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PubMed2001

Pneumoperitoneum: an absolute indication for surgery in infants with necrotizing enterocolitis?: Report of a case.

It is generally agreed that neonates with necrotizing enterocolitis (NEC) and pneumoperitoneum should be treated surgically. We report herein the case of a 3-day-old male newborn with NEC in whom a pneumoperitoneum subsequently developed without any cause found at laparotomy. This case is presented to discuss the nonsurgical management of pneumoperitoneum in selected patients.

Emergencies↗
PubMed2005

Portal venous gas and surgical outcome of neonatal necrotizing enterocolitis.

PURPOSE: The prognostic significance of portal venous gas (PVG) in neonatal necrotizing enterocolitis (NEC) for operative intervention (OP), neonatal complications, and mortality remains uncertain. The authors designed a long-term prospective study to describe the natural history of PVG related to these outcomes and to test the hypothesis that PVG does not mandate OP. METHODS: All infants admitted to a single center between October 1991 and February 2003 were evaluated weekly to identify all cases of NEC (defined as Bell stage II or higher). Demographic, radiological, surgical, and outcome data were abstracted prospectively. Radiographic studies were performed at the onset of illness and at subsequent 6- to 8-hour intervals or as clinically indicated. A single pediatric radiologist reviewed all radiographs. Values are expressed as mean +/- SD. Odds ratios and relative risk ratios are reported with 95% CIs. The level of significance was P < or = .05. RESULTS: After the exclusion of 24 infants with lethal diseases, major congenital or chromosomal anomalies, or recurrent episodes of NEC, 194 of 5891 infants developed NEC. The overall incidence of NEC was 3.7%. In 194 infants with NEC, the incidence of PVG was 33% (n = 64). Gestational age (30.8 +/- 4 vs 29.3 +/- 4.2 weeks; P = .02) but not birth weight (1609 +/- 761 vs 1434 +/- 810 g; P = NS) was greater in infants with PVG compared with infants without PVG (n = 130). Sixty-six (34%) infants with NEC underwent OP. Operative intervention occurred more frequently in infants with PVG compared with infants without PVG (OR, 2.5; CI, 1.37-4.76; P = .003)--only 48% of infants with PVG underwent OP. Among the variables, gestational age, severe NEC (Bell stage III), severe intramural gas (in all 4 abdominal quadrants), and the presence of PVG, severe NEC was most highly associated with OP (OR, 77.47; CI, 10.36-580.16; P < .0001). Bell stage III NEC was present in 98% of infants who underwent OP compared with 40% of infants without OP ( P < .0001). Of all infants with NEC, 37 (19%) died. Mortality was higher among infants who underwent OP (33% vs 12%; P < .0003). A multivariate regression model identified Bell stage III (OR, 3.74; CI, 1.20-11.62; P = .02), but neither PVG nor OP, to be significantly associated with mortality. Of interest is that survival in infants with PVG was greater (but not significantly so) than in infants without PVG in both OP (74% vs 59%) and non-OP (91% vs 87%) groups. Furthermore, 30 of 64 (47%) infants with PVG survived without OP, and of all 33 infants with PVG who did not undergo OP, 30 (91%) infants survived. CONCLUSIONS: Decision for OP should be based on the severity of NEC and not on the presence of PVG alone because nearly half of infants with PVG survive without OP. Overall, the presence of PVG does not increase the risk of mortality among infants with NEC. Severe NEC, but not OP, is associated with higher mortality.

Chi-Square Distribution↗
PubMed2005

Ischemia and necrotizing enterocolitis: where, when, and how.

