BURNS

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CHAPTER 79 BURNS

The frequency of burn injury and its subsequent multisystem effects make the treatment of burn patients a commonly encountered management challenge for the trauma/critical care surgeon. The emergency surgery components of initial burn care include fluid resuscitation and ventilatory support, as well as preservation and restoration of remote organ function. Following appropriate resuscitation, burn patient management is focused on wound care and provision of the necessary metabolic support. The involvement of the emergency/trauma surgeon in burn wound management is dependent on the extent and depth of the wound and the rapid identification of those patients who are best cared for at a burn center.

INCIDENCE

The precise number of burns that occur in the United States each year is unknown because only 21 of 50 states mandate the reporting of burn injury. An estimated total number of burns has been obtained by extrapolation of those data. At present, 1.25 million is regarded as a realistic estimate of the annual incidence of burns in the United States, 80% of which involve less than 20% of the total body surface. Approximately 190–263 patients per million population are estimated to require admission to a hospital for burn care each year. In the population of burn patients requiring hospital care, there is a smaller subset of approximately 20,000 burn patients who, as defined by the American Burn Association (Table 1), are best cared for in a burn center each year. This subset consists of 42 patients per million population with major burns, and 40 patients per million population having lesser burns but a complicating cofactor.

Table 1 Burn Center Referral Criteria

a If the mechanical trauma poses the greater immediate risk, the patient may be stabilized and receive initial care at a trauma center before transfer to a burn center.

Adapted with permission from Stabilization, Transfer and Transport, Chapter 8. In Advanced Life Burn Support Course Instructors Manual. Chicago, American Burn Association, 2001, pp. 73–78.

MECHANISM OF INJURY

Certain populations are at high risk for specific types of injuries that require treatment by the trauma/critical care surgeon. Scald burns are the most frequent form of burn injury overall, causing 58% of burn injuries and over 100,000 emergency department visits annually. Sixty-five percent of children age 4 and under who require hospitalization for burn care have scald burns, the majority of which are due to contact with hot foods and liquids. The occurrence of accidental tap water scalds can be minimized by adjusting the temperature settings on hot water heaters or by installing special faucet valves that prevent delivery of water at unsafe temperatures. Scald burns with injury typically involving the feet, posterior legs, buttocks, and sometimes the hands are most often caused by immersion in scalding water by an abusive caretaker. It is important that the trauma/critical care surgeon identify and report child abuse, because when abuse is undetected and the child is returned to the abusive environment, repeated abuse is associated with a high risk of fatality.

Fire and flame sources cause 34% of burn injuries and are the most common causes of burns in adults. One-fifth to one-quarter of all serious burns are related to employment. Kitchen workers are at relatively high risk for scald injury, and roofers and paving workers are at greatest risk for burns due to hot tar. Workers involved in plating processes and the manufacture of fertilizer are at greatest risk for injury due to strong acids, and those involved with soap manufacturing and the use of oven cleaners are at greatest risk of injury due to strong alkalis.

Electric current causes approximately 1000 deaths per year. Young children have the highest incidence of electric injury caused by household current as a consequence of inserting objects into an electrical receptacle or biting or sucking on electric cords and sockets. Adults at greatest risk of high-voltage electric injury are the employees of utility companies, electricians, construction workers (particularly those manning cranes), farm workers moving irrigation pipes, oil field workers, truck drivers, and individuals installing antennae. Lightning strikes result in an average of 107 deaths annually. The vast majority (92%) of lightning-associated deaths occur during the summer months among people engaged in outdoor activities such as golfing or fishing.

Abuse is a special form of burn injury, affecting the extremes of age. Child abuse is typically inflicted by parents but also perpetrated by siblings and child care personnel. The most common form of thermal injury abuse in children is caused by intentional application of a lighted cigarette. Burning the dorsum of a hand by application of a hot clothing iron is another common form of child abuse. Scald burns, as previously discussed, are also common. In recent years, elder abuse by caretakers or family members has become more common, and it too should be reported and the victim protected.

PATHOPHYSIOLOGY

Local Effects

The cutaneous injury caused by a burn is related to the temperature of the energy source, the duration of the exposure, and the tissue surface involved. At temperatures less than 45° C, tissue damage is unlikely to occur even with an extended period of exposure. In the adult, exposure for 30 seconds when the temperature is 54° C will cause a burn injury, while an identical burn will occur with only a 10-second exposure in a child. When the temperature is elevated to 60° C, a common setting for home water heaters, tissue destruction can occur in less than 5 seconds in children. It is not surprising, therefore, that significant injury can occur when patients come in contact with boiling liquids or live flames.

Burn injury causes three zones of damage. Centrally located is the zone of coagulation. In a full-thickness burn, the zone of coagulation involves all layers of the skin, extending down through the dermis and into the subcutaneous tissue. In partial-thickness injuries, this zone extends down only into the dermis, and there are surviving epithelial elements capable of ultimately resurfacing the wound. Surrounding the zone of coagulation is an area of lesser cell injury, the zone of stasis. In this area, blood flow is altered but is restored with time as resuscitation proceeds. If patients are inadequately resuscitated, thrombosis can occur and the zone of stasis can be converted to a zone of coagulation. The most peripheral zone is an area of minimally damaged tissue, the zone of hyperemia, which abuts undamaged tissue. The zone of hyperemia is best seen in patients with superficial partial-thickness injuries as occur with severe sun exposure.

Along with the changes in wound blood supply, there is significant formation of edema in the burn-injured tissues. Factors elaborated in the damaged tissues and released as local mediators include histamine, serotonin, bradykinin, prostaglandins, leukotrienes, and interleukin-1, all of which cause alterations in local tissue homeostasis and increases in vascular permeability. Complement is also activated which can further modify transcapillary fluid flux. The net effect of these various changes is significant movement of fluid into the extravascular fluid compartment. Maximum accumulation of both water and protein in the burn wound occurs at 24 hours post injury and can persist beyond the first week post-burn. Additionally, patients who have greater than a 20%–25% body surface burn have similar fluid movement in undamaged tissue beds. This may be related in part to the changes in transcapillary fluid flux and also may be in response to the volume of resuscitation fluids administered.

