Care of the Child with Burns

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20 Care of the Child with Burns

John B. Pietsch, Dai H. Chung

Pearls

• Intentional injury (child abuse) should be considered and ruled out as a cause of burns and scalds in children.

• Burns are painful; therefore analgesia should be provided and supplemented as needed before burn care.

• Formulas developed to estimate burn size in adults should not be used to calculate the burn surface area and fluid resuscitation requirements for children.

• Children with large burns should receive nursing and medical care in units with nurses and physicians who have pediatric expertise. Strong consideration should be given to transfer of a child to a pediatric critical care unit when large burns or complicating factors, such as smoke inhalation, are present.

Introduction

The incidence of pediatric burn injuries has declined as a result of preventive measures and legislation. However, more than 1 million burn injuries still occur each year in the United States. Although most of these burn injuries are minor, each year in the United States approximately 45,000 patients suffer moderate to severe burns that require hospitalization. Of these cases, 67% are young males, and 40% are children younger than 15 years.^31a Burns are the second leading cause of unintentional death in children younger than 5 years. It is estimated that the number of serious disabilities from burns is triple the number of deaths. Three fourths of these burns are thought to be preventable.²²

Eighty-five percent of thermal injuries in children occur at home, usually in the kitchen or bathroom. Infants and toddlers are injured most frequently by scald burns (Table 20-1),¹ whereas contact burns become more common once the infant is crawling or walking. Flame burns are seen in children 2 to 4 years of age and older and are the most common cause of burn injury in children 5 to 18 years of age. Electrical and chemical burns are uncommon in children and can be lethal if they are severe.¹²⁸

Table 20-1 Epidemiology of Pediatric Burns

Inflicted injury is an additional cause of thermal injury in infants and children. These injuries often have a typical pattern of delayed presentation for medical care, bilateral symmetry of the burn, or a stocking or glove distribution.

The purpose of this chapter is to discuss the normal functions of the skin and the pathophysiologic changes that occur as a result of a burn injury. The management of thermal injuries, complications of burns and burn therapy, and nursing interventions in the care of the child with burns will be presented.

Essential anatomy and physiology

The skin is the largest organ of the body, amounting to 4 to 5 square feet in the child. Children have larger skin surface area to volume ratios than adults. As a consequence, the child has relatively greater daily fluid requirement and evaporative water loss per kilogram of body weight.

The skin is composed of three layers: epidermis, dermis, and subcutaneous tissues (Fig. 20-1). The epidermis is a superficial layer of stratified epithelial tissue that is composed of five microscopic levels of maturing cells. The epidermis is thinner in infants than in older children, and its thickness also varies over parts of the body. This layer is constantly shed to the environment, so that it regenerates continually. After a superficial burn, the epidermis will regenerate because portions of the epidermal appendages are present.

Fig. 20-1 Anatomy of the skin.

(From Thibodeau GA, Patton KT: Anatomy and physiology, ed 5, St Louis, 2003, Mosby.)

The dermis layer is thicker than the epidermis and composes the bulk of the skin; it consists of connective tissue containing nerve endings, blood vessels, hair follicles, the lymph spaces, and the sebaceous and sweat glands. When the entire layer of dermis is burned, all epithelial elements are destroyed, and the skin cannot heal or regenerate spontaneously.

The subcutaneous tissue, located below the dermis, contains collagen and adipose tissue. This layer can be damaged by deep burns that leave bones, tendons, and muscles exposed. In third-degree burns, eschar (thick, coagulated particles from destroyed dermis) attaches to this subcutaneous layer and may be difficult to remove.

Functions of the Skin

The skin has multiple functions. It provides a protective barrier, and it assists in the maintenance of fluid and electrolyte balance and thermoregulation. In addition, the skin is an excretory and a sensory organ. The skin also participates in vitamin D production and determines appearance. All these functions are threatened after a burn.

When the skin is intact, it forms a protective barrier against bacteria and pathogenic organisms; disruption of this barrier leaves the patient vulnerable to infection. The skin also limits evaporative fluid losses. When a burn occurs, the transmission of water vapor to the environment will increase; this evaporative water loss is proportional to the extent and depth of injury in burns affecting up to 50% of body surface area, and then it plateaus.

A third function of the skin is temperature control. Normally, body temperature can be maintained despite a mild reduction in the environmental temperature, because blood flow to the skin is reduced and the subcutaneous fat provides insulation. When the skin is burned, heat loss to the environment is significant, and body temperature (particularly in small children) may decrease.

The skin functions as an excretory organ when perspiration occurs. When deep burns are present, sweat glands are destroyed and this ability is lost. The skin also functions as the largest sensory organ of the body. Receptors located in the skin enable detection of pain and pressure. When moderate burns are present, nerve endings are exposed to the surface, which is extremely painful; deep burns destroy nerve endings, and sensation is lost.

A sixth function of the skin is the production of vitamin D, which is essential for bone growth. Vitamin D is absorbed by the skin and promotes calcium and phosphate deposition in bones. This function is compromised in second-degree burns, and completely lost in third-degree burns. The skin also determines physical appearance and identity. The alteration in appearance caused by a burn can be extremely stressful.

Severity and Classification of Injury

Depth of Burn

The severity of the burn injury is determined by estimating the depth and extent of the injury. The degree of tissue destruction is affected by the burning agent, its temperature, and the duration of exposure to the heat source. Healthy skin can tolerate brief exposure to temperatures up to 40° C (104° F) without injury, but higher temperatures will produce burns. Severity of the injury increases as the temperature and duration of contact increase.¹⁸⁰

Significant variations in skin thickness throughout the body also influence the depth of the burn. Where the epithelium is thin (such as over the ears, genitalia, medial portions of upper extremities, and in very young patients), even a brief exposure to a heat source can result in a full-thickness injury.

