1. NECROTIZING ENTEROCOLITIS
Janice Nicklay Catalan M.D.

2. 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

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

4. 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

5. 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

6. 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

7. NECROTIZING ENTEROCOLITIS
Pathophysiology:
UNKNOWN CAUSE…….

8. MUCOSAL INJURY CIRCULATORY INSTABILITY
Hypoxic-ischemic event Polycythemia
PRIMARY INFECTIOUS AGENTS
Bacteria, Bacterial toxin, Virus, Fungus
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

9. 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

10. RISK FACTORS Infectious Agents: usually occurs in clustered epidemics
normal intestinal flora
E. coli
Klebsiella spp.
Pseudomonas spp.
Clostridium difficile
Staph. Epi
Viruses

11. 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

12. 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

13. 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

14. RISK FACTORS Enteral Feedings: immature mucosal function
malabsorption
breast milk may have a protective effect
IGA
macrophages, lymphocytes
complement components
lysozyme, lactoferrin
acetylhydrolase

15. 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

16. CLINICAL PRESENTATION
Gastrointestinal:
Feeding intolerance
Abdominal distention
Abdominal tenderness
Emesis
Occult/gross blood in stool
Abdominal mass
Erythema of abdominal wall
Systemic
Lethargy
Apnea/respiratory distress
Temperature instability
Hypotension
Acidosis
Glucose instability
DIC
Positive blood cultures

17. CLINICAL PRESENTATION
Sudden Onset:
Full term or preterm infants
Acute catastrophic deterioration
Respiratory decompensation
Shock/acidosis
Marked abdominal distension
Positive blood culture
Insidious Onset:
Usually preterm
Evolves during 1-2 days
Feeding intolerance
Change in stool pattern
Intermittent abdominal distention
Occult blood in stools

18. BELL STAGING CRITERIA

19. 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

20. 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

21. RADIOLOGICAL FINDINGS
Pneumoperitoneum
free air in the peritoneal cavity secondary to perforation
falciform ligament may be outlined
“football” sign
surgical emergency

22. LABORATORY FINDINGS CBC Acidosis Hyperkalemia neutropenia/elevated WBC
thrombocytopenia
Acidosis
metabolic
Hyperkalemia
increased secondary to release from necrotic tissue

23. LABORATORY FINDINGS
DIC
Positive cultures
blood
CSF
urine
stool

24. TREATMENT Stop enteral feeds Nasogastric decompression Antibiotics
re-start or increase IVF
Nasogastric decompression
low intermittent suction
Antibiotics
Amp/Gent; Vanc/Cefotaxime
Clindamycin
suspected or proven perforation

25. 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

26. TREATMENT Labs: q6-8hrs X-rays: q6-8hrs Supportive Therapy
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

27. PROGNOSIS Depends on the severity of the illness
Associated with late complications
strictures
short-gut syndrome
malabsorption
fistulas
abscess
* MOST COMMON