Systemic Response

The physiologic response to a major burn injury results in some of the most profound changes that a patient is capable of enduring. The magnitude of the response is proportional to the burn size, reaching a maximum at about a 50% body surface area burn. The duration of the changes is related to the persistence of the burn wound and therefore resolves with wound closure. The organ-specific response follows the pattern that occurs with other forms of trauma, with an initial level of hypofunction, the “ebb phase,” followed by a hyperdynamic “flow” phase.

Changes in the cardiovascular response are critical and directly impact the initial care and management of the burn patient. Immediately following burn injury, there is a transient period of decreased cardiac performance and elevated peripheral vascular resistance, which can be exacerbated by inadequate volume replacement. Systemic hypoperfusion can result in further increases in systemic vascular resistances and reprioritization of regional blood flow. Failure to adequately resuscitate a burn patient worsens myocardial performance. Conversely, adequate resuscitation restores normal cardiac performance values within 24 hours of injury, and by the second 24 hours those values further increase to supranormal levels, resulting in a hyperdynamic state, which will revert back to more normal levels with wound closure.

Pulmonary changes following burn injury are the consequences of direct parenchymal damage that occurs with inhalation injury. In patients without inhalation injury, pulmonary changes following burn injury are reflective of the generalized hyperdynamic state of the patient. Lung ventilation increases in proportion to the total body surface area of the burn, with increases in both respiratory rate and tidal volume. Worsening of the burned patient’s respiratory status should indicate a supervening process, including sepsis, pneumonia, occult pneumothorax, pulmonary embolism, congestive heart failure, or an acute intra-abdominal process. In patients without these events, pulmonary gas exchange is relatively preserved, and there is little change in pulmonary mechanics.

The renal response to burn injuries is largely dependent on the cardiovascular response. Initially there is a reduction in renal blood flow, which is restored with resuscitation. If a patient is underresuscitated, renal hypoperfusion will persist, with early onset renal dysfunction secondary to renal ischemia. This can be exacerbated if the patient exhibits myoglobinuria or hemoglobinuria, either of which is capable of causing direct tubular damage.

Burn injury is capable of affecting both gastrointestinal motility and mucosal integrity, usually as a result of underresuscitation leading to intestinal hypoperfusion. Conversely, patients who are massively resuscitated will have significant edema of the retroperitoneum, bowel mesentery, and bowel wall contributing to a paralytic ileus. With near-immediate initiation of enteral feedings, gastrointestinal motility can be preserved, mucosal integrity protected, and effective nutrient delivery achieved. Delay in the initiation of enteral feeding is associated with the onset of ileus, which can also occur when the burn resuscitation has been complicated.

From a neuroendocrine standpoint, burn injury results in an elevated hormonal and neurotransmitter response similar in magnitude to that of the “fight or flight” response. The duration of the neurohumoral response is prolonged and is exacerbated by surgical stress. The increases in glucocorticoids and catecholamines are necessary to support the stress response of the injured patient. When there is an insufficient stress hormone response, an otherwise survivable insult can become fatal. Many of the multisystem changes occurring post-burn can be related in part to the alterations in catecholamine secretion, particularly the changes in resting metabolic expenditures, substrate utilization, and cardiac performance. As wound closure is accomplished, the increased neurohumoral response abates and anabolic hormones become predominant.

Burn injury affects the hematopoietic system, resulting in the loss of balance in both leukocyte and erythrocyte production and function. Burns of greater than 20% of total body surface area are associated with both alterations in red cell production and increases in red cell destruction at the level of the cutaneous circulation, resulting in anemia. Such anemia can be further compounded by frequent phlebotomy, surgical blood loss, hemodilution due to resuscitation, and transient alterations in erythrocyte membrane integrity. Longer-term changes appear to be related to hyporesponsiveness of the erythroid progenitor cells in the bone marrow to erythropoietin. During the early stages of resuscitation, reductions in platelet number, depressed fibrinogen levels, and alterations in coagulation factors return to normal or near normal values with appropriate resuscitation. Changes in white cell number occur early, with an increase in neutrophils due to demargination and accelerated bone marrow release. With uncomplicated burn injury, bone marrow myelopoiesis is preserved.

In addition to the changes occurring in the bone marrow, there are significant further depressions in the immune response. Burn injury causes a global impairment in host defense. Alterations of the humoral immune response include reductions in IgG and IgM secretion, decreased fibronectin levels, and increases in complement activation. Cellular changes include alterations in T-cell responsiveness and cell populations, leading to alterations in antigen presentation and impairment of delayed-type hypersensitivity reactions. Leukocyte function is adversely affected. Granulocytes have been noted to have impaired chemotaxis, decreased phagocytic activity, decreased antibody-dependent cell cytotoxicity, and a relative impairment in their capacity to respond to a second challenge. The clinical significance of these observations is that the burn patient is at significant risk for post-burn infectious complications.

GRADING OF BURN WOUND DEPTH

The injuries that will be apparent on examination are the consequences of the level of tissue destruction. Wounds that are superficial are associated with hyperemia, fine blistering, increased sensation, and exquisite pain upon palpation. The wounds are hyperemic, warm, and readily blanch. These types of injuries represent firstdegree burns or are alternatively termed superficial partial-thickness injuries. With a second degree or deeper partial-thickness burn, the wound presents with intact or ruptured blisters or is covered by a thin coagulum termed “pseudoeschar.” The key physical finding is preservation of sensation in the burned tissue, although it is reduced (Table 2). With proper care, superficial and even deeper partial-thickness injuries are capable of spontaneous healing without grafting. The risk of infection in deep partial-thickness wounds is significant, and if an infection develops it can lead to a greater depth of skin loss. A full-thickness wound occurs when the injury penetrates all layers of the skin or extends into the subcutaneous or deeper tissues. These wounds will appear pale or waxy, be anesthetic, dry, and inelastic, and contain thrombosed vessels. Occasionally in children or young women, the initial appearance of a wound may be more that of a brick red coloration. Such wounds will have significant edema and are inelastic and insensate. Full-thickness wounds are infection-prone wounds, as they no longer provide any viable barrier to invading organisms and if left untreated become rapidly colonized and a portal for invasive burn wound sepsis.

Table 2 Clinical Characteristics of Burn Injuries

RESUSCITATION PRIORITIES

Fluid Administration

Immediately following burn injury, the changes induced in the cardiovascular system must receive therapeutic priority. In all patients with burns of more than 20% of the total body surface area and those with lesser burns in whom physiologic indices indicate a need for fluid infusion, a large-caliber intravenous cannula should be placed in an appropriately sized peripheral vein, preferably underlying unburned skin. If there are no peripheral veins available, central venous access is indicated. Lactated Ringer’s solution should be infused at an initial rate of 1 liter/hr in the adult and 20 ml/kg/hr for children who weigh 50 kg or less. That infusion rate is adjusted following estimation of the fluid needed for the first 24 hours following the burn.

