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.

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