Necrotising Enterocolitis (in the Newborn)

NEC is an inflammatory bowel necrosis seen in infants, and is the most common gastrointestinal emergency in preterm neonates.


  • More common in infants <32 weeks gestation and/or <1500g.
  • Occurs in 1-3/1000 live births
    • >90% of cases in preterm infants
    • 4-11% of preterm infants get NEC
    • Very/Extremely low birth weight infants have both higher incidence and higher mortality/morbidity
  • Major cause of morbidity/mortality


  • Prematurity
    • Most important/significant factor
    • Due to gut immaturity, particularly in motility, digestion, perfusion, barrier function and immune defenses.
  • NEC most commonly occurs in infants who are receiving enteral feeds
    • More common also in formula fed infants (cf breast-fed infants)
      • ?due to osmotic forces/injury
      • ?due to increased splanchnic blood flow and ischaemia of underperfused areas
      • ?due to stasis and bacterial overgrowth caused by immature motility of the gut
      • ?inflammatory response to feed
  • Mucosal injury is thought to be an early event, followed by an uncontrolled inflammatory response involving a cascade of inflammatory mediators (e.g. IL1, IL6, IL8, IL10, IL12 and IL18; TNFa and PAF; NO)
    • Lack of gut flora diversity and immature of the gut barrier function may also contribute to this response
  • The disease is commonly localised to the ileocolic region, although the colon may be involved, particularly in term infants.
    • The four major findings histopathologically, are
      • coagulative necrosis
      • bacterial overgrowth
      • pneumatosis intestinalis (gas cysts in the bowel)
      • inflammation
    • Some infants can develop total gut necrosis (severe disease)


  • Onset can be insidious or sudden/catastrophic.  Typically around 2-4 weeks old.
  • Often presents with nonspecific signs
    • tachycardia, apnoea, lethargy, unstable temperature (i.e. raised NEWS/PEWS scores)
  • GI signs include
    • vomiting, abdominal distention, tenderness, ileus (with hypoactive bowel sounds),
    • bloody stools only occur in around 25%
    • in patients with an OG tube, increased prefeed residuals may be present


  • Bell’s criteria
  • cdscds
  • Radiography
    • Main diagnostic feature is pneumotosis intestinalis (air in the bowel wall)
      • can be linear or cystic
  • Blood tests may show thrombocytopenia, neutropenia, coagulopathy or acidosis (all signs of more significant disease)
    • However, most a non-specific (particularly a raised CRP) and should be analysed accordingly


  • Nil by mouth/OG/NG tube + decompression of the GI tract (by OG/NG)
    • 3-5 days in stage I and 10-14 days in stages II/III
    • IV fluid replacement and TPN feeding
  • IV antibiotics (usually for 10-14 days)
    • Amoxicillin, Metronidazole and Gentamycin (typically, but consult local advice)
      • Antifungals should be considered if infant is unresponsive to these
  • Around 20-40% will require surgery
    • Any perforation, failure of medical management, single fixed bowel loop (on X-ray), abdominal wall erythema or palpable mass are all relative indications
    • Peritoneal drainage is thought to be as effective as laparotomy although there is concern about subsequent neurodevelopmental impairment in the former.


  • Steroids, minimal enteric feeding and breastfeeding have all been shown to reduce the risk of NEC.  However, with the exception of breastfeeding, the risks often outweigh the benefits if to administer these prophylactically
  • Note that slow advancement of feeding has not been shown to be effective
  • Antibiotics, recombinant growth factor and pre/probiotics may be useful in protecting against NEC


  • Mortality rates range between 20% and 50%.
  • Approximately 20-40% of affected infants may require surgery, and as many as 50% infants may die in the postoperative period.
  • Subacute complications include
    • strictures
    • dysmotility
    • malabsorption
    • short gut syndrome.
  • Severe NEC has been associated with growth delay that can persist beyond infancy into childhood and poor neurodevelopmental outcome at a corrected gestational age of 18–22 months.

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