Pathophysiology of Necrotising Enterocolitis

Necrotising enterocolitis is a multifactorial disease. We know that prematurity, enteral feeding (especially with cows’ milk-derived formula), colonisation of the intestine with pathogenic bacteria and congenital cardiac disease are all risk factors for NEC. Detailed studies have also shown that immunological dysfunction leads to intestinal inflammation and that ischaemia-reperfusion injury plays a part as well, resulting in ischaemic necrosis of the bowel. NEC pathophysiology is best understood by the interaction of all these factors. Bacterial colonisation occurs prior to the onset of NEC but many babies will be colonised without going on to develop the disease. Formula feeds promote bacterial overgrowth. Bacterial invasion of the intestinal wall occurs and causes inflammation. The premature intestine does not regulate its blood flow properly, meaning that it is not always able to increase intestinal perfusion in response to feeding. The premature intestine is also more prone to inflammation than the term infant’s. Inflammation increases the metabolic demand and can lead to relative ischaemia. Once injury occurs, there is a vicious cycle as inflammation causes ischaemia which damages the intestinal wall and causes more inflammation. Breakdown in the intestinal barrier increases the risk of bacterial invasion. Bacterial invasion causes inflammation, ultimately resulting in ischaemic necrosis of the bowel. In severe cases, the infants become unwell with a systemic inflammatory response due to the severe inflammation and bowel perforation occurs leading to contamination of the peritoneum with intestinal contents.