Jong O. Lee and David N. Herndon
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
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.
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.22These 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.24Increased 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.
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.
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 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
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.
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 In addition to the preceding measures, adequate humidification and treatment of bronchospasm with β-agonists is indicated.
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/min) with smaller high-frequency respirations (200–500 breaths/min) and has been shown to permit adequate ventilation and oxygenation in patients who had failed conventional ventilation. An explanation for the greater utility of this method is the ability to recruit alveoli at lower airway pressures.38 This ventilator method may also have a percussive effect to loosen inspissated secretions and improve pulmonary hygiene.
Prompt treatment is imperative in minimizing tissue damage in chemical burns. A chemical burn should be copiously irrigated with water, and 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 of 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 until removal. Emergent operative debridement with pH testing of each tangential slice may be necessary to ensure no further injury after exposure to solutions with a high pH. 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 that causes severe burns and systemic effects, yet it is used widely in industrial and domestic settings.39 When 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 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 also be closely monitored.
Electrical burns are unique in that the location of the injury may be mostly internal. Electrical current proceeds down the path of least resistance, which is via nerves, blood vessels, and muscle, thus sparing 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 entire extremities. Electrical injury may be associated with blunt trauma from tetanic contractions of muscles or a fall.
With any significant electrical injury, vigorous IV resuscitation should be given with attention to myoglobinuria from muscle damage. Urine output should be maintained at greater than 1 mL/kg per hour with administration of fluids and an osmotic diuresis using mannitol to increase renal tubular flow if needed. The administration of IV bicarbonate to alkalinize the urine should be considered to decrease precipitation of hemochromogens 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. Debridement of nonviable tissue is appropriate. 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, so close ophthalmologic follow-up is necessary.
Care of Burn Wound
Improvements in the treatment of burn wounds and utilization of antimicrobial dressings have dramatically decreased the incidence of fatal sepsis in burned patients.40 The previous technique of allowing separation of eschar with lysis by bacterial enzymes has given way to wound closure using early excision and grafting. In those wounds that will heal spontaneously without skin grafts, topical antimicrobial agents 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 thoroughly cleaned and debrided, the management phase begins. Each wound should be dressed with an appropriate covering that serves three functions. First, it protects the damaged epithelium and dermis. Second, the dressing should be occlusive to reduce evaporative heat loss. Third, the dressing should provide 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 topical salves to decrease pain and keep the skin moist. Second-degree wounds can be treated by daily dressing changes with an antibiotic ointment such as silver sulfadiazine covered with several layers of gauze under elastic wraps. Alternatively, the wounds can be covered with a temporary biological 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 losses. They may also have the added benefit of not inhibiting epithelialization, a feature of most topical antimicrobial agents. These coverings include allograft (cadaver skin), porcine xenograft (pigskin), and Biobrane (Bertek, Morgantown, West Virginia).41,42 The advantages and disadvantages of the various coverings are listed in Table 48-4. These should generally be applied within 24 hours of the burn before bacterial colonization of the wound occurs. As synthetic coverings such as Biobrane have no antimicrobial property, close observation is required.
TABLE 48-4 Advantages and Disadvantages of Alternative Wound Coverings
Surgical Management of Burn Wound
Full-thickness burns will not heal in a timely fashion without autografting, and the same is true for some deep partial-thickness burns. These burned tissues serve as a nidus for inflammation and infection that can lead to death of the patient. Early excision and grafting of these wounds is now practiced by most burn surgeons in response to reports showing benefits over serial debridement in terms of survival, blood loss, and length of hospitalization.43–45
These excisions can be performed with tourniquet control or with application of topical epinephrine and thrombin to minimize blood loss. After a burn wound has been excised, the wound must be covered with either autograft skin or some other covering. This covering is ideally the patient’s own skin. Wounds less than 20–30% TBSA can usually be closed in one operation with autograft skin taken from the patient’s available normal nonburned skin (donor site). In these operations, the skin grafts are either not meshed or meshed with a narrow ratio (2:1 or less). In major burns, donor site 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 autografts (4:1 or greater ratio) covered with allograft skin to completely close the wounds. 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. Massively burned patients are profoundly immunosuppressed, and rejection of allograft skin is rarely a problem. Portions of the wound that cannot be covered with widely meshed autograft are covered with allograft skin temporarily in preparation for autografting when donor sites are healed and ready. 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 and face.
