Burn Injury: Thermal and Electrical - examdev.theaba.org · gases and products of incomplete combustion; when present, an inhalation injury is associated with increased mortality

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63Burn Injury: Thermal and ElectricalWinston t. RichaRds, david J. hall, MaRtin d. Rosenthal, and david W. Mozingo

InTroducTIon

Burn injury accounts for 40,000 hospital admissions/year, including 30,000 admissions to hospitals with specialized burn centers. More than 60% of the 40,000 hospitalizations for burn injuries in the United States each year are now admit-ted to 127 hospitals with specialized burn centers. Thirty-eight percent of the admissions exceeded 10% total body surface area (TBSA), and 10% exceeded 30% TBSA involvement. Most included severe burns of such vital body areas as the face, hands, and feet; interestingly, 69% of burn patients were male. Data from the National Hospital Discharge survey of 2010, as well as the National Inpatient Sample 2012, and the American Burn Association National Burn Repository 2013 report suggest that the causes of the burns include fire (43%), scald (34%), contact with a hot object (9%), electrical (4%), and chemical (3%) (1).

Burn injury has a systemic effect on the patient, and each organ system responds to this injury in a predictable man-ner proportional to the extent of burn. The current literature supports the following physiologic responses in each organ system.

Burn PhysIology and ThE EffEcTs on organ sysTEms

Cardiovascular System

Immediately after a burn injury cardiac output (CO) becomes depressed, systemic vascular resistance (SVR) increases, and the patient’s capillary permeability increases. Each of these occurs in a burn size- and time-dependent fashion.

During the late 1960s and early 1970s, animal studies by Moncrief, Asch, and Wilmore clearly defined the physiologic response of the heart and systemic and pulmonary vascula-ture to burn injury (3–4). These experiments showed a burn size- and severity-dependent depression in CO, which resolved over time, and could be altered with fluid resuscitation and the addition of vasoactive medications. They also showed a time-dependent increase in SVR and pulmonary vascular resistance (PVR), which resolved with fluid resuscitation as well as with the administration of vasoactive medication.

Burn injury causes loss of the skin’s fluid barrier func-tion. These resultant fluid losses, as well as increased capil-lary permeability, lead to hypovolemia and burn shock. The loss of fluid leads to decreased cardiac preload and ultimately, decreased CO. Integumentary fluid losses and tissue edema drive the cardiovascular response to burn injury, but improve-ment in cardiac function parameters achieved by fluid resusci-tation do not fully resolve this deficit; there is evidence linking a myocardial depressant factor to multiple inflammatory medi-ators (5–8).

Cardiac depression after a thermal injury is mediated by the interaction of multiple inflammatory and anti- inflammatory molecular signals. Early and late inflammatory mediators influence myocardial contraction and relaxation in the first 24 to 48 hours after burn injury (9,10). Factors including tumor necrosis factor-α (TNF-α), Fas ligand, interleukin (IL)-1, IL-18, IL-6, macrophage migration inhibitory factor (MIF), high mobility group box 1 (HMGB-1) chemokines, and caspase-1 have been implicated in the loss of cardiac contractility as well as myocardial relaxation, leading to decreased CO after injury. By contrast, the anti-inflammatory pathways involving IL-10, transforming growth factor (TGF)-β, and soluble TNF recep-tor lead to the resolution of the initial myocardial depression.

Resuscitation of the burn patient addresses the cardiac depression, with administered fluid bolstering the intravascu-lar volume by replacing losses and anticipating future deficits. Multiple resuscitation strategies exist for fluid management in the burn patient, which are discussed separately below. Myocardial depression can be marginally supported pharma-cologically with the use of inotropic agents. Further research toward more direct management of the decreased contractil-ity could target the inflammatory mediators released after burn injury (8).

Pulmonary System

Burn injury has multiple effects on the pulmonary system. Depending on the mode of injury, including inhalation and direct burns to the chest wall, these effects may be manifest as alterations in respiratory rate, tidal volume, gas exchange, and even long-term effects on pulmonary function. Burn injury not only affects the lungs in a direct manner, but complications of these injuries may add to further dysfunction. Pneumonia and tracheal irritation from prolonged intubation are some of the complicating factors that affect the burn patient (2).

The pulmonary response to burn injury is characterized by transient pulmonary hypertension, decreased lung compliance, and hypoxia. These functional changes are mediated by multiple factors including inflammation, acid–base imbalance, airway injury, and chest wall restriction. The body’s pH balance high-lights the close interaction between the pulmonary and renal systems in addressing disturbances caused by burn injury. Stud-ies of anti-inflammatory treatment prior to burn injury altered the pattern of decreased compliance, pulmonary hypertension, and hypoxia, suggesting a cause-and-effect relationship (11).

With relatively small TBSA burns, respiratory rates increased, peaking by postburn day 8 and returning to control levels by about 3 weeks postburn. Along with these respira-tory rate changes, an increase in tidal volume and minute ven-tilation were also recorded; these returned to control levels in approximately 3 weeks (11).

Chest burns with their concurrent edema formation showed notable restrictive effects on pulmonary function during the

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676 SECTion 6 the suRgical Patient

first 3 days postinjury; these effects resolved over time. Dur-ing the patient’s initial resuscitation, decreased chest wall compliance may lead to restricted ventilation and increased airway pressures; burn wound escharotomy of the chest wall is indicated in these situations to improve chest wall compliance.

Further effects of burn injury on pulmonary function have been attributed to burn wound infection, which may lead to lung dysfunction secondary to inflammatory mediator release from around the burned tissue, possibly mediated by throm-boxane A2; management of the inflammatory process initiated by burn injury may prove to be helpful in modulating this effect (12).

Complications associated with intubation after burn inju-ries include ventilator-associated pneumonia (VAP) and tra-cheal stenosis. Protocols for the reduction/prevention of VAP have been extensively reviewed and are currently being used in many hospitals. The judicious management of ventila-tor support and endotracheal intubation addresses postin-jury tracheal stenosis. Tracheal decannulation at the earliest opportunity afforded by the patient’s physiology is important in reducing this complication. Presently, a generalized benefit from the VAP bundle has not been clearly defined in the burn patient population, and requires further study (13–15).

Smoke inhalation injury affects between 10% and 30% of burn patients. This injury is caused by the inhalation of hot gases and products of incomplete combustion; when present, an inhalation injury is associated with increased mortality up to 20% over that predicted by age and extent of burn alone. Although in the past, increased fluid resuscitation was advo-cated for patients with inhalation injury, this did not correlate well with fluid requirements during resuscitation; interestingly, a low initial PaO2/FiO2 ratio does so correlate. An increased TBSA injury is associated with increased pneumonia rates, and the presence of pneumonia in patients with an inhala-tion injury results in a higher mortality rate. Pneumonia and inhalation injury increase length of stay over inhalation injury alone; this is discussed further below (16).

In the late 1980s, high-frequency percussive ventilation (HFPV) was used to treat patients with severe inhalation injury; the results were promising, and further studies fol-lowed. By 2007, it had been noted that HFPV for inhalation injury did not change mean ventilator days, intensive care unit (ICU) length of stay, hospital length of stay, or incidence of pneumonia. Despite the similarities in the HFPV and conven-tional ventilator groups, a decrease in both overall morbidity and mortality in a subset of patients with less than or equal to 40% TBSA burned was noted. This finding led to the recom-mendation for further study in a randomized and controlled fashion (17–28).

Renal System

Renal failure has been reported in up to 20% of burn injury patients, with a clinical picture related to the size and sever-ity of burn injury. Multifactorial in nature, the time course of renal failure falls into early or late categories. The mor-tality of patients developing severe renal failure with burn injury approaches 80%. Early acute renal failure appears to be directly associated with clinical events such as delayed resusci-tation, under-resuscitation, hypotension, and rhabdomyolysis.

Increased burn severity is associated with a higher incidence of acute renal failure. Rhabdomyolysis, a rare consequence of

flame burns, but often associated with electrical injury, has a direct association with renal failure. Late episodes of acute renal failure are more commonly associated with sepsis, toxic drugs, and pre-existing medical conditions.

Treatment of acute renal failure in the burn patient and other patient populations involves multiple steps. Adequate fluid resuscitation initiated as early as possible during the time course of the burn injury will reduce the presentation of early acute renal failure. Monitoring urine output as a measure of renal perfusion allows the clinician to maintain adequate fluid input. Late episodes of acute renal failure can be addressed by treating the underlying cause. Sepsis from invasive vascular access, wounds, pneumonia, or urinary tract should be con-trolled by replacing the lines, excising the burn wound, and providing adequate antibiotic therapy for pneumonia and uri-nary tract infection. When needed, renal replacement therapy should be instituted and has shown benefit. The application of CVVH in adult patients with severe burns and acute kidney injury was associated with a decrease in 28-day and hospital mortality (29).

Gastrointestinal Tract and Liver

Ileus presents in patients with burns exceeding 20% TBSA. Despite this problem, using the gut with some—even minimal—level of feeding is advocated early after injury, and is usually well tolerated. Tube feeding should be instituted for patients with large burns where the patient is unable to tolerate sufficient intake by mouth to sustain the markedly increased nutritional requirements (30).

