eMedicine Specialties > Radiology > Pediatrics

Necrotizing Enterocolitis

Author: Beverly P Wood, MD, MS, PhD, Professor, Departments of Radiology and Pediatrics, Division of Medical Education, Keck School of Medicine, University of Southern California
Contributor Information and Disclosures

Updated: Nov 10, 2008

Introduction

Background

Image 1.


The radiograph demonstrates multiple dilated loops in the large bowel and small bowel. Note the pneumatosis intestinalis with bubbly and linear gas collections in the bowel wall.

Image 4.


Portal venous air is present in a patient with pneumatosis intestinalis.

Presentation

Demographics

The incidence of necrotizing enterocolitis (NEC) varies from isolated cases to nursery epidemics. The population group most often affected is ill, preterm neonates.⁵

The incidence rates of necrotizing enterocolitis are similar in all developed countries in which high-quality health care is available for premature infants.

The incidence in premature neonates is highest in those with very low birth weights.⁶ NEC is less commonly seen in premature neonates with higher birth weights and in full-term neonates.

Currently, the mortality rate of patients with necrotizing enterocolitis is less than 20% when infants are treated early in the course of the illness. Without treatment, the mortality rate is extremely high.

Morbidity associated with NEC includes bowel stricture, peritoneal adhesions, and bowel perforation. If perforation occurs, the necrotic bowel is surgically resected. Resection of large lengths of bowel may result in short-bowel syndrome.

Necrotizing enterocolitis exhibits no sexual predilection.
 

Presentation

The onset of necrotizing enterocolitis may occur from 2 weeks to several months after birth. The meconium is usually passed normally. The initial signs of NEC include abdominal distention and gastric retention of fluid. Manifestations of the disease develop after enteric feedings begin.

The onset of NEC may be insidious, and sepsis may occur before any intestinal abnormality is noted. The spectrum of presentations ranges from mild NEC with guaiac-positive stool to severe NEC with peritonitis, bowel perforation, shock, and possible death. The progression of NEC may be rapid; however, progression of the disease usually occurs after 72 hours.

Obviously bloody stool is observed in approximately 25% of patients.

The distal ileum and proximal colon are most commonly involved in necrotizing enterocolitis, although any region of the bowel may be involved. The stomach may be involved as well.

Pneumatosis is a late finding in NEC and usually indicates some necrosis of the bowel wall. The presence of irritability and bowel distention, especially when associated with bloody stool, is pathognomonic of NEC.^7,8


Natural History

Several factors contribute to the development of neonatal necrotizing enterocolitis. The underlying pathology is one of gas accumulation in the submucosal layers of the bowel wall that progresses to necrosis. Eventual necrosis of the bowel loops, perforation, systemic sepsis, and death may result from NEC. The bowel regions most often affected are the right side of the colon and the distal ileum, although any portion of the bowel is susceptible.

The major or most common contributor to NEC is sepsis; however, indwelling vascular catheters, the use of assisted ventilation, respiratory acidosis, and hypoxemia are contributing factors as well. NEC is primarily a complication of premature birth, which may be associated with hypoxemia, acidosis, hypotension, sepsis, and stress. NEC may occur in ill full-term neonates, particularly those with a history of sepsis, hypoxia, asphyxia, or difficult resuscitation.

Polycythemia, the use of hypertonic formulas or medicines, and too-rapid feeding may cause mucosal injury. Epidemics of NEC have been documented, and infectious agents such as Clostridium perfringens, Escherichia coli, Staphylococcus epidermidis, and rotavirus have been identified in association with NEC. Most often, no pathogen is identified.^{9,10,11,12,13}

The presence of free air indicates a bowel perforation; in such cases, surgical exploration and resection of necrotic bowel is needed. Intensive therapy is started immediately. Feeding is stopped, nasogastric decompression is performed, and intravenous fluids are administered. Once cultures of blood, stool, and cerebrospinal fluid are obtained, systemic antibiotics are started; these may include anti-Pseudomonas medications and an aminoglycoside.¹⁴

When present, umbilical catheters are removed; assisted ventilation should be initiated if distention contributes to hypoxia. If hypotension develops, resuscitation is initiated with the administration of blood, plasma, crystalloid, and/or dopamine, as indicated. The patient's course is monitored with frequent radiography, including cross-table lateral views, to evaluate perforation.

Treatment

Medical treatment fails in approximately 20% of patients who have associated pneumatosis intestinalis. Pneumatosis intestinalis is lethal in at least 25% of these patients.

Strictures develop at the site of the necrotizing lesion in approximately 10% of patients. Resection of the stricture is curative.

Complications that may occur after massive intestinal resection include short-bowel syndrome, cholestatic jaundice, and conditions related to total parenteral alimentation via central venous catheters.¹⁵  Complications may be prevented with judicious feeding and the use of breast milk.¹⁶

Differential Diagnoses

Other Problems to Be Considered

Obstruction resulting from tenacious intestinal content in infants who are fed high-energy formulas
Hirschsprung disease
Intestinal hypoperistalsis syndromes
Adynamic ileus

• Search for CME/CE on This Topic »