Most surgeons excise the full-thickness burn wound within the first week, sometimes in serial operations, removing 20% of the burn wound at a time per operation on subsequent days. Others remove the total burn wound in one operative procedure; however, this can be difficult in patients with large burns and complicated by the development of hypothermia or massive blood loss. It is the authors’ practice to perform the excision immediately after stabilization of the patient, because blood loss diminishes if the operation can be performed the first day after injury. 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 a considerable problem.
Early excision should be reserved for full-thickness burn typically 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, or Biobrane, allowing the wound, which will heal, to be protected. 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 with conservative therapy with late skin grafting with scald burns showed that patients undergoing early excision 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.46
Loss of a skin graft after an operation is 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, or “rolling” of nonmeshed grafts postoperatively and/or use of a bolster dressing over the graft minimizes fluid collections. Shearing is decreased by immobilization of the grafted area. Inadequately excised wound beds are uncommon in the practice of experienced surgeons. Punctate bleeding or color of the dermis or fat in areas excised under a tourniquet denotes the proper level of excision.
Control of Infection
Decreased invasive infections in burn wounds are due to 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.
Topical antibiotic salves include 8.5% mafenide acetate (Sulfamylon), 1% silver sulfadiazine (Silvadene), 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 also has the advantage of penetration of eschar. 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 sulfate is typically reserved for small full-thickness injuries 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. Some Pseudomonas species, however, possess plasmid-mediated resistance. It is painless on application and is easy to use. 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 of this problem. Petroleum-based antimicrobial ointments with polymyxin B, neomycin, and bacitracin are clear on application, painless, allow for observation of the wound, 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, 0.5% sodium hypochlorite, 5% acetic acid, and 5% mafenide acetate solution. 0.5% silver nitrate has the advantage of painless application and almost complete antimicrobial coverage. The 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. 0.5% hypochlorite is a basic solution with effectiveness against most microbes, but it has a cytotoxic effect on wounds, thus inhibiting healing. Low concentrations of sodium hypochlorite (0.025%) have less cytotoxic effects while maintaining the antimicrobial effects. In addition, hypochlorite ion is inactivated by contact with protein, so the solution must be continually changed. The same is true for acetic acid solutions, although this solution may be more effective against Pseudomonas. Mafenide acetate solution has the same characteristics as the mafenide acetate cream.
The use of perioperative systemic antimicrobials has a role in decreasing sepsis in the burn wound until it is healed, also. 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 burn wounds, as well.
Management of Organ Systems
Major burns result in a number of effects to organ systems in addition to injury 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 wounds including the area of burn and any donor sites remain high. Many of these patients are placed in air-fluidized beds to decrease shearing of grafts, which also increases evaporative losses. Approximately 3,750 mL/m2 per day of free water is lost through open wounds, and an additional 1 L/m2 per day is lost through continuous airflow past open wounds if treated in an air-fluidized bed. 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 phosphate are also lost into burn wounds and will require constant monitoring and replacement.
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.47,48 Treatment is as with any cause for renal failure. Indications for dialysis include life-threatening congestive heart failure, pulmonary edema, hyperkalemia, and metabolic acidosis refractory to medical management. Continuous venovenous hemodialysis (CVVHD) may have some advantages over routine hemodialysis because of slower fluid fluxes. Peritoneal dialysis is an option in these patients as well, with the same advantages as CVVHD. Catheters for any of these approaches can be placed through burned tissue, although intact skin is preferable.
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 also common. A striking finding associated with larger burns is the development of a fatty liver, which can increase hepatic size 2- to 3-fold.49 The primary determinant seems to be a relative decrease in efficiency of the very-low-density lipoprotein system to handle the massive increase in delivery of free fatty acids 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 production of coagulation factors, thrombocytopenia, or dilutional effects of massive blood transfusions can occur after a major burn. Treatment is directed toward prevention of massive blood loss through the use of tourniquets, epinephrine application, and thrombin topical sprays.
