Chapter 124

Burns and Post-Burn Care: 

Anesthetic Considerations 

Marc-André Bernath, Pascal Stucki, and Mette M. Berger 

124 

CHAPTER 

INTRODUCTION 

Burn injury is frequent in the pediatric population. It ranks among 

the highest causes of death, usually after motor vehicle accidents, 

in both industrialized and developing countries worldwide: 1–6 the 

majority of victims are preschool-age males of low socioeconomic 

income. Most burn cases are scalds and involve only the skin, but 

some patients have an additional inhalation syndrome or multiple 

injuries that worsen prognosis. 

Although mortality has decreased over the last two decades, 

except for one study on a restricted number of patients concluding 

that young age is not a predictor of mortality in burns, 7 studies on 

larger cohorts found that equivalent burn injuries in children 

2050 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations 

TABLE 124-1. Physiologic Differences Between Children and Adults Affecting Burn Care 

System Characteristics Consequences 

Anatomy 

Fluid homeostasis 

Respiratory 

Cardiovascular 

Metabolism 

Renal 

Immunity 

Central nervous system 

Psychological 

Higher body surface to weight ratio 

Larger head compared to the rest of the body 

(19% in 4 years old vs 9% in adults) 

Larger fluid content, with larger extracellular 

compartment and larger circulating volume 

Narrow airways 

Limited respiratory reserve 

Large cardiovascular reserve (except for young 

infants and in case of previous cardiopathy) 

Lower systemic vascular resistances 

Higher basal metabolic rate 

Growth in process 

Greater sensitivity to osmolarity changes 

Lower sodium clearance (infancy) 

Immune response not mature 

Stronger acute phase response (except during the 

first months) 

Better tolerance to hypoxia 

Greater cerebral plasticity 

Difficulty to express pain and emotional reactions 

Larger evaporation: administration of 

fluids must be extremely precise 

Different estimation of burned surface 

(normograms) 

More sensitive to fluid shifts and overload 

High risk of airway obstruction 

Higher rates of respiratory failure 

Good hemodynamic tolerance to fluids 

Left ventricle more susceptible to hypertension 

Larger energy and nutrient requirements 

per kg 

Risk of stunting, delayed bone formation 

More difficult management of hypernatremia 

Greater susceptibility to infection 

Fewer neurologic sequelae 

Difficulty in pain assessment 

Undertreatment of pain 

where K f 

= capillary filtration coefficient an index of the total 

number of filtering pores; P c 

and P if 

= the hydrostatic pressures of, 

respectively, intracapillary and interstitial spaces; s = the osmotic 

reflection coefficient, an index of the microvascular permeability 

to proteins; and π p 

– π if 

= the oncotic pressures of, respectively, 

plasma and interstitial fluid. Burn injury is unique in that it 

significantly modifies all these factors toward increased susceptibility 

of edema formation (Figure 124–1): indeed, K f 

, P c 

and 

π if 

increase as s, P if 

,andπ p 

decrease. 

Generalized edema will occur with large burns and will most 

often develop over the first 12 to 24 hours following the injury. 

The net water accumulation arises from an increased filtration rate 

with a decrease in both fluid reabsorption and lymph flow at the 

whole body level. 14 This fluid extravasation causes a hypovolemic 

shock. At the cellular level, a decrease in skeletal muscle membrane 

potential has been documented in patients with burns 

involving 20 to 55% BSA, in parallel with decreases in muscle 

intracellular sodium levels and increases in intracellular potassium 

and water contents. These alterations result from a decreased cell 

membrane adenosine triphosphatase activity. 15 The changes affect 

nearly any organ, and alterations of membrane potential have been 

measured in the hepatocyte, the enterocyte, the heart, and skeletal 

muscle. Investigators utilizing animal models and clinical studies 

involving human primates have produced a large body of information 

suggesting that apoptosis is associated with most of the 

tissue damages triggered by severe thermal injuries. 16 

Inflammatory and Immune Response 

Any aggression induces an inflammatory response, which 

constitutes an organized defense mechanisms intended to protect 

the body from further damage, to restore homeostasis and to 

promote wound repair. It includes a local reaction to injury, a systemic 

response (tachycardia, tachypnea, fever), cytokine production, 

leukocyte changes, endocrine changes, protein alterations 

with a reprioritization of hepatic synthesis, and redistribution of 

the micronutrients, including trace elements from the vascular 

compartment to the liver and reticuloendothelial system. Cytokine 

production is strongly enhanced after major burns, the balance 

between proinflammatory and anti-inflammatory mediators in 

acute injury being lost; 17 the phenomenon is further increased in 

case of infection. The intensity of this reaction is correlated with 

mortality. 18 Although the initial acute phase response is perceived 

as beneficial, its persistence for prolonged periods of time causes 

progressive loss of lean body cell mass, particularly of skeletal 

muscle, and an increased susceptibility to infection. It will favor 

organ dysfunction, and eventually organ failure. 

In clinical settings, the detectable changes are increases in 

C-reactive protein, ceruloplasmin, and fibrinogen, associated with 

decreases in transferrin, prealbumin, and albumin. It is important 

to suspect infection as coresponsible for this unspecific response, 

to identify the responsible microorganism, and to treat the infection. 

19 During the acute phase, reactive oxygen species (ROS, also 

called free radicals) production is markedly increased. ROS are 

produced primarily by the mitochondrial respiratory chain, and by 

the activated leukocytes. This is a normal phenomenon favoring 

bacterial destruction and cell signaling. The endogenous antioxidant 

defense mechanisms are usually sufficient to cope with 

moderate overproduction. When this defense is overwhelmed, as 

in severe burns, the deleterious effects of ROS appear, with 

proximity oxidation of nucleotides, proteins, and lipids. Burns are 

characterized by an intense lipid peroxidation, due partially to the 

direct effect of the burn on the lipids contained in skin, but also 

through an increased production of free radicals (mainly the anion

CHAPTER 124 ■ Burns and Post-Burn Care: Anesthetic Considerations 2051 

Figure 124-1. Schematic diagram of edema 

formation after burns. Under normal conditions, 

there is a slight imbalance of the Starling 

equation favoring filtration (flow across the 

capillary wall = Jv), which is entirely evacuated 

by the lymphatic flow (J L 

). After burns, the various 

factors of the equation increase, inducing 

an increase in net filtration in excess of lymph 

flow capacity and resulting in edema formation. 

The interstitial proteins undergo transformations 

contributing to the increase in oncotic 

pressure. (P c 

and P if 

= capillary and interstitial 

hydrostatic pressures). 

OH–). Topical antioxidant treatments have been proposed but 

have not entered routine protocols. Other therapeutic tools are 

under investigation (see “Metabolic and Nutritional support”). 

Damage to distant tissues occurring with burns is partly attributable 

to the lipid peroxides generated in the burn wound. This 

favors occurrence of organ dysfunction. Early wound excision has 

been advocated on this basis to reduce the release of lipid peroxide. 

Early debridement has contributed to the reduction of burn 

mortality. 

Immune System 

An overall depression of the immune system starts within the first 

hours of burn injury. Both humoral and cellular responses are 

strongly depressed, 20 with reduced numbers of lymphocytes, 

reduced macrophage and neutrophil counts (and activity), and 

decreased concentrations of opsonins, immunoglobulins, and 

chemotactic factors. These alterations persist for weeks and render 

the burned patient particularly sensitive to infections. Aseptic 

handling is therefore mandatory, requiring nurses and doctors to 

perform strict aseptic techniques. Early and daily hydrotherapy 

consists of extensive wound scrubbing in a bath. This is usually 

undertaken under heavy sedation or general anesthesia. Many 

attempts have been made at restoring immunity. Surgery is an 

important contributing factor: early excision has been shown to 

accelerate the normalization of antibody synthesis. 21 Trace element 

deficiencies have long been known to decrease immune response. 

Restoring the copper, selenium, and zinc level using large supplements 

during the first week postinjury leads to an improved 

neutrophil response and to a reduction in infectious complications, 

particularly of pneumonia. 22 

Cardiovascular System 

Almost immediately after injury, massive fluid shifts occur due to 

the loss of vascular and endothelial integrity. The magnitude of 

the capillary leak is such that proteins up to 300,000 Kd pass the 

endothelial barrier during the first hours postinjury. Impermeability 

to albumin-sized molecules is restored only by 36 hours 

post-burn. 23 The total amount of fluid lost as exudates is about 

1 L/10% BSA in adults, with a protein content reaching 30 g/L. 14 

This protein loss via the wound exceeds normal protein intake in 

healthy subjects. Some of the exudate evaporates from the wound, 

leading to more fluid loss. These fluid losses will rapidly cause 

hypovolemia with circulatory failure, which, depending on the 

burn size and initial resuscitation, may persist for 72 hours post– 

initial burn injury. 24 

The hemodynamic evolution is summarized in Table 124–2. 

Burn shock is characterized by a profound reduction in cardiac 

output (carbon monoxide, CO) that occurs within minutes of 

injury. Initially, the systolic blood pressure and heart rate (HR) are 

preserved, while the systemic vascular resistance increases twoor 

threefold, the pulmonary vascular resistance increasing even 

more. 23 This early vasoconstrictive response is mediated by 

catecholamines, vasopressin, and thromboxane A 2 

(TXA 2 

). The 

loss of intravascular volume causes a reduction of ventricular 

filling pressure, resulting in low CO. Loss of myocardial con- 

TABLE 124-2. Summary of Hemodynamic and Metabolic 

Changes After Major Burns 

Variable 

0–24 Hours 24–72 Hours* >72 Hours 

Hemodynamics 

MAP no no, ↓ ↓, no, ↑ 

Heart rate ↑↑ ↑ no, ↑ 

CVP ↓ no, ↓ no, ↑ 

SVR + PVR ↑↑↑ ↑, no no, ↓ 

Vascular permeability ↑↑↑ ↑ no 

Cardiac output + CI ↓↓ no, ↑ no, ↑ 

SVI + LVSWI ↓↓ no no 

Metabolism 

VO 2 

↓ ↑ ↑↑↑ 

Energy expenditure ↓ no, ↑ ↑↑↑ 

Core temperature no, ↓ no, ↑ ↑↑ 

*Expected changes in case of successful resuscitation. In case of delayed fluid 

resuscitation or with heart failure, the picture differs. 

MAP = mean arterial pressure; CVP = central venous pressure; CI = cardiac 

index; SVR = systemic vascular resistances; PVR = pulmonary vascular 

resistance; SVI = stroke volume index; LVSWI = left ventricular stroke work 

index; VO 2 

= oxygen consumption.


tractility, alteration of ventricular compliance, and increase of 

afterload further contribute to the reduction of cardiac output. 

The reduction in cardiac output is detectable within minutes, 

before any decrease in plasma volume is detectable, implicating 

some form of direct myocardial depression in addition to the 

catecholamine effect. Plasma levels of cardiac troponin l (cTnI), a 

marker of nonischemic cardiac injury, was found to be elevated in 

burned subjects between the 5th and the 14th day postinjury. 25 

Animal studies suggest that humoral factors are involved; 26 a 

myocardial depressant factor has indeed been isolated in the 

serum of injured animals. Likely depressant humoral mediators 

are tumor necrosis factor (TNF), interleukins, vasopressin, and 

oxygen free radicals. Mechanisms of burn-related cardiac dysfunction 

may involve mitochondrial injury from oxidative stress. 

Membrane potential depression in heart and skeletal muscle fibers 

initiating shock can indeed be counteracted by the administration 

of free radical scavengers, such as glutathione peroxidase, catalase, 

and superoxide dismutase. 15,27 Mesenteric lymph from burn 

animals used at concentrations varying from 0.1 to 5%, but not 

from control sham-burn animals, induced dual positive and 

negative inotropic effects depending on the concentrations used. 

These burn lymph-induced changes in cardiac myocyte Ca 2+ 

handling can contribute to burn-induced contractile dysfunction 

and ultimately to heart failure. 28 Animal studies have confirmed 

clinical findings, that the association of burn, with either smoke 

inhalation, sepsis, or exposure to lipopolysaccharides enhance 

myocardial dysfunction. 29–33 

At the microcirculatory level, loss of plasma causes increased 

viscosity with a high hematocrit. This is an additional cause of the 

observed reduction in coronary blood flow, shifting the myocardium 

towards anaerobic metabolism. 

The myocardial depression is mainly left-sided: the cardiac 

index (CI), stroke volume index (SVI), and left ventricular stroke 

work index (LVSWI) are severely depressed. It has been implicated 

in adults as contributing to refractory burns shock, and occurs in 

pediatric patients as well. 34 In summary, the acute phase of burns 

combines features of both hypovolemic and cardiogenic shock, 

which must be considered during resuscitation (see “Fluid Resuscitation”). 

