Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.


PART THREE – Clinical Management of Special Surgical Problems

Chapter 29 – Anesthesia for Children with Burns

John E. McCall,Carl G. Fischer



Pathophysiology of the Burn Patient, 976



Respiratory Derangements, 976



Burn Shock and Hemodynamic Derangements,979



Hematologic Derangements, 981



Metabolic and Nutritional Derangements, 981



Renal Derangements, 981



Hepatic Derangements, 981



Pharmacologic Considerations in the Burn Patient, 982



Muscle Relaxants, 982



Analgesics, 982



Anxiolytics, 983



Anesthetics, 983



Resuscitation and Initial Management of the Burn Patient, 983



Airway and Ventilatory Management,983



Fluids, 984



Early Nutrition and Metabolic Needs,984



Escharotomies, 984



Associated Injuries, 984



Special Considerations for Electrical Burns, 984



Perioperative Management, 985



Perioperative Evaluation, 986



Induction and Airway Management,986



Maintenance of Anesthesia, 986



Intraoperative Blood Loss, 987



Postoperative Pain Control, 987



Surgical Reconstructive Phase of Burn Care, 987



Summary, 988

Children are often the victims of burns and scalds. Burns are the leading cause of accidental in-home deaths for children less than 15 years of age, with the peak incidence occurring in children aged 1 to 5 years, mostly due to scalds. In the United States, there is a 1:70 lifetime chance of being hospitalized for a burn injury, and an average of 12,000 burn fatalities are reported in the United States each year (Lloyd, 1977 ). Only motor vehicle trauma causes more accidental deaths than burns ( Feck and Baptiste, 1979 ).

Burns can be inflicted by various modalities including radiation, electrical, thermal, and caustic chemicals. The causes of thermal burns are scald, contact, and/or flame ( Parks et al., 1977 ).

Burns are classified as follows ( Table 29-1 ):



A first-degree burn involves only the epithelial layer of the skin; these burns are erythematous and may be quite painful but heal with no scarring. These injuries are typical of sunburn ( Fig. 29-1A ).



A second-degree burn involves the epithelial layer and to a varying degree the underlying dermis. These burns are characterized by the formation of blisters or a pink, moist appearance. Pain is an important component. Reepithelialization occurs because of sparing of the dermal appendages. The amount of pain and scarring produced depends on the depth of the dermal injury. Healing, if it occurs, should be complete in 7 to 14 days ( Fig. 29-1B ).



A deep dermal or deep second-degree burn involves most of the dermis, resulting in survival of few dermal appendages. Blister formation is seldom seen due to the thickness of the dead tissue. These burns are characterized by red or white, depending on depth of injury, colorless skin. These burns may be indistinguishable from third-degree burns. This may be unimportant as excision and grafting almost certainly are needed ( Fig. 29-1C ).



A third-degree or full-thickness burn involves the entire skin thickness, epidermis as well as dermis. It has the waxy white appearance of avascular tissue. Excision and grafting are mandated, or scarring will be severe ( Fig. 29-1D ).



Fourth-degree burns are full-thickness burns that extend into the supporting structures under the fascia.

To assess the total surface area of burn involvement, various tools and diagrams have been used. The diagram and chart in Figure 29-2 are of great use and require little learning curve.

The exact classification of burn injury may not be defined on the first examination; this is especially true of scald injuries. Watchful waiting eventually gives a true picture of the severity and extent of the injury and clarifies the extent of surgery that might be required. The amount of physiologic derangement, morbidity, and even mortality associated with a burn depends on the size and depth of injury. An inhalation injury adds to this derangement. Burn severity can be classified as minor, moderate, and major as originally determined by the American Burn Association and the American College of Surgeons Committee on Trauma ( Table 29-2 ).

Abnormalities seen in burn patients include metabolic derangements, neurohumoral responses, massive fluid shifts, possible sepsis, and systemic effects of massive tissue destruction ( Szyfelbein et al., 1993 ). Even minor burns may be associated with some systemic effects. The anesthesiologist who cares for these patients must be well versed in the treatment of these potentially altered pathophysiologic, pharmacologic, and anatomic derangements seen in burn patients.

Burn care has improved with resulting increase in survival rates even with extremely large burns. Now patients with burns of 80% have a survival rate of over 50%, and in adolescents and young adults this estimate probably is too low ( Saffle, 1998 ). In this chapter we hope to convey the information that has made many of these advances possible.

TABLE 29-1   -- Burn wound classification

First degree



Involves epithelial layer of skin only



Erythematous in appearance—typical of sunburn



Pain (+)



Heals without scarring

Second degree



Involves epithelial layer plus varying degree of underlying dermis






Uniformly pink, moist



Pain (+/+)



Heals within 2 weeks without scarring or functional impairment






White or mottled red, fairly dry. May be difficult to differentiate from third degree



Pain (+/-)



Most often will need excision and grafting or will have scarring

Third degree



Involves epithelial as well as full dermal layer



White, cherry red, or black



Elasticity of skin missing



Dry, hard, leathery appearance



Pain (+/-)



Need excision and grafting or will have major scarring

Fourth degree

• Full-thickness extending into the supporting structures under the fascia

Modified from De Campo T. Aldrete JA: The anesthetic management of the severely burnted patient. Intensive Care Med 7:55, 1981.





FIGURE 29-1  Degrees of burn severity. A, Patient with a first-degree burn. B, Patient with a second-degree burn. C, Patient with a deep second-degree burn. D, Patient with a third-degree burn.




FIGURE 29-2  Burn size estimate diagram, age versus area.  (Redrawn from Lund CC, Browder NC: The estimation of areas of burns. Surg Gynecol Obstet 79:352-357, 1994; now J Am Coll Surg.)




TABLE 29-2   -- Burn definitions


Burn Classification


Superficial burns of less than 15% TBSA (total body surface area)




Superficial burns of 15-25% TBSA in adults



Superficial burns of 10-20% TBSA in children



Full-thickness burns of less than 10% TBSA and burns not involving the eyes, ears, face, hands, feet, or perineum




A second-degree burn greater than 25% TBSA



A third-degree burn greater than 10% TBSA



Any size burn with accompanying inhalation injury



Electrical burns



Any complicated burn injury, ie., patients with underlying disease, patients with burns to the eyes, ears, face, hands, feet, or perineum

Modified from De Campo T, Aldrete JA: The anesthetic management of the severely burned patient. Intensive Care Medi':55, 1981.

As adapted from criteria of the American Burn Association and the American College of Surgeons Committee on Trauma.






Airway Injury

The air temperature in a room containing a fire may exceed 1000°F ( Trunkey, 1978 ). Due to the combination of efficient heat dissipation in the upper airway, low heat capacity of air, and reflex closure of the larynx, superheated air usually causes thermal injury only to airway structures above the carina ( Pruitt et al., 1979 ). Thermal injury to these airway structures may result in massive swelling of the tongue, epiglottis, or aryepiglottic folds with the resultant airway obstruction. These injuries are poorly tolerated, especially by infants and young children who have small airway size in absolute terms, high minute ventilation, and poorly developed respiratory muscles that fatigue easily ( Keens et al., 1978 ). This scenario is further complicated by the possibility that the anatomic distortion caused by the massive swelling makes intubation very difficult. Because airway swelling develops over a matter of hours as fluid resuscitation is ongoing, the initial evaluation of the child might not provide a good indication of the severity of obstruction that may occur later. A high index of suspicion must be maintained and the child's respiratory status must be continuously monitored to assess the need for airway control and ventilator support. If the history and initial examination lead one to suspect significant thermal injury to the upper airway, intubation or tracheostomy for airway protection and possible ventilatory support should be considered early rather than later.

Inhalation Injury

In addition to the upper airway injury mentioned, the child with a burn may also have an inhalation injury. Inhalation injury is produced by the exposure of the lower respiratory tract to smoke, carbon monoxide, hydrogen cyanide, or, more commonly, a combination of these elements. A history of exposure to a closed space fire, loss of consciousness, and the presence of chemical irritants, along with a physical examination revealing carbonaceous sputum and singed nasal or facial hair, are all suggestive of inhalation injury. The presence of inhalation injury increases fluid requirements for resuscitation from burn shock by approximately 50% ( Navar et al., 1985 ) and is a major source of mortality in burn patients ( Thompson et al., 1986 ).

Smoke Inhalation

The chemical injury due to smoke inhalation occurs when toxic particles or gases are inhaled and damage small airways and alveoli. The combustion of most substances generates materials that are toxic to the respiratory tract. For example, burning rubber and plastic products produce sulfur dioxide, nitrogen dioxide, ammonia, and chlorine, which form strong acids or alkali when combined with water in the airways and alveoli. Glues in laminated furniture and wall paneling may release cyanide gas, which is rapidly absorbed. Burning cotton or wool produces aldehydes that precipitate pulmonary edema ( Fein et al., 1980 ).

Almost all smoke-related toxins damage both airway epithelial and capillary endothelial cells. Histologic changes resemble those seen with tracheobronchitis. Mucociliary transport is destroyed, inhibiting the clearance of secretions, debris, and bacteria. The early inflammatory changes that occur in the airway are followed by a period of diffuse exudate formation ( Herndon et al., 1986 ). Alveolar macrophages are damaged and produce chemotaxins, further enhancing the inflammatory response ( Loke et al., 1984 ). Bronchiolar edema may become quite severe. The combination of the resulting necrotizing bronchitis, bronchial swelling, and bronchospasm results in obstruction of both large and small airways. Wheezing occurs as a result of bronchial swelling and irritant receptor stimulation. Alveolar collapse and atelectasis occur due to surfactant loss ( Herndon et al., 1985 ). A generalized increase in capillary permeability aggravates airway and pulmonary edema.

