CHAPTER OBJECTIVES
At the end of this chapter, the learner will be able to:
Classify burn wounds according to the depth of tissue injury using the American Burn Association terminology.
Estimate the percentage of total body surface area of a burn using the “Rule of Nines.”
Appreciate the different mechanisms of burn injuries.
Recognize the critical aspects of the initial evaluation and assessment of a burn injury.
Estimate the fluid and caloric requirements of a burn patient.
Understand the different nonsurgical and surgical treatment modalities for burns and identify when surgical treatment is required.
Distinguish the discrete complications that can occur after a burn injury and discuss how they are managed.
Address the major physical and psychological objectives of rehabilitation in a burn patient.
The World Health Organization estimates that almost 200,000 deaths annually are attributed to burns, and the vast majority of burn morbidity worldwide is related to nonfatal burn injuries.1 In the United States alone over 45,000 patients each year require hospitalization for burns,2 creating a significant burden for the health care system. Over 90% of the burn injuries are deemed preventable occurrences. Mortality has significantly decreased with the development of regional burn units, establishment of multidisciplinary treatment teams, and improved critical care strategies focused on optimizing resuscitation, early surgical interventions, infection control, and nutrition. The American Burn Association reports the current survival rates are greater than 96%.2 With increasing survival of this patient population, greater emphasis has been placed on long-term rehabilitation geared at restoration of function and activities of daily living, correction of esthetic deformities, and improvement of the psychosocial well-being. With this paradigm shift in burn care toward emphasis on optimizing post-burn quality of life, newer interventions are being developed and applied even during the acute phase of burn care to facilitate such improvements for burn survivors.
The term burn injury is often employed as an umbrella term that encompasses a vast array of unique mechanistic etiologies which eventually result in injury to skin and underlying structures. These mechanisms are classically separated into four main categories: thermal, chemical, radiation, and electrical. Thermal etiologies include flame, contact, scald, and frostbite. Thermal injury to the skin is the result of the direct energy transfer to the tissue in relation to temperature and contact time. Temperature is in actuality a derivative of the average kinetic energy of the molecules within a system, or in the case of burn injury, a substance (ie, boiling water), such that the temperature of any substance represents a potentially transferable molecular kinetic energy (KEavg = 3/2 κT; κ = Boltzmann’s constant, T = Kelvin) to some other substance (ie, skin). Transfer of this stored kinetic energy to cellular structures of the skin results in denaturation of proteins, vaporization of water, and thrombosis of cutaneous blood vessels, thus resulting in tissue and cell death. The rapid coagulation of protein occurs in the setting of irreversible thermal cross-linking that may limit depth progression when compared to other burn mechanisms such as that seen with chemical and radiation. This process may be immediate in the case of high temperature and/or prolonged contact time, but may also be potentiated by the patient’s premorbid condition, injury status, and local inflammatory factors. The delineation between hot and cold thermal mechanisms (ie, flame, contact, scald) strictly translates to the interface through which the stored kinetic energy is transferred and has implications with respect to the contact time required to facilitate such a transfer. For example, contact burns occur when a solid substance (ie, hot iron) contacts skin; a burn injury of a specific depth will occur at a much shorter exposure interval than to that of a liquid or gas of the same temperature. This is because the solid substance has a significantly greater molecular energy density, which allows it to transfer a greater magnitude of energy across the contact interface in a short period of time in comparison to less energetically dense liquid and gas. This means that in order for liquid and gas to achieve the same depth burn as that of a contact mechanism, a higher temperature or longer contact time would be required. This nuance is important to keep in mind when comparing the burn mechanism to the pattern of a burn injury. For example, a mixed mechanism such as hot noodles (boiling liquid and hot solid) will often result in variable burn depths despite both components of the substance having the same “temperature.” This delineation also plays an important role when examining burn patterns and comparing observations to the reported mechanism for investigations related to burn abuse and neglect. Other mechanisms of burn injury related to chemicals, electricity, and radiation will be discussed in further detail later in the chapter as tissue damage in these instances is not always a direct result of kinetic energy but rather more complex biochemical and electrophysical interactions.