Hypermetabolism in Burns
Patients with major burn injury have the highest metabolic rate of all critically ill or injured patients.50 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, immune depression, and delayed wound healing.51,52 This response is mediated by increases in circulating levels of the catabolic hormones including catecholamines, cortisol, and glucagon.52,53
Marked wasting of lean body mass occurs within a few weeks of injury. Modern techniques using immediate total burn excision, rapid wound closure, adequate early enteral feeding, critical care, and control of infection have resulted in a significant reduction in mortality. Hypermetabolism and catabolism of muscle protein continue up to 6–9 months after a severe burn.54 Therefore, nutritional support of burn patients becomes an essential part of treatment during their hospitalization.
Pharmacological agents have been used to attenuate catabolism and to stimulate growth after burn injury. Erosion of lean body mass can be further minimized through the use of anabolic hormones such as growth hormone, insulin, insulin-like growth factor (IGF)/IGF-binding protein-3, oxandrolone, and fenofibrate as well as catecholamine antagonists such as propranolol. These agents contribute to maintenance of lean body mass and promote wound healing.55–61
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.62,63 Early enteral feeding preserves gut mucosal integrity, improves intestinal blood flow and motility, and decreases translocation of intestinal bacteria.62 Therefore, nasoduodenal or nasojejunal tube feeding should be commenced as early as within the first 6 hours postburn as long as the patient is not in hypovolemic shock.
The caloric requirements needed to reach weight and nitrogen balance have been calculated from linear regression analysis of weight change versus predicted dietary intakes in adults at 25 kcal/kg plus 40 kcal/% TBSA burn for 24 hours (Table 48-5).64 Nutritional requirements for pediatric patients are based on body surface area (Table 48-6).65–70
TABLE 48-5 Curreri Formula for Estimating Caloric Requirements for Adult Burn Patients64
TABLE 48-6 Formulas for Estimating Caloric Requirements for Pediatric Burn Patients65–70 (Shriners Hospitals for Children at Galveston, Texas)
Our society has used radioactivity to its benefit as an energy source, defensive weapon, and diagnostic and therapeutic medical tool since the discovery of radiation by Becquerel over 100 years ago. With these benefits come hazards in the form of accidents in nuclear power plants, threat of nuclear war, terrorist acts, and potential for radiation injuries from improper use of radioactive isotopes and ionizing radiation. The threat of nuclear or radiation accidents resulting in mass casualties is real and has never been greater as radiation sources are ubiquitous and are available from industrial, military, and medical sources. Major industrial accidents at Three Mile Island, Chernobyl, Goiania, Brazil, and the Tukushima Oaichi Nuclear Power Plant on the eastern shore of Japan after the tsunami on March 11, 2011 have highlighted the need for knowledge of radiation effects and treatment.
Exposure to radiation can be classified into the following three types:71
1. Small, contained events affecting one or more persons, either localized or affecting the whole body, for example, laboratory accident or damage from x-ray machines
2. Industrial accidents affecting large numbers of people with varying degrees of severity, for example, meltdown of a nuclear power plant
3. Detonation of a nuclear device with injuries to hundreds or thousands of people with associated trauma
Specific changes noted in association with radiation make these injuries unique and require consideration as a separate form of trauma.72 In explosions, however, the release of kinetic energy can cause other more standard injuries commonly associated with blunt mechanisms. The patients may present with trauma and burns in addition to radiation exposure and explosions. The intent of this part of the chapter is to provide information regarding the terminology associated with radiation, pathophysiology of injury, and diagnosis and treatment of these injuries, including triage and decontamination.
Radiation incidents within the United States must be reported to the Radiation Emergency Assistance Center/Training Site (REAC/TS) at the Oak Ridge Institute for Science and Education, Oak Ridge Associated Universities in Oak Ridge, Tennessee (http://www.orau.gov/reacts). This agency is funded by the U.S. Department of Energy and provides assistance in the response to all types of radiation accidents or incidents on a 24 hour per day basis. The agency has the capability of providing medical attention and should be contacted to both inform and receive advice about specific incidents. They can assist with calculations of absorbed dose. The telephone number for REAC/TS is (865) 576-1005.
