Chapter 48: Burns and Radiation

Introduction

Approximately 1.25 million people burned annually in the United States, where 30,000 patients require admissions to burn centers every year and about 3400 die.^1,2 Burns requiring hospitalization typically include burns greater than 10% of the total body surface area (TBSA) or significant burns of the face, hands, feet, or perineum.

The highest incidence of burn injury occurs during the first few years of life and between 20 and 59 years of age. The major causes of severe burn injury in younger patients are liquid scalds, and flame burns are more common in adult patients.² Most burn deaths are caused by flame burns, while liquid scald burns account for the second largest number of deaths.

Between 1971 and 1991, burn deaths decreased by 40% with a concomitant 12% decrease in deaths associated with inhalation injury.³ Since 1991, burn deaths per capita have decreased 25% according to statistics from the Centers for Disease Control and Prevention (www.cdc.gov/ncipc/wisqars). These improvements were in part due to prevention strategies resulting in fewer burns of lesser severity as well as significant advances in treatment techniques particularly in children. In 1949, Bull and Fisher first reported the expected 50% mortality rate for burn sizes in several age groups based upon data from their unit.⁴ They reported that approximately one-half of children aged 0–14 years with 49% TBSA burns die.⁴ This dismal statistic has dramatically improved, with the latest reports indicating 50% mortality for 98% TBSA burns in children 14 years and younger.^5,6 A healthy child with any size burn might be expected to survive.⁷ Nevertheless, a 60% TBSA burn has been shown to be an important threshold that, if exceeded, can increase the risk of death.^8,9 The same cannot be said, however, for those aged 45 years or older, where improvements have been more modest. This is especially true in patients over 65 years of age, where a 35% burn still kills half of the patients.¹⁰

These dramatic improvements in mortality after massive burns are due to better resuscitation, improvements in wound coverage by early excision and grafting, better support of the hypermetabolic response to injury, early nutritional support, more appropriate control of infection, and improved treatment of inhalation injuries. Future breakthroughs in the field are likely to be in the area of faster and better return of function and improved cosmetic outcomes.

Burn Center Referral Criteria

Some burn patients benefit from treatment in specialized burn centers. These centers have dedicated resources and the required multidisciplinary approach to maximize outcomes from such devastating injuries.¹¹ The American Burn Association and the American College of Surgeons Committee on Trauma have established guidelines to identify patients who should be transferred to a specialized burn center as follows¹²:

• Partial-thickness burns greater than 10% TBSA.

• Burns that involve the face, hands, feet, genitalia, perineum, or major joints.

• Third-degree burns in any age group.

• Electrical injury, including lightning injury.

• Chemical burns.

• Inhalation injury.

• Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality.

• Any patient with burns and concomitant trauma in which the burn injury poses the greatest risk of morbidity or mortality.

• Burned children in hospitals without qualified personnel or equipment for the care of children.

• Burn injury in patients who will require special social, emotional, or rehabilitative intervention.

Pathophysiology

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

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

The skin generally provides a barrier to limit transfer of heat energy to underlying tissues; however, after the source of burn is removed, the response of local tissues can lead to further injury. The necrotic area of a burn is termed the “zone of coagulation.” The area immediately surrounding the necrotic zone has a moderate degree of injury that initially causes a decrease in tissue perfusion. This area is termed the “zone of stasis” and, depending on the environment of the wound, can progress to coagulative necrosis if local blood flow is not maintained. Thromboxane A₂, a potent vasoconstrictor, is present in high concentrations in burn wounds, and local application of thromboxane inhibitors has been shown to improve blood flow and may decrease this zone of stasis.^13,14 Antioxidants^15,16 and inhibition of neutrophil-mediated processes¹⁷ may also improve blood flow, preserve this tissue, and affect the depth of injury. Endogenous vasodilators such as calcitonin gene-related peptide and substance P, whose levels are increased in the plasma of burn patients,¹⁸ may play a role, also. The last area, the zone of hyperemia, is formed as a result of vasodilation from inflammation surrounding the burn wound. This zone contains clearly viable tissue from which the healing process begins (Fig. 48-1).

Inflammatory Response

The hypermetabolic response and massive release of inflammatory mediators in the wound and in other tissues is seen with a significant burn. This hypermetabolism is associated with alterations in blood serum glucose as well as lipids, and it typically occurs in the ebb phase (first 14 hours) and flow phase (until 5 days post burn).^19,20,21 Many mediators have been proposed to explain the changes in permeability after burns, including prostaglandins, catecholamines, histamine, bradykinin, vasoactive amines, leukotrienes, and activated complement.²² Mast cells in the burned skin release histamine in large quantities immediately after injury,²³ causing a characteristic response in venules by increasing the space in intercellular junctions.²⁴ The use of antihistamines in the treatment of burn edema, however, has had limited success with the possible exception of H₂-receptor antagonists.²⁵ In addition, aggregated platelets release serotonin, which plays a major role in the formation of edema. This agent acts directly to increase pulmonary vascular resistance and indirectly aggravates the vasoconstrictive effects of various vasoactive amines. Serotonin blockade has been shown to improve cardiac index, decrease pulmonary artery pressure, and decrease oxygen consumption after burns.²⁶

As previously noted, another mediator likely to play a major role in changes in vascular permeability and tone is thromboxane A₂. Levels of thromboxane increase dramatically in the plasma and wounds of burn patients.^27,28 This potent vasoconstrictor leads to platelet aggregation in the wound, contributing to expansion of the zone of stasis. It also causes prominent mesenteric vasoconstriction and decreased blood flow to the gut in animal models with compromised gut mucosal integrity and immune function.²⁹

Patients with major burn injury have the highest metabolic rate of all critically ill or injured patients.³⁰ The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, loss of lean body mass and body weight, accelerated breakdown of glycogen and protein, lipolysis, and immune depression.^31,32 This response is mediated by increases in circulating levels of catabolic hormones including catecholamines, cortisol, and glucagon.^32,33

Pharmacological agents have been used to attenuate catabolism and to stimulate growth after burn injury. To further minimize erosion of lean body mass, administration of anabolic hormones such as growth hormone, insulin, insulin-like growth factor (IGF)/IGF-binding protein-3, oxandrolone, fenofibrate, and catecholamine antagonists such as propranolol has been studied. These agents contribute to maintenance of lean body mass and promote wound healing.^{34,35,36,37,38,39,40}