In 1953, Douglas M. Jackson published a classic article in the British Journal of Surgery describing three histological zones of dermal burn injury. These “zones of injury” have been adapted by burn literature and are still applicable (FIGURE 10-1).3 Zone 1 is the Zone of Coagulation and refers to the area of burned tissue that is irreversibly damaged and is no longer viable. Depending on burn size and depth, this area may be addressed with immediate mechanical or subsequent operative debridement. Zone 2 is the Zone of Stasis which refers to the area of burned tissue that is potentially reversible if appropriate and expedient post-burn interventions are administered. In particular, adequate intravascular resuscitation, infection prevention, early removal of necrotic or non-viable tissues, nutrition optimization, and restoration of physiologic core body temperature are all components of the treatment algorithm that can minimize conversion of Zone 2 to irreversible Zone 1 injury. Zone 3 is the Zone of Hyperemia, which is the area of “unburned” tissue surrounding Zone 2 that is exposed to the nearby release of inflammatory cytokines (eg, interleukins, prostaglandins, bradykinin, substance P, histamine) and subsequently develops vasodilation and increased capillary permeability leading to “hyperemia.” As there is no direct tissue injury, Zone 3 is completely reversible unless infection of adjacent Zone 2 burn results in inflammatory sequelae of the Zone 3 tissue.
FIGURE 10-1
Jackson’s concentric zones of burn tissue Jackson’s burn theory classifies three concentric zones in relation to the potential viability of the tissue. These regions from the center of the wound to the periphery were labeled as the zone of coagulation, zone of stasis, and the zone of hyperemia. The center zone of coagulation is the area of maximum contact to the thermal source. Tissues in this area undergo a coagulation necrosis as proteins of the extracellular matrix are denatured and vascularity is impaired. Cells will not recover and emphasis is placed on early debridement and prevention of infection. The intermediate zone of stasis is characterized by hypoperfusion and hypometabolism as the numbers of viable cells are substantially reduced. Phenotypically this area appears as blanching erythema when pressure is applied. There is a risk of tissue progression to necrosis if proper care is not taken to preserve tissue perfusion by adequate fluid resuscitation, avoidance of vasoconstrictors, and prevention of infection. Patients with significant comorbidities that impair blood flow such as diabetes, peripheral vascular disease, and tobacco use are at increased risk for irreversible injury. The outer zone of hyperemia also appears as erythema as the result of local vasodilatation. Cells in this zone are completely viable and will recover if protected from further trauma and/or infection.
The severity of the burn injury and treatment algorithm is determined by the depth of penetration and the surface area of injured skin in relationship to the total body surface area (TBSA) of the patient. The previous designation of first-, second-, and third-degree burns has been replaced by the designations of superficial, partial thickness, and full thickness, respectively, because of the heterogeneity within the spectrum of burn depth. While researchers and clinicians have transitioned to the aforementioned depth descriptors, medical coding still utilizes the degree system, so it is important for practitioners treating burn wounds to understand both systems and the translation between the two.
Superficial injuries are burns limited to the epidermis without disruption of epithelial integrity (FIGURE 10-2). This injury was previously designated first-degree burn. These injuries are characterized by erythema of the skin secondary to vasodilatation of local capillaries. Sunburns are examples of superficial burns and after 3–4 days, the damaged epithelium desquamates and is replaced by regenerating keratinocytes.4 Importantly, superficial or first degree burns are not included in TBSA calculations as this injury does not violate the dermis and therefore the physiologic derangements from such burns are inconsequential during the treatment of deeper burns. Often, referring providers will incorrectly include superficial or first-degree burns in TBSA calculations, which leads to burn size overestimation, excessive or unnecessary treatments, and inappropriate initiation of Parkland resuscitation.
Partial-thickness, previously second-degree, burns are heterogeneous in nature due to the differences in dermal thickness regionally, and in pathophysiology related to differences in superficial and deep injuries to the dermis. The primary state of a partial-thickness burn is that dermal structures are still intact and thus spontaneous healing may occur through migration of epithelial progenitor cells from dermal appendages. However, the healing potential of superficial partial-thickness burn may be much better than a deep partial-thickness burn because of the absolute amount of dermis that is viable. This heterogeneity difference in healing potential and the correlating need for possible excision and grafting have resulted in the designation of superficial partial-thickness and deep partial-thickness injury.
