As depicted in Figure 1 acute diarrhea causes the host to undergo a sequence of hormonal, metabolic and immunologic responses, all of which have a nutritional cost. The impact will be more significant in the debilitated or marginally nourished child. From a nutritional point of view this process of nutrient loss and redistribution has the potential for being exploited to the benefit of the host. Two treatment techniques could be used to improve the host response to infection. Nutrients which are essential for optimal immune function and which are rapidly being metabolized may be selectively replaced, while nutrients that the offending organism needs may be withdrawn or temporarily withheld. A better understanding of the physiologic response and nutritional consequences of diarrhea should permit us to further improve the outcome of this and other infectious diseases.
PIP: A better understanding of the physiologic response to and nutritional consequences of acute diarrhea can facilitate an improved outcome for this and other infectious diseases. Acute diarrhea causes the host to undergo a sequence of hormonal, metabolic, and immunologic responses, all of which have nutritional consequences. Its most profound effect is on the malabsorption of water and electrolytes by the intestinal epithelial cell, the electrolyte, leading to dehydration. Diarrhea is defined as any alteration of fluid and electrolyte movement that results in increased fecal water due to an excessive amount of solute in the stool. Infectious agents that damage the enteric mucosa cause villous atrophy, which is accompanied by increased proliferation, migration, and extrusion of epithelial cells; this results in alterations of fluid and electrolyte movement and is the final common pathway to the development of diarrhea. During the acute stages of diarrhea, there are increased losses of fecal weight and volume as well as sodium and chloride and the level of disaccharidase enzymes is depressed. Different bacteria affect different parts of the gastrointestinal tract. After bacterial adherence and surface colonization of the intestinal epithelium, diarrhea can result from any of 3 major mechanisms: 1) production and release of enterotoxins, 2) direct invasion of the mucosa or submucosa, and 3) adhesion and cytotoxic disruption of the microvilli of the enterocyte. There is evidence of diarrhea-associated changes in the plasma concentration of certain gastrointestinal hormones and indications that calcium plays a key role in the intracellular regulation of electrolyte transport. The impact of diarrhea will be more significant in the debilitated or marginally nourished child. To improve the host response to infection, nutrients that are essential for optimal immune function and are rapidly being metabolized should be selectively replaced, while nutrients needed by the offending organism can be withheld.