Q.

NECROTIZING ENTEROCOLITIS ➔ Aggressive enteral feeding: predispose to

➔ Most common life-threatening emergency of development of NEC
GI tract in the newborn period ➔ 90% cases occur in preterm infants; but can
➔ Characterized by various degrees of mucosal or occur in full-term neonates
transmural necrosis of the intestine ➔ NEC in term infants: secondary disease; seen
➔ Cause is unclear but most likely multifactorial more frequently in infants w/ history of:
➔ 5-10% in infants w/ birth weight <1500 g ◆ Birth asphyxia
➔ 20-30% mortality rate ◆ Down syndrome
➔ 50% mortality in infants who require surgery ◆ Congenital heart disease
➔ Incidence & case fatality rate increase w/ ◆ Rotavirus infections
decreasing birthweight & gestational age ◆ Gastroschisis
◆ Hirschsprung disease
Pathology and Pathogenesis
➔ Factors that contribute to the development of Clinical Manifestations
NEC: Onset usually in 2nd or 3rd week of life; can be
◆ Mucosal ischemia & subsequent as late as 3 months in VLBW infants
necrosis Age of onset: inversely related to gestational
◆ Gas accumulation in submucosa of age
bowel wall (pneumatosis intestinalis) First signs of impending disease:
◆ Progression of necrosis to perforation, ◆ Lethargy
peritonitis, sepsis, & death ◆ Temperature instability
➔ Distal part of ileum & proximal segment of ◆ Abdominal distention
colon: most frequently involved ◆ Feeding intolerance
➔ Gangrene may extend from stomach to rectum ◆ Bloody stools
in fatal cases (NEC totalis) Sepsis may be suspected before NEC due to
➔ 3 major risk factors: nonspecific signs
◆ Prematurity Mild disease w/ guaiac-positive stools → severe
◆ Bacterial colonization of the gut illness w/ bowel perforation, peritonitis, SIRS,
◆ Formula feeding shock, & death
➔ NEC develops primarily in premature infants w/ Laboratory derangements:
exposure to metabolic substrate in context of ◆ Neutropenia
immature intestinal immunity, microbial ◆ Anemia
dysbiosis, & mucosal ischemia ◆ Thrombocytopenia
➔ Underlying genetic predisposition: ◆ Coagulopathy
◆ variants in genes regulating ◆ Metabolic acidosis
immunomodulation & inflammation Hypotension & respiratory failure: common
(toll-like receptor 4, IL-6), apoptosis, & Progression may be rapid but unusual for
cellular repair (platelet-activating disease to progress from mild to severe after 72
factor), & oxidant stress (vascular hrs.
endothelial growth factor, arginine,
nitric oxide) Check Table 123.1 (Nelson’s, page 951)
➔ Greatest risk factor for NEC: prematurity
➔ NEC rarely occurs before the initiation of enteral Diagnosis
feeding & much less common in infants fed ➔ Very high index of suspicion in treating preterm
human milk at-risk infants is crucial
➔ Plain abdominal radiographs: essential
 ➔ Pneumatosis intestinalis: air in the bowel wall;
confirms clinical suspicion of NEC & is
diagnostic
➔ 50-75% of px have pneumatosis when
treatment is started
➔ Portal venous gas: sign of severe disease
➔ Pneumoperitoneum: indicates perforation
➔ Ultrasound w/ Doppler flow assessment:
evaluate for free fluid, abscess, & bowel wall
thickness, peristalsis, & perfusion
➔ Differential diagnosis:
◆ Specific infections (systemic or
intestinal)
◆ GI obstruction
◆ Volvulus
◆ Isolated intestinal perforation
● Idiopathic focal intestinal
perforation: occur
spontaneously or after the early
use of postnatal corticosteroids
& indomethacin
● Pneumoperitoneum develops in
such px; less ill than those w/
NEC
Check Fig. 123.5, 123.6, 123.7 (Nelson’s page 952)
Treatment
➔ Rapid initiation of therapy: required for infants
w/ suspected & proven NEC
➔ NO definitive treatment for NEC