Superficial partial-thickness burns are dermal injuries that extend into the papillary dermis (FIGURE 10-3). These wounds are sensate to nociceptive, proprioceptive, and light touch stimuli, blanch with pressure, and typically result in blistering as a result of the local inflammatory process between the dermis and the epidermis. In particular, blistering in superficial partial-thickness burns is the result of exudative accumulation at the site of the damaged epidermal–dermal interface and these blisters often remain intact at time of presentation. The blistering is often serous in nature; thus, a hemorrhagic appearance often correlates with deeper partial-thickness burns. These wounds heal within 2–3 weeks by re-epithelialization from retained dermal appendages (i.e. bulge stem cells from base of hair follicles) and rarely form hypertrophic scarring and/or wound contracture; therefore, they do not require excision and grafting.
FIGURE 10-3
A. Superficial partial-thickness burns Superficial partial-thickness burns involve the epidermis and the superficial dermis. They are characterized by intense pain, blanching with pressure, and blistering as a result of the local inflammatory process between the dermis and epidermis. These wounds heal within 2–3 weeks by epithelization and rarely form hypertrophic scarring and/or wound contracture. A scald burn on the lower extremity with sloughing of the epidermis is an example of a superficial partial-thickness burn; the areas that are mottled and nonblanching are deep partial-thickness burns. B. Superficial partial-thickness burn re-epithelializing The thermal burn on the plantar foot is superficial partial thickness, and islands of new epithelium can be observed in the middle of the wound. The blistered tissue was debrided, but the wound healed without grafting.
Deep partial-thickness burns extend into the reticular dermis and are nociceptively insensate, have a mottled white appearance, and do not blanch with pressure as the result of impaired vascularity and capillary refill (FIGURE 10-4). Because the free nerve endings responsible for nociception are more superficial within the dermis compared to the other somatosensory nerve receptors contained within skin, often deep partial burns will remain sensate to light touch (ie, Merkel’s cells, Meissner’s corpuscles), vibration and rapid pressure (Pacinian corpuscle), and stretch and sustained pressure (ie, Ruffini’s corpuscles) even when no longer sensitive to pain. This delineation of the type of sensation that is lost within a burn wound helps further clarify the depth of burn when a mixed clinical exam is present. Furthermore, deep partial burns may also be pink rather than white but blanching will be diminished compared to other more superficial areas and there is often a transition point rather than clear demarcation. The reticular dermis contains skin appendages, and injury in this area can cause permanent damage to hair follicles and sebaceous glands, two critical sources of epidermal stem cells required for re-epithelialization. Furthermore, the reticular dermis possesses a distinct lineage of fibroblasts compared to those of the papillary dermis that are specifically responsible for deposition of new extracellular matrix proteins. Deep partial-thickness burns, therefore, damage this fibroblast population that is crucial for wound healing. As a result of damage to stem cell-containing hair follicles and sebaceous glands as well as loss of reticular fibroblasts, deep partial-thickness burns heal in 3–9 weeks by contraction rather than re-epithelialization, which results in significant hypertrophic scarring and wound contracture. Because of the sequelae of delayed healing in deep partial-thickness burns that are allowed to heal by contracture—causing hypertrophic scarring and contractures with significant cosmetic and functional impairments—they are best treated by debridement of necrotic tissue and autologous skin grafting.
FIGURE 10-4
Deep partial-thickness burn Deep partial-thickness injuries extend into the reticular dermis and are insensate, have a mottled white appearance, and do not blanch with pressure as the result of impaired vascularity and capillary refill. Deep partial-thickness burns heal in 3–9 weeks, sometimes with significant hypertrophic scarring and wound contracture; therefore, they are best treated by debridement of necrotic tissue and skin grafts.
Full-thickness burns are cutaneous injuries extending through the entire dermis and across the subdermal plexus, owing to complete loss of skin’s barrier function (FIGURE 10-5). The previous designation was a third-degree burn. This designation also implies that there is no possibility of healing from the wound base, as all dermal regenerative cells have been obliterated. The physical appearance is often leathery brown or black eschar with no capillary refill, although pink and white colors may be present. The key delineation is that pigmentation is fixed in full thickness injuries because no blanching is present with coagulation of the subdermal plexus. Furthermore, full thickness burn tissue is dead and therefore shrinks or contracts as opposed to partial-thickness tissue which is damaged, not dead, and therefore swells. The saying “dead tissue shrinks, damaged tissue swells” is a helpful one to remember when assessing burn depth. The wounds are insensate with respect to all forms of somatosensation and treatment is focused on early excision and grafting to prevent infection, hypertrophic scarring, and wound contracture. Depending on size and location, most full-thickness injuries are treated with excision and grafting procedures, although excision and delayed primary closure or more complex reconstructive options such as local or free vascularized tissue transfer may be employed when critical structures are exposed or ideal graft-receptive wound beds are not available.
