Cardiac

Immediately after an injury, cardiac output is dramatically reduced.^22,23 This decrease is often related to the rapid reduction in circulating blood volume and the severe compressive effects of circumferential burns on the abdomen and chest that impair venous return.²⁴ Despite adequate cardiac filling pressures, cardiac output often remains reduced. This may result from other factors, such as direct myocardial depression from the burn injury. Some investigators have described circulating myocardial depressant factors such as interleukins, tumor necrosis factors, or oxygen free radicals existing in subjects with extensive third-degree burns.^25–28 Transesophageal echocardiography may be helpful in guiding supportive care in the early phase.²⁹ At our institution, acutely burned children frequently require inotropic support during the acute period of depressed cardiac function. Carefully titrated inotropic support improves cardiac output, without the need for volume overload–mediated improvement in cardiac function.

Children develop a hypermetabolic state 3 to 5 days after a burn injury. This state is associated with a twofold to threefold increase in cardiac output, which persists for weeks to months, depending on the extent of the injury and the time needed for wound closure; heart rate, cardiac output, cardiac index, and rate-pressure-product are increased for at least 2 years after burns that involve 40% or greater of body surface area.³⁰ Some children develop a reversible cardiomyopathy.³¹ Hypertension has been reported to occur during this hypermetabolic period. The most common cause of the hypertension in this period is inadequate pain control, and this should be ruled out. However, other circulating mediators such as increased catecholamines, atrial natriuretic factor, renin-angiotensin, endothelin-1, and vasopressin and other circulating vasoactive mediators can cause intermittent or persistent hypertension in patients with burn injuries.^32–36 If decreased cardiac output is observed during this hypermetabolic state, gram-negative sepsis or hypovolemia should be suspected. Closure of the burn wound usually decreases metabolic demand, resulting in a concomitant reduction in cardiac output.^37,38 Some children may benefit from treatment with propranolol, which reduces cardiac work and decreases the systemic inflammatory response.^39,40

Pulmonary

Pulmonary function may be adversely affected from the upper airway to terminal alveoli. The upper airway is an excellent heat exchanger; just as it warms cold air, it cools hot air. The cooling of hot inspired air may cause a thermal injury to the tissues of the larynx; the air in a closed space (e.g., house or automobile fire) may reach 538° C (1000° F) 2 feet above floor level. Inspiration of superheated air damages the upper airway. Airway obstruction occurs as a result of massive edema formation involving laryngeal and tracheal structures above the carina (see later). The thermal insult also may injure the ciliated epithelium and mucosa in the proximal bronchi. The inhalation of toxic fumes, such as nitrogen dioxide and sulfur dioxide released from burning plastic, which combine with water in the tracheobronchial tree to form nitric and sulfuric acids, may damage the distal bronchi and alveoli. Thus upper airway injury is usually a thermal insult, whereas lower airway injury is a chemical or toxic insult. Acid gases such as hydrochloric acid, sulfuric acid, and phosgene form small aerosolized particles that penetrate deep into the tracheobronchial tree, damaging the alveolar membranes and surfactants.⁴¹ Wool and cotton combustion forms aldehydes, which may cause pulmonary edema in concentrations as small as 10 ppm.⁴² Combustion of synthetic materials (insulation, wall paneling) releases hydrogen cyanide. Although cyanide is a rare toxin in fires,⁴³ cyanide poisoning can lead to histotoxic hypoxia and death,⁴⁴ mimicking carbon monoxide (CO) poisoning. Inhalation of hydrogen cyanide is an often unrecognized cause of immediate death.

The overall effect of a pulmonary inhalation injury is necrotizing bronchitis, bronchial swelling, alveolar destruction, exudation of protein, loss of surfactant, loss of the protective bronchial lining, and bronchospasm, all of which contribute to the development of bronchopneumonia (Figs. 34-2 and 34-3). Inhalation of particulate matter (smoke, soot) and lower airway edema also obstruct the airway mechanically. Edema of the bronchi, combined with loss of integrity of the pulmonary capillary endothelium, decrease pulmonary compliance. Circumferential chest burns may have a tourniquet-like effect that decreases chest wall compliance.²⁴ All of these injuries lead to clinically important ventilation-perfusion abnormalities and right-to-left intrapulmonary shunting, with hypoxemia and hypercarbia. In adults, the Pao₂/Fio₂ ratio and baseline carboxyhemoglobin concentrations are predictive of mortality.⁴⁵ One pediatric trial of inhaled heparin and acetylcysteine suggested a benefit with decreased airway cast formation and mucus plugging.⁴⁶ However, subsequent studies have yielded contradictory results.^47,48 CO inhalation can further compromise both hemoglobin’s oxygen (O₂)-carrying capacity and its ability to deliver O₂ to tissues. CO also impairs O₂ usage at the cellular level (cellular respiration). Severe smoke inhalation alone may occur without externally visible injuries.⁴⁹ One clue that smoke inhalation has occurred is the presence of singed nasal hairs or nasal passages. Extrapulmonary factors such as changes in cardiac output also can contribute to hypoxemia. Blood gas analysis alone may not indicate these factors. Rational therapy of arterial O₂ desaturation requires evaluation of both extrapulmonary and intrapulmonary factors,^21,50 including cardiac output, mixed venous O₂ content or saturation, and shunt fraction.²² In general, the prognosis of cutaneous burn is compounded by the presence of an inhalation injury; the presence of an inhalational injury doubles the mortality rate from cutaneous burns,⁴¹ with pediatric mortality reported to be approximately 16%.⁵¹