While it is accepted that ischemia contributes to the pathogenesis of necrotizing enterocolitis (NEC), three important questions regarding this role subsist. First, where within the intestinal circulation does the vascular pathophysiology occur? It is most likely that this event begins within the intramural microcirculation, particularly the small arteries that pierce the gut wall and the submucosal arteriolar plexus insofar as these represent the principal sites of resistance regulation in the gut. Mucosal damage might also disrupt the integrity or function of downstream villous arterioles leading to damage thereto; thereafter, noxious stimuli might ascend into the submucosal vessels via downstream venules and lymphatics. Second, when during the course of pathogenesis does ischemia occur? Ischemia is unlikely to the sole initiating factor of NEC; instead, it is more likely that ischemia is triggered by other events, such as inflammation at the mucosal surface. In this context, it is likely that ischemia plays a secondary, albeit critical role in disease extension. Third, how does the ischemia occur? Regulation of vascular resistance within newborn intestine is principally determined by a balance between the endothelial production of the vasoconstrictor peptide endothelin-1 (ET-1) and endothelial production of the vasodilator free radical nitric oxide (NO). Under normal conditions, the balance heavily favors NO-induced vasodilation, leading to a low resting resistance and high rate of flow. However, factors that disrupt endothelial cell function, eg, ischemia-reperfusion, sustained low-flow perfusion, or proinflammatory mediators, alter the ET-1:NO balance in favor of constriction. The unique ET-1-NO interaction thereafter might facilitate rapid extension of this constriction, generating a viscous cascade wherein ischemia rapidly extends into larger portions of the intestine.

Endothelin-1↗
PubMed2002

Revisiting ischemia and reperfusion injury as a possible cause of necrotizing enterocolitis: Role of nitric oxide and superoxide dismutase.

BACKGROUND/PURPOSE: The pathogenesis of necrotizing enterocolitis (NEC) is unknown. Ischemia and reperfusion (I/R) injury has been considered a major contributing factor. Nitric oxide (NO) and superoxide dismutases (SODs) have been shown to protect bowel from I/R injury. This study aims to assess (1) the ability of premature intestine to resist I/R injury compared with mature intestine and (2) the possible role of NO and SODs in modulating such response. METHODS: Intestines from 5 groups of rats (n = 6 for each study group) were studied: (1) premature, gestational age 20 days; (2) premature, gestational age 22 days; (3) full-term, newborn; (4) infant, day 15; (5) infant, day 30. EXPERIMENTS: (1) The degrees of I/R injury after 0, 30, 60, 90 and 120 minutes, respectively, of ischemia and 25 minutes of I/R were assessed histologically by a pathologist who was unaware of the operative details. (2) Tissue NO and copper levels were measured by electroparamagnetic resonance (EPR) study; and nitric oxide synthases, copper zinc (CuZn) SODs and manganese (Mn) SODs were examined immunohistochemically. (3) and (4) I/R injury was assessed in rats that had received intraperitoneal injections of L-arginine (NO donor) and L-NAME (NO antagonist), respectively. RESULTS: For premature (1,2), newborn (3) and mature (4,5) intestines, grades of injury at maximum I/R period studied (120 minutes of ischemia, 25 minutes of reperfusion) were 0, 0, and 3, respectively (P <.05); NO levels were 1 u +/- 1.5, 3 +/- 2.5, and 22 u +/- 3.5, respectively (P <.05); Cu levels were 150 u +/- 15, 200 u +/- 41 and 12 u +/- 2, respectively (P <.05); NOS in intestines were +, +, +++ and CuZnSODs were ++, +++, +, respectively; and MnSODs were +++, ++, -, respectively. No change in NO levels was detected in groups (1), (2), or (3) after L-arginine and L-NAME injections. CONCLUSIONS: Premature rat intestine is highly resistant to I/R injury, which may indicate that I/R alone, in the absence of other predisposing factors (eg, bacterial colonization) may not be sufficient in causing NEC. Nitric oxide does not have a protective role for immature and newborn intestines in I/R as in mature intestine. The high level of SODs of the immature and newborn intestine may play an important role in its high resistance to I/R injury.

Animals↗
PubMed2005

Comparative study between isolated intestinal perforation and necrotizing enterocolitis.