The end result of smoke inhalation is pulmonary failure occurring 12 to 48 hours after the smoke exposure and is due to a decrease in lung compliance, an increase in airway and tissue resistance, an increase in ventilation/perfusion mismatch, and an increase in dead space ventilation. In several days, the injury may progress to sloughing of airway mucosa and intrapulmonary hemorrhage, which may result in mechanical obstruction of the lower airways and flooding of the alveoli. Air trapping, occurring distal to airway obstruction, may result in volutrauma and ventilator-induced lung injury. Due to ulceration and extensive necrosis of the respiratory epithelium, children with an inhalation injury may be predisposed to secondary bacterial invasion and subsequent development of a superimposed bacterial pneumonia several days after injury ( Pruitt et al., 1975 ; Boutros and Hoyt, 1976 ; Rue et al., 1993 ). Although treatment is mainly supportive with mechanical ventilation, inhaled bronchodilators and mechanical methods of enhancing clearance of debris from the lower airways may be beneficial. If the child survives, pulmonary function may not return to normal for several months ( Madden et al., 1986 ).

Carbon Monoxide/Cyanide Poisoning

Carbon monoxide is an odorless, tasteless, nonirritating gas that is a product of incomplete combustion. Children exposed to a closed-space fire have a high likelihood of carbon monoxide poisoning even if they have no thermal burns. Carbon monoxide levels may exceed 10% in a closed space with a fire; significant injury may occur in a short period of time with exposure to as little as 1% ( Fig. 29-3 ). Carbon monoxide poisoning is a major source of early morbidity in the burned child, with many fatalities occurring at the scene of the fire ( Trunkey, 1978 ). With an affinity for hemoglobin 200 times greater than that for oxygen, carbon monoxide effectively competes with oxygen for hemoglobin binding. This not only shifts the oxyhemoglobin dissociation curve to the left but also alters its shape. Oxygen delivery to tissues is severely compromised due to both the reduced oxygen-carrying capacity of blood and the less efficient dissociation of oxygen from hemoglobin at the tissue level ( Fig. 29-4 ). In addition, carbon monoxide competitively inhibits intracellular cytochrome oxidase enzyme systems, most notably cytochrome P-450, resulting in an inability of cellular systems to utilize oxygen (Goldbaum et al., 1976 ). Inhaled hydrogen cyanide, which is produced during the combustion of numerous household materials, also affects the cytochrome oxidase system and thus may have a synergistic effect with carbon monoxide, producing an increase in tissue hypoxia and acidosis as well as a decrease in cerebral oxygen consumption and metabolism ( Moore et al., 1991 ).


FIGURE 29-3  Hemoglobin is rapidly converted to carboxyhemoglobin in the presence of carbon monoxide.  (Modified from Stewart RD, Stewart RS, Stamm W, et al.: Rapid estimation of carboxyhemoglobin level in fire fighters. JAMA 235:390, 1976.)





FIGURE 29-4  Carboxyhemoglobin-induced changes in the oxygen-hemoglobin dissociation curve.  (From Fein A, Leff A, Hopewell PC: Pathophysiology and management of the complications resulting from fire and the inhaled products of combustion: review of the literature. Crit Care Med 8:94, 1980.)




Carbon monoxide poisoning may be difficult to detect. The absorbance spectra of carboxyhemoglobin and oxyhemoglobin are very similar. Pulse oximeters cannot distinguish between the two forms of hemoglobin, and oximeter readings are normal even when lethal amounts of carboxyhemoglobin are present. A PaO2 obtained from an arterial blood gas measures the amount of oxygen dissolved in the plasma but does not quantitate hemoglobin saturation, which is the true measure of the oxygen-carrying capacity of the blood. Carboxyhemoglobin levels may be measured directly, but this test is rarely available at the scene. Due to the inevitable time delay between exposure and testing, levels measured on arrival at a health care facility do not reflect the true extent of poisoning, especially when the child has been breathing high concentrations of oxygen.

The half-life of carboxyhemoglobin is 250 minutes for the victim breathing room air; this is reduced to 40 to 60 minutes with the inhalation of 100% oxygen ( Crapo, 1981 ). Any child suspected of carbon monoxide exposure should receive high levels of oxygen until carbon monoxide poisoning has been ruled out. If the patient is unconscious or cyanotic, intubation for the administration of high oxygen concentrations is indicated.

While hyperbaric oxygenation further reduces the half-life of carboxyhemoglobin, the hyperbaric chamber is a difficult environment in which to monitor the patient and to perform fluid resuscitation and early burn care such as escharotomies and dressing changes. It is the opinion of most burn experts that hyperbaric oxygen treatment should be reserved for the child with minimal to no cutaneous burns or other injuries ( Grube et al., 1988 ).

Additional External Factors

Circumferential burns of the chest may cause a mechanical restrictive effect and further compromise ventilation. Escharotomies in the anterior axillary lines, in conjunction with appropriately placed transverse escharotomies, may allow some patients to avoid mechanical ventilation.


Proper fluid management is critical to the survival of the child with a major burn. Although we have a better understanding of the massive fluid shifts and vascular changes that occur during burn shock than in the past, inadequate fluid resuscitation remains one of the most common causes of death within the first 10 days after burn injury ( Artz and Moncrief, 1969 ). Further complicating the alterations in fluid homeostasis, children with major burns commonly exhibit systemic inflammatory response syndrome (SIRS), which ranges in severity from the presence of tachycardia, tachypnea, fever, and leukocytosis to refractory hypotension and, in its most severe form, shock and multiple organ dysfunction syndrome (MODS). Table 29-3 summarizes the systemic effects of burn injury ( Szyfelbein et al., 1993 ).

TABLE 29-3   -- Systemic effects of burn injury





↓ CO due to decreased circulating blood volume, myocardial depressant factor

↑CO due to sepsis

↑CO 2 to 3 times > baseline for months (hypermetabolism)


Upper airway obstruction due to edema
Lower airway obstruction due to edema, bronchospasm, particulate matter



Tracheal stenosis

↓ Pulmonary compliance

↓ Chest wall compliance

↓ Chest wall compliance



(a) Secondary to ↓ circulating blood volume

↑GFR secondary to ↑CO

(b) Myoglobinuria

Tubular dysfunction

(c) Hemoglobinuria


Tubular dysfunction



↓ Function due to ↓ circulating blood volume, hypoxia, hepatotoxins


↑Function due to hypermetabolism, enzyme induction, ↑CO

↓ Function due to sepsis, drug interaction


↓ Red blood cell mass


↓ Platelets

↑Clotting factors

↑Fibrin split products, consumptive coagulopathy, anemia

Possible AIDS, hepatitis







ICU psychosis


↑Heat, fluid, electrolyte loss

Contractures, scar formation


↓ Ionized calcium

↑Oxygen consumption


↑Carbon dioxide production


↓ Ionized calcium


Altered volume of distribution

↑Tolerance to narcotics, sedatives


Altered protein binding

Enzyme induction, altered receptors

Altered pharmacokinetics

Drug interaction

Altered pharmacodynamics


Reproduced with permission from Szyfelbein SK, Martyn JA, Coté CJ: Burn injuries. In Coté CJ, Ryan JF, Todre ID, Goudsouzian NG, editors: A practice of anesthesia for infants and children, 2nd ed. Philadelphia, 1993, WB Saunders Co.

↓, Decrease in; ↑, increase in; AIDS, acquired immunodeficiency syndrome; CO, cardiac output; FRC, functional residual capacity; GFR, glomerular filtration rate; ICP, intracranial pressure; ICU, intensive care unit.




Proinflammatory cytokines, chemokines, and noncytokine inflammatory mediators all play a role in the pathophysiology of SIRS and MODS. Tumor necrosis factor-α (TNFα), which is released from macrophages in response to local or systemic injury, is a classic mediator of systemic inflammation, and modulates a variety of immunologic and metabolic events ( Spooner et al., 1992 ). The release of TNFα activates antimicrobial defense mechanisms and tissue repair, but paradoxically it may begin a sequence of events leading to tissue injury, organ dysfunction, and even apoptosis in a variety of cell types ( Voss and Cotton, 1998 ). In addition, TNFα leads to the release of other mediators such as interleukins (IL-1, IL-6, and others) and interferon γ (IFNγ). Interleukins potentiate the destructive effects of TNFα and elevated levels may be predictive of a poor outcome ( Van der Poll and van Deventer, 1999 ). IFNγ stimulates cytokine secretion, phagocytosis, and the respiratory burst activity of macrophages, thus amplifying the inflammatory response ( Tominaga et al., 2000 ). Chemokines, such as IL-8, function as chemoattractants for leukocytes and play a role in tissue destruction ( Laffon et al., 1999 ). Nuclear factor-κB (NFκB) is a transcription factor that may regulate many of the previously mentioned factors through transcription of a number of cytokine, chemokine, adhesion molecule, and enzyme genes leading to the clinical manifestation of SIRS. NFκB may be associated with poor outcome in patients with sepsis ( Bohrer et al., 1997 ). It has been demonstrated that NFκB plays a key role in the molecular and cellular events leading to acid-induced lung injury ( Madjdpour et al., 2003 ); a similar role in SIRS can be hypothesized. Noncytokine factors, such as platelet activation factor, eicosanoids, leukotrienes, and thromboxane A2, also play a role in SIRS and MODS. Additionally, complement activation causes leukocyte attraction and activation, leading to cellular destruction through the release of reactive oxygen intermediates and proteases ( Czermak et al., 1999 ). This hyperactive inflammatory response, with its numerous and complex interacting mediators, results in alterations of cardiovascular, metabolic, gastrointestinal, and coagulation systems. (A more detailed discussion of the subject is beyond the scope of this text.)

Burn shock is a combination of hypovolemic and cellular shock and is characterized by changes that include decreases in cardiac output and plasma volume resulting in decreased blood flow to major organs. In burn shock, resuscitation is complicated by massive transvascular fluid shifts that are unique to thermal trauma ( Warden, 2002 ). Fluid requirements are initially increased due to a marked increase in vascular permeability in the area of the burn; however, this increased permeability becomes generalized in a patient with burns of greater than 30% of the body surface area ( Moncrief, 1973 ). Edema occurs due to local thermally induced changes in the microcirculation and an increase in total body capillary permeability. The failure of semipermeable membranes leads to tremendous loss of fluids, electrolytes, and plasma proteins from the intravascular space. Maximum edema formation occurs from 8 to 24 hours after the burn, and the progression of edema is dependent on the adequacy of resuscitation. As in other types of shock, the primary goal is to restore and preserve tissue perfusion in order to avoid ischemia. Inadequate resuscitation results in severe depletion of plasma volume, which in turn increases morbidity and mortality due to adverse effects on cardiac output, renal function, and perfusion of burn wounds.

