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:
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

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

BELL STAGING CRITERIA

STAGE I. Suspect NEC II. Definite NEC CLINICAL
Mild abdominal distention Poor feeding Emesis The above, plus Marked abdominal distention GI bleeding

X-RAY TREATMENT
Mild ileus Medical Work up for Sepsis

Significant Ileus Pneumatosis Intestinalis PVG PneumoPeritoneum

Medical

III. Advanced NEC

The above, plus Unstable vital signs Septic Shock

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