Part 1. Current Controversies in the Understanding of Necrotizing Enterocolitis

Barbara Noerr, RNC, MSN, CRNP


Adv Neonatal Care. 2003;3(3) 

In This Article

Risk Factors: The Clear Link with Prematurity

Historically, the frequency of NEC evolved with the establishment of NICUs in the 1960s. The disease continued to escalate as neonatal care improved and the survival and absolute number of pre-term neonates increased.[4,8] Countries with low rates of preterm births (eg, Japan, Sweden) have a correspondingly low prevalence of NEC.[4] Table 2 highlights risk factors for NEC. Prematurity is the major risk.

The specific vulnerabilities of the preterm infant's GI tract to NEC, although not completely understood, are likely related to an immature GI mucosal barrier and immune response, along with impaired circulatory dynamics from hypoxic-ischemic insults.[8] Premature infants may experience vasoconstriction, hypotension, and thrombosis leading to decreased GI perfusion and GI mucosal injury.[3] Indwelling umbilical artery catheters (UAC) may decrease blood vessel diameter and flow, leading to GI ischemia.[4] The potential for UAC-induced arterial spasm or microemboli formation is a well-documented risk of therapy. Small emboli may cause visible blanching or cyanosis of a neonate's lower extremity. However, decreased GI perfusion may be clinically silent, until clinical symptoms of NEC appear.

Preterm infants commonly have a patent ductus arteriosus (PDA) with its inherent left-to-right shunt, diminishing blood flow to the mesenteric vascular bed.[13] Treatment of the PDA with indomethacin, a highly effective, potent vasoconstrictor, is associated with numerous adverse effects including GI bleeding, isolated ileal perforation, and NEC.[15]

The efficacy of indomethacin therapy and the risk of NEC were evaluated by retrospective data analysis of 250 preterm neonates with echocardiogram-confirmed PDA who were treated with indomethacin.[15] Closure of the PDA was achieved in 89% of cases. Ninety infants developed NEC, with 34 of these requiring surgical intervention. NEC was associated with younger gestational age (P < 0.04), lower birth weight (P < 0.001), and prolonged ventilator support (P < 0.02).

The authors then compared these infants with a matched control group without PDA or indomethacin therapy.[15] The incidence of NEC in control infants was 13.7% compared with 35% in the study group (P < 0.02). The need for surgical intervention and mortality was similar between groups. Perforation rates in the control group were 12.3% compared with 30% in those treated with indomethacin (P < 0.05). A 16% decrease in mesenteric blood flow was observed after indomethacin administration.[15] This was of concern because GI hypoperfusion with resultant mucosal hypoxia is implicated in gastric perforation and NEC. Ischemia and ulceration may follow hypoperfusion, allowing for bacterial invasion, the setup for NEC.

In summary, caregivers must be aware of both the risks of an untreated PDA and those associated with treatment. Both the left-to-right shunt and mesenteric steal associated with PDA and the acute decreased blood flow associated with indomethacin increase the preterm infant's risk for NEC.


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