In the United States of America 2 million burn injuries occur each year, prompting 80 000 hospital admissions, and result in 6500 deaths and much disability. Up to 80 per cent of these injuries may have been prevented: prevention is ideal, but burn injuries nonetheless persist. Survival rates have improved over the past few decades. In the 1950s and early 1960s, survival from a 30 per cent body surface area burn injury at any age was almost unprecedented. Today children survive burns affecting more than 90 per cent of the body surface area, and young and middle-aged adults with more than 70 per cent burns survive routinely. These dramatic improvements have come from the recognition that destroyed and damaged tissues must be removed promptly after the injury and that the wound must be physiologically closed immediately thereafter. As the size of the burn injury increases, surgical strategies must be altered to accomplish the surgical goal of tissue excision and immediate wound closure.

The direct injury caused by a burn produces an initial volume of irreversibly damaged tissue, surrounding which is a region of tissue that has suffered reversible injury. The final depth and extent (lateral extension) of the injury depends upon the extent to which these adjacent sublethally injured tissues recover: survival of these adjacent tissues is influenced by the host's physiological response, which includes tissue oedema and ischaemia, the host's inflammatory response, and by environmental factors, including infections and the efficacy of topical treatment. The evolution of the depth and extent of the wound requires frequent observation by a knowledgeable clinician over the initial 3 to 5 days following injury so that the damage can be accurately assessed: accurate estimation of depth is important in determining treatment and prognosis.

When a burn wound heals spontaneously the dead tissue separates as new epithelium covers the injured area. When burns are superficial regeneration occurs rapidly from uninjured epidermal elements, hair follicles, and sweat glands within the injured tissue; since dermis remains intact, little scarring results unless infection intervenes. When burns are deep, however, the epidermis and much of the dermis is destroyed, and epithelialization starts from the edges of the wound or from the scattered integumental remains. Because this process is exceptionally slow excessive granulation tissue forms before the wound can be covered by epidermis. Wounds like these eventually contract dramatically; unless skin grafting is prompt, disfiguring or disabling scars result.

Grading of a burn as first, second, third, or fourth degree refers to the depth of the irreversible tissue damage (Fig. 1) 2889. The depth of injury can be determined from the appearance of the wound (Table 1) 709. Distinguishing first degree and superficial second degree injuries is usually simple; operative intervention is rarely required. A distinction between deep second degree and third degree burns can often not be made until after 3 to 5 days of observation; however, in either case surgery is the optimal treatment. Fourth degree burns are readily apparent upon observation; they are always treated surgically.

Elderly patients and young children require additional consideration since they have thin skin, and are therefore more likely to suffer full-thickness injuries when exposed to burning agents that would create only partial-thickness injuries in other individuals. This point is particularly important when assessing scald burns, which occur relatively frequently in toddlers. These indeterminant injuries are usually deeper than is initially apparent, and this becomes obvious after 3 to 5 days of observation.

The overall extent of the burn injury is best estimated by recording the affecting areas on a burn diagram and estimating the percentage of the body surface area using the ‘rules of nines’ in the adult (Table 2) 710 or using the Lund–Browder chart in children (Fig. 2) 2890. Special consideration is necessary in children, in whom the head represents a much greater percentage of the total body surface area, while the lower extremities represent a lower percentage than in adults.

The physiological impact of the injury or severity of the burn can be judged from the quantity of tissue involved in the injury (Table 3) 711. This assessment is represented by the percentage of the body surface area burned and by the depth of the burn. A small injury will generally require little treatment and often does not greatly alter the cardiovascular and metabolic state. Moderate and large injuries require resuscitation of the patient and have potentially dire cardiovascular and metabolic consequences.

Electrical burns occur when electrical current passes through the body, and severe internal damage may occur even when the most obvious cutaneous manifestations are only small wounds of entrance and exit. The two major additional effects of electrical injury are the effect of the electric current upon normal cardiac electrical conductivity and the fact that electrical current tends to cause more damage to deep tissues than to superficial tissues. Continuous cardiac monitoring is mandatory for at least the first 24 h after an electrical burn. Damage to deep tissues can be assessed by frequent observation by knowledgeable observers and ultimately by sequential operative debridement of devitalized tissues in the wound and in adjacent subfascial compartments.