Gastroduodenal stress ulceration has been a hallmark of early burn care, with significant bleeding or perforation complicating the care of extensively burned individuals. This complication markedly decreased with the use of ant-acids, H2-antagonists, and proton pump inhibiting medica-tions; their use has become routine in the management of the thermally injured patient (31).

Perforation

Poor perfusion of the gut during resuscitation may lead to seg-mental ischemia in the watershed areas of the intestine. With this condition, there is a risk for developing necrosis and sub-sequent perforation; vasoactive medications used during burn resuscitation or during prolonged septic events may increase this risk (32). Clinicians may use physical examinations, labo-ratory studies, and x-rays to monitor this complication.

Normal gut flora has been identified as an infection source in the burn patient as well as in other critically injured patients (33–35). Maintaining gut integrity with nutritional support in the form of glutamine supplementation has been proposed and studied in the burn patient. A second approach to this prob-lem, selective gut decontamination, has been proposed and tested in animal models (36–38). Selective gut decontamina-tion has been shown to reduce bacterial translocation from the gut in burned rats (39). With this reduction in translocation, immunosuppression was reduced and the cardiac response to subsequent septic challenge was improved. Clinical success with this approach is not well documented (40–44).

Intra-abdominal hypertension, as defined by a bladder pres-sure of 30 mmHg or greater is the precursor to the abdominal compartment syndrome. Respiratory compromise with increas-ing peak airway pressures, renal compromise with decreased

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CHAPTER 63 Burn injury: thermal and electrical 677

renal perfusion and urine output, and increased mortality among burn patients are the features of this syndrome (45). Burn patients with 30% or greater TBSA injury, requiring fluid resuscitation over and above the standard calculated rates are at risk for this complication (46). We recommend monitoring bladder pressures in each patient with burns greater than 30% and initiating therapeutic maneuvers for those patients with pressures of greater than 30 mmHg (47).

Therapy for intra-abdominal hypertension follows a graded response. Reduced fluid administration, sedation, and neuromuscular blocking agent (NMBA) use for the patient are the initial treatments. Escharotomies and peritoneal drainage make up the next most invasive line of management and, ulti-mately, abdominal decompression through a laparotomy inci-sion may be needed to relieve the symptoms. In the severely burned population, abdominal compartment syndrome has a high mortality rate and should be addressed urgently when recognized (48–50).

Central Nervous System

Burn injury and resuscitation in an ovine model showed that cerebral autoregulation adjusted to the hemodynamic changes caused by burn injury. Autoregulation of cerebral blood flow was effective to a point and then began to fail as resuscitation proceeded, suggesting that the cerebrovascular system has a limited reserve to tolerate the effects of burn injury (51–53).

Endocrine System

There is a graded response of the endocrine system after burn injury. Hormone levels are directly related to the TBSA involved; these levels rise and fall in a time-dependent fash-ion from the onset of injury. Burn injury is characterized by a painful incident followed by a significant inflammatory response, with fluid losses and shifts occurring both near the burn wound itself and systemically. Each part of the endocrine system reacts to regain or maintain its preburn state.

The hypothalamus responds by secreting antidiuretic hor-mone (ADH) which acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood. This reduces the volume of urine formed while retaining water in response to losses of fluid from the intravascular space. The anterior pituitary releases adrenal corticotropic hormone (ACTH), which stimulates the release of the mineralocor-ticoid aldosterone and glucocorticoid cortisol. Aldosterone acts on the kidney to promote retention of sodium ions in the blood. Water follows the salt and helps maintain normal blood volume and pressure. Glucocorticoids increase blood sugar levels through the stimulation of gluconeogenesis. This elevation in blood glucose levels is thought necessary to supply the increased metabolic demand of the injured body. Cortisol and other glucocorticoids also have a potent anti-inflamma-tory effect on the body (54–62). They depress the immune response, especially cell-mediated immune responses.

The adrenal medulla releases the tyrosine-derived neu-rotransmitters adrenaline and noradrenaline into the blood. This response is associated with the autonomic nervous system—sometimes called the fight or flight response—and leads to multiple effects, some of which are an increase in the rate and strength of the heartbeat, resulting in increasing

blood pressure, and the shunting of blood from the skin to the skeletal muscles, coronary arteries, liver, and brain. With the release of adrenaline and noradrenaline, blood sugar rises and the metabolic rate is increased; bronchial dilation occurs; pupils dilate; and blood clotting time is decreased. This auto-nomic response also leads to increased ACTH secretion from the anterior lobe of the pituitary.

The elevations in stress-related hormones are noted in a time- and burn size–dependent manner after injury. This hormone response follows a pattern associated with the ebb and flow of the burn injury process. An initial increase in the hormone levels in response to fluid shifts and inflammation resolves over time as the patient’s fluid balance returns to normal, and the burn wounds close.

Several medications are available that can modify the endocrine response to burn injury. A recent prospective, double-blind, randomized single-center study on the effect of oxandrolone on the endocrine, inflammatory, and hypermeta-bolic responses during the acute phase of burn injury suggested that this treatment shortened the length of acute hospital stay, maintained lean body mass, and improved body composition and hepatic protein synthesis while having no adverse effects on the endocrine axis postburn. This study, and another using beta-blockade to modify the metabolic response after burn injury, are at the heart of attempts to improve the outcome of patients after a severe burn injury (63,64).

Hematopoietic System

Typically, the red blood cell (RBC) mass in the burn patient declines in a burn size- and severity-dependent fashion. This is initially related to the burn injury itself and thereafter decreased RBC production, increased RBC damage, and RBC losses from therapeutic interventions. Although surgery and phlebotomy account for the iatrogenic loss of RBCs, several possible causes have been explored for the injury-related loss of blood in the burn patient. Initial heat injuries to the RBCs, as well as sequestration of blood in the burn eschar, are early factors in the loss of RBCs and the decline in hemoglobin and hematocrit. Damage to RBCs secondary to the inflammatory response to the burn wound is a later developing cause for blood loss in these patients (65–70).

In 1973, Loebl (69) described studies of RBC half-life in burn victims and healthy volunteers. RBCs from the burn patient had a normal half-life when transfused into healthy volunteers. The same RBCs had a decreased half-life in the burn victim and, when normal RBCs were transfused into a burn victim, they acquired a similar decrease in their half-life; this study suggested a humoral or inflammatory process driving the loss of red cells.

Later studies have linked this loss in RBCs to a process mediated by inflammation and the release of toxic oxygen–free radicals, representing a nonspecific mechanism for the destruction of red cells. Immune system–mediated processes for the destruction of RBCs in burn patients have also been postulated, but Coombs testing in these patients has failed to reveal a definite link to immune-mediated blood loss. Studies by Posluszny et al. in a mouse model show a decrease in bone marrow hematopoetic commitment to erythroid cells and an increase in myeloid cells. This accounted for a decrease in RBC production after burn injury. Further study is needed to identify the same patterns in burn patients (71,72).

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Immune System

Infection remains a major complicating factor of burn injury (73–76). Burned skin loses its barrier function against the environment, and normal skin flora and environmental patho-gens are able to gain access to the system. Risk of infection and its complications are directly related to the size of the burn injury and additional factors, such as inhalation injury and pre-existing medical conditions. Burn injury leads to compro-mised immune function, resulting in increased susceptibility to sepsis and multiple organ system failure.

Immune system dysfunction occurs on the cellular and humoral levels. Multiple avenues for this effect have been investigated. Currently, macrophages, T cells, other lympho-cyte subpopulations, and humoral factors such as opsonins, immunoglobulins, protease inhibitors, toll-receptors, and che-motactic factors have been implicated in the process. Some combination of all of the above factors, related to their natural interaction, produces a weakened immune system susceptible to infection entering through multiple avenues (77–79).

In general, burn patients are assailed by bacteria from mul-tiple directions. Damaged skin, its barrier function destroyed, is the most obvious portal. Burn-related hypotension and peripheral vasoconstriction may permit intestinal hypoperfu-sion, with normal gastrointestinal flora becoming a source of proinflammatory mediators, pathogens, and toxins that con-tribute to multi-organ failure. Other clinically relevant path-ways include cannulation of the respiratory, vascular, and genitourinary systems, providing ready access for bacteria into the compromised host; these are considered nosocomial infections (80).

