Why the study?
Does the type and emergence from anesthesia affect the neuroendocrine stress response in children undergoing abdominal surgery?
Does the type and emergence from anesthesia affect the neuroendocrine stress response in children undergoing abdominal surgery?
This editorial emphasizes that the neuroendocrine stress response during surgery is significantly influenced by anesthesia and emergence, factors that must be accounted for in surgical stress studies.
I was saddened to note that the first scientific paper in Anaesthesia in the new millennium made little reference to anaesthesia itself. Bozkurt et al. (Anaesthesia 2000; 55: 5–9) studied the endocrine and metabolic responses of 29 children undergoing operations for abdominal pain. The paper discusses various factors affecting the responses to surgery including the size of the skin incision, the amount of tissue damage and the effects of the pneumo-peritoneum. However, the effects of anaesthesia are ignored. It has been known for some time that in the early peri-operative period regional anaesthesia attenuates (or may even abolish) the neuroendocrine response to surgery [1, 2] compared with patients undergoing the same operation but with a general anaesthetic. The metabolic profiles tend to become similar by 24 h, perhaps because of the effects of fasting and/or tissue damage. Barker et al. [3] showed that even in operations where there was virtually no tissue damage, there might be a doubling of the plasma cortisol concentration from a baseline before anaesthesia started until 60 min after the end of surgery. The same group [4] subsequently showed that the emergence from anaesthesia itself has a significant effect on the plasma cortisol level that had previously been masked by the stress response to surgery. They compared three groups undergoing cataract surgery. Two of the groups had general anaesthesia alone (GA) and retrobulbar block alone (RB). The third group (GA + RB) had a general anaesthetic followed by a retrobulbar block before surgery. There was no significant difference in cortisol levels between group GA + RB and group RB until the end of surgery. However, the serum cortisol level in group GA + RB then doubled in the first 30 min post surgery until there was no significant difference compared with group GA. Bozkurt et al. measured the cortisol levels from 5 min after induction until extubation. All the metabolic indicators that they measured were within the normal ranges and there were no significant differences between the final values in the two groups of patients. Induction and emergence are possibly the most important parts of anaesthesia and the neuroendocrine markers of the response to ‘operations’ seem to underline this point. Perhaps if the anaesthetists hadn't been outnumbered as authors then this point would have been addressed. It is clear that certain types of laparoscopic surgery offer significant advantages to patients in terms of recovery and complication rate when compared with the ‘open’ alternatives. However, what still remains far from clear is the meaning of the changes in various metabolic markers as a consequence of surgery and anaesthesia.
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D. J. Dalgleish (2000) studied this question.
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