Resuscitation fluid needs are proportional to the extent of the burn (combined extent of partial- and full-thickness burns expressed as a percentage of total body surface area) and are related to body size (most readily expressed as body weight) and age (the surface area per unit of body mass is greater in children than in adults). The patient should be weighed on admission and the extent of partial- and full-thickness burns estimated according to standard nomograms (Figure 1). The fluid needs for the first 24 hours can be estimated on the basis of the Advanced Burn Life Support and Advanced Trauma Life Support consensus formula (Table 3).

Figure 1 Example of a form used for documenting extent of burn. Figure outlines are filled in with a blue pencil and a red pencil to indicate distribution of partial-thickness and full-thickness burns, respectively. Note the columns indicating how the percentage of total body-surface area represented by body-part surface changes with time.

(Used with permission from Martin RR, Becker WK, Cioffi WG, and Pruitt BP Jr: Thermal Injuries. In Wilson RF and Walt AJ, editors: Mangement of Trauma: Pitfalls and Practice, 2nd ed. Baltimore, Williams and Wilkins, 1996, p. 765.)

Table 3 Fluid Required for the First 24 Hours Post-Burn

Adults = 2–4 ml LR/%TBSAB/Kg, BW

Children = 3–4 ml LR/%/TBSAB/Kg, BW + maintenance in children <30 kg

BW, Body weight; LR, lactated Ringer’s; TBSAB, total body surface area burned.

Because of the greater surface area per unit of body mass in children, the volume of fluid required for the first 24 hours is relatively greater than that for an adult. In all patients, one-half of the estimated volume should be administered in the first 8 hours after the burn. If the initiation of fluid therapy is delayed, the initial half of the volume estimated for the first 24 hours should be administered in the hours remaining before the 8th post-burn hour. The remaining half of the fluid is administered over the subsequent 16 hours.

The limited glycogen stores in a child may be rapidly exhausted by the marked stress hormone response to burn injury. Serum glucose levels in the burned child should be monitored, and 5% dextrose in lactated Ringer’s administered if serum glucose decreases to hypoglycemic levels. In the case of small children with small burns, the resuscitation fluid volume as estimated on the basis of burn size may not meet normal daily metabolic requirements. In such patients, maintenance fluids should be added to the resuscitation regimen.

The infusion rate is adjusted according to the individual patient’s response to the injury and the resuscitation regimen. The progressive edema formation in burned and even unburned limbs commonly make measurements of pulse rate, pulse quality, and even blood pressure difficult and unreliable as indices of resuscitation adequacy. Therefore, hourly urine output should be used as a measure of the adequacy of resuscitation. The fluid infusion rate is adjusted to obtain 30 ml of urine per hour in the adult and 1 mg/kg of body weight per hour in children weighing less than 30 kg. The administration of fluid is increased or decreased only if the hourly urinary output is one-third or more below, or 25% or more above, the target level for 2 successive hours. If in either adults or children the resuscitation volume infused in the first 12 hours will result in administration of 6 ml or more per percent of body surface area burned per kilogram of body weight in the first 24 hours, human albumin diluted to a physiologic concentration in normal saline should be infused and the volume of crystalloid solution reduced by a comparable amount.

Restoration of functional capillary integrity occurs at or near 24 hours after burn injury. Consequently, the volume of fluid needed for the second 24 hours post-burn is less, and colloidcontaining fluids can be infused to reduce further volume and salt loading. Human albumin diluted to physiologic concentration in normal saline is the colloid-containing solution of choice, infused in a dosage of 0.3 ml per percent of burn per kilogram of body weight for patients with 30%–50% burns, 0.4 ml per percent of burn per kilogram of body weight for patients with 50%–70% burns, and 0.5 ml per percent of burn per kilogram of body weight for patients whose burns exceed 70% of the total body surface area. Water containing 5% dextrose is also given in the amount necessary to maintain an adequate urinary output. The colloid-containing fluids for children are estimated according to the same formula, but half normal saline is infused to maintain urinary output and avoid inducing physiologically significant hyponatremia by infusion of large volumes of electrolyte-free fluid into the relatively small intravascular and interstitial volume of the child. Fluid infusion “weaning” should also be initiated during this time period, to further minimize volume loading. In a patient who is assessed to be adequately resuscitated, the volume of fluid infused per hour should be arbitrarily decreased by 25%–50%. If urinary output falls below target level, the prior infusion rate should be resumed. If urinary output remains adequate, the reduced infusion rate should be maintained over the next 3 hours, at which time another similar fractional reduction of fluid infusion rate should be made. This decremental process will establish the minimum infusion rate that maintains resuscitation adequacy in the second post-burn day.

Fluid management after the first 48 hours post-burn should permit excretion of the retained fraction of the water and salt loads infused to achieve resuscitation, prevent dehydration, and electrolyte abnormalities, and allow the patient to return to pre-burn weight by post-burn day 8–10. Infusion of the large volumes of lactated Ringer’s required for resuscitation commonly produces a weight gain of 20% or more and a reduction of serum sodium concentration to approximate that of lactated Ringer’s—that is, 130 mEq/l. Correction of that relative hyponatremia is facilitated by the prodigious evaporative water loss from the surface of the burn wound, which is the major component of the markedly increased insensible water loss that is present following resuscitation. Inadequate replacement of insensible water loss makes hypernatremia the most commonly encountered electrolyte disturbance in the extensively burned patient following resuscitation. Such hypernatremia should be managed by provision of sufficient electrolyte-free water to allow excretion of the increased total body sodium mass and replace insensible water loss to the extent needed to prevent hypovolemia.

Electrolyte abnormalities are frequently encountered in the immediate post-burn period. Hyperkalemia is frequently encountered and is typically a laboratory sign of hemolysis but may also be a sign of muscle destruction by high-voltage electric injury or a particularly deep thermal burn. Hyperkalemia may also occur in association with acidosis in patients who are grossly under-resuscitated. In the case of patients with high-voltage electric injury, emergency debridement of nonviable tissue and even amputation may be necessary to remove the source of the potassium. Hypophosphatemia is also extremely common after burn resuscitation due to either prolonged administration of parenteral nutrition or failure to supply sufficient phosphate to meet the needs of tissue anabolism following wound closure. Hypophosphatemia can be prevented and treated by appropriate dietary phosphate supplementation.