Classically, description of burn injury refers to the three concentric zones of tissue damage.^143,¹⁸⁰ The central area of the burn wound, called the zone of coagulation, is injured most severely and is characterized by coagulation necrosis. The zone of stasis is an area of direct but milder injury, which can be damaged further if ischemia develops.²³² The zone of hyperemia is the area of tissue most peripheral to the initial burn and is injured only minimally.

A second method of burn classification describes the specific depth of injury (Table 20-2). A first-degree burn involves the top portion of the epidermis and does not extend into the dermis layer (Fig. 20-2). The burn area is characterized by erythema, mild edema, pain, and blanching with pressure. There is no vesicle formation. First-degree burns (e.g., sunburn) heal spontaneously without scarring in 7 to 10 days.

Table 20-2 Characteristics of Burn Injury

Fig. 20-2 Classification of burn depth. First-degree burns involve the epidermis, second-degree burns involve the epidermis and dermis, and third-degree burns penetrate to the subcutaneous tissue.

From Garner WL: Thermal burns. In Achauer BM, Eriksson E, editors: Plastic surgery: indications, operations, and outcomes, St Louis, 2000, Mosby.

A second-degree burn (i.e., a partial thickness burn) involves the entire epidermis and part of the dermis layer of the skin. These burns can be classified further as superficial partial thickness or deep partial thickness, depending on the amount of dermis injured. Superficial second-degree burns are limited to the papillary dermis and are typically erythematous and painful with blisters. These burns spontaneously reepithelialize in 10 to 14 days from retained epidermal structures and may leave only slight skin discoloration. Deep second-degree burns extend into the reticular layer of the dermis. The deep epidermal appendages allow some of these wounds to heal slowly over several weeks, often with significant scarring.

A full-thickness, or third-degree burn, encompasses the entire epidermis and dermis layers. The wound surface, called eschar, will appear dry and leathery, with a waxy-white or black color produced by particles from destroyed dermis. Thrombosed vessels may be seen beneath the surface of the burn. The patient with a third-degree burn experiences little or no pain, because the nerve endings in the dermis layer have been destroyed. This type of burn will require surgical repair. Fourth-degree burns, typically resulting from profound thermal or electrical injury, involve organs beneath the layers of the skin, such as muscle and bone.

An accurate and rapid determination of burn depth is vital to the proper management of burn injuries. In particular, the distinction between superficial and deep dermal burns is critical, because it dictates whether the burn can be managed without surgical procedures. Unfortunately, the determination of whether an apparent deep dermal burn will heal in 3 weeks is approximately 50% accurate, even when made by an experienced surgeon. Early excision and grafting provide better results than nonoperative therapy for such indeterminate burns.

Extent of Injury

A variety of methods have been developed for determination of the extent of any burn injury, but most involve expression of the burn as a percent of the total body surface area (TBSA) involved. Accurate calculation of the surface area of the burn is required to estimate fluid losses and fluid requirements.

A rapid method of calculating burn area in adolescents and adults, developed in the 1940s by Pulaski and Tennison,^174a is called the rule of nines (Fig. 20-3).¹ In the rule of nines, each upper extremity and the head constitute 9% of the TBSA, and the lower extremities and the anterior and posterior trunks are each 18% of TBSA. The perineum, genitalia, and neck comprise the remaining 1% of the TBSA. A quick estimate of burn size can also be obtained by using the patient’s palm to represent 1% of TBSA and transposing that measurement to estimate the wound size.

Fig. 20-3 Estimation of extent of burn injury: rule of nines applied to adult patient (see far right) and modified rule of nines for pediatric patients. Note that the numbers on the chest represent the combined estimate of total body surface area (TBSA) of the chest plus the back. These numbers should be divided by 2 (i.e., 16% of TBSA) to estimate the TBSA of either the front or the back.

(From Herndon DN, editor: Total burn care, ed 2, Philadelphia, 2002, WB Saunders.)

Use of the rule of nines can be misleading in children because the child’s body proportions differ from those in adolescents and adults. In children, the head and neck constitute a relatively larger portion of the TBSA, and the lower extremities constitute a smaller portion. For example, an infant’s head constitutes 19% of TBSA, compared with 9% in an adult. Thus, a modified rule of nines, based on the anthropomorphic differences of infancy and childhood, is generally used to assess pediatric burn size (see Fig. 20-3). Clinical criteria can also be used to estimate the percentage of TBSA burned, based on the patient’s age and the body part burned (see Classification of Burns).

Another widely used method of determining the extent of pediatric burn injury is the Lund and Browder method (Fig. 20-4). This method allows for changes in body surface area as the average-sized child grows.¹¹⁹

Fig. 20-4 A, The Lund and Browder charts are somewhat more accurate than the rule of nines in estimating the total body surface area (TBSA) burned. B, The proportion of TBSA of individual areas, according to age. Compared with adults, children have larger heads and smaller legs. Other areas are relatively equivalent throughout life. The adult rule of nines is not accurate for determining the percentage of TBSA burned in children.

(From Bethel CA, Mazzeo AS: Burn care procedures. In Roberts JR, editor: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, WB Saunders.)

Computer-generated estimates of burn injury size are available. Such programs are gaining in popularity, because they can provide estimates of fluid requirements and drug doses.

Factors Influencing Severity of Burn

To appreciate the significance of a burn, other factors in addition to the depth and extent of the injury must be considered. The age and underlying clinical condition of the child and the location of the injury also must be evaluated. Complications related to fluid resuscitation and organ system failure are most common in children younger than 2 years. Children with underlying organ system failure also will be less tolerant of fluid shifts associated with the burn and fluid resuscitation.

