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 2.
Anteroposterior image shows necrotizing enterocolitis with pneumatosis intestinalis.
Image 3.
Lateral abdominal image shows pneumatosis intestinalis.
Image 4.
Portal venous air is present in a patient with pneumatosis intestinalis.
Necrotizing enterocolitis (NEC) is a serious gastrointestinal disease of neonates. Its etiology is unknown. NEC is characterized by mucosal or transmucosal necrosis of part of the intestine. Infants born before term who are undersized and ill are most susceptible to NEC; the incidence of NEC is increasing because of the improved survival rate in the high-risk group of premature infants.1,2,3,4 (See Images 1-4 above.)
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Necrotizing Enterocolitis (from Pediatrics, Cardiac Disease and Critical Care Medicine)
Necrotizing Enterocolitis: Surgical Perspective
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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
More on Necrotizing Enterocolitis |
 Overview: Necrotizing Enterocolitis |
| Imaging: Necrotizing Enterocolitis |
| Multimedia: Necrotizing Enterocolitis |
| References |
| Further Reading |
| Next Page » |
References
Chung DH, Ethridge RT, Kim S, Owens-Stovall S, Hernandez A, Kelly DR, et al. Molecular mechanisms contributing to necrotizing enterocolitis. Ann Surg. Jun 2001;233(6):835-42. [Medline].
Claud EC, Walker WA. Hypothesis: inappropriate colonization of the premature intestine can cause neonatal necrotizing enterocolitis. FASEB J. Jun 2001;15(8):1398-403. [Medline].
Di Lorenzo M, Krantis A. Altered nitric oxide production in the premature gut may increase susceptibility to intestinal damage in necrotizing enterocolitis. J Pediatr Surg. May 2001;36(5):700-5. [Medline].
Duro D, Kamin D, Duggan C. Overview of pediatric short bowel syndrome. J Pediatr Gastroenterol Nutr. Aug 2008;47 Suppl 1:S33-6. [Medline].
Hunter CJ, Upperman JS, Ford HR, Camerini V. Understanding the Susceptibility of the Premature Infant to Necrotizing Enterocolitis (NEC). Pediatr Res. Dec 10 2007;[Medline].
Manogura AC, Turan O, Kush ML, Berg C, Bhide A, Turan S. Predictors of necrotizing enterocolitis in preterm growth-restricted neonates. Am J Obstet Gynecol. Jan 11 2008;[Medline].
Buchheit JQ, Stewart DL. Clinical comparison of localized intestinal perforation and necrotizing enterocolitis in neonates. Pediatrics. Jan 1994;93(1):32-6. [Medline].
Casey L, Lee KH, Rosychuk R, Turner J, Huynh HQ. 10-year review of pediatric intestinal failure: clinical factors associated with outcome. Nutr Clin Pract. Aug-Sep 2008;23(4):436-42. [Medline].
Cakmak Celik F, Aygun C, Cetinoglu E. Does early enteral feeding of very low birth weight infants increase the risk of necrotizing enterocolitis?. Eur J Clin Nutr. Nov 28 2007;[Medline].
Premji S, Chessell L. Continuous nasogastric milk feeding versus intermittent bolus milk feeding for premature infants less than 1500 grams. Cochrane Database Syst Rev. 2001;(1):CD001819. [Medline].
Ververidis M, Kiely EM, Spitz L, Drake DP, Eaton S, Pierro A. The clinical significance of thrombocytopenia in neonates with necrotizing enterocolitis. J Pediatr Surg. May 2001;36(5):799-803. [Medline].
Hunter CJ, Petrosyan M, Ford HR, Prasadarao NV. Enterobacter sakazakii: An Emerging Pathogen in Infants and Neonates. Surg Infect (Larchmt). Aug 7 2008;[Medline].
Gagliardi L, Bellù R, Cardilli V, De Curtis M. Necrotising enterocolitis in very low birth weight infants in italy: incidence and non-nutritional risk factors. J Pediatr Gastroenterol Nutr. Aug 2008;47(2):206-10. [Medline].
Bury RG, Tudehope D. Enteral antibiotics for preventing necrotizing enterocolitis in low birthweight or preterm infants. Cochrane Database Syst Rev. 2001;(1):CD000405. [Medline].
Sigalet DL. Short bowel syndrome in infants and children: an overview. Semin Pediatr Surg. May 2001;10(2):49-55. [Medline].
Ng E, Shah VS. Erythromycin for the prevention and treatment of feeding intolerance in preterm infants. Cochrane Database Syst Rev. Jul 16 2008;CD001815. [Medline].
Saxena A, Galwa RP. Sonographic findings and outcome in necrotizing enterocolitis. Pediatr Radiol. Nov 2007;37(11):1180. [Medline].
Further Reading
Evidence-based care guideline for necrotizing enterocolitis (NEC) among very low birth weight infants.
Cincinnati Children's Hospital Medical Center. 2005 Jul 14 (revised 2007 Feb). 12 pages. NGC:005522
Keywords
necrotizing enterocolitis, NEC, neonatal colitis, neonatal enteritis, necrotic appendicitis of the newborn, neonatal gastrointestinal disease, complication of prematurity
