Approximately 1.25 million people burned annually in the United States, where 30,000 patients require admissions to burn centers every year and about 3400 die.1,2 Burns requiring hospitalization typically include burns greater than 10% of the total body surface area (TBSA) or significant burns of the face, hands, feet, or perineum.
The highest incidence of burn injury occurs during the first few years of life and between 20 and 59 years of age. The major causes of severe burn injury in younger patients are liquid scalds, and flame burns are more common in adult patients.2 Most burn deaths are caused by flame burns, while liquid scald burns account for the second largest number of deaths.
Between 1971 and 1991, burn deaths decreased by 40% with a concomitant 12% decrease in deaths associated with inhalation injury.3 Since 1991, burn deaths per capita have decreased 25% according to statistics from the Centers for Disease Control and Prevention (www.cdc.gov/ncipc/wisqars). These improvements were in part due to prevention strategies resulting in fewer burns of lesser severity as well as significant advances in treatment techniques particularly in children. In 1949, Bull and Fisher first reported the expected 50% mortality rate for burn sizes in several age groups based upon data from their unit.4 They reported that approximately one-half of children aged 0–14 years with 49% TBSA burns die.4 This dismal statistic has dramatically improved, with the latest reports indicating 50% mortality for 98% TBSA burns in children 14 years and younger.5,6 A healthy child with any size burn might be expected to survive.7 Nevertheless, a 60% TBSA burn has been shown to be an important threshold that, if exceeded, can increase the risk of death.8,9 The same cannot be said, however, for those aged 45 years or older, where improvements have been more modest. This is especially true in patients over 65 years of age, where a 35% burn still kills half of the patients.10
These dramatic improvements in mortality after massive burns are due to better resuscitation, improvements in wound coverage by early excision and grafting, better support of the hypermetabolic response to injury, early nutritional support, more appropriate control of infection, and improved treatment of inhalation injuries. Future breakthroughs in the field are likely to be in the area of faster and better return of function and improved cosmetic outcomes.
Burn Center Referral Criteria
Some burn patients benefit from treatment in specialized burn centers. These centers have dedicated resources and the required multidisciplinary approach to maximize outcomes from such devastating injuries.11 The American Burn Association and the American College of Surgeons Committee on Trauma have established guidelines to identify patients who should be transferred to a specialized burn center as follows12:
Partial-thickness burns greater than 10% TBSA.
Burns that involve the face, hands, feet, genitalia, perineum, or major joints.
Third-degree burns in any age group.
Electrical injury, including lightning injury.
Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality.
Any patient with burns and concomitant trauma in which the burn injury poses the greatest risk of morbidity or mortality.
Burned children in hospitals without qualified personnel or equipment for the care of children.
Burn injury in patients who will require special social, emotional, or rehabilitative intervention.
Burns are classified into six causal categories, three zones of injury, and five depths of injury (Table 48-1). The causes include fire, scald, contact, chemical, electrical, and radiation. Fire burns can be divided into flash and flame burns, while scald burns can be divided into those caused by liquids, grease, or steam. Liquid scald burns can be further divided into spill and immersion scalds.
TABLE 48-1Definition of Burn Types, Zones, and Depth of Injury ||Download (.pdf) TABLE 48-1 Definition of Burn Types, Zones, and Depth of Injury
|Burn ||Categories ||Zones of injury ||Burn depth |
|Fire ||Flash ||Zone of coagulation ||First degree (superficial) |
| ||Flame |
|Scald ||Liquid ||Zone of stasis ||Superficial second degree (superficial partial thickness) |
| ||– Spill || || |
| ||– Immersion || || |
| ||Grease ||Zone of hyperemia ||Deep second degree (deep partial thickness) |
| ||Steam || ||Third degree (full thickness) |
|Contact ||Fourth degree (deep organ involvement) |
Flame, scald, and contact burns cause cellular damage primarily by the transfer of energy that induces coagulative necrosis. On the other hand, direct damage to cellular membranes is the cause of injury in chemical and electrical burns.
The skin generally provides a barrier to limit transfer of heat energy to underlying tissues; however, after the source of burn is removed, the response of local tissues can lead to further injury. The necrotic area of a burn is termed the “zone of coagulation.” The area immediately surrounding the necrotic zone has a moderate degree of injury that initially causes a decrease in tissue perfusion. This area is termed the “zone of stasis” and, depending on the environment of the wound, can progress to coagulative necrosis if local blood flow is not maintained. Thromboxane A2, a potent vasoconstrictor, is present in high concentrations in burn wounds, and local application of thromboxane inhibitors has been shown to improve blood flow and may decrease this zone of stasis.13,14 Antioxidants15,16 and inhibition of neutrophil-mediated processes17 may also improve blood flow, preserve this tissue, and affect the depth of injury. Endogenous vasodilators such as calcitonin gene-related peptide and substance P, whose levels are increased in the plasma of burn patients,18 may play a role, also. The last area, the zone of hyperemia, is formed as a result of vasodilation from inflammation surrounding the burn wound. This zone contains clearly viable tissue from which the healing process begins (Fig. 48-1).
Zones of injury after burn. Factors likely to affect the zone of stasis determine the extension of injury from the original zone of coagulation.
