Carbon Monoxide Poisoning

Carbon monoxide (CO) is produced in almost every fire, and CO poisoning can cause immediate death during the fire or death during the first 12   hours after a burn. CO has much higher affinity for hemoglobin than does oxygen; as a result, it will bind tightly with hemoglobin, forming carboxyhemoglobin (COHb). Each gram of hemoglobin bound to CO is unable to carry oxygen, so impaired oxygen transport, decreased oxygen delivery, tissue hypoxia, and metabolic acidosis will result if CO levels are high. COHb levels greater than 40% usually produce significant tissue and organ ischemia and dysfunction, and levels greater than 60% are usually fatal.^78,216

It is important to note that pulse oximeters will not reflect the severity of CO poisoning because they do not recognize CoHb. As a result, the pulse oximeter will indicate only the saturation of normal hemoglobin. If CO poisoning is suspected, the child’s oxyhemoglobin saturation must be measured by cooximeter.

Initiation of Therapy

Adequate fluid resuscitation and replacement in a severely burned child is critical to ensure survival. Initial fluid resuscitation is designed to restore adequate intravascular volume and maintain effective tissue and organ perfusion. In addition, electrolyte and acid-base balance must be maintained, and excessive fluid administration must be avoided.

Repeated bolus administration of isotonic fluid (20   mL/kg administered over 5 to 20 minutes) may be necessary until systemic perfusion and urine output are restored. Next, the volume and content of the fluid deficit is calculated (based on the child’s body surface area and the size of the burn), and maintenance fluid requirements are estimated.

If the burn totals less than 15% TBSA, it may be possible to replace the deficit by providing oral fluids, including protein supplements, milk products, and clear liquids. Throughout fluid administration, the effectiveness of the child’s perfusion is closely monitored, and urine volume and fluid balance must be evaluated regularly.

Intravenous Access and Monitoring

When the burn totals 15% or more of TBSA, intravenous therapy will be mandatory to restore intravascular volume and maintain fluid and electrolyte balance. Major peripheral veins should be cannulated using large-bore catheters. A urinary catheter should be inserted to enable continuous monitoring of urine output.

Whenever a major burn is present or systemic perfusion is compromised significantly, insertion of a central venous catheter (into the subclavian, internal jugular, or femoral vein) should be considered to provide reliable, large-bore venous access. Use of a multilumen central venous catheter will provide two or more ports to facilitate fluid administration and central venous pressure (CVP) monitoring. Any central venous catheter must be inserted under strict sterile conditions and cared for using strict aseptic technique (see Chapter 21 and Box 22-6).

Determination of Fluid Requirements

A variety of formulas have been developed to assist in determining fluid losses and requirements in patients with burns (Table 20-3). Many formulas, however, have been designed for use in adult patients and are based solely on body weight and percentage of TBSA burned. Use of these adult formulas will result in inadequate pediatric fluid resuscitation.^62,135

The most popular formula for use in adolescent and adult patients with burns is the Parkland (by Baxter), formula.¹⁰ Modification of the Parkland formula for children provides for crystalloid administration during the first 24   hours of therapy. The volume administered during this time is based on the burn surface area (4   mL/kg per percent of TBSA burned) plus maintenance fluid requirements (1500   mL/m² BSA).²¹⁵ Half of this calculated fluid is administered during the first 8   hours of therapy, and the remaining half is administered during the next 16   hours of therapy.

The child’s fluid resuscitation requirements should be based on body surface area rather than weight. Because children have a greater body surface area in relation to weight, weight-based formulas can underestimate the fluid requirements of children with minor burns and may grossly overestimate the fluid requirements of those with extensive burns.⁷⁹ TBSA can be rapidly estimated from height and weight using standard nomograms (see inside back cover of this text).

The Galveston formula²⁶ (developed by Carvajal at the Shriners Hospital for Children in Galveston, Texas) provides 5000   mL/m² BSA burned plus 2000   mL/m² BSA of lactated Ringer’s solution given over the first 24   hours after the injury, with half the volume administered during the first 8   hours and the remaining half over the next 16   hours. The Carvajal formula²⁶ recommends crystalloid and colloid administration based on the absolute surface area of the child’s burn, plus generous maintenance fluid administration.

The formula selected for burn resuscitation usually is based on physician preference or burn unit protocols. Any fluid resuscitation formula, however, should serve only as a guide for initiation of therapy. Ongoing assessment of systemic perfusion, intravascular volume status, and fluid and electrolyte balance should be used to modify therapy.

Selection of Fluid Content

There is continued debate regarding the relative benefits of crystalloid versus colloid administration during burn resuscitation.^27,42,51,176 Proponents of crystalloids advocate the use of isotonic or hypertonic crystalloids because they are physiologic, inexpensive, and readily available.

Critics of crystalloid administration note that immediately after administration, isotonic crystalloids will equilibrate between the intravascular and interstitial spaces, and only a fraction of administered intravenous crystalloids will remain in the vascular space.¹⁷⁸ Therefore, large quantities of crystalloids generally are required to restore intravascular volume. In addition, the fluid that moves into the interstitial space may contribute to worsening systemic edema. Pulmonary interstitial water usually does not increase substantially during this time, because pulmonary capillary permeability remains normal unless significant inhalation injury occurs. In addition, lymph flow is usually proportional to the amount of pulmonary interstitial water movement.

Colloid resuscitation may restore intravascular volume and pressure more efficiently than will crystalloid administration. If capillary permeability is normal, administered colloids will remain in the vascular space for several hours, exerting oncotic pressure. This oncotic pressure will increase intravascular volume and maintain intravascular osmolality, so that continued fluid shift from the vascular space is less likely. Because colloids are thought to diffuse more slowly into the interstitial space, colloid resuscitated patients may develop less edema than crystalloid-resuscitated patients.¹⁶³ Adequate fluid resuscitation should be possible with relatively small volumes of colloids,^86,201 so that the patient receives a small volume and salt load.

Critics of colloid administration note that membrane permeability is not normal in patients immediately after burns, and proteins may move from the vascular to the interstitial space during the first 24   hours after a burn.⁹ Movement of administered colloids into the interstitial space can increase interstitial oncotic pressure, enhancing the fluid shift from the intravascular space into the interstitial space.

Colloid administration during the first day after a burn was avoided in the past, based on the fear that it would increase the severity of third-spacing of fluid.¹⁸² However, the validity of this criticism has been challenged during the last decade. Although albumin may leave the vascular space, an equal amount of albumin may be returned to the vascular space by lymphatics approximately 8   hours or more after a burn. Therefore many institutions have successfully added small amounts of colloids to their early burn resuscitation protocols.

In general, adequate resuscitation can be provided if isotonic crystalloids are administered in sufficient quantity.⁴⁸ Lactated Ringer’s (LR) solution, an isotonic crystalloid, is the most widely used solution for burn resuscitation. The composition of LR’s solution closely mimics extracellular (including intravascular) fluid composition (Table 20-4); therefore LR’s solution is ideal for replenishing intravascular water and electrolytes. In addition, LR’s solution contains lactate, which is metabolized to bicarbonate, so it will buffer mild acidosis. Lactated Ringer’s solution is inexpensive, readily available, and effective in the treatment of nonhemorrhagic hypovolemia.

Normal saline (0.9% sodium chloride) can be used as an alternative to lactated Ringer’s solution for isotonic crystalloid resuscitation. Because normal saline contains no potassium, use of normal saline may be ideal for the patient with hyperkalemia or renal failure. Potassium chloride (20-40   mEq/L) is usually added to normal saline if renal function is adequate and the child’s serum potassium is acceptable. Normal saline does not contain lactate or other buffers.

During fluid resuscitation, the child’s systemic perfusion and urine output must be monitored closely. These parameters should improve if fluid administration is adequate (Table 20-5). The serum hemoglobin concentration, electrolyte balance, and acid-base status (including serum lactate) must also be monitored closely.

Table 20-5 Clinical Responses to Fluid Resuscitation in Burned Patients

BSA, Body surface area.

