PATHOGENETIC CONCEPTIONS ABOUT NEONATAL N ECROTIZING ENTEROCOLITIS

The pathogenesis of neonatal necrotizing enterocolitis is still unknow n today. Only prematurity has been confirmed as a primary risk factor. Previous studies demonstrated the special pathophysiological conditio ns in prematurity. Differences in intestinal permeability, blood flow in anemia and hypoxemia, the uptake, transport, delivery and consumpti on of oxygen, the digestion of carbohydrates and proteins and in intes tinal motility between premature and term infants exist. The diving-re flex too is important for intestinal pathophysiology in these patients . The central key of the pathogenesis is the evident vascular damage. Infectious agents, inflammatory mediators, circulatory insufficiency, feeding excess is followed by the initial mucosal damage. This results in an increased intestinal permeability also for inflammatory mediato rs, endotoxins, bacteria and gas. Ileus, stasis and gas production cau se endotoxinemia and abdominal distension. Increased intraluminal pres sure with or without activation of inflammatory mediators leads to an important vascular dysregulation. Consecutively these multiple facts c ause the ''ischemic looking'' hemorrhagic necrosis, we call necrotizin g enterocolitis.