Changes in Organ Function

Major burn injury results in multiple organ dysfunction. Cardiac effects include marked loss of plasma volume, increased peripheral vascular resistance, and decreased cardiac output.^41,42,43,44 Pulmonary effects include a decrease in pulmonary static compliance.⁴⁵ These changes are associated with mild direct cardiac damage.⁴⁶ Renal blood flow decreases with a fall in glomerular filtration rate, which may result in renal dysfunction. Metabolic changes are characterized by an early depression followed by a marked, sustained increase in resting energy expenditure as well as increased lipolysis, proteolysis, and oxygen consumption. This is driven, in part, by an increase in production of catecholamines, cortisol, and glucagon.⁴⁷ Increased peripheral lipolysis results in hepatic steatosis, and a fatty liver is caused by breakdown of triglycerol into free fatty acids. Like steatosis, peripheral lipolysis contributes to morbidity and mortality through fatty infiltration of various organs. All burn-related metabolic responses last more than 2 years post burn.²¹ There is a generalized impairment in host defenses, with depressed production of immunoglobulin, decreased opsonic activity, and depressed bactericidal activity.⁴⁸ This leads to an increased susceptibility to infections.

Initial Care

The patient should be removed from the source of the burn to stop the burning process, and clothing and jewelry should be immediately removed. The patient should be kept warm by being wrapped in a clean sheet or blanket. The immediate treatment of a burn patient should proceed as with any trauma patient, and any potential life-threatening injuries should be identified and treated.

Assessment of the patient starts with the airway. One hundred percent oxygen is administered, and oxygen saturation is monitored. Stridor, wheezing, tachypnea, and hoarseness indicate impending airway obstruction due to an inhalation injury or edema, and immediate treatment is required. If the patient has labored breathing or signs of obstruction, immediate intubation should be performed with in-line stabilization of the neck if an injury to the cervical spine is suspected.

Arterial blood gas and carboxyhemoglobin (COHb) levels should be obtained when inhalation injury is suspected. Carbon monoxide (CO) has an affinity for hemoglobin (Hb) that is 210–280 times that of oxygen, and COHb can falsely elevate oxygen saturation levels determined colorimetrically. Therefore, use of a pulse oximeter may not be effective, as patients with CO poisoning may show falsely normal oxygen saturation levels. Use of a pulse CO-oximeter enables measurement of absorption at several wavelengths to distinguish oxyhemoglobin from COHb saturation and determines blood oxygen saturation more reliably including the total amount of Hb, COHb, met-Hb, and reduced Hb.⁴⁹

The treatment for CO inhalation is 100% O₂ by endotracheal tube or face mask. This will decrease the half-life of CO from 4–6 hours at room air to 40–80 minutes with 100% O₂. In three atmosphere absolute 100% oxygen in a hyperbaric chamber, the half-life decreases further to 15–30 minutes. In addition, full-thickness circumferential burns of the chest can interfere with ventilation. Bilateral expansion of the chest should be observed to document equal air movement. If the patient is on a ventilator, airway pressure and Pco₂ should be monitored. Rising airway pressure and Pco₂ indicates compromised ventilation, and an escharotomy should be performed to allow better movement of the chest and improve ventilation.

Noninvasive measurement of blood pressure may be difficult in patients with burned extremities, and these individuals may need an arterial line so that their blood pressure can be monitored during transfer or resuscitation. A radial arterial line may not be reliable in patients with upper extremity burns and is difficult to secure. Therefore, the insertion of a femoral arterial line may be more appropriate.

Abdominal injuries and fractures may be present in patients who have been burned, as well. Each patient should be fully assessed for associated injuries that may be more immediately life-threatening. The burn wounds can be addressed after standard evaluation.

As previously noted, burn patients should initially be placed on sterile or clean sheets. Cold water and ice may, in large burns, harm patients by inducing hypothermia and should be avoided. The patient should be kept warm and the wounds clean until assessment by the physicians responsible for definitive care of the burns. A nasogastric tube and bladder catheter are placed to decompress the stomach and to monitor urine output.

Fluid Resuscitation

After a large burn, there is a systemic capillary leakage that increases with burn size. Capillaries usually regain competence after 18–24 hours if resuscitation has been successful. Waiting for longer times until initiating resuscitation of burn patients results in poorer outcomes, and delays should be minimized.⁵⁰ The best intravenous (IV) access can be obtained with short large-bore peripheral catheters through unburned skin; however, veins beneath burned skin can be accessed to avoid a delay in obtaining IV access. Central venous lines are required when peripheral IV access is difficult. Intraosseous access is another option until IV access is accomplished. Lactated Ringer’s solution without dextrose is the fluid of choice except in children less than 2 years. Infants should receive some 5% dextrose in intravenous solutions to prevent hypoglycemia because they have limited glycogen stores. This can be accomplished by giving 5% dextrose as maintenance fluid and lactated Ringer’s solution as resuscitation fluid.

The initial rate can be rapidly estimated by multiplying the estimated TBSA burned by the weight in kilograms, which is divided by 4 to get an hourly rate for the first eight hours (ie, a rearrangement of the Parkland formula). Thus, the rate of infusion for an 80-kg man with a 40% TBSA burn would be 40% TBSA × 80 kg /4 = 800 mL/h for the first 8 hours.

