Critical illness causes a profound increase in the inflammatory response that subsequently leads to metabolic and neurohormonal responses. The metabolic event responses that characterise the stress response are hypermetabolism, dyslipidaemia, hyperglycaemia and increased protein turnover.
Whole-body oxygen consumption and energy expenditure are generally increased in paediatric burn patients, paediatric neurotrauma patients and in neonatal sepsis, whereas in critically ill children with other diagnoses (including sepsis) the energy expenditure shows a substantial variability but in general is not increased.
Dyslipidaemia is characterised by increased lipolysis and hypocholesterolaemia. This leads to increased plasma concentrations of triglycerides and free fatty acids and a decreased cholesterol content.
Hyperglycaemia is very frequently seen and is associated with a worse outcome. The mechanism of hyperglycaemia seems more complicated than mere insulin resistance and there is still debate about the beneficial effects of insulin treatment in critically ill children to maintain normoglycaemia.
Increased protein turnover is the result of increased hepatic protein synthesis at the cost of muscle protein. There is an increased visceral hepatic protein synthesis of acute phase proteins (eg, C-reactive protein). Recovery of the acute stress response can be expressed by the decline in C-reactive protein level, which dictates the changes in thyroid hormone and insulin-like growth factor type 1 levels. In the recovery phase protein intake up to 4 g/kg per day can be necessary.
Nutritional support can slow down the catabolic phase but is difficult in a highly inflammatory condition. Administration of adequate amounts of amino acids and/or insulin stimulates protein anabolism.