Necrotizing enterocolitis (NEC) Flashcards
What is Necrotizing Enterocolitis (NEC)?
NEC is a bacteria-mediated inflammatory condition of the neonatal bowel that leads to sepsis and bowel necrosis.
Why is NEC significant in neonates?
NEC is the most common cause of peritonitis in neonates and a major cause of morbidity and mortality.
How common is NEC?
It occurs in 1 in 1000 live births and affects up to 10% of very low birth weight (VLBW) infants (<1500g).
What is the most important risk factor for NEC?
Prematurity – 90% of affected neonates are preterm.
What causes NEC?
NEC is due to an uncontrolled inflammatory response to pathogenic bacteria in the gut lumen, occurring in the setting of an immature immune system.
What is the most important risk factor for NEC?
Prematurity – 90% of affected neonates are preterm.
How does lack of human breast milk contribute to NEC?
Breast milk provides protective factors, including antibodies and beneficial bacteria that help strengthen gut immunity. Formula feeding lacks these benefits, increasing NEC risk.
How does NEC lead to sepsis and bowel necrosis?
Bacteria breach the gut mucosal barrier, enter circulation, and trigger sepsis and coagulative necrosis of the gut.
What maternal conditions increase the risk of NEC?
Maternal diabetes, chorioamnionitis, HIV (neonatal infection), and fluid overload.
How does maternal diabetes contribute to NEC?
Hyperglycemia and vascular dysfunction increase fetal inflammation and gut immaturity.
Why does lack of antenatal steroids increase NEC risk?
Antenatal steroids promote lung and gut maturity; without them, preterm neonates have weaker gut barriers.
How can NEC risk be reduced antenatally?
Antenatal care, maternal steroids if <34 weeks, HIV treatment (PMTCT/ HAART), and conservative IV fluids.
What conditions cause perinatal ischaemia, increasing NEC risk?
Pre-eclampsia, maternal vasoactive drug use (cocaine, opiates), hypoxic-ischaemic encephalopathy (HIE), PDA, and blood transfusion.
Why does a patent ductus arteriosus (PDA) increase NEC risk?
Steals blood flow from the gut, causing gut hypoxia and necrosis.
How can perinatal ischaemia-related NEC be prevented?
Good obstetric care, avoiding NSAIDs for PDA, pausing feeds during blood transfusions, and using erythropoietin instead of transfusions when possible.
How does an altered microbiome contribute to NEC?
Pathogenic Gram-negative bacteria overgrowth damages the gut and increases inflammation.
What factors disrupt the neonatal microbiome?
NICU bacterial outbreaks, formula feeding, rapid feed escalation, prolonged antibiotic use, and perinatal sepsis.
How can NEC be prevented through microbiome protection?
Hand hygiene, exclusive breast milk feeding, kangaroo mother care, safe formula prep, and use of probiotics/prebiotics.
What triggers inflammation in NEC?
Pathogenic gut bacteria trigger an uncontrolled inflammatory response in the immature gut.
What happens to the gut barrier?
Increased permeability → Bacteria invade → Coagulative necrosis of bowel wall
How does NEC lead to bowel perforation?
Full-thickness necrosis → Bowel wall weakens → Perforation in 15-50%
Which part of the bowel is most affected?
Terminal ileum & ascending colon (vascular compromise may contribute)
Why is NEC so deadly?
Bacterial translocation → Sepsis + Pro-inflammatory cytokine storm → Multi-organ failure
What is the mortality rate?
30-50% (higher if perforation and septic shock occur)
How does SIP (spontaneous intestinal perforation) differ from NEC?
Most common in extremely low birth weight babies (<1000g)
✅ Absence of metabolic acidosis or inflammatory signs
✅ No pneumatosis intestinalis or bowel thickening on x-rays
✅ Prognosis slightly better than NEC
What causes bowel obstruction in neonates?
✅ Volvulus (twisting of the intestine), adhesive bands (post-op), incarcerated inguinal hernia
✅ Presents with bilious vomiting & abdominal distension
How is GERD different from NEC?
✅ Non-bilious vomiting & apnoea
✅ Typically resolves with conservative management
What other infections may present with ileus and non-specific sepsis signs?
✅ Pneumonia, meningitis, or urinary tract infection
✅ Need to rule out with clinical signs and cultures
What are some causes of bloody stools or vomiting in neonates?
