prepared from clohorty some slides were taken from dr. Padmesh Vadakepat presentation

1. Necrotizing enterocolitis
- Dr.Raghavendra Babu S
DNB year II
JLNH&RC

2. Necrotizing Enterocolitis:
􀂾 an acquired neonatal acute intestinal
necrosis of unknown etiology
􀂾 NEC is neither a uniform nor a well-defined
disease entity
Acquired neonatal intestinal diseases (ANIDs)
Wider umbrella, includes different pathologies
affecting gastrointestinal tract in preterm and term
infants. Some which do lead to the common final
pathology of NEC and some which do not.
􀂾 Includes:
􀂾 NEC
􀂾 SIP (isolated spontaneous intestinal perforation)
􀂾 Viral enteritis of infancy
􀂾 Cow’s milk protein allergy

3. Epidemiology
Incidence: 0.3-2.4 / 1000 live births
2-5 % of all NICU admissions
5-10 % of VLBW infants
 Over 90 % of cases occur in preterm babies
About 10 % occur in term newborns: essentially
limited to those that have some underlying illness or
condition requiring NICU admission
 Sex, race, geography, climate has no role in
determining the incidence of NEC
 Prematurity is the single greatest risk factor

4. Intestinal ischemia (injury)
Enteral nutrition
Pathogenic
organisms

5. Risk factors influencing NEC prediposition
• Prematurity:
 inflamatory propensity of the immature gut.
 Decreases intestinal barrier function.
 Decreased gut motility and abberent vascular regulation.
• Enteral feeding:
 Aggressive advancement of feeding.
 Non human milk feeding
• Abnormal bacterial colonization:
 Prolonged emperical antibiotic therapy
 Decreased commensal flora
 Increased pathogenic bacteria
Maternal cocaine abuse – 2.5 times increases risk

6. Risk Factors: in Term Babies
Limited to those that have some underlying illness or
condition requiring NICU admission.
• Congenital Heart Disease
• Intrauterine growth restriction
• Polycythemia
• Hypoxic-ischemic events
• The mean gestational age of infants with NEC is 30 to 32
weeks, and the infants generally are weight appropriate
for gestational age.
• Postnatal age at onset is inversely related to birth weight
and gestational age with mean age at onset of 12 days

7. PRIMARY INFECTIOUS AGENTS
Bacteria, Bacterial toxin, Virus,
Fungus
CIRCULATORY INSTABILITY
Hypoxic-ischemic event
Polycythemia
MUCOSAL INJURY
INFLAMMATORY MEDIATORS
Inflammatory cells (macrophage)
Platelet activating factor (PAF)
Tumor necrosis factor (TNF)
Leukotriene C4, Interleukin 1; 6
ENTERAL FEEDINGS
Hypertonic formula or
medication Malabsorption,
gaseous distention H2 gas
production, Endotoxin
production

8. pathogenesis

9. Microbiologic Flora and Infection
Several organisms have been accused, but non has been
proven to be causative:
– Enterobacteriaceae
– Enterobactersakazakii
– Coagulase-negative staphylococci: SIP
– Closrtidium perfringens
– Candida species: SIP
– Cytomegalovirus
– Torovirus
– HIV
– Mucormycosis

10. Cytokines and Inflammatory Mediators
– Platelet Activating Factor (PAF)
– Tumor Necrosis Factor (TNF)
– High-mobility group box 1 protein (HMGB 1)
– Interferon-gamma (INF-gamma)
– Interleukins (ILs)
– Matrix metalloproteinases(MMPs)

11. Clinical Presentation
• Course of the disease
Fulminant presentation
Slow, paroxysmal presentation
• The onset of NEC usually occurs in the 1st 2 weeks of
life (with a mean age at onset of 12 days) but can be as
late as 3 months of age in VLBW infants

12. • The 1st signs of impending disease may be
-Nonspecific including lethargy and temperature
instability or
-Related to gastrointestinal pathology such as
abdominal distention and gastric retention.
• Obvious bloody stools are seen in 25% of patients.
The spectrum of illness is broad and ranges from
-Mild disease with only guaiac-positive stools
to
-Severe illness with bowel perforation, peritonitis,
systemic inflammatory response syndrome, shock, and
death.

13. • Abdominal (enteric)
signs:
– Distension
– Tenderness
– Gastric aspirate,
vomiting
– Ileus
– Abdominal wall
erythema, induration
– Ascites
– Abdominal mass
– Bloody stool
• Systemic signs:
– Respiratory distress,
apnea, bradycardia
– Lethargy, irritability
– Temp. instability
– Poor feeding
– Hypotension
– Acidosis
– Oligurea
– Bleeding diathesis

15. Laboratory features
• No lab test is specific for NEC
• The most common triad:
– Thrombocytopenia
– Persistent metabolic acidosis
– Severe refractory hyponatremia
Serial measurements of CRP – diagnostic and
prognostic
• ↑WBC, ↓WBC, ↓PMN
• Hyperkalemia
• Stool: reducing substances, occult blood

16. Blood studies:
Thrombocytopenia
COMMON TRIAD
OF SIGNS
Persistent
Hyponatremia
Severe Refractory
Metabolic Acidosis

17. Radiology studies
• Abdominal X-ray:
•
•
•
•
•
Abnormal gas pattern, ileus
Bowel wall edema
Pneumatosis intestinalis
Fixed position loop
Intra hepatic-portal venous gas ( in the absence of
UVC)
• Pneumoperitonium - left lateral decubitus or crosstable lateral views

21. •
•
Intestinal perforation.
Abdominal Xray in NEC demonstrates marked distention and massive
pneumoperitoneum
Free air below the anterior abdominal wall.

