Acute management of burn/electrical injuries

18 Acute management of burn/electrical injuries








History


Since man first learned to make fire (ca.500 000 bce), fire was metaphorically a multiedged sword. By controlling fire, man could throw off many shackles but once the use of fire was incorporated into daily life, accidental burns became an inevitable cause of common and severe injuries. Man began to search their environment for soothing burn medications. The difficulties in the treatment of burns have been lamented by all writers for millennia.


About 4000 bce the Shumerian civilization emerged upon the flood plain of the lower reaches of the Tigris and Euphrates rivers. One of the greatest finds of archaeology was the ruins of a library assembled in Nineveh by Ashurbanipal. The library included a medical section with Shumerian medical texts dealing with the diagnosis and bultiti (’therapy’) of burns written on tablets of moist clay in cuneiform script. An anonymous Shumerian physician, who lived toward the end of the 3rd millennium bce, prepared a tablet 9.5 × 16 cm in size and wrote down a number of remedies for burns, based on plant extracts. This clay document, the oldest medical handbook known to man, lay buried in the Nippur ruins for more than 5000 years, until it was excavated and taken to Philadelphia.


The next data on the treatment of burns is recorded in Ebers Papyrus in 1500 bce, where initial topical treatment of burns was a frog warmed in oil and rubbed on the burned surface, and later treatment included lemon strips in an oily lixture or black mud, boiled cow dung and goose.


Sushruta Samhita (ca.800 bce) used clarified butter mixed with red ochre or the bark of a fig tree. He recommended debridement of severe burns with ‘loose skin and flesh.’ In the Sushruta Samhita, we find the first description of the classical symptoms of a typical burn case – the enormous thirst and fever are mentioned. The Old Testament (Leviticus 13: 24–28) lists burn-injury of the skin among other dermatological illnesses.


Hippocrates (460–377 bce) wrote a whole chapter on burns in his book Peri Elkeon (‘About Ulcers’). Burns were systematically described as kavma or pyrikafston. He realized the significance of loss of fluids from the burn surface by pointing out in his book Peri Himon (‘About Humors’) that “fluids (exudates) coming out of the vessels are forming blisters, as in burn wounds, and should be emptied” and advised as treatment, “lots of fluids and diluted honey by mouth for the patient.” In his fourth book, Kat’ Iitrion (‘In the Medical Office’), which is similar to the operating theater of today’s medicine, he clarified local treatment of wounds under aseptic conditions. He demonstrated that wound management and dressing changes should be “as quick as possible, painless, comfortable, and presentable, while the bandage should be soft, light, and clean.” He urged his colleagues to work under as clean conditions as possible and to wear clean and properly tailored garments. Finally, according to the Hippocratic Aphorisms, surgery remained the ultimate solution for treatment, since “what drugs do not cure, iron may cure; what iron doesn’t. …”


Pliny the Elder (23–79 ce) used goat’s dung, gluebristles, wax and bone marrow. Application of animals’ dung is still popular in various parts of the world. Apart from the excision of contracted scars described by Celsus, surgery had no place in the treatment of burns in Greek and Roman medicine.


Around 500 bce, the Chinese were using a mixture of tea leaves (tannic acid) to treat burns, but the oldest preserved written Chinese scientific description of burn wound treatment dates back to Hong Ge (281–341 ce). His book Zhou Hou Fang (Prescriptions for Emergency) suggested the topical application of two different prescriptions: old (imperative) calcarea optionally blended with plant oil, or the use of pig fat cooked with willow bark. The application of these mixtures resulted in reduced numbers of wound infections and has to be regarded as the oldest preserved Chinese description of an anti-infectious astringent to be used in thermal injuries.


Paulus Aegineta (625–690 ce) recommended applications of moderately detergent materials, which were not definitely heating or cooling: “Light earths mixed with vinegar to prevent blisters from forming.” Rhazes (850–923 ce) of the Arabian School of Medicine introduced the popular ‘white ointment,’ composed of white lead, oil of roses and wax. Furthermore, he wrote about the effect of application of cold water in relieving the pain of an acute burn. Thus, Rhazes advised rose water, cooled with snow, and Avicenna (980–1037 ce) advocated icy water. Valesco de Tarenta of Montpellier in his Textbook of Surgery (1490) described how to avoid syndactyly in the burnt hands. Bouisson of Montpellier was the originator of the exposure method in treating burns: “… in burns the ventilation can supersede other methods … it substitutes dry for a moist surface diminishing the chances of infection”.