Children who are inadequately resuscitated from burn shock may not be able to increase their cardiac output to the extent needed to maintain arterial pressure in the face of excessive vasodilation and therefore exhibit signs of hypotension and shock. These patients may demonstrate a reduced vascular responsiveness to vasoconstrictors. It has been hypothesized that the presence of endotoxin or bacteria in the blood plays a role in this clinical picture ( Traber et al., 1988 ). Proinflammatory cytokines, chemokines, noncytokine inflammatory mediators, and vasoactive substances with potentially deleterious effects are released from burned tissue, including vasoconstricting and vasodilating prostaglandins, kinins, serotonin, histamine, oxygen radicals, and lipid peroxidases ( Demling, 1985 ). Administration of adequate volumes of fluid, during resuscitation as well as in the operating room, is of paramount importance.

Once adequate fluid resuscitation has been completed, the clinical picture of the burned child is that of a patient with a hyperdynamic circulation characterized by low systemic vascular resistance and high cardiac output. Blood flow to all major organs is increased ( Wilmore et al., 1980 ). The degree of increase in cardiac output is a function of wound size. As the child stabilizes in the early postburn shock period, sustained hypertension is frequently present, probably mediated by renin, antidiuretic hormone (ADH), or catecholamines ( Falkner et al., 1978 ).


A major burn also causes significant hematologic derangements in a characteristic biphasic response. Initial anemia is due to erythrocyte loss, the degree of which is proportional to the burn size. The loss occurs due to a number of etiologies. Red blood cell destruction occurs as a direct result of the burn injury and due to loss into capillary thrombi, which are produced through burn activation of the complement and coagulation cascades. Burn injury also induces alterations in the erythrocytes, via release of oxygen free radicals and proteases, which lead to their destruction ( Heatherill et al., 1986 ). Red cell loss may approach 20% in the first 24 hours after a major burn and may continue at a rate of 1% to 2% per day until the wounds are grafted ( Deitch and Sittig, 1993 ). If an increase in hemoglobin is observed during burn resuscitation, this is due to hemoconcentration and is an indication for an increase in fluid administration. During recovery from burn injury, anemia is due to a decrease in production of red cells. Erythropoietin levels are elevated, but the bone marrow remains hyporesponsive, possibly due to high circulating levels of various cytokines and other inflammatory mediators ( Jelkmann et al., 1990 ).

Thrombocytopenia occurs early after burn injury due to increased platelet aggregation, consumption during the formation of microemboli, and dilution during fluid resuscitation ( Lawrence and Atac, 1992). At 10 to 14 days postinjury, an increase in platelet count occurs, which may last several months ( Heideman, 1979 ).

Burn patients experience activation of both the thrombotic and fibrinolytic pathways. This may increase the likelihood of disseminated intravascular coagulation (DIC) early in the course of patients with major burns ( Kowal-Vern et al., 1992 ). As the child recovers from burn injury, factors V, VII, and VIII and fibrinogen may be elevated for several months; however, the child does not become hypercoagulable ( Simon et al., 1977 ).


The metabolic consequences of major burn injury in a child are profound and constitute a major challenge to effective treatment. Metabolic rates of children with burns can be twice normal and three to four times that of an unburned adult. Catabolic activity and nitrogen losses are greater than are seen with any other catastrophic illness ( Wilmore and Aulick, 1978 ). Elevated levels of epinephrine and norepinephrine are present for a prolonged period after burn injury. Derangements in other hormones such as glucagon, glucocorticoids, growth hormone, and thyroid hormone are also present ( Wilmore et al., 1974 ). Manifestations of hypermetabolism include persistent hyperpyrexia, tachycardia, hyperpnea, body wasting, increased oxygen consumption, and increased carbon dioxide production. The degree of hypermetabolism correlates with burn size. Protein catabolism, ureagenesis, lipolysis, accelerated gluconeogenesis, skeletal muscle proteolysis, elevated free fatty acids, glycogen mobilization, insulin resistance, and glucose intolerance are all indicators of the hypermetabolic state ( De Campo and Aldrete, 1981 ).


The renal function of a child with a major burn may be impaired due to hypovolemia, hypotension, hypoxemia, myoglobinuria, hemoglobinuria, or a combination. Oliguria during burn resuscitation is due to a decrease in renal blood flow ( Aikawa et al., 1990 ). Inadequate resuscitation early in burn shock exacerbates renal damage; fluid therapy should be directed toward the maintenance of 0.5 to 1.0 mL/kg per hr of urine output. Stress-induced elevation of serum glucose levels may cause an osmotic diuresis even in the face of hypovolemia; adequate urine output may give the false impression that renal blood flow is adequate as well. Children with burns of greater than 40% of the total body surface area (TBSA) may have tubular dysfunction as evidenced by an inadequate renal response to ADH and aldosterone ( Moncrief and Teplitz, 1964 ).

The renal system may be further compromised by other factors. High levels of stress hormones and impairment of atrial natriuretic polypeptide secretion may contribute to reduced renal function ( Aikawa et al., 1990 ). The kidneys may be exposed to nephrotoxic antibiotics as well as other nephrotoxins such as free hemoglobin ( Sawada et al., 1984 ). Most cases of renal failure occur 5 days or more after burn injury; four fifths of these patients have inhalation injury as well ( Holm et al., 1999 ). Even after the completion of resuscitation from burn shock, the pharmacology of drugs excreted by the kidney may be altered in an unpredictable fashion ( Loirat et al., 1978 ).


Like the kidneys, the liver of the child with a major burn may experience insults due to hypovolemia, hypotension, hypoxemia, inflammation, or a combination. Other potential insults include drug toxicity, sepsis, and infection due to exposure to multiple blood products. Liver damage may be manifest by hepatic edema and release of hepatic enzymes ( Jeschke et al., 2001 ). Liver injury may be due to hypoperfusion as well as insult from inflammatory cytokines such as IL-1 and TNFα ( Jeschke et al., 1999 ).

In the early stages of burn resuscitation hepatic blood flow is decreased; once burn shock has resolved, the child enters the hypermetabolic phase and liver blood flow increases along with an increase in the metabolism of glucose and fats. The increased hepatic flow increases drug delivery to the liver ( Martyn, 1986 ); protein binding may be altered, so pharmacokinetics of various drugs may be altered in an unpredictable fashion ( Wilmore et al., 1980 ). Hepatic protein synthesis shifts from constitutive proteins such as albumin, prealbumin, and transferrin to acute phase proteins ( Jeschke et al., 2001 ); albumin falls to critically low levels during the acute phase. In most cases, liver function returns to normal within 1 week of burn injury unless further insults occur.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


Burns involving more than 10% to 15% of the TBSA in patients give rise to a cascade of systemic and localized physiologic responses (Demling, 1984, 1985 [11] [12]). These responses include alterations in metabolic rate and cardiac output, alterations in fluid compartments, glomerular filtration, hepatic perfusion, reduction in serum albumin levels, and increases in α1-acid glycoproteins. The greater the magnitude of the burn, the more profound are these changes. The response to medication in any patient may be unpredictable, but this is especially true in major burn patients and thus it is necessary to titrate to effect any and all medications given. This subject has been well reviewed ( Martyn, 1986 ).

There are multiple other factors that may interact to alter pharmacokinetics. These may include sepsis, other drugs that may induce or inhibit metabolic pathways, drugs that are hepatotoxic or nephrotoxic, malnutrition, and parenteral nutrition. In addition, there may be burn-induced hepatic, renal, and pulmonary dysfunction.

In the early or acute stage of burn injury, known as the resuscitative phase, blood flow is decreased to organs and tissue for several reasons, including increased blood viscosity, hypovolemia, and decreased cardiac function secondary to circulating proinflammatory and vasoactive substances. Especially in this phase, only the intravenous route of medication administration should be used, titrating the desired effect of the medication with small repetitive doses. Subcutaneous and intramuscular routes of administration should be avoided due to variable uptake.

In the second stage of burn injury, known as the hypermetabolic phase, hypermetabolism and increased blood flow to all major organs are predominant ( Wilmore et al., 1980 ). In this phase, it is not clear if drug metabolism is increased ( Martyn, 1986 ). Many drugs are bound to plasma proteins, albumin for acidic drugs, and α1-acid glycoproteins for basic drugs; binding to other proteins occurs to a much smaller extent. This binding is usually reversible and drugs compete with one another for binding sites. Examples of drugs bound to proteins include benzodiazepines and antiepileptics, which are acidic and when bound to albumin have an increased free component in the acute stages, and basic drugs such as tricyclic antidepressants and neuromuscular relaxants, which bind to α1-acid glycoprotein and have a decreased free component in this phase ( Martyn et al., 1984 ). In most instances, increased protein-binding leads to a decreased volume of distribution for any given drug ( Stanski and Watkins, 1982 ).


Because of the well-known response of hyperkalemia with the use of succinylcholine in the burn patient ( Gronert and Theye, 1975 ; Tolmie et al., 1967 ) and the controversy over when this response becomes manifest ( MacLennan et al., 1998 ; Gronert, 1999 ; Martyn, 1999 ) this drug should not be stocked in any operating room in which a burn patient is to have surgery. The onset of hyperkalemia is as early as 24 to 48 hours after injury and may continue for up to 2 years after the burn injury ( Martyn et al., 1982 ). Although the duration of the hyperkalemic response is controversial, it can easily be avoided with the use of fairly rapid-onset nondepolarizing agents.