Musculoskeletal System

Loss of muscle mass and bone are notable in severely burned patients. Bone loss is, in part, due to an increase in gluco-corticoids that inhibit bone formation and osteoblast differ-entiation, hypercalciuria secondary to hypoparathyroidism, and vitamin D deficiency. Muscle loss is secondary to an intense catabolic state initiated by the inflammatory response to burn injury and is fueled by the need to repair the sur-face injury suffered. Propranolol administration in pediatric patients reduces thermogenesis, cardiac work, resting energy expenditure, and peripheral lipolysis; it also increases skeletal muscle protein anabolism. These effects are being studied in adult burn patients (81–86). A randomized, double-blinded, placebo-controlled study by Klein and Herndon (82) sug-gested that intravenous pamidronate administration may help preserve bone mass in children with over 40% TBSA burns. Follow-up to that study 2 years later showed a sus-tained improvement in bone mineral content as measured by dual-energy radiograph absorptiometry (83). This effect was attributed to a decrease in the glucocorticoid-mediated effect on bone mass.

fluId rEsuscITaTIon

Fluid resuscitation addresses the clinical picture of burn shock. Multiple resuscitation regimens have been developed to over-come the cardiac depression, vasoconstriction, and hypovole-mia associated with acute burn injury. Most, if not all, of the

current formulae have been developed through retrospective review of the fluid requirements of burn patients. Aided by the use of the rule of nines and Lund-Browder charts, a patient’s TBSA burn and weight measurements are used to determine their initial fluid requirement. One-half of the fluid require-ments calculated are given in the first 8 hours after the burn injury, with the remaining amount administered over the sub-sequent 16 hours. A slight variation in the composition of the resuscitation fluid is present in the different formulae; there are also differences in the addition of colloid to the initial resusci-tation scheme (87–98); the most commonly used formulae are noted in Table 63.1.

Colloid infusion during the resuscitation of acutely injured patients has been debated for some time. Acute burn injury leads to capillary permeability, which allows loss of intravas-cular albumin into the interstitial spaces of the acutely injured patient. Currently, the application of albumin or fresh-frozen plasma is considered after the initial 8-hour period postburn in an attempt to avoid loss of the colloid secondary to capillary permeability (99–102).

Adequate resuscitation is measured by end-organ perfu-sion. Currently, exact measures of end-organ perfusion are being developed and tested. A surrogate measure of the success of fluid administration is the measurement of urine output. Renal function is highly dependent on renal blood flow, which can be adequately assessed by the rate of urine output. Most practitioners view a urine production rate of 0.5 to 1.0 mL/kg ideal (or adjusted) body weight per hour as adequate. Second-ary measures of perfusion are also important in the resusci-tation plan. The combination of blood pressure, heart rate, oxygenation, and central venous pressure are used in tandem to determine the adequacy of treatment.

Measures of adequate resuscitation, such as blood pres-sure, heart rate, and central venous pressure used alone, must be monitored cautiously. Postburn tissue edema will decrease the accuracy of cuff blood pressure measurements, and the vasoconstriction caused by catecholamine release will adversely affect the accuracy of indwelling arterial lines. Cen-tral venous pressure measurements require the interaction of multiple physiologic and environmental parameters to provide the practitioner with meaningful measurements.

Patients who begin to lag in their urine output during resus-citation should have their fluid rates adjusted. Urinary rates of less than one third the predicted value based on the patient body weight over two consecutive hours should prompt an increase in intravenous fluid administration. On the other hand, patients running one third or more over their expected urine output may benefit from decreased fluid administra-tion. A graded increase or decrease of the intravenous fluid rate of 20% per hour is a measured and conservative response to these situations. Those patients who do not respond as expected to calculated fluid administration or who require more than 6 mL/kg per percent TBSA fluid administration

TABLE 63.1 The Common Resuscitation Formulae

Evans Formula Brooke Formula Parkland Formula

colloid 1.0 ml/kg/% 0.5 ml/kg/% none

crystalloid 1.0 ml/kg/% 1.5 ml/kg/% 4.0 ml/kg/%

Free water

2,000 ml 2,000 ml none

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should be considered for more invasive monitoring, such as pulse-waveform analysis (FlowTrack, PICCO, LiDCO, and bedside Echo) or pulmonary artery catheter monitoring. With measurements obtained through this more advanced moni-toring, a decision can be made to either support the CO or reduce the SVR, or both. Small doses of hydralazine may be used to reduce peripheral resistance in situations where the CO remains low. Hydralazine doses on the order of 0.5 mg/kg have been shown to be effective when used in this situation. In animal models of burn injury, sodium nitroprusside and vera-pamil decreased SVR and supported CO with good effect. This approach should be used with caution in the severely burn-injured patient to avoid further tissue hypoperfusion, which may exacerbate the condition of the partially burned tissues, increase fluid creep, worsen tissue edema, and may precipitate abdominal compartment syndrome (103).

At-risk patients for volume over-resuscitation include pediatric patients with an increased TBSA to weight, patients with inhalation injuries, electrical injuries, intoxication, and delayed fluid resuscitation. Fluid creep during resuscitation is worsened by exceeding the Parkland formula early or pushing high urine output during goal-directed therapy. Other factors that contribute to increased fluid administration include seda-tion and pain management with opioids, propofol, and benzo-diazepines, or patient factors like morbid obesity (104–106).

Insensible water losses become more significant with larger TBSA burns. Evaporative water losses from the open wounds/burns usually peak on the third day postburn and then trail off until the wounds are completely closed. An estimation of insensible water losses may be calculated as follows:

Insensible water loss (in mL/h) = (125 + %TBSA burned) × BSA (in m2).

The body surface area may be estimated using the formula of DuBois and DuBois as follows:

BSA = (W0.425 × H0.725) × 0.007184

where W is the weight in kilograms and H is the height in centimeters. Initially, the replacement fluid is free water ini-tially and then it is altered based on electrolyte measurements (107,108).

ElEcTrIcal Injury

Electrical injuries can be divided into those due to low voltage (<1,000 volts) and those due to high voltage (≥1,000 volts) (109). These injuries have varying patterns: Low-voltage injuries range from the circumoral injuries noted in children who have bitten home electrical cables to deaths caused by dropping electrical appliances in a bathtub full of water; high-voltage injuries have a range that includes the more severe episodes of instant death, massive tissue loss, and secondary clothing ignition. Some of the less dramatic injuries include thermal injury, central nervous system–related trauma, and fractures. With high-voltage injuries, there is a high ratio of limb amputations, highlighting the danger of this modern-day source of power. Herein, we will concentrate on high-voltage injuries.

Electrical energy interacts with human anatomy follow-ing the basic principles of physics. Current flowing through tissue is related to the voltage drop across the resistance of

that tissue. Heat produced by this current can be represented mathematically as follows:

J (heat in Joules) = I2 × R × T

where I is the current, R is the resistance, and T is the time in seconds. Body tissues have differing electrical resistances. Given the above equation, it appears that differing tissues would create varying degrees of heat and subsequent damage; interestingly, clinical findings do not wholly support this con-cept. The highest resistance is found in the bone, fat, and ten-dons, whereas the lowest resistance has been identified in the muscles, blood, and nerves; skin has an intermediate resis-tance. Clinical findings in electrically injured patients support the idea that the body represents a volume conductor with a resistance on the order of 500 to 1,000 ohms. In this model, the relative differences in tissue resistance are small enough that the body is considered a single resistor. Heat generated by the current flowing through the resistor is related to the cross-sectional area of the entry or exit wound and the local anatomy.

Contact wounds on the hands and feet are common. Each of the contact areas might have a low cross section, releasing more heat in that area; as the current crosses the “bottleneck” areas of the ankles and wrists, there may be more tissue dam-age generated at those sites. At its most extreme, heat released by high-voltage injuries produces coagulation necrosis of the tissues and varying other effects on the organs as the electricity passes through.

Arc injuries are less common, but just as destructive. Elec-tricity can travel 2 to 3 cm/10,000 volts, and may travel 10 ft or more to its target. Temperatures at the contact points range from 2,000 to 4,000°C, with spikes of up to 20,000°C; this intense temperature leads to severe and deep tissue damage.

Electrical injuries have specific organ effects in addition to the thermal injury described above. With high-voltage inju-ries, cardiac standstill and ventricular fibrillation are the most lethal cardiac injuries. Other electrocardiographic (ECG) findings and rhythm changes that have been reported include atrial fibrillation, focal ectopic arrhythmias, supraventricular tachycardia, right bundle branch block, and nonspecific ST-T segment changes. These clinical findings are thought to be associated with direct myocardial muscle damage, coronary vasospasm, and coronary endarteritis.

Renal injury may be direct, although this is rare, or may take on the more familiar form of acute renal failure second-ary to rhabdomyolysis. Large quantities of muscle protein, hemoglobin, and other tissue proteins released from the tis-sues coagulated by high voltage and current are filtered into the renal tubules, causing acute renal failure with oliguria or polyuria. Up to 15% of patients injured in high-voltage accidents will suffer from this type of renal injury.

Central nervous system injury ranges from the devastating effect of high voltage and current on the brain and brainstem, leading to instant death or to more subtle findings. Altered levels of consciousness with varying degrees of recovery have been reported, while progressive neurologic deterioration has been noted in both the central and the peripheral nervous sys-tems. With high-voltage injuries, progressive deterioration of the microvascular nutrient vessels to the nerves has been iden-tified, and is thought to lead to ischemia, necrosis, and fibrosis of the injured nerve; progressive loss of function can be seen as a late developing problem (110).

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Other organ systems may be directly affected by the pas-sage of current through them. Each is susceptible to both the current and the resistance-induced production of high tem-peratures and tissue damage. Cataracts may form in the eyes of a patient who has had an electrical injury in which the cur-rent pathway is through the orbits; this complication has been reported in up to 30% of patients suffering from this injury (111,112).

