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Necrotizing Enterocolitis-NEC

Necrotizing Enterocolitis - NEC

necrotizing enterocolitis




•Necrotizing enterocolitis (NEC) is the most
common gastrointestinal emergency of the
•It is characterized by various degrees of mucosal or
transmural necrosis of the intestine.
•Despite advances in neonatology over the last few
decades, mortality and morbidity secondary to NEC
remains high.
•Current clinical practice is directed towards
prompt, early diagnosis and institution of
proper intensive care management.


•NEC is the most common surgical disorder among
infants in Neonatal Intensive Care Unit (NICU) with
an incidence that varies from center to center and
from year to year.
•In most centers, NEC occurs in 2-5% of all NICU
admissions, and 5-10% of very low birth weight
•Sex, race, geography, climate, and season do not
play any determining role in the incidence or
course of NEC.

•Several studies have been carried out to
uncover the causes/risk factors associated with
NEC and hence improve outcome in the
management of NEC.
•A study by Abdulkadir et al in Katsina, Nigeria in
2018 on “Necrotizing enterocolitis associated
with dysbiosis of preterm gut microbiome: A
review” concluded that NEC results from
dysbiosis of gut microbiome.

•Herrmann et al performed a clinical control trial in
2014 on 162 babies, of which 148 (91%) received
exclusive human milk (mother’s milk &/or donor
human milk), & only 1% had NEC when compared
to 3.4% of the control cohort.
•“Neonatal necrotizing enterocolitis in Lagos” a
study by Adeyemi et al on 14 babies diagnosed
with NEC within 6years (1978-1984), showed a
79% mortality as only 3 neonates survived
following medical management.


1. Prematurity – is the greatest risk factor.
Decreasing gestational age in associated with an
increased risk of NEC, with a mean GA of 30-
32weeks and a mean age of onset of 12 days.
2. Enteral feeding – is the next greatest risk factor.
>90% of infants have been fed before the onset
of NEC. The risk is least with infants who are
exclusive breastfed. Bovine milk-based products
may increase the risk of NEC.
3. Antenatal steroids – Randomized controlled
trials have shown reduced incidence of NEC
among infants treated with antenatal
4. Infants exposed to cocaine have a 2.5times
increased risk of developing NEC due to it’s
vasoconstrictive effects, causing intestinal
5. Use of H2 blockers have been implicated in a
higher risk of NEC in extremely low birth weight
(ELBW) infants, suggesting that an acidic
gastrointestinal environment may be protective.
6. ~10% of infants with NEC are full term. These
infants have other risk factors such as congenital
heart disease, polycythaemia, sepsis, hypotension
and asphyxia which all result in splanchnic

Maternal factors
Cocaine abuse
In-utero growth restriction
Lack of prenatal steroids
Placental abruption

•Main risk factors
Low birth weight
Formula feeding
Intestinal dysbiosis

Other risk factors
Acid-suppressing medications
Acute hypoxia
Antibiotic exposure
Blood transfusions
Cardiac anomalies
Neonatal anemia
Poor intestinal perfusion
Prolonged use of indomethacin for PDA


•The pathogenesis of NEC is multifactorial.
•The TRIAD of;
a) Intestinal ischemia (injury)
b) Enteral nutrition (metabolic substrate)
c) Bacterial translocation
has been classically linked to NEC.
• Aggressive enteral feeding may predispose to the
development of NEC.

•Bacterial and viral agents implicated are;
Escherichia coli, Klebsiella, Clostridium
perfringens, Staphylococcus epidermidis,
astrovirus, norovirus, and rotavirus.
• In most situations, a pathogen may not be
•There is release of endotoxins and cytokines by
proliferating colonizing bacteria and bacterial
fermentation with gaseous distension results.

• Evidence supports a critical role for
inflammatory mediators. Platelet-activating
factor (PAF), endotoxin lipopolysaccharide
(LPS), tumor necrosis factor-a (TNF-a),
interleukins, and nitric oxide are some of the
inflammatory mediators that have been
suspected to have a role in the pathophysiology
of NEC.
•The distal part of the ileum and proximal
segment of the colon are most frequently
•In fatal cases, gangrene may extend from the
stomach to the rectum.

