Critical Care Management of the Severely Burned Patient

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Critical Care Management of the Severely Burned Patient

Jeffrey R. Saffle

Chapter Outline

Introduction

Patients suffering major burn injuries present unique challenges in both the types and magnitude of management problems. Fluid resuscitation, pulmonary dysfunction, metabolic stress, and infections complicating burns may surpass similar problems in other intensive care unit (ICU) populations, and treatment is further complicated by abnormal drug pharmacology, severe pain, and psychosocial stress, all superimposed on the need for multiple major surgical procedures and prolonged rehabilitation.

This chapter will review the critical care management of burned adults. It will be apparent that in many areas existing literature is neither comprehensive nor rigorously “evidence-based.”¹ In providing a rationale for treatment, therefore, it is often necessary to extrapolate from studies in other disorders, particularly trauma. This may or may not be valid, particularly in such “burn-specific” areas as fluid resuscitation, inhalation injury, and nutritional support. These issues will be discussed as they arise, but readers will need to interpret this information for themselves.

Incidence and Survival from Burn Injury

The incidence of burn injury has declined in the United States throughout recent decades. From the 1960s to the early 1990s, reported burns decreased from 10.2 to approximately 4.2 injuries per 1000 Americans annually, or about 1.25 million injuries ²; hospitalizations decreased from over 90,000 to approximately 52,000/year; and deaths decreased at least 40%, from 9000/year to 5500/year. These trends are likely to continue.

Simultaneously, survival from burns has improved dramatically. During World War II, burns of 40% total body surface area (TBSA) produced a 50% mortality rate; today a similar mortality rate is seen with burns of over 80% TBSA.³ Survival rate is lower—though still improved—for the elderly, and even higher for children and young adults.⁴ These accomplishments are due to cumulative advances in fluid resuscitation, critical care, nutrition, surgery, and skin substitutes. However, it has been the organization of specialized burn centers around a consolidated team of experts that has made this success possible.⁵

Burn survival has been repeatedly shown to correlate with three major factors: patient age, burn size, and the presence of inhalation injury. Pulmonary damage from smoke inhalation is itself a serious injury, and can as much as double the mortality rate from cutaneous burns alone.3,5 Ryan and colleagues found that burn size 40% TBSA or greater, age 60 years or older, and inhalation injury contributed to the mortality rate in a stepwise manner; patients with all three had a mortality rate of 90% (Table 67.1).⁶

Table 67.1

Risk Factors for Death from Burn Injuries *

TBSA, total body surface area.

^*This table indicates the three risk factors universally accepted to affect burn patient mortality rate, their prevalence, and relative contribution to mortality rate. These data are similar to those from many modern burn centers. Note that overall mortality rate is only 4% and that most patients are relatively young and have limited burn wounds, placing them at little risk of dying.

Adapted with permission from Ryan CM, Schoenfeld DA, Thorpe WP, et al: Objective estimates of the probability of death from burn injuries. N Engl J Med 1998;338(6):362-366. Copyright ©1998, Massachusetts Medical Society. All rights reserved.

This experience has two important implications for current and future burn treatment. First, mortality risk for many patients is now so low that almost no injury is too large to preclude survival. The decision to intentionally withhold treatment is now rare and is based on predicted quality of life rather than predicted fatality itself. Second, it has necessitated unprecedented research and interest on the rehabilitation of patients who increasingly survive catastrophic injuries. Functional outcomes of burn treatment, including quality of life and return to work, are now the most relevant measures of successful care for all patients.7,8

However, the decline in burns has had other unintended consequences, which create challenges to the provision of effective burn care in many areas. As burns have decreased, so has the number of burn centers in the United States. There are now over 25% fewer burn centers than in 1970 ⁹; only 60 facilities in the United States are currently verified by the American Burn Association (ABA) and American College of Surgeons (ACS).¹⁰ This reduced number limits access to specialized burn care for many Americans. For the same reason, the experience of most physicians with even basic burn care has been dramatically reduced; many U.S. doctors—even surgeons—receive little or no burn training. As a result, important errors in initial burn assessment are made commonly by primary care providers,^11–13 leading to significant under- or (mostly) overtriage, care that is sometimes inadequate, and further stress on the few remaining centers, which now must cover larger referral areas.^14,15

Pathophysiology of Burns

Although the term burn strictly denotes injury caused by heat from flames and scalding liquids, other agents including chemicals, electric current, ionizing radiation, and friction produce nearly identical coagulative necrosis of tissues. The magnitude of such injury depends on the intensity of the source (temperature, voltage, pH, etc.) and the duration of contact, and the clinical severity of a burn is a function of the depth and extent of injury; these factors determine what skin structures are destroyed, the magnitude of response, and the ability of the wound to heal. Accurate assessment of burn wounds is essential in determining appropriate treatment and in predicting outcome.

The outermost epidermis of the skin is a thin layer of metabolically active cells that provides a specialized barrier to moisture, bacteria, and chemicals. Burns limited to the epidermis display redness and mild pain without blisters. The underlying dermis is much thicker, containing large amounts of structural proteins, which provide strength and flexibility to the skin. Burns extending into the dermis (second-degree, or partial-thickness burns) can vary greatly in appearance and severity. Superficial dermal burns are red, painful, and moist, with prominent fluid-filled blisters, but coagulative necrosis of deeper injuries effectively seals off the skin surface, producing a dry wound. Hair follicles and sweat glands lined with epidermis penetrate through the dermis and serve as a source of epidermal regeneration as partial-thickness injuries heal. Full-thickness or third-degree burns destroy the entire dermis. Such injuries may be a variety of colors, but are invariably dry and relatively insensate. The coagulated dermis is constricted and rigid; as fluid accumulates beneath it, tissue pressure can increase to a dangerous degree, causing vascular compromise and compartmental compression (see later).

Cutaneous injury generates intense inflammation with protean systemic manifestations that persist even after wound coverage is attained. Immediately following injury, release of inflammatory mediators causes widespread loss of capillary integrity and depletion of intravascular volume, as well as depressed myocardial contractility, increased peripheral vascular resistance, and systemic hypoperfusion. This shock state can be rapidly lethal, but with adequate support, hemodynamic stability is restored within 24 to 48 hours and is thereafter characterized by increased cardiac output and decreased vascular resistance. This process is fueled by a cascade of local and systemic inflammatory mediators and includes sustained release of epinephrine, cortisol, and glucagon, which generate hypermetabolism, autocannibalism of body protein stores, and glucose intolerance, which persist well into rehabilitation (see “Metabolic Support and Gastrointestinal Management,” later).

An even more obvious consequence of burn injury is the burn wound itself. Burned skin quickly accumulates a coating of tenacious eschar comprising dried serum and necrotic dermis. Minor burn injuries can often be allowed to heal spontaneously as eschar sloughs and new epidermis emerges from deep appendages to cover the wounds. But the eschar of deep or extensive injuries is extremely susceptible to infection, which has historically been a frequent cause of death. Prompt removal of eschar and coverage with intact skin is essential to control sepsis, ameliorate inflammation, reduce scarring, and optimize functional long-term outcomes. This is a major goal of early burn treatment.

Acute Care of the Burned Patient

Acute burn treatment can be divided into four phases, which are outlined in Figure 67.1. Initial assessment is the process of stabilizing the acutely injured patient, treating immediate life-threatening injuries, and preparing for inpatient care. The first 48 hours following injury constitute acute resuscitation, focused on initial assessment, airway support, and fluid replacement. The wound coverage phase then ensues, in which the major goal of treatment is surgical excision and closure of burn wounds. Ventilator management, metabolic support, control of infection and pain, physical therapy, and other supportive measures are essential adjuncts during this period. The goals of the final rehabilitation phase include scar control, optimizing function, and return to independent living. This period can last for months and continue long past discharge. Obviously these phases overlap: discoveries made during initial assessment may require prolonged management; many units begin surgical excision even before resuscitation is completed, and several aspects of rehabilitation—physical therapy, psychosocial support, nutrition, etc.––should start essentially at the time of injury.

Figure 67.1 Schematic representation of acute burn treatment. Initial assessment and triage should follow the principles of advanced trauma life support, but particular attention must be paid to burn-specific conditions, including protection from additional injury and the presence of inhalation injury, acute edema formation, and major fluid requirements. Following this immediate care, ongoing burn treatment consists of acute fluid resuscitation, wound coverage, and rehabilitation. These phases are shown in overlapping boxes to indicate that, even though the importance of each varies as burn care proceeds, they are often performed simultaneously, and consideration of the importance of each should be borne in mind throughout the course of treatment. See text for additional details.

Initial Assessment

Initial assessment of burn victims should follow the universally accepted protocol of the American College of Surgeons’ Advanced Trauma Life Support (ATLS) course.¹⁶ In doing so, attention must be paid to several burn-specific issues, but it must be remembered that other types of trauma or preexisting conditions can always be present, emphasizing the importance of systematic patient evaluation.

Scene Safety: Stop the Burning Process

Though many burned patients receive appropriate on-scene care from first responders, remember that patients can suffer ongoing injury from smoldering clothing, caustic chemicals, and the like. Initial assessment of every patient should begin by assuring that the patient and care providers are protected from further harm. Awareness of the threat of terrorist incidents or mass casualties mandates that these principles be practiced consistently.

The Primary Survey and Inhalation Injury

In burn patients, assessment of airway, breathing, and circulation must include evaluation for signs and symptoms of inhalation injury. Carbon monoxide (CO) poisoning and asphyxia cause the vast majority of scene and emergency room fatalities, and up to 80% of fire-related deaths.17,18 Inhalation injury and its management are covered in Chapter 48.