* See normal blood pressure and heart rate ranges for age in Tables 1-1 and 1-3 (and on pages inside front cover).

Because only a portion of administered isotonic crystalloids will remain in the vascular space, generous crystalloid administration is needed to restore effective or adequate intravascular volume. Systemic edema should be anticipated, because some of the administered volume moves into the interstitial space. It is important to note that the development of such edema does not indicate that fluid resuscitation is adequate; titration of fluid administration should be based on assessment of perfusion and intravascular volume status.

Pulmonary edema usually is not problematic during early burn resuscitation. However, because respiratory failure can develop for a variety of reasons, the patient’s respiratory function must be monitored closely, and appropriate support (with intubation, mechanical ventilatory support, and positive end expiratory pressure) must be provided as needed.

Hypotonic crystalloids should not be used for fluid resuscitation, because such fluid will tend to lower intravascular sodium concentration and osmolality and enhance the fluid shift from the vascular space. Hypoosmolality will worsen systemic edema and may contribute to the development of cerebral edema. Furthermore, the fluids will not assist in the restoration of intravascular volume.

Hypertonic saline resuscitation can be beneficial in treating burn-induced shock.^16,17,64,84 This process maintains intravascular volume more effectively because it induces movement of free water from the interstitial to the intravascular space, thus decreasing generalized tissue edema. However, hypertonic saline is not widely used because of the potential risk of hypernatremia, hyperosmolarity, renal failure, and alkalosis.^98,173,222 Some favor the use of a modified hypertonic solution—adding an ampule of sodium bicarbonate to each liter of lactated Ringer’s solution during the first 24   hours of resuscitation.¹⁹

Routine Care

Regardless of the type of resuscitation fluid being used, the nurse must closely monitor the patient’s response to volume resuscitation (see Table 20-5). Adequate systemic perfusion, demonstrated by warm extremities, brisk capillary refill, strong peripheral pulses, and adequate (1-2   mL/kg body weight per hour) urine volume should be observed.

The child’s level of consciousness should be appropriate for clinical condition. Irritability may be an early sign of cardiovascular or neurologic deterioration,¹⁵⁰ and lethargy or decreased response to painful stimulation is abnormal and requires investigation.

Tachycardia may continue despite adequate fluid resuscitation, but it should not be extreme, and the blood pressure should be appropriate for age. Extreme tachycardia, thready peripheral pulses, hypotension, and metabolic acidosis indicate serious compromise in cardiac output and systemic perfusion, as well as a probable urgent need for volume administration.

During fluid resuscitation, the nurse should be alert for the development of pulmonary edema, and the team should have a plan for a sequence of appropriate respiratory support. Elective intubation should be performed before decompensation occurs (see Respiratory Failure in this chapter and Chapter 9).

Urine volume should be recorded every hour, and urine specific gravity should be determined every 2 to 4   hours. Frequency of assessment of serum electrolytes, hematocrit, and blood gases during the first hours of therapy will be determined by patient condition; hourly evaluation may be required for the patient in unstable condition.

Pulse oximetry should be used for continuous monitoring of arterial oxyhemoglobin saturation. Additional monitoring, including the use of near-infrared spectroscopy (NIRS) and monitoring of exhaled carbon dioxide (P_ETCO₂) should be used based on unit protocols.

During fluid resuscitation of the infant, the serum glucose concentration should be monitored closely. Young infants may rapidly develop hypoglycemia during stress, so it is necessary to provide a continuous source of glucose intake and monitor point-of-care (e.g., bedside) or intravascular glucose concentration frequently.

Once the child’s condition is stable, hematocrit, hemoglobin, blood urea nitrogen (BUN), creatinine, electrolytes, glucose, serum osmolality, and urine sodium are monitored daily—more often if abnormalities are present. The hematocrit and BUN often rise immediately after a burn, but sustained and significant increase in these values usually suggests the need for further volume administration. An increase in the serum creatinine often indicates the presence of renal failure.

The urine sodium may also be monitored. Normal urinary excretion of sodium is approximately 60 to 100   mEq/L. A low urine sodium (less than 40   mEq/L) usually results from aldosterone secretion in the presence of inadequate intravascular volume¹²³ and indicates the need for further volume administration.

The rate, content, and function of each fluid infusion system should be checked hourly, and each infusion site should be examined. Intravenous tubing must be changed using strict aseptic technique. Intravenous catheters must be taped or sutured securely, so that kinking or dislodgement is impossible.

The child’s daily weight without dressings should be recorded accurately using the same scale or method at the same time each day. The child’s weight immediately after the burn should be used as the baseline weight. If the child is not weighed until fluid resuscitation is underway, estimation of the preburn weight should be made after an interview with the parents. During this period, the child’s weight typically will increase by 10% to 20% or more.

Evaluation of Therapy

There is no single parameter that will indicate effectiveness of postburn resuscitation. Systemic perfusion and neurologic function must be maintained at satisfactory levels. Mean arterial pressure should be appropriate for age. Whereas hypotension certainly indicates cardiovascular compromise and the need for further resuscitation, a normal mean arterial pressure may be present despite significant hypovolemia and shock. Acidosis should be absent or mild and improving if resuscitation is effective.

Urine volume and CVP should also be monitored closely, but they will fluctuate significantly during resuscitation. It is usually advisable to evaluate the average urine volume over 2-hour periods to better monitor fluid balance and adjust fluid administration. Low urine volume usually indicates the need for additional fluid administration. Diuretic therapy should not be provided during the initial phase of standard burn resuscitation, because it may contribute to intravascular volume depletion. Mannitol administration may be necessary after severe electrical injuries to enhance clearance of myoglobin.

Increased fluid administration is probably necessary if inadequate systemic perfusion and continuing acidosis are associated with a low CVP. Vasoactive drug therapy will not improve systemic perfusion produced by hypovolemia. Poor systemic perfusion and extreme acidosis despite adequate fluid administration indicate severe shock and are associated with a high mortality (see Shock in Chapter 6).

Fluid and Electrolyte Therapy

Fluid loss during this period will consist of continued evaporative water losses from the burn surface and basal metabolic (insensible) water losses (Box 20-5). Evaporative water losses become significant approximately 24   hours after the burn, and they may be as high as 2000   mL/day in the child. Because fluid lost by evaporation is predominantly water, replacement with 5% dextrose and 0.45% sodium chloride solution is provided.

Hypokalemia is more likely to develop if dextrose-containing intravenous fluids are used, because such fluids will enhance intracellular movement of potassium. Supplementary potassium administration should be planned to maintain normal serum potassium concentration.

Colloids are often administered to maintain intravascular oncotic pressure and enhance the interstitial-to-intravascular fluid shift. Usually a volume of colloid equivalent to 20% of the circulating blood volume is administered over 24   hours.

Blood administration may be necessary if significant anemia develops. The hematocrit should be maintained at approximately 25% to 30%, using whole blood or packed RBCs. Administration of 10   mL/kg of packed RBCs will increase the hematocrit by approximately 10 percentage points (e.g., from 25% to 35%). This volume should be administered over 3 to 4   hours, and patient tolerance of the volume should be assessed constantly during the transfusion. A diuretic may be administered immediately before the transfusion to prevent hypervolemia (for further information regarding transfusion therapy, see Chapter 15).

Routine Care

Continuous evaluation of systemic perfusion is required. Color, peripheral perfusion, oxygenation, and level of consciousness should remain excellent. A mild tachycardia may continue. Urine volume should exceed 1 to 2   mL/kg body weight per hour with a specific gravity of less than 1.020 as intravascular volume is restored.

Urine volume should be totaled hourly, and urine specific gravity should be recorded every 2   hours. Assessment of fluid balance should be made at these times. A urine specific gravity greater than 1.025 usually indicates the need for additional fluid administration.

The child’s hematocrit, hemoglobin, BUN, creatinine, electrolytes, glucose, serum osmolality, and urine sodium should continue to be monitored. A fall in hemoglobin, hematocrit, and serum sodium and osmolality typically are observed during this phase of therapy. A rise in serum BUN and creatinine may indicate renal dysfunction. The urine sodium may rise (above the normal 60-100   mEq/L) as renal sodium excretion increases.

