Chapter 21 Burns

More than 500,000 burn injuries occur annually in the United States.1 Although most of these burn injuries are minor, approximately 40,000 to 60,000 burn patients require admission to a hospital or major burn center for appropriate treatment. The devastating consequences of burns have been recognized by the medical community and significant amounts of resources and research have successfully improved these dismal statistics.2 Specialized burn centers (Box 21-1) and advances in therapy strategies, based on improved understanding of resuscitation, enhanced wound coverage, more appropriate infection control, improved treatment of inhalation injury, and better support of the hypermetabolic response to injury have further improved the clinical outcome of this unique patient population.3 However, severe burns remain a devastating injury, affecting almost every organ system and leading to significant morbidity and mortality.4,5


There is no greater trauma than a major burn injury, which can be classified according to different burn causes and different depths (Box 21-2). Of all cases, almost 4000 people die of complications related to thermal injury.6 As in all trauma-related deaths, burn deaths generally occur immediately after the injury or weeks later as a result of multisystem organ failure. Of all burns, 66% occur at home and fatalities are predominant in the extremes of age, the very young and older adults. The most common causes are flame and scald burns.7 Scald burns are most common in victims up to 5 years of age. There is a significant percentage of burns in children that are caused by child abuse. There are a number of risk factors that have been linked to burn injury—specifically age, location, demographics, and low economic status.8 These risk factors underscore the fact that most burn injuries and fatalities are preventable and mandate intervention and prevention strategies. Overall, no single group is immune to the public health debt caused by burns.

Location plays a major role in the risk and treatment of burn. The available resources in a given community greatly influence morbidity and mortality. A lack of adequate resources affects the education, rehabilitation, and survival rates of burn victims. Someone with a severe burn in a resource-rich environment can receive care within minutes, whereas a burned individual in an austere environment may suffer for an extended period waiting for care. The ideal treatment of burns requires the collaboration of surgeons, anesthesiologists, occupational therapists, physiotherapists, nurses, nutritionists, rehabilitation therapists, and social workers just to accommodate the basic needs of a major burn survivor.9 Any delay in reaching these resources compounds a delay in resuscitation and thus adds to the mortality risk.10 For those who have access to adequate burn care, survival from a major burn is the rule, no longer the exception. The survival rate for all burns is 94.6%, but for at-risk populations, in communities lacking medical, legal, and public health resources, survival can be almost impossible.7

Pathophysiology of Burn Injuries

Local Changes

Locally, thermal injury causes coagulative necrosis of the epidermis and underlying tissues, with the depth of injury dependent on the temperature to which the skin is exposed, the specific heat of the causative agent, and the duration of exposure. Burns are classified into five different categories of cause and depth of injury. The causes include injury from flame (fire), hot liquids (scald), contact with hot or cold objects, chemical exposure, and/or conduction of electricity (Box 21-2). The first three induce cellular damage by the transfer of energy, which induces coagulation necrosis. Chemical burns and electrical burns cause direct injury to cellular membranes in addition to the transfer of heat and can cause a coagulation or colliquation necrosis.

The skin, which is the largest organ on the human body, provides a staunch barrier in the transfer of energy to deeper tissues, thus confining much of the injury to this layer. Once the inciting focus is removed, however, the response of local tissues can lead to injury in the deeper layers. The area of cutaneous or superficial injury has been divided into three zones—zone of coagulation, zone of stasis, and zone of hyperemia (Fig. 21-1). The necrotic area of burn where cells have been disrupted is termed the zone of coagulation. This tissue is irreversibly damaged at the time of injury. The area immediately surrounding the necrotic zone has a moderate degree of insult, with decreased tissue perfusion. This is termed the zone of stasis and, depending on the wound environment, can survive or go on to coagulative necrosis. The zone of stasis is associated with vascular damage and vessel leakage. Thromboxane A2, a potent vasoconstrictor, is present in high concentrations in burn wounds, and the local application of inhibitors improves blood flow and decreases the zone of stasis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressures also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Treatment directed at the control of local inflammation immediately after injury may spare the zone of stasis, indicated by studies demonstrating the blockage of leukocyte adherence with anti-CD18 or anti-intercellular adhesion molecules; monoclonal antibodies improve tissue perfusion and tissue survival in animal models. The last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. This region contains the clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis.