Over the next days (2 to 5 days after the initial insult), 

depending on the efficiency of the initial resuscitation, the patient 

will develop a hypermetabolic state, called the flow phase. This 

may result in a two- to threefold increase in CO and oxygen consumption, 

which will persist for weeks. It is generally associated 

with a moderate reduction in systemic vascular resistances, but 

may become very severe in the presence of sepsis. This second 

phase has hemodynamic features similar to those of a septic shock, 

with increased CI, normal SVI, and low systemic vascular 

resistance. In children, episodic or persistent arterial hypertension 

is frequent both during the acute and the convalescence phases; it 

is frequently associated with hypervolemia and is possibly related 

to increased renin and catecholamine production. 35 

Respiratory System 

Inhalation Injury 

Smoke inhalation and respiratory complications are still major 

causes of mortality in severely burned patients. Respiratory distress 

occurs through one or several of the following mechanisms: 

mechanical (airway obstruction), toxic (corrosion and intoxication), 

inflammatory (cytokines), and infectious. 36 Inhalation 

injury is defined as acute respiratory tract damage of variable 

severity caused by inspiration of steam or toxic inhalants such as 

fumes (small particles dispersed in air), gases and mists (aerosolized 

irritants or cytotoxic liquids; Table 124–3). 37 The diagnosis 

is suspected clinically on the basis of history and physical 

examination and can be confirmed by bronchoscopy. Respiratory 

failure in burned patients occurs through a number of associated 

mechanisms. Acute respiratory distress syndrome (ARDS) is a 

common early complication. Tracheal stenosis can occur as a late 

complication of prolonged mechanical ventilation. Clinical and 

experimental studies have shown that damage to the mucosal 

barrier and the release of inflammatory mediators are the most 

important pathophysiologic events following smoke inhalation. 

Manipulation of the inflammatory response following inhalation 

may become a future treatment option. 36 

Even in the absence of inhalational injury, acute lung injury is 

a common cause of morbidity and mortality for patients sustaining 

severe burns. A review in 2002 of numerous clinical and 

laboratory studies have implicated TNF-α and neutrophils as 

important participants in the pathogenesis of burn-induced lung 

injury. The mechanism by which these and other proinflammatory 

mediators affect the movement of fluid and protein across the 

microvascular barrier into the interstitium of lung remained 

unclear. 38 

A recent study on adult burned patients requiring mechanical 

ventilation found a correlation between early onset of ARDS, 

changes in white blood cell count and organ dysfunction. Although 

multifactorial, the pathogenesis of post-burn respiratory dysfunction 

favors an inflammatory process mediated by the effect of 

the burn itself, rather than being secondary to sepsis. 39 

The lung plays a major role in post injury multiple organ failure 

(MOF). In a prospective study on 1344 trauma patients at risk for 

postinjury MOF, lung dysfunction was observed in 94% of patients 

presenting with one or more organ dysfunctions and in 99% of 

patients with two or more organ dysfunctions. The severity of 

other organ dysfunction related directly to the severity of respiratory 

dysfunction. 40 

Renal System 

Acute renal failure (ARF) occurring after burn injuries is a threatening 

complication, since it is still related with a high mortality 

rate. Aggressive fluid resuscitation remains the best preventive tool 

of ARF. 41 Before 1983, mortality was 100% in burned children with 

concomitant ARF, and has decreased to 56% since 1984. 42 Indeed 

ARF occurs in 14.5% of patients with electrical burns 43 (see 

“Electrical Injuries”), and a mortality rate of 59% remains similar 

to other causes of ARF despite intensive care support including 

hemodialysis or peritoneal dialysis. Delayed initiation of intravenous 

fluid resuscitation is an important causing factor of ARF 

and is related to overall mortality. 41,44 

After burn injury, there is an immediate reduction in renal 

blood flow mediated by TXA 2 

which lasts a few hours. 45 Hypovolemia 

and decreased cardiac output further decrease the renal 

blood flow and cause filtration failure and tubular dysfunction. In 

response to hypovolemia, fluid retention mechanisms are activated, 

with elevation of antidiuretic hormone, aldosterone, and 

renin activity. 46 Free hemoglobin and myoglobin further contribute 

to tubular dysfunction. Rhabdomyolysis occurs to some 

extent in any burn patient, but is particularly pronounced in case 

of crush syndrome or electrical burns.

TABLE 124-3. Principal Toxic Gases 

Acrolein 

Acrylonitriles 

Aldehydes 

Ammonia (NH 3 

) 

Chlorine (Cl 2 

) 

Cyanide 

Hydrogen cyanide (HCN) 

Formaldehyde 

Nitrogen oxides (NO, NO 2 

) 

Phosgen (COCl 2 

) 

Sulfide dioxide (SO 2 

) 


Characteristic Origin Acute Effects 

Highly irritating to mucous 

membranes 

Colorless, highly-water 

soluble gas. Forms 

ammonium hydroxide: 

highly irritating to any 

mucous membrane 

Heavy, greenish yellow gas, 

highly reactive 

Colorless, water soluble gas, 

bitter almond smell 

Colorless, dense, nonflammable 

gas 

Red-brown, heavy, insoluble, 

irritating gas 

Colorless, heavy, insoluble gas. 

Hydrolyses to form HCl, 

extremely irritating 

Colorless, heavy, irritating gas, 

pungent odor 

Cellulose from paper, wood, 

cotton, jute. Acrylics in 

textiles, wall coverings, 

paintings. Polyurethane, 

home furnishing 

Polyamide in carpets, closing. 

Wool, nylon and silk in 

blankets, clothing, and 

furniture 

Mixing of household products 

Polyamide and polyurethane 

from insulation material 

Melamine resins in household 

and kitchen goods, foam 

insulation 

Fabrics and nitrocellulose films 

Floor, wall, furniture coverings, 

wrappings, wire/pipe coating 

Rubber in tires and toys 

Severe inflammatory reaction: 

tracheobronchitis 

Airway obstruction, pulmonary 

edema, bronchopneumonia 

Airway obstruction, pulmonary 

edema, ulcerative tracheobronchitis 

Asphyxia 

Irritating 

Acute pulmonary edema 

bronchiolitis 

Atelectasis, acute pulmonary 

edema, bronchiolitis, 

ulcerative bronchiolitis 

Bronchoconstriction, mucosal 

sloughing, alveolar edema 

and hemorrhage 

Splanchnic Compartment 

The gut has long been identified to be directly affected by burn 

injury, with the description of Curling ulcer in the 1970s. 47 The 

abdominal compartment syndrome (ACS) has become a matter 

of concern in both adult and pediatric burns. 48,49 In one report, 

eight out of 48 patients with a mean total BSA (TBSA) burned of 

46% developed ACS. All patients with ACS received resuscitation 

volumes of 300 mL/kg per day or greater. 49 The other report 

compared hypertonic resuscitation with “Parkland” resuscitation 

in terms of decreasing the risk for ACS. The hypertonic group 

maintained adequate urine output with lower volumes of resuscitation 

and had a lower incidence of intra-abdominal hypertension 

(2/14 vs 11/22). As in their other report, the critical volume 

associated with development of intra-abdominal hypertension was 

approximately 300 mL/kg per day—this number is now called the 

Ivy index. 

Alterations in distribution of blood flow occur in the early postburn 

period and are caused by neurogenic and humoral release of 

catecholamines and prostanoids. Initially, splanchnic blood flow is 

reduced, except for flow to the adrenals and to the liver. TXA 2 

is 

likely to play a major role in gut dysfunction, promoting mesenteric 

vasoconstriction, and decreasing gut blood flow. Poorly 

perfused organs shift towards anaerobic glycolysis, promoting 

metabolic acidosis. With aggressive fluid resuscitation, perfusion 

can be restored to a great extent. The gastrointestinal function, 

including the pyloric function, is depressed immediately after 

burns. A true paralytic ileus will install for many days if the gastrointestinal 

tract is not used; early gastric nutrition is associated 

with maintenance of pyloric function. 50 Opiates and sedatives 

further depress the gastrointestinal function. Stress ulcer prophylaxis 

is mandatory from puberty on (e.g., sucralfate), since 

the bleeding risk is elevated in burn injuries and may be lifethreatening. 

47 

Metabolism and Thermal Regulation 

Energy expenditure follows the classical biphasic pattern after 

burns: the first 24 to 48 hours, called ebb phase, are characterized 

by an intense sideration with depressed energy expenditure and 

oxygen consumption. The subsequent flow phase is characterized 

by a strong and prolonged increase in resting metabolic rate. 51,52 A 

significant proportion of the mortality and morbidity of severe 

burns is attributable to this hypermetabolic response, which 

can last for as long as 1 year after injury and is associated with 

impaired wound healing, increased infection risks, erosion of lean 

body mass, hampered rehabilitation, and delayed reintegration of 

burn survivors into society. 53 

Hypermetabolism is mainly caused by cytokines and stress 

hormone release. The stress hormones (i.e., catecholamines, 

glucocorticoids and glucagons) are massively released, causing 

severe changes in substrate metabolism: ureagenesis, glucogenolysis, 

gluconeogenesis, and lipolysis are strongly stimulated, promoting 

catabolism. 54 These processes produce extensive body 

wasting, resulting in net body-weight loss; this state can persist for 

weeks or months, and is particularly deleterious in a growing 

child. The occurrence of hyperthermia and sepsis further modify 

the metabolic response in an unpredictable direction.


Enlargement of the liver with fatty infiltration is a complication 

found at autopsy and has been reported repeatedly since the 1970s 

in children with extensive burns; 52,55 it is only reported occasionally 

in European settings. Liver enlargement starts early 

on during the first week, peaking at 2 weeks after burn. The 

enlargement is associated with impairment of protein synthesis. 52 

This type of complication is associated with hypercaloric nutrition 

using large amounts of glucose. This may be related to the more 

frequent use of high loads of carbohydrates during parenteral 

nutrition in North America. Indeed fatty-liver development is 

considered to be secondary to the overload of normal processing 

enzymes by the massive peripheral lipolysis, or to the downregulation 

of the fatty acid–handling mechanisms as a result of 

hormonal or cytokine changes associated with burns. 56 It has been 

shown in adult trauma patients that high loads of carbohydrates 

cause de novo lipogenesis. 57 

Thermal Regulation 

After major burns, temperature regulation is seriously altered. The 

patients not only lose the insulating properties of the skin, but they 

usually strive for a temperature of 38.0 to 38.5°C 58 due to an 

increase of their hypothalamic temperature set point. Catecholamine 

production contributes to the changes in association with 

various cytokines, including interleukin-1 and interleukin-6. Any 

attempt to lower the basal temperature by external means will 

result in augmented heat loss, thus increasing metabolic rate. 

Ambient temperature should be set at 28 to 33°C to limit the 

metabolic response. 58 Another cause of increased metabolic rate 

is evaporation of exudates from the wounds, which consumes 

energy, again causing heat loss. The evaporation causes extensive 

fluid losses from the wounds, approximating 4000 mL/m 2 BSA 

burns. Every liter of evaporated fluid corresponds to a caloric 

expenditure of about 600 kcal. Finally, burned patients are 

frequently infected and exhibit highly febrile states. Extensively 

burned patients frequently experience hypothermia (defined as 

core temperature below 35°C). Surgery under general anesthesia, 

which inhibits the heat-conserving and heat-generating mechanisms, 

frequently results in hypothermia. Time to recover from 

hypothermia has been shown to be predictive of outcome in 

adults, 59 time to revert to normothermia being longer in nonsurvivors. 

Considering that hypothermia favors infections and 

delays wound healing, the maintenance of perioperative normothermia 

is of utmost importance. 60 

Platelets 

The early phase is characterized by a fall in platelet count secondary 

to dilution, consumption, increased platelet aggregation, and 

to lung trapping. This is followed by thrombocytosis starting 

during the 2nd week after injury. This elevation depends on burn 

size and may persist for weeks or months. 

Clotting Factors 

The alterations observed after burns are complex and can be 

summarized as follows. During the early phase after burns, fibrin 

split products increase. Dilution and consumption explain low 

prothrombin time (PT) values. Thereafter, as part of the acute 

phase response, fibrin increases, as well as factors V and VIII; 

these alterations may last 2 to 3 months. 

Central Nervous System 

Neurologic disturbances are commonly observed in burned 

patients. Several pathophysiologic mechanisms are involved 62 

including cerebral glucose metabolism alterations as shown in 

animal models. 63,64 Inhalation of neurotoxic chemicals, of carbon 

monoxide, or hypoxic encephalopathy may adversely affect the 

central nervous system as well as arterial hypertension. 62 Other 

factors include hypo- and hypernatremia, hypovolemic shock, 

sepsis, antibiotic overdosage (e.g., penicillin), and possible oversedation 

or withdrawal effects of sedative drugs. The possibility 

of cerebral edema and raised intracranial pressure must be 

considered during the early resuscitation phase, especially in the 

case of associated brain injury. 

ELECTRICAL BURN INJURIES 

Electrical injury may be extremely devastating and destructive 

(Figure 124–2). It encompasses different types of injury, depending 

on the level of energy involved, and can result in severe 

surface and deep tissue injury associated with the passage of 

electricity. 65 Associated lesions to the spine must be considered. 

