Chapter 8: Burns

1. Follow American Burn Association criteria for transfer of a patient to a regional burn center.

2. Never administer prophylactic antibiotics other than tetanus vaccination.

3. Early excision and grafting of full-thickness and deep partial-thickness burns improve outcomes.

4. Intravenous fluid resuscitation for patients with burns greater than 20% of total body surface area (children with burns >15% of total body surface area) should be titrated to mean arterial pressure (MAP) greater than 60 mmHg and urine output greater than 30 mL/h.

Surgical care of the burned patient has evolved into a specialized field incorporating the interdisciplinary skills of burn surgeons, nurses, therapists, and other healthcare specialists. However, recent mass casualty events have been a reminder that healthcare systems may be rapidly pressed to care for large numbers of burn patients. Naturally, general surgeons may be at the forefront in these events, so it is crucial that they are comfortable with the care of burned patients and well equipped to provide standard of care.

Burn injury historically carried a poor prognosis. With advances in fluid resuscitation¹ and the advent of early excision of the burn wound,² survival has become an expectation even for patients with severe burns. Continued improvements in critical care and progress in skin bioengineering herald a future in which functional and psychological outcomes are equally important as survival alone. With this shift in priority, the American Burn Association (ABA) has emphasized referral to specialized burn centers after early stabilization. Specific criteria should guide transfer of patients with more complex injuries or other medical needs to a burn center (Table 8-1). The ABA has published standards of care³ and created a verification process to ensure that burn centers meet those standards.⁴ Because of increased prehospital safety measures, burn patients are being transferred longer distances to receive definitive care at regional burn centers⁵; recent data from one burn center with a particularly wide catchment area confirmed that even transport times averaging 7 hours did not affect the long-term outcomes of burn patients.⁶

Initial evaluation of the burned patient involves four crucial assessments: airway management, evaluation of other injuries, estimation of burn size, and diagnosis of CO and cyanide poisoning. With direct thermal injury to the upper airway or smoke inhalation, rapid and severe airway edema is a potentially lethal threat. Anticipating the need for intubation and establishing an early airway are critical. Perioral burns and singed nasal hairs are signs that the oral cavity and pharynx should be further evaluated for mucosal injury, but these physical findings alone do not indicate an upper airway injury. Signs of impending respiratory compromise may include a hoarse voice, wheezing, or stridor; subjective dyspnea is a particularly concerning symptom and should trigger prompt elective endotracheal intubation. In patients with combined multiple trauma, especially oral trauma, nasotracheal intubation may be useful but should be avoided if oral intubation is safe and easy.

Burned patients should be first considered trauma patients, especially when details of the injury are unclear. A primary survey should be conducted in accordance with Advanced Trauma Life Support guidelines. Concurrently with the primary survey, large-bore peripheral intravenous (IV) catheters should be placed and fluid resuscitation should be initiated; for a burn larger than 40% total body surface area (TBSA), two large-bore IVs are ideal. IV placement through burned skin is safe and effective but requires attention to securing the catheters. Central venous access may provide useful information as to volume status and be useful in severely burned patients. Rarely, IV resuscitation is indicated in patients with burns smaller than 15% who can usually hydrate orally. Pediatric patients with burns larger than 15% may require intraosseous access in emergent situations if venous access cannot be attained. An early and comprehensive secondary survey must be performed on all burn patients, but especially those with a history of associated trauma such as with a motor vehicle collision. Also, patients from structural fires in which the manner of egress is not known should be carefully evaluated for injuries from a possible jump or fall. Urgent radiology studies, such as a chest x-ray, should be performed in the emergency department, but nonurgent skeletal evaluation (i.e., extremity x-rays) can be done in the intensive care unit (ICU) to avoid hypothermia and delays in burn resuscitation. Hypothermia is a common prehospital complication that contributes to resuscitation failure. Patients should be wrapped with clean blankets in transport. Cooling blankets should be avoided in patients with moderate or large (>20% TBSA) burns.

Patients with acute burn injuries should never receive prophylactic antibiotics. This intervention has been clearly demonstrated to promote development of fungal infections and resistant organism and was abandoned in the mid-1980s. A tetanus booster should be administered in the emergency room.

The importance of pain management for these patients has been widely recognized over the past 25 years. However, we must also consider treatment of long-term anxiety. Therefore, it is important to administer an anxiolytic such as a benzodiazepine with the initial narcotics.

Most burn resuscitation formulas estimate fluid requirements using the burn size as a percentage of TBSA (%TBSA). The “rule of nines” is a crude but quick and effective method of estimating burn size (Fig. 8-1). In adults, the anterior and posterior trunk each account for 18%, each lower extremity is 18%, each upper extremity is 9%, and the head is 9%. In children under 3 years old, the head accounts for a larger relative surface area and should be taken into account when estimating burn size. Diagrams such as the Lund and Browder chart give a more accurate accounting of the true burn size in children. The importance of an accurate burn size assessment cannot be overemphasized. Superficial or first-degree burns should not be included when calculating the %TBSA, and thorough cleaning of soot and debris is mandatory to avoid confusing soiled skin with burns. Examination of referral data suggests that physicians inexperienced with burns tend to overestimate the size of small burns and underestimate the size of large burns, with potentially detrimental effects on pretransfer resuscitation.⁷

An important contributor to early mortality in burn patients is carbon monoxide (CO) poisoning resulting from smoke inhalation. The affinity of CO for hemoglobin is approximately 200 to 250 times more than that of oxygen, which decreases the levels of normal oxygenated hemoglobin and can quickly lead to anoxia and death.⁸ Unexpected neurologic symptoms should raise the level of suspicion, and an arterial carboxyhemoglobin level must be obtained because pulse oximetry can be falsely elevated. Administration of 100% oxygen is the gold standard for treatment of CO poisoning and reduces the half-life of CO from 250 minutes in room air to 40 to 60 minutes on 100% oxygen.⁹ Some authors have proposed hyperbaric oxygen as an adjunctive therapy for CO poisoning.¹⁰ However, the data are mixed regarding the success of hyperbaric oxygen, and its associated logistical difficulties and complications have limited its usefulness for patients with moderate or large burns.^11,12 Patients who sustain a cardiac arrest as a result of their CO poisoning have an extremely poor prognosis regardless of the success of initial resuscitation attempts.¹³ Hydrogen cyanide toxicity may also be a component of smoke inhalation injury. Afflicted patients may have a persistent lactic acidosis or ST elevation on electrocardiogram (ECG).¹⁴ Cyanide inhibits cytochrome oxidase, which is required for oxidative phosphorylation.¹⁵ Treatment consists of sodium thiosulfate, hydroxocobalamin, and 100% oxygen. Sodium thiosulfate works by transforming cyanide into a nontoxic thiocyanate derivative, but it works slowly and is not effective for acute therapy. Hydroxocobalamin quickly complexes with cyanide, is excreted by the kidney, and is recommended for immediate therapy.⁹ In the majority of patients, the lactic acidosis will resolve with ventilation, and sodium thiosulfate treatment becomes unnecessary.¹⁶