Inhalation injury should be suspected in all patients exposed to flames or smoke, especially if the patient was unconscious or trapped in a closed space. Physical findings include facial burns, singed nasal hairs or eyebrows, wheezing or stridor, carbonaceous sputum, hoarseness, and anxiety. These findings should alert the examiner to the possible need for airway support.¹⁹

Inhalation injury is classically considered to consist of three distinct entities: CO poisoning, upper airway injury, and lower airway injury (the “true” inhalation injury). Although patients can frequently present with a combination of all three problems, this classification is worthwhile because of the different pathologic processes and time courses with which these injuries present.

Carbon Monoxide Poisoning

CO is a product of incomplete combustion, and its highest concentrations occur in indoor fires, where its effects may be amplified by flame-induced oxygen depletion.²⁰ CO displaces oxygen binding, producing systemic hypoxia despite normal oxygen tension. The most common symptoms are mental status changes, varying from headache to coma, which can present without burn injuries or respiratory distress and be overlooked easily. Classic “cherry red cyanosis” appearance is absent in many victims or can be obscured by soot or burns. Importantly, pulse oximetry is inaccurate in the presence of CO. Direct measurement of carboxyhemoglobin concentration should be performed but should never delay treatment. Patients are at greatest risk on presentation, and immediate application of oxygen is often definitive. As reviewed in Chapter 48, the use of hyperbaric oxygen for acute CO poisoning is controversial; it should probably be reserved for severe cases with neurologic compromise, when its use will not interfere with other essential components of acute burn care.

Smoke contains many other toxic chemicals, including cyanide. Cyanide poisoning has been documented in burn victims and does not always correlate with CO exposure.²¹ Because blood levels cannot be obtained immediately, empiric treatment using cyanide antidote kits has been advocated in patients with unusually severe acidosis or shock.²² The recent availability of hydroxocobalamin as a cyanide antidote, which has few side effects, has led to both renewed interest in the treatment of cyanide toxicity and aggressive marketing of the drug. However, a recent review points out that confirmed cases of significant cyanide poisoning following smoke exposure are rare.²³ At present, treatment of suspected cyanide toxicity in acutely burned patients is controversial, and indications are unclear.²⁴ High-flow oxygen coupled with aggressive resuscitation and cardiovascular support remain the mainstays of treatment.

Upper Airway Injury

Patients with extensive or deep burns to the face, or who have breathed substantial quantities of hot gases or soot, are at risk of airway occlusion from progressive pharyngeal or supraglottic edema and facial swelling. This swelling can occur even without flame injury in children with scalds or severe chemical burns. Edema formation can be extremely rapid and progress for at least 24 hours. Patients must be followed serially, and intubated early and electively if evidence of progressive airway compromise occurs. Figure 67.2 illustrates such a case.

Figure 67.2 This young man was burned playing with matches and gasoline, sustaining burns to 60% total body surface area, including his entire face. On presentation, he was alert and breathing comfortably. Arterial blood gases (including carboxyhemoglobin) and chest x-ray findings were normal. Based on the extent and location of his injuries, elective nasotracheal intubation was performed. Six hours later, the patient displays massive facial edema. Eyes are swollen shut, and oral excursion is severely restricted. If he lost his endotracheal tube at this point, his airway could not be maintained. Note that the tube is tied around his head securely, not taped in position. He will need to remain intubated for at least 3 to 5 days until most of this edema resolves.

Indications for Intubation

Awareness of the potential for acute airway compromise following burn injury has led to a liberal attitude toward intubation that is probably appropriate. “When in doubt, intubate” expresses many physicians’ attitude toward this problem. However, this dictum has sometimes led to indiscriminate and unnecessary intubation of patients with even minor facial burns.²⁵ The presence of inhalation injury does not mandate intubation, and airway compromise can be life-threatening even in the absence of inhalation injury. Indications for intubation, as in all trauma patients, are based on symptoms found on initial assessment, including altered mental status, refractory hypoxemia, and signs of impending airway obstruction including wheezing, stridor, dyspnea, and progressive facial swelling. Emergency tracheostomy or cricothyroidotomy, which should rarely be needed if intubation is performed in a timely manner, can be an extremely challenging procedure in the setting of massive head and neck swelling.

Pulmonary (“True”) Inhalation Injury

Exposure of the bronchi and small airways to toxic smoke causes chemical injury to the epithelium, which can progress to mucosal sloughing, mucous plugging, bronchiectasis, hypoxemia, and pneumonia. Clinical signs of this problem may be absent for up to 72 hours after exposure, and initial chest radiographs are usually normal.²⁶ Patients with immediate respiratory distress, stridor, or hypoxemia are much more likely to have upper airway injury. Even in the absence of symptoms, patients suspected of having inhalation injury require hospital admission and close observation. Fiberoptic bronchoscopy demonstrating carbonaceous debris, erythema, or mucosal sloughing is highly sensitive for diagnosis of inhalation injury and can facilitate immediate intubation if injury is confirmed²⁷ (Fig. 67.3). Inhalation injury is discussed further in Chapter 48.

Figure 67.3 Bronchoscopic appearance of the carina of a man who was dragged unconscious from a burning house. Carbonaceous deposits are apparent in his trachea, and more extensively in the mainstem bronchi. This finding is diagnostic of inhalation injury.

The combined mortality rates for burns and trauma appear to be at least additive compared to either injury alone.29,30 Thorough evaluation of all potential injuries according to ATLS guidelines is imperative and can be challenging in burn patients: the discoloration, pain, and swelling of burn wounds, for example, can conceal underlying fractures³¹; and burns of the torso or acute inhalation injury can obscure a pneumothorax or other injuries. For this reason, it is important not to focus too heavily on burn injuries in performing the secondary survey.

In addition, care should be provided by a multispecialty team with expertise in managing all injuries. Treatment of many traumatic injuries takes priority over definitive burn care and mandates immediate operation. Because fresh burn wounds are initially—and briefly—free of bacteria, laparotomy, craniotomy, repair of lacerations, and operative fixation of fractures should be performed immediately, and no later than 12 to 24 hours after burn.32,33 This approach will minimize risk of infections, permit early mobilization, and facilitate access to burn wounds for dressings and surgery. These interventions can be performed safely provided essential components of burn care—including airway support, temperature control, and aggressive fluid resuscitation—are instituted immediately and continued through surgery. Close coordination between the burn center and trauma center will optimize outcome for these patients.

The Resuscitation Phase

Burn Shock

Following initial evaluation, the primary focus of early burn treatment is fluid resuscitation. The goals of resuscitation are to support organ function while avoiding complications of over- or underadministration of fluid.³⁴ This task can be challenging given the huge fluid shifts and cardiovascular effects of acute burns. Development of effective protocols for resuscitation represents one of the major advancements in burn care in this century.

The magnitude of fluid shifts following a major burn can exceed those of any other injury. At the cellular level, burn injury immediately impairs membrane adenosine triphosphatase (ATPase) activity and reduces transmembrane potential,35,36 resulting in increased intracellular sodium and extracellular potassium concentrations, cellular swelling, and acidosis. Fluid resuscitation only partially corrects these abnormalities, which may require several days to resolve completely as local inflammation subsides.

These events present clinically as a profound inflammatory response, causing increased capillary permeability and massive tissue edema at the expense of intravascular volume. Immediate release of histamine and serotonin increase local perfusion, initiate capillary leakage, and potentiate vasoconstriction caused by massive catecholamine secretion.36–38 Tumor necrosis factor (TNF)-α produces myocardial depression and activates a number of other vasoactive mediators.³⁹ Prostaglandins, leukotrienes, oxygen radicals, products of platelet activation and coagulation, and a cascade of cytokines also contribute to these abnormalities.^40,41 Alterations in local blood flow increase arteriolar tone and pressure and dilate postcapillary venules, causing local capillary perfusion to become less selective and increased, favoring extensive edema formation.

The forces that control transcapillary fluid flux are summarized in Starling’s equation ⁴²; their alterations in burn injury have been reviewed by Demling⁴³ (Table 67.2). The greatest edema formation occurs almost immediately within the wound, caused by near-total permeability to even very large (35 nm) molecules,⁴⁴ and permitting protein-rich plasma to pour into the interstitium.⁴⁵ Maximum protein extravasation occurs within the first hour of injury, and both its duration and magnitude are proportional to burn size.^46,47

Table 67.2

Starling Forces and Capillary Permeability *

^*See discussion in Demling RH: The burn edema process: Current concepts. J Burn Care Rehabil 2005;26:207-227.

Adapted with permission from Ryan CM, Schoenfeld DA, Thorpe WP, et al: Objective estimates of the probability of death from burn injuries. N Engl J Med 1998;338:362-366. Copyright ©1998, Massachusetts Medical Society. All rights reserved.

Even after local capillary integrity normalizes within 8 to 12 hours, edema formation continues in unburned as well as burned tissues.⁴⁸ Depletion of intravascular proteins, further diluted by crystalloid resuscitation,⁴⁹ eliminates the oncotic pressure gradient (see πp − πi in Table 67.2), which maintains intravascular volume. Hypoproteinemia alone can mimic burn edema, and infusions of colloid can almost completely prevent edema in unburned tissues.^50,51 Progressive edema also alters the configuration of interstitial collagen and hyaluronic acid, which are normally densely coiled to limit fluid influx.⁵² Burn injury disrupts this “safety valve” configuration, increasing compliance, producing osmotically active molecular fragments, and generating negative (“sucking”) interstitial pressure⁵³ and extremely rapid fluid sequestion.⁴⁸ Though this gradient is neutralized within a few hours, compliance continues to increase as interstitial gel is hydrated, allowing liters of fluid to accumulate with little change in hydrostatic pressure⁵⁴ and permitting edema to persist for weeks following injury.