High-voltage current (>1000 V) results in the most extensive 

Hematologic Effects 

Hematologic alterations are extensive, appear during the first 

hours after injury, and will persist for weeks. 61 

Erythrocytes 

Anemia invariably occurs in the course of burns, arising from 

multiple factors (enhanced erythrocyte destruction or decreased 

bone marrow production). Thermal or electrical injuries induce 

direct and delayed destruction of erythrocytes. Other factors such 

as blood sampling for laboratory tests, surgery, or gastrointestinal 

bleeding play an important role. Reduced or delayed production 

of erythrocytes is caused by the inflammatory response, infection, 

iron deficiency, and other nutritional deficiencies such as copper 

deficiency. 

Figure 124-2. Child with an oral electrical burn injury (courtesy 

B. Bissonnette).


damage. In high-voltage injury, three types of injuries are observed: 

entry and exit wounds, arc burns, and surface burns resulting from 

ignition of clothes or objects in the environment (usually deep 

burns). Low-voltage current (domestic accidents) causes 

physiologic alterations due to the passage of current flow through 

the cardiovascular system, and especially the heart. Alternating 

current (50–60 Hz) is more dangerous than direct current, because 

it causes tetanic muscle contractions that “freeze” the victim to the 

source of the current. Electrical injuries are deep by nature, 

involving muscle and other fluid-rich structures. Their demarca - 

tion is slow, rendering full assessment difficult. Cardiac arrhythmia 

(ventricular fibrillation) and cardiac arrest are common, 66 especi - 

ally in injuries from low-voltage alternating current. Vascular 

complications include delayed hemorrhage and thrombosis. 

Neurologic complications are also frequent (loss of consciousness, 

seizures, spinal cord lesions, deafness, peripheral nerve injury). 

Gastrointestinal complications include bowel perforations, as well 

as ulcers at various levels of the gut. Acute renal failure is a 

common complication of electrical injury, due to rhabdomyolysis 

or to renal injury directly related to the electrical current. 

RESUSCITATION 

Initial Evaluation 

On the site of an accident, the initial evaluation must be quick and 

address life support. As with all traumatic injuries, the first 

concern is the patency of the airway (the ABC [airway, breathing, 

circulation] of advanced trauma life support). The immediate 

institution of intravenous fluid resuscitation is the next high 

priority: delays in resuscitation are predictors of poor outcome in 

massive burns. A secondary assessment will be carried out in the 

hospital emergency department or, better, in the burns facility. As 

in adults, the assessment of the burn injury involves the determination 

of the total burned surface, using the normograms 

adapted for age. It also involves the recognition of associated 

injuries and of comorbidity. Burn victims require a detailed and 

thorough examination to appreciate the extent of the damage, as 

well as a complete history for determination of adequate therapy. 

Airway and Inhalation Injury 

General Management of the Patient 

In children, the risk of acute and rapid airway obstruction is 

particularly high, due to the very rapid development of laryngeal 

edema. Any sign that the airway is threatened or compromised is 

an indication for immediate endotracheal intubation. Otherwise 

it is appropriate to provide oxygen through a face mask until the 

resuscitation phase is completed. An initial bronchoscopy is 

required for the diagnosis of inhalation. In case of mucosal lesions, 

sloughing may require repeated suctioning. Total tracheal tube 

obstruction by debris (occurring more frequently in small 

children) must be recognized immediately, with prompt removal 

and replacement of the tube. If acute respiratory failure occurs, 

consensus treatment strategies for acute lung injury (ALI)/ARDS 

should be applied. 

Carbon Monoxide Poisoning 

Measurement of the peripheral oxygen saturation (SpO2) is not 

helpful for the detection of CO poisoning. Carboxyhemoglobin 

TABLE 124-4. Symptoms of Carbon Monoxide (CO) 

Poisoning 

CO Hemoglobin, % 

0–10 

10–20 

20–30 

30–40 

40–50 

50–60 

60–70 

70–80 

Clinical Signs 

None (angina pectoris in patients with 

ischemic coronaropathy) 

Headache, cutaneous vasodilatation 

(flushing), dyspnea on vigorous 

exercise 

Pulsatile headache, dyspnea on 

moderate exercise 

Intense headache, nausea, vomiting, 

irritability 

Generalized weakness, dizziness, 

blurred vision, confusion 

Fainting on exertion 

Tachycardia, dyspnea at rest, loss of consciousness 

Tachycardia, tachypnea, Coma, con - 

vulsions, Cheyne–Stokes breathing 

pattern 

Coma, convulsions, cardiovascular and 

respiratory depression 

Possible death 

Refractory shock, death 

(COHb) levels must be measured directly. Symptoms are not 

specific (Table 124–4). Because COHb elimination half-life is 

dependent on oxygen tension and time, 100% oxygen should be 

provided to accelerate the dissociation of CO from hemoglobin 

and to increase the amount of dissolved O 2 

in the blood, 

improving oxygenation. In adults, hyperbaric oxygen may reduce 

the incidence of neurologic sequelae 67 by shortening the halflife 

of carboxyhemoglobin from 320 minutes to approximately 

60 minutes. The therapeutic target is to reduce COHb below 5%. 

In children with neurological symptoms or COHb concentration 

greater than 40%, hyperbaric oxygen should be considered despite 

the lack of clear data on its effectiveness in children. 68 

Cyanide Poisoning 

Cyanide uncouples oxidative phosphorylation at the mitochondrial 

level. Cyanide binds reversibly to the ferric ion (Fe 3+ ) of 

cytochrome oxidase, the terminal oxidase of the mitochondrial 

electron transport chain, inhibiting this enzyme and halting 

aerobic metabolism. This binding blocks the major pathway of 

high-energy phosphate production, resulting in anaerobic 

metabolism, decreased adenosine triphosphate (ATP) production 

and thus, rapid depletion of cellular energy stores. Glycolysis 

continues with further pyruvate production, since it can no 

longer be incorporated in the tricarboxylic acid cycle. Instead, it 

is reduced to lactate, which accumulates rapidly. This causes 

systemic hyperlactatemia and metabolic acidosis with an increased 

anion gap. Cyanide poisoning causes tissue hypoxia by decreasing 

extraction of the transported oxygen and by inhibition of the 

central respiratory centers, which causes hypoventilation. Normally, 

the body’s natural defense is the enzyme rhodanese, which 

catalyses the complexing of cyanide with sulfur, forming the much 

less toxic thiocyanate ion (SCN–). The sulfur pool is limited and,


therefore, is the rate-limiting factor for endogenous cyanide 

detoxification. 

Inhalation of high airborne cyanide concentrations may result 

in loss of consciousness after only a few breaths. Patients with 

acute poisoning present with headache, vomiting, hypotension, 

and cardiac arrhythmias, which rapidly progress to coma, convulsions, 

shock, respiratory failure, and death. Specific therapy for 

cyanide poisoning is controversial, because of absence of consensus 

on the incidence of clinically important exposure. 37 

Antidotes are indicated in patients with suspected important 

exposure, or in case of severe lactic acidosis (>10 mmol/L). 69 In 

adults, hydroxocobalamin was shown to reduce mortality among 

victims of cyanide inhalation poisoning and is well tolerated with 

few side effects. 70 It may be safely administered very early even by 

the rescue team. 71 Other antidotes may be used depending on their 

specific risk-benefit ratio (e.g., thiosulfate, cobalt, amyl nitrite, or 

sodium nitrite, methemoglobin forming agents). 69 

In smoke inhalation, carbon monoxide and cyanide poisoning 

may be combined; the treatment should target both toxic agents, 

combining cyanide antidotes and normobaric or hyperbaric oxygen. 

Circumferential Chest Burns 

Extensive third-degree burns to the thorax, especially if circumferential, 

may result in impaired thoracic wall motion with 

reduced compliance. If early escharotomy is not performed, precipitation 

into respiratory failure may occur even in the absence of 

any other risk factor. 

Fluid Resuscitation and 

Hemodynamic Support 

General Principles of Fluid 

and Drug Administration 

Fluid resuscitation is a major determinant of outcome in children 

with burn. 41 It requires special care in children, because some 

formulas may underestimate their requirements, especially in 

small patients (40% BSA). Pediatric 

patients require more fluid for resuscitation than adults (Table 

124–5, Figure 124–3): this results form the high volume-to-surface 

area ratio in infants and children. In children, the separate calculation 

of daily maintenance fluids provided, in addition to the 

burns resuscitation fluids, is recommended. 72 Current formulas, 

which are derived from experimental studies, are successful in 

preventing or reversing burn shock in 70 to 95% of cases. 41,44 

The principles of fluid resuscitation were developed in the early 

1950s. It was shown that exudates and edema fluid found in burn 

wounds was isotonic, containing same amounts of electrolytes and 

protein as plasma does. Studying hemodynamic effects of various 

regimes, using different proportions of colloids and crystalloids 

resulted finally in the development of the Parkland Hospital 

formula. 73 No single fluid resuscitation formula has proven to be 

superior, but the Parkland formula probably remains the easiest 

and therefore the safest for extended use. 

In burns below 5% BSA, fluid resuscitation can be done by the 

oral route. Above 5% BSA, an intravenous resuscitation is required 

under normal civilian condition. The first half of the fluids 

calculated with the Parkland formula is usually administered over 

8 hours, the remainder being given in 16 hours. Other treatment 

strategies recommend even a faster infusion rate in the first 

4 hours. The crystalloid resuscitation results in large increase of 

total body sodium and water contents, with fluid retention and 

massive interstitial edema. Nevertheless, liberal fluid administration 

is associated with several possible complications such as an 

increasing need for tracheostomies, pulmonary edema, and ACS 

with raised intra-abdominal pressure. Therefore, a strict control of 

fluid administration is required. After the first 24 hours, fluid and 

sodium administration is drastically reduced by 50 to 70% compared 

to the first day to cover daily maintenance requirements. 

The use of colloids is controversial. It is generally accepted that 

liberal colloid use results in increased morbidity and delayed 

healing. Colloid use should be avoided as much as possible. 

Albumin 5% may be considered if severe hypoalbuminemia is 

present (albuminemia 15–20g/L). Indication to fresh frozen 

plasma should be limited to correction of coagulation defects. 

Below burns 30–40% BSA, a central venous catheter is usually 

sufficient to guide hemodynamic resuscitation. In larger burns, 

a arterial catheter is helpful to adjust vasopressor therapy. In 

recent years, minimally invasive hemodynamic monitoring has 

been made available. Pulse contour analysis associated with 

TABLE 124-5. Resuscitation Formulas for Pediatric Patients 

Author Formula Time Partition Fluid Pediatric Specific 

Evans,1952 

Carvajal 

Shriners’ Burns Unit, 

Galveston 

Shriners’ Burns Unit, 

Cincinnati 

Baxter, 1968, 

Parkland 

Sick Kids Hospital, 

Toronto 

1 mL/kg/1% BSA + 

1 mL/kg/1% BSA 

5000 mL/m 2 BSA burn 

+ 2000 mL/m 2 

5000 mL/m 2 BSA burn 

+ 2000 mL/m 2 

4 mL/kg/1% BSA burn 

+ 1500 mL/m 2 

4 mL/kg/1% BSA burn 

6 mL/kg/% BSA burn 

0–24 h 

0–24 h 

0–24 h 

0–24 h 

0–24 h 

0–8 h 50% 

8–16 h 25% 

16–24 h 25% 

0–24 h 

0–8 h 50% 

8–24h 50% 

0–8 h 50% 

8–24 h 50% 

RL 

colloid 

RL 

RL 

+ 12.5 g albumin 

RL + 50 mmol NaHCO 3 

RL 

RL + 12.5 g albumin 

RL 

RL 

No 

Yes 

Yes 

Yes 

No 

Yes 

RL = Ringer lactate.


Time 

Variable 

Therapeutic options 

Result 

adequate 

not achieved 

Admission 

RL 4 ml x kg -1 x burned %BSA-1 in 24 hr 

50% in 4 hours 

Antioxidant micronutrients (IV) 

At 4 hours 

Assess 

Urine output 

MAP 

pHa 

1ml 

stable 

7.3 

< 1ml 

unstable 

< 7.3 

achieved 

continue 

Start EN 

not ok 

RL: 1 ml x kg -1 x %BSA -1 

At 8 hours 

Re-Assess 

As above + CVP 

Albumin 

10 mmHg 

15 ml x kg -1 

> 10 mmHg 

< 15 ml x kg-1 

achieved 

not ok 

continue 

RL: 1 ml x kg -1 x %BSA -1 

colloids 10 ml x kg -1 

At 12 hours 

As above 

achieved 

Re-Assess 

not ok 

continue 

dobutamine 5 µg x kg -1 /min 

consider PAC 

At 18 hours 

Re-Assess 

At 24 hours 

As above + SvO 2 

PaO 2 /FIO 2 

65% 

200 

achieved 

continue 

< 65% 

< 200 

not ok 

Shift fluid composition 

to glucose 5%, or glucosaline 

prescribe 50% of first 24 hrs' fluid intake 

use PAC 

dobutamine 

Re-Assess 

As above 

achieved 

continue 

not ok 

dobutamine 

colloids 10 ml x kg-1 

Figure 124-3. Resuscitation algorithm (see legend for Figure 124–1). 

thermodilution cardiac output measurement (PiCCO) provides 

accurate cardiac output assessment even in small children and 

gives important parameters to guide hemodynamic resuscitation. 74 

Some laboratory routines are useful particularly during the 

first weeks after a major burn injuries; these are summarized in 

Table 124–6. 