Burn Depth

The depth of burn varies, depending on the degree of tissue damage. Burn depth is classified into degree of injury in the epidermis, dermis, subcutaneous fat, and underlying structures (Fig. 21-2). First-degree burns are, by definition, injuries confined to the epidermis. First-degree burns are painful, erythematous, and blanch to the touch, with an intact epidermal barrier. Examples include sunburn or a minor scald from a kitchen accident. These burns do not result in scarring, and treatment is aimed at comfort with the use of topical soothing salves, with or without aloe, and oral nonsteroidal anti-inflammatory drugs (NSAIDs).

Second-degree burns are divided into two types, superficial and deep. All second-degree burns have some degree of dermal damage, by definition, and the division is based on the depth of injury into the dermis. Superficial dermal burns are erythematous, painful, blanch to touch, and often blister. Examples include scald injuries from overheated bathtub water and flash flame burns. These wounds spontaneously reepithelialize from retained epidermal structures in the rete ridges, hair follicles, and sweat glands in 1 to 2 weeks. After healing, these burns may have some slight skin discoloration over the long term. Deep dermal burns into the reticular dermis appear more pale and mottled, do not blanch to touch, but remain painful to pinprick. These burns heal in 2 to 5 weeks by reepithelialization from hair follicles and sweat gland keratinocytes, often with severe scarring as a result of the loss of dermis.

Third-degree burns are full-thickness burns through the epidermis and dermis and are characterized by a hard, leathery eschar that is painless and black, white, or cherry red. No epidermal or dermal appendages remain; thus, these wounds must heal by reepithelialization from the wound edges. Deep dermal and full-thickness burns require excision with skin grafting from the patient to heal the wounds in a timely fashion.

Fourth-degree burns involve other organs beneath the skin, such as muscle, bone, and brain.

Currently, burn depth is most accurately assessed by the judgment of experienced physicians. Accurate depth determination is critical to wound healing because wounds that will heal with local treatment are treated differently than those requiring operative intervention. Examination of the entire wound by the physicians ultimately responsible for their management is the gold standard used to guide further treatment decisions. Newer technologies, such as the multisensor laser Doppler flowmeter, hold promise for determining burn depth quantitatively. Several studies have claimed superiority of this method over clinical judgment in the determination of wounds requiring skin grafting for timely healing, which may lead to a change in the standard of care in the future.

Systemic Changes

Severe burns covering more than 40% of the TBSA are typically followed by a period of stress, inflammation, and hypermetabolism, characterized by a hyperdynamic circulatory response with increased body temperature, glycolysis, proteolysis, lipolysis, and futile substrate cycling (Fig. 21-4). These responses are present in all trauma, surgical, and critically ill patients, but their severity, length, and magnitude are unique for burn patients.4

Hypermetabolic Response to Burn Injury

Marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are thought to initiate the cascade of events leading to the acute hypermetabolic response, with its ensuing catabolic state.11 The cause of this complex response is not well understood. However, interleukin-1 (IL-1) and IL-6, platelet-activating factor, tumor necrosis factor (TNF), endotoxins, neutrophil-adherence complexes, reactive oxygen species, nitric oxide, coagulation, and complement cascades have also been implicated in regulating this response to burn injury.12 Once these cascades are initiated, their mediators and byproducts appear to stimulate the persistent and increased metabolic rate associated with altered glucose metabolism seen after severe burn injury.

The postburn metabolic phenomena occur in a timely manner, suggesting two distinct patterns of metabolic regulation following injury. The first phase occurs within the first 48 hours of injury and has been called the ebb phase, characterized by decreases in cardiac output, oxygen consumption, and metabolic rate, as well as impaired glucose tolerance associated with its hyperglycemic state. These metabolic variables gradually increase within the first 5 days postinjury to a plateau phase (the flow phase), characteristically associated with hyperdynamic circulation and the hypermetabolic state.11,13 Insulin release during this period was found to be twice that of controls in response to glucose load and plasma glucose levels are markedly elevated, indicating the development of an insulin resistance.14 It is currently thought that these metabolic alterations resolve soon after complete wound closure. We have found that the hypermetabolic response to burn injury may last for more than 12 months after the initial event; in our recent studies,15 we noted that sustained hypermetabolic postburn alterations, as shown by persistent elevations of total urine cortisol, serum cytokine, and catecholamine levels, and basal energy requirements, were accompanied by impaired glucose metabolism and insulin sensitivity that persisted for up to 3 years after the initial burn injury.

