Risk factors

Children under 5 years old are a vulnerable group, susceptible to injury and especially to burns. The two most common causes of burns are scalds and contact burns. The latter play a minor role since they imply injury of small extent and rarely require admission to hospital. On the other hand, scalds are often accidents of such a severity that hospitalization and resuscitation are required. In children, scald burns accounted for about two-thirds of burn injuries and in those <5 years old, scalds caused 75% of all burn injuries, most commonly occurring in the kitchen. In adults, predisposing factors to scalding include alcoholism, senility, psychiatric disorders, and neurological disease such as epilepsy.

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

Flash and flame burns

Flash and flame burn injuries are the most common cause of adult burn admissions. In general, flash burns reach progressive layers of the dermis in proportion to the amount and kind of fuel that explodes. In contrast to flash injuries, flame burns are invariably deep dermal if not full-thickness because of more prolonged exposure to intense heat and are often associated with inhalational injury and other concomitant trauma. Patients whose bedding or clothes have been on fire rarely escape without some full-thickness 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.

Fig. 18.1 The burn wounds may give clues to the mechanism of injury. The burn tideline associated with sitting in a bath of hot water.

Contact burns

In order to get a burn from direct contact, the object touched must either have been extremely hot or the contact abnormally long. The latter is a more common reason, and these types of burns are commonly seen in people with epilepsy or those who misuse alcohol or drugs. They are also seen in elderly people after a loss of consciousness; such a presentation requires a full investigation as to the cause of the blackout (Fig. 18.2). Contact burns commonly result from hot metals, plastics, glass or hot coals. Burns from brief contact with very hot substances are usually due to industrial accidents. Although generally small in size, contact burns are challenging in that the injury tends to be deep dermal or full thickness.

Fig. 18.2 Direct contact burn.

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.

Chemical burns

See ‘Cold and chemical injury to the upper extremity,’ Chapter 20 for details of chemical burns.

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

Fig. 18.3 Electrical burn wounds.

Fig. 18.4 Entry site for an electrical burn.

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.

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.

Mediators of burn injury

Apart from the burn shock mechanism already described, burn injury produces a veritable cornucopia of local and circulating mediators that are produced in the blood or released by cells after thermal injury. These mediators clearly play important, but complex roles in the pathogenesis of edema and the cardiovascular abnormalities of burn injury. Osteo-muscular proteolysis, lipolysis, gluconeogenesis, increased metabolic rate, and a severe systemic inflammatory response are induced by local infections or surgical procedures. The increased vascular permeability post-burn is mediated by histamine and numerous vasoactive substances, including serotonin, bradykinin, prostaglandins, leukotrienes, and platelet activating factor. Hyper-metabolism is mediated by hormones such as catecholamines, glucagon, and particularly cortisol.

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).

Fig. 18.5 Burns patients often have other injuries that require attention.

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.

Fig. 18.6 The airway must be secured early in cases of airway involvement.

Fig. 18.7 Inhalation injury necessitates aggressive airway interventions, here nasopharyngeal suction.

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.

Table 18.2 Typical findings in burn injuries

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.

Box 18.6

Burn reconstruction priorities

Urgent and important procedures

• Deformities affecting vital function (e.g., airway, oral continence, protection of the eye, and hand function)

• Compression/entrapment or neurovascular bundles

• Severe contractures

Important procedures

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