboratory Findings

There is no characteristic pattern to the electrolyte changes. The serum sodium concentration may be normal or high, and the potassium concentration is usually low on admission or at some point during resuscitation. In the first few days, the aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase (CK) may be elevated, especially in exertional heat stroke. Proteinuria and granular and red cell casts are seen in urine specimens collected immediately after diagnosis. If the urine is dark red or brown, it probably contains myoglobin. The blood urea nitrogen and serum creatinine rise transiently in most patients and continue to climb if renal failure develops. Hematologic findings may be normal or may be typical of disseminated intravascular coagulation (ie, low fibrinogen, increased fibrin split products, slow prothrombin and partial thromboplastin times, and decreased platelet count).

C. Prevention

For the most part, heat stroke in military recruits and athletes in training is preventable by adhering to a graduated schedule of increasing performance requirements that allows acclimatization over 2-3 weeks and increasing fluid replacement using water and some electrolytes, especially sodium. Heat produced by exercise is dissipated by increased cardiac output, vasodilation in the skin, and increased sweating. With acclimatization, there is increased efficiency for muscular work, increased myocardial performance, expanded extracellular fluid volume if hydration is maintained, greater output of sweat for a given amount of work (releasing more heat), a lower salt content of sweat, and a lower central temperature for a given amount of work.

Access to drinking water should be unrestricted during vigorous physical activity in a hot environment. Free water is preferable to electrolyte-containing solutions. Clothing and protective gear should be lightened as heat production and air temperature rise, and heavy exercise should not be scheduled at the hottest times of day, especially at the beginning of a training schedule.

Treatment

The patient should be cooled rapidly. The most efficient method is to induce evaporative heat loss by spraying the patient with water at 15°C and fanning with cool air. Immersion in an ice water bath or the use of ice packs is also effective but causes cutaneous vasoconstriction and shivering and makes patient monitoring more difficult. Monitor the rectal temperature frequently. To avoid overshooting the end point, vigorous cooling should be stopped when the temperature reaches 38.9°C. Shivering should be controlled with parenteral phenothiazines. Oxygen should be administered, and if the Pao₂ drops below 65 mm Hg, tracheal intubation should be performed to control ventilation. Fluid, electrolyte, and acid-base balance must be controlled by frequent monitoring. Intravenous fluid administration should be based on the central venous or pulmonary artery wedge pressure, blood pressure, and urine output; overhydration must be avoided. Intravenous mannitol (12.5 g) may be given early if myoglobinuria is present to avoid renal dysfunction. Disseminated intravascular coagulation may require treatment with heparin. Occasionally, inotropic agents (eg, isoproterenol, dopamine) may be indicated for cardiac insufficiency, which should be suspected if hypotension persists after hypovolemia has been corrected.

Prognosis

Bad prognostic signs are temperature of 42.2°C or more, coma lasting over 2 hours, shock, hyperkalemia, and an AST greater than 1000 units/L during the first 24 hours. The death rate is about 10% in patients who are correctly diagnosed and treated promptly. Deaths in the first few days are usually due to cerebral damage; later deaths may be from bleeding or may be due to cardiac, renal, or hepatic failure.

FROSTBITE

Frostbite involves freezing of tissues. Ice crystals form between and in the cells and grow at the expense of intracellular water. The resulting ischemia due to vasoconstriction and increased blood viscosity is the mechanism of tissue injury. Skin and muscle are considerably more susceptible than tendons and bones to freezing damage due to a lower oxygen requirement, which explains why the patient may still be able to move severely frostbitten digits.

Frostbite is caused by cold exposure, the effects of which can be magnified by moisture or wind; for example, the chilling effects on skin are the same with an air temperature of 6.7°C and a 40-mph wind as with an air temperature of −40°C and only a 2-mph wind. Contact with metal or gasoline in very cold weather can cause virtually instantaneous freezing; skin will often stick to metal and be lost. The risk of frostbite is increased by generalized hypothermia, which produces peripheral vasoconstriction as part of the mechanism for preservation of core body temperature.

Two related injuries, trench foot and immersion foot, involve prolonged exposure to wet cold above freezing (eg, 10°C). The resulting tissue damage is produced by tissue ischemia.

