Special Interest Topics
Burn and Other Exposure Injuries
Man’s primitive fascination with fire has led to affliction with burn injuries since the dawn of our history. Therapy has evolved from the application of mud and excrement in Egyptian times, to dressings impregnated with pig fat and resin in the Roman era, to the emergence of a relatively modern concept of first aid from the military battlefield.1 Still today, burn injuries and their sequelae represent one of the most potentially devastating and challenging conditions in medicine. Over one million burns occur annually in the United States, with the majority being treated in an outpatient setting. Children up to 4 years of age and working age adults comprise nearly 90% of patients with burn injuries. Injuries to children largely involve scald injuries whereas flame burns are predominant in the working age population.2 Presentation may vary considerably, from simple sunburns requiring no more than counseling and a topical agent to extensive tissue loss resulting in multi-organ system failure and a protracted ICU course. In more serious cases, it is imperative that burn care extend far beyond the initial insult. Burns can significantly alter quality of life and are a common cause of disability. Debilitating contractures and cosmetically unacceptable scars may have long-lasting physical and psychological consequences, requiring continued physician involvement and support.
Burns occur via numerous etiologic insults and may damage the skin and appendageal structures at various depths. Skin may be harmed by contact with heat, noxious chemicals, and/or electrical current.
With the exception of minor injuries, all burn patients should be treated as trauma patients. Initial evaluation should assess life-threatening conditions and focus on the airway, vital signs, neurological status, etc. A careful history identifying the cause, type, and exact time of injury is paramount in determining initial fluid resuscitation, expected clinical course, and disposition.
Exposure to smoke or heated gas may cause airway edema which can quickly progress to obstruction. Facial burns, carbonaceous sputum, elevated blood carboxyhemoglobin, and tachypnea should raise concern for airway injury. Progressive hoarseness often indicates impending airway obstruction. Intubation by an experienced anesthesiologist or emergency room physician should be ideally performed prior to the development of a complete obstruction. A history of smoke exposure in an enclosed space or for a prolonged time merits screening for carbon monoxide poisoning via measurement of blood levels. Although standard blood tests suffice, non-invasive pulse carbon monoxide oximetry should be used where available. The clinician should be aware that standard pulse oximetry and arterial blood gases erroneously report normal oxygen levels in the setting of carbon monoxide poisoning. Specific and severe burn injuries require immediate transfer to a burn center once the patient has been stabilized (table 12.1).3
A thorough full-body assessment is critical in major injuries to avoid missing any areas of soft tissue damage. For electrical injuries, potentially hidden points of entry and exit should be sought. These commonly occur on the palms and soles since electrical cables are inadvertently grasped and the current travels to the ground. In these cases, damage along the path of the current is hidden but should be suspected.
Depth of burn injury
Careful assessment of burn depth is the next critical step in determining appropriate management and can help predict prognosis and long-term scarring. It is important to keep in mind that most burns represent a mixture of different depths. Superficial or first-degree burns involve only the epidermis. They are painful and have an erythematous, glistening appearance without blister formation. Capillary refill is brisk, as is bleeding on pin-prick. The classic example is a sunburn, although superficial burns are frequently caused by flash burns (i.e., brief, intense thermal exposure) as well.
Partial-thickness or second-degree burns involve the epidermis and part of the dermis. They are further subdivided into superficial and deep partial thickness burns depending on the depth of dermal involvement. Superficial partial-thickness burns are pink and painful with delayed capillary refill. They will generally heal in 2 to 3 weeks without significant scarring, although depigmentation of the affected skin is possible. Scald burns typically result in superficial partial-thickness burns.
Deep partial-thickness burns are characterized by injury extending into the reticular dermis. They appear “cherry red” or pale and dry with mottling (figure 12.1). The neural plexus in the deep dermis is often injured resulting in variable sensation and burns that are generally less painful to touch. They will not blanch with gentle pressure, and bleeding from pin-prick will be delayed. The rate of healing is variable depending on the number of intact adenxal structures left in the skin. As a result, thin, hairless skin (e.g. eyelids) will heal more slowly than thick or hairy skin (e.g. back, scalp). Typically, these burns will heal in 1 to 3 months, but with a significant amount of scarring and possible contractures because follicular structures needed for re-epithelialization may be destroyed. Often, they are best treated by excision and grafting.
