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The metabolic response to trauma and sepsis

  • Erie County Medical Center
  • SUNY Buffalo

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

The metabolic response of the body to trauma and sepsis is the summed response of the organs. Net catabolism of the muscles of ambulation is particularly important in providing the other organs with a source of amino acids for protein synthesis and, therefore, anabolism. This net catabolism of muscle is based upon decreased physical activity, the net effects of the neuroendocrine system, and the consequences of local amino acid concentration changes within muscle, particularly of leucine. Secondary to these changes, previously healthy humans sustaining acute short-term trauma of fairly major degree do not require exogenous supplies of amino acid even though the patient has a short-term negative nitrogen balance. In contrast, the septic patient has, in addition to the preceding changes, activation of phagocytosis with release of phagocytic factors that mobilize white cells, increase body temperature, and further modulate the metabolism of muscle and probably all other organs. Since these changes are induced by phagocytosis, which may be activated by retained dead tissues of all kinds, the basic attributes of the septic state may be activated in the absence of bacteria. The retained dead tissue makes bacterial growth much more likely. The septic state, therefore, has as its hallmark all of the changes of the trauma state, plus a prolonged enhanced catabolism of all amino acids, which leads to protein malnutrition with its overt manifestation of multiple systems organ failure. These patients require calories only 10 to 50% in excess of the requirement of normal humans, but a great increase in amino acid intake (up to 2.5% to 3 g/kg per day). This support will purchase more time in which to treat the underlying sepsis.

Original languageEnglish
Pages (from-to)125-131
Number of pages7
JournalWorld Journal of Surgery
Volume7
Issue number1
DOIs
StatePublished - Jan 1983

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