A 10- to 50-fold elevation of plasma catecholamine and corticosteroid levels occurs in major burns, which persist up to 3 years post-injury.4,13,15 Cytokine levels peak immediately after the burn injury, approaching normal levels only after 1-month postinjury. Constitutive and acute-phase proteins are altered beginning 5 to 7 days postburn and remain abnormal throughout the acute hospital stay. Serum insulin-like growth factor I (IGF-I), IGF-binding protein 3 (IGFBP3), parathyroid hormone, and osteocalcin levels decrease immediately after the injury 10 fold, and remain significantly decreased up to 6 months postburn compared with normal levels. Sex hormone and endogenous growth hormone levels decrease at approximately 3 weeks postburn (Fig. 21-5).

For severely burned patients, the resting metabolic rate at a thermal neutral temperature (30° C) exceeds 140% of normal at admission, reduces to 130% once the wounds are fully healed, and then to 120% at 6 months after injury and 110% at 12 months postburn.13 Increases in catabolism result in loss of total body protein, decreased immune defenses, and decreased wound healing.4

Immediate postburn patients have low cardiac output characteristic of early shock. However, 3 to 4 days postburn, the cardiac output is more than 1.5 times that of a nonburned healthy volunteer.13 Heart rates of pediatric burn patients approach 1.6 times those of nonburned, healthy volunteers.11 Postburn patients have increased cardiac work.4 Myocardial oxygen consumption surpasses that of marathon runners and is sustained well into the rehabilitative period.

There is profound hepatomegaly after injury. The liver increases its size by 225% of normal by 2 weeks postburn and remains enlarged at discharge at 200% of normal.13

Postburn, muscle protein is degraded much faster than it is synthesized.16 The net protein loss causes loss of lean body mass and severe muscle wasting, leading to decreased strength and failure to rehabilitate fully. Significant decreases in lean body mass related to chronic illness or hypermetabolism can have dire consequences. A 10% loss of lean body mass is associated with immune dysfunction. A 20% loss of lean body mass positively correlates with decreased wound healing. A loss of 30% of lean body mass leads to increased risk for pneumonia and pressure sores. A 40% loss of lean body mass can lead to death. Uncomplicated severely burned patients can lose up to 25% of total body mass after acute burn injury.13 Protein degradation persists up to almost 1 year after severe burn injury, resulting in significant negative whole-body and cross-leg nitrogen balance (Fig. 21-6).4 Protein catabolism has a positive correlation with increases in metabolic rates. Severely burned patients have a daily nitrogen loss of 20 to 25 g/m2 of burned skin.4 At this rate, a lethal cachexia can be reached in less than 1 month. Burned pediatric patients’ protein loss leads to significant growth retardation for up to 24 months postinjury.15

Elevated circulating levels of catecholamines, glucagon, and cortisol after severe thermal injury stimulate free fatty acids and glycerol from fat, glucose production by the liver, and amino acids from muscle (Fig. 21-7).4,11 Specifically, glycolytic-gluconeogenic cycling is increased 250% during the postburn hypermetabolic response, coupled with an increase of 450% in triglyceride fatty acid cycling. These changes lead to hyperglycemia and impaired insulin sensitivity related to postreceptor insulin resistance, as demonstrated by elevated levels of insulin and fasting glucose, and significant reductions in glucose clearance. Whereas glucose delivery to peripheral tissues is increased up to threefold, glucose oxidation is restricted. Increased glucose production is directed, in part, to the burn wound to support the relatively inefficient anaerobic metabolism of fibroblasts and endothelial and inflammatory cells. The end product of anaerobic glucose oxidation, lactate, is recycled to the liver to produce more glucose via gluconeogenic pathways. Serum glucose and insulin levels increase postburn and remain significantly increased through the acute hospital stay. Insulin resistance appears during the first week postburn and persists significantly after discharge, up to 3 years postburn.13,15

Septic patients have a profound increase in metabolic rates and protein catabolism, up to 40% more compared with those with burns of a similar size who do not develop sepsis.17,18 A vicious cycle develops, because catabolic patients are more susceptible to sepsis caused by changes in immune function and immune response. The emergence of multidrug resistant organisms has led to increases in sepsis, catabolism, and mortality (Fig. 21-8). Modulation of the hypermetabolic hypercatabolic response, thus preventing secondary injury, is paramount for the restoration of structure and function of severely burned patients.