Different formulas have been devised to assist the clinician in determining the proper amount of resuscitation fluid. Early work by Baxter and Shires formed the basis for modern fluid resuscitation protocols.⁵¹ They showed that edema fluid in burn wounds is isotonic and contains the same amount of protein as plasma and that the greatest loss of fluid is into the interstitial fluid compartment. They used various volumes of intravascular fluid to determine the optimal delivered amount in terms of cardiac output and extracellular volume in a canine burn model. These findings led to a successful clinical trial of the “Parkland formula” in resuscitating burn patients (Table 48-2). From their findings, they also concluded that colloid solutions should not be used in the first 24 hours until capillary permeability returns closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after a burn (8 hours) and, thus, colloids could be used earlier.⁵²

Moncrief and Pruitt studied the hemodynamic effects of fluid resuscitation in burns, which resulted in the Brooke formula (Table 48-2). They showed that fluid loss in moderate burns results in an obligatory 20% decrease in both extracellular fluid and plasma volume during the first 24 hours after injury. In the second 24 hours, plasma volume returns to normal with the administration of colloid. Cardiac output is low on the first post burn day in spite of resuscitation, but subsequently increases to supernormal levels as the flow phase of hypermetabolism is established.²² Since these studies, it has been found that much of the fluid needs are due to capillary leakage that permits passage of large molecules and water into the interstitial space. Intravascular volume follows the gradient into the burn wound and non-burned tissues. Approximately 50% of fluid resuscitation needs are sequestered in nonburned tissues in 50% TBSA burns.⁵³

Hypertonic saline solutions have theoretic advantages in the resuscitation of burn patients. As these solutions have been shown to decrease net fluid intake,⁵⁴ decrease edema,⁵⁵ and increase lymph flow by transferring volume from the intracellular space to the interstitium. During the use of these solutions, care must be taken to avoid serum sodium concentrations greater than 160 mEq/dL.²² Of note, it has been shown that patients with over 20% TBSA burns and randomized to resuscitation with either hypertonic saline or lactated Ringer’s solution do not have significant differences in total volume requirements or in changes in percent weight gain in the days following the burn.⁵⁶ Other investigators have found an increase in renal failure with hypertonic solutions that has tempered further enthusiasm for their use in resuscitation.⁵⁷ Some burn centers have successfully used a modified hypertonic solution by adding one ampule of sodium bicarbonate to each liter of lactated Ringer’s solution.⁵⁸ Further research will need to be conducted to determine the optimal formula to reduce over-resuscitation and maintain adequate cellular function.⁵⁹

Of interest, it has been shown that resuscitation volumes required in the severely burned patient decrease when high-dose intravenous ascorbic acid is administered during resuscitation. This is associated with decreased weight gain and improved oxygenation.⁶⁰

Most burn centers use guidelines similar to the Parkland or Brooke formulas, with varying amounts of crystalloid and colloid solutions being administered for the first 24 hours post burn (see Table 48-2). These formulas are guidelines to the amount of fluid necessary to maintain adequate perfusion.

In pediatric burns, the commonly used formulas are modified to account for changes in surface area-to-mass ratios. Compared to adults, children have a larger body surface area relative to their weight and generally have greater fluid needs during resuscitation. The Galveston formula for children based on body surface area uses 5000 mL/m² TBSA burned for resuscitation + 1500 mL/m² TBSA for maintenance in the first 24 hours (Table 48-2). This formula accounts for both the resuscitation fluid requirements and maintenance needs of children with burns.

All these formulas calculate the amount of volume given in the first 24 hours, with half being given in the first 8 hours and the other half being given over the next 16 hours.

Both under- and over-resuscitation should be prevented. Under-resuscitation may lead to multiple organ failure caused by decreased perfusion; however, under-resuscitation is uncommon.⁶¹ On the other hand, over-resuscitation (so called “fluid creep”⁵⁹) may result in pulmonary edema, extremity and abdominal compartment syndromes, as well as pericardial effusions which may increase risk of acute respiratory distress syndrome (ARDS).^62,63,64,65 Over-resuscitation can be prevented by monitoring urine output, which should be maintained at 0.5 mL/kg/h in adults and 1.0 mL/kg/h in children. Other parameters such as heart rate, blood pressure, mental status, and peripheral perfusion should be monitored, also. The rate of intravenous fluid infusion should be adjusted hourly based on the patient’s response to the particular fluid volume administered.

Determination of Burn Depth

The depth of burn determines the outcome in terms of survival and scarring. Though technologies such as laser Doppler imaging^66,67 with multiple sensors hold promise for quantitatively determining burn depth, it is most accurately assessed by the judgment of experienced physicians. These measurements may give objective evidence of tissue loss and assist the physician in the proper choice of treatment. Determination of depth is critical in the treatment plan, as there are wounds that will heal with only local treatment and those that will require operative intervention for timely healing. Being able to identify patients who will need operative intervention will facilitate care.

Superficial burns (first-degree) are confined to the epidermis. These burns are painful, erythematous, and blanch to the touch with an intact epidermis without blister. Examples include sunburn and a minor scald or flash burn. These burns will heal in 3–5 days, will not result in scarring, and treatment is aimed at comfort with the use of topical soothing salves with or without aloe and nonsteroidal anti-inflammatory drugs or acetaminophen.

Partial-thickness (second-degree) burns are divided into two types (Figs. 48-2 and 48-3), superficial and deep. All partial-thickness burns have some degree of dermal injury, and the division is based on the depth of injury into this level. Superficial partial-thickness burns are erythematous, painful, and wet. They blanch to touch and often form blisters. Blistering may not occur for some hours following injury. Burns thought to be first degree may subsequently be diagnosed as partial-thickness burns by the second day. These wounds will spontaneously reepithelialize in 7–14 days from epidermal structures retained in the rete ridges, hair follicles, and sweat glands. Deep partial-thickness burns extending into the reticular dermis will appear dry, paler than pink, or mottled. They may not blanch to touch, but will remain painful to pinprick. In deeper partial-thickness burns, sensation becomes blunted (less sensitive to pinprick than surrounding normal skin). Capillaries may refill slowly after compression or not at all. These burns will heal in 21–28 days or longer, depending on the depth of burn, by reepithelialization from hair follicles and keratinocytes in sweat glands. Nevertheless, deep partial-thickness burns may require skin grafting to facilitate healing. The longer the wound takes to heal, the worse the scarring will be.

Full-thickness (third-degree) burns are burns that extend through the dermis down to the subcutaneous tissue. They are characterized by a firm leathery eschar that is painless and yellow, grey, white, or cherry red in color (Figs. 48-3 and 48-4). The eschar is insensitive to pinprick but may be sensitive to pressure on palpation. No epidermal or dermal appendages remain, and these wounds must heal by reepithelialization from the wound edges by contraction, which takes a protracted time. Full-thickness burns require excision and skin grafting with autograft skin so that they can heal in a timely fashion.

