NECROTIZING

ENTEROCOLITIS
Presenter’s name: Sultan Neazy 1

Supervisor’s name: Dr ABDULRAHMAN MIRZA

 1College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia 2 King Abdullah International Medical
Research Center, Jeddah, Saudi Arabia
Foregut
• NORMAL EMBRYOLOGY OF THE GI TRACT

• BLOOD SUPPLY TO GI TRACT

• NECROTIZING ENTEROCOLITIS
 Normal Embryology
Endoderm
Epithelial lining and glands

Mesoderm
Lamina propria, muscularis mucosa, submucosa, muscularis externa
and serosa

Ectoderm
Enteric nervous system and posterior luminal digestive structures
 Normal Embryology
Primitive Gut Tube:

Incorporation of the yolk sac during craniocaudal and

lateral folding of the embryo.
Foregut
Midgut
Hindgut
 Canalization
Week 5 - Endoderm portion of GI tract proliferates

Week 6 - Occlusion of the lumen

Week 8 - Recanalization due to cell degeneration

Abnormalities in this process will lead to

Stenosis/Atresia
Duplications
Foregut
• Foregut gives rise to:
• Esophagus
• Stomach
• Liver
• Gallbladder and bile ducts
• Pancreas
• Upper Duodenum
Midgut
• Lower Duodenum – Cranial portion of the midgut.
• Jejunum, ileum, cecum, appendix, ascending colon, and
proximal 2/3 of transverse colon – Develop as the midgut
loop herniates through the primitive umbilical ring during
umbilical herniation at week 6.
• The loop then rotates 270 degrees counterclockwise around
the superior mesenteric artery and returns to the abdominal
cavity.
 Enteric Nervous System
• Collection of neurons in the GI tract.

• Controls motility, exocrine and endocrine secretion

and microcirculation.

• Regulates immune and inflammatory process.

• Functions independent of CNS.

 Development of Enteric Nervous System
• Primarily derived from the vagal segment of neural crest cells.

• Cells initially migrate to the cranial section and then caudally

• Hindgut ganglia receive contributions of cells from the cranial and

sacral segments of the neural crest cells

• Interstitial cells of Cajal arise from the local gut mesenchyme

Development of Enteric Nervous System
• Nerve cell bodies are grouped into ganglia
• Ganglia are connected to bundles of nerves forming two plexus
• Myenteric (Auerbach’s)
• Submucosal (Meissner’s)
Enteric Nervous System
• Myenteric plexus
• Lies between the circular and longitudinal
muscles
• Regulates
• Motility
• Secretomotor function to mucosa
• Connections to
• gallbladder and pancreas
• sympathetic ganglia
• esophageal striated muscle
Enteric Nervous System
• Submucosal plexus
• Lies between circular muscle layer and the muscularis mucosa
• Regulates:
• Glandular secretions
• Electrolyte and water transport
• Blood flow
• Similar structure found in gallbladder, cystic duct,
common bile duct and the pancreas
 Blood Supply to the GI tract
Proximal Esophagus
Inferior Thyroid Artery
Thoracic Esophagus
Terminal bronchial arteries
Distal Esophagus
Left gastric and left phrenic
arteries
Stomach
Celiac artery
Small intestine
Superior mesenteric artery
Large intestine
Superior and Inferior
mesenteric arteries
Blood Supply to the GI tract
 NECROTIZING
ENTEROCOLITIS
Definition of necrotizing enterocolitis

Hemorrhagic necrotizing inflammation of the intestinal wall

Acquired inflammatory disease that affects the gut of newborn

infants nearly exclusively.

The Most Common newborn Surgical Emergency.

Definition of necrotizing enterocolitis

Most commonly affects the distal ileum and proximal colon

Pan involvement (pannecrosis, NEC totalis): Necrosis of at least

75%of the gut

Accounts for 19% of all cases of surgically treated NEC and most of
the deaths.
Definition of necrotizing enterocolitis
Epidemiology of necrotizing enterocolitis

NEC is a disease of premature LBW infants rather than those who are
small for gestational age.

Only 7-13% of all NEC cases occur in full-term infants. (CVDs)

The mortality rate was higher in patients with early-onset disease.

90% of NEC cases develop in infants after feedings are initiated.

Epidemiology of necrotizing enterocolitis

The incidence approximately 1~3 cases per 1000 live births.

The incidence varies according to degree of prematurity and

birth weight .

1-7 % of NICU admission - VLBW 10 ~12 %

Inverse relation between NC and GA / onset of NEC and GA.

 Pathophysiology of necrotizing enterocolitis

The causes of necrotizing enterocolitis are not fully

understood but multiple factors contribute to the
development of the condition. 
• Intestinal wall perfusion and motility disorders
• Defective or underdeveloped immune system
• Intestinal microbial overgrowth
• Formula feeding
• Rapid increase of enteral nutrition 
Clinical features of necrotizing enterocolitis
Clinical features of necrotizing enterocolitis
 diagnosis of necrotizing enterocolitis
History:
onset that ranges from 1-3 days - 1 month

Hx of systemically illness:
birth asphyxia
respiratory distress
congenital heart disease
metabolic abnormalities
History of abnormal fetal growth pattern.