The content, infusion rate, and infusion system for each intravenous line should be checked at least every hour. The infusion site also should be checked hourly, and the catheter and tubing should be secured to prevent dislodgement or kinking. The tubing must be changed using strict aseptic technique.

The child’s daily weight should be recorded accurately, and weight changes should be evaluated. The child’s weight typically falls during this time; it may return to near baseline values by the sixth day after the burn.

Evaluation of Therapy

If cardiorespiratory function remains adequate, systemic perfusion should continue to improve. If hypervolemia is present, the child will demonstrate high CVP, and hepatomegaly and pulmonary edema may develop or persist (Table 20-6).

Table 20-6 Clinical Parameters Indicating Hypervolemia During Fluid Resuscitation 24-48   h after Burn Injury

BSA, Body surface area.

* See Box 20-4 for desirable responses.

† See normal blood pressure and heart rate values for age in Tables 1-1 and 1-3 and on pages inside front cover.

If cardiovascular dysfunction is associated with the hypervolemia, poor systemic perfusion will be noted in addition to the signs of pulmonary and systemic edema, and oliguria may be present. Ventricular dilation and reduced contractility will be apparent on echocardiography. In these patients, diuretic therapy and support of cardiovascular function should be intensified, and vasoactive drug therapy probably is necessary. See Chapters 6 and 8 for further information about management of shock and congestive heart failure.

If urine volume does not improve and the serum BUN and creatinine rise during this time, renal failure may be present. See Chapter 13 for information regarding management of renal failure.^198,211

Airway Obstruction

The child with airway obstruction will demonstrate tachypnea, nasal flaring, and retractions. Upper airway obstruction will produce drooling and stridor with prolonged inspiratory time. Lower airway obstruction will produce wheezing and prolonged expiratory time. If a significant increase in respiratory effort is noted within the first hours after a burn, severe airway obstruction is probably present and will likely increase in severity over the course of the first 8   hours following the burn. If evidence of respiratory fatigue (including irritability or decreased responsiveness, severe retractions, or slowing of respiratory rate), hypoxemia, or hypercarbia is observed, respiratory arrest is probably imminent and urgent support of airway, oxygenation and ventilation is needed.

Acute Respiratory Distress Syndrome

The first signs of respiratory failure related to increased capillary permeability pulmonary edema (i.e., ARDS) usually include tachypnea and hypocapnia, with a resultant respiratory alkalosis. Although the chest radiograph may initially be normal, reticular infiltrates indicative of interstitial pulmonary edema are often apparent within 8   hours of the inhalation, the burn, or the development of sepsis.

Within 24 to 96   hours after the pulmonary insult, the child with ARDS will demonstrate clinical evidence of significant pulmonary edema and decreased pulmonary compliance (tachypnea with increased respiratory effort). Crackles often are noted on clinical examination. Arterial blood gases or pulse oximetry will demonstrate hypoxemia, which is not relieved by supplementary oxygen administration.¹⁸⁴

Carbon Monoxide Poisoning

CO poisoning should be suspected in any child who has been burned in a fire involving wood or furniture. The presence of carbonaceous material in the sputum will confirm the inhalation of smoke and possible CO poisoning.

CO poisoning will produce a fall in measured hemoglobin saturation if a cooximeter (e.g., Corning IL282 or Corning 2500; Corning, N.Y.) is used for blood-gas analysis. The hemoglobin saturation obtained by pulse oximetry can be normal despite significant CO poisoning, because the COHb is not recognized as functioning hemoglobin by the oximeter. If the hemoglobin saturation from a blood gas sample is calculated based on the child’s arterial oxygen tension and pH, a normal saturation may be derived despite progressive hypoxemia.⁴³ Dissolved oxygen in the arterial blood may produce a normal arterial oxygen tension, even in the presence of significant compromise in arterial oxygen content and tissue oxygenation. For these reasons the arterial oxyhemoglobin saturation should be measured with a cooximeter.

To determine the presence and severity of CO poisoning, COHb levels should also be determined, and the hemoglobin saturation should be measured. In addition, the child’s arterial pH and serum lactate should be closely monitored, because they will reflect the severity of tissue hypoxia. COHb levels begin to fall within hours of CO exposure; therefore low COHb levels may be obtained in the child with severe CO poisoning if blood sampling is delayed.

Mild CO poisoning will produce headache and shortness of breath, but CO toxicity will result in cardiorespiratory distress, coma, severe metabolic acidosis, and multisystem organ failure (Table 20-9). Significant CO toxicity produces vasodilation and a characteristic cherry red color in the mucous membranes and cheeks. Late neurologic dysfunction following CO inhalation has been reported in children and includes headache, personality and behavioral changes, memory loss, and poor school performance; this dysfunction is thought to result from hypoxic injury to the cerebral cortex.¹¹²

Table 20-9 Relationship Between Blood Carboxyhemoglobin Levels and Clinical Signs and Symptoms

COHb, Carboxyhemoglobin.

Airway Obstruction

Specific signs of airway obstruction and the need for intubation include the development of severe respiratory distress or failure, fatigue, or inability to cry forcefully or speak. Hypoxia will be only a very late sign of critical airway obstruction and often indicates that respiratory arrest is imminent. Succinylcholine should not be used for intubation of burn patients, because it may produce potassium release from muscles and severe hyperkalemia (particularly 48 or more hours after a burn).

Occasionally, severe upper airway edema makes intubation difficult, and a tracheostomy may be necessary. However, early elective intubation, rather than late emergency intubation may preclude the need for tracheostomy and its potential complications.¹³²

Maintenance of proper tube placement is essential for the child with critical airway obstruction. If severe facial burns are present, facial tape cannot be used to secure the endotracheal tube. Twill tape can be wrapped around the neck and the endotracheal tube to secure the tube. The twill tape should be placed above one ear and under the other ear to minimize nasal distortion.² Commercial tube holders may also be used.

Sedation or pharmacologic paralysis (with analgesia) may be necessary to maintain endotracheal tube position until edema subsides. For unknown reasons, patients with extensive burns usually are resistant to all but extremely high doses of nondepolarizing neuromuscular blocking agents.

Acute Respiratory Distress Syndrome

If the child develops permeability pulmonary edema and ARDS, then intubation and mechanical ventilation will be required.¹⁸⁴ Mechanical ventilation support must be skilled, and high inspired oxygen concentration and titrated positive end-expiratory pressure (PEEP) may be required to achieve optimal oxygen delivery.

PEEP effectively reduces intrapulmonary shunting because it expands atelectatic areas of the lung and improves functional residual capacity.¹⁸⁸ In addition, PEEP probably moves edema fluid to harmless areas of the lung.

Titration of PEEP is designed to ensure maximal oxygen delivery—optimal arterial oxygen content without significant depression of cardiac output. Ideally, titration of PEEP will enable reduction of potentially harmful levels of inspired oxygen and will improve arterial oxygen content and lung compliance. However, it is important to note that high levels of PEEP may produce barotrauma, which can be as harmful to the lung as high levels of inspired oxygen. High PEEP can also reduce systemic venous return and cardiac output, with resultant reduction in oxygen delivery. Therefore the levels of inspired oxygen and PEEP should be the lowest levels consistent with satisfactory oxygen delivery and end organ function. For further information about the management of ARDS, see Acute Respiratory Distress Syndrome in Chapter 9.

Carbon Monoxide Poisoning

The only widely accepted treatment for CO poisoning is administration of 100% oxygen. A high concentration of inspired oxygen will break the CO hemoglobin bond, and hyperoxemia will reduce the half-life of CO. Monitor COHb levels; they typically begin to fall 45 to 60 minutes after CO exposure, and reach normal within 8 to 12   hours. High inspired oxygen should be provided until the COHb level falls to less than 5% to 10% of total hemoglobin.