The hypermetabolic response and massive release of inflammatory mediators in the wound and in other tissues is seen with a significant burn. This hypermetabolism is associated with alterations in blood serum glucose as well as lipids, and it typically occurs in the ebb phase (first 14 hours) and flow phase (until 5 days post burn).19,20,21 Many mediators have been proposed to explain the changes in permeability after burns, including prostaglandins, catecholamines, histamine, bradykinin, vasoactive amines, leukotrienes, and activated complement.22 Mast cells in the burned skin release histamine in large quantities immediately after injury,23 causing a characteristic response in venules by increasing the space in intercellular junctions.24 The use of antihistamines in the treatment of burn edema, however, has had limited success with the possible exception of H2-receptor antagonists.25 In addition, aggregated platelets release serotonin, which plays a major role in the formation of edema. This agent acts directly to increase pulmonary vascular resistance and indirectly aggravates the vasoconstrictive effects of various vasoactive amines. Serotonin blockade has been shown to improve cardiac index, decrease pulmonary artery pressure, and decrease oxygen consumption after burns.26
As previously noted, another mediator likely to play a major role in changes in vascular permeability and tone is thromboxane A2. Levels of thromboxane increase dramatically in the plasma and wounds of burn patients.27,28 This potent vasoconstrictor leads to platelet aggregation in the wound, contributing to expansion of the zone of stasis. It also causes prominent mesenteric vasoconstriction and decreased blood flow to the gut in animal models with compromised gut mucosal integrity and immune function.29
Patients with major burn injury have the highest metabolic rate of all critically ill or injured patients.30 The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, loss of lean body mass and body weight, accelerated breakdown of glycogen and protein, lipolysis, and immune depression.31,32 This response is mediated by increases in circulating levels of catabolic hormones including catecholamines, cortisol, and glucagon.32,33
Pharmacological agents have been used to attenuate catabolism and to stimulate growth after burn injury. To further minimize erosion of lean body mass, administration of anabolic hormones such as growth hormone, insulin, insulin-like growth factor (IGF)/IGF-binding protein-3, oxandrolone, fenofibrate, and catecholamine antagonists such as propranolol has been studied. These agents contribute to maintenance of lean body mass and promote wound healing.34,35,36,37,38,39,40
Changes in Organ Function
Major burn injury results in multiple organ dysfunction. Cardiac effects include marked loss of plasma volume, increased peripheral vascular resistance, and decreased cardiac output.41,42,43,44 Pulmonary effects include a decrease in pulmonary static compliance.45 These changes are associated with mild direct cardiac damage.46 Renal blood flow decreases with a fall in glomerular filtration rate, which may result in renal dysfunction. Metabolic changes are characterized by an early depression followed by a marked, sustained increase in resting energy expenditure as well as increased lipolysis, proteolysis, and oxygen consumption. This is driven, in part, by an increase in production of catecholamines, cortisol, and glucagon.47 Increased peripheral lipolysis results in hepatic steatosis, and a fatty liver is caused by breakdown of triglycerol into free fatty acids. Like steatosis, peripheral lipolysis contributes to morbidity and mortality through fatty infiltration of various organs. All burn-related metabolic responses last more than 2 years post burn.21 There is a generalized impairment in host defenses, with depressed production of immunoglobulin, decreased opsonic activity, and depressed bactericidal activity.48 This leads to an increased susceptibility to infections.
The patient should be removed from the source of the burn to stop the burning process, and clothing and jewelry should be immediately removed. The patient should be kept warm by being wrapped in a clean sheet or blanket. The immediate treatment of a burn patient should proceed as with any trauma patient, and any potential life-threatening injuries should be identified and treated.
Assessment of the patient starts with the airway. One hundred percent oxygen is administered, and oxygen saturation is monitored. Stridor, wheezing, tachypnea, and hoarseness indicate impending airway obstruction due to an inhalation injury or edema, and immediate treatment is required. If the patient has labored breathing or signs of obstruction, immediate intubation should be performed with in-line stabilization of the neck if an injury to the cervical spine is suspected.
Arterial blood gas and carboxyhemoglobin (COHb) levels should be obtained when inhalation injury is suspected. Carbon monoxide (CO) has an affinity for hemoglobin (Hb) that is 210–280 times that of oxygen, and COHb can falsely elevate oxygen saturation levels determined colorimetrically. Therefore, use of a pulse oximeter may not be effective, as patients with CO poisoning may show falsely normal oxygen saturation levels. Use of a pulse CO-oximeter enables measurement of absorption at several wavelengths to distinguish oxyhemoglobin from COHb saturation and determines blood oxygen saturation more reliably including the total amount of Hb, COHb, met-Hb, and reduced Hb.49
The treatment for CO inhalation is 100% O2 by endotracheal tube or face mask. This will decrease the half-life of CO from 4–6 hours at room air to 40–80 minutes with 100% O2. In three atmosphere absolute 100% oxygen in a hyperbaric chamber, the half-life decreases further to 15–30 minutes. In addition, full-thickness circumferential burns of the chest can interfere with ventilation. Bilateral expansion of the chest should be observed to document equal air movement. If the patient is on a ventilator, airway pressure and Pco2 should be monitored. Rising airway pressure and Pco2 indicates compromised ventilation, and an escharotomy should be performed to allow better movement of the chest and improve ventilation.
Noninvasive measurement of blood pressure may be difficult in patients with burned extremities, and these individuals may need an arterial line so that their blood pressure can be monitored during transfer or resuscitation. A radial arterial line may not be reliable in patients with upper extremity burns and is difficult to secure. Therefore, the insertion of a femoral arterial line may be more appropriate.
Abdominal injuries and fractures may be present in patients who have been burned, as well. Each patient should be fully assessed for associated injuries that may be more immediately life-threatening. The burn wounds can be addressed after standard evaluation.
As previously noted, burn patients should initially be placed on sterile or clean sheets. Cold water and ice may, in large burns, harm patients by inducing hypothermia and should be avoided. The patient should be kept warm and the wounds clean until assessment by the physicians responsible for definitive care of the burns. A nasogastric tube and bladder catheter are placed to decompress the stomach and to monitor urine output.