INTRODUCTION: Intestinal perforations in the neonatal period are usually related to necrotizing enterocolitis (NEC) or intestinal occlusion. Intestinal perforation in the absence of these conditions is called isolated perforation (IP). Several risk factors and pathogenic mechanisms have been suggested, and most of them are common to those classically attributed to NEC. AIM: To identify and compare the clinical and pathological features of IP and NEC. MATERIAL AND METHODS: We reviewed all cases of neonatal intestinal perforation and NEC in the last five years. Thirty-three patients were retrospectively classified into Group NEC: 24 cases, and Group IP: 9 cases. We collected multiple data as study variables: 1) General features; 2) Obstetric history; 3) Neonatal treatment; 4) Comorbidity; 5) Perforation features; 6) Treatment and outcome. RESULTS: Comparing the groups, we found statistical significant differences in isolated perforation cases with these risk factors: extreme prematurity, very low birth weight, abruptio placenta, intubation and neonatal mechanical ventilation, umbilical catheterization, precocious sepsis, and indomethacin therapy. A more precocious operation and a good prognosis also reached statistical significance. In the other hand, we found statistically significant differences in NEC with congenital cardiopathy (excluding isolated patent ductus arteriosus), with intestinal pneumatosis, with diffuse bowel involvement and a worse prognosis. Risk factors and pathologic findings seem to support an ischaemic pathogenesis in both diseases.

Enterocolitis, Necrotizing↗
PubMed2004

Necrotizing enterocolitis: the evidence for use of human milk in prevention and treatment.

Necrotizing enterocolitis (NEC) is one of the diagnoses for which donor human milk is regularly prescribed. The role of human milk in both prevention and treatment of NEC has long been recognized. Human milk, whether mother's own or donor, provides significant protection against many of the known risk factors of NECas well as therapeutic protection for the infant recovering from NEC. In the absence of mother's own milk, donor human milk could be life saving to fragile preterm infants, who are at highest risk of developing NEC.

Adult↗
PubMed2000

Necrotizing enterocolitis in neonates with congenital heart disease: risk factors and outcomes.

OBJECTIVE: Necrotizing enterocolitis (NEC) is primarily a disease of the premature infant. Among children born at term, however, congenital heart disease may be an important predisposing factor for this condition. To determine risk factors for NEC in patients with congenital heart disease, we conducted a case-control study of neonates with cardiac disease admitted to the cardiac intensive care unit at our center during the 4-year period from January 1995 to December 1998. METHODS: Cardiac diagnosis and age at admission were analyzed for association with NEC among the 643-patient inception cohort. Demographic, preoperative, and operative variables were recorded retrospectively in 21 neonates with congenital heart disease who developed NEC and 70 control neonates matched by diagnosis and age at admission. Using parametric and nonparametric analysis, cases and controls were compared with respect to previously identified risk factors for NEC. RESULTS: Among the entire cohort of 643 neonates with heart disease admitted to the cardiac intensive care unit, diagnoses of hypoplastic left heart syndrome (odds ratio [OR] = 3.8 [1.6-9.1]) and truncus arteriosus or aortopulmonary window (OR = 6.3 [1.7-23.6]) were independently associated with development of NEC by multivariable analysis. In the case-control analysis, earlier gestational age at birth (36.7 +/- 2. 7 weeks vs 38.1 +/- 2.3 weeks), prematurity (OR = 3.9 [1.2-12.5]), highest dose of prostaglandin >0.05 microg/kg/minute (OR = 3.9 [1. 2-12.5]), and episodes of low cardiac output (meeting specific laboratory criteria) or clinical shock (OR = 6.5 [1.8-23.5]) correlated with the development of NEC. Earlier gestational age and episodes of low output were the only factors that remained significantly associated with NEC by multivariable analysis. Although there was no difference in hospital mortality between patients with and without NEC, mean hospital stay was significantly longer in those who developed NEC (36 +/- 22 days vs 19 +/- 14 days). CONCLUSIONS: The risk of NEC in neonates with congenital heart disease is substantial. Factors associated with an elevated risk of NEC in infants with heart disease include premature birth, hypoplastic left heart syndrome, truncus arteriosus, and episodes of poor systemic perfusion or shock. Heightened suspicion is warranted in newborns with these risk factors.

Case-Control Studies↗
PubMed2002

Protective effects of recombinant human interleukin-10 on intestines of hypoxia-induced necrotizing enterocolitis in immature rats.

