Bowel Perforation in Premature Infants with Necrotizing Enterocolitis: Risk Factors and Outcomes

Abstract

We aim to determine risk factors and clinical outcomes for bowel perforation in premature infants with NEC. We analyzed clinical data of 57 cases of premature infants with NEC at our NICU between January 2010 and December 2012. Based on the presence of bowel perforation, we divided these infants into two groups: perforated NEC group (n = 10) and nonperforated NEC group (n = 47). We compared general information, clinical characteristics, and laboratory findings between groups. The perforated NEC group, compared to the nonperforated NEC group, had significantly lesser gestational age, lower birth weight, higher prevalence of apnea, mechanical ventilation, sepsis and shock, lower blood pH, higher levels of blood glucose, abnormal WBC count and thrombocytopenia, and elevated CRP (all P < 0.05). Moreover, the perforated NEC group had significantly longer durations of fasting and TPN usage, higher incidences of EUGR and cholestasis, longer duration of antibiotics, higher frequency of advanced antibiotics use, and poorer prognosis than the nonperforated NEC group (all P < 0.05). Bowel perforation in premature infants with NEC was associated with multiple risk factors. Early identification of some of these risk factors in premature infants with NEC may help implement early intervention to reduce the incidence of bowel perforation and thereby improve the prognosis.

Estimation of Neonatal Intestinal Perforation Associated with Necrotizing Enterocolitis by Machine Learning Reveals New Key Factors

“…The relative contribution of each predictor variable also allowed to verify that the models are doing what they are intended to do (estimation of intestinal perforation diagnosis), by finding variables involving literature-known factors, that may allow an early diagnosis and follow-up of premature neonates. With respect to previously described risk factors for intestinal perforation associated with NEC, lower birth weight [ 32 , 33 , 34 ], decreased gestational age [ 32 , 33 ], apnea episode [ 32 ], presence of sepsis [ 32 ], lower platelet count [ 6 , 32 , 35 ] were also obtained by our models. Risk factors contained in the final GutCheck model included gestational age, packed red blood cells transfusion, unit NEC rate, late-onset sepsis, multiple infections, hypotension treated with inotropic medications, Black or Hispanic race, birth in a different NICU and metabolic acidosis [ 13 ].…”

Necrotizing enterocolitis: It’s not all in the gut

“…7,8,11 These systemic and local factors leave the intestine, specifically the distal ileum and proximal colon, susceptible to inflammatory processes and perforation leading to pneumoperitoneum. 55,56 Finally, advanced NEC (Bell’s Stage III) requiring surgical intervention is characterized by bowel perforation with resultant pneumoperitoneum, hypotension, signs of peritonitis, and severe metabolic acidosis. 7,8,11 Gestational age must also be taken into account when considering the diagnosis of NEC, where gestational age and the onset and severity of NEC symptoms have an inverse correlation.…”

“…Surgical treatment of NEC typically includes resection of ischemic bowel portions; the long-term outcome of these patients is dependent on the length of remaining intestine and its ability to absorb nutrients adequately. 18,55–57 Specifically, ileal resection may lead to GI dysmotility, abnormal mucosa, bacterial overgrowth, and vitamin B 12 or enzyme deficiency, causing malabsorption of nutrients. 18,55–57 Furthermore, NEC is the most common cause of SBS in neonates, which can lead to GI complications such as gastric acid hyper-secretion, bacterial overgrowth, D-lactic acidosis, translocation of enteric bacteria to the bloodstream, and intestinal failure-associated liver disease.…”

“…18,55–57 Specifically, ileal resection may lead to GI dysmotility, abnormal mucosa, bacterial overgrowth, and vitamin B 12 or enzyme deficiency, causing malabsorption of nutrients. 18,55–57 Furthermore, NEC is the most common cause of SBS in neonates, which can lead to GI complications such as gastric acid hyper-secretion, bacterial overgrowth, D-lactic acidosis, translocation of enteric bacteria to the bloodstream, and intestinal failure-associated liver disease. 18,55–57,98 Clinical management of SBS requires a multi-disciplinary approach to ensure that the neonate receives sufficient nutrition for growth, to maximize intestinal adaptation, and to minimize fluid, electrolyte, and nutritional losses.…”

Non-intervention observation: Dynamic evolution laws of inflammatory response in necrotizing enterocolitis

“…Newborns with asphyxia, hypoxia, hypotension, acidosis, and shock upon birth, are prone to defensive reflex blood redistribution, decreased mesenteric blood flow and intestinal mucosal ischemia and necrosis ( 6 ). Furthermore, the weakened intestinal mucosal barrier functions result in the propagation and translocation of a large number of intestinal pathogenic bacteria, and the release of a large number of toxic substances, such as endotoxin, IL-6, TNF-, and IL-4 ( 7 ). These inflammatory factors also promote the cascade reaction of intestinal mucosal inflammation, cause more extensive mucosal necrosis, enable more toxic substances to enter into the circulation of the blood, and lead to bacteremia, sepsis and shock ( 8 ).…”