Burns are commonly classified as thermal, electrical, or chemical burns, with thermal burns consisting of flame, contact, or scald burns. Flame burns are not only the most common cause for hospital admission of burns, but also have the highest mortality. This is primarily related to their association with structural fires and the accompanying inhalation injury and/or CO poisoning.¹⁷

Electrical burns make up only 4% of U.S. hospital admissions but have special concerns including the potential for cardiac arrhythmias and compartment syndromes with concurrent rhabdomyolysis. A baseline ECG is recommended in all patients with an electrical injury, and a normal ECG in a low-voltage injury may preclude hospital admission. Because compartment syndrome and rhabdomyolysis are common in high-voltage electrical injuries, vigilance must be maintained for neurologic or vascular compromise, and fasciotomies should be performed even in cases of moderate clinical suspicion. Long-term neurologic and visual symptoms are not uncommon with high-voltage electrical injuries, and ophthalmologic and neurologic consultation should be obtained to better define a patient’s baseline function.¹⁸

Chemical burns are less common but potentially severe burns. The most important components of initial therapy are careful removal of the toxic substance from the patient and irrigation of the affected area with water for a minimum of 30 minutes, except in cases of concrete powder or powdered forms of lye, which should be swept from the patient to avoid activating the aluminum hydroxide with water. The offending agents in chemical burns can be systemically absorbed and may cause specific metabolic derangements. Formic acid has been known to cause hemolysis and hemoglobinuria, and hydrofluoric acid causes hypocalcemia. Hydrofluoric acid is a particularly common offender due to its widespread industrial uses. Calcium-based therapies are the mainstay of treating hydrofluoric acid burns, with topical application of calcium gluconate onto wounds¹⁹ and IV administration of calcium gluconate for systemic symptoms. Intra-arterial calcium gluconate infusion provides effective treatment of progressive tissue injury and intense pain.^20,21 Patients undergoing intra-arterial therapy need continuous cardiac monitoring. Persistent refractory hypocalcemia with electrocardiac abnormalities may signal the need for emergent excision of the burned areas.

Based on the original burn depth classification by Dupuytren in 1832,²² burn wounds are commonly classified as superficial (first-degree), partial-thickness (second-degree), full-thickness (third-degree), and fourth-degree burns, which affect underlying soft tissue. Partial-thickness burns are classified as either superficial or deep partial-thickness burns by depth of involved dermis. Clinically, first-degree burns are painful but do not blister, second-degree burns have dermal involvement and are extremely painful with weeping and blisters, and third-degree burns are leathery, painless, and nonblanching. Jackson described three zones of tissue injury following burn injury.²³ The zone of coagulation is the most severely burned portion and is typically in the center of the wound. As the name implies, the affected tissue is coagulated and sometimes frankly necrotic, much like a third- or fourth-degree burn, and will need excision and grafting. Peripheral to that is a zone of stasis, with variable degrees of vasoconstriction and resultant ischemia, much like a second-degree burn. Appropriate resuscitation and wound care may help prevent conversion to a deeper wound, but infection or suboptimal perfusion may result in an increase in burn depth. This is clinically relevant because many superficial partial-thickness burns will heal with expectant management, and the majority of deep partial-thickness burns require excision and skin grafting. The last area of a burn is called the zone of hyperemia, which will heal with minimal or no scarring and is most like a superficial or first-degree burn.

Unfortunately, even experienced burn surgeons have limited ability to accurately predict the healing potential of partial-thickness burns soon after injury; one reason is that burn wounds evolve over the 48 to 72 hours after injury. Numerous techniques have been developed with the idea that better early prediction of burn depth will expedite appropriate surgical decision making. One of the most effective ways to determine burn depth is full-thickness biopsy, but this has several limitations; not only is the procedure painful and potentially scarring, but accurate interpretation of the histopathology requires a specialized pathologist and may have slow turnaround times.²⁴ Laser Doppler can measure skin perfusion to predict burn depth with a positive predictive value of up to 80% in some studies.^25,26 Noncontact ultrasound has been postulated as a painless modality to predict nonhealing wounds and has the advantage of easily performed serial measurements.²⁷ Unfortunately, none of these newer therapies have proven adequately superior to justify their cost and as yet have not substituted serial examination by experienced burn surgeons.

The Baux score (mortality risk equals age plus %TBSA) was used for many years to predict mortality in burns. Analysis of multiple risk factors for burn mortality has validated age and %TBSA as the strongest predictors of mortality.²⁸ Advancements in burn care have lowered overall mortality to the point that the Baux score may no longer be accurate. However, age and burn size, as well as inhalation injury, continue to be the most robust indicators for burn mortality.²⁹ Age even as a single variable strongly predicts mortality in burns,³⁰ and in-hospital mortality in elderly burn patients is a function of age regardless of other comorbidities.³¹ In nonelderly patients, comorbidities such as preinjury human immunodeficiency virus (HIV), metastatic cancer, and kidney or liver disease may influence mortality and length of stay.³² A recent large database study of 68,661 burn patients found that the variables with the highest predictive value for mortality were age, %TBSA, inhalation injury, coexistent trauma, and pneumonia.³³

A myriad of formulas exist for calculating fluid needs during burn resuscitation, suggesting that no one formula benefits all patients. The most commonly used formula, the Parkland or Baxter formula, consists of 3 to 4 mL/kg/% burn of lactated Ringer’s, of which half is given during the first 8 hours after burn and the remaining half is given over the subsequent 16 hours. The concept behind continuous fluid requirements is simple. The burn (and/or inhalation injury) drives an inflammatory response that leads to capillary leak; as plasma leaks into the extravascular space, crystalloid administration maintains the intravascular volume. Therefore, if a patient receives a large fluid bolus in a prehospital setting or emergency department, that fluid has likely leaked into the interstitium and the patient still requires ongoing burn resuscitation according to the estimates. Continuation of fluid volumes should depend on the time since injury, urine output, and mean arterial pressure (MAP). As the leak closes, the patient will require less volume to maintain these two resuscitation endpoints. Children under 20 kg have the additional requirement that they do not have sufficient glycogen stores to maintain an adequate glucose level in response to the inflammatory response. Specific pediatric formulas have been described, but the simplest approach is to deliver a weight-based maintenance IV fluid with glucose supplementation in addition to the calculated resuscitation fluid with lactated Ringer’s.

