Necrotizing Enterocolitis

Case Presentation
This is a case of a live baby boy, born preterm to a 26 year-old G2P2 (1102) via E LTCS x preterm labor
Mother revealed use of cocaine during the perinatal period Three days prior to delivery, mother was given indomethacin because of preterm labor Baby was delivered by emergency cesarean section because of late decelerations

Case Presentation
APGAR Scores
1, i, 3, 7

Birth weight
1150 kg

Case Presentation
Because of worsening respiratory distress, an umbilical arterial line was placed at L4. A CBC obtained from the UA was remarkable for a Hct = 71%. On day one of life, the infant was placed on TPN Within 72 hours, feedings were begun The baby was advanced to full feedings over 3 days

Case Presentation
On day 4 of life, a murmur was heard and an echocardiogram and chest x-ray were obtained. Total fluid intake at that time was 185 ml/kg day

Case Presentation
On day 10 of life, he needed NaHCO3 because of a mild metabolic acidosis. Gastric aspirates increased in volume and were blood tinged. A CBC was remarkable for leukopenia and thrombocytopenia. On day 11, he became distended & developed erythema of the abdominal wall.

Definition
Infection of the mucosal lining of the bowel. An idiopathic coagulation necrosis and inflammation of the intestine in a neonatal patient. Ischemic and inflammatory necrosis of the bowel primarily affecting premature neonates after the initiation of enteral feeding.

Epidemiology
Most common life-threatening emergency of the gastrointestinal tract in the newborn period Incidence: 6-10% in VLBW infants < 1500 grams Inverse relationship with gestational age Males and females equally effected

Epidemiology
Mean age at diagnosis 20 days (premature) vs. 7 days (term) 10% term infants (usually in those with preexisting illness) Overall mortality of 10-30%

Causes
Strongly associated with feeding initiation Low intestinal immune function Bacterial invasion Umbilical artery catheterization Hyperviscosity Cardiovascular and pulmonary disorders

Pathophysiology

UNKNOWN CAUSE.

Pathophysiology

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

Clinical Presentation

Clinical Presentation

Bells Staging Criteria

Stage I (suspected NEC) Stage II (definite NEC) Stage III (advanced NEC, severely ill)
IIIA (without perforation) IIIB (with perforation)

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

Administration of intravenous fluids with careful attention to respiratory status, coagulation profile, and acid-base and electrolyte balance

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

Outcome
Depends on the severity of the illness Associated with late complications
* Strictures (most common) short-gut syndrome malabsorption fistulas abscess

Complications
Mortality is 30-60% Stricture formation is 25-35% Bowel obstruction in 5% Enterocutaneous fistulas FTT secondary to short bowel syndrome and malabsorption TPN related cholestasis Central line sepsis

Outcome
Infants treated medically survival is > 95% Infants requiring surgery survival is 70-75%

Prevention
Antenatal steroids decreased the incidence of NEC in randomized blinded studies Use of human milk (1.2% incidence vs. 7.2% incidence in formula feed premies) GI priming with cautious advancement of enteral feeding
Minimal enteric feedings (gut stimulation) prior to bolus feedings may reduce the incidence of NEC; early initiation of aggressive feeding protocols may increase its incidence in VLBW infants