1. NECROTIZING
ENTEROCOLITIS
Dr Varsha Shah

2. OBJECTIVES
• Ability to diagnose and treat the signs and
symptoms of NEC
• Ability to evaluate radiographs for the
classic findings of NEC
• List several long-term complications
associated with NEC

3. NECROTIZING
ENTEROCOLITIS
• Epidemiology:
– most commonly occurring gastrointestinal
emergency in preterm infants
– leading cause of emergency surgery in neonates
– overall incidence: 1-5% in most NICU’s
– most common in VLBW preterm infants
• 10% of all cases occur in term infants

4. NECROTIZING
ENTEROCOLITIS
• Epidemiology:
– 10x more likely to occur in infants who have
been fed
– males = females
– blacks > whites
– mortality rate: 25-30%
– 50% of survivors experience long-term
sequelae

5. NECROTIZING
ENTEROCOLITIS
• Pathology:
– most commonly involved areas: terminal ileum
and proximal colon
– GROSS:
• bowel appears irregularly dilated with hemorrhagic
or ischemic areas of frank necrosis
– focal or diffuse
– MICROSCOPIC:
• mucosal edema, hemorrhage and ulceration

6. NECROTIZING
ENTEROCOLITIS
• MICROSCOPIC:
– minimal inflammation during the acute phase
• increases during revascularization
– granulation tissue and fibrosis develop
• stricture formation
– microthrombi in mesenteric arterioles and
venules

7. NECROTIZING
ENTEROCOLITIS
• Pathophysiology:
UNKNOWN
CAUSE…….

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

9. RISK FACTORS
• Prematurity:
* primary risk factor
– 90% of cases are premature infants
– immature gastrointestinal system
• mucosal barrier
• poor motility
– immature immune response
– impaired circulatory dynamics

10. RISK FACTORS
• Infectious Agents:
– usually occurs in clustered epidemics
– normal intestinal flora
• E. coli
• Klebsiella spp.
• Pseudomonas spp.
• Clostridium difficile
• Staph. Epi
• Viruses

11. RISK FACTORS
• Inflammatory Mediators:
– involved in the development of intestinal injury
and systemic side effects
• neutropenia, thrombocytopenia, acidosis,
hypotension
– primary factors
• Tumor necrosis factor (TNF)
• Platelet activating factor (PAF)
• LTC4
• Interleukin 1& 6

12. RISK FACTORS
• Circulatory Instability:
– Hypoxic-ischemic injury
• poor blood flow to the mesenteric vessels
• local rebound hyperemia with re-perfusion
• production of O2 radicals
– Polycythemia
• increased viscosity causing decreased blood flow
• exchange transfusion

13. RISK FACTORS
• Enteral Feedings:
– > 90% of infants with NEC have been fed
– provides a source for H2 production
– hyperosmolar formula/medications
– aggressive feedings
• too much volume
• rate of increase
– >20cc/kg/day

14. RISK FACTORS
• Enteral Feedings:
– immature mucosal function
• malabsorption
– breast milk may have a protective effect
• IGA
• macrophages, lymphocytes
• complement components
• lysozyme, lactoferrin
• acetylhydrolase

15. From UpToDate online, Adapted from Kliegman, RM, Pediatr Res 1993; 34:701.

16. CLINICAL PRESENTATION
Gestational age: Age at diagnosis:
< 30 wks 20 days
31-33 wks 11 days
> 34 wks 5.5 days
Full term 3 days
*Time of onset is inversely related to gestational age/birthweight

17. CLINICAL PRESENTATION
Gastrointestinal: Systemic
Feeding intolerance Lethargy
Abdominal distention Apnea/respiratory distress
Abdominal tenderness Temperature instability
Emesis Hypotension
Occult/gross blood in stool Acidosis
Abdominal mass Glucose instability
Erythema of abdominal wall DIC
Positive blood cultures