The child may survive the initial CO exposure, but die from progressive hypoxic cerebral edema 48 to 72   hours after exposure. During this time, careful neurologic assessment should be performed. Signs of increased intracranial pressure include: deterioration in level of consciousness (progressive irritability, then lethargy), decreased spontaneous movement or reduced movement in response to pain, inability to follow commands, and pupil dilation with decreased response to light. Bradycardia, systolic hypertension, and altered respiratory pattern (with possible apnea) may be only late signs of increased intracranial pressure, when cerebral herniation is imminent.

Unfortunately, the development of increased intracranial pressure following cerebral hypoxia is usually a sign of devastating neurologic insult, which is typically unresponsive to conventional therapy for increased intracranial pressure. For further information regarding assessment and management of increased intracranial pressure, see Chapter 11.

Use of hyperbaric oxygen (HBO) has been advocated as a treatment for CO poisoning,^78,234 although its efficacy has not been studied in controlled clinical trials. Brief (30-90-minute) periods in HBO (at 2.5-3.0 times atmospheric pressure) will approximately double the amount of dissolved oxygen present in the blood, so oxygen delivery will improve. In addition, HBO therapy displaces CO from hemoglobin, myoglobin, and cells; this reduces the half-life of carboxyhemoglobin to approximately 20 to 30 minutes, compared with approximately 5 to 6   hours in room air and 80 to 90 minutes in 100% oxygen. HBO therapy also results in rapid removal of CO from intracellular cytochromes, so effects of cellular hypoxia may be halted.²¹⁶

HBO therapy is performed in designated HBO units. If the child’s condition is unstable, a multiplace chamber must be used to allow constant attendance by physicians and nurses. HBO is used most frequently for treating patients with isolated CO poisoning, particularly if COHb levels are high (exceeding 25%-30%). HBO therapy may be effective even after COHb levels have returned to normal. Several pediatric case reports have noted promising results of this therapy.⁷⁸

If evidence of inhalation injury is present, elective intubation should be performed before evidence of respiratory function deterioration develops. Humidification of inspired air and suctioning will facilitate removal of airway secretions, but bronchoscopy may be necessary to confirm the diagnosis and to remove carbonaceous material or sloughed epithelium.

Evaluation of Therapy

If airway patency is maintained and inhalation injury is mild, the child should demonstrate effective, spontaneous respiratory effort throughout care. If significant hypoxemia or increased work of breathing is observed, increasing levels of respiratory support (increased inspired oxygen concentrations, intubation, mechanical ventilation, and titration of PEEP) must be provided until oxygen delivery is acceptable.

If burns are extensive, respiratory function is likely to deteriorate during the first days of hospitalization. As a result, continuous assessment of respiratory function and evaluation of the effectiveness of mechanical ventilation support is mandatory. If high concentrations of inspired oxygen and PEEP are required to maintain oxygenation, severe parenchymal injury is probably present, and prolonged mechanical ventilation support may be required (refer to Chapter 9 for treatment of ARDS).

Late deterioration in respiratory function most likely is caused by secondary pneumonia. Appropriate mechanical ventilation support and antibiotic therapy will be required.

Normal Inflammatory Response

The burn wound is the most common site of infection in patients with burns who develop sepsis. For infection to occur, a microorganism must colonize the wound and survive local conditions at the site of entry,¹⁵³ then the organism or its toxins must disseminate into the surrounding tissue.

Once the organism enters the body, it triggers a local inflammatory response that includes vasodilation and increased capillary permeability (for further information, see Septic Shock in Chapters 6 and 16, and Septic Shock: Mediators of the Septic Cascade in the Chapter 6 Supplement on the Evolve Website). The inflammatory response is designed to deliver white blood cells (WBCs; particularly the neutrophils) to the area of infection. The organism also may be ingested by macrophages or eliminated by circulating neutrophils.

The complement system is a network of serum proteins that normally are present in the inactive form; activation of any of the complement proteins will result in activation of a series of proteins in a cascading fashion. The complement proteins contribute to the inflammatory process and immunity when they bind with invading organisms, facilitating phagocytosis in a process called opsonization.⁸⁸ In addition, activation of the complement system results in stimulation of the clotting cascade and may result in changes in vascular tone and alteration in platelet function.

Enzymes and granules released by macrophages and WBCs will also contribute to the inflammatory response and destruction of the organism.^45,221 A specific immune response may be initiated by the lymphocytes to enable the development of immunity.

If the organism is not destroyed at the tissue level, it may enter the blood stream; at this point, bacteremia is present (if the organism is a fungus, fungemia is present; if the organism is a virus, viremia is present). As blood passes through lymph tissue, specific antibodies and lymphocytes may combat the infection.²⁰³ The success of the response to an invading organism will depend on the virulence of the organism itself and the strength of the body’s lymphocyte and immune response.²²³

Effects of Thermal Injury

Thermal injury activates the body’s inflammatory response and creates changes in immune function. The ability of the body to fight infection is compromised by decreased neutrophil phagocytosis, alteration in complement function, circulation of burn generated toxins, suppression of lymphocyte function, and administration of antimicrobial agents (especially tetracycline).^157,159 The extent of postburn immunosuppression depends on a variety of factors, including the severity of the burn, the patient’s nutritional status, and the patient’s hormonal balance.

Neutrophil phagocytic function is typically normal immediately after a burn. However, approximately 5 or more days after the burn, phagocytic function may be normal, depressed, or increased.^46,80 Because neutrophils provide the first-line response to infection, neutrophil depression can significantly increase the patient’s risk of infection.

Circulating immunosuppressive substances are present in patients with burns. These substances appear within 24   hours of injury and may persist until the wound is closed.¹⁵² The origin of these suppressors is not known, although substances secreted from WBC granules or membranes have been implicated.^{4,5a,36,53,87,154,160,209} Burn toxin, a high-molecular-weight protein, is known to contribute to postburn immunosuppression.^108,109,158

The complement system may be activated after a burn; this can produce blood pressure instability, fever, peripheral vasodilation with increased capillary permeability, changes in leukocyte function, coagulopathies, and microcirculatory obstruction.²²⁰ The complement system also may be dysfunctional after a thermal injury.

Immediately after a burn, lymphocyte response to antigen usually is depressed.¹⁵⁶ This depression lasts approximately 48   hours and may compromise the patient’s immune response.

General Findings

Burn wound sepsis is the most serious complication of burn injury and is defined as a bacterial count of greater than 10⁵ organisms per gram of tissue associated with invasion of viable tissue beneath the eschar.¹⁹⁴ Infections and sepsis also may be caused by other organisms, including Candida species, other fungi,^49,208 or viruses.

Signs of possible local burn wound infection are listed in Box 20-6; they include a change in wound appearance or drainage, vesicular or coloration changes in the skin surrounding the burn, and the presence of a distinctive odor. If any of these changes are noted, burn wound infection should be suspected, and a wound biopsy should be performed.¹⁸⁹

Signs of sepsis in the burned child are listed in Box 20-7 and include alteration in neurologic, gastrointestinal, and skin perfusion, subtle changes in vital signs (including unexplained tachycardia and early tachypnea or the need for increased oxygen or mechanical ventilation support), alteration in temperature (fever or hypothermia) and alteration in WBCs.¹⁶⁵ Clinical and laboratory evidence of end organ dysfunction (e.g., lactic acidosis, oliguria, disseminated intravascular coagulation) will be observed when septic shock develops (see, also, Boxes 6-2 and 6-3).

Initially the child with sepsis may demonstrate peripheral vasodilation with increased capillary permeability similar to that seen during the third-spacing phase following a burn. Increased fluid administration suddenly may be necessary to maintain systemic perfusion, and systemic and pulmonary edema may develop. In addition, laboratory findings may indicate nonspecific signs of stress, including hyperglycemia (or hypoglycemia in infants), early disseminated intravascular coagulation (particularly thrombocytopenia), and metabolic acidosis. Leukocytosis or leukopenia may develop. When septic shock develops, cardiovascular dysfunction (e.g., hypotension and signs of poor perfusion, such as lactic acidosis) and other organ failure will develop (see Septic Shock in Chapter 6 and Box 6-3).