Chemicals continue to destroy tissue while they remain in contact with the skin; the best treatment for chemical injuries is to flush the surface immediately with copious amounts of water, to remove or dilute the chemical agent. Powdered chemicals may be brushed from the skin and then flushed from the body surface. Chemicals in contact with the eyes should be thoroughly irrigated with clean water subsequently evaluation by an ophthalmologist is required.

Chemical agents designed for warfare which require further consideration include nerve agents (tabun, sarin, soman, and VX), blistering agents (mustard and nitrogen mustard), choking agents (phosgene), blood poison or anoxia agents (hydrocyanic acid and cyanogen chloride), and phosphorus. Nerve agents are volatile liquid organophosphates that may be inhaled or absorbed through the skin at ambient temperatures. They act primarily by inhibiting acetylcholinesterase at cholinergic receptor sites and result in cholinergic (muscarinic and nicotinic) hyperactivity without serious skin injury. The actions of these agents can be blocked by atropine, pyridostigmine bromide (Mestinon), and anticonvulsants. Choking agents are intended to be inhaled and produce upper airway irritation, bronchospasm, and bronchorrhoea without skin injury. The anoxia agents are also inhaled, and interfere with the oxygen utilization by the tissues. They do not cause cutaneous injury, but lead to deep coma and death within minutes. Other warfare agents, such as mustard, nitrogen mustard, and phosphorus burn skin: exposure should be treated by copious water flushes to dilute and remove the agent.

The initial approach to management of the patient with a major burn is similar to that of any other major trauma patient, as suggested by the American College of Surgeons in the Advanced Trauma Life-Support Course. Assessment begins with a primary survey including evaluation of the ‘A, B, C’ of resuscitation (Airway with cervical spine immobilization, Breathing, and Circulation). Later, a complete secondary survey should be conducted from head to toe to identify associated injuries: although the burn may often be the most obvious injury, other serious and life-threatening injuries can also be present. As part of the secondary survey, a pertinent history of past illnesses should be elicited, with emphasis on details of the accident.

The patient must have an adequate airway free of any obstruction and be able to breathe adequately (Table 4) 712. If the airway is adequate and the patient is breathing, administration of oxygen by face mask or by nasal cannulas may be sufficient. However, if the patient is not breathing well because of either an obstructed upper airway or a depressed depth or frequency of breathing, endotracheal intubation is necessary. This is best performed through the nose, although orotracheal intubation can be a reasonable alternative. Emergency tracheostomy should be avoided unless it is absolutely necessary. For patients with associated cervical spine injuries, stability should be evaluated with at least a cross-table lateral cervical spine radiograph prior to intubation: until the cervical spine is evaluated fully, all manipulations of the head and neck must be performed with immobilization of the head and neck in the axis of the body. Although these safeguards do not eliminate spinal cord injury, they lower the potential risk to an acceptable and reasonable level. Proper alveolar ventilation can be usually achieved once the patient is safely intubated.

As part of the primary survey, adequacy of the peripheral circulation can be determined early after the burn injury by palpatation of peripheral pulses. All clothing should be completely removed before the patient reaches hospital, or in the receiving hospital's emergency room. This allows a rapid determination of the extent of injury and adequacy of peripheral circulation, and stops the burning process by removing smouldering or chemical-laden clothing. Rings, watches, and other jewellery should be removed from any injured limbs: constriction of an oedematous extremity by jewellery can result in distal ischaemia.

Fluid is transferred to the area of injury from the vascular space within minutes of thermal injury. This fluid loss may result in hypovolaemic shock; the greater the surface area involved, the more extensive the hypovolaemia. Initial volume resuscitation should begin immediately, following the introduction of at least two large-bore intravenous catheters—ideally into non-burned upper or lower extremities, but through burned tissues if necessary. In hospitals equipped to manage complications of central venous cannulation, placement of a central venous catheter is preferred when extremities are circumferentially burned; ‘cut-downs’ should be avoided unless absolutely necessary. Since patients with moderate burns often have an ileus that persists beyond the early days of treatment, a nasogastric tube should be used to decompress the bowel. A Foley catheter is necessary to allow measurement of urine output accurately.