FIGURE 34-2 A, Cross section of a normal bronchiole. Note the ciliated epithelial layer. B, Compare with a cross section of a distal bronchiole from a child who died of an inhalation injury. Note the marked thickening of the bronchial wall, the massive inflammatory cell infiltrate, the sloughing of the mucosa, and the total destruction of the ciliated columnar epithelium.

FIGURE 34-3 A, Normal alveoli. B, Inhalation alveolar injury is generally related to noxious fumes such as nitrogen dioxide and sulfur dioxide that are carried far down the tracheobronchial tree, combine with exhaled water, and form nitric acid and sulfuric acid, resulting in pulmonary congestion, alveolar injury, and hyaline membrane formation.

Renal

Renal function may be adversely affected soon after injury, primarily as a result of myoglobinuria and hemoglobinuria.⁵² The former is most common after electrical injury,^53,54 whereas the latter is common after severe cutaneous burns of 40% or greater of body surface area. Hypovolemia, hypotension, and hypoxemia may further aggravate renal dysfunction, leading to acute tubular necrosis. Catecholamines, angiotensin, and vasopressin production increase, leading to systemic vasoconstriction, compounding the renal insufficiency.^55,56 Release of vasoactive peptides such as endothelin-1 may cause acute vasoconstriction, which also may adversely affect renal function.^57,58 Fluid retention is common during the first 3 to 5 days after injury and is followed by diuresis thereafter. Thus renal function may be impaired soon after the injury, delaying the excretion of some drugs or their active metabolites. At 3 to 7 days after the burn injury, glomerular filtration rate increases pari passu with an increased cardiac output and metabolic rate.⁵⁹ The serum half-life of many antibiotics and other medications that depend on renal excretion may be altered as a result of changes (increased or decreased) in the glomerular filtration rate.^60–64 Children who sustain a burn that covers greater than 40% of their body surface area demonstrate renal tubular dysfunction, in the form of an inability to concentrate the urine.²⁰ Even during hyperosmolar states, antidiuresis is not observed, suggesting an inadequate renal response to antidiuretic hormone and aldosterone. Thus an adequate urine output may be observed even in the presence of hypovolemia.⁶⁵ Episodic or persistent hypertension is frequent in children, in part mediated by an increase in renin and catecholamine production.^66,67 If hypertension persists, treatment that decreases stress on the cardiovascular system or reduces the potential for hypertensive encephalopathy should be instituted.

Hepatic

The liver may be damaged by hypoxemia or hypoperfusion during the early postburn phase as a result of inhaled or absorbed chemical toxins, hypovolemia, or hypotension.^68,69 Reperfusion injury may harm the liver when adequate circulation is reestablished. Delayed hepatic dysfunction may result from drug toxicity, sepsis, the hypermetabolic response to burns, or blood transfusions.⁷⁰ Studies in adults have found increased hepatic blood flow, increased protein synthesis and breakdown, and increased hepatic gluconeogenesis during the hypermetabolic phase of burn injury. With the onset of sepsis, hepatic glucose output and alanine uptake may decrease sharply but hepatic blood flow and O₂ usage can remain increased.^68,71 Fatty infiltration of the liver also has been reported.⁷² Sustained increases in hepatic blood flow deliver more drug to the liver; this effect, combined with drug-induced enzyme induction, may decrease the half-life of drugs that are perfusion limited.⁷³ Although all studies of animals suggest decreased clearance of drugs after burn injury, clinical studies of the capacity of the liver to metabolize drugs are conflicting, even for the same class of drugs.^74–79 The magnitude of the burn, the time after injury, and the effects of co-administered drugs, alone or in combination, as well as alterations in protein binding and volume of distribution, may have a role in these conflicting reports.

