Metabolic alterations in the critically ill child

Abstract

The metabolic response to critical illness is characterized by changes in energy metabolism and distribution of substrates and nutrients to sustain cellular function, repair, and to support the immune response and growth. Such response is regulated by simultaneous neurohormonal and inflammatory responses mediated by neurotransmitters, cytokines, hormones, and metabolic signals. The stress-mediated changes in energy expenditure (EE) are characterized by an initial phase of decreased followed by an increased EE. Inflammation triggered by cytokines is divided in several categories: interleukins, chemokines, interferons, tumor necrosis factor, and growth factors. The interleukins are divided into pro-inflammatory (responsible for cell activation, tissue damage and necrosis) and anti-inflammatory interleukins (involved in dampening and reversing the inflammatory process. The counter-regulatory response is characterized by increased concentrations of catecholamines, glucagon, and cortisol and oppose the effects of insulin. Those same elements that regulate stress, inflammation and energetic failure also induce an increase in whole-body protein synthesis, intensification of muscle protein catabolism, and a reduction in muscle protein synthesis to support a surge of amino acids (AA) released into the systemic circulation to serve as biochemical precursors, signals and structural substrates and oxidation for energy if needed. Both energetic and macronutrient processes interact and regulate themselves to establish a new homeostatic situation suited to fight infections, sustain life, and promote recovery. Due to current advances in intensive care, and modern life sustaining therapies, a prolongation of the inflammatory and catabolic state and nitrogen loss occurs, rendering the individual resistant to traditional nutrition support therapies.