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Abstract SUMMARY Persistent diarrhea (PD) is still a major cause of morbidity and mortality in the developing world and usually follows acute infectious diarrhea. PD is commonly seen in association with significant malnutrition, and the relationship between persistent diarrhea and malnutrition is bidirectional. PD should be differentiated with other chronic diarrheal diseases. Progression from acute to persistent diarrhea is due to an interaction between several complex pathophysiological mechanisms. Small bowel injury has been incriminated as the central mechanism in PD. In PD, chronic inflammation and defective intestinal repair result in abnormal mucosal morphology, leading to poor absorption of luminal nutrients and increased permeability of the bowel to abnormal dietary or microbial antigens. The severity of these changes is greater in younger children due to delayed intestinal mucosal maturation. Micronutrient deficiencies contribute to poor intestinal repair and immunological responses that may result in prolongation of mucosal injury and delayed intestinal repair mechanisms. The influence of hyperbaric oxygen on bodily organs and tissues is multidirectional. In the conditions of high partial concentrations, oxygen becomes a drug inducing numerous significant phenomena in the body of a sick child, the most important of which is the effect on cellular metabolism. The use of hyperbaric oxygen is known to: increase the antimicrobial activity of leukocytes; reduces the adhesion of neutrophils to the vascular walls thereby limiting endothelial damage. It also leads to vasocontriction in areas with a regular oxygen concentration without causing changes in circulation in the areas with an impaired flow; restores fibroblast growth and collagen production and ATP storage which reduces tissue oedema; limits some |