Central Nervous System

The central nervous system (CNS) may be adversely affected by inhalation of neurotoxic chemicals or by hypoxic encephalopathy; other contributing factors include sepsis, hyponatremia, and hypovolemia.⁸⁰ CNS dysfunction includes hallucinations, personality changes, delirium, seizures, abnormal neurologic symptoms, and coma.⁸¹ These effects may be due to the burn injury or to the administration of drugs necessary for sedation, anxiolysis, and analgesia.⁸² Such effects usually clear after several weeks. Abnormalities of CNS neurotransmitters have been postulated to mediate the anorexia associated with extensive burn injury.⁸³ The possibility of cerebral edema and increased intracranial pressure also must be considered during the initial phases of burn injury. Under such circumstances, the usual measures for treating increased intracranial pressure would be instituted (see Chapter 24). Data suggest that rapid overcorrection of hyponatremia also may be associated with cerebral injury.⁸⁴

Hematologic

Blood viscosity may increase as a result of hemoconcentration secondary to fluid shifts and because of alterations in plasma protein content.⁸⁵ The hematopoietic system is also adversely affected. Ongoing microangiopathic hemolytic anemia secondary to the burn injury is common.⁸⁶ An inhibitor of erythroid stem cells has been found in the sera of burn patients, which may in part contribute to the anemia of burn injury. Another study has demonstrated a normal erythropoietin response to anemia in patients with burn injury.⁸⁷ The half-life of red blood cells is diminished in burn patients, and multiple blood draws may contribute to the development of anemia.^88,89 The possible role of recombinant erythropoietin in the care of children with burns has yet to be defined.^90,91 One study in adults reported no reduction in either mortality or blood transfusion requirements in patients who received recombinant erythropoietin compared with controls.⁹²

In the early stage, thrombocytopenia secondary to increased platelet aggregation and trapping of platelets in the lungs is followed by an increase in platelet count 10 to 14 days after the burn injury. A prolonged period of thrombocytopenia and reduced nadir in platelet count compared to survivors are both associated with increased mortality.⁹³ This thrombocytopenia may persist for several months.^89,93 An increase in fibrin split products (disseminated intravascular coagulopathy), which lasts for 3 to 5 days, may occur.⁶² Factors V, VII, and VIII and fibrinogen are also increased several-fold over baseline for the first 3 months after severe injury uncomplicated by sepsis.^94,95 Children with increased platelet counts (>1 million/mm³) who then developed sepsis in our unit experienced a marked decrease in the platelet count. The sudden onset of thrombocytopenia should prompt an evaluation of the child for sepsis.⁹⁶ Likewise, large swings in the fibrinogen concentration can occur (up to 2 g/dL),⁹⁷ although these do not appear to herald an increase in the incidence of thrombotic events.

Gastrointestinal

Gastrointestinal function is diminished immediately after thermal injury secondary to the onset of gastric stasis and intestinal ileus.⁹⁸ Because of the risk of pulmonary aspiration of gastric contents during this time, the stomach should be adequately vented and appropriate gastric acid ulcer prophylaxis instituted. At 48 to 72 hours after a burn injury, when generalized edema is resolving, gastrointestinal function usually resumes. Enteral feeding should be established at this time to provide calories, to blunt the hypermetabolic response, and to attenuate gluconeogenesis and stress ulceration.^85,99,100 Early enteral feeding has the added advantages of diminishing muscle catabolism, reducing bacterial translocation through the intestinal mucosa and is associated with reduced mortality.^101–104

In children who do not tolerate enteral feeding, parenteral nutrition must be initiated.^99,105–107 Stress ulcers (Curling ulcers) are associated with any burn injury and may be life-threatening, although the incidence has decreased in critically ill patients, in part because of improved pharmacologic control of gastric acidity.¹⁰⁸ Prospective studies of pediatric and adult burn patients and patients in intensive care indicate that cimetidine or ranitidine in the usual doses does not adequately protect critically ill patients from increases in gastric acidity.^60,61 The increased requirement for drugs is due to differences in their pharmacokinetics.⁶⁰ Therefore frequent feedings when tolerated and the liberal use of antacids, combined with larger or more frequent doses of H₂-receptor antagonists (or proton pump inhibitors), may be required to prevent development of stress ulcers.^60,85,98

Endocrine

The endocrinologic response to acute thermal injury is complex, involving most organ systems. Stimuli that trigger endocrine responses include the thermal injury itself and subsequent fluid shifts, as well as the stress responses that are associated with critical illness.¹⁰⁹ These may include decreased circulating hormone concentrations (e.g., triiodothyronine, dehydroepiandrosterone, and testosterone), as well as increased concentrations of other hormones (antidiuretic hormone, catecholamines, renin, angiotensin II, and cortisol).¹¹⁰ Replacement therapy with synthetic androgenic steroids (e.g., oxandrolone) shortens acute hospital stay and improves body composition (lean body mass) and hepatic protein synthesis.^111,112 Glucose control may be poor, owing to the increased levels of cortisol and insulin resistance.¹¹³ Tight control of hyperglycemia may improve mitochondrial oxidative capacity,¹¹⁴ decrease the incidence of urinary tract infection, and improves the survival of critically ill burn patients, although the last finding resulted from a single study.^115,116 Avoiding hyperglycemia may attenuate the risk of cerebral injury from hypoperfusion states (see Chapters 24 and 39); one group recommends a target blood glucose level of 130 mg/dL.¹¹⁶ Blocking the renin-angiotensin system may improve the insulin response after burn injury.¹¹⁷ It should be noted that insulin resistance might persist for 6 to 9 months after discharge.¹¹⁴

