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Malabsorption and Villous Atrophy in Patients Receiving Enteral Feeding

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

Geoff Chu, MB, BS

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

Logan Faust, MD

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

George Chandy, MD

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

John Argyrides, MB, BS

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

Trevor Robb, BSc

Department of Gastroenterology, Women's and Children's Hospital, North Adelaide, South Australia

Peter Wilson, MB, BS

Gastroenterology Unit, The Queen Elizabeth Hospital, Woodville South

Background: The purpose of this study was to assess the structure and function of the small intestine before and after enteral feeding given via a percutaneous feeding gastrostomy (PEG). It is not known whether this method of feeding provides a good luminal drive to the small intestine. Methods: Studies were performed of patients at the time of PEG placement, in a cross-sectional group after a period of feeding and in a smaller longitudinal subgroup. Enteral feeds were adjusted in volume and caloric content for each patient. Duodenal biopsies were taken during endoscopy for quantitative morphometry, and lactulose-rhamnose permeability tests were performed during the next day. Duodenal fluid was cultured quantitatively in the first study, and disaccharidases determined in the second study. Results: The first study of 15 patients, who had enteral feeding for a median (range) period of 13 (8 to 104) weeks, showed partial villous atrophy with normal crypt length, no increase in duodenal bacteriology, and abnormal lactulose-rhamnose sugar permeability due to rhamnose malabsorption. These changes were also present in 38 similar patients before enteral feeding. A second study before enteral feeding showed lowered maltase activity (24 patients), and similar intestinal permeability findings (22 patients). Twelve of these patients were followed longitudinally for 3 months of enteral feeding that maintained but did not improve nutrition, as assessed by body mass index and mid-arm muscle circumference, and there was no change in duodenal morphometry (11 patients), rhamnose malabsorption (4 patients), or disaccharidases (11 patients). Conclusions: These studies suggest villous atrophy was not due to an inflammatory enteropathy but resulted from a poor luminal "drive" associated with the enteral feeding. Enteral feeding maintained but did not improve nutrition status. (Journal of Parenteral and Enteral Nutrition 19:193-198, 1995)

Journal of Parenteral and Enteral Nutrition, Vol. 19, No. 3, 193-198 (1995)
DOI: 10.1177/0148607195019003193


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