As noted, the increased levels of α1-acid glycoprotein leads to lower free fractions of muscle relaxants in the plasma. Resistance to atracurium ( Dwersteg et al., 1986 ), vecuronium ( Mills and Martyn, 1989), curare ( Martyn et al., 1980 ), and pancuronium ( Martyn et al., 1983 ) has been demonstrated. Table 29-4 demonstrates this very well using vecuronium as an example ( Mills and Martyn, 1989 ). A major reason may also be the increased number of receptors on the muscle membranes ( Martyn et al., 1980 ). Most experts believe that altered pharmacokinetics and increased plasma protein binding contribute little to the phenomenon ( Leibel et al., 1981 ; Martyn et al., 1982 ). The larger the burn, the more this effect is noted. The effect is noted beginning about the sixth day, peaks at days 15 to 40, and has decreased by day 70 after the burn; however, some resistance may be seen at 500 days after the burn ( Dwersteg et al., 1986 ; Martyn et al., 1982 ). As an example, patients with burns of 50% to 60% may require doses 2.5 to 5 times that in nonburned patients. Interestingly, despite the large doses used, the serum half-life is unchanged and the reversal of nondepolarizing muscle relaxants using the usual drugs is accomplished without a problem.

TABLE 29-4   -- Emergency department values of vecuronium in burn patients and control patients

Study Group (%TBSA burn)




17.6 (15.4–19.9)

35.3 (30.6–42.3)


34.0[*] (29.3–38.7)

68.2[*] (59.8–79.9)


55.4[*] (48.1–62.1)

111.1[*] (99.8–126.2)


64.5* (57.4–71.9)

129.4[*] (113.0–154.0)

From Mills AK, Martyn JA: Neuromuscular blockade with vecuronium in paediatric patients with burn injury Br J Clin Pharm 28:155, 1989.

Numbers in parentheses represent lower and upper 95% confidence limits.

TBSA, total body surface area.

The effective doses for 50% and 95% twitch suppression (ED50and ED95f or vecuronium are significantly increased in burned children compared with controls. The shift in the dose response curve is related to the magnitude of burn.



Significantly different from controls, P < 0.01.




Pain control in burn patients is a major issue that in the past has received little attention in the literature. In many instances, pain control has been woefully neglected, especially in children who are too young to speak or are intubated and cannot speak. Concerns with possible addiction or the impaired drug elimination in these patients are some of the reasons given for this and leads to severe undermedication. In a survey of multiple burn centers, no cases of such addiction have been discovered ( Perry and Heidrich, 1982 ).

It is a well-known phenomenon with practitioners who routinely work with burn patients that the opioid requirements for pain relief are often increased. This may be due to changes in pharmacokinetic and pharmacodynamic factors. Tolerance to opioids develops quickly, but addiction develops very rarely in patients treated with opioids for pain relief ( Porter and Hick, 1980 ). Withdrawal is usually not a problem in that opioids are gradually tapered as the healing takes place and the number of procedures is reduced.

The main drugs in the armamentarium for pain management remain morphine and fentanyl. A continuous infusion of morphine for pain control is preferred when necessary, and fentanyl is usually used only intraoperatively. Although remifentanil is an excellent agent with fast awakening, the painful procedures that many burn patients undergo make this agent less than ideal.


Sedatives and anxiolytics are often administered to burn patients, especially those on ventilators. In burn patients given a single dose of diazepam, there is a rapid fall in drug concentration in the plasma and the therapeutic effect is short lived. This is due to the rapid uptake of the drug by the tissue and the high lipid solubility of the medication ( Greenblatt et al., 1983 ). In those patients on diazepam for prolonged periods, high levels of parent drug have been found in the plasma for up to 2 weeks after the last dose. Active metabolites were found after an even longer period ( Martyn et al., 1983 ). Lorazepam may be better used in burn patients due to its alternate metabolic pathway and due to the fact that the clearance is unimpaired even in the face of altered volume of distribution ( Greenblatt et al., 1983 ).


Inhaled Anesthetics

Halothane is and has been used extensively in many pediatric burn centers. It is often switched to isoflurane for the maintenance phase, especially in older children and adolescents. The newer anesthetics, including sevoflurane, have not played a major role, other than being used for a “smoother and faster” induction. In the same way that inductions are faster, awakening is equally as rapid. In many burn cases a slower emergence is preferred. The same can be said about the use of remifentanil. Both of these agents are excellent when one wants a rapid onset and an early awakening. However, due to the residual pain involved in acute burn surgery, the residual effects of the older inhalation agents and the lingering effects of morphine and even fentanyl are of some benefit. Although sevoflurane and remifentanil certainly may have a place during the reconstructive phase of burn anesthesia and surgery, they have not become important agents in the burn unit. There is little in the literature that promotes these agents or techniques for use in the acute phase of burn anesthesia.

Multiple administrations of halothane have not led to profound liver dysfunction ( Gronert et al., 1967 ) or to an increased risk of halothane hepatitis in this population ( Martyn, 1986 ). If indeed halothane hepatitis is due to an allergic phenomenon, the anergic state of the burn patient may in part be responsible for its absence.

Most inhalation agents have been clinically studied in the burn patient, but there are little data concerning uptake, distribution, and elimination ( Martyn, 1986 ). Further discussion of these agents is given in the anesthetic management section.


There is a large body of literature documenting the use of ketamine in burn patients as both an induction agent and one used for the maintenance of anesthesia. Ketamine is well known for its cardiovascular stimulating properties, its analgesic effects, and its versatility ( Slogoff et al., 1974 ). Tolerance may be exhibited ( White et al., 1982 ), and high doses may prolong awakening in some patients. Dosing, as stated for all drugs in the burn patient, must be individualized. Side effects may be the same as in nonburned patients and, when used, may cause hallucinations and other untoward effects. These effects may be minimized by a small dose of benzodiazepine preceding the ketamine. It should also be mentioned that ketamine in the volume-depleted patient may cause hypotension.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier



As with any severely injured child, airway management is of utmost importance in the child with a major burn. Initial assessment should include a brief but directed history and physical examination. The history should focus on the mechanism of injury and underlying risk factors. Salient points include exposure to smoke in a closed space (i.e., car, house, or trailer fire), loss of consciousness at the scene with the resultant loss of protective airway reflexes, and a history of reactive airway disease, bronchitis, or other chronic diseases of the airways.

Physical examination of the child with an acute burn should focus on assessment of the risk of airway obstruction, respiratory failure, or both and the need for early establishment of an artificial airway. A child with an inhalation injury may develop massive swelling of the airway within a matter of hours after the injury as fluid resuscitation contributes to edema formation in thermally injured tissues of the upper airway. The extent of airway edema correlates with the body surface area burned. Not only does edema have the potential to cause mechanical obstruction of the supraglottic airway (see section on pathophysiology), it also makes endotracheal intubation extraordinarily difficult. Clinical suspicion of inhalation injury should be aroused by the above-mentioned risk factors in the history, as well as clinical features such as burns of the face and neck, singed nasal hairs, carbonaceous sputum, and hoarseness. Fiberoptic bronchoscopy may contribute to the diagnosis ( Hunt et al., 1975 ) but should not take the place of clinical judgment. Blood gases may be normal for the first few hours after injury and thus may not be helpful, especially before fluid resuscitation is complete. Intubation and mechanical ventilation may also be indicated in a child with carbon monoxide poisoning and depressed airway reflexes, even without thermal injury.

Some authors believe that intubation of an inflamed airway increases the risk of damage to the larynx ( Colice et al., 1986 ). Not every child with a face burn requires intubation; as mentioned, a delay in establishing an airway may result in a much more difficult scenario several hours later. The risk of losing an airway is much greater in attempting intubation after airway edema has resulted in severe distortion of airway structures, as in a child with acute epiglottitis. Although fiberoptic intubation figures prominently in the American Society of Anesthesiologists—difficult airway algorithm, if intubation of the burned child is delayed to the point where airway edema has developed to any significant degree, use of a fiberoptic technique is not helpful, as airway edema and secretions immediately obscure the endoscopic view.

Direct laryngoscopy with a rigid blade allows for mechan-ical displacement of edematous tissues and affords the best possible view of the airway. These children should not be given muscle relaxants as their use is likely to lead to a “cannot intubate, cannot ventilate” situation. Awake intubation is not a viable option in most children, including those with burns. Judicious administration of intravenous ketamine (1 to 1.5 mg/kg) allows one to sedate the child while maintaining spontaneous ventilation. Whether airway reflexes are maintained with ketamine is subject to debate; however, aspiration has not been reported as a problem during early airway management of burned children. Because the airway obstruction is the result of supraglottic edema, the laryngeal mask airway (LMA) may in theory provide a useful temporary airway until intubation or a surgical airway is accomplished. The use of the LMA in this situation has not been reported in the literature.

If intubation is predicted to be or proves to be impossible, a tracheostomy may be considered. In the past, authors have stated that a tracheostomy in a child with a burned airway was associated with a mortality of close to 100% ( Eckhauser et al., 1974 ). Later studies have refuted this statement ( Palmieri et al., 2002 ; Saffle et al., 2002 ) and proved that tracheostomy is safe and may actually improve patient comfort. A tracheostomy is the airway of choice for a child with deep burns of the lower face, where an endotracheal tube would complicate skin grafting, and for patients who are anticipated to require greater than 2 to 3 weeks of mechanical ventilation.


Many have debated the most appropriate type of fluid for resuscitation of the patient in burn shock; however, the adequacy of volume of fluid and replacement of extracellular salt lost into the burned tissue are the most reliable predictors of successful resuscitation ( Neely et al., 1988 ). Crystalloid, in particular lactated Ringer's solution and Normosol, are the most popular resuscitation fluids currently used (Warden, 2002 ). The modified Parkland formula recommends 4 mL/kg per percent burn in the first 24 hours with one half administered in the first 8 hours. To this amount is added to 1500 mL/m2 to account for normal maintenance ( Merrell et al., 1986 ). Studies indicate that hypertonic saline may be beneficial in modulating the inflammatory cascade and restoring hemodynamic parameters and microcirculatory flow ( Junger et al., 1997 ).