After a large burn, there is a systemic capillary leakage that increases with burn size. Capillaries usually regain competence after 18–24 hours if resuscitation has been successful. Waiting for longer times until initiating resuscitation of burn patients results in poorer outcomes, and delays should be minimized.50 The best intravenous (IV) access can be obtained with short large-bore peripheral catheters through unburned skin; however, veins beneath burned skin can be accessed to avoid a delay in obtaining IV access. Central venous lines are required when peripheral IV access is difficult. Intraosseous access is another option until IV access is accomplished. Lactated Ringer’s solution without dextrose is the fluid of choice except in children less than 2 years. Infants should receive some 5% dextrose in intravenous solutions to prevent hypoglycemia because they have limited glycogen stores. This can be accomplished by giving 5% dextrose as maintenance fluid and lactated Ringer’s solution as resuscitation fluid.
The initial rate can be rapidly estimated by multiplying the estimated TBSA burned by the weight in kilograms, which is divided by 4 to get an hourly rate for the first eight hours (ie, a rearrangement of the Parkland formula). Thus, the rate of infusion for an 80-kg man with a 40% TBSA burn would be 40% TBSA × 80 kg /4 = 800 mL/h for the first 8 hours.
Different formulas have been devised to assist the clinician in determining the proper amount of resuscitation fluid. Early work by Baxter and Shires formed the basis for modern fluid resuscitation protocols.51 They showed that edema fluid in burn wounds is isotonic and contains the same amount of protein as plasma and that the greatest loss of fluid is into the interstitial fluid compartment. They used various volumes of intravascular fluid to determine the optimal delivered amount in terms of cardiac output and extracellular volume in a canine burn model. These findings led to a successful clinical trial of the “Parkland formula” in resuscitating burn patients (Table 48-2). From their findings, they also concluded that colloid solutions should not be used in the first 24 hours until capillary permeability returns closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after a burn (8 hours) and, thus, colloids could be used earlier.52
TABLE 48-2Resuscitation Formulas ||Download (.pdf) TABLE 48-2 Resuscitation Formulas
|Formula ||Crystalloid volume ||Colloid volume ||Free water |
|Parkland ||4 mL/kg/% TBSA burn ||None ||None |
|Brooke ||1.5 mL/kg/% TBSA burn ||0.5 mL/kg/% TBSA burn ||2.0 L |
|Galveston (pediatric) ||5000 mL/m2 burned + 1500 mL/m2 total ||None ||None |
Moncrief and Pruitt studied the hemodynamic effects of fluid resuscitation in burns, which resulted in the Brooke formula (Table 48-2). They showed that fluid loss in moderate burns results in an obligatory 20% decrease in both extracellular fluid and plasma volume during the first 24 hours after injury. In the second 24 hours, plasma volume returns to normal with the administration of colloid. Cardiac output is low on the first post burn day in spite of resuscitation, but subsequently increases to supernormal levels as the flow phase of hypermetabolism is established.22 Since these studies, it has been found that much of the fluid needs are due to capillary leakage that permits passage of large molecules and water into the interstitial space. Intravascular volume follows the gradient into the burn wound and non-burned tissues. Approximately 50% of fluid resuscitation needs are sequestered in nonburned tissues in 50% TBSA burns.53
Hypertonic saline solutions have theoretic advantages in the resuscitation of burn patients. As these solutions have been shown to decrease net fluid intake,54 decrease edema,55 and increase lymph flow by transferring volume from the intracellular space to the interstitium. During the use of these solutions, care must be taken to avoid serum sodium concentrations greater than 160 mEq/dL.22 Of note, it has been shown that patients with over 20% TBSA burns and randomized to resuscitation with either hypertonic saline or lactated Ringer’s solution do not have significant differences in total volume requirements or in changes in percent weight gain in the days following the burn.56 Other investigators have found an increase in renal failure with hypertonic solutions that has tempered further enthusiasm for their use in resuscitation.57 Some burn centers have successfully used a modified hypertonic solution by adding one ampule of sodium bicarbonate to each liter of lactated Ringer’s solution.58 Further research will need to be conducted to determine the optimal formula to reduce over-resuscitation and maintain adequate cellular function.59
Of interest, it has been shown that resuscitation volumes required in the severely burned patient decrease when high-dose intravenous ascorbic acid is administered during resuscitation. This is associated with decreased weight gain and improved oxygenation.60
Most burn centers use guidelines similar to the Parkland or Brooke formulas, with varying amounts of crystalloid and colloid solutions being administered for the first 24 hours post burn (see Table 48-2). These formulas are guidelines to the amount of fluid necessary to maintain adequate perfusion.
In pediatric burns, the commonly used formulas are modified to account for changes in surface area-to-mass ratios. Compared to adults, children have a larger body surface area relative to their weight and generally have greater fluid needs during resuscitation. The Galveston formula for children based on body surface area uses 5000 mL/m2 TBSA burned for resuscitation + 1500 mL/m2 TBSA for maintenance in the first 24 hours (Table 48-2). This formula accounts for both the resuscitation fluid requirements and maintenance needs of children with burns.
All these formulas calculate the amount of volume given in the first 24 hours, with half being given in the first 8 hours and the other half being given over the next 16 hours.
Both under- and over-resuscitation should be prevented. Under-resuscitation may lead to multiple organ failure caused by decreased perfusion; however, under-resuscitation is uncommon.61 On the other hand, over-resuscitation (so called “fluid creep”59) may result in pulmonary edema, extremity and abdominal compartment syndromes, as well as pericardial effusions which may increase risk of acute respiratory distress syndrome (ARDS).62,63,64,65 Over-resuscitation can be prevented by monitoring urine output, which should be maintained at 0.5 mL/kg/h in adults and 1.0 mL/kg/h in children. Other parameters such as heart rate, blood pressure, mental status, and peripheral perfusion should be monitored, also. The rate of intravenous fluid infusion should be adjusted hourly based on the patient’s response to the particular fluid volume administered.
Determination of Burn Depth
The depth of burn determines the outcome in terms of survival and scarring. Though technologies such as laser Doppler imaging66,67 with multiple sensors hold promise for quantitatively determining burn depth, it is most accurately assessed by the judgment of experienced physicians. These measurements may give objective evidence of tissue loss and assist the physician in the proper choice of treatment. Determination of depth is critical in the treatment plan, as there are wounds that will heal with only local treatment and those that will require operative intervention for timely healing. Being able to identify patients who will need operative intervention will facilitate care.
