NEONATAL NECROTIZING
ENTEROCOLITIS
MR. NYAMAI S.M
Introduction:
NEC is the most common life-threatening
emergency of the gastrointestinal tract in the
newborn.
◦ Various degrees of mucosal or transmural
necrosis of the intestine occurs.
◦ The incidence of NEC is 1–10% of infants in
NICU.
◦ Although rare, the disease does occur in
term infants (10%)
◦ The mortality rates vary from 10% to 50%
Low Birth Weight and Low Gestational
Age<28 wk have high incidence and
fatality
Def. of NEC
Is an acquired neonatal disorder
representing an end expression of
serious intestinal injury after a
combination of vascular, mucosal, and
metabolic(and other unidentified)
insults to a relatively immature gut.
Risk factors
Prematurity
Asphyxia and acute cardiopulmonary
collapse,
Enteral feeding: NEC is rare in unfed
infants. About 90-95% of infants with NEC
received at least one enteral feeding.
Polycythymia and hyperviscosity
syndrome.
Exchange transfusion.
Large feeding volumes and rapid
advancement of enteral feedings.
Enteric pathogenic organisms
ETIOLOGY:
◦
Etiology of NEC is unclear; May be
multifactorial.
Prematurity is the single greatest
risk factor.
Infants exposed to cocaine have a
2.5 times increased risk of developing
NEC.
The mean gestational age of infants
with NEC is 30 to 32 weeks
PATHOLOGY AND
PATHOGENESIS:
Intestinal ischemia ( injury)
Enteral nutrition
Pathogenic organisms
( metabolic substrate
Risk factors for NEC- Triad
PATHOLOGY AND PATHOGENESIS: contd..
NEC probably results from an interaction between loss of
mucosal integrity due to factors like ischemia, infection,
inflammation, and the host's response to that injury like
circulatory, immunologic, inflammatory responses resulting
in necrosis of the affected area.
Various bacterial and viral agents, including E.coli, Klebsiella,
Clostridium perfringens,Staph. epidermidis, and rotavirus
NEC rarely occurs before initiation of enteral feeding
Aggressive enteral feeding may predispose to the
development of NEC.
Uniqueness of Preterm Gut
Decreased IgA
Decreased Intestinal T lymphocytes
Poor Antibody Response
Higher Membrane Permeability of GI
epithelial lining
Lower Gastric Motility
More Scant and More Permeable
Mucin Blanket
Uniqueness of Preterm Gut contd…
Proposed Mechanism for NEC
• Enteral feeding induces bacterial proliferation
• Hypoxia or mild infection induces mild
mucosal damage
• This allows bacterial adhesion to Toll-like
receptors 4
• This adhesion cause local inflammation and
infiltration by PMN and monocytes with
release of inflammatory mediators- TNF, PAF
• TNF and PAF cascades the inflammatory
process
• Increased membrane permeability allows
bacterial invasion
• Splanchnic constriction causes hypoxia with
development of o2 radicals
CLINICAL MANIFESTATIONS:
Onset can be insidious or rapid.
Onset time: The onset of NEC varies; in very
low birth weight (VLBW)infants, NEC is usually
diagnosed between 14-20 days of life.
In full-term infants, the age of onset is usually
during the first week of life.
The postnatal age at onset is inversely
related to birth weight and gestational age.
It is unusual for the disease to progress from
mild to severe after 72 hr.
CLINICAL MANIFESTATIONS:
The 1st signs of impending disease may be
-Nonspecific including lethargy and temperature
instability
or
• -Related to gastrointestinal pathology such as
abdominal distention and gastric retention.
• Obvious bloody stools are seen in 25% of patients.
• The spectrum of illness is broad and ranges from
• -Mild disease
• -Severe illness with bowel perforation, peritonitis, systemic
inflammatory response syndrome, shock, and death.
CLINICAL MANIFESTATIONS:
Martin Bell’s Staging (1978)
• The original clinical criteria was based on:
1. Systemic Signs
2. Intestinal Signs
3. Radiological Signs
• Classified into:
• I. Suspected:
• II. Definite :
• A (Mildly ill) ,
• B (Moderately ill)
• III. Advanced:
• A (Severely ill, bowel intact),
• B (Severely ill, bowel perforated)
Modified Bell’s staging for NEC
Diagnosis of NEC
Very high index of suspicion.
1. Plain abdominal x-rays :
Pneumatosis intestinalis (air in the bowel wall) is
diagnostic;
Portal venous gas is a sign of severe disease, and
Pneumoperitoneum indicates a perforation.
2. Hepatic ultrasonography:
May detect portal venous gas despite normal
abdominal radiograph.
3. Analysis of stool for blood and
carbohydrate
Carbohydrate malabsorption - positive stool
Clinitest result, can be a frequent and early
indicator of NEC.
