Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter III.12. Necrotizing Enterocolitis
Kelly S. Yamasato
October 2002

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This is a 14 day old infant female born to a 24 year old G1P1 mother at 30 weeks gestation via spontaneous vaginal delivery. Birthweight was 1340 g. Apgar scores were 6 and 7 at 1 and 5 minutes. Her early hospital course was remarkable for respiratory distress syndrome and patent ductus arteriosus. Recent problems include apnea and bradycardia of prematurity and feeding intolerance. Her nutritional needs have been met by advancing enteral feedings of preterm formula supplemented with parenteral hyperalimentation. On the day prior to the onset of symptoms, she was no longer receiving hyperalimentation and she was feeding 30 cc every 3 hours. Today she presents with abdominal distention and bilious vomiting. Her stool color has darkened and her urine output is reduced. She is also having more apnea and bradycardia events.

Exam: VS T 36, HR 180, RR 60, BP 63/40, weight 1425 grams. She is lethargic, slightly toxic, and poorly perfused. Cardiac exam demonstrates tachycardia and no murmurs. Lungs are clear. Her abdomen is tympanitic, distended, and questionably tender, with hypoactive bowel sounds. Stool is guaiac positive.

Abdominal radiographs demonstrate pneumatosis intestinalis. She is made NPO and a nasogastric tube is placed to suction. Following an intravenous bolus of normal saline, her tachycardia resolves and she is placed on maintenance intravenous fluids at 150 cc/kg/day. Empiric antibiotic therapy of ampicillin and gentamicin is started. Serial abdominal radiographs and examinations are regularly performed to monitor her status. She begins to show improvement shortly after the initiation of therapy, and enteral feeding is reintroduced 10 days later. Her feedings are slowly advanced. She is discharged from the hospital at 6 weeks of age. She is evaluated for intestinal stricture later in infancy and none is found.

Necrotizing enterocolitis (NEC) is a fulminant syndrome causing bowel wall necrosis, which can lead to air in the intestinal wall, portal venous system, or peritoneal cavity (1). It occurs in 1-5% of neonatal intensive care unit admissions and is the most common GI emergency in neonates (2,3). NEC may affect the gastrointestinal (GI) tract from the stomach to the rectum, although the distal ileum and proximal colon are the segments most commonly involved (2). The incidence of this disease is 1 to 3 per 1000 live births, with 75-95% of cases occurring in premature infants (4,5). Onset is most common between 3 to 10 days of age, with the age of onset inversely related to gestational age at birth (6). The overall mortality rate in NEC may be as high as 30% (7). NEC in full-term infants is associated with a lower mortality rate than that of premature infants (5).

Prematurity and low birthweight (<1500 grams) are important risk factors for NEC. Although findings vary widely, an estimated 10% of infants with birth weights less than 1500 grams develop NEC (7). Enteral feeding is also a suspected risk factor, as more than 90% of infants who develop NEC have been enterally fed (6). Aggressive enteral feeding rates (greater than 20 cc's/kg per day) and the use of formula rather than breast milk are particularly associated with increased NEC incidence (8). Other suggested risk factors include conditions that increase the risk of infection or hypoxia, such as maternal infections during delivery, exchange transfusion via the umbilical vein, polycythemia, congenital heart disease, perinatal asphyxia, and respiratory distress (1,5).

NEC is a multifactorial disease with an unclear pathophysiology. The pathogenesis of NEC is believed to involve triggers such as bacterial colonization, intestinal ischemia, and formula feeding, that activate proinflammatory mediators (7). These mediators lead to intestinal epithelial cell necrosis and ischemic injury (secondary to vasoconstriction) (8), producing the epithelial disruption and bowel necrosis characteristic of NEC. Some of the mediators suspected to play a role include platelet activating factor, nitric oxide, and interleukin-8 (7). Infants with NEC also show increased cyclooxygenase-2 expression, suggesting involvement of this pathway (3). Rapid enteral feeding (2) and increased intraluminal pressure (1) may also contribute to intestinal damage. Immature GI tracts are especially susceptible to the proinflammatory mediator damage that appears to contribute to NEC. Intestinal defenses against inflammatory injury are not completely developed (7,8). For example, premature infants may have deficiencies in protective compounds such as erythropoietin, epidermal growth factor, and intestinal trefoil factor (7). In addition, premature infants display under-developed immunologic and digestive functions, increasing their risk of intestinal infection. Decreased small intestine motility in premature infants may also contribute to NEC by facilitating bacterial overgrowth and bowel distention (8). Although bacteria such as Pseudomonas, Klebsiella, some E. coli strains, Salmonella, and Clostridium butyricum are suspected to have a role in NEC (1), no pathogen is identified in most cases (2). The role of intestinal hypoxia in NEC has not been established (8), however, congenital heart disease or a patent ductus arteriosus may contribute to the development of NEC by reducing gut perfusion (ischemia) (9).

