NECROTIZING ENTEROCOLITIS

 NEC is a syndrome of intestinal injury and is

the most common intestinal emergency
occurring in preterm infants admitted to the
neonatal ICU.

 Prematurity is the most consistent and

significant factor associated with neonatal
NEC.
 The disease occurs in 10% of infants who weigh
less than 1500 g at birth.

 NEC is infrequent among term infants (<10% of

affected infants).

 Most cases of NEC occur in premature infants born

before 34 weeks' gestation who have been fed
enterally.
NEC
Usually occurs sporadically, occasional in clusters
Occurs infrequently and earlier in term infants
Almost always occurs after enteral feeding
More common with formula feeds vs. breast milk feeds
Most often affects distal ileum, ascending colon
May involve entire GI tract

Mortality: 25- 30% (primarily with surgical NEC)

Long-term morbidity: 25-50%
PATHGENESIS
 Prematurity is associated with immaturity of the
gastrointestinal tract, including
 decreased integrity of the intestinal mucosal
barrier, depressed mucosal enzymes,
 suppressed gastrointestinal hormones,
 suppressed intestinal host defense system,
 decreased coordination of intestinal motility, and
differences in blood flow autoregulation, which is
thought to play a significant role in the
pathogenesis of NEC.
 Superinfection that leads gas formation within the bowel
wall– causes extensive bowel necrosis and septicemia---
perforation and peritonitis.
 Platelet activating factor, TNF play a role in bowel
necrosis.
 More than 90% of infants diagnosed with NEC have
been fed enterally; however, NEC has been
reported in infants who have never been fed.

 Feeding hypotheses have considered formula

osmolality and strength, rate and route of feeding
administration, bolus versus continuous feeds, and
formula versus human milk.

 Only human milk has shown a beneficial role in

reducing the incidence of NEC.
 It also is theorized that compromised intestinal
blood flow contributes to NEC.

 The pathogenesis of NEC also has been attributed

to an ischemic insult to the gastrointestinal tract,
although most infants with NEC have not had an
obvious hypoxic-ischemic event.
 Preterm infants in a neonatal ICU exhibit a different
intestinal microflora than healthy infants.

 Primary invasion of the gut by bacteria is an

alternative mechanism in the pathogenesis of NEC.

 Approximately 20% to 30% of infants with NEC

have associated bacteremia with enteric organisms.
 NEC: PATHOLOGICAL FINDINGS
Intestinal mucosa: edema, hemorrhage inflammation,
necrosis, perforation

Subserosal gas bubbles

May be transmural

Perforation, large necrotic areas

Usually involves distal ileum  proximal colon, ileocecal

valve. May involve entire GI tract from stomach to rectum
NEC
SUBMUCOSAL AIR AND NECROSIS
 Radiographic
Pneumotosis
intestinalis

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NEC: RISK FACTORS

INCREASED RISK

Asphyxia
Prematurity/LBW
IUGR
Polycythemia
PDA
Indomethacin
Fetal cocaine exposure
Low cardiac output states
Enteral feeding (formula)
NEC: RISK FACTORS

No effect on risk Decreased risk

Fast vs. slow feeding volume Term gestation

advance Antenatal steroids
Continuous vs. bolus feeds ? Trophic feeding
Delayed feeding
Human milk feeds
HUMAN MILK FEEDS

Reduces overall risk from 5% to 1%

Exclusive HM feeding (BW<1250) reduces risk NEC

(166%) and need for surgery (102%) compared to
feeding bovine-based milk

Sullivan S, et al. J Peds 2010;156:562

HUMAN MILK: BENEFICIAL EFFECTS
Supports normal intestinal biome by growth of appropriate
bacterial flora (bifidobacteria and lactobacillus) with
diversity of species
Inhibits growth of and kills pathogens
Maintains mucosal integrity
Prevents tissue penetration of pathogens
Decreases inflammatory response
Maintains systemic immune function
CLINICAL MANIFESTIONS
 Early clinical signs of NEC include
 abdominal distention,

 feeding intolerance/increased gastric residuals,

 emesis, rectal bleeding, and occasional diarrhea.