Mass Casualty 

When fire or burn disasters cause mass fatalities, most or all 

of the fatalities occur on-scene, during transit, or soon after 

hospital arrival. Civilian accidents generally involve a constant 

proportion of children and adolescents, particularly when


TABLE 124-6. Proposed Minimum Laboratory Monitoring Routines in Patients With Major Burns (>40% Body Surface Area) 

During Acute Phase (First 2 Weeks) 

Hemoglobin, hematocrit, 

Na, K, glucose 

Mg (ionized), P 

Ca (ionized) 

pH, anion gap, lactate, 

blood gases 

Albumin 

Prealbumin 

Leukocyte count 

C-reactive protein 

ASAT, ALAT, γ-GT, 

alkaline phosphatase 

Frequency 

6 hourly during the first 72 h, or 24 h after the 

surgical sessions 

Daily during the first week 

Then, 2–3 times weekly 

After transfusion 

Weekly during parenteral nutrition and with 

prolonged bed rest 

Twice per day 

Every 12 hours during the first 72 h, then daily 

during first week 

Once weekly 

Daily during first 72 h 

Daily in case of fever 

Weekly with parenteral or enteral nutrition, or 

in case of suspicion of overfeeding 

Comment 

Very low levels are very common 

In respiratory failure, may require more 

frequency 

Helps assess response to feeding 

After resuscitation according to clinical 

signs of infection 

Remains elevated during the first 10 days. 

Changes help to assess presence of 

infection 

Often slightly increased without any 

clinical relevance 

Beware of increasing values with artificial 

nutrition 

ASAT = aspartate transaminase; ALAT = alanine aminotransferase; γ-GT = gamma glutamyl transferase. 

discotheques are involved. Burn patients requiring hospitalization 

are usually distributed across several hospitals on the day of 

a disaster. 75 

It is important to keep in mind that in case of mass causality, 

oral fluid resuscitation is an alternative with burns up to 40% 

BSA; 76 the volume of fluid required to achieve stability is about 

15 to 20% of body weight during the first 24 hours, which corresponds 

to 10.5 to 14 liters per day in a 70-kg patient—it is enormous. 

Salt water must be avoided, because it generates nausea and 

vomiting. Practically, salt tablets are added to water or any other 

fluid (5–7.5 g/L). 77 

Hospitalized burn patients are resource- intensive and have 

longer lengths of stay when compared with other disaster victims. 

In addition to patients received directly on the day of the disaster, 

burn centers should anticipate additional admissions in the first 

week following the disaster, as other hospitals appropriately 

request transfer of admitted thermally injured patients. 

ANESTHETIC MANAGEMENT 

General Considerations 

Successful anesthesia for hydrotherapy, excision, and grafting of a 

burn requires planning. Patients with burns involving


Tracheal Intubation 

An important airway management decision must be made as soon 

as the patient arrives in the hospital. Edema associated with 

massive fluid resuscitation may compromise the airway and make 

delayed tracheal intubation difficult. As a general rule, it is better 

to tracheally intubate the burn patient early rather than late. For 

children, an inhalational induction with oxygen and a volatile 

agent such as sevoflurane before airway manipulation is probably 

the safest technique. 72 Nasotracheal intubation is the preferred 

route for prolonged tracheal intubation in infants and small 

children, because it is more secure and less irritant to the trachea 

with head movement. Uncuffed tubes have been and may remain 

the first choice in children and infants. Classically, the tube size 

is chosen to permit an air leak as of an airway pressure of 18 to 

25 cmH 2 

O. On the rare occasions with concomitant ARDS, cuffed 

tubes may be needed to ensure high airway pressure ventilation 

for adequate oxygenation. During the first 72 hours postinjury, 

edema of the tracheal mucosa may be severe, and may require 

reduction in tube diameter. However, changing the tracheal tube 

at this stage may be life-threatening, as usually the face and upper 

airway are also extensively swollen, rendering visibility and access 

to intubation very difficult. If children are critically burned and 

expected to require more than transient mechanical ventilation 

support, low-pressure cuffed endotracheal tubes should be placed, 

regardless of the child’s age. 82 Because accidental extubation may 

be fatal at this stage, particular care should be taken to secure 

properly the tracheal tube (lace around the head) associated to 

deep sedation. In particular cases, utilizing a suture to maintain 

the tube can be considered. At any stage in the course of a burn 

injury involving the face or neck, the airway may be significantly 

compromised. In patients with burns involving the neck, the upper 

thorax, and the inferior part of the face, scarring with associated 

tissue retraction may lead to difficult debridement. It affects 

airway management; intubation of a previously easy airway may 

become extremely difficult after a few weeks. Ketamine anesthesia 

is an alternative for the release of neck contractures before 

intubation. Even when available, fiberoptic-aided intubation may 

fail; a laryngeal mask can offer a temporary rescue solution. 

Monitoring 

Standard monitoring may be extremely difficult to obtain in major 

burns. A useful means of monitoring may be by esophageal 

stethoscope, as it practically always allows hearing both heart and 

ventilation sounds. Peripheral pulse oximetry may be difficult to 

obtain from a finger, toe, or ear, but alternative sites such as, nose, 

or tongue may be helpful. Monitoring temperature is mandatory, 

as heat loss may be massive. Capnography is mandatory with all 

forms of ventilation, whether mechanical or spontaneous, especially 

for patients with their trachea intubated or for those 

breathing through a laryngeal mask. Blood pressure is measured 

by cuffs, adapted to any limb for minor burns, or monitored 

invasively in major burn patients. In children, arrhythmias are 

mainly of three types: sinus tachycardia, almost universal, and 

(rarely) ventricular fibrillation or cardiac arrest. An echocardiogram 

(ECG) is sometimes very difficult to obtain, especially when 

the patient is rotated during surgery. Alternative electrode sites 

should be tried. If no ECG trace is obtainable, consider placement 

of sterile subcutaneous or intradermal pace maker wires in the 

surgical field or needles with crocodile grips; extensively burned 

patients are at high risk of hemodynamic instability, with an 

increased risk of problems presented by arrhythmias. As mentioned 

above, severely burned patients with hemodynamic 

instability are monitored with central lines and may even require 

pulse contour cardiac output monitoring 74 to help guide the fluid 

and pharmacologic therapy. Urine output should be measured and 

maintained >0.5 mL/kg/h throughout the surgical and anesthetic 

procedure. 

Heat Loss 

Temperature control is mandatory, and maintaining temperature 

is a serious concern. A study of patients with a mean burn size 

of 44% TBSA showed that patients at thermoneutral ambient 

temperature (28–32°C) had metabolic rates 1.5 times those of 

nonburned controls. 83 However, when ambient temperature was 

decreased to 22–28°C, the metabolic rate increased in proportion 

to burn size. Thus, ambient temperatures less than the thermoneutral 

range should be avoided, whether in the burn unit or in the 

operating room. The four classical routes for temperature loss are 

convection, conduction, evaporation, and radiation. During burn 

excision/grafting sessions, large areas of skin are exposed, leading 

to extensive evaporative and convective heat losses. The main 

factors affecting heat loss are the burned area surface, the donor 

site area for grafts, wet packs, a cool operating room, and anesthesia, 

which causes vasodilatation. Heat loss can hence be 

reduced by raising room temperature and closing doors to limit 

draughts, using a warming blanket or an overhead heater, covering 

the nonoperated areas, warming blood and infused solutions, 

warming and humidifying inspired gases, and using warm packs. 

Using a forced-air convection system is usually not possible with 

extensive burns, as the remaining available surface after surgical 

preparation is very limited. However, it is recommended for 

surgery limited to the extremities or small burned surface areas. 

Pharmacology and Choice 

of Anesthetic Agents 

Burns involving >10% BSA cause large changes in fluid compartments 

and alter pulmonary, hepatic, and renal functions considerably. 

Uptake, volume of distribution, and clearance of many drugs 

are affected. 84 The major changes in plasma proteins will affect the 

pharmacokinetics of the medications such as benzodiazepines 

with strong protein binding. The two most important proteins 

in this respect are alpha1-acid glycoprotein and albumin: the 

first increases, and albumin, the most important quantitatively, 

decreases after major burns, modifying the proportion of free 

drugs in an unpredictable way. Because most anesthetic drugs are 

not highly protein bound, the impact of these changes is minimal. 

Inhalation Agents 

The pharmacokinetics of inhalation anesthetics are least altered 

amongst anesthetic drugs. All halogenated agents have been used 

for anesthetizing burn patients with no major problems. Many 

anesthesiologists however, prefer total intravenous anesthesia 

(TIVA), considering inhalational techniques unfit for burns 

because of their undesired side effects. For instance, halogenated 

agents cause peripheral vasodilatation with enhanced cooling and 

increased bleeding, postoperative rigidity, and shivering (source 

of graft displacement and pain), They are contraindicated with 

certain vasoconstrictor regimes used for surgery (halothane


combined with epinephrine). Halothane has been extensively used 

in burned children. There is no evidence that its repeated use is 

associated with additional risk of halothane hepatitis. 84 The lower 

solubility of sevoflurane, combined with minimal airway irritation, 

offers the advantage of a more rapid induction. The same 

mentioned undesired effects apply to this inhalation agent except 

that it is less feared in presence of epinephrine. Isoflurane has no 

advantage on either halothane or sevoflurane for induction. 

Moreover of the three halogenated agents, it is the most potent 

vasodilator. Entonox, a mixture of oxygen and nitrous oxide, has 

been used extensively for dressings in burned children. Although 

very effective, long-term use is associated with bone marrow 

depression. 85 

Intravenous Agents 

KETAMINE: Some procedures like hydrotherapy or bandaging can 

be performed using ketamine anesthesia or sedation. This agent is 

particularly versatile, having both analgesic and anesthetic effects. 

The most important adverse effects are hallucinations and excessive 

increases in blood pressure and heart rate. These reactions 

can be attenuated or avoided by combining ketamine with sedative 

or hypnotic drugs like midazolam and/or propofol. 86 Dreams and 

psychic problems seem to be less common in patients with severe 

burns, 78 possibly from the frequent use of benzodiazepines for 

their basal sedation in the intensive care unit (ICU). It can be 

administered by both intramuscular and oral routes, making it 

advantageous when venous access is difficult. Following intravenous 

administration, a rapid onset of action is seen within 1 minute 

lasting for about 10 minuts. The use of the pure S-ketamine 

enantiomer, which is more potent than the racemic solution, 

allows the dose to be reduced. Anesthesia can be initiated by 

incremental I.V. doses of midazolam up to about 0.1 mg/kg 

or until the child looks sleepy, followed by I.V. injection of 

S-ketamine at a dose of 0.5-1 mg/kg, repeated every 10 to 15 

minutes (representing a 50% dose reduction compared to racemic 

ketamine). Ketamine with propofol is hemodynamically neutral. 

Combining (S)-ketamine to midazolam for analgosedation in the 

ICU reduces exogenous catecholamine requirements. Moreover, 

the effects on intestinal motility are superior to opiates. 86 In a 

randomized, double blind trial on burned children, propofolketamine 

combination was superior to propofol-fentanyl because 

of more restlessness in patients given propofol–fentanyl. 87 

Ketamine is proposed as first choice for anesthesia in burned 

patients, for its many advantages: 88 rapid onset and short duration 

of action, its wide safety margin, its direct stimulation effect on 

central sympathetic tone which is threefold in burned patients, its 

faculty of retaining protective airway reflexes, its prolonged 

analgesic effect, and its capacity to reduce systemic inflammation 

and ischemia–reperfusion damage. 

PROPOFOL: The use of propofol has gained wide acceptance 

among pediatric anesthesiologists over the last decade. 89,90 Clinical 

studies have shown that infants and young children require larger 

doses than older children and adults for both induction and 

maintenance. A pharmacokinetic study done on children 1 to 

3 years of age with minor burns (48 hours) at high doses (>4 mg/kg/h) may cause a rare 

but frequently fatal complication known as propofol infusion 

syndrome (PRIS). PRIS is characterized by metabolic acidosis, 

rhabdomyolysis of both skeletal and cardiac muscle, arrhythmias 

(bradycardia, atrial fibrillation, ventricular and supraventricular 

tachycardia, bundle branch block and asystole), myocardial failure, 

renal failure, hepatomegaly and death. PRIS must be kept in mind 

as a rare, but highly lethal, complication of propofol use, not 

necessarily confined to its prolonged use. If PRIS is suspected, 

propofol must be stopped immediately and cardiocirculatory 

stabilization and correction of metabolic acidosis initiated. 92 In 

view of the poor prognosis and availability of alternative forms of 

sedation, propofol is not recommended for long-time infusion. 93 

Prolonged infusions should also be avoided considering the 

possibility of direct neurotoxicity through an effect on the 

γ-aminobutyric acid (GABA)ergic neurons. 94 However, propofol 

remains suitable for short-term perioperative sedation or anesthesia 

associated with high-dose opiate analgesia or with ketamine. 

