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THE RADIOLOGY OF NECROTIZING ENTEROCOLITIS - 07/09/11

Doi : 10.1016/S0033-8389(05)70256-6 
Carlo Buonomo, MD *

Résumé

Necrotizing enterocolitis (NEC), a broad term that has been used to describe many inflammatory conditions of the intestine, has come in modern pediatric practice to refer almost exclusively to the idiopathic, often severe enterocolitis that occurs in premature infants in neonatal intensive care units. Much progress has been made in understanding NEC since the first comprehensive description of the syndrome in 19646; the precise origin of NEC, however, remains unclear. Historically, NEC has been thought to be caused by the combination of hypoxia, infection, and enteral feeding. This model is supported by the observations that the pathology of NEC resembles that of ischemic necrosis, that NEC often occurs in epidemics, and that NEC usually develops only after the institution of feeding. It is clear, however, that some of the so-called risk factors for the development of NEC are common to all neonates, most of whom do not develop NEC, and that NEC occurs in infants who do not have any identifiable risk factors. It may be that the primary pathologic event in NEC is injury to the intestinal mucosa and that this injury can be caused by different factors in different patients.22

The only definite risk factor for the development of NEC is prematurity. The great majority of cases occur in infants who weigh less than 2000 g, and both the incidence and mortality of NEC increase with decreasing birthweight and gestational age.17 Advances in neonatology have led to improved survival of very-low-birthweight (less than 1000 g) infants; consequently, there has been an increase in the mortality from NEC in the last decade despite an overall decrease in neonatal mortality.17

NEC may also occur in full-term infants. Specific risk factors, such as polycythemia, can frequently be identified in full-term children. Newborns who have had cardiac surgery or abdominal surgery, particularly repair of gastroschisis or intestinal atresia, are also at risk for NEC.1 Babies born to mothers who abuse cocaine also may have a higher incidence of NEC.12 There may be an increase in the incidence of NEC in preterm infants treated with indomethacin for patent ductus arteriosus15; however, this has not been definitely established.

In NEC there is inflammation of the intestine, which begins in the mucosa and which may then extend through the bowel wall. Involvement may be diffuse and contiguous, or patchy. The distal ileum and proximal colon are involved more frequently than other sites, although any portion of the intestine may be affected.4

Most infants develop NEC within the first few days of life. The age of onset of NEC, however, is inversely proportional to gestational age; very premature infants may not develop NEC until the second or third week of life, or even later.40 The clinical signs of NEC are varied and nonspecific. Gastrointestinal symptoms include abdominal distention, feeding intolerance, vomiting, blood in the stool, and diarrhea. Systemic signs are lethargy, temperature and blood pressure instability, and apnea. Advanced disease may present as shock. Physical signs, specifically in advanced disease, include erythema of the body wall and palpable distended bowel loops. The mortality of NEC is probably about 20% to 40% and, as noted previously, increases as the birthweight decreases.

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 Address reprint requests to Carlo Buonomo, MD, Department of Radiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115


© 1999  W. B. Saunders Company. Publié par Elsevier Masson SAS. Tous droits réservés.© 1998 
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Vol 37 - N° 6

P. 1187-1198 - novembre 1999 Retour au numéro
Article précédent Article précédent
  • IMAGING OF NEONATAL GASTROINTESTINAL OBSTRUCTION
  • Marta Hernanz-Schulman
| Article suivant Article suivant
  • SONOGRAPHY OF THE NEONATAL GENITOURINARY TRACT
  • David E. Blews

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