Pediatric Burns
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Pediatric Burns By Bradley J. Phillips

Chapter 2:  Principles of Pediatric Burn Injury
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obtained. Quantitative cultures of the wound are useful to differentiate infection from colonization. Broad-spectrum antibiotic coverage should be started immediately and continued until culture sensitivities can further direct treatment. If no infection is found, then antibiotics may be stopped after 48 to 72 hours to avoid overuse of broad-spectrum antibiotics. Preventative protocols, such as the scheduled rotation of central venous catheters, also help to reduce the prevalence of sepsis.20

Antibiotics/Antifungals

There is no role for systemic antibiotic prophylaxis in burn care. Antibiotics should only be initiated to treat known or suspected infections and continued as directed by culture sensitivities.12 Prudent, sensitivity-driven antibiotic use is important in limiting antibiotic resistance in a population very prone to sepsis and infection. Fungal wound infections are very common in large burns and typically occur at day 16 following injury.28 Because these infections are associated with a very high mortality rate, oral prophylaxis with antifungal agents is appropriate and has been shown to decrease the incidence of fungal infections.29

Nutrition and Metabolism

Patients with large burns experience a hypercatabolic state over an extended period, well beyond their initial injury.30 This state is characterized by increased insulin resistance, gluconeogenesis, and protein catabolism.3 In injuries involving greater than 40% TBSA, a patient’s resting energy expenditure is 150% to 200% higher than normal.31 In these large burns, patients can lose up to 25% of their preburn body weight by the third week following their injury.32 The effects of hypercatabolism include loss of lean body mass and growth delay for up to 2 years.25 As bone mineral density is chronically lower in children with severe burns, these patients have an increased lifelong risk of osteoporosis. The goal of nutrition and metabolism in the acute phase is to maintain preadmission weight, which may be difficult to assess initially due to fluctuations in fluid status. Laboratory findings are also unreliable in the acute phase and cannot be used in the evaluation of nutritional status. Hypoalbuminemia is expected acutely as the liver shifts production in favor of acute phase reactants such as C-reactive protein.33 Early excision of injured tissue helps to decrease catabolism, presumably by removing a major source of inflammatory mediators. Early initiation of nutrition is an important component in counteracting catabolism.34 Delays in initiating nutritional support have been shown to exacerbate catabolism, impair wound healing, and increase the risk of infection.8 Therefore, a nasogastric tube should be placed early in order to begin a high caloric diet with carbohydrates as the main source of calories. Early enteral feeding has also been shown to maintain the gut barrier, prevent gut atrophy, and potentially decrease enterogenic infections. Care should be taken to avoid overfeeding, which can lead to hepatic dysfunction, hyperglycemia, and increased carbon dioxide production. When initiating enteral feedings in the acute phase, patients should be monitored for hypotension, splanchnic hypoperfusion, and intestinal necrosis.30

Therapy, in addition to nutrition, can help to attenuate lean body mass loss. While aerobic exercise is effective for older children in maintaining lean body mass, muscle strength, and power, it has limited use in infants and toddlers.31 Anabolic agents have also been shown to benefit pediatric burn patients. Oxandrolone given orally twice daily at a dose of 0.1 mg/kg will increase protein synthesis and decrease loss of lean body mass. Insulin supplementation can help overcome burn-induced insulin resistance. When titrated between 400 mU/ml and 900 mU/ml to control blood glucose levels for 7 days, patients demonstrate improved healing time and increased muscle protein synthesis.31

Catabolism-blocking agents can also be useful in these patients. Propanolol, a beta blocker, can attenuate the stress-induced hypermetabolism. When titrated to decrease the patient’s baseline heart rate by 20% for several weeks, beta blockade is able to decrease excess thermogenesis, tachycardia, cardiac work, and superphysiologic resting energy expenditure.35

Rehabilitation and Reintegration

Improved resuscitation, along with early excision and grafting, permits most pediatric patients to survive deep burns. Currently, even a child with a large burn of up to 60% TBSA may be expected to survive with appropriate care in a specialized burn center.36 With more severely burned children surviving their injuries, the focus has shifted to improving their quality of life.37 The morbidity of these burns is significant and includes common complications such as scarring, contraction, and weakness from loss of muscle. The ultimate goal of this phase is to facilitate psychological and functional recovery, and is best accomplished in the multidisciplinary setting of a specialized burn center.

Hypertrophic Scarring

Hypertrophic scarring is a common complication of burns and occurs most often in deep dermal burns that are left to heal spontaneously over a protracted period of greater than 3 weeks.1 Hypertrophic areas have an exaggerated inflammatory response which stimulates excess growth