There is no single laboratory or clinical finding that confirms the presence of sepsis.^2a A wound biopsy will aid in identifying an infecting organism and its sensitivities, and histologic examination will determine whether bacterial invasion of healthy tissue has occurred.¹⁸⁹ In addition, sepsis caused by gram-positive, gram-negative, and fungal infections can produce characteristic clinical findings. The characteristics of potential infections and resulting sepsis are summarized briefly here (Table 20-10).

Gram-Positive Infections and Sepsis

Group A streptococcus is a gram-positive, highly transmissible pathogen. Gram-positive infection typically develops during the first week after a burn and also may invade freshly grafted wounds and donor sites, potentially causing graft loss and conversion of donor sites to full-thickness injuries.

This infection is characterized by wound erythema, pain, induration, and swelling. The erythema may extend from the margin of the burn wound, indicating streptococcus invasion of normal tissue.¹²⁴

Staphylococcus aureus and Staphylococcus epidermidis are also gram-positive organisms; they are easily transmitted by contact or airborne routes. These infections usually have an insidious course, and 2 to 5 days may elapse between the onset of signs of infection and the development of sepsis. Staph wound infections are characterized by microabscesses, tissue necrosis, and increased exudate,²⁹ and they may cause graft loss. Staph sepsis will produce high fever and leukocytosis, and a gastrointestinal ileus is often present.

Gram-Negative Infections and Sepsis

Pseudomonas aeruginosa is an opportunistic gram-negative organism that rarely causes infection in healthy individuals. Because it grows well in moist, open wounds, it frequently invades immunosuppressed patients with burns. This infection results in a green, foul-smelling wound discharge over a 2- to 3-day period. The eschar may become dry with a green exudate, often progressing to patchy areas of necrosis. Occasionally, when Pseudomonas species sepsis is present, a spidery lesion (ecthyma gangrenosum) develops in healthy tissue. The patient with a Pseudomonas species infection often has hypothermia with a depressed WBC count. A paralytic ileus may develop.

Other gram-negative organisms, including Escherichia coli, Klebsiella, Proteus, Enterobacter, and Providencia species have been observed with increasing frequency in burn units. These infections usually colonize the wound from the patient’s own flora and produce infection when other organisms are eliminated by antibiotic therapy.³ Translocation of gram-negative bacteria or endotoxin from the patient’s own gastrointestinal tract can also contribute to the development of gram negative sepsis.

Fungal Infections and Sepsis

Candida albicans, a fungal infection, most frequently develops in patients with extensive burns after prolonged broad-spectrum antibiotic therapy. The antibiotics suppress the child’s normal bacterial flora, so that susceptibility to fungal infection increases. If a Candida species infection develops on a granulating wound, the wound becomes dry and flat with a yellow or orange color. A wound biopsy will be necessary to confirm the diagnosis. Systemic candidiasis is a common complication.

Prevention

The most important actions to prevent burn infection are good hand-washing technique and the use of topical antimicrobials. In burn units, cross-contamination (infection spreading from patient to healthcare workers to patient) will occur if healthcare workers fail to wash hands before and after patient contact. Burn care should always be performed using strict clean or aseptic technique, with clean gown, gloves, mask, and hat (or according to unit policy). In addition, strict aseptic technique must be practiced during catheter and intravenous tubing changes, and sterile technique during procedures.

Topical antimicrobial agents are applied to prevent colonization of the wound. In addition, providing early and adequate nutrition will help maintain adequate immune function.

Some physicians advocate excising the burn eschar within 72   hours of injury to reduce the possibility of burn wound sepsis.^61,137,196 Early excision is thought to be effective, because it enables early closure of the wound (with biologic dressings or grafting), eliminates the potential source of immunosuppressive factors, stops the consumption of immune defense factors, reduces the length of hospital stay (see Management of Escharotomy), and provides better functional and cosmetic results.

Care of an Infected Wound

Once a burn wound infection develops, appropriate antimicrobial agents are provided. In addition, the wound is extensively debrided, and topical antimicrobial agents and systemic antibiotics are administered in an attempt to gain bacteriologic control of the wound.

Aggressive debridement of devitalized and infected tissue can eliminate the source of bacteria and produce marked improvement in patient condition. Following debridement, continuous monitoring is required to detect reappearance of infection.

Once the infectious organism is identified, careful adherence to hospital and Centers for Disease Control (CDC) infection precautions is mandatory. Caution is required to prevent contamination of noninfected areas with soiled dressings or wash solutions.

Application of topical antibiotics will reduce the bacteria present in the wound and may prevent bacterial invasion of healthy tissue. During use of topical antibiotics, the wound appearance must be monitored closely to detect the development of secondary infections.

Treatment of Sepsis

Once sepsis is suspected, blood cultures are obtained and systemic antibiotics are administered. In addition, providers should closely monitor for the development of shock and provide shock resuscitation and support of cardiopulmonary function and oxygen delivery when indicated.

Initially, broad-spectrum antibiotics are prescribed until results of blood cultures and sensitivity studies are available; more specific antibiotics are then used. If aminoglycoside antibiotics are administered, peak and trough levels are monitored to ensure effective blood concentrations (see Chapter 4).

Occasionally, antibiotics may be injected or infused into the wound itself in an attempt to eliminate the infection at its site.^142,174 This therapy is controversial, however, because it may increase the formation of resistant organisms.

Detailed discussion of the treatment of septic shock is included in Chapter 6 (see Fig. 6-8). Aggressive fluid resuscitation (with administration of bolus therapy) is indicated; typically three or four boluses of 20   mL/kg are administered in the first hour after the development of signs of septic shock, unless signs of heart failure (e.g., hepatomegaly, pulmonary edema, and respiratory distress) suggestive of myocarditis develop. Beta-adrenergic and vasoactive drug support should be initiated if shock persists, and support of the airway, oxygenation, and ventilation are required.

Evaluation of Therapy

Throughout therapy the burn wounds should be inspected to determine progress in healing.¹⁵⁰ When sepsis is present, intravenous catheters should be changed every 72   hours, and more often if sites appear inflamed. Routine culture of catheter tips was shown to have no demonstrable benefit,¹⁹⁰ because these tips often are contaminated during removal. However, if catheter infection is suspected, tip culture may aid in confirmation of the diagnosis. Meticulous catheter care should be performed at least every 24 to 48   hours, using aseptic technique per unit policy (See Box 22-6).

Metabolic Rate and Oxygen Consumption

After a burn, catecholamine secretion in response to stress will stimulate metabolic rate, oxygen consumption, heat production, and substrate mobilization.⁷⁰ When a major burn is present, the basal metabolic rate may be twofold higher than normal. The actual metabolic rate can be determined by measuring the exchange of respiratory gases and calculating heat production from oxygen consumption and carbon dioxide production (see Indirect Calorimetry, later in this section).²⁰⁶

Oxygen consumption increases when the metabolic rate increases. However, this increase in oxygen consumption varies in different tissue beds after a burn. Despite the fact that blood flow to the burn wound is enhanced,⁷³ the burn uses little or no oxygen for its metabolic processes. As a result, anaerobic burn metabolism can produce localized metabolic acidosis. Visceral oxygen consumption increases markedly with a burn injury, whereas peripheral oxygen uptake remains a fixed percentage of total aerobic metabolism.²⁰⁶

A 1 to 2° C elevation in skin and core temperature frequently is observed immediately after a burn, as the result of increased heat production. Central thermoregulation is altered at this time to maintain this higher temperature. The child is usually asymptomatic, with a mild elevation in body temperature.

Glucose and Fat Metabolism

Hyperglycemia is observed after a burn, resulting from accelerated gluconeogenesis, reduced insulin levels, and abnormal glucose utilization. Hepatic gluconeogenesis is stimulated by catecholamine release, and the quantity of glucose made is directly related to the extent of the injury.²⁰⁷

Glucose utilization is not uniform throughout the body after a burn. The net glucose flux across healthy tissues and skeletal muscles is low, whereas glucose uptake by burned tissue is extremely high. In addition, injured tissues release large quantities of bacteria, which consume most of the available glucose.²⁰⁶ Renal glucose consumption is also elevated, whereas central nervous system glucose consumption remains normal.

