NEC is a devastating condition affecting premature infants. It involves necrosis of the intestinal tissue. Key factors that increase risk are prematurity, enteral feeding, and circulatory instability in the intestines. Clinically, infants may experience apnea, feeding intolerance, and abdominal distension. Diagnosis involves blood tests showing infection and inflammation as well as imaging showing abnormalities in the intestines. Treatment involves bowel rest, antibiotics, and sometimes surgery. Outcomes depend on severity but mortality can be over 40% in very premature infants and survivors face long-term complications.

1. Case
Presentation

2. • B/o Sabiya Banu,32 wks,1.7kg,admitted on 2HOL
with provisional diagnosis of MPT/LBW/Moderate
RDS.
• H/o PPROM>72 hours,no antenatal steroids.
• CPAP started at 2 HOL,recieved late rescue
surfactant at 4HOL ,INSURE .
• Removed from CPAP at 48 HOL.
• Initial septic screen was negative.
• Baby on 2nd line Ab as per protocol.

3. • Baby started with feeds 3ml/3hrly RTF of EBM on D3 of life.
• Feeds gradually increased twice daily
increment(30ml/kg/day)
• On D7 of life baby on 23ml RTF,developed abdominal
distension,residual feeds.AG-27cm.
• Abdomen –Soft,mild distension,non tender,Bowel sounds –
heard.No abdomen wall edema/erythema.
• Investigations-TLC-10,590/cumm,
Plt-12,000/cumm.CRP-62.5mg/dl. Serum Na-124mEq/dl.
• Stool occult blood-positive
• Diagnosis of NEC stage 1A was made .
• Baby kept NPO and Ab’s changed to Meropenem &
ofloxacin
• In view of broad spectrum Ab’s and other risk factors
Flucanozole was added.

4. • Surgical consultation –advised for medical line of
management.
• After 48hrs of bowel rest,Repeat invetsigations requested
showed-TLC-7870/cumm,PLT-40000/cumm and CRP of
94.1mg/L.
• In view of persistent distension and RTA baby was kept NPO
for 5days.
• Baby was restarted on feeds after 5 days of bowel
rest.(D=9)
• Baby started with 3ml RTF/3hrly and gradually increased
with once daily increment.
• After 3 days of feed on 10ml/EBM 3 hrly,baby had repeat
bout of feed intolerance.(D=12 )
• Repeat counts D12-Hb-11.3Gm%,TLC-10,720 and
platelet -35,000/cumm. CRP-53.2mg/L.
• USG abdomen D15-Minimal turbid ascites,small bowel
edema,no pneumobilia.
• Diagnosis was revised to NEC stage 2B.

5. • Baby kept NBM and continued with same
antibiotics.
• On D19 baby noticed to have significant
tachycardia 190bpm,bounding periphreal pulses
and PSM.Screening echo showed PDA 4mm with L
to R shunt.(RFT-WNL,Plt-75,000/cumm)
• Received Oral Ibubrofen for 3days.
• Baby restarted on feeds after 7 days of bowel rest
D21 of life RTF EBM 3ml/3hrly.

6. MODERATE PT(32WK)/LBW/MODERATE
RDS/STAGE 2B NEC/HS PDA 4MM L TO
R SHUNT.

7. NEC

8. • Most common GI emergencies in the newborn
infant.
• Defined as:
Transmural coagulative necrosis of the
intestinal mucosa,with invasion of enteric gas
forming organisms, and dissection of gas into
the muscularis and portal venous system .

9. Epidemology:
• 1 -3 /1000 live births and 1 -7.7 % of admissions to
NICUs .
• Rates were inversely related to BW
401 to 750 g – 11.5%
751 to 1000 g – 9 %
1001 to 1250 g – 6 %
1251 to 1500 g – 4 %
• Mortality rates range from 15- 30% and are inversely
related to GA and BW.
• Approximately 13 % of cases occur in term,have a pre
existing illness- IUGR,congenital heart disease ,
respiratory distress , sepsis , birth asphyxia , and
polycythemia .

10. Pathology:
• The terminal ileum and colon are MC involved,
entire GI tract is affected in severe cases.
• On gross examination- the bowel distended and
hemorrhagic. Subserosal collections of
gas,gangrenous necrosis and perforation may be
present.
• Histologic findings in NEC -mucosal edema,
hemorrhage, and transmural coagulative
necrosis.
-secondary bacterial infiltration, and collections of
gas.

11. Gross Microscopy

12. Pathogenesis:Factors implicated in NEC
• Prematurity
• Enteral nutrition
• Circulatory instability of the intestinal tract.
• Microbial bowel overgrowth
• Medications that cause intestinal mucosal injury or enhance
microbial overgrowth-Antibiotics,H2 blockers.
• Maternal choriamniotis.
• IUGR with doppler changes.
• Maternal smoking,coccaine use.
• Polycythemia
• Anemia ,PRBC transfusion.
• Umbilical cathetristaion
• Oral indomethacin

13. Pathogeneis:

14. Prematurity:
• Immature mucosal barrier with increased
permeability
• Immature local host defenses.
• Immature bowel motility and function.