The location of the burn can have a significant effect on morbidity and mortality. A thermal injury to the face, hands, or feet can result in serious sequelae, particularly loss of function. Burns of the face may be associated with severe edema and airway occlusion. Skin over the ears and perineum is relatively thin, so injuries sustained in these areas can result in a full-thickness injury.

Full-thickness circumferential burns to the extremities produce a constricting eschar, which can result in vascular compromise to the distal tissues, including nerves. Accumulation of tissue edema beneath the nonelastic eschar impedes venous outflow, resulting in a compartment syndrome and eventually affecting arterial flow. When distal pulses are absent on palpation or Doppler examination and a central circulation problem has been ruled out, an escharotomy is performed to avoid vascular compromise of the limb tissues.

Classification of Burns

After providing first aid and initiating appropriate fluid resuscitation, providers should consider transferring the patient to a tertiary burn center. Burn units with experienced multidisciplinary teams are best prepared to treat patients with major burns. In addition to physicians and nurses, respiratory and rehabilitation therapists play a critical role in managing acute burns. Any patient who sustains a major burn injury, as defined by the American Burn Association (Box 20-1), should be transferred to a nearby burn center for further care.

Pathophysiology of a Burn

Pathophysiologic changes resulting from a thermal injury can affect all organs and systems of the body. The severity of the injury determines the significance of the changes.

Local Circulatory Destruction

Immediately after the burn, major circulatory destruction occurs at the burn site. The severity of the damage depends on the extent of the burn injury and might not be immediately apparent.

The vessels supplying the burned skin are occluded, and there is reduction in or cessation of blood flow through the arteries and veins. Release of vasoactive substances (especially histamine) from injured cells will produce vasoconstriction,¹⁴³ and peripheral vessel thrombosis ultimately may occur. The reduction in skin perfusion can produce tissue necrosis and increase the depth of the burn.

When a partial thickness burn is present, rapid restoration of arterial and venous circulation is observed within 24 to 48 hours. Cellular necrosis beyond the immediate area of the burn is prevented, and reepithelialization occurs from viable dermal elements. When a full-thickness burn is present, progressive tissue necrosis occurs over 3 to 4 weeks, because blood vessels in the dermis have been destroyed. This destruction ceases only after new vessels (the neovasculature) arise from underlying tissue.

Capillary Permeability (Third-Spacing) Period

When the child sustains a major burn, normal fluid homeostasis is altered, and intravascular volume and cardiac output will be affected. The first 12 to 36 hours after a burn are characterized by fluid shift from the intravascular to the interstitial space as a result of increased capillary permeability. This fluid shift is known as third-spacing of fluid, because the fluid is located in neither the intravascular nor the intracellular space—it is in a third space, in this case it moves to the surface of the burn and to the interstitial space. With third spacing of fluid, a significant volume of fluid is unavailable to the circulation to support cardiac output and systemic perfusion. Third-spacing is most significant during the first 12 hours after a burn.

Normally, intravascular proteins remain in the vascular space, because they are too large to escape through capillary pores. The increased capillary permeability associated with a thermal injury allows intravascular proteins and fluid to escape the vascular space. The amount of fluid shift that occurs is determined by the extent and severity of the burn injury. Burns affecting 15% or less of the TBSA produce minor fluid shifts, whereas large burns not only result in fluid loss from the surface of the burn, the burn affects capillary permeability in noninjured tissues, resulting in a major loss of intravascular fluid. If the intravascular fluid loss is not replenished, hypovolemia will result in compromise of systemic perfusion.

As protein rich fluids, electrolytes, and plasma escape into the interstitial space, peripheral edema develops. Movement of proteins into the interstitial space will increase tissue colloid osmotic pressure, enhancing the intravascular-to-interstitial fluid shift.¹³⁶

Pulmonary capillary permeability is typically normal unless severe inhalation injury is present or fluid administration is excessive. When pulmonary edema develops, it is often temporary, because pulmonary lymph flow often increases proportionately and rapidly eliminates the pulmonary interstitial fluid.

Fluid lost from the vascular space is relatively isotonic; therefore if it is replaced with isotonic or hypertonic fluids, electrolyte balance should be maintained. Dilutional hyponatremia, hypocalcemia, and hypomagnesemia are seen occasionally,²¹³ particularly if antidiuretic hormone secretion is significant (antidiuretic hormone secretion causes water retention in excess of sodium—see Chapter 12). It is rarely necessary to replace these electrolytes if isotonic fluids are administered; however, electrolyte balance should be monitored closely. Hypotonic fluids (e.g., 5% dextrose and water or 5% dextrose and 0.45% sodium chloride) should not be administered during this period.

Potassium is released from injured cells into the extracellular fluid. For this reason, supplementary potassium chloride may not be required in resuscitation fluids. If fluid resuscitation is inadequate, or renal failure develops, hyperkalemia may be problematic.

The concentration of base bicarbonate in the extracellular fluid decreases after a burn, and fixed acids are released from the injured tissues into the extracellular fluid, including the plasma. These acids normally are excreted by the kidney and buffered by respiratory compensation. If fluid resuscitation is inadequate, or respiratory function is compromised, the patient may develop metabolic acidosis. Young infants are less able to compensate for significant metabolic acidosis, because the infant kidneys are unable to excrete large quantities of acids or absorb large quantities of bicarbonate.¹⁷⁹

During the third-spacing period, hemoconcentration develops and the viscosity of the blood increases. This hemoconcentration can produce sluggish blood flow through small vessels and platelet and leukocyte accumulation in capillaries. Red blood cell (RBC) destruction also is enhanced. Rapid and accurate fluid resuscitation should minimize hemoconcentration.

