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Year : 2019  |  Volume : 32  |  Issue : 2  |  Page : 745-747

Early onset necrotizing enterocolitis in a full-term neonate

Department of Pediatric Surgery, SMS Medical College, Jaipur, Rajasthan, India

Date of Submission04-Oct-2017
Date of Acceptance06-Dec-2017
Date of Web Publication25-Jun-2019

Correspondence Address:
Aditya P Singh
Near The Mali Hostel, Main Bali Road, Falna, Pali District, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mmj.mmj_695_17

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We are presenting a case of necrotizing enterocolitis (NEC) in a full term neonate.
NEC usually affect the preterm baby while in our case baby was full term neonate.
A 2 days old male neonate who had diagnosis of NEC, was managed by us.
Baby had the involvement of large bowel with sever faecal peritonitis and baby was expired due to septicemia.
NEC may occurs in full term baby with large bowel involvement. Resection of the gangrenous colon and rectoascending anastomosis with protective ileostomy was done. Baby was expired after 3 days due to septicemiasepticemia.

Keywords: colon, full term, necrotizing enterocolitis, neonate

How to cite this article:
Singh AP, Gupta AK, Pardeshi R, Mathur V. Early onset necrotizing enterocolitis in a full-term neonate. Menoufia Med J 2019;32:745-7

How to cite this URL:
Singh AP, Gupta AK, Pardeshi R, Mathur V. Early onset necrotizing enterocolitis in a full-term neonate. Menoufia Med J [serial online] 2019 [cited 2020 May 27];32:745-7. Available from: http://www.mmj.eg.net/text.asp?2019/32/2/745/260913

  Introduction Top

Necrotizing enterocolitis (NEC) is the most common and frequently dangerous gastrointestinal emergency in premature infants in the neonatal ICU. Although 90% of infants who develop NEC are born premature, full-term and near-term infants also develop the disease[1]. The etiology and pathophysiology of primary NEC remains to be fully elucidated, but it is likely multifactorial leading to intestinal mucosal injury[2],[3]. The most important risk factor for NEC is prematurity and the earliest infants are at the greatest risk. Multiple factors, including hypoxia, feeding, sepsis, abnormal colonization of the bowel, and the release of inflammatory mediators stimulated by an ischemic–reperfusion injury in an immature gut are thought to lead to NEC[1],[4]. We present here a case of NEC in a 2-day-old neonate with colon involvement, which highlighted the different presentation of the NEC.

  Case Report Top

A 2-day-old male neonate was presented to us with complaints of bilious vomiting since 1 day. The baby had normal vaginal birth and had nonconsanguineous parents. Antenatal ultrasounds were normal. Baby was full term weighed 2.8 kg. Baby had respiratory distress after delivery. Baby was put on an oxygen hood and intravenous antibiotics were started. Only routine resuscitation was provided in the delivery room. The baby was fed on mother's milk after 1 day. He fed once, and after that the baby started bilious vomiting. There was no history of mother's illness or drug intake. Baby had bloody stool with firm abdomen, redness present, and tenderness on palpation. Routine blood investigations were within normal limits including complete blood counts, renal function test, and serum electrolytes except a total leukocyte count of 17 000/cm. Serum bilirubin was 8 mg/dl. Breast milk was withheld, and an oral gastric tube was used for gastric decompression. Radiographic study of the abdomen showed pneumatosis intestinalis without any gas under both domes of the diaphragm [Figure 1]. Blood culture was negative. On exploration, there was gross fecal peritonitis with gangrene and large perforations throughout the colon. The rectum, cecum with a 2 cm part of the ascending colon, and small bowel were spared [Figure 2]. Resection of the gangrenous colon and rectoascending anastomosis with protective ileostomy was done. Baby was shifted on ventilator postoperatively and expired after 3 days due to septicemia.
Figure 1: An erect radiographic study of the abdomen show pneumatosis intestinalis.

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Figure 2: Photograph showing the excised gangrenous large bowel.

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  Discussion Top

NEC is the most common gastrointestinal emergency and cause of significant morbidity and mortality in preterm infants. The incidence of NEC is inversely related to an infant's birth gestation, but marked variability is evident across neonatal ICUs and countries[4],[5],[6]. Such events may include hypoxia in utero or sepsis. The release of inflammatory mediators signals neutrophil activation, increased permeability of the vasculature, release of reactive oxygen species, and ultimately vasoconstriction with ischemic–reperfusion injury[1],[4]. As the mucosal barrier breaks down and NEC becomes severe, it can lead to overwhelming sepsis and death in worst cases[1],[4]. In our case, it may also have started in utero, so presentation was within 2 days.

Late preterm infants, in particular, are more likely to develop NEC if they have other risk factors, including intrauterine growth retardation, polycythemia, hypoglycemia, sepsis, exchange transfusions, umbilical lines, gestational diabetes, and being born to a mother with chorioamnionitis[7].

Early onset sepsis, drug exposure, and respiratory distress were all associated with NEC, and those who developed NEC were significantly less likely to have received breast milk and more likely to have been fed only formula[8].

The possible risk factors present in the prenatal course include maternal drug use (specifically cocaine), maternal hypertensive disease including pregnancy-induced hypertension[7], maternal infections, and problems related to placental blood flow that may result in a growth-restricted newborn[7]. Placental disease restricts the quality and quantity of nutrition to the developing fetus, leads to a growth-restricted newborn, and may lead to metabolic compromise if combined with other risk factors[7].

