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Neonatal Necrotizing Enterocolitis
1. PAEDIATRICS AND CHILD HEALTH
• NEONATOLOGY
• Neonatal Necrotizing Enterocolitis (NEC)
Dr. Chongo Timothy Shapi (BSc.HB, MBChB)
- Medical Doctor.
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
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2. Introduction
• NEC is the most common life-threatening
emergency of the GIT in the newborn period
• The disease is characterized by various degrees of
mucosal or transmural necrosis of the intestine
• The cause of NEC remains unclear but is most
likely multifactorial
• The incidence of NEC is 1–5% of infants in NICU
• Preterm babies and SGA are susceptible to NEC
• Rare in term babies
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
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3. Pathology and Pathogenesis
• Multifactorial
• There is :
1. Development of a necrotic segment of intestine
2. Gas accumulation in the submucosa of the bowel
wall (pneumatosis intestinalis)
3. Progression of the necrosis to perforation,
peritonitis, sepsis, and death
• NEC affects mostly the terminal ileum and the
proximal segment of colon
• In fatal cases, gangrene may extend from the
stomach to the rectum
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4. Pathology and Pathogenesis
• Though a multifactorial disease primarily
associated with intestinal immaturity, the
concept of “risk factors” for NEC is controversial
• The following triad is classically been linked to
NEC:
1. Intestinal ischemia (injury)
2. Enteral nutrition (metabolic substrate)
3. Pathogenic micro-organisms
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6. Pathology and Pathogenesis
• NEC probably results from an interaction
between:
1. Loss of mucosal integrity due to a variety of
factors (ischemia, infection, inflammation) and
2. The host's response to that injury (circulatory,
immunologic, inflammatory)
• Coagulation necrosis is the characteristic
histologic finding of intestinal specimens
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7. Pathology and Pathogenesis
• Clustering of cases suggests a primary role for an infectious
agent
• Pathogenic agents include:
1. Escherichia coli
2. Klebsiella
3. Clostridium perfringens
4. Staphylococcus epidermidis
5. Rotavirus
• Nonetheless, in most situations, no pathogen is identified
• NEC rarely occurs before the initiation of enteral feeding
and is much less common in infants fed human milk
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8. Clinical Manifestations
• Onset
- Usually occurs in the 1st 2 wk of life
- But can be as late as 3 mo of age in VLBW infants
• Age of onset is inversely related to gestational age
• Initial symptoms:
Mainly GIT:
- Feeding intolerance (unable to breastfeed)
- Temperature instability
- Delayed gastric emptying
- Vomiting
- Abdominal distension
- Abdominal tenderness
- Ileus/decreased bowel sounds
- Abdominal wall erythema
- Bloody stools
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Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
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10. Bell’s Clinical Staging
Stage I: suspecting disease
- IA: Infant with suggestive clinical signs but X-ray is
non-diagnostic
- IB: As in IA plus bloody stools
Stage II: definite disease, infant with pneumatosis
intestinalis
- IIA: Mildly ill infant
- IIB: Moderately ill
Stage III: advanced disease
- IIIA: critical with impending perforation
- IIIB: critical with proven perforation
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11. • Because of nonspecific signs, sepsis may be
suspected before NEC
• NEC can progress rapidly from mild abdominal
to fullness to septic shock and necrosis of the
entire intestine
• Management requires a high index of
suspicion
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12. Investigations
• FBC/DC
• Blood for MCS
• Stool MCS
• Abdominal X-ray in the left lateral decubitus
• Abdominal USS targeting the liver
• U/Es + Creatinine
• Blood gases
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13. Diagnosis
• A very high index of suspicion in treating preterm at-
risk infants is crucial
• Plain abdominal X-rays are essential to make a
diagnosis of NEC
• The finding of pneumatosis intestinalis (air in the
bowel wall) confirms the clinical suspicion of NEC and
is diagnostic
• Portal venous gas is a sign of severe disease, and
pneumoperitoneum indicates a perforation
• Hepatic ultrasonography may detect portal venous gas
despite normal abdominal roentgenograms (X-rays)
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15. X-ray Findings
• Grade I: thickening of the bowel wall +/- dilatation
of the gut
• Grade II: bowel wall gas (pneumatosis intestinalis)
• Grade III: gas in the liver and biliary tree
• Grade IV: gas within the peritoneum
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17. Treatment
• Rapid initiation of therapy is required for
suspected as well as proven NEC cases
• There is no definitive treatment for established
NEC
• Therapy is directed at supportive care and
preventing further injury with:
- Stopping feeding
- Nasogastric decompression
- Administration of IVFs (crystalloids e.g. ¼ SD in
10% dextrose or blood products)
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Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
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18. Treatment
- Poor perfusion with HCT > 40% give ordinary plasma
at 20 ml/kg, if HCT < 40% give packed RBCs 10-15
ml/kg
- Give antibiotics as soon as the blood for
investigations has been collected
- Initially, give BSA (cefotaxime plus metronidazole)
and then change to drugs that are sensitive
according to the lab results
- Correct haematologic, metabolic and electrolyte
abnormalities
- Intubate when in respiratory failure or worsening
acidosis
- Surgery when indicated
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19. Treatment
• Monitor the patient's course closely by:
- Performing frequent physical assessments
- Sequential AP and cross-table lateral or lateral
decubitus abdominal x-rays to detect intestinal
perforation
- Serial determination of hematologic, electrolyte,
and acid-base status
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20. Treatment
• Indications for surgery include:
- Evidence of perforation on abdominal roentgenograms
(pneumoperitoneum)
- Positive abdominal paracentesis (stool or organism on
Gram stain from peritoneal fluid)
- Failure of medical management, a single fixed bowel
loop on roentgenograms, abdominal wall erythema, or
a palpable mass are relative indications for exploratory
laparotomy
NB: Surgery should be performed after intestinal
necrosis develops, but before perforation and peritonitis
occurs
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21. Prognosis
• Medical management fails in about 20–40%
Early postoperative complications include:
- Wound infection
- Wound dehiscence
- Stomal problems (prolapse, necrosis)
Late complications include:
- Intestinal strictures
- Short-bowel syndrome (malabsorption, growth failure,
malnutrition)
- Complications related to central venous catheters (sepsis,
thrombosis), and cholestatic jaundice
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22. Prevention
• Exclusive breast-feeding has a reduced risk of NEC
• Minimal enteral feeds followed by judicious
volume advancement
- Remember, early initiation of aggressive feeding
protocols increases the risk of NEC in VLBW infants
• Probiotic preparations (a probiotic is a substance
that stimulates the growth of micro-organisms
especially beneficial ones = normal flora)
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