Paré (1510–1590 ce) clearly described the differences between second-degree and third-degree burns, early excision of the burn wound, and those burns that frequently developed contractures. “One must be careful if burns affect the palpebres or the legs or the fingers or the throat or the axilla or the joint of the knee or of the arm for these joints should not stick together”. Fabricius Hildanus (1560–1634 CE) wrote the first book devoted entirely to burns: De Combustionibus (1607) and insisted that the classification of burns should be a guide for treatment: “Gradus et distributio combustionurn in tres species item ex quibus indicationes.” A more extensive survey was written in 1622 by Hornung. Richard Wiseman in 1676 wrote several ‘chirurgical treatises’ and discussed splinting to avoid contractures. He advised refrigerants or calefactive medicaments.


Richter (1788) wrote on the relation between burn wound size and the patient’s prognosis. Edward Kentish (1769–1797) in his essay on burns (1797) described warm stimulating remedies for the treatment of frostbite. Baron Guillaume Dupuytren (1775–1835) classified burns into six degrees. Jean Petit wrote about burns in the Dictionare des Sciences Medicales, which was published in 1812. He clearly delineated three degrees of burns, based on depth, as erythema, blistering, and full-thickness skin injury, including tendon or muscle. Samuel Cooper’s surgical dictionary of 1830 referred to the three-degree classification based on inflammation and appearance, rather than burn depth.


In a landmark decision in 1848, Syme at the Royal Infirmary in Edinburgh designated one building for all burn cases, and this became known as the Burn Hospital. The 19th century presented two basic important principles for the local treatment of burns. Pollock (1817–1897) used in 1871 skin grafts for burns, after Reverdin’s famous publication on skin grafting technique in Paris in 1869.


In 1875, Joseph Lister recommended boric acid and carbolic acid for burn wounds to kill bacteria. In 1881, Tappeiner of Munich studied autopsies of burn deaths and recognized the concentration of blood, increased hemoglobin concentration, and decreased blood and water volume. In spite of a speech by Robert Hornby in 1833 to the Royal Medical Society, in which he recognized burn shock as similar to shock seen with acute peritonitis, and in which he argued against bleeding and purging, these practices persisted through the latter part of the 19th century. The appreciation by Tappeiner of burn pathology, however, was a significant event. In 1905, Sneve noted the importance of intravenous saline for resuscitation and wrote an article in the Journal of the American Medical Association advocating early skin grafting.


The first person to suggest excision of the burnt tissue was Lusgarten (1871), however, Wilms (1901) was the first to carry it out, but he never grafted the excised areas. In Vienna, Weidenfeld and Zumbusch (1905) performed excision of burnt areas in the acute period, either on admission or during the first 3 days. In 1968, Janžekovič revived the idea of early excision of burnt tissue and immediate skin grafting and thus laid the cornerstone to the contemporary principle of early tangential excision and early grafting.



Epidemiology


The incidence of burn injuries varies from country to country, typically peaking during the country’s holiday period. According to the most recent statistics compiled by the World Health Organization and the World Fire Statistics Center, fires caused 6.6 million major burn injuries and 400 000 deaths every year.1 The burden of burn injury falls predominantly on the world’s poor; 95% of fire-related burns occur in low- and middle-income countries where prevention programs are almost nonexistent and open fires for cooking, lighting or heating are commonplace. The average death rates are about three fire deaths per 100 000 inhabitants and one fire death per 100 fires. However, this average conceals a more than 100-fold variation in death rates from country to country. A better indication of typical fire risk is the median fire death rate per 100 000 inhabitants by country, which was 0.9 in 2004. In addition, the WFSC released fire-related death data by country (from lowest to highest number of deaths per 100 000 person) from 2002–2004. The countries with the lowest incidences include Singapore (0.08) and Switzerland (0.51). Those with the highest include Finland (2.08) and Hungary (2.10).The cost to society in terms of lost wages, vocational rehabilitation, and need for long-term care is staggering. Worldwide, severe burns cause disabilities that cost $80.2 billion a year in lost productivity (wages and skills) alone; medical expenses would add millions more. Lost productivity costs the world billions of dollars annually. In 2009, the WFSC noted that the cost of direct fire losses ranged from 0.06–0.26% of countries’ gross domestic product (GDP) and the cost of indirect fire losses ranged from 0.002–0.95% of countries’ GDP.