Early signs and symptoms of NEC involve abdominal distention with gastric retention, episodes of apnea, and vomiting (1,6). Visible blood in the stool occurs in about 25% of patients (2), while occult blood occurs more frequently. NEC often progresses rapidly and may quickly lead to intestinal perforation, shock, and septicemia (1). Pneumatosis intestinalis (gas in the bowel wall) is nearly diagnostic of NEC and is estimated to occur in about 75% of cases. Portal venous gas (PVG), another virtually pathognomonic sign, is seen about 10-30% of the time, as gas lucencies visible over the liver on x-ray, or air bubbles imaged on ultrasound. PVG usually indicates more severe disease (10).

NEC is most commonly staged using the following system proposed by Bell, et al (6,8,11):

Stage 1: Suspected NEC involving a wide range of nonspecific symptoms such as mild abdominal distention, apnea, guaiac-positive stools, lethargy, and bradycardia.

Stage 2: NEC is proven, primarily by the detection of intestinal dilatation and pneumatosis intestinalis through abdominal radiography. Stage 2 NEC mortality rates approximate 15%.

Stage 3: Advanced NEC possibly involving septic shock, respiratory and metabolic acidosis, disseminated intravascular coagulation, neutropenia, and ascites. Pneumoperitoneum may be present. The mortality rate for stage 3 NEC is approximately 60%.

One of the primary diagnostic tools in NEC is the abdominal radiograph. The abdominal radiograph may be used to detect nonspecific early signs of NEC, such as diffuse intestinal gaseous distention or asymmetric bowel gas patterns. However, its major use is to confirm or monitor for the development of NEC by detecting pneumatosis intestinalis. Suspected NEC usually warrants a series of abdominal films every 12 to 24 hours for a minimum of 2 to 3 days to monitor for pneumatosis intestinalis. Contrast enemas are not commonly used in the diagnosis of NEC, but may prove useful when abdominal radiographs are unclear. A contrast enema in an infant with NEC may display mucosal irregularity and edema (10).

The differential diagnosis of NEC includes systemic and intestinal infections, congenital intestinal obstruction (e.g., volvulus, pyloric stenosis, ileal atresia, Hirschsprung's disease), neonatal appendicitis, spontaneous bowel perforation, and pseudomembranous colitis or ecchymotic colitis (1,5,9).

Aggressive treatment is indicated in all suspected cases of NEC. Such measures include oral feeding cessation, nasogastric decompression, and intravenous fluid therapy. Systemic antibiotics, usually ampicillin or an anti-pseudomonas penicillin with an aminoglycoside, are administered following blood culture collection. Umbilical catheters should also be removed. Respiratory status, coagulation profile, and acid-base electrolyte balance should be carefully monitored. Abdominal radiographs may be taken every six hours and the patient's general condition assessed every 4-6 hours (6).

Early consultation with a surgeon is advised in all cases of NEC. Conservative treatment is insufficient in 20-40% of cases (9). Surgical procedures may include exploratory laparotomy, necrotic bowel resection, and external stoma diversion. Intraperitoneal drainage is another option that is often used on patients who may not be able to tolerate a laparotomy and resection (9). Indications for surgical intervention include failure of medical management, pneumoperitoneum (an indication of perforation), abdominal wall cellulitis, and signs of gangrenous intestine (e.g., fixed intestinal loop, ascites) (6). Mortality rates in NEC cases involving surgery range from 20-50% (9).

The elusiveness of the etiology of NEC has made it difficult to establish effective preventive measures. The use of total parenteral nutrition with slow progression to enteral feeding rather than a rapid enteral feeding protocol may be one such measure. Studies also suggest that dopamine and dobutamine may reduce the risk of NEC by improving mesenteric blood flow and cardiovascular function (9). The use of human breast milk, rather than formula, may reduce the incidence of NEC by providing phagocytic cells, lymphocytes, neutrophils, and IgA (6,8).

