British journal of anaesthesia
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In the past two to three decades, advancing knowledge in the areas of physiology, pharmacology and scientific technology have allowed diversification from the purely technical aspects of administration of anaesthesia towards more accurate assessment of outcome for the individual in terms of both anaesthetic-induced morbidity and mortality. In addition, elucidation of the aetiology of the morbidity and mortality produced by anaesthesia, as opposed to that from surgery or concomitant medical or surgical disease processes, is assuming increased importance as a result of the expansion in medical litigation, where anaesthetists find themselves amongst the higher risk specialties in medicine. The morbidity produced by anaesthesia is relatively easy to define for specific populations, but the prediction of risk in an isolated individual remains elusive. ⋯ However, perhaps one of the more valuable aspects of this type of methodology is its potential use in quality control and audit within departments. There are undoubted problems and universally acknowledged difficulties in epidemiological research into anaesthetic mortality. Comparison of data between studies is rendered difficult owing to variations in procedure, including its prospective or retrospective nature, the definition of death, the perioperative time period studied, and the patient and hospital populations encompassed.(ABSTRACT TRUNCATED AT 400 WORDS)
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Randomized Controlled Trial Clinical Trial
Fentanyl and the beta-endorphin, ACTH and glucoregulatory hormonal response to surgery.
The effect of the supplementation of nitrous oxide-oxygen anaesthesia with either fentanyl 15 micrograms kg-1 or 0.5% halothane on the beta-endorphin, ACTH, glucoregulatory hormonal and metabolic response to pelvic surgery was investigated. Fentanyl inhibited the increases in circulating beta-endorphin, ACTH, growth hormone, cortisol and glucose concentrations found in the patients receiving halothane. Changes in circulating beta-endorphin concentrations during surgery probably reflect alterations in pituitary secretion and appear to have no major metabolic effects. The suppression of pituitary secretion persisted for at least 4 h after the start of surgery.