Exogenous glucose from intravenous fluids is not utilized appropriately at this time, so serum glucose concentration often remains elevated long after glucose administration. Hepatic gluconeogenesis will continue despite exogenous glucose administration.²²⁶

Major thermal injury and hypermetabolism produce an increase in serum free fatty acids. Hydrolysis of stored triglycerides is accelerated, and mobilization of fat stores is stimulated by catecholamine secretion and elevated glucagon levels.²⁵ Postburn hypoalbuminemia also contributes to the elevation in free fatty acids,⁷⁵ because the serum albumin is not available to transport free fatty acids across cell membranes. Albumin administration at this time may help reduce serum free fatty acids.

Negative Nitrogen Balance

A thermal injury results in the breakdown of protein from skeletal muscle in burned and unburned areas.²¹⁸ This muscle breakdown provides amino acids for gluconeogenesis and fuel sources for local tissue needs.⁶⁹ If protein intake and synthesis do not increase and protein breakdown from skeletal muscle continues, a marked negative nitrogen balance ensues and nitrogen is excreted with urea in the urine. Urinary nitrogen loss is related primarily to the metabolic rate of the child, but is also affected by the child’s nutritional status and muscle mass.

Approximately 20% of daily nitrogen losses occur from the surface of the burn wound itself. If appropriate nutrition is not provided, lean body mass and total body weight may decrease as much as 30%. Such massive protein loss will result in accelerated tissue destruction, delayed wound healing, graft failure, and increased susceptibility to infection.

Physical Assessment of Nutritional Status

A variety of parameters must be examined to determine the child’s nutritional status (Table 20-11). However, these standard parameters do not allow for the effects of a large burn and its therapy on metabolic rate, so the child’s nutritional support must be evaluated constantly.

Anthropometric measurements include daily weight, triceps skin fold, and middle upper arm circumference.³³ The most useful of these measurements is the daily weight.

Laboratory analysis of serum (visceral) proteins and lymphocyte counts, and calculations made from urine creatinine clearance and urea also can be used to evaluate nutritional status. However, each measurement or calculation has its limitations and will be useful only for evaluating changes in patient body mass or fat stores. It is imperative that the measurements be obtained under identical conditions each time and that several parameters be used to determine the effectiveness of nutritional therapy.

If the critical care unit bed does not allow immediate determination of the child’s weight, the child should be weighed as soon as possible after the burn injury to determine a baseline weight. Once fluid resuscitation and fluid accumulation have occurred, the child’s weight will increase significantly. Daily weight measurements should be recorded. The daily weight should be obtained using the same process or scale at the same time of day, without dressings or splints, if possible. All catheters and tubing should be factored into the weight or elevated off the scale, so they do not influence weight measurement.

Daily weights should be recorded on a weight chart. A weight change of 10% or more is significant and requires evaluation of caloric and fluid intake. Weight loss of 5% or more of baseline body weight usually indicates inadequate nutritional support.²⁰⁶ A weight gain can indicate fluid retention, early sepsis, or muscle or fat accumulation. Changes in weight will most accurately reflect nutritional status late after a burn, once edema has disappeared.

Laboratory Evaluation of Nutritional Status

Laboratory evaluation of nutritional status can be an extremely helpful adjunct to the clinical assessment.

Calorie Count

An accurate and comprehensive record of the child’s daily caloric intake is a relatively simple method of evaluating the child’s nutritional status. All food, beverages, and parenteral nutrition the child receives are recorded by the bedside nurse. The caloric content of the intake can then be calculated by a nurse or dietician.

Determining Nutritional Requirements

The child’s nutritional requirements are determined by the amount of calories, nitrogen, and protein needed for normal homeostasis, plus those needed during burn-induced catabolism and healing of the burn wound.²¹⁸ Initial estimate of nutritional requirements is made at the time of admission. A variety of equations are available to determine nutritional requirements; all pediatric equations use the child’s age, body weight or body surface area (see BSA nomogram on inside back cover of this text), and the percent of TBSA burned. Nutritional requirement equations developed for use in adult patients are not suitable for use in pediatric patients.^40,85,117

The most popular pediatric formula for determining nutritional needs of children with burns is the Polk formula (Box 20-8); it provides for basal metabolic requirements plus additional calories based on the percent of the child’s body surface area burned.⁷⁴ Alternative formulas calculate basal metabolic requirements based on the child’s body surface area with additional fluid requirements based on burn surface area.⁹⁶ Use of body surface area provides a more accurate estimation of caloric requirements than those based on weight alone.

Regardless of the type of formula used, any calculation of nutritional requirements should serve only to provide a baseline estimate of nutritional needs. Nutritional therapy must then be individualized after consideration of the child’s preburn nutritional status, associated injuries and therapy, and the child’s weight gain and nutritional progress.

Additional Nutritional Requirements

High protein intake will be required after a burn to replace protein lost as a result of the increased metabolic rate, through the burn wound itself, and from tissue breakdown and infection. Protein intake can be calculated based on urinary nitrogen excretion, because 1   g of urinary nitrogen represents the loss of 30   g of lean body tissue, or 6.25   g of protein.⁷⁰ An estimate of protein requirements also can be made from the child’s weight (3   g protein required per kilogram body weight) plus percent of TBSA burned (1   g protein required per 1% of TBSA burned). Serum protein measurements are unreliable as parameters to guide protein replacement.⁵

Approximately 20% to 30% of the child’s total caloric intake should be in the form of proteins, and approximately 50% to 60% of total calories should be administered as carbohydrates. Fats should constitute approximately 5% to 15% of nonprotein caloric intake.¹³⁸ It is now thought that W-3 fatty acids, such as those derived from fish oil, are the most desirable form of fat supplement.⁷⁶ Excessive carbohydrate intake can result in hyperglycemia,¹² and excessive fat intake can result in immunosuppression, hyperlipidemia, and hepatic dysfunction.^207,209

Vitamin and mineral supplementation is necessary, although specific requirements after a burn injury have not been determined. Fat-soluble vitamins (A, D, E, and K) are stored in fat deposits and are depleted during prolonged feeding without supplementation. Water-soluble vitamins (B and C) are not stored in large quantities, so they also are depleted rapidly. Although vitamin and mineral deficiency can impair healing,⁹⁹ excessive vitamin administration also may be toxic.^52,225 National Academy of Science³⁴ and American Medical Association⁶ recommendations should be followed until more specific information is known about vitamin and mineral requirements after a burn.

Indirect Calorimetry

Indirect calorimetry has only recently been used to determine caloric requirements in children.^102,193 This technique determines kilocalories of energy expenditure based on the measurement of oxygen consumption (VO₂) and carbon dioxide production (VCO₂).²⁰⁰ An accurate weight measurement is also required.

Although calorimetry is often performed when the child is at rest, more accurate caloric requirements are calculated from measurements performed during typical periods in the child’s day. Particularly stressful procedures (e.g., dressing changes, suctioning) should not be performed for 30 min before calorimetry.

The child must be intubated if he or she is unable to cooperate and follow directions. If the child is intubated, the ventilator circuit is connected to the calorimetry circuit (e.g., Waters Instruments, Rochester, MN or Sensormedics, San Diego, CA). Air leaks around the endotracheal tube must be eliminated for accurate results; this may require temporary replacement of the child’s tube with a cuffed tube or a larger tube.

If the child is breathing spontaneously, the child inspires and exhales into the calorimetry circuit through a mouthpiece or face mask. If the mouthpiece is used, a nose clip is placed to prevent inadvertent nasal breathing.

The amount of oxygen consumed and carbon dioxide produced is determined by the difference in concentration of these gases between inspiration and exhalation.¹¹⁷ Energy expenditure is calculated by means of standard equations.²³ Anything that interferes with gas exchange in the lungs (e.g., pneumothorax) or gas conduction to the calorimetry circuit will produce inaccurate results.

