Burns and Radiation

Jong O. Lee and David N. Herndon

BURNS

Epidemiology

While the number of burn injuries is decreasing in the United States, nearly 1.25 million people are burned every year.¹ Of these, 60,000–80,000 patients per year require hospitalization due to burn injuries, and about 5,500 of these patients 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 29 years of age. The major causes of severe burn injury are flame burns, which cause most of the burn deaths, and liquid scalds.

From 1971 to 1991, burn deaths decreased by 40%, with a concomitant 12% decrease in deaths associated with inhalation injury.² Since 1991, burn deaths per capita have decreased another 25% according to statistics from the Centers for Disease Control and Prevention (www.cdc.gov/ncipc/wisqars). These improvements are due to prevention strategies resulting in fewer burns of lesser severity, as well as significant improvements in the care of severely burned patients, especially children. In 1949, Bull and Fisher first reported the expected 50% mortality rate for burn sizes in several age groups based on data from their unit.³ They reported that approximately one half of children aged 0–14 years with burns of 49% TBSA would die.³ This dismal statistic has dramatically improved, with the latest reports indicating 50% mortality for 98% TBSA burns in children 14 years and under.^4,5 A healthy young patient with any size burn might be expected to survive.⁶ The same cannot be said, however, for those aged 45 years or older. Improvements in this group have been much more modest, especially in patients over 65 years of age where a 35% burn still kills half of the patients.⁷ The improved survival figures after massive burns are due to advances in understanding of 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. Aggressive treatment of patients with severe burns has improved outcomes to the point that survival in massive injuries is common. Future breakthroughs in the field are likely to be in the area of faster and better return of function and improved cosmetic outcomes.

Criteria for Referral to Burn Centers

Some burn patients benefit from treatment in specialized burn centers. These centers have dedicated resources and the expertise of all the required disciplines to maximize outcomes from such devastating injuries.⁸ The American Burn Association and the American College of Surgeons Committee on Trauma have established guidelines about which patients should be transferred to a specialized burn center. Patients meeting the following criteria should be treated at a designated burn center:

1. Second- and third-degree burns of greater than 10% TBSA

2. Full-thickness burns in any age group

3. Any burn involving the face, hands, feet, eyes, ears, or perineum that may result in cosmetic or functional disability

4. Electrical injury

5. Inhalation injury or associated trauma

6. Chemical burns

7. Burns in patients with significant comorbid conditions (e.g., diabetes mellitus, chronic obstructive pulmonary disease, cardiac disease)

Patients meeting the following criteria can be treated in a general hospital setting:

1. Second-degree burns of less than 10% TBSA

2. No burns to areas of special function or risk and no significant associated or premorbid conditions

Pathophysiology

Burns are classified into six causal categories, three zones of injury, and five depths of injury (Table 48-1). The causes include injury due to fire, scald, contact, chemicals, electrical current, and radiation. Fire burns are divided into flash and flame burns; scald burns into those caused by liquids, grease, or steam; and liquid scald burns can be further divided into spill and immersion scalds.

TABLE 48-1 Definition of Burn Types, Zones, and Depth of Injury

Flame, scald, and contact induce cellular damage primarily by the transfer of energy that induces coagulative necrosis, while direct injury to cellular membranes is the cause of injury in chemical and electrical burns.

The skin generally provides a barrier to limit transfer of energy to deeper tissues. After the source of burn is removed, however, the response of local tissues can lead to further injury. The necrotic area of a burn is termed the zone of coagulation in the center. 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.⁹ Antioxidants¹⁰ and inhibition of neutrophil-mediated processes¹¹ 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 burned patients,¹² may also play a role. The last area is the zone of hyperemia related to vasodilation from inflammation surrounding the burn wound. This zone contains the clearly viable tissue from which the healing process begins (Fig. 48-1).

FIGURE 48-1 Illustration of the zones of injury after burn. Factors likely to affect the zone of stasis determine the extension of injury from the original zone of coagulation.

Inflammatory Response

Massive release of inflammatory mediators is seen with a significant burn, both in the wound and in other tissues. These mediators produce vasoconstriction and vasodilation, increased capillary permeability, and edema locally and in distant organs. Many mediators have been proposed to explain the changes in permeability after burns, including prostaglandins, catecholamines, histamine, bradykinin, vasoactive amines, leukotrienes, and activated complement.¹³ Mast cells in the burned skin release histamine in large quantities immediately after injury,¹⁴ which will cause a characteristic response in venules by increasing the space in intercellular junctions.¹⁵ The use of antihistamines in the treatment of burn edema, however, has had limited success with the possible exception of H₂-receptor antagonists.¹⁶ 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.¹⁷