Skin

Extensive skin destruction results in the inability to regulate body heat, conserve fluids and electrolytes, and protect against bacterial invasion. Permeability of burned tissues is markedly increased and proportional to the number of layers of tissue damaged.¹¹⁸ Because children have a much greater ratio of body surface area to weight compared with adults, they are even more likely to become hypothermic (see Fig. 34-1). Thus it is important to keep these children covered as much as possible, to increase the environmental temperature, and to use radiant warmers, plastic wrap around extremities, reflective insulated blankets, artificial “noses” (in-line moisture and heat exchangers), and hot-air heating blankets. Late complications affecting the skin include progressive scar formation, which results in movement-restricting contractures.^24,119 Topical antibiotic and antibacterial therapy is necessary to prevent burn wound sepsis.^120–125

Metabolic

Many metabolic alterations follow extensive burn injury. Increased usage of glucose, fat, and protein results in greater O₂ demand and increased carbon dioxide (CO₂) production.* Mediators that have been implicated in these metabolic changes include interleukin-1, tumor necrosis factor, catecholamines, prostanoids, and other stress hormones.^2,133 Centrally mediated or sepsis-induced hyperthermia also increases O₂ consumption and CO₂ production. Some of these abnormalities may persist even after complete closure of the burn wounds, when metabolic demand is already reduced.^† Intravenous alimentation, particularly with increased glucose concentrations, may also increase CO₂ production and therefore increase ventilatory requirements.¹⁰⁵ Increase in O₂ demand¹³⁵ and CO₂ production must be compensated for during controlled mechanical ventilation. Treatment of fever reduces metabolic demand.¹³⁶

Calcium Homeostasis

The ionized calcium concentrations in many acutely burned patients are dramatically decreased. Marked abnormalities in the indices of calcium and magnesium metabolism, including hypoparathyroidism in both acute and recovery phases, may persist for weeks after injury (E-Fig. 34-1).^137,138 One study suggested that short-term therapy with pamidronate, a drug that inhibits bone resorption, conserves bone mass after burn injury in children.¹³⁹ Hypophosphatemia and hypermagnesemia revert toward normal during the latter phase of recovery from the acute injury. The usual reciprocal relationship between calcium and inorganic phosphate is not evident in those with major burns. Therefore supplemental calcium therapy is extremely important, particularly when rapid colloid infusions are required intraoperatively during burn surgeries, because ionized hypocalcemia dramatically impairs cardiovascular homeostasis. In general, frequent small boluses of calcium are safer and more effective than intermittent large boluses (see also Figs. 10-8 and 10-9).¹⁴⁰ Doses of 2.5 mg/kg calcium chloride or 7.5 mg/kg calcium gluconate ionize at equivalent rates and produce equivalent increases in calcium concentration. After recovery from burn injury, vitamin D supplements are strongly recommended to offset the decreased conversion of 7-dehydrocholesterol to previtamin D₃.¹⁴¹

E-FIGURE 34-1 Ionized calcium values from burned children and adults are plotted for the first 35 days after burn injury. Note that the majority of values are abnormally low; shaded blue area = range of normal values.

(From Szyfelbein SK, Drop LJ, Martyn JA. Persistent ionized hypocalcemia during resuscitation and recovery phases of body burns. Crit Care Med 1981;9:454-8.)

Psychiatric

It is imperative to recognize that physical trauma is not the only trauma sustained by the pediatric burn patient; psychological trauma and its associated long-term sequelae is also common.^142,143 A large percentage of acutely burned children present with acute stress or develop posttraumatic stress disorders.^142–145 Risk factors for developing acute stress disorders include the size of burn, the degree of pain, the pulse rate, and parental issues.¹⁴⁶ Treatment with fluoxetine or imipramine may ameliorate these stress disorders,^147–149 although one randomized controlled study found no difference from placebo.¹⁵⁰ Another study found risperidone to be of value in reducing stress symptoms.¹⁵¹ There is an increased incidence of attention-deficit disorders in pediatric burn patients, likely owing to impulsivity.^152,153 Finally, the normal psychosocial support network may be impaired in the families of the burn patient, even before the burn injury.^154–156

