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Necrotising Enterocolitis 417

Among the most accepted and consistently recognised risk factors
for developing NEC are prematurity and timing and content of
gastrointestinal feeding (i.e., formula concentration). Certain aspects
of prematurity have been recognised that would appear to place these
children at increased risk for NEC development. Among these are
immaturity of gastrointestinal motility, digestive ability, circulatory
regulation, intestinal barrier function along with abnormal colonisation
by pathologic bacteria, and underdeveloped intestinal defense
mechanisms. Other risk factors implicated in the pathogenesis of NEC
22
include bacterial infection, the presence of pathogenic bacteria in the
23
ICU (the so-called NEC epidemics), intestinal ischaemia, 24,25 certain
pharmacologic agents, 26,27 and a host of inflammatory mediators, 28,29
although their relative contributions remain unclear. Other factors
particularly pertinent to developing nations include antenatal factors,
such as impaired umbilical artery flow, multiple pregnancy, and
maternal infections, including HIV. Nevertheless, despite these
30
numerous recognised associations, no clear pathway of pathogenesis
has been identified.
Figure 70.1: Small intestine showing necrosis, haemorrhage and congestion
with a focal area of re-epithelisation of the mucosa (right). Original Pathology
magnification, 20x. NEC usually begins in the mucosal layer of the bowel. Intramural pro-
gression may be recognised by the frequent association of pneumatosis
intestinalis, which represents bacterial hydrogen gas in the intestinal
wall (Figure 70.2). This gas may extend into the vessels and into the
portal vein and may be visualised radiographically as portal venous gas.
Macroscopically, there is considerable variation in the degree of bowel
involvement from a fairly minor inflammatory response of the bowel
to full thickness necrosis, which may involve large segments of intes-
tine (Figure 70.3). The terminal ileum and caecum are most commonly
affected, but NEC represents a spectrum of disease; in its severest form,
it may affect the entire bowel and parts of the stomach (NEC totalis).
The affected bowel frequently extends beyond the macroscopic disease
seen at surgery.
At surgery, the serosal surface is characterised by patches of full-
thickness necrosis, oedema, and subserosal haemorrhages in affected
portions of bowel. Pneumatosis intestinalis may be seen and felt
in the bowel wall and may extend into the mesentery. Perforation
of transmural necrotic patches is common, with subsequent gross
contamination and peritonitis. Surgical intervention is required in
at least 40% of patients with NEC due to intestinal necrosis with or
without perforation. The objectives of surgical management are to
Figure 70.2: Frontal abdominal radiograph showing pneumatosis intestinalis in remove the necrotic bowel, preserve bowel length, divert the faecal
the right colon (arrow). stream if required, and control sepsis.
Clinical Presentation
Infants with acute NEC usually present with both specific gastroin-
testinal signs as well as nonspecific physiologic signs often indicative
of generalised infection. The classic history for a patient with NEC is
a premature infant within 2 weeks of delivery who begins to develop
feeding intolerance, distention, and/or blood per rectum after the
initiation of formula feeds. The most common gastrointestinal signs
reported are abdominal distention and blood per rectum. Others include
feeding intolerance, bilious emesis, haematemesis, and guaic positive
stools. Some of the nonspecific signs include lethargy, temperature and
glucose instability, hypotension, and apnoeic spells associated with
bradycardia (Table 70.1).
Initial physical exam findings are often subtle, significant only
for mild distention and tenderness. As the disease progresses, the
abdominal exam often reveals significant tenderness, palpable bowel
loops, and an inflammatory mass, along with erythema or oedema of
the abdominal wall.

Figure 70.3: Segments of small bowel showing hyperaemia and an area of full-
thickness necrosis (arrow).