Cardiac output falls within minutes of injury, reaching 50% to 60% of normal within an hour, although systemic vascular resistance (SVR) increases dramatically. Both changes occur far faster than the depletion of intravascular volume 45,55 and regardless of fluid resuscitation. Release of catecholamines and other vasoactive mediators clearly increases SVR, but the decrease in cardiac output is harder to explain. Researchers have long postulated the existence of a “myocardial depressant factor,”⁵⁶ though no such substance has been isolated. It seems more likely that cardiac output is impaired by the combination of increased SVR, volume depletion, and actions of TNF-α, endotoxin, and other chemicals. One clinically important side effect of capillary permeability is hemoconcentration—a marked rise in hematocrit as plasma is sieved out of the bloodstream into the interstitium—which increases blood viscosity and further impairs cardiac output.

Cardiac output begins to recover within a few hours of injury and requires 12 to 24 hours to normalize, even with vigorous resuscitation. SVR follows an opposite course, peaking quickly and then declining to near-normal within 24 to 48 hours (Fig. 67.5). Following these initial changes a chronic hyperdynamic circulation is maintained, with cardiac output persisting well above normal, and marked vasodilation and decreased SVR often persisting even after wound coverage is attained.

Figure 67.5 This classic graph shows characteristic postburn changes in cardiac output and peripheral vascular resistance in a group of seven patients (mean burn size 64.5% total body surface area [TBSA]) resuscitated with the Brooke formula (lactated Ringer’s [LR] solution, 1.5 mL/kg/%TBSA, albumin, 0.5 mL/kg/%TBSA, plus 2000 mL dextrose/water in the first 24 hours). Cardiac output falls acutely, before blood volume has changed appreciably, then rebounds gradually, with return to normal by 24 to 36 hours, and thereafter remaining above normal. Peripheral vascular resistance shows an opposite effect. (From Pruitt BA Jr, Mason AD Jr, Moncrief JA: Hemodynamic changes in the early postburn patient: The influence of fluid administration and of a vasodilator (hydralazine). J Trauma 1971;11:36-46.)

Fluid Resuscitation of Burn Patients

Before World War II, patients with even moderate burns usually died within a few days because of progressive shock and renal failure. In 1942, surgeons Oliver Cope and Francis Moore designed the first formal resuscitation regimen to treat victims of the Cocoanut Grove nightclub fire, with substantial improvements in survival.³⁶ With continued refinements, today almost all patients can be resuscitated successfully, and renal failure complicating burn injury is rare. A host of formulas have been developed, almost all based on body weight and burn size, and utilizing various combinations of crystalloid and colloid solutions. The archetype and most widely used of such regimens is the Parkland formula, designed by Baxter.³⁵ He demonstrated that a volume of lactated Ringer’s (LR) solution equal to 4 mL per kilogram body weight for each percent TBSA burned (4 mL/kg/%TBSA), given in the first 24 hours after injury, would maintain urine output of 50 to 70 mL/hour, replete blood volume, and restore cellular transmembrane potential and cardiac output in most patients. Half this calculated volume is given in the first 8 hours after burn, the remainder over the next 16 hours. The intravenous rate is adjusted hourly to maintain urine output and is decreased gradually until a “maintenance” rate is reached at approximately 24 hours.

Maintenance requirements for burn patients are also increased due to ongoing evaporative and metabolic losses, and continued fluid support is essential even after resuscitation is complete. A popular formula to estimate these requirements is that developed by Warden:⁵⁷

In this equation,

Evaporative water losses = (35 + %TBSA burn) × m² × 24 hours

Normal insensible losses = (1500 × m²) per 24 hours

m² = body surface area in square meters

This experience forms the basis of modern burn resuscitation. But despite widespread acceptance of the principles of fluid replacement, disagreement persists over almost every aspect of practical management, and the practice of resuscitation varies significantly among units. One example exists in defining the end points of resuscitation. Successful resuscitation requires meticulous monitoring and adjustment of resuscitation based on patient response. Traditional resuscitation relies almost exclusively on hourly urine output for this purpose, so the amount of fluid required for resuscitation depends partly on the urine output targeted. Baxter used an output of 50 to 70 mL/hour; several other formulas that accept outputs of 0.5 mL/kg/hour (1.0 mL/kg/hour in children) call for LR infusion rates between 2 and 3 mL/kg/%TBSA, and are also in widespread use.^34,36

The Phenomenon of “Fluid Creep”

Clinicians have long accepted the consensus that patients should receive as little fluid as possible to maintain organ perfusion.⁵⁸ But several patient groups routinely require more resuscitation fluid than predicted by the Parkland formula, including patients with inhalation injury,⁵⁹ those with multiple trauma and electrical burns, patients in whom resuscitation is substantially delayed,⁴ and patients with alcohol or drug abuse.⁶⁰ Inexperienced clinicians often make substantial errors in estimating burn size, which can result in significant under- or overestimation of fluid requirements.¹¹ Careful monitoring of resuscitation and individualized fluid therapy can often obviate these problems.

But in recent years a widespread tendency for patients to receive increasing quantities of resuscitation fluid has been observed, a phenomenon dubbed “fluid creep” by Pruitt.⁶¹ Cancio and associates found that 63% of their recent patients required a mean of 6.1 ± 0.22 mL/kg/%TBSA for resuscitation despite very modest urine output.⁶² Others have documented such increased fluid requirements in up to 100% of patients.^63–65 The potential complications of fluid creep are far from benign, including extremity and abdominal compartment syndromes, worsening pulmonary dysfunction, and more frequent and prolonged endotracheal intubation. Figure 67.6 illustrates the actual resuscitation of a child who required an excessive amount of crystalloid to achieve successful resuscitation and maintain adequate urine output.

Figure 67.6 Time course of fluid resuscitation for a 6-year-old boy (20 kg) with 33% total body surface area (TBSA) scald burns. He arrived at the burn center 6 hours after injury, having received 900 mL of lactated Ringer’s (LR) solution prior to arrival. Fluid resuscitation was started according to the Parkland formula (heavy dashed line); nurses were instructed to maintain urine output between 0.9 and 1.8 mL/kg/hour (dotted line). Initial resuscitation was close to Parkland guidelines, but beginning at about 10 hours after burn, fluid requirements increased progressively until about 22 hours, when urine output finally began to rise, and fluids were tapered in a stepwise manner according to protocol. The patient reached his calculated maintenance fluid rate of 106 mL/hour at hour 36. Total resuscitation received was 11.38 mL/kg/%TBSA. He had no difficulties with compartment syndromes or respiratory distress. This case illustrates the occurrence of “fluid creep” that has been experienced frequently in modern burn care.

This departure from tradition is probably due to several influences. First, the successful resuscitation of patients with massive burns appears to routinely require increased fluid volumes.⁶² In Baxter’s initial report of 277 patients, 89% of those with burns 60% TBSA or greater died.⁴⁵ However, modern survival is much better and owes some of its success to persisting with aggressive fluid resuscitation beyond the confines of the Parkland formula.

Second, it appears that fluid creep perpetuates itself. Overly zealous initial fluid administration—often performed in the field—increases serum protein depletion, generating a vicious circle of reduced oncotic pressure and enhanced edema, which in turn increases crystalloid requirements. This mechanism also helps explain the occurrence of resuscitation failure, in which fluid requirements actually escalate despite adequate—or excessive—crystalloid administration.⁶⁶ The use of colloid-containing fluids can arrest this cycle and restore oncotic pressure but adds to overall fluid requirements as well.

Fluid creep has probably also been encouraged by resuscitation trends in other ICU populations. Traditional burn resuscitation formulas permit significant deficits in vascular volume and cardiac output to persist until the end of 24 hours.⁴⁵ The routine observation of hematocrits as high as 70% during resuscitation is consistent with this concept. Both lactic acid (LA) and base deficit (BD) remain elevated throughout traditional resuscitation,⁶⁷ which also fails to reflect changes in cardiac output and oxygen delivery (VO₂).⁶⁸ In contrast, resuscitation in other shock states has been increasingly directed at normalizing LA and BD, and optimizing cardiac output, VO₂, and pulmonary wedge pressure.^69,70 As this concept gained acceptance in critical care, burn clinicians have become more inclined to monitor these parameters and to respond to abnormalities by increasing fluid support.

However, this approach may not be valid in burns. Although it is accepted that patients’ ability to achieve optimal values of cardiac output and VO₂ correlates strongly with outcome, it is less clear whether exaggerated fluid infusion, invasive monitoring, and inotropic support can change nonresponders into responders and thus improve survival.⁷¹ Optimizing VO₂ and improved survival in one group of patients with severe burns,⁷² but both Kaups and colleagues⁶⁴ and Choi and coworkers⁶⁵ were unable to determine if resuscitation aimed at normalizing elevated BD was effective or beneficial. In other studies of goal-directed therapy in burns, attaining target values of cardiac output, VO₂, or wedge pressure routinely required more fluid—as much as four times Parkland calculations—without obvious improvement in survival,^73,74 and potential increase in edema-related complications, which appear directly related to the fluid volume administered.^75,76

It is clear that the optimal method of monitoring and delivering burn resuscitation has yet to be determined. Although fluid creep is widespread, most burn centers still base fluid administration primarily on urine output. Invasive hemodynamic monitoring does not appear beneficial for routine use, though it may be helpful in guiding therapy in individuals who are clearly failing to respond to traditional resuscitation, including elderly patients or those with massive injuries, cardiac disease, associated multiple trauma, or severe pulmonary dysfunction.

