Abstract
The usual characterization of sepsis is that it is a disease process caused by infectious organisms. However, recent evidence suggests that sepsis is rather an acquired disease of intermediary metabolism induced by the host response to invasion by infectious agents.The characteristics and the magnitude of this metabolic disorder are not specific for particular infectious agents, but occur with bacterial, fungal and viral organisms. The metabolic dysfunction which is initiated by sepsis induces a shift in the pattern of physiologic abnormalities and dynamic metabolic interrelations which are involved in the regulation of energetic substrate flux between skeletal muscle, liver and adipose tissue. This altered regulation modifies the normal balance of control by neuro and endocrine mechanisms.
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References
Siegel JH, Cerra FB, Coleman B, et al (1979) Physiological and metabolic correlations in human sepsis. Surgery 86(2):163–193
Siegel JH, Giovannini I, Coleman B (1979) Ventilation: perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis. J Trauma 19(6):432–460
Siegel JH, Giovannini I, Coleman B, Cerra FB, Nespoli A (1982) Pathologic synergy modulation of the cardiovascular, respiratory and metabolic response to injury by cirrhosis and/or sepsis: a manifestation of a common metabolic defect? Arch Surg 117:225–238
Sganga G, Siegel JH, Brown G, et al (1985) Reprioritization of hepatic plasma protein release in trauma and sepsis. Arch Surg 120:187–199
Pittiruti M, Siegel JH, Sganga G, et al (1985) Increased dependence of leucine in post-traumatic sepsis: leucine/tyrosine clearance ratio as indicator of hepatic impairment in septic multiple organ failure syndrome. Surgery 98(3):378–387
Vary T, Siegel JH, Nakatani T, Sato T, Aoyama H (1986) Regulation of glucose metabolism by altered pyruvate dehydrogenase activity I. Potential site of insulin resistance in sepsis JPEN 10(4):351–355
Vary TC, Siegel JH, Nakatani T, Sato T, Aoyama H (1986) A biochemical basis for depressed ketogenesis in sepsis. J Trauma 26:419–425
Siegel JH, Vary TC (1987) Sepsis, abnormal metabolic control and the multiple organ failure syndrome. In: Siegel JH (ed) Trauma: Emergency Surgery and Critical Care. Churchill-Livingstone, New York, pp 411–501
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© 1987 Springer-Verlag Berlin Heidelberg
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Siegel, J.H. (1987). Abnormal Metabolic Control in Septic Multiple Organ Failure. In: Vincent, J.L. (eds) Update 1987. Update in Intensive Care and Emergency Medicine, vol 3. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83042-6_2
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DOI: https://doi.org/10.1007/978-3-642-83042-6_2
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-17576-6
Online ISBN: 978-3-642-83042-6
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