COMMON TRIAD
OF SIGNS ‘HAT’
• 4. Blood studies:
Thrombocytopenia
Persistent Metabolic Severe Refractory
Acidosis Hyponatremia
Abdominal radiograph
Pneumoperitoneum
“football” sign
◦ The median umbilical ligament and
falciform ligament are sometimes
included in the description of this sign
Pneumoperitoneum
/scrotum
Intestinal perforation
Abdominal X-ray in NEC
demonstrates marked
distention and massive
pneumoperitoneum
There is Free air below the
anterior abdominal wall
Differential diagnosis of
NEC :
• infections (systemic or intestinal)-
Pneumonia, Sepsis.
• ◦ Gastrointestinal obstruction, volvulus,
malrotation,
• ◦ Isolated intestinal perforation.
• ◦ Metabolic disorders. (e.g., galactosemia
with Escherichia coli sepsis)
• ◦ Feeding intolerance
• ◦ Severe allergic colitis
• ◦ Idiopathic focal intestinal perforation
TREATMENT: Basic NEC protocol
• Treat suspected as well as proven NEC cases.
For established NEC, therapy is directed at
supportive care and preventing further injury
through:
• -Cessation of feeding,
• -Nasogastric decompression, and
• -Administration of intravenous fluids.
• Start on systemic antibiotics : ampicillin +
gentamicin or cefotaxime , add metronidazole
or clindamycin if peritonitis or perforation is
suspected
Basic NEC protocol …..continued
• Monitor for GI bleeding
• Fluid balance: maintain urine output 1-3 ml/kg/hr
• Lab.: CBC, PLT, electrolytes q 8-12 hrs
• PT, PTT, LFT’s as indicated
• CRP
• Radiology: serial AXR q 6-8 hrs in the first 2-3 days
• Family support
PourcyrousM et al. C-reactive protein in the diagnosis, management, and prognosis of neonatal necrotizing
enterocolitis. Pediatrics. 2005 Nov;116(5):1064-9.
TREATMENT: Contd..
• ◦Remove umbilical catheters if present.
• Ventilation should be assisted as required.
• Intravascular volume replacement with
crystalloid or blood products.
• Cardiovascular support with volume and/or
inotropes.
• Correction of hematologic, metabolic, and
electrolyte abnormalities.
• Monitor respiratory status, coagulation
profile, and acid-base and electrolyte balance
Algorithm for the treatment of NEC
MONITORING:
• Sequential anteroposterior and cross-
table lateral or lateral decubitus
abdominal x-rays to detect intestinal
perforation;
• ◦ Serial determination of hematologic
status,
• ◦ Serial determination of electrolyte
status, and
• ◦ Serial determination of acid-base
status.
Indications for surgery :
• Absolute indications:
• Evidence of perforation on abdominal
x- ray or
• Positive abdominal paracentesis
• Relative indications:
• ◦ Failure of medical management,
• ◦ Single fixed bowel loop on x ray,
• ◦ Abdominal wall erythema, or
• ◦ A palpable mass.
PROGNOSIS
• Medical management fails in about 20–40%
of patients with pneumatosis intestinalis at
diagnosis; of these, 10–30% die.
• Early postoperative complications :
Wound infection, dehiscence, and stomal
problems (prolapse, necrosis).
• Later complications : Intestinal
strictures develop at the site of the
necrotizing lesion in about 10% of
surgicallyor medically managed patients.
PROGNOSIS….
• After massive intestinal resection,
• -short-bowel syndrome
• Adverse neurodevelopmental outcome.
• The overall mortality is 9% to 28%
Soraisham AS et al. Does necrotisingenterocolitis impact the neurodevelopmental and growth outcomes
in preterm infants with birthweight< or =1250 g?. J PaediatrChild Health. 2006 Sep;42(9):499-504.
PREVENTION:
• Exclusively breast-fed Newborns.
• ◦ Early initiation of aggressive feeding may increase the risk
of NEC in VLBW infants.
• ◦ Gut stimulation protocol of minimal enteral feeds followed
by judicious volume advancement may decrease the risk.
• ◦ Probiotic preparations have also decreased the incidence
of NEC. .
• Induction of GI maturation.
• ◦ Incidence of NEC is significantly reduced after prenatal
steroid therapy.
• ◦ Alteration of the immunologic status of the intestine using
immunoglobulin A (IgA) and immunoglobulin G (IgG)
supplementation.
References
• 1. MarkelTA et al. Cytokines in necrotizing enterocolitis. Shock. 2006 Apr;25(4):329-37.
• 2. Quigley M et al. Formula milk versus donor breast milk for feeding preterm or low birth weight infants.
Cochrane Database SystRev. 2007 Oct 17;(4):CD002971.28
• 3. NowickiPT. Ischemia and necrotizing enterocolitis, Where, when, and how. Seminars in Pediatric
Surgery (2005) 14, 152-158.
• 4. Dempsey EM, Barrington K. Short and long term outcomes following partial exchange transfusion in
the polycythaemicnewborn: a systematic review. Arch DisChild Fetal Neonatal Ed. 2006 Jan;91(1):F2-6.
• 5. EpelmanM et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with pathologic
correlation. RadioGraphics2007; 27:285–305.
6. Xavier Demestreet al Peritoneal drainage as primary management in necrotizing enterocolitis: A
prospective study, J PediatrSurg. 2002 Nov •Volume 37 •Number 11 •p1534 to p1539.