The majority of incidents are associated with sealed highly radioactive sources often used in industrial radiography followed by those associated with x-ray machines or the use of unsealed radioisotopes in medicine and uranium products. When fissionable material, usually enriched uranium, has enough neutron flux to undergo a spontaneous nuclear reaction, the material has reached “critical mass,” with the release of uncontrolled radiation. The majority of deaths from radiation incidents occurred after 1975, with most (>40) being associated with the Chernobyl incident in 1986.
The most devastating loss of life associated with radiation was with the detonation of atomic bombs in Nagasaki and Hiroshima in World War II. Fifty percent of the deaths were related to burn injuries, 30% of which were flash burns from the explosion. Physicians caring for the patients noticed that the burns began to heal, and then, at 1–2 weeks after the injury, began to deteriorate with infection and disordered formation of granulation tissue. A gray, greasy coating of the wounds was described. Associated thrombocytopenia caused bleeding into the wounds and gastrointestinal tract with the ultimate demise of most of these patients. These observations have led to studies into the pathophysiology of these injuries.
Measuring Exposure to Radiation
Radiation consists of both particles (α, β, and neutrons) and photons (γ and x-rays), which have specific energies and tissue penetrance (Table 48-7). Ionizing radiation can strip electrons from atoms to cause chemical change, resulting in biological damage. The potential for biological injury for each of these depends on the amount of energy transmitted by the particle or photon when it interacts with the target. Each type of radiation has different qualities, and each will be absorbed in differing amounts in tissue.
TABLE 48-7 Types of Radiation, Relative Energies, Penetrance, and Relative Hazard
Distance, time, and shielding can reduce exposure from a radiation source. The delivered dose of radiation diminishes over distance from its source by the inverse law.73 If the distance between an object and the source of exposure is doubled, exposure is reduced to one fourth its original value.
Dosimetry is the measurement of radiation exposure by detectors that indicate the type, quality, flux, and rate of exposure dependent on the distance of the detector from the source. Geiger–Müller instruments detect β and γ radiation and are useful in the assessment of the effectiveness of decontamination procedures.74 These instruments read counts per minute or milliroentgens per hour of β and γ irradiation. Individual exposure to radiation can be determined using radiation badges that contain a thermoluminescent dosimeter to record the cumulative dose of ionizing radiation on a photographic emulsion.
Cell damage from radiation is caused by the transfer of kinetic energy from particles or photons to existing molecules, causing ionization of mostly oxygen and formation of free radicals such as the hydroxyl radical. These highly toxic compounds react with normal biological molecules to cause cellular damage, mostly to the phospholipid membranes and deoxyribonucleic acid.75 Cell types have different sensitivities to radiation based on individual characteristics. Cells with high proliferation rates are the most sensitive, while those with low proliferation rates are relatively resistant (Table 48-8). For organs made up of resistant cells, most of the effects are on the microvasculature.
TABLE 48-8 Radiosensitivity of Human Cell Types
The overall effect depends on the extent of cellular mass exposed, the duration of exposure, and the homogeneity of the radiation field. Radiation injuries are either localized or whole body, depending on the circumstances of the exposure. The term localized radiation injury refers to an injury involving a relatively small portion of the body that does not lead to systemic effects.73 This is mostly associated with local exposure to low-energy radiation, such as handling of sealed radiation sources of 60Cobalt or 192Iridium for industrial purposes or inadvertent exposure to x-ray beams.74
Dose of exposure determines injury severity. Erythema of the skin is often the first sign, and the sooner its appearance, the higher the dose of exposure. It often appears as a superficial burn at the following intervals of time: (a) early, which will be transitory and short-lived; (b) secondarily, often 2–3 weeks after exposure and immediately preceding moist desquamation; and (c) late, 6–18 weeks after exposure, heralded by vasculitis, swelling, and pain. Depilation is also used to determine the extent of localized injury and may occur as early as 7 days after exposure. It is usually associated with doses of 7–10 Gy, and the hair loss is permanent. Alternatively, with lower doses of 3–5 Gy, depilation occurs at 18–30 days and the hair loss is temporary.