Clinical Findings

Frostnip, a minor variant of this syndrome, is a transient blanching and numbness of exposed parts that may progress to frostbite if not immediately detected and treated. It often appears on the tips of fingers, ears, nose, chin, or cheeks and should be managed by rewarming through contact with warm parts of the body or warm air.

Frostbitten parts are numb, painless, and of a white or waxy appearance. With superficial frostbite, only the skin and subcutaneous tissues are frozen, so the tissues beneath are still compressible with pressure. Deep frostbite involves freezing of underlying tissues, which imparts a wooden consistency to the extremity.

After rewarming, the frostbitten area becomes mottled blue or purple and painful and tender. Blisters appear that may take several weeks to resolve. The part becomes edematous and to a varying degree painful.

Treatment

The frostbitten part should be rewarmed (thawed) in a water bath at 40-42.2°C for 20-30 minutes. Thawing should not be attempted until the victim can be kept permanently warm and at rest. It is far better to continue walking on frostbitten feet even for many hours than to thaw them in a remote cold area where definitive care cannot be provided. If a thermometer is unavailable, the temperature of the water should be adjusted to be warm but not hot to a normal hand. Never use the frozen part to test the water temperature or expose it to a source of direct heat such as a fire. The risk of seriously compounding the injury is great with any method of thawing other than immersion in warm water.

After thawing has been completed, the patient should be kept recumbent and the injured part left open to the air, protected from direct contact with sheets, clothing, or other material. Blisters should be left intact and the skin gently debrided by immersing the part in a whirlpool bath for about 20 minutes twice daily. No scrubbing or massaging of the injured part should be allowed, and topical ointments, antiseptics, and so on, are of no value. Vasodilating agents and surgical sympathectomy do not appear to improve healing.

The tissue will heal gradually, and any dead tissue will become demarcated and usually slough spontaneously. Early in the course, it is nearly impossible, even for someone with considerable experience in the treatment of frostbite, to judge the depth of injury; most early assessments tend to overestimate the extent of permanent damage. Therefore, expectant treatment is the rule, and surgical debridement should be avoided even if evolution of the injury requires many months. Surgery may be indicated to release constricting circumferential eschars, but rarely should the process of spontaneous separation of gangrenous tissue be surgically facilitated. Even in severe injuries, amputation is rarely indicated before 2 months unless invasive infection supervenes. Nuclear scans may be useful to delineate tissue viability.

Concomitant fractures or dislocations create challenging and complex problems. Dislocations should be reduced immediately after thawing. Open fractures require operative reduction, but closed fractures should be managed with a posterior plastic splint. Anterior tibial compartment syndrome, which may develop in patients with associated fractures, may be diagnosed by arteriography and treated by fasciotomy.

After the eschar separates, the skin is noted to be thin, shiny, tender, and sensitive to cold; occasionally it exhibits a tendency to perspire more readily. Gradually, it returns toward normal, but pain on exposure to cold may persist indefinitely.

Prognosis

The prognosis for normal function is excellent if appropriate treatment is provided. Individuals who have recovered from frostbite have increased susceptibility to another frostbite injury on exposure to cold.

ACCIDENTAL HYPOTHERMIA

Accidental hypothermia consists of the uncontrolled lowering of core body temperature below 35°C by exposure to cold. The syndrome may be seen, for example, in elderly people living alone in inadequately heated homes, in alcoholics exposed to the cold during a binge, in those engaged in winter sports, and in people who become lost in cold weather. Alcohol facilitates the induction of hypothermia by producing sedation (inhibiting shivering) and cutaneous dilation. Other sedatives, tranquilizers, and antidepressants are occasionally implicated. Diseases that predispose to hypothermia include myxedema, hypopituitarism, adrenal insufficiency, cerebral vascular insufficiency, mental impairment, and cardiovascular disorders.

The heart is the organ most sensitive to cooling and is subject to ventricular fibrillation or asystole when the temperature drops to 21-24°C. Hypothermia affects the oxyhemoglobin dissociation curve, so less oxygen is released to the tissues. Cardiac standstill may cause death in less than 1 hour in shipwreck victims immersed in cold water (6.7°C). Increased capillary permeability, manifested by generalized edema and pulmonary, hepatic, and renal dysfunction, may develop as the patient is rewarmed. Coagulopathies and disseminated intravascular coagulation are seen occasionally. Pancreatitis and acute renal failure are common in patients whose temperature on admission is below 32°C.

