A narrative review of skeletal muscle atrophy in critically ill children: pathogenesis and chronic sequelae.

Muscle wasting is now recognized as a growing, debilitating problem in critically ill adults, resulting in long-term deficits in function and an impaired quality of life. Ultrasonography has demonstrated decreases in skeletal muscle size during pediatric critical illness, although variations exist. However, muscle protein turnover patterns during pediatric critical illness are unclear. Understanding muscle protein turnover during critical illness is important in guiding interventions to reduce muscle wasting. The aim of this review was to explore the possible protein synthesis and breakdown patterns in pediatric critical illness. Muscle protein turnover studies in critically ill children are lacking, with the exception of those with burn injuries. Children with burn injuries demonstrate an elevation in both muscle protein breakdown (MPB) and synthesis during critical illness. Extrapolations from animal models and whole-body protein turnover studies in children suggest that children may be more dependent on anabolic factors (e.g., nutrition and growth factors), and may experience greater muscle degradation in response to insults than adults. Yet, children, particularly the younger ones, are more responsive to anabolic agents, suggesting modifiable muscle wasting during critical illness. There is a lack of evidence for muscle wasting in critically ill children and its correlation with outcomes, possibly due to current available methods to study muscle protein turnover in children-most of which are invasive or tedious. In summary, children may experience muscle wasting during critical illness, which may be more reversible by the appropriate anabolic agents than adults. Age appears an important determinant of skeletal muscle turnover. Less invasive methods to study muscle protein turnover and associations with long-term outcome would strengthen the evidence for muscle wasting in critically ill children.