NEC outbreaks have been reported, and epidemic precautions and infection-control measures are indicated in a suspected outbreak. Prophylactic antibiotics have been employed in the past; however the possibility of developing resistant organisms has discouraged their routine use (8).

NEC has a recurrence rate of about 4% in infants (6). About 10% of patients will develop strictures due to scarring and fibrosis of the bowel (6). Even mild cases of NEC can result in strictures (10). Intestinal resection may lead to short bowel syndrome and the many complications associated with the prolonged use of parenteral alimentation such as central venous catheter related sepsis and thrombosis, and cholestatic jaundice (2). NEC may also lead to enterocolonic fistulas, possibly through the adherence of inflamed bowel to adjacent bowel segments or through a previously closed perforation (9).


1. True/False: The majority of patients with NEC have visible blood in the stool.

2. Which of the following has not been suspected as a risk factor for NEC?
. . . . . a. aggressive enteral feeding
. . . . . b. maternal infections during delivery
. . . . . c. dopamine administration
. . . . . d. umbilical vein catheters
. . . . . e. all of the above have been considered as risk factors

3. True/False: Prophylactic antibiotics are a commonly used measure to prevent NEC.

4. How is the reduced intestinal motility of premature infants thought to contribute to the development of NEC?

5. A premature infant is suspected to have NEC. Name three initial treatment measures that should be employed.

Related x-rays

Newborn radiographs: Available online at:

NEC radiographs: Yamamoto LG. Hematemesis in a 6-Day Old Infant. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1995, volume 2, case 14. Available online at:

Older infant with pneumatosis intestinalis: Yamamoto LG. Bloody Diarrhea and Dehydration In a 5-Month Old. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1999, volume 6, case 14. Available online at:


1. Guerrant RL, Lima AAM. Chapter 85 - Inflammatory Enteritides. In: Mandell GL, Bennett JE, Dolin R (eds). Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 5th edition. 2000, Philadelphia: Churchill Livingstone, pp. 1130-1132.

2. Stoll BJ, Kliegman RM. Chapter 98 - Digestive System Disorders. In: Behrman RE, Kliegman RM, Jenson HB (eds). Nelson Textbook of Pediatrics, 16th edition. 2000, Philadelphia: W.B. Saunders Company, pp. 513-514.

3. Chung DH, Ethridge RT, Kim S, et al. Molecular mechanisms contributing to necrotizing enterocolitis. Ann Surg 2001;233(6):835-848.

4. Sanderson IR. The physicochemical environment of the neonatal intestine. Am J Clin Nutr 1999;69(suppl):1028S-1034S.

5. Ng SCY. Necrotizing enterocolitis in the full-term neonate. J Paediatr Child Health 2001;37:1-4.

6. Kirse Coit A. Necrotizing Enterocolitis. J Perinat Neonat Nurs 1999;12(4):53-66.

7. Caplan MS, Jilling T. New concepts in necrotizing enterocolitis. Curr Opin Pediatr 2001;13(2):111-115.

8. Neu J, Weiss MD. Necrotizing Enterocolitis: Pathophysiology and Prevention. J Parenteral Enteral Nutr 1999;23(5 suppl):S13-S17.

9. Engum SA, Grosfeld JL. Necrotizing enterocolitis. Curr Opin Pediatr 1998;10(2):123-130.

10. Buonomo C. The radiology of necrotizing enterocolitis. Radiol Clin North Am 1999;37(6):1187-1191,vii.

11. Bell MJ, Ternberg J, Fengin R, et al. Neonatal necrotizing enterocolitis: Therapeutic decisions based on clinical staging. Ann Surg 1978;187:1-7.

Answers to questions

1. False, an estimated 25% show visible bloody stool.

2. c. Dopamine may actually reduce the risk of NEC by increasing mesenteric blood flow.

3. False, the development of resistant organisms presently discourages routine prophylactic antibiotic use.

4. Reduced intestinal motility increases the chances of bacterial overgrowth.

5. Acceptable answers include: 1) oral feeding cessation, 2) nasogastric decompression, 3) intravenous fluid therapy, 4) systemic antibiotics, 5) umbilical catheter removal, 6) acid-base electrolyte balance monitoring, 7) early consultation with a surgeon.

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