Superficial burns (first-degree) are confined to the epidermis. These burns are painful, erythematous, and blanch to the touch with an intact epidermis without blister. Examples include sunburn and a minor scald or flash burn. These burns will heal in 3–5 days, will not result in scarring, and treatment is aimed at comfort with the use of topical soothing salves with or without aloe and nonsteroidal anti-inflammatory drugs or acetaminophen.
Partial-thickness (second-degree) burns are divided into two types (Figs. 48-2 and 48-3), superficial and deep. All partial-thickness burns have some degree of dermal injury, and the division is based on the depth of injury into this level. Superficial partial-thickness burns are erythematous, painful, and wet. They blanch to touch and often form blisters. Blistering may not occur for some hours following injury. Burns thought to be first degree may subsequently be diagnosed as partial-thickness burns by the second day. These wounds will spontaneously reepithelialize in 7–14 days from epidermal structures retained in the rete ridges, hair follicles, and sweat glands. Deep partial-thickness burns extending into the reticular dermis will appear dry, paler than pink, or mottled. They may not blanch to touch, but will remain painful to pinprick. In deeper partial-thickness burns, sensation becomes blunted (less sensitive to pinprick than surrounding normal skin). Capillaries may refill slowly after compression or not at all. These burns will heal in 21–28 days or longer, depending on the depth of burn, by reepithelialization from hair follicles and keratinocytes in sweat glands. Nevertheless, deep partial-thickness burns may require skin grafting to facilitate healing. The longer the wound takes to heal, the worse the scarring will be.
Right hand showing superficial partial-thickness burn; the typically occurring blister has been removed. Superficial partial-thickness burn has a wet, pink, and moist appearance.
Left hand showing deep partial-thickness burn, typically with mottled pink or white areas.
Full-thickness (third-degree) burns are burns that extend through the dermis down to the subcutaneous tissue. They are characterized by a firm leathery eschar that is painless and yellow, grey, white, or cherry red in color (Figs. 48-3 and 48-4). The eschar is insensitive to pinprick but may be sensitive to pressure on palpation. No epidermal or dermal appendages remain, and these wounds must heal by reepithelialization from the wound edges by contraction, which takes a protracted time. Full-thickness burns require excision and skin grafting with autograft skin so that they can heal in a timely fashion.
Left hand showing full-thickness burn. Grey, yellow, and cherry-red areas can be defined as full-thickness burns.
Fourth-degree burns involve other tissues beneath the skin, such as muscle, tendon, and bone. They have a charred appearance that usually results from high-voltage electrical injury or from prolonged duration of contact with fire or an object such as a hot muffler.
Determination of Burn Size
The most commonly used method of determining the burn size in adults is the “rule of nines” (Fig. 48-5). Each upper extremity and the head and neck are 9% of the TBSA. Each lower extremity, the anterior trunk, and posterior trunk are 18% each. Finally, the perineum and genitalia are 1% of the TBSA. Another method of estimating burn size is using the patient’s open hand including the digits, which is approximately 1% TBSA.
Determining burn size by the “rule of nines.”
The Berkow formula or Lund Browder chart can be helpful in determining burn size in children (Table 48-3). Children have a relatively larger portion of body surface area in the head and neck and a smaller surface area in the lower extremities. Infants have 21% of the TBSA in the head and neck and 14% in each leg, which incrementally approaches adult proportions with increasing age.
TABLE 48-3Berkow Chart for Estimation of Burn Size in Children ||Download (.pdf) TABLE 48-3 Berkow Chart for Estimation of Burn Size in Children
|Area ||1 y ||1–4 y ||5–9 y ||10–14 y ||15 y |
|Head ||19 ||17 ||13 ||11 ||9 |
|Neck ||2 ||2 ||2 ||2 ||2 |
|Ant. trunk ||13 ||13 ||13 ||13 ||13 |
|Post. trunk ||13 ||13 ||13 ||13 ||13 |
|Buttock ||2.5 ||2.5 ||2.5 ||2.5 ||2.5 |
|Genitalia ||1 ||1 ||1 ||1 ||1 |
|Upper arm ||4 ||4 ||4 ||4 ||4 |
|Forearm ||3 ||3 ||3 ||3 ||3 |
|Hand ||2.5 ||2.5 ||2.5 ||2.5 ||2.5 |
|Thigh ||5.5 ||6.5 ||8 ||8.5 ||9 |
|Leg ||5 ||5 ||5.5 ||6 ||6.5 |
|Foot ||3.5 ||3.5 ||3.5 ||3.5 ||3.5 |
Overestimation of burn size is common.68,69 Precise estimation of burn size is important, as an inaccurate estimation may lead to an inadequate fluid resuscitation or over-resuscitation.70 In the future, computer-aided systems or smartphones may aid estimation of burn size and improve accuracy.71
With circumferential constricting burns (deep partial- and full-thickness burns) to an extremity, peripheral circulation to the limb can be compromised with edema. Development of generalized edema beneath a non-yielding eschar impedes venous outflow and will have a tourniquet effect on the arterial inflow to the distal beds. This can be recognized by numbness and tingling in the limb and increased pain in the digits. Arterial flow can be assessed by pulse oximetry and determination of Doppler signals in the digital arteries and the palmar and plantar arches in affected extremities. Capillary refill is assessed, also. The release of a burn eschar is performed by making lateral and medial incisions on the affected extremity using the electrocautery. The entire constricting eschar must be incised to relieve the obstruction to blood flow. If the hand is involved, two incisions are made on the dorsal surface and along the medial or lateral sides of the digits, taking care not to damage the neurovascular bundles. These bundles are located slightly to the palmar side of the digit.
