Necrotizing Enterocolitis (nec)

Ira Shah
Consultant Pediatrician, B.J.Wadia Hospital for Children, Mumbai, India
First Created: 01/07/2004 

Introduction

NEC is a syndrome of acute intestinal necrosis. The etiology is unknown and pathogenesis is complex and multifactorial. It is the most common serious surgical disorder among infants in the NICU & a significant cause of neonatal morbidity and mortality. It is seen in 2.5% of all NICU admissions and has an overall mortality rate of 30-40% with mortality increasing to more than 80% in neonates less than 1 kg.

Pathology: Common sites are the terminal ileum and ascending colon.

Predisposing Factors

  • Prematurity: Seen commonly at a mean gestational age of 30-32 wks. (AGA). It is the single greatest risk factor. Incidence of NEC increases as gestational age decreases.
  • In Term infants & near terms: Conditions predisposing to decreased gastrointestinal oxygen delivery
  • Perinatal asphyxia (lower 1 minute apgar score)
  • Lower cord PH (acidosis)
  • Polycythemia
  • RDS/apnea
  • Shock
  • Umbilical artery catheterization
  • Early or large volume nasogastric feeding
  • Congenital heart disease

Pathogenesis

  • Role of immature Gastrointestinal host defenses
  • Role of infectious agents & bacterial toxins
  • Role of inflammatory mediators
  • Role of oxygen radicals & ischemia reperfusion injury

Clinical Staging Of NEC


Stage Clinical features X-ray Survival (%)
  • Suspect NEC
  • Mild abdominal distension
  • Stasis
  • Vomiting
  • Poor feeding
  • Mild ileus

100%
  • Definite NEC
  • Marked abdominal distension
  • GI bleeding
  • Definite ileus
  • Pneumatosis intestinalis

95%
  • Advanced NEC
  • DIC
  • Shock
  • Sclerema
  • Brownish Peritoneal aspirate
  • Fixed dilated loop of intestine
  • Portal vein gas
  • Pneumoperitoneum

50%

Clinical Features

  • Symptoms may appear within 96 hrs after initiation of feeds
  • Majority of cases occur within first 10 days of life
  • Onset may be insidious/explosive/delayed
  • Earliest signs: abdominal distension, retention of milk in a sick-looking LBW infant.
  • Clinical triad: Abdominal. Distension + GI bleeding + Pneumatosis intestinalis
  • Signs of functional Intestinal obstruction: Abdominal distension, progressive decreased peristalsis, bilious vomiting, hematemesis and blood in stools
  • Signs of peritonitis & perforation: Ascites, erythema & edema of abdominal wall, localized mass or rigidity
  • Systemic signs respiratory distress, apnea, bradycardia, lethargy, thermal instability, irritability, poor feeding, hypotension (shock), oliguria, bleeding diathesis, sclerema

Investigations

  • Serial X-rays of abdomen: Fixed bowel loop, appearance of mass, pneumatosis intestinalis, portal or hepatic venous air, pneumoperitoneum
  • Stool examination: Occult blood, reducing substances for unabsorbed lactose, culture for aerobic/anaerobic bacteria
  • Blood: Electrolytes, hematocrit, coagulation status, culture, ABG. Watch for triad of thrombocytopenia, severe refractory hyponatremia and acidosis.
  • USG: Micro bubbles of gas in portal vein
  • Hydrogen breath test

Management


Medical Surgical
Respiratory:
  • Supplement O2
  • Mechanical ventilatory support
CVS:
  • Fresh frozen plasma
  • Low doses dopamine
Metabolic:
  • NaHCO3
Nutrition:
  • Stop oral feedings (7-14 days)
  • TPN instituted (90-110 cal/kg/d)
Antibiotics- For 7-14 days. Broad spectrum

Hematological:
  • Platelet transfusions
  • Packed RBCs
  • Vitamin K
CNS:
  • Treat IVH, meningitis, seizures
Renal:
  • Fluid therapy
Indications:
  • Bowel perforation
  • Full thickness necrosis of bowel wall as evidenced by dilated loop of intestine unchanged in position > 24 hrs.
  • Peritonitis. Aspiration of brown colored fluid is indicative of intestinal gangrene.
Surgical treatment:
Excision of necrotic area & end-to-end anastomosis

Differential Diagnosis

  • Pneumonia & sepsis

  • Surgical abdominal catastrophes

    • Malrotation with obstruction
    • Malrotation with midgut volvulus
    • Intusussception
    • Ulcer
    • Gastric perforation
    • Mesenteric vessel thrombosis

  • Infections enterocolitis with diarrhea
  • Inherited metabolic disease
  • Feeding intolerance
  • Systemic candidiasis

Prevention

Corticosteroids - Prenatal/Postnatal

  • Lower incidence of NEC in mothers of preterm who received dexamethasone antenatally.

Feeding regimen

  • Breast feeding
  • Acidified feeds
  • Small iso-osmolar feeds with gradual increase in feeds

Oral Immunoglobulins (IgA & IgG)

  • Enhances intestinal immune defenses

Reduce incidence of:

  • Preterm delivery
  • Prevent predisposing factors

Prognosis

Recurrent NEC is 4%

Sequelae

  • Strictures (20%) most common in large bowel
  • Enteric fistulas
  • Short bowel syndrome (following surgery)
  • Malabsorption & chronic diarrhea
  • Dumping syndromes: loss of terminal ileum
  • Fluids electrolyte losses (with ileostomy)
  • Parenteral nutrition associated hepatic disease
  • Developmental delay


Necrotizing Enterocolitis (NEC) Necrotizing Enterocolitis (NEC) Necrotizing Enterocolitis (NEC) 01/07/2004
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