Endocrine Metabolic Effects

Henrik Kehlet P. Prithvi Raj

Physical injury is followed by a coordinated set of responses characterized by increased fuel production and an increased rate of metabolism, fuel utilization, and catabolism.

Although the secondary end-organ responses to injury have been well characterized in years, the biochemical basis of the stress response is still poorly understood, in part because of the complexity of events triggered by the various stimuli. In surgical patients, injury, pain, hemorrhage, infection, and anxiety are common stimuli that may elicit the response, additional factors are fluid loss and tissue damage. The mediators involved in setting the injury response in train to these stimuli are primarily neural and humoral stimuli ( Fig. 23-1 ). Afferent or efferent neural blockade or both by various techniques of regional anesthesia, may, therefore, alter the response to surgical injury.

Figure 23-1 Release mechanisms of the injury response. The primary mediators are afferent neural stimuli, humoral mediators (monokines [e.g., interleukin, TNF]), arachidonic cascade metabolites, and plasma protease. Secondary factors are anxiety, pain, hemorrhage, fluid loss, and infection (endotoxin)fFrom Kehlet H: Endocrine-metabolic effects. In Raj PP [ed]: Clinical Practice of Regional Anesthesia. New York, Churchill Livingstone, 1991, p 188.)

The injury response is generally considered a defensive maneuver, although if continued or amplified, it may have detrimental effects because of increased demands on various organs, catabolism, and muscle wasting, and impaired immunofunction, among other factors.[1

This chapter updates current information regarding the modifying effect of regional anesthetic techniques on the surgical stress response, with an emphasis on the differential effect of anesthetic techniques during various surgical procedures. However, clinical implications of regional anesthesia in modifying the stress response are only briefly addressed in this chapter. No attempt is made to review the general aspects of surgical injury, for which the reader is referred to recent reviews.^ [3] [4] [5] Furthermore, specific references are only given in some areas of current interest, because the topic has been reviewed in detail.13 [fl Q

The modifying effect of regional anesthesia on the endocrine-metabolic response to surgery is variable and depends on the technique of regional anesthesia ( Fig. 23-2 ). Each technique is described.

Figure 23-1 Release mechanisms of the injury response. The primary mediators are afferent neural stimuli, humoral mediators (monokines [e.g., interleukin, TNF]), arachidonic cascade metabolites, and plasma protease. Secondary factors are anxiety, pain, hemorrhage, fluid loss, and infection (endotoxin)fFrom Kehlet H: Endocrine-metabolic effects. In Raj PP [ed]: Clinical Practice of Regional Anesthesia. New York, Churchill Livingstone, 1991, p 188.)

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