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

Determination of Burn Size

The most commonly used method of determining the burn size in adults is the “rule of nines” (Fig. 48-5). Each upper extremity and the head and neck are 9% of the TBSA. Each lower extremity, the anterior trunk, and posterior trunk are 18% each. Finally, the perineum and genitalia are 1% of the TBSA. Another method of estimating burn size is using the patient’s open hand including the digits, which is approximately 1% TBSA.

The Berkow formula or Lund Browder chart can be helpful in determining burn size in children (Table 48-3). Children have a relatively larger portion of body surface area in the head and neck and a smaller surface area in the lower extremities. Infants have 21% of the TBSA in the head and neck and 14% in each leg, which incrementally approaches adult proportions with increasing age.

Overestimation of burn size is common.^68,69 Precise estimation of burn size is important, as an inaccurate estimation may lead to an inadequate fluid resuscitation or over-resuscitation.⁷⁰ In the future, computer-aided systems or smartphones may aid estimation of burn size and improve accuracy.⁷¹

Escharotomies

With circumferential constricting burns (deep partial- and full-thickness burns) to an extremity, peripheral circulation to the limb can be compromised with edema. Development of generalized edema beneath a non-yielding eschar impedes venous outflow and will have a tourniquet effect on the arterial inflow to the distal beds. This can be recognized by numbness and tingling in the limb and increased pain in the digits. Arterial flow can be assessed by pulse oximetry and determination of Doppler signals in the digital arteries and the palmar and plantar arches in affected extremities. Capillary refill is assessed, also. The release of a burn eschar is performed by making lateral and medial incisions on the affected extremity using the electrocautery. The entire constricting eschar must be incised to relieve the obstruction to blood flow. If the hand is involved, two incisions are made on the dorsal surface and along the medial or lateral sides of the digits, taking care not to damage the neurovascular bundles. These bundles are located slightly to the palmar side of the digit.

If vascular compromise has been prolonged, reperfusion after an escharotomy may cause reactive hyperemia and further edema in the muscle, making continued surveillance of the distal extremities necessary. Increased pressures in the underlying musculofascial compartments may necessitate fasciotomies.

Extremity compartment syndrome can also develop in patients receiving large amounts of resuscitation fluids or in severe burns such as electrical injuries. In such patient, a standard fasciotomy should be performed instead of an escharotomy.

A circumferential burn of the chest with a constricting eschar can cause a similar phenomenon, except the effect is to decrease ventilation by limiting excursion of the chest wall. Any decline in ventilator parameters such as an increase in peak airway pressure and Pco₂ should prompt inspection of the chest with appropriate escharotomies. Escharotomies should be made in the lateral chest bilaterally with a connecting incision being introduced across the chest to relieve constriction and allow adequate ventilation.

Inhalation Injury

Inhalation injuries occur in 8% of cutaneous burn injuries and are one of the factors that contributes to mortality in burns by adding another inflammatory focus and impeding normal gas exchange. The presence of such an injury can be used as a significant predictor of outcome in massive burns. Inhalation injuries used to be associated with high mortality, but the last few decades have seen improved survival with early diagnosis, better airway management, gentle ventilation, and pulmonary hygiene.⁷² Early diagnosis and prevention of complications are necessary to decrease morbidity and mortality related to inhalation injury.

In most inhalation injuries, damage is caused primarily by inhaled toxins. Heat is generally dispersed in the upper airways, whereas cooled smoke particles and released toxins are carried distally into the bronchi and alveoli. The injury is principally chemical in mechanism, and the response is an immediate increase in blood flow in the bronchial arteries with formation of edema and increases in lung lymph flow. The lung lymph in this situation is similar to serum, indicating that permeability at the capillary level is markedly increased. The resulting edema is associated with an increase in lung neutrophils, and it is postulated that these cells may be the primary mediators of pulmonary damage with this injury.⁷³ Neutrophils release proteases and reactive oxygen species that can produce conjugated dienes by lipid peroxidation. High concentrations of these conjugated dienes are present in the lung lymph and pulmonary tissues after inhalation injury, suggesting that increased neutrophils are active in producing cytotoxic materials.³⁷

Another hallmark of inhalation injury is separation of the ciliated epithelial cells from the basement membrane followed by formation of exudate within the airways. The exudate consists of proteins found in the lung lymph and eventually coalesces to form fibrin casts.⁷⁴ Clinically, these fibrin casts can be difficult to clear with standard airway suction, and bronchoscopy is often required. These casts can also add barotrauma to localized areas of the lung by forming a “ball-valve.” During inspiration, the airway diameter increases, and air flows past the cast into the distal airways. During expiration, the airway diameter decreases, and the cast effectively occludes the airway, preventing the inhaled air from escaping. Increasing volume leads to localized increases in pressure that are associated with numerous complications, including pneumothorax and decreased lung compliance. Therapy aimed at clearing the airway and minimizing complications would likely improve outcomes.

Patients with smoke inhalation often present with a history of exposure to smoke in a closed space, stridor, hoarseness, wheezing, carbonaceous sputum, facial burns, and singed nasal vibrissae. Each of these findings has poor sensitivity and specificity⁷⁵; therefore, the diagnosis is often established with bronchoscopy. Bronchoscopy can reveal early inflammatory changes such as erythema, edema, ulceration, sloughing of mucosa, and prominent vasculature in addition to infraglottic soot.⁷⁶ Mechanical ventilation may be needed to maintain gas exchange, and repeated bronchoscopies may reveal continued ulceration of the airways with the formation of granulation tissue and exudate, inspissation of secretions, and edema.

Management of an inhalation injury is directed at maintaining open airways, clearing secretions, and maximizing gas exchange while the lungs heal. A coughing patient with a patent airway can clear secretions very effectively, and efforts should be made to treat patients without mechanical ventilation, if possible. If respiratory failure is imminent, intubation should be instituted early, with frequent chest physiotherapy and suctioning being performed to maintain pulmonary hygiene. Frequent bronchoscopies may be needed to clear inspissated secretions. Mechanical ventilation should be used to provide gas exchange with as little barotrauma as possible. Inhalation treatments have been effective in improving the clearance of tracheobronchial secretions and decreasing bronchospasm.

