Critically ill patients frequently suffer from gastrointestinal dysfunction as the intestine is a vulnerable organ. In critically ill patients who require nutritional support, the current guidelines recommend the use of enteral nutrition within 24–48 h and advancing towards optimal nutritional goals over the next 48–72 h; however, this may be contraindicated in patients with acute gastrointestinal injury because overuse of the gut in the acute phase of critical illness may have an adverse effect on the prognosis. We propose that trophic feeding after 72 h, as a partial gut rest strategy, should be provided to critically ill patients during the acute phase of illness as an organ-protective strategy, especially for those with acute gastrointestinal injury.

The mechanism behind the beneficial effects of enteral nutrition (EN) for patients with acute pancreatitis (AP) is largely unknown. Adipokines, as mediators of metabolism and inflammation, may be a possible mechanism. The study aimed to investigate the effect of EN on adipokines early in the course of AP. Patients with AP were randomised to EN or nil-by-mouth (NBM). Blood samples were taken on the first 4 d of admission and adipokine concentrations for adiponectin, leptin, omentin, resistin and visfatin were determined by ELISA assays. A linear mixed model analysis was run to determine differences in adipokine concentrations between the two study groups. A total of thirty-two patients were included in the study. Omentin concentrations were significantly higher in patients who received EN compared with NBM across the first 4 d of admission (mean difference: 11·6 (95 % CI 1·0, 22·3) ng/ml; P = 0·033). Leptin concentrations were significantly higher in patients who received EN compared with NBM after adjusting for age, sex and BMI (mean difference: 2·3 (95 % CI 0·1, 4·5) ng/ml; P = 0·037). No significant difference in adiponectin, resistin or visfatin concentrations were observed between the two study groups. EN significantly increases omentin and leptin concentrations in AP. Future research should be directed towards understanding whether these adipokines are responsible for the therapeutic benefits of EN.

Enteral nutrition (EN) reduces infectious complications and mortality compared with parenteral nutrition (PN) in patients with predicted severe acute pancreatitis. However, to date the complications attributable to the administration of EN and PN in this patient group have not been comprehensively studied. The aim of the study was to systematically review the complications related to the use of nutrition in patients with predicted severe acute pancreatitis receiving EN v. PN. The Cochrane Library, MEDLINE and Scopus were searched. Randomised controlled trials (RCT) of EN v. PN in predicted severe acute pancreatitis were selected. Pooled estimates of complications were expressed as OR with corresponding 95 % CI. Data from five RCT were meta-analysed. Diarrhoea occurred in six of ninety-two (7 %) patients receiving PN and twenty-four of eighty-two (29 %) patients receiving EN (OR 0·20; 95 % CI 0·09, 0·43; P < 0·001). Hyperglycaemia developed in twenty-one of ninety-two (23 %) patients receiving PN and nine of eighty-two (11 %) receiving EN (OR 2·59; 95 % CI 1·13, 5·94; P = 0·03). Given a significant reduction in infectious complications and mortality associated with the use of EN over PN that has been consistently demonstrated in previous studies, the former should be the treatment of choice in acute pancreatitis. Further clinical studies should investigate the strategies to mitigate the complications of enteral tube feeding in patients with acute pancreatitis.

Artificial nutrition is an inherent part of management in acute pancreatitis. However, there is no consensus regarding the optimal time of the commencement of feeding in these patients. Our aim was to compare the effect of enteral v. parenteral nutrition with regard to the time points when they were administered in the randomised controlled trials. The search was undertaken in the Cochrane Central Register of Controlled Trials, MEDLINE and Science Citation Index as well as in the proceedings of major gastroenterology meetings. The summary estimate of the effect associated with artificial nutrition was calculated using a random-effects model and presented as a risk ratio (RR) and 95 % CI. A total of eleven randomised controlled trials were included. When started within 48 h of admission, enteral nutrition, in comparison with parenteral nutrition, resulted in a statistically significant reduction in the risks of multiple organ failure (RR 0·44; 95 % CI 0·23, 0·84), pancreatic infectious complications (RR 0·46; 95 % CI 0·27, 0·77) and mortality (RR 0·46; 95 % CI 0·20, 0·99). After 48 h of admission, enteral nutrition, in comparison with parenteral nutrition, did not result in a statistically significant reduction in the risks of multiple organ failure (RR 0·73; 95 % CI 0·33, 1·63), pancreatic infectious complications (RR 0·31; 95 % CI 0·07, 1·34) and mortality (RR 0·67; 95 % CI 0·22, 2·10). Enteral nutrition is more effective than parenteral nutrition in reducing the risk of multiple organ failure, pancreatic infectious complications and mortality in patients with acute pancreatitis. The magnitude of these benefits may depend on the timing of the commencement of nutrition.

We present a case of severe acute pancreatitis in a 14-year-old boy that may have been caused by hyperparathyroidism. The clue to finding the parathyroid adenoma was the hypercalcaemia. Although the patient did have acute pancreatitis, no therapy had been effective until the discovery of the parathyroid adenoma. After the excision of the parathyroid adenoma, the function of the pancreas and serum calcium returned to normal. This result suggests a certain cause and effect relationship between hyperparathyroidism and acute pancreatitis.