Hx of Maternal risk factors that reduce fetal gut blood flow:

pregnancy-induced hypertension
chronic disease (diabetes)
maternal cocaine abuse
diagnosis of necrotizing enterocolitis

Pre-Term:
• Hx of indomethacin Use
• Hx of PDA treated with surgical ligation
• Hx of Feeding intolerance while advancing on
enteral feeding
• Hx of transfusion
 diagnosis of necrotizing enterocolitis

Complete blood count: 

• Neutrophil counts < 1500/μL are associated with a poor
prognosis.
• The degree of thrombocytopenia correlates with the severity
of NEC.
•↑ Inflammatory markers
•Check for signs of DIC 
•Arterial blood gas analysis: Metabolic acidosis is associated with
advanced NEC.
 diagnosis of necrotizing enterocolitis

Blood cultures:
Positive in 30% to 35% of patients.
K. pneumoniae and E. coli cause most positive blood cultures.

Stool cultures:
E. coli, K. pneumoniae, Enterococcus cloacae …. Others

Peritoneal cultures:
Most commonly grow Klebsiella species, E. coli, coagulase
negative staphyl, Enterobacter species, and yeast
 diagnosis of necrotizing enterocolitis

•Abdominal radiography
• Pneumatosis intestinalis: bubbles of gas within the wall of
the intestine  
• Portal venous gas (pneumatosis hepatis) 
• Increased intestinal wall thickness
• Dilated intestinal loops 
• Air‑fluid levels
• Pneumoperitoneum as a result of intestinal perforation 
 diagnosis of necrotizing enterocolitis

•Abdominal ultrasound
• Indication: Ultrasound may be helpful for diagnosing
NEC when abdominal radiography is inconclusive.
• Findings
• Pneumatosis intestinalis
• Portal venous gas
• Increased intestinal wall thickness
• Decreased intestinal wall perfusion
Duke Abdominal Assessment Scale (DAAS)

Ultrasound examination: fifty one

sonographic examinations were
performed bedside, by two
radiologists, blind of clinical
findings except for NEC, using
TOSHIBA NEMIO XG ultrasound
device, equipped with a high-
resolution linear transducer of 5–
10 MHz and a convex 2–4 MHZ
sector probe.
Fig. 1. A 20 days female patient, clinically diagnosed as NEC stage III B, by US the
following were seen (A) thickened echogenic bowel loops wall with loss of typical gut
signature, intramural air (pneumatosis) echogenic air foci (arrow) as well as intervening
free fluid (yellow arrow). (B) Turbid free fluid collection with echogenic foci (arrow). 
(C) dilated bowel with anechoic content. (D) color Doppler revealed characteristic
hyperemic y-shaped flow pattern. 
(E) Absent color doppler flow in a different bowel loop with still detected arterial flow
 in a distal mesenteric vessel. (F) Linear sub-diaphragmatic echogenic lines (arrow)
representing free intraperitoneal air.
 (G) Abdominal radiograph
obtained at the same setting
showed a rim of central free
intraperitoneal air (arrow) (DAAS
10).
DDX of necrotizing enterocolitis
 Management of necrotizing enterocolitis

Treatment should be initiated promptly when NEC is suspected to

prevent complications such as perforation, peritonitis, and sepsis.
•Supportive care: 
• Stop enteral feeding → parenteral feeding and substitution of
fluids
• Gut decompression via nasogastric tube

•IV broad-spectrum antibiotics: e.g., ampicillin, gentamicin, and 

metronidazole for anaerobic coverage
Management of necrotizing enterocolitis

•Radiographic monitoring: plain supine abdominal

radiographs every 6–12 hours in the initial phase of the
disease

•Surgery: primary peritoneal drainage
and/or laparotomy with necrotic bowel excision
• Indications: perforation, peritonitis and/or clinical
worsening despite medical therapy
 Surgical intervention of necrotizing enterocolitis

Absolute Indications:
Evidence of intestinal perforation on an abdominal
radiograph, paracentesis that is positive for stool or bile and
fluid with gram positive stain
 
Clinical deterioration despite maximal medical therapy.

More than 2 relative indications.

 Surgical intervention of necrotizing enterocolitis

Relative Indications:
•Positive paracentesis and massive ascites.
• Palpable abdominal mass.
• Abdominal wall erythema.
• Portal venous gas.
• Fixed dilated intestinal loop.
• Extensive pneumatosis intestinal.
primary peritoneal drainage
Management of necrotizing enterocolitis
Management of necrotizing enterocolitis

Stoma closure in NEC:

In general, stoma may be safely closed anytime after 4 weeks. Before
Stoma closure, contrast study to rule out a stricture or strictures in
the distal defunctionalized bowel.
Stoma complications
Complications of necrotizing enterocolitis

•Intestinal perforation:
• Abdominal radiography: pneumoperitoneum
• Treatment: surgery
•Short bowel syndrome
•Peritonitis
•Sepsis

•Mortality rate: approx. 10–30%

 References:

References
 NECROTIZING
ENTEROCOLITIS
Presenter’s name: Sultan Neazy 1

Supervisor’s name: Dr ABDULRAHMAN MIRZA

 1College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia 2 King Abdullah International Medical
Research Center, Jeddah, Saudi Arabia