In addition, mucosal oedema and reduced splanchnic blood flow may contribute to reduced absorption. Abnormal small intestinal motility may also be important [24] and accelerated transit would reduce the time for absorption. However, to date, small intestinal transit has not been formally Rucaparib side effects examined in the critically ill population. It is possible that some critically ill patients have significant malabsorption and cannot be fed enterally. This needs further investigation and, if confirmed, methods to identify these patients clinically need to be developed.In health and some disease states, GE is both determined by, and a determinant of, blood glucose concentrations [4]. This study found that slower GE was associated with a smaller increment in blood glucose in the healthy subjects, consistent with previous observations [25].

Although no relation between postprandial blood glucose concentrations and GE was demonstrated in the critically ill patients in this study, the postprandial increment in blood glucose was related to glucose absorption.Hyperglycaemia occurs frequently in critical illness, has been attributed to insulin resistance, as well as abnormalities in the release and action of other regulatory hormones and the presence of inflammatory cytokines [8], and is associated with a worse clinical outcome [9,26]. The close relation between GE and glucose absorption suggests that, if GE is accelerated by the use of prokinetics, or if the stomach is bypassed and nutrient is placed directly into the small intestine, the rate of glucose absorption may be increased.

This could have the undesirable effect of increasing blood glucose concentrations. However, it is unclear how important this effect is in patients receiving continuous infusions of enteral feeding because in this study the nutrient was delivered as a single naso-gastric bolus, which is likely to cause a greater increment in blood glucose concentration. This warrants further investigation.Acute elevations in blood glucose concentration slow GE in healthy humans and patients with type 1 diabetes. Hyperglycaemia (about 15 mMol/l) markedly slows GE [5,27,28], but even changes in blood glucose concentrations within the normal postprandial range (4 to 8 mmol/l) can have a significant impact [29-31].

Consistent with these findings, this study found an inverse relation between baseline blood glucose concentrations and subsequent GE in the patients, such that higher blood glucose was associated with slower GE. The absence of a relation in healthy subjects is not surprising given that blood glucose concentrations were much lower (maximum 6.4 mMol/l). Hence, it is possible that in ICU patients glycaemia influences GE. However, the causes of delayed GE are likely to be multifactorial and the relative importance of changes in blood glucose concentrations is Cilengitide as yet unclear.