FIGURE 10-5
Full-thickness burn Full-thickness burns extend through the entire dermis and into the subcutaneous tissue. The appearance is leathery brown or black eschar with no capillary refill. The wounds are insensate and treatment is focused on early excision and grafting to prevent infection, hypertrophic scarring, and wound contracture. This foot with extensive eschar and exposed subcutaneous tissue is an example of a full-thickness burn.
The extent of burn penetration may not be readily apparent at the time of initial evaluation because the burn eschar often impairs delineation of true depth. Although many tools have been used as predictive indicators of depth of injury (eg, biopsy, ultrasound, infrared, or perfusion techniques), none has proven to be as reliable as a physical examination at 48–72 hours postinjury.5 The initial non-surgical debridement of burn wounds with mechanical methods such as rigorous scrubbing to remove blisters, exudate, coagulum, and eschar is crucial to the accurate assessment of the burn depth.
An estimate of the burn wound surface area in proportion to the TBSA is used to estimate the total fluid and caloric requirements and is a predictor of morbidity and mortality. For an adult patient, the burn area is often generalized utilizing the “Rule of Nines” for rapidity and ease of assessment (FIGURE 10-6). When assessing burn size for patients with BMIs greater than 35, adaptation of the Rule of Nines to the Rule of Sevens is indicated to reduce inaccuracies that occur when generalizing the Rule of Nines to obese patients. In particular, the anterior and posterior torsos represent 28% TBSA, respectively, whereas the lower extremities are 14% and the upper extremities 7%. While the Rule of Nines and Sevens are useful for larger, contiguous burns, the Palmar Surface Area (PSA) technique which equates the patient’s own palm and fingers to 1% TBSA is best used for smaller and scattered patterns. It is important to note that age, gender, and BMI all impact PSA relative to TBSA, and can result in twofold errors in estimation when not accounted for by the practitioner. More sophisticated charts such as the Lund–Browder chart are available for more accurately estimating the body surface in relationship to age and may be more useful particularly in the pediatric population (TABLE 10-1). The Lund–Browder chart, although more accurate, is more time-consuming in application and is often not employed by non-burn and pre-hospital providers. In order to ameliorate the significant errors that may occur in TBSA estimation, computer- and mobile app–based methods such as Burn Case 3D6 have been devised. The depths of penetration as well as the TBSA burn are major determinants by the American Burn Association for referral to a regional burn center for a higher level of care (TABLE 10-2).
FIGURE 10-6
Rule of Nines The Rule of Nines is used to determine total body surface area that is burned and estimates that each upper extremity accounts for 9% of the total burn surface area or TBSA, and each lower extremity, 18%. In addition, the anterior and posterior trunk is predicted to be 18%, the head and neck 18%, and the perineum 1%. For burns spanning anatomical regions, the volar surface area of the hand may be considered 1% of the TBSA.
| American Burn Association Criteria for Referral to Regional Burn Unit |
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When a patient first enters a burn center and the initial burn evaluation is completed, prognostication is performed to facilitate a better understanding of injury severity as well as discussions with the patient and family members regarding overall prognosis. Initially, when the Parisian surgeon Serge Baux first devised his mortality scoring system in 1961, this calculated score (ie, Baux Score = patient age + % TBSA) translated directly to the patient’s mortality rate. In other words, a 60-year-old patient with a 40% TBSA burn had a 100% mortality rate. However, due to significant advances in burn critical care and surgical management, this score is now used as a marker of injury severity but not as a direct measure of mortality risk. Recently, to account for the influence of inhalation injury on mortality in burn injury, the Revised Baux Score (rBaux) was formulated by Osler et al. in 2010.7 This method calculates a score by summating a patient’s age, % TBSA, and adding an additional 17 points in the presence of any inhalation injury. For example, a 50-year-old patient with a 30% TBSA burn and inhalation injury would have a total Revised Baux Score of 97 (50 + 30 + 17). With the rBaux, a conversion nomogram may be used to determine predicted mortality. While the rBaux provides a relatively accurate estimate of predicted mortality after severe burn injury, it does not account for other clinical indicators of prognosis such as comorbidities or concomitant trauma.