✅ Cows-milk protein allergy, maternal swallowed blood, midgut volvulus
✅ Differentiate based on history and clinical presentation
What are the DDx of NEC
- Spontaneous intestinal perforation
- Bowel obstruction
- GERD
- Pneumonia, meningitis, UTI
- Allergy due to cows milk protein allergy, maternal swallowed blood and midgut volvulus
When do premature neonates typically present with NEC?
First week of life
✅ 2-3 weeks after birth in some cases
When do term neonates usually present with NEC?
✅ 10% of cases present within 2-3 days after birth
✅ Often with a history of infectious, hypoxic, or metabolic insults
What are the early features of NEC?
✅ Subtle and can be difficult to differentiate from other neonatal sepsis causes
✅ Fulminant progression: Can lead to death within 24 hours of symptom onset in over 1/3 of affected infants
What are the risk factors for a poor outcome?
✅ Diffuse patchy or multiple areas of small bowel necrosis
✅ Pan-involvement (over 75% of bowel involvement)
What might a discoloured abdominal wall indicate in extremely low birth weight neonates?
Bowel perforation
✅ Common in infants <1000g birth weight
✅ Pneumoperitoneum (air in the peritoneum) from bowel perforation
What is the clinical significance of a discoloured abdominal wall?
✅ Discolouration (often blue or reddish) may indicate peritonitis or subcutaneous emphysema from air escaping into the abdominal wall
✅ Signs of sepsis and abdominal distension usually accompany bowel perforation
How can bowel perforation in such a baby be differentiated from other conditions?
✅ X-ray findings: Look for pneumoperitoneum (free air)
✅ Absence of pneumatosis intestinalis or bowel thickening (in contrast to NEC)
What is the prognosis in bowel perforation in extremely low birth weight babies?
✅ Slightly better prognosis than NEC, but remains a serious condition
✅ Immediate surgical intervention is often required to manage perforation and prevent further complications
What are the clinical features of Stage I (Suspected NEC)?
Non-specific signs of sepsis, such as temperature instability, glucose instability, and apnoea.
Non-specific signs of ileus, including abdominal distension, increased gastric residual volumes (aspirated before orogastric tube feeds), milk/bilious vomiting, and faecal occult blood.
What are the radiological features (AXR) of Stage I (Suspected NEC)?
Non-specific bowel distension and thickening.
What are the management principles for Stage I (Suspected NEC)?
- Bowel rest (gastric tube drainage, nil per mouth).
- Treat sepsis with broad-spectrum antibiotics.
- Administer intravenous fluids.
- Provide high-care monitoring of vital signs.
- Monitor electrolytes carefully and blood cell counts
What are the clinical features of Stage IIa (Definite NEC - early)?
Specific features of gastrointestinal sepsis, including bloody stool/vomitus, progressive distension, absent bowel sounds, abdominal tenderness, and palpable bowel loops.
What are the radiological features (AXR) of Stage IIa (Definite NEC - early)?
Pneumatosis intestinalis (air in the bowel wall).
Tubular thickened bowel loops.
What is the management for Stage IIa (Definite NEC - early)?
As per Stage I: Bowel rest (gastric tube drainage, nil per mouth), treat sepsis with broad-spectrum antibiotics, intravenous fluids, high-care monitoring of vital signs, and electrolyte monitoring.
What are the clinical features of Stage IIb (Definite NEC - moderate)?
As Stage IIa, with additional alterations in haemodynamic status (e.g., tachycardia).
Thrombocytopaenia, hyponatraemia, and mild acidosis.
What are the radiological features (AXR) of Stage IIb (Definite NEC - moderate)?
Ascites
What is the management for Stage IIb (Definite NEC - moderate)?
As per Stage IIa, but with intensive care monitoring, support, and surgical consultation.
What are the clinical features of Stage IIIa (Severe NEC with organ dysfunction)?
Deteriorating vital signs, including septic shock with organ dysfunction, hypotension, apnoea, disseminated intravascular coagulopathy (DIC), progressive metabolic acidosis, peritonitis, and a tender mass (usually in the right iliac fossa) from sealed-off bowel perforation.
What are the radiological features (AXR) of Stage IIIa (Severe NEC with organ dysfunction)?
White-out of the abdomen (ascites).
Persistent fixed loop of bowel for >24 hours.