Hypoxic insult
Splanchnic vasoconstriction
Reduced mesenteric flow
Bowel mucosa hypoxia
Gas accumulation in submucosa
(Pneumatosis intestinalis)
Perforation with pneumoperitoneum
Peritonitis, sepsis, and death

•Factors that have been considered as regards
enteral formula feeds include; the osmolality of
formula, the lack of immunoprotective factors in
formula, the timing, volume, and rate of feeding.
• Some case control studies suggest that judicious
introduction of feedings and avoidance of large
day-to-day volume increases may lower the
incidence of NEC.

• However, the rate of daily feeding increment
that may protect infants from developing
NEC has not been identified, and the
mechanism by which larger volumes may
predispose to the development of NEC is not


•Diagnosis of NEC requires a very high index of
•It is suspected from clinical presentation but
must be confirmed by diagnostic
radiographs, surgery or autopsy


•This can be divided into systemic or abdominal
A) SYSTEMIC – Lethargy, apnea/respiratory
distress, temperature instability, irritability,
acidosis, glucose instability, poor
perfusion/shock, & DIC.

B) ABDOMINAL – Abdominal distension or
tenderness, gastric aspirates (feeding
residuals/intolerance), vomiting, ileus,
bloody stools, abdominal wall erythema,
abdominal mass.
• The onset of NEC is usually in the 2nd or 3rd
week of life but can occur as late as 3months
in very low birth weight infants.

•Age of onset is inversely related to gestational
•The spectrum of NEC is broad and ranges from
mild disease with only guaiac positive stools, to
severe illness with bowel perforation,
peritonitis, shock and death.
•Progression from mild to severe disease may be



•Radiology studies – plain abdominal x-ray, both
AP and cross-table lateral views may reveal bowel
wall oedema, pneumatosis intestinalis (air in the
bowel wall – radiologic hallmark), portal venous
gas (is a sign of severe disease) and
pneumoperitoneum (gas under the diaphragm).
•Hepatic sonography may also detect portal
venous gas in some infants with normal
abdominal x-rays.

radiology features of nec


• No laboratory tests are specific for NEC, though
they are valuable in confirming diagnosis.
• Blood and serum studies – thrombocytopenia,
persistent metabolic acidosis, and severe
refractory hyponatremia constitute the most
common triad of signs. Blood cultures may
reveal bacteremia with a pathogenic organism.
•Stool analysis – bloody stools may be an
indication of NEC (25%). Occult
hematochezia does not correlate well with
NEC and hence routine test for faecal occult
blood is not recommended.

• Bell staging is not a continuum; babies may
present with advanced NEC, without earlier
signs and symptoms.
• STAGE 1 (Suspect) – clinical signs and
symptoms, including abdominal signs and
nondiagnostic radiographs.
• STAGE 2 (Definite) – clinical signs and symptoms,
pneumatosis intestinalis and portal venous gas on
*Stage 2a – Mildly ill
*Stage 2b – Moderately ill with systemic
• STAGE 3 (Advanced) – clinical signs and symptoms,
pneumatosis intestinalis on radiograph and critically
*Stage 3a – Impending intestinal
*Stage 3b – Proven intestinal perforation.


1. Sepsis
2. Intestinal obstruction
3. Malrotation with midgut volvulus
4. Isolated intestinal perforation – also known as
asymptomatic pneumoperitoneum. It occurs in
2% of extreme low birth weight infants, occurs at
an earlier age than NEC and is not associated
with feeding.
5. Infectious enterocolitis – diarrhea is
6. Severe allergic colitis – presents with
abdominal distension and bloody stools. Xrays and laboratory studies are normal.
7. Feeding intolerance.