InhalaTIon Injury

The pathophysiology associated with smoke inhalation injury falls into three broad categories: (i) upper airway injury; (ii) asphyxiant gases and hypoxic environments; and (iii) carbo-naceous particle deposition (113–116).

The diagnosis of inhalation injury is based on several site-specific and clinical findings surrounding each burn patient. For example, closed space injuries or explosions are some of the circumstances surrounding inhalation injury. Noxious fumes noted at the scene by the scene responders, as well as facial burns noted on the patient, are other findings consis-tent with inhalation injury. Clinical findings on examination, such as large burns, carbonaceous sputum, hoarseness, or an abnormal lung examination, are associated with this injury, and elderly patients are more susceptible to inhalation injury.

Once inhalation injury is suspected, upper airway pathol-ogy should be expected. Heated smoke or ambient air may injure the supraglottic airway from the lips to the vocal cords. This injury may occur abruptly, leading to significant edema and swelling of the face and oropharynx, as well as affecting the region around the vocal cords.

True heat injury below the cords is rare, with the excep-tion of steam injuries or ignition of flammable gases in the airway. Signs and symptoms of a true airway burn injury include hoarseness; stridor and/or wheezing; carbonaceous sputum; singed nasal hair, eyebrows, or facial hair; and edema or inflammatory changes in the upper airway. The resultant upper airway edema formation can threaten the airway and the patient’s breathing.

Asphyxiant gases and hypoxic environments lead to the second area of pathology associated with inhalation injury. In fires involving structures, the ambient oxygen level markedly decreases; this lack of oxygen may lead to carbon monox-ide generation, as this molecule is a byproduct of incomplete combustion in the burning structure. Carbon monoxide binds tightly to hemoglobin, reducing the amount of oxygen deliv-ered to end organs, which may cause a hypoxic injury. Aside from carbon monoxide, other toxic gases can be released by the flames. Cyanide generation is associated with burning plastics; this molecule is highly lethal. Treatment of carbon monoxide intoxication includes a high concentration of oxy-gen and, sometimes, hyperbaric oxygen. Cyanide poisoning treatment includes delivery of oxygen, as well as a three-part regimen to bind the cyanide compound in the blood.

The third broad area of pathology associated with smoke inhalation injury is related to the deposition of carbonaceous particles in the airway. The flame-generated toxins that are bound to the carbon particles will slowly be released after the latter are deposited in the lungs, inducing a chemical tracheal bronchitis. This effect is manifested by impaired ciliary func-tion and edema, significant inflammation, and ulceration or

necrosis of the respiratory epithelium. The clinical sequelae of tracheal bronchial injury include bronchorrhea, broncho-spasm, distal airway obstruction, and atelectasis, as well as pneumonia. Epithelial injury leads to sloughing of the mucosa and blockage of the airways with this cellular debris. Air trap-ping in this situation leads to atelectasis and the development of barotrauma and pneumonia.

Treatment for each area of pathology is based on stan-dard clinical practice. When presented with a patient who is suspected of having an inhalation injury and upper airway edema, endotracheal intubation to protect the airway should be performed early to avoid the consequences of airway com-promise. Patients suffering from carbon monoxide exposure, and showing clinical signs of intoxication, should be treated with 100% oxygen to displace the molecule from hemoglo-bin. If immediately available, and if the patient is stable, high levels of carboxyhemoglobin and severe neurologic symp-toms should be treated with hyperbaric oxygen therapy. The tracheal-bronchial injury associated with inhalation injury and carbonaceous particle deposition should be treated with humidified oxygen by face mask, and frequent examination of the airway should be performed to evaluate for signs of compromise that may require endotracheal intubation.

Cyanide toxicity presents clinically with lethargy, nau-sea, headache, weakness, and coma. Cyanide combines with cytochrome oxidase, thereby blocking oxygen use and inhib-iting high-energy phosphate compound production. Cyanide toxicity begins at 0.1 μg/mL of serum and quickly leads to death at concentrations of 1 μg/mL. Laboratory studies show a decreased arteriovenous oxygen difference with severe metabolic acidosis; this acidosis is unresponsive to fluids and oxygen administration.

S-T segment elevations may be seen on the patient’s elec-trocardiogram, mimicking a myocardial infarction. Treatment of this condition includes the administration of 100% oxygen and a three-part medication regimen. Initially, the administra-tion of amyl nitrate pearls, by inhalation for 15 to 30 sec-onds every minute, is followed by 10 mL 3% sodium nitrate solution (300 mg) intravenously over 3 minutes, repeated at one-half the dosage in 2 hours if symptoms persist or recur-rent signs of toxicity are present. Sodium thiosulfate is the final medication, given in a dose of 50 mL of a 25% solution (12.5 g) intravenously over 10 minutes, repeated at half the dosage in 2-hour intervals if persistent or recurrent signs of toxicity are present.

InfEcTIon conTrol

Historically, mortality from burn injury was associated with burn shock (117–119); the loss of fluid through the burned and damaged skin, as well as fluid shifts related to the release of inflammatory mediators, led to hypovolemia and unrecov-erable end-organ failure. As our understanding of the injury suffered during burns improved, so did the survivability of these injuries. Currently, burn shock is well controlled by our fluid resuscitation regimens. The new challenge in burn injury is the concurrent development of infection in a compromised host. Burn injury is associated with a burn size–dependent depression in the immune system in which bacterial, fungal, and viral elements are better able to breach the defense mecha-nisms of the body, thereby worsening the injury.

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As fluid resuscitation techniques advanced, wound coloni-zation and sepsis became a leading factor in morbidity and mortality. The advent of topical antibiotic/anti-infective agents addressed this new area of pathology. Subsequent movement toward early wound excision and skin grafting led to improve-ments in the rates of wound sepsis and its complications. Although the burn wound has become less of a risk for infec-tion, other portals of entry have persisted in plaguing the burn patient. With our current methods of intubating the respira-tory, vascular, and genitourinary systems, we expose the burn patient to other portals of entry for pathogens.

nuTrITIon

Burn patients present to the ICU in a severe inflammatory state. This state, along with a wide variety of prehospital fac-tors and premorbid conditions, provides the practitioner with a challenging nutritional problem. Nutritional support for the burn patient can be addressed in several steps: first, an assessment of the patient’s initial nutritional status, and sec-ond, monitoring of his or her nutritional status throughout the hospital course, and adjustments based on the monitor-ing measures. By using a combination of variables, including burn size and severity, time from injury, physical parameters such as age, weight, and the presence of other medical factors, nutrition support can be tailored to each burn patient.

Nutritional assessment begins with measurement of the patient’s weight, estimation of the patient’s calorie and protein needs, measurement of the patient’s serum albumin, prealbu-min, and C-reactive protein levels (120–133). Pre-existing ill-nesses should prompt the practitioner to make adjustments in the rate of feeding, use of additional medications, and the need for additional nutrient support.

Glutamine supplementation has been shown to improve morbidity and mortality when administered to critically ill patients. This response appears to improve with increas-ing doses of the amino acid, and parenteral administration appears to have an improved response over enteral adminis-tration. Not all of the trials reported to date have shown a definitive benefit, and the general consensus is that a large ran-domized controlled trial would be needed to confirm or refute the benefits of glutamine administration (134,135).

Physiologically, glutamine affects the immune system, the anti-oxidant status, glucose metabolism, and heat shock protein response. These physiologic effects appear to provide benefit with regard to gastrointestinal mucosal integrity, wound heal-ing, gram-negative bacteremia and infection—including with Pseudomonas—as well as a reduction in mortality, and possi-bly cost savings to burn patients. At the time of this writing, a consensus has not been reached on the length of time for gluta-mine therapy, the optimal dose, and definite safety aspects of the supplementation of glutamine in critically ill and burn patients. Most studies suggest that clinically important differences appear to commence at doses over 0.2 g/kg body weight per day, and most trials have used 15 to 30 g/day glutamine supplementation.

Wound managEmEnT

With the exception of chemical burns, for which prompt water irrigation to remove the offending agent is required, no specific

treatment of the thermal burn wound is needed in the prehos-pital setting (113,136,137). The patient should be covered with a clean sheet and blanket to conserve body heat and minimize burn wound contamination during transport to the hospital. The application of ice or cold-water soaks, when initiated within 10 minutes after burning, may reduce tissue heat content and lessen the depth of thermal injury. If cold therapy is used, care must be taken to avoid causing hypothermia; this is accomplished by limiting this form of therapy to 10% or less of the body surface and only for the time required to produce analgesia.

Following admission to the burn center, definitive care of the burn wound can begin. Daily wound care involves cleans-ing, debridement, and dressing of the burn wound. On the day of injury, the burn wound is best cleansed by means of hydrotherapy, a practice that has been used in the treatment of burn patients for many years and remains an integral part of current treatment plans. Hydrotherapy is accomplished by means of showering or use of a spray table. Showering is often used for ambulatory patients who remain capable of indepen-dent, or near-independent, wound care. Patients who are near to discharge are encouraged to use the shower, especially if showering is to be used at home.