Clinical Findings

A. Symptoms and Signs

The patient is mentally depressed (somnolent, stuporous, or comatose), cold, and pale to cyanotic. The clinical findings are not always striking and may be mistaken for the effects of alcohol. The core temperature ranges from 21°C to 35°C. Shivering is absent when the temperature is below 32°C. Respirations are slow and shallow. The blood pressure is usually normal and the heart rate slow. When the core temperature drops below 32°C, the patient may appear to be dead. The extremities may be frostbitten or frozen.

B. Laboratory Findings

Dehydration may increase the concentration of various blood constituents. Severe hypoglycemia is common, and unless detected and treated immediately, it may become dangerously worse as rewarming produces shivering. The serum amylase is elevated in about half of cases, but autopsy studies show that it does not always reflect pancreatitis. Diabetic ketoacidosis becomes a management problem in some patients whose amylase values are elevated on entry. The AST, LDH, and CK enzymes are usually elevated but are of no predictive significance. The electrocardiogram shows lengthening of the PR interval, delay in interventricular conduction, and a pathognomonic J wave at the junction of the QRS complex and ST segment.

Treatment

Hypothermic patients should never be considered dead until all measures for resuscitation have failed, because cardiopulmonary arrest in severe hypothermia is still compatible with some recovery.

Mild hypothermia (body temperature 32-35°C) can be treated in most cases by passive rewarming (heavy clothing and blankets in a warm environment) for a few hours—especially when the patient is shivering. The patient’s temperature should be continuously monitored with a rectal or esophageal probe until body temperature reaches normal. Since the volume of intravenous fluids required for resuscitation is often substantial, their temperature can affect the outcome. Consequently, intravenous fluids should be warmed with a heat exchanger during administration.

Active rewarming is indicated for temperature below 32°C, cardiovascular instability, or failure of passive rewarming. The methods include immersion in a warm water bath, inhalation of heated air, pleural lavage, and blood warming with an extracorporeal bypass machine. Active external rewarming is most often performed by immersion in a warm (40-42°C) water bath, which will raise body temperature at a rate of 1-2 degrees per hour. A disadvantage of this method is that the core temperature may continue to decline after initiation of the rewarming efforts (known as afterdrop), which is associated with worsening cardiovascular function.

Closed pleural irrigation should be performed by flushing the right hemithorax with warm (40-42°C) saline solution through two large thoracostomy tubes, one anterior and the other posterior. Rewarming by peritoneal lavage involves giving warm (40-45°C) crystalloid solutions, 6 L/h, which raises core temperature by 2-4 degrees per hour.

Active core rewarming with partial cardiopulmonary bypass, the most efficient technique, is indicated for patients with ventricular fibrillation and severe hypothermia or those with frozen extremities. At a flow rate of 6-7 L/min, core temperature can be raised by 1-2°C every 3-5 minutes.

In severe cases, endotracheal intubation should be used for better management of ventilation and protection against aspiration, a common lethal complication. Arterial blood gases should be monitored frequently. Bretylium tosylate in an initial dose of 10 mg/kg is the best drug for ventricular fibrillation. Antibiotics are often indicated for coexisting pneumonitis. Serious infections are often unsuspected upon admission, and delay in appropriate therapy may contribute to the severity of the illness. Hypoglycemia calls for intravenous administration of 50% glucose solution. Fluid administration must be gauged by central venous or pulmonary artery wedge pressures, urine output, and other circulatory parameters. Increased capillary permeability following rewarming predisposes to the development of pulmonary edema and compartment syndromes in the extremities. To minimize these complications, the central venous or wedge pressure should be kept below 12-14 cm water. Drugs should not be injected into peripheral tissues, because absorption will not take place while the patient is cold and because drugs may accumulate to produce serious toxicity as rewarming occurs.

As rewarming proceeds, the patient should be continually reassessed for signs of concomitant disease that may have been masked by hypothermia, especially myxedema and hypoglycemia. Any inexplicable failure to respond should suggest adrenal insufficiency.

Prognosis

Survival can be expected in only 50% of patients whose core temperature drops below 32.2°C. Coexisting diseases (eg, stroke, neoplasm, myocardial infarction) are common and increase the death rate to 75% or more. Survival does not correlate closely with the lowest absolute temperature reached. Death may result from brain damage pneumonitis, heart failure, or renal insufficiency.