Another mediator likely to play a major role in changes in vascular permeability and tone is thromboxane A₂. It has been shown that levels of thromboxane increase dramatically in the plasma and wounds of burned patients.^18,19 This potent vasoconstrictor leads to platelet aggregation in the wound, contributing to expansion of the zone of stasis. Also, it causes prominent mesenteric vasoconstriction and decreased blood flow to the gut in animal models that compromise gut mucosal integrity and immune function.²⁰

Changes in Organ Function

Cardiac effects include marked loss of plasma volume, increased peripheral vascular resistance, and decreased cardiac output,²¹ and pulmonary effects include a decrease in pulmonary static compliance.²² These changes are associated with mild direct cardiac damage.²³ Renal blood flow decreases with a fall in glomerular filtration rate, which may result in renal dysfunction. Metabolic changes are highlighted by an early depression followed by a marked, sustained increase in resting energy expenditure, increased lipolysis and proteolysis, and an increase in oxygen consumption. This is driven in part by an increase in production of catecholamines, cortisol, and glucagon.²⁴ Increased peripheral lipolysis results in hepatic steatosis. There is a generalized impairment in host defenses with depressed production of immunoglobulin, decreased opsonic activity, and depressed bactericidal activity,²⁵ and these cause the burned patient to become especially prone to infection.

Initial Care

The burning process is stopped by removing the patient from the source of burn, and clothing and jewelry are removed immediately (see Chapter 10). The patient is 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 using pulse oximetry. 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 orotracheal 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 levels are obtained when appropriate. The presence of carbon monoxide (CO) in the blood, which has an affinity 210–280 times that of oxygen for hemoglobin (Hb), can falsely elevate oxygen saturation levels that are determined colorimetrically. Use of a pulse oximeter may not be effective, as patients with CO poisoning may have a normal oxygen saturation level on the device. Use of a pulse CO-oximeter measures absorption at several wavelengths to distinguish oxyhemoglobin from carboxyhemoglobin saturation and determines the blood oxygen saturation more reliably using the total amount of Hb, including carboxyhemoglobin, met-Hb, and reduced Hb.

The treatment for CO inhalation is 100% O₂ by endotracheal tube or face mask. This will decrease the half-life of CO from 4 to 6 hours at room air to 40–80 minutes with 100% O₂. In 3 atm absolute 100% oxygen in a hyperbaric chamber, the half-life decreases further to 15–30 minutes. Full-thickness circumferential burns of the chest can interfere with ventilation, so 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. If ventilation is compromised with a rising airway pressure and pCO₂, an escharotomy on the chest should be performed to allow better movement of the chest and improve ventilation. Measurement of a noninvasive blood pressure may be difficult in patients with burned extremities, and such patients may need an arterial line to monitor their blood pressure 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 temporary femoral arterial line may be more appropriate.

Fluid Resuscitation

After a serious burn, there is a systemic capillary leak that increases with burn size. Capillaries usually regain competence after 18–24 hours if resuscitation has been successful. Increased times to beginning resuscitation of burned patients result in poorer outcomes, and delays should be minimized.²⁶ The best intravenous (IV) access is with short peripheral catheters through unburned skin; however, veins beneath burned skin can be used to avoid a delay in obtaining IV access. Central venous lines are required when peripheral IV access is difficult. In children, intraosseous access can be utilized in the proximal tibia until IV access is accomplished. Lactated Ringer’s solution without dextrose is the fluid of choice except in children under 2 years of age, who should receive some 5% dextrose in the lactated Ringer’s solution. 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, using a modified formula developed at Parkland Memorial Hospital in Dallas, Texas, by multiplying the estimated TBSA burned by the weight in kilograms, which is divided by 4 for the first 8 hours. Thus, the rate of infusion for an 80-kg man with a 40% TBSA burn would be for the first 8 hours.

Different formulas, all originating from experimental studies on the pathophysiology of burn shock, have been devised to assist the clinician in determining the proper amount of resuscitation fluid. Early work by Baxter and later by G. T. Shires established the basis for modern protocols for fluid resuscitation.²⁷ 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 varying 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 burned patients (Table 48-2). Also, it was shown that changes in plasma volume were not related to the type of resuscitation fluid used in the first 24 hours but colloid solutions could increase plasma volume after this time. From these findings, it was concluded that colloid solutions should not be used in the first 24 hours until capillary permeability returned closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after a burn (6–8 hours) and therefore, suggest that colloids can be used at this point.²⁸

TABLE 48-2 Resuscitation Formulas

Moncrief and coworkers also studied the hemodynamic effects of fluid resuscitation in burns, which resulted in the Brooke formula²¹ (Table 48-2). They showed that fluid loss in moderate burns resulted 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 returned to normal with the administration of colloid. Cardiac output was low the first day in spite of resuscitation but subsequently increased to supernormal levels as the flow phase of hypermetabolism was established.²¹ Since these studies, it has been found that much of the fluid needs are due to capillary leak that permits passage of large molecules and water into the interstitial space. Intravascular volume follows the gradient into the burn wound and nonburned tissues. Approximately 50% of fluid resuscitation needs are sequestered in nonburned tissues in 50% TBSA burns.²⁹