Scald burns are the result of contact with hot liquids and are the most common burn etiology in developed countries. The extent of injury is dependent on the temperature and viscosity of the liquid and the duration of exposure, in addition to patient factors and anatomical location. Exposure to hot water above 60°C for 3 seconds can result in deep partial-thickness or full-thickness injury. These injuries typically appear less severe in exposed areas of the body. Clothed areas typically have more extensive injuries because clothing absorbs the heated liquid, prevents evaporative heat dissipation, and maintains contact with the skin for a longer duration of time. In the pediatric population, immersion scald burns with a symmetric distribution and linear demarcations of the upper extremity or lower extremity and/or crease-sparing of perineal and buttocks should warrant suspicion of abuse, and health care professionals are required to notify appropriate child protective agencies (FIGURE 10-7). While not within the scope of this chapter, a detailed discussion on the evaluation and management of suspected abuse and negligent burns may be found in “Negligent and Inflicted Burns in Children” by Collier et al. in the July 2017 issue of Clinics in Plastic Surgery.8
FIGURE 10-7
Scalding burn This toddler’s hand is an example of a superficial partial-thickness burn due to scalding water. The depth of tissue injury depends on the liquid temperature and time of exposure. Any suspicion of child abuse with this type of burn should be reported to the Children’s Protective Services.
Scald burns from grease may result in more severe injuries as grease is more viscous than water, therefore resulting in a longer duration of contact from decreased evaporative losses and difficulty removing the offending agent. Although grease can reach higher temperatures (usually around 200°C) compared to water, water has a significantly higher heat capacitance and therefore contains more stored thermal energy for a given temperature. As a result, water can transfer greater energy in a given period of time and cause greater damage per second of exposure. The combination of boiling water and oil results in the greatest degree of damage compared to either in isolation as the oil prevents evaporation of water which facilitates prolonged delivery of stored thermal energy in water to the contacted tissues. These burns therefore frequently result in deep partial-thickness to full-thickness injuries.
Tar is a unique type of scald burn that requires specialized management because it becomes adherent to the skin as it cools and creates a secondary alkaline chemical injury. Treatment is initially focused on rapidly cooling the tar with ice packs to reduce continued thermal injury followed by the slow removal of the tar with petroleum-based ointment such as Neosporin (Johnson & Johnson, New Brunswick, NJ) and Medi-sol (Medi-sol, Oklahoma City, OK) or simple mineral oil. The ointment or oil may need to be applied multiple times in order to totally dissolve the tar. Rapid intervention is warranted even after cooling measures have stopped thermal-based injury, as the alkaline composition of tar can continue to cause underlying liquefactive necrosis. Once dissolved, appropriate assessment can be made regarding the depth of penetration and extent of injury.
Flame injuries are the second most common mechanism of burns and the most common mechanism requiring hospitalization. Flame injuries account for 44% of burn admissions in the United States annually.2 The incidence of flame burns has significantly decreased with the implementation of prevention programs and improved detection methods such as smoke detectors and fire alarms. The major determinant of morbidity and mortality in this patient population is the presence of concomitant inhalation injury.9 Inhalation injury should be suspected if the burn occurred within an enclosed space or if physical examination reveals singed nasal hair, voice changes (eg, coarse or hoarseness), inspiratory stridor, and/or carbonaceous sputum.
Electrical burns have been described as the most devastating burn injuries because they not only involve the skin, but underlying organ systems as well (eg, the cardiovascular and nervous systems). Electrical burn pathophysiology, like that of chemical injury, has a mixed contribution from direct and indirect mechanisms to create tissue injury to both cutaneous and deeper structures. Electrical current is directly damaging to cell membranes as the flow of electrons will generate heat as they flow through relative “high resistance” of these cellular structures. This mechanism creates the entry and exit wounds often seen in electrical injury. As electrical energy travels through the body, it is converted to heat, and the severity of injury is dependent on voltage, magnitude, and type of current (alternating vs direct), the pathway traveled through the victim’s body, and the electrical resistance of tissues through which the electricity passes [least-to-most resistance: blood vessels, nerves, muscle, skin (wet < dry), tendon, fat, and bone]. Bone has a relatively high resistance compared to other tissues and heats up with conduction of electrical current such that thermal injury to adjacent muscle can be severe and lead to occult compartment syndrome which is hard to recognize and can be fatal if missed.