15. Enteral nutrition
• More than 90 percent of infants who develop NEC have
received milk feeding
• Incompletely digested carbohydrates and lipids in the
intestine of preterm infants cause mucosal injury .
• Human milk, protective :PAF acetylhydrolase, S IgA, IL-
10, IL-11, EGF , nucleotides, glutamine, and
antioxidants such as vit E, carotene, and glutathione.

16. Anemia & RBC transfusion:
• Multicenter observational’ cohort study
reported that severe anemia and not RBC
transfusion was associated with NEC.
• Clinically-significant anemia is associated with
an increased risk for NEC, and that RBC
transfusion is only a surrogate marker for
anemia
‘Patel RM, Knezevic A, Shenvi N, et al. Association of Red Blood Cell Transfusion, Anemia, and
Necrotizing Enterocolitis in Very Low-Birth-Weight Infants. JAMA 2016; 315:889

17. Medications
• Hyperosmolar medications and formulas can
cause mucosal injury and may result in NEC-
oral theophylline, multivitamins,
or phenobarbitone.
• Cimetidine, ranitidine, and famotidine, are
associated with higher rates of NEC.
• Antibiotic administration greater than five
days duration is associated with an increased
risk of NEC or death

18. Clinical Presentation:
• Majority of premature infants who develop
NEC are healthy, feeding well, and growing
babies.
• Onset of symptoms varies and is inversely
related to gestational age
GA< 26 weeks-23 days,
GA >31 weeks- 11 days.
• Indian data peak age –end of 1stwk to 2nd
week

19. Systemic Signs
• Apnea,Bradycardia
• Respiratory distress
• Lethargy
• Poor feeding
• Temperature instability.
• Hypotension
• Bleeding diathesis with
consumption coagulopathy.
Abdominal Signs
• Gastric retention
• Abdominal Distension
• Abdominal redness &
tenderness
• Vomiting.
• Diarrhea.
• Rectal bleeding
(hematochezia)
• Bilious drainage from
enteral feeding tubes

20. Modified Bells staging for NEC:
• Bell staging criteria (Walsh & Kleigman)
provide a uniform definition of NEC based
upon the severity of systemic, intestinal, and
radiographic findings.
1. Stage I/suspected NEC
2. Stage II/proven NEC
3. Stage III/advanced NEC

21. Bells Staging Criteria

22. Investigations:
Abdomen X ray
• Abnormal gas pattern with dilated loops of bowel -ileus, early stages
of NEC.
• Bowel wall edema
• Pneumatosis intestinalis, the hallmark of NEC, appears as bubbles of
gas in the small bowel wall, stages II and III NEC .
• Gasless abdomen indicating ascites.
• Pneumoperitoneum bowel perforation occurs , IIIB NEC.
-"football" sign on a supine radiograph,large hypolucent area in the
central abdomen with markings from the falciform ligament.
• Sentinel loops, a loop of bowel that remains in fixed position, is
suggestive of necrotic bowel and/or perforation in the absence of
pneumatosis intestinalis.
In EPT, treatment -clinical suspicion as confirmatory
radiographic findings may not be present

24. USG abdomen:
• USG more sensitive method to detect
intramural air and portal venous gas .
• USG can detect intermittent gas bubbles in
liver parenchyma and the portal venous
system that are not detected by radiographs
• Color Doppler USG more sensitive than
abdominal radiography in detecting bowel
necrosis and alterations in bowel wall
perfusion

25. Blood and serum studies:
• WBC count <1500/cumm –poor prognostic factor
• Thrombocytopenia, persistent metabolic acidosis, and severe
refractory hyponatremia triad of signs and help to confirm the
diagnosis.
• Serial measurements of CRP - diagnosis and assessment of
response to therapy of severe NEC.
• Blood cultures are positive in ˜40% of cases
Analysis of stool:
• Grossly bloody stools may be an indication of NEC, routine
testing of stool for occult blood has no value .
• 60% of infants will have Hemoccult-positive stools at any
given time during hospitalization without any evidence for
NEC

26. D/D’s
1. Sepsis with Ileus
2. Infectious enteritis
3. Spontaneous intestinal perforation of the
newborn
4. Intestinal obstruction –enterocolitis in
Hirschsprung disease, ileal atresia, volvulus,
meconium ileus, and intussusception.
5. Anal fissures
6. Neonatal appendicitis
7. Cow's milk protein allergy

27. Management:
• Medical management
-Supportive care
-Antibiotics
-Radilogical and lab monitoring
• Surgical management
-Primary peritonael drainage
-Laprotomy

28. Supportive Care:
• Bowel rest with gastrointestinal decompression
with intermittent nasogastric suction.
• Total parenteral nutrition
• Fluid replacement to correct third space losses
• Support of both the cardiovascular( inotropes)
and respiratory systems (O2 & Ventilation as
needed).
• Correction of hematologic (DIC) and metabolic
abnormalities (metabolic acidosis).