Of this volume, 50 per cent must be given in the first 8 h following the injury (note: this first 8-h period begins at the time of injury, not with the initiation of resuscitation). The remaining fluid is given over the next 16 h. In this calculation, the percentage body surface area burned includes the sum of partial- and full-thickness injury: the fluid requirement in the second 24 h is usually approximately 50 per cent of the calculated resuscitation volume. Monitoring of vital signs is required to maintain an adequate urine output of at least 0.5 ml/kg.h. This guideline provides an initial estimate of fluid replacement; however, only close monitoring during initial treatment can direct the treatment of an individual patient.

The secondary survey begins with a detailed physical examination from head to toes which aims to detect any associated injuries (Table 5) 713. A history is taken during the examination, and details regarding the accident should be obtained, including information about the burning agent, the location of the injury (closed versus open space), the possibility of smoke inhalation, exposure to noxious chemicals, and the possibility of any related trauma. A history of pre-existing illnesses such as diabetes, hypertension, and cardiac or renal disease should be elicited. Use of regular medications, alcohol, or drugs should be identified. Allergies or other sensitivities should be identified, and a history of tetanus immunizations should be obtained.

Following both the primary and secondary surveys, definitive resuscitation therapy should be instituted. Morphine may be used for pain management; however, full-thickness burns are painless because nerve fibres have been destroyed. Narcotics and other parenteral medications that are administered should be given intravenously, not intramuscularly, since drugs are poorly absorbed from muscular tissues during hypovolaemic shock, but they may be absorbed rapidly once circulation is restored.

Patients who have undergone previous tetanus active immunization and have had a toxoid booster injection within 1 year of the injury require no further prophylaxis unless they have an associated tetanus-prone wound, when they should receive a toxoid booster injection. Patients who received their most recent booster injection more than 1 year before injury should be given a booster dose of toxoid; those who have not received prior immunization should be given human antitetanus globulin and an immunizing dose of toxoid, followed by the usual immunizing dosage schedule of toxoid established for non-immunized people.

Initially the burn wound should simply be covered with a clean, dry sheet with no creams or other medications. Covering the wound excludes air from partial-thickness injuries and may diminish pain. Application of ice is neither useful nor recommended. Initial laboratory studies that should be undertaken include haematocrit, glucose, electrolytes, blood urea nitrogen, urinalysis, and chest radiograph. In patients with large burns or possible inhalation injuries, arterial blood gases, an electrocardiogram, and a measurement of blood carboxyhaemoglobin should also be obtained.

Oedema may develop underneath circumferential burns of extremities and compromise the arterial circulation to more distal aspects of the extremities. Early after the injury, the adequacy of the peripheral circulation can usually be assessed by palpation of the peripheral pulses. However, these pulses frequently become impossible to identify as oedema develops under a circumferential eschar. Increased compartment pressures can completely obstruct arterial inflow, leading to distal ischaemia, necrosis, and gangrene. Signs and symptoms of peripheral ischaemia can be difficult to identify in patients with large burns, who are often intubated, receiving narcotics, and have peripheral oedema due to administration of resuscitation fluid. The classic signs and symptoms of peripheral ischaemia (pain, paraesthaesias, pallor, pulselessness, and paralysis) may therefore be masked, and Doppler ultrasound is the only reliable method for its early detection. When vascular compromise occurs escharotomies (incisions made through burned epidermis and dermis) are necessary to restore both arterial and venous circulation.

Circumferential chest burns may similarly restrict chest wall excursion and minute-alveolar ventilation; escharotomies of the chest wall may be required when supranatural inspiratory pressure is required to ventilate the lungs. Escharotomies should be carried out in these patients after consultation with regional burn care centres.

Fasciotomy is usually not necessary, except in patients with very deep extremity burns and burns from electrical injuries. The volar compartments of the forearm and anterior, lateral, and posterior compartments of the leg are the important regions to consider for decompression by fasciotomy. The clinical indication for fasciotomy is similar to that for escharotomy, but the confining tissue is the deep fascia and not the eschar. Escharotomy will often decompress the compartmental pressures sufficiently to obviate the need for fasciotomy. The use of devices to determine the need for fasciotomy based upon compartmental pressures is investigational and the decision to perform a fasciotomy should be made on clinical grounds.

