Burns

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Burns

Over the past several decades, burn-related hospital admissions and deaths have decreased by 50% in large part due to advancements in burn care, introduction of topical antimicrobial agents, and a better understanding of fluid resuscitation and aggressive surgical management.13 Despite these advances, nearly 100,000 children age 14 years and under were treated for burns in hospital emergency rooms in 2007. Of these, 20% occurred in children less than 4 years old.4 Thus, burns remain a leading cause of morbidity and mortality in children. Optimal management requires a team of health care providers, therapists, and social workers.

Pathophysiology

Skin is a complex, multilayer organ with a surface area ranging from 0.2–0.3 m2 in the newborn to 1.5–2.0 m2 in the adult. An understanding of its basic structure and regenerating ability is critical to burn management. The skin provides protection, participates in thermoregulation and vitamin D production, and is involved in sensation. The epidermis is the avascular and aneural superficial layer made up of keratinocytes (95%), melanocytes, Langerhans cells, and Merkel cells. Desquamation of cells formed at the basal layer takes 2 to 4 weeks. The entire epidermis is replaced by new cells every 48 days. The dermis has a deep reticular layer and a superficial papillary region that are connected to the epidermis via the basement membrane. Composed primarily of collagen and elastin from fibroblasts, the dermis provides support for the skin.

The mechanism of any burn plays an important role in how deep and severe the injury will extend as well as how it is treated. The extent of injury is determined by the temperature, duration of exposure, skin thickness, and specific heat of the causative agent. Grease burns result in deeper injury than water of the same temperature, since lipid has a higher specific heat. Scald burns constitute 70% of pediatric burns with the majority occurring in toddlers. Whether due to spilling hot drinks or hot tap water, they tend to be superficial dermal burns. Flame burns are more common in adolescents and can result in deep injury. Contact burns are also common in children and may be caused by touching a hot oven door, an iron, or even hot pavement.

In 1953, Jackson described the zones of burn injury that remain important to the understanding and management of burns today (Fig. 13-1).5 The zone of coagulation occurs at the site of maximal damage and is defined by irreversible tissue loss due to protein coagulation. The zone of stasis surrounds this area and has decreased tissue perfusion, but remains salvageable with aggressive resuscitation. Outside the zone of stasis is the zone of hyperemia where tissue perfusion is increased and often survives unless faced with infection or hypotension.

The systemic response to burn injury is mediated by the release of inflammatory mediators such as thromboxane A2, bradyknin, oxidants, and cytokines which can impair flow to the zone of stasis through thrombosis, vasoconstriction, and capillary blockage.6 The administration of antioxidants, bradykinin antagonists, and thromboxane A2 inhibitors can improve blood flow and mitigate injury.79 In addition, the administration of β-glucan, through its immunomodulatory effects, antioxidant properties, and ability to reduce the inflammatory response, has been shown to improve re-epithelialization in a rat model of burn injury.10

The systemic effects of burn injury extend beyond these three zones and can potentially lead to multiorgan dysfunction. The cardiovascular system can experience myocardial depression and hypovolemia. Pulmonary vasoconstriction and edema lead to respiratory failure.11 Splanchnic vasoconstriction can result in gut dysmotility and malabsorption by causing epithelial apoptosis and decreased epithelial proliferation.1214 This results in atrophy of small bowel mucosa, increased intestinal permeability, bacterial translocation, and sepsis.15 Splanchnic vasoconstriction and activation of stress-induced hormones and mediators, such as angiotensin, aldosterone, and vasopressin, leads to a decrease in renal perfusion that can lead to oliguria.16 When unrecognized, this can progress to acute tubular necrosis, renal failure, and, ultimately, death.17,18 Finally, there is a systemic decrease in immune function due to impaired production and function of neutrophils, macrophages and T-lymphocytes, placing the patient at risk for infectious complications.19,20