Hypertonic Resuscitation

Crystalloid solutions remain the mainstay of all resuscitation regimens as they are inexpensive, well tolerated, readily available, and easily mobilized and excreted. The effective component of crystalloid is sodium,⁷⁷ which has led to the use of hypertonic saline solutions to satisfy capillary and cellular leakage while minimizing fluid volume and edema.^78,79 Solutions containing as much sodium as 300 mEq/L result in delivery of almost identical quantities of sodium as LR solution with substantially less volume.⁸⁰ Hypertonic saline resuscitation has been advocated for children⁸¹ and the elderly,⁸² who tolerate under- and overresuscitation poorly, as well as for patients with head injuries,⁸³ and for field and combat resuscitation when the weight of available solutions must be minimized.^84,85

Hypertonic saline resuscitation carries the risk of significant hypernatremia, hyperchloremia, acidosis, and hyperosmolarity, and requires careful monitoring. In addition, savings in initial fluid requirements may be balanced by increased free water retention later.⁸⁶ Hypertonic saline has been associated with increased mortality risk in at least one study, possibly related to increased renal failure.⁸⁶ However, it is still used selectively in some burn centers^79,87 and remains an option in acute burn management.

Crystalloid Versus Colloid

Because of the indiscriminate nature of early postburn capillary leakage, colloids are not superior to crystalloids in initial burn resuscitation.⁵⁵ For this and other reasons, colloid use in resuscitation of all types has been condemned.⁸⁸ However, capillary integrity is largely restored by the end of 24 hours after injury, and colloids given at this time can effectively restore oncotic pressure, expand plasma volume, and reduce secondary edema in unburned tissue,^35,51 including possible prevention of abdominal compartment syndrome.⁸⁹

Colloids used in burn resuscitation have included albumin, plasma protein fraction (Plasmanate), fresh frozen plasma, and the synthetic colloids dextran and hetastarch. Routine albumin administration is a component of the traditional Evans and Brooke formulas 36,55 and was originally used at the end of Parkland resuscitation.³⁵ In a widely quoted randomized trial, Goodwin and associates found that albumin-based resuscitation required less total fluid than solution alone but was associated with a sustained increase in extravascular lung water.⁹⁰ Critics have also pointed out that routine albumin supplementation has no apparent benefits.⁹¹ Nonetheless, albumin remains a popular colloid; its current use varies among burn centers from routine administration within 8 to 12 hours of injury,^50,57 to selective use as “rescue” in problem resuscitations, to near-total interdiction. Fresh frozen plasma has also been used successfully⁹²; its colloid effect probably explains much of the efficacy of plasma exchange therapy in complex burn resuscitations.⁹³ Both low-molecular-weight dextran and hetastarch have been used in burn resuscitation and appear as effective as albumin in maintaining oncotic pressure and limiting edema in unburned tissues.^51,94,95 They offer advantages of long shelf life, availability, freedom from disease transmission, and lower cost. However, hetastarch has been associated with rare anaphylaxis and dose-dependent coagulopathy and bleeding, which limits is use in large volumes.⁹⁶

Colloid is probably unnecessary for resuscitation of most patients with uncomplicated injuries. With increasing burn size, the benefits of colloid administration, restricted to use after the first 8 to 12 hours after burn, may be significant in reducing total fluid requirements and edema-related complications. Many centers now utilize LR solution for the first hours after injury, followed by hypertonic saline, colloid, or both to reduce edema as resuscitation is completed.⁵⁷ The patient illustrated in Figure 67.6 would be a very appropriate candidate for this form of “rescue” therapy, which would likely have reduced his ongoing fluid requirements. This area of resuscitation is extremely controversial and will benefit from randomized multicenter trials.

Pharmacologic Manipulation of Resuscitation

Improved understanding of the pathophysiology of burn shock has led investigators to attempt to reduce its severity by blocking some of its specific chemical mediators. These efforts have included use of vasodilators such as hydralazine, histamine blockade using cimetidine, the serotonin antagonist ketanserin, and anti-inflammatory drugs such as hydrocortisone and ibuprofen.43,55,97–99 Large doses of the antioxidant vitamin C has been shown to decrease fluid requirements in clinical burn resuscitation.¹⁰⁰ Many of these efforts have shown modest benefits, though none has found its way into widespread clinical use. The possibility of developing an effective “cocktail” to ameliorate the effects of burn shock holds promise for the future.

Practicing Effective Resuscitation

A bewildering array of regimens (and opinions) are in current use for burn resuscitation. In attempting to practice resuscitation effectively, the clinician must decide on a protocol that is uniform and easy to apply by nurses, yet flexible enough to permit individualized therapy and provide appropriate “escapes” for patients who are unstable.

An example of the protocol used at the University of Utah is included in Figure 67.7. The protocol is based on the Parkland formula, but contains an option for the use of LR/albumin to arrest escalating fluid requirements. It requires nurses to adjust infusions based on hourly urine output, but mandates that physicians be contacted if worrisome parameters develop. We have found this protocol effective in resuscitating the vast majority of patients without frequent input from physicians. Similar protocols are in use in a number of burn centers.

Figure 67.7 Burn fluid resuscitation protocol used at the University of Utah. Physicians order an initial infusion rate of lactated Ringer’s solution based on Parkland calculations, and indicate the target maintenance rate. Nursing staff measures hourly urine output, and increases or decreases fluids based on this response. If patients develop unexpected changes in vital signs, or fail to respond appropriately, physicians are contacted. An option for the use of colloid-containing resuscitation is included for patients whose requirements fail to decline. This regimen permits close titration of fluids without requiring hourly physician input.

Complications of Edema

Although the quantity of edema in both burned and unburned tissue is affected by fluid resuscitation, it is also true that substantial swelling occurs regardless of the resuscitation used. Swelling within the face, eyes, extremities, and torso can have catastrophic consequences if untreated, and it is essential to remember that edema is progressive for 24 hours following burn injury; an area that is soft and pliable on admission may become tensely swollen within hours or overnight. Clinicians must be aware of the potential for these complications, follow serial examinations, and treat them as they develop.

Facial Swelling

Full-thickness facial burns can swell massively and produce complete airway obstruction within an hour or 2 of injury, as illustrated in Figure 67.2. As discussed under initial assessment, endotracheal intubation is essential in this setting and should be performed early and electively.

Continued facial swelling may preclude safe extubation for several days following injury, and inadvertent extubation in this period can be disastrous. Tubes must be secured carefully; patients may require sedation or paralysis to ensure this. As edema begins to resolve within 48 to 72 hours, extubation should not be attempted until patients can open their eyes and breathe spontaneously and an air leak can be demonstrated with the cuff deflated. Early tracheostomy may provide a more comfortable and secure airway for patients with large injuries.

Ocular Swelling

Elevated intraocular pressures (IOPs) have been documented in burn patients and appear to correlate with resuscitation volume. No data exist on the consequences of this phenomenon, but the risk of optic nerve ischemia and permanent visual loss may exist. Lateral canthotomy has been recommended for patients with persistently high IOPs.101,102 Measurement of IOP during acute burn resuscitation may be warranted in patients with severe facial injuries and eyelid edema.

Extremity Compartment Syndromes

Burns probably constitute the most common cause of extremity compartment syndromes. The pathophysiology is identical to that which accompanies fractures, crush injuries, and so on with the notable exception that in burn patients the constricting layer is the burn eschar, not the underlying fascia, so that incision through the burn wound—“escharotomy”—is required to relieve compression.

Failure to diagnose circulatory embarrassment of a burned extremity can lead to progressive ischemia, myonecrosis, and amputation. Because this can develop insidiously in burned extremities that are soft on presentation, a high index of suspicion and performance of serial examinations are essential. Compartmental compression is most likely following full-thickness, circumferential extremity burns but can develop in the absence of these findings, even in unburned extremities in patients who require excessive resuscitation volumes, particularly children.

Swollen extremities should be initially treated with elevation and avoidance of constricting dressings. Classic findings of pain, paralysis, pallor, paresthesia, pulselessness (the “five Ps”) may be difficult beneath burn injuries or in intubated patients, and may not develop until irreversible ischemia has occurred. Similarly, limb-threatening compression can exist despite persistent palpable or Doppler pulses.¹⁰³ For these reasons, some authorities perform escharotomies based on a general impression of extremity swelling, or even prophylactically. Alternatively, many clinicians monitor intramuscular pressure to determine the need for decompression. This procedure is easily done by inserting a large-bore (18-gauge) needle attached to a pressure transducer through the eschar into the underlying muscle. Pressures that exceed 30 cm H₂O in the relaxed extremity indicate compromised capillary perfusion and mandate decompression.¹⁰⁴ Measurements should be repeated following escharotomy; pressures that remain elevated indicate the need to deepen or extend incisions or to proceed with fasciotomy. This may be particularly likely in patients with very deep burns, associated trauma, or electrical injury (Fig. 67.8).

Figure 67.8 Massively swollen forearm following high-voltage electrocution injury. Simple escharotomy of the distal forearm and hand failed to decompress the extremity, so extensive fasciotomy was performed to above the elbow. The skin edges are widely separated by edema. Proximal forearm muscles are viable, but tissues distal to the drawn line—the line of anticipated amputation—are clearly necrotic. The wrist and fingers are “frozen” in flexion caused by contraction of damaged muscles.