Ventilatory Support

The most critical factor in the initial assessment of a burn patient is the patency of the airway and the ability of the patient to maintain and protect the airway. Standard criteria should be used to determine the need for mechanical stabilization of the airway, also keeping in mind the systemic response to a major burn and the local response to an airway injury which may combine to cause progressive airway swelling and edema that will impair air flow. Circumferential torso burns will further impair the ability of the patient to respire. Allowing airway compromise to proceed to a critical state before intubating the patient and stabilizing the airway is not appropriate care. The safest approach when there is concern about the airway, particularly in a patient needing transport for definitive care, is to perform early intubation.

Patients suffering both inhalation injuries and thermal burns have a significantly increased incidence of complications and probability of death. While an inhalation injury alone carries a mortality of 5%–8%, a combination of a thermal injury plus inhalation injury can easily result in a mortality 20% above that predicted on the basis of age and burn size. Injuries to the airway are due to the direct damage by the inhaled products of combustion that cause inflammation and edema. Damage to the oropharynx and upper airway is related to the heat content of the inhaled material. In the distal airways, however, injury is principally related to the particulate material contained within the smoke and the chemical composition of inhaled materials. Moist heat, which occurs with steam, has 4000 times the heat-carrying capacity of dry smoke and is capable of causing more extensive thermal damage of the tracheobronchial tree.

Presenting signs and symptoms of an inhalation injury are stridor, hypoxia, and respiratory distress. The probability that a patient has suffered an inhalation injury is highly correlated with being burned in an enclosed space, having burns of the head and neck, and having elevated carbon monoxide levels. The extent and severity of the inhalation injury are directly related to the duration of exposure and the types of toxins contained within the smoke, and exacerbates the ensuing host inflammatory response. Activation of the inflammatory cascade results in the recruitment of neutrophils and macrophages which propagate the injury. Altered surfactant release causes obstruction and collapse of distal airway segments. As part of the response to injury, there is a marked and near-immediate increase in bronchial artery blood flow, which is associated with marked alterations in vascular permeability within the lung. The net effect is that extensive destruction and inflammation reduce pulmonary compliance and impair gas exchange, resulting in altered pulmonary blood flow patterns and ventilation perfusion mismatches.

Part of the initial management of the patient with inhalation injury should include a thorough evaluation of the airway, including bronchoscopy. The clinical findings of an inhalation injury on bronchoscopy include airway edema, inflammation, increased bronchial secretions, presence of carbonaceous material which can diffusely carpet the airway, mucosal ulcerations and even endoluminal obliteration due to sloughing mucosa, mucous plugging, and cast formation. Signs of gastric aspiration may also be evident. Repeat bronchoscopy can be performed for removal of debris and casts as well as surveillance for infection.

Carbon monoxide and cyanide gases are present in smoke and when inhaled are rapidly absorbed and cause systemic toxicity as well as impaired oxygen utilization and delivery. Carbon monoxide is an odorless, nonirritating gas that rapidly diffuses into the bloodstream and has a 240-fold greater affinity for hemoglobin than does oxygen, thus easily displacing oxygen. The diagnosis of carbon monoxide poisoning is made in a burn patient on the basis of circumstances of injury, physical findings, and the measurement of blood carboxyhemoglobin level. It is important to note that pulse oximetry values do not differentiate between carboxyhemoglobin and oxyhemoglobin. Patients with significant carbon monoxide intoxication can have normal oxygen saturations but will not have satisfactory blood oxygen content. Signs and symptoms of carbon monoxide poisoning are typically mild to absent when carbon monoxide-hemoglobin (carboxyhemoglobin) levels are 10% or less. When carboxyhemoglobin levels are between 10% and 30%, symptoms are present and often manifested by headache and dizziness. Severe poisoning is seen in patients with carboxyhemoglobin levels of greater than 50%, which may be associated with syncope, seizures, and coma. The primary treatment modality for carbon monoxide intoxication is the administration of increased levels of inspired oxygen.

Cyanide poisoning, which can occur in combination with carbon monoxide intoxication, disrupts normal cellular utilization of oxygen by binding to the cytochrome oxidase and resulting in cellular lactic acid production and greater cellular dysfunction due to uncoupling of the oxidative phosphorylation system. Blood concentrations of cyanide greater than 0.5 mg/l are toxic. Treatment of cyanide poisoning includes the administration of oxygen as well as decontaminating agents such as amyl and sodium nitrates. These compounds induce the formation of methemoglobin, which can act as a scavenger of cyanide. Hydroxycobalamin is the antidote of choice.

The goal of mechanical ventilation following inhalation injury is to minimize further damage to the airway and lung parenchyma while providing adequate gas exchange. This is best achieved through careful control of airway pressures, thereby limiting ventilationinduced barotrauma. Lung damage following burn injury is not homogeneous but patchy in distribution and requires that the level of positive end expiratory pressure (PEEP) used to maximize airway recruitment be limited to avoid ventilator-induced lung injury. In severe lung injury, mechanical ventilation can lead to increases in alveolar sheer forces and changes in pulmonary blood flow. This, in association with reductions in elasticity and alterations in lung compliance, results in further lung injury and ventilation perfusion abnormalities.

For patients who have signs of inhalation injury on bronchoscopy, it is beneficial to initiate aggressive management of retained secretions with the use of bronchodilators and mucolytic agents. Meticulous control of airway pressure should be practiced, with the early performance of torso escharotomies and prompt treatment of abdominal compartment syndrome. Mean airway pressures should be maintained at less than 32–34 cm of water and chemical paralysis liberally used, with a low threshold for conversion to pressurecontrolled ventilation with titration of tidal volumes to lessen further the risk of ventilator-induced barotrauma. This may require the acceptance of smaller than usual tidal volumes and permissive hypercapnia, which is acceptable as long as arterial blood pH is above 7.26 and the patient is hemodynamically stable.