Initial Management

The majority of pediatric burns are minor, often resulting from scald accidents and affecting less than 10% total body surface area (TBSA), or from thermal injuries isolated to the hands. Such burns are usually limited to partial-thickness injury of the skin and can be managed on an outpatient basis, which is beyond the scope of this chapter. Unfortunately, larger burns require inpatient treatment and special attention. The initial step is completion of the primary and secondary surveys.21 Issues with airway, breathing, and circulation should be addressed immediately. Signs and symptoms including increased respiratory effort, wheezing, stridor, and tachypnea should raise concern for impending loss of the airway. The decision to intubate a patient with a tenuous airway should be made early. Inhalation injury can result in edema that may worsen over the first few hours, so repeated evaluations of the airway are important. Burn injuries can have a negative effect on breathing mechanics through smoke inhalation, a blast injury causing blunt chest trauma, and the restrictive effects of a burn eschar that limits full chest expansion. Escharotomy should be performed for the latter. Patients need support with 100% supplemental oxygen. If inhalation injury is suspected, arterial blood gas analysis and carboxyhemoglobin level are needed. Two large bore IVs should be placed and aggressive fluid resuscitation is important. When extremity burns limit peripheral IV access or if there is difficulty obtaining central venous access, intraosseus access should be utilized as a temporary (<24 hours) alternate route for fluid administration. A urinary catheter should be inserted, and heart rate, blood pressure and urine output should be monitored as tachycardia and low urine output signal a low intravascular volume state.

The source of thermal injury needs to be removed from the patient as quickly as possible, even during the primary survey, if not done before. Active cooling may limit the depth of the burn but can result in hypothermia. Chemicals need to be removed from the skin and the area should be thoroughly irrigated with water. Neutralization of chemicals is not needed and may produce additional heat that could lead to a deeper burn. Care should be taken to keep the patient warm as the risk of hypothermia increases with increasing burn area.

A decision should be made after initial evaluation, resuscitation, and wound dressing as to whether or not the patient needs to be transferred to a burn center. The American Burn Association and American College of Surgeons have clear recommendation regarding which patients should be referred to these centers (Box 13-1).22 However, a recent study raises concern that resources are often wasted by transferring less severe injuries to burn centers.23

There are several techniques to estimate the TBSA of the burn. The Wallace rule of nines estimates burn area fairly well for adolescents. Each upper extremity and the head represent 9% of the TBSA. The lower extremities and the anterior and posterior trunks are 18% each. The perineum, genitalia, and neck each measures 1%. Due to differences in body proportions for infants and children, the rule of nines has been modified to more accurately determine burn area in these patients. In this modification, the head represents 18% of the TBSA and each leg is 13.5%. Other modifications have been proposed to better estimate TBSA burn in obese patients.24 The Lund and Browder chart may provide more accurate determination of burn area in children as it compensates for variations in body shape and proportions (Fig. 13-2). For a rapid estimation of burn size, the palmar method can be used. The palmar surface is approximately 1% of the TBSA and is best used for estimating small surface area burns. First-degree burns should not be included in burn size calculations using any of these techniques. A recent study found that estimates of burn area are inaccurate in approximately 80% of children with the majority being overestimated.25 The authors concluded that this may be due to the variety of techniques used, or inclusion of first-degree burns in the calculation. This can also lead to unnecessary transfer of patients to burn care centers as discussed previously.

A key component to the initial management of the severely burned patient includes escharotomy when indicated (Fig. 13-3). Full-thickness circumferential burns on the extremities can produce a constricting eschar which, together with the associated edema, can impede venous outflow and impair arterial flow. If pulses are absent, a bedside escharotomy should be performed with a scalpel or electrocautery along the lateral and medial aspects of the affected extremity. Incisions can be carried onto the hypothenar and thenar eminences and dorsolateral aspects of the digits if the hands or fingers are involved (Fig. 13-4). The resulting ischemia reperfusion injury and edema can cause significant increases in fascial compartment pressures. Although rare, fasciotomy may be necessary to relieve pressure and prevent necrosis of the underlying muscles and neurovascular bundles.

Fluid Resuscitation

Once adequate intravenous or intraosseous access is obtained, fluid resuscitation is initiated. There are several formulas available to guide this resuscitation (Table 13-1). The Parkland formula is the most widely used, but is not as applicable in young children because children have greater TBSA relative to their body weight than adults. As a result, weight-based formulas can under-resuscitate children with minor burns and can grossly over-resuscitate children with extensive burns.26 TBSA-based formulas, such as the Shriners–Galveston formula, are therefore better at estimating fluid requirements in children less than 20 kg.27 TBSA is assessed from height and weight using standard nomograms or calculated using formulas (Table 13-2). Dextrose-containing solutions, such as 5% dextrose with 0.25 to 0.5 normal saline, are used as the primary solution. Children younger than 2 years of age are susceptible to hypoglycemia due to limited glycogen stores. Therefore, lactated Ringer’s solution with 5% dextrose is given during the first 24 hours in these patients.