Intrapartum risk factors may include maternal cardiac arrest, umbilical cord prolapse, placental abruption, and chorioamnionitis. Maternal infections that develop during the intrapartum period may also be suspect.

NEC appears to occur earlier in full-term infants. Ruangtrakool studied 16 full-term infants; among them, NEC developed 8.6 days after birth, in comparison to 12.8 days after birth in preterm controls[9].

Most of these infants had colon involvement, making this location typical among this group as compared with the preterm group, where the most common site is the jejunum and the ileum[10].

Infants with NEC present with clinical symptoms of abdominal distension, feeding intolerance, bilious vomiting, and bloody stools, and with laboratory derangements characterized by neutropenia, thrombocytopenia, metabolic acidosis, and high C-reactive protein levels[11]. In some infants, NEC progresses to peritonitis, intestinal perforation, septic shock, disseminated intravascular coagulation, and death.

Plain radiography is the cornerstone of NEC diagnosis and staging[11]. The pathognomonic radiological finding of NEC is that of pneumatosis intestinalis, defined as gas in the bowel wall originating from pathogenic bacteria. Other findings that are seen in more severe forms of NEC are ascites and portal venous gas. Pneumoperitoneum resulting from intestinal perforation is indicative of intestinal perforation and/or necrosis.

Doppler ultrasonography, especially aimed at measuring blood flow velocity in the celiac trunk and superior mesenteric artery, has been used to identify patients at risk of developing NEC, as well as to assess the bowel viability in those infants with established NEC[9]. In particular, sonographic findings of free gas, focal fluid collection, increased bowel wall echogenicity, absent bowel perfusion, portal venous gas, bowel wall thinning or thickening, and pneumatosis intestinalis are associated with an adverse outcome.

Other imaging modalities could provide more information and help diagnosis and follow-up of infants with NEC; like magnetic resonance imaging scan, near-infrared spectroscopy is a noninvasive real-time method of measuring local tissue oxygenation that is being evaluated as a predictive diagnostic modality for NEC.

Most infants with suspected (Bell's stage I) or confirmed (Bell's stage II) NEC are managed nonoperatively. Nonoperative treatment includes withholding feeds, ventilatory support, fluid resuscitation, inotropic support, correction of acid–base imbalance, coagulopathy and/or thrombocytopenia, bowel rest, and antibiotics.

A proportion of medically managed infants with NEC require acute surgical intervention, due to clinical deterioration or intestinal perforation. These include requirement of inotropes, worsening abdominal findings, hemodynamic instability, worsening laboratory values (intractable acidosis, persistent thrombocytopenia, rising leukocytosis, or worsening leukopenia), and/or sonographic evidence of decreased or absent bowel perfusion.

  Conclusion Top

In our view, NEC can be suspect in a full-term neonate in the early neonatal period. We can prevent morbidity and mortality in these neonates due to NEC by early diagnosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their conse nt for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Neu J, Mshvildadze M, Mai V. A roadmap for understanding and preventing necrotizing enterocolitis. Curr Gastroenterol Rep 2008; 10:450–457.  Back to cited text no. 1
Gordon PV, Swanson JR. Necrotizing enterocolitis is one disease with many origins and potential means of prevention. Pathophysiology 2014; 21:13–19.  Back to cited text no. 2
Neu J, Walker WA. Necrotizing enterocolitis. N Engl J Med 2011; 364:255–264.  Back to cited text no. 3
Patole SK. Prevention and treatment of necrotizing enterocolitis in preterm neonates. Early Hum Dev 2007; 83:635–642.  Back to cited text no. 4
Gagliardi L, Bellu R, Cardilli V, De Curtis M. Network Neonatale Lombardo. Necrotising enterocolitis in very low birth weight infants in Italy: incidence and non-nutritional risk factors. J Pediatr Gastroenterol Nutr 2008; 47:206–210.  Back to cited text no. 5
Christensen RD, Gordon PV, Besner GE. Can we cut the incidence of necrotizing enterocolitis in half – today? Fetal Pediatr Pathol 2010; 29:185–198.  Back to cited text no. 6
Manogura AC, Turan O, Kush ML, Berg C, Bhide A, Turan S, et al. Predictors of necrotizing enterocolitis in preterm growth-restricted neonates. Am J Obstetr Gynecol 2008; 198:638.e1–638.e5.  Back to cited text no. 7
Stout G, Lambert DK, Baer VL, Gordon PV, Henry E, Wiedmeier SE, et al. Necrotizing enterocolitis during the first week of life: a multicentered case-control and cohort comparison study. J Perinatol 2008; 28:556–560.  Back to cited text no. 8
Yikilmaz A, Hall NJ, Daneman A, Gerstle JT, Navarro OM, Moineddin R, et al. Prospective evaluation of the impact of sonography on the management and surgical intervention of neonates with necrotizing enterocolitis. Pediatr Surg Int 2014; 30:1231–1240.  Back to cited text no. 9
Fanaroff AA, Martin RJ. Neonatal-perinatal medicine. 7th ed. London: Mosby; 2002; 1 & 2:1298–1300.  Back to cited text no. 10
Kim SS, Albanese CT. Necrotizing enterocolitis. In: O'Neill JA, Coran AG, Fonkalsrud E, Grosfeld JL. Pediatric surgery. 6th ed. St. Louis: Mosby; 2003; 2:1427–1452.  Back to cited text no. 11


  [Figure 1], [Figure 2]


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