FACULTY OF HEALTH SCIENCES, McMaster University

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Necrotizing Enterocolitis (NEC)

Introduction & Epidemiology
Theories on Pathogenesis
Risk Factors
Clinical Manifestations
Clinical Staging
Treatment
Random Thoughts

 

 

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Introduction and Epidemiology

Necrotizing Enterocolitis:

A disease of the GI tract that predominately affects premature infants
Acute, necrotizing inflammation of the small and large intestine
Path. Shows edema, hemorrhage and necrosis of the mucosa => inflamed and gangrenous bowel.
1% and 5% of all NICU admissions
62 - 94% are premature

Onset

- 3- 10 days after birth (24 hrs à 3 months)

 

What it is NOT

socioeconomic status
seasonal pattern
sex association

 

Pathogenesis

1. Hypoxic – Ischemic Injury (Diving reflex)

mesenteric ischemia?
Stresses: hypotension, hypothermia, hypoxia, feeds, anemia, uvc
Reduced or absent neonatal intestinal blood flow regulation/oxygenation
Mucosal injury from hypoxia and oxygen radicals

2. Enteral Alimintation (feeding diathesis)

Substrate for bacterial overgrowth?
Increases oxygen demand and metabolic demand
Immature immune system, functional immaturity of the gut
? benefit to breast milk (Ig, lactobacilli, lysozyme, etc..)

3. Infectious Disease

NEC does appear in epidemics / NICU’s (temporal / geographic)
? bacterial/viral à clotridial exotoxins
assoc. w/ outbreaks à klebsiella, e.coli, clotridia, staph, rotavirus, coronavirus, etc…

4. Others

smaller bile salt pool (which neutralizes exotoxins)
antenatal steroids increase bile salt pools and hasten gut maturation

 

 

 

 

Risk Factors

Purported Risk Factors

1.Prematurity

2.Perinatal asphyxia

3.RDS

4.Umbilical catheterization

5.Hypothermia

6.Shock

7.Hypoxia

8.PDA

9.Cyanotic congenital heart disease

10.Polycythemia

11.Thrombocytosis

12.Anemia

13.Exchange transfusion

14.Congenital GI anomalies

15.Chronic diarrhea

16.Non-breast milk formula

17.Naso-jejunal (NJ) feedings

18.Hypertonic formula

19.Too much formula - too fast

20.Hospitalization during an epidemic

21.Colonization with necrogenic bacteria

In summary, the available information supports the notion that the development of NEC involves multiple factors in the setting of a stressed gut with immature protective mechanisms. The primary initiator(s) of the disease remain unknown.

 

 

Clinical Manifestations

- signs of NEC are indistinguishable from sepsis

- ranging from feeding intolerance to evidence of a

- fulminant intraabdominal catastrophe (sepsis, shock, peritonitis à death.)

GI signs- abdominal distension, gastric aspirates, bilious vomiting, and bloody stools

- acute abodmen (tender, guarding, wall erythema)

Systemic Signs- Lethargy, apnea, and hypoperfusion

 

Symptoms Associated with NEC

Gastrointestinal Systemic
Abdominal distension Lethargy
Abdominal tenderness Apnea/respiratory distress
Feeding intolerance Temperature instability
Delayed gastric emptying "Not right"
Vomiting Acidosis (metabolic /respiratory)
Occult/gross blood in stool Glucose instability
Change in stool pattern/diarrhea Poor perfusion/shock
Abdominal mass DIC
Erythema of abdominal wall Positive blood cultures

 

Courses of the Illness

Sudden Insidious
Full-term or preterm infants Usually preterm
Acute catastrophic deterioration Evolving during 1 to 2 days
Respiratory decompensation Feeding intolerance
Shock/acidosis Change in stool pattern
Marked abdominal distension Intermittent abdominal distension
Positive blood culture Occult blood in stool

 

Clinical Staging

A clinical staging system for NEC was devised by Bell et al:

 

Stage IA - Suspected NEC:
Systemic signs: temperature instability, apnea, bradycardia, lethargy
Intestinal signs: Elevated pre-gavage residuals, mild abdominal distension, emesis, heme-positive stools
Radiologic signs: Normal or intestinal dilatation, mild ileus
Treatment: NPO, antibiotics x 3 days pending culture

 

Stage IB - Suspected NEC:
Intestinal signs: bright red blood from rectum

 

Stage IIA - Definite NEC (mildly ill):
Intestinal signs: Same as stage IA, plus absent bowel sounds, +/- abdominal tenderness
Radiologic signs: intestinal dilatation, ileus, pneumatosis intestinalis
Treatment: NPO, antibiotics 7-10 days if exam is normal in 24 to 48 hours