TABLE 13-1

Burn Resuscitation Formulas

Formula First 24 Hours Fluid Solution
Parkland 4 mL/kg per %TBSA burn Lactated Ringer’s (LR)
Brooke 1.5 mL/kg per %TBSA burn LR + colloid 0.5 mL/kg per %TBSA burn
Shriners–Galveston 5000 mL/m2 burned + 2000 mL/m2 total LR + 12.5 g albumin

TBSA, total body surface area

TABLE 13-2

Formulas for Body Surface Area (BSA)

Dubois Formula BSA (m2) = height (cm)0.725 × weight (kg)0.425 × 0.007184
Jacobson Formula BSA (m2) = [height (cm) + weight (kg) − 60]/100

Regardless of which formula is utilized, there must be close monitoring of the patient’s physiologic response to the fluid administration. Urine output should be maintained at 1 mL/kg/h. Inadequate resuscitation can result in hypoperfusion to the zone of stasis, with subsequent deepening of the burn, as well as hypoperfusion of major organs. During the first six to 12 hours, capillary permeability is increased and fluid moves from the intravascular space to the interstitial tissues with worsening edema. Overly aggressive fluid administration can result in significant tissue edema, tissue hypoxia, and elevated compartment pressures.28

Several authors have shown that the addition of colloid solutions such as albumin can reduce crystalloid requirements and more rapidly establish a balanced fluid intake to output ratio.29,30 However, a 2011 Cochrane database review found that albumin does not lower mortality in adults with major burns.31 Thus, the benefit of the more expensive albumin instead of standard crystalloid solutions is questionable. Other solutions, such as hypertonic saline, have been used in an effort to provide a high osmotic pressure which is thought to keep more volume in the intravascular space. Hypertonic saline also may have anti-inflammatory effects. However, it should be used with caution as it causes hypernatremia, and has not been shown to improve outcomes for hypotensive trauma patients.32

Unlike adults, children do not show hemodynamic changes reflecting hypovolemia until they are significantly volume depleted. Tachycardia may be a sign of compensation for a low volume state or stress response to injury. Signs of inadequate perfusion include lethargy and decreased capillary refill with cool, clammy extremities. Laboratory tests should be performed along with serial clinical exams to follow the response to resuscitation. Resolving acidosis, for example, may serve as an objective marker of improvement. Hyponatremia is a frequent complication in pediatric burn patients after aggressive fluid resuscitation, and correction is required to avoid severe electrolyte imbalance.

An increased incidence of pneumonia, bloodstream infection, acute respiratory distress syndrome (ARDS), multiple-organ failure, and death may be associated with over-resuscitation during the first 24 hours postburn.33 Interestingly, ‘permissive hypovolemia’ helps avoid these complications and has been shown to decrease multiple-organ dysfunction.34

Inhalation Injury

While inhalation injury is less common in children than adults, the mortality increases to nearly 40% when it occurs.35 The heat of inhaled gas causes upper airway injury. Inhaled toxins can result in upper airway injury in addition to causing tracheobronchial irritation and bronchoconstriction. Damaged epithelium releases vasoactive substances (thromboxanes A2, C3a, and C5a) that lead to hypoxia, increased airway resistance, decreased pulmonary compliance, increased alveolar epithelial permeability, and increased pulmonary vascular resistance.36 Carbon monoxide (CO) is produced during combustion and can contribute to the inhalational injury by displacing oxygen from hemoglobin-binding sites. The oxyhemoglobin dissociation curve is shifted to the left as the ability of hemoglobin to unload oxygen in the tissues is decreased. Secondary injury is due to impaired ciliary clearance of airway debris. Neutrophil infiltration occurs, macrophages are destroyed, and bacteria accumulate leading to pneumonia.

