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PubMed2001

Controversies in the management of necrotizing enterocolitis.

BACKGROUND: Necrotizing enterocolitis (NEC) is the most frequent and lethal disease that affects the gastrointestinal tract of the premature infant. Controversy persists as to the most appropriate management once the diagnosis is confirmed. METHODS: Review of the pertinent medical literature. RESULTS: The incidence of NEC is increasing, but the survival rate is not. Initial management of NEC consists of bowel rest, orogastric decompression, intravenous hydration, and broad-spectrum antibiotics; surgical intervention is typically reserved for infants with advanced disease or evidence of intestinal perforation. There is no consensus in the literature regarding the optimal treatment strategy for patients who require surgical intervention. There exists a lack of randomized trials comparing definitive intestinal resection with or without primary anastomosis, intestinal diversion with limited resection, or peritoneal drainage without resection. CONCLUSION: An individualized approach must be taken to achieve optimum survival for patients with NEC. Isolated perforation, in our opinion, is best managed with resection and enterostomy, whereas pan-intestinal involvement is best managed with proximal diversion alone.

Attitude of Health Personnel↗
PubMed2001

Hypothesis: inappropriate colonization of the premature intestine can cause neonatal necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a major cause of morbidity in preterm infants. We hypothesize that the intestinal injury in this disease is a consequence of synergy among three of the major risk factors for NEC: prematurity, enteral feeding, and bacterial colonization. Together these factors result in an exaggerated inflammatory response, leading to ischemic bowel necrosis. Human milk may decrease the incidence of NEC by decreasing pathogenic bacterial colonization, promoting growth of nonpathogenic flora, promoting maturation of the intestinal barrier, and ameliorating the proinflammatory response.

Digestive System↗
PubMed2005

Matrilysins-1 and -2 (MMP-7 and -26) and metalloelastase (MMP-12), unlike MMP-19, are up-regulated in necrotizing enterocolitis.

OBJECTIVES: Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants characterized histologically by extensive tissue injury and inflammation. Matrix metalloproteinases (MMP) are involved in tissue remodeling and cell migration, both being important aspects of inflammatory disease. The aim of this study was to investigate whether MMPs play a role in the pathogenesis of NEC. METHODS: Expression of MMP-1, -7, -9, -10, -12, -19 and -26 was studied using in situ hybridization/immunohistochemistry in samples intestinal tissue removed from 15 patients with NEC; in 7 of them control samples were obtained at closure of stomas. Six intestinal samples from patients with intestinal atresia and four samples of necrosis were also included in the material examined. Laminin-5 was immunostained to find migrating enterocytes and cytokeratin to delineate mucosal epithelium. RESULTS: MMP-7 protein was upregulated in the epithelium of 12/18 NEC samples. MMP-26 was induced in stromal cells of 12/17 NEC specimens. Stromal expression was found for MMP-1 and -12 mRNAs in 7/18 samples. MMP-1 was also detected in the epithelium of regenerating areas. Both NEC and stoma samples expressed MMP-9 in inflammatory cells. Epithelial MMP-19 was downregulated in NEC. CONCLUSIONS: Our results suggest that several MMPs may be major factors in tissue destruction and remodeling in NEC. Targeted inhibition of matrilysins, using synthetic MMP inhibitors or blockers of their signal transduction pathways, may represent a novel therapeutic option for the treatment of intestinal inflammation associated with NEC.

Case-Control Studies↗
PubMed2002

Role of platelet-activating factor in the pathophysiology of necrotizing enterocolitis.

UNLABELLED: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal illness that affects predominantly preterm infants. Treatment options are limited and NEC remains a significant cause of morbidity and mortality. The precise aetiology of NEC remains unclear but evidence strongly suggests that the cause is multifactorial and there are four main aetiological factors: prematurity, hypoxia, enteral feeding and bacterial colonization. The presence of similar intestinal lesions, regardless of aetiological trigger, strongly implicates a final common pathway in the pathogenesis. There is now a substantial body of evidence to indicate that endogenous inflammatory mediators, particularly platelet-activating factor (PAF), play a vital role in this final pathway. CONCLUSION: The use of agents that antagonize PAF may provide therapeutic options in the management of NEC.

Animals↗
PubMed2003

The role of dietary supplementation with L-glutamine in inflammatory mediator release and intestinal injury in hypoxia/reoxygenation-induced experimental necrotizing enterocolitis.