Males account for approximately two-thirds of the total costs of fire/burn injuries and females account for the remaining third. Fatal fire and burn injuries cost 2% of the total costs of all fatal injuries. Hospitalized fire and burn injuries are 1% of the total cost of all hospitalized injuries. Nonhospitalized fire and burn injuries cost 2% of the total cost of all non-hospitalized injuries.




Mechanisms of thermal injury



Types of burns


The body has very few specific protective and repair mechanisms for thermal, electrical, radiation and chemical burns. Heat changes the molecular structure of tissue and denaturation of proteins is a common effect of all types of burns. The extent of burn damage depends on the temperature of agent, concentration of heat and the duration of contact.



Thermal burns




Scalds

Hot water scalds are the most common cause of pediatric burn admissions. They also often occur in elderly people. The common mechanisms are spilling hot drinks or liquids or being exposed to hot bath water (Fig. 18.1). The depth of scald injury depends on the water temperature, the skin thickness and the duration of contact. Water at 60°C creates a deep dermal burn in 3 s but will cause the same injury in 1 s at 69°C. Boiling water often causes a deep dermal burn, unless the duration of contact is very short. Grease and hot oils will generally cause deep dermal or deeper burns.





Tar

Tar is usually used as a protective coating in surfacing pavement and roads, roofing and other industrial applications. It is made from distillates of petroleum and is composed of long-chain hydrocarbons and waxes, which have a high boiling point. The boiling points of paving tar and roof tiling tar are 140°C and 232°C, respectively. Hence, accidents involving tar, tend to be associated with deeper burns.


When tar splatters, it cools rapidly to between 93°C and 104°C before landing. When hot tar makes contact with the skin it cools, solidifies and sticks. The tar usually retains sufficient heat to produce a significant burn by prolonged heat transfer to the skin. Once cooled, the tar quickly hardens and adheres to the skin. The aim of first aid at the scene is to reduce the effects of thermal insult. In order to expedite the cooling and solidification process one should apply cold water. Often, the tar is cool by the time the patient arrives at the medical facility. If not, the tar should be actively cooled to terminate thermal damage with room temperature water and prevent the further spread of the tar. Care must be taken not to develop hypothermia in major burns and adherent tar should not be removed in the field, but only by qualified personnel at a medical facility. The injuries are typically over the exposed skin of the face and extremities and the burn is of variable depth but is often deep second degree or third degree. Tar which has just been heated is sterile, skin is not. So, colonization of the wound from the surrounding intact skin may develop.


Burns due to hot tar are difficult to manage because of the difficulty in removing the tar without inflicting further injury to the underlying burn. As it is difficult to remove the tar rapidly and there is no pressing medical need to do so, it is best to treat the injury as a deep burn with appropriate fluid resuscitation or preparation for skin grafting as needed. Removal of the tar is not essential but it improves patient comfort and allows early assessment of the underlying tissue damage. This approach carries the risk of infection and the potential conversion of a partial thickness injury to a full thickness injury.


Numerous substances have been used in the past with variable results and selection of the appropriate agent for the removal of adherent tar is still challenging. Polyoxyethylene sorbitan, an emulsifying agent commonly used as a base in ointments, separates the tar from the skin and, as it is water soluble, easily washes off.2


Alternatively silver sulfadiazine, neosporin ointment (with polyoxyethylene sorbitan as a base), polysorbate or De-Solv-It (a citrus petroleum distillate with surfactant and lanolin) may be left on the burn, which is then bandaged. The tar comes away with the bandages when they are removed the next day. These may be used by themselves or in combination with an antibiotic ointment.3 With some of these agents, it is recommended to leave it on for 12–48 h at a time until the tar has dissolved.


Organic solvents, such as alcohol, acetone, aldehydes, ether, gasoline and kerosene have had limited use. Some of these substances are relatively ineffective, have a slow solvent action, which requires continual rubbing and repeated applications and can induce further local tissue damage as well as the possibility of systemic toxicity through absorption, so these are not recommended for removing tar.


Common household agents, such as mayonnaise (15–30 min), butter (20–30 min), sunflower seed oil (20–30 min), and baby oil (1–1.5 h) placed on sterile gauze and onto the tar, have been promoted to remove tar effectively, rapidly and without further damage, over the aforementioned time periods. When large amounts of tar are present, the technique may need to be repeated. The burn depth can then be evaluated and managed by early surgical intervention if required. Organic, nonsterile agents are easy to acquire and are available in large quantities, but they carry the risk of promoting wound infection or allergic reaction. Bacterial or fungal growth can occur if the tar is not completely removed and the organic agent is not completely rinsed off.