Moist desquamation is equivalent to a partial-thickness burn. This develops over a period of 3 weeks and occurs with doses of 12–20 Gy. The latency period is shorter with higher doses. Full-thickness ulceration and necrosis are caused by doses in excess of 25 Gy, and the onset varies from weeks to months after exposure. The microvasculature changes in a characteristic pattern, with surviving superficial vessels becoming telangiectatic and deeper vessels developing obliterative endarteritis. Occlusion of deeper vessels results in full-thickness necrosis.
Acute Radiation Syndrome
Detonation of a nuclear device can result in enough radiation exposure to cause immediate death for exposed individuals within the lethal area of the blast. The severity of injury from the acute radiation exposure is directly related to the effective dose of radiation to the whole body. Radiation exposure to less than 1 Gy is associated with minimal symptoms and no mortality, but exposure to greater than 8 Gy has 100% mortality.76
LD50/60 is a lethal dose required to kill 50% of the population within 60 days. LD50/60 for human beings is 250–450 rad. The hematopoietic and gastrointestinal systems are affected by radiation because they have rapidly dividing cells. Loss of stem cells and rapidly dividing cells from hematopoietic and gastrointestinal tissues can lead to bleeding, infection, and diarrhea.
Acute radiation syndrome has four phases of severity of signs and symptoms (Table 48-9). In the prodromal phase, onset is related to total dose of radiation received. It can be minutes, if a lethal dose (>8 Gy) is received, to hours if <2 Gy is received. Fever, nausea, vomiting, and anorexia may last for 2–4 days or longer if a higher dose is received. Gastrointestinal symptoms appearing within 2 hours of radiation usually indicate a fatal outcome. When signs and symptoms regress, the latent phase starts. This may last a few hours to 2–3 weeks or longer depending on the dose of radiation. As the dose of radiation increases, the latent phase becomes shorter. Symptoms of hematopoietic, gastrointestinal, and neurologic syndromes are expressed in a manifest phase following the latent phase. Nausea, vomiting, diarrhea, and bleeding characterize this phase. A recovery phase follows the manifest phase. This phase is variable and may last weeks to months, and if the dose is high enough, death ensues.
TABLE 48-9 Four Phases of Acute Radiation Syndrome
Effects of whole-body exposure depend on the dose of radiation absorbed by all tissues of the body. As opposed to local exposure to just the skin, whole-body exposure will lead to much more absorption of energy. For instance, a 5 Gy exposure to the skin of a finger (10 g of tissue) will be a total amount of absorbed energy equaling 500,000 erg. For an absorbed dose of 5 Gy over the whole body , the absorbed energy will total 5,000,000,000 erg. Thus, a lower absorbed dose may actually mean a much higher amount of absorbed energy when considered over the whole body. The effects are primarily on the cardiovascular, hematopoietic, gastrointestinal, and central nervous systems. With relatively lower doses, bleeding, infection, and loss of electrolytes can occur from damage to the intestinal mucosa and blood cell components. Higher doses will cause cardiovascular collapse and circulatory failure.
The dose absorbed will determine one of the following three courses:
1. Hematopoietic syndrome—Exposure to 1–4 Gy causes pancytopenia with an onset of 48 hours and a nadir at 30 days. Spontaneous bleeding can occur from thrombocytopenia, and opportunistic infections can occur from granulocytopenia.
2. Gastrointestinal syndrome—Exposure to 8–12 Gy will cause gastrointestinal symptoms in addition to pancytopenia. Severe nausea, vomiting, abdominal pain, and watery diarrhea occur within hours of the exposure. This resolves, and then the mucosa of the intestine sloughs in 4–7 days, which causes bloody diarrhea and loss of the intestinal barrier and translocation of bacteria. Sepsis and massive fluid losses ensue and cause hypovolemia, acute renal failure, and death.
3. Neurovascular syndrome—An exposure to >15 Gy causes immediate total collapse of vascular tone that is superimposed on the preceding syndromes. This may be caused by the massive release of vasodilatory mediators or destruction of the endothelium.77 This progresses rapidly to shock and death.
Regardless of the dose, the first symptom encountered is usually nausea and vomiting, which may resolve before the onset of the other symptoms.
Need for effective field triage and evacuation of casualties is important. In addition, an effective decontamination plan is essential.