If vascular compromise has been prolonged, reperfusion after an escharotomy may cause reactive hyperemia and further edema in the muscle, making continued surveillance of the distal extremities necessary. Increased pressures in the underlying musculofascial compartments may necessitate fasciotomies.
Extremity compartment syndrome can also develop in patients receiving large amounts of resuscitation fluids or in severe burns such as electrical injuries. In such patient, a standard fasciotomy should be performed instead of an escharotomy.
A circumferential burn of the chest with a constricting eschar can cause a similar phenomenon, except the effect is to decrease ventilation by limiting excursion of the chest wall. Any decline in ventilator parameters such as an increase in peak airway pressure and Pco2 should prompt inspection of the chest with appropriate escharotomies. Escharotomies should be made in the lateral chest bilaterally with a connecting incision being introduced across the chest to relieve constriction and allow adequate ventilation.
Inhalation injuries occur in 8% of cutaneous burn injuries and are one of the factors that contributes to mortality in burns by adding another inflammatory focus and impeding normal gas exchange. The presence of such an injury can be used as a significant predictor of outcome in massive burns. Inhalation injuries used to be associated with high mortality, but the last few decades have seen improved survival with early diagnosis, better airway management, gentle ventilation, and pulmonary hygiene.72 Early diagnosis and prevention of complications are necessary to decrease morbidity and mortality related to inhalation injury.
In most inhalation injuries, damage is caused primarily by inhaled toxins. Heat is generally dispersed in the upper airways, whereas cooled smoke particles and released toxins are carried distally into the bronchi and alveoli. The injury is principally chemical in mechanism, and the response is an immediate increase in blood flow in the bronchial arteries with formation of edema and increases in lung lymph flow. The lung lymph in this situation is similar to serum, indicating that permeability at the capillary level is markedly increased. The resulting edema is associated with an increase in lung neutrophils, and it is postulated that these cells may be the primary mediators of pulmonary damage with this injury.73 Neutrophils release proteases and reactive oxygen species that can produce conjugated dienes by lipid peroxidation. High concentrations of these conjugated dienes are present in the lung lymph and pulmonary tissues after inhalation injury, suggesting that increased neutrophils are active in producing cytotoxic materials.37
Another hallmark of inhalation injury is separation of the ciliated epithelial cells from the basement membrane followed by formation of exudate within the airways. The exudate consists of proteins found in the lung lymph and eventually coalesces to form fibrin casts.74 Clinically, these fibrin casts can be difficult to clear with standard airway suction, and bronchoscopy is often required. These casts can also add barotrauma to localized areas of the lung by forming a “ball-valve.” During inspiration, the airway diameter increases, and air flows past the cast into the distal airways. During expiration, the airway diameter decreases, and the cast effectively occludes the airway, preventing the inhaled air from escaping. Increasing volume leads to localized increases in pressure that are associated with numerous complications, including pneumothorax and decreased lung compliance. Therapy aimed at clearing the airway and minimizing complications would likely improve outcomes.
Patients with smoke inhalation often present with a history of exposure to smoke in a closed space, stridor, hoarseness, wheezing, carbonaceous sputum, facial burns, and singed nasal vibrissae. Each of these findings has poor sensitivity and specificity75; therefore, the diagnosis is often established with bronchoscopy. Bronchoscopy can reveal early inflammatory changes such as erythema, edema, ulceration, sloughing of mucosa, and prominent vasculature in addition to infraglottic soot.76 Mechanical ventilation may be needed to maintain gas exchange, and repeated bronchoscopies may reveal continued ulceration of the airways with the formation of granulation tissue and exudate, inspissation of secretions, and edema.
Management of an inhalation injury is directed at maintaining open airways, clearing secretions, and maximizing gas exchange while the lungs heal. A coughing patient with a patent airway can clear secretions very effectively, and efforts should be made to treat patients without mechanical ventilation, if possible. If respiratory failure is imminent, intubation should be instituted early, with frequent chest physiotherapy and suctioning being performed to maintain pulmonary hygiene. Frequent bronchoscopies may be needed to clear inspissated secretions. Mechanical ventilation should be used to provide gas exchange with as little barotrauma as possible. Inhalation treatments have been effective in improving the clearance of tracheobronchial secretions and decreasing bronchospasm.
For the pharmacological treatment of inhalation injury, beta-agonists, nebulized acetylcysteine and heparin, and nebulized racemic epinephrine have been beneficial as has adequate humidification of ventilated air.9,77,78
In addition to conventional ventilator methods, novel ventilator therapies such as high-frequency percussive ventilation have been devised to minimize barotrauma. This method combines standard tidal volumes and respirations (ventilator rates 6–20 breaths/minute) with smaller high-frequency respirations (200–500 breaths/minute) and has been shown to permit adequate ventilation and oxygenation in patients who have failed conventional ventilation. An explanation for the greater utility of this method is the ability to recruit alveoli at lower airway pressures.79 This ventilator method may also have a percussive effect that loosens inspissated secretions and improves pulmonary hygiene.
Prompt treatment is imperative in minimizing tissue damage in chemical burns, and the area of the burn should be copiously irrigated with water. Care must be taken to direct the drainage of the irrigating solution away from unburned areas to limit the area of skin exposed to chemicals. If the chemical composition is known, monitoring the irrigated solution pH will give an indication of the effectiveness of the irrigation. Attempts at neutralization of either acidic or basic solutions can result in heat production and extend the injury. Generally, acids cause coagulative necrosis and are confined to the skin, while basic solutions cause liquefactive necrosis and extend further into the tissues. After the chemical injury has been controlled, the remaining burn is treated in the same way as thermal injuries. Assessment of burn depth is often difficult, but is typically deeper than it appears.
