Burns

Burn injury historically carried a poor prognosis. With advances in fluid resuscitation and the advent of early excision of the burn wound, 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 psychologic outcomes are equally important as survival alone. With this shift in priority. Because of increased prehospital safety measures, burn patients are transferred longer distances for definitive care at regional burn centers6; data from one burn center with a particularly wide catchment area confirmed that even transport times averaging several
hours did not affect the long-term outcomes of burn patients.

Initial evaluation

Initial evaluation of the burned patient should follow the same initial priorities of all trauma patients and 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 potentially lethal.
Anticipating the need for intubation and establishing an early airway are critical. Signs of impending respiratory compromise include a hoarse voice, wheezing, or stridor; subjective dyspnea is a particularly concerning symptom and should trigger prompt elective endotracheal intubation. Perioral burns and singed nasal hairs alone do not indicate an upper airway injury, but are signs
that the oral cavity and pharynx should be further evaluated for mucosal injury. Orotracheal intubation is the preferred method for securing the airway. Nasotracheal intubation may be useful for patients with associated facial trauma when experienced providers are present, but it should be avoided if oral intubation is safe and easy. 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 and intraosseous (IO) access should be considered when peripheral access cannot be easily obtained. 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 IO access in emergent situations if venous access cannot
be attained. 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 delayed resuscitation. Hypothermia is a common prehospital complication that contributes to resuscitation failure. Patients should be wrapped with clean blankets in transport. Cooling 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 organisms and was abandoned in the mid-1980s. A tetanus booster should be administered in the emergency department depending on patient immunization status.
The importance of pain management for these patients has been widely recognized over the past 25 years. While pain management is a priority for burn patients, it is important to acknowledge the opioid crisis and the recent push toward decreasing opiate use in general. In order to limit opiate-related morbidity, we recommend responsible opiate use in conjunction with mutimodal pain control and development of a weaning plan starting at opioid commencement. Clear expectations around pain medication use should be set with patients. Anxiety is another component of the psychological response of burn patients, seen with both wound care and general postinjury hospital course.
Benzodiazepines are a staple in the treatment of acute anxiety;however, they can contribute significantly to hospital delirium. We recommend conservative benzodiazepine use to mitigate
the effects of anxiety while minimizing deliriogenic effects of benzodiazepines. Most burn resuscitation formulas estimate fluid requirements based on burn size measured as a percentage of TBSA (%TBSA). The “rule of nines” is a crude but quick and effective method of estimating burn size. 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. For smaller or odd-shaped burns, the “rule of the palm” where the palmar surface of the hand, including the digits, is 1% TBSA is useful. Diagrams such as the Lund and Browder chart give a more accurate accounting of the true burn size in children and adults. The importance of an accurate burn size assessment cannot be overemphasized. Superficial or first-degree burns should not be included when calculating burn size, 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.

Burn classification

Burns are commonly classified as thermal, electrical, or chemical burns, with thermal burns consisting of flame, contact, or scald burns. Flame burns are the most common cause for hospital admission of burns, and have the highest mortality. This is primarily related to their association with structural fires and the accompanying inhalation injury and/or CO poisoning. Electrical burns make up 3% of U.S. hospital admissions but have special concerns, including cardiac arrhythmia and
compartment syndrome with concurrent rhabdomyolysis. A baseline ECG is recommended in all patients with an electrical injury, and a normal ECG in a low-voltage injury (<1000 V)
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 symptoms and cataract development are not uncommon with high-voltage electrical injuries, and neurologic and ophthalmologic consultation should be obtained to define baseline patient function.
Chemical burns also comprise 3% of admitted burn patients and result in potentially severe burns. Typically, acid chemical burns result in coagulation necrosis and alkali chemical burns cause liquefactive necrosis (with an exception of hydrofluoric acid, which also causes liquefactive necrosis).

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.
in cases of exposure to dry chemicals, such as concrete or powdered forms of lye, the substance should be swept from the patient to avoid a thermal reaction 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 wounds and IV administration of calcium gluconate for
systemic hypocalcemia symptoms. Intra-arterial calcium gluconate infusion provides effective treatment of progressive tissue injury and intense pain. 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.