Inflammation and Edema

Significant burns are associated with a massive release of inflammatory mediators, both in the wound and in other tissues. These mediators produce vasoconstriction and vasodilation, increased capillary permeability, and edema locally and in distant organs. The generalized edema is in response to changes in Starling forces in burned and unburned skin. Initially, the interstitial hydrostatic pressures in the burned skin decrease, and there is an associated increase in nonburned skin interstitial pressures. As the plasma oncotic pressures decrease and interstitial oncotic pressures increase because of increased capillary permeability-induced protein loss, edema forms in the burned and nonburned tissues. The edema is greater in the burned tissues because of lower interstitial pressures.

Many mediators have been proposed to account for the changes in permeability after burns, including histamine, bradykinin, vasoactive amines, prostaglandins, leukotrienes, activated complement, and catecholamines. Mast cells in the burned skin release histamine in large quantities immediately after injury, which elicits a characteristic response in venules by increasing intercellular junction space formation. The use of antihistamines for the treatment of burn edema, however, has had limited success. In addition, aggregated platelets release serotonin, which plays a major role in edema formation. This agent acts directly to increase pulmonary vascular resistance and indirectly aggravates the vasoconstrictive effects of various vasoactive amines. Serotonin blockade improves the cardiac index, decreases pulmonary artery pressure, and decreases oxygen consumption after burn. When the antiserotonin methysergide was given to animals after scald injury, wound edema formation decreased as a result of local effects.

Another mediator likely to play a role in changes in permeability and fluid shifts is thromboxane A2; its level increases dramatically in the plasma and wounds of burn patients. This potent vasoconstrictor leads to vasoconstriction and platelet aggregation in the wound, contributing to expansion of the zone of stasis. It has also caused prominent mesenteric vasoconstriction and decreased gut blood flow in animal models, which compromised gut mucosal integrity and decreased gut immune function.

Effects on the Gastrointestinal System

The gastrointestinal response to burn is highlighted by mucosal atrophy, changes in digestive absorption, and increased intestinal permeability. Atrophy of the small bowel mucosa occurs within 12 hours of injury in proportion to the burn size and is related to increased epithelial cell death by apoptosis. The cytoskeleton of the mucosal brush border undergoes atrophic changes associated with vesiculation of microvilli and disruption of the terminal web actin filaments. These findings are most pronounced 18 hours after injury, which suggests that changes in the cytoskeleton, such as those associated with cell death by apoptosis, are processes involved in the changed gut mucosa. Burn also causes reduced uptake of glucose and amino acids, decreased absorption of fatty acids, and reduction in brush border lipase activity. These changes peak in the first several hours after burn and return to normal at 48 to 72 hours after injury, a timing that parallels mucosal atrophy.

Intestinal permeability to macromolecules, which are normally repelled by an intact mucosal barrier, increases after burn. Intestinal permeability to polyethylene glycol 3350, lactulose, and mannitol increases after injury, correlating with the extent of the burn. Gut permeability increases even further when burn wounds become infected. A study using fluorescent dextrans has shown that larger molecules appeared to cross the mucosa between the cells, whereas the smaller molecules traversed the mucosa through the epithelial cells, presumably by pinocytosis and vesiculation. Mucosal permeability also paralleled increases in gut epithelial apoptosis.

Changes in gut blood flow are related to changes in permeability. Intestinal blood flow was shown to decrease in animals, a change associated with increased gut permeability at 5 hours after burn. This effect was abolished at 24 hours. Systolic hypotension has been shown to occur in the hours immediately after burn in animals with a 40% TBSA full-thickness injury. These animals showed an inverse correlation between blood flow and permeability to intact Candida spp.