During stabilization of the patient, information about the incident including the type of radiation, the duration of the exposure, and the distance from and direct contact with the source should be obtained. This information will be necessary to calculate the dose of radiation. Other important information is the background radiation level of the involved area at the time of a radiation incident. Average radiation background in the United States is 360 mrem per year. Any radiation above background level is considered contamination. The history should also include any previous exposures to ionizing radiation.
The individual radiation dose is assessed by determining the time to onset and severity of nausea and vomiting, decline in absolute lymphocyte count over several hours or days after exposure, and appearance of chromosomal aberrations including dicentric and ring forms in lymphocytes in peripheral blood. Documentation of clinical signs and symptoms affecting the hematopoietic, gastrointestinal, neurovascular, and cutaneous systems over time is essential for triage of victims, selection of therapy, and assignment of prognosis.
A complete blood count with differential should be performed as soon as possible and every 4 hours, with particular attention to the total lymphocyte count (TLC) as the most accurate indication of radiation injury. The rate of decrease in TLC varies inversely with the dose of radiation and therefore, portends the prognosis. A decrease in the TLC by 50% or an absolute TLC of <1,200/mm3 within 48 hours of exposure indicates that at least a moderate dose of radiation has been encountered (Table 48-10).78 Increases in serum amylase and diamine oxidase (specific to enterocytes) may be helpful in determining injury to the intestinal mucosa.79 In patients who have received a large dose of radiation, chromosome dicentric counting should be obtained. Chromosomal analysis of lymphocytes allows for accurate prediction of the received dose of radiation at 48 hours; however, this is impractical in determining the dose acutely.80
TABLE 48-10 Significance of Absolute Lymphocyte Count on Prognosis
Doses under 1 Gy usually will cause no symptoms and do not require admission to the hospital. In similar fashion, patients who are asymptomatic for 24 hours have no major injury.
Like other disaster situations, major radiation accidents and exposures can quickly overwhelm any response system. Treatment facilities may be destroyed, supply distribution may be hampered, and health care workers can be among the injured. For these reasons, triage with resources directed toward those likely to survive is paramount to limit casualties. Unfortunately, the extent of radiation injury may not be initially apparent.
Victims should be evacuated as quickly as possible to limit exposure. The patient’s injuries including burns or traumatic injury should be treated, and then symptomatic treatment for the radiation illness should commence.
Thermal burns are likely to occur in combination with radiation injury, which makes for a deadly combination. Over 50% of the deaths in Hiroshima and Nagasaki were from thermal burns.81 A thermal burn and radiation injury are synergistic, as animals that receive both injuries have a higher mortality beyond that expected for these injuries either alone or added together.82,83 In case of a nuclear explosion, it has been proposed that patients with burns alone between 20% and 70% should receive the most attention, as they can be expected to survive with adequate treatment. With the addition of a significant radiation injury, only those with less than 30% could be expected to survive.84Therefore, available resources should be directed at this group if the system is overwhelmed.
Under most circumstances, the immediate resuscitation and treatment of life-threatening injuries supersedes treatment for radiation exposure, as the effects of radiation are relatively delayed.
The first priority in treatment of radiation injury is the stabilization of the patient. Once the resuscitation has begun and the initial assessment is complete, decontamination should be started. Decontamination should occur before access to hospital or treating facility to reduce continued radiation exposure to the patient and eliminate radiation risk to others. Removal of clothing and jewelry and irrigation or washing of the body is an effective way of removing any radioactive contamination. Simply removing the clothes eliminates 90% of the contamination. Decontamination begins with the areas of highest levels of contamination. Contaminated wounds should be decontaminated prior to decontaminating intact skin. Nasal swabs from each nostril and a throat swab are performed to detect inhalation or radioactive contaminants. If patient has ingested or inhaled radioactive material, urine and stool samples are obtained to measure insoluble radioactive isotopes.
Open wounds should be covered with a clean dressing. These wounds are assumed to be contaminated with radioactive material and should be gently irrigated with copious amounts of water, saline, or 3% sodium hydroxide solution. The irrigant should be rinsed to a safe drain with the goal of diluting any radioactive particles without spreading them to adjacent uncontaminated areas. Irrigation is continued until the area indicates a steady state or absence of radiation with a Geiger counter or reaches the background radiation level.