Mechanical or manual debridement is painful, relatively ineffective, and results in the removal of underlying viable skin and hair follicles, thus extending the depth and area of the dermal injury. In addition, a degree of autodebridement will occur. Debriding is a balance between removing the tar and exposing the injured skin for evaluation and treatment. Judgment should be exercised as to how much debridement is appropriate in the emergency setting, as extensive debridement may require moderate-to-deep sedation. If the skin has a light coat of tar and the patient does not complain about the underlying skin or surrounding tissue, leaving the asymptomatic tar in place may be acceptable.4 It has been reported that early excision and grafting may be required in some patients and this will decrease the hospitalization times. Tar that is part of an obvious burn, blister, or tissue loss should be removed and conjunctival tar, should be removed by an ophthalmologist.




Electrical burns


Thermal injury due to electrical current is defined as tissue injury by exposure to supraphysiological electrical currents (Table 18.1). Electrical burns (Figs 18.3, 18.4) are classified as high voltage (≥1000 V), low voltage (<1000 V), ‘flash burn’ (in which there is no electrical current flow through the body of the patient) and burns caused by lightning.


Table 18.1 Physiologic effects of different electrical currents





















  Effect current (milliamps)
Tingling sensation/perception 1–4
Let-go current 3–9
Skeletal muscle tetany 16–20
Respiratory muscle paralysis 20–50
Ventricular fibrillation 50–120



Low voltage injuries rarely cause significant damage beyond a small deep partial thickness burn at contact points. High-voltage injuries are more apt to cause deep tissue destruction. In fact, most electrical burns are work related (i.e., construction workers, linemen, utility and electrical workers). Typically, high-voltage injury causes extensive skin injury with necrosis at the contact point and deeper structures, resulting in a large area of necrosis. The electricity flows through the tissues and generates heat, which damages them. The resistance of tissues increases gradually from nerves to vessels, muscles, skin, tendons, fat and bone. Bones are more resistant to the flow of electricity, producing the highest amount of heat with the same current, in accordance with the Joule effect. Because of this phenomenon, multi-organ injury can occur with significant electrical burns. This multiorgan injury (e.g., heart, kidney, nerves, eyes) must be promptly identified, controlled and treated. In addition, it is important to note that high voltage electrical injuries resemble a crush syndrome and require suitable decompression. Therefore, the degree of tissue damage is more extensive than that perceived on initial examination due to the progressive and continuing tissue necrosis. In high-voltage injuries, the victim usually does not continue to grasp the conductor. Often, these patients are thrown away from the electric circuit, which leads to traumatic injuries (e.g., multiple orthopaedic injuries, cranio-encephalic trauma). As a result of these associated injuries, these patients must be considered as polytraumatized.


Despite great advances in the treatment modalities of electrical injuries in the recent decades, the magnitude of the problem remains very high both for the victim and the treating surgeon. Most of them succumb to it due to systemic effect; many of those who survive, lose one or more limbs and present with complicated defects involving different tissues at different parts of the body. These wounds are often potentially life-threatening and some are functionally disabling.


The contact wounds are usually present at the entry and exit points and the injuries are more severe at these two points. The terminology of entry and exit point, however, is an archaic term for the simple reason that they are applicable to direct current, whereas in an alternate current the exit point becomes the entry (re-entry) point also. The resultant damage is more severe.


The victims of electrical burns show certain specific features with regard to therapy and the evolution of the pathology. The very nature of electrical burns is its vascular damage leading to progressive tissue necrosis, often seen in skin and muscles. Soft tissue damage in the extremities can precipitate compartment syndrome requiring fasciotomy. This results in a gross limitation on manipulation of local tissues for reconstruction.


The damage to the tissues is three-dimensional with the current producing extensive necrosis of the tissues at different levels from skin to bone. The site and extent of tissue necrosis can be clearly identified by 99 T Cm-MDP bone scans. The optimal management of these wounds therefore has evolved into a plan of early primary debridement, suitable decompression, including fasciotomy, an aggressive but cautious revision debridement and early skin cover, often composite, with an aim to preserve vital structures. Serial and multiple debridements of wounds, including superficial and deep muscles must be performed but nerves, tendons, joints and bones even if denatured can be preserved as they can partially regenerate if covered with vascularized skin.