Full-thickness or third-degree burns extend through the entirety of the dermis (figure 12.2). They appear dry, leathery and can be white, brown, or black. These wounds are insensate, do not blanch, and do not bleed upon pin-prick. Thrombosed vessels may be visible and are pathognomonic for third-degree burns. Fourth degree burns extend completely through the skin and subcutaneous tissues, affecting underlying muscle and bone.4
Assessing burn depth requires experience and often takes several days of observation to determine the appropriate management. Patients may be admitted for observation and re-examined every day as the appearance of the wound becomes clearer. Serial debridement of necrotic tissue may be required to accurately assess the degree of injury. Generally, the wounds that appear likely to heal within three weeks can be managed conservatively, whereas those that will take longer are best treated by excision and grafting.
Determining total burn surface area
Calculating total burn surface area (TBSA) is the next critical step as it serves to guide initial fluid resuscitation, nutritional requirements, and appropriate triage. Of note, partial thickness burns covering more than 10% of TBSA and those in anatomically sensitive areas (i.e., genitalia, hands, crossing joints) should be immediately referred to a burn center (table 12.1). It can be estimated by either of two methods. Regardless of the technique employed, it is important to note that only areas of partial- and full-thickness injury (second and third degree burns) should be counted. Superficial burns involving only the epidermis (i.e., first-degree burns) need not be considered. The “rule of nines” is the most popular method and divides the adult body into anterior torso (18%), posterior torso (18%), legs (18% each), arms (9% each), head/neck (9%), hands (1% each), and perineum (1%) (figure 12.3). The percentage assigned to a body area reflects its total area, therefore a burn involving one-third of the leg should be considered a 6% TSBA burn. A modified rule of nines is used for children dividing the body into anterior torso (18%), posterior torso (18%), head/neck (18%), legs (13.5% each), arms (9% each), hands (1% each), and perineum (1%). Because the proportions for infants and children differ significantly from each other and adults, Lund and Browder charts are available to provide a more precise estimate of TBSA based on the patient’s age. For small or scattered burns, a second technique for calculating burn area involves using the patient’s hand (note: not the examiner’s). The patient’s hand represents approximately 1% of the body surface area and can be used to estimate TBSA by counting how many “hands” are required to cover the area of a burn.5
Zones of injury
The initial effect caused by a burn can be generally divided into three distinct zones based on histology, degree of tissue damage, and blood flow. The zone of coagulation is the portion of the wound that was most directly affected by the insult and is characterized by irreversible tissue damage. The zone of stasis is the surrounding ischemic area that is potentially salvageable. Fluid resuscitation seeks to increase perfusion in this area and prevent progression to skin necrosis. The zone of hyperemia is the most peripheral area and is characterized by inflammation leading to increased blood flow and increased vascular permeability causing edema. This area invariably recovers rapidly over the course of a few days.2
Historically, high early mortality rates seen following burn injury were in part related to unrecognized fluid loss and inadequate resuscitation. Hypovolemia develops quickly due to evaporation from a compromised skin barrier and extravastion of fluid into unburned tissue. Today, burns of significant size (greater than 10% total body surface area) are managed with fluid replacement according to one of several described protocols. The more widely used Parkland Formula calculates the amount of total fluid requirement over the first 24-hour period following the injury. Total fluid volume is calculated as the patient’s weight in kilograms multiplied by four and then by the total body surface area of second and third-degree burns in percentage points. One-half the calculated volume is given over the first eight hours from the time of injury (not from the time of evaluation). The second half is given over the next 16 hours (Table 12.2). Regardless of the formula used, the clinician should bear in mind that any mathematical calculation of fluid requirements is merely an estimate. Close monitoring of the response to fluid administration and physiologic tolerance of the patient is crucial. Fluid management in the pediatric population can be challenging, especially in infants where lack of renal maturation and reduced GFR makes resuscitation more delicate. Adequacy of resuscitation should be carefully monitored in multiple ways via heart rate, blood pressure, mental status, acid-base balance, etc. Among these methods, urine output is the most accurate. A urine output of 0.5-1.0 ml/kg/hr indicates that hydration is appropriate. Higher urine outputs may be desired in patients with crush or high-voltage electrical injuries where myoglobinuria can damage the renal tubules.
