Necrotizing Enterocolitis

NECROTIZING ENTEROCOLITIS
Necrotizing enterocolitis (NEC) is a medical condition primarily seen in premature infants, where
portions of the bowel undergo necrosis (tissue death). It occurs postnatally (i.e. it is not seen in stillborn
infants) and is the second most common cause of morbidity in premature infants, causing 355 deaths
per year in the United States in 2013, down from 484 in 2009. Rates per 100,000 live births were almost
three times higher for blacks than for whites
Signs and symptoms
The condition is typically seen in premature infants, and the timing of its onset is generally inversely
proportional to the gestational age of the baby at birth (i.e. the earlier a baby is born, the later signs of
NEC are typically seen). Initial symptoms include feeding intolerance, increased gastric residuals,
abdominal distension and bloody stools. Symptoms may progress rapidly to abdominal discoloration
with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support.
Diagnosis
The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities,
most commonly radiography. Specific radiographic signs of NEC are associated with specific Bell’s stages
of the disease:
Bell's stage 1/Suspected disease:
 Mild systemic disease (apnoea, bradycardia, temperature instability)
 Mild intestinal signs (abdominal distention, gastric residuals, bloody stools)
 Non-specific or normal radiological signs
Bell's stage 2/Definite disease:
 Mild to moderate systemic signs
 Additional intestinal signs (absent bowel sounds, abdominal tenderness)
 Specific radiologic signs (pneumatosis intestinalis or portal venous air)
 Laboratory changes (metabolic acidosis, thrombocytopaenia)

Bell's stage 3/Advanced disease:
 Severe systemic illness (hypotension)
 Additional intestinal signs (striking abdominal distention, peritonitis)
 Severe radiologic signs (pneumoperitoneum)
 Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular

coagulation
More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC
before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless
abdomen, or a sentinel loop. Diagnosis is ultimately made in 5–10% of very low-birth-weight infants
(<1,500g).
Treatment
Treatment consists primarily of supportive care including providing bowel rest by stopping enteral feeds,
gastric decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and
third-space losses, support for blood pressure, parenteral nutrition, and prompt antibiotic therapy.
Monitoring is clinical, although serial supine and left lateral decubitus abdominal x-rays should be
performed every six hours. Where the disease is not halted through medical treatment alone, or when
the bowel perforates, immediate emergency surgery to resect the dead bowel is generally required,
although abdominal drains may be placed in very unstable infants as a temporizing measure. Surgery
may require a colostomy, which may be able to be reversed at a later time. Some children may suffer
from short bowel syndrome if extensive portions of the bowel had to be removed.
Prevention
Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC.
Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. In a
2012 policy statement, the American Academy of Pediatrics recommended feeding preterm infants
human milk, finding "significant short- and long-term beneficial effects," including reducing the rate of
NEC by a factor of two or more.
A study by researchers in Peoria, IL, published in Pediatrics in 2008, demonstrated that using a higher
rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in
zero infants developing NEC in the experimental group, compared with 14% with NEC in the control
group.
Neonatologists at the University of Iowa reported on the importance of providing small amounts of
trophic oral feeds of human milk starting as soon as possible, while the infant is being primarily fed
intravenously, in order to prime the immature gut to mature and become ready to receive greater oral
intake. Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut
mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in
very premature infants, where the blood supply is limited due to immature development of the
capillaries, so nutrients from the lumen of the gut are needed.
A Cochrane review published in April 2014 has established that supplementation of probiotics enterally
"prevents severe NEC as well as all-cause mortality in preterm infants."
Increasing amounts of milk by 30 to 35 ml/kg is safe in infant who are born weighing very little or are
premature. Not beginning feeding an infant by mouth for more than 4 days does not appear to have
protective benefits.
Data from the NICHD Neonatal Research Network's Glutamine Trial showed that the incidence of NEC
among extremely low birthweight (ELBW, <1000 g) infants fed with more than 98% human milk from
their mothers was 1.3%, compared with 11.1% among infants fed only preterm formula, and 8.2%
among infants fed a mixed diet, suggesting that infant deaths could be reduced by efforts to support
production of milk by mothers of ELBW newborns.
Prognosis
Typical recovery from NEC if medical, non-surgical treatment succeeds, includes 10–14 days or more
without oral intake and then demonstrated ability to resume feedings and gain weight. Recovery from
NEC alone may be compromised by co-morbid conditions that frequently accompany prematurity. Long-
term complications of medical NEC include bowel obstruction and anemia.
Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving,
with survival rates of 70–80%. "Surgical NEC" survivors are at-risk for complications including short
bowel syndrome and neurodevelopmental disability

Necrotizing Enterocolitis

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NECROTIZING ENTEROCOLITIS

Signs and symptoms

Bell's stage 1/Suspected disease:

 Mild systemic disease (apnoea, bradycardia, temperature instability)

 Mild intestinal signs (abdominal distention, gastric residuals, bloody stools)

 Non-specific or normal radiological signs

Bell's stage 2/Definite disease:

 Mild to moderate systemic signs

 Additional intestinal signs (absent bowel sounds, abdominal tenderness)

 Specific radiologic signs (pneumatosis intestinalis or portal venous air)

 Laboratory changes (metabolic acidosis, thrombocytopaenia)

 Severe systemic illness (hypotension)

 Additional intestinal signs (striking abdominal distention, peritonitis)

 Severe radiologic signs (pneumoperitoneum)

 Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular

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