Electrical injuries are classified as low voltage (<1000 V) and high voltage (≥1000 V). Low voltage typically involves tissues immediately surrounding the point of initial contact, while high voltage usually results in penetration to deeper organ systems. High-voltage injuries, especially from alternating current sources, create significant tetany that may result in skeletal fracture, even of the spine, and the sustained high-intensity contractions can lead to myocyte necrosis. This muscle damage causes myoglobinuria that can result in renal failure and hyperkalemia, which in turn may lead to life-threatening arrhythmias. Alternating current causes tetanic contractions that can prevent the victim from releasing the source, called the no-let-go-phenomenon, thereby resulting in prolonged contact with the electricity and thus more devastating injuries. Smaller body parts such as the hands, fingers, and feet generate more heat because they dissipate less heat to the surrounding tissues, and in many cases injuries to these structures result in complete necrosis (FIGURE 10-8).
An electrical burn typically has three injury components that need to be evaluated: a true electrical energy injury from current flow, an arc or flash flame injury by a current arcing at a temperature around 7200°F from the source to the ground, and a flame injury via ignition of clothing. The extent of injury can be easily underestimated because the cutaneous phenotypic appearance may be limited, while underlying muscle necrosis may be extensive. Complications of electrical injuries include rhabdomyolysis leading to hyperkalemia, cardiac injury and arrhythmias, metabolic acidosis, myoglobinemia, and renal failure.
Treatment of electrical burns is focused on aggressive fluid hydration, correction of electrolyte abnormalities, and diuresis. Muscle edema may also lead to compartment syndrome and should be suspected if the patient complains of progressive pain on passive extension and/or paresthesia. In these cases, an emergent fasciotomy is required to prevent progressive tissue hypoperfusion and necrosis. Cardiac arrest, ventricular fibrillation, and cardiac arrhythmias are common within the first 48 hours and can be life-threatening. Indications for cardiac monitoring are documented ECG abnormalities, observed arrhythmias, post-injury electrolyte disturbances, high voltage (≥1,000 V) mechanism, large TBSA burn, and/or advanced age. In addition, transient and permanent nerve injuries, including peripheral neuropathy, delayed transverse myelitis, and anterior spinal syndrome, have been reported.
Lightning strikes are a rare type of electrical injury resulting from a direct current that can generate heat as high as 50,000°F. Due to the short duration of action, usually of 1–2 milliseconds, frank skin necrosis is uncommon. Patients typically demonstrate superficial skin manifestations of a fernlike pattern, termed Lichtenberg figures, that are related to the flow of electrons over the body surface (FIGURE 10-9). These lesions are transient, lasting only for 24 hours, and death is usually the result of cardiac arrest and apnea from direct effects of the current on the central nervous system. Lightning can also cause punctate wounds as seen in FIGURE 10-10.
FIGURE 10-9
Lichtenberg figures with lacy ferning pattern seen on the upper chest (Used with permission from Zafren K, Thurman R, Jones ID. Environmental conditions. In: Knoop KJ, Stack LB, Storrow AB, Thurman R, eds. The Atlas of Emergency Medicine, 3rd ed. New York, NY: McGraw-Hill; 2010:chap. 16.)
Chemical burns occur secondary to the contact of the skin with strong acids or bases. Concentration of the agent, quantity, duration of contact, and the mechanism of action in a biological system are factors that determine the severity of the chemical burn injury. Acidic burns tend to be less severe as contact results in a coagulation necrosis of the tissue that creates a denatured protein eschar which then impairs further penetration of the acid. However, basic agents result in a liquefaction necrosis of tissue, which causes a deeper extension of injury due to protein hydrolysis and fat saponification, thereby creating a liquified area of damage that allows the base to penetrate to underlying tissue. Hydrofluoric acid (HF) is unique in that it also causes liquefactive necrosis and penetrates much deeper than other types of acid.
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