Use of a spray table is generally reserved for newly admitted patients, those with limited mobility, or those with large open wounds. The patient is placed on the table, and the wounds are washed and rinsed with running water. As an alternative, a stretcher or plinth can be placed over a Hubbard tank. The patient is placed on the stretcher, and the wounds are washed and rinsed as described previously.

Wound debridement involves the removal of all loose tissue, wound debris, and eschar (nonviable tissue); debridement of a burn wound is accomplished through mechanical, chemical (enzymatic), or surgical means.

Surgical, or sharp, debridement requires the use of scalpels and scissors to debride wounds of loose, necrotic tissue. Care must be taken to avoid excessive debridement that results in bleeding and pain. Bleeding may indicate injury to the healthy underlying tissue. In most instances, sharp debride-ment should be carried out in the operating room to ensure adequate debridement and hemostasis. Definitive management of third-degree burn wounds and deep second-degree injuries may require tangential excision of the eschar or necrotic tissue followed by wound closure with skin grafts or other wound closure adjuncts. This process will not be reviewed here.

Multiple topical antimicrobial agents are used in burn wound care. Mafenide acetate (Sulfamylon), silver sulfadiazine (Silvadene), and silver nitrate are the three most commonly used topical antimicrobial agents for burn wound care. Each agent has specific limitations and advantages with which the physician must be familiar to ensure patient safety and optimal benefit. Mafenide acetate and silver sulfadiazine are available as topical creams to be applied directly to the burn wound, whereas silver nitrate is applied as a 0.5% solution in occlusive dressings. Either cream is applied in a half-inch (about one-third of a centimeter) layer to the entire burn wound in an asep-tic manner after initial debridement, and reapplied at 12-hour intervals or as required to maintain continuous topical cover-age. Once daily, all of the topical agents should be cleansed from the patient using a surgical detergent disinfectant solution and the burn wounds examined by the attending physician. Silver nitrate is applied as a 0.5% solution in multilayered occlusive dressings that are changed twice daily.

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Mafenide acetate burn cream is an 11.1% suspension in a water-soluble base. This compound diffuses freely into the eschar, owing to its high degree of water solubility. Mafenide is the preferred agent if the patient has heavily contaminated burn wounds or has had burn wound care delayed by several days. This agent has the added advantage of being highly effec-tive against gram-negative organisms, including most Pseudo-monas species. Physicians using this agent must be aware of several potential clinical limitations associated with its use. Hypersensitivity reactions occur in 7% of patients, and pain or discomfort of 20 to 30 minutes duration is common when it is applied to partial-thickness burn wounds. This agent is also an inhibitor of carbonic anhydrase, and a diuresis of bicar-bonate is often observed after its use. The resultant metabolic acidosis may accentuate postburn hyperventilation, and sig-nificant acidemia may develop if compensatory hyperventila-tion is impaired. Inhibition of this enzyme rarely persists for more than 7 to 10 days, and the severity of the acidosis may be minimized by alternating applications of mafenide with silver sulfadiazine cream every 12 hours (138).

Silver sulfadiazine burn cream is a 1% suspension in a water-miscible base. Unlike mafenide, silver sulfadiazine has limited solubility in water and, therefore, limited ability to penetrate into the eschar. The agent is most effective when applied to burns soon after injury to minimize bacterial proliferation on the wound’s surface. This agent is painless on application, and serum electrolytes and acid–base balance are not affected by its use. Hypersensitivity reactions are uncommon; an erythema-tous maculopapular rash sometimes seen subsides on discon-tinuation of the agent. Silver sulfadiazine occasionally induces neutropenia by a mechanism thought to involve direct bone marrow suppression; white blood cell counts usually return to normal following discontinuation. With continual use, resis-tance to the sulfonamide component of silver sulfadiazine is common, particularly in certain strains of Pseudomonas and many Enterobacter species. However, the continued sensitiv-ity of microorganisms to the silver ion of this compound has maintained its effectiveness as a topical antimicrobial agent.

A 0.5% silver nitrate solution has a broad spectrum of antibacterial activity imparted by the silver ion. This agent does not penetrate the eschar, because the silver ions rapidly precipitate on contact with any protein or cationic material. Use of this agent is not associated with more intense wound pain, except from the mechanical action required for dress-ing changes. The dressings are changed twice daily and moist-ened every 2 hours with the silver nitrate solution to prevent evaporation from increasing the silver nitrate concentration to cytotoxic levels within the dressings. Transeschar leaching of sodium, potassium, chloride, and calcium should be antici-pated, and these chemical constituents should be appropri-ately replaced. Hypersensitivity to silver nitrate has not been described. Mafenide acetate, silver sulfadiazine, and 0.5% silver nitrate are effective in the prevention of invasive burn wound infection; however, because of their lack of eschar pen-etration, silver nitrate soaks and silver sulfadiazine burn cream are most effective when applied soon after burn injury.

PaIn managEmEnT

Because burn pain is variable in its degree and time course, reliance on a single analgesic regimen is unreliable at best and

unsuccessful at worst. Conversely, the diverse spectrum of burn patients—adult versus children, large burns versus small, ICU nursing versus ward setting—makes the routine individualiza-tion of analgesic plans overwhelming and impractical. Our recommendation is to determine an analgesic regimen for each individual patient based on two broad categories: the assessed clinical need for analgesia and the limitations imposed by the patient.

The first step is to address background, procedural, postoperative, and breakthrough pain treatment separately, and then consider individual drug choices based on patient limitations. To reinforce this type of approach to analgesic management, detailed institutional guidelines to help physi-cians and nurses choose and administer specific analgesics are recommended.

Background Pain

In general, because it is a pain of continuous nature, back-ground pain is best treated with mild-to-moderately potent, longer-acting analgesics administered so that plasma drug concentrations remain relatively constant throughout the day. Examples include the continuous IV infusion of fen-tanyl or morphine (with or without patient-controlled anal-gesia [PCA]), oral administration of long-acting opioids with prolonged elimination (methadone) or prolonged enteral absorption (sustained-release morphine, sustained-release oxycodone), or oral administration on a regular schedule of short-acting oral analgesics (oxycodone, hydromorphone, codeine, acetaminophen). Such analgesics should almost never be administered on an as-needed (PRN) basis during the early and middle phases of hospitalization.

Procedural Pain

In contrast, procedural pain is significantly more intense but shorter in duration; therefore, analgesic regimens for proce-dural pain are best composed of more potent opioids that have a short duration of action. Intravenous access is help-ful in this setting, with short-acting opioids (fentanyl) offering a potential advantage over more longer-acting agents (mor-phine, hydromorphone). When intravenous access is not pres-ent, orally administered opioids (morphine, hydromorphone, oxycodone, codeine) are commonly used, although their rela-tively long duration of action (2 to 6 hours) may potentially limit postprocedure recovery for other rehabilitative or nutri-tional activities. Oral transmucosal fentanyl and nitrous oxide are useful agents when IV access is not present due to their rapid onset and short duration of action.

Postoperative Pain

Postoperative pain deserves special mention because increased analgesic needs should be anticipated following burn wound excision and grafting. This is particularly true when donor sites have been harvested, as these are often the source of increased postoperative pain complaints. In contrast, pain from excised/grafted burns may increase, decrease, or not change postop-eratively compared to preoperatively. Typically, this increased analgesic need in the postoperative period is limited to 1 to 4 days following surgery before returning to, or falling below, preoperative levels.

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Breakthrough Pain

Breakthrough pain occurs at rest when background analgesic therapy is inadequate. Breakthrough pain occurs commonly in burn patients, particularly in early stages of hospitalization until a stable, appropriate, and individualized pharmacologic regimen can be determined for each patient. Analgesia for breakthrough pain can be provided with IV or oral opioids. When breakthrough pain occurs repeatedly, it is an indication to re-evaluate and likely increase the patient’s background pain analgesic regimen, as it may be inadequate in terms of analge-sic dose and/or frequency. Tolerance develops rapidly in these patients and may initially manifest as breakthrough pain.

Patient Limitations

As stated above, the presence of intravenous access directly influences analgesic drug choice, particularly in children. Simi-larly, patients who are endotracheally intubated and venti-lated are somewhat protected from the risk of opioid-induced respiratory depression; thus, opioids may be more generously administered in these individuals, as is often required for pain-ful burn debridements. Also, individual differences in opioid efficacy should be considered in all patients, including opioid tolerance in patients requiring prolonged opioid analgesic therapy or in those with pre-existing substance abuse histories.

An appropriate rationale is to titrate the drug dose to the desired effect, rather than to rely on a particular textbook dose for all patients. Because of the development of drug tolerance with prolonged medical use or recreational abuse of opioids (i.e., increasing drug doses are required to attain adequate levels of analgesia), opioid analgesic doses needed for burn analgesia may exceed those recommended in standard dosing guidelines. Furthermore, because of cross-tolerance, tolerance to one opioid analgesic usually implies tolerance to all opioid analgesics. One clinically relevant consequence of drug toler-ance is the potential for opioid withdrawal to occur during inpatient burn treatment. Thus, the period of inpatient burn care is not an appropriate time to institute deliberate opioid withdrawal or detoxification measures in tolerant patients, because such treatment ignores the very real analgesic needs—background pain and procedural pain—of these patients. Sim-ilarly, when reductions in analgesic therapy are considered as burn wounds close, reductions should occur by careful taper-ing, rather than abrupt discontinuation of opioids, to prevent the acute opioid withdrawal syndrome.