87,95 In an animal model of burn injury propofol anesthesia 

offered a possible protection against apoptosis of enterocytes 

and reduced serum TNF-α levels, when compared to ketamine 

anesthesia. 96 This would be an argument to use propofol for the 

first anesthetic post burn injury, ignoring the viewpoint that its 

use should be avoided in the first 48 hours, period of major 

hemodynamic instability. 89 Patient-controlled sedation with 

propofol has been validated as safe and effective for burn dressings 

provided no lockout interval was used. 97 This may well be applied 

to older children. 

Muscle Relaxants 

Burned patients respond abnormally to both depolarizing and 

nondepolarizing muscle relaxants. This is related to changes in the 

muscle membrane observed in burns of less than 10% BSA. 

Neuromuscular dysfunction is proportional to burn size and to the 

degree of hypermetabolism: it is related to changes in the nicotinic 

acetylcholine receptors. Immature nicotinic receptors appear in 

the neuromuscular junction and are generalized to the entire 

skeletal muscles. The absolute number of receptors increases, and 

they differ from mature receptors with respect to their half-life, the 

duration of their ionic canal permeability, their affinity for agonists, 

and their sensitivity to antagonists. 98 Immobilization further 

contributes to these changes in acetylcholine receptor subunit 

mRNA, but the changes after burns differ from those seen after 

denervation. 99 A decrease in plasma cholinesterase activity is also 

observed. 

DEPOLARIZING AGENTS: The response to succinylcholine is 

increased, with a marked increase in kalemia. Cardiac arrest 

following normal doses of succinylcholine has repeatedly been 

reported. 100–103 The rise in kalemia is related to the burn size, the 

dose of succinylcholine, and the time elapsed since the injury. It 

appears after 3 to 4 days; duration of the phenomenon is related to 

the burn size and to the duration of immobilization in bed. The


acute sensitivity to succinylcholine was demonstrated on electromyographic 

investigations using doses as small as 0.1 mg/kg. 

Patients may become paralyzed with very small doses at the time 

of maximum sensitivity. Succinylcholine can be used in the 

immediate postburn period (


TABLE 124-7. Simplified Sedation Score 

Level 

Clinical Sign 

0 Agitated 

1 Awake 

2 Drowsy, roused by voice 

3 Roused by strong stimuli (tracheal suction) 

4 Not arousable 

5 Anesthetized or paralyzed 

Adapted from Addenbrooke’s Sedation Score. 153 

the perception of pain. Assessment can be done by using questionnaires 

or visual analogue scales (VASs) in adults. In children, the 

Children’s Hospital of Eastern Ontario’s Pain Score (CHEOPS) 

score, a visual analog scale, and the pain thermometer developed 

in Montreal can be used. 111 Frequent pain assessment with valid 

patient self-report measures should be the basis for documenting 

pain treatment. Whenever sedation is used in the ICU, there is a 

risk of oversedation, because it is easier to nurse a sleeping patient. 

Oversedation has a cost and must be avoided. Therefore, the depth 

of sedation must be regularly assessed (Table 124–7), and patients 

should always remain arousable. 

Hypnosis 

This form of pain control has been increasingly included in the 

multimodal pain management of burned patients. 123,124 Case 

reports in children are generally positive, but authors report it to 

be more difficult in preschool-aged children, whereas children 

aged 6 years and older respond very well. 

Regional Anesthesia 

Limited burns to limbs may be managed by an anesthetic 

technique that associates regional blocks with either propofol 

sedation or light inhalational anesthesia. This technique is very 

useful for skin grafting. The following blocks for the lower limb are 

easy to perform and often useful. The femoral nerve block will 

provide analgesia for the anterior aspect of the thigh and leg. The 

lateral cutaneous block will provide analgesia to the lateral aspect 

of the thigh. For the upper limb, the most performed block is the 

axillary plexus block. Central blocks such as caudals, epidurals, or 

spinals are seldom used in the initial post-burn phase, because of 

the loss of sympathetic tone exacerbating hypotension and heat 

loss. Although continuous peripheral blocks such as the facia iliaca 

compartment block prove to be efficacious for pain relief on donor 

sites after skin grafting in burned patients, 125 the same but singleblock 

technique has the same morphine sparing-effect during a 

72-hour postoperative period with limited side effects, compared 

to the continuous technique. 126 

Hematologic Management Strategies 

Morbidity with homologous blood transfusion is low but well 

documented. Transfusion of blood products should be limited. 

Surgical blood losses are maximal during the first 2 weeks postburn 

injury, 127 during which the inflammatory response is 

maximal. The losses range from 4 to 15% of the patient’s blood 

volume for every percent of skin debrided. In a more recent 

retrospective chart review of consecutive pediatric burn surgeries 

the average blood loss per percent TBSA treated was 15 mL (range: 

0.7–37 mL) and the average percent of total blood volume loss per 

percent of TBSA treated was only 0.76%. The protocol to reduce 

intraoperative blood loss consisted of the debridement of fullthickness 

burns with electrocautery and partial-thickness burns 

with dermabrasion. All debrided or harvested surgical sites were 

treated immediately with epinephrine solution-soaked pads. All 

graft harvest sites were injected with an epinephrine solution 

before harvesting split-thickness skin grafts. 128 The advantages of 

both early tangential excision and split-skin grafting for surgical 

burns are well established. In a cohort of pediatric patients with 

massive burns delays in excision were associated with longer 

hospitalization and delayed wound closure, as well as increased 

rates of invasive wound infection and sepsis. 

Early excision within 48 hours was considered optimal. 129 

However, because of the important associated blood loss, this 

technique requires an experienced team which may only be 

available in a few centers worldwide: other centers may have to 

limit the excision to as little as 10 to 30% BSA per session. The 

estimation of blood loss is quite difficult and requires clinical 

expertise. It is based practically on the close observation of the 

surgical field, associated with the integration of each of the values 

provided by the various monitoring devices mentioned above. A 

rising of both diastolic blood pressure and heart rate associated 

with a drop in the pulse oximeter amplitude is an early sign 

of hypovolemia and is usually treated with administration of 

crystalloid solutions. A drop in systolic blood pressure with a 

disappearing pulse oximeter trace denotes severe hypovolemia 

requiring the administration of colloids. Very severe hypovolemia 

must be suspected when capnography reveals a drop in end tidal 

CO 2 

. At this stage, if the previous mentioned filling strategies have 

been provided, only blood transfusion will permit restoration of 

hemodynamic stability. Characteristic blood clotting changes are 

also clinically observable; diffuse bleeding usually reflects massive 

hemodilution and, less frequently, a clotting disorder. 

What is the acceptable hemoglobin level? There is yet no 

definitive answer to this question, although levels of 70 to 80 g/L 

of hemoglobin appear safe in children and healthy adults; much 

lower levels have been associated with survival in Jehovah‘s 

Witnesses. 60 A large trial in critically ill adult patients showed 

that a conservative blood transfusion policy as above is safe and 

is possibly even associated with lower mortality than a more 

liberal transfusion policy. 130 Early administration of recombinant 

erythropoietin (300 U/kg of recombinant erythropoietin within 

72 hours of admission, and daily for 7 days, followed by 150 U/kg 

for 2 weeks) does not prevent post-burn anemia, nor does it 

decrease transfusion requirements. 67 Moreover, failure to provide 

iron supplementation in patients receiving recombinant erythropoietin 

can lead to a rapid depletion of iron stores and may 

contribute to an immune dysfunction. 131 The different treatment 

strategies are summarized in Table 124–8. 

In large burns (>20 to 30% BSA; depending on site and degree 

of burn), it is mandatory to monitor blood pressure invasively; 

indeed, rapid changes in volemia are diagnosed at a glance, correlated 

with changes in the surface area under the pressure curve. 

Moreover, left ventricular contractility can be estimated on the 

upstroke limb of the pressure curve. A second transducer committed 

to on-line central venous pressure measurement is 

mandatory in infants and small children, since even small volumes 

may lead to cardiac dilatation through overload. Changes in 

heart rate may be the only available observation. Repeated


TABLE 124-8. Treatment Strategies for Hematologic Disorders 

Hematologic Disorder Suggested Management Comment 

Anemia 

Prevention during surgery 

Established anemia: 

Ht


is highly recommended. General strategies of lung protective 

ventilation and treatment should be applied, including positive 

end-expiratory pressure (PEEP), low tidal volume target, permissive 

hypercapnia, and permissive hypoxemia. 

Prolonged intubation and ventilatory support may be required 

with severe burns, especially those involving the face with inhalation 

injury. The risks involved are associated with the small size 

of the pediatric tubes and the difficulty in suctioning secretions, as 

well as the risk of accidental extubation and long-term sequelae 

(subglottic stenosis). In patients requiring long term ventilatory 

support, tracheostomy may be a way to avoid these complications. 

134 

Metabolic and Nutritional Support 

During the last 3 decades, awareness of the importance of nutritional 

support in burn patients has grown rapidly. This aspect is 

particularly critical in patients with prolonged hospital stays. One 

half of the children admitted to a burn center will stay up to 

1 month, and 25% will require up to 3 months. 135 

Antioxidant Micronutrient Therapy— 

Reinforcing Endogenous Defenses 

The normally effective endogenous antioxidant defense system is 

overwhelmed after major burns. In experimental burns, antioxidant 

vitamin supplements have been shown to limit the endothelial 

injury and capillary leak. Large supraphysiologic doses of 

vitamin C administered over the first 24 hours reduce post-burn 

fluid requirement by an antioxidant mechanism. 136 In animals, 

selenium supplements limit the peroxidative damage caused by 

burns. 137 In adults, supplementation with trace elements, particularly 

with selenium, reduces the lipid peroxidation process 

during the first week and reinforces endogenous antioxidant and 

immune defenses, 138 but has no impact on early fluid requirements. 

Data in children are still missing, although trace element 

deficiency has been shown to be caused by cutaneous exudative 

losses as in adults. 22 

Energy Expenditure 

Energy expenditure undergoes major changes over time after burn 

injury, in both adult and pediatric patients. The increase in resting 

energy expenditure starts around the 5th day, peaking between 

the 2nd and 4th week depending on burn size, then reverting 

progressively towards normal about 2 years after injury. 52 In 

children, the changes have been shown to be sex dependent, with 

a significantly lower energy expenditure in girls at any time after 

injury. 52 The endocrine response was also gender linked: girls had 

significantly higher levels of insulin-like growth factor 1, insulinlike 

growth factor binding protein 3, free thyroxin index, T4, and 

insulin compared with boys (P < .05). 

Post-burn oxandrolone has become part of the supportive 

metabolic treatment in major burns. In a randomized trial 

including 235 children with burns of more than 40% BSA, length 

of ICU stay was significantly decreased in the oxandrolone-treated 

patients (0.48 ± 0.02 days/1% burn) compared with controls (0.56 

± 0.02 days/1% burn) (P < .05). 52 Control patients lost 8 ± 1% of 

their lean body mass, whereas oxandrolone-treated patients had 

preserved lean body mass (9 ± 4%, P < .05). Oxandrolone significantly 

increased serum prealbumin, total protein, testosterone, and 

aspartate transaminase (ASAT)/alanine aminotransferase (ALAT), 

whereas it significantly decreased alpha 2-macroglobulin and 

complement C3 (P < .05). Oxandrolone had no adverse effect on 

the endocrine and inflammatory response (no significant dif - 

ference was observed between groups). 

For nearly 50 years, standard clinical management of burned 

patients included high-calorie and high-protein input to promote 

healing and maintain body weight. Overfeeding however, should 

be avoided as strongly as underfeeding. Recent evidence confirms 

the inadequacy of the hypercaloric formulas: all overestimate 

requirements and none take into account the evolution of energy 

expenditure over time. The strongest recommendations are produced 

by the Galveston center. They propose the Galveston formula 

to initiate nutrition according to age as a first step, followed 

by targeted adaptations according to indirect calorimetry measurements. 

The outdated Currerri formula should no longer be 

used. The variability of energy expenditure is such, that all 

respectable centers now recommend using indirect calorimetry 

and accordingly adapt feeding for prolonged periods. 

Nutrient Delivery 

Pediatric patients require artificial nutrition whenever burns 

exceed 20% BSA, even less with face or inhalation involvement. 

Early enteral nutrition has become a routine in most burn centers. 

Gastric or postpyloric feeding is started within 12 hours of injury 

by a nasoenteric tube. It is widely and successfully used in North 

American Centers. 139 Maintaining continuous enteral nutrition 

during surgical procedures contributes to increase energy intake, 

but this must be weighed against the risk of bronchoaspiration. In 

severe burns, percutaneous endoscopic gastrostomy may be a 

good alternative to nasoenteric tubes to facilitate nursing. The 

diets are those used in other pediatric trauma patients, i.e., highenergy 

and high-protein diets. Total parenteral nutrition is 

indicated for patients presenting contraindications to enteral 

nutrition or in whom the gut function is compromised. Parenteral 

nutrition requires giving particular attention to the energy target, 

since it is frequently easier to administer the nutrients by this route 

than by the enteral approach. A study in burned adults reported a 

higher rate of infectious complications in patients receiving 

parenteral nutrition supplements compared with those on 

pure enteral nutrition (63% vs 26%, respectively). 140 These data 

should be regarded with caution, since the parenteral supplements 

resulted in very large energy intakes, i.e., overfeeding. The 

deleterious effects may actually be related to this excessive caloric 

intake and not to the intravenous technique. Enteral nutrition is 

not always easy in the severely critically ill patient. It may result in 

insufficient energy intakes, with a risk of developing malnutrition. 