Capillary Healing Period: Fluid Remobilization (or Diuresis)

Injured capillaries heal approximately 24 to 36 hours after a burn, so intravascular fluid loss typically ceases at this time, and fluid begins to shift back into the intravascular compartment. This stage is called the fluid remobilization period. If the patient tolerates the fluid shift, fluid and electrolyte balance is maintained. Renal blood flow and urine formation increase, and diuresis is observed. Edema subsides and body weight returns to normal.

The fluid administration rate must be tapered during this period. If excessive fluids are administered, or if renal or cardiovascular function is impaired, signs of hypervolemia (including progressive myocardial dysfunction and pulmonary edema) will be noted. If diuresis is not observed, renal damage should be suspected.

Hyponatremia is likely to develop approximately 24 to 36 hours after a burn, because renal sodium excretion is enhanced during diuresis. Normal serum sodium concentration should be restored approximately 72 to 96 hours after the burn. Hypokalemia may be observed as potassium returns to the intracellular compartment. The serum potassium concentration should be monitored closely, and potassium supplementation may be required.

Anemia frequently develops as a result of hemodilution and, to a lesser extent, from enhanced RBC destruction. As much as 10% of the patient’s erythrocytes may be destroyed immediately after a burn, but transfusion is rarely necessary.

Cardiovascular Dysfunction

Cardiac output falls after a burn as the result of decreased intravascular volume and the development of myocardial dysfunction.¹²³ Myocardial dysfunction after a burn is not explained entirely by intravascular fluid loss. Within 30 minutes after a large burn (i.e., 50% or more of TBSA), cardiac output may decrease to 30% of preburn levels and may remain depressed for 18 to 36 hours. Cardiac output returns to normal levels long before plasma volume has been restored completely.⁴⁷

The fall in cardiac output after a burn has been attributed to the presence of circulating myocardial depressant factor or the development of a catecholamine (stress induced) increase in systemic and pulmonary vascular resistances and increased ventricular afterload.²²⁹ Treatment of low cardiac output requires supportive care; the efficacy of vasoactive (inotropic) drug therapy in the treatment of this cause of myocardial dysfunction has not been determined.

Immediately after a burn, catecholamine secretion can produce an increase in systemic and pulmonary vascular resistances. Although vasoconstriction may help to maintain mean arterial pressure in the face of a fall in cardiac output and extravascular fluid shifts, it also may contribute to increased ventricular afterload and increased ventricular work. The relative significance of this vasoconstriction in pediatric patients is unknown.

In general, treatment of inadequate cardiovascular function requires support of maximal oxygen delivery (including support of oxygenation, ventilation, and cardiac output) with titration of intravenous volume administration. The effectiveness of vasoactive agents for children with significant burns has not been studied (refer to discussion of shock in Chapter 6).

Cardiac output may increase to high levels (as much as 300% of normal values) about 36 or more hours after a burn. Increased metabolic rate and anemia contribute to this hyperdynamic state.

Pulmonary Injuries

Respiratory insufficiency can result from the inhalation of superheated air, steam, toxic fumes, or smoke, and it is a major cause of morbidity and mortality in burned children.^94,^97,^126,^146,¹⁹⁷ This respiratory failure may result from airway edema or obstruction or from microcirculatory changes and increased capillary permeability. Pulmonary edema can result from inhalation injuries, excessive volume administration during resuscitation, or sepsis.

Inhalation of smoke, steam or other irritants will produce upper airway edema, erythema, and blistering. Progressive edema can cause upper airway obstruction. Ciliated epithelial cells may be damaged during inhalation, so that foreign particles can enter the bronchi. The damaged mucosal layer may slough 48 to 72 hours after a burn, producing acute airway obstruction.^30,⁹⁴

Damage to the pulmonary parenchyma can result from an inhalation injury and can complicate shock and fluid resuscitation (see Respiratory Failure, later in this chapter and Acute Respiratory Distress Syndrome in Chapter 9). Increased alveolar capillary membrane permeability will produce pulmonary edema with resultant intrapulmonary shunting and hypoxemia, decreased lung compliance, and increased work of breathing.¹¹⁸

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.

Gastrointestinal Dysfunction

When cardiac output falls after a burn, blood flow is diverted from the liver, kidney, and gastrointestinal circulations to maintain blood flow to the brain and heart. This decrease in gastrointestinal perfusion results in impaired gastrointestinal motility. Severe compromise in motility results in further reduction in blood flow, so severe gastrointestinal ischemia can develop.

Gastrointestinal ischemia can increase the permeability of gastrointestinal mucosa to gram-negative bacteria and endotoxins. As a result, translocation of gram-negative bacteria or endotoxin can occur and may precipitate gram-negative sepsis (see Septic Shock in Chapter 6, and Septic Shock: Mediators of the Septic Cascade in the Chapter 6 Supplement on the Evolve Website).

When gastrointestinal motility is reduced, mucosal secretions and gases can accumulate in the intestine and stomach, causing severe abdominal distension. Gastrointestinal perfusion and motility should return to normal when hypovolemia is corrected and cardiac output is restored.

Curling’s ulcer, or acute ulcerative gastroduodenal disease, may develop after a burn. The etiology of this condition is unknown, but it relates to compromised gastrointestinal perfusion and resultant mucosal damage. The mucous membrane ordinarily prevents autodigestion, because it acts as a barrier to the absorption of hydrogen ions that are secreted into the gastric lumen. An alteration in gastric mucosal function can compromise this barrier and increase the production of hydrogen ions, so that gastric and duodenal ulcerations may develop.