Escharotomies can often be done at the bedside using electrocautery and appropriate analgesia. Longitudinal incisions should run the length of the burn wound, be placed medially and laterally on the supinated limb to avoid major nerves and vessels, and facilitate resurfacing with skin grafts. Incisions must penetrate through the burn until the wound edges “pop open,” and pressure is clearly relieved. Incisions in burned hands should extend at least to the metacarpophalangeal joints; performance of individual digit escharotomies has some support ¹⁰⁵ but is often omitted. As an alternative, the use of enzymatic debriding agents to provide chemical escharotomy is popular in some centers.¹⁰⁶

Torso Compartment Syndromes

Recent awareness of massive abdominal swelling as a cause of cardiorespiratory compromise has led to protocols for monitoring intra-abdominal pressure and performing decompressive laparotomy in many ICU populations. In burn patients, occurrence of abdominal compartment syndrome has accompanied reports of fluid creep, as discussed earlier,⁷⁵ though it can clearly develop in the absence of excessive resuscitation. Patients with major (≥25% TBSA) burns and extensive torso injuries or who require large resuscitation volumes (≥500 mL/hour⁷⁶) should have routine monitoring of bladder pressures.^76,107 The finding of intra-abdominal hypertension in the absence of clinical symptoms should prompt other measures to reduce abdominal pressure.¹⁰⁸ There is evidence that both hypertonic saline and colloid-based resuscitation can prevent the development of abdominal compartment syndrome^79,89; removal of peritoneal fluid with dialysis catheters has also been effective.¹⁰⁹ Unfortunately, many patients with abdominal compartment syndrome present with diffuse retroperitoneal swelling rather than free peritoneal fluid; diagnostic ultrasound can make this decision and guide catheter placement if free fluid is seen.

Like other edema-related complications, abdominal hypertension can develop insidiously and then present precipitously with oliguria and critical hypotension and respiratory embarrassment. In patients with deep burns of the chest or abdomen, performance of torso escharotomy—sometimes repeatedly—will often improve ventilation and obviate laparotomy. Patients in whom other measures fail or symptoms progress rapidly should undergo immediate decompressive laparotomy, at the bedside if necessary. Delayed decompression may worsen shock and even lead to intestinal necrosis, although prompt decompression will both improve survival and reduce ongoing resuscitation requirements.¹¹⁰ Containment of the exposed viscera by mesh or plastic silos may be needed following laparotomy, as widely used “vac-pack” dressings¹¹¹ may be impossible to secure over burn eschar. As edema resolves, every effort should be made to reduce abdominal contents and obtain fascial closure through repeated wound revisions. Figure 67.9 illustrates a patient in whom numerous complications of edema—massive facial swelling, extremity compartment syndromes, and abdominal compartment syndrome—have occurred simultaneously. Although the mortality rate of abdominal compartment syndrome in burn patients is high,¹¹² this likely reflects the severity of the underlying burn more than this complication itself.

Figure 67.9 Complications of edema in an elderly man with 70% total body surface area burns. Facial edema is massive; tracheostomy has been performed to provide secure, long-term airway support. Escharotomies on upper extremities and multiple torso escharotomies have resulted in increased swelling and separation of wound edges. Despite these measures, abdominal compartment syndrome necessitated bedside laparotomy and placement of a synthetic mesh “silo” to contain eviscerated abdominal contents. As edema resolved over several days, viscera were gradually returned to the abdomen and the silo was trimmed, until closure of the fascia was possible. The other escharotomy wounds were covered with skin grafts.

Acute Renal Failure

The development of effective protocols for fluid resuscitation has greatly reduced the incidence of acute renal failure (ARF) during initial burn treatment. ARF may still develop if resuscitation is delayed or inadequate,¹¹³ particularly in patients with high-voltage electrical injuries or extremely deep burns, in whom pigment-induced nephropathy from myoglobin/hemoglobin is possible. Patients with visibly red or black urine should have resuscitation increased to produce urine outputs of 50 to 100 mL/hour. A one-time initial dose of an osmotic diuretic such as mannitol to stimulate urine production, and alkalinization of the urine by adding bicarbonate to intravenous fluids, is also widely practiced.^114,115

ARF in burn patients is now most often a late complication of infection or dehydration and continues to have a high mortality rate.¹¹⁶ Clearly its prevention is the best management strategy through meticulous fluid management and infection control. When ARF develops, patients should be treated with dialysis according to standard indications. Continuous renal replacement therapy can be particularly effective in managing patients who tolerate intermittent dialysis poorly.¹¹⁷ Nutritional support should not be reduced in this setting; rather, patients should continue to receive the calories and protein they require and undergo dialysis as needed.

Electrolyte Abnormalities

Although almost any disturbance of electrolytes can occur during the course of an acute burn, several characteristic patterns are seen. Most frequent are disturbances in serum sodium concentration. Massive resuscitation with LR solution (sodium content 130 mEq/L) results in the infusion of a large sodium load. Following resuscitation, urine output will be less reflective of intravascular volume, and serum sodium concentration will reflect free water balance. The formula given previously for maintenance fluids following resuscitation provides only a rough estimate of individual requirements, which can also be affected by fever, ventilator support, hyperglycemia, and other abnormalities. Progressive hyponatremia should prompt a reduction in total free water intake, although hypernatremia should be treated with increased free water. Dehydration can develop insidiously despite adequate daily urine output.

Hypokalemia may occur immediately after burn related to epinephrine release from injury,¹¹⁸ although hyperkalemia can result from cellular injury and acidosis. Both are usually short-lived and rarely require treatment. Thereafter, potassium levels often drop below normal, and patients may require substantial supplementation. Elevated aldosterone secretion following burn injury contributes to chronic hypokalemia and alkalosis.¹¹⁹ Magnesium levels also commonly drop, and supplementation of both potassium and magnesium is required as part of the “refeeding” effect of aggressive nutritional support.

Hypophosphatemia is also extremely common from multiple causes including catecholamine secretion, metabolic alkalosis, impaired renal phosphate absorption, and increased excretion during postresuscitation diuresis.¹²⁰ Phosphate levels typically reach a nadir 2 to 5 days after injury, and afterward rebound slowly. Significant hypophosphatemia can lead to cardiac dysfunction, reduced red blood cell survival, and neurologic abnormalities, particularly during refeeding. Substantial phosphate supplementation may be needed throughout the wound coverage phase of burn treatment. Routine monitoring and replacement of all electrolytes should be performed at least until patients no longer require intravenous fluids.

The Wound Coverage Phase

Surgical Treatment of Burn Patients

Although effective fluid resuscitation has reduced the acute mortality risk of burned patients, aggressive surgery has produced the greatest advancement in overall survival from burns. Early excision of wounds and coverage with skin or skin substitutes work to remove burn eschar as a major source of infection, shorten the period of severe hypermetabolism, relieve pain, improve function, and permit earlier mobilization and preservation of muscle mass.

Burn eschar left in place eventually separates from underlying tissue through the action of leukocyte enzymes. Bacterial infection facilitates this process, and burn eschar is an ideal medium for bacterial growth. In the era before routine excision, many patients died from sepsis while awaiting eschar separation while experiencing unremitting pain and prolonged muscle wasting. Surgical excision of burns was first practiced in the early twentieth century but produced high mortality rates from blood loss and anesthesia. Beginning in the 1970s, improved support has permitted aggressive excision of major burns with increased survival and decreased length of stay.121,122–124 Early excision is now considered a standard of care. A detailed discussion of these techniques is beyond the scope of this chapter. However, intensivists must be aware of the principles of surgical treatment and be able to support patients pre- and postoperatively.¹²⁵

Indications and Timing of Surgery

The larger the burn injury, the more acute the need for early excision. Patients with small (<10-15% TBSA) burns can be followed for up to 14 days to evaluate healing, but when burn size exceeds 25% to 30% TBSA, a widely accepted goal is removal of essentially all of the burn wound within 7 days of injury. Muller and Herndon excise the entire wound in a single procedure even while fluid resuscitation is ongoing,¹²⁶ but most units practice a staged approach, removing 15% to 20% TBSA at each operation.

En bloc excision of skin and subcutaneous tissue to vascularized fascia is rapid and relatively bloodless and creates a reliable bed for skin grafting. It is often practiced in the elderly and for particularly deep burns. However, fascial excisions are disfiguring and cause substantial problems with joint stiffness and pain. Far more common today is “tangential excision,” in which thin slices of tissue are removed until a viable bed of dermis or subcutaneous fat is reached. This requires more skill and time and produces more blood loss, but long-term results are unquestionably superior.

Unless covered, excised wounds will desiccate and develop a new layer of necrotic tissue—in essence, a second eschar—with attendant metabolic stress, pain, and infection. The ultimate goal of excision is autografting—coverage with the patient’s own skin. Burns excised within 7 to 10 days of injury are usually quite clean, and are often autografted immediately, providing prompt wound closure and facilitating early mobility. If donor sites are limited, autografts can be meshed to expand and cover more area. Excised wounds can be covered with antibiotic-soaked dressings to maintain tissue viability and combat infection for a few days. In recent years, a variety of skin substitutes have been utilized when donors are not available or if burns appear infected or poorly vascularized. The most widely used material is cadaver allograft skin obtained from tissue banks. Like autograft, allograft permits vascular ingrowth and take—sometimes for weeks—though this tissue is always eventually rejected. Allograft placement reduces bacterial colonization and pain, retards wound contraction, creates a clean, vascular bed, and can serve as a test for subsequent autografting. Cultured epithelial autografts (cultured skin) can be used to cover extensive areas but are expensive, fragile, and prone to loss from infection. They are best used over a scaffolding of intact or allograft dermis, and meticulous wound care is essential for success. A variety of synthetic and processed skin are also available, including synthetic dermis (Integra), acellular dermal matrix (Alloderm), amniotic membrane, collagen-bound polymer membranes (Biobrane, Transcyte), and others. Products still in development combine synthetic dermis with cultured epidermis, providing the potential for future one-step complete skin replacement.¹²⁷ All of these products require experience and skill to utilize successfully.

