Part 1. Current Controversies in the Understanding of Necrotizing Enterocolitis

Authors and Disclosures

Barbara Noerr, RNC, MSN, CRNP, Neonatal Intensive Care Unit, Penn State Milton S. Hershey Medical Center, Hershey, PA

Sidebar 1: NEC in Full-Term Infants

NEC is rare in full-term infants. Over a 25-year period in one institution, only 23 of 226 cases of NEC occurred in full-term infants.^[4] NEC is described as a different disease in the full-term infant, with direct injury to the GI mucosa playing an important role.^[2,54] Congenital heart disease (CHD), hypothyroidism, Down syndrome, small bowel atresia, and gastroschisis are often present in full-term infants with NEC.^{[54,55,56,57,58]}

Neonates with CHD have a 10-fold increased risk for the development of NEC.^[54] Recent review of a database including 643 neonates with CHD admitted over a 4-year period reported NEC in 21 (3.3%).^[54] Thirteen infants presented with NEC before surgical intervention for CHD. The majority (10 of 21) had hypoplastic left heart syndrome, with an overall NEC incidence of 7.6% among neonates with this complex lesion.

Alterations in mesenteric blood flow make infants with CHD vulnerable to NEC.^[54] Neonates with many forms of CHD (eg, hypoplastic left heart syndrome, coarctation of the aorta, truncus arteriosus) have a widened pulse pressure and low diastolic pressure leading to retrograde diastolic flow in the descending aorta with the potential for mesenteric ischemia.^[57] Surgical intervention requiring cardiopulmonary bypass adds to the potential for low perfusion states leading to mesenteric ischemia.^[56]

There are minor variations in the clinical presentation of NEC between preterm and full-term infants.^[4,58] In full-term infants, the age of onset of symptoms tends to be earlier and occurs more rapidly, with signs and symptoms as early as the first day of life.^[2] Thrombocytopenia and acidosis are not outstanding features in these infants when compared with the preterm infant.^[4] There may be fewer systemic manifestations, and pneumatosis intestinalis occurs less frequently. The mortality rate for NEC is also lower in the full-term infant.

Sidebar 2: A Brief Review of Intestinal Anatomy

Approximately 85% of fluids ingested and those secreted by the GI tract on a daily basis are absorbed via the small intestine. During fetal development, the small intestine undergoes several invaginations, where the small bowel becomes ensheathed. The result is formation of multiple villi and microvilli. Intestinal villi, with their branching projections and folds, increase the surface area for absorption tremendously. With a combination of the villi and microvilli in the small intestine, it is estimated there is an absorptive surface equal to that of a tennis court in adults.

(Enlarge Image)

The villus is the functional unit of the small intestine, specifically designed for its important role of absorption of nutrients. Located over the entire surface of the small intestine, the villus can be found from about the common bile duct to the ileocecal valve. A single layer of columnar epithelium containing capillaries and lymphatic vessels lines the villus. Each epithelial cell has a characteristic brush border area containing as many as 1,000 microvilli in adults. The brush border protrudes into the GI chyme.

There are 3 layers of smooth muscle in the small intestine. One is circular and the other 2 run longitudinally. The wall of the small intestine is lined by mucosa, or mucous membrane and serosa, or serous membrane. The mucosal layer contains the villi. The serosa continues onto the mesentery, the peritoneal fold that encircles most of the small intestine and connects it to the posterior abdominal wall. Nerve fibers, lymphatic, and blood vessels are located in the mesentery.