Hydrofluoric acid is a highly dangerous substance, yet it is used widely in industrial settings. It causes severe burns and systemic effects.80 When it is exposed to biological tissues, the fluoride ion precipitates calcium and may cause systemic hypocalcemia. This may occur even with a very small burn. Management of burns caused by this substance differs from burns caused by other acids. In addition to undergoing copious irrigation of the burned area, the exposed skin should be treated with 2.5% calcium gluconate gel to provide pain relief and limit the spread of the fluoride ion. For hand burns, even intra-arterial calcium gluconate has been advocated. Patients should be monitored closely for prolongation of the QT interval, torsade de pointes, or ventricular fibrillation. Changes in the QT interval should be treated with 20 mL of 10% calcium gluconate repeated as needed to maintain normal levels of serum calcium. Other serum electrolytes such as magnesium must be closely monitored, also.
Electrical injuries are unique in that the location of the injury may be mostly internal as the current proceeds down the path of least resistance via the nerves, blood vessels, and muscle. This spares the skin, except at the contact points of the electrical current. If the resistance of contact sites of high-voltage current is high, the local injury may be extensive, with loss of digits or even the entire extremity. In addition, an electrical injury may be associated with blunt trauma from titanic contractions of muscles or falls.
With any significant electrical injury, vigorous intravenous resuscitation should be given with attention to myoglobinuria from muscle damage. Urine output should be maintained at greater than 1 mL/kg/h with fluid administration and mannitol to increase renal tubular flow if needed. The administration of intravenous bicarbonate to alkalinize the urine should be considered to decrease precipitation and deposition of myoglobin in the renal tubules, but it has not been proven in prospective studies. Patients should be monitored for cardiac arrhythmias for 24 hours after admission.
Serial examinations of the extremities are necessary to detect any vascular compromise, and fasciotomies of the involved limbs are often necessary. If operative exploration is necessary, complete fasciotomies with inspection of deep tissues should be undertaken. Acute and chronic neuropathies are common and may be permanent. Development of cataracts is also common after severe electrical injury and may be delayed for months; therefore, close ophthalmologic follow-up is necessary.
Improvements in the treatment of burn wounds and use of antimicrobial dressings have dramatically decreased the incidence of wound infection and sepsis in burn patients.81 The old technique of allowing separation of eschar with lysis by bacterial enzymes has given way to wound closure using early excision and skin grafting.82 In wounds that will heal spontaneously without skin grafts, topical antimicrobial agents or silver-based dressings limit wound contamination and provide a moist environment for healing. Current therapy for burn wounds can be divided into the following three stages: assessment, management, and rehabilitation. Once the extent and depth of the wounds have been assessed and the wounds have been thoroughly cleaned and debrided, the management phase begins. Each wound should be dressed with an appropriate covering that protects the damaged epithelium and dermis, prevents infection, and provides comfort over the painful wound.
The choice of dressing should be individualized based on the characteristics of the burn. First-degree burns are minor with minimal loss of barrier function. These wounds require no dressing and are treated with lotion to keep the skin moist. Second-degree burns can be treated by an antibiotic ointment such as silver sulfadiazine and covered with gauze under elastic wraps. Alternatively, the wounds can be covered with a temporary biologic or synthetic covering to close the wound. These coverings eventually slough as the wound reepithelializes underneath. These types of dressings provide stable coverage with decreased pain and a barrier to evaporative loss. They may also have the added benefit of not inhibiting epithelialization, a feature of most topical antimicrobial agents. These coverings include biological materials such as allograft skin, porcine xenograft skin, human amniotic membranes,83 and synthetic materials such as Biobrane (Smith and Nephew, Andover, MA, USA) and various silver impregnated dressings such as Mepilex (Mölnlycke Health Care, Gothenburg, Sweden).83,84,85,86 The advantages and disadvantages of the various coverings are listed in Table 48-4. These should be applied within 24 hours of the burn before bacterial colonization of the wound occurs.
TABLE 48-4Advantages and Disadvantages of Alternative Wound Coverings ||Download (.pdf) TABLE 48-4 Advantages and Disadvantages of Alternative Wound Coverings
|Covering ||Material ||Advantages ||Disadvantages |
|Allograft ||Amnion ||Low antigenicity, antimicrobial potential, good wound adherence ||Expensive, limited availability |
|Allograft ||Cadaver skin (fresh or frozen) ||Reduces bacterial colonization, vascularizes ||Expensive, limited availability |
|Xenograft ||Pigskin ||Readily available, less expensive than allograft ||Does not resist infection |
|Biobrane ||Synthetic nylon and silicon ||Readily available ||Must be placed early, nonantimicrobial |
|Mepilex ||Silver impregnated foam dressing ||Readily available, antimicrobial ||More expensive than silver sulfadiazine |
Surgical Management of Burn Wound
Deep partial-thickness burns may not heal and full-thickness burns will not heal in a timely fashion without autografting. Also, burned tissues serve as a nidus for infection and inflammation. Early excision and skin grafting of these wounds is now practiced by most burn surgeons in response to literature showing benefit over serial debridements in terms of survival, blood loss, and length of hospitalization.87,88,89
These excisions can be performed under tourniquet control or with application of topical epinephrine to minimize blood loss. After a burn wound has been excised, the wound must be covered with either autograft skin or another covering, such as allograft skin. Wounds less than 20% TBSA can usually be closed in one operation with autograft skin taken from the patient’s available normal skin (donor site). In these operations, the skin grafts are either unmeshed or meshed with a narrow ratio (2:1 or less). In major burns, donor sites may be limited to the extent that the entire wound cannot be covered with autograft skin in one operation. The availability of allograft skin to cover these wounds has changed the course of modern treatment for massive burns. A typical method of treatment is to use widely expanded autograft skin (4:1 or greater ratio) covered with allograft skin to completely close the wounds.90 The 4:1 expended autograft skin heals underneath the allograft skin by reepithelialization in approximately 21 days, and the allograft skin will slough as autograft skin heals underneath it. Portions of the wound that cannot be covered with widely meshed autograft skin due to scarcity of available autograft skin are temporarily covered with allograft skin in preparation for autografting when donor sites are healed and available. Ideally, areas with less cosmetic importance are covered with the widely meshed skin to close most of the wound prior to using nonmeshed grafts for the cosmetically important areas such as the hands, face, and neck.