About 85 per cent of burns are small and can be treated in out-patient facilities. Patients with more severe burns require admission and consideration for treatment in a specialized burn facility after initial assessment and treatment has been provided. The types of injuries that should be referred to a specialized treatment centre are shown in Table 6 714.

Patients with pre-existing cardiovascular and renal disease present special problems. Since most cardiac arrhythmias are caused by hypovolaemia, hypoxia, acidosis, or hyperkalaemia, these metabolic disorders should be sought and corrected in addition to the use of drugs to rectify cardiac problems as necessary. Fluid, electrolyte, and colloid administration should be limited to amounts sufficient to produce a urinary output of 0.5 to 1 ml/kg.h in adults and 0.5 ml/kg.h in children. Pulse, blood pressure, temperature, electrocardiogram, and arterial blood gases should be monitored, particularly in elderly patients and in those with moderate or larger injuries.

Hypokalaemia is common in the early resuscitation period: many patients present with depleted K⫀ stores secondary to prior diuretic therapy and K⫀ is not generally included in the early vigorous fluid replacement. Serum potassium levels should be aggressively maintained above 4 mEq/l. If 0.5 per cent silver nitrate topical solution is used as a topical antibacterial agent, one should remember that this hypotonic solution leeches Na⫀ and Cl&sub-;, and possibly K⫀, from the tissues into the wet dressings; additional supplementation of these electrolytes may be necessary to avoid severe hyponatraemia, hypochloraemia, and hypochloraemic alkalosis.

Hypoalbuminaemia results from a combination of the dilutional effects of crystalloid replacement therapy and enhanced loss of protein into the subeschar oedema fluid. Parenteral administration of colloid solution should be continued throughout the resuscitation period to maintain albumin levels at or above 1.5 g/dl. Since most calcium in the serum is reversibly bound to albumin, hypocalcaemia may be a result of hypoalbuminaemia. Although the ionized fraction of serum calcium is usually normal, it should be measured periodically. Replacement quantities of calcium, phosphate, and magnesium may be given daily.

Generalized poor tissue perfusion resulting from hypovolaemia or cardiac failure causes metabolic acidosis. A blood pH measurement of less than 7.2 should prompt consideration of intravenous sodium bicarbonate treatment; the underlying aetiology of the metabolic acidosis must be identified and treated vigorously. Focal poor tissue perfusion can result from constricting eschar or fascia; it should be treated surgically. Metabolic acidosis can also result from the inhibition of carbonic anhydrase activity by topical sulphamylon; the contribution of this to the overall metabolic acidosis can be dramatic.

Because thermally injured skin loses core body heat more rapidly than normal skin, maintenance of body temperature is important. Hypothermia below 97°F (36°C), can be associated with poor peripheral perfusion and cardiac arrhythmias. Rewarming patients from temperatures below 91°F (33°C) can be associated with fatal arrhythmias; these patients should be warmed slowly and monitored continuously.

Myoglobinuria can result from ischaemic constriction of muscle, deep thermal injury, or electrical burns of muscle. It should be treated by alkalinization of the urine with sodium bicarbonate with frequent monitoring of both serum and urinary pH to allow adjustments to treatment; the goal is a urinary pH above 8. Intravenous mannitol may be needed to promote osmotic diuresis if myoglobinuria is severe. Haemoglobinuria may result from erythrocyte destruction following burns; its treatment is identical to that for myoglobinuria. Both abnormalities may result in renal tubular necrosis if not promptly and accurately managed.

Injuries of the respiratory tract of burn patients are a heterogeneous group of pulmonary complications and they increase the risk of mortality by 20 per cent for a given cutaneous injury. Respiratory injuries are clinically divided into asphyxia, pharyngeal-glottic and upper airway injuries (upper airway obstruction), and respiratory bronchiolar-alveolar injury (gas exchange difficulties).