Anxiolysis in the Treatment of Burn Pain

Current aggressive therapies for cutaneous burns, together with the qualities of background and wound care pain, make burn care an experience that normally induces anxiety in a large proportion of adult and pediatric patients. Anxiety, in itself, can exacerbate acute pain. This has led to the common practice in many burn centers of using anxiolytic drugs in combination with opioid analgesics. Intuitively, this practice seems particularly useful in premedicating patients for wound care, to diminish the anticipatory anxiety experienced by these patients prior to and during debridement. Low-dose benzo-diazepine administration significantly reduces burn wound care pain scores and narcotic requirements. It appears that the patients most likely to benefit from this therapy are not those

with high trait or premorbid anxiety, but rather those with high state or the time of the procedure anxiety, or those with high baseline pain scores. Other nonpharmacologic anxioly-sis techniques, such as hypnosis and behavioral therapy, could also be considered.

TEam aPProach To Burn PaTIEnTs

The management of the burned patient is a multidisciplinary effort of burn care professionals to provide optimal care to the burn patient. This multidisciplinary care spans the early resuscitative phases of care through the long-term rehabilita-tion and reconstructive phases. The Burn Center Director coordinates all activities of the multidisciplinary care of the critically ill burn patients. Team members include burn sur-geons, plastic and reconstructive surgeons, critical care spe-cialists, anesthesiologists, critical care burn nurses, physical therapists, occupational therapists, clinical nutritional special-ists, psychologists, social workers, and pastoral care support personnel. This multidisciplinary approach affords the patients and their families state-of-the-art resources for optimal out-come, education, and rehabilitation. This concept of team care, originating in the 1950s when the first burn centers opened, has persisted to this day and is a model of coordinated, interdisci-plinary, outcome-driven patient care.

• Role of inflammation and inflammatory mediators in the depression of cardiac function and increase in capil-lary permeability.

• Smoke inhalation and its effect on mortality from burn injury.

• Renal replacement therapy and its potential role in modulating the inflammatory effects of burn injury.

• Modulating the hypermetabolic response to burn injury medically as well as reducing the loss of bone density in patients with severe burn injuries.

• Addressing the effects of burn injury on the immune system and reducing the incidence of infection through VAP bundles, catheter management, and improving the rate of wound closure. Further study in supporting the immune system despite the burn injury.

Key Points

References 1. Bessey PQ, Phillips BD, Lentz CW, et al. Synopsis of the 2013 annual

report of the national burn repository. J Burn Care Res. 2014;35 Suppl 2: S218–S234.

2. Moncrief JA. Effect of various fluid regimens and pharmacologic agents on the circulatory hemodynamics of the immediate postburn period. Ann Surg. 1966;164(4):723–750.

3. Asch MJ, Feldman RJ, Walker HL, et al. Systemic and pulmonary hemo-dynamic changes accompanying thermal injury. Ann Surg. 1973;178(2): 218–221.

4. Wilmore DW, Aulick LH, Mason AD, Pruitt BA. Influence of the burn wound on local and systemic responses to injury. Ann Surg. 1977;186(4):444–456.

5. Kuntscher MV, Germann G, Hartmann B. Correlations between cardiac output, stroke volume, central venous pressure, intra-abdominal pressure and total circulating blood volume in resuscitation of major burns. Resus-citation. 2006;70(1):37–43.

LWBK1580_C63_p675-686.indd 683 29/07/17 11:20 AM


6. Cioffi WG, DeMeules JE, Gamelli RL. Vascular reactivity following ther-mal injury. Circ Shock. 1988;25(4):309–317.

7. Lund T, Reed RK. Acute hemodynamic effects of thermal skin injury in the rat. Circ Shock. 1986;20(2):105–114.

8. Hilton JG. Effects of verapamil on the thermal trauma depressed car-diac output in the anaesthetized dog. Burns Incl Therm Inj. 1984;10(5): 313–317.

9. Carlson DL, Horton JW. Cardiac molecular signaling after burn trauma. J Burn Care Res. 2006;27:669–675.

10. Horton JW, Sanders B, White DJ, Maass DL. The effects of early excision and grafting on myocardial inflammation and function after burn injury. J Trauma. 2006;61(5):1069–1077.

11. Tripathi FM, Pandey K, Paul PS, et al. Blood gas studies in thermal burns. Burns Incl Therm Inj. 1983;10(1):13–16.

12. Iglesias G, Zeigler ST, Lentz CW, et al. Thromboxane synthetase inhibition and thromboxane receptor blockade preserve pulmonary and circulatory function in a porcine burn sepsis model. J Am Coll Surg. 1994;179(2):187–192.

13. Shi Z, Xie H, Wang P, et al. Oral hygiene care for critically ill patients to prevent ventilator-associated pneumonia. Cochrane Database System Rev. 2013;8:CD008367.

14. Wang L, Li X, Yang Z, et al. Semi-recumbent position versus supine position for the prevention of ventilator-associated pneumonia in adults requiring mechanical ventilation. Cochrane Database System Rev. 2016;1:CD009946.

15. Tokmaji G, Vermeulen H, Müller MC, et al. Silver-coated endotracheal tubes for prevention of ventilator-associated pneumonia in critically ill patients. Cochrane Database System Rev. 2015;8:CD009201.

16. Shirani KZ, Pruitt BA Jr, Mason AD Jr. The influence of inhalation injury and pneumonia on burn mortality. Ann Surg. 1987;205(1):82–87.

17. Nieminen S, Fraki J, Niinikoski J, et al. Acute effects of burn injury on tissue gas tensions in the rabbit. Scand J Plast Reconstr Surg. 1977;11(1): 69–74.

18. Mlcak R, Desai MH, Robinson E, et al. Lung function following thermal injury in children: an 8-year follow up. Burns. 1998;24(3):213–216.

19. Whitener DR, Whitener LM, Robertson KJ, et al. Pulmonary function measurements in patients with thermal injury and smoke inhalation. Am Rev Respir Dis. 1980;122(5):731–739.

20. Tripathi FM, Pandey K, Paul PS, et al. Respiratory functions in thermal burns. Burns Incl Therm Inj. 1983;9(6):401–408.

21. Demling RH, Wenger H, Lalonde CC, et al. Endotoxin-induced pros-tanoid production by the burn wound can cause distant lung dysfunction. Surgery. 1986;99(4):421–431.

22. Demling RH, Wong C, Jin LJ, et al. Early lung dysfunction after major burns: role of edema and vasoactive mediators. J Trauma. 1985; 25(10):959–966.

23. Demling RH. Effect of early burn excision and grafting on pulmonary function. J Trauma. 1984;24(9):830–834.

24. Tasaki O, Goodwin CW, Saitoh D, et al. Effects of burn on inhalation injury. J Trauma. 1997;43(4):603–607.

25. Teixidor HS, Novick G, Rubin E. Pulmonary complications in burn patients. J Can Assoc Radiol. 1983;34(4):264–270.

26. Pruitt BA Jr, Erickson DR, Morris A. Progressive pulmonary insuffi-ciency and other pulmonary complications of thermal injury. J Trauma. 1975;15(5):369–379.

27. Endorf FW, Gamelli RL. Inhalation injury, pulmonary perturbations, and fluid resuscitation. J Burn Care Res. 2007;28(1):80–83.

28. Petroff PA, Hander EW, Mason AD Jr. Ventilatory patterns following burn injury and effect of sulfamylon. J Trauma. 1975;15(8):650–656.

29. Chung KK, Lundy JB, Matson JR, et al. Continuous venovenous hemo-filtration in severely burned patients with acute kidney injury: a cohort study. Crit Care. 2009;13(3):R62.

30. McDonald WS, Sharp CW Jr, Deitch EA. Immediate enteral feeding in burn patients is safe and effective. Ann Surg. 1991;213(2):177–183.

31. Alhazzani W, Alenezi F, Jaeschke RZ, et al. Proton pump inhibitors ver-sus histamine 2 receptor antagonists for stress ulcer prophylaxis in criti-cally ill patients: a systematic review and meta-analysis. Crit Care Med. 2013;41(3):693–705.

32. Moore LJ, Kowal-Vern A, Latenser BA. Cecal perforation in thermal injury: case report and review of the literature. J Burn Care Rehabil. 2002;23(6): 371–374.

33. Manson WL, Klasen HJ, Sauer EW, Olieman A. Selective intestinal decon-tamination for prevention of wound colonization in severely burned patients: a retrospective analysis. Burns. 1992;19(2):98–102.

34. Mackie DP, van Hertum WA, Schumburg TH, et al. Reduction in Staphy-lococcus aureus wound colonization using nasal mupirocin and selective decontamination of the digestive tract in extensive burns. Burns. 1994;20 (Suppl 1):S14–S17.

