Chapter 98. Burns: Resuscitation Phase (0 to 36 Hours)

• A burn patient is a trauma patient; therefore, other injuries should be expected and sought.
• Endotracheal tubes should be large enough to allow ventilation and pulmonary toilet.
• Hypothermia is a major concern, and early, aggressive attempts at prevention are required.
• Modification of the standard lactated Ringer's resuscitation is often necessary in the massive burn or inhalation injury patient or in the very young and old. Additions of colloid, blood, and inotropes are often very useful in restoring hemodynamic stability. Fluid formulas should not be rigid.
• It is important to watch for local perfusion problems and chest wall restriction caused by the burn.
• The burn itself is a low priority for initial care.

Care of the burn patient has improved dramatically over the past 10 to 15 years, resulting in a marked decrease in mortality and morbidity, as well as improved functional outcome. The major reason for this improvement is the multidisciplinary approach by a team that has the clinical decision-making skills, experience, and scientific background to render care in a manner that avoids the predictable pitfalls while also maintaining critical care monitoring. A burn center is the best environment to provide this care.

The burn patient's condition changes dramatically over the course of the injury. The initial postburn period is characterized by cardiopulmonary instability caused by fluid shifts and direct smoke injury to the airways. With the onset of intense wound inflammation, immunosuppression, and infection, physiologic and metabolic parameters change substantially from those seen initially. Treatment therefore must be based on a clear understanding of these changes over time.1,2 This discussion thus will be divided into three time periods—the initial resuscitation period (0 to 36 hours; this chapter), the early postresuscitation period (2 to 6 days; Chap. 99), and the inflammation-infection period, which is usually most evident after the first week (Chap. 100).

Monitoring requirements are no different from those for any other ICU patient. However, vascular access is much more of a problem, and noninvasive measures are often all that are available. A typical burn unit has a procedure room for wound care and often an operating room, but wound care in the ICU is very feasible and actually essential in the unstable patient. Hyperbaric oxygen chambers are not a necessary component and are really only indicated in patients with such severe carbon monoxide exposure that the cytochrome system is saturated with carbon monoxide, which is not readily displaced with 100% oxygen alone (see Chap. 102). It is safe to say that 99% of patients with major burns and some degree of carbon monoxide inhalation do not benefit from hyperbaric oxygen. The secret to a successful patient outcome, however, remains in the knowledge base, judgment, and decision-making skills of the personnel, not in the external environment.1,2

Cardiopulmonary instability characterizes the resuscitation phase. Life-threatening airway and breathing problems are major concerns at this time, with carbon monoxide poisoning, upper airway edema, and the immediate effect of smoke inhalation injury being the most common. The initial phase is also characterized by hypovolemia because plasma volume is lost into the burn tissue. The burn itself is of less immediate concern, with initial treatment of pulmonary and circulatory abnormalities taking first priority. Any early management error will lead to a dramatic increase in morbidity and mortality during the subsequent injury phases. It is of critical importance to remember that the burn patient is a trauma patient with the potential for many other injuries. The standard approach to trauma resuscitation therefore must be followed, including assessment for cervical spine and head injuries, pulmonary and abdominal trauma, fractures, and so on. Management of these problems is the same as in the nonburn patient.

Abnormalities of ventilation and oxygenation are common in the immediate postburn period. Several fairly distinct critical disease processes must be recognized and managed aggressively.3 The first three are associated with the inhalation injury complex and are presented below in the approximate order in which symptoms will develop (carbon monoxide toxicity, upper airway obstruction, and chemical burn to the lung). These sections are followed by discussions of lung changes due to the skin burn and, finally, of the effects of impaired chest wall compliance.

Smoke Inhalation Injury Complex

Pulmonary insufficiency caused by the inhalation of heat and smoke is the major cause of mortality among fire victims, accounting for over 50% of fire-related deaths.4,5 The exposure time, concentration of fumes, elements released, and degree of accompanying body burn are critical variables in determining outcome.

Carbon Monoxide and Cyanide Toxicity

Carbon monoxide, a by-product of incomplete combustion, is one of the leading causes of death in fires. Hydrogen cyanide is also a well-recognized cause of morbidity and mortality, especially with burning of synthetics such as polyurethane.