The incidence of Curling’s ulcer is unknown, because it typically is diagnosed at autopsy. Superficial gastric and duodenal mucosal changes are common in children with major burns,⁶⁷ but ulcer prophylaxis has ensured that clinically significant bleeding and ulceration are still relatively uncommon.

Gastrointestinal ulceration may produce pain, hemorrhage, or perforation. Gastric suction and stool samples should be tested for the presence of blood (heme protein), and the use of antacids or sucralfate (a hydrogen ion diffusion barrier) should be considered.¹³¹ Administration of histamine receptor antagonists (e.g., cimetidine or ranitidine) is controversial, because the morbidity of these drugs may be higher than the risk of stress ulceration. Severe pneumonias may result from aspiration of gastric bacteria that can flourish after these drugs are administered. The gastric pH should be maintained at 3.5 to 5.0 (see Chapter 14).

Metabolic Changes

The patient with a burn is in a hypermetabolic state, with high oxygen consumption and caloric requirements. Metabolic rate reaches its peak at double (or more) normal values approximately 4 to 12 days after a burn.⁵^b Catecholamine secretion activates the stress response, and heat production and substrate mobilization will result in protein and fat catabolism, increased urinary nitrogen losses, and rapid utilization of glucose and calories.⁷⁰ An increased metabolic rate continues until after the burn is healed or covered by graft.

Central thermoregulation is altered at this time, and the hypermetabolic condition often produces a low-grade fever.²⁰⁵ In contrast, heat loss and a fall in body temperature may be observed in the very young child with an extensive burn.

Because a burn is a major body stress, muscle protein catabolism increases to provide amino acids for gluconeogenesis and fuel sources for local tissue needs.⁶⁹ Insufficient protein administration and nutrition will result in a marked catabolic state (negative nitrogen balance) and major muscle loss. Large amounts of urea in the urine indicate increased nitrogen loss.²¹⁸

Thermal injury and hypermetabolism result in increased serum free fatty acids. Hydrolysis of stored triglycerides is accelerated, and catecholamine secretion stimulates mobilization of fat stores. Hypoalbuminemia results from increased protein loss at the burn surface and can, in turn, reduce fatty acid transport.⁷⁵

Compromise in Immune Function

A thermal injury destroys the protective barrier of the skin, creating an open wound. The burn activates the inflammatory response, but may compromise immune function, leaving the patient at risk for infection.

After a burn, several circulating immunosuppressive substances are present. Nonspecific suppressor T cells compromise lymphocyte response for approximately 48 hours.¹⁵⁴ Leukocyte phagocytosis is reduced, and the reticuloendothelial system is often depressed.²²⁰ Burn toxin, a high-molecular-weight protein, is thought to contribute to postburn immunosuppression. The patient’s immune function may be compromised further by the application of topical antimicrobial agents and the insertion and contamination of intravascular catheters.

A burn activates the complement system. This system consists of a series of circulating proteins that are present in an inactive form. Some of these proteins coat invading organisms, rendering them susceptible to phagocytosis. In addition, the complement system participates in the coagulation cascade.

Infection or injury can activate the complement system, resulting in a normal inflammatory response.⁸⁸ Extensive burns result in a decrease in serum complement levels and a potential reduction in the inflammatory response during infection (see Septic Shock in Chapter 6, and Septic Shock: Mediators of the Septic Cascade in the Chapter 6 Supplement on the Evolve Website).

Common clinical conditions

Care of the child with burns requires support of cardiorespiratory function, prevention of infection, and preparation of the burn surface for healing or grafting. In addition, potential complications of the burn and its treatment must be prevented. An overview of this nursing care is provided in the nursing care plan (Box 20-2), and the major potential patient problems are reviewed in the following discussion.

Box 20-2 Nursing Care of the Child with Thermal Injuries

Inadequate Cardiac Output and Tissue Perfusion (Alteration in Tissue Perfusion) Related to: Extravascular Fluid Shift and Relative Hypovolemia, Inadequate or Delayed Fluid Resuscitation, Constriction of Eschar

Expected Patient Outcome

Patient will demonstrate adequate tissue perfusion as evidenced by:

• Persistence or return of peripheral pulses

• Brisk capillary refill, warm extremities with no evidence of compartment syndrome (see Chapter 19)

• Pink mucous membranes, nail beds

• Effective cardiac output and organ perfusion

• Absence of metabolic acidosis

• Urine volume averaging 1 mL/kg per hour or more

Nursing Activities

• Constantly assess fluid balance, systemic perfusion. Monitor for signs of hypovolemic shock, including: tachycardia, oliguria, cool skin and cool extremities, weak peripheral pulses, altered level of consciousness, negative fluid balance, low central venous or pulmonary artery wedge pressure, development of lactic acidosis, and absence of hepatomegaly (by clinical examination) and of cardiomegaly (on chest radiograph).

• Calculate fluid replacement requirements and discuss inadequate fluid administration or excessive fluid losses with the on-call provider immediately.

• Administer fluid boluses and maintenance fluids as needed to restore adequate intravascular volume and systemic perfusion and to replace ongoing fluid losses.

• Assess perfusion and appearance of and movement and sensation in extremities and digits.

Report decreased or absent peripheral pulses, delayed capillary refill, edema, cyanosis, or cool extremities or digits to the on-call provider immediately.

Assess blood flow to extremities using Doppler; if Doppler indicates low flow to extremities, monitoring of compartment pressures may be ordered (see Chapter 19).

• Assist with escharotomies or fasciotomies on arms, legs, and chest as needed.

