Necrotizing Enterocolitis [NEC] is a common disease process and complication found in preterm neonates (Bell, 2004; Carter, 2007; Carter & Holditch-Davis, 2008; Gregory, 2008; Kawase et al. , 2006; Thompson & Bizarro, 2008; Yeo, 2006). It is a multifactorial disease process affecting the gastrointestinal [GI] tract of neonates and infants that may result in mucosal and/or transmural necrosis of the intestines (Carter, 2007, p. 1228; Yeo, 2006, p. 46. ). Primarily a condition of prematurity, NEC occurs in term newborns only rarely.
There are no documented in utero cases of NEC simply due to the fact that the neonate’s bowels are sterile before birth. NEC is known to affect 5% to 10% of very low-birth-weight [VLBW] newborns and extremely low-birth-weight [ELBW] newborns. Those weighing less than 1000g and less than 28 weeks’ gestational age are found to be most susceptible. NEC occurs in 1% to 5% of newborns in the NICU and in 1 to 3 per 1000 live births. For known and unknown reasons, NEC incidence is unit dependent.
The overall mortality rate for the disease is 25% and can be as high as 66% for VLBW newborns (Yeo, 2006, p. 46). The etiology of the disease is still predominantly unknown (Bell, 2004; Carter, 2007; Carter & Holditch-Davis, 2008; Gregory, 2008; Kawase et al. , 2006; Thompson & Bizarro, 2008; Yeo, 2006) however, several risk factors are found to be associated with the disease. The primary or key risk factor associated with the disease is prematurity (Gregory, 2008, p. 260; Yeo, 2006, p.
46) since premature newborns have a high risk for developing pathological processes such as infections and complications that increases length of stay in the neonatal intensive care unit (NICU). Furthermore, “preterm infants have altered host defenses, abnormal peristalsis due to bacterial overgrowth in the intestines, and poor autoregulation of blood flow. They [also] have a different inflammatory response, microbial flora, and feeding patterns than those of the term newborns” (Yeo, 2006, p. 46-47).
Additionally, it was found that premature infants were 13 times more likely to develop NEC if the infant required increased respiratory support to maintain oxygenation during the early neonatal period and 6. 4 times more likely to develop NEC if the infant did not receive nutritionally fortified enteral feedings of breast milk. When both factors were present, the odds of NEC increased 28. 6 times when compared with infants without these factors. (Gregory, 2008, p. 260).
However, the general consensus is that NEC is a multi-factorial disease process with various triggering events associated with/or in the form of ischemia of the GIT, infectious causes and enteral feedings (Bell, 2004, p. 173; Carter & Holditch-Davis, 2008, p. 286; Yeo, 2006, p. 46).
Additional risk factors discussed by other researches include physiological immaturity of the GI tract, alterations in the normal microbiological flora (Carter, 2007, p. 1228), infants who experienced early nasal continuous positive airway pressure [ENCPAP] failure (Aly, Massaro & El-mohandes, 2005, p. 1660), race [blacks], gender [males] (Carter & Holditch-Davis, 2008, p. 287; Thompson & Bizarro, 2008, p. 1230), birth weight, need for mechanical ventilation, infections before NEC diagnosis (Carter & Holditch-Davis, 2008, p. 287), maternal risk factors such as placental insufficiency from chronic disease and cocaine use, and peri- and postnatal factors [hypoxia, ischemia, umbilical vein catheters, hyperviscosity, cardiovascular abnormalities, ischemia of the intestinal mucosa, hyperosmolar formula and medications, and cleanliness of the NICU] (Yeo, 2006, p. 46).