Combining parenteral nutrition with enteral nutrition may 

actually be required to reach a reasonable energy target in a 

minority of patients. Daily close monitoring of energy delivery is 

therefore required, and modern computerized systems facilitate 

the metabolic management as shown in Figure 124–4. 

Impact on Liver Function 

Hepatic homeostasis and metabolism are essential for survival in 

critically ill and severely burned patients. The liver undergoes 

hypertrophy after burn. In a trial including 102 children with 

major burns, liver size was measured by means of ultrasound, and 

liver weight was calculated weekly during hospital stay and at 6, 9, 

and 12 months after burn. The liver size was then compared with


Figure 124-4. Monitoring of fluid and energy balances with help of computerized systems facilitates decision making. For every 

24 hours (24 h per column), the figure shows energy target, enteral and intravenous energy delivery, energy balances, indirect 

calorimetry determinations, and protein intakes. The upper graph show daily energy balances and plasma albumin values, and 

the lower shows the fluid balance (full line) and evolution of weight curve. 

the predicted value for each individual. 52 Liver size and weight 

increased significantly during the first week after burn (mean 

85%), peaking at 2 weeks after burn (mean 126%): at discharge, 

the increase was still 89%. At 6, 9, and 12 months, the liver weight 

remained elevated by 40 to 50% compared with the predicted liver 

weight. The hepatic protein synthesis was affected up to 9 months 

after burn. 

Liver dysfunction is clearly multifactorial—high dose insulin 

and glucose have been blamed, as well as peripheral lipolysis. 54 

Some years back an isotopic investigation in 6 patients with severe 

burns showed that despite a glucose delivery rate similar to 100% 

in excess of energy requirements, did not alter total hepatic very 

low-density protein (VLDL) triglyceride (TG) secretion rate, 

plasma TG concentration, nor plasma VLDL TG concentration. 141 

Instead, the high-carbohydrate delivery in conjunction with 

insulin therapy nearly tripled the proportion of de novo– 

synthesized palmitate in VLDL TG front, with a corresponding 

decreased amount of palmitate from lipolysis. A 15-fold increase 

in plasma insulin concentration did not change the rate of release 

of FA into plasma. The peripheral release of FA represents a far 

greater potential for hepatic lipid accumulation in burn patients 

than the endogenous hepatic fat synthesis, even during excessive 

carbohydrate intake in conjunction with insulin therapy 

Control of hyperglycemia has been shown to decrease 

mortality in some categories of surgical critically ill adults, 142 

whereas data in children remain few but encouraging. A study 

in burned children with a before and after design including 

64 children, 143 targeted glucose 90 to 120 mg/dL in the interven - 

tion group showed that intensive insulin therapy was safe: it was 

associated with lower infection rates (urinary tract infections) and 

improved survival. 

Anabolic Agents 

A continued catabolic state results in weight loss, lean muscle loss, 

immunologic compromise, and poor or delayed wound healing 

with prolonged recovery times. Various efforts have been made to


promote anabolism. Recombinant human growth hormone 

(rhGH) therapy has been extensively investigated: in GH-deficient 

children, rhGH therapy improved nitrogen balance, increased 

body cell mass, and promoted bone formation. 144 These effects 

make GH a candidate for anabolism stimulation. Supplementation 

studies in burned pediatric patients have shown a decrease in 

donor-site healing times and length of hospital stay per 1% burned 

BSA, and attenuation of hypermetabolism and of inflammation 

particularly when used in combination with propranolol. 145 

Although safe in children, the use of rhGH in critically ill adult 

patients is not warranted, because it doubles mortality, mainly 

from multiple organ dysfunction and septic shock. 146 

Insulin has well-known anabolic properties, as it promotes 

protein synthesis. In a group of adolescent patients, high-dose 

intravenous glucose along with insulin was associated with a 

2-day reduction in the donor-site healing time. 147 However, recent 

data show that high loads of glucose promote de novo lipogenesis 

in the critically ill. 57 In combination with data published regarding 

liver fat deposits on postmortem pathologic evaluation in patients 

receiving large glucose loads, 55 the de novo lipogenesis data 

indicate that using high glucose loads along with insulin should be 

restricted until further studies prove its safe use. 

Micronutrients 

Trace element deficiencies (particularly copper, iron, and zinc) 

have been known to occur in burned children since the 1970s. 138 

They are largely explained by exudative cutaneous losses which 

have now been confirmed in children. 22 Copper, which plays an 

essential role in collagen synthesis, wound repair, and immunity, 

is strongly depleted in burns. 138 Early trace element supplementation 

is associated with improved wound healing, decreased 

protein catabolism, decreased pulmonary infection, and shortened 

ICU stay. 138 During artificial nutrition, special attention should be 

given to all micronutrients; trace element and vitamin contents of 

enteral nutrition or of standard parenteral nutrition additives are 

insufficient to cover the increased requirements after burns. The 

standard recommendations for pediatric parenteral supplements 

are provided in Table 124–9. 148 Additional intravenous vitamin C, 

vitamin E, copper, selenium, and zinc supplements should be 

provided. 22 Doses and combinations of micronutrients used in our 

institution, calculated by adapting the adult doses to the weight of 

the pediatric patients, are proposed in the same Table 9. Some 

micronutrient supplements may be provided by either the enteral 

or intravenous routes. On the other hand, because there is competition 

and antagonism for intestinal transmucosal transport, 

copper and zinc are best provided by the intravenous route. 

Calcium and Bone Metabolism 

Calcium, magnesium, and phosphorus homeostasis are severely 

altered after trauma and particularly after burns. 149 The changes 

are long-lasting and continue into the recovery period, many years 

after the injury. Bone formation is reduced both in adults and 

children when burns exceed 40% BSA. Bone mineral density is 

significantly lower in burned children compared with the same 

age-related normal children. Girls have improved bone mineral 

content and percentage fat compared with boys. 52 The consequences 

are increased risk of fractures, decreased growth velocity 

and, finally, stunting. 144 The bone is affected for multiple reasons, 

such as alteration of mineral metabolism, elevated cytokine and 

corticosteroid levels, decreased GH, nutritional deficiencies, and 

interoperative immobilization. Cytokines contribute to the 

alterations, particularly interleukin-1β and interleukin-6, which 

are greatly increased in burns, and stimulate osteoblast-mediated 

bone resorption. Cortisol production is increased in burns, 

leading to decreased bone formation. Low GH levels fail to 

promote bone formation. 144 Various studies suggest that immobilization 

plays a primary role in the pathogenesis of burnassociated 

bone disease. 150 Alterations of magnesium and calcium 

homeostasis constitute another cause. Hypocalcemia and hypomagnesemia 

are constant findings, and ionized calcium remains 

low for weeks 35 ; the alterations are partly explained by large 

TABLE 124-9. Recommended Daily Intravenous Micronutrient Supplements After Burn Injury Versus in Patients 

Without Burns 

Daily Intravenous Supplements 

Micronutrient Dose: Major Burns (Nonburned Patient) Comment 

Magnesium 

Multitrace element solution 

Additional trace element 

supplement 

Multivitamin preparation 

Additional vitamin E 

Additional ascorbic acid 

0.25 mmol/kg 

Many brands available 

Administer daily requirements according to label 

4 mL per kg of a 250 mL solution containing: 

• Copper 3.75 mg → 60 mg/kg (20 mg/kg) 

• Selenium 375 µg → 6 µg/kg(1.5 µg/kg) 

• Zinc 37.5 mg → 600 µg/kg (100 µg/kg) 

• Glu-1-P 1200 mg → 19 mg/kg 

Many brands available 

Administer daily requirement according to label 

1.5 mg/kg 60 kg: maximum 100 mg 

15 mg/kg maximum 40 kg: 500 mg 

from 60 kg: 1000 mg 

BSA = body surface area; Glu-1-P = glucose-1-phosphate; arrow = yield. 

Both basic requirements and supplements should be administered as of admission. 

Partially adapted from Greene et al. 148 

May be given by the enteral route 

Start on admission 

Start on admission and pursue 

according to burns for: 

BSA 30%: 15 days 



May be given by the enteral route 

Start on admission


exudative magnesium and phosphorus losses. 149 A close followup 

of ionized calcium, magnesium, and inorganic phosphate is 

mandatory, since burn patients usually require substantial supplementation 

by intravenous or enteral routes. 

Heterotopic ossification, which is encountered only occasionally 

in children, is an alteration of calcium metabolism 

associated with an invalid state. It has not been entirely elucidated; 

new bone is formed in tissues that do not normally ossify. The 

condition is favored by immobilization. Nutritional supplements 

have been implicated and reported to mobilize calcium and to 

increase calciuria. 151 Overzealous joint manipulation causing 

microtrauma to the musculotendinous apparatus is also probably 

involved. 152 

Septic Complications 

Due to an overall depression of the immune defense system, burn 

patients have a high incidence of septic complications. Pulmonary 

and cutaneous infections are the most frequent, followed by 

urinary and blood stream infections. The use of prophylactic 

antibiotherapy in acute burns enhances the development of 

resistant organisms, although only minimally reducing the 

incidence of sepsis. There are no data showing a reduction of 

wound infections due to prophylaxis. Therefore, antibiotic treatment 

must be directed against identified germs. Children frequently 

have other sources of infections (e.g., upper respiratory 

tract infections, otitis media) that require appropriate treatment. 

Ethical Issues 

Therapy withdrawal or withholding is a sensitive question all over 

the world. It becomes even more difficult when children are 

concerned. Very little literature exists in this area. The national 

legislations vary from complete interdiction to tolerance of therapy 

withholding or withdrawal. There are, in addition, important 

cultural, religious, and individual factors involved that explain the 

large variability. Whatever the attitude toward these issues, any 

intensivist would agree that some victims of burns are identified 

early as probable nonsurvivors. Major burns involving more than 

80% BSA with extensive destruction of face and limbs, extremes of 

age, and unprecedented survival in an institution may call for such 

reflection. Under certain circumstances, the decision to withhold 

curative treatment and to focus on the patient’s comfort may be 

considered a treatment option, applying to both children and 

adults. Some institutions have communication protocols that 

facilitate the discussion of the topic, but most do not. Implementing 

“do not resuscitate” order guidelines must be based on 

the particular center’s experience as well as on its cultural and 

legislative background. When legally possible, decisions not to 

resuscitate or to withhold further treatment should be based on a 

multidisciplinary approach. 

CONCLUSION 

Care of the burned patients involves detailed knowledge of the 

pleiomorphic effects of burn injuries on all the organ systems. The 

extensive alterations will modify pharmacokinetics and pharmacodynamics 

of anesthetic agents. Burns are a devastating event 

in a child’s life: adequate analgesia and sedation and safe repeated 

anesthetic care, together with concern and understanding of the 

psychological aspects, maintenance of metabolic support to limit 

stunting observed after major burns, all contribute to limit the 

negative impact of severe burn injury on a young life. The management 

of these patients therefore requires a multidisciplinary 

approach and the constitution of a true burn team. 

REFERENCES 

1. Franco MA, Gonzales NC, Diaz ME, et al. Epidemiological and clinical 

profile of burn victims: Hospital Universitario San Vicente de Paul, 

Medellin, 1994–2004. Burns. 2006;32:1044–1051. 

2. Holland AJ. Pediatric burns: the forgotten trauma of childhood. Can J 

Surg. 2006;49:272–277. 

3. Langer S, Hilburg M, Drucke D, et al. Analysis of burn treatment for 

children at Bochum University Hospital. Unfallchirurg. 2006;109:862–866. 

4. Rawlins JM, Khan AA, Shenton AF, et al. Epidemiology and outcome 

analysis of 208 children with burns attending an emergency department. 

Pediatr Emerg Care. 2007;23:289–293. 

5. Roudsari BS, Shadman M, Ghodsi M. Childhood trauma fatality and 

resource allocation in injury control programs in a developing country. 

BMC Public Health. 2006;6:117. 

6. Xin W, Yin Z, Qin Z, et al. Characteristics of 1494 pediatric burn patients 

in Shanghai. Burns. 2006;32:613–618. 

7. Sheridan RL, Weber JM, Schnitzer JJ, et al. Young age is not a predictor 

of mortality in burns. Pediatr Crit Care Med. 2001;2:223–224. 

8. Thombs BD, Singh VA, Milner SM. Children under 4 years are at greater 

risk of mortality following acute burn injury: evidence from a national 

sample of 12,902 pediatric admissions. Shock. 2006;26:348–352. 

9. Young AE, Chambers TL. Standards for care of critically ill children with 

burns. Lancet. 2005;365:1911–1913. 

10. Finnerty CC, Herndon DN, Przkora R, et al. Cytokine expression profile 

over time in severely burned pediatric patients. Shock. 2006;26:13–19. 