Burn depth

Based on the original burn depth classification by Dupuytren in 1832, 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. Fifth-degree burns (through muscle to bone) and sixth degree burns (charring bone) were also described although are less common. 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. 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 full thickness 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 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 nonoperative management, and the majority of deep partial-thickness burns benefit from excision and skin grafting. The outermost area of a burn is called the zone of hyperemia, which will heal with minimal or no scarring and is most like a superficial partial thickness burn 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 burn depth assessment tools have been developed with the idea that earlier burn depth definition 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. Laser Doppler can measure skin perfusion to predict burn depth with sensitivities and specificity of up to 83% and 97%, respectively. Noncontact ultrasound has been postulated as a painless modality to predict nonhealing wounds and has the advantage of easily performed serial measurements.

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.

Prognosis

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 burn size as the strongest predictors of mortality. Advancements in burn care have lowered overall mortality to the point that the original Baux score may no longer be accurate. However, the Revised Baux Score, which accounts for age, burn size, and inhalation injury, has been found to be independently
associated with mortality. As such, age, burn size, and inhalation injury continue to be the most robust indicators for burn mortality. Age even as a single variable strongly predicts mortality in burns, and in-hospital mortality in elderly burn patients is a function of age regardless of other comorbidities. 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. A
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.
A more recent study analyzing 506,628 burn inpatients between 1998 and 2008 demonstrated an association between burn size, age, inhalation injury, and mortality. Other factors associated
with mortality included African American race, female gender, and treatment in urban private hospitals (as opposed to urban academic hospitals). Mortality is not the only outcome of interest in the burn population. Burn injury can significantly impact the subsequent quality of life for survivors, including but not limited to appearance, mobility, functional status, and ability to work. One study
found that burn injury reduces short term quality of life by 30% and long-term quality of life by approximately 11%.35 Predictors of poorer physical and mental health 12 months removed
from burn injury include older age, female gender, and greater %TBSA burn size. One factor impacting quality of life is itching—a late and bothersome consequence of burn injury that
affects both adult and pediatric population. Other factors discussed later in this chapter include hypertrophic scarring, contracture, and heterotopic ossification. Finally, return to work or school has been a useful tool to evaluate recovery and prognosis. A recent meta-analysis found that approximately 28% of burn survivors never return to work. A recent study using an interventional bundle involving the patient, the employee, worker’s compensation, and burn clinic staff demonstrated a return to work rate of 93%. 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 reentry to school.
It is important to recognize these potential quality-of-life issues in burn patients and take necessary steps to diminish the impact that burn injury has on quality of life both in the hospital and
following discharge

Resuscitation

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 per % 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 most recent American Burn Association consensus formula recommends 2 mL/kg per % burn of Lactated
Ringers given the tendency toward excessive fluid administration with the traditional formulas.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, the 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 capillary 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 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 response to therapy. 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 out
put should be 30 mL/h in adults and 1 to 1.5 mL/kg per 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, and others have found that base deficit predicts eventual organ dysfunction and mortality. 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. 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. Actual administrated fluid volumes typically exceed volumes predicted by standard formulas. One survey of burn centers showed that 58% of patients end up getting more fluids than would be predicted by Baxter’s formula. Comparison of modern-day patients with historical controls shows that over
resuscitation may be a relatively recent trend. One theory is that increased opioid analgesic use results in peripheral vasodilation and hypotension and the need for greater volumes of bolused resuscitative fluids. A classic study by Navar et al showed that burned patients with inhalation injury required an average of 5.76 mL/kg per % burn, vs. 3.98 mL/kg per % burn for patients without inhalation injury, and this has been corroborated by subsequent studies. Prolonged mechanical
ventilation may also play a role in increased fluid needs. A 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. 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. A recent meta-analysis accounting for statistical heterogeneity among studies included demonstrated a trend toward mortality benefit for patients receiving albumin. However, albumin use has never been shown to definitively improve mortality in burn
patients and has controversial effects on mortality in critically ill patients. Still, many burn centers including ours continue to use albumin as an adjunct during burn resuscitation. Attempts
to minimize fluid volumes in burn resuscitation have included study of hypertonic solutions. A recent meta-analysis evaluating hyperosmotic vs. isoosmotic fluid resuscitation demonstrates decreased total fluid load (vol/%TBSA per weight) over the first 24 hours with use of hyperosmotic fluid with no difference in total fluid, urine output, creatinine, or mortality. A described downside of hypertonic fluid administration is hyperchloremic acidosis. 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, although no mortality
benefit has been noted thus far in two trials.67,68 Plasmapheresis has also been associated with decreased fluid requirements and increased urine output in patients who require higher resuscita
tive 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. One adjunct that has found increasing utility in surgical ICUs has been the application of bedside ultrasound. 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: parasternal long axis, parasternal short axis, and apical four-chamber views. Whereas no study has used ultrasound to guide fluid resuscitation in burn patients, volume status can be estimated by examination of cardiac function and evaluation of the inferior vena cava (IVC) diameter with changes in respiration, as has been done in patients with hemorrhage and shock. Ultrasound also allows timely diagnosis of pneumothorax. 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 ultrasoundin burned patients. Machine learning and bedside computer decision support are other adjuncts gaining traction in caring for burn patients. These modalities can enhance patient care and aid in diagnosis, treatment, and research. The use of bedside computer decision support has been particularly appealing for resuscitation of burn patients in the first 48 hours and has been shown to improve fluid management during initial resuscitation. the role of blood transfusion in critically injured patients has undergone a reevaluation in recent years. Blood transfusions are considered to be immunomodulatory and potentially immunosuppressive, which is one explanation to the links
between blood transfusions and increased infection and shorter time to recurrence after oncologic surgery. 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.A follow-up study implementing 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. A recent randomized control trial in patients with >20% TBSA compared outcomes of a restrictive to a liberal red blood cell transfusion strategy. There were no differences in blood stream infection, organ dysfunction, ventilator days, time to wound healing, or 30-day mortality betweenboth groups. These data, in concert with other reported compli
cations such as transfusion-related lung injury, 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. Promising animal studies demonstrating
erythropoietin-mediated prevention of secondary burn progression have yet to be validated in humans.