Initial Wound Care

Initial wound care is focused on preventing further injury. Burning clothing should be removed, contact disrupted with metal objects that may retain heat, and only molten materials adherent to the skin surface should be cooled. Attempted cooling of burn wounds should not done, as local vasoconstriction can impair wound blood flow and extend the depth of the injury, as well as exacerbate systemic hypothermia. Patients being prepared for transport or admitted for definitive care should be placed in sterile or clean, dry dressings and be kept warm. Items of clothing or jewelry should be removed prior to the onset of burn wound edema to prevent further compromise of the circulation. In cases of chemical injury, the removal of contaminated clothing with copious water lavage of liquid chemicals and removal by brushing of powdered materials at the scene can limit the extent of the resultant burn injury. No attempt should be made at chemical neutralization, as such treatment would result in an exothermic reaction and cause additional tissue damage. The care provider must exercise extreme caution when working with victims of chemical injury to prevent self-contamination and personal injury.

After admission to the hospital and as soon as resuscitative measures have been instituted, the burn wounds should cleansed with warm fluids and a detergent disinfectant like chlorhexidine gluconate, which has an excellent antimicrobial spectrum. During cleansing, hypothermia must be avoided. Materials that are densely adherent to the wound, such as wax, tar, plastic, and metal, should be gently removed or allowed to separate during the course of subsequent dressing changes. Sloughing skin, devitalized tissue, and ruptured blisters should be gently trimmed from the wound. Careful wound cleansing should be done at each dressing change, with serial debridement of devitalized tissue performed as necessary. The wound should be monitored for signs of infection and change in depth from the initial assessment.

The damaged skin surface can serve as the portal for microbial invasion if it becomes progressively colonized. As microbial numbers increase within the wound to levels of 100,000 organisms per gram of tissue, an invasive wound infection and ultimately systemic sepsis may occur. Topically applied antimicrobial agents, which penetrate the burn eschar, are capable of achieving sufficient levels to control microbial proliferation within the wound. Systemic antibiotics are not indicated, as they do not adequately penetrate eschar. Topical antimicrobial agents are used in the prophylactic treatment of the burn wound and as a part of the management of burn wound infections. Topical agents do not heal the wound but prevent local burn wound infection from destroying viable tissue in wounds capable of spontaneous healing.

Silver sulfadiazine, the most widely used agent, is available as a 1% suspension in a water-soluble micronized cream base. The cream is easily applied and causes little or no pain on application. The cream can be directly applied to the wound as a continuous layer and covered over with a dressing. At each dressing change, the cream should be totally removed and not allowed to form a caseous layer that will obscure the wound bed. The most common toxic side effect of silver sulfadiazine is a transient leukopenia which, when it does occur in up to 15% of treated patients, resolves spontaneously without discontinuation of the drug. Silver sulfadiazine is active against a wide range of microbes, including Staphylococcus aureus, Escherichia coli, Klebsiella sp., many but not all Pseudomonas aeruginosa, Proteus sp., and Candida albicans.

Mafenide acetate was one of the first effective topical agents introduced for the management of the burn wound. It was initially available as Sulfamylon® Burn Cream, which is highly effective against Gram-positive and Gram-negative organisms but provides little antifungal activity. Mafenide acetate readily diffuses into the eschar and is the agent of choice for significant burns of the ears because it is also capable of penetrating cartilage. Drawbacks with the use of mafenide acetate include pain on application to partial-thickness burns, and limited activity against methicillin-resistant S. aureus. Mafenide acetate also inhibits carbonic anhydrase and may cause a self-limiting hyperchloremic acidosis. Mafenide acetate has more recently become available as a 5% aqueous solution and is an excellent agent to use on freshly grafted wounds and is not associated with the problems found with the cream formulation.

Silver nitrate as a 0.5% solution is effective against Gram-positive and Gram-negative organisms but does not penetrate the eschar. Silver nitrate solution leaches sodium, potassium, chloride, and calcium from the wound, in association with transeschar water absorption which can result in mineral deficits, alkalosis, and water loading. Those side effects can be minimized by giving sodium and other mineral supplements and modifying fluid therapy. These problems and the labor required to use silver nitrate effectively limit its routine use, and most see silver sulfadiazine as a highly acceptable alternative.

Silver-impregnated dressings have recently become available for clinical use. When the fabric base is in contact with wound fluids, the silver is released continuously and serves as the antimicrobial agent deposited onto the wound. The treatment interval with such a composite may extend up to several days depending on the fabrication design, with dressing changes needed only once or twice per week. The effectiveness of this membrane in treating extensive full-thickness burns is unconfirmed, and at present it is used to treat partialthickness burns.

In superficial partial-thickness burns, the use of bacitracin ointment represents a satisfactory alternative, particularly in patients with a known sulfa allergy. It may be used open, especially with superficial facial burns or as a component of a closed dressing. Other topical agents include antibiotic combinations such as triple antibiotic ointment (neomycin, bacitracin zinc, and polymyxin B) and Polysporin (bacitracin zinc and polymyxin B). In the case of methicillin-resistant staphylococci, mupirocin is a useful agent.

The application of topical antimicrobial agents to the burns of patients who will be transferred to a burn center may preclude the use of biological membrane dressings that must adhere to the wound surface to be effective. Additionally, as soon as a patient is admitted to a burn center, any previously placed dressing must be removed to permit the burn team to make a precise assessment of the extent of the burn and the depth of injury. Unless there will be an extended period of time before the patient is transferred to a burn center, the preferred initial management entails placing the patient in a dry dressing, particularly one with a nonadherent lining, and keeping the patient warm.

Burn Wound Excision and Grafting

Excision of the burned tissue and grafting are required for wounds that are full thickness in depth; this treatment is also now considered the optimum management of wounds with a mixed depth of injury. Wounds that are capable of spontaneous closure within 2–3 weeks post-injury can be managed expectantly, provided the cosmetic and functional outcomes will be acceptable. Wounds needing excision and closure should undergo excision as soon as possible, as this reduces the period of disability and the overall cost of the injury. In patients with a large burn wound, the timing and extent of the surgery are based on the patient’s relative physiologic stability and his or her capacity to undergo a major operative procedure. Early burn wound excision and closure in patients with large wounds shortens the length of hospitalization, reduces cost, and favorably impacts overall burn mortality.

Wounds that are small or linear in shape can be managed by excision of the burn and primary wound closure. This is useful in burns of the upper inner arm in the elderly, localized burns of a pendulous breast, abdominal burns, buttock injuries, and thigh burns. This approach works quite well when these wounds are excised early, before significant microbial colonization of the wound occurs.