Measurements obtained during calorimetry also can be used to calculate the respiratory quotient (RQ). RQ is the ratio of oxygen consumption to carbon dioxide production, and it is useful in assessing energy expenditure. The RQ will vary with the adequacy of feeding and the type of fuel used as energy. An RQ of 0.70 is seen in starvation, and an RQ greater than 1.0 suggests that overfeeding has occurred, with resultant pure carbohydrate metabolism and fat synthesis.¹⁹²

The use of indirect calorimetry still requires refinement. Because oxygen consumption can vary significantly throughout the day as the result of activity, pain, and change in temperature, all measurements must be performed under identical conditions. In addition, calculated allowances (available from the manufacturer) for activity are not accurate for pediatric patients.²⁰⁰ Calorimetry does not measure nitrogen balance, so it is usually necessary to continue to monitor urinary nitrogen excretion.

Oral Feeding

Although oral feeding is the preferred route of nutrition, only children with uncomplicated burns totaling 15% or less of TBSA can be expected to ingest sufficient calories by this route. To maximize effectiveness of oral feeding, every attempt must be made to maximize the quantity and content of the child’s caloric intake. The child’s likes and dislikes must be noted, and favorite foods must be available at all times on the unit.²²⁴ When the child is thirsty, high-calorie liquids, including fruit juices, fortified milk drinks, and commercial oral feeding preparations, should be offered instead of water. Commercial nitrogen and caloric supplements should be added to food and beverages to optimize intake. Mealtimes should be made special, and strenuous activity and therapy should not be scheduled immediately before or after eating.

Tube or Enteral Feeding

Whenever possible, the child’s gut should be used for feeding. Oral and gastric feeding preserve gut mucosal mass and maintain digestive enzyme control.²¹⁸ Tube feeding may be used to supplement oral intake, if the child is unable to ingest at least 75% of caloric requirements.¹⁶⁴ Tube feedings should be planned for any child with burns in excess of 15% of TBSA. Feeding should begin as soon as possible after the burn, because delayed feedings are associated with loss of mucosal mass, elevated catabolic hormones, increased metabolic rate, and decreased feeding tolerance.^54,139 Enteral feeding may prevent or minimize translocation of gram-negative bacteria and endotoxin across the gastrointestinal mucosa.⁶³

Continuous tube feedings usually are required to provide maximal caloric intake. Nasogastric feeding may be provided as long as active bowel sounds are present, usually within 48 to 72   hours after a burn injury. Nasoduodenal feeding can begin immediately after a burn, even if bowel sounds are absent, so this method of feeding has recently become popular.^76,77,107 Intravenous albumin administration may help to maintain serum albumin soon after a burn until the child demonstrates ability to tolerate tube feeding.

A nasogastric or nasoduodenal tube should be small (8-10 French), soft, and pliable. A Silastic catheter (e.g., Frederick-Miller tube, Cook, and Dobbhoff) is preferred, because it can remain in place for a month or longer. If a nasoduodenal tube is inserted, fluoroscopy is recommended to ensure proper placement. A nasogastric tube should also be placed to allow the detection of residual feeding or displacement of the duodenal tube into the stomach.

Tube feeding should be started with a small volume of formula, and the hourly feeding volume is increased gradually as tolerated every 4 to 8   hours. The head of the child’s bed should be elevated to reduce the risk of regurgitation. Infusion pumps should be used to ensure consistent feeding volume and rate. Intermittent bolus feedings should be avoided, because they are associated with a higher incidence of gastric cramping, diarrhea, gastric distension, regurgitation, and aspiration.^95,99

Ultimately, tube feeding should contain 1 to 2 calories/mL, with protein, fats, carbohydrates, vitamins, and minerals. Modular feedings have recently become popular, because they allow adjustment of the quantity of specific nutrients according to patient need and because they are thought to reduce the incidence of diarrhea.

Commercial tube feedings designed for adults are inappropriate for use in young infants, because they contain amounts of protein that are excessive for immature kidneys.⁷⁶ Infant formulas such as Similac (Abbott, Abbott Park, IL) or Enfamil (Mead Johnson Nutrition, Glenview, IL) are preferred. Caloric content of these formulas can be increased gradually from 20 calories/ounce to 24-27 calories/ounce as tolerated, using commercial feeding supplements if needed.

Isotonic commercial tube feeding preparations (such as Isocal [Mead Johnson Nutrition, Glenview, IL] and Osmolite [Abbott, Abbott Park, IL]) can be used for children older than 1 year; they may be enriched with additional protein (e.g., whey or Pro-mix) to provide additional protein caloric intake.¹⁷² High-nitrogen content formulas, including Isocal HN, have been developed to meet the high nitrogen needs of burn and trauma patients.

Daily multivitamin and mineral supplements including ascorbic acid and zinc sulfate should be administered. Administration of intravenous or enteral glutamine may reduce translocation of gram-negative bacteria across gastrointestinal mucosa during parenteral nutrition. The efficacy of this therapy is under evaluation.⁶³

Potential complications of tube feeding include gastric distension, aspiration, respiratory infection, nausea, vomiting, and diarrhea. Abdominal girth should be measured hourly when feedings are initiated or increased and every 2 to 4   hours during feeding. If gastric distension develops, regurgitation and aspiration may occur.

Gastric residual volume should be checked every 4   hours and again as needed. If residual volume during gastric feeding equals more than half of the previous 2-hour feeding, reduction in feeding volume or concentration may be required. If residual gastric volume is present during duodenal feeding, the duodenal tube may have slipped into the stomach, and it must be repositioned.

Diarrhea may develop during tube feeding. It can be caused by excessive feeding volume or a rapid increase in feeding concentration. Other potential causes of diarrhea that should be considered include infection, hypoalbuminemia, lactose intolerance, and inappropriate formula. If diarrhea develops, temporary reduction in the volume of feeding or administration of antidiarrheal agents (e.g., paregoric, loperamide, lomotil) may be necessary. Alteration in the protein content of the formula also may be needed to reduce diarrhea. A variety of formulas (e.g., Reabilan, Clintec Nutrition Company, Deerfield, IL) are available that contain small peptides that can be absorbed more efficiently in the intestine. In addition, these peptide formulas can enhance fluid reabsorption from the gut, so that diarrhea is reduced.

Once the child begins to tolerate oral feeding, he or she can be weaned gradually from tube feeding. When oral intake begins, it is helpful to interrupt the tube feeding for a few hours before meals, so that the child feels hungry before eating. The tube should not be removed until the child has demonstrated adequate oral intake.

Parenteral Feeding

Parenteral alimentation will be required if adequate caloric intake through tube feeding cannot be ensured; it may be used to supplement tube feeding and caloric intake, or as the sole means of nutritional support. Parenteral alimentation should be considered if the child requires more than 3000 calories/day (or 3000   kCal/day).

The term hyperalimentation should not be applied to parenteral alimentation. This form of feeding is not better (or hyper) when compared with oral or tube feeding. In fact, parenteral feeding is more expensive, with less effective utilization of nutrients, and presents a higher risk of infection than does oral or tube feeding. If parenteral alimentation is begun, daily assessment of the child’s nutritional status and requirements must be performed, and the alimentation content or volume should be modified accordingly.

Parenteral alimentation generally is provided through a central venous catheter so that maximum glucose and protein concentration can be delivered. Peripheral alimentation is used only for supplementary feeding because the maximum glucose concentration tolerated through a peripheral venous catheter will be 12.5% dextrose.

Central venous alimentation solutions consist of 20% to 25% dextrose and 25% crystalline amino acids. This solution normally provides approximately 7   g of protein (4   kCal/g) and 800 to 1000   kCal/L. Water- and fat-soluble vitamins, trace elements, and electrolytes must be added to the solution. Lipid solutions (e.g., INTRALIPID 10% or INTRALIPID 20%, Baxter Healthcare Corporation, Clintec Nutrition Division, Deerfield, IL) usually are infused during parenteral alimentation to provide fat calories (9   kCal/g, or 1.1   kCal/mL of 10% lipid solution).

Because hypertonic glucose is an excellent growth medium, strict aseptic technique must be maintained when changing alimentation tubing and catheter entrance site dressings. Ideally, parenteral alimentation catheters should be used only for alimentation and not for drug administration or blood sampling. Potential complications of parenteral alimentation include metabolic imbalance and sepsis.¹³⁴ For further information regarding parenteral alimentation, see Chapter 14.