Airway and Oxygenation

Every burn patient, especially those with inhalation injuries, must be considered hypoxemic and exposed to carbon monoxide (CO). Therefore during transport to the hospital and on admission, administration of high inspired concentrations of O₂ is mandatory, pending evaluation of the severity of CO poisoning and pulmonary injury (see later).¹⁸¹ Direct injury to the airway and alveoli occurs in children who have sustained pulmonary injury from the inhalation of smoke, flames, noxious gases, heated air, or steam.^{42,51,133,182–211} When a child is burned in an enclosed space (house, automobile) or if thermal burns or carbonaceous materials are evident about the mouth and nose, inhalational injury is probable.^192,212 Upper airway obstruction caused by edema of the lips, nose, tongue, pharynx, glottis, and subglottis is very common. The resultant airway obstruction can be compared with the combined effects of acute macroglossia, epiglottitis, macro uvula, and laryngotracheobronchitis. The decreasing patency of the airway resulting from rapidly increasing edema, beginning in the first hours after the injury and lasting several days, makes delayed intubation hazardous if not impossible (Fig. 34-4). Prophylactic intubation should be performed in any case of severe facial burns or when pulmonary burn and upper airway inhalation injury are suspected. The severity of adverse outcomes is related to the presence or absence of inhalation injury.^{51,200–211,213}

FIGURE 34-4 A, A young child who had just sustained a facial burn in a closed space. Note the early onset of facial edema. B, Several hours later there is massive edema that extends into the oropharynx, larynx, and trachea (similar to the combined effects of macroglossia, epiglottitis, and laryngotracheobronchitis). Early prophylactic intubation is mandatory in any facial burn or in any child when there is potential for inhalation injury. Note that the cuffed endotracheal tube was changed from an oral to a nasal position and that it is secured with cloth tape rather than adhesive tape.

Control of the airway in children is usually accomplished under general anesthesia. In the case of pure inhalational injury without facial or upper airway burns, the need for intubation should be considered on a case-by-case basis. Early clinical experience at our hospital showed that tracheal tubes could be left in place in these children for weeks with fewer risks than the alternative, tracheostomy.^214,215 Tracheostomy in thermally injured children was associated with high mortality rates; in one pediatric series the death rate approached 100%.²¹⁶ However, in recent years there has been a move back to performing tracheostomy for children who are expected to require long-term ventilatory management. Although one review of burn centers in North America found that the practice of performing a tracheostomy in burned children was variable, there has been increasing tendency to perform a tracheostomy in children over age 7. ²¹⁷ Some report that an early tracheostomy secures the airway and reduces the risk of subglottic stenosis.^218,219 When early airway instrumentation is indicated, a cuffed tracheal tube is preferred to reduce the need for changing the tube to deliver high peak inspiratory pressures should they be required.²²⁰ Traditionally, cuffed tracheal tubes have not been used in children younger than 8 years. This practice may not be necessary with proper attention to leak pressures (pressure at which gas can be heard “leaking” around the tracheal cuff by auscultating over the trachea while administering positive pressure) or the use of the MICROCUFF (Kimberly-Clark, Roswell, Ga.) tube (see later), although long-term studies with these tubes are needed (see Chapter 12).^221,222 We routinely use cuffed tracheal tubes, appreciating the added flexibility they offer in not requiring replacement because of decreasing edema (with associated increased leak if uncuffed tubes were used). Another important means of minimizing barotrauma is the use of permissive hypercarbia.²²³ New tracheal tubes that are designed to have the cuff located more distally and made of thinner material (MICROCUFF) may also reduce the potential for airway injury (see also Figs. 12-15 and 12-17), although in the hot environment of a burn unit they may have a greater tendency toward kinking.^224–228

Carbon Monoxide Poisoning and Cyanide Poisoning

The majority of smoke inhalation victims have CO poisoning. Direct measurement of carboxyhemoglobin (COHb) is an important guide to the adequacy of treatment. Estimates of the COHb concentration may be derived by measuring (not calculating) O₂ saturation or arterial O₂ content. The half-life of COHb is approximately 5 hours when the patient is breathing room air but decreases to 90 minutes when 100% O₂ is administered.^229,230 Immediate administration of O₂ is therefore essential to achieve the maximum possible level of O₂ in the blood; positive-pressure ventilation may be indicated in severe cases.^231–233 Hyperbaric oxygen may be a useful adjunct for this purpose (see later).