It is important to remember that any formula for burn resuscitation is merely a guideline, and fluid must be titrated based on appropriate measures of adequate resuscitation. A number of parameters are widely used to gauge burn resuscitation, but the most common remain the simple outcomes of blood pressure and urine output. As in any critically ill patient, a target MAP of 60 mmHg ensures optimal end-organ perfusion. Goals for urine output should be 30 mL/h in adults and 1 to 1.5 mL/kg/h in pediatric patients. Because blood pressure and urine output may not correlate perfectly with true tissue perfusion, the search continues for other adjunctive parameters that may more accurately reflect adequate resuscitation. Some centers have found serum lactate to be a better predictor of mortality in severe burns,^34,35 and others have found that base deficit predicts eventual organ dysfunction and mortality.^36,37 Because burned patients with normal blood pressure and serum lactate levels may have compromised gastric mucosal perfusion, continuous measurement of mucosal pH with its logistical difficulties has garnered limited popularity.^38,39 Invasive monitoring with pulmonary artery catheters typically results in significant excessive fluid administration without improved cardiac output or preload measurements; use of invasive monitoring seems to have variable effects on long-term outcomes.⁴⁰

Actual administrated fluid volumes typically exceed volumes predicted by standard formulas.⁴¹ One survey of burn centers showed that 58% of patients end up getting more fluids than would be predicted by Baxter’s formula.⁴² Comparison of modern-day patients with historical controls shows that over-resuscitation may be a relatively recent trend.⁴³ One theory is that increased opioid analgesic use results in peripheral vasodilation and hypotension and the need for greater volumes of bloused resuscitative fluids.⁴⁴ A classic study by Navar et al showed that burned patients with inhalation injury required an average of 5.76 mL/kg/% burn, vs. 3.98 mL/kg/% burn for patients without inhalation injury, and this has been corroborated by subsequent studies.^45,46 Prolonged mechanical ventilation may also play a role in increased fluid needs.⁴⁷ A recent multicenter study found that age, weight, %TBSA, and intubation on admission were significant predictors of more fluid delivery during the resuscitation period. Those patients receiving higher fluid volumes were at increased risk of complications and death.⁴⁸ Common complications include abdominal compartment syndrome, extremity compartment syndrome, intraocular compartment syndrome, and pleural effusions. Monitoring bladder pressures can provide valuable information about development of intra-abdominal hypertension.

The use of colloid as part of the burn resuscitation has generated much interest over the years. In late resuscitation when the capillary leak has closed, colloid administration may decrease overall fluid volumes and potentially may decrease associated complications such as intra-abdominal hypertension.⁴⁹ However, albumin use has never been shown to improve outcomes in burn patients and has controversial effects on mortality in critically ill patients.^50,51 Attempts to minimize fluid volumes in burn resuscitation have included study of hypertonic solutions, which appear to transiently decrease initial resuscitation volumes, with the downside of causing hyperchloremic acidosis.⁵²

Other adjuncts are being increasingly used during initial burn resuscitation. High-dose ascorbic acid (vitamin C) may decrease fluid volume requirements and ameliorate respiratory embarrassment during resuscitation.⁵³ Plasmapheresis may also decrease fluid requirements in patients who require higher volumes than predicted to maintain adequate urine output and MAP. It is postulated that plasmapheresis may filter out inflammatory mediators, thus decreasing ongoing vasodilation and capillary leak.⁵⁴

One recent adjunct that has found increasing utility in other surgical ICUs has been the application of bedside thoracic ultrasound.⁵⁵ Ultrasound offers the potential to make rapid, noninvasive assessments during acute changes in clinical condition. For burn patients, bedside ultrasonography may be indicated for evaluation of volume status, gross assessment of cardiac function, and diagnosis of pneumothorax. Determining patient cardiac function and volume status may guide fluid resuscitation. Cardiac function can be evaluated with three common heart views: the parasternal long axis, parasternal short axis, and apical four-chamber views.⁵⁶ Volume status can be estimated by examination of cardiac function, evaluation of the inferior vena cava (IVC) diameter, and changes with respiration. Ultrasound also allows timely diagnosis of pneumothorax.⁵⁷ A high-frequency probe with an adequate window between ribs permits identification of lung parenchyma against the chest well. A pneumothorax appears as a transition on ultrasound between lung parenchyma, which has a heterogeneous appearance, and air, which has a hypoechoic appearance. Further studies are warranted to identify indications for the use of ultrasound in burned patients.