Hemodynamic Support

In acutely burned patients blood pressure is sustained by elevated catecholamine levels, though blood volume may remain below normal and hematocrit artificially high. With induction of anesthesia, adrenergic blockade and vasodilation can produce sudden hypotension as these hidden hypovolemia and anemia are revealed. In addition, surgical excision of old or infected burn wounds may stimulate bacteremia and potentiate hemodynamic instability.¹²⁸ The surgical team should prepare for these contingencies by continuing liberal fluid infusions during surgery and anticipating blood loss. Major burn excisions produce significant bleeding, which is often underestimated by surgeons. The blood loss from excision of 1% of the body surface area of an adult has been estimated at approximately 100 mL.¹²⁹ Use of tourniquets for excision, performance of staged excisions, and use of subdermal clysis of epinephrine-containing solutions—the Pitkin procedure—can all help reduce intraoperative bleeding.¹³⁰

Temperature Control

Burn patients often display mild to moderate fever secondary to hypermetabolism and also have accelerated evaporative heat loss. In the operating room, exposure and suppression of metabolism increase the risk of hypothermia, which can be very hard to correct. Temperature should be monitored carefully, patient warming devices should always be used in the operating room, and the room itself should be kept warm. Limiting operations to 2 to 3 hours is also helpful in avoiding hypothermia.

Burn Pharmacology and Anesthesia

Depolarizing muscle relaxants (succinylcholine) should not be used in patients with acute injuries,¹³¹ but burn patients are also relatively resistant to nondepolarizing agents and frequently require increased dosage. Induction agents that produce vasodilation, such as propofol, may potentiate hypotension, and should be used with caution. Ketamine maintains hemodynamic stability, and can be used effectively in surgery or for bedside procedures and dressing changes.¹³² Pharmacokinetics and dynamics of many other drugs are also significantly altered in burn patients.¹³³ Increased volume of distribution, decreased albumin binding, and increased renal blood flow necessitate monitoring and individualized dosing of many drugs.¹³⁴

Pain Control

Pain management is notoriously difficult in burn patients, who often require remarkable quantities of narcotics and sedatives throughout their hospital course. Although altered pharmacology undoubtedly plays a role in this process, extreme levels of sustained pain are typical, and tachyphylaxis often develops during long-term administration of opioids. Patient-controlled analgesia (PCA) can be effective, but use may be limited by impaired consciousness and hand function.¹³⁵ Nonopioid analgesics such as ibuprofen and toradol can be useful adjuncts in patients with cutaneous injuries. Finally, behavior modifications such as relaxation therapy, hypnosis, and virtual reality can be extremely helpful in overcoming the anxiety of dressing changes and physical therapy. Careful assessment of pain and anxiety and individualized dosing regimens are essential for successful management of burn patients.¹³⁶

Pulmonary Management

A variety of pulmonary problems occur frequently in burn patients and can require simultaneous treatment. Initial airway compromise, discussed previously, can be isolated and self-limited, but frequently contributes to pulmonary infection and inflammation. Acute respiratory distress syndrome (ARDS) can occur in the absence of inhalation injury, or components of both disorders can coexist and complement each other. Pulmonary edema or large pleural effusions can complicate fluid resuscitation. Aspiration, narcotic-induced respiratory depression, atelectasis and immobilization from bed rest, associated chest trauma, pulmonary thromboembolism, barotrauma, and pneumothorax/hemothorax following central line placement are all encountered in the management of major burns.

Chapter 48 provides a detailed discussion of the pathophysiology and treatment of the pulmonary complications of burn injury. Recent evidence suggests that inadequate fluid resuscitation may actually accentuate pulmonary damage¹³⁷; burn patients with inhalation injuries require increased resuscitation volumes⁵⁹ and should be resuscitated at least as aggressively as other burn patients. Pulmonary artery catheterization may be helpful in patients with severe lung injuries who require high ventilator pressures. Although colloid-based resuscitation may be associated with persistently increased extravascular lung water,⁹⁰ this does not appear to be the case with crystalloid, even in patients who require substantially more fluid than Parkland requirements.⁷⁴

A number of reports have focused on techniques to improve oxygenation in burn patients with severe acute lung injury, including extracorporeal membrane oxygenation,¹³⁸ inhaled nitric oxide,¹³⁹ and novel ventilator strategies such as high-frequency volume diffusive,¹⁴⁰ oscillation,¹⁴¹ or percussive ventilation.¹⁴² However, these modalities are limited in their availability and usefulness, and clear-cut indications for each have not been developed. The use of permissive hypercapnia may be beneficial,¹⁴³ though other protective lung strategies have not been evaluated in burns. The vast majority of burn patients can be managed effectively with conventional ventilation techniques, and death purely from hypoxia is rare.

Multiple organ failure is the most common cause of death in burn patients,144,145 very frequently triggered by ongoing pulmonary infection, which can be severe and persistent.¹⁴⁶ This pneumonia is usually ventilator associated; intubation facilitates contamination of the lower airways already primed for infection by the mucosal sloughing, mucous plugging, and atelectasis caused by inhalation injury. Frequent cultures and aggressive antibiotic use are necessary for successful treatment. The use of ventilator bundles, including frequent suctioning and chest physiotherapy, elevation of the head of the bed, closed suction techniques, postpyloric feeding, and frequent oral care, may also be helpful.¹⁴⁷ The use of heparin and acetylcysteine aerosols—sometimes combined with bronchodilators—to liquefy and mobilize casts and debris has shown some promise in pediatric patients.¹⁴⁸ Improved mobilization of secretions may also be the mechanism by which percussive or oscillatory ventilation is beneficial.¹⁴² Fiberoptic bronchoscopy and bronchoalveolar lavage can be used both for diagnosis of pneumonia and as a therapeutic maneuver to clear tenacious plugs and improve ventilation.¹⁹ Based on limited evidence, neither corticosteroids nor prophylactic antibiotics appear to be helpful in treating respiratory failure or preventing pneumonia.¹⁴⁹ The performance of tracheostomy in patients who fail initial attempts at extubation may or may not reduce infections¹⁵⁰ but unquestionably provides a more comfortable and secure airway for long-term ventilator support.

Cardiovascular Complications and Care

As mentioned previously, the immediate response to burn injury consists of reduced cardiac output and increased peripheral resistance, followed by gradual return of both values to near-normal at the end of resuscitation, after which markedly elevated cardiac output and reduced peripheral resistance persists through wound coverage and into rehabilitation (see Fig. 67.5). This response is so characteristic that invasive hemodynamic monitoring is rarely needed during resuscitation.

Catecholamine stimulation of cardiac function often results in hypertension, which can be difficult to manage, as well as sustained tachycardia and tachyarrhythmias. Beta blockade is useful in treating these problems, and may be indicated for routine administration as well. Beta blockers are tolerated well in this situation, and may even contribute to improved outcomes.¹⁵¹

Hypotension can also occur in burn patients during acute care. Obligatory postresuscitation diuresis coupled with increased evaporative and metabolic fluid losses favors development of occult volume depletion. Progressive hypernatremia or azotemia and sustained tachycardia provide clues to this diagnosis, which may require aggressive fluid support. Persistent hypotension should lead to a search for sepsis. Invasive monitoring may be helpful in this setting as well; however, the classic hemodynamic picture of sepsis—increased cardiac output and reduced peripheral resistance—is also the characteristic postburn response, so that such monitoring will likely be more useful in guiding therapy than in diagnosis.

Adrenal Insufficiency

Recent studies have demonstrated a surprisingly high frequency of absolute or relative adrenal insufficiency in critical care patients, including burns, which may increase mortality risk from shock and sepsis.152,153 However, the quoted incidence of this problem has varied greatly, depending on the diagnostic criteria used and the populations studied.^154–157 No systematic evaluation of adrenal insufficiency has been conducted in burn patients. The incidence of this complication remains unknown,¹⁵⁸ but may be more common than previously suspected, and should be considered in burn patients with refractory hypotension.

Infection Control

Burn Wound Infections

Historically overwhelming burn wound sepsis was a major cause of death in patients who survived resuscitation. Over the past 50 years, the use of systemic and topical antibiotics coupled with surgical excision and skin grafting has dramatically decreased this problem. However, infection in burn wounds remains an important source of morbidity and mortality risks. As with other infections, the development of increasingly effective antibiotics has been matched by rapid adaptation of microbial pathogens. The initial use of antibiotics in World War II controlled Streptococcus and Staphylococcus infections, but these were supplanted by gram-negative organisms, particularly Pseudomonas. In the 1960s and 1970s, development of silver nitrate solution, mafenide acetate (Sulfamylon) and silver sulfadiazine (Silvadene, Thermazene) were effective in combating these infections, but microflora continued to evolve. Today, burn wound infections are increasingly caused by multiply resistant gram-negative organisms, Acinetobacter, methicillin-resistant Staphylococcus, Candida, and fungi.¹⁵⁹ Individual patients may display a similar progression of wound colonization as therapy and antibiotic administration continue.

Established principles of infection control remain a critical component of burn care. Essentially every open wound should be treated with topical agents until healed. The time-tested agents sulfadiazene and mafenide remain effective against a wide range of bacteria, and still constitute the first line for acute burn treatment despite some limitations. Silver sulfadiazine has been associated with neutropenia, though this is usually a transient phenomenon in the early postburn period (see later). Mafenide is a carbonic anhydrase inhibitor that can generate significant metabolic acidosis if used on large areas and has also been linked to the emergence of fungal infections.¹⁶⁰ A number of newer topical agents are now available, including silver-containing dressings (Acticoat, Acquacel-Ag), cerium-silver nitrate, mupirocin (Bactroban), chlorhexidine, betadine, and others. The choice of agent and technique should be adjusted based on culture results and wound appearance, and can often be reduced as wounds heal. Silver-containing agents and topical antifungals such as nystatin are effective against yeast and mold infections, and antibiotic solutions including mafenide and silver nitrate are widely used to soak fresh skin grafts and some skin substitutes. The so-called melting graft syndrome has been attributed to chronic infection with Staphylococcus species¹⁶¹; topical mupirocin may be particularly effective in this setting.