Standard pulse oximeters do not differentiate between oxyhemoglobin and COHb; in contrast, transcutaneous O₂ analyzers and cooximeters are useful.²³⁴ Thus pulse oximetry cannot be used to accurately monitor the oxygenation of patients with CO poisoning because COHb produces an overestimation of O₂ saturation; the photo detector is “fooled” into interpreting COHb as oxyhemoglobin.^234–236 A more recent eight-wavelength pulse oximeter capable of measuring COHb and methemoglobin may prove useful in the management of burn patients^237,238; however, the sensors are quite expensive and likely should be reserved for use in those with an established diagnosis, unless arterial blood gas analysis is not immediately available.²³⁹

COHb is produced by the combination of CO with the iron of the heme radical at the O₂-binding site. CO combines more slowly with hemoglobin than O₂ but is bound 200 times more firmly.^240,241 Inhalation of 1% CO for 2 minutes can result in COHb values of 30% (E-Fig. 34-2).²⁴² The toxic effects of CO poisoning are due to tissue, organ, and cellular hypoxia from decreased O₂ delivery. Decreased delivery occurs because CO reduces O₂ binding capacity both to the hemoglobin molecule at the tissue level and to cytochromes in the respiratory chain at the cellular level; even in small amounts, COHb shifts the O₂-dissociation curve to the left (E-Fig. 34-3), thus reducing release of O₂ from hemoglobin.^{42,181,231,241–245} For example, if an individual had 40% carboxyhemoglobin, this would reduce O₂ carrying capacity from 20 mL/100 g of hemoglobin to 12 mL/100 g and with the leftward shift further compromise O₂ delivery.

E-FIGURE 34-2 Note the rapid rise in carboxyhemoglobin values when just 1% carbon monoxide is inhaled.

E-FIGURE 34-3 The changes in the oxygen-hemoglobin dissociation curve that occur with carbon monoxide poisoning. The oxygen-hemoglobin dissociation curve is altered in shape and shifted to the left. Therefore less oxygen is available for delivery to tissues and the oxygen carried by hemoglobin is more tightly bound.

(Modified from Douglas CG, Haldane JS, Haldane JBS. The laws of combination of hemoglobin with carbon monoxide and oxygen. J Physiol 1912;44:275-304.)

The evidence supporting the use of hyperbaric oxygenation (HBO) therapy as an adjunct therapy for burns remains controversial.^85,246–250 A Cochrane review of six randomized controlled trials with 1361 patients concluded that at present insufficient data exist to demonstrate reduced adverse neurologic outcomes with HBO therapy and that additional research is needed to “better define the role, if any, of HBO in the treatment of patients with CO poisoning.”²⁵¹ The most common indication for hyperbaric therapy in burned children is concomitant CO poisoning.^42,252,253 As previously mentioned, CO binds avidly to hemoglobin²⁵⁴ and other iron-containing enzymes, such as intramitochondrial cytochromes, interfering with the delivery and usage of O₂, respectively.^255,256 Children suffering significant CO exposure are at risk of developing both acute and delayed neurologic sequelae. The pathophysiology of neurologic sequelae is not known, although imaging studies suggest a potentially reversible demyelinating process.^257,258 Data supporting the use of hyperbaric O₂ to prevent and treat these complications may be weak^259–266 but cannot be discounted, given the seriousness of these sequelae.^{248,249,267,268}

The important practical question is whether hyperbaric treatment will decrease the frequency and severity of delayed neurologic sequelae in burned children with concomitant CO poisoning. This is a difficult question because the incidence of delayed sequelae is unknown and determining the severity of an individual exposure is often not possible. Delayed sequelae include headaches, irritability, personality changes, confusion, memory loss, and gross motor deficits. The frequency with which those exposed develop symptoms is unknown, although they are reported to occur in approximately 10% of patients with serious exposures.²⁴³ A symptom-free interval of several days is commonly reported. Delayed hyperbaric treatment may relieve symptoms, and spontaneous resolution of delayed sequelae may be expected in up to 75% of patients within 1 year.^269–275 The severity of the CO poisoning is often difficult to pinpoint because there is a poor correlation between serum COHb and degree of CO exposure.^276,277 Neuropsychiatric testing has been proposed as a more accurate way to determine this,²²⁹ but such detailed examinations are difficult in burned children secondary to pain medications and hemodynamic instability. Some clinicians believe that a history of unconsciousness indicates that an exposure has been severe enough to warrant treatment.^{271,278–280} However, the relatively few randomized prospective studies evaluating this have returned conflicting results.^262,266 Hyperbaric O₂ treatment is not without expense, inconvenience, and risk, and the indications for treatment of burned children with concomitant CO poisoning are debated.^256,281 One study described complications during treatment of a heterogeneous groups of patients: emesis (6%), seizures (5%), agitation requiring restraints or sedation (2%), cardiac dysrhythmias or cardiac arrests (2%), arterial hypotension (2%), and tension pneumothorax (1%).²⁵⁶ Complications may be expected more frequently in the critically ill.²⁸²

Hyperbaric O₂ treatment is probably appropriate in burned children with documented or strongly suspected serious CO poisoning who are hemodynamically stable, not requiring ongoing burn resuscitation, and not wheezing or air trapping and in whom such treatment does not require interfacility transport, which is inconsistent with good general burn treatment.

