Metabolic basis of starvation diarrhoea: implications for treatment

Abstract

The terminal diarrhoea of kwashiorkor or marasmus may be due largely to malnutrition of the intestinal epithelium. Experimental data suggest that the first days of treatment should be devoted to restoration of epithelial function, to prevent worsening of diarrhoea by osmotic food loads.

PIP: Diarrhea or respiratory infection constitutes the terminal illness in most starved children and adults. A major component of starvation diarrhea appears to be an organ-specific malnutrition of the inestinal epithelium, not bacterial overgrowth. Faced with an overburden of nutrients on refeeding, the intestine cannot salvage ions because its epithelium has insufficient energy to control absorption effectively. In many cases, patients have a worsening of diarrhea and die within the 1st few days of oral refeeding. Antibiotics are particularly detrimental in starvation because they prevent effective bacterial fermentation and thus production of substrates for mucosal growth and sodium absorption. Oral rehydration thereapy uses glucose to drive sodium absorption in the small intestine mucosa, but it provides little energy to the mucosa. Nutrition of the small bowel mucosa is promoted by increasing the vascular supply of amino acids. Once nutrition of the intestinal mucosa has been restored, absorption of orally supplied nutrients becomes efficient. Refeeding diets in starvation should have a relatively high content of ferementable complex polysaccharides and dietary fiber and smaller amounts of milk fats and glucose than are normally provided to severely malnourished children. The starved intestinal epithelium returns to functional capacity after 5-7 days. As a result of the therapeutic implications in severely malnourished children, it is essential that cases of infective diarrhea and starvational diarrhea be differentiated from each other.