For the pharmacological treatment of inhalation injury, beta-agonists, nebulized acetylcysteine and heparin, and nebulized racemic epinephrine have been beneficial as has adequate humidification of ventilated air.^9,77,78

In addition to conventional ventilator methods, novel ventilator therapies such as high-frequency percussive ventilation have been devised to minimize barotrauma. This method combines standard tidal volumes and respirations (ventilator rates 6–20 breaths/minute) with smaller high-frequency respirations (200–500 breaths/minute) and has been shown to permit adequate ventilation and oxygenation in patients who have failed conventional ventilation. An explanation for the greater utility of this method is the ability to recruit alveoli at lower airway pressures.⁷⁹ This ventilator method may also have a percussive effect that loosens inspissated secretions and improves pulmonary hygiene.

Chemical Burns

Prompt treatment is imperative in minimizing tissue damage in chemical burns, and the area of the burn should be copiously irrigated with water. Care must be taken to direct the drainage of the irrigating solution away from unburned areas to limit the area of skin exposed to chemicals. If the chemical composition is known, monitoring the irrigated solution pH will give an indication of the effectiveness of the irrigation. Attempts at neutralization of either acidic or basic solutions can result in heat production and extend the injury. Generally, acids cause coagulative necrosis and are confined to the skin, while basic solutions cause liquefactive necrosis and extend further into the tissues. After the chemical injury has been controlled, the remaining burn is treated in the same way as thermal injuries. Assessment of burn depth is often difficult, but is typically deeper than it appears.

Hydrofluoric acid is a highly dangerous substance, yet it is used widely in industrial settings. It causes severe burns and systemic effects.⁸⁰ When it is exposed to biological tissues, the fluoride ion precipitates calcium and may cause systemic hypocalcemia. This may occur even with a very small burn. Management of burns caused by this substance differs from burns caused by other acids. In addition to undergoing copious irrigation of the burned area, the exposed skin should be treated with 2.5% calcium gluconate gel to provide pain relief and limit the spread of the fluoride ion. For hand burns, even intra-arterial calcium gluconate has been advocated. Patients should be monitored closely for prolongation of the QT interval, torsade de pointes, or ventricular fibrillation. Changes in the QT interval should be treated with 20 mL of 10% calcium gluconate repeated as needed to maintain normal levels of serum calcium. Other serum electrolytes such as magnesium must be closely monitored, also.

Electrical Injuries

Electrical injuries are unique in that the location of the injury may be mostly internal as the current proceeds down the path of least resistance via the nerves, blood vessels, and muscle. This spares the skin, except at the contact points of the electrical current. If the resistance of contact sites of high-voltage current is high, the local injury may be extensive, with loss of digits or even the entire extremity. In addition, an electrical injury may be associated with blunt trauma from titanic contractions of muscles or falls.

With any significant electrical injury, vigorous intravenous resuscitation should be given with attention to myoglobinuria from muscle damage. Urine output should be maintained at greater than 1 mL/kg/h with fluid administration and mannitol to increase renal tubular flow if needed. The administration of intravenous bicarbonate to alkalinize the urine should be considered to decrease precipitation and deposition of myoglobin in the renal tubules, but it has not been proven in prospective studies. Patients should be monitored for cardiac arrhythmias for 24 hours after admission.

Serial examinations of the extremities are necessary to detect any vascular compromise, and fasciotomies of the involved limbs are often necessary. If operative exploration is necessary, complete fasciotomies with inspection of deep tissues should be undertaken. Acute and chronic neuropathies are common and may be permanent. Development of cataracts is also common after severe electrical injury and may be delayed for months; therefore, close ophthalmologic follow-up is necessary.

Care of the Burn Wound

Improvements in the treatment of burn wounds and use of antimicrobial dressings have dramatically decreased the incidence of wound infection and sepsis in burn patients.⁸¹ The old technique of allowing separation of eschar with lysis by bacterial enzymes has given way to wound closure using early excision and skin grafting.⁸² In wounds that will heal spontaneously without skin grafts, topical antimicrobial agents or silver-based dressings limit wound contamination and provide a moist environment for healing. Current therapy for burn wounds can be divided into the following three stages: assessment, management, and rehabilitation. Once the extent and depth of the wounds have been assessed and the wounds have been thoroughly cleaned and debrided, the management phase begins. Each wound should be dressed with an appropriate covering that protects the damaged epithelium and dermis, prevents infection, and provides comfort over the painful wound.

The choice of dressing should be individualized based on the characteristics of the burn. First-degree burns are minor with minimal loss of barrier function. These wounds require no dressing and are treated with lotion to keep the skin moist. Second-degree burns can be treated by an antibiotic ointment such as silver sulfadiazine and covered with gauze under elastic wraps. Alternatively, the wounds can be covered with a temporary biologic or synthetic covering to close the wound. These coverings eventually slough as the wound reepithelializes underneath. These types of dressings provide stable coverage with decreased pain and a barrier to evaporative loss. They may also have the added benefit of not inhibiting epithelialization, a feature of most topical antimicrobial agents. These coverings include biological materials such as allograft skin, porcine xenograft skin, human amniotic membranes,⁸³ and synthetic materials such as Biobrane (Smith and Nephew, Andover, MA, USA) and various silver impregnated dressings such as Mepilex (Mölnlycke Health Care, Gothenburg, Sweden).^83,84,85,86 The advantages and disadvantages of the various coverings are listed in Table 48-4. These should be applied within 24 hours of the burn before bacterial colonization of the wound occurs.

