In fact, according to the findings of B. M. Carter and D. Holditch-Davis (2008), black infants exhibit increased rates of NEC that could not be explained by correlations of race with birth weight, infections, or days of mechanical ventilation – indicating that race (blacks) is a risk factor that is currently inexplicable. In fact, the frequency with which black infants were diagnosed with NEC was significantly higher than that of other races.
Investigations of the role of race in the development of NEC extend to maternal factors to understand the level of contribution. For example, Group Beta Streptococcus (GBS) colonization was found to occur often in black women and this colonization was found to contribute to decreased oxygenation to the bowel or proliferation of bacteria, which eventually can contribute to NEC in the preterm infant (p. 289). Furthermore, the authors found that as the number of infections increased, the risk for NEC also increased.
The idea is that NEC could be caused by the verutilization of antibiotics which leads to the overgrowth of pathogens, signifying that infections prior to NEC potentially decreases infants’ immunological competence, thereby increasing vulnerability to succeeding pathogens ((B. M. Carter and D. Holditch-Davis, 2008, p. 288). The authors also explained that the risk of NEC also increases with the need for mechanical ventilation.
They explain that though initial survival often depends on intubation at birth, intubation and the indwelling endotracheal tube insertion, however, can possibly destroy the integrity of the infant’s esophageal mucosal barriers, increasing the risk of contracting infections. Ironically, having NEC also increases the need for mechanical ventilation due to the intestinal inflammation caused by NEC which increases metabolic demands causing respiratory decompensation, which can lead to intubation (B. M. Carter and D. Holditch-Davis, 2008, p. 289).
Furthermore, the frequency and severity of NEC was also found to increase with decreasing birth weight. Infants with lower birth weight (<1000 g) revealed to have had more episodes of nosocomial sepsis than those of higher birth weight (>1000 g) and were found to require more mechanical ventilation. This findings support the fact that infants who are of lower birth weight present with multiple risk factors associated with NEC (B. M. Carter and D. Holditch-Davis, 2008, p. 289). Though gender has not been recognized as a risk factor of NEC, other studies, however, have found that there are more male than female infants who develop NEC.
Also, the same data imply that the mortality for NEC is higher in male infants than female infants (B. M. Carter and D. Holditch-Davis, 2008, p. 289). NEC primarily presents in the first two weeks of life of the preterm (Thompson & Bizarro, 2008, p. 1230). Clinical presentation may span from mild illness, which can be resolved within a few days of antibiotics use and gastric decompression, to life-threatening conditions accompanied by thrombocytopenia, acute respiratory failure, and cardiovascular collapse (Yeo, 2006, p. 47).
However, some signs and symptoms of early NEC can be nonspecific and are common to other neonatal disease processes thus requiring varying management strategies (Thompson & Bizarro, 2008, p. 1230). Typically, early signs include lethargy, poor feeding, temperature instability, and bilious emesis. Other possible indicators identifiable are abdominal distention, increasing prefeeding residuals, and gross or occult blood in the stool.
Physical assessments usually include findings such as green or bluish hue on the abdomen caused by meconium visibility through the abdominal wall (Yeo, 2006, p. 47) as well as abdominal signs associated with the pathophysiology of the GI tract such as abdominal distension and tenderness, absent bowel sounds, presence of blood in the stool, emesis and increased gastric feeding residuals (Thompson & Bizarro, 2008, p. 1230). Systemic signs on the otherhand include increased apnea, bradycardia and/or episodes of oxygen desaturation, onset of lethargy or irritability, and temperature instability (Thompson & Bizarro, 2008, p. 1230).