An inhalation injury should be recognized early through a detailed history of the burn and the initial evaluation. On examination, patients may be found to have facial burns, singed hairs in the nose, eyebrows or head, and/or carbonaceous sputum. Patients with inhalation injury who are obtunded are likely to have a carboxyhemoglobin level greater than 10%. Additional signs of significant injury are an altered voice along with hoarseness and stridor. Airway security in these patients is imperative. Fiberoptic bronchoscopy continues to be the preferred technique for documenting inhalation injury. Inflammatory changes in the tracheal mucosa such as edema, hyperemia, mucosal ulceration, and sloughing can be visualized. A ventilation scan with xenon-133 can also identify regions of inhalation injury by assessing respiratory exchange and excretion of xenon-133 from the lungs.37 When combined, bronchoscopy and xenon-133 scanning are over 90% accurate in the diagnosis of inhalation injury. However, the clinical applicability of xenon-133 scans remains unclear due to false positives in children with pulmonary disease.38,39 They may also be potentially dangerous due to the need to transport a critically ill burn patient to a nuclear medicine suite. Chest radiographs are not useful as they are often normal immediately following injury.38,40 Bedside bronchoscopy and a heightened clinical suspicion remain paramount in the diagnosis and treatment of these injuries.

After the airway is secured, an inhalation treatment protocol is utilized in the intensive care unit that focuses on the clearance of secretions and control of bronchospasm. One hundred per cent high flow, humidified oxygen should be administered to displace CO from hemoglobin. Early and aggressive pulmonary therapy consisting of chest physiotherapy, frequent suctioning, and early mobilization of the patient should be started. Bronchodilators and racemic epinephrine are used to treat bronchospasm. Clearance of secretions can be assisted with inhalation treatments composed of heparin and acetylcysteine. Human autopsy and animal models have shown nebulized heparin (5000–10,000 units/3 mL of NS q5 hours) to reduce tracheobronchial cast formation improves minute ventilation and decreases peak inspiratory pressures after smoke inhalation.4143 The addition of 20% acetylcysteine (3 mL q4 hours) also improves the clearance of tracheobronchial secretions and minimizes bronchospasm. Pediatric and adult studies have shown this combination of medications to decrease reintubation rates and reduce mortality.4446

Assessment of Burn Depth

Burn injury may involve one or both layers of the skin and may even extend to the subcutaneous fat, muscle, and bone.47 First-degree burns involve the epidermis. They are erythematous and very painful. Most sunburns fit this category of superficial, epidermal injury. For first-degree burns, topical ointments may be used for symptom relief and the involved areas should be kept out of the sunlight.

Superficial second-degree burns (superficial dermal burns) extend into the papillary dermis. They characteristically form blisters, but these blisters may not immediately follow the injury, making determination of depth difficult (Fig. 13-5). These wounds are painful when uncovered. The wound blanches with pressure due to increased vascularity secondary to vasodilatation. Superficial second-degree burns are managed with daily dressing changes with topical antimicrobials. They may also be treated with application of petroleum gauze or a synthetic dressing to allow for rapid spontaneous re-epithelialization. With appropriate care, these wounds will heal spontaneously within two to three weeks without the need for excision and grafting.

Deep second-degree burns (deep dermal burns) extend into the reticular dermis and healing takes several weeks. These burns also blister, but the surface of the wound remains mottled and white (Fig. 13-6). Blanching occurs very slowly. Patients complain of pressure and discomfort rather than pain. These burns will require operative treatment if healing does not occur by 3 weeks.

Third-degree or full-thickness burns involve the entire dermis and extend into the subcutaneous tissue. These appear charred, leathery, and firm (Fig. 13-7). Patients typically are insensate in the burned regions and may not feel pressure. Blanching does not occur when pressure is applied. Full-thickness injuries should be excised and grafted early.48

Determination of burn wound depth can sometimes be difficult. Initial evaluation by an experienced surgeon as to whether an indeterminate dermal burn will heal in three weeks is only about 50–70% accurate.4951 Scald injuries are particularly difficult to assess for depth and extent of injury. A number of techniques or tools have been described to improve accuracy. These techniques utilize the physiology of the skin and the alterations that occur with burn injury. Detection of dead cells or denatured collagen using ultrasound, biopsy, or vital dyes has been trialed.5255 Other technologies such as analyzing altered blood flow using fluorescein, laser doppler imaging, and thermography have shown some promise.5658 Unfortunately, many of these techniques have not been adopted due to variable reproducibility. Laser Doppler imaging has been shown to increase the accuracy of burn depth assessment when compared with experienced burn surgeons.59 Videomicroscopy has also been found to be accurate, especially when used after the first 24 hours.60 This technique is relatively inexpensive and easy to learn.