Symptoms of carbon monoxide toxicity usually are not present until the carboxyhemoglobin concentration exceeds 15%. Symptoms are those of decreased tissue oxygenation, with the initial manifestations being neurologic. Cyanide toxicity presents in a very similar fashion, with severe metabolic acidosis and obtundation. Diagnosis, however, is more difficult because measurement of cyanide levels is not always readily available or very reliable. Normal levels are less than 0.1 mg/L (even in smokers). A level near 1 mg/L is lethal. Neurologic dysfunction also can be caused by factors other than carbon monoxide toxicity, such as alcohol or drug intoxication or blunt head trauma. A toxicology screen therefore is warranted. The indications for obtaining a computed tomographic (CT) scan of the head are the same as for other trauma patients.

The persistence of a metabolic acidosis in a patient with adequate volume resuscitation and cardiac output suggests that oxygen transport and use are being impaired by carbon monoxide or cyanide. PaO2 can remain relatively normal because the chemical alteration of hemoglobin by carbon monoxide will not affect the amount of oxygen dissolved in arterial plasma. A high carboxyhemoglobin level also indicates a significant smoke exposure and, therefore, a chemical burn to the airways. Treatment of carbon monoxide toxicity is covered more fully elsewhere in this text; briefly, it consists of the early displacement of carbon monoxide from hemoglobin by administration of 90% to 100% oxygen (see Chap. 102). Treatment of cyanide toxicity involves restoration of hepatic blood flow to clear the cyanide. In addition, [dx id=""]sodium nitrite[/dx] is given, followed by sodium thiosulfate. Hyperbaric oxygen is best used in patients who show severe neurologic compromise with a high carboxyhemoglobin level (>50%) but no major burns and who are not responding to high-flow oxygen. The vast majority of patients can be managed successfully using simply 90% to 100% oxygen.

Upper Airway Obstruction from Airway Edema

Heat produces an immediate injury to the airway mucosa, resulting in edema, erythema, and ulceration. Although these mucosal changes may be present anatomically shortly after the burn, physiologic alterations will not be present until the edema is sufficient to produce clinical evidence of impaired upper airway patency. This may not occur for 12 to 18 hours. The presence of a body burn magnifies the effects of airway injury in direct proportion to the size and depth of the skin burn. The massive amount of fluid administered is in part responsible. A face or neck burn will accentuate these problems by producing marked anatomic distortion and, in the case of a deep neck burn, external compression of the larynx. The airway edema and the external burn edema have a parallel time course so that by the time symptoms of airway edema develop, external and internal anatomic distortion is extensive. The local edema usually resolves in 4 to 5 days.

Inspection of the oropharynx for soot or evidence of a heat injury should be routine in every burn victim. Numerous techniques have been used in further assessing the degree of injury and in determining the need for endotracheal intubation. Fiberoptic bronchoscopy or laryngoscopy will show whether physical evidence of pharyngeal or laryngeal mucosal injury is present. Laryngoscopy will demonstrate the presence of mucosal irritation at and above the cords and provide information about the need for endotracheal intubation.4,5 Unfortunately, unless serial studies are performed, none of these tests can predict the severity of subsequent airway compromise accurately because the edema progresses during the first 18 to 24 hours. Repeated examinations for airway compromise are feasible in patients without facial burns. However, in the presence of a large burn, it is best to proceed with intubation if there is any concern.

An early decision regarding the need for airway intubation is crucial. When there is doubt, it is safer to intubate. A patient with a significant inhalation injury and deep facial burns usually should be managed by early endotracheal intubation. There are many other indications for intubation in burn patients besides airway edema, such as hemodynamic instability and impaired consciousness. A large orotracheal tube (at least 7 mm in internal diameter) should be used in adults because very thick secretions develop. If the initial tube is too small, it will be dangerous to change once massive facial and airway edema develops. An algorithm for this approach is presented in Fig. 98-1.