BACKGROUND/AIMS: Necrotizing enterocolitis (NEC) is a multifactorial syndrome in the neonate. Enteral feeding practices are an important component of gastrointestinal injury in neonatal NEC. In the present study, we examined the protective effect of oral supplementation with L-glutamine, an important specific fuel for the enterocytes, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. METHODS: Young mice were divided into four groups: group 1 mice (untreated) underwent H/R; group 2 mice were supplemented with L-glutamine in drinking water (0.5 g/dl) for 3 days, and group 3 mice were supplemented with L-glutamine (3 g/dl) for 10 days. Group 4 mice served as control. Hypoxia was induced by placing the young mice in a 100% CO(2) chamber for 5 min. After hypoxia, they were reoxygenated for 10 min with 100% oxygen. We examined the intestinal lesions with light microscopy and measured intestinal generation of PAF and TNF-alpha in the H/R-induced model of NEC. RESULTS: In group 3 mice, NEC-induced intestinal tissue damage was greatly attenuated with necrosis limited partially to the mucosa. Both intestinal tissue PAF and TNF-alpha concentrations were significantly higher in the untreated group than in controls (p < 0.001). Group 3 mice (3 g/dl supplemented) showed a significant decrease in intestinal TNF-alpha concentration compared with young group 1 and group 2 mice (p < 0.05 and p < 0.05, respectively). On the other hand, no significant difference was observed in the intestinal generation of PAF between H/R groups (p > 0.05). CONCLUSION: The present study suggests that H/R plays an important role in the pathogenesis of NEC and supports the hypothesis that especially PAF and TNF-alpha are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with L-glutamine reduces the histologic evidence of H/R-induced intestinal injury. Based on these findings, beneficial effects of L-glutamine in this model of NEC are mediated via mechanisms inhibiting intestinal cytokine release.

Administration, Oral↗
PubMed2000

Intestinal transplantation for short gut syndrome attributable to necrotizing enterocolitis.

BACKGROUND: Necrotizing enterocolitis (NEC) is a life-threatening condition of the neonatal age, which frequently requires surgical intervention. After extensive bowel resection, a small proportion of these patients may develop chronic short gut syndrome (SGS) and require chronic total parenteral nutrition (TPN) use. Intestinal transplantation has been performed in these patients as a life-saving option. This study reviews our experience with intestinal transplantation for SGS attributable to NEC emphasizing the mode of presentation, natural history, timing, and outcome. METHODS: A retrospective chart review was performed for all pediatric patients who underwent small bowel transplantation for NEC at the University of Miami between August 1994 and March 1999. RESULTS: Eleven transplants were performed for 10 patients with NEC (8 male and 2 female; median age: 1.75 years [range: 10 months to 10. 1 years]). Procedures performed were isolated intestinal transplants (n = 2), combined liver-intestinal transplants (n = 6), and multivisceral transplants (n = 3). All patients were born prematurely with median birth weight of 1.640 kg (range: 810 g to 2. 730 kg). They developed NEC in the first few days of life and subsequently underwent an average of 5 surgeries per patient before transplant. Transplant was indicated for liver failure in 8 patients and recurrent central line sepsis in 2 others. At present, 6 patients are alive with an overall 1-year and 3-year actuarial survival of 60% and a median follow-up of 29 months (range: 9-46 months). Six children have been weaned off TPN after a median time of 71 days (range: 19-131) from transplantation. All survivors are at home with functional grafts. CONCLUSION: Intestinal transplantation provided a reasonable outcome in patients with NEC-associated SGS who had already developed life-threatening complications related to TPN. Intestinal transplantation replaced the diseased intestine and liver, enfranchised patients from TPN, and conferred improved quality of life. These patients should be actively considered for intestinal transplantation and referred to a transplant center as soon as possible.

Child↗
PubMed2005

Neurodevelopmental and growth outcomes of extremely low birth weight infants after necrotizing enterocolitis.