11. Demling R, LaLonde C, Knox J, et al. Fluid resuscitation with deferoxamine 

prevents systemic burn-induced oxidant injury. J Trauma. 1991; 

31:538–544. 

12. Lund T, Wiig H, Reed RK. Acute postburn edema: role of strongly 

negative interstitial fluid pressure. Am J Physiol. 1988;255:H1069–1074. 

13. Kramer GC, Nguyen TT. Pathophysiology of burn shock and burn edema. 

In: Herndon D, editor. Total Burn Care. London: Saunders;1996. p. 44–52. 

14. Arturson G. Fluid therapy of thermal injury. Acta Anaesthesiol Scand. 

1985;29:55–59. 

15. Barber AE, Shires GT. Cell damage after shock. New Horizons. 1996;4: 

161–166. 

16. Gravante G, Delogu D, Sconocchia G. “Systemic apoptotic response” after 

thermal burns. Apoptosis. 2007;12:259–270. 

17. Carlson DL, Horton JW. Cardiac molecular signaling after burn trauma. 

J Burn Care Res. 2006;27:669–675. 

18. Marano MA, Fong Y, Moldawer LL, et al. Serum cachectin: tumor 

necrosis factor in critically ill patients with burns correlates with infection 

and mortality. Surg Gynecol Obstet. 1990;170:32–38. 

19. Marshall JC, Vincent JL, Fink MP, et al. Measures, markers, and mediators: 

toward a staging system for clinical sepsis. A report of the Fifth 

Toronto Sepsis Roundtable, Toronto, Ontario, Canada, October 25–26, 

2000. Crit Care Med. 2003;31:1560–1567. 

20. Allgöwer M, Schoenenberger GA, Sparkes BG. Burning the largest 

immune organ. Burns. 1995;21:S7–S47. 

21. Yamamoto H, Siltharm S, deSerres S, et al. Immediate burn wound excision 

restores antibody synthesis to bacterial antigen. J Surg Res. 1996;63:157–162. 

22. Berger MM. Acute copper and zinc deficiency due to exudative losses— 

substitution versus nutritional requirements. Burns. 2006;32:393. 

23. Demling RH. Fluid replacement in burned patients. Surg Clin North Am. 

1987;67:15–30. 

24. Carleton SC. Cardiac problems associated with burns. Cardiol Clin. 

1995;13:257–262. 

25. Zeng L, Chen Y, Wu M. Cardiac troponin I: a marker for detecting nonischemic 

cardiac injury. Zhonghua Yi Xue Za Zhi. 2001;81:393–395. 

26. Raffa J, Trunkey DD. Myocardial depression in acute thermal injury. 

J Trauma. 1978;18:90–93. 

27. Zang Q, Maass DL, White J, et al. Cardiac mitochondrial damage and loss 

of ROS defense after burn injury: the beneficial effects of antioxidant 

therapy. J Appl Physiol. 2007;102:103–112.


28. Yatani A, Xu DZ, Irie K, et al. Dual effects of mesenteric lymph isolated 

from rats with burn injury on contractile function in rat ventricular 

myocytes. Am J Physiol Heart Circ Physiol. 2006;290:H778–785. 

29. Goto M, Samonte V, Ravindranath T, et al. Burn injury exacerbates 

hemodynamic and metabolic responses in rats with polymicrobial sepsis. 

J Burn Care Res. 2006;27:50–59. 

30. Niederbichler AD, Westfall MV, Su GL, et al. Cardiomyocyte function 

after burn injury and lipopolysaccharide exposure: single-cell contraction 

analysis and cytokine secretion profile. Shock. 2006;25:176–183. 

31. Quinn DA, Moufarrej R, Volokhov A, et al. Combined smoke inhalation 

and scald burn in the rat. J Burn Care Rehabil. 2003;24:208–216. 

32. Ren J, Wu S. A burning issue: do sepsis and systemic inflammatory 

response syndrome (SIRS) directly contribute to cardiac dysfunction? 

Front Biosci. 2006;11:15–22. 

33. White J, Thomas J, Maass DL, et al. Cardiac effects of burn injury 

complicated by aspiration pneumonia-induced sepsis. Am J Physiol Heart 

Circ Physiol. 2003;285:H47–58. 

34. Reynolds EM, Ryan DP, Sheridan RL, et al. Left ventricular failure 

complicating severe pediatric burn injuries. J Pediatr Surg. 1995;30:264– 

269; discussion 269–270. 

35. Szyfelbein SK, Drop LJ, Martyn JAJ. Persistent ionized hypocalcemia in 

patients during resuscitation and recovery phases of body burns. Crit Care 

Med. 1981;9:454–458. 

36. Bargues L, Vaylet F, Le Bever H, et al. Respiratory dysfunction in burned 

patients. Rev Mal Respir. 2005;22:449–460. 

37. Fitzpatrick JC, Cioffi WG. Inhalation injury. Trauma Quart. 1994;11:114– 

126. 

38. Turnage RH, Nwariaku F, Murphy J, et al. Mechanisms of pulmonary 

microvascular dysfunction during severe burn injury. World J Surg. 

2002;26:848–853. 

39. Steinvall I, Bak Z, Sjoberg F. Acute respiratory distress syndrome is as 

important as inhalation injury for the development of respiratory 

dysfunction in major burns. Burns. 2008;. 

40. Ciesla DJ, Moore EE, Johnson JL, et al. The role of the lung in postinjury 

multiple organ failure. Surgery. 2005;138:749–757; discussion 757–748. 

41. Barrow RE, Jeschke MG, Herndon DN. Early fluid resuscitation improves 

outcomes in severely burned children. Resuscitation. 2000;45(2):91–96. 

42. Jeschke MG, Barrow RE, Wolf SE, et al. Mortality in burned children with 

acute renal failure. Arch Surg. 1998;133:752–756. 

43. Haberal MA. An eleven-year survey of electrical burn injuries. J Burn 

Care Rehabil. 1995;16:43–48. 

44. Gore DC, Hawkins HK, Chinkes DL, et al. Assessment of adverse events 

in the demise of pediatric burn patients. J Trauma-Injury Infect Crit Care. 

2007;63:814–818. 

45. Myers SI, Minei JP, Casteneda A, et al. Differential effects of acute thermal 

injury on rat splanchnic and renal blood flow and prostanoid release. 

Prostaglandins Leukotrienes Essential Fatty Acids. 1995;53:439–444. 

46. Gore DC, Dalton JM, Gehr TWB. Colloid infusions reduce glomerular 

filtration in resuscitated burn victims. J Trauma. 1996;40:356–360. 

47. Pruitt BA Jr, Foley FD, Moncrief JA. Curling’s ulcer: a clinical-pathology 

study of 323 cases. Ann Surg. 1970;172:523–539. 

48. Namias N. Advances in burn care. Curr Opin Crit Care. 2007;13(4):405– 

410. 

49. Ivy ME, Atweh NA, Palmer J, et al. Intra-abdominal hypertension and 

abdominal compartment syndrome in burn patients. J Trauma. 

2000;49:387–391. 

50. Raff T, Hartmann B, Germann G. Early intragastric feeding of seriously 

burned and long-term ventilated patients: a review of 55 patients. Burns. 

1997;23:19–25. 

51. Cunningham JJ. Factors contributing to increase energy expenditure in 

thermal injury: a review of studies employing indirect calorimetry. JPEN. 

1990;14:649–656. 

52. Jeschke MG, Finnerty CC, Suman OE, et al. The effect of oxandrolone on 

the endocrinologic, inflammatory, and hypermetabolic responses during 

the acute phase postburn. Ann Surg. 2007;246:351–360; discussion 360– 

352. 

53. Pereira CT, Murphy KD, Herndon DN. Altering metabolism. J Burn Care 

Rehabil. 2005;26(3):194–199. 

54. Aarsland A, Chinkes D, Wolfe RR, et al. Beta-blockade lowers peripheral 

lipolysis in burn patients receiving growth hormone. Ann Surg. 

1996;223:777–789. 

55. Burke JF, Wolfe RR, Mullany CJ, et al. Glucose requirements following 

burn injury. Ann Surg. 1979;190:274–285. 

56. Wolfe RR, Klein S, Herndon DN, et al. Substrate cycling in thermogenesis 

and amplification of net substrate flux in human volunteers and burned 

patients. J Trauma. 1990;30:S6–S9. 

57. Tappy L, Schwarz JM, Schneiter P, et al. Effects of isoenergetic glucosebased 

or lipid-based parenteral nutrition on glucose metabolism, de novo 

lipogenesis, and respiratory gas exchanges in critically ill patients. Crit 

Care Med. 1998;26:860–867. 

58. Wolf SE, Debroy M, Herndon DN. The cornerstones and directions of 

pediatric burn care. Pediatr Surg Int. 1997;12:312–320. 

59. Shiozaki T, Kishikawa M, Hiraide A, et al. Recovery from postoperative 

hypothermia predicts survival in extensively burned patients. Am J Surg. 

1993;165:326–330. 

60. Donner B, Tryba M, Kurz-Muller K, et al. Anesthesia and intensive care 

management of severely burned children of Jehovah’s Witnesses. 

Anaesthesist. 1996;45:171–517. 

61. Harries RHC, Phillips LG. Hematologic and acute phase response. In: 

Herndon D, editor. Total Burn Care. London: Saunders;1996. p. 293–301. 

62. Belmonte Torras JA, Marin de la Cruz D, Sune Garcia JM, et al. Burns 

produced by lighters. An Pediatr (Barc). 2006;64:468–473. 

63. Carter EA, Tompkins RG, Babich JW, et al. Decreased cerebral glucose 

utilization in rats during the ebb phase of thermal injury. J Trauma. 

1996;40:930–935. 

64. Zhang Q, Carter EA, Ma B, et al. Burn-related metabolic and signaling 

changes in rat brain. J Burn Care Res. 2008;29:346–352. 

65. Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of 

burns. BMJ. 2004;328:1427–1429. 

66. Chen EH, A Sareen. Do children require ECG evaluation and inpatient 

telemetry after household electrical exposures? Ann Emerg Med. 2007; 

49:64–67. 

67. Still JM Jr, Belcher K, Law EJ, et al. A double-blinded prospective 

evaluation of recombinant human erythropoietin in acutely burned 

patients. J Trauma. 1995;38:233–236. 

68. Scalfaro P, Haenggi MH, Roulet E, et al. Carbon monoxide poisoning in 

children: never trivialize. Rev Med Suisse Romande. 2000;120:259–262. 

69. Megarbane B, Delahaye A, Goldgran-Toledano D, et al. Antidotal 

treatment of cyanide poisoning. J Chin Med Assoc. 2003;66:193–203. 

70. Borron SW, Baud FJ, Barriot P, et al. Prospective study of hydroxocobalamin 

for acute cyanide poisoning in smoke inhalation. Ann Emerg 

Med. 2007;49:794–801, 801 e791–792. 

71. Fortin JL, Giocanti JP, Ruttimann M, et al. Prehospital administration of 

hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 

8 years of experience in the Paris Fire Brigade. Clin Toxicol (Phila). 2006;44 

Suppl 1:37–44. 

72. MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major thermal 

injury. Anesthesiology. 1998;89:749–770. 

73. Warden GD. Fluid resuscitation and early management. In: Herndon D, 

editor. Total Burn Care. London: Saunders;1996. p. 53–60. 

74. Fakler U, Pauli Ch, Balling G, et al. Cardiac index monitoring by pulse 

contour analysis and thermodilution after pediatric cardiac surgery. 

J Thorac Cardiovasc Surg. 2007;133(1):224–228. 

75. Barillo DJ. Planning for burn mass casualty incidents. J Trauma. 2007;62 

(suppl):S68. 

76. Sørensen B. Management of burns occurring as mass casualties after 

nuclear explosion. Burns. 1980;6. 

77. Berger MM, Eggimann P, Heyland DK, et al. Reduction of nosocomial 

pneumonia after major burns by trace element supplementation: aggregation 

of two randomised trials. Crit Care. 2006;10:R153:e-pub 2 Nov. 

78. Brown TCK, Fisk GC. Burns. In: Brown T, Fisk G, editors. Anesthesia for 

Children. 2nd ed. London: Blackwell Scientific Publication; 1992. p. 281–290. 

79. Pearson KS, From RP, Symreng T, et al. Continuous enteral feeding and 

short fasting periods enhance perioperative nutrition in patients with 

burns. J Burn Care Rehabil. 1992;13:477–481. 

80. Snelling CFT. Quantitative evaluation of blood loss during debridement 

and grafting in burns. Can J Surg. 1982;25:416–417. 

81. Goldstein B, Doody D, Briggs S. Emergency intraosseous infusion in 

severely burned children. Pediatr Emerg Care. 1990;6:195–197. 

82. Sheridan RL. Uncuffed endotracheal tubes should not be used in seriously 

burned children. Pediatr Crit Care Med. 2006;7:258–259. 

83. Milner EA, Cioffi WG, Mason AD, et al. A longitudinal study of resting 

energy expenditure in thermally injured patients. J Trauma. 1994;37:167– 

170. 

