Objective: Inadequate nutrition is common in critical illness due in part to gastric stasis. However, recent data suggest that altered small intestinal mucosal function may be a contributing factor. The aim of this study was to examine the effects of critical illness on sucrose absorption, permeability, and mucosal morphology.
Design: Prospective, observational study.
Setting: Tertiary critical care unit.
Subjects: Twenty mechanically ventilated patients (19 men; 52.2 ± 20.5 yr; 9 feed intolerant; Acute Physiology and Chronic Health Evaluation II score 16.2 ± 6.0) and 20 healthy subjects (14 men; 51.6 ± 21.5 yr).
Interventions: Following a 4-hr fast, a “meal” (100 kcal Ensure, 20-g enriched 13C-sucrose, 1.1 g rhamnose, 7.5 mL lactulose) was administered into the small intestine. Sucrose absorption was evaluated by analyzing 13CO2 concentration (cumulative percent of administered 13C dose recovered) in expiratory breath samples taken at timed intervals. At 90 minutes, a plasma lactulose/rhamnose concentration was also measured, with lactulose/rhamnose ratio, a marker of small intestinal mucosal permeability. When possible duodenal biopsies were taken in critically ill patients on insertion of the small intestinal feeding catheter and examined for disaccharidase levels and histology. Data are mean ± SD.
Results: When compared with healthy subjects, critically ill patients had significantly reduced cumulative 13CO2 recovery (90 min: 1.78% ± 1.98% vs. 8.04% ± 2.55%; p < 0.001) and increased lactulose/rhamnose ratio (2.77 ± 4.24 vs.1.10 ± 0.98; p = 0.03). The lactulose/rhamnose ratio was greater in feed-intolerant patients (4.06 ± 5.38; p = 0.003). In five patients, duodenal mucosal biopsy showed mild to moderate epithelial injury. Sucrase levels were normal in all patients.
Conclusions: Sucrose absorption is reduced and intestinal permeability increased in critically ill patients, possibly indicating an impairment of small intestinal mucosal function. These results, however, are discordant with duodenal mucosal histology and sucrase levels. This may reflect an inactivation of sucrase in vivo or inadequate nutrient exposure to the brush border due to small intestinal dysmotility.
1Departments of Gastroenterology and Hepatology, Royal Adelaide Hospital Adelaide, South Australia.
2Investigation and Procedures Unit, Repatriation General Hospital Adelaide, South Australia.
3Critical Care Services, Royal Adelaide Hospital Adelaide, South Australia.
4Discipline of Acute Care Medicine, University of Adelaide, Adelaide, South Australia.
5Discipline of Medicine, University of Adelaide, Adelaide, South Australia.
6Centre for Paediatric and Adolescent Gastroenterology, Women’s and Children’s Hospital, Adelaide, South Australia.
7Anatomical Pathology, Flinders Medical Centre, Adelaide, South Australia.
This work was performed at the Royal Adelaide Hospital, South Australia. Breath test analysis was conducted at the Women’s and Children’s Hospital, South Australia.
Supported, in part, by a Clinical Project Grant, Royal Adelaide Hospital.
The authors have disclosed that they do not have any potential conflicts of interest.
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