Effects on the Immune System

Burns cause a global depression in immune function, which is shown by prolonged allograft skin survival on burn wounds. Burn patients are then at great risk for a number of infectious complications, including bacterial wound infection, pneumonia, and fungal and viral infections. These susceptibilities and conditions are based on depressed cellular function in all parts of the immune system, including activation and activity of neutrophils, macrophages, T lymphocytes, and B lymphocytes. With burns of more than 20% TBSA, impairment of these immune functions is proportional to burn size.

Macrophage production after burn is diminished, which is related to the spontaneous elaboration of negative regulators of myeloid growth. This effect is enhanced by the presence of endotoxin and can be partially reversed with granulocyte colony-stimulating factor (G-CSF) treatment or inhibition of prostaglandin E2. Investigators have shown that G-CSF levels actually increase after severe burn. However, bone marrow G-CSF receptor expression is decreased, which may in part account for the immunodeficiency seen in burns. Total neutrophil counts are initially increased after burn, a phenomenon related to a decrease in cell death by apoptosis. However, neutrophils that are present are dysfunctional in terms of diapedesis, chemotaxis, and phagocytosis. These effects are explained, in part, by a deficiency in CD11b/CD18 expression after inflammatory stimuli, decreased respiratory burst activity associated with a deficiency in p47-phox activity, and impaired actin mechanics related to neutrophil motile responses. After 48 to 72 hours, neutrophil counts decrease, similar to macrophages with similar causes.

Helper T cell (Th cell) function is depressed after a severe burn associated with polarization from the IL-2 and interferon-γ (IFN-γ) cytokine-based Th1 response toward the Th2 response. The Th2 response is characterized by the production of IL-4 and IL-10. The Th1 response is important in cell-mediated immune defense, whereas the Th2 response is important in antibody responses to infection. As this polarization increases, so does the mortality rate. Administration of IL-10 antibodies and growth hormone has partially reversed this response and improved mortality rate after burn in animals. Burn also impairs cytotoxic T lymphocyte activity as a function of burn size, thus increasing the risk of infection, particularly from fungi and viruses. Early burn wound excision improves cytotoxic T cell activity.


Basic Treatment

Initial Assessment

As with any trauma patient, the initial assessment of a burn patient is done by primary and secondary surveys. In the primary survey, immediate life-threatening conditions are quickly identified and treated. In the secondary survey, a more thorough head to toe evaluation of the patient is undertaken.

Exposure to heated gases and smoke results in damage to the upper respiratory tract. Direct injury to the upper airway results in edema, which, in combination with generalized whole-body edema associated with severe burn, may obstruct the airway. Airway injury must be suspected with facial burns, singed nasal hairs, carbonaceous sputum, and tachypnea. Upper airway obstruction may develop rapidly, and respiratory status must be continually monitored to assess the need for airway control and ventilatory support. Progressive hoarseness is a sign of impending airway obstruction, and endotracheal intubation should be instituted early, before edema distorts the upper airway anatomy. This is especially important in patients with massive burns, who may appear to breathe without problems early in the resuscitation period until several liters of volume have been given to maintain homeostasis, resulting in significant airway edema.

The chest should be exposed to assess breathing; airway patency alone does not ensure adequate ventilation. Chest expansion and equal breath sounds with CO2 return from the endotracheal tube ensure adequate air exchange.

Blood pressure may be difficult to determine in burn patients with edematous or charred extremities. The pulse rate can be used as an indirect measure of circulation; however, most burn patients remain tachycardic, even with adequate resuscitation. For the primary survey of burn patients, the presence of pulses or Doppler signals in the distal extremities may be adequate to determine adequate circulation of blood until more effective monitoring modalities, such as arterial pressure measurements and urine output, can be established.

In patients who have been in an explosion or deceleration accident, a possibility exists for spinal cord injury. Appropriate cervical spine stabilization must be accomplished by whatever means necessary, including using cervical collars to keep the head immobilized until the condition can be evaluated.