BACKGROUND/PURPOSE: The role of cytokines in the pathogenesis of hemodynamic instability or tissue destruction in patients with necrotizing enterocolitis (NEC) remains undefined. The aim of this study was to determine the effects of recombinant human interleukin-102 (rhIL-10) on intestines of hypoxia-induced necrotizing enterocolitis in immature rats. METHODS: The study was performed on 1-day-old Sprague Dawley rat pups. Group 1 (n = 8) served as nonhypoxic controls. Group 2 (untreated, n = 11) rats were subjected to hypoxia-reoxygenation (H/O) and then were returned to their mothers. Group 3 (rhIL-10 treated, n = 10) rats were subjected to H/O, were returned to their mothers, and were treated with rhIL-10 (75 microgram/kg subcutaneously) for the next 3 days. All animals were killed on day 4, and intestine specimens were obtained to determine the tissue level of malondialdehyde (MDA) and histologic changes. RESULTS: The microscopic lesions in the untreated rats were virtually the same as those seen in neonatal NEC, with destruction of villi and crypts, and in some cases extension to the muscularis. In contrast, in the rats treated with rhIL-10, lesions were limited essentially to the very tips of the villi. Intestinal injury score was significantly less in the rhIL-10-treated rats than in the untreated rats (P <.05). In the rhIL-10-treated group, Malondialdehyde (MDA) levels were not significant in comparison to the control group. In the untreated group, MDA levels were significantly increased when compared with the control and the rhIL-10-treated groups (P <.001 and P <.05, respectively). CONCLUSION: RhIL-10 has a protective effect on intestinal injury in NEC in an experimental model.

Animals↗
PubMed1999

Interleukin-10 inhibits inducible nitric oxide synthase in an animal model of necrotizing enterocolitis.

BACKGROUND: Nitric oxide (NO) and its role in surgical inflammation are well documented; demonstrating the role of NO in necrotizing enterocolitis (NEC) and ways in which it may be suppressed may provide avenues for immune modulation in the treatment of NEC. AIMS: We sought to demonstrate an increase in inducible nitric oxide synthase (iNOS) mRNA and nitric oxide in an experimental model of necrotizing enterocolitis. In addition, we hypothesized that interleukin-10 (IL-10) would attenuate this response. METHODS: Newborn rats were treated with 25 microliters intraperitoneal IL-10 or vehicle prior to laparotomy, 1 h superior mesenteric artery (SMA) occlusion, 50 micrograms/kg intraluminal platelet activating factor administration, and SMA reperfusion. iNOS mRNA and nitric oxide levels were measured in the liver, small bowel, and serum and compared using Student's t-test. RESULTS: Small bowel iNOS mRNA increased after NEC induction from 0.058 +/- 0.02 to 0.144 +/- 0.05 relative intensity units (RIU) at 2 h (p < 0.01) and from 0 to 0.09 +/- 0.02 RIU at 6 h (p < 0.03). Liver mRNA increased from 0.026 +/- 0.002 to 0.485 +/- 0.09 RIU (p < 0.002) and from 0 to 0.069 +/- 0.02 RIU (p < 0.0001) at 2 and 6 h, respectively. Serum nitric oxide increased in NEC induced animals at 2 h from 28.04 +/- 10.5 to 45.18 +/- 6.8 microM (p < 0.001). IL-10 suppressed iNOS mRNA and nitric oxide expression at 2 h in small bowel, liver, and serum by 60%, 89%, and 11%, respectively. CONCLUSIONS: IL-10 decreases iNOS mRNA response in experimental NEC. This down-regulation may be an avenue for anti-inflammatory intervention in NEC.

Animals↗
PubMed1993

Necrotizing enterocolitis: research agenda for a disease of unknown etiology and pathogenesis.

Necrotizing enterocolitis (NEC) is a significant neonatal public health problem that affects low-birth weight infants in neonatal intensive care units throughout the country. As the survival rate of low-birth weight infants continues to increase and as the number of low-birth weight births remains unchanged, we can anticipate that NEC will continue to be a cause of significant morbidity and mortality in the future. Despite many reports about NEC that describe demographic risk factors and short-term or long-term outcome, there is a paucity of basic science information about neonatal gastrointestinal physiology and pathophysiology in human preterm and even full-term infants. It has become increasingly evident that we need a much better understanding about the developmental aspects of gastrointestinal function in health and disease before we can achieve further advances in our understanding of and thus rational therapy for and prevention of NEC. The purpose of the National Institute of Child Health and Human Development conference "Necrotizing Enterocolitis: Basic Science Approaches to Gut Maturation and Pathogenesis" was to bring together basic science investigators, clinical epidemiologists, and clinical scientists to identify important areas of research that need to be applied to the problem of NEC. The concept of applying the "bench to bedside" type of collaborative research was emphasized and encouraged because many clinical neonatologists may have little scientific interaction with basic scientists. In addition, many basic scientists may be unaware of NEC and the implications for targeted research related to this disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Digestive System↗
PubMed2007

