The state of hypercatabolism has been associated with severe complications after major trauma, related to hyperglycemia, hypoproteinemia, and immunosuppression. This hypercatabolic condition leads to a significantly increased oxygen consumption and energy expenditure. In contrast, the 'flow' phase occurs after resuscitation from a state of shock, which leads to an increased metabolic turnover, activation of the innate immune system and induction of the hepatic acute-phase response. The brief duration of this phase limits its clinical relevance. The ' ebb' phase is associated with a decline in body temperature and oxygen consumption, presumably aimed at reducing posttraumatic energy depletion. He characterized the 'ebb' and the 'flow' phases of posttraumatic metabolic alterations. In 1942, Cuthbertson was the first to describe distinct phases of the metabolic changes which occur after major trauma. This process creates a capillary bed that facilitates tissue repair and regeneration. This phase is characterized by a return of oxidative metabolism, favoring angiogenesis in damaged tissues and organs. The third ('angiogenic') phenotype is defined as the late (or 'endocrine') phase of systemic response to injury. The resulting post-shock hypercatabolism and hypermetabolism is related to a hyperdynamic response with increased body temperature, increased oxygen consumption, glycogenolysis, lipolysis, proteolysis and futile substrate cycling. This phase is characterized by leukocytic and bacterial infiltration of previously damaged tissues, which occurs in an edematous, oxygen-poor environment.

The second ('leukocytic') phenotype, is characterized as the intermediate (or 'immune') phase of the metabolic response to trauma. This phase is characterized by regulating the metabolic supply to cells via the least elaborate mechanism: diffusion. The first ('ischemia/reperfusion') phenotype represents the immediate, nervous system-related alteration in response to injury, in which neuronal and humoral responses and edema formation predominate.

Using this innovative classification concept, the authors explain the metabolic alterations in association with the 'classical' progression of posttraumatic inflammation. The authors classified the metabolic changes after injury into three distinct phenotypes: (1) the 'ischemia/reperfusion phenotype' (2) the 'leukocytic phenotype' and (3) the 'angiogenic phenotype'. In a recent article published in the Journal, Aller and colleagues propose a modern perspective on the metabolic events associated with the inflammatory response to major trauma, which should guide therapeutic strategies. The potential clinical impact of metabolic staging, and of an appropriately adapted 'metabolic control' and nutritional support, remains to be determined. Recently, the concept of 'metabolic staging' has been advocated, which takes into account the distinct inflammatory phases and metabolic phenotypes after major trauma, including the 'ischemia/reperfusion phenotype', the 'leukocytic phenotype', and the 'angiogenic phenotype'.

A proactive concept of early enteral 'immunonutrition' in severely injured patients, is aimed at counterbalancing the negative aspects of hyperinflammation and hypercatabolism in order to reduce the risk of late complications, including infections and posttraumatic organ failure. This hypercatabolic state must be recognized early and mandates an early nutritional management strategy. The early posttraumatic stress response is associated with a state of hyperinflammation, with increased oxygen consumption and energy expenditure. Metabolic changes after major trauma have a complex underlying pathophysiology.

Catabolic phase