Adequate resuscitation of the burn patient depends on the establishment and maintenance of reliable IV access. Increased times to beginning resuscitation of burn patients result in poorer outcomes and delays should be minimized. Venous access is best attained through short peripheral catheters in unburned skin; however, veins in burned skin can be used and are preferable to no IV access. Superficial veins are often thrombosed in full-thickness injuries and therefore are not suitable for cannulation. Saphenous vein cutdowns are useful in cases of difficult access and are used in preference to central vein cannulation because of lower complication rates. In children younger than 6 years, experienced physicians can use intraosseous access in the proximal tibia until IV access is accomplished. Lactated Ringer’s solution without dextrose is the fluid of choice, except in children younger than 2 years, who should receive 5% dextrose Ringer’s lactate. The initial rate can be rapidly estimated by multiplying the TBSA burned by the patient’s weight in kilograms and then dividing by 8. The rate of infusion for an 80-kg man with a 40% TBSA burn can be calculated by the following formula:


This rate should be continued until a formal calculation of resuscitation needs is performed.

Many formulas have been devised to determine the proper amount of fluid to give a burn patient, all originating from experimental studies on the pathophysiology of burn shock. These experimental studies established the basis for modern fluid resuscitation protocols. It was shown that edema fluid in burn wounds is isotonic and contains the same amount of protein as plasma, and that the greatest loss of fluid is into the interstitium.22 Various volumes of intravascular fluid were used to determine the optimal amount in terms of cardiac output and extracellular volume in a canine burn model; this was applied to the clinical setting by the Parkland formula (Table 21-2). Plasma volume changes were not related to the type of resuscitation fluid in the first 24 hours, but thereafter colloid solutions could increase plasma volume by the amount infused. From these findings, it was concluded that colloid solutions should not be used in the first 24 hours until capillary permeability returns closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after burn (6 to 8 hours), and therefore colloids could be used earlier.

Concurrently, researchers have shown the hemodynamic effects of fluid resuscitation in burns, which culminated in the Brooke formula (see Table 21-2). It was found that fluid resuscitation causes an obligatory 20% decrease in extracellular fluid and plasma volume that concludes after 24 hours. In the second 24 hours, plasma volume returns to normal with the administration of colloid. Cardiac output is low in the first day despite resuscitation, but it subsequently increases to supernormal levels as the flow phase of hypermetabolism is established. Since these studies, it has been found that much of the fluid needs are caused by leaky capillaries that permit passage of large molecules into the interstitial space to increase the extravascular colloid osmotic pressure. Intravascular volume follows the gradient to tissues, both into the burn wound and nonburned tissues. Approximately 50% of fluid resuscitation needs are sequestered in nonburned tissues in 50% TBSA burns.

Hypertonic saline solutions have theoretical advantages in burn resuscitation. These solutions decrease net fluid intake, decrease edema, and increase lymph flow, probably by the transfer of volume from the intracellular space to the interstitium. When using these solutions, hypernatremia must be avoided, and it is recommended that serum sodium concentrations should not exceed 160 mEq/dL. However, it must be noted that for patients with more than 20% TBSA burns who are randomized to hypertonic saline or lactated Ringer’s solution, resuscitation does not have significant differences in volume requirements or changes in percentage of weight gain. Other investigators have found an increase in renal failure with hypertonic solutions that has tempered further efforts in this area of investigation. Some burn units successfully use a modified hypertonic solution of one ampule of sodium bicarbonate (50 mEq) in 1 liter of lactated Ringer’s solution. Further research should be done to determine the optimal formula to reduce edema formation and maintain adequate cellular function.

Most burn units use something similar to the Parkland or Brooke formula, which calls for administering varying amounts of crystalloid and colloid for the first 24 hours. The fluids are generally changed in the second 24 hours, with an increase in colloid use. These are guidelines to direct resuscitation of the amount of fluid necessary to maintain adequate perfusion. Studies have shown that the Parkland formula often underestimates the volume of crystalloid received in the first 24 hours after severe burn, a phenomenon termed fluid creep. No single cause has clearly been identified. More liberal use of opioid analgesic and positive pressure ventilation has been suggested.23 The increased fluid volumes are not without consequence; increased compartment pressures in the extremities, abdomen and, most recently, the orbit24 have been suggested as requiring monitoring and possible release to prevent increased morbidity and mortality. The abdominal compartment is clinically monitored via the Foley catheter. When the pressure increases toward and above 30 mm Hg, complete abdominal escharotomy is ensured and paralytics are considered. If the increased abdominal pressure persists (>30 mm Hg), an improved outcome is based on the performance of a decompressive laparotomy. However, patients who require this procedure have mortality rates of 60% to almost 100%, depending on the series. Therefore, monitoring of the resuscitation is crucial to ensure an acceptable outcome. This is easily done in burn patients with normal renal function by following the volume of urine output, which should be 0.5 mL/hr in adults and 1.0 mL/kg/hr in children. Changes in IV fluid infusion rates should be made on an hourly basis, determined by the response of the patient to the particular fluid volume administered. The exact formulas are shown in Table 21-2.