35. Mackie DP, van Hertum WA, Schumburg T, et al. Prevention of infection in burns: preliminary experience with selective decontamination of the digestive tract in patients with extensive injuries. J Trauma. 1992;32(5): 570–575.

36. Horton JW, Maass DL, White J, Minei JP. Reducing susceptibility to bacte-remia after experimental burn injury: a role for selective decontamination of the digestive tract. J Appl Physiol. 2007;102(6):2207–2216.

37. Yao YM, Lu LR, Yu Y, et al. Influence of selective decontamination of the digestive tract on cell-mediated immune function and bacteria/endotoxin translocation in thermally injured rats. J Trauma. 1997;42(6):1073–1079.

38. Yao YM, Yu Y, Sheng ZY, et al. Role of gut-derived dedotoxaemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract. Burns. 1995;21(8):580–585.

39. Baron P, Traber LD, Traber DL, et al. Gut failure and translocation follow-ing burn and sepsis. J Surg Res. 1994;57(1):197–204.

40. Taylor N, van Saene HK, Abella A, et al. Selective digestive decontamina-tion. why don’t we apply the evidence in the clinical practice? Med Inten-siva. 2007;3193:136–145.

41. de La Cal MA, Cerda E, Garcia-Hierro P, et al. Survival benefit in critically ill burned patients receiving selective decontamination of the digestive tract: a randomized, placebo-controlled, double-blind trial. Ann Surg. 2005;241(3): 424–430.

42. Szanto Z, Pulay I, Kotsis L, Dinka T. Selective bowel decontamination. Orv Hetil. 2006;147(14):643–647.

43. Barrett JP, Jeschke MG, Herndon DN. Selective decontamination of the digestive tract in severely burned pediatric patients. Burns. 2001; 27(5):439–445.

44. Verwaest C, Verhaegen J, Ferdinande P, et al. Randomized, controlled trial of selective digestive decontamination in 600 mechanically ventilated patients in a multidisciplinary intensive care unit. Crit Care Med. 1997;25(1):63–71.

45. Tuggle D, Skinner S, Garza J, et al. The abdominal compartment syndrome in patients with burn injury. Acta Clin Belg Suppl. 2007;(1):136–140.

46. Oda J, Yamashita K, Inoue T, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns. 2006;32(2):151–154.

47. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174(6):667–672.

48. Hobson KG, Young KM, Ciraulo A, et al. Release of abdominal compart-ment syndrome improves survival in patients with burn injury. J Trauma. 2002;53(6):1129–1133.

49. Hershberger RD, Hunt JL, Arnoldo BD, Purdue GF. Abdominal compart-ment syndrome in the severely burned patient. J Burn Care Res. 2007; 28(5):708–714.

50. Wise R, Jacobs J, Pilate S, et al. Incidence and prognosis of intra-abdom-inal hypertension and abdominal compartment syndrome in severely burned patients: Pilot study and review of the literature. Anaesthesiol Intensive Ther. 2016;48(2):95–109.

51. Khedr EM, Khedr T, El-Oteify MA, Hassan HA. Peripheral neuropathy in burn patients. Burns. 1997;23(7–8):579–583.

52. Shin C, Kinsky MP, Thomas JA, et al. Effect of cutaneous burn injury and resuscitation on the cerebral circulation in an ovine model. Burns. 1998;24(1):39–45.

53. Maybauer DM, Maybauer MO, et al. Effects of severe smoke inhalation injury and septic shock on global hemodynamics and microvascular blood flow in sheep. Shock. 2006;26(5):489–495.

54. Finfer S. Corticosteroids in septic shock. N Engl J Med. 2008;358(2):188–190. 55. Jeschke MG, Boehning EF, Finnerty CC, Herndon DN. Effect of insulin

on the inflammatory and acute phase response after burn injury. Crit Care Med. 2007;35(9 Suppl):S519–523.

56. Matsui M, Kudo T, Kudo M, et al. The endocrine response after burns. Agressologie. 1991;32(4):233–235.

57. Murton SA, Tan ST, Prickett TCR, et al. Hormone responses to stress in patients with major burns. Br J Plast Surg. 1998;51:388–392.

58. Smith A, Barclay C, Quaba A, et al. The bigger the burn, the greater the stress. Burns. 1997;23(4):291–294.

59. Sprung CL, Annane D, Keh D, et al, for the CORTICUS Study Group. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358(2):111–124.

60. Sedowofia K, Barclay C, Quaba A, et al. The systemic stress response to thermal injury in children. Clin Endocrinol. 1998;49:335–341.

61. Jeschke MG, Finnerty CC, Suman OE, et al. The effect of xyandrolone on the endocrinologic, inflammatory, and hypermetabolic responses during the acute phase postburn. Ann Surg. 2007;246(3):351–362.

62. Wick S. Endocrinology: hormone effects. University of Nebraska at Omaha, Human Physiology and Anatomy Laboratories, August 1997.

LWBK1580_C63_p675-686.indd 684 29/07/17 11:20 AM


63. Jeschke MG, Norbury WB, Finnerty CC, et al. Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children. J Trauma. 2007;62(3):676–681.

64. Norbury WB, Jesche MG, Herndon DN. Metabolism modulators in sep-sis: propranolol. Crit Care Med. 2007;35(9 Suppl):S616–620.

65. Wong CH, Song C, Heng KS, et al. Plasma free hemoglobin: a novel diag-nostic test for assessment of the depth of burn injury. Plast Reconstruct Surg. 2006;117(4):1206–1213.

66. Lawrence C, Atac B. Hematologic changes in massive burn injury. Crit Care Med. 1992;20(9):1284–1288.

67. Endoh Y, Kawakami M, Orringer EP, et al. Causes and time course of acute hemolysis after burn injury of the rat. J Burn Care Rehab. 1992;13 (2 Pt 1):203–209.

68. Hatherill JR, Till GO, Bruner LH, Ward P. Thermal injury, intravascular hemolysis, and toxic oxygen products. J Clin Invest. 1986;78:629–636.

69. Loebl EC, Baxter CR, Curreri PW. The mechanism of erythrocyte destruc-tion in the early post-burn period. Ann Surg. 1973;178(6):681–686.

70. Kawakami EY, Orringer EP, Peterson HD, Meyer AA. Causes and time course of acute hemolysis after burn injury in the rat. J Burn Care Rehabil. 1992;12(2 Pt 1):203–209.

71. Posluszny JA Jr, Muthumalaiappan K, Kini AR, et al. Burn injury dampens erythroid cell production through reprioritizing bone marrow hematopoi-etic response. J Trauma. 2011;71(5):1288–1296.

72. Howell K, Posluszny J, He LK, et al. High MafB expression following burn augments monocyte commitment and inhibits DC differentiation in hemopoietic progenitors. J Leukoc Biol. 2012;91(1):69–81.

73. Griswold JA. White blood cell response to burn injury. Semin Nephrol. 1993;13(4):409–415.

74. Oberbeck R, Schmitz D, Wilsenack K, et al. Adrenergic modulation of survival and cellular immune functions during polymicrobial sepsis. Neu-roimmunomodulation. 2004;11(4):214–223.

75. Schmitz D, Wilsenack K, Lendemanns S, et al. Beta-adrenergic block-ade during systemic inflammation: impact on cellular immune func-tions and survival in a murine model of sepsis. Resuscitation. 2007; 72(2):286–294.

76. Alexander M, Chaudry IH, Schwacha MG. Relationships between burn size, immunosuppression, and macrophage hyperactivity in a murine model of thermal injury. Cell Immunol. 2002;220(1):63–69.

77. Schwacha MG, Chaudry IH. The cellular basis of post-burn immunosup-pression: macrophages and mediators. Int J Mol Med. 2002;10(3):239–243.

78. Kobayashi M, Jeschke MG, Shigematsu K, et al. M2b monocytes pre-dominated in peripheral blood of severely burned patients. J Immunol. 2010;185(12):7174-7179.

79. Schwacha MG, Zhang Q, Rani M, et al. Burn enhances toll-like recep-tor induced responses by circulating leukocytes. Int J Clin Exp Med. 2012;5(2):136–144.

80. Moore FA. The role of the gastrointestinal tract in postinjury multiple organ failure. Am J Surg. 1999;178(6):449–453.

81. Klein GL. Burn-induced bone loss: importance, mechanisms, and manage-ment. J Burns Wounds 2006;5:32–38.

82. Klein GL, Herndon DN, Goodman WG, et al. Histomorphometric and biochemical characterization of bone following acute severe burns in chil-dren. Bone. 1995;17(5):455–460.

83. Przkora R, Herndon DN, Sherrard DJ, et al. Pamidronate preserves bone mass for at least 2 years following acute administration for pediatric burn injury. Bone. 2007;41:279–302.

84. Klein GL, Wimalawansa SJ, Kulkarni G, et al. The efficacy of acute administration of pamidronate on the conservation of bone mass follow-ing severe burn injury in children: a double-blind, randomized, controlled study. Osteoporos Int. 2005;16(6):631–635.