Surgical Management of Burn Wound

Deep partial-thickness burns may not heal and full-thickness burns will not heal in a timely fashion without autografting. Also, burned tissues serve as a nidus for infection and inflammation. Early excision and skin grafting of these wounds is now practiced by most burn surgeons in response to literature showing benefit over serial debridements in terms of survival, blood loss, and length of hospitalization.^87,88,89

These excisions can be performed under tourniquet control or with application of topical epinephrine to minimize blood loss. After a burn wound has been excised, the wound must be covered with either autograft skin or another covering, such as allograft skin. Wounds less than 20% TBSA can usually be closed in one operation with autograft skin taken from the patient’s available normal skin (donor site). In these operations, the skin grafts are either unmeshed or meshed with a narrow ratio (2:1 or less). In major burns, donor sites may be limited to the extent that the entire wound cannot be covered with autograft skin in one operation. The availability of allograft skin to cover these wounds has changed the course of modern treatment for massive burns. A typical method of treatment is to use widely expanded autograft skin (4:1 or greater ratio) covered with allograft skin to completely close the wounds.⁹⁰ The 4:1 expended autograft skin heals underneath the allograft skin by reepithelialization in approximately 21 days, and the allograft skin will slough as autograft skin heals underneath it. Portions of the wound that cannot be covered with widely meshed autograft skin due to scarcity of available autograft skin are temporarily covered with allograft skin in preparation for autografting when donor sites are healed and available. Ideally, areas with less cosmetic importance are covered with the widely meshed skin to close most of the wound prior to using nonmeshed grafts for the cosmetically important areas such as the hands, face, and neck.

As autologous skin grafts are still the gold standard for the treatment of full-thickness burns and donor sites can be limited after large burns, dermal and epidermal substitutes have received considerable attention. Dermal replacements such as Integra (Integra LifeSciences Corporation, Plainsboro, NJ, USA) and Alloderm (LifeCell Corporation, Branchburg, NJ, USA) are commercially available.^91,92,93 For the epidermal replacement, cultured epithelial autografts are available; however, these are expensive to use and prone to breakdown and infections.⁹⁴ A more affordable approach for epithelial autografts might be ReCell (Avita Medical, Royston, UK). The ReCell system can be easily generated within the operating room and applied after 15 minutes. Large prospective randomized controlled trials are warranted to determine its effectiveness.^86,95

Most surgeons are in favor of early excision as previously noted. Full thickness burn wounds are excised within the first week, sometimes in serial operations, removing 20% of the burn wound at each operation on subsequent days. Others remove the total burn wound in one operative procedure under good anesthesia support; however, this can be difficult in patients with large burns and complicated by the development of hypothermia or massive blood loss. Performing excision immediately after stabilization of the patient is recommended, as blood loss diminishes if the operation can be performed the first day after injury.⁸⁸ This may be due to the relative predominance of vasoconstrictive substances such as thromboxane and catecholamines in the circulation and the natural edema planes that develop immediately after the injury. When the wound becomes hyperemic after 2 days, blood loss during excision can be considerable.

Early excision should typically be reserved for full-thickness burns caused by flame. This is highlighted because scald burns are very common. These injuries are often partial thickness or a mixture of partial and full thickness and should be covered with substances such as allograft, porcine xenograft, human amnion, Biobrane, or silver-impregnated dressings. A deep partial-thickness burn can appear clinically to be a full-thickness burn at 24–48 hours after injury, particularly if it has been treated with topical antimicrobials that combine with wound drainage to form a pseudoeschar. A randomized prospective study comparing early excision versus conservative therapy with late skin grafting of scald burns showed that those excised early had more wound excised, more blood loss, and more time in the operating room. No difference in hospital length of stay or rate of infection was seen.⁹⁶

Skin graft loss after an operation is typically due to one or more of the following reasons: presence of infection, fluid collection under the graft, shearing forces that disrupt the adhered graft, or an inadequate excision of the wound bed leaving residual necrotic or nonviable tissue. Infection is controlled by the appropriate use of perioperative antibiotics and covering the grafts with topical antimicrobial agents at the time of surgery. Meticulous hemostasis, appropriate meshing of grafts, aspiration of a hematoma or seroma under a non-meshed graft postoperatively, and/or use of a bolster dressing over the graft minimize fluid collection. Shearing is decreased by immobilization of the grafted area. Inadequately excised wound beds are uncommon in the practice of experienced surgeons.

Control of Infection

Invasive infections in burn wounds can be reduced by early excision and closure and the timely and effective use of antimicrobials. The antimicrobials that are used can be divided into those given topically and those given systemically.

Available topical antibiotics can be divided into salves and soaks. Salves are generally applied directly to the wound with dressings placed over them, and soaks with antimicrobial solutions are generally poured into dressings on the wound. Each of these classes of antimicrobials has its advantages and disadvantages. Salves may be applied once or twice a day but may lose their effectiveness in between dressing changes. Soaks will remain effective because antimicrobial solution can be added without removing the dressing; however, the underlying skin can become macerated.

Some of the topical antibiotic salves include 8.5% mafenide acetate, 1% silver sulfadiazine, polymyxin B, neomycin, bacitracin, and mupirocin. No single agent is completely effective, and each has advantages and disadvantages. Mafenide acetate has a broad spectrum of activity through its sulfa moiety, particularly for Pseudomonas and Enterococcus species. It has the advantage of being able to penetrate eschar, also. Disadvantages include pain on application, an allergic skin rash, and inhibition of carbonic anhydrase activity that can result in a metabolic acidosis when applied over large surfaces. For these reasons, mafenide acetate is typically reserved for small full-thickness burns and ear burns to prevent chondritis. Silver sulfadiazine, the most frequently used topical agent, has a broad spectrum of activity from its silver and sulfa moieties that covers gram-positive organisms, most gram-negative organisms, and some fungi. It is painless upon application. Occasionally, patients will complain of some burning sensation after it is applied, and some patients will develop a transient leukopenia 2–4 days following its continued use. This leukopenia is generally harmless and resolves with cessation of treatment in 2–3 days. When the leukopenia resolves, silver sulfadiazine may be reapplied without recurrence. Petroleum-based antimicrobial ointments with polymyxin B, neomycin, and bacitracin are clear on application and allow for observation of the wound, are painless, and provide a moist environment. These agents are commonly used for the treatment of facial burns, graft sites, healing donor sites, and small partial-thickness burns. Mupirocin is an ointment that has improved activity against gram-positive bacteria, particularly methicillin-resistant Staphylococcus aureus. Nystatin in powder form can be applied to wounds to control fungal growth, and it can be combined with topical agents such as polymyxin B to decrease colonization of both bacteria and fungi.