Chemical Burns of the Upper and Lower Airways

Toxic gases contained in smoke, as well as carbon particles coated with irritating aldehydes and organic acids, can injure both upper and lower airways (Table 98-1). The location of injury will depend on the duration of exposure, the size of the particles, and the solubility of the gases.

Breath holding and laryngospasm are protective mechanisms against excessive exposure in the conscious patient. The unconscious patient, however, loses this protection and sustains more severe injury to the lower airways. Information regarding loss of consciousness at the scene should be sought in the history.

Symptoms may well be absent on admission, with the true magnitude of injury becoming evident only after 24 to 48 hours. Early symptoms usually consist of wheezing and bronchorrhea. This intense initial bronchorrhea caused by irritation of the airway mucosa in combination with increased oral and nasal secretions can give the false appearance of fulminant pulmonary edema. Soot in the lung secretions is certain evidence of smoke exposure but is not always present.

Early bronchospasm and bronchiolar edema initiated by the irritant gases cause a marked decrease in dynamic lung compliance with increased work of breathing. Impaired clearance of secretions will accentuate this problem.

Impairment of gas exchange is due to ventilation/perfusion (V̇/Q̇) mismatching related to airway injury rather than to alveolar edema.6–8 A body burn markedly potentiates the inhalation-induced lung dysfunction caused by chemical injury. The combination of a major burn and smoke inhalation is more lethal than either injury alone.

Initial treatment of this component consists of an aggressive approach to upper airway maintenance and pulmonary support that includes maintenance of small-airways patency and removal of soot and mucopurulent secretions. Careful, well-monitored fluid resuscitation is necessary to avoid accentuation of the process. The addition of positive end-expiratory pressure (PEEP) frequently is necessary to maintain small-airways patency and an adequate functional residual capacity (FRC), assisting in holding the edematous airway open until edema resolves. Endotracheal intubation and PEEP have been reported to decrease the rate of early pulmonary death after severe burns and smoke inhalation.9

Beginning about 18 to 24 hours after a burn, increasing airway resistance is often due to bronchiolar edema and airway plugging rather than to bronchospasm. The associated impairment of gas exchange often responds to further increases in PEEP in addition to bronchodilator administration. The injured airway mucosa frequently becomes colonized with bacteria. Prophylactic antibiotic administration only selects for resistant organisms and therefore is not indicated. Corticosteroids increase morbidity and mortality in the presence of a body burn and are, therefore, contraindicated.10

Impaired Chest Wall Compliance

Respiratory excursion can be impaired markedly by a burn to the chest wall, especially a circumferential third-degree burn.11,12 The loss of chest wall compliance increases the work of breathing. Symptoms may not be evident until edema formation peaks. The first clinical evidence of chest wall restriction is often labored breathing, followed by rapid respiratory deterioration, particularly in the patient who is not receiving ventilatory support. Clearance of secretions can be impaired owing to the inability to generate enough hyperinflation to cough well.

Treatment involves surgical decompression or escharotomy of the chest wall. Longitudinal incisions placed in the midaxillary lines should be connected across the lower chest wall. Bleeding usually is controlled easily if the incisions stay within the margins of the third-degree burn because the dermal vessels are thrombosed. The incision must extend into the subeschar area to allow adequate chest wall expansion. Escharotomies usually are not required in a second-degree burn unless the edema is so massive that the burned skin is tight. (This approach is diagrammed in Fig. 98-2.)

Massive fluid shifts occur during the resuscitation phase of burn injuries and can lead to severe impairment in oxygen delivery to tissues. An understanding of these early fluid shifts is necessary to avoid hemodynamic instability and to initiate appropriate treatment.

Pathophysiology of Burn Shock

With a major burn, intravascular volume is lost into burned tissue as well as nonburned tissue. Increased vascular permeability, the increased osmotic forces in burned tissue, and cellular swelling contribute.14 The most pronounced shift occurs in the first several hours as a result of the increased protein permeability and the apparent increase in burn tissue osmotic pressure.15 The fluid and protein shifts are the greatest in the first several hours because of the combined effect of increased permeability and an imbalance of osmotic forces. Subsequently, the quantity of edema depends on the adequacy of the fluid resuscitation. Severe hypoproteinemia also occurs as a result of the loss of protein into the wound. The major protein losses occur in the first 6 to 8 hours, during the period of peak fluid loss. Plasma proteins can decrease to less than 50% of normal. Resolution of edema depends on restoration of lymphatic patency, which may take a number of days to weeks. Edema in deeper burns resolves more slowly than in superficial burns.