The role of blood transfusion in critically injured patients has undergone a reevaluation in recent years.^58,59 Blood transfusions are considered to be immunosuppressive, which is one explanation for the common responses seen to blood transfusions, such as increased infection and shorter time to recurrence after oncologic surgery.⁶⁰ A large multicenter study of blood transfusions in burn patients found that increased numbers of transfusions were associated with increased infections and higher mortality in burn patients, even when correcting for burn severity.⁶¹ A follow-up study implanting a restrictive transfusion policy in burned children showed that a hemoglobin threshold of 7 g/dL had no more adverse outcomes vs. a traditional transfusion trigger of 10 g/dL. In addition, costs incurred to the institution were significantly less.⁶² These data, in concert with other reported complications such as transfusion-related lung injury,⁶³ have led to recommendations that blood transfusions be used only when there is an apparent physiologic need. Attempts to minimize blood transfusion in nonburned critically ill patients have led to use of erythropoietin by some centers. However, burn patients often have elevated erythropoietin levels, and a randomized study in burn patients showed that recombinant human erythropoietin did not effectively prevent anemia or decrease the number of transfusions given.⁶⁴

Inhalation injuries are commonly seen in tandem with burn injuries and are known to increase mortality in burned patients.⁶⁵ Smoke inhalation is present in as many as 35% of hospitalized burn patients and may triple the hospital stay compared to isolated burn injuries.⁶⁶ The combination of burns, inhalation injury, and pneumonia increases mortality by up to 60% over burns alone.⁶⁷ Subsequent development of the adult respiratory distress syndrome (ARDS) is common in these patients and may be caused in part by recruitment of alveolar leukocytes with an enhanced endotoxin-activated cytokine response.⁶⁸ When ARDS complicates burns and inhalation injury, mortality approaches 66%; in one study, patients with burns ≥60% TBSA in combination with inhalation injury and ARDS had 100% mortality.⁶⁹

Smoke inhalation causes injury in two ways: by direct heat injury to the upper airways and inhalation of combustion products into the lower airways. Direct injury to the upper airway causes airway swelling that typically leads to maximal edema in the first 24 to 48 hours after injury and often requires a short course of endotracheal intubation for airway protection. Combustion products found in smoke, most commonly from synthetic substances in structural fires, cause lower airway injury. These irritants cause direct mucosal injury, which in turn leads to mucosal sloughing, edema, reactive bronchoconstriction, and finally obstruction of the lower airways. Injury to both the epithelium and pulmonary alveolar macrophages causes release of prostaglandins, chemokines, and other inflammatory mediators; neutrophil migration; increased tracheobronchial blood flow; and finally increased capillary permeability. All of these components of acute lung injury increase the risk of pneumonia and ARDS following an inhalation injury.

The physiologic effects of smoke inhalation are numerous. Inhalation injury decreases lung compliance⁷⁰ and increases airway resistance work of breathing.⁷¹ Inhalation injury in the presence of burns also increases overall metabolic demands.⁷² The most common physiologic derangement seen with inhalation injury is increased fluid requirement during resuscitation. Since severe inhalation injury may result in mucosal sloughing with obstruction of smaller airways, bronchoscopy findings including carbon deposits, erythema, edema, bronchorrhea, and a hemorrhagic appearance may be useful for staging inhalation injury. Furthermore, bronchoalveolar lavage within 24 hours after an inhalation injury demonstrates a high rate of positive quantitative cultures,⁷³ suggesting that pneumonia develops soon after the acute lung injury. Because bronchoscopy is an invasive test, attempts have been made to utilize other diagnostic modalities, such as thoracic computed tomography (CT) scans⁷⁴ and xenon ventilation-perfusion scanning.⁷⁵ Decreased Pao₂:Fio₂ ratio (<200) on admission may not only predict inhalation injury but also indicate increased fluid needs more accurately than bronchoscopic grading of the severity of inhalation.⁷⁶

Treatment of inhalation injury consists primarily of supportive care. Aggressive pulmonary toilet and routine use of nebulized bronchodilators such as albuterol are recommended. Nebulized N-acetylcysteine is an antioxidant free radical scavenger designed to decrease the toxicity of high oxygen concentrations. Aerosolized heparin aims to prevent formation of fibrin plugs and decrease the formation of airway casts. These agents seem to improve pulmonary toilet but have no demonstrated effect on mortality.⁷⁷ Aerosolized tissue plasminogen activator⁷⁸ and recombinant human antithrombin⁷⁹ have shown promise in sheep models, but have not yet seen widespread clinical use. Administration of intrabronchial surfactant has been used as a salvage therapy in patients with severe burns and inhalation injury.⁸⁰ Inhaled nitric oxide may also be useful as a last effort in burn patients with severe lung injury who are failing other means of ventilatory support.⁸¹ The use of steroids has traditionally been avoided due to worse outcomes in burn patients,⁸² but new promising data in late ARDS have prompted scientific review of steroid use.⁸³

New ventilator strategies have contributed to the improved mortality with ARDS. Although ARDS still contributes to mortality in burn patients, treatments have improved so that mortality is primarily from multisystem organ failure rather than isolated respiratory causes.⁸⁴ The ARDS Network Study finding that low tidal volume (6 cc/kg) or “lung-protective ventilation” had a 22% lower mortality than patients with traditional tidal volumes (12 cc/kg)⁸⁵ has dramatically changed the management of patients with acute lung injury. A similar approach had previously been shown to improve outcomes in pediatric burn patients.⁸⁶ In patients with refractory hypoxemia despite lung-protective ventilation, prone positioning may improve oxygenation but has not shown a definitive effect on mortality.⁸⁷ No specific studies have examined prone positioning in burned patients, and caution must be used in patients with facial burns who are already at risk for loss of the endotracheal tube. High-frequency percussive ventilation (HFPV) has shown early promise in patients with inhalation injury.⁸⁸ One study showed notable decreases in both morbidity and mortality with HFPV, especially in patients with burns less than 40% TBSA and inhalation injury.⁸⁹ A related technique is high-frequency oscillatory ventilation, which has been used primarily as a salvage modality in patients refractory to more conventional measures.⁹⁰ Extracorporeal membrane oxygenation (ECMO) is typically reserved for salvage situations, and experience with this modality is limited to small numbers of patients.⁹¹ A promising area of future study may be arteriovenous carbon dioxide removal, a technique that has proven superior to both low tidal volume ventilation and HFPV in a sheep model but has not yet transitioned from bench to bedside.⁹²

Multitudes of topical therapies exist for the treatment of burn wounds. Silver sulfadiazine is one of the most widely used in clinical practice. Silver sulfadiazine has a wide range of antimicrobial activity, primarily as prophylaxis against burn wound infections rather than treatment of existing infections. It has the added benefits of being inexpensive and easily applied and has soothing qualities. It is not significantly absorbed systemically and thus has minimal metabolic derangements. Silver sulfadiazine has a reputation for causing neutropenia, but this association is more likely due to neutrophil margination from the inflammatory response. True allergic reactions to the sulfa component of silver sulfadiazine are rare, and at-risk patients can have a small test patch applied to identify a burning sensation or rash. Silver sulfadiazine destroys skin grafts and is contraindicated on burns or donor sites in proximity to newly grafted areas. Also, silver sulfadiazine may retard epithelial migration in healing partial-thickness wounds.