Hypertonic saline solutions have theoretic advantages in the resuscitation of burned patients. These solutions have been shown to decrease net fluid intake,³⁰ decrease edema,³¹ and increase lymph flow probably by the transfer of volume from the intracellular space to the interstitium. When using these solutions, one must take care to avoid serum sodium concentrations greater than 160 mEq/dL.¹³ Of note, it has been shown that patients with over 20% TBSA burns who were randomized to resuscitation with either hypertonic saline or lactated Ringer’s solution did not have significant differences in total volume requirements or in changes in percent weight gain over the days after the burn.³² Other investigators have found an increase in renal failure with hypertonic solutions that has tempered further enthusiasm for their use in resuscitation.³³ Some burn units have successfully used a modified hypertonic solution by adding one ampule of sodium bicarbonate to each liter of lactated Ringer’s solution.³⁴ Further research will need to be done to determine the optimal formula to reduce formation of edema as well as maintain adequate cellular function.

Of interest, it has been shown that resuscitation volumes required in the severely burned patient decreased when high-dose IV ascorbic acid was administered during resuscitation. This was associated with decreased weight gain and improved oxygenation.³⁵

Most burn centers around the country use something similar to the Parkland or Brooke formula in which varying amounts of crystalloid and colloid solutions are administered for the first 24 hours postburn (Table 48-2). IV fluids are generally changed in the second 24 hours to more hypotonic solutions. These formulas are guidelines to the amount of fluid necessary to maintain adequate perfusion. This is monitored in burned patients by following the volume of urine output, which should be maintained at 0.5 mL/kg per hour in adults and 1.0 mL/kg per hour in children. Other parameters such as heart rate, blood pressure, mental status, and peripheral perfusion are monitored, also. Changes in the rates of infusion of IV fluids should be made on an hourly basis as determined by the response of the patient to the particular fluid volume administered.

In pediatric burns, the commonly used formulas are modified to account for changes in surface area to mass ratios. Children have a larger body surface area relative to their weight than do adults and generally have somewhat greater fluid needs during resuscitation. The Galveston formula is based on body surface area and uses 5,000 mL/m² TBSA burned for resuscitation + 1,500 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 a child with burn. All of these formulas calculate the amount of volume given in the first 24 hours, one half of which is given in the first 8 hours and next one half of which is given over next 16 hours. Some dextrose is added to the resuscitation fluid in children under 2 to prevent hypoglycemia because they have limited glycogen stores. It is best to use two IV fluids in infants, lactated Ringer’s solution for resuscitation and 5% dextrose in lactated Ringer’s solution for maintenance.

Other Injuries

Other traumatic injuries may be present in patients who have been burned. Each patient should be fully evaluated for associated injuries that may be more immediately life threatening, and the burn wounds can be addressed after standard evaluation and resuscitation. Burned 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 the definitive care of the burn. Nasogastric tubes and bladder drainage catheters are placed in patients requiring transfer to a burn center to decompress the stomach and to monitor the progress of resuscitation.

Determination of Burn Depth

The depth of burn determines outcome in terms of survival and scarring. Although technologies such as the laser Doppler flow meter with multiple sensors hold promise for quantitatively determining burn depth, it is most accurately assessed by the judgment of experienced physicians. Determination of depth is critical in the treatment plan as there are wounds that will heal with local treatment versus those that will require operative intervention for timely healing. Being able to determine who will need operative intervention will facilitate care.

Superficial (first-degree) burns are confined to the epidermis. These burns are painful, erythematous, and blanch to the touch with an intact epidermis without blister. Examples include sunburn, a minor scald, or flash burn. These burns will heal in 3–6 days and will not result in scarring. 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, superficial and deep. All partial-thickness burns have some degree of dermal damage, and the division is based on the depth of injury into this layer. Superficial partial-thickness burns are erythematous, painful, wet, blanch to touch, and often form blisters, although 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 from retained epidermal structures in the rete ridges, hair follicles, and sweat glands in 7–14 days. The injury may cause skin discoloration over the long term. Deep partial-thickness burns into the reticular dermis will appear dry, more pale than pink, or mottled. They may not blanch to touch but will remain painful to pinprick. In deeper partial-thickness burns, the 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, often with hypertrophic scars. The longer the wound takes to heal, the worse the scarring will be.