In addition to topical antibiotics, meticulous wound cleansing and debridement should be performed at least daily and wounds inspected carefully. Findings suggestive of invasive infection include green or black discoloration, purulent exudate, extending erythema or tissue necrosis, conversion of superficial-appearing burns to deep wounds, development of satellite lesions (ecthyma gangrenosum), and loss of vascularized skin grafts. Any of these findings should prompt careful culturing of wounds, escalating or changing topical and systemic antibiotics, and possibly surgery.

Surface cultures of burn wounds will identify dominant organisms, but cannot distinguish between invasive infection and colonization. Burn wound biopsies can be obtained for quantitative culture; bacterial counts of 10⁵ per gram of tissue or more has been used as a criterion for invasive burn wound sepsis. However, false-positive results are frequent; wounds may be heavily colonized without bacterial invasion, and biopsies must be obtained in exactly the right place.¹⁶² Histologic demonstration of organisms penetrating into viable tissue and capillaries remains a valid diagnostic finding.¹⁵⁹ However, many centers lack an experienced pathologist to read these samples accurately, so routine biopsies are now used infrequently. Daily examination of wounds and clinical suspicion remain the most important tools for prompt diagnosis of burn wound infection. Once detected, burn wound sepsis is best treated by aggressive, total wound excision, broad-spectrum systemic coverage, and topical antibiotic soaks in preparation for allograft or autograft placement. Burn wound sepsis is an extremely serious complication and should involve every member of the burn team.

Other Infections

Modern methods of infection prevention and control have contributed to decreased rates of many types of infections in burn patients. With the decline in burn wound infections, pneumonia has emerged as the most common infection in burn patients. Central venous catheter infections—particularly from Candida—also remain a constant threat ¹⁶³ and can contribute to bacterial endocarditis, particularly if lines are allowed to reach the atrium or ventricle.¹⁶⁴ Neither routine catheter changes nor rewires have been shown to decrease infectious risks.¹⁶⁵ The current use of peripherally inserted central catheters (PICC lines) may or may not reduce the risks of catheter-related infection,¹⁶⁶ but regardless of the line or site used, adherence to accepted principles of catheter placement and care¹⁶⁷ and prompt removal of catheters when possible should be practiced. Improved wound management, nutrition, and hygiene have all but eliminated such historically important infections as suppurative thrombophlebitis, chondritis of the ear, and suppurative parotitis as clinical problems.

Diagnosis of infection can be difficult in burn patients. Fever, leukocytosis, and tachycardia are all normal consequences of acute burn injury, and standard criteria for the diagnosis of systemic inflammatory response syndrome (SIRS) and sepsis are difficult to interpret.¹⁶⁸ Low-grade fever may be sustained during acute treatment, but any increase in temperature above 38.5° C, especially when accompanied by increases in white blood cells (WBCs) or heart rate, should prompt an evaluation for infection, including appropriate cultures. The once-common policy of obtaining routine surveillance cultures of blood, urine, or wounds has been shown to have relatively low yield and a high incidence of false-positive results.¹⁶⁹ Some units use swab cultures to detect colonization and to track dominant flora for epidemiologic reasons. The value of measuring specific biomarkers to detect infection, including C-reactive protein and procalcitonin, has been inconsistent and remains controversial.^170,171

Systemic prophylactic antibiotics have not been shown to reduce burn wound or other infections and should not be used.172,173 As in all ICU patients, antibiotic use should be guided by the clinical situation and culture results. As noted previously, burn patients often exhibit abnormal drug kinetics and require increased antibiotic dosing and careful monitoring of antibiotic efficacy. The clinical pharmacist is an essential member of the burn team for this and other reasons. The isolation of burn patients through universal precautions and the separation of infected patients by cohort nursing should be practiced as routine components of infection control. The practice of selective digestive decontamination in burn patients is controversial; although some centers report benefits,¹⁷⁴ and some no effect,¹⁷⁵ from this time-consuming technique, it is not routinely practiced in U.S. burn centers.

Metabolic Support and Gastrointestinal Management

The Hypermetabolism of Burn Injury

Burns induce the greatest hypermetabolic response of any injury. This response typically follows the ebb and flow pattern described over 70 years ago,¹⁷⁶ in which initial (24-72 hours) reduced energy expenditure is followed by increasing metabolism, which peaks 10 to 14 days after injury and then tapers slowly as wound healing progresses. The degree of hypermetabolism correlates with burn size but appears to level off with burns of 40% to 50% TBSA, above which no further increase is seen.¹⁷⁷ This response is sustained by the secretion of catecholamines, cortisol, and glucagon that persists until after wounds are closed. Together these hormones accelerate catabolism through breakdown of skeletal muscle, reduced uptake of fats, and opposition to the effects of insulin.^178,179 The result is obligatory muscle wasting to support gluconeogenesis; lipids have very little protein-sparing effect, and even exogenous glucose is limited in its ability to prevent protein wasting.¹⁸⁰

In the 1970s burn patients frequently demonstrated prolonged calorie and protein consumption that exceeded twice normal and caused fatal inanition within a few weeks of injury.181–184 Modern burn treatment—aggressive excision and wound coverage, control of sepsis and pain, mechanical ventilation, and improved environmental control—have all helped reduce both the duration and magnitude of this response.^177,185,186 Nonetheless, significant hypermetabolism persists well after burn wounds are closed, and careful nutritional support is a requirement for the successful care of burn patients.¹⁸⁷

Route and Timing of Nutritional Support

The superiority of enteral nutrition is widely accepted,¹⁸⁸ and may be especially true for burn patients. Enteral nutrition nourishes bowel mucosa, preserves blood supply, reduces permeability, and improves associated immune function.^189–191 In trauma and ICU patients, early and aggressive enteral nutrition appears to decrease infectious complications, but total parenteral nutrition (TPN) has been associated with an increased mortality rate in burn patients,^192,193 and it also promotes development of fatty liver.¹⁹⁴ It may even be preferable to withhold nutrition entirely for limited periods, rather than use TPN.

Enteral feeding should begin as quickly as practical following injury, especially if patients will not be able to eat within 5 to 7 days. In contrast to early studies,¹⁹⁵ immediate enteral feedings have not been consistently shown to reduce hypermetabolism,¹⁹⁶ but do decrease calorie deficit and improve nitrogen balance.^197,198 Feedings can be started within a few hours of injury, and continued even through surgical procedures.¹⁹⁹ The routine use of promotility agents has not been studied in burn patients²⁰⁰; it is also unclear whether small intestinal feedings are superior to gastric feedings; both can have complications, and both require careful monitoring.

Energy Requirements

Dozens of regimens have been used to estimate the caloric needs of burn patients, including the famous Curreri formula.²⁰¹ However, static formulas cannot accommodate the major fluctuations that occur over time and between individuals of different ages and burn sizes.²⁰² In addition, because modern burn treatment has reduced hypermetabolism, older formulas overestimate requirements significantly.²⁰³ Current recommended caloric intake for adults with major burns is 120% to 150% of Harris-Benedict estimates of basal needs.²⁰⁴ Many centers also use indirect calorimetry to measure energy expenditure and to detect significant under- or overfeeding.²⁰⁵ Regardless, support should still be increased during periods of peak energy expenditure to avoid underfeeding, and reduced later to avoid overfeeding.

Whatever regimen is chosen, the practical difficulties of delivering nutritional support are substantial.206,207 Interruptions in feedings, fluctuations in energy consumption caused by fever and activity, and delivery of empty calories in glucose solutions all frustrate attempts to tailor individual nutrition exactly, which may explain why the superiority of indirect calorimetry-based nutrition has not been proved.²⁰² Involvement of the team—including a dietician—in implementing, assessing, and adjusting feedings is probably more important than adherence to predetermined estimations.²⁰⁸

Enteral Formulas

Chapter 82 provides details on the composition of many commercially available enteral formulas which can be used in burn patients. Specific components of effective enteral formulas include the following:

Carbohydrates and Glucose Control

The catabolism of burn injury makes carbohydrates the preferred energy source, but also worsens hyperglycemia. Recent studies have demonstrated the value of meticulous glucose control in ICU populations in reducing organ failure, length of stay, and inflammation.209,210 These benefits are likely seen in burn patients as well,²¹¹ but hormonally mediated resistance to insulin—the so-called diabetes of injury—makes attaining control a major challenge. Many burn units use hyperglycemia protocols, which require frequent (or continuous) dosing of insulin and careful monitoring. Oral hypoglycemics appear helpful in this effort²¹²; in addition, giving limited calories as fat helps reduce the glucose burden required by these patients.

Fat

A certain (small) quantity of dietary fat is an essential nutrient. Lipolysis is suppressed in burn patients, as is the ability to utilize exogenous fat as an energy source. Fat intake should be restricted to less than 30% of total nonprotein calories, or about 1 g/kg/day ²¹³ or less^214,215; withholding fat entirely from TPN for substantial periods may be beneficial.^188,216 In addition, products high in ω-3 free fatty acids (FFAs) and correspondingly low in ω-6 FFAs may improve glucose control and reduce infections.^217,218 Most clinical experience has been obtained with the use of immune-enhancing diets (IEDs) (see later) in which the effects of individual components have been difficult to assess.

Protein

Accelerated proteolysis is often the most important characteristic of burn-induced hypermetabolism. A major goal of nutrition is to reduce or replace protein losses, which can exceed lb of lean body mass per day. Providing adequate calories alone will not reduce muscle breakdown,²¹⁹ so increased protein must be provided as well. Protein requirements increase with burn size^220,221; appropriate provision of dietary protein has resulted in reduced infections and a lower mortality rate in patients with major injuries.²²² Current recommendations are 1.5 to 2.0 g of protein/kg/day (up to 3.0 g/kg/day in children),^205,208,223 which corresponds to a nonprotein calorie/nitrogen ratio of 100 : 1 or less. Nitrogen balance should be monitored regularly.