Generalized tissue edema in nonburned tissues is evident in patients with burns covering more than 30% of the total body surface area (TBS). The edema appears to be due, at least in part, to the low protein content.16

Cardiac output is depressed initially, primarily as a result of hypovolemia. Afterload is also increased owing to a marked increase in systemic vascular resistance (SVR) elicited by vasoactive mediators such as catecholamines. A decrease in cardiac contractility17 is most evident in third-degree burns covering more than 40% of the TBS and is probably due to myocardial edema rather than to a circulating factor. All these contributors to impaired perfusion are summarized in Fig. 98-3.

Management of the Circulation

Intravenous Access

A peripheral vein catheter through nonburned tissue is the preferred route for fluid administration. A central line or pulmonary artery line, preferably through nonburned tissue, is needed only occasionally to monitor the patient during the initial resuscitation period and is removed as soon as it is no longer needed.

Monitoring lines are required primarily for elderly patients or patients with severe heart disease. Because of the high infection rate, an intravenous catheter should not be placed through burn tissue unless no other possible route exists. Some centers rotate central line sites regularly (e.g., every 3 days) to minimize the risk of catheter sepsis, but any benefits may be offset by the risks of repeated procedures.

What to Monitor

No one parameter of perfusion in a burn patient is a completely reliable indicator of tissue oxygenation (perfusion). The increased sympathetic tone characteristic of this early period makes arterial pressure an insensitive measure of volume status. However, a minimum perfusion pressure—e.g., a mean arterial pressure of more than 85 mm Hg—must be maintained.

Tachycardia is inevitable owing to hypovolemia and catecholamine release. In most patients, a pulse rate of less than 120 beats per minute usually indicates adequate volume, whereas a pulse rate of more than 130 beats per minute usually indicates that more fluid is needed.

Renal blood flow is another reflection of the adequacy of systemic perfusion during this early phase of injury. A urine output of 0.5 to 1 mL/kg per hour normally reflects adequate renal blood flow, assuming that there are no factors such as hyperglycemia, mannitol, or alcohol to alter the relationship between renal perfusion and urine output. A value greater than 1.0 mL/kg per hour usually means that too much fluid is being given and that excess edema therefore is being produced.

The measurement of base deficit is extremely useful for the assessment of tissue oxygenation. A base deficit during this phase usually reflects impaired tissue oxygenation due to hypovolemia or carbon monoxide (or cyanide) toxicity, and a progressive decrease in base deficit is a very sensitive indicator of the adequacy of restoration of perfusion.

Burn patients are very prone to hypothermia during this early period, especially with infusion of cool fluids. A decrease in temperature will lead to further hemodynamic instability and impaired perfusion. The external environment must be altered to allow for maintenance of a normal temperature (37 to 37.5° C) for this period.

The filling pressures in a large burn at this stage are usually low even with adequate fluid resuscitation because the rate of fluid loss increases markedly with small rises in capillary pressure. Use of an arbitrary filling pressure as an end point of resuscitation should be avoided.

Only older patients with massive burns or smoke inhalation are typically monitored with a central catheter. Hypoperfusion is almost always due to hypovolemia. Measurement of the mixed venous oxygen tension, however, can assist greatly in this determination.

Choice of Resuscitation Fluid

In general, fluids that contain at least as much salt as is present in plasma are appropriate in resuscitation.16a Restoration of sodium lost into the burn is essential. Fluids should be free of glucose (except in the treatment of small children) because glucose intolerance characteristically is present. Blood volume can be restored more effectively as the leakage decreases at about 24 to 36 hours. Volume infusion above the amount necessary for adequate perfusion can accentuate edema-related complications markedly.