➔ Therapy is directed at supportive care &
preventing further injury:
◆ Cessation of feeding
◆ Nasogastric decompression
◆ Administration of IV fluids
➔ Careful attention to respiratory status,
coagulation profile, & acid-base & electrolyte
balances
➔ Systemic antibiotics:
◆ started immediately once blood has
been drawn out for culture
◆ broad coverage based on antibiotic
sensitivity patterns of gram-positive,
gram-negative, anaerobic organisms in
NICU
➔ Umbilical catheters removed; good IV access
maintained
➔ Ventilation should be assisted if there is apnea
or if abdominal distention is contributing to
hypoxia & hypercapnia
➔ Stabilize the infant w/ NEC:
◆ Intravascular volume replacement w/
crystalloid or blood products
◆ Cardiovascular support w/ fluid boluses
and/or inotropes
◆ Correction of hematologic, metabolic, &
electrolyte abnormalities
➔ Patient’s course should be monitored closely by:
◆ frequent physical assessments
◆ sequential anteroposterior &
cross-table lateral or lateral decubitus
abdominal radiographs: detect
intestinal perforation
◆ Serial determinations of hematologic,
electrolyte & acid-base status
➔ Gown & glove isolation & grouping of infants at
similar increased risks into cohorts separate
from other infants: contain an epidemic
➔ Surgeon: consulted early in the course of
treatment
➔ ONLY ABSOLUTE INDICATION FOR SURGERY:
evidence of perforation on abdominal
radiograph (pneumoperitoneum) present in
less than half of infants w/ perforation or
necrosis at operative exploration
➔ Indications for exploratory laparotomy:
◆ Progressive clinical deterioration
despite maximal medical management
◆ Single fixed bowel loop on serial
radiographs
◆ Abdominal wall erythema
➔ Surgery: AFTER intestinal necrosis develops but
BEFORE perforation & peritonitis occur
➔ Surgical treatment:
◆ Primary peritoneal drainage (PDD)
◆ Exploratory laparotomy w/ resection of
necrotic intestine & usually stoma
creation
➔ Surgical approach depends on surgeon
preference & physiologic status of the patient.
Prognosis ◆ IL-8
➔ Medical management fails in 20-40% of px w/ ◆ Heart rate characteristics (HRC) index
pneumatosis intestinalis at diagnosis; 20-50% ➔ Near-infrared spectroscopy (NIRS): promising
die predictive diagnostic modality for NEC
➔ Early postoperative complications:
◆ Wound infection
◆ Dehiscence
◆ Stomal problems (prolapse, necrosis)
➔ Later complications:
◆ Intestinal strictures: occur in 10% of
surgically or medically managed px
➔ Complications after massive intestinal resection:
◆ Short bowel syndrome (malabsorption,
growth failure, malnutrition)
◆ Complications related to central
catheters (sepsis, thrombosis)
◆ Cholestatic jaundice
➔ Preterm infects w/ NEC who require surgical
intervention: increased risk for adverse growth
& neurodevelopmental outcomes

Prevention
➔ Most effective preventive strategy: use of
human milk
➔ Newborns exclusively breastfed: reduced risk of
NEC
➔ Fortification: essential for preterm infants since
human milk does not provide complete
nutritional support
➔ Exclusive human milk diet: using human rather
than bovine fortifiers may reduce risk of NEC
➔ Probiotics, prebiotics & synbiotics: may prevent
NEC
➔ Inhibitors of gastric acid secretion (H2-receptor
blockers, proton pump inhibitors) or prolonged
empirical antibiotics in early prenatal period:
increased risk of NEC; should be avoided
➔ Early detection & treatment: prevent late
deleterious consequences of NEC
➔ Biomarkers for early identification of NEC:
◆ CRP
◆ Urinary intestinal fatty acid-binding
protein (I-FABP)
◆ Claudin-3 (tight junction protein)
◆ Fecal calprotectin
◆ Acylcarnitine
◆ IL-6