Specific Amino Acids

The amino acids arginine (Arg) and glutamine (Glu) play enhanced roles in critical illness. Both are depleted rapidly in burn patients, and are considered conditionally essential.219,224 Glutamine is important in energy transport, as a precursor of glutathione²²⁵ and as a nutrient for enterocytes, helping to preserve bowel integrity and limit permeability.^226–228 In burn patients provision of up to 25 g Glu/day, given parenterally²²⁹ or enterally,²³⁰ has been associated with improved visceral protein levels and reduced infectious mortality rate and length of stay. Glutamine supplementation has been recommended¹⁸⁸ but is not routinely practiced. Glutamine is almost totally absent from TPN formulas, which may explain some of the benefits of enteral nutrition in burn patients.

Arginine enhances natural killer cell function and nitric oxide (NO) synthesis, promoting inflammation and resistance to infection.231,232 Specific studies of arginine supplementation have not been performed in burn patients, but arginine has been incorporated into complex immune-enhancing diets (IEDs) containing ω-3 FFAs, arginine, glutamine, and RNA, among other components.²³³ These diets have shown benefits in some surgical populations,²³⁴ but deleterious or no effects in patients with sepsis or pneumonia,²³⁵ and their widespread use has been questioned.¹⁸⁸ Few data are available on IEDs in burn patients,²³⁶ but the mixed results in other groups suggest that components should be studied separately before incorporating them into cocktails with even more unpredictable effects. Most burn centers simply use high-protein diets rather than these specialized and expensive formulas.

Other Nutrients

A number of micronutrients—including vitamins A, C, and D, iron, zinc, and others—are important in wound healing and may be depleted following burn injury,²³⁷ and some supplementation has been recommended.²³⁸ Many centers simply administer multivitamins, which is probably adequate.^178,239 Commercial enteral formulas also contain far more than the recommended daily dietary allowances of many vitamins and trace elements.

Monitoring Nutritional Support

Because burn injury alters many parameters of nutritional status, monitoring nutrition can be as difficult as providing it. For example, substantial weight gain invariably accompanies fluid resuscitation,²⁴⁰ although overfeeding can increase body fat even as protein stores are depleted.^241,242 As a result, patients have often lost more lean body mass than is reflected by weight alone.²⁴³ Nitrogen balance studies can be useful, but sedation and bed rest make attaining positive nitrogen balance difficult,²⁴⁴ emphasizing the need to continue physical therapy even during acute care. Serum protein markers are often distorted; levels of albumin,²⁴⁵ prealbumin, and transferrin^205,246 fall quickly following injury, and recover only very slowly even with appropriate nutrition. Perhaps the best marker of nutritional adequacy in burn patients is their overall status, including vital signs, wound healing, and functional improvement. Body weight, nitrogen balance, and protein markers may be most useful in tracking trends in individuals.²⁴⁷

Modulation of Hypermetabolism

Burn-related hormonal changes complicate the provision of nutritional support, but also provide mechanisms by which hypermetabolism can be manipulated. Recent studies have shown promising results, and suggest that manipulation of the metabolic response to injury may become routine in the future. A variety of approaches have been utilized, including beta blockade with propranolol, low-dose insulin infusions, use of counterregulatory hormones such as insulin-like growth factor-1 (IGF-1), or anabolic agents such as testosterone and oxandrolone.²⁴⁸ The use of propranolol appears to be a safe, low-cost way to ameliorate both the cardiovascular response and hypermetabolic muscle wasting that occur during acute burn care.²⁴⁹ Administration of the synthetic oral androgen oxandrolone has been shown to reduce muscle breakdown, speed rehabilitation, and lead to decreased length of stay in hospitalized patients.^250,251 Although none of these therapies is now routine, they are becoming more widespread. Recommendations for their routine use will need to await larger controlled trials to demonstrate efficacy.

Gastrointestinal Complications in Burn Patients

Although the incidence of most gastrointestinal (GI) complications has decreased dramatically with improved resuscitation and control of infection, a number of problems are frequent or serious enough to deserve discussion.

Acute Cholecystitis

Cholecystitis—usually acalculous—can have a number of causes, including gallbladder ischemia from shock and dehydration,²⁵² biliary stasis from narcotics and TPN, bile pigment loads from hemolysis and transfusion, and bacterial seeding from sepsis. With more effective control of these factors, acute cholecystitis is now rare; a recent review documented just 20 cases among 10,762 acutely burned patients (0.18%), with progressive declines in recent years.²⁵³ Fever, leukocytosis, feeding intolerance, and abdominal pain are characteristic findings, though they may be difficult to sort out in acutely ill patients. Ultrasound and computed tomography (CT) scanning are preferred for confirmation of diagnosis; biliary scintigraphy can have a high false-positive rate. Treatment has traditionally consisted of prompt cholecystectomy, though placement of cholecystostomy tubes under ultrasound guidance can provide definitive treatment in many patients.²⁵⁴ With prompt diagnosis, the mortality rate from this complication should be low.

Hepatic Enzyme Elevation

Immediately following burn injury, hemolysis and ileus can contribute to a cholestatic picture, which should resolve within a few days. Some degree of chronic fatty infiltration of the liver may be inevitable in patients with major burns, and mild enzyme elevations are often seen, which is exacerbated by overfeeding and the use of TPN.¹⁹⁴ Severe hepatic steatosis may be both a cause and consequence of sepsis, and correlates with increased mortality rate.

Pancreatitis

Pancreatitis can also result from systemic hypoperfusion and secondary sepsis. In contrast to cholecystitis, the incidence of pancreatitis may be increasing as more severely injured patients now survive burn shock. Ryan and colleagues documented hyperamylasemia in 40% of patients with large burns, with an associated increased mortality rate and length of stay,²⁵⁵ although pancreatic pseudocysts and abscesses were quite rare. Pancreatic enzymes should be measured in patients with feeding intolerance, abdominal pain, or nausea; in many cases, transient bowel rest and fluid support will be effective treatment. Use of TPN should be avoided unless pancreatitis is unusually severe and prolonged.

Gastrointestinal Bleeding

Although the time-honored eponym Curling’s ulcer has sometimes been considered a unique entity, burn patients develop the stress ulcerations typical among acutely ill patients. Mucosal erosions and atrophy can occur within 72 hours of injury and progress to large (often multiple) ulcerations of the prepyloric area or duodenum. Their primary cause is thought to be gastric mucosal hypoperfusion from shock or sepsis; the role of Helicobacter pylori infection is unclear.256,257 Modern treatment strategies including aggressive fluid resuscitation, suppression or neutralization of gastric acid, and early enteral feeding have resulted in a dramatic decline in the incidence of this complication from as high as 86% in early postmortem studies²⁵⁸ to less than 2% today. Bleeding is more frequent with large injuries and in patients with coagulopathy, prolonged mechanical ventilation, and sepsis. Aggressive evaluation of any observed GI bleeding should be undertaken. Most patients can be controlled with endoscopic maneuvers and continuous proton pump inhibitors. Surgery for acute upper GI bleeding is now rarely required.²⁵⁹

Ileus and Intestinal Necrosis

Ileus occurs routinely following acute burns, and oral intake should be withheld at least until resuscitation is completed. Impaired intestinal motility can be aggravated by narcotics, infection, and ventilatory support. Severe colonic ileus—Ogilvie’s syndrome—can occur in this setting,²⁶⁰ and overly aggressive enteral feeding can rarely lead to bowel distention, ischemia, necrosis, perforation, and death.^261,262 For this reason, feedings should be monitored carefully, and held if obstipation, distention, or pain becomes significant. CT scanning can confirm bowel dilatation or free air, in which case immediate laparotomy is mandatory.

Diarrhea

Diarrhea is extremely common with enteral feedings, and can be a major problem in management. The cause is often multifactorial,²⁶³ including high osmotic loads, overfeeding, enteral medications, and infections including Cytomegalovirus and Clostridium difficile.²⁶⁴ Treatment options include enteral opiates such as Imodium or paregoric or the use of fiber-containing products. However, fiber can clog small-diameter tubes and has been blamed for intestinal distention and necrosis,²⁶⁵ and slowing intestinal transit can potentiate infectious diarrhea. Often simply holding feedings for a few hours will suffice; diarrhea unresponsive to simple measures should prompt a search for infectious causes, inside or outside the bowel.²⁶⁶

Hematologic Considerations

Red Blood Cells

Hemoconcentration, which accompanies burn shock, can result in hematocrits of 70% or higher. This will theoretically produce sludging and increased vascular resistance, though clinical problems with thrombosis are rare. As resuscitation proceeds hematocrits fall progressively, and are usually below normal by the end of 48 hours. Thereafter, anemia often persists or worsens until wound coverage is obtained. Several mechanisms contribute to this finding.²⁶⁷ First, burn injury destroys red blood cells directly; significant hemolysis can occur within minutes of injury and produce hemoglobinuria or jaundice. Burn-induced alterations in red blood cell metabolism result in spherocytosis, increased membrane fragility, and shortened red blood cell survival. Erythropoietic response is blunted, apparently at the stem cell level,²⁶⁸ and erythropoietin supplementation is not helpful.²⁶⁹ Acute hemorrhage from surgery, and more gradual blood loss from wound debridements add to these effects.

The issue of appropriate transfusion trigger is controversial in burn patients. No systematic trial of transfusion thresholds has been performed, and no standard is universally accepted,²⁷⁰ though limited evidence supports the practice of conservative transfusion in burn patients as in other ICU populations. In a multicenter review, Palmieri and coworkers found that transfusions correlated with both mortality risk and infectious episodes in major burns,²⁷¹ which underscores that transfusions should be based on physiologic assessment and not given routinely.