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Special Feature
February 1999

Radiological Case of the Month

Arch Pediatr Adolesc Med. 1999;153(2):199-200. doi:
Denouement and Discussion: Necrotizing Enterocolitis in a Term Infant

Figure 1. Abdominal radiograph (supine view) showing distended loops of bowel, and a bowel pattern of bubbles present in the right iliac fossa (arrows).

Figure 2. Abdominal radiograph (left lateral decubitus view) showing distended loops of bowel and pneumatosis intestinalis present on the right side. There is no evidence of intraperitoneal air or portal venous air.

Vomiting in the initial days of life is suggestive of an obstruction of the gastrointestinal tract, but it also may represent a nonspecific symptom of sepsis. Bile-stained vomitus in the newborn is a surgical emergency and should be considered a sign of an intestinal obstruction beyond the second portion of the duodenum until proven otherwise. Intestinal obstruction occurs in approximately 1 of every 1000 newborns, with signs of vomiting, abdominal distension, and delayed passage of meconium. Abdominal radiographs (supine and cross-table lateral views) are obtained to detect air-fluid levels, distended loops of bowel, pneumoperitoneum, characteristic patterns of obstruction, or pneumatosis intestinalis, indicating necrotizing enterocolitis.

Necrotizing enterocolitis represents the most common gastrointestinal emergency seen in the neonatal intensive care unit, and affects almost 2000 neonates in the United States each year.1 The etiology for necrotizing enterocolitis is multifactorial, and no universal theory of pathogenesis has been accepted. Risk factors include birth asphyxia, shock, hyaline membrane disease, apnea, presence of a patent ductus arteriosus, and use of umbilical artery and vein catheters.2 However, there is no difference in the incidence of these risk factors between infants with necrotizing enterocolitis compared with infants of similar birth weight and gestation without necrotizing enterocolitis.35

The disease has diverse clinical manifestations, ranging from a relatively mild course characterized by feeding intolerance, abdominal distension, hematochezia, and vomiting to a more fulminant course characterized by intestinal necrosis, perforation, sepsis, and death. Newborns may initially display abdominal distension and marked gastric residual fluid or vomiting. Occultly positive for blood or grossly bloody stools may be present. Frequently, affected infants have nonspecific signs and symptoms of sepsis. The initial findings from the physical examination are nonspecific, but as the disease progresses, the abdomen becomes firm and discolored, and visible loops of bowel are seen.

Necrotizing enterocolitis usually affects premature infants. In a review of 123 affected infants, the mean gestational age was 31 weeks, with an average birth weight of 1460 g. Only 7.3% of the reported patients were term births.6 In another review, however, 13 (20%) of the 64 infants were term births. While the histopathologic observations do not differ between term and preterm infants, the classic radiographic features are encountered less frequently in term infants.7 Other investigators have suggested that infants with symptoms of necrotizing enterocolitis during the first 1 to 2 days of life are larger weight, more mature, and less frequently asphyxiated than infants with the onset of necrotizing enterocolitis presenting later.8

The treatment of necrotizing enterocolitis, in the absence of signs of intestinal necrosis or perforation, is medical and includes nasogastric decompression and institution of broad-spectrum systemic antibiotic therapy. Serial abdominal radiographs are obtained to document progression or resolution of the disease. Early surgical consultation should be obtained. Intestinal perforation or disease refractory to medical management requires surgical intervention.9

Necrotizing enterocolitis is a serious and potentially life-threatening disease that affects primarily preterm infants. The pathogenesis of this disorder appears to be multifactorial, and term infants may suffer from a histopathologically and etiologically similar disease, although term infants are more likely to present with these symptoms within the first several days of life. Term infants are less likely to exhibit the classic radiologic manifestations of this disease, and thus a high index of suspicion is required to ensure timely intervention.

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Article Information

Accepted for publication February 2, 1998.

Reprints: Derek S. Wheeler, MD, US Naval Hospital, Department of Pediatrics, PSC 490, Box 221, FPO AP, Guam 96538 (e-mail: dwheeler@gam10.med.navy.mil).

References
1.
Wilson  RKanto  WP  JrMcCarthy  BJ  et al.  Epidemiologic characteristics of necrotizing enterocolitis: a population-based study. Am J Epidemiol. 1981;114880- 887
2.
Amoury  RA Necrotizing enterocolitis: a continuing problem in the neonate. World J Surg. 1993;17363- 373Article
3.
Yu  VYHTudehope  DI Neonatal necrotizing enterocolitis: 2 perinatal risk factors. Med J Aust. 1977;1688- 693
4.
Kliegman  RMHack  MJones  PFanaroff  AA Epidemiologic study of necrotizing enterocolitis among low-birth-weight infants. J Pediatr. 1982;1200440- 444Article
5.
Virnig  NLReynolds  JW Epidemiologic aspects of neonatal necrotizing enterocolitis. AJDC. 1974;128186- 190
6.
Kliegman  RMFanaroff  AA Neonatal necrotizing enterocolitis: a nine-year experience. AJDC. 1981;135603- 607
7.
Polin  RAPollack  PFBarlow  B  et al.  Necrotizing enterocolitis in term infants. J Pediatr. 1976;89460- 462Article
8.
Thilo  EHLazarte  RAHernandez  JA Necrotizing enterocolitis in the first 24 hours of life. Pediatrics. 1984;73476- 480
9.
Cikrit  DMastandrea  JWest  KWSchreiner  RIGrosfeld  JL Necrotizing enterocolitis: factors affecting mortality in 101 surgical cases. Surgery. 1984;96648- 655
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