 

Stage IIB - Definite NEC (moderately ill):
Systemic signs: Same as stage IIA, plus mild metabolic acidosis, mild thrombocytopenia
Intestinal signs: Same as stage IIA, plus absent bowel sounds, definite abdominal tenderness, +/- abdominal cellulitis or right lower quadrant mass
Radiologic signs: Same as stage IIA plus portal vein gas, +/- ascites
Treatment: NPO, antibiotics x 14 days. Bicarb for acidosis

 

Stage IIIA - Advanced NEC (severely ill, bowel intact):
Systemic signs: Same as stage IIB, plus hypotension, bradycardia, severe apnea, combined respiratory and metabolic acidosis, DIC, neutropenia
Intestinal signs: Same as stage IIB, plus signs of generalized peritonitis, marked tenderness, and distension of abdomen
Radiographic signs: Same as stage IIB, plus definite ascites
Treatment: Same as stage IIB, plus 200 cc/kg fluids, inotropic agents, ventilation therapy, paracentesis

 

Stage IIIB - Advanced NEC (severely ill, bowel perforated):
Radiologic signs: Same as stage IIB, plus pneumoperitoneum
Treatment: Same as above, plus surgical intervention

Diagnosis

Labs – sepsis (cbc, blood gases)

Xrays – pneumotosis intestinalis (air within subserosal bowel wall)

- pneumoperitonium / perforation

- large distended, immobile intestinal loops à gangrenous

- air in portal venous system

Gross Path

- affects jejunum, ileum and colon mostly

- distended loops of intestine

- spotty intramural hemorrhage and areas of necrosis

- areas of subserosal gas collection\

- cloudy à turbid peritoneal fluid

 

 

Briefly on Treatment

Medical

iv fluid resuscitation
correction of anemia / hematocrit, platelets
bowel rest (ng. Decompression)
abdo xray q6h (in acute phase ? perforation)
if apneic à intubate and ventilate
stable à TPN nutrition
no enteral feedings until > 5d of normalized GI function (10-14 days from onset)
Antibiotic therapy is empirically started

 

Surgical

Highly specific indications

Pneumoperitoneum
Positive paracentesis
Fixed loop on serial radiographs
Erythema on the abdominal wall
Abdominal mass
Portal venous gas

Nonspecific supportive findings

Abdominal tenderness
Persistent thrombocytopenia (<100,000/mm3)
Progressive neutropenia
Clinical deterioration
Severe GI bleeding

* life threatening hemolysis after transfusion has been reported with NEC

 

Prognosis

- NEC is most common cause of death in neonates undergoing surgery

- mortality is 30-40% in this group (surgical)

- stricture formation in 25-35% of survivors

Late complications: FTT, feeding problems, diarrhea, bowel obstruction

Stricture
Fistula
Abscess
Recurrent NEC
Short-gut syndrome
Malabsorption
Cholestasis
Enterocyst formation

 

 

 

Obstetric Tidbit

Journal of Pediatrics, 1990 Jul

"Prenatal and postnatal corticosteroid therapy to prevent neonatal necrotizing enterocolitis: a controlled trial"

Pop = 466 women in premature labor

Maneuver = assigned to placebo vs. betamethasone prenatal

= those assigned placebo prenatally were further assigned to dexamethasone in first 7 days of life)

 

Exclusion: expected to deliver in less than 24 hours,

- severe medical complications

- IUGR, PROM

- newborns with malformations, cong. Infected, growth-retarded

Groups (A= placebo, B= betamethasone)

NEC Mortality

A1 (postnatal dex) 6.9% 11%

A2 (placebo) 14.4% 56%

(10.4%)

B 3.4% 0%, no surgery

 

 

 

 

A decreased incidence of necrotizing enterocolitis after prenatal x

glucocorticoid therapy. x

Source x

Pediatrics. 73(5):682-8, 1984 May.

In a large multicentered, collaborative randomized and blinded trial x

utilizing antenatal corticosteroids, the goals included determining the

effectiveness of these agents in accelerating lung maturation, as well as w

monitoring any short-term or long-term adverse effects of this treatment x

on the parturient, fetus, and/or infant. More than 100 specific items, x

pertaining to diagnoses, complications, and outcomes were recorded for the x

696 mothers enrolled in the study and their 745 infants. A significantly x

decreased incidence of necrotizing enterocolitis (P = .002) was found in x

the infants treated with steroids. The possibility of accelerated x

intestinal maturation induced by antenatal maternal steroid therapy x

exists. This treatment regimen is particularly attractive as adverse x

aspects of steroid therapy at the dosage utilized have not been x

demonstrated.