Inhalation injury an ventilator management

Inhalation injuries are commonly seen in tandem with burn injuries and are known to increase mortality in burned patients. Smoke inhalation is present in as many as 35% of hospitalized burn patients and may triple the hospital stay compared to isolated burn injuries. Mortality for inhalation injury has been reported to be as high as 25%, with this increasing to 50% in patients with ≥20% TBSA burns. The pneumonia rate in patients with inhalation injury has been reported to be three
times higher than those without inhalation injury, and it has been associated with increased length of stay, increased ventilator days, and need for tracheostomy. The combination of burns, inhalation injury, and pneumonia increases mortalty by up to 60% over burns alone.93 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. When ARDS complicates burns and inhalationinjury, mortality approaches 66%; in one study, patients with burns ≥60% TBSA in combination with inhalation injury and ARDS had 100% mortality. 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 compliance and increases airway resistance work of breathing. Inhalation injury in the presence of burns also increases overall metabolic demands. 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. The
Abbreviated Injury Score—a scale from 0 to 4, with 0 representing no injury and 4 representing massive injury—is commonly used for grading inhalation injury. Higher grades of bronchoscopic
inhalation injury have been associated with increased incidence of ARDS, increased ventilator days, higher rate of multiple organ dysfunction syndrome, and higher mortality. Bronchoscopic evaluation can also help isolate organisms early in the course of a potential pneumonia. Bronchoalveolar lavage (BAL) within 24 hours after an inhalation injury. demonstrates a high rate of positive quantitative cultures, suggesting that pneumonia develops soon after the acute lung injury. Bacterial contamination from urgent intubation may contribute to early development of pneumonia in patients with inhalation injury. Early evaluation with bronchoscopy can identify causative organisms and
guide appropriate antibiotic therapy. Because bronchoscopy is an invasive test, attempts have
been made to utilize other diagnostic modalities, such as thoracic computed tomography (CT) scans and xenon ventilation-perfusion scanning. However, these are generally not utilized unless otherwise indicated, and the best tools available for diagnosing inhalation injury remain clinical presentation and bronchoscopic evaluation. Decreased PaO2: FiO2ratio (<350) on admission may not only predict inhalation injury but also indicate increased fluid needs more accurately than bronchoscopic grading of the severity of inhalation. 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 and has been associated with increased number of ventilator-free days. A recent meta analysis demonstrated improved mortality with the use of inhaled anticoagulation regimens. Aerosolized tissue plasminogen
activator and recombinant human antithrombin 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. Inhaled nitric oxide may also be useful as a last effort in burn patients with severe lung injury who are failing other means of ventilator support. The use of steroids has traditionally been avoided due to the worse outcomes in
burn patients; however, some data demonstrate selectively improved outcomes with septic shock requiring vasopressor circulatory. An important contributor to early mortality in burn patients
and often seen in patients with inhalation injury is carbon monoxide (CO) poisoning. This clear, odorless gas has an affinity for hemoglobin is approximately 200 to 250 times more than
that of oxygen. Carboxyhemoglobin decreases the levels of normal oxygenated hemoglobin and can quickly lead to anoxia and death. CO also causes uncoupling of oxidative phosphorylation in mitochondria, free radical generation, and increased systemic inflammatory response via platelet activation—all of which may increase cardiac and neurologic morbidity and mortality in CO toxicity. Unexpected neurologic or cardiac 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% normobaric oxygen is the gold standard for treating CO poisoning and
reduces the half-life of CO from 250 minutes in room air to 40 to 60 minutes. Some authors have proposed hyperbaric oxygen as an adjunctive therapy for CO poisoning. However, a recent meta-analysis offers mixed results regarding the success and long-term outcomes of hyperbaric oxygen, and its associated logistical difficulties and complications have limited its usefulness for patients with moderate or large burns. 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.