Attention should then be turned to the intact skin, where decontamination involves gentle scrubbing of the contaminated sites with a soft brush under a steady stream of water. A 3- to 4-minute scrub with a mild soap or detergent is adequate, also. Following this, an application of povidone iodine or hexachlorophene solution and a 2-minute scrub is recommended. This should be repeated until the skin has a steady state of radiation. After two rounds of the preceding treatment, a diluted mixture of 1 part commercial bleach to 10 parts water can be used to remove further radioactive particles.
Management of Local Injuries
Most radiation injuries are local injuries, frequently involving the hands. These local injuries seldom cause the classical signs and symptoms of the acute radiation syndrome. Local injuries to the skin evolve very slowly over time, and symptoms may not occur for days to weeks after the exposure.
Mild erythema should be treated conservatively with dressings, if needed. The lesion may progress to ulceration or chronic radiodermatitis. If no signs or symptoms develop in the first 48 hours, a less severe course can be expected. Dry desquamation can be treated with lotions to moisturize the skin. Moist desquamation should be treated as a second-degree wound with daily dressing changes and topical antimicrobials. Wounds with high radiation exposure may ultimately convert to full-thickness necrosis from obliterative endarteritis and may require skin grafting, flap coverage, or amputation. Early skin grafts may be successfully used on injuries from β radiation, as these particles do not penetrate as deeply. For other types of radiation, vascularized tissue is preferable to skin grafts laid on a wound bed with a questionable long-term blood supply. The decision regarding operative treatment of these wounds is difficult due to the slow progression of the injury. If intervention is performed too early, failure may occur due to progression of the injury. If intervention is performed too late, a chronic wound that may be associated with an increased risk of infection will result.
Management of Whole-Body Injuries
The management of whole-body irradiation is aimed primarily at symptoms of cellular loss until these systems can regenerate themselves. Except for removal of internal radiation, no treatment can interrupt the process. Antiemetics to provide symptomatic relief from nausea and vomiting are indicated. Resuscitation may be needed to maintain euvolemia because of volume losses.
Patients with exposure to less than 1 Gy can be treated in the outpatient setting if there are no other injuries. For patients with more than 1 Gy exposure, admission to the hospital is indicated until symptoms have subsided. Gastrointestinal bleeding, diarrhea, infections, anemia, and diffuse bleeding from pancytopenia may occur with varying degrees of severity. If the exposure is more than 2 Gy, a bone marrow transplant as a salvage maneuver should be considered. This treatment is performed within 5 days of exposure (transplant will not function for 10–14 days) in a designated center. The blood analysis and cell typing should be completed promptly. A unique and important feature of radiation injury is that a severe exposure may so rapidly deplete the peripheral lymphocytes that none remain to serve as a basis for identification of a donor after the process has begun.85
Infections become problematic in these patients who are profoundly immunosuppressed. Opportunistic organisms are often the cause, and a thorough search for these should ensue when an infection develops. Treatment by physicians experienced in the management of profoundly immunosuppressed patients, particularly those with transplants, is important for success in these situations. All blood products should be irradiated to prevent graft versus host disease. Transplants should be performed at the peak of immunosuppression, which is between 3 and 5 days after a high-dose exposure. The use of hematopoietic growth factors such as granulocyte colony-stimulating factor (G-CSF) and granulocyte–macrophage colony-stimulating factor (GM-CSF) has been shown to decrease recovery time, return levels of granulocytes to normal after irradiation, and increase survival in animals and primates.86 Because G-CSF approved for clinical use is readily available, it could be used for radiation victims. GM-CSF is approved for clinical use to increase recovery after bone marrow transplantation.87
The treatment of burns and radiation injuries is complex. Knowledgeable physicians can treat minor injuries in the community. Moderate and severe injuries, however, require treatment in dedicated facilities with resources to maximize the outcomes from these often devastating injuries. The care of patients has markedly improved over the last 40 years, and most patients with massive injuries now survive. Challenges for the future will be in modulation of scar formation and in shortening the time to a functional and visually appealing outcome.
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