It is important to realize that regardless of the resuscitation formula and fluid that are used, these formulas are only guidelines and provide a starting point. Rates of fluid administration should be titrated to maintain a urine output of 1 mL/kg per hr. Central venous pressures may also be useful in guiding fluid therapy, providing the tip of the catheter is properly placed in the central circulation. Femoral catheters are usually too short to reach the level of the diaphragm and therefore do not adequately reflect true right heart filling pressures. Once resuscitation is complete, fluids can be decreased to a maintenance rate that takes into account the burn size and extra evaporative losses that are expected ( Warden, 2002 ). Using the following formula, daily maintenance fluids (in milliliters per 24 hours) can be calculated:

[(% TBSA burned + 35) × body surface area (m2) × 24] + 1500 mL/m2

As with resuscitation fluids, it must be remembered that formulas only provide a starting point; the actual rate of fluid administration must be dictated by patient response (i.e., urine output). The importance of maintaining a normal circulating blood volume cannot be overemphasized.


The child with a major burn, even if he or she is able to eat, rarely is able to consume an adequate number of calories. Despite the ileus, which is almost universally present in the first few days after a major burn, it has been demonstrated that enteral feedings can be started safely within hours of burn injury. Early enteral feeding improves nitrogen balance and overall nutrition ( McDonald et al., 1991 ) and reduces the incidence of stress ulceration ( Demling, 1985 ). Tube feedings administered through nasal jejunal tubes do not need to be stopped before surgery but can be continued throughout the perioperative period without increased risk of aspiration or other complications ( Jenkins et al., 1994 ). This reduces interruptions in feedings and therefore ensures adequate nutrition for patients undergoing multiple procedures and may also reduce infectious complications.

Failure to recognize and satisfy these exaggerated metabolic needs results in impaired wound healing, cellular dysfunction, and decreased resistance to infection. Environmental stress adds significantly to metabolic rate. Maintaining a high ambient temperature and humidity may reduce caloric requirements by up to 20% ( Wilmore et al., 1974 ) and should be a standard of care in all burn centers as well as in the operating room. In addition, whether inside or outside the hospital, meticulous attention must be paid to the maintenance of normothermia during transport of the burned child. Metabolic needs do not return to normal until all burn wounds are covered and healed.


Burned tissue becomes inelastic. If a patient has a circumferential burn, the inelastic eschar will not expand to accommodate the inevitable tissue swelling occurring beneath it and tissue pressures increase. If the circumferential burn involves a limb, a compartment syndrome may develop. If the chest is involved, a restrictive pattern of ventilatory failure may develop. If the abdomen is involved, elevated intra-abdominal pressures may result in an intra-abdominal compartment syndrome, leading to a decrease in venous return, a decrease in urine output, and respiratory failure. With any of these scenarios, urgent escharotomies are required (Figs. 29-5 and 29-6 [5] [6]). This can be accomplished in the operating room, or often more readily at the bedside using ketamine for sedation and analgesia. If electrocautery is used to perform the procedure, blood loss is usually minimal.


FIGURE 29-5  Escharotomy sites.  (Redrawn from Pruitt BA, Dowling JA, Moncrief JA: Escharotomy in early burn care. Arch Surg 96:502, 1968.)





FIGURE 29-6  Extensive escharotomies required in a child with a major burn.




When caring for the child with a major burn, associated injuries are easily overlooked. Although management of the child's airway and volume status is a top priority, other injuries should be sought if a history of trauma is elicited, such as burns associated with a motor vehicle accident or a fall from a burning building. Long bone fractures, closed head injury, skull fracture, and intra-abdominal hemorrhage may complicate burn injury. In the older child and teenager, the presence of alcohol or illicit drugs may complicate management. A rapid yet thorough physical examination accompanied by a focused history should help to elucidate any additional injuries.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


Electrical burns are truly a unique form of thermal injury. They may be classified into low voltage (≤400 V) and high voltage (>1000 V) injuries. Low voltage injuries are commonly seen in home settings, and high voltage injuries in industrial settings ( Warden, 2003 ).

One type of injury is a purely contact burn in which there is no true entrance or exit wound. They are usually full-thickness burns due to prolonged contact with the element. They are treated as a true thermal burn, are usually caused by low voltage contact, and are of a limited extent. Of these, the most devastating are probably those in small children who bite an electric cord, causing injury to either one or both of the commissures of the mouth.

Another type is the electrical flash. These are not truly burns but rather injury due to an electrical discharge. They also may be treated as though a thermal burn.

The most devastating type of electrical burn is caused by high-voltage injuries. These injuries result from true electrical damage to a vast area of tissues and organs, including the heart, respiratory system, circulatory system, central nervous system, peripheral nervous tissue, eyes, kidney, and the integument and bones. The visible injury may be only the tip of the iceberg, with the major injury being to the underlying structures.

Lightning strikes remain a significant problem to the population, causing approximately 1320 deaths from 1980 through 1995; of these deaths, 85% occurred in males. The greatest number of deaths occurred in the 15- to 19-year-old group (Morbidity Mortality Weekly Report, 1998). Almost 30% of the people struck by lightening die, especially those with cranial and/or burns of the feet. As in electrical burns, the observed peripheral injury may be only the tip of the iceberg as many underlying structures may be involved.

In patients with low-voltage injuries, the deep burn usually corresponds to the area of superficial involvement. This is usually not the case with high-voltage injuries. In the latter injuries, the current often passes up the center of the limb as if it were a conducting cable causing extensive damage to vessels, muscles, and nerves. Nevertheless, vascular damage may be present in any of these injuries, causing problems to structures distal to the involved site.

Early major problems in patients with major electrical/lightening burns may be cardiac arrhythmias and/or damage to muscle with release of free hemoglobin and myoglobin with subsequent hemoglobinuria and myoglobinuria. The latter is manifest by red to red-black urine and must be treated by maintaining high urine output. A urine output of 1 to 2 mL/kg per hr must be maintained until the pigment load is decreased, or there may be serious tubular damage to the kidneys resulting in oliguric renal failure. Mannitol is often added to the resuscitation fluids, in these cases, in order to increase urine output. Some clinicians also add sodium bicarbonate to the intravenous solutions to alkalinize the urine ( Warden, 2003 ). This is one of the few burn problems that may be taken to the operating room within the first 24 hours of injury before stabilization is complete. The usual reason is for decompression of the extremity or extremities to maintain circulation. The decompression is necessary due to tissue swelling as well as injury to the blood vessels (the path of least resistance) from the current. Often, these patients need to return to the operating room at frequent intervals, even in the first 24 to 48 hours, to have the nonviable tissue débrided. This nonviable tissue may underlie normal skin ( Warden, 2003 ).

This section is not meant to be a complete guide to treatment of severe electrical burns and thus a textbook of burn surgery should be referenced for a more thorough treatment of severe electrical injuries. Suffice it to say that on a percent burn injury, major electrical burns may be more devastating than a pure thermal burn.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


Once initial resuscitation and stabilization are complete, patients with full-thickness or deep partial-thickness burns begin a series of trips to the operating room for wound excision and coverage, either with autograft or with a temporary covering such as cadaver skin. Early excision of burn tissue may result in fewer complications, especially those due to infection ( Demling, 1985 ). The child presenting to the operating room for excision, grafting of burn wounds, or both almost always require general anesthesia.


During the preanesthetic evaluation of a child with a major burn, special attention should be focused on areas most likely to be adversely affected by the burn injury. These include the airway, respiratory system, cardiovascular system, and volume status. The physical examination should include an assessment of sites for monitoring blood pressure, electrocardiography, pulse oximetry, and temperature. A review of the past anesthetic records is always helpful, especially if the child has undergone prior anesthetics during the current admission. Ventilator settings should be noted and a determination made as to whether the intensive care unit ventilator should be brought into the operating room. Intravenous access must be adequate in view of the blood and fluid requirements likely to be encountered. Laboratory values should be checked, with special attention to the acid-base balance, hematocrit, calcium, and electrolytes. If a large blood loss is anticipated, consider initiating transfusion in advance of the procedure. A recent chest radiograph should be reviewed.

Most important, the time should be taken to discuss the proposed anesthetic management with the child and his or her family. The risks and benefits should be discussed along with a nontechnical explanation of anesthetic and operating room procedures. The child and family should be reassured that the child's safety and comfort are of utmost importance and will be maintained intraoperatively and postoperatively to the greatest degree possible.


Transport to the operating room should be well planned and efficient. Preoperative sedation and analgesia should be provided if tolerated by the patient, as the trip to the operating room may be anxiety provoking and painful. Measures to prevent heat loss should be instituted prior to transport, as children with burns are especially susceptible to hypothermia and do not tolerate caloric stress well. If the patient is dependent on mechanical ventilation, current settings, including peak end-expiratory pressure (PEEP), should be duplicated during transport.

The child with burns should have standard monitors placed before induction. Sites for monitors may be problematic. Blood pressure cuffs usually continue to function adequately even when placed over dressings. Because extensive burns often involve the hands and feet, sites for an oximeter probe are often scarce. Probes may be placed on the tongue, lip, or any other novel site that produces an adequate signal. Additional monitors, such as invasive arterial and/or venous pressure monitoring or bladder catheterization, may be considered but possibly delayed until after induction. Alligator clips attached to wet dressings usually provide adequate electrocardiographic tracings; these may be changed to needle electrodes once the child is anesthetized.

If possible, induction of anesthesia prior to transfer to the operating table is more comfortable for the child. If volume status is adequate, any induction agent may be used with careful titration to effect. If the patient has any evidence of myocardial depression or decreased intravascular volume, ketamine may be the preferred induction agent due to its sympathomimetic effects. High concentrations of volatile agents should be used with caution while monitoring for myocardial depression. In any case, induction agents should be carefully titrated to effect.