In selected cases, the injury may be such that amputation of the burned part is most appropriate. In the patient with significant multisystem trauma, the expeditious removal of the burn injury might be the best option for the patient’s overall survival. A mangled extremity, which has also suffered a severe burn that is deemed nonsalvageable, should undergo early amputation. It is not necessary to extend the amputation to a level that allows closure with unburned tissue. If viable muscle is available to close the amputation site, that wound bed can be resurfaced with an autogenous skin graft. A grafted amputation site can, with a modern prosthesis, function as a durable stump. In a patient who is paraplegic and suffers an extensive, deep lower extremity burn injury, amputation can be a viable alternative to excision and grafting. A similar option may need to be considered for the patient in whom significant pre-existing peripheral vascular disease makes the likelihood of a healed and functional extremity very low.

Excision and grafting will be required for wounds not amenable to primary closure. The extent of the procedure that a patient can undergo is related to the patient’s age and physiologic status. Implicit in this approach is the use of experienced operating teams, an anesthesiologist who thoroughly understands the unique problems of the patient with a major body surface-area burn, and an operating room fully equipped to treat such a patient, as well as ready availability of blood products and the capacity to care for the patient postoperatively. A patient having this extent of surgery in essence undergoes a doubling of the surface area of “injury”—the now excised and grafted wound along with the partial-thickness wound produced by the donor site. In patients with wounds of a larger size (>30% total body surface area) or those who cannot tolerate a single procedure to achieve closure, staged excision of burned tissue is performed and the resulting wounds are closed with available cutaneous autografts or a biologic dressing.

The technique of burn wound excision is based on the depth of the wound and anatomic site to be excised. The most common method of excision is tangential. Excision of deep partial-thickness wounds to the level of a uniformly viable bed of deep dermis by tangential technique and immediate coverage with cutaneous autograft results in rapid wound closure with a typically excellent result. Optimally, the desired wound bed is achieved in one pass of the Weck blade as evidenced by diffuse bleeding. A frequent error is attempting this technique in wounds of an inappropriate depth and assuming that punctuate bleeding indicates a viable bed. Such wounds will heal with a poor take, as the bed contains marginally viable tissue incapable of supporting the cutaneous autograft. During the performance of this procedure, the amount of blood loss can be minimized with the use of a tourniquet on extremity burns or subeschar clysis containing epinephrine. An alternative to tangential excision is fascial excision, which involves excision of the burn wound to fascia or deep subcutaneous tissue. Viability of the fascia should be carefully assessed, and if the viability is questionable, the excision should be carried down to the underlying muscle prior to grafting.

The blood loss occurring with burn wound excision is related to the time of excision post-burn, the area to be excised, the presence of infection, and the type of excision. Donor sites can also represent a significant portion of the blood loss. The quantity of blood loss has been estimated to range from 0.45 to 1.25 ml/cm² of burn area excised. Adjunctive measures that can be used to control blood loss include elevation of limbs undergoing excision, applications of topical thrombin and/or vasoconstrictive agents in solutions to the excised wound and donor site, clysis of skin graft harvest sites and/or the eschar prior to removal, and application of tourniquets. Spray application of fibrin sealant can also reduce bleeding from the excised wound after release of the tourniquet. Blood loss will be compounded if the patient becomes coagulopathic, hypothermic, or acidotic during the procedure, a triad that can be avoided by partnership with an experienced anesthesiologist.

Grafting of the burn wound is usually done at the time of excision. However, there are instances where it advisable to stage the skin grafting procedure. The surgeon must be aware of the patient’s status throughout the surgical procedure and, if necessary, truncate the procedure. It may be best to perform only the excision, and stage the timing of the grafting. Additionally, if the viability of the wound bed is suspect, only excision should be performed. The wound can be dressed with a 5% Sulfamylon solution dressing or covered with a skin substitute and subsequently re-evaluated.

Several skin substitutes exist. The two most commonly used naturally occurring biologic dressings are human cutaneous allograft and porcine cutaneous xenograft. Both of these preparations are capable of becoming vascularized. Allograft skin can provide wound coverage for 3–4 weeks before rejection. Xenograft tissue is available as reconstituted sheets of meshed porcine dermis or as fresh or prepared split-thickness skin. Xenograft skin can be used to cover partial-thickness injuries or donor sites, which re-epithelialize beneath the xenograft. Additionally, various synthetic membranes have been developed that provide wound protection and possess vapor and bacterial barrier properties. Either Biobrane™ (Dow-Hickham, Sugarland, TX) or Integra™ (Integra LifeScience Corporation, Plainsboro, NJ) can be placed over freshly excised full-thickness wounds, and once fully vascularized, the epidermal analog is removed and the vascularized “neodermis” covered with a thin split-thickness cutaneous autograft. A permanent skin substitute for burn care victims continues to represent the holy grail. Presently, cultured epithelial autografts are commercially available but are limited in their use because of suboptimal graft take, fragility of the skin surface, and high cost. Use of any biologic dressing requires that the excised wound and the dressing that has been applied be meticulously examined on at least a daily basis. Submembrane suppuration or the development of infection necessitates removal of the dressing, cleansing of the wound with a surgical detergent disinfectant solution, and even re-excision of the wound if residual nonviable or infected tissue is present.

The proper management of the patient’s burn wounds is critical to achieve the optimum cosmetic and functional outcome and the timely return of the patient to full activity. In patients with major burns, the wound must be properly cared for and closure achieved expeditiously to lessen the level of physiologic disruption that accompanies a major burn. Failure to do so can result in invasive wound infection, chronic inflammation, erosion of lean body mass, progressive functional deficits, and even death.

Specialized Injuries: Electrical Burns

The principal mechanism by which electricity damages tissue is by conversion to thermal energy. Currents of 1000 volts and above are classified as high voltage. Upon contact with such currents, the body acts as a volume conductor. The electric current may induce cardiac and/or respiratory arrest, necessitating cardiopulmonary resuscitation at any time after injury. Arrhythmias may also occur, necessitating electrocardiogram monitoring for at least 24 hours after the last recorded episode of arrhythmia.

