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PubMed1998

High morbidity of enterostomy and its closure in premature infants with necrotizing enterocolitis.

OBJECTIVE: To review the morbidity and mortality among 68 premature infants treated with enterostomy for necrotizing enterocolitis. DESIGN: Data were collected retrospectively from hospital medical records to include the period between January 1, 1987, and September 30, 1997. SETTING: Tertiary care children's hospital. PATIENTS: A group of 68 infants aged 2 to 35 days (mean age, 12.5 days), weighing 1500 g or less, with necrotizing enterocolitis necessitating surgical enterostomy for treatment. INTERVENTIONS: Creation of any enterostomy during exploratory laparotomy for necrotizing enterocolitis and subsequent closure. MAIN OUTCOME MEASURES: