ABSTRACT
Necrotizing enterocolitis is the most common gastrointestinal emergency of the neonate, affecting 5-10% of infants, yet the pathogenesis remains unclear. Widely accepted risk factors include prematurity, enteral feeds, bacterial colonization and mucosal injury. How these or other yet identified factors come together to create the classic clinical and pathologic features is the subject of much research. The activation of the cytokine cascade, in part by bacterial ligands, appears to play a key role in mucosal injury. Two mediators that may also contribute are platelet activating factor and intestinal toll-like receptors. Short chain fatty acids, the products of bacterial fermentation of carbohydrates, have been thought to cause mucosal injury. Overgrowth of pathogenic bacteria in the face of a decreased commensal population may play a key role. A current focus of clinical research involves probiotics, enterally fed forms of commsenal bacteria. This may set the stage for a healthier intestinal ecosystem and possibly, decreased risk of NEC.