Aggressive treatment including surgical debridement of devitalized tissues, or those with doubtful viability, frequently exposes vital structures in patients who have suffered high-voltage burns. The problem of ‘high risk’ wounds warranting priority in providing an early and emergency cover compounded with paucity and limitations of choice of procedures throw a great challenge to the surgeon. These require a higher necessity of flaps when compared with other burn groups, due to the characteristic compromising of deeper structures. High complication rates are reported with electrical injury including partial or complete flap failure. This fact, associated with the need to preserve the vital organs and structures like vessels, bones, tendons and nerves justifies the aforementioned cautious reconstructive approach with serial examination and debridement prior to a definitive surgery. The vascular damage and resulting thrombotic phenomenon abates during second week and tissues become healthy. This is the time when tissues around the wound withstand manipulation for a local, regional, axial or free flap. The mortality rate of patients who suffer high-voltage burns ranges from 0 to 21.7%; their main cause of death is multiorgan failure secondary to sepsis of cutaneous origin.5,6


Myonecrosis, with severe myoglobinemia as a result of a massive muscular destruction can lead to acute renal failure, despite aggressive volemic replacement. As the extent of injury cannot be quantified as in a cutaneous burn, fluid resuscitation must be adjusted to urine output. The treatment of myoglobinuria includes initial stabilization and resuscitation of the patient while concomitantly attempting to preserve renal function. Early aggressive fluid replacement is beneficial in minimizing the occurrence of renal failure. While osmotic diuretics (e.g., mannitol) and alkalinizing agents (e.g., bicarbonate) are considered the standard of care in preventing acute renal failure in patients with myoglobinuria, there is little clinical evidence to support the use of these agents.7


Cardiac dysfunction, such as atrial fibrillation or supraventricular arrhythmias, are observed in up to one-third of patients who suffered from electrical burns. Electrical function of the heart should be assessed by an initial electrocardiogram and continuous cardiac rhythm monitoring for the first 24 h after injury. According to the majority of publications, these complications are transitory and no patients were noted to have developed late cardiac complications. Chronic complications that persist after the hospitalization period, include the occurrence of peripheral nerve injuries, mainly sensory deficits such as dysesthesias and paraesthesias and cataracts.


A wide spectrum of abdominal visceral complications occur following high-voltage electrical injury. These injuries result either from direct injuries to intra-abdominal structures from the contact points over the abdomen or are a result of current passing through the abdominal viscera from more distant entrance and exit wounds. In treating high-voltage electric accidents, anticipate the entire spectrum of anatomic and pathologic alterations to the abdominal viscera. Therefore, these injuries of the abdomen warrant early exploration to determine whether there is injury of the viscera. Distribution of intravenously injected fluorescein dye may prove helpful in demarcating devascularized bowel.




Pathophysiology


The skin is the largest organ of the body. While not very active metabolically, the skin serves multiple functions essential to our survival, functions that are compromised in the presence of a burn. These functions include: (1) Thermal regulation and prevention of fluid loss by evaporation. (2) Hermetic barrier against infection. (3) Sensory receptors that provide information about environment.


The skin is divided into three layers: (1) Epidermis: This is the outermost layer of skin composed of cornified epithelial cells. Outer surface cells die and are sloughed off as newer cells divide at the stratum germinativum. The outer epidermal layer provides critical barrier functions and is composed of an outer layer of dead cells and keratin, which present a barrier to bacterial and environmental toxins. The basal epidermal cells supply the source of new epidermal cells. (2) Dermis: This is the middle layer of skin composed of primarily connective tissue. It contains capillaries that nourish the skin, nerve endings, and hair follicles. The inner dermal layer has a number of essential functions, including continued restoration of the epidermis. The dermis is divided into the papillary dermis and the reticular dermis. The former is extremely bioactive; the latter, less bioactive. This difference in bioactivity within the dermis is the reason that superficial partial-thickness burns generally heal faster than deeper partial-thickness burns; the papillary component is lost in the deeper burns. (3) Hypodermis: This is a layer of adipose and connective tissue between the skin and underlying tissues.


Much of the treatment of burns is predicated on the depth and extent (percentage total body surface area, TBSA) of the initial burn injury. In this way the severity can be clarified and the treatment designed. The classification of burn depths should be referred to as:



It is critical to understand the clinical implications of accurate evaluation of the injury so that consistent and timely therapy can be instituted.


Burn injuries of the skin result in both local tissue destruction and systemic responses. Loss of the normal skin barrier function causes the common complications of burn injury. These include infection, loss of body heat, increased evaporative water loss, and change in key interactive functions such as touch and appearance.



Local response


The three mechanisms by which energy is transferred are conduction, convection and radiation. All of these mechanisms affecting heat transfer may deliver heat to, or away from, living tissues. Sustained temperatures result in cellular dysfunction and early denaturation of protein. As the temperature or the time of exposure increases, cell damage increases.