85. Núñez-Villaveirán T, Sánchez M, Millán P, García-de-Lorenzo A. System-atic review of the effect of propanolol on hypermetabolism in burn inju-ries. Med Intensiva. 2015;39(2):101–113.

86. Finnerty CC, Herndon DN. Is propranolol of benefit in pediatric burn patients? Adv Surg. 2013;47:177–197.

87. Tanaka H, Matsuda T, Miyagantani Y, et al. Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administra-tion. Arch Surg. 2000;135:326–331.

88. Klein MB, Hayden D, Elson C, et al. The association between fluid adminis-tration and outcome following major burn. Ann Surg. 2007;245(4):622–628.

89. Hoskins SL, Elgjo GI, Lu J, et al. Closed-loop resuscitation of burn shock. J Burn Care Res. 2006;27(3):377–385.

90. Berger MM, Bernath MA, Chiolero RL. Resuscitation, anesthesia and anal-gesia of the burned patient. Curr Opin Anaesthesiol. 2001;14:431–435.

91. Mansfield MD. Resuscitation and monitoring. Ballieres Clin Anesthesiol. 1997;11(3):369–384.

92. Demling RH. The burn edema process: current concepts. J Burn Care Rehab. 2005;26:207–277.

93. Bert J, Gyenge C, Bowen B, et al. Fluid resuscitation following a burn injury: implications of a mathematical model of microvascular exchange. Burns. 1997;23(2):93–105.

94. Ampratwum RT, Bowen BD, Lund T, et al. A model of fluid resuscitation following burn injury: formulation and parameter estimation. Comput Methods Programs Biomed. 1995;47:1–19.

95. Lund T, Bert JL, Onarheim H, et al. Microvascular exchange during burn injury. I. A review. Circ Shock. 1989;28(3):179–197.

96. Bert JL, Bowen BD, Gu X, et al. Microvascular exchange during burn injury: ii. formulation and validation of a mathematical model. Circ Shock. 1989;28(3):199–219.

97. Bowen BD, Bert JL, Gu X, et al. Microvascular exchange during burn injury. III. Implications of the model. Circ Shock. 1989;28(3):221–233.

98. Bert JL, Bowen BD, Reed RK, Onarheim H. Microvascular exchange during burn injury: iv, fluid resuscitation model. Circ Shock. 1991;34(3):285–297.

99. O’Mara MS, Slater H, Goldfarb IW, Caushaj PF. A prospective, random-ized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma. 2005;58(5):1011–1018.

100. Tricklebank S. Modern trends in fluid therapy for burns. Burns. 2009;35(6):757–767.

101. Cochran A, Morris SE, Edelman LS, Saffle JR. Burn patient charac-teristics and outcomes following resuscitation with albumin. Burns. 2007;33(1):25–30.

102. Lawrence A, Faraklas I, Watkins H, et al. Colloid administration normal-izes resuscitation ratio and ameliorates “fluid creep”. J Burn Care Res. 2010;31(1):40–47.

103. Lavrentieva A, Palmieri T. Determination of cardiovascular param-eters in burn patients using arterial waveform analysis: a review. Burns. 2011;37(2):196–202.

104. Greenhalgh DG. Burn resuscitation. J Burn Care Res. 2007;28(4):555–565. 105. Saffle JI. The phenomenon of “fluid creep” in acute burn resuscitation.

J Burn Care Res. 2007;28(3):382–395. 106. Sullivan SR, Friedrich JB, Engrav LH, et al. “Opioid creep” is real and may

be the cause of “fluid creep.” Burns. 2004;30(6):583–590. 107. Cancio LC, Chávez S, Alvarado-Ortega M, et al. Predicting increased

fluid requirements during the resuscitation of thermally injured patients. J Trauma. 2004;56(2):404–413.

108. Namdar T, Stollwerck PL, Stang FH, et al. Transdermal fluid loss in severely burned patients. Geriatr Med Sci. 2010;8:Doc28.

109. Remensnyder JP. Acute electrical injuries. In: Martyn JAJ, ed. Acute Man-agement of the Burned Patient. Philadelphia, PA: WB Saunders Company, 1990:66–86.

110. Kwon KH, Kim SH, Minn YK. Electrodiagnostic study of peripheral nerves in high-voltage electrical injury. J Burn Care Res. 2014;35(4): e230–e233.

111. Korn BS, Kikkawa DO. Images in clinical medicine. Ocular manifestation of electrical burn. N Engl J Med. 2014;370(4):e6.

112. Boozalis GT, Purdue GF, Hunt JL, McCulley JP. Ocular changes from elec-trical burn injuries: a literature review and report of cases. J Burn Care Rehab. 1991;12(5):458–462.

113. Mozingo DW, Cioffi WG Jr, Pruitt BA Jr. Burns. In: Bongard FS, Sue DY, eds. Current Critical Care Diagnosis & Treatment. 2nd ed. New York: Lange Medical Books/McGraw-Hill, 2002:799–828.

114. Elderman DA, Khan N, Kempf K, White MT. Pneumonia after inhalation injury. J Burn Care Res. 2007;28(2):241–246.

115. Cioffi WB, Graves TA, McManus WF, Pruitt BA Jr. High-frequency per-cussive ventilation in patients with inhalation injury. J Trauma. 1989; 29(3):350–354.

116. Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive ventilation in inhalation injuries. J Burn Care Res. 2007;28(3):396–400.

117. O’grady NP, Alexander M, Dellinger EP, et al. Healthcare infection con-trol practices advisory committee: guidelines for the prevention of intra-vascular catheter-related infections. Am J Infect Control. 2002;30(8): 476–489.

118. Tompkins RG, Burke JF, Schoenfeld DA, et al. Prompt eschar excision: a treatment system contributing to reduced burn mortality. Ann Surg. 1986;204(3):272–280.

119. Gastmeier P, Geffers C. Prevention of ventilator-associated pneumonia: analysis of studies published since 2004. J Hosp Infect. 2007;67(1):1–8.

120. Purdue GF. American Burn Association presidential address 2006 on nutri-tion: yesterday, today, and tomorrow. J Burn Care Res. 2006;28(1):1–5.

121. Juang P, Fish DN, Jung R, MacLaren R. Enteral glutamine supplementa-tion in critically ill patients with burn injuries: a retrospective case-control evaluation. Pharmacotherapy. 2007;27(1):11–19.

LWBK1580_C63_p675-686.indd 685 29/07/17 11:20 AM


122. Peng YZ, Yuan ZQ, Ciao GX. Effects of early enteral feeding on the prevention of enterogenic infection in severely burned patients. Burns. 2001;27(2):145–149.

123. Chen Z, Wang S, Yu B, Li A. A comparison study between early enteral nutrition and parenteral nutrition in severe burn patients. Burns. 2007;33(6):708–712.

124. Prelack K, Dylewski M, Sheridan RL. Practical guidelines for nutritional management of burn injury and recovery. Burns. 2007;33:14–24.

125. Berger MM, Shenkin A. Trace element requirements in critically ill burned patients. J Trace Elements. 2007;SI:44–48.

126. Wolf SE. Nutrition and metabolism in burns: state of the science, 2007. J Burn Care Res. 2007;28(4):572–576.

127. Windle EM. Glutamine supplementation in critical illness: evidence, rec-ommendations, and implications for clinical practice in burn care. J Burn Care Res. 2006;27(6):764–772.

128. Bongers T, Griffiths RD, McArdle A. Exogenous glutamine: the clinical evidence. Crit Care Med. 2007;35(9):S545–S552.

129. Druml W. Protein metabolism in acute renal failure. Miner Electrolyte Metab. 1998;24(1):47–54.

130. Druml W. Nutritional management of acute renal failure. Am J Kidney Dis. 2001;37(1 Suppl 2):S89–94.

131. Chan L. Nutritional support in acute renal failure. Curr Opin Clin Nutr Metab Care. 2004;7:207–212.

132. Cynober L. Amino acid metabolism in thermal burns. J Parenter Enteral Nutr. 1989;12(2):196–205.

133. Windle EM. Glutamine supplementation in critical illness: evidence, rec-ommendations, and implications for clinical practice in burn care. J Burn Care Res. 2006;27(6):764–772.

134. Tao KM, Li XQ, Yang LQ, et al. Glutamine supplementation for critically ill adults. Cochrane Database Systemat Rev. 2014;9:CD010050.

135. Tan HB, Danilla S, Murray A, et al. Immunonutrition as an adju-vant therapy for burns. Cochrane Database Systemat Rev. 2014;12: CD007174.

136. Nguyen TT, Gilpin DA, Meyer NA, Herndon DN. Current treatment of severely burned patients. Ann Surg. 1996;223(1):14–25.

137. Murphy KD, Lee JO, Herndon DN. Current pharmacotherapy for the treatment of severe burns. Exp Opin Pharmacother. 2003;4(3):369.

138. Brown TP, Cancio LC, McManus AT, Mason AD Jr. Survival benefit con-ferred by topical antimicrobial preparations in burn patients: a historical perspective. J Trauma. 2004;56(4):863-866.

LWBK1580_C63_p675-686.indd 686 29/07/17 11:20 AM

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