Burn wound infections
Diagnosing burn wound infections by regular monitoring of vital signs and frequent wound inspection prevents delays in wound healing and potential systemic sequelae such as bacteremia, sepsis, and multi-organ dysfunction syndrome. Minimizing exposure to pathogens and treating infections early are critical to successful burn management as infection remains responsible for the majority of mortalities. Although wound infections are common, many burn patients are also at risk for pneumonia if they are intubated, immobile, or septic, or if they have suffered an inhalation injury or chest wall injury that limits thoracic cage excursion.
Although burn wounds are initially sterile, gram-positive bacteria may survive within the sweat glands and hair follicles and will quickly colonize the wound within 24-48 hours if no anti-microbial agent is used. At approximately one week post-injury, the wound may be colonized by an assortment of gram-positive bacteria, gram-negative bacteria, and yeast or fungi. Microbes that colonize the wound may arise from the host’s own gastrointestinal or respiratory flora, or they may originate from the hospital environment.
Staphylococcus aureus is a common etiologic agent of burn wound infections, particularly ones arising soon after injury. However, Pseudomonas aeruginosa has become the predominant agent overall in a number of burn centers. It is often characterized by a greenish-blue discharge and a characteristic grape-like odor. Gram-negative bacteria have become a more frequent cause of invasive infections as a result of their numerous virulent factors and antimicrobial resistance traits. Anaerobes are a less common source of infection and typically occur in the setting of electrical injury or when open wound dressings are used.6
Fungi and yeast tend to colonize wounds later, and patients on broad-spectrum antibiotics may be at increased risk. Fungal wound infections are associated with a high mortality and their resistance to topical antimicrobials highlights the importance of aggressive wound debridement.
Topical burn care
Burn care is largely dependent on the depth, size, and location of the burn sustained. It is imperative that the treating clinician be mindful of the fact that each burn may vary in depth and, therefore, require different treatment. Initial treatment for all but superficial burns remains the same. Clothing, jewelry, and debris should be gently removed. Mineral oil can be applied to painlessly remove charred clothing adherent to a burn. Wounds should be cleansed with soap and water to remove smaller debris and loose tissue. Intact bullae are best left alone whereas burst, flaccid blisters and frankly necrotic tissue should be scraped off or debrided sharply to prevent infection and accurately assess burn depth. A minimally adherent dressing such as Vaseline-impregnated gauze should be applied to minimize contamination and evaporative loss.
Topical agents play an important role in burn care by their ability to augment wound healing and prevent infection. Given the variety of agents available, one needs to understand their subtle nuances in order to maximize their potential. Superficial, partial thickness burns that should heal without surgical intervention should be dressed with an easy-to-apply, topical antimicrobial agent. It is important to keep in mind that although burn wounds can be initially considered sterile they are typically colonized quickly by both gram-positive and gram-negative bacteria, necessitating the need for broad-spectrum topical antimicrobial coverage. Parenteral agents are not recommended in the absence of multi-organ system involvement. Deeper, partial thickness burns should generally be treated by tangential excision and grafting. In a similar fashion, full-thickness burns should be treated with an antimicrobial topical agent capable of eschar penetration until excision is appropriate.