Available agents for application as a soak include 0.5% silver nitrate solution, 0.025% sodium hypochlorite, 5% acetic acid, and 5% mafenide acetate solution. 0.5% silver nitrate has the advantages of painless application and almost complete antimicrobial coverage. Disadvantages include its staining of surfaces to a dull gray or black when the solution is exposed to light. The solution is hypotonic, and continuous use can cause leaching of electrolytes, with rare methemoglobinemia as another complication. Hypochlorite is a basic solution with effectiveness against most microbes, but it also has cytotoxic effects on wounds, thus inhibiting healing. Low concentrations of sodium hypochlorite (0.025%) have less cytotoxic effects and maintain antimicrobial effects. In addition, hypochlorite ion is inactivated by contact with protein. Therefore, the solution must be continually changed. The same is true for acetic acid solutions, though this solution may be more effective against Pseudomonas. Mafenide acetate solution has the same characteristics as mafenide acetate cream.

Perioperative systemic antimicrobials are useful in decreasing sepsis in the burn wound. Common organisms that must be considered when choosing a perioperative regimen include S. aureus and Pseudomonas sp, which are prevalent in wounds. Acinetobacter sp has emerged as a significant organism in the burn wounds, also.

Management of Organ Systems

Major burns affect a number of organ systems in addition to the skin. The immense inflammatory focus incited by the burn causes the release of numerous cytokines and inflammatory mediators that have many systemic effects and, ultimately, may result in multiorgan dysfunction and death. The systemic inflammatory response syndrome is present in every major burn, but with differing severity, and the kidneys, liver, heart, lungs, hematopoietic system, and coagulation system may be affected. Each of these systems must be supported through the course of the burn injury.

After resuscitation and stabilization, evaporative losses through open wounds including the area of the burn and any donor sites remain high. Approximately 3750 mL/m²/d of free water is lost through open wounds. These insensible losses must be added to urine output, stool volume, and respiratory losses in determining fluid balances. Daily weights are useful in determining the response to fluid management. Sodium, potassium, calcium, magnesium, and phosphorus are lost into burn wounds, as well, and require constant monitoring and replacement.

In the acute phase and up to 2 years post injury, cardiac output and heart rate remain elevated.⁴⁴ Accordingly, a clinical trial was undertaken to investigate the effects of a non-selective beta-receptor antagonist on cardiac dysfunction and showed a significant reduction in both heart rate and resting energy expenditure at 12 months follow-up.⁹⁷

Renal failure after a burn occurs in a bimodal fashion, with an early peak that is due to acute tubular necrosis from inadequate early resuscitation and a later peak at 2–4 weeks that is likely due to sepsis and nephrotoxic medications.^98,99 Treatment is as with renal failure of any other cause. Indications for dialysis include life-threatening congestive heart failure, pulmonary edema, hyperkalemia and metabolic acidosis refractory to medical management. Catheters can be placed through burned tissue, although intact skin is preferable, and continuous venovenous hemodialysis may have some advantages over routine hemodialysis because of slower fluid fluxes.

Hepatic dysfunction can occur because of toxins associated with chemical injury or flame burns in which the patient was doused with chemicals, particularly gasoline. The direct hepatotoxicity that results is manifested by early increases in hepatocellular enzymes. Support through the recovery period is indicated. Later evidence of hepatic dysfunction from sepsis is common, also. A striking finding associated with larger burns is the development of a fatty liver, which can increase hepatic size two- to threefold.¹⁰⁰ The primary cause seems to be a relative decrease in efficiency of the very low density lipoprotein system to handle massive increases in free fatty acids, which arise from peripheral lipolysis induced by sustained elevations in serum catecholamines. Fat that cannot be exported is deposited in the liver.

Coagulopathies from decreased hepatic synthetic function of coagulation factors, thrombocytopenia, or dilutional effects of massive blood transfusions can occur after a major burn, as well.

Nutritional Management of Burn Patients

Nutritional support of severely burned patients is best accomplished by early enteral nutrition that can abate the hypermetabolic response to a burn.^101,102 Early enteral feeding preserves gut mucosal integrity, improves intestinal blood flow and motility, and decreases translocation of intestinal bacteria.¹⁰¹ Therefore, nasoduodenal or nasojejunal enteral tube feeding should be commenced as early as within the first 6 hours post burn, as long as the patient is not in hypovolemic shock.¹⁰³

The caloric requirements needed to reach nitrogen balance in burn patients have been calculated from linear regression analysis of weight change versus predicted dietary intakes in adults and are equivalent to 25 kcal/kg plus 40 kcal/% TBSA burned per day (Table 48-5).¹⁰⁴ Nutritional requirements for pediatric burn patients are based on body surface area (Table 48-6).^{105,106,107,108,109,110}

Marked loss of lean body mass occurs within a few weeks of injury but modern techniques using immediate total burn excision, rapid wound closure, nutritional support, critical care, and infection control have significantly reduced mortality.¹¹¹ Even so, burn-induced hypermetabolism lasts a much longer time, up to 2 years after burn, as previously noted.^20,21,112 Therefore, nutritional support of burn patients becomes an essential part of treatment during their hospitalization and should be continued after discharge.

The plasma concentration of trace elements and vitamins is generally decreased over a long period after burn.²¹ Berger et al^113,114 reported that substituting these micronutrients in burn patients reduces morbidity.

Introduction

Radioactivity has been used as an energy source, defensive weapon, and diagnostic and therapeutic medical tool since its discovery 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 (USA, 1979), Chernobyl (Ukraine, 1986), Goiânia (Brazil, 1987), and Fukushima Daiichi (Japan, 2011) have highlighted the need for knowledge of radiation effects and treatment.

Exposure to radiation can be classified into the following three types¹¹⁵:

1. Small, contained events affecting one or more persons, either localized or affecting the whole body; for example, a laboratory accident or damage from x-ray machines.

2. Industrial accident affecting large numbers of people with varying degrees of severity.

3. Detonation of a nuclear device with injuries to hundreds or thousands of people.

Specific changes associated with radiation make these injuries unique and necessitate their consideration as a separate form of trauma.¹¹⁶ In explosions, however, the release of kinetic energy can cause other more standard injuries commonly associated with blunt mechanisms. Patients may present with trauma and burns in addition to radiation exposure and explosions. The intent of this portion of the chapter is to provide information on radiation terminology, pathophysiology of injury, and diagnosis and treatment of these injuries, including triage and decontamination.

