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Background: In health, the hormones amylin and glucagon-like peptide-1 (GLP-1) slow gastric emptying (GE) and modulate glycaemia. The aims of this study were to determine amylin and GLP-1 concentrations in the critically ill and their relationship with GE, glucose absorption and glycaemia., Methods: In fasted critically ill and healthy subjects (n = 26 and 23 respectively), liquid nutrient, containing 100 mg (13) C-sodium octanoate and 3 g 3-O-methlyglucose (3-OMG), was administered via a nasogastric tube. Amylin, GLP-1, glucose and 3-OMG concentrations were measured in blood samples taken during fasting, and 30 min and 60 min after the 'meal'. Breath samples were taken to determine gastric emptying coefficient (GEC). Intolerance to intragastric feeding was defined as a gastric residual volume of ≥ 250 ml and/or vomiting within the 24 h prior to the study., Results: Although GE was slower (GEC: critically ill 2.8 ± 0.9 vs. health, 3.4 ± 0.2; P = 0.002), fasting blood glucose was higher (7.0 ± 1.9 vs. 5.7 ± 0.2 mmol/l; P = 0.005) and overall glucose absorption was reduced in critically ill patients (3-OMG: 9.4 ± 8.0 vs. 17.7 ± 4.9 mmol/l.60 min; P < 0.001), there were no differences in fasting or postprandial amylin concentrations. Furthermore, although fasting [1.7 (0.4-7.2) vs. 0.7 (0.3-32.0) pmol/l; P = 0.04] and postprandial [3.0 (0.4-8.5) vs. 0.8 (0.4-34.3) pmol/l; P = 0.02] GLP-1 concentrations were increased in the critically ill and were greater in feed intolerant when compared with those tolerating feed [3.7 (0.4-7.2) vs. 1.2 (0.7-4.6) pmol/l; P = 0.02], there were no relationships between GE and fasting amylin or GLP-1 concentrations., Conclusion: In the critically ill, fasting GLP-1, but not amylin, concentrations are elevated and associated with feed intolerance. Neither amylin nor GLP-1 appears to substantially influence the rate of GE., (© 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.)

The motor dysfunctions underlying delayed gastric emptying (GE) in critical illness are poorly defined. Our aim was to characterize the relationship between antro-duodenal (AD) motility and GE in critically ill patients. AD pressures were recorded in 15 mechanically ventilated patients and 10 healthy volunteers for 2 h (i) during fasting, (ii) following an intragastric nutrient bolus with concurrent assessment of GE using the (13)C-octanoate breath test and (iii) during duodenal nutrient infusion. Propagated waves were characterized by length and direction of migration. Critical illness was associated with: (i) slower GE (GEC: 3.47 +/- 0.1 vs 2.99 +/- 0.2; P = 0.046), (ii) fewer antegrade (duodenal: 44%vs 83%, AD: 16%vs 83%; P < 0.001) and more retrograde (duodenal: 46%vs 12%, AD: 38%vs 4%; P < 0.001) waves, (iii) shorter wave propagation (duodenal: 4.7 +/- 0.3 vs 6.0 +/- 0.4 cm; AD: 7.7 +/- 0.6 vs 10.9 +/- 0.9 cm; P = 0.004) and (iv) a close correlation between GE with the percentage of propagated phase 3 waves that were antegrade (r = 0.914, P = 0.03) and retrograde (r = -0.95, P = 0.014). In critical illness, the organization of AD pressure waves is abnormal and associated with slow GE.

Objective: Delayed gastric emptying (GE) is common both in critical illness and in patients with diabetes mellitus (DM). The effect of DM on the incidence of slow GE in these patients is unknown. We evaluated the effect of DM on liquid GE in critically ill patients., Methods: Retrospective analysis of GE using a standard [13C]octanoic acid breath test in 12 type 2 DM patients compared with (a) 44 critically ill patients without DM, including (b) a subgroup of 15 age- and sex-matched patients and (c) 15 healthy volunteers. We determined the gastric emptying coefficient (GEC) and the gastric half-emptying time (t50). Mean APACHE II scores, blood glucose levels and use of morphine were similar between patient groups., Results: GE was faster in critically ill patients with DM (t50 122 +/- 11 min, GEC: 3.8 +/- 0.3) than in patients without DM (t50 168 +/- 16 min, GEC 2.8 +/- 0.1) and in age- and sex-matched controls (t50 165 +/- 13 min, GEC 2.7 +/- 0.2) and was similar to that in healthy volunteers (t50 148 +/- 13 min, GEC 3.5 +/- 0.1). The proportion of patients with slow emptying (GEC < 3.2) was greater in non-DM (all = 56%, matched = 60%) than in DM patients (25%) and healthy subjects (26%)., Conclusion: Long-standing type diabetes mellitus is not a risk factor for slow GE in critically ill patients.