Hydrogen cyanide toxicity may also be a component of an overwhelming smoke inhalation injury. Cyanide inhibits cytochrome oxidase, which is required for oxidative phosphorylation. Afflicted patients may have a persistent, severe lactic acidosis, neurologic symptoms, pulmonary edema, or cardiac sequelae (ST elevation on electrocardiogram). Classic signs of cyanide poisoning—including bitter almond breath and cherry red skin changes—are rare and should not be used as the sole
diagnostic criteria. Treatment consists of sodium thiosulfate, hydroxocobalamin, and 100% oxygen. Sodium thiosulfate works as a substrate for the metabolism cyanide into a nontoxic derivative, but it works slowly and is not effective for acute therapy. Hydroxocobalamin—a vitamin B12 precursor—quickly complexes with cyanide, is excreted by the kidney, and is recommended for immediate therapy. In the majority of patients, lactic acidosis will resolve with ventilation, and sodium thiosulfate treatment becomes unnecessary. Given the unknown side-effects of hydroxocobalamin administration, it should be reserved only for patients with a strong suspicion of cyanide poisoning.
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. 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)124 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. In patients with refractory hypoxemia despite lung-protective ventilation, prone positioning may improve oxygenation and mortality. No specific studies have examined prone positioning in burned patients, and in fact exclusion criteria from a large prone positioning trial included patients with ≥20% TBSA.127 Select reports demonstrate the feasibility of prone positioning in burn patients, although they present logistical challenges and caution must be used in patients
with frontal and facial burns who are already at risk for loss of the grafts, invasive catheters, and the endotracheal tube. High-frequency percussive ventilation (HFPV) has shown early promise in patients with inhalation injury. One study showed notable decreases in both morbidity and mortality with HFPV, especially in patients with burns <40% TBSA and inhalation injury. A randomized controlled trial between low-tidal volume ventilation and HFPV in burn patients requiring mechanical ventilation demonstrated no significant difference in primary clinical outcomes. A related technique is high-frequency oscillatory ventilation (HFOV), which has been used primarily as a salvage modality in patients refractory to more conventionalmeasures.132 However, two recent studies and a recent meta-analysis have concluded that HFOV yields no mortality benefit and in fact may actually increase patient mortality in patients with ARDS. Extracorporeal membrane oxygenation (ECMO) is typically reserved for salvage situations, although utilization of ECMO for burn patients is increasing and out comes have been shown to be similar to other ECMO patients

Treatment of the burn wound

Multitudes of topical therapies exist for the treatment of burn wounds, many of which contain antimicrobial properties. A recent Cochrane Database Review nicely summarizes the data surrounding antisepsis for burns; however, much of the data is inconclusive. 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, being easily applied, and having 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 following burn injury. 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. As mafenide is a carbonic anhydrase inhibitor, a historically described side effect is metabolic acidosis. However, multiple studies have been performed using mafenide to treat burn wounds without any significant incidence of metabolic
acidosis. 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. Although there is no definitive evidence regarding use in the burn population, Dakin’s solution (0.5% sodium hypochlorite solution) is an acceptable alternative 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. Recent media coverage of 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 are increasingly being used for donor sites, skin grafts, and partial-thickness burns because of their potential to avoid daily dressing changes. These may be more comfortable for the patient, reduce the number of dressing changes, and shorten hospital length of stay, but they limit serial wound examinations. Biologic membranes such as Biobrane (Smith & Nephew Global Products) 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.

Nutrition

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%. This can lead to catabolism of muscle proteins and decreased lean body mass that may delay functional recovery. Early enteral