Silver sulfadiazine (Silvadene®) remains one of the most popular agents. It is formulated as a white, water-soluble cream with broad-spectrum antimicrobial coverage (including Pseudomonas). Its application is painless and often found to be soothing. However, silver sulfadiazine is not able to penetrate a burn eschar, limiting its use in such wounds. A transient, self-limiting leukopenia develops in 3 to 5% of patients and should not require discontinuation. A small test dose on normal skin should be applied first only in patients with a known sulfa allergy.
Mafenide sodium (Sulfamylon®) is available as a water-soluble cream or solution. Like silver sulfadiazine, it has broad-spectrum antimicrobial coverage but unlike other topical agents, mafenide has excellent penetration, making it the “gold standard” for burns of the ear or in the presence of a burn eschar. In such cases, twice daily application is necessary. Application tends to be painful, potentially limiting its use. Mafenide is a potent carbonic anhydrase inhibitor that can cause metabolic acidosis, in addition to osmotic diuresis and electrolyte abnormalities.5
Silver nitrate is available as a solution-soaked dressing, and as such, dressings need to be changed frequently (3 to 6 times per day) to keep the wound moist. Application is painless although care must be taken as silver nitrate stains clothing and linens black. It too has broad-spectrum antimicrobial coverage. Silver nitrate is prepared as a hypotonic solution, which can result in electrolyte abnormalities, most commonly hyponatremia or hypochloremia, requiring frequent monitoring for those with large wounds. The silver ions in both silver nitrate and silver sulfadiazine can rarely cause methemeglobinemia. Should this develop, any silver containing agents should be immediately discontinued.
Other topical anti-microbial agents
Over-the-counter ointments, such as bacitracin, neomycin and polymyxin, are commonly used for superficial partial-thickness burns, especially on the face, as mentioned previously. These products carry a low risk of allergic dermatitis. Of note, mupirocin (Bactroban®) is the only agent in this class to be bactericidal against methicillin-resistant staphylococcus aureus (MRSA).
Topical debriding agents
Ointments containing collagenase or papain-urea stand apart from the previously mentioned agents due to their ability to enzymatically debride non-viable tissue. They are an excellent choice in burn wounds with mild necrotic or fibrinous material. In these wounds, they can result in a clean dermis earlier, leading to faster re-epithelialization.5
Significant burn injury results in a large-volume fluid shifts and a systemic inflammatory response that affects nearly all organ systems. As a result, burn patients may present with or develop hypothermia during their hospital course. Forced-air warming blankets and gently heated intravenous fluids should be used to achieve or maintain normothermia. Hypothermia has been associated with increased mortality rates and a higher incidence of acute lung injury.
Severe burns results in a hypermetabolic state, which may last several months. The increase in energy expenditure is proportional to burn surface area and can lead to a doubling of the basal metabolic rate in severe burns. Enteral nutrition should be started early and is preferable as parenteral nutrition is associated with immunosuppresion and higher mortality rates. Generally, patients with a total body burn surface area of greater than 20% should undergo tube feeding to ensure caloric needs are met. Close attention must be paid to changes in nutritional status as the patient recovers.
Basal energy expenditure (BEE) determines the required caloric intake and can be estimated using the Harris-Benedict equation (table 12.3).4 BEE is then multiplied by a factor based upon the severity of the stress (i.e., in large burns this factor is 1.8-2.1). Indirect calorimetry is a more accurate way of measuring caloric expenditure by determining measured oxygen consumption and carbon dioxide production in ventilated patients.
Caloric intake should be appropriately balanced between lipids, carbohydrates, and proteins with the assistance of nutritionist. Highly stressed patients have higher protein needs, and may require up to 2g/kg/day (assuming normal renal function) to prevent muscle breakdown. In addition, critically ill patients benefit from tight glucose control and therefore require regular monitoring of blood glucose levels. Adequate levels of vitamins and minerals are provided in most commercially available enteral feeding formulas. However, administering supernormal levels of certain nutrients (termed immunonutrition) may be beneficial. For example, omega-3-fatty acids can suppress proinflammtory cytokines, arginine can enhance lymphocyte function, and glutamine can improve gut barrier function.4
Burn injury can cause renal failure from myoglobinuria secondary to muscle breakdown or hemolysis. Inadequate urine output despite adequate fluid resuscitation often heralds renal failure. Dialysis may be required and should not be delayed. In the presence of myoglobinuria, urine output must be kept high with intravenous fluids,and diuretic use should be considered.