18. CLINICAL PRESENTATION
ABDOMINAL DISTENSION

19. CLINICAL PRESENTATION
SEVERE ABDOMINAL DISTENSION

20. CLINICAL PRESENTATION
Sudden Onset: Insidious Onset:
Full term or preterm infants Usually preterm
Acute catastrophic deterioration Evolves during 1-2 days
Respiratory decompensation Increase desaturations
Shock/acidosis
Feeding intolerance (regurgitation,
Marked abdominal distension
high/green aspirates)
Positive blood culture
Change in stool pattern
Intermittent abdominal
distention,loops,crepitus
Occult blood in stools
Poor perfusion, lethargy

21. 12.52 pm AXR

22. • ADDENDUM
• Review of the images reveal air lucency noted in both hypochondrial regions
which
• are worrisome for free gas. There is also suggestion of portal venous gas.
• ***FINAL ADDENDUM***
Verified by: Dr PCC, Registrar,
• Amended Date/Time: 30-MAR-2005 09:27
• ORIGINAL REPORT
• HISTORY
• High NG aspirates
• REPORT
• The small bowel loops are dilated and there is faecal material noted in the large
• colon but not much in the rectum. However, no definite pneumotosis intestinalis
• is seen. Tip of the NG tube is in the distal oesophagus rather than the stomach
• and should be adjusted.
• CONCLUSION
• The small bowel is dilated. The cause however is not visualised in the study.

23. 15.52 pm AXR

24. • ORIGINAL REPORT
• HISTORY
• ? sepsis. Growing prem. Abdominal distension.
• REPORT
• CXR - MOBILE SUPINE AP
• Compared with CXR from 14/12/2004.
• NG tube is again noted. There is now bilateral perihilar peribronchial thickening.
• Cardiac size is unremarkable.
• The intestinal loops remained gaseously distended though faecal matter is seen within
• the colon. There is a lack of rectal air through a catheter is seen in the lower
• pelvic cavity.

25. 22.40 pm

26. • ORIGINAL REPORT
• HISTORY
• Septicaemia. NEC. Intubated.
• REPORT
• MOBILE SUPINE (CHEST AND ABDOMEN)
• The tip of the NG tube is projected over the distal esophagus. The tip of the ETT
• is about 0.6cm from the carina.
• A tube is projected over the rectal area.
• There is diffuse haziness of both lungs. The heart size cannot be assessed.
• There are multiple gas distended intestinal loops and intraperitoneal free gas present
• which appears worse when compared to the last AXR.

27. 1.44 am

28. 1.44 am

29. • ORIGINAL REPORT
• HISTORY
• NEC, septic shock on CPAP, IA and IV lines.
• REPORT
• AXR - SUPINE AP
• Compared with AXR taken 10 hours earlier.
• The nasogastric tube is now seen projected over the left hypochondrium. There is
• interval worsening of the gaseously distended intestinal loops. Faecal matter is
• again seen in the proximal colon. No air or faecal matter seen in the pelvic cavity.
• There is free extraluminal air within the peritoneal cavity, outlining the liver.
• Rigler's sign is noted, consistent with intestinal perforation.

34. Blood in stool at 4 am, axr 6 am

35. Blood in stool AXR 10. 30 am,

36. Blood in stool AXR 14.24 pm,

38. Portal Air
Dilated stomach &
loops of bowel

39. Neonatal NEC Pathology
Pneumatosis
Necrosis

41. Rigler sign
Rigler's sign, also known as the double wall sign, is seen on
an x-ray of the abdomen when air is present on both sides of
the intestine, i.e. when there is air on both the luminal and
peritoneal side of the bowel wall.

