While several studies [53, 54] and expert advisory groups [55, 56] have shown that early enteral feeding is beneficial in the management of critically ill patients, no study has addressed the question of whether the avoidance of pancreatic stimulation during feeding early in the course of acute pancreatitis hastens the resolution of the acute inflammatory response and the duration of disease. The observation by the Glasgow group  that outcome was no different whether patients were fed by stomach or 'jejunum' [(it is likely that most patients received duodenal feeding] does not address this concern, as our
investigations have shown that the stimulatory effect of feeding is no different whether the diet is taken as a drink or infused directly into the duodenum , and studies of Vu et al. showed that feeding in the proximal jejunum still stimulates secretion . Consequently, both forms of feeding were stimulatory, and it remains possible that neither were better than no feeding, particularly in view of the observed high mortality rates of 20-30%. Although clinical deterioration has not been commonly recognized in the enteral vs. parenteral feeding trials, we published compelling evidence of exacerbation in a patient with necro-tizing disease during advancement of enteral feeding, based on the combination of clinical signs (abdominal pain), blood tests (increased WBC) and CT scanning (extension of necrosis) . Furthermore, objective evidence that the injured pancreas can still respond to enteral stimulation was obtained from our measurements of secretion in patients with severe necrotizing disease fed by enteral and parenteral nutrition . We are not alone in observing exacerbation of disease during enteral feeding . Following from this, we are concerned that conventional enteral feeding may be providing a mixed bag of benefits and risks in patients with acute pancreatitis.
Finally, it must be remembered that enteral feeding, like TPN, has its own difficulties and complications. We are surprised that the Glasgow group did not encounter problems when trying to feed patients with necrotizing disease by NG tube, as it is our experience that most have gastric outlet obstruction due to compression of the distal stomach and duodenum by the inflammatory mass (Fig. 5.5). Unless a second decompression tube is used, which would also be counter-productive as it would prevent effective feeding, the risk of aspiration and pulmonary complications in ICU patients would be greatly increased [40, 57].
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