Two characteristics of high-voltage electric injury increase the incidence of acute renal failure in patients. First, there is often extensive unapparent subcutaneous tissue injury in a limb underlying unburned skin. The limited cutaneous injury may lead to gross underestimation of resuscitation fluid needs. Second, the mass of muscle injured by the electric current may cause rhabdomyolysis, resulting in direct damage to the renal tubules. Resuscitation fluids should be based on the extent of burn visible plus the estimated daily needs of the patient, adjusted according to the patient’s response. If the urine contains hemochromogens (dark red pigments), fluid should be administered to obtain 75–100 ml of urine per hour, with sodium bicarbonate added to the fluids to alkalinize the urine. If the hemochromogens do not clear promptly, or the patient remains oliguric, 25 g of mannitol should be given as a bolus and 12.5 g of mannitol added to each liter of lactated Ringer’s until the pigment clears. The addition of mannitol, an osmotic diuretic, makes measurements of urine output unreliable as a monitor of the adequacy of resuscitation, and central venous monitoring is indicated.

When the body functions as a volume conductor, current flow is proportional to the cross-sectional area of the body part involved. Consequently, severe tissue destruction may occur in a limb with a relatively small cross-section area, whereas relatively little tissue damage may occur as current flows through the trunk. Damage to the muscle in a limb is often associated with marked increase in the pressure within the compartment containing the damaged muscle, which, if unrelieved, may cause further tissue necrosis. A limb compartment, which is hard to palpation, should alert one to the need for immediate surgical exploration. Operative intervention and extensive fasciotomy are mandated by extensive deep tissue necrosis, compartment syndrome, or persistent or progressively severe hyperkalemia. The extent of destruction may necessitate amputation at the time of exploration, particularly if the nonviable muscle is the source of persistent hyperkalemia. Following debridement or amputation, the wound should be dressed open. The patient is returned to the operating room in 24–36 hours for reinspection and further debridement of nonviable tissue if necessary. When all tissue in the wound is viable, it may be closed definitively.

Tissue damage can also be caused by low-voltage or house current. Burns of the oral commissure occur in young children who bite electric cords or suck on the end of a live extension cord or an electric outlet. The lesion may have the characteristics of full-thickness tissue damage, but early surgical debridement may only accentuate the defect and should be avoided. These injuries will usually heal with minimal cosmetic sequelae, which can be addressed electively if needed.

Specialized Injuries: Chemical Injuries

A variety of chemical agents can cause tissue injury as a consequence of an exothermic chemical reaction, protein coagulation, desiccation, and delipidation. The severity of a chemical injury is related to the concentration and amount of chemical agent and the duration with which it is in contact with tissue. Consequently, initial wound care to remove or dilute the offending agent takes priority in the management of patients with chemical injuries, brushing away dry material and instituting immediate, copious water lavage. For patients in whom extensive surface injury has occurred, the irrigation fluid should be warmed to prevent the induction of hypothermia.

The appearance of skin damaged by chemical agents can be misleading. In the case of patients injured by strong acids, the involved skin surface may have a silky texture and a light brown appearance, which may be mistaken for a sunburn rather than the full-thickness injury that it is. Skin injured by delipidation caused by petroleum distillates may be dry, show little if any inflammation, and appear to be undamaged but yet found to be a full-thickness injury on histologic examination.

Specialized Injuries: Cold Injuries

Injuries occurring secondary to environmental exposure can result in local injuries, frostbite, or systemic hypothermia. The pathophysiology of frostbite is crystal formation due to freezing of both extracellular and intracellular fluids. Patients presenting with frostbite will have coldness of the injured body part, with loss of sensation and proprioception. On initial examination, the limb may well appear pale, cyanotic, or have a yellow-white discoloration. During rapid rewarming at 40°–42° C in water for 15–30 minutes, hyperemia will occur followed by pain, paresthesias, and sensory deficits. Greater than 1 week may pass before a true determination of the depth and extent of the injury can be obtained. The injured extremity should be elevated in an attempt to control edema and padded to avoid pressure-induced ischemia as a secondary insult. Frostbite wounds are tetanus-prone wounds, and therefore tetanus toxoid should be administered based on the patient’s immunization status.

MORBIDITY AND COMPLICATIONS MANAGEMENT

Early Complications

As resuscitation proceeds and edema forms beneath the inelastic eschar of encircling full-thickness burns of a limb, blood flow to underlying and distal unburned tissue may be compromised. Cyanosis of distal unburned skin and progressive paresthesias, particularly unrelenting deep tissue pain, which are the most reliable clinical signs of impaired circulation, may become evident only after relatively long periods of relative or absolute ischemia. Since the full-thickness eschar is insensate, the escharotomy can be performed as a bedside procedure without anesthesia, using a scalpel or an electrocautery device. On an extremity, the escharotomy incision, which is carried only through the eschar and the immediately subjacent superficial fascia, is placed in the mid-lateral line and must extend from the upper to the lower limit of the burn wound (Figure 2). The circulatory status of the limb should then be reassessed. If that escharotomy has not restored distal flow, another escharotomy should be placed in the mid-medial line of the involved limb. A fasciotomy may be needed when there has been a delay in restoring the patient’s limb circulation and in particular if the patient is receiving a massive fluid load.

Figure 2 The dashed lines indicate the preferred sites of escharotomy incisions for the limbs (mid-lateral and mid-medial lines), thorax (anterior axillary lines and costal margin), and neck (lateral aspect). The thickened areas of the lines on the limbs emphasize the importance of carrying the incisions across involved joints.

(Used with permission from Martin RR, Becker WK, Cioffi WG, and Pruitt BP Jr: Thermal Injuries. In Wilson RF and Walt AJ, editors: Management of Trauma: Pitfalls and Practice, 2nd ed. Baltimore, Williams and Wilkins, 1996, p. 765.)

Edema formation beneath encircling full-thickness truncal burns can restrict the respiratory excursion of the chest wall. If the limitation of chest wall motion is associated with hypoxia and elevated peak inspiratory pressure, chest escharotomy is indicated to restore chest wall motion and improve ventilation. These escharotomy incisions are placed in the anterior axillary line bilaterally, and if the eschar extends onto the abdominal wall, the anterior axillary line incisions are joined by a costal margin escharotomy incision (see Figure 2).

The timely administration of adequate fluid as detailed previously has essentially eliminated acute renal failure after burn injury. Far more common today are the complications of excessive resuscitation—that is, compartment syndromes and pulmonary compromise. Compartment syndromes can be produced in the calvarium, muscle compartments beneath the investing fascia, and the abdominal cavity.