A poor mask fit due to facial edema, burns, or bulky dressings may complicate management of an already difficult airway. Due to airway edema, intubation may be difficult for the first 5 to 7 days after acute burn injury, especially if the patient has sustained an inhalation injury (see sections on pathophysiology and airway management). Inelastic eschar around the mouth of a child with facial burns may limit mouth opening and jaw mobility. If difficult airway maintenance or intubation is anticipated, spontaneous ventilation should be maintained until the airway is secured. Judicious use of ketamine or a controlled inhalation induction may be useful in this regard.

Staged early excision and grafting require numerous trips to the operating room, possibly four or five times in a week. While data are sparse, there is concern that the repetitive intubation/extubation sequence has the potential to cause laryngeal injury, especially to the already inflamed airway ( Colice et al., 1986 ). With this in mind, McCall and others (1999) advocate the use of the LMA for intraoperative airway management of these patients whenever possible. In their study, using the LMA in 88 pediatric burn patients for 141 general anesthetics, 20% of the patients required a minor intraoperative airway intervention (most commonly reseating or repositioning of the LMA after intraoperative patient position changes), but only 2% required LMA removal and intubation ( McCall et al., 1999 ). Of note, no patient sustained airway injury or aspirated, despite the fact that many patients were placed in the lateral or prone position.

Whether airway maintenance is performed with an endotracheal tube or an LMA, it is often difficult to secure the device due to facial burns and/or dressings. Twill tape may be tied around the child's neck, or cloth tape may be stapled to the face. Staples leave very little in the way of scarring, especially when used in an area that is to be excised in the future. During the course of burn surgery, the child may be repositioned on the operating table numerous times; the airway must be well secured. If long-term intubation is anticipated, a nasal endotracheal tube may be preferable for patient comfort, stability, mouth care, and potential ability to communicate by lip reading.

The child with a major burn has a high cardiac output and increased levels of oxygen consumption and CO2 production requiring the minute ventilation at least twice normal. Failure to adjust intraoperative ventilation accordingly leads to hypercapnia and hypoxemia. The child with an inhalation injury or acute respiratory distress syndrome may have noncompliant lungs; the child with an extensive burn of the trunk may have a noncompliant chest wall. Both conditions require higher-than-usual airway pressures and PEEP to maintain acceptable ventilation and gas exchange. End-tidal PCO2 monitoring may underestimate arterial PCO2 due to an increase in physiologic dead space and shunt. If the anesthesia machine ventilator is not capable of delivering the required pressures, an intensive care unit ventilator may be used. In the burned child with respiratory failure, it may be necessary to use a noncompliant anesthesia circuit and a cuffed endotracheal tube to allow delivery of adequate ventilator pressures.


Maintenance of anesthesia may be accomplished by a number of techniques, including nitrous oxide/opioid, ketamine, propofol, volatile anesthetic agent, or a combination dictated by the child's overall clinical condition. If opioids, benzodiazepines, vasopressors, or inotropic agents are infused preoperatively, they most likely should be continued into the intraoperative and postoperative periods. When dosing analgesics and muscle relaxants, it must be remembered that the child with a burn may have increased requirements due to altered metabolism, pharmacokinetics, and pharmacodynamics. If ketamine is used for maintenance during long procedures, it may result in prolonged emergence. Hallucinations and other unpleasant emergence phenomena may occur, especially in the older child and teenager who receive ketamine; the incidence of these side effects may be reduced by the addition of a benzodiazepine or propofol.

The metabolic demands of the child must be met even while in the operating room. The child must be kept warm, as each calorie lost to the environment is a calorie lost to wound healing. The operating room must often be kept uncomfortably warm; fluids and blood must also be warmed. Consideration should also be given to using warming blankets and warmed and humidified inspired gases and covering the child with plastic or thermal blankets (especially the head). Forced warm air devices are difficult to use in this environment due to the large amount of body surface exposed.

Nutrition must be maintained as well as possible to minimize protein catabolism and promote wound healing. Children with extensive burns require enteral feedings. Nutrition is usually supplied through a nasoduodenal tube. In this setting, because this tube exits distal to the pylorus, feedings can be continued throughout the perioperative period including the intraoperative period as long as the nasogastric tube aspirate does not contain tube-fed material. This practice is essential to maintain caloric balance in these hypermetabolic children and has not led to an increase in aspiration or other complications. Adequate pain control, a warm environment, and early wound closure all help reduce the catabolic state of these children.


Blood loss during burn excision is likely to be rapid and extensive. Quantity of loss is difficult to estimate because much of the hemorrhage ends up on the table, in the drapes, or on the floor. One may calculate appropriate preoperative blood ordering by estimating that 3% of the child's blood volume is lost for every 1% of the body surface excised ( Housinger et al., 1993 ). Thus, an excision of a 20% TBSA burn results in a loss of 60% of the child's blood volume. Burns of the face, head, and neck produce even greater blood loss when excised. During skin grafting, which typically occurs 1 day after excision, one should expect the blood loss to be two thirds the amount that occurred during the prior excision (i.e., 2% of blood volume lost for every 1% of the body grafted). As blood loss occurs quickly, transfusion should begin before the patient arrives in the operating room and additional units of blood should be immediately available and checked. Needless to say, blood and blood products should be warmed due to the rapidity of transfusion. Adequacy of transfusion may be assessed by clinical signs such as blood pressure, heart rate, peripheral perfusion, urine output, and arterial or central venous pressure monitoring.

If transfusion exceeds one blood volume, one must consider the alterations in coagulation and metabolism that may occur. Administration of calcium may be required due to the quantity of citrate preservative in the banked blood. Platelets, fibrinogen, and other clotting factors may require replacement. The complications of major transfusion are discussed in detail elsewhere (see Chapter 12 , Blood Conservation). Intraoperative laboratory determination of hemoglobin level may be helpful but should be repeated several hours postoperatively, as blood loss and other major fluid shifts may continue during this time. Although attempts are made to limit transfusion as much as possible, a hematocrit of at least 30% is recommended in children with large burns to maintain adequate oxygen-carrying capacity.

Adequate venous access is mandatory. Catheters must be as large as possible. Peripheral venous access is acceptable, but sites are limited in children with major burns. Central venous catheters are preferable and lead to few complications provided they are moved to a new site on a regular basis. Central venous catheters may be inserted through burned tissue if necessary.

The surgeon may be able to decrease blood loss to some extent by the subcutaneous infusion of an isotonic crystalloid solution into the burn wound to be excised. This solution is infused by roller pump and contains 1 to 2 mg of epinephrine/L, thus decreasing blood flow to the area via a hydrostatic and a vasoconstrictor mechanism. The amount of this solution infused may exceed the patient's blood volume, but despite the massive amount of volume and epinephrine delivered, few adverse effects are noted clinically, probably due to the loss from the surgical site and the slow uptake of the solution. This same solution is also used to prepare intact skin for harvest of split-thickness skin grafts.

In summary, the key to maintaining adequate circulating blood volume during a major burn excision is to anticipate the need for rapid transfusion. Beginning transfusion before surgery may be justified, even if the preoperative hematocrit is above 30%. Published studies have demonstrated complications related to blood loss may be reduced by limiting the length of the procedure to less than 2 hours, the area excised to less than 15% of the body surface area, and the blood loss to less than 50% of the patient's blood volume ( Engrav et al., 1983 ). These are practical suggestions, but they are often difficult to carry out in practice.


High levels of postoperative pain must be anticipated. Preoperative infusions of opioids, anxiolytics, and other sedatives should be continued throughout the perioperative period. Additional opioids and sedatives should be titrated intraoperatively according to patient response, keeping in mind the increased dosing requirements and altered pharmacokinetics of the child with a major burn.

It is well recognized that donor site pain is the most intense that the burned child experiences. As mentioned, an isotonic crystalloid solution is infused into donor site tissues prior to skin harvesting. In order to decrease postoperative pain from these donor sites, an addition of 2 to 2.5 mg/kg of bupivacaine to the solution to be infused is recommended. The safety and efficacy of this practice have been confirmed through assays of bupivacaine blood levels and effective postoperative pain control (unpublished observations). Even very dilute solutions of subcutaneous bupivacaine are found to be very effective in reducing donor site pain.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


As one can well imagine, major burns, especially in children, in some respects may present a lifetime of care due to the need for scar revisions, psychological support, and in many cases cosmetic surgery to help make the patient more comfortable in the acts of daily living.

These patients with burns continue to present the anesthesiologist/anesthetist with potentially serious problems in the operating room; especially those who have had major burns of the face and head come readily to mind. There may be contractures of the mouth, making access for the airway extremely difficult. Neck contractures can significantly impede visualization of the glottis and intubation. One must plan ahead in preparing for a procedure that includes various means and instruments to aid in securing a safe, effective airway.

In cases of microstomia with scarred nares or marked scarring in the oropharynx ( Fig. 29-7 ), a technique of anesthetic care might be needed in which the mouth opening is enlarged prior to endotracheal intubation. One approach is a technique of intravenous sedation, including ketamine, and then injections of local anesthetic with epinephrine into the oral commissures and cheek. The surgeon then makes surgical incisions in order to enlarge the mouth opening, making oral intubation possible. This technique, although not presented in the literature, has worked well at the institution where surgeons and anesthesiologists have worked together for many years. One must be aware in using this technique, however, that if the condition has persisted for a long time, the temporomandibular joint may be involved and there may still be limitations in the mouth opening.


FIGURE 29-7  Marked scarring of the oropharynx after lye ingestion. Oral opening 6 mm by 10 mm. The child could only eat “one half of an M and M” according to the mother.



Many of these children have undergone numerous surgical procedures in the past, including those during the acute phase of treatment. Many are, therefore, very anxious preoperatively and need reassurance as well as satisfactory preoperative medications. Intravenous access can also be a challenge in these patients, due to the burns and grafting procedures that obliterate peripheral sites. As in many children, these individuals often are afraid of needles and a mask induction may be preferred.

In the reconstructive phase of burn treatment, anesthetic choices are those preferred by the anesthesiologist and the patient and those that are compatible with the procedure being performed. These choices include any and all that would be used in the everyday anesthetic management of the child.