As autologous skin grafts are still the gold standard for the treatment of full-thickness burns and donor sites can be limited after large burns, dermal and epidermal substitutes have received considerable attention. Dermal replacements such as Integra (Integra LifeSciences Corporation, Plainsboro, NJ, USA) and Alloderm (LifeCell Corporation, Branchburg, NJ, USA) are commercially available.91,92,93 For the epidermal replacement, cultured epithelial autografts are available; however, these are expensive to use and prone to breakdown and infections.94 A more affordable approach for epithelial autografts might be ReCell (Avita Medical, Royston, UK). The ReCell system can be easily generated within the operating room and applied after 15 minutes. Large prospective randomized controlled trials are warranted to determine its effectiveness.86,95
Most surgeons are in favor of early excision as previously noted. Full thickness burn wounds are excised within the first week, sometimes in serial operations, removing 20% of the burn wound at each operation on subsequent days. Others remove the total burn wound in one operative procedure under good anesthesia support; however, this can be difficult in patients with large burns and complicated by the development of hypothermia or massive blood loss. Performing excision immediately after stabilization of the patient is recommended, as blood loss diminishes if the operation can be performed the first day after injury.88 This may be due to the relative predominance of vasoconstrictive substances such as thromboxane and catecholamines in the circulation and the natural edema planes that develop immediately after the injury. When the wound becomes hyperemic after 2 days, blood loss during excision can be considerable.
Early excision should typically be reserved for full-thickness burns caused by flame. This is highlighted because scald burns are very common. These injuries are often partial thickness or a mixture of partial and full thickness and should be covered with substances such as allograft, porcine xenograft, human amnion, Biobrane, or silver-impregnated dressings. A deep partial-thickness burn can appear clinically to be a full-thickness burn at 24–48 hours after injury, particularly if it has been treated with topical antimicrobials that combine with wound drainage to form a pseudoeschar. A randomized prospective study comparing early excision versus conservative therapy with late skin grafting of scald burns showed that those excised early had more wound excised, more blood loss, and more time in the operating room. No difference in hospital length of stay or rate of infection was seen.96
Skin graft loss after an operation is typically due to one or more of the following reasons: presence of infection, fluid collection under the graft, shearing forces that disrupt the adhered graft, or an inadequate excision of the wound bed leaving residual necrotic or nonviable tissue. Infection is controlled by the appropriate use of perioperative antibiotics and covering the grafts with topical antimicrobial agents at the time of surgery. Meticulous hemostasis, appropriate meshing of grafts, aspiration of a hematoma or seroma under a non-meshed graft postoperatively, and/or use of a bolster dressing over the graft minimize fluid collection. Shearing is decreased by immobilization of the grafted area. Inadequately excised wound beds are uncommon in the practice of experienced surgeons.
Invasive infections in burn wounds can be reduced by early excision and closure and the timely and effective use of antimicrobials. The antimicrobials that are used can be divided into those given topically and those given systemically.
Available topical antibiotics can be divided into salves and soaks. Salves are generally applied directly to the wound with dressings placed over them, and soaks with antimicrobial solutions are generally poured into dressings on the wound. Each of these classes of antimicrobials has its advantages and disadvantages. Salves may be applied once or twice a day but may lose their effectiveness in between dressing changes. Soaks will remain effective because antimicrobial solution can be added without removing the dressing; however, the underlying skin can become macerated.
Some of the topical antibiotic salves include 8.5% mafenide acetate, 1% silver sulfadiazine, polymyxin B, neomycin, bacitracin, and mupirocin. No single agent is completely effective, and each has advantages and disadvantages. Mafenide acetate has a broad spectrum of activity through its sulfa moiety, particularly for Pseudomonas and Enterococcus species. It has the advantage of being able to penetrate eschar, also. Disadvantages include pain on application, an allergic skin rash, and inhibition of carbonic anhydrase activity that can result in a metabolic acidosis when applied over large surfaces. For these reasons, mafenide acetate is typically reserved for small full-thickness burns and ear burns to prevent chondritis. Silver sulfadiazine, the most frequently used topical agent, has a broad spectrum of activity from its silver and sulfa moieties that covers gram-positive organisms, most gram-negative organisms, and some fungi. It is painless upon application. Occasionally, patients will complain of some burning sensation after it is applied, and some patients will develop a transient leukopenia 2–4 days following its continued use. This leukopenia is generally harmless and resolves with cessation of treatment in 2–3 days. When the leukopenia resolves, silver sulfadiazine may be reapplied without recurrence. Petroleum-based antimicrobial ointments with polymyxin B, neomycin, and bacitracin are clear on application and allow for observation of the wound, are painless, and provide a moist environment. These agents are commonly used for the treatment of facial burns, graft sites, healing donor sites, and small partial-thickness burns. Mupirocin is an ointment that has improved activity against gram-positive bacteria, particularly methicillin-resistant Staphylococcus aureus. Nystatin in powder form can be applied to wounds to control fungal growth, and it can be combined with topical agents such as polymyxin B to decrease colonization of both bacteria and fungi.
Available agents for application as a soak include 0.5% silver nitrate solution, 0.025% sodium hypochlorite, 5% acetic acid, and 5% mafenide acetate solution. 0.5% silver nitrate has the advantages of painless application and almost complete antimicrobial coverage. Disadvantages include its staining of surfaces to a dull gray or black when the solution is exposed to light. The solution is hypotonic, and continuous use can cause leaching of electrolytes, with rare methemoglobinemia as another complication. Hypochlorite is a basic solution with effectiveness against most microbes, but it also has cytotoxic effects on wounds, thus inhibiting healing. Low concentrations of sodium hypochlorite (0.025%) have less cytotoxic effects and maintain antimicrobial effects. In addition, hypochlorite ion is inactivated by contact with protein. Therefore, the solution must be continually changed. The same is true for acetic acid solutions, though this solution may be more effective against Pseudomonas. Mafenide acetate solution has the same characteristics as mafenide acetate cream.