Excessively high temperatures cause graded tissue injury radiating from the point of contact and become progressively less severe at the periphery. The increased temperature kills cells in the immediate area and coagulates and denatures the surrounding extracellular matrix proteins (zone of coagulation). Circulation to this area ceases immediately. The area surrounding the injury is characterized by decreased tissue perfusion (zone of stasis). The tissue in this zone is potentially salvageable. The main aim of burn resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults, such as prolonged hypotension, infection, or edema, can convert this zone into an area of complete tissue loss. With proper wound care, however, these pathophysiological changes may be reversed. The zone of stasis is surrounded by a zone of hyperemia. In this outermost zone, tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion. The three zones of a burn were described by Jackson in 1947. These three zones of a burn are three-dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.


Primary tissue loss in burn injury occurs as a result of protein denaturation secondary to thermal, chemical, electrical, friction, or ultraviolet radiation induced insults. This process is rapidly followed by activation of toxic inflammatory mediators, especially in the perfused subsurface. Oxidants and proteases further damage skin and capillary endothelial cells, potentiating ischemic tissue necrosis Burn wound conversion is also attributed to the secondary consequences of burn injury. Sequelae such as edema, infection, and altered perfusion promote progression of injury beyond the degree of initial cell death. Burn-induced disruption of collagen cross-linking abolishes the integrity of osmotic and hydrostatic pressure gradients, resulting in local edema and larger scale fluid shifts. In addition, damage to cell membranes results in a dynamic cascade of inflammatory mediators that exacerbate already abnormal cell-to-cell permeability, worsening fluid regulation and systemic inflammatory responses. At the molecular level, both complement activation and intravascular stimulation of neutrophils result in the production of cytotoxic oxygen free radicals. Increased histamine activity, enhanced by the catalytic properties of xanthine oxidase, causes progressive local increases in vascular permeability. Toxic byproducts of xanthine oxidase, including hydrogen peroxide and hydroxyl radicals, appear to directly damage dermal structures. One major component of burn shock is the increase in total body capillary permeability. Direct thermal injury results in marked changes in the microcirculation. Most of the changes occur locally at the burn site, when maximal edema formation occurs at about 8–12 h post-injury in smaller burns and 12–24 h post-injury in major thermal injuries. The rate of progression of tissue edema is dependent upon the adequacy of resuscitation.


The temperature of the heat source and the length of exposure determine the extent of tissue destruction (time-temperature curve). Patients burned by higher temperatures (molten metal, hot grease, or flammable clothing) have deeper burns than those burned with hot water. The effect also varies over different types and parts of the body. The result of heat injury is affected by variables such as skin thickness. The thicker, glabrous skin of the palms and soles is more resistant to full-thickness injury than is the thinner skin of the eyelid or dorsum of the hand. Infant skin is also thinner than adult skin and more likely to sustain full-thickness injury from the same temperature.


The depth of any injury is not always obvious initially, and observers often disagree. Many methods have been proposed to predict the depth of the injury immediately or soon after injury (ultrasound examination, intravenous fluorescent probes), but none has been as reliable as serial examination of the wound over time. The final depth of the injury typically becomes obvious 48–72 h after injury. Very rarely does the thermal injury penetrate into the subcutaneous or deep tissue.



Systemic response


The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% TBSA. Cutaneous thermal injury greater than one-third of the TBSA invariably results in the severe and unique derangements of cardiovascular function called burn shock. Shock is an abnormal physiologic state in which tissue perfusion is insufficient to maintain adequate delivery of oxygen and nutrients and removal of cellular waste products. Unresuscitated burn shock correlates with increased hematocrit values in burned patients, which are secondary to fluid and electrolyte loss after burn injury. Increased hematocrit values occurring shortly after severe burn injury result from fluid and protein translocation into both burned and non-burned tissues.


Burn shock is a complex process of circulatory and microcirculatory dysfunction that is not easily or fully repaired by fluid resuscitation. Severe burn injury results in significant hypovolemic shock and substantial tissue trauma, both of which cause the formation and release of many local and systemic mediators. Burn shock results from the interplay of hypovolemia and the release of multiple mediators of inflammation with effects on both the microcirculation and the function of the heart, large vessels and lungs. Subsequently, burn shock continues as a significant pathophysiologic state, even if hypovolemia is corrected. Increases in pulmonary and systemic vascular resistance (SVR) and myocardial depression occur despite adequate preload and volume support. Such cardiovascular dysfunctions can further exacerbate the whole body inflammatory response into a vicious cycle of accelerating organ dysfunction.