Asphyxia seriously contributes to mortality from burn injuries: there are 3000 to 4000 deaths from carbon monoxide poisoning or asphyxia in the United States each year, and the majority of these patients die at the scene of the accident. Death occurs from the decreased availability of haemoglobin for oxygen binding and, therefore, a decreased oxygen carrying capacity and oxygen delivery. The target organs are the brain and myocardium and victims present with myocardial ischaemia and neurological depression. Cyanide exposure may also contribute to asphyxia and should be considered in patients with a history of exposure to burning plastics.

Glottic and airway injuries may be present in up to one-third of burn patients and may result from a combination of thermal and chemical damage. These injuries have a variable presentation: onset of airway oedema and resultant obstruction is occasionally sudden, but an insidious and delayed onset of respiratory complications, including tracheobronchial infection, is more common. Few gases have sufficient heat capacity to produce thermal damage below the level of the trachea and direct thermal injury usually only affects the uppermost airway. The exceptions to this are superheated steam and explosions occurring within the airway itself.

The diagnosis of inhalation injury is usually made by clinical suspicion and bronchoscopy; chest radiography and arterial blood gases may initially be normal. Inhalation injury can often be confirmed by ¹³³Xe lung scans and by pulmonary function testing. The treatment of acute pulmonary injuries and their respiratory complications is entirely symptomatic: little is known about the mechanism of injury or repair. The consensus is against the continuous use of corticosteroids or prophylactic antibiotics for inhalation injuries in the early post-burn period. Surveillance for infection should be employed, along with maximal pulmonary physiotherapy.

Prompt excision and immediate wound closure removes devitalized tissue and replaces it with either autografts or acceptable skin substitutes such as allografts or artificial skin. Prompt excision and immediate wound closure consists of the surgical removal of all areas of the burn (both deep dermal and full-thickness injury) that will require more than 3 weeks to heal spontaneously. Separate surgical procedures begin as soon as possible after injury and are continued until all devitalized tissue (eschar) is excised. In massive burn injuries the first surgical procedure includes harvesting of all available donor sites, excising the largest burned areas that have the highest likelihood of successful graft take, and immediately closing the excised area with autografts. Excision and autografting of the back is often chosen as the first procedure because this shows reliable skin graft take and such treatment greatly simplifies the patient's clinical care once a graft has taken. The physical state of the resuscitated patient does not recover after the injury but steadily deteriorates until wound closure is complete. Therefore the operative procedures should begin as soon after injury as possible when the physiology of the patient is closer to normal: extensive operative procedures performed in the first week after injury are frequently safer than those undertaken in the third week. It is equally important to harvest the autograft donor sites soon after injury. Since donor sites heal and may be reharvested in 2 weeks, the sites harvested on the first day after injury can usually be reharvested on about day 14. This plan minimizes both the time required for autograft closure and length of hospital stay.

There are two critical problems for the nutritional management of an injured patient. First, what level of caloric intake will be required to allow the patient to meet the caloric needs in response to his or her injury? Second, what mixture of substrates (proteins, carbohydrates, and fats) will meet the caloric requirements and optimally satisfy metabolic needs without incurring a negative nitrogen balance?

Oxygen consumption studies have shown that the metabolic rate of burn patients does not exceed twice the patient's normal basal metabolic rate as predicted by the Harris–Benedict Table of Correlations for adults and children above 2 years old. Usually, the metabolic rate does not exceed a 50 per cent increase above the normal basal rate. The Harris–Benedict correlation considers age, sex, height, and weight as factors which determine basal caloric requirements: Equation 38

where BMR is normal basal metabolic rate in kcal, W is ideal body weight in kg, H is height in cm, and A is age in years. Age, sex, height, and weight normally control individual metabolic rates. Studies have demonstrated that although the size of the open burn wound and body temperature contribute to hypermetabolism, their contribution is small and for clinical purposes their contribution can be neglected in determining daily caloric requirements of burn patients. Since doubling the BMR overestimates the effect of even the largest burn, one may elect to ignore burn size and body temperature to simplify the clinical calculation of caloric need. The daily caloric need for a seriously burned patient who is performing no muscular exercise may therefore be calculated using the simple formula: Equation 39

The total caloric requirement is met by provision of carbohydrate, protein, and fat. A carbohydrate delivery rate of 5 mg/kg.min provides enough calories to minimize the utilization of amino acids as an energy source and approximates the maximum rate of glucose oxidation for an injured patient remaining in bed. Additional exogenous glucose delivered to a patient at rest is not used for ATP production but is simply converted to fat. At the infusion rate of 5 mg/kg.min, the respiratory quotient is just below unity, indicating that glucose is being oxidized to CO&sub2;, H&sub2;O, and energy and is not being stored as fat.

