The Quest to Preserve Muscle Mass—Lessons From Pediatric Burn Injury*

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Excerpt

The stress response to critical illness is characterized by increases in both protein synthesis and protein breakdown, with predominance of breakdown that could result in net muscle loss (1). The evolutionary response to severe burn injury (affecting greater than 40% body surface area) in humans represents the most stereotypic and profound example of this phenomenon. Prolonged protein catabolism with muscle protein loss has been demonstrated for up to 2 years after the initial thermal injury in children (2, 3). The net loss of muscle protein is associated with decline in total body lean mass and function. Hence, a variety of strategies such as testosterone, oxandrolone, human recombinant growth hormone, insulin, metformin, and propranolol have been studied in the acute hypermetabolic phase of the injury, to improve skeletal muscle protein net balance in patients with severe burns (4). Attenuation of muscle catabolism or increase in muscle synthesis using pharmacologic and nonpharmacologic therapies could help ameliorate net muscle loss, improve strength and function, hasten wound healing, and positively impact outcomes.
In this issue of Pediatric Critical Care Medicine, Cambiaso-Daniel et al (5) describe the degree of change in body composition over time in different anatomical regions (upper extremity, lower extremity, and truncal) in children with severe burns in their PICU. In their retrospective study, the authors identified patients with severe burns at their institution with two dual x-ray absorptiometry (DXA) scans that were at least 2 weeks apart. The patients received therapies according to the institutional protocols, but those randomized to experimental anabolic drugs or early interventional programs were excluded. The final cohort included 24 children 10 ± 5 years old, with total body surface area burn of 59% ± 17%, who had two DXA scans performed approximately at 34 ± 21 days interval. The patients had significant loss of lean mass (3%) in the whole body; the lean mass loss was significantly greater in the upper extremities (17%) than in the lower extremities (7%). Fat mass increase in whole body was significant and was greater in the truncal region and in the lower limbs. Enteral nutrition was preferred and started soon after admission to achieve energy delivery guided by measured energy expenditure with stress factor added. The diet consisted of 82% carbohydrates, 15% protein, and 3% fat. The major limitation of this study (5) is the highly selective and nonrandom sample of only 24 patients over 15 years. Of the hundreds of patients with burn injury treated at their institution, 210 had DXA scans in the ICU, of which 186 patients were excluded due to nonavailability of scans at appropriate periods or inclusion in trials of anabolic therapies. The small sample size and other limitations of this study (5) will preclude generalizations to all pediatric burn patients, and the observations will need to be repeated in a larger study. Furthermore, the authors did not examine the impact of potential confounders such as nutritional intake, route of nutrition delivery, physical therapy, and early mobilization strategies on body composition. However, the authors must be commended for their study, which adds to our understanding of the effects of severe burns on body composition. The differential effect of burn injury on lean mass in upper versus lower extremities will likely help guide physical therapies in this population. Furthermore, the routine nutritional and physical therapies that were employed in routine care of these children are worth exploring here. Enteral nutrition was started early, and the prescription was adjusted after measuring resting energy expenditure. Regular physical therapy included range of motion, passive exercises and limb stretching in these acutely ill children.

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