Wound Care

Most partial-thickness burns can be managed nonoperatively for ten to 14 days with topical therapies and dressings. Using this strategy, the goal of burn care is to provide an optimal environment for re-epithelialization by providing a warm and moist environment, removal of exudate and potentially contaminated or necrotic material (eschar), and control of bacterial proliferation. Burns should be excised and grafted if there are no signs of healing by three weeks. Desai et al confirmed the validity of this strategy with scald injuries in a randomized trial.61

Antimicrobial agents

The initial treatment of partial-thickness burns is debridement and coverage with a topical agent that has antibacterial properties and allows for separation of the burn eschar.6264 Various topical antimicrobial agents have been used (Table 13-3). These agents decrease bacterial content, but they do not eradicate or prevent colonization. In general, quantitative wound biopsy cultures that exceed 100,000 organisms per gram are consistent with, although not diagnostic of, invasive infection.

Silver sulfadiazine (Silvadene, Monarch Pharmaceuticals Inc., Bristol, TN) is currently the most commonly used topical antimicrobial agent for burn care. It is a white, highly insoluble compound synthesized from silver nitrate and sodium sulfadiazine.65 It has a broad spectrum of efficacy including Staphylococcus aureus, Escherichia coli, Klebsiella, Pseudomonas, and Proteus species. It also possesses an analgesic effect but does not penetrate eschar well. The combination of silver sulfadiazine with nystatin has significantly reduced the incidence of Candida infection in burned patients.66 The most common side effect from silver sulfadiazine is leukopenia which is caused by margination of leukocytes and is usually transient.67 It occurs somewhere between 5–15% of patients treated.68 Changing to another topical antimicrobial agent usually resolves this side effect.

Mafenide acetate (Sulfamylon, UDC Laboratories, Inc, Rockford IL) was introduced as a topical burn agent in the mid-1960s. It is more effective in penetrating eschar and is frequently used in third-degree burns. It has broad activity against most Gram-negative and Gram-positive pathogens, but unfortunately has minimal antifungal activity.69 The application of Sulfamylon can be painful which limits its practical use in the outpatient setting. Sulfamylon is a potent carbonic anhydrase inhibitor and can therefore cause metabolic acidosis.70 This side effect can usually be avoided by limiting its use to only 20% TBSA at any given time, and rotating application sites every several hours with another topical antimicrobial agent.

Silver nitrate (0.5%) was also introduced in the mid-1960s. It is typically used to soak gauze dressings thereby avoiding frequent dressing changes with the potential loss of grafts or healing cells. Silver nitrate is painless on application and has broad coverage. Unfortunately, the compound can cause hyponatremia and hypochloremia while also creating dark gray or black stains. Another important but infrequent complication is methemoglobinemia, which occurs as a result of nitrate reduction by wound bacteria followed by the systemic absorption of the toxic nitrite. Dressings containing biologically active silver ions (Aquacel, ConvaTec Ltd., UK; Acticoat, Smith & Nephew, London, UK) hold promise for retaining the effectiveness of silver nitrate but without its side effects. Several favorable clinical trials utilizing these products have been conducted and have found these products to be as effective as traditional dressings utilizing silver nitrate. The products were also noted to be less painful than traditional dressings when applied and removed, and also were associated with decreased burn wound cellulitis.7173

Facial burns, small areas of partial-thickness burns, and healing donor sites require special mention. On superficial facial wounds, silver sulfadiazine may retard epithelialization and is not usually placed on the face.74 An alternative is petroleum-based antimicrobial ointments. These include polymyxin B, bacitracin, and polysporin. Their application is painless and transparent which allows for easier monitoring. These agents are mostly effective against Gram-positive organisms.