Radiation Incidents

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 US Department of Energy and provides assistance in response to all types of radiation accidents or incidents on a 24-h/d basis. The agency has defined three types of nuclear/radiological catastrophes as follows: detonation of a “dirty bomb,” explosive destruction of a nuclear reactor, and detonation of a nuclear weapon.¹¹⁷ Furthermore, it has the capability of providing medical attention and should be contacted to both inform and receive advice about specific incidents. It 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 unsealed radioisotopes used 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 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, with 30% being attributable to 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 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 changes that result 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 is absorbed into tissue to varying degrees.

Distance, time, and shielding are the ways to reduce exposure from a radiation source. The delivered dose of radiation diminishes over distance from its source by the inverse law.¹¹⁸ That is, if the distance between an object and the source of exposure is doubled, exposure is reduced to one-fourth its original value. Safe distances can be accurately determined using Newton’s inverse-square law [Intensity at point 1/Intensity at point 2 = (Distance at point 1)²/(Distance at point 2)²].

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-Mueller instruments detect β and γ radiation and are useful in the assessment of the effectiveness of decontamination procedures.¹¹⁹ 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. When in contact with contaminated victims or working with radiation, individuals should wear dosimeters under protective clothing.

Pathophysiology

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 biologic molecules to cause cellular damage, primarily to phospholipid membranes and deoxyribonucleic acid.¹²⁰ Different cell types have different sensitivities to radiation. 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 effects are seen on the microvasculature.

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.¹¹⁸ 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.¹¹⁹

Dose of exposure determines injury severity. The onset of vomiting could be useful for estimating the dose received from a single exposure. Vomiting in the first 10 minutes of the exposure means that the dosage was more than 8 Gy; within 10–30 minutes, 6–8 Gy; within 1 hour, 4–6 Gy; within 1–2 hours, 2–4 Gy; and over 2 hours, less than 2 Gy.¹²¹ Aside from vomiting, erythema of the skin can be an initial sign of exposure, and the sooner the appearance of erythema, the higher the dose of exposure. It often appears as a superficial burn at the following intervals of time: early, which will be transitory and short-lived; secondarily, often 2–3 weeks after exposure and immediately preceding moist desquamation; and 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.

Acute Radiation Syndrome

Detonation of a nuclear device can result in enough radiation exposure to cause immediate death for individuals within the lethal area of the blast. The severity of injury from 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.¹²²

LD_50/60 is a lethal dose required to kill 50% of the population within 60 days. LD_50/60 for human beings is 250–450 rad. The hematopoietic and gastrointestinal systems are affected by radiation because they have rapidly dividing cells. Therefore, 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). Onset of the first “prodromal” phase is related to the total dose of radiation received. It can be minutes if a lethal dose (>8 Gy) is received to hours if less than 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. Recovery is variable and may last weeks to months. If the dose is high enough, death ensues.

Whole-Body Exposure

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, exposing the skin of a finger (10 g of tissue) to 5 Gy will yield a total amount of absorbed energy equaling 500,000 ergs. For an absorbed dose of 5 Gy over the whole body (100 kg = 100,000 g), the absorbed energy will total 5,000,000,000 ergs. Thus, a lower absorbed dose may actually mean a higher amount of absorbed energy when considered over the whole body. Effects are primarily seen 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 lead to one of the three following 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 the mucosa of the intestine then sloughs in 4–7 days, causing bloody diarrhea, 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 more than 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.¹²³ This progresses rapidly to shock and death.

Regardless of the dose, the first symptom encountered is usually nausea and vomiting that may resolve before the onset of the other symptoms.

Assessment

Need for effective field triage and evacuation of casualties is important. In addition, effective decontamination is essential and should be performed as soon as possible.

During stabilization of the patient, information about the incident should be obtained, including the type of radiation, the duration of the exposure, the distance from the source, and whether direct contact with the source occurred. 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. The average radiation background in the United States is 360 mrem/y. Any radiation above the background level is considered contamination. The history should include any previous exposures to ionizing radiation, also.

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), which is 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 50% decrease in the TLC or an absolute TLC of less than 1200 mm³ within 48 hours of exposure indicates that at least a moderate dose of radiation has been encountered (Table 48-10).¹²⁴ Increases in serum amylase and diamine oxidase (specific to enterocytes) may be helpful in determining injury to the intestinal mucosa.¹²⁵ In patients who 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.¹²⁶

Triage

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 healthcare 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 burn 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.¹²⁷ Thermal burns and radiation injuries are synergistic, as animals that receive both injuries have a higher mortality beyond that expected for either alone or added together.^128,129 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.¹³⁰ Therefore, 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.

Decontamination

The first priority in the 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 the 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. For example, simply removing the clothes eliminates 90% of the contamination. Decontamination begins with the most highly contaminated areas. Contaminated wounds should be decontaminated prior to intact skin. Nasal swabs from each nostril and a throat swab are performed to detect inhalation or radioactive contaminants. If the 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 amount 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 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 level of radiation. After two rounds of the preceding treatment, a diluted mixture of one 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 lotion to moisturize the skin. Moist desquamation should be treated as a partial-thickness 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 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 performed too late, it will result in a chronic wound and may be associated with an increased risk of infection.

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 are given to provide symptomatic relief from nausea and vomiting. Resuscitation may be needed to maintain euvolemia because of volume losses.

Exposure to less than 1 Gy can be treated on an outpatient basis if there are no other injuries. Those with more than 1 Gy exposure should be admitted to a hospital until the symptoms have subsided. Gastrointestinal bleeding, diarrhea, infection, 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 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.¹³¹

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. 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 hemopoietic growth factors such as granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to speed restoration of granulocytes to normal levels after irradiation and increase survival in animals.¹³² 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.¹³³

The treatment of burns and radiation injuries is complex. Knowledgeable physicians can treat minor injuries in the community; however, moderate and severe injuries 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 the scar formation and in shortening the time to a functional and visually appealing outcome. Furthermore, improvement of rehabilitation and social reintegration should be the goal.