Mafenide acetate, either in cream or solution form, is an effective topical antimicrobial. It is effective even in the presence of eschar and can be used in both treating and preventing wound infections; the solution formulation is an excellent antimicrobial for fresh skin grafts. Use of mafenide acetate may be limited by pain with application to partial-thickness burns. Mafenide is absorbed systemically, and a major side effect is metabolic acidosis resulting from carbonic anhydrase inhibition.

Silver nitrate has broad-spectrum antimicrobial activity as a topical solution. The solution used must be dilute (0.5%), and prolonged topical application leads to electrolyte extravasation with resulting hyponatremia. A rare complication is methemoglobinemia. Although inexpensive, silver nitrate solution causes black stains, and laundry costs may offset any fiscal benefit to the hospital. Increasingly, Dakin’s solution (0.5% sodium hypochlorite solution) is being used as an inexpensive topical antimicrobial.

For smaller burns or larger burns that are nearly healed, topical ointments such as bacitracin, neomycin, and polymyxin B can be used. These are also useful for superficial partial-thickness facial burns as they can be applied and left open to air without dressing coverage. Meshed skin grafts in which the interstices are nearly closed are another indication for use of these agents, preferably with greasy gauze to help retain the ointment in the affected area. All three have been reported to cause nephrotoxicity and should be used sparingly in large burns. The recent media fascination with methicillin-resistant Staphylococcus aureus (MRSA) has led to widespread use by community practitioners of mupirocin for new burns. Unless the patient has known risk factors for MRSA, mupirocin should only be used in culture-positive burn wound infections to prevent emergence of further resistance.

Silver-impregnated dressings such as Acticoat (Smith & Nephew, London, United Kingdom), Aquacel Ag (Convatec, Princeton, NJ), and Mepilex Ag (Mölnlycke Health Care US, LLC, Norcross, GA) are increasingly being used for donor sites, skin grafts, and partial-thickness burns. These may be more comfortable for the patient, reduce the number of dressing changes, and shorten hospital length of stay, but they do limit serial wound examinations. Biologic membranes such as Biobrane (Dow-Hickham, Sugarland, TX) provide a prolonged barrier under which wounds may heal. Because of the occlusive nature of these dressings, these are typically used only on fresh superficial partial-thickness burns that are clearly not contaminated.

Nutritional support may be more important in patients with large burns than in any other patient population. Not only does adequate nutrition play a role in acute issues such as immune responsiveness, but the hypermetabolic response in burn injury may raise baseline metabolic rates by as much as 200%.⁹³ This can lead to catabolism of muscle proteins and decreased lean body mass that may delay functional recovery.⁹⁴ Early enteral feeding for patients with burns larger than 20% TBSA is safe and may reduce loss of lean body mass,⁹⁵ slow the hypermetabolic response,⁹⁶ and result in more efficient protein metabolism.⁹⁷ If the enteral feeds are started within the first few hours after admission, gastric ileus can be avoided. Adjuncts such as metoclopramide promote gastrointestinal motility; if other measures for gastric feeding are unsuccessful, advancing the tube into the small bowel with nasojejunal feeding can be attempted.⁹⁸ In endotracheally intubated patients, trips to the operating room do not necessitate holding enteral feedings.⁹⁹ Immune-modulating supplements such as glutamine may decrease infectious complications and mortality in burn patients,¹⁰⁰ likely via prevention of T-cell suppression in mesenteric lymph nodes.¹⁰¹

Calculating the appropriate caloric needs of the burn patient can be challenging. A commonly used formula in nonburned patients is the Harris-Benedict equation, which calculates caloric needs using factors such as gender, age, height, and weight. This formula uses an activity factor for specific injuries, and for burns, the basal energy expenditure is multiplied by two. The Harris-Benedict equation may be inaccurate in burns of less than 40% TBSA, and in these patients, the Curreri formula may be more appropriate. This formula estimates caloric needs to be 25 kcal/kg/d plus 40 kcal/%TBSA/d. Indirect calorimetry can also used to calculate resting energy expenditure, but in burn patients, a “metabolic cart” has not been documented to be more beneficial than the predictive equations.¹⁰² Titrating caloric needs closely is important, because overfeeding patients will lead to storage of fat instead of muscle anabolism.¹⁰³

Modifying the hypermetabolic response is an area of intense study with several recent findings. β-Blocker use in pediatric patients decreases heart rate and resting energy expenditure and abrogates protein catabolism, even in long-term use.¹⁰⁴ There may be benefits to β-blockade in adult patients,¹⁰⁵ and many centers use β-blockers routinely in the adult population with limited safety and efficacy data. The anabolic steroid oxandrolone has been extensively studied in pediatric patients as well, and has demonstrated improvements in lean body mass and bone density in severely burned children.¹⁰⁶ The weight gain and functional improvements seen with oxandrolone may persist even after stopping administration of the drug.¹⁰⁷ A recent double-blind, randomized study of oxandrolone showed decreased length of stay, improved hepatic protein synthesis, and no adverse effects on endocrine function, although the authors noted a rise in transaminases with unclear clinical significance.¹⁰⁸ Intensive insulin therapy in critically ill patients has shown benefit, presumably from avoidance of hyperglycemia.¹⁰⁹ However, in burn patients, the insulin itself may have a metabolic benefit, with improvements in lean body mass and amelioration of the inflammatory response to burn injury.^110,111 Oral hypoglycemic agents such as metformin also help to avoid hyperglycemia and may contribute to prevention of muscle catabolism.¹¹²