Positioning

If the anterior neck is burned, the use of pillows should be avoided, and the child’s neck should be kept straight or slightly extended. Doughnut pillows placed under the head or linen rolls placed under the shoulders work well. Because this position will facilitate aspiration if vomiting occurs, the child must be monitored closely.

Hands should be splinted in the position of function, with the wrist dorsiflexed at 45 degrees or neutral, according to the physical therapist’s preference. Burns in the area of the axillae frequently result in severe contractures. When axillary burns are present, the arms should be positioned at 90-degree angles from the body.⁶⁰

The foot should be positioned at a 90-degree angle from the leg, avoiding both dorsiflexion and plantar flexion. If the feet are not burned, the use of high-topped athletic shoes will facilitate proper positioning. Splints or footboards also may be used. Knees should remain extended, and hips should not be flexed.¹⁹⁹

Traction, splints, and dressings can be used to maintain appropriate positioning during the acute phase. Active and passive range-of-motion exercises are imperative to avoid the development of joint stiffness and contractures.

Evaluation of Therapy

Constant and thorough assessment of joint function and range of motion is needed to identify any signs of contraction and prevent contracture development. Interruption of the program may be necessary during grafting procedures, but it is imperative that it be resumed as soon as possible after graft stabilization.^{38,39,55,83,116,133,166,195}

Care of Excision Sites

If grafting is performed later on the day of excision, bleeding must be stopped before grafting occurs. Gauze soaked with 1/10,000 strength epinephrine in normal saline, thrombin, or Neo-Synephrine (or other vasoconstrictor or coagulant) is applied over the newly exposed tissue to stop bleeding. Extremities are wrapped with elastic bandages and elevated above the level of the heart; they may be suspended from intravenous poles as long as care is taken to avoid nerve stretch injuries (especially of the brachial plexus). Pressure is applied to dressings over the trunk. The dressings are removed with saline irrigation after 10 to 15 minutes. Any remaining bleeding vessels are cauterized, and grafting can be performed.

If grafting is not performed immediately after excision, the newly exposed dermis, subcutaneous fat, or fascial layer must be kept moist until grafting occurs. Layers of gauze are placed over the tissue, and irrigation catheters are placed between layers of gauze. The entire irrigation dressing is covered with an elastic bandage to keep the dressing intact and to reduce bleeding. Normal saline or an antimicrobial solution is flushed through the catheters every 2 to 4   hours and as needed to keep the gauze moist.

Donor Sites

Patient donor sites should resemble the area to receive the graft, so that hair growth and skin texture will conform to that surrounding the wound.⁴⁴ Ideally, the donor sites should be covered by clothing or regrowth of hair, so that any scarring will not be visible. The scalp is an excellent donor site for children, because the head has a large available surface area and hair growth will cover the donor site. Small burns can also be covered with skin removed from the anterior or lateral surfaces of the upper thighs and lower abdomen.

The donor skin is removed using a power-driven dermatome. A full-thickness skin graft consists of the entire donor epithelium and dermis. This type of graft generally is used for reconstruction. Because the graft is thick (0.035   inches or more), the donor site also must be grafted or closed primarily, or it will not heal spontaneously.

A split thickness skin graft (STSG) consists of only the epithelium and part of the dermis. If the graft will be placed as a sheet, only a thin (0.004-0.008   inch) graft will be required. If the donor skin will be meshed (to expand the area covered), a thicker (0.010-0.020   inch) graft will be removed. If a mesh is created from donor skin, the surface covered can be expanded to 1.5 to 9 times the size of the original donor area through use of a Tanner mesher. However, the greater the expansion of the donor skin, the more fragile the skin mesh. Generally, expansions of 1.5 to 3 times are preferred. The STSG donor site can heal by epithelialization and contraction.

Postoperatively, the split-thickness donor site should be treated as a partial thickness burn injury.⁵⁷ A wide variety of care modalities have been used with comparable results. The site may be covered with dry or antimicrobial-permeated gauze, polyurethane, or a silver sulfadiazine dressing. Gauze is left in place for 2 to 3 weeks, until it naturally separates from the site as the area heals. This technique is relatively simple for the nurse, but is usually uncomfortable for the child, because the gauze tends to pull as it dries and mobility at the donor site is compromised.

If a polyurethane dressing is applied without wrinkles or gaps, it can remain in place for 10 to 14 days. If the donor site is covered with silver sulfadiazine, dressing changes should be performed two or three times per day.

With proper care, the donor site should heal quickly. Complications at the site include hypertrophic scarring, pigmentation, and blistering. The donor site also may become infected or separate. Application of elastic bandages can prevent or minimize hypertrophic scarring and blistering.

Postoperative Care

Once the donor skin is obtained and prepared, it is placed over the clean, granulating burn surface and secured. Staples usually are used to secure the graft, and they can be reinforced with sutures or steri-strips.

The grafted skin must remain in constant contact with the tissue bed to receive nutrients and oxygen supply. Once the graft is applied, a fibrin layer forms between the granulating bed and the graft. Capillary action allows absorption of serum from the bed into the graft during the first days after grafting. Capillary buds then form a fine network of vascular channels to the fibrin layer,²²⁸ and blood flow to the graft is present within 3 days. Complete capillary ingrowth will be established approximately 7 to 10 days after grafting. It is imperative that the graft be secure (e.g., by wrapped dressings), without stress or shear forces applied during this time, to ensure delivery of nutrients to the graft and to prevent the disruption of the fragile capillary network.

Expanded (mesh) grafts are used most commonly because they cling to the recipient bed more easily than do sheet grafts. Epithelial tissue will grow between the interstices of the expanded graft to provide full coverage. In addition, expanded grafts heal by contraction.

Postoperatively, an occlusive dressing usually is applied to an expanded graft, and moist occlusive dressings are usually preferred. Fine mesh gauze soaked in normal saline or antimicrobial solution is applied over the fresh graft, and these are covered with dry gauze. Catheters can be incorporated into the gauze dressings to allow irrigation every 2 to 4   hours. The entire dressing is secured with an elastic bandage to stabilize the dressing and maintain graft position.

Splints should be applied if needed to prevent movement of and tension on the graft site. The dressing is changed 48 to 96   hours after surgery, and the site is inspected. Clean dressings are then applied and changed daily for 2 to 4 days. Dressings are discontinued if the graft is healing well by the sixth postoperative day. A lubricating cream can be applied to keep the graft moist and to prevent cracking.

Sheet grafts are used most frequently over the face and hands, because they provide the best cosmetic results. Sheet grafts also retain moisture, so they are used over exposed arteries, veins, or nerves. In addition, they are usually placed over joints or areas of flexion creases to limit graft contraction.

Sheet grafts are usually left open to the air, without dressings, for the first days after surgery. Serum and exudate that accumulate under the graft must be evacuated, or the graft may fail.¹⁶⁸ The serum may be allowed to seep from under the surface of the graft via small slices in the graft (similar to the small slices on a pie crust). Alternatively, the serum may be aspirated or expressed. Serum aspiration is accomplished with a needle and syringe. To express the serum, a sterile cotton applicator is rolled gently over the sheet graft from the center of the graft toward the nearest incision. The rolling technique should only be performed over a small amount of tissue, without application of pressure, because extensive or firm rolling might interrupt capillary development and blood flow to the graft.

All graft sites must be monitored closely for evidence of erythema, purulent drainage, odor, or sloughing. Folliculitis and pruritus may also develop under skin grafts.

Often, the child is fitted with special elastic (compression) garments to minimize scar formation. All necessary measurements should be recorded as soon wounds are healed so that the garments are available for use before the child is discharged.

Skin grafts speed healing and reduce scarring for children with burns. However, multiple grafting procedures are frequently necessary to complete the burn repair. During this time, children will require extensive rehabilitation and psychosocial support to help them return successfully to a normal life and to cope with changes in appearance resulting from the injury.