22. • Abdominal ultrasound:
– Thick-walled loops of bowel with hypomotility.
– Intraperitonealfluid is often present.
– Intramural gas can be identified in early-stage NEC
– In the presence of pneumatosisintestinalis, gas is
identified in the portal venous circulation within the
liver.
– Color Doppler US is more accurate than abdominal
radiography in depicting bowel necrosis in NEC.

23. • Differential diagnosis of NEC :
• Specific infections (systemic or intestinal)- Pneumonia,
Sepsis.
• Gastrointestinal obstruction, volvulus, malrotation,
• Isolated intestinal perforation.
• Severe Inherited Metabolic disorders. (e.g., galactosemia
with Escherichia coli sepsis)
• Feeding intolerance
• Severe allergic colitis
• Idiopathic focal intestinal perforation can occur
spontaneously or after the early use of postnatal steroids
and indomethacin.

24. • MODIFIED BELL’S STAGING OF NEC:
Based on:
1. Systemic Signs
2. Intestinal Signs
3. Radiological Signs
Classified into:
I. Suspected:
II. Definite :
A (Mildly ill) ,
B (Moderately ill)
III. Advanced:
A (Severely ill,bowel intact),
B (Severely ill,bowel perforated)

26. • TREATMENT:
• Rapid initiation of therapy is required for suspected as well
as proven NEC cases.
• There is no definitive treatment for established NEC and,
therapy is directed at supportive care and preventing
further injury with
-Cessation of feeding,
-Nasogastric decompression, and
-Administration of intravenous fluids.
• Once blood has been drawn for culture, systemic
antibiotics (with broad coverage for gram-positive, gramnegative, and anaerobic organisms) should be started
immediately.

27. • TREATMENT: Contd..
• Umbilical catheters if present should be removed.
• Ventilation should be assisted as required.
• Intravascular volume replacement with crystalloid or blood
products.
• Cardiovascular support with volume and/or inotropes.
• Correction of hematologic, metabolic, and electrolyte
abnormalities.
• Careful attention to respiratory status, coagulation profile,
and acid-base and electrolyte balance are important.

28. • MONITORING:
• Sequential abdominal grith measuremet
• Sequential anteroposterior and cross-table lateral or lateral
decubitus abdominal x-rays to detect intestinal perforation;
• Serial determination of hematologic status,
• Serial determination of electrolyte status, and
• Serial determination of acid-base status.

29. • Indications for surgery :
• Absolute indications:
• Evidence of perforation on abdominal roentgenograms
(pneumoperitoneum) or
• Positive abdominal paracentesis (stool or organism on
Gram stain from peritoneal fluid).
•
•
•
•
•
Relative indications:
Failure of medical management,
Single fixed bowel loop on roentgenograms,
Abdominal wall erythema, or
A palpable mass.

30. • Ideally, surgery should be performed after
intestinal necrosis develops, but before
perforation and peritonitis occurs.
• Peritoneal drainage may be helpful for
patients with peritonitis who are too unstable
to undergo surgery. Peritoneal drainage is
more successful in patients with isolated
intestinal perforation.

31. Initial signs of possible NEC (bell’s stage I )
•NPO
•GI decompression- low constant sucton, replace output with electrolytes
•CBC with differentials, blood culture, CRP, S.Electrolytes
•Abdominal radiograph
•Begin antibiotics
Mild to Moderate (Bell’s stage II)
Advanced (Bell’s Stage III)
•Serial abdominal radiographs
•Serial abdominal radiographs
•Broad spectrum antibiotics for 7- 10 days •Broad spectrum antibiotics for 7- 10 days
•NPO for 5-10 days, parentaral nutrition •NPO for 10-14 days, parentaral nutrition
•Monitor electrolytes
•Monitor electrolytes
•Serial CBCs every 12h to 24h for 2-3 days
•Serial CBCs every 12h to 24h for 2-3 days
•Co-mangement with paediatric surgeon
•Hemodynamic support
•Monitor coagulation abnormalities and
correct
Indications for surgery
•Intestinal perforation
•Fixed adynamic loop – necrotic gut
•Signs suggestive of necrotic gut –persistent severe thrombocytopenia, severe
metabolic acidosis

32. • PROGNOSIS.:
• Medical management fails in about 20–40% of patients
with pneumatosis intestinalis at diagnosis; of these, 10–
30% die.
• Early postoperative complications : Wound infection,
dehiscence, and stomal problems (prolapse, necrosis).
• Later complications : Intestinal strictures develop at the site
of the necrotizing lesion in about 10% of surgically or
medically managed patients.

33. • PROGNOSIS….
• After massive intestinal resection,
-Complications from postoperative NEC include
short-bowel syndrome (malabsorption, growth failure,
malnutrition),
• Premature infants with NEC who require surgical
intervention or who have concomitant bacteremia are at
increased risk for adverse growth and neurodevelopmental
outcome.
• The overall mortality is 9% to 28% regardless of surgical or
medical intervention.

34. • PREVENTION:
• Always better than cure!
• Newborns exclusively breast-fed have a reduced risk of NEC.
• Early initiation of aggressive feeding may increase the risk of NEC
in VLBW infants.
• Gut stimulation protocol of minimal enteral feeds followed by
judicious volume advancement may decrease the risk.
• Probiotic preparations have also decreased the incidence of NEC.
. Induction of GI maturation.
• Incidence of NEC is significantly reduced after prenatal steroid
therapy.
• Alteration of the immunologic status of the intestine using
immunoglobulin A (IgA) and immunoglobulin G (IgG)
supplementation.