Proteolytic enzymatic agents have been utilized to debride wounds, including proteases (sultilains) elaborated from Bacillus subtilis, collagenase, and papaine-urea. Collagen is a protein that is found normally in skin (~75% of dry weight of skin) and is the dominant protein that must be lysed to allow for eschar separation. Collagenase is an exogenous enzyme that breaks down denatured collagen but does not lyse healthy, normal collagen. Collagenase Santyl ointment (Healthpoint Biotherapeutics, Fort Worth, TX) is used in many burn units for the treatment of partial-thickness burns. A multicenter trial of 79 patients ranging in age from 5 to 60 years suggested a slight acceleration of wound closure compared to silver sulfadiazine.75 A recent prospective randomized study in children comparing collagenase to silver sulfadiazine showed equivalent outcomes with regards to skin graft rates, hospitalization, and hospital charges.76

Burn Wound Dressings

The concept of an ‘optimal environment’ is derived from the work carried out by Winter in 1962.77 In young pigs, he found that partial-thickness wounds that were kept moistened with polyethylene film epithelialized twice as fast as those left exposed to air. Hinman and Maiback confirmed this observation with a series of human volunteers.78 Therefore, for 50 years, it has been felt that a burn dressing should provide an ‘optimal environment’ while also possessing bacterial inhibition. Typically, burn dressings consist of mesh that either contains or are placed over antimicrobial compounds. Nonadherent dressings such as Telfa (Tyco Healthcare Group LP, Mansfield, MA), Xeroform (Tyco Healthcare Group LP, Mansfield, MA), Adaptic (Johnson & Johnson, New Brunswick, NJ), or Mepitel (Molnlycke Health Care AB Gothenburg, Sweden) can be placed directly on the wound to help reduce both the pain associated with dressing changes and the friction associated damage to the wound or skin graft. The nonadherent dressing and antimicrobial compound serve to provide the ‘optimal environment’ for re-epithelialization.

Further advancements with burn dressings have recently led to a number of synthetic mesh products designed to adhere to wounds until epithelialization has occurred. The benefits of these dressings include less pain related to fewer dressing changes. These dressings are very effective for superficial partial-thickness wounds. Deep wounds and those with excessive drainage do not allow adherence, and therefore, negate the benefits of these synthetic dressings.

An example of a synthetic mesh product is Biobrane (UCL Laboratories, Rockford IL). It is a bilaminate thin membrane composed of thin semipermeable silicone bonded to a layer of nylon mesh, which is coated with a monomolecular layer of type I collagen of porcine origin. This dressing provides a hydrophilic coating for fibrin ingrowth which promotes wound adherence. The dressing is placed on a clean fresh superficial second-degree burn wound and can be secured using steri-strips and/or bandages. This dressing is easily removed from the wound bed as the wound epithelializes underneath it. Fluid can accumulate under the dressing and can be aspirated if needed. However, if a foul-smelling exudate is detected, the Biobrane should be removed and an antimicrobial dressing applied. Biobrane is now widely used in the management of superficial second-degree burns as it reduces pain, fluid, and electrolyte loss. These advantages make it an ideal dressing for use in the outpatient setting.79

Dressings that are commonly utilized for coverage of postoperative incisions may also be used as small superficial second-degree burn dressings. These alternatives include Duoderm (ER Squibb & Sons, Inc. Princeton NJ), Opsite (Smith & Nephew, London, UK), and Tegaderm (3M Pharmaceuticals, St Paul MN). Despite lacking special biological factors (collagen and growth factors), these dressings provide a cheap and transparent alternative to more expensive dressings. Also, Duoderm has been found to be less expensive than Biobrane and therefore could be a first-line treatment option for intermediate thickness burn wounds in children.80

The disfigurement resulting from full-thickness burns has been decreased with the advent of combined synthetic and biologic materials. Integra (Integra LifeSciences Corp, Plainsboro NJ) has an inner layer composed of a porous matrix of bovine collagen and the glycosaminoglycan chrondroitin-6-sulfate which facilitates fibrovascular ingrowth.81 The outer layer is a polysiloxane polymer with vapor transmission characteristics similar to normal epithelium. Integra acts as a dermal replacement. It provides a matrix for the infiltration of fibroblasts, macrophages, lymphocytes, and capillaries from the wound bed, and promotes rapid neo-dermis formation. Approximately two weeks after engraftment, the outer silicone layer is removed and is replaced with an epidermal split thickness autograft (Fig. 13-8). Integra covered wounds have less scarring, but are susceptible to infection and must be monitored carefully. Its advantages were validated in a randomized study in children with large TBSA burns.82 Children treated with Integra demonstrated significantly decreased resting energy expenditure as well as increased bone mineral content and density. Also, improved scarring was found at 24 months after burn injury.