29. Antibiotics:
• After obtaining appropriate specimens for
culture, broad spectrum antibiotic treatment
should be initiated for suspected or proven
NEC.
• Regimens should provide coverage for
pathogens that cause late-onset bacteremia.
• Anaerobic coverage considered-peritonitis or
pneumoperitoneum, suggesting intestinal
perforation.

30. • Lack of consensus, and the choice of
antibiotic regimen varies among NICU
1. Ampicillin, gentamicin ,and metronidazole
2. Ampicillin, gentamicin, and clindamycin
3. Ampicillin, cefotaxime, and metronidazole
4. Piperacillin.tazobactam and gentamicin
5. Vancomycin, piperacillin-tazobactam,
and gentamicin.
6. Meropenem

31. Surgical management:
Indications
• Perforation on abdominal X
ray(pneumoperitoneum)
• Positvie test on paracentesis(stool ,organism)
• Failure of medical management.
• Single fixed bowel loop on radiograph
• Abdominal wall erythema.
• Palpable mass

32. • Ideally surgery performed after intestinal necrosis
but before perfoartion and peritonitis develop.
• Surgical procedures- exploratory laparotomy with
resection of the affected intestinal region, or
primary peritoneal drainage (PPD).
• PPD may be the preferred initial surgical
procedure in extremely low birth weight (ELBW)
infants and unstable premature infants.

33. Complications:
Early:
• Infectious complications – Sepsis, meningitis,
peritonitis, and abscess formation
• Disseminated intravascular coagulation- intestinal or
extraintestinal bleeding
• Respiratory and cardiovascular complications –
Hypotension, shock, and respiratory failure
• Metabolic complications – Hypoglycemia and
metabolic acidosis
Late:
• Stricture formation(9-36%)
• Short bowel syndrome.(9% surgical operated cases)

34. Mortality:
71,808 premature infants who were born between January 2005 and
December 2006 -Vermont Oxford Network
Fitzgibbons SC, Ching Y, Yu D, et al. Mortality of necrotizing enterocolitis expressed by birth weight categories. J
Pediatr Surg 2009; 44:1072
 BW 501 to 750 g – 42 %
 BW 751 to 1000 g – 29 %
 BW 1001 to 1250 g – 21 %
 BW 1251 to 1500 g – 16 %
• Mortality rate is higher in infants with more severe disease requiring
surgical intervention(30.8 versus 6.8 percent).
• Radiographic evidence of portal venous air, an increase in feeding volume
that was greater than 20 mL/kg per day, and an increase in the
concentration of HMF within 48 hours of developing NEC .
• Hematocrit < 22 % ,I:T ratio > 0.5, and total lymphocyte count
below 4000/microlt

35. Long term outcome:
• Approximately one-half of survivors have no long-term sequel.
• 10% infants will have late gastrointestinal morbidity-
persistent loose stools or frequent bowel movements
• Infants with NEC were at increased risk for cerebral palsy, and
cognitive and severe visual impairment.
• Patients who were surgically treated had poorer
neurodevelopmental outcome than those treated medically.
• ELBW infants who required surgical care were more likely to
have significant growth delay and poorer developmental
outcome at 18 to 22 months.
Hintz SR, Kendrick DE, Stoll BJ, et al. Neurodevelopmental and growth outcomes of extremely low birth weight
infants after necrotizing enterocolitis. Pediatrics 2005; 115:696.

36. Prevention of NEC:
• Antenatal corticosteroids reduced the risk for NEC
approximately by half.
• Human milk compared with formula is the most important strategy
associated with a lower risk of NEC( 2.8 times risk in formula fed)
• TIMING AND ADVANCEMENT OF FEEDING
 The optimal timing of initiation of minimal enteral (trophic) feeding
remains uncertain and its association with NEC is lacking.
 Advancement of enteral feed volumes at daily increments of 30 to
40 mL/kg compared to lower volumes of 15 to 24 mL/kg did not
increase the risk of NEC or death in VLBW infants (BW <1500 g)
Morgan J, Young L, McGuire W. Slow advancement of enteral feed volumes to prevent necrotising enterocolitis in very
low birth weight infants. Cochrane Database Syst Rev 2015; :CD001241

37. Prevention of NEC:
• Routine use of probiotic –not recomended, the lack of an established
regimen of optimal strain and dosing, and the absence of quality
control regulation to ensure consistency and safety of product.
• Oral immunoglobulins may reduce NEC by inhibiting the release of
proinflammatory cytokines ,meta analysis administration of oral IgG
or IgG/IgA combination did not reduce the incidence .
• Lactoferrin,Arginine,Glutamine ,HMO-proven to be beneficaial in
some studies but not routinely recommended.

38. Prevention of NEC:
• Avoidance of histamine 2 blockers:Immunity provided
by gastric acid may be important in preventing the
cascade of infectious and inflammatory events.
• Avoidance of prolonged empirical antibiotic use :use of
prolonged initial empiric antibiotic (≥5 days duration)
started in the first three days of life was associated
with an increased risk of NEC or death.
• Unproven as measures to prevent NEC:use of feeding
protocols, judicious advancement of feeding, avoidance
of hypertonic formulas and contrast agents, and
prompt treatment of polycythemia.