Hypovolemia and fluid extravasation


Burn injury causes extravasation of plasma into the burn wound and the surrounding tissues. Extensive burn injuries are hypovolemic in nature and characterized by the hemodynamic changes similar to those that occur after hemorrhage, including decreased plasma volume, cardiac output, urine output, and an increased systemic vascular resistance with resultant reduced peripheral blood flow. However, as opposed to a fall in hematocrit with hemorrhagic hypovolemia, due to transcapillary refill an increase in hematocrit and hemoglobin concentration will often appear even with adequate fluid resuscitation. As in the treatment of other forms of hypovolemic shock, the primary initial therapeutic goal is to quickly restore vascular volume and to preserve tissue perfusion to minimize tissue ischemia. The critical concept in burn shock is that massive fluid shifts can occur even though total body water remains unchanged. What actually changes is the volume of each fluid compartment, intracellular and interstitial volumes increasing at the expense of plasma volume and blood volume. In extensive burns (>25% TBSA), fluid resuscitation is complicated not only by the severe burn wound edema, but also by extravasated and sequestered fluid and protein in nonburned soft tissue. Large volumes of resuscitation solutions are required to maintain vascular volume during the first several hours after an extensive burn. Multiple formulae have been published with variations in both the volumes per weight suggested and the type or types of crystalloid or crystalloid-colloid combinations administered to approximate the fluid need of a burn patient. To date, no single recommendation has been distinguished as the most successful approach. A detailed description of various formulae appears later in this chapter. It should be emphasized that blind adherence to any formula can result in ‘overresuscitation’ and thereby to massive volume overload and edema. All formulae represent only a rough guideline to estimate the fluid need. Successful fluid resuscitation has to be adapted to the clinical need and to the monitoring (urinary output, sufficient mean arterial pressure). Data suggest that despite fluid resuscitation normal blood volume is not restored until 24–36 h after large burns. Edema formation often follows a biphasic pattern. An immediate and rapid increase in the water content of burn tissue is seen in the first hour after burn injury. A second and more gradual increase in fluid flux of both the burned skin and nonburned soft tissue occurs during the first 12–24 h following burn trauma.


The tissues in ischemic areas can potentially be salvaged by proper resuscitation in the initial stages and by proper burn wound excision and antimicrobial therapy in the convalescent period. Underresuscitation can convert this area into deep dermal or full-thickness burns in areas not initially injured to that extent. Reevaluation of these threatened areas over the first several days is used to determine when the first burn excision should be performed (i.e., when the depth of burn has become apparent and decisions about which areas are deep dermal or full thickness are clear).


A new area of interest with immediate resuscitation is the use of negative pressure dressings on affected areas. Animal models and early clinical work suggest that this treatment may limit the conversion of zones of hyperemia to zones of ischemia by removing edematous fluid and allowing salvage of areas that would otherwise need excision and grafting.




Initial evaluation and treatment


Treatment of a burned patient starts at the scene of injury with the safe removal of the patient from the cause of the burn. In all cases (especially if chemical or electrical burns), care must be taken to avoid personal injury by checking the area is safe and that appropriate protective clothing is worn if necessary. Priority should be given to assessing the person’s airway, breathing, and circulation, and presence of any coexisting injuries which may require more urgent treatment than the burn. Belts, clothes, jewelry and watches that can retain heat and cause constriction should be removed and the patient kept aware. An inhalation injury should be assumed and airway should checked and oxygen given. Heat can be dissipated from the burn wound by cooling with water but cold water and ice should not be used as they can cause rapid hypothermia. A quick assessment should be made for associated trauma and the patient transported to the nearest burn unit for definitive management (Box 18.1, Fig. 18.5).



Box 18.1


Burn injuries that should be referred to a burn unit




1. Partial thickness burns >10% TBSA and patients requiring burn shock resuscitation


2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints


3. Deep partial thickness burns and full thickness burns in any age group


4. Circumferential burns in any age group


5. Electrical burns, including lightning injury


6. Chemical burns


7. Burns with a suspicion of inhalation injury


8. Burns of any size with concomitant trauma or diseases which might complicate treatment, or prolong recovery, or affect mortality


9. Diseases associated to burns such as toxic epidermal necrolysis, necrotizing fasciitis, staphylococcal scalded child syndrome etc., if the involved skin area is 10% for children and elderly and 15% for adults or any doubt of treatment


10. Any patients with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols


11. Any type of burns if any doubt about the treatment


12. Burned children in hospitals without qualified personnel or equipment for the care of children


13. Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention


14. Suspected nonaccidental injury.


Modified from: European Burns Association. European Practice Guidelines for Burn Care & Guidelines for the Operations of Burn Units; 2002:55–62; Resources for Optimal Care of the Injured Patient; 1999; Committee on Trauma, American College of Surgeons; 1999.