OBJECTIVES: Necrotizing enterocolitis (NEC) is a significant complication for the premature infant. However, subsequent neurodevelopmental and growth outcomes of extremely low birth weight (ELBW) infants with NEC have not been well described. We hypothesized that ELBW infants with surgically managed (SurgNEC) are at greater risk for poor neurodevelopmental and growth outcomes than infants with medically managed NEC (MedNEC) compared with infants without a history of NEC (NoNEC). The objective of this study was to compare growth, neurologic, and cognitive outcomes among ELBW survivors of SurgNEC and MedNEC with NoNEC at 18 to 22 months' corrected age. METHODS: Multicenter, retrospective analysis was conducted of infants who were born between January 1, 1995, and December 31, 1998, and had a birth weight <1000 g in the National Institute of Child Health and Human Development Neonatal Research Network Registry. Neurodevelopment and growth were assessed at 18 to 22 months' postmenstrual age. chi2, t test, and logistic regression analyses were used. RESULTS: A total of 2948 infants were evaluated at 18 to 22 months, 124 of whom were SurgNEC and 121 of whom were MedNEC. Compared with NoNEC, both SurgNEC and MedNEC infants were of lower birth weight and had a greater incidence of late sepsis; SurgNEC but not MedNEC infants were more likely to have received a diagnosis of cystic periventricular leukomalacia and bronchopulmonary dysplasia and been treated with postnatal steroids. Weight, length, and head circumference <10 percentile at 18 to 22 months were significantly more likely among SurgNEC but not MedNEC compared with NoNEC infants. After correction for anthropometric measures at birth and adjusted age at follow-up, all growth parameters at 18 to 22 months for SurgNEC but not MedNEC infants were significantly less than for NoNEC infants. SurgNEC but not MedNEC was a significant independent risk factor for Mental Developmental Index <70 (odds ratio [OR]: 1.61; 95% confidence interval [CI]: 1.05-2.50), Psychomotor Developmental Index <70 (OR: 1.95; 95% CI: 1.25-3.04), and neurodevelopmental impairment (OR: 1.78; 95% CI: 1.17-2.73) compared with NoNEC. CONCLUSIONS: Among ELBW infants, SurgNEC is associated with significant growth delay and adverse neurodevelopmental outcomes at 18 to 22 months' corrected age compared with NoNEC. MedNEC does not seem to confer additional risk. SurgNEC is likely to be associated with greater severity of disease.

Cerebral Palsy↗
PubMed1997

[Necrotizing enterocolitis (NEC)].

Necrotizing enterocolitis is a serious abdominal disease in infants during the first 2 months of life. The earliest radiographic finding on frontal abdominal films is initially distension of the small bowel, secondly of the colon, and pneumatosis intestinalis. Pneumatosis intestinalis is not pathognomonic for necrotizing enterocolitis; it can occur throughout life in different abdominal diseases. It can be a serious prognostic sign for abdominal ileus, but it may also occur in non-critically ill patients. Radiographic diagnosis in childhood is achieved with a frontal film of the abdomen in the prone position, and to detect a possible perforation, a left lateral abdominal decubitus exposure is necessary. Sonography and duplex sonography are helpful in evaluating progressive changes, the clinical course and the differential diagnosis.

Diagnosis, Differential↗
PubMed1996

Intestinal glycosaminoglycans in neonatal necrotizing enterocolitis.

Advanced necrotizing enterocolitis (NEC) is a common neonatal surgical emergency of unknown aetiology. Despite improvements in the prognosis, the aggressive form of the disease is still associated with significant rates of morbidity and mortality. Recent evidence indicates that the extracellular matrix (ECM) is important in gastrointestinal development and glycosaminoglycans, major constituents of the ECM, are attenuated in inflammatory bowel disease. The hypothesis of this study was that changes in the nature and distribution of intestinal glycosaminoglycans occur in NEC. The distribution and nature of glycosaminoglycans were determined in 31 sections of well preserved resection margins and severely diseased bowel from eight neonates affected by NEC. An established histological method of glycosaminoglycans analysis using cationic gold with silver enhancement was employed in this study. The identity of specific glycosaminoglycans was also elucidated using a combination of cationic gold staining and glycanase digestion. In well preserved tissue, staining was seen throughout the full thickness of the bowel. The epithelial basement membrane and basolateral surfaces, lamina propria and submucosa were particularly prominent. In moderate disease, patchy loss of anionic sites was frequently observed with glycosaminoglycans-deficient areas adjacent to intact sites. In severe NEC, there was extensive loss of glycosaminoglycans in most of the sections examined. Glycanase analysis revealed that the glycosaminoglycans in well preserved tissue were sensitive to chondroitinase ABC and only vascular sites were sensitive to heparinase III. The consequences of glycosaminoglycans loss in NEC as demonstrated in this study are not known but modulation of gastrointestinal glycosaminoglycans could be important in the pathogenesis of NEC and may underlie some of the clinical manifestations of this condition.