Perioperative systemic antimicrobials are useful in decreasing sepsis in the burn wound. Common organisms that must be considered when choosing a perioperative regimen include S. aureus and Pseudomonas sp, which are prevalent in wounds. Acinetobacter sp has emerged as a significant organism in the burn wounds, also.
Management of Organ Systems
Major burns affect a number of organ systems in addition to the skin. The immense inflammatory focus incited by the burn causes the release of numerous cytokines and inflammatory mediators that have many systemic effects and, ultimately, may result in multiorgan dysfunction and death. The systemic inflammatory response syndrome is present in every major burn, but with differing severity, and the kidneys, liver, heart, lungs, hematopoietic system, and coagulation system may be affected. Each of these systems must be supported through the course of the burn injury.
After resuscitation and stabilization, evaporative losses through open wounds including the area of the burn and any donor sites remain high. Approximately 3750 mL/m2/d of free water is lost through open wounds. These insensible losses must be added to urine output, stool volume, and respiratory losses in determining fluid balances. Daily weights are useful in determining the response to fluid management. Sodium, potassium, calcium, magnesium, and phosphorus are lost into burn wounds, as well, and require constant monitoring and replacement.
In the acute phase and up to 2 years post injury, cardiac output and heart rate remain elevated.44 Accordingly, a clinical trial was undertaken to investigate the effects of a non-selective beta-receptor antagonist on cardiac dysfunction and showed a significant reduction in both heart rate and resting energy expenditure at 12 months follow-up.97
Renal failure after a burn occurs in a bimodal fashion, with an early peak that is due to acute tubular necrosis from inadequate early resuscitation and a later peak at 2–4 weeks that is likely due to sepsis and nephrotoxic medications.98,99 Treatment is as with renal failure of any other cause. Indications for dialysis include life-threatening congestive heart failure, pulmonary edema, hyperkalemia and metabolic acidosis refractory to medical management. Catheters can be placed through burned tissue, although intact skin is preferable, and continuous venovenous hemodialysis may have some advantages over routine hemodialysis because of slower fluid fluxes.
Hepatic dysfunction can occur because of toxins associated with chemical injury or flame burns in which the patient was doused with chemicals, particularly gasoline. The direct hepatotoxicity that results is manifested by early increases in hepatocellular enzymes. Support through the recovery period is indicated. Later evidence of hepatic dysfunction from sepsis is common, also. A striking finding associated with larger burns is the development of a fatty liver, which can increase hepatic size two- to threefold.100 The primary cause seems to be a relative decrease in efficiency of the very low density lipoprotein system to handle massive increases in free fatty acids, which arise from peripheral lipolysis induced by sustained elevations in serum catecholamines. Fat that cannot be exported is deposited in the liver.
Coagulopathies from decreased hepatic synthetic function of coagulation factors, thrombocytopenia, or dilutional effects of massive blood transfusions can occur after a major burn, as well.
Nutritional Management of Burn Patients
Nutritional support of severely burned patients is best accomplished by early enteral nutrition that can abate the hypermetabolic response to a burn.101,102 Early enteral feeding preserves gut mucosal integrity, improves intestinal blood flow and motility, and decreases translocation of intestinal bacteria.101 Therefore, nasoduodenal or nasojejunal enteral tube feeding should be commenced as early as within the first 6 hours post burn, as long as the patient is not in hypovolemic shock.103
The caloric requirements needed to reach nitrogen balance in burn patients have been calculated from linear regression analysis of weight change versus predicted dietary intakes in adults and are equivalent to 25 kcal/kg plus 40 kcal/% TBSA burned per day (Table 48-5).104 Nutritional requirements for pediatric burn patients are based on body surface area (Table 48-6).105,106,107,108,109,110
TABLE 48-5Curreri Formula for Estimating Caloric Requirements for Adult Burn Patients104 ||Download (.pdf) TABLE 48-5 Curreri Formula for Estimating Caloric Requirements for Adult Burn Patients104
|16–60 y ||25 kcal/kg/d 40 kcal/% burn/day |
|>60 y ||25 kcal/kg/d 65 kcal/% burn/day |
TABLE 48-6Formulas for Estimating Caloric Requirements for Pediatric Burn Patients105,106,107,108,109,110 (Shriners Hospitals for Children at Galveston, Texas) ||Download (.pdf) TABLE 48-6 Formulas for Estimating Caloric Requirements for Pediatric Burn Patients105,106,107,108,109,110 (Shriners Hospitals for Children at Galveston, Texas)
|0–1 y ||2100 kcal/m2 TBSA/day + 1000 kcal/m2 TBSA burn/day |
|1–11 y ||1800 kcal/m2 TBSA/day + 1300 kcal/m2 TBSA burn/day |
|12–18 y ||1500 kcal/m2 TBSA/day + 1500 kcal/m2 TBSA burn/day |
Marked loss of lean body mass occurs within a few weeks of injury but modern techniques using immediate total burn excision, rapid wound closure, nutritional support, critical care, and infection control have significantly reduced mortality.111 Even so, burn-induced hypermetabolism lasts a much longer time, up to 2 years after burn, as previously noted.20,21,112 Therefore, nutritional support of burn patients becomes an essential part of treatment during their hospitalization and should be continued after discharge.
The plasma concentration of trace elements and vitamins is generally decreased over a long period after burn.21 Berger et al113,114 reported that substituting these micronutrients in burn patients reduces morbidity.