42. Foot ball sign

44. BELL STAGING CRITERIA
STAGE CLINICAL X-RAY TREATMENT
I. Suspect Mild abdominal Mild ileus Medical
distention Work up for
NEC Poor feeding Sepsis
Emesis
II. Definite The above, plus Significant Medical
Marked abdominal Ileus
NEC distention Pneumatosis
GI bleeding Intestinalis
PVG
III. Advanced The above, plus Pneumo- Surgical
Unstable vital signs Peritoneum
NEC Septic Shock

46. RADIOLOGICAL FINDINGS
• Pneumatosis Intestinalis
– hydrogen gas within the bowel wall
• product of bacterial metabolism
a. linear streaking pattern
• more diagnostic
b. bubbly pattern
• appears like retained meconium
• less specific

47. RADIOLOGICAL FINDINGS
• Portal Venous Gas
– extension of pneumatosis intestinalis into the
portal venous circulation
• linear branching lucencies overlying the liver and
extending to the periphery
• associated with severe disease and high mortality

48. RADIOLOGICAL FINDINGS
• Pneumoperitoneum
– free air in the peritoneal cavity secondary to perforation
• falciform ligament may be outlined
– “football” sign
• Ultrasound
– Good for bedside demonstration of ascites
– May show portal air more clearly than KUB
– surgical emergency

49. LABORATORY FINDINGS
• FBC
– neutropenia/elevated WBC
– thrombocytopenia
• Acidosis
– metabolic
• Hyponatreamia
• Hyperkalemia
– increased secondary to release from necrotic
tissue

50. LABORATORY FINDINGS
• DIC
• Positive cultures
– Blood culture aerobic, anaerobic
– CSF
– urine
– Stool culture, aerobic, rotavirus

51. MEDICAL TREATMENT
• Stage Ia
– NPO x 3 days
• Stage Ib - IIb/IIIa
– NPOX 7 days since blood in stool
– Broad spectrum antibiotics
• Cover Gram +, Gram - & Anaerobes, Ampi/Amikacin/Flagyl
• Ib = 3 days, IIa = 7-10 d, IIb & up = 14 d
– Follow KUB for resolution
• Resume enteral feeds 10-14 days after radiographic resolution
– May require paracentesis if IIIa

52. SURGICAL CONSULT and
TREATMENT
• Surgical Consult
– suspected or proven NEC
– indications for surgery:
• portal venous gas; pneumoperitoneum
• clinical deterioration
– despite medical management
• positive paracentesis
• fixed intestinal loop on serial x-rays
• erythema of abdominal wall

53. TREATMENT
• Labs: q6-8hrs
– FBC PLT, Electrolytes, DIC panel (PT, PTT), blood
gases
• X-rays: q6-8hrs
– AP, left lateral decubitus or cross-table lateral
• Supportive Therapy
– fluids, blood products (PCT< FFP< PLT), Inotropes,
mechanical ventilation (May need long line, ETT,IA
line)

54. Surgical treatment
• Stage IIIa - IIIb
– Laparotomy
• Resection of necrotic bowel
• Ileostomy with mucous fistula
– Subsequent re-anastamosis
• May result in strictures requiring further surgery later
– Peritoneal drain
• Placement in NICU under local anesthetic
• Used when infant is too clinically unstable for surgery
• May help stabilize pt for subsequent surgery

55. Histopathology
Normal NEC:
small Hemorrhagic
bowel necrosis
beginning at
the mucosa
and working
its way down
into the wall
http://library.med.utah.edu/WebPath/PEDHTML/PED045.html

56. Histopathology
Pneumatosis in
the submucosa
of the small
bowel
http://library.med.utah.edu/WebPath/PEDHTML/PED049.html

57. PROGNOSIS
• Depends on the severity of the illness
• Associated with late complications
* strictures
– short-gut syndrome
– malabsorption
– fistulas
– abscess
* MOST COMMON

58. Outcomes
• Mortality varies with birth weight:
– <1000 g = 40-100%
– <1500 g = 10-44%
– >2500 g = 0-20%
• Morbidity/Mortality vary with severity:
– Resection -> Short gut -> FTT, malabsorbtion
– Strictures -> further surgery in medical and surgical
NEC
– Prolonged NPO status on TPN -> cholestasis &
metabolic abnormalities