Heart failure is a potential complication from circulating myocardial depressants (namely lipopolysaccharide) after a major burn. Diastolic dysfunction predominates and should be treated by administering an inotropic agent. Drugs should be chosen that minimize vasoconstriction so as to avoid worsening already hypoxic wounds.
Distal perfusion after an extremity burn may be compromised by compartment syndrome, a condition characterized by increased compartment pressures secondary to edema. Pain out of proportion to the injury and aggravated by passively stretching muscles within the compartment is often reported early and nearly universal. Paresthesia and loss of pulses are much later findings. Although generally clinical examination is sufficient for diagnosis, intra-compartment pressures of greater than 30 mm Hg are confirmatory. Fasciotomies of the affected extremity are indicated to prevent muscle necrosis and limb loss.
Burn injury may also cause acute damage to regions distal to the injury as a result of circumferential compression to either the trunk and/or an extremity due to necrotic skin and soft tissue. Full-thickness injury can produce a tough eschar that may compromise distal perfusion of an extremity or ventilation by limiting thoracic cage excursion. In either situation, an escharotomy is indicated. This should be done soon after the initial assessment as fluid resuscitation may worsen the problem. Because the skin is insensate, this can often be done at the bedside with hand-held electrocautery through the eschar and into the subcutaneous adipose. The skin should subsequently spread restoring distal perfusion. Eventual coverage may be completed with autologous split and full thickness grafts, xenografts, cultured cells, or alloplastic dressings.
Following an adequate period of time to allow for fluid resuscitation and demarcation of areas of questionable depth, the patient may undergo tangential excision of those areas deemed too deep to heal within a reasonable period of time. Damage to the appendageal structures in these deep partial thickness burns limits their ability to reepithelialize. The skin is excised using a thin blade with an overlying guard until viable tissue is encountered. A tourniquet may or may not be used on an extremity since punctate bleeding determines adequate perfusion.
Skin is harvested from donor sites that are relatively flat and unnoticeable, such as the lateral thigh, lower back, or scalp. Split thickness skin is harvested at a depth of roughly 8 to 12/1000 of an inch using an electric dermatome that moves a thin blade side to side between a guarded handle (figure 12.4). Firm, consistent pressure is used to harvest skin of suitable quality. Skin grafts may be placed through a mesher, which punches small holes in the graft at regularly spaced intervals in order to increase the total surface area. A graft that is meshed either 1 ½ or 3 times is valuable when larger amounts of skin are needed. Care must be taken with grafts meshed at a 3:1 ratio since the resultant skin bridges may rotate to the dermal side when the graft is placed on the recipient site. A meshed graft also minimizes fluid accumulation beneath the graft. Unmeshed grafts are preferred in cosmetically sensitive areas such as the face since meshed grafts have a hatched or waffle pattern once they heal. To prevent accumulation of fluid beneath unmeshed grafts, multiple incisions may be made to allow egress of serum or blood.
The skin graft may be affixed to the periphery of the debrided area using sutures, staples, or tape. Several sutures should also be placed icentrally to minimize shearing forces. For added support, a tie-over bolster, circumferential dressing or negative pressure sponge should be used. If the latter is chosen, pressure should be low enough to allow for ingrowth of blood vessels. A splint is also helpful for burns on an extremity to limit movement and, therefore, shearing forces on the graft. The dressing is changed in three to five days to confirm take of the graft. Longer times until the first dressing change may be appropriate for meshed grafts with adequate postoperative compression since fluid accumulation is rarer. The first dressing change should occur earlier for unmeshed grafts which may not have ideal compression. At three days, fluid may be aspirated from beneath a skin graft without affecting its viability. Graft survival is much less likely if aspiration is delayed. Care should be exercised such that the graft is not inadvertently removed with the dressing. Failure of graft take is due to one or more complications, including an inadequately vascularized wound bed, infection, seroma or hematoma formation, and movement of the graft (i.e., shear forces).