• Treatment should begin promptly when NEC is
A. Immediate medical management – here, attention
to respiratory, cardiovascular, and hematologic
resuscitation is given, as well as correction of
electrolyte abnormalities.
1. Secure airway and support breathing - Abdominal
distension may compromise breathing and baby
may require artificial ventilation.
2. Circulation –
•establish intravascular access for infusion of
•give intravascular volume replacement (saline,
blood, fresh frozen plasma) – this treats
hypoperfusion/hypovolemic shock.
•correct metabolic acidosis - Improves organ and
tissue perfusion.
3. Place large‐bore naso/orogastric tube for
intestinal decompression & bowel rest.
4. NPO (nil by mouth) – start parenteral
nutrition. This supports nutritional demands
for growth.
5. Broad‐spectrum antibiotics against
gram‐positive, gram‐negative and anaerobic
organisms (ampicillin, gentamicin, and
clindamycin or metronidazole). Also consider
antifungal agents.
6. Treat coagulopathy (fresh frozen plasma,
platelets, cryoprecipitate). This avoids
bleeding complications.
7. Monitor regularly – clinical, radiographic and
laboratory investigations, as NEC can worsen
very quickly to bowel perforation.

B. Surgical intervention –
*Indications – bowel perforation or failure of NEC to
resolve on medical treatment and a positive result of
abdominal paracentesis.
Options are;
1. Peritoneal drainage at bedside
2. Exploratory laparotomy – resection of non‐viable
bowel and anastomosis or ileostomy or colostomy.

NOTE: Peritoneal drainage alone is associated
with worse neurodevelopmental outcome than
•A large randomized trial showed that a majority
of infants who were initially treated with
peritoneal drains required a delayed secondary


•Medical management fails in approximately 20-
40% of patients with pneumatosis intestinalis at
diagnosis; of these, 10-30% die.
•Early postoperative complications include;
* wound infection
* wound dehiscence
* stomal problems (prolapse, necrosis).

•Later complications include;
*Intestinal strictures - which develop at the site
of the necrotizing lesion in approximately 10%
of surgically or medically managed patients.
Resection of the obstructing stricture is curative.
*Short-bowel syndrome (malabsorption,
growth failure, malnutrition),
•Complications related to the use of central
venous catheters – sepsis and thrombosis
•Cholestatic jaundice.
•Preterm infants with NEC who require surgical
intervention or who have concomitant
bacteremia are at increased risk for adverse
growth and neurodevelopmental outcome.


• Prevention of NEC is the ultimate goal.
•Unfortunately, this can best be accomplished
only by preventing premature birth. If
prematurity cannot be avoided, several
preventive strategies may be of benefit.
1. Induction of GI maturation - The incidence of
NEC is significantly reduced after prenatal
steroid therapy
2. Exclusive feeding of human milk-based diet
- Premature infants who are fed exclusively
with expressed human milk are at decreased
risk for developing NEC. Mothers should be
strongly encouraged to provide expressed milk
for their premature babies when able. Donor
human milk can also be given.
3. Optimization of enteral feedings – Because
of the lack of adequately sized randomized
trials in ELBW infants, currently there is not
enough evidence to support either early
versus delayed feedings, or an optimum rate
of advancement of feedings.
~ However, from the available evidence, it is
clear that adoption and strict adherence to a
particular standardized feeding regimen
significantly reduces the risk of NEC; therefore,
individual NICUs should agree on a feeding
regimen and monitor adherence.

4. Enterally fed probiotics are a promising new
approach to the prevention of NEC. Probiotics
fed to preterm infants may help to normalize
intestinal microflora colonization.
A recent meta-analysis has shown reduced
incidence of NEC by over 50% in infants fed
probiotics (e.g., Lactobacillus GG,
Bifidobacterium breve, Saccharomyces
boulardii, Lactobacillus acidophilus) compared
with controls.

~ Until further evidence is available to help
determine the most effective probiotic(s),
their optimum dosage, and long and shortterm safety, the use of probiotics in the
prevention and treatment of NEC should
be confined to carefully monitored trials.



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