Cyanide toxicity may occur in inhalational burn injuries as well.²⁸³ If cyanide poisoning is confirmed in the child’s blood, administration of hydroxycobalamin or sodium thiosulfate, alone or in combination, is warranted (see Chapter 10).²⁸⁴ HBO therapy has been shown to facilitate movement of cyanide out of tissues and into blood, thereby potentially facilitating treatment,²⁸³ although the use of HBO for treatment remains investigational.

Adequacy of Circulation

The various formulas for determining fluid replacement are estimates and often need modification, depending on clinical and laboratory findings.* The most widely accepted fluid protocols in current use are the Parkland (Baxter) and Brooke formulas. All formulas and guidelines for fluid therapy require modification according to the individual child, depending on the child’s response (Table 34-1).⁶ The most important metric of fluid homeostasis remains a good urine output (0.5 to 1 mL/kg/hr).

TABLE 34-1 Parkland and Brooke Formulas

Both formulas provide estimates of the fluid volume required for resuscitation, in addition to the calculated normal maintenance fluid requirement for each day. These formulas are of great value in guiding the fluid resuscitation of older children; however, serious underestimation of the fluid volume may occur if applied to infants weighing less than 10 kg. In such infants, it is reasonable to estimate the normal hourly maintenance fluid requirements and then add to this the fluid volume of the Parkland or Brooke formula.² Alternatively, the crystalloid fluid regimen for resuscitation can be increased to 6 mL/kg × the percent surface area burn per 24 hours.^297,298

The degree of edema depends on the volume and composition of the resuscitation fluid administered. Consequently, colloids or hypertonic saline (with or without albumin) are used in some burn centers during early burn wound resuscitation.²⁹⁹ These modified regimens have been shown to be particularly effective in the very young and the elderly.^† The purported advantage is less tissue edema. It is of interest that a Cochrane review of 15 studies using hypertonic saline in 614 patients found that less intravenous fluid was needed for resuscitation and higher sodium values occurred, although the overall morbidity and mortality was unchanged.³⁰¹

A growing practice in burn programs has been to begin the fluid resuscitation with colloid, usually 5% albumin, early during resuscitation of seriously burned children.³⁰² No consensus has been reached on such a colloid protocol.³⁰³ In seriously burned children in our unit, we begin with a 5% albumin solution at a maintenance rate immediately on admission. We administer an amount equal to that of their calculated crystalloid requirements, tapering the crystalloid first, and continuing albumin fusion for 48 hours. Further work is required before advocating hypertonic fluid regimens in burned children routinely.³⁰⁴

The syndrome of hyperosmolar hyperglycemic nonketotic coma (severe dehydration, marked hyperglycemia, serum hyperosmolality, and coma in the absence of ketoacidosis) may be associated with burns. Avoiding this syndrome is critically important because it carries a high mortality.²⁸⁵ Glucose-containing solutions should be restricted at all times, particularly during the initial volume resuscitation. Serum glucose concentrations should be measured frequently during this period. Blood glucose concentrations should be managed with insulin with a target blood glucose of 130 mg/dL.¹¹⁶

The general appearance of the child and his or her sensorium provide important guides to the effectiveness of the resuscitative therapy. In addition, urine output is a useful metric to determine the need for additional fluid administration, recognizing that antidiuretic hormone secretion may be increased and renal tubular dysfunction may be present.^20,158 Every effort must be made to protect kidney function by providing adequate fluid replacement.^2,304 Renal failure in the presence of a major burn is usually lethal. However, overly aggressive fluid administration may induce pulmonary and tissue edema. Therefore, when a burned child is being volume resuscitated, all fluids to replace the circulating blood volume must be carefully titrated. Commonly used end points of satisfactory fluid resuscitation include heart rate, systemic arterial blood pressure, urinary output, central venous pressure, arterial oxygenation, and pH. Cardiovascular function estimated by transthoracic or transesophageal echocardiography²⁹ and technetium-99m ventriculography may be of value in critically ill patients.^305,306 These advanced cardiac evaluations are not required in most children; they are mostly useful in the presence of cardiovascular compromise and a need to consider the use of a vasopressor or additional volume loading.

In a child, the evaporative fluid losses exceed 4000 mL/m² of burn surface each day, compared with only 2500 mL/m² in an adult.²⁹⁰ Concomitantly, for each square meter of burn surface, 2500 to 4000 kcal of heat is lost each day. Minimizing caloric expenditure and providing caloric supplementation simultaneously are the only ways to minimize catabolism of body tissues. The tendency for children to be poikilothermic, particularly in the absence of protective skin as a result of the burn injury, causes profound temperature derangements. Efforts to maintain a normal body temperature are essential in both the operating room and the intensive care unit. These measures are especially important during the initial volume resuscitation and in the operating room when dressings are removed for examination and excision (Fig. 34-5).