For areas prone to complications due to secondary skin contraction with healing (e.g., the lower eyelid), full thickness grafts should be used. These are generally harvested by hand using a scalpel just above the level of the subcutaneous fat. Any remaining fat is then removed with a sharp, fine scissor from the undersurface of the graft prior to placement.
In the absence of sufficient healthy skin for grafting, a small amount of epithelial cells may be harvested from an unburned area such as the perineum or inner thigh and grown in a laboratory as cultured sheets. Use of cultured epithelial cells is indicated for very large burns where donor area is limited. Unfortunately, high cost and lower strength are barriers to more widespread use.
Xenografts (tissues from other species) have held the promise of a natural replacement material in large supply. They have been used for years but still are complicated by immunologic rejection. Today, pig skin is used for large burns as a temporary occlusive dressing or as a test graft for wounds of questionable vascularity. If the xenograft fails to take, the wound bed is presumed to be inadequate for more valuable autogenous skin. However, if the xenograft successfully takes, it may be completely removed in favor of an autogenous skin graft. Another option is to remove the antigenic epidermis from the inert dermis by dermabrasion replacing it with a thinner skin graft. This allows the epidermis to regenerate more rapidly and and subsequently becoming quickly available for repeat harvest.
Synthetic skin may also be used but is not able to completely obviate the need for an autogenous graft. Integra™ (Life Sciences) is composed of collagen fibrils bound to a silicone sheet replicating the dermal and epidermal elements of natural skin. The collagen fibrils are incorporated into the healing wound bed to recreate the dermis, while the silicone acts as a temporary barrier to fluid loss similar to a natural epidermis. In two or more weeks, the silicone sheet is removed and a thinner skin graft than normal may be applied.
Caring for healed wounds
Caring for a burn does not end once the wound has been successfully grafted or re-epithelialized (figure 12.5). Nutrition plays a large role in healing and adequate caloric intake following injury must be monitored. Healing wounds are sensitive to ultraviolet (UV) rays, and protection from the sun is critical. Patients must be reminded to use sunscreen or clothing that covers the wound when outdoors. Sun exposure can lead to hyperpigmentation of the graft or wound.
Pruritus is a common complaint since healed wounds lack adnexal structures needed to keep skin moist. A mild alcohol- and fragrance-free moisturizer should be applied daily and after washing. Despite liberal moisturizer use, many patients still complain of iprutitus. In these cases, an oral anti-histamine may be beneficial.
Epidermal inclusion cysts can develop when skin grafts are placed over a wound bed that contains intact dermal structures or small, microscopic patches of epidermis that were not visible to the surgeon at the time of graft placement. Inclusion cysts may be treated by incision and drainage. Larger cysts may require excision.2
Burn scar contractures are one of the most devastating sequelae of severe injuries. They result from prolonged healing, delayed re-epithelialization, or excessive immobility in a flexed position. Compression dressings, massage, silicone sheets, and active and passive range of motion activities can reduce long-term scar formation. Severe contractures are both physically and psychologically debilitating. Such patients should be referred to a plastic surgeon experienced in burn reconstruction for further management.
Electrical injuries represent an uncommon but potentially devastating event that can affect multiple organs outside of the area directly affected. It should be noted that tissue damage results from a combination of both thermal and non-thermal energy via protein denaturation and altering the permeability of the cell plasma membrane (i.e., electroporation). Electrical injuries are classically divided into low-voltage (less than 1,000 volts) and high-voltage (greater than 1,000 volts). Electrical injuries in the home are usually low-voltage, while high-voltage injuries typically occur at factory or construction sites. This distinction dictates subsequent management. Low-voltage injuries may generally be treated on an outpatient basis, assuming there are no significant injuries or arrhythmias.