Crystalloid

Crystalloid, in particular lactated Ringer's solution, is the most popular resuscitation fluid in the United States. The amount of isotonic crystalloid required in the first 24 hours is adjusted on the basis of the parameters used to monitor the adequacy of resuscitation (see below). If a hypertonic solution is used, the serum sodium level should not be allowed to exceed 160 mEq/L.15

Colloid

Since nonburned tissue appears to regain normal permeability very shortly after injury, and since hypoproteinemia may accentuate the edema in nonburned tissue, protein restoration beginning at about 8 to 12 hours with 6% albumin seems appropriate if edema in noninjured tissue and total fluid requirements are to be minimized. The use of fresh frozen plasma should be reserved for correction of documented clotting abnormalities.

[dx id=""]Hetastarch[/dx], a 6% starch solution, has colloid properties similar to those of a 6% protein solution and generates an oncotic pressure comparable with that of protein. The molecules are much larger than those of most dextrans, and vascular clearance therefore is much slower. As with dextran, volumes exceeding several liters can lead to clotting abnormalities and to the potential for immune dysfunction from reticuloendothelial blockade.

Blood

Because there is no early red blood cell deficit with a burn alone (unless severe hemolysis occurs), blood replacement usually is not needed.

Rate of Infusion

An initial rate can be estimated using the size of the burn (combined second and third degree) relative to the TBS and body weight:

However, the volume of fluid required is that necessary to maintain perfusion. Any formula is only an initial guide. Approximately half the fluid requirements for the first 24 hours need to be given in the first 8 hours. Beginning at 8 to 10 hours, an attempt should be made to decrease the rate of fluid administration gradually to the lowest level that maintains adequate perfusion.

Indication for Inotropic Support

Inotropic support to supplement fluids is indicated if adequate perfusion cannot be maintained without excessive fluid administration. In contrast to nonburned patients, it is very difficult to increase preload to values above normal levels in order to increase cardiac output in burned patients. Hemodynamic management is summarized in Fig. 98-4.

A number of hematologic disorders are seen after major burns.18 Hemolysis occurs commonly after deep third-degree burns or any prolonged exposure to a heat source. In addition, red blood cell fragility is increased markedly. Increased cell wall lipid peroxidation is evident, and fragmented cells are seen often on smears. The injured red blood cells will have a markedly shortened life span, leading to an anemia beginning in the first week. Red blood cell hematopoiesis is also markedly impaired and remains so until the burn is closed, resulting in a persistent anemia. A leukocytosis is also characteristic during this early phase. A marked consumption of platelets, fibrinogen, and plasminogen is seen in the burn wound, as well as a marked depletion of hemostatic components. A hypercoagulable state may be seen in the initial period in moderate burn injuries. A hypocoagulable state, resulting from depletion of clotting factors, is seen frequently with massive burns. Thrombocytopenia also will be evident in the latter group. It most likely results from the tremendous stimulus to clotting created by the large area of injured collagen tissue.

Anatomy and Function of the Skin

The skin is the largest organ of the body, ranging in area from 0.25 m2 in newborns to over 2 m2 in adults. It consists of two layers, epidermis and dermis (or corium). The outermost cells of the epidermis are dead cornified cells that act as a tough protective barrier against the environment. The second, thicker layer, the corium (0.06 to 0.12 mm thick), is composed chiefly of fibrous connective tissue. The dermis contains the blood vessels to the skin and the epithelial appendages of specialized function. The nerve endings that mediate pain are also found in the dermis. Partial-thickness injuries are extremely painful because the nerve endings are exposed. Full-thickness burns usually are anesthetic because the nerves have been destroyed by heat. The skin is also the barrier that prevents loss of body fluids through evaporation and limits the loss of body heat. In addition, the skin is the primary protective barrier against penetration of microorganisms into the subdermal tissues. Loss of this function results in increased risk of invasive infection.

Depth of Burn Injury

Traditionally, burn depth has been classified in degrees of injury based on the amount of epidermis and dermis injured. At present, depth is estimated by physical appearance, pain, and skin texture or pliability. A first-degree burn involves only the thin outer epidermis and is characterized by erythema and mild discomfort, healing rapidly.