Colon↗
PubMed1984

Laboratory basis for the medical management of necrotizing enterocolitis (NEC).

Necrotizing enterocolitis (NEC) is a serious condition affecting the neonate that may be responsive to medical management. This study evaluates the efficacy of supplemental oxygen (FiO2 40% and 50%), systemic antibiotics (ampicillin and gentamicin, cephamandole) and oral antibiotics (trimethoprim-sulfamethoxazole, neomycin and gentamicin) in a weanling rat bowel ischemia model induced by a transient (one minute) occlusion of the superior mesenteric artery. Animals were evaluated for overall survival, duration of survival, presence of bowel necrosis or perforation at seven days. Mortality in ischemic controls was 83.8%. This was reduced to 52% by FiO2 of 50%, and 40% with systemic ampicillin and gentamicin (with or without FiO2 50%) (P less than .001). Length of survival was 3.4 days in controls and increased from 5.4 to 5.9 days in rats given FiO2 50% and/or ampicillin and gentamicin (P less than .001). The incidence of bowel necrosis in controls was 60% and was reduced to 25% in rats given systemic ampicillin and gentamicin and 23.3% with 50% FiO2 and the same antibiotics (P less than .001). Systemic cephamandole and oral antibiotics had no beneficial effects.

Animals↗
PubMed1998

Alterations in respiratory status: early signs of severe necrotizing enterocolitis.

BACKGROUND: Necrotizing enterocolitis (NEC) presents with well-recognized signs of intestinal inflammation such as bilious vomiting, bloody stool, abdominal distension, and tenderness. The authors observed otherwise unexplained changes in the respiratory status requiring increased respiratory support during the 24 hours before direct evidence of the intestinal disorder in patients with severe NEC. METHODS: To study this observation the authors collected data on 10 consecutive patients in whom NEC required an operation. RESULTS: Eight of these patients were recovering from respiratory distress syndrome (RDS). During the 24 hours before any direct sign of intestinal dysfunction seven of these eight had a respiratory prodrome needing increased respiratory support. Two patients required intubation and mechanical ventilation. Five needed increased supplemental oxygen. This prodrome included decreased oxygenation in seven, increased respiratory rate in five, and increased PCO2 in five, preceded by hypocarbia in three. CONCLUSIONS: These changes in the respiratory condition revisit the concept of high output respiratory failure. This term was introduced to describe the respiratory failure in adult patients who suffer acute intestinal illness. Increased metabolic demand from the intestinal illness was thought to stress the ability of the patient to delivery oxygen and remove carbon dioxide. The ability of the respiratory system to meet the increased demands is limited by the intestinal dysfunction itself (abdominal pain and distension). In our patients recovering from RDS the pulmonary reserve is inherently limited. Because they are carefully monitored, it is easy to retrieve evidence of respiratory changes that precede the direct signs of intestinal disease. In the earliest stages of intestinal illness before the direct signs of intestinal dysfunction, these patients often manifest unexplained signs of respiratory compensation and decompensation and require increased respiratory support. Regardless of the pathophysiology, these alterations in respiratory status represent an early warning sign of NEC.

Enterocolitis, Pseudomembranous↗
PubMed1994

The radiology of necrotizing enterocolitis.

Imaging of necrotizing enterocolitis is frustrating, with no single imaging test that is both sensitive and specific for the diagnosis. Early, nonspecific findings on plain abdominal films before development of pneumatosis intestinalis is enough evidence in the proper clinical setting to institute medical treatment of necrotizing enterocolitis. Subsequent development of pneumatosis intestinalis will help confirm the clinical diagnosis, but treatment should not be withheld for its development. Delayed complications of necrotizing enterocolitis can be diagnosed by contrast enema examinations, and ultrasound is a helpful additional test in equivocal cases.

Abdomen↗
PubMed2004

Necrotizing enterocolitis: preventative strategies.

Necrotizing enterocolitis (NEC) remains a major cause of morbidity and mortality in premature infants. Although the pathogenesis of NEC is unclear, prevention strategies have been developed based on clinical observations and epidemiologic and experimental data. Most current strategies have centered on feeding practices (eg, institution of feeds, advancement of feeds, composition of feeds, and standardization of feeding practices). Emerging strategies include amino acid supplementation, the use of platelet-activating factor(PAF) antagonists or PAF-acetylhydrolase administration, polyunsaturated fatty acid administration, epidermal growth factor administration, and the use of pre- and probiotics.

