Protein Anabolism in Critically Ill Children: Pathophysiological aspects and interventional challenges

Critical illness can be defi ned as “a life threatening medical or surgical condition usually requiring intensive care unit (ICU) level care“ [1]. It mostly results from infection, sepsis and trauma (including surgery and burns). Th ese conditions are accompanied by similar physiological and biochemical responses, which have been termed the systemic infl ammatory response syndrome (SIRS) [2]. Th e associated major metabolic changes are also known as the acute stress response. From an evolutionary point of view these responses are required for the “fi ght, fl ight, fright” reaction when encountering a thread, to mobilise fuels for tissues that are activated [3-5]. A key feature is increased sympathetic nervous system activity, resulting in increased levels of adrenaline and glucocorticoids. Subsequently, immune cells are activated and pro-infl ammatory cytokines secreted, which trigger further metabolic changes. In addition, insulin secretion is increased as well as the counter regulatory hormones glucagon, cathecholamines, cortisol and growth hormone. As a result, glucose production is increased via increased glycogenolysis and gluconeogenesis and insulin resistance develops, leading to hyperglycemia. Also, fat is mobilised (lipolysis) and fat oxidation and ketone body formation are increased, while muscle protein breakdown is stimulated to provide amino acids for protein synthesis in proliferating cells, the production of acute phase proteins and other peptides (e.g. cytokines) and for gluconeogenesis. Th us, protein turnover is increased, with both increased protein breakdown and protein synthesis. Protein synthesis, however, is stimulated to a lesser extent than protein breakdown, resulting in net protein loss, i.e. protein catabolism. In addition, the increased substrate cycling results in increased energy expenditure, because both protein synthesis and breakdown consume ATP

Volvulus as a complication of chronic intestinal pseudo-obstruction syndrome

Chronic intestinal pseudo-obstruction syndrome (CIPS) is a severe motility disorder of the gastrointestinal tract that presents with continuous or recurrent symptoms and signs of intestinal obstruction without evidence of a structural lesion occluding the intestinal lumen. Mechanical obstruction might occur in these patients as well but is typically difficult to distinguish from an exacerbation of CIPS. We report two pediatric cases in which mechanical obstruction by volvulus mimicked an exacerbation of CIPS, requiring surgical intervention. Conclusion: Awareness of the possibility of true mechanical obstruction in CIPS patients during an exacerbation episode is needed, as this is a severe condition and usually requires surgical intervention

Arginine appearance and nitric oxide synthesis in critically ill infants can be increased with a protein-energy-enriched enteral formula

Background: Arginine is considered an essential amino acid during critical illness in children, and supplementation of arginine has been proposed to improve arginine availability to facilitate nitric oxide (NO) synthesis. Protein-energy-enriched enteral formulas (PE-formulas) can improve nutrient intake and promote anabolism in critically ill infants. However, the effect of increased protein and energy intake on arginine metabolism is not known Objective: We investigated the effect of a PE-formula compared with that of a standard infant formula (S-formula) on arginine kinetics in critically ill infants Design: A 2-h stable-isotope tracer protocol was conducted in 2 groups of critically ill infants with respiratory failure because of viral bronchiolitis, who received either a PE-formula (n = 8) or S-formula (n = 10) in a randomized, blinded, controlled setting. Data were reported as means 6 SDs Results: The intake of a PE-formula in critically ill infants (aged 0.23 6 0.14 y) resulted in an increased arginine appearance (PEformula: 248 6 114 mmol $kg21$ h21; S-formula: 130 6 53 mmol $kg21$ h21; P = 0.012) and NO synthesis (PE-formula: 1.92 6 0.99 mmol $kg21$ h21; S-formula: 0.84 6 0.36 mmol $kg21$ h21; P = 0.003), whereas citrulline production and plasma arginine concentrations were unaffected Conclusion: In critically ill infants with respiratory failure because of viral bronchiolitis, the intake of a PE-formula increases arginine availability by increasing arginine appearance, which leads to increased NO synthesis, independent of plasma arginine concentrations