There are several complications commonly associated with treatment of burn patients. Though not always avoidable, maintaining vigilance for typical complications and using appropriate techniques for prevention may limit the frequency and severity of complications. Ventilator-associated pneumonia, as in all critically ill patients, is a significant problem in burned patients. However, it is so common in patients with inhalation injury that a better nomenclature may be postinjury pneumonia. Unfortunately, commonly used scores in critical illness such as the Clinical Pulmonary Infection Score (CPIS) have not been shown to be reliable in burn patients. Quantitative bronchoscopic cultures in the setting of clinical suspicion of pneumonia should guide treatment of pneumonia.¹¹³ Simple measures such as elevating the head of the bed and maintaining excellent oral hygiene and pulmonary toilet are recommended to help decrease the risk of postinjury pneumonia. There is some question as to whether early tracheostomy decreases infectious morbidity in burn patients and whether it improves long-term outcomes. There do not seem to be any major differences in the rates of pneumonia with early tracheostomy, though there may be reduced development of subglottic stenosis compared with prolonged endotracheal intubation.^114,115 Practical considerations such as protection of facial skin grafts may influence the decision for tracheostomy placement. One major consideration in deciding whether to perform a tracheostomy has been the presence of eschar at the insertion site, which complicates tracheostomy site care and increases the risk of airway infection. Bedside percutaneous dilatational tracheostomy is a facile method for performing tracheostomy and is reported to be as safe as open tracheostomy in the burn population.¹¹⁶

Massive resuscitation of burned patients may lead to an abdominal compartment syndrome characterized by increased airway pressures with hypoventilation, and decreased urine output and hemodynamic compromise. Decompressive laparotomy is the standard of care for refractory abdominal compartment syndrome but carries an especially poor prognosis in burn patients.¹¹⁷ Adjunctive measures such as minimizing fluid, performing torso escharotomies, decreasing tidal volumes, and chemical paralysis should be initiated before resorting to decompressive laparotomy. Patients undergoing massive resuscitation also develop elevated intraocular pressures and may require lateral canthotomy.¹¹⁸

Deep vein thrombosis (DVT) has been commonly believed to be a rare phenomenon in burned patients, and there is a paucity of controlled studies regarding heparin prophylaxis in this population.¹¹⁹ However, recent data show that up to 25% of burn patients develop DVT, and fatal pulmonary emboli have been reported in burn patients.^120,121 A large retrospective study in patients with routine prophylaxis found DVT in only 0.25% of patients and reported no bleeding complications.¹²² Thus, it appears that heparin prophylaxis is safe in burn patients and may help prevent thrombotic complications.

Unfortunately, the use of both prophylactic and therapeutic heparin may be associated with heparin-associated thrombocytopenia (HIT). One study of HIT in burn patients showed an incidence of 1.6% in heparinized burn patients. Thrombotic complications included DVT, pulmonary embolus, and even arterial thrombosis requiring limb amputation. Nonheparin anticoagulation for HIT commonly caused bleeding complications requiring transfusion.¹²³ Although rare, a high index of suspicion for HIT should be maintained in thrombocytopenic burn patients, particularly if the platelet counts drop at hospital days 7 to 10.

Burn patients often require central venous access for fluid resuscitation and hemodynamic monitoring. Because of the anatomic relation of their burns to commonly used access sites, burn patients may be at higher risk for catheter-related bloodstream infections. The 2009 Centers for Disease Control and Prevention National Healthcare Safety Network report (http://www.cdc.gov/nhsn/dataStat.html) indicates that American burn centers have higher infectious complication rates than any other ICUs. Because burn patients may commonly exhibit leukocytosis with a documented bloodstream infection, practice has been to rewire lines over a guide wire and to culture the catheter tip. However, this may increase the risk of catheter-related infections in burned patients, and a new site should be used if at all possible.¹²⁴

Full-thickness burns with a rigid eschar can form a tourniquet effect as the edema progresses, leading to compromised venous outflow and eventually arterial inflow. The resulting compartment syndrome is most common in circumferential extremity burns, but abdominal and thoracic compartment syndromes also occur. Warning signs of impending compartment syndrome may include paresthesias, pain, decreased capillary refill, and progression to loss of distal pulses; in an intubated patient, the surgeon should anticipate the compartment syndrome and perform frequent neurovascular evaluations. Abdominal compartment syndrome should be suspected with decreased urine output, increased ventilator airway pressures, and hypotension. Hypoventilation, increased airway pressures, and hypotension may also characterize thoracic compartment syndrome. Escharotomies are rarely needed within the first 8 hours following injury and should not be performed unless indicated because of the terrible aesthetic sequelae. When indicated, they are usually performed at the bedside, preferably with electrocautery to minimize blood loss. Extremity incisions are made on the lateral and medial aspects of the limbs in an anatomic position and may extend onto thenar and hypothenar eminences of the hand. Digital escharotomies do not usually result in any meaningful salvage of functional tissue and are not recommended. Inadequate perfusion despite proper escharotomies may indicate the need for fasciotomy, but this procedure should not be routinely performed as part of the eschar release. Thoracic escharotomies should be placed along the anterior axillary lines with bilateral subcostal and subclavicular extensions. Extension of the anterior axillary incisions down the lateral abdomen typically will allow adequate release of abdominal eschar.

The strategy of early excision and grafting in burned patients revolutionized survival outcomes in burn care. Not only did it improve mortality, but early excision also decreased reconstruction surgery, hospital length of stay, and costs of care.^125,126 Once the initial resuscitation is complete and the patient is hemodynamically stable, attention should be turned to excising the burn wound. Burn excision and wound coverage should ideally start within the first several days, and in larger burns, serial excisions can be performed as patient condition allows. Excision is performed with repeated tangential slices using a Watson or Goulian blade until viable, diffusely bleeding tissue remains. It is appropriate to leave healthy dermis, which will appear white with punctate areas of bleeding. Excision to fat or fascia may be necessary in deeper burns. The downside of tangential excision is a high blood loss, though this may be ameliorated using techniques such as instillation of an epinephrine tumescence solution underneath the burn. Pneumatic tourniquets are helpful in extremity burns, and compresses soaked in a dilute epinephrine solution are necessary adjuncts after excision. A fibrinogen and thrombin spray sealant (Tisseel Fibrin Sealant; Baxter, Deerfield, IL) also has beneficial effects on both hemostasis and graft adherence to the wound bed. The use of these techniques has markedly decreased the number of blood transfusions given during burn surgery.¹²⁷ For patients with clearly deep burns and concern for excessive blood loss, fascial excision may be employed. In this technique, electrocautery is used to excise the burned tissue and the underlying subcutaneous tissue down to muscle fascia. This technique markedly decreases blood loss but results in a cosmetically inferior appearance due to the loss of subcutaneous tissue. For excision of burns in difficult anatomic areas such as the face, eyelids, or hands, a pressurized water dissector may offer more precision but is time consuming, has a steep learning curve, and is expensive.¹²⁸

