THE RADIOLOGY OF NECROTIZING ENTEROCOLITIS

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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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RADIOLOGY

Once NEC is suspected, a regular routine of abdominal films is instituted. We obtain supine films of the abdomen every 12 to 24 hours depending on the clinical status of the baby. In more ill children, the supine film is accompanied by one obtained by a horizontal beam for detection of free air. Either a supine cross-table lateral view or a left-side-down decubitus view may be obtained. Both are extremely sensitive for the detection of free air (see later). The cross-table lateral is easier to

COMPLICATIONS

Babies who survive NEC, both those treated medically and surgically, may develop a number of late complications. Infants who have had extensive bowel resection may develop short-gut syndrome with its attendant complications. Survivors treated both medically and surgically may develop intestinal strictures. The babies with strictures may be asymptomatic but most develop signs and symptoms of bowel obstruction weeks to months after the initial diagnosis of NEC. About 10% to 20% of babies with NEC

FOCAL INTESTINAL PERFORATION WITHOUT NECROTIZING ENTEROCOLITIS

NEC is the most common cause of intestinal perforation in the newborn period. Other common causes include intestinal obstruction, idiopathic gastric perforation, and iatrogenic causes, such as malpositioned nasogastric tubes.16 In recent years, there have been many reports of neonates who have developed focal perforations of the intestine without evidence of NEC.2, 8, 15, 31, 33, 34, 38, 44, 47 Focal perforation without NEC, in fact, probably represents the second most common cause of

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

    *

    Children's Hospital; and the Department of Radiology, Harvard Medical School, Boston, Massachusetts

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