What is the management for Stage IIIa (Severe NEC with organ dysfunction)?
As per Stage IIb, with multisystem support such as ventilation, inotropes.
Consider paracentesis of ascites (look for bacteria or “prune juice” of necrotic bowel).
Possible surgical exploration to exclude dead bowel.
What are the clinical features of Stage IIIb (Severe NEC with perforation)?
As per Stage IIIa, with additional features including frank peritonitis.
May have oedema, redness, and blue-black discolouration of the abdominal wall.
Hyperkalaemia and refractory metabolic acidosis.
What are the radiological features (AXR) of Stage IIIb (Severe NEC with perforation)?
Pneumoperitoneum (often best visualized on lateral shoot-through X-ray).
Rigler’s sign, football sign, liver lucency, etc.
What is the management for Stage IIIb (Severe NEC with perforation)?
As per Stage IIIa, but with surgery, including peritoneal drainage and/or laparotomy.
What can an AP abdominal film, aided by a lateral shoot-through, reveal in cases of NEC?
- Tubular distension of bowel loops.
- Thickened loops of bowel and free fluid, causing bowel loops to be displaced from each other.
- Pneumatosis intestinalis (gas within the bowel wall).
- Portal vein gas outlining the portal veins in the liver.
-The gas is hydrogen produced by bacteria in the bowel wall.
What is Pneumatosis intestinalis, and how can it be identified on radiology?
Pneumatosis intestinalis is gas within the bowel wall.
It can be submucosal (“soapy bubbles”) or intermuscular with a linear configuration (“tram-track”: black line between white lines).
In older children, it may mimic the appearance of stool, but faecal loading should not normally be seen in a child on milk feeds.
What radiological features can be seen in the liver related to NEC?
Liver lucency and outlining of the falciform ligament with gas create the “football” sign.
What is Pneumoperitoneum, and how is it visualized on X-ray?
Pneumoperitoneum is the presence of air in the peritoneal cavity.
It may be seen on lateral shoot-through X-ray.
“Rigler’s sign” is a feature of pneumoperitoneum, where gas outlines both sides of the bowel wall.
In which stages of NEC is surgical intervention required, and what is the rate of surgery in these cases?
Surgical intervention is required in all Stage 3b cases and many Stage 3a cases.
Surgery occurs in 30 to 50% of cases, although lower rates are reported in highly developed, high-income settings.
What is the role of initial peritoneal drainage in NEC management
Initial peritoneal drainage may help release abdominal compartment syndrome.
In selected extremely low birth weight (ELBW) babies, peritoneal drainage might be the only intervention required, as the underlying small, spontaneous perforation may seal off without further intervention in a third of ELBW babies.
What are the goals of surgery once the baby has stabilized in Stage 3a or 3b NEC?
- Confirmation of bowel viability.
- Resection of necrotic bowel.
- Evacuation of stool from the peritoneal cavity in the case of perforation with soiling.
- Re-establishment of intestinal continuity, which may involve staging with an initial stoma in the case of diseased distal bowel or damage-control surgery in very sick infants.
- Preservation of bowel length if intestinal recovery is expected.
When is stoma reversal feasible in infants with NEC, and what needs to be excluded before reversal?
Stoma reversal is often feasible 4-6 weeks after surgery in thriving infants.
Before reversal, distal bowel strictures due to fibrosis from partial bowel necrosis should be excluded by contrast enema.
What are some common complications associated with stoma formation in NEC?
30% stoma problems including:
High output
Prolapse
Stenosis
Anastomotic leak at reversal
What are the common wound complications after NEC surgery?
10-25% wound problems, including:
Wound breakdown
Infection
What intestinal complications can arise after NEC?
10% intestinal strictures following surgery.
What are the long-term neurological outcomes for babies with NEC?
Poor long-term neurological outcomes are common:
- 30-50% of babies with NEC experience brain injury and developmental delay.
- This is often associated with prolonged intensive care and poor nutritional intake (especially in babies with short bowel syndrome or high output stomas).
- As many as 50% may experience permanent neurological damage, including severe cerebral palsy.
- Normal neurodevelopment is seen in less than a quarter of survivors.
What is the mortality rate for babies with NEC, and what factors influence it?
Mortality rates:
- 15% in high-income settings.
- 30-50% in middle-income settings.
- Up to 90% in low-income settings.
Lower gestational age is associated with higher mortality.