• Perform passive and active range-of-motion exercises to extremities as ordered.

• Position patient carefully to prevent compromised blood flow to extremities.

Potential Hypovolemia or Inadequate Fluid Volume Related to: Fluid Loss Through Evaporation from Burn Surface, Increased Capillary Permeability and Extravascular Fluid Shift, Inadequate Fluid Administration, Excessive Fluid Losses Through Fever, Diarrhea

Expected Patient Outcomes

• Patient will demonstrate adequate intravascular volume as evidenced by: effective systemic perfusion, balanced fluid intake and output (with consideration of fluid loss from surface of burn), urine volume of 1 mL/kg per hour, electrolyte balance, central venous pressure or pulmonary artery wedge pressure of approximately 2 to 5 mm Hg (or higher as needed to maintain adequate systemic perfusion), normal arterial pH, and normal serum lactate.

• Patient will demonstrate no signs of hemoconcentration or dehydration, such as dry mucous membranes, poor skin turgor, increase in serum electrolyte concentration and hematocrit, sunken fontanelle (in infants), and oliguria with increased urine specific gravity.

Nursing Activities

• Monitor patient systemic perfusion: signs of hypovolemia include signs of poor systemic perfusion associated with a low central venous pressure or pulmonary artery wedge pressure, small heart size on chest radiograph, and absence of hepatomegaly. Report these findings to the on-call provider immediately.

• Monitor for signs of dehydration, including: sunken fontanelle in infants, dry mucous membranes, poor skin turgor, evidence of weight loss, rise in serum electrolyte concentration, and increase in hematocrit. Report findings to the on-call provider.

• Monitor urine output and fluid balance every hour; report oliguria or negative fluid balance to the on-call provider (consider fluid loss through burn).

• Titrate fluid administration as needed (and with physician or other provider order) to maintain systemic perfusion.

• Monitor heart size and evidence of pulmonary edema on chest radiograph; discuss these findings with on-call provider.

• Monitor electrolyte balance, serum albumin, and hematocrit.

• Obtain daily weights, report them to the on-call provider, and discuss changes in fluid requirements.

Potential Hypervolemia or Fluid Volume Excess Related to Excessive Fluid Administration and Renal Failure

Expected Patient Outcomes

• Patient will demonstrate no evidence of hypervolemia, such as signs of congestive heart failure, pulmonary edema, or hemodilution.

• Patient will maintain electrolyte balance.

Nursing Activities

• Monitor systemic perfusion and fluid balance; report signs of congestive heart failure (tachycardia, tachypnea, periorbital edema, hepatomegaly, increased respiratory effort, cardiomegaly, and oliguria), excessive weight gain, or positive fluid balance to the on-call provider (note that most patients will demonstrate weight gain following fluid resuscitation after a burn).

• Assess for evidence of pulmonary edema, including crackles and increased respiratory effort; be prepared to support oxygenation and ventilation as needed.

• Palpate liver margin; report the presence or progression of hepatomegaly to the on-call provider.

• Monitor electrolyte balance; report a fall in electrolyte concentration or hematocrit to the on-call provider.

• Administer diuretic as ordered.

Potential Airway Obstruction Related to: Airway Inflammation, Pulmonary Interstitial Edema, Reduced Ciliary Function Following Inhalation Injury, Altered Level of Consciousness

Expected Patient Outcomes

• Patient will demonstrate patent airway as demonstrated by: normal spontaneous respiratory rate and effort, adequate depth of respirations and air movement, effective oxygenation and carbon dioxide removal (per arterial blood gases, pulse oximetry and exhaled carbon dioxide tension [P_ETCO₂]), and absence of crackles and stridor

• If patient develops airway obstruction, intubation and appropriate support will be provided immediately.

Nursing Activities

• Monitor patient respiratory rate, effort, and air movement. Notify on-call provider of signs of airway obstruction, including tachypnea, retractions, nasal flaring, stridor, or weak cry. Be prepared to assist with emergency intubation as needed. Resuscitation bag and mask with oxygen source should be available at the bedside.

• Note that the diagnosis of respiratory failure from airway obstruction is a clinical diagnosis and can be present despite normal arterial blood gases and pulse oximetry. Hypoxemia and hypercarbia will only be late signs of airway obstruction, and intubation should be accomplished before these develop.

• Monitor for evidence of inhalation injury, including singed nasal hairs, excessive secretions, progressive respiratory distress; report these findings to the on-call provider immediately.

• Provide oxygen therapy as needed and monitor the effect on systemic oxygenation, including pulse oximetry and arterial blood gases.

• Perform tracheal suctioning as needed to maintain a clear upper airway.

• Encourage the alert patient (as age-appropriate) to take deep breaths and cough as needed to clear the airway.

• Insert oral or nasal airway as needed (and ordered by on-call provider).

• Position child to maintain airway patency (particularly important if level of consciousness is impaired).

• Assess patient responsiveness; discuss elective intubation if the patient is obtunded or demonstrates decreased response to stimulation

• Relieve pain and discomfort as needed.

• Assist with escharotomies of the chest as needed.

Hypoxemia, Hypoxia and Impaired Gas Exchange Related to: Airway Obstruction, Inhalation Injury, Pulmonary Edema, Acute Respiratory Distress Syndrome, Carbon Monoxide Poisoning, Impaired Level of Consciousness

Expected Patient Outcomes

• Patient will demonstrate adequate respiratory function as evidenced by: appropriate respiratory rate, depth and effort; patent airway; normal arterial blood gases; COHb level less than 10%; absence of crackles or pulmonary edema on chest radiograph.