Once the patient arrives at the emergency room, an evaluation of the Airway, Breathing, and Circulation (the ABCs) should receive first priority (Box 18.2). It is also important to exclude associated trauma. The history should include the time, location and circumstances of the injury, where the patient was found, and their condition (Box 18.3). Past medical and social history, current medication usage, drug allergies, and tetanus status should be rapidly determined. It is also important to consider the possibility of nonaccidental burns or scalding (Box 18.4).





A thorough assessment of a person with a burn should then take into account:




The airway should be secured because upper airway obstruction can develop quickly (Fig. 18.6). Smoke inhalation causes more than 50% of fire-related deaths. Patients sustaining an inhalation injury may require aggressive airway intervention (Fig. 18.7). Most injuries result from the inhalation of toxic smoke; however, super-heated air may rarely cause direct thermal injury to the upper respiratory tract (see complications, below). Patients who are breathing spontaneously and at risk for inhalation injury should be placed on high-flow humidified oxygen. Patients trapped in buildings or those caught in an explosion are at higher risk for inhalation injury. These patients may have facial burns, singeing of the eyebrows and nasal hair, pharyngeal burns, carbonaceous sputum, or impaired mentation. A progressive change in voice quality or hoarseness, stridorous respirations, or wheezing may be noted. The upper airway may be visualized by laryngoscopy, and the tracheobronchial tree should be evaluated by bronchoscopy. Chest radiography is not sensitive for detecting inhalation injury. Patients who have suffered an inhalation injury are also at risk for carbon monoxide poisoning. The pulse oximeter is not accurate in patients with carbon monoxide poisoning because only oxyhemoglobin and deoxyhemoglobin are detected. Co-oximetry measurements are necessary to confirm the diagnosis of carbon monoxide poisoning. Other pulmonary assessments include arterial blood gas measurements and bronchoscopy. Patients exposed to carbon monoxide should receive 100% oxygen using a nonrebreather facemask.





Burn assessment


After completion of the primary survey, a secondary survey must include assessment of the depth and TBSA burned (Figs 18.8–18.10).






Diagnosis/patient presentation


Accurate assessment of burn depth on admission is important in making decisions about dressings and surgery (Table 18.2). However, the burn wound is a dynamic living environment that will alter depending on both intrinsic factors (such as release of inflammatory mediators, bacterial proliferation) and extrinsic factors (such as dehydration, systemic hypotension, cooling). There is much evidence to demonstrate the beneficial effects of cooling on reducing tissue damage and wound healing time. Although immediate cooling is preferable, even a 30 min delay in application of cooling is still beneficial to the burn wound but the application of cooling 60 min after injury, does not demonstrate any benefit.8 Tetanus prophylaxis must be considered wherever there is tissue damage, and particularly in elderly patients. It is therefore important to review the wound at regular intervals until healing.



Optimum treatment of the wound reduces morbidity and, in larger injuries, mortality. It also shortens the time for healing and return to normal function and reduces the need for secondary reconstruction (Box 18.6). When epithelialization is delayed beyond 3 weeks, the incidence of hypertrophic scarring rises. Hypertrophic scars occur in 60% of burned children aged under 5 years. Optimal burn care requires early excision and grafting of all burns that will produce hypertrophic scars (typically those that will not or have not healed within 3 weeks of the injury), so an accurate estimation of burn depth is crucial. Early grafting of those burns that have not healed at three weeks has been shown to improve the result, but because of delays in the referral process, all injuries, which show no sign of healing by 10 days, should be referred for assessment. The appearance of the wound – and the apparent burn depth – changes dramatically within the first 7–10 days. A burn appearing shallow on day 1 may appear considerably deeper by day 3. This demarcation of the burn is a consequence of thrombosis of dermal blood vessels and the death of thermally injured skin cells. Superficial burns may convert to deeper burns due to infection, desiccation of the wound, or the use of vasoactive agents during resuscitation from shock.


Feb 21, 2016 | Posted by in General Surgery | Comments Off on Acute management of burn/electrical injuries
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