NECROTIZING

ENTEROCOLITIS

Janice Nicklay Catalan M.D.

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

NECROTIZING
ENTEROCOLITIS
Epidemiology:
most commonly occurring gastrointestinal
emergency in preterm infants
leading cause of emergency surgery in neonates
overall incidence: 1-5% in most NICUs
most common in VLBW preterm infants
10% of all cases occur in term infants

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

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

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

NECROTIZING
ENTEROCOLITIS
Pathophysiology:

UNKNOWN
CAUSE.

PRIMARY INFECTIOUS AGENTS

Bacteria, Bacterial toxin, Virus, Fungus

CIRCULATORY INSTABILITY
Hypoxic-ischemic event
Polycythemia

MUCOSAL INJURY
INFLAMMATORY MEDIATORS
Inflammatory cells (macrophage)
Platelet activating factor (PAF)
Tumor necrosis factor (TNF)
Leukotriene C4, Interleukin 1; 6

ENTERAL FEEDINGS
Hypertonic formula or medication
Malabsorption, gaseous distention
H2 gas production, Endotoxin
production

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

RISK FACTORS
Infectious Agents:
usually occurs in clustered epidemics
normal intestinal flora

E. coli
Klebsiella spp.
Pseudomonas spp.
Clostridium difficile
Staph. Epi
Viruses

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

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

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

RISK FACTORS
Enteral Feedings:
immature mucosal function
malabsorption

breast milk may have a protective effect

IGA
macrophages, lymphocytes
complement components
lysozyme, lactoferrin
acetylhydrolase

CLINICAL PRESENTATION
Gestational age:
< 30 wks
31-33 wks
> 34 wks
Full term

Age at diagnosis:
20 days
11 days
5.5 days
3 days

*Time of onset is inversely related to gestational age/birthweight

CLINICAL PRESENTATION
Gastrointestinal:

Systemic

Feeding intolerance
Abdominal distention
Abdominal tenderness
Emesis
Occult/gross blood in stool
Abdominal mass
Erythema of abdominal wall

Lethargy
Apnea/respiratory distress
Temperature instability
Hypotension
Acidosis
Glucose instability
DIC
Positive blood cultures

CLINICAL PRESENTATION
Sudden Onset:

Insidious Onset:

Full term or preterm infants

Acute catastrophic deterioration
Respiratory decompensation
Shock/acidosis
Marked abdominal distension
Positive blood culture

Usually preterm
Evolves during 1-2 days
Feeding intolerance
Change in stool pattern
Intermittent abdominal
distention
Occult blood in stools

BELL STAGING CRITERIA

STAGE

CLINICAL

X-RAY TREATMENT

I. Suspect
NEC

Mild abdominal
distention
Poor feeding
Emesis

Mild ileus

Medical
Work up for
Sepsis

II. Definite
NEC

The above, plus

Marked abdominal
distention
GI bleeding

Significant
Ileus
Pneumatosis
Intestinalis
PVG

Medical

III. Advanced
NEC

The above, plus

Unstable vital signs
Septic Shock

PneumoPeritoneum

Surgical

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

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

RADIOLOGICAL FINDINGS
Pneumoperitoneum
free air in the peritoneal cavity secondary to
perforation
falciform ligament may be outlined
football sign

surgical emergency

LABORATORY FINDINGS
CBC
neutropenia/elevated WBC
thrombocytopenia

Acidosis
metabolic

Hyperkalemia
increased secondary to release from necrotic
tissue

LABORATORY FINDINGS
DIC
Positive cultures

blood
CSF
urine
stool

TREATMENT
Stop enteral feeds
re-start or increase IVF

Nasogastric decompression
low intermittent suction

Antibiotics
Amp/Gent; Vanc/Cefotaxime
Clindamycin
suspected or proven perforation

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

TREATMENT
Labs: q6-8hrs
CBC, electrolytes, DIC panel, blood gases

X-rays: q6-8hrs
AP, left lateral decubitus or cross-table lateral

Supportive Therapy
fluids, blood products, pressors, mechanical
ventilation

PROGNOSIS
Depends on the severity of the illness
Associated with late complications
*

strictures
short-gut syndrome
malabsorption
fistulas
abscess
* MOST COMMON