For burned children, formulas are commonly used that are modified to account for changes in surface area–to–mass ratios. These changes are necessary because a child with a comparable burn to that of an adult requires more resuscitation fluid per kilogram. The Galveston formula uses 5000 mL/TBSA burned (in m2) + 2000 mL/m2 total for maintenance in the first 24 hours. This formula accounts for maintenance needs and the increased fluid requirements of a child with a burn. All the formulas listed in Table 21-2 calculate the amount of volume given in the first 24 hours, with half is given in the first 8 hours.

The use of albumin during IV resuscitation has been debated. In a meta-analysis of 31 trials, it was shown that the risk of death is higher in burn patients receiving albumin compared with those receiving crystalloid, with a relative risk of death of 2.40 (95% confidence interval [CI], 1.11 to 5.19). Another meta-analysis of all critically ill patients refuted this finding, showing no differences in relative risk between albumin-treated and crystalloid-treated groups. As quality of the trials improved, the relative risks were reduced. Additional evidence has suggested that albumin supplementation, even after resuscitation, does not affect the distribution of fluid among the intracellular and extracellular compartments. What we can conclude from these trials and meta-analyses is that albumin used during resuscitation is at best equal to crystalloid and at worst detrimental to the outcome of burn patients. Thus, we cannot recommend the use of albumin during resuscitation.

To combat any regurgitation with an intestinal ileus, a nasogastric tube should be inserted in all patients with major burns to decompress the stomach. This is especially important for patients being transported in an aircraft at high altitudes. Also, all patients should be restricted from taking anything by mouth until the transfer has been completed. Decompression of the stomach is usually necessary because the apprehensive patient will swallow considerable amounts of air and distend the stomach. Additionally, a Dobhoff tube should be placed into the first (superior) part of the duodenum to feed the severely burned patient continuously.

Recommendations for tetanus prophylaxis are based on the condition of the wound and the patient’s immunization history. All patients with burns of more than 10% of the TBSA should receive 0.5 mL of tetanus toxoid. If prior immunization is absent or unclear, or the last booster dose was more than 10 years ago, 250 U of tetanus immunoglobulin is also given.


When deep second- and third-degree burn wounds encompass the circumference of an extremity, peripheral circulation to the limb can be compromised. The development of generalized edema beneath a nonyielding eschar impedes venous outflow and eventually affects arterial inflow to the distal beds. This can be recognized by numbness and tingling in the limb and increased pain in the digits. Arterial flow can be assessed by the determination of Doppler signals in the digital arteries and the palmar and plantar arches in affected extremities. Capillary refill can also be assessed. Extremities at risk are identified on clinical examination or on measurement of tissue pressures higher than 40 mm Hg. These extremities require escharotomies, which are releases of the burn eschar performed at the bedside by incising the lateral and medial aspects of the extremity with a scalpel or electrocautery unit. The entire constricting eschar must be incised longitudinally to relieve the impediment to blood flow completely (Fig. 21-9). The incisions are carried down onto the thenar and hypothenar eminences and along the dorsolateral sides of the digits to open the hand completely, if it is involved. If it is clear that the wound will require excision and grafting because of its depth, escharotomies are safest to restore perfusion to the underlying nonburned tissues until formal excision. If vascular compromise has been prolonged, reperfusion after an escharotomy may cause reactive hyperemia and further edema formation in the muscle, making continued surveillance of the distal extremities necessary. Increased muscle compartment pressures may necessitate fasciotomies. The most common complications associated with these procedures are blood loss and the release of anaerobic metabolites, causing transient hypotension. If distal perfusion does not improve with these measures, central hypotension because hypovolemia should be suspected and treated.

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Aug 1, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Burns
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