With its high morbidity and mortality rates, NEC has emerged as one of the most destructive diseases in neonatal intensive care units. Although the exact etiology of NEC remains unknown, research states that it is multifactorial, with intestinal ischemia as one of the factors. There was a perception that the mode of delivery could be a contributing factor to ischemic trauma; however, studies have failed to find a connection between the mode of delivery and NEC [15]. It has been confirmed by our study that infants with cardiogenic and classical NEC are not different in their modes of delivery, and that therefore mode of delivery alone does not constitute a risk factor for the development of NEC in patients with CHD.

Another critical factor affecting the development of NEC is nutrition. Breast milk is a known protective factor in the prevention of NEC (this may be due to the presence of bioactive substances with bactericidal and immune-modulating properties) [6], and feeding with breast milk during the first week can lower the frequency of NEC that occurs in the early period [16]. In another study, preoperative feeding with breast milk was found to reduce the occurrence of NEC in infants with CHD [5]. Therefore, in our hospital, infants with CHD whose preoperative condition is stable and preterm and term infants are routinely fed breast milk. Additionally, equal importance is given to nutrition in the early postcardiac surgery period. Our research did not indicate any difference in patients’ nutritional patterns in the cardiogenic and classical groups. In several studies, it has been demonstrated that both preterm and term infants with CHD are at a higher risk of developing NEC as a result of intestinal hypoxia and ischemia during the first few days after birth [9, 10]. In term infants with CHD, persistent retrograde diastolic flow in the abdominal aorta is associated with an increased risk of NEC [17]. In our study, 28% of patients in the cardiogenic group developed intestinal hypoxia due to cyanotic heart disease. Moreover, the number of patients in the cardiogenic group was higher than that in the classical group, which indicates that CHD directly increases the frequency of NEC.

A comparison was also made between the gestational age of infants in the cardiogenic and classical groups. Pickard et al. reported no difference in the gestational age of NEC infants with or without CHD [11]. Another study found that infants with CHD who developed NEC had a greater gestational age than those without CHD who developed NEC [8]. There is no doubt that infants with very low birth weights are at an increased risk of developing NEC. In their study, Fisher et al. reported that the frequency of NEC is inversely proportional to birth weight in infants with CHD [9]. In the present study, the results indicate that the gestational age and birth weight of term and near-term infants with CHD differ significantly from those observed in infants without CHD [8]. The results of our study suggest that NEC cases accompanied by CHD have a different clinical course than classical NEC cases. Based on these findings, it can be concluded that the molecular mechanisms responsible for the development of NEC are different in patients with CHD.

NEC appears to present at 12 days in preterm infants [15], 8 days in term infants, and 26 days in term infants with CHD [18]. According to Lambert et al., the onset of NEC in infants with CHD occurs seven days after birth [19]. In some studies, as in our study, the age of onset of NEC was found to be higher in infants with CHD than in infants without CHD [8, 11]. Therefore, as per our study, infants with CHD should be actively monitored in the third week of life to develop NEC.

It is well known that cardiac surgery increases the risk of developing NEC, although some infants with CHD develop NEC prior to surgery as a result of reduced mesenteric perfusion [8]. Many factors contribute to this increased risk, such as stress following cardiac surgery, systemic inflammatory responses, hypothermia, decreased blood flow to the intestinal mucosa, and an increase in intestinal permeability postoperatively [8, 13, 20]. However, in our study, only two patients developed NEC after cardiac surgery. Therefore, we concluded that the risk of NEC in infants with CHD is higher even without surgery.

Different opinions have been expressed regarding the localization of NEC in infants with CHD. Some studies indicate no difference in the localization of NEC in infants with and without CHD [8, 21], whereas Diez et al. reported that the small intestine is more affected in infants with CHD [22]. However, in another study, NEC was most frequently observed in the colon of infants with CHD [23]. There may be several reasons for this, including pulmonary steal and ischemia-sensitive intestines distal to the splenic flexure and rectosigmoid arteries [10, 23]. The results of our study also indicate no relationship between NEC localization and CHD. Nevertheless, our research findings are limited to observations made on operated patients. Hence, to determine the localization of NEC in infants with CHD, further studies are needed in which the affected bowel segment can be evaluated in nonoperated patients.

Complications, such as perforation and stricture, are more common in classical NEC patients because the preterm infants’ intestines are immature and more fragile; infants with CHD are often at or near term, thereby reducing the requirement for surgical treatments [8]. Another study reported that the prevalence of CHD in NEC patients did not affect the rate of surgery, complications, or mortality [23]. However, in our study, more surgical treatments were performed in infants with CHD. Our results indicate that bedside drain installation was higher in the noncardiogenic group. This was because the general condition of the noncardiogenic NEC group cases was too bad to be anesthetized. Therefore, it can be concluded that NEC infants with CHD have a different course of the disease and require different surgical interventions than those with classical NEC.

Some studies have reported that the mortality rate of NEC patients is higher in infants with NEC and severe CHD [8, 13, 18]. Kesler et al. found that patients with NEC accompanied by CHD had longer hospitalization [24], and their mortality rate was sevenfold higher than that of patients with NEC. Pickard et al. demonstrated that infants with CHD had superior short-and long-term outcomes [11]. Our study found that the mortality rate of the cardiogenic group was higher than that of the classical group. In NEC patients, the mortality rate increases with comorbid diseases, such as CHD.