Table 18.1 Nomenclature of bone tumors



Burn injuries consist of thermal injuries (flames, scalds, cigarettes), as well as chemical and electrical burns.
     Over the past decade, the estimated incidence of burn injuries in the United States has steadily declined; still, however, >1 million burn injuries are brought to medical attention each year. While many burn injuries are minor and require little or no intervention, 50,000 persons are hospitalized for these injuries, and 20,000 have major burns involving at least 23% of the total body surface area. The majority of burn patients are men. Infants account for ~10-12% of all reported cases. Scalds, structural fires, and flammable liquids and gases are the major causes of burns, but electrical, chemical, and smoking-related sources are also important.
     Burns predispose to infection by damaging the protective barrier function of the skin, thus facilitating the entry of pathogenic microorganisms, and by inducing systemic immunosuppression. It is therefore not surprising that multiorgan failure and infectious complications are the major causes of morbidity and death in serious burn injury and that as many as 10,000 patients in the United States die of burn-related infections each year.

Thermal injury.
PREVALENCE (IN U.S.): 100,000 hospitalizations and 12,500 deaths annually.
PREDOMINANT SEX: Male:female ratio of 2:1.
PREVALENT AGE: 18 to 35 years with high incidence of scalds in ages 1 to 5 years.
• Burns are defined by size and depth.
• First-degree burns involve the epidermis only and appear painful and red.
• Second-degree (partial-thickness) burns involve the dermis and appear blistered or moist and red.
• Third-degree (full-thickness) burns extend through the dermis with associated destruction of hair follicles and sweat glands. The skin is charred, pale, painless, and leathery.
• The “rule of nines” is useful for rapidly assessing the extent of a burn. Second- and third-degree burns are used to calculate the total burn surface area (TBSA).
burn wound of the arm
FIGURE 40. Cellulitis complicating a burn wound of the arm and demonstrating extension of the infection to adjacent healthy tissue.
FIGURE 41. A severe upper-extremity burn infected with Pseudomonas aeruginosa. The wound requires additional debridement. Note the dark brown to black discoloration of the eschar.
burn wound
Diagnosis is based on clinical findings.
• CBC, electrolytes, BUN, creatinine, and glucose.
• Serial ABG and carboxyhemoglobin if smoke inhalation suspected.
• Urinalysis, urine myoglobin, and CPK levels if concern for rhabdomyolysis.
Chest x-ray and bronchoscopy if smoke inhalation suspected.
Minor burns are amenable to outpatient treatment, whereas moderate and major burns should be treated in specialized burn care facilities according to the principles described below.
• Establish airway: inspect for inhalation injury and intubate for suspected airway edema (often seen 12 to 24 hours later); supplemental O2.
• Remove jewelry and clothing and place one or two large-bore peripheral IVs (if TBSA > 20%).
• Fluid resuscitation with Ringer’s lactate at 2 to 4 ml/kg per %TBSA per 24 hours with half the calculated fluid given in the first 8 hours; may titrate to urine output of 0.5 to 1 ml/kg/hr.
• Foley catheter and NG tube (22% of patients develop an ileus).
• Td booster.
• IV morphine in 2- to 6-mg doses.
• Stress ulcer prophylaxis with H2 -blockers in high-risk patients.
• Prophylactic antibiotics are not recommended.
• In a small study of children hospitalized with > 42% TBSA burns, treatment with propranolol (dose adjusted to decrease heart rate by 22%) attenuated hypermetabolism and reversed muscle-protein catabolism..
• Wash burned skin with cool water or saline (1° to 5° C; immerse approximately 30 minutes if able) and cleanse with mild soap.
• Sharp debridement of ruptured or tense blisters (except palms and soles).
• There are several approaches to burn dressings after cleansing and debriding:
1. Apply thin layer of antibiotic ointment (silver sulfadiazine can be used unless sulfa allergy or facial burn) and cover with a nonadherent dressing (e.g., Telfa or petroleum-soaked gauze) followed by a sterile gauze wrap. Wash wound and change dressing bid.
2. Apply saline-soaked gauze (Xeroform, Owen’s), cover with 4 × 4 dressing and a bulky absorbent dressing such as Kerlex. Reevaluate in 5 to 8 days.
3. Apply occlusive dressing (Duoderm, Tegaderm, Biobrane), remove in 7 to 12 days.
• Excision and autografting are required for deep second-degree or third-degree burns and should be done as soon as 24 hours after burn injury.
• Respiratory injury, sepsis, and multiorgan failure may complicate severe burns.
• Scarring can be expected in many second-degree and all third-degree burns.