The incidence of nausea and vomiting is extremely high in the postoperative period in this patient population. In the scalp-expander group, prior to instituting a rigorous regimen of antiemetic drugs, the incidence was nearly 100% ( Stubbs, 1999) . However, this problem is seen in many pediatric hospitals where the incidence of nausea and vomiting is reported to be high, especially with certain procedures such as tonsillectomy/adenoidectomies (40% to 88%) ( Carithers et al., 1987 ; Sukhani et al., 2002 ) and strabismus surgery (50% to 80%) ( Watcha et al., 1991 ; Gurkan et al., 1999 ). The propofol-based anesthetic technique has markedly decreased postoperative nausea and vomiting, even with a background infusion of 10 to 20 mcg/kg per min.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


Care of the burn patient, especially those children with major burns, demands a meticulous approach by a multidisciplinary team of physicians, nurses, pharmacists, physical therapists, blood bank and laboratory technicians, and social workers. These children and their families require multiple hours of attention for not only their medical care but also for the psychologic support of both the patient and his or her family. This is important during the acute phases of burn care but also may stretch into many years of contact during the physical maturing of the burn scars, with the attendant releases mandated not only by dense scar tissue but also the psychologic maturing of both the patient and his or her family. Although these patients may be readily accepted in the hospital setting, returning to community living presents its own problems for both the patient and the family. The anesthetic management must be geared to the constantly changing physical condition of the patient. Even the burn patient who returns after the acute phase of treatment for reconstructive procedures may well challenge the anesthesiologist in safely securing the airway and certainly in being able to secure vascular access. Although most anesthesiologists have limited contact and experience with burn patients, it must be kept in mind that they might be called on, at any time, to help in the initial resuscitation of a burn victim as well as in securing the airway.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


We offer special thanks to Ms. Linda Holbrook for her excellent administrative support.

Copyright © 2008 Elsevier Inc. All rights reserved. -

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier


Aikawa et al., 1990. Aikawa N, Wakabayashi G, Ueda M, et al: Regulation of renal function in thermal injury.  J Trauma  1990; 30:S174.

Artz and Moncrief, 1969. Artz CP, Moncrief JA: The burn problem.   In: Artz CP, Moncrief JA, ed. The treatment of burns,  Philadelphia: WB Saunders; 1969:1-22.

Bohrer et al., 1997. Bohrer H, Qui F, Zimmerman T, et al: Role of NFκB in the mortality of sepsis.  J Clin Invest  1997; 100:972.

Boutros and Hoyt, 1976. Boutros AR, Hoyt JR: Management of carbon monoxide poisoning in the absence of hyperbaric oxygen chamber.  Crit Care Med  1976; 4:144.

Carithers et al., 1987. Carithers JS, Gebhart DE, Williams JA: Postoperative risks of pediatric tonsilloadenoidectomy.  Laryngoscope  1987; 97:422.

Colice et al., 1986. Colice GL, Munster AM, Haponik EF: Tracheal stenosis complicating cutaneous burns: An underestimated problem.  Am Rev Respir Dis  1986; 134:1315.

Crapo, 1981. Crapo RO: Smoke inhalation injuries.  JAMA  1981; 246:1694-1696.

Czermak et al., 1999. Czermak BJ, Sarma V, Pierson CL, et al: Protective effects of C5a blockade in sepsis.  Nature Med  1999; 5:788.

de Campo and Aldrete, 1981. de Campo T, Aldrete JA: The anesthetic management of the severely burned patient.  Intensive Care Med  1981; 7:55-62.

Deitch and Sittig, 1993. Deitch EA, Sittig KM: A serial study of the erythropoietic response to thermal injury.  Ann Surg  1993; 217:293.

Demling, 1984. Demling RH: Effect of early burn excision and grafting on pulmonary function.  J Trauma  1984; 24:830.

Demling, 1985. Demling RH: Burns.  N Engl J Med  1985; 313:1389.

Dwersteg et al., 1986. Dwersteg JF, Pavlin EG, Heimbach DM: Patients with burns are resistant to atracurium.  Anesthesiology  1986; 65:517.

Eckhauser et al., 1974. Eckhauser FE, Billote J, Burke JF, et al: Tracheostomy complicating massive burn injury. A plea for conservatism.  Am J Surg  1974; 127:418.

Engrav et al., 1983. Engrav LH, Heimbach DM, Reus JL, et al: Early excision and grafting vs. nonoperative treatment of burns of indeterminate depth: A randomized prospective study.  J Trauma  1983; 23:1001.

Falkner et al., 1978. Falkner B, Roven S, DeClement FA, et al: Hypertension in children with burns.  J Trauma  1978; 18:213.

Feck and Baptiste, 1979. Feck G, Baptiste MS: The epidemiology of burn injury in New York.  Public Health Rep  1979; 94:312.

Fein et al., 1980. Fein A, Leff A, Hopewell PC: Pathophysiology and management of the complications resulting from fire and the inhaled products of combustion: review of the literature.  Crit Care Med  1980; 8:94.

Goldbaum et al., 1976. Goldbaum LR, Orellano T, Dergal E: Mechanism of the toxic action of carbon monoxide.  Ann Clin Lab Sci  1976; 6:372.

Greenblatt et al., 1983. Greenblatt DJ, Shader RI, Abernethy DR: Current Status of benzodiazepines.  N Engl J Med  1983; 309:354.

Gronert, 1999. Gronert GA: Succinylcholine hyperkalemia after burns.  Anesthesiology  1999; 91:320.

Gronert et al., 1967. Gronert GA, Schaner PJ, Gunther RD: Multiple halothane anesthesia.  Pacif Med Surg  1967; 75:28.

Gronert and Theye, 1975. Gronert GA, Theye RA: Pathophysiology of hyperkalemia induced by succinylcholine.  Anesthesiology  1975; 43:89.

Grube et al., 1988. Grube BJ, Marvin JA, Heimbach DM: Therapeutic hyperbaric oxygen: Help or hindrance in burn patients with carbon monoxide poisoning?.  J Burn Care Rehabil  1988; 9:249.

Gurkan et al., 1999. Gurkan Y, Kilickan L, Toker K: Propofol-nitrous oxide versus sevoflurane-nitrous oxide for strabismus surgery in children.  Paediatr Anaesth  1999; 9:495.

Heatherill et al., 1986. Heatherill RJ, Till GO, Burner LH, et al: Thermal injury, intravascular hemolysis, and toxic oxygen products.  J Clin Invest  1986; 78:629.

Heideman, 1979. Heideman M: The effect of thermal injury on hemodynamic, respiratory and hematologic variables in relationship to complement activation.  J Trauma  1979; 19:239.

Herndon et al., 1985. Herndon DN, Thompson RB, Traber DL: Pulmonary injury in burned patients.  Crit Care Clin  1985; 1:79.

Herndon et al., 1986. Herndon DN, Traber LD, Linares H, et al: Etiology of the pulmonary pathophysiology associated with inhalation injury.  Resuscitation  1986; 14:43.

Holm et al., 1999. Holm C, Horbrand E, von Donnersmarch GH, et al: Acute renal failure in severely burned patients.  Burns  1999; 25:171.

Housinger et al., 1993. Housinger TA, Lang D, Warden GD: A prospective study of blood loss with excisional therapy in pediatric burn patients.  J Trauma  1993; 34:262.

Hunt et al., 1975. Hunt JL, Agee RN, Pruitt BA: Fiberoptic bronchoscopy in acute inhalation injury.  J Trauma  1975; 15:641.

Jelkmann et al., 1990. Jelkmann W, Wolff M, Fandrey J: Modulation of the production of erythropoietin by cytokines: in vitro studies and their clinical implications.  Contrib Nephrol  1990; 87:68.

Jenkins et al., 1994. Jenkins M, Gottschlich AM, Mayes T, et al: Enteral feeding during operative procedures.  J Burn Care Rehabil  1994; 15:199.

Jeschke et al., 1999. Jeschke MG, Herndon DN, Wolf SE, et al: Recombinant human growth hormone alters acute phase reactant proteins, cytokine expression and liver morphology in burn rats.  J Surg Res  1999; 83:22.

Jeschke et al., 2001. Jeschke MG, Low JFA, Spies M, et al: Cell proliferation, apoptosis, NF-kappaB expression, enzyme, protein, and weight changes in livers of burned rats.  Am J Physiol Gastrointest Liver Physiol  2001; 280:G1314.

Junger et al., 1997. Junger WG, Coimbra R, Liu FC, et al: Hypertonic saline resuscitation: A tool to modulate immune function in trauma patients?.  Shock  1997; 8:235.

Keens et al., 1978. Keens TG, Bryan AC, Levison H, et al: Developmental pattern of muscle fiber types in human ventilatory muscles.  J Appl Physiol  1978; 44:909.

Kowal-Vern et al., 1992. Kowal-Vern A, Gamelli RL, Walenga JM, et al: The effect of burn wound size on hemostasis: A correlation of the hemostatic changes to the clinical state.  J Trauma  1992; 33:50.

Laffon et al., 1999. Laffon M, Pittet J, Modelska K, et al: Interleukin-8 mediates injury from smoke inhalation to both the lung endothelial and alveolar epithelial barriers in rabbits.  Am J Respir Crit Care Med  1999; 160:1443.

Lawrence and Atac, 1992. Lawrence C, Atac B: Hematologic changes in massive burn injury.  Crit Care Med  1992; 20:1284.

Leibel et al., 1981. Leibel WS, Martyn JA, Szyfelbein SK, et al: Elevated plasma binding cannot account for the burn related d-tubocurarine hyposensitivity.  Anesthesiology  1981; 54:378.

Lightning-associated deaths–United States, 1980–1995. Lightning-associated deaths–United States, 1980–1995.  Morb Mortal Wkly Rep  1998; 47:391-394.

Lloyd, 1977. Lloyd JR: Thermal trauma: Therapeutic achievements and investigative horizons.  Surg Clin North Am  1977; 57:121.