Since full-thickness burns are impractical for most burn wounds, split-thickness sheet autografts harvested with a power dermatome make the most durable wound coverings and have a decent cosmetic appearance. In larger burns, meshed ­autografted skin provides a larger area of wound coverage. This also allows drainage of blood and serous fluid to prevent accumulation under the skin graft with subsequent graft loss. Areas of cosmetic importance such as the face, neck, and hands should be grafted with nonmeshed sheet grafts to ensure optimal appearance and function. Unfortunately, even extensive meshing of skin grafts in patients with limited donor sites may not provide adequate amounts of skin. Options for temporary wound coverage include human cadaveric allograft, which is incorporated into the wound but is rejected by the immune system and must be eventually replaced. This allows temporary biologic wound coverage until donor sites heal enough so that they may be reharvested. Xenograft appears to function as well as allograft for temporary wound coverage and is considerably less ­expensive.

The search for a perfect permanent synthetic skin substitute remains elusive. Integra (Integra LifeSciences Corporation, Plainsboro, NJ) is a bilayer product with a porous collagen-chondroitin 6-sulphate inner layer that is attached to an outer silastic sheet, which helps prevent fluid loss and infection as the inner layer becomes vascularized, creating an artificial neodermis. At approximately 2 weeks after placement, the silastic layer can be removed and a thin autograft can be placed over the neodermis. This results in faster healing of the more superficial donor sites and seems to be associated with hypertrophic scarring and improved joint function.¹²⁹ Alloderm (LifeCell Corporation, The Woodlands, TX) is another dermal substitute consisting of cryopreserved acellular human dermis. This must also be used in combination with thin split-thickness skin grafts.¹³⁰

Epidermal skin substitutes such as cultured epithelial autografts are an option in patients with massive burns and very limited donor sites.¹³¹ Their clinical use has been limited by a long turnaround time for culturing, as well as the fragility of the cultured skin, which creates great difficulty with intraoperative handling and graft take. There are promising developments in skin culturing techniques and engineered skin development, but no other products are Food and Drug Administration approved and commercially available.¹³²

Thighs make convenient anatomic donor sites; they are easily harvested and relatively hidden from an aesthetic standpoint. The thicker skin of the back is useful in older patients, who have thinner skin elsewhere and may have difficulty with healing of donor sites. The buttocks are an excellent donor site in infants and toddlers; silver sulfadiazine can be applied to the donor site with a diaper as coverage. The scalp is also an excellent donor site; the skin is thick and the many hair follicles allow rapid healing, with the added advantage of being completely hidden once hair regrows. Epinephrine tumescence is necessary for harvesting the scalp, for both hemostasis of this hypervascular area and also to create a smooth contoured surface for harvesting.

The list of commonly used donor site dressings is long and includes simple transparent films to hydrocolloids, petrolatum gauzes, and silver-impregnated dressings. Donor sites close to fresh grafts may be dressed with a porous nonadherent gauze, and both the donors and grafts are soaked with an antimicrobial solution. Principals behind choosing a dressing should balance ease of care, comfort, infection control, and cost. The choice of donor site dressing is largely institution dependent, and few data support the clear superiority of any single treatment plan.

Rehabilitation is an integral part of the clinical care plan for the burn patient and should be initiated on admission. Immediate and ongoing physical and occupational therapy is mandatory to prevent functional loss. Patients who are unable to actively participate should have passive range of motion done at least twice a day. This includes patients with burns over joints, such as with hand burns. Patients should be taught exercises they can do themselves to maintain full range of motion. Patients with foot and extremity burns should be instructed to walk independently without crutches or other assistive devices to prevent extremity swelling, desensitize the burned areas, and prevent disuse atrophy; when patients are not ambulating, they must elevate the affected extremity to minimize swelling. If postoperative immobilization is used for graft protection, the graft should be evaluated early and at frequent intervals so that active exercise can be resumed at the earliest possible occasion. The transition to outpatient care should also include physical and occupational therapy, with introduction of exercises designed to accelerate return to activities of daily living as well as specific job-related tasks. Tight-fitting pressure garments provide vascular support in burns that are further along in the healing process. Whether they prevent hypertrophic scar formation has been long debated. However, they do provide vascular support that many patients find more comfortable.

Once patients have recovered from their acute burns, many face management of the hypertrophic burn scars. In patients with healed burns or donor sites, hypertrophic scar-related morbidity includes pruritus, erythema, pain, thickened tight skin, and even contractures. Within these scars, there is believed to be an increased inflammatory response that has increased neovascularization, abundant collagen production, and abnormal extracellular matrix structure. Treatment for these scars has included nonsurgical therapies such as compression garments, silicone gel sheeting, massage, physical therapy, and corticosteroid. Surgical excision and scar revision represent more invasive scar management approaches that are often necessary for functional and aesthetic recovery.

Laser-based therapies provide addition treatment options for symptomatic hypertrophic scars. Two of the most common ones are the pulsed dye laser (PDL) and the ablative carbon dioxide (CO₂) laser. The PDL causes photothermolysis of hemoglobin, resulting in coagulative necrosis.¹³³ It obliterates small capillaries close to the skin and has had success treating congenital, cutaneous vascular malformations. The CO₂ laser has been used for treatment of acne and recently has been gaining increasing acceptance for its use to treat hypertrophic burn scars.¹³⁴ It works by ablating microscopic columns of tissue to flatten scars and is also believed to stimulate matrix metalloproteinases and other signaling pathways to induce collagen reorganization. Lasers are believed to help with scar remodeling and collagen reorganization. Outpatient and office-based treatment sessions are tolerated well by most patients. There is wide practice variation on when to start therapy and the number of treatments, but the literature has general support for starting treatment at 6 to 12 months and offering three treatments. More research is needed to determine the full potential of laser therapy to provide burn survivors a less invasive treatment of hypertrophic scars with improved symptoms and quality of life.