Second-degree burns are defined as those in which the entire epidermis and variable portions of the dermis are destroyed. A superficial second-degree burn involves heat injury to the upper third of the dermis. The microvessels perfusing this area are injured, and permeability is increased, resulting in the leakage of large amounts of plasma into the interstitium. This fluid lifts off the thin, heat-destroyed epidermis, causing blister formation. Despite loss of the entire basal layer of the epidermis, a burn of this depth will heal in 7 to 14 days.

A deep dermal(or deep second-degree) burn extends well into the dermal layer, and fewer viable epidermal cells remain. Therefore, reepithelialization is extremely slow, sometimes requiring months. The wound surface usually is red, with white areas in deeper parts. Because the remaining blood supply is marginal, there is a high probability that the tissue damage will deepen with time.

A full-thickness (or third-degree) burn occurs with destruction of the entire epidermis and dermis, leaving no residual epidermal cells to repopulate the burned area. The portion of the wound not closed by wound contraction will require skin grafting. The exact depth of many deep burns cannot be defined on first appearance. A zone of ischemia is present between the dead superficial tissue and the deeper living tissue. This marginally viable tissue can be readily converted to nonviable tissue by infection or a further decrease in blood flow.

Severity of Injury

The size of the burn is defined as a percentage of the TBS. A useful initial guide is the rule of nines, which divides the body into areas that each represent 9% of the TBS. The head and each arm are considered 9% of the total, whereas the chest and abdomen, the back, and each lower extremity are considered to be 18% of the TBS. However, the Lund and Browder chart (Fig. 98-5) is more accurate and should be used for more precise calculation. The surface area of the body involved, the depth and location of injury, the patient's age, and the presence of associated injuries determine morbidity and mortality.1 Age and the presence of associated injury appear to be the most significant parameters affecting the chance of survival (Table 98-2).

The early treatment focuses on neutralizing the source of burn injury, avoiding excess heat loss, determining the extent of injury, cleaning and débriding the wound, controlling infection, and maintaining tissue perfusion.

Avoiding Excess Heat Loss

With a deep burn, the barrier to evaporative water loss is markedly impaired. As a consequence, the barrier to heat loss is also impaired, a fact that is extremely important to recognize in the resuscitation period. Heat loss can be decreased by closing the wound under dressings, thereby limiting air movement and decreasing the air-to-wound temperature gradient. Therefore, the burn is only cooled initially to neutralize excessive heat and to control pain in superficial second-degree burns covering less than 15% of the TBS.21 Patients with major burns must be placed in a warmed external environment to minimize heat loss. Wound débridement and washing should not be initiated on a large burn until the external temperature is controlled.19

Determining the Extent of Injury

The wound can be categorized on the basis of size, depth, age, and other complicating factors. Table 98-3 presents the standard categorization used by the American Burn Association.

Controlling Infection

The management of the burn wound itself depends on the status of initial cardiopulmonary function. Adequate control of the airway, maintenance of adequate gas exchange, and restoration of fluid loss must precede attempts at wound cleaning and débridement. Initial débridement consists of the elimination only of superficial, easily removed dead tissue; once this is accomplished, control of potential infection in the injured tissue is the next priority. Tetanus prophylaxis is necessary. Numerous studies have demonstrated that prophylactic systemic antibiotics in patients with either minor or major burns are of no benefit in decreasing the rate of wound infection.22

The recommendation for the use of topical antibiotics is based on the fact that nonviable tissue is present and will act as a nidus for infection and on the lack of effectiveness of systemic antibiotics.

Impaired Distal Perfusion and Need for Escharotomy

As subeschar edema develops under the burn tissue, pressure increases. This development is of particular concern in extremities with a circumferential burn, where the increasing pressure cannot be dissipated by expansion of neighboring tissue. The pressure impedes blood flow. Perfusion to the distal extremity must be monitored closely. Pain and color are unreliable indicators of perfusion in the presence of a burn. The use of a Doppler flowmeter is the most practical means of assessing perfusion. Decreasing distal flow with a proximal deep burn is also an indication for escharotomy. Wound management is summarized in Fig. 98-6.