FIGURE 34-5 Children with extensive burn injury can be kept warm by having the extremities wrapped with sterile plastic bags. Covering the head is also an important method of heat preservation.

Associated Injury

Associated injuries such as a tension pneumothorax, a ruptured spleen or liver, long-bone fractures, or head injury may be missed, especially during the initial assessment and early phase of burn wound fluid resuscitation. Taking a detailed history, especially from the emergency medical personnel and family, combined with a careful physical examination, is mandatory during the initial resuscitation because such injuries may compound or be hidden by the need for an increased volume of resuscitation fluids. The type of burn injury (e.g., explosion, electrical) may trigger concerns for associated injuries (e.g., shrapnel wounds).

Circumferential Burns

Adverse cardiovascular and respiratory responses are immediate to circumferential burns of the chest, abdomen, and extremities.^2,24,196,197 Circumferential burns of the thorax can restrict respiratory effort, resulting in respiratory failure as a result of decreased chest wall compliance. Functional residual capacity is reduced with airway closure and atelectasis, resulting in profound hypoxemia.^{42,183–187,190–198,307} Deep circumferential burns of the chest and abdomen may generate excessive intrathoracic and intraabdominal pressure, which, in addition to restricting diaphragmatic movement, may further reduce the already decreased cardiac output by impairing venous return (Fig. 34-6).^24,196,197 When this occurs, both extrapulmonary and intrapulmonary factors can contribute to arterial desaturation.⁵⁰

FIGURE 34-6 A, Circumferential chest burns result in severe impairment of respirations secondary to the tourniquet effect of the shrinking eschar and subcutaneous edema. The widely separated escharotomy lines indicate the severity of the constriction. B, Similar effects occur in circumferentially burned extremities. Early escharotomy may help to preserve blood flow and obviate amputation.

The edema of damaged tissues also can generate severe compressive forces, restricting or occluding the blood flow to burned extremities. The net result may be ischemia of the limb, which if left untreated, may lead to partial or total amputation. Escharotomies of circumferential burns of the chest, abdomen, and extremities must be performed urgently because impaired hemodynamics and respiratory mechanics can cause irreversible damage within hours of the burn injury. Escharotomy is often undertaken without the need for general anesthesia because a full-thickness burn usually destroys skin innervation. Abdominal compartment syndrome may develop in children who require large volume resuscitation. To detect any evolving compartment syndrome, some burn centers advocate routine monitoring of bladder pressure.^307,308

Electrical Burns

Electrical burns occur with household voltage (electric cords and sockets) and nonhousehold high-voltage current (power line or lightning). Children often disconnect extension cords by stabilizing one end in their mouths and pulling the other end with a hand, resulting in circumoral and lingual burns.^4,53,309,310 High-voltage injuries are often associated with loss of limbs and other injuries that are not immediately obvious.^311–314 The extent of this injury is unpredictable. The surface injury is often small, but the extent of underlying tissue damage and necrosis is massive. Such an injury is a combination of electrical and thermal damage.^314,315 Victims often have concurrent injuries such as fractures of vertebrae or long bones, ruptured organs, myocardial injury, or numerous contusions. Even children with low-voltage injuries may have abnormalities of cardiac conduction.³¹² Children with electrical burns may be comatose or have sustained seizures at the time of admission to the hospital. Muscle tissue adjacent to bone is usually more damaged than superficial muscles because bone is a poor conductor of electrical current, and therefore heats up when high currents are passed through it, resulting in damage to the muscles surrounding bone. Early fasciotomy may be needed to preserve the blood flow to extremities (Fig. 34-7). Myonecrosis necessitates general anesthesia during the first day of injury at the time when fluid shifts, hyperkalemia, and myoglobinuria are maximal. Massive myonecrosis and hemolysis may result in hyperkalemia, as well as myoglobinuria and hemoglobinuria. In the presence of hemoglobinuria or myoglobinuria, increased fluids and mannitol will ensure a continuous urine output (>1 mL/kg/hr).^316,317 Alkalization of the urine may prevent these proteins from precipitating in the renal tubules. Follow-up of patients with electrical injuries often reveals unpredictable sequelae, which may manifest months to years later. These injuries may occur in organs or areas that do not appear abnormal during the acute course of illness. These late complications most frequently include neurologic dysfunction, ocular damage, damage to the gastrointestinal tract, circumoral strictures, changes in the electrocardiogram, and delayed hemorrhage from large vessels.^315,317

FIGURE 34-7 Electrical injuries tend to follow neurovascular structures and have an entry as well as an exit wound. The skin might appear normal but the underlying structures may have had extensive injury. These children require a fasciotomy rather than just a simple escharotomy to preserve blood flow to the deep structures. In general, this is required on the first day of injury for best results in tissue preservation.