High-voltage injuries are typically arc-mediated, meaning the patient is unlikely to have had direct contact with the electrical source. Since electrical energy travels along the path of least resistance, one should look carefully for entrance and exit sites on initial evaluation. Cutaneous burns do not necessarily reflect deep tissue damage, and, as a result, these patients may have extensive muscle and nerve injury. Electrical burns often do not fully declare themselves at first and the extent of soft tissue injury often extends beyond what is initially evident. Muscle injury and edema can result in increased compartment pressures and, ultimately, compartment syndrome. Consequently, patients at risk should have serial neurologic exams. Myoglobinuria from muscle necrosis results in tea-colored urine and necessitates maintaining a high urine output (approximately 100cc/hr) to prevent renal damage. If the urine does not clear despite adequate fluid resuscitation, mannitol can be administered. In addition, some advocate the alkalinization of urine to prevent precipitation of myoglobulin in kidney tubules.
Given the propensity of cardiac arrythmias as a result of electrical injuries, all patients should, at a minimum, have an electrocardiogram. Although not evidence-based, cardiac monitoring for 24 hours is protocol at some institutions.
Electrical injuries can result in significant long-term sequelae. Most commonly, neurological deficits involving either the peripheral (i.e., peripheral neuropathy) or central nervous system (i.e., cognitive changes, poor motor skills) which can occur even months after the injury. In addition, cataracts occur in approximately 5% of electrical injury patients, with other ocular injuries occurring less frequently.
Chemical injuries constitute only 3% of cutaneous burns; however, they account for 30% of burn deaths.7 They are broadly classified into acid or alkali (base) burns. Alkali burns have a more insidious course and generally cause more injury than acid burns as a result of liquefaction necrosis, allowing the alkali to penetrate deeper into the tissues. Acid burns, on the other hand, cause immediate, more-limited tissue damage. Coagulation necrosis results in eschar formation, which prevents further penetration of the acid.
The first step in treatment should be removal of the inciting agent. This includes discarding contaminated clothing. Healthcare workers must take appropriate precautions as some chemicals can erode through standard protective equipment. The affected skin should be copiously irrigated for at least 30 minutes to an hour with room temperature water. Irrigation should be avoided in the presence of chemicals that ignite upon contact with water (e.g., elemental sodium, potassium and lithium). Neutralizing the chemical agent should not be attempted, as an exothermic reaction often develops, potentially causing further injury. Depending on the inciting agent, patients should be monitored for systemic effects. For example, phenol causes central nervous system depression and cardiopulmonary collapse. Although hundreds of chemicals can cause burns, a few deserve specific mention for their unique treatments.
Hydrofluoric acid, commonly found in industrial cleaning solutions and frequently used in the glass and silicon chip industries, penetrates skin and tissue until its fluoride ion chelates with a calcium source, usually bone. Subsequent hypocalcemia may result in dysrhythmias. A topical calcium gluconate gel may prevent further damage and is most effective when applied soon after exposure. Subcutaneous injection of calcium gluconate can also be beneficial, although one must be cautious in its administration as it may cause skin necrosis. As a last resort, calcium gluconate can be injected intra-arterially. A marked decrease in pain signifies effective treatment.7
Alkali burns tend to penetrate deeper, causing more severe burns than acids. However, their course is more insidious, and treatment should assume that burns will progress significantly in depth during the 24 hours after injury. Unlike acids, which result in coagulation necrosis, alkali burns are characterized by liquefaction necrosis and fat saponification. Prolonged vigorous water lavage for 60 minutes or more is necessary. Lye (found in drain cleaners and paint thinners) and cement are the most common agents causing alkali burns.7
Tar and Grease
Tar and grease burns are two of the more commonly encountered chemical burns and should be initially treated by applying cold water to the hot, adherent material. In order to easily remove the tar, bacitracin, mineral oil, or Neosporin should be applied and washed off 12 hours later.