Heparin-binding epidermal growth factor-like growth factor promotes enterocyte migration and proliferation in neonatal rats with necrotizing enterocolitis.

PURPOSE: We have shown that heparin-binding epidermal growth factor-like growth factor (HB-EGF) decreases experimental necrotizing enterocolitis (NEC). Intestinal epithelial cell (IEC) migration (restitution) and proliferation are key elements in recovery from intestinal injury. Here, we investigated whether the beneficial effects of HB-EGF are mediated, in part, by its ability to affect these processes. METHODS: Necrotizing enterocolitis was induced in newborn rats by exposure to stress (hypoxia, hypothermia, hypertonic feedings, and lipopolysaccharide), with pups receiving different doses of HB-EGF (0, 25, 50, 100, 200, 400, 600, and 800 microg/kg). To investigate the effect of HB-EGF on enterocyte proliferation and migration, bromodeoxyuridine was administered intraperitoneally 18 hours before sacrifice, with intestine subjected to bromodeoxy-uridine immunohistochemistry. RESULTS: The incidence and severity of experimental NEC decreased, and the survival rate increased, with increasing doses of HB-EGF. Results were confirmed using scanning electron microscopy. Migration of IEC in breast-fed pups was 7.07 microm/h, decreased significantly to 2.29 microm/h in stressed pups, and was significantly improved at 5.95 microm/h in pups subjected to stress but treated with HB-EGF (P < .05). Quantification of IEC proliferation revealed 208 (+) cells per high-power field (HPF) in breast-fed pups, which decreased significantly to 99 (+) cells per HPF in stressed pups and increased to 190 (+) cells per HPF in stressed pups treated with HB-EGF (P < .05). CONCLUSIONS: These results demonstrate that HB-EGF protects newborn rats from experimental NEC in a dose-dependent fashion. The ability of HB-EGF to protect the intestines from NEC is due, in part, to the ability of HB-EGF to preserve enterocyte migration and proliferation.

Animals↗
PubMed2004

Bladder wall necrosis in an extremely low-birth-weight infant: a thought-provoking complication of necrotizing enterocolitis.

An 879-g baby boy had catastrophic necrotizing enterocolitis (NEC) at 29 days of life and underwent surgical laparotomy with a subsequent ileostomy and peritoneal drain placement. The infant was subsequently stable until 42 days of life when a spontaneous perforation of the bladder apex was diagnosed by a suprapubic cystogram. Laparotomy on day of life 46 found a loop of dead bowel herniating into a necrotic hole of the bladder dome. This case shows a previously unreported complication of NEC and discusses the possibility that prolonged use of a peritoneal drain may have permitted its genesis.

Atrophy↗
PubMed1982

Critical evaluation of the persistent loop sign in necrotizing enterocolitis.

A review of the records and radiographs of 21 newborn infants with necrotizing enterocolitis and 10 control infants was performed to test the significance of the persistent loop sign in necrotizing enterocolitis. Twelve clinical and laboratory variables were compared with the persistent loop sign. None of the control infants and seven of the 21 study infants had a persistent loop sign. Four of the seven infants were proven to have necrotic bowel. All four died. Four of the 14 study patients without the persistent loop sign had necrotic bowel. Two of these four infants died. The findings of this study do not support the use of a persistent segmental loop of bowel as a single criterion for surgical intervention.

Enterocolitis, Pseudomembranous↗
PubMed1994

Acute tubular necrosis in a newborn suffering from neonatal necrotizing enterocolitis.