Psychological rehabilitation is equally important in the burn patient. Depression, posttraumatic stress disorder, concerns about image, and anxiety about returning to society constitute predictable barriers to progress in both the inpatient and outpatient setting. Psychological distress occurs in as many as 34% of burn patients and persists in severity long after discharge.¹³⁵ Despite this, many patients will be able to quickly return to work or school, and goals should be set accordingly. The return to school for pediatric patients is actually very prompt, averaging about 10 days after discharge. However, further study is needed to determine whether attendance and performance suffer despite early re-entry to school.¹³⁶ The involvement of clinical psychologists and psychiatrists is invaluable in providing guidance and coping techniques to lessen the significant psychological burden of burn injury.

Despite many areas of progress in prevention, burns continue to be a common source of injury. Some successful initiatives have included community-based interventions targeting simple home safety measures. Smoke alarms are known to decrease mortality from structural fires, but not all homes are equipped with proper smoke alarms, particularly in low-income households. Mandatory smoke alarm installation via community initiatives can be successful, but seems to be contingent on close long-term follow-up to ensure proper maintenance and function.^137,138 Regulation of hot water heater temperatures has had some success and may be even more effective in conjunction with community-based programs emphasizing education and in-home inspections.^139,140

Interest in mass burn casualty disaster planning invariably includes a discussion of radiation burns. The 1945 nuclear bombing on Hiroshima and Nagasaki provided several important lessons for healthcare providers. First, the proximity to the detonated bomb directly impacted mortality. The fatality rate at 0.6 miles from ground zero was 86%, decreased to 27% at 0.6 to 1.6 miles, and was 2% for patients 1.6 to 3.1 miles away. Over 122,338 individuals died in Hiroshima, and 68,000 of these deaths occurred in the first 20 days. Of the survivors, 79,130 people were injured and 118,613 remain uninjured. Estimates of the injuries at Hiroshima suggest that 90% of patients had burns, 83% sustained traumatic injuries, and 37% had radiation injuries.^141,142

The mechanism of the explosion explains how radioactive material is distributed. A 20-kiloton nuclear device generates 180 mph winds 0.8 miles from the epicenter. The explosion results in a direct pressure wave and an indirect wind drag. The direct pressure can destroy windows and buildings, rupture eardrums, and cause pulmonary contusions, pneumothoraces, and hemothoraces. Radiation travels linearly, resulting in varying degree of burns depending on the distance from ground zero and time of exposure. A fireball at detonation sends radioactive material into the air and follows wind patterns settling to the ground in a predictable pattern. Thermal injuries near ground zero result in 100% fatalities due to incineration.^141,142

Radioactive material results in both acute injury from immediate exposure and more prolonged injury from delayed exposure to radioactive fallout or contamination. When a 10-kiloton nuclear bomb is detonated, people at a distance 0.7 miles from ground zero absorb 4.5 Gy. At 60 days, the medial lethal radiation dose (LD₅₀) is 3.5 Sv; with aggressive medical care, this dose might be doubled to nearly 7 Sv. To put this in context, radiation exposure from a diagnostic CT of the chest or abdomen is 5 mSv, and the average annual background absorbed radiation dose is 3.6 mSv. Radiation is known to impact several organ systems and result in several syndromes based on increasing exposure doses. These syndromes include hematologic (1–8 Sv exposure), gastrointestinal (8–30 Sv exposure), and cardiovascular/neurologic syndromes (>30 Sv exposure), with the latter two being nonsurvivable.^141,142,143

After initial evaluation and decontamination by removing clothing, a useful way to estimate exposure is by determining the time to emesis. Patients who do not experience emesis within 4 hours of exposure are unlikely to have severe clinical effects. Emesis within 2 hours suggests a dose of at least 3 Sv, and emesis within 1 hour suggests at least 4 Sv. The hematologic system follows a similar dose-dependent temporal pattern for predicting radiation exposure, mortality, and treatment. These have been determined based on the Armed Forces Radiobiology Research Institute’s Biodosimetry Assessment Tool, which can be downloaded from www.afrri.usuhs.mil.

The combination of radiation exposure and burn wounds has the potential to increase mortality compared with traditional burns. Early closure of wounds before radiation depletes circulating lymphocytes may be needed for wound healing (which occurs within 48 hours). Also, in radiation injuries combined with burn or trauma, laboratory lymphocyte counts may be unreliable.^{141,142,143,144} A significant difference between burn/traumatic injuries and radiation injures is that burn/traumatic injuries can result in higher mortality when not treated within hours.

Decontamination and triage are vital to maximize the number of survivors. Initial decontamination requires removal of clothing and washing wounds with water. Irrigation fluid should be collected to prevent radiation spread into the water supply. Work by many professional organizations, including the ABA, has focused on nationwide triage for disasters and will be vital to save as many lives as possible. Yet, it is likely that expectant or comfort care could be offered to more patients than typically seen in civilian hospitals, due to resource availability after the disaster.

It has long been anecdotally noted that two patients of similar ages and burn size may have very divergent responses to their burn injuries. Attention is being increasingly turned to identifying genetic differences among burn patients and how they affect response to injury. Specific allele variants have been linked with increased mortality in burned patients.¹⁴⁵ It may be that genetic differences may predispose burn patients to severe sepsis,¹⁴⁶ perhaps by downregulating the immune response.¹⁴⁷ The Inflammation and the Host Response to Injury trial was a prospective, multicenter, federally funded study that aimed to define specific genetic pathways that differ in the response to both burns and traumatic injury.¹⁴⁸ Blood and tissue samples from a strictly defined patient population were analyzed using gene arrays to determine whether differential expression in certain genetic pathways affects clinical outcomes.¹⁴⁹ Although data from this study are still being analyzed, some interesting findings suggest that sepsis, trauma, and burn patients share common gene expression patterns, starting early after injury. These genes can upregulate proinflammatory pathways as well as disrupt antigen presentation pathways. A better understanding of these common genomic responses may allow for the targeted treatment of immunologic and signal pathways to help improve patient survival from burn injuries.

With the dramatic progress in improving survival following a major burn injury during the twentieth century, understanding and addressing functional and psychological outcomes is critical to the well-being of burn survivors. Since 1993, the National Institute of Disability and Rehabilitation Research has funded four burn model systems to identify long-term sequelae of burn injuries and to develop ways to improve outcomes for survivors. Ongoing outcome studies are crucial for dismantling barriers that our patients face in returning to their communities and to the workplace or to school.