Excessive fluid administration may also cause formation of enough ascitic fluid and edema of the abdominal contents resulting in intra-abdominal hypertension. The abdominal compartment syndrome represents progression of intra-abdominal hypertension to the point of organ dysfunction, including decreased cardiac output with resultant hypotension, increased peak airway pressures, oliguria, and worsening metabolic acidosis due to hypoperfusion. Bladder pressure measurements serve as an indirect measurement of intra-abdominal pressures. Elevation of the bladder pressure above 25 mm Hg should prompt therapeutic intervention, beginning with adequate sedation, reduction of fluid infusion rate, diuresis, and paracentesis. If organ failure becomes evident, decompressive laparotomy is indicated.

Compartment syndromes may also occur in the muscle compartments underlying the investing fascia of the limbs of burn patients, even in limbs that are unburned. To assess compartment pressure, the turgor of the muscle compartments should be assessed on a scheduled basis by simple palpation. A stony hard compartment is an ominous finding which should prompt direct measurement of intracompartmental pressure. A muscle compartment pressure of 25 mm of mercury or more necessitates performing a fasciotomy of the involved compartment in the operating room using general anesthesia.

Metabolic and Nutritional Support

Burn injury alters the distribution and utilization of nutrients as well as the metabolic rate. All of these post-burn metabolic changes must be considered in planning nutritional support of the hypermetabolic burn patient. This is necessary to minimize loss of lean body mass, accelerate convalescence, and restore physical abilities. Bedside indirect calorimetry is the most accurate means of determining metabolic rate and nutritional requirements, but bedside metabolic care may not always be available. A rule of thumb estimate for nutritional needs of patients whose burns exceed 30% of the body surface area is 2000–2200 kcal and 12–18 g of nitrogen per square meter of body surface per day.

At the time of admission, patients should have a nasogastric or nasoduodenal tube placed. It is preferable to start enteral feedings as soon as possible after the patient is admitted. When feedings are initiated early, the desired rate of administration can typically be reached within 24–48 hours after admission. If the patient is intolerant to gastric feedings, the administration of metoclopramide will often resolve the problem. If a patient fails to respond to metoclopramide, an attempt should be made to pass a feeding tube distal to the ligament of Treitz. In patients who become intolerant of enteral feedings, or who develop gastrointestinal complications that prevent enteral feeding, total parenteral nutrition will be required.

Burn injury induces insulin resistance, which may lead to hyperglycemia. The maintenance of blood glucose values below 120 mg/dl with aggressive insulin infusion has been demonstrated to have a favorable impact on the outcome of critically ill patients. Potassium and phosphorous must also be given to meet the patient’s needs, which often exceed initial estimates, particularly when large loads of glucose are being given with exogenous insulin. Over the course of the patient’s care, as the open wound area decreases and the hypermetabolic state slowly resolves, the nutrient load should be adjusted so that balance is maintained between metabolic needs and substrate delivery, preventing overfeeding.

TRANSPORTATION AND TRANSFER

Many important advances have been made in the care and management of burn-injured victims during the past 50 years. One of the more significant advances has been the recognition of the benefits of a team approach in the care of critically injured burn patients. The American College of Surgeons and the American Burn Association have developed optimal standards for providing burn care and a burn center verification program that identifies those units that have undergone peer review of their performance and outcomes. Patients with burns and/or associated injuries and conditions listed in Table 1 should be referred to a burn center.

Once the decision has been made to transfer a patient to a burn center, there should be physician-to-physician communication regarding the patient’s status and need for transfer. It is critical that the patient be properly stabilized in preparation for the transfer. During transport the need to perform life-saving interventions such as endotracheal intubation or re-establishing vascular access may be very difficult to accomplish in the relatively unstable and limited space of a moving ambulance or a helicopter in flight. That difficulty makes it important to institute hemodynamic and pulmonary resuscitation and to achieve “stability” prior to undertaking transfer by either aeromedical or ground transport. A secure large-bore intravenous cannula must be in place to permit continuous fluid resuscitation. Patients should be placed on 100% oxygen. If there is any question about airway adequacy, an endotracheal tube should be placed and mechanical ventilation instituted. The hourly urinary output should also be monitored, with fluid infusion adjusted as necessary. All patients should be placed NPO, and those with a greater than 20% body surface area burn require placement of a nasogastric tube. The burn wound should be covered with a clean and/or sterile dry sheet. The application of topical antimicrobial agents is contraindicated prior to transfer, since they will have to be removed on admission to the burn center. Maintenance of the patient’s body temperature is vital. The patient should be covered with a heat-reflective space blanket to minimize heat loss. Burn wounds, as tetanus-prone wounds, mandate immunization in accordance with the recommendations of the American College of Surgeons.

MORTALITY

Early post-burn renal failure as a consequence of delayed and/or inadequate resuscitation has been eliminated, and inhalation injury as a comorbid factor has been tamed. Invasive burn wound sepsis has been controlled, and early excision with prompt skin grafting and general improvements in critical care have reduced the incidence of infection, eliminated many previously life-threatening complications, and accelerated the convalescence of burn patients. Mortality for various ages and burn sizes is reported in Table 4. Not only has survival improved, but the elimination of many life-threatening complications and advances in wound care have improved the quality of life of even those patients who have survived extensive, severe thermal injuries.

Table 4 Changes in Burn Patient Mortality at U.S. Army Burn Center, 1945–1991

Age Group	Percentage of Body Surface Burn Causing 50% Mortality (LA₅₀)
	1945–1957	1987–1991
Children (0–14)	51	72 ^a
Young adults (15–40)	43	82 ^b
Young adults (15–40)	43	73 ^c
Older adults	23	46 ^d

Source: Pruitt BA Jr, Gamelli RL: Burns. In Britt LD, Trunkey DD, Organ CH, Feliciano DV, editors: Acute Care Surgery. New York, Springer, 2006, p. 155, with permission.

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INCIDENCE

MECHANISM OF INJURY

PATHOPHYSIOLOGY

Local Effects

Systemic Response

GRADING OF BURN WOUND DEPTH

RESUSCITATION PRIORITIES

Fluid Administration

Ventilatory Support

Initial Wound Care

Burn Wound Excision and Grafting

Specialized Injuries: Electrical Burns

Specialized Injuries: Chemical Injuries

Specialized Injuries: Cold Injuries

MORBIDITY AND COMPLICATIONS MANAGEMENT

Early Complications

Metabolic and Nutritional Support

TRANSPORTATION AND TRANSFER

MORTALITY

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