Administration, Oral↗
PubMed2003

Current controversies in the understanding of necrotizing enterocolitis. Part 1.

Necrotizing enterocolitis (NEC) has widespread implications for neonates. While mostly affecting preterm neonates, full-term neonates, especially those with congenital heart disease, are also at risk. Although the exact pathogenesis of NEC remains elusive, three major factors, a pathogenic organism, enteral feedings, and bowel compromise, coalesce in at-risk neonates to produce bowel injury. Initiation of the inflammatory cascade likely serves as a common pathway for the disorder. Clinical signs and symptoms range from mild feeding intolerance with abdominal distension to catastrophic disease with bowel perforation, peritonitis, and cardiovascular collapse. Vigilant assessment of at-risk neonates is crucial. When conservative medical management fails to halt injury, surgical intervention is often needed. Strategies to decrease the incidence and ultimately prevent NEC loom on the horizon, such as exclusive use of human breastmilk for enteral feedings and administration of probiotics.

Australia↗
PubMed2006

Bile acids induce ileal damage during experimental necrotizing enterocolitis.

BACKGROUND & AIMS: Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of premature infants. While the effect of bile acids (BAs) on intestinal mucosal injury is known, we investigated the contribution of BAs during the development of NEC in neonatal rats. METHODS: Premature rats were fed with cow's milk-based formula and subjected to asphyxia and cold stress to develop NEC. Jejunal and ileal luminal BAs, portal blood BAs, and messenger RNA and protein for the apical sodium-dependent bile acid transporter, the ileal bile acid binding protein, and the heteromeric organic solute transporter (Ostalpha/Ostbeta)were evaluated. RESULTS: Ileal luminal BAs levels were increased significantly during disease development and the removal of ileal BAs significantly decreased the incidence and severity of disease. Furthermore, when NEC was reduced via treatment with epidermal growth factor (EGF), BA levels were reduced significantly. Jejunal luminal BA levels were similar between animals with NEC and controls, but portal/ileal luminal BA ratios were decreased significantly in animals with NEC. The apical sodium-dependent bile acid transporter was up-regulated at the site of injury in animals with NEC and decreased after EGF treatment; however, the ileal bile acid binding protein was up-regulated only in the NEC and EGF group. Ostalpha/Ostbeta expression was low in all groups, and only slightly increased in the NEC group. CONCLUSIONS: These data strongly suggest that BAs play a role in the development of ileal damage in experimental NEC and that alterations in BA transport in the neonatal ileum may contribute to disease development.

Animals↗
PubMed1999

Klebsiella pneumoniae with extended spectrum beta-lactamase activity associated with a necrotizing enterocolitis outbreak.

BACKGROUND: Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in newborn infants, affecting primarily premature neonates. Clustering of cases in epidemics is well-described; many are associated with an identifiable pathogen. PATIENTS AND METHODS: Case reports are presented of six neonates seen with NEC during a 2-month period in 1998. All bacterial isolates were subjected to antibiotic testing, determination of MIC and molecular fingerprinting. RESULTS: Klebsiella pneumoniae with extended spectrum beta-lactamase production was isolated from blood cultures of all six patients. In five patients the isolate appeared to be a single clone. The onset of NEC in the patients was earlier, more rapid and more severe than usual. Four of the six required surgery and five required mechanical ventilation. Two of the six patients died, but only one was directly related to a complication of NEC. All of the patients developed severe thrombocytopenia (platelet count <20 x 10(9)/l), and three developed hepatitis. The K. pneumoniae proved difficult to eradicate. Extended courses of multiple antibiotics were administered and measures were introduced to reduce overcrowding and improve infection control. CONCLUSION: The isolation of a single clone of K. pneumoniae with extended spectrum of beta-lactamase activity during an NEC outbreak highlights the need for strict infection control. This organism caused significant morbidity and was difficult to treat.

Anti-Bacterial Agents↗
PubMed2005

Neonatal necrotizing enterocolitis: an update.

Necrotizing enterocolitis (NEC) is a leading cause of mortality and morbidity in neonatal intensive care units. Here we review selected manifestations of NEC, risk factors involved in its pathophysiology as well as putative mechanisms associated with how an immature gut might be more susceptible to NEC. Treatment and potential preventive strategies are discussed.

Diagnosis, Differential↗