 As the disease progresses, patients may develop marked

abdominal distention,
 bilious emesis,

 ascites,

 bloody stools

 abdominal wall erythema, lethargy, temperature instability,

increased episodes of apnea/bradycardia, disseminated
intravascular coagulation, and shock.
 With abdominal perforation, the abdomen may develop a
bluish discoloration.
CLINICAL PRESENTATION NEC: SYSTEMIC SIGNS

apnea and bradycardia (sudden onset or increase in

frequency/severity)
tachycardia
lethargy
temperature instability (hypothermia)
poor perfusion
pallor
shock
NEC: CLINICAL PRESENTATION
Classic triad:
feeding intolerance
abdominal distention,
grossly bloody stools

Systemic signs of sepsis

IMAGING
 Radiographic imaging is essential to the
diagnosis of NEC. The earliest radiographic finding
is intestinal ileus, often associated with thickening
of the bowel loops and air-fluid levels. The
pathognomonic radiographic finding is
pneumatosis intestinalis caused by hydrogen
gas production from pathogenic bacteria present
between the subserosal and muscularis layers of
the bowel wall.
 Radiographic findings also may include a fixed or
persistent dilated loop of bowel, intrahepatic
venous gas, and pneumoperitoneum seen with
bowel perforation.
NORMAL PLAIN FILM OF NEWBORN
ABDOMEN
NECROTIZING ENTEROCOLITIS

Bowel loops may

become thickened and
tubular

A persistently fixed
dilated loop may be
evident on consecutive
films
Pneumatosis intestinalis: gas formed in the intestinal wall by bacteria
(“Frothy” or “soap bubble” pattern); bowel distention;
 X-ray Abdominal Findings
 Pneumatosis –intestinals (gas in the intestinal wall)
which is pathognomic
 Intrahepatic portal venous gas
 Pneumo-peritoneum (gas under the diaphragm)
NEC: DIAGNOSTIC EVALUATION
CBC with differential
Platelet count
Serial abdominal X-ray
Electrolytes
Blood gas
Blood culture
LABORATORY FINDINGS IN NEC
 wbc with left shift
Thrombocytopenia
Metabolic acidosis usual triad.
Hyponatremia
Hyperkalemia
 CRP/ESR
Bacteremia
NEC: COMPLICATIONS
Perforation
Abscess formation
Recurrent NEC
Subacute or intermittent obstruction
Malnutrition
Chronic malabsorption, FTT
Short gut
Fistula formation
Strictures/Intestinal obstruction
 The differential diagnosis of NEC includes sepsis
with intestinal ileus or a volvulus. Both conditions can
present with systemic signs of sepsis and abdominal
distention.

 The absence of pneumatosis on abdominal

radiographs does not rule out the diagnosis of NEC;
however, other causes of abdominal distention and
perforation (gastric or ileal perforation) should be
considered and investigated.

 Patients diagnosed with Hirschsprung enterocolitis or

severe gastroenteritis may present with pneumatosis
intestinalis.
 The management of NEC includes
 the discontinuation of enteral feedings,
gastrointestinal decompression with nasogastric
suction,
 fluid and electrolyte replacement,
 total parenteral nutrition, and
 systemic broad-spectrum antibiotics.

 When the diagnosis of NEC is made, consultation with

a pediatric surgeon should be obtained.

 Even with aggressive and appropriate medical

management, 25% to 50% of infants with NEC require
surgical intervention.
NEC: TREATMENT COURSE
Symptoms improve in 48-72 hours following treatment unless
bowel necrosis, perforation occur

NPO X 10 days after signs of NEC resolve

Continue antibiotics for NEC X 14 days

Antibiotics X 3 days if NEC ruled out

 NEC TREATMENT
NPO 3  14 days
NG decompression Until no gastric residuals
Antibiotics 3  10 days
ampicillin
+gentamicin /cephalosproin
+metronidazole
Abdominal x-rayrepeat q 6-24 hours until stable
Volume NS, LR, FFP, D10W
Pressors dopamine, dobutamine, epinephrine
Blood products PRBC, platelets, FFP
Nutrition TPN (Cho, protein,lipid)
 SURGICAL TREATMENT OF NEC

Paracentesis diagnostic (perforation)

peritoneal drainage

Laparotomy intestinal resection, ileostomy,

peritoneal drain
 The decision to perform surgery is obvious when
the presence of a pneumoperitoneum is observed
on abdominal radiograph.
 Other, not so obvious indications for surgical
intervention include rapid clinical deterioration
despite medical therapy, rapid onset and
progression of pneumatosis, abdominal mass, and
intestinal obstruction.

 The surgical procedure of choice is laparotomy

with removal of the frankly necrotic and nonviable
bowel.