Protein should be infused at a rate of 1.5 to 2.5 g/kg.day, depending on the size of injury and the presence of sepsis. This rate of administration has been shown to maintain a positive nitrogen balance in adults and in children, but neither the exact protein requirements nor the optimal mixture of amino acids required by seriously injured patients are known. Unfortunately, nitrogen balance studies do not produce the exact information necessary to determine the quantity and composition of the proteins required. Until rates of synthesis of muscle protein, collagen components of host defence, and other proteins can be accurately measured in vivo, this protein replacement rate remains only an estimate.

Calculating the caloric equivalent received by a seriously burned patient given glucose at 5 mg glucose/kg. min and protein at 2.5 g/kg.day shows that the patient's caloric requirement (calculated as BMR × 2) is not achieved. Fats are therefore given to meet the remaining caloric requirement, via either the enteral or parenteral route. These fats supply calories and minimize the need for mobilization of endogenous proteins for energy and gluconeogenesis; they also provide essential fatty acids. Administration of parenteral lipids in the form of intravenous fat emulsions should be used with caution in burn patients: this has been associated with thrombocytopenia, particularly in infants and children.

Early, aggressive metabolic support with amino acids begins within hours after the injury in patients with burns affecting greater than 20 per cent of the body surface area, pre-existing malnutrition, patients with complications such as sepsis or associated injuries, and those admitted late after a burn and who have already lost more than 10 per cent of their premorbid weight. Nutritional support is begun as soon as possible after the injury, but not later than 24 h after completion of the immediate post-burn resuscitation phase or within 12 h after injury. This support is accomplished by oral feeding, enteral feeding, or total parenteral nutrition, depending on the patient's condition. The enteral route is preferred since it is associated with fewer complications and is cheaper than parenteral feeding. However, anorexia, facial burns, or dysphagia may make oral feeding difficult or impossible and enteral feedings may need to be given via tubes. If gastric emptying is delayed but intestinal absorption is normal, continuous enteral feeding can be given using post-pyloric feeding tubes. Total parenteral nutrition is used if intestinal motility or absorption is abnormal or if multiple operative procedures are anticipated over the first weeks of the admission, inhibiting normal gastrointestinal absorptive function.

Infection of the burn wound is a major cause of complications and death in burn patients: the best approach to the problem is the prevention of wound infection. Infection is most likely to affect a large open wound containing necrotic tissue; susceptibility is increased by the lowered host resistance that results from serious trauma, and this is more important than the virulence of most infecting bacteria in determining the seriousness of the infection. Decreased host resistance must be corrected or prevented. Necrotic tissue must be removed and wounds properly closed. Secondary derangements in physiology and metabolism leading to caloric and protein starvation must be corrected. Cross-contamination of wounds must be prevented, and antibiotic treatment to prevent invasive infections should be administered only at times of increased patient risk.

Prompt excision of necrotic tissue and immediate closure of the wound with skin graft is essential in preventing infection. Protection of the wound from cross-contamination is promoted by maintaining the patient in a isolated environment and by following standard precautions. An additional and important adjunct is the use of topical antibacterial agents such as 0.5 per cent silver nitrate, 10 per cent mafenide acetate (sulphamylon), or silver sulphadiazine to reduce bacterial colonization of the burn wound.

Before application of a topical agent, all grease, oil, loose skin, burned clothing, and other contaminants should be removed. The advantages and disadvantages of commonly used topical agents are shown in Table 7 715. If 0.5 per cent silver nitrate is to be used, a thick layer of wide mesh gauze dressing is placed on the wound and saturated with the agent, which not only markedly decreases bacterial growth on the burn wound, but also minimizes evaporative water loss, thereby conserving energy. Silver nitrate is not used on the perineum or face because of the potential for ingestion and likelihood of staining of mucous membranes. For these areas, silver sulphadiazine has been used. Dressings should be soaked with the solution every 2 h to maintain a 0.5 per cent concentration at the wound surface. A lower concentration is not bacteriostatic; a higher concentration can damage viable skin. Rarely, methaemoglobinaemia can be produced when nitrates are reduced by certain unusual strains of Escherichia coli and Klebsiella in wounds.

The two other topical agents frequently used are creams of sulphamylon and silver sulphadiazine. They are applied twice daily directly to the burn wound after the initial removal of wound contaminants. All previously applied sulphamylon or silver sulphadiazine must be removed before a fresh layer is applied. As previously mentioned, sulphamylon is a carbonic anhydrase inhibitor and can cause a severe metabolic acidosis. Allergic reactions and haemolysis may develop in patients deficient in glucose 6-phosphate treated with either sulphamylon or silver sulphadiazine.

Routine administration of systemic antibiotics throughout the burn illness does not prevent burn wound infection and should not be used. The use of antibiotics for indiscriminate periods in an effort to avoid infection is actually an ineffective and dangerous approach that alters the normal flora and causes allergic reactions, renal, otic, or other organ injury, and wound colonization by resistant bacterial strains. Nevertheless, routine antibiotic administration can, in specific instances and for short intervals, supplement the patient's natural ability to fight invasive infection. Antibiotics are of considerable importance for two general indications: in prevention of infection during specific periods of reduced host resistance and in established infections.

Prophylactic antibiotics may be useful immediately after injury, when host defence is reduced. Wound cellulitis caused by &bgr;-haemolytic streptococci can be prevented by administration of anti-streptococcal agents for 3 days after injury in all patients with serious second degree or with third degree burns. Prophylactic antibiotics may also be appropriate to prevent the high incidence of bacteraemia which occurs during and after excision of colonized burn eschar. Treatment should begin immediately before the operation and last through the immediate postoperative period, until normal cardiovascular haemodynamics are restored (usually within 24 h) and other normal physiological signs return. The perioperative antibiotic given should be chosen on the basis of previous burn wound culture results and sensitivities of the organisms. If these are unavailable, general antimicrobial coverage for both Gram-positive cocci and Gram-negative rods is recommended. Intravenous antibiotics should be directed toward the commonly encountered Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Klebsiella, Acinetobacter, and Proteus spp. Both vancomycin and aminoglycoside serum levels should be measured when these antibiotics are used perioperatively but continued for more than 48 to 72 h.

Identification of invasive infections requiring antibiotic treatment is often difficult because burn wounds are not normally sterile and therefore, wound bacteriology will not alone distinguish between wound colonization and invasive infection requiring treatment. Once a diagnosis of invasive infection has been established, however, prompt systemic antibiotic therapy is required. Indications for antibiotic treatment in burn patients are outlined in Table 8 716.

The best indicator of invasive infection of a burn wound is histological evidence of bacterial invasion of viable tissue at the base of the wound. Biopsy of the wound should be performed to include the viable wound base, and the specimen should be subjected to grinding and bacterial quantitation, as well as to routine morphology, including the proper stains for bacteria and yeast. Quantitative burn wound cultures and histological evaluation is difficult to perform in the course of routine burn care and is not usually useful clinically.

The infecting organism can usually be predicted by referring to the most recent surveillance cultures of the burn wound, urine, and respiratory tract secretions. In large burn injuries, surveillance cultures of body fluids should be taken on a regular basis at least weekly: the last strain cultured from the burn wound is often responsible for the invasive infection. More definitive information can be obtained from blood cultures obtained at the first clinical indication of invasive infection.

Pathogenic Gram-negative bacteria, especially E. coli and Klebsiella and Enterobacter spp., are usually responsible for invasive infections. These organisms are best managed on the basis of individual sensitivity testing of the particular isolate. If the pathogen cannot be identified, both an aminoglycoside and penicillinase-resistant penicillin should be given to allow wide spectrum coverage until more specific antibiotic therapy can be designed. In patients with large, open wounds, and especially in children, drug leakage from the wound greatly complicates accurate therapy that is based on body size, and serum antibiotic levels should be monitored to ensure that therapeutic drug levels are maintained.

Bronchogenic infections or pneumonia occur frequently, usually accompany inhalation injury, and are commonly due to the organism colonizing the burn wound. Long-term prophylactic corticosteroid therapy is detrimental, and preventive antibiotics are probably ineffective after inhalation injury. Daily sputum cultures are appropriate in the susceptible patient and dictate the choice of antibiotic if pneumonia does occur. Attention to pulmonary therapy and toilet is also indicated.

The adult respiratory distress syndrome occurs frequently in thermally injured patients, but is particularly difficult to distinguish from inhalation injury. In addition, cardiogenic pulmonary oedema, bronchopneumonia, and severe tracheobronchial infection need to be excluded. The typical chest radiograph findings and pulmonary gas exchange abnormalities usually confirm the diagnosis in the absence of significant inhalation injury and infectious processes. Treatment is supportive, as in other critically ill patients with associated organ failures.

The incidence of pulmonary emboli in thermally injured patients is low. The embolic pathogenesis is similar to other patient populations. Generally, the asymptomatic burn patient is not given prophylactic anticoagulants.

Pulmonary oedema may occur following inhalation injury or fluid overload, particularly in patients lacking cardiac reserve. Close attention should be given to arterial O&sub2; tension, respiratory mechanics, and the administered fluid load. Intubation, positive end-expiratory pressure, and pharmacological intervention may become necessary. When pulmonary oedema occurs immediately after the burn, extensive parenchymal chemical damage has probably occurred and the prognosis is guarded. Atelectatic changes and pneumonitis may also occur. Atelectasis and aspiration can be prevented and treated as in other hospitalized patients.

Curling first noted the association between bleeding duodenal ulcers and burn injury in 1842. The incidence of diagnosed gastric or duodenal ulceration in burn patients was about 10 per cent in 1970; however, ulcer-related complications have markedly decreased in the last decade, probably due to the advent of continuous tube feedings and exacting control of gastric pH. The pathophysiology of the initial mucosal injury appears to be related to mucosal hypoxia which increases susceptibility to damage by normal concentrations of gastric acid. This hypoxia may be due to diminished organ blood flow or submucosal arteriovenous shunting.

The other notable gastrointestinal complication is impaired motility involving the gastrointestinal tract and the biliary system. Acute gastric dilation and intestinal paralytic ileus are commonly seen and are probably the result of frequent anaesthesia, sepsis, fluid overload, and electrolyte imbalances. Delayed gastric emptying and ileus frequently limit the success of enteral alimentation. Acute acalculous cholecystitis is common in these critically ill patients. It usually manifests as sepsis, right upper quadrant pain and mass, and liver function abnormalities. An ultrasound examination or radionuclide scan usually supports the diagnosis. Cholecystitis can often be treated by antibiotics plus cholecystectomy, cholecystostomy, or percutaneous drainage.

Acute renal failure may be secondary to hypoperfusion and hypoxia occurring before plasma volume was replaced in resuscitation. Failure may also be exacerbated by precipitation of free haemoglobin from damaged red blood cells or muscular myoglobin from crush or electrical injuries; or it may be a result of nephrotoxic drugs, particularly antimicrobial agents, which are administered to these patients. These insults may also be superimposed on pre-existing renal compromise. Oliguric or non-oliguric acute tubular necrosis can result, with the additive attendant clinical problems of acute renal failure in combination with management of the burn injury.

Congestive heart failure occurs either in the acute phase of the burn injury or during the mobilization of the peripheral oedema. Endocarditis may also complicate burn sepsis and should be kept in mind as an infrequent cause of infection. The use of digitalis and antiarrhythmics may become necessary in specific patients.

Burn encephalopathy encompasses a wide range of cerebral compromise syndromes whose aetiologies include water intoxication, acute hypertension, drug narcosis, septicaemia, hyperpyrexia, and dehydration. Necropsy at the end stage of this encephalopathic picture reveals cerebral oedema and uncal or cerebellar herniation.