84. Martyn J. Clinical pharmacology and drug therapy in the burned patient. 

Anesthesiology. 1986;65:67–75.


85. Fee JP, Thompson GH. Comparative tolerability profiles of the inhaled 

anaesthetics. Drug Saf. 1997;16:157–170. 

86. Adams HA, Werner C. From the racemate to the eutomer: (S)-ketamine. 

Renaissance of a substance? Anaesthesist. 1997;46:1026–1042. 

87. Tosun Z, Esmaoglu A, Coruh A. Propofol-ketamine vs propofol-fentanyl 

combinations for deep sedation and analgesia in pediatric patients 

undergoing burn dressing changes. Paediatr Anaesth. 2008;18:43–47. 

88. Ceber M, Salihoglu T. Ketamine may be the first choice for anesthesia in 

burn patients. J Burn Care Res. 2006;27:760–762. 

89. Carsin H. Use of Diprivan in burn patients. Ann Fr Anesth Reanim. 

1994;13:541–544. 

90. Murat I, Billard V, Vernois J, et al. Pharmacokinetics of propofol after a 

single dose in children aged 1–3 years with minor burns. Comparison of 

three data analysis approaches. Anesthesiology. 1996;84:526–532. 

91. Han TH, Lee JH, Kwak IS, et al. The relationship between bispectral 

index and targeted propofol concentration is biphasic in patients with 

major burns. Acta Anaesthesiol Scand. 2005;49:85–91. 

92. Fodale V, La Monaca E. Propofol infusion syndrome: an overview of a 

perplexing disease. Drug Saf. 2008;31:293–303. 

93. Bray RJ. Propofol infusion syndrome in children. Paediatr Anaesth. 

1998;8:491–499. 

94. Honnegger P, Matthieu JM. Selective toxicity of the general anesthetic 

propofol for GABAergic neurons in rat brain cell cultures. J Neuroscience 

Res. 1996;45:631–636. 

95. Escarment J, Cantais E, Le Dantec P, et al. Propofol and ketamine for 

dressing in burnt patients. Can Anesthesiol. 1995;43:31–34. 

96. Yagmurdur H, Akca G, Aksoy M, et al. The effects of ketamine and 

propofol on bacterial translocation in rats after burn injury. Acta 

Anaesthesiol Scand. 2005;49:177–182. 

97. Coimbra C, Choiniere M, Hemmerling TM. Patient-controlled sedation 

using propofol for dressing changes in burn patients: a dose-finding 

study. Anesth Analg. 2003;97:839–842. 

98. Martyn JA, White DA, Gronert GA, et al. Up-and-down regulation of 

skeletal muscle acetylcholine receptors. Effects on neuromuscular 

blockers. Anesthesiology. 1992;76:822–843. 

99. Ward JM, Rosen KM, Martyn JAJ. Acetylcholine receptor subunit 

mRNA changes in burns are different from those seen after denervation: 

The 1993 Lindberg award. J Burn Care Rehabil. 1993;14:595–601. 

100. Belin RP, Karleen CI. Cardiac arrest in the burned patient following 

succinyldicholine administration. Anesthesiology. 1966;27:516–518. 

101. Bush GH, Graham HA, Littlewood AH, et al. Danger of suxamethonium 

and endotracheal intubation in anaesthesia for burns. Br Med J. 1962; 

2:1081–1085. 

102. Forrest T. A report on two cases of cardiac arrest. Brit J Anaesth. 1959;31: 

277–279. 

103. Tolmie JD, Joyce TH, Mitchell GD. Succinylcholine danger in the burned 

patient. Anesthesiology. 1967;28:467–470. 

104. Moore GP, Pace SA, Busby W. Comparison of intraosseous, intramuscular, 

and intravenous administration of succinylcholine [Letters]. 1989; 

5:209–210. 

105. Mills AK, Martyn JAJ. Neuromuscular blockade with vecuronium in 

paediatric patients with burn injury. Br J Clin Pharmacol. 1989;28:155– 

159. 

106. Badetti C, Pascal L, Bernini V, et al. Resistance to vecuronium in burnt 

patients. Influence of the burnt surface on the effectiveness of the dose. 

Ann Fr Anesth Reanim. 1996;15:135–141. 

107. Uyar M, Hepaguslar H, Ugur G, et al. Resistance to vecuronium in 

burned children. Paediatr Anaesth. 1999;9:115–118. 

108. Han T, Kim H, Bae J, et al. Neuromuscular pharmacodynamics of rocuronium 

in patients with major burns. Anesth Analg. 2004;99:386–392. 

109. Werba AE, Neiger FX, Bayer GS, et al. Pharmacodynamics of mivacurium 

in severely burned patients. Burns. 1995;22:62–64. 

110. Martyn JAJ, Szyfelbein SK, Sheridan R, et al. Burned patients are not 

resistant to the neuromuscular effetcs of mivacurium. Europ J Anaesth. 

1997;14 (Suppl.6):1. 

111. Choinière M. Pain of burns. In: Wall P, Melzack R, editors. Textbook of 

Pain. 3rd ed. London: Churchill Livingstone; 1994. 

112. Ashburn M. A. Burn pain: the management of procedure-related pain. 

J Burn Care Rehabil. 1995;16:365–371. 

113. Friedland LR, Pancioli AM, Duncan KM. Pediatric emergency 

department analgesic practice. Pediatr Emerg Care. 1997;13:103–106. 

114. Zernikow B, Burk G, Michel E. Pain therapy in acute pediatric diseases 

and vaccination. Schmerz. 2000;14:319–323. 

115. Jellish WS, Gamelli RL, Furry PA, et al. Effect of topical local anesthetic 

application to skin harvest sites for pain management in burn patients 

undergoing skin-grafting procedures. Ann Surg. 1999;229:115–120. 

116. Beushausen T, Mucke K. Anesthesia and pain management in pediatric 

burn patients. Pediatr Surg Int. 1997;12:327–333. 

117. Foyatier JL, Latarjet J, Comparin JP, et al. Treatment of burns in infants. 

Arch Pediatr. 1995;2:1000–1006. 

118. Hughes J, Leach HJ, Choonara I. Hallucinations on withdrawal of 

isoflurane used as sedation. Acta Paediat. 1993;82:885–886. 

119. Cederholm I, Bengtsson M, Björkman S, et al. Long term high dose 

morphine, ketamine and midazolam infusion in a child with burns. 

Br J Clin Pharmacol. 1990;30:901–905. 

120. Martyn J, Greenblatt DJ. Lorazepam conjugation is unimpaired in burn 

trauma. Clin Pharmacol Ther. 1988;43:250–255. 

121. Rice TL, Kyf JV. Intranasal administration of midazolam to a severely 

burned child. Burns. 1990;16:307–308. 

122. Choinière M, Grenier R, Paquette C. Patient-controlled analgesia: a 

double-blind study in burn patients. Anaesthesia. 1992;47:467–472. 

123. Patterson DR, Hoffman HG, Weichman SA, et al. Optimizing control of 

pain from severe burns: a literature review. Am J Clin Hypn. 2004;47:43–54. 

124. de Jong AE, Middelkoop E, Faber AW, et al. Non-pharmacological 

nursing interventions for procedural pain relief in adults with burns: a 

systematic literature review. Burns. 2007;33:811–827. 

125. Cuignet O, Pirson J, Boughrouph J, et al. The efficacy of continuous 

fascia iliaca compartment block for pain management in burn patients 

undergoing skin grafting procedures. Anesth Analg. 2004;98:1077–1081. 

126. Cuignet O, Mbuyamba J, Pirson J. The long-term analgesic efficacy of a 

single-shot fascia iliaca compartment block in burn patients undergoing 

skin-grafting procedures. J Burn Care Rehabil. 2005;26:409–415. 

127. Steadman PB, Pegg SP. A quantitative assessment of blood loss in burn 

wound excision and grafting. Burns. 1992;18:490–491. 

128. Losee J.E, Fox I, Hua LB, et al. Transfusion-free pediatric burn surgery: 

techniques and strategies. Ann Plast Surg. 2005;54:165–171. 

129. Xiao-Wu W, Herndon DN, Spies M, et al. Effects of delayed wound excision 

and grafting in severely burned children. Arch Surg. 2002;137:1049–1054. 

130. Hébert PC, Blajchman MA, Marshall J, et al. A multicenter, randomized, 

controlled clinical trial of transfusion requirements in critical care. New 

Engl J Med. 1999;340:409–417. 

131. Fleming RY, Herndon DN, Vaidya S, et al. The effect of erythropoietin 

in normal healthy volunteers and pediatric patients with burn injuries. 

Surgery. 1992;112:424–431; discussion 431–422. 

132. Cartotto R, Kadikar N, Musgrave MA, et al. What are the acute 

cardiovascular effects of subcutaneous and topical epinephrine for 

hemostasis during burn surgery? J Burn Care Rehabil. 2003;24:297–305. 

133. McGill V, Kowal-Vern A, Gamelli RL. A conservative thermal injury 

treatment protocol for the appropriate Jehovah’s Witness candidate. 

J Burn Care Rehabil. 1997;18:133–138. 

134. Barret JP, Desai MH, Herndon DN. Effects of tracheostomies on 

infection and airway complications in pediatric burn patients. Burns. 

2000;26:190–193. 

135. Murphy J, Purdue G, Hunt J, et al, editors. Burn Injury. 2nd ed. New 

York: Churchill Livingstone; 1997. 

136. Tanaka H, Matsuda T, Miyagantani Y, et al. Reduction of resuscitation 

fluid volumes in severely burned patients using ascorbic acid administration. 

Arch Surg. 2000;135:326–331. 

137. Agay D, Sandre C, Ducros V, et al. Optimization of selenium status by a 

single intra-peritoneal injection of Se in Se deficient rat: possible application 

to burned patient treatment. Free Rad Biol Med. 2005;39:762–768. 

138. Berger MM, Baines M, Raffoul W, et al. Trace element supplements after 

major burns modulate antioxidant status and clinical course by way of 

increased tissue trace element concentration. Am J Clin Nutr. 2007;85: 

1293–1300. 

139. Greenhalgh DG, Housinger TA, Kagan RJ, et al. Maintenance of serum 

albumin levels in pediatric burn patients: a prospective randomized trial. 

J Trauma. 1995;39:67–74. 

140. Herndon DN, Barrow RE, Stein M, et al. Increased mortality with 

intravenous supplemental feeding in severely burned patients. J Burn 

Care Rehabil. 1989;10:309–313. 

141. Aarsland A, Chinkes DL, Sakurai Y, et al. Insulin therapy in burn patients 

does not contribute to hepatic triglyceride production. J Clin Invest. 

1998;101:2233–2239. 

142. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy 

in critically ill patients. New Engl J Med. 2001;345:1359–1367.


143. Pham TN, Warren AJ, Phan HH, et al. Impact of tight glycemic control 

in severely burned children. J Trauma. 2005;59:1148–1154. 

144. Klein GL, Wolf SE, Langman CB, et al. Effect of therapy with recombinant 

human growth hormone on insulin-like growth factor system 

components and serum levels of biochemical markers of bone formation 

in children after severe burn injury. J Clin Endocrinol Metab. 1998;83: 

21–24. 

145. Jeschke MG, Finnerty CC, Kulp GA, et al. Combination of recombinant 

human growth hormone and propranolol decreases hypermetabolism 

and inflammation in severely burned children. Pediatr Crit Care Med. 

2008;9:209–216. 

146. Takala J, Ruokonen E, Webster NR, et al. Increased mortality associated 

with growth hormone treatment in critically ill adults. New Engl J Med. 

1999;341:785–792. 

147. Pierre EJ, Barrow RE, Hawkins HK, et al. Effects of insulin on wound 

healing. J Trauma. 1998;44:342–345. 

148. Greene HL, Hambidge KM, Schanler R, et al. Guidelines for the use 

of vitamins, trace elements, calcium, magnesium, and phosphorus in 

infants and children receiving total parenteral nutrition: Report of the 

subcommittee pn pediatric parenteral nutrition from the Committee on 

Clinical Practice Issues of the American Society for Clinical Nutrition. 

Am J Clin Nutr. 1988;48:1324. 

149. Berger MM, Rothen C, Cavadini C, et al. Exudative mineral losses after 

serious burns: a clue to the alterations of magnesium and phosphate 

metabolism. Am J Clin Nutr. 1997;65:1473–1481. 

150. Klein GL, Kikuchi Y, Sherrard DJ, et al. Burn-associated bone disease in 

sheep: roles of immobilization and endogenous corticosteroids. J Burn 

Care Rehabil. 1996;17:518–521. 

151. Evans B. Heterotopic bone formation in thermal burns. Clin Orthop 

Related Res. 1991;263:94–101. 

152. Peterson SL, Mani MM, Crawford CM, et al. Postburn heterotopic 

ossification: insights for management decision making. J Trauma. 1989; 

29:365–369. 

153. Weinbroum AA, Helpern P, Rudick Sorkine, P, et al. Midazolam versus 

proprofol for long-term sedation in the ICU: a randomized prospective 

comparison. Intensive Care Med. 1997;23:1258–1263.

Chapter 124

Create successful ePaper yourself

Delete template?

Save as template?