• If patient demonstrates hypoxemia despite oxygen therapy, or ineffective ventilation, support of airway, oxygenation, and ventilation will be provided,

• Patient will remain alert and oriented with adequate respiratory rate and effort.

Nursing Activities

• Monitor respiratory rate and effort, and notify a provider of development of respiratory distress.

• Monitor pulse oximetry, exhaled carbon dioxide (P_ETCO₂), and arterial blood gases; notify a provider of any development of hypoxemia or hypercarbia.

• Monitor for evidence of inhalation injury, including headache, dizziness, confusion, flushed appearance (late finding), visual disturbance, seizures, and metabolic acidosis. Report these findings to the on-call provider immediately.

If inhalation injury and carbon monoxide poisoning are suspected, obtained blood gas specimen for qualification of COHb level; notify on-call provider of result (COHb levels greater than 10% can be associated with significant compromise of oxygen delivery).

Severe carbon monoxide poisoning may be present despite a normal oxyhemoglobin saturation as measured by pulse oximetry, because the pulse oximeter does not recognize COHb. To determine actual hemoglobin saturation, the hemoglobin saturation must be measured using a cooximeter in the blood gas laboratory.

• Administer oxygen as ordered, and monitor the patient’s response.

• Be prepared to assist with non-invasive positive-pressure ventilation, hyperbaric oxygen therapy or intubation and mechanical ventilation as needed. Ensure that emergency equipment is readily available.

Pain Related to Burn, Multiple Invasive or Painful Catheters, and Painful Dressing Changes and Procedures

Expected Patient Outcomes

• Patient will demonstrate no pain, as evidenced by verbal reports of pain (as age-appropriate), facial expression, crying or whining, and increased heart rate and blood pressure.

• Patient will demonstrate relaxed body position, relaxed facial expression, ability to sleep when undisturbed, and appropriate heart rate and blood pressure for age and clinical condition.

• Patient will indicate reduction or elimination of pain as indicated and quantified using consistent pain assessment tools (see Chapter 5).

Nursing Activities

• Assess nature, location, quality, and intensity of pain every hour and as needed using consistent pain assessment tool (see Chapter 5).

• Monitor patient closely for nonverbal evidence of pain, including: restlessness, guarding of burned areas, wrinkled brow, clenched fingers, reluctance to move, facial pallor or flushing, diaphoresis, tachycardia or hypertension, pupil dilation.

• Assess analgesic administration and discuss modification of analgesic dose, schedule, or type with a physician or other on-call provider if pain persists.

• Administer analgesics as ordered and evaluate effectiveness; if continuous infusion medications are ordered, ensure that bolus administration of the drug is used to initiate infusion therapy and achieve therapeutic drug levels. Bolus therapy may also be required if dose of drug is increased (see Chapter 5). Ensure adequate analgesia before painful procedures.

• Identify factors that aggravate or alleviate pain and modify patient support accordingly.

• Assist with nonpharmacologic methods of pain relief.

• Ensure uninterrupted periods of rest.

Potential Burn Wound Infection or Septic Shock Related to: Open Wound, Presence of Multiple Invasive Catheters, Compromise in Immune Function

Expected Patient Outcomes

• Patient will demonstrate no signs of infection, including fever or hypothermia, leukocytosis or leukopenia, wound erythema, wound drainage, or positive blood cultures.

• If infection develops, it will be promptly treated with antibiotics and the patient will be closely monitored for evidence of sepsis.

• Burn wound and graft sites will heal within appropriate interval.

Nursing Activities

• Assess wound appearance for evidence of local signs of infection, including: erythema; change in color, appearance, odor, or amount of wound drainage; change in color of wound to black or dark brown, progression of burn to full thickness injury; sloughing of graft or wound breakdown after closure.

• Monitor patient temperature and white blood cell count and differential; notify the on-call provider of changes.

• Obtain blood cultures as ordered.

• Administer antibiotics as ordered (precisely on time) and monitor for side effects.

• Ensure strict aseptic technique during all invasive procedures; ensure clean technique during all noninvasive procedures including wound care.

• Maintain closed delivery system for all intravenous lines.

• Ensure good hand-washing technique by all members of the healthcare team before and after patient contact.

• Monitor the patient closely for signs of sepsis, including fever, hypothermia, tachycardia, tachypnea, alteration in responsiveness, leukocytosis, leukopenia, metabolic acidosis, evidence of organ system dysfunction (e.g., oliguria, diarrhea or vomiting, abdominal distension, elevation in liver transaminases), evidence of relative hypovolemia (and increased intravascular fluid requirements to maintain perfusion), and signs of septic shock (sepsis plus cardiovascular and one other organ system failure). See Boxes 6-2 and 6-3.

Potential Temperature Instability Related to Heat Loss Through Burn Surface

Expected Patient Outcomes

• Patient will maintain normal body temperature with absence of shivering and chills.

• Patient skin temperature will remain normal and extremities will be warm to the touch.

Nursing Activities

• Monitor body temperature hourly initially, then every 2 to 4 hours when the patient’s condition is stable.

• Monitor for signs of cold stress, including shivering or chills, or tachycardia, tachypnea and hypoxemia in young infant.

• Use a heat shield, over bed warmer, or warming blanket as needed to maintain the patient’s body temperature.

• Keep ambient air warm, and prevent any room draft.

• Use warmed (not hot) solution during burn care.

• Perform burn care under a heat shield or overbed warmer for infants or young children and as needed for older children.

• Minimize patient exposure during treatments or wound care (e.g., perform burn care on one extremity at a time, and redress that extremity before the next extremity is unwrapped).

• Consider warming of intravenous fluids and blood products; warming should be performed according to hospital policy for infants and young children.

