Some aspects of the metabolic response to surgical trauma

Abstract

The metabolic response to trauma is characterized by hypermetabolism, increased N excretion, accelerated fluxes of substrates (particularly glucose) between organs, and anorexia (Wilmore & Kinney, 1981). The combination of hypermetabolism and anorexia leads to negative energy and N balance. In the case of patients undergoing surgery, this situation is often superimposed on a state of nutritional depletion caused by pre-existing disease. The result is the high incidence of malnutrition among surgical patients which has been reported frequently over the past 30 years (Bistrian et al. 1974; Hill, 1977; McWhirter & Pennington, 1994), and which is known to cause a longer stay in hospital, a greater risk of infectious complications and an increase in the post-operative mortality rate. Although this area has been the subject of considerable research in recent years, the relative importance of the acute response to surgical trauma, compared with the chronic disease-induced depletion, in causing malnutrition and hence adverse clinical consequences is still far from clear. Furthermore, it is not clear whether the existence of previous under-nutrition affects the magnitude of the acute metabolic response to surgery, and if it does, how this affects the ultimate clinical outcome. One of the difficulties in carrying out these investigations has been assembling homogeneous groups of patients with the same severity of disease, nutritional depletion, surgical intervention and presence of septic complication. Moreover , metabolic studies have rarely been carried out longitudinally, yet this is crucial to understanding both the immediate effect of surgery and the longer-term consequences. Under these circumstances it can be useful to employ animal models, and there are reports in the literature of studies ranging from the relatively mild effects of single-impact blunt trauma (Fisher et al. 1991) to the severe effects of extensive bums (Al-Shamma et al. 1979). Our own studies have concentrated on the effects of moderate surgery in the form of hysterectomy in rats. The present paper will review some of the effects of surgical trauma on food intake, body composition, energy expenditure and fuel utilization in both human and animal studies, with some comments on their interaction with malnutrition. Food intake after injury It is generally accepted that injury causes anorexia, but there are surprisingly few studies which document the magnitude of this effect. This may be partly due to the difficulty of measuring food intake reliably. Some studies in which energy intake was measured over periods from 7 to 12d after gastrointestinal surgery are listed in Table 1. The results show a considerable degree of consistency. It should be noted that in most of these studies there had been a period of approximately 5 d immediately after the operation during which intake was zero or minimal, before the measurements began. Studies of non-gastrointestinal surgery have shown similarly low food intakes, although the period of post-operative starvation would have been shorter (Manners, 1974; Hessov, 1977; Walesby et al. 1979). The studies were all uncontrolled, and indeed it is difficult to identify appropriate control data with which to compare these values, but these results seem to indicate that many patients experience a deficit of at least 50 % in food intake over a 2-3 week post-operative period. The study by Keele et al. (1 997) also showed that the anorexia lasts for a considerable time after the immediate post-operative period, as intakes continued to rise during the second month after discharge from hospital. Studies in rats have shown a much greater range of responses (Table 21, although the time frame is much shorter. Burn injuries appear to cause only minor and transient decreases in food intake, in contrast with the prolonged elevation of energy expenditure and negative energy balance reported in these animals (Al-Shamma et al. 1979). Blunt trauma to the limbs had no effect on food intake, whereas abdominal surgery depressed food intake for several days. There is some evidence that the magnitude of the decrease is related to the severity of the operation, with hysterectomy (Bosagh Zadeh & Emery, 1997) causing a greater and more prolonged reduction in food intake than simple laparotomy (Emery & Ghusain-Choueiri, 1994). Food intake is controlled by a variety of physiological and psychological mechanisms. We have begun to investigate the causes of surgical anorexia by measuring average meal size and meal frequency, and have found that