Full-thickness (third-degree) burns are burns through the dermis down to the subcutaneous tissue and are characterized by a firm leathery eschar that is painless and black, white, or cherry red in color. An eschar is insensitive to pinprick but may feel 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 grafting with autograft skin to heal the wounds in a timely fashion and to decrease scarring. Deep partial-thickness burns often require grafting to facilitate healing, as well.

Fourth-degree burns involve other tissues or organs beneath the skin, such as muscle, tendon, and bone. They have a charred appearance that usually results from prolonged duration of contact with fire or an object such as a hot muffler or from high-voltage electrical injury.

Determination of Burn Size

The most commonly used method of determining the burn size in adults is the “rule of nines” (Fig. 48-2). Each upper extremity and the head and neck are 9% of the TBSA; each lower extremity, the anterior trunk, and posterior trunk are 18%; and the perineum and genitalia are assumed to be 1% of the TBSA. For smaller burns, burn size can also be estimated by examining the area of the patient’s open hand, which is approximately 1% TBSA, and visually transposing this onto the wound to determine burn size.

FIGURE 48-2 Determining burn size by the “rule of nines.”

Children have a relatively larger portion of the body surface area in the head and neck and smaller surface area in the lower extremities. Infants have 21% of the TBSA in the head and neck and 13% in each leg, with these proportions incrementally approaching adult proportions as age increases. The Berkow formula or Lund Browder chart can be helpful in determining burn size in children (Table 48-3).

TABLE 48-3 Berkow Chart for Estimation of Burn Size in Children

Escharotomies

With circumferential constricting deep partial- and full-thickness burns to an extremity, peripheral circulation to the limb can be compromised by edema. Development of generalized edema beneath a nonyielding eschar impedes venous outflow and will eventually affect 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. Extremities at risk are identified on clinical examination, which mandate an escharotomy performed at the bedside. The release of a burn eschar is performed by lateral and medial incisions on the extremity with an 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 with care not to damage the neurovascular bundles. These bundles are located slightly to the palmar side of the digit. If it is clear that the wound will require excision and grafting because of its depth of injury, escharotomies are the safest route to restore perfusion to the underlying nonburned tissues. If vascular compromise has been prolonged, reperfusion after an escharotomy may cause a reactive hyperemia and further formation of edema in the muscle, making continued surveillance of the distal extremities necessary. Increased pressures in the underlying musculofascial compartments are treated with standard fasciotomies.

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 decrease in ventilation documented by an increase in peak airway pressure and pCO₂ of a burned patient should be followed by inspection of the burn on the chest wall. When necessary, escharotomies are performed in the lateral chest bilaterally with a connecting incision across the chest to relieve the constriction and allow for adequate ventilation.

Inhalation Injury

An associated inhalation injury is one of the factors that contributes to mortality in burns. Inhalation injury adds another inflammatory focus to the burn and impedes the normal gas exchange that is vital for critically injured patients. The presence of such an injury can be used as a significant predictor of outcome in massive burns. In one study, the amount of time spent on a ventilator in the first 28 days was the strongest predictor of mortality in a group of children with over 80% TBSA burns. As expected, inhalation injury was present in the majority of these children.²⁶

In most inhalation injuries, damage is caused primarily by inhaled toxins. Heat is generally dispersed in the upper airways, whereas the cooled particles of smoke and toxins are carried distally into the bronchi and alveoli. The injury is principally chemical in nature. The response is an immediate increase in blood flow in the bronchial arteries to the bronchi 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 edema that results is associated with an increase in neutrophils in the lung, and it is postulated that these cells may be the primary mediators of pulmonary damage with this injury. Neutrophils release proteases and oxygen-free radicals 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.³⁶

Separation of the ciliated epithelial cells from the basement membrane followed by formation of exudate within the airways is another hallmark of inhalation injury. The exudate consists of proteins found in the lung lymph that eventually coalesce to form fibrin casts. Clinically, these fibrin casts can be difficult to clear with standard techniques of airway suction, and bronchoscopy is often required. These casts can also add barotrauma to localized areas of 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 after this injury.

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 specificity; therefore, the diagnosis is often established by the use of bronchoscopy. Bronchoscopy can reveal early inflammatory changes such as erythema, edema, ulceration, sloughing of mucosa, and prominent vasculature in addition to infraglottic soot. 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 inhalation injury is directed at maintaining open airways, clearing secretions, and maximizing gas exchange while the lung heals. 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 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. IV heparin has been shown to reduce the formation of tracheobronchial casts, minute ventilation, and peak inspiratory pressures after smoke inhalation. When heparin was administered directly to the lungs in a nebulized form to reduce bleeding complications, it was shown to have similar effects on casts without causing a systemic coagulopathy.

When N-acetylcysteine treatments are added to nebulized heparin in burned children with inhalation injury, reintubation rates and mortality are decreased.³⁷

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