Potential for Inadequate Nutrition Related to: Excessive Caloric Requirements, Inadequate Caloric Intake, Altered Metabolism

Expected Patient Outcome

• Patient will demonstrate adequate nutritional status as evidenced by no weight loss, good wound healing and skin turgor, absence of nausea and vomiting, adequate recorded caloric intake.

Nursing Activities

• Calculate the patient’s caloric and protein needs and notify the on-call provider if these are not being met. Monitor patient tolerance of tube, oral, or parenteral feedings. Ensure appropriate distribution of calories within protein, fat, and carbohydrates.

• Begin enteral feedings as ordered; notify a provider of feeding intolerance (including abdominal distension, vomiting, diarrhea, increased residual volume after gastric feeding, reflux). For additional information, see Chapter 14.

• Implement measures to reduce nausea and vomiting as needed, including position changes and administering an antiemetic.

• Ensure adequate oral intake when tolerated; calculate caloric intake and ensure provision of multiple opportunities to eat a wide variety of appetizing foods.

Determine the child’s preferences and encourage the parents to bring the child’s favorite foods.

Allow adequate time for meals uninterrupted by treatments or examinations.

• Obtain daily weight; notify a provider of weight loss or failure to gain weight.

• Obtain consultation with dietician as needed. Evaluate oxygen and caloric expenditure using calorimetry as needed.

Additional Potential Problems

• Fear and anxiety

• Potential alteration in self-concept

COHb, Carboxyhemoglobin.

Inadequate Intravascular Volume and Cardiac Output: Third-Spacing Phase

Etiology and Pathophysiology

The child with burns loses a large amount of fluid from the burn surface itself. In addition, increased capillary permeability produces third-spacing of fluid. Significant unreplaced intravascular volume loss will result in a fall in cardiac output and a compromise in systemic perfusion.

The magnitude of the intravascular volume deficit will depend on the depth and surface area of the injury and the time elapsed before adequate fluid resuscitation.²⁸ In general, deeper and larger (15% or more of TBSA) burns are associated with more significant fluid shifts and circulatory complications.

Clinical Signs and Symptoms

After a significant burn, intravascular volume loss will eventually produce signs of hypovolemia (Box 20-3). Children often do not exhibit significant signs of hypovolemia, including hypotension until more than 25% of the circulating volume is depleted and complete cardiovascular collapse is imminent.

Tachycardia reflects a compensatory response to hypovolemia, but caution is needed to avoid overinterpreting this finding, because reflex tachycardia from postinjury catecholamine response is common. A lethargic child with tachycardia plus decreased capillary refill and cool, clammy extremities needs prompt attention, because shock is likely to be present.

Significant hypovolemia will compromise systemic perfusion and may produce shock. Such hypovolemia will produce tachycardia, prolonged capillary refill time, and cold extremities. Anuria is often present. The development of a metabolic acidosis (i.e., fall in arterial pH, rise in serum lactate) indicates critical compromise in tissue perfusion. The young infant in shock often will demonstrate temperature instability and hypoglycemia. Hypotension may develop only as a late sign of shock.⁴⁷

Following the stress of the burn, antidiuretic hormone secretion is enhanced, so urine volume usually is reduced even if fluid resuscitation is adequate. Hour-to-hour fluctuations in urine volume are common during this time.

Interstitial fluid accumulation can produce diffuse peripheral (systemic) edema. Such edema will be most severe in dependent areas. If pulmonary edema develops, it will produce intrapulmonary shunting. The resultant hypoxemia will be detected with pulse oximetry or arterial blood gases. Tachypnea, nasal flaring, and retractions will indicate decreased lung compliance and increased work of breathing. Crackles may be heard, and pulmonary edema also will be noted on a chest radiograph. If the child is intubated, frothy secretions may be suctioned from the tube.

Management

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

Table 20-3 Recommendations for Fluid Administration Rate for Patients with Burns

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 formula ²⁶ (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.

Table 20-4 Composition of Resuscitation Solutions

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

Parameter	Desirable Response (Fluid Resuscitation Adequate)	Undesirable Response (Fluid Administration Inadequate)
Urine output	1 mL/kg per hour (up to 30 kg, then 25-30 mL/h)	<1 mL/kg per hour (for children above 30 kg, less than 25 mL/h)
Specific gravity	1.010-1.025	>1.025
Weight	Preburn level	10% less than preburn level
Blood pressure	Normal for age or high*	Low for age*
Pulse	Normal for age*	Normal or high*
Level of consciousness	Alert, clear, and lucid	Lethargic and stuporous
Hematocrit	35%-45%	48%-55%
Serum sodium	135-145 mEq/L	>150 mEq/L
Blood urea nitrogen	5-20 mg/dL	>25 mg/dL
Creatinine	0.8-1.4 mg/dL	>2.0 mg/dL
Osmolality (serum)	275-295 mOsm/L	>300 mOsm/L
Urine sodium	60-100 mEq/L	≤40 mEq/L
Blood pH	7.20-7.50	<7.20
Serum lactate	Venous: 0.5-2.2 mmol/L Arterial: 0.5-1.6 mmol/L	>4 mmol/L
Peripheral circulation	Brisk capillary refill; normal color in unburned areas	Cyanosis; prolonged capillary refill
Central venous pressure (CVP)	4-8 mmHg	<2-4 mmHg
Pulmonary artery pressure (PAP)	Systolic, 20-30 mmHg	Systolic, <20 mmHg
	Diastolic, 5-15 mmHg	Diastolic, <5 mmHg
Cardiac index	3.0-4.5 L/min per m² BSA	<3.0 L/min per m² BSA

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