Biological dressings include xenografts from swine and allografts from cadaver donors, such as Alloderm (LifeCell Corp., Branchburg, NJ). They are especially useful for coverage of large full-thickness burns. The dressings are eventually rejected by the patient’s immune system and slough. The wound beds become excellent recipient beds for subsequent autografts. Although extremely rare, the transmission of viral diseases from the allograft is a potential concern. These dressings are useful adjuncts when autografts are not available or time is needed for donor sites to heal before being used again for grafting.

Excision and Grafting

Prompt burn excision and grafting has been shown to improve survival, decrease length of hospitalization, and reduce costs in burn patients of all ages. Children particularly have benefited from more timely and extensive operative management.8186 Once a burn is considered ‘deep’ or fails to heal with topical care, tangential excision is needed. This technique was originally described by Janzekovic in 1970.87 The eschar is sequentially shaved using a dermatome, knife blade or, more recently, a Versajet (Smith & Nephew, Inc., London, UK) water dissector until a viable tissue bed is obtained.88 In a prospective randomized trial, the Versajet technique was shown to produce a more precise and faster excision than hand-held dermatome escharectomy.89

After excision, coverage is ideally completed with an autograph. Split-thickness autografts (0.008–0.010 inch thickness) are harvested and utilized as a sheet (unmeshed) or meshed graft. Sheet grafts provide better long-term aesthetic outcomes, but are complicated by the development of a seroma or hematoma and also limited coverage. Narrow meshed autografts (1 : 1 or 1 : 2) have the advantages of limiting the total surface area of donor harvest and allowing better drainage of fluid under the grafted sites. In larger burns (>20–30%), coverage may require a combination of meshed autograft and allografts. The meshed autografts (4 : 1 to 6 : 1) can be covered with meshed allograft (2 : 1) overlays.90 Alternatively, grafting with sequential harvesting of split-thickness autograft from limited donor sites until the entire burn wound is covered may be needed. The use of a widely meshed graft is avoided on the face and functionally important parts of the hand. Full-thickness grafts that include both dermal and epidermal components are commonly obtained from the lower abdomen, groin, or upper arm. These grafts provide the best outcome for wound coverage with diminished contracture and a better pigment match, but their use is generally limited due to the lack of donor sites.

Nonthermal Injuries

Chemical Burns

Cleaning products pose a risk for accidental exposure and chemical burns. The chemical agent responsible for the injury should be identified. Contacting poison control is often necessary. During the initial evaluation, all caustic material should be flushed from the skin with copious amounts of water. Chemicals are classified as either alkali or acid. Alkalis, such as lime, potassium hydroxide, sodium hydroxide, and bleach are the common agents involved in chemical injury and cause liquification necrosis in deep burns. Acid burns are less common and cause coagulation necrosis. Formic acid injuries are rare but can result in multiple systemic organ failure with metabolic acidosis, renal failure, intravascular hemolysis, and ARDS. Hydrofluoric acid burns are managed with copious water irrigation and neutralization of the fluoride ion using topical 2.5% calcium gluconate gel. Without this management, free fluoride ion causes liquefaction necrosis of the affected soft tissues, including bones. Because of potential hypocalcemia, patients should be closely monitored for prolonged QT intervals.

Electrical Burns

Three to 9% of all admitted burn patients are injured from electrical contact.91 Electrical burns are categorized into low- and high-voltage injuries. Low voltage (<1000 V) injuries typically occur at home where electrical cords are bitten especially by younger children (Fig. 13-9). High-voltage (>1000 V) injuries may result from power lines or lightning strikes, and are characterized by a varying degree of local burn with destruction of deep tissues.92 The electrical current enters the body and travels preferentially through the low resistance tissues (nerves, blood vessels, and muscles). As skin has high resistance, it is mostly spared leaving little visible evidence of injury. Primary and secondary surveys, including electrocardiography, are very important. If the initial electrocardiogram is normal, further cardiac monitoring is not needed. However, any abnormal findings require continued monitoring for 48 hours and appropriate management of dysrhythmias if detected.93 Injuries to deep tissues and organs must be identified and treated. As tissue edema worsens, patients may develop compartment syndromes requiring fasciotomy to avoid limb loss. Myoglobinuria can lead to renal failure and should be treated with vigorous hydration with sodium bicarbonate and mannitol. Low-voltage injury is typically limited to superficial thermal burn and can be treated with topical wound care.

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