Necrotizing enterocolitis

(NEC)
 Introduction
• Necrotizing enterocolitis (NEC)  is one of the
most common reasons for surgical consultation
in neonates and is the most common GI
emergency in the neonatal population.
• NEC remains one of the most challenging
diseases confronted by pediatric surgeons and
still carries a mortality rate of 30-50% when a
perforation occurs.
 Introduction
• Although various clinical and radiographic
signs and symptoms are used to make the
diagnosis, the classic clinical triad consists of
abdominal distension, bloody stools, and
pneumatosis intestinalis. Occasionally, signs
and symptoms include temperature instability,
lethargy, or other nonspecific findings of
sepsis.
 Pathogenesis
• Despite recent insights into the multifactorial
pathogenesis of NEC, a complete understanding of its
pathophysiology remains elusive. Cause is uncertain.
• The classic histologic findings of inflammation and
coagulation necrosis are presenting over 90% of
surgical specimens. Likely multifactorial- intestinal
ischemia and infection central to process
• Preterm infants- incidence inversely related to
gestational age. Incidence and severity higher in
neonates with smaller birth weights
 RISK FACTORS
• Infectious Agents:
– NEC most commonly is diagnosed during the second week of life,
after intestinal colonization has been established.
– normal intestinal flora (E. Coli, Klebsiella spp., Pseudomonas spp.,
Clostridium difficile, Staph. Epi, Viruses)
– usually occurs in clustered epidemics
• 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
• 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)
– immature mucosal function (malabsorption)
 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
 CLINICAL PRESENTATION

Gastrointestinal: Systemic
Feeding intolerance Lethargy
Abdominal distention Apnea/respiratory distress
Abdominal tenderness Temperature instability
Emesis Hypotension
Occult/gross blood in stool Acidosis
Abdominal mass Glucose instability
Erythema of abdominal wall DIC
Positive blood cultures
Abdominal Distension
 LABORATORY FINDINGS
• DIC
• Positive cultures (blood, CSF, urine, stool)
• CBC
– neutropenia/elevated WBC
– thrombocytopenia
• Acidosis
– metabolic
• Hyperkalemia
– increased secondary to release from necrotic tissue
 Radiographic presentation
• Usually followed by KUB & Lateral Decubitus radiograph
– Pneumatosis
– Dilated loops of bowel
– Free air (if perforated) / Pneumoperitoneum
• Lateral decub is particularly helpful
• free air in the peritoneal cavity secondary to perforation
– 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
 surgical emergency
• Ultrasound
– Good for bedside demonstration of ascites
– May show portal air more clearly than KUB
Dilated loops & Portal Air

Portal Air

Dilated
stomach &
loops of
bowel

http://www.adhb.govt.nz/newborn/TeachingResources/Radiology/AXR/NEC/NECwithPortalGasAP1.jpg
 A Bad Case of NEC

Abdominal
free air
Portal Air

Pneumatosis

http://www.medicine.cmu.ac.th/dept/radiology/pedrad/case8ans.html
 Pathology
• Most common site of
involvement is the
terminal ileum followed
by the colon
• Disease can involve
single or multiple
segments of bowel
• Pan-necrosis in 19%,
mortality 100%
Pneumatosis

Necrosis
 Modified Bell Staging for NEC
Stage & Systemic Signs Abdominal Signs Radiographic Signs
Severity
Stage Ia Temp changes, apnea, Distension, gastric Normal, or intestinal
Suspected NEC bradycardia, lethargy retention, emesis, heme dilation
positive stool Mild ileus

Stage Ib Same as Ia Ia + grossly bloody Same as Ia

Suspected NEC stool

Stage IIa Same as Ia Ib + absent bowel Intestinal dilation,

Definite Mild NEC sounds +/- abdominal ileus, pneumatosis
tenderness intestinalis

Stage IIb Ia + mild metabolic IIa + definite IIa + ascites

Definite Moderate NEC acidosis, tenderness, +/- abd
thrombocytopenia cellulitis, RLQ mass

Stage IIIa IIb, but more severe, + IIb + peritonitis, Same as IIb
Advanced, Severe NEC combined respiratory & marked distension and
Bowel Intact metabolic acidosis, tenderness
neutropenia, & DIC
Stage IIIb Same as IIb Same as IIIa IIIa +
Advanced Severe NEC pneumoperitoneum
Bowel Perforated

Adapted from sources showing Bell Staging

 TREATMENT
• Stop enteral feeds
– re-start or increase IVF
– Follow KUB for resolution
• Resume enteral feeds 10-14 days after radiographic resolution
• Nasogastric decompression
– low intermittent suction
• Antibiotics
– Broad spectrum antibiotics Cover Gram +,
Gram - & Anaerobes
Amp/Gent; Vanc/Cefotaxime;Clindamycin
 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
 Surgical Treatment
• Laparotomy
• Resection of necrotic bowel
• Ileostomy with mucous fistula
– Subsequent re-anastamosis
• May result in strictures requiring further
surgery later
• Peritoneal drain
• Placement in NICU under local anesthetic
• Used when infant is too clinically unstable for
surgery
• May help stabilize pt for subsequent surgery
 Complications
• Sepsis, meningitis, abscess formation
• DIC
• Hypotention, shock
• Respiratory failure
 PROGNOSIS
• Depends on the severity of the illness
• Associated with late complications
– Strictures (MOST COMMON)
– short-gut syndrome
– malabsorption
– fistulas
– abscess
 Outcomes
• Mortality 20-40%
Mortality varies with birth weight:
– <1000 g = 40-100%
– <1500 g = 10-44%
– >2500 g = 0-20%
• Morbidity/Mortality vary with severity:
– Resection -> Short gut -> FTT, malabsorbtion
– Strictures -> further surgery in medical and surgical NEC
– Prolonged NPO status on TPN -> cholestasis &
metabolic abnormalities
 Prevention
• Encourage breast feeding
– Breast fed babies have lower incidence than formula
fed
– breast milk may have a protective effect (IGA,
macrophages, lymphocytes ,complement components,
lysozyme, lactoferrin, acetylhydrolase)
• No evidence shows that late initiation of enteral
feeding or slow rate of feeding makes any
difference
• Maintain high level of suspicion
– Feeding babies with NEC worsens the disease