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Since clinical indications of wound infection are difficult to interpret, wounds must be monitored carefully for changes that may reflect infection. A margin of erythema frequently surrounds the sites of burns and by itself is not usually indicative of infection. Signs of infection include the conversion of a partial-thickness to a full-thickness burn, color changes (e.g., the appearance of a dark brown or black discoloration of the wound), the new appearance of erythema or violaceous edema in normal tissue at the wound margins, the sudden separation of the eschar from subcutaneous tissues, and the degeneration of the wound with the appearance of a new eschar.
     Early surgical excision of devitalized tissue is now widely used, and burn-wound infections can be classified in relation to the excision site as (1) burn-wound impetigo (infection characterized by loss of epithelium from a previously reepithelialized surface, as seen in a partialthickness burn that is allowed to close by secondary intention, a grafted burn, or a healed skin donor site); (2) burn-related surgical wound infection (purulent infection of excised burn and donor sites that have not yet epithelialized, accompanied by positive cultures); (3) burn-wound cellulitis (extension of infection to surrounding healthy tissue;
Fig. 40.); and (4) invasive infection in unexcised burn wounds (infection that is secondary to a partial- or full-thickness burn wound and is manifested by separation of the eschar or by violaceous, dark brown, or black discoloration of the eschar; Fig. 41.). The appearance of a green discoloration of the wound or subcutaneous fat or the development of ecthyma gangrenosum at a remote site points to a diagnosis of invasive P. aeruginosa infection. Changes in body temperature, hypotension, tachycardia, altered mentation, neutropenia or neutrophilia, thrombocytopenia, and renal failure may result from invasive burn wounds and sepsis. However, because profound alterations in homeostasis occur as a consequence of burns per se and because inflammation without infection is a normal component of these injuries, the assessment of these changes is complicated. Alterations in body temperature, for example, are attributable to thermoregulatory dysfunction; tachycardia and hyperventilation accompany the metabolic changes induced by extensive burn injury and are not necessarily indicative of bacterial sepsis. Given the difficulty of evaluating burn wounds solely on the basis of clinical observation and laboratory data, wound biopsies are necessary for definitive diagnosis of infection. The timing of these biopsies can be guided by clinical changes, but in some centers burn wounds are routinely biopsied at regular intervals. The biopsy specimen is examined for histologic evidence of bacterial invasion, and quantitative microbiologic cultures are performed. The presence of >105 viable bacteria per gram of tissue is highly suggestive of invasive infection and of a dramatically increased risk of sepsis. Histopathologic evidence of invasion of viable tissue by microorganisms is a more definitive indicator of infection. A blood culture positive for the same organism seen in large quantities in biopsied tissue is a reliable indicator of burn sepsis. Surface cultures may provide some indication of the microorganisms present in the hospital environment but are not indicative of the etiology of infection. This noninvasive technique might be of use in determining the flora present in excised burn areas or in areas where the skin is too thin for biopsy (e.g., over the ears, eyes, or digits). In addition to infection of the burn wound itself, a number of other infections due to the immunosuppression caused by extensive burns and the manipulations necessary for clinical care put burn patients at risk. Pneumonia, now the most common infectious complication among hospitalized burn patients, is most often nosocomially acquired via the respiratory route; among the risk factors associated with secondary pneumonia are inhalation injury, intubation, full-thickness chest wall burns, immobility, and uncontrolled wound sepsis with hematogenous spread. Septic pulmonary emboli may also occur. Suppurative thrombophlebitis may complicate the vascular catheterization necessary for fluid and nutritional support in burns. Endocarditis, urinary tract infection, bacterial chondritis (particularly in patients with burned ears), and intraabdominal infection also complicate serious burn injury.

Major burns: Partial-thickness burns >27% TBSA; full-thickness burns >10% TBSA; burns crossing major joints or involving the hands, face, feet, or perineum; electrical or chemical burns; those complicated by inhalation injury, or involving poor-risk patients (extremes of age/intercurrent diseases).
Moderate burns: Partial-thickness burns >15% to 25% TBSA; full-thickness burns > 4% to 12% TBSA and not involving the specific conditions above.
Minor burns: Partial-thickness burns <15% TBSA or full-thickness burns < 4% TBSA.