Loirat et al., 1978. Loirat P, Rohan J, Baillet A, et al: Increased glomerular filtration rate in patients with major burns and its effect on the pharmacokinetics of tobramycin.  N Engl J Med  1978; 299:915.

Loke et al., 1984. Loke J, Paul E, Virgulto JA, et al: Rabbit lung after acute smoke inhalation.  Arch Surg  1984; 119:956.

MacLennan et al., 1998. MacLennan N, Heimbach DM, Cullen BF: Anesthesia for major thermal injury.  Anesthesiology  1998; 89:749.

Madden et al., 1986. Madden MR, Finkelstein JL, Goodwin CW: Respiratory care of the burn patient.  Clin Plast Surg  1986; 13(1):29.

Madjdpour et al., 2003. Madjdpour L, Kneller S, Booy C, et al: Acid induced lung injury.  Anesthesiology  2003; 99:1323.

Martyn, 1986. Martyn JA: Clinical pharmacology and drug therapy in the burned patient.  Anesthesiology  1986; 65:67.

Martyn, 1999. Martyn JA: Succinylcholine hyperkalemia after burns.  Anesthesiology  1999; 91:321.

Martyn et al., 1984. Martyn JA, Abernethy DR, Greenblatt DJ: Plasma protein binding of drugs after severe burn injury.  Clin Pharmacol Ther  1984; 35:534.

Martyn et al., 1983. Martyn JA, Greenblatt DJ, Quinby WC: Diazepam kinetics following burns.  Anesth Analg  1983; 51:293.

Martyn et al., 1983. Martyn JA, Liu LM, Szyfelbein SK, et al: The neuromuscular effects of pancuronium in burned children.  Anesthesiology  1983; 59:561.

Martyn et al., 1982. Martyn JA, Matteo RS, Lebowitz PW, et al: Pharmacokinetics of d-tubocurarine in patients with thermal injury.  Anesth Analg  1982; 61:241.

Martyn et al., 1982. Martyn JA, Matteo RS, Szyfelbein SK, et al: Unprecedented resistance to neuromuscular blocking effects of metocurine with persistence after complete recovery in a burned patient.  Anesth Analg  1982; 61:614.

Martyn et al., 1980. Martyn JA, Szyfelbein SK, Ali HH, et al: Tubocurarine requirement following major thermal injury.  Anesthesiology  1980; 52:352.

McCall et al., 1999. McCall JE, Fischer CG, Schomaker E, et al: Laryngeal mask airway use in children with acute burns: intraoperative airway management.  Paediatr Anaesth  1999; 9:515.

McDonald et al., 1991. McDonald W, Sharp D, Deitch E: Immediate enteral feeding in burn patients is safe and effective.  Ann Surg  1991; 213:177.

Merrell et al., 1986. Merrell SW, Saffle JR, Sullivan JJ, et al: Fluid resuscitation in thermally injured children.  Am J Surg  1986; 152:664.

Mills and Martyn, 1989. Mills AK, Martyn JA: Neuromuscular blockade with vecuronium in paediatric patients with burn injury.  Br J Clin Pharm  1989; 28:155.

Moncrief, 1973. Moncrief JA: Burns.  N Engl J Med  1973; 288:444.

Moncrief and Teplitz, 1964. Moncrief JA, Teplitz C: Changing concepts in burn sepsis.  J Trauma  1964; 4:233.

Moore et al., 1991. Moore SJ, Ho IK, Hume AS: Severe hypoxia produce by concomitant intoxication with sublethal doses of carbon monoxide and cyanide.  Toxicol Appl Pharmacol  1991; 109:412.

Navar et al., 1985. Navar PD, Saffle JR, Warden GD: Effect of inhalation injury on fluid resuscitation requirements after thermal injury.  Am J Surg  1985; 150:716.

Neely et al., 1988. Neely A, Nathen P, Highsmith R: Plasma proteolytic activity following burns.  J Trauma  1988; 28:362.

Palmieri et al., 2002. Palmieri TL, Jackson W, Greenhalgh DG: Benefits of early tracheostomy in severely burned children.  Crit Care Med  2002; 4:922.

Parks et al., 1977. Parks DH, Carvajal HF, Larson DL: Management of burns.  Surg Clin North Am  1977; 57:875.

Perry and Heidrich, 1982. Perry S, Heidrich G: Management of pain during débridement: A survey of U.S. burn units.  Pain  1982; 13:267.

Porter and Hick, 1980. Porter J, Hick H: Addiction rare in patients treated with narcotics.  N Engl J Med  1980; 302:123.

Pruitt et al., 1975. Pruitt BA, Erickson DR, Morris A: Progressive pulmonary insufficiency and other pulmonary complications of thermal injury.  J Trauma  1975; 15:369.

Pruitt et al., 1979. Pruitt BA, Flemma RJ, Divincenti , et al: Complications in burn patients.  J Thorac Cardiovasc Surg  1979; 59:7.

Roughton and Darling, 1944. Roughton FJW, Darling RC: The effect of carbon monoxide on the oxyhemoglobin dissociation curve.  Am J Physiol  1944; 141:17.

Rue et al., 1993. Rue III LW, Cioffi Jr WG, Mason Jr AD, et al: Improved survival of burned patients with inhalation injury.  Arch Surg  1993; 128:772.

Saffle et al., 2002. Saffle JR, Morris SE, Edelman L: Early tracheostomy does not improve outcome in burn patients.  J Burn Care Rehabil  2002; 23:431.

Saffle, 1998. Saffle JR: Predicting outcomes of burns.  N Engl J Med  1998; 338:387.

Sawada et al., 1984. Sawada Y, Momma S, Takamizawa A, et al: Survival from acute renal failure after severe burns.  Burns  1984; 11:143.

Simon et al., 1977. Simon TL, Curreri PW, Harder LA: Kinetic characterization of hemostasis in thermal injury.  J Lab Clin Med  1977; 89:702.

Slogoff et al., 1974. Slogoff S, Allen GW, Wessels JV, et al: Clinical experience with subanesthetic ketamine.  Anesth Analg  1974; 53:356.

Spooner et al., 1992. Spooner C, Markowitz N, Saravolatz L: The role of tumor necrosis factor in sepsis.  Clin Immunol Immunopathol  1992; 62:S11.

Stanski and Watkins, 1982. Stanski DR, Watkins DW: Drug disposition in anesthesia,  New York, Grune & Stratton, 1982.

Stewart et al., 1976. Stewart RD, Stewart RS, Stamm W, et al: Rapid estimation of carboxyhemoglobin level in fire fighters.  JAMA  1976; 235:390.

Stubbs et al., 1999. Stubbs TK, Saylors S, Jenkins M, et al: Pediatric patients experiencing postoperative nausea and vomiting after burn reconstruction surgery: an analysis.  J Burn Care Rehabil  1999; 20:236.

Sukhani et al., 2002. Sukhani R, Pappas AL, Lurie J, et al: Ondansetron and dolasetron provides equivalent postoperative vomiting control after ambulatory tonsillectomy in dexamethasone pretreated children.  Anesth Analg  2002; 95:1230.

Szyfelbein et al., 1993. Szyfelbein SK, Martyn JA, Coté CJ: Burn injuries.   In: Coté C, Ryan J, Todres I, et al ed. A practice of anesthesia for infants and children,  Philadelphia: WB Saunders; 1993:357-376.

Thompson et al., 1986. Thompson PB, Herdon DN, Traber DL, et al: Effect on mortality of inhalation injury.  J Trauma  1986; 26:163.

Tolmie et al., 1967. Tolmie JD, Joyce TH, Mitchell GD: Succinylcholine danger in the burned patient.  Anesthesiology  1967; 28:467.

Tominaga et al., 2000. Tominaga K, Yoshimoto T, Torigoe K, et al: IL-1 synergizes with IL-8 or IL-1β for IFN-γ production from human T cells.  Int Immunol  2000; 12:151.

Traber et al., 1988. Traber DL, Redl H, Schlag G, et al: Cardiopulmonary responses to continuous administration of endotoxin.  Am J Physiol  1988; 254:H833.

Trunkey, 1978. Trunkey DD: Inhalation injury.  Surg Clin North Am  1978; 58:1133.

Van der Poll and van Deventer, 1999. Van der Poll T, van Deventer S: Cytokines and anticytokines in the pathogenesis of sepsis.  Infect Dis Clin North Am  1999; 13:403.

Voss and Cotton, 1998. Voss M, Cotton M: Mechanisms and clinical implications of apoptosis.  Hosp Med  1998; 59:924.

Warden, 2002. Warden G: Fluid resuscitation and early management.   In: Herndon D, ed. Total burn care,  2n ed.. London: WB Saunders; 2002:88-90.

Warden et al., 1983. Warden GD, Stratta RJ, Laffle JR, et al: Plasma exchange therapy in patients failing to resuscitate from burn shock.  J Trauma  1983; 23:9456.

Warden, 2003. Warden GD: Words of wisdom,  8th ed.. Shriners Hospital for Children, 2003.

Watcha et al., 1991. Watcha MF, Simeon RM, White PF, et al: Effect of propofol on the incidence of postoperative vomiting after strabismus surgery in pediatric outpatients.  Anesthesiology  1991; 75:204.

White et al., 1982. White PF, Way WL, Trevor AJ: Ketamine: Its pharmacology and therapeutic uses.  Anesthesiology  1982; 56:119.

Wilmore et al., 1974. Wilmore D, Long J, Mason A, et al: Catecholamines: Mediators of the hypermetabolic response to thermal injury.  Ann Surg  1974; 180:653.

Wilmore and Aulick, 1978. Wilmore DW, Aulick LH: Metabolic changes in burned patients.  Surg Clin North Am  1978; 58:1173.

Wilmore et al., 1980. Wilmore DW, Goodwin CW, Aulick LH, et al: Effect of injury and infection on visceral metabolism and circulation.  Ann Surg  1980; 192:491.


If you find an error or have any questions, please email us at Thank you!