The case history of a newborn who at birth had a necrotizing enterocolitis, worsened by an acute tubular necrosis and anuresis, is presented. A continuous arteriovenous hemofiltration was instituted for the baby, who had previously undergone abdominal surgery with resection of the necrotic bowel. The hypothesis that necrotizing enterocolitis could be the cause of acute tubular necrosis in infancy is discussed.

Enterocolitis, Pseudomembranous↗
PubMed1992

Necrotizing enterocolitis in infancy.

The most common gastrointestinal emergency in the newborn is necrotizing enterocolitis. Premature babies are the most likely victims, but it also occurs in full-term infants. Although great strides have been made in elucidating some of the factors responsible for necrotizing enterocolitis, such as intestinal ischemia, bacterial overgrowth, and feeding dysfunction, the exact etiology is as yet unclear. The timing and indications for surgery differ from institution to institution, but the long-term outcome is similar in most large series. The overall mortality rate remains about 20% to 40%, and of the survivors, about one half seem to have no sequelae, the remaining infants having neurologic and gastrointestinal deficits of various degrees of significance.

Enterocolitis, Pseudomembranous↗
PubMed1980

Feeding and necrotizing enterocolitis.

Twenty-six infants had necrotizing enterocolitis (NEC) in the neonatal unit of the Long Island Jewish-Hillside Medical Center, New Hyde Park, NY, between 1964 and 1976; 25 of these cases occurred between 1973 and 1976. The relationship of feeding practices to this clustering of NEC cases was investigated in two ways: (1) A 10% sample of all admissions, 1964 to 1976, was studied. A striking correlation was found between the yearly incidence of NEC and the percentage of infants in that year who had received large increases in daily feeding volume. The highest mean daily feeding volume occurred in 1974 and 1975, the two years of peak NEC incidence. (2) The feeding records of the 26 NEC cases were studied. Thirteen NEC patients had had large increases in feeding volume within two days of NEC onset. Seven others received greater than 150 mL of formula per kilogram per day prior to NEC onset. Rapid increase in feeding volume and the use of large volumes are suggested as important etiologic factors of NEC.

Enteral Nutrition↗
PubMed1984

The role of host factors in an outbreak of necrotizing enterocolitis.

During an outbreak investigation of necrotizing enterocolitis (NEC) in a neonatal intensive care unit, we identified nine definite and six suspected cases of NEC on the basis of histopathologic, clinical, and roentgenographic findings. Neonates of low birth weight (less than 1,250 g) had the highest incidence of NEC, supporting a role for prematurity in this disease. Patients with definite NEC and those with severe clinical features had significantly lower birth weights and postconception ages (gestational age at birth plus postnatal age at onset of NEC) than the patients with suspected NEC. In a case-control study using birth weight-matched control subjects, maternal toxemia was identified as a possible protective factor for NEC. To our knowledge, this is the first report of the relationship between NEC disease severity and postconception age. These findings also suggest that toxemia may be an important protective factor in NEC and should be examined in subsequent studies.

Disease Outbreaks↗
PubMed1987

Analysis of bowel perforation in necrotizing enterocolitis.

The most severe complication of necrotizing enterocolitis (NEC) is bowel perforation. Identification of neonates at high risk for perforation and optimization of radiologic imaging to identify bowel perforation are necessary to reduce the high mortality rate associated with this catastrophic event. One hundred and fifty-five cases of NEC were seen at our institution during a 5.5-year period. Nineteen (12%) progressed to perforation. A review of surgical findings, autopsy results and radiographs from these patients shows only 63% had radiographic evidence of free air in the peritoneal cavity at the time of perforation. Twenty-one percent had radiographic evidence of ascites but no pneumoperitoneum, and 16% had neither free air nor ascites. Thus purely radiographic criteria for bowel perforation in NEC are imprecise, and paracentesis is mandatory in NEC patients with ascites or clinical findings indicative of peritonitis. Timing of radiographic studies and site of bowel involvement are also important. Seventy-nine percent of perforations occurred by 30 h from confirmation of diagnosis (by clinical or radiographic criteria). Surgery or autopsy revealed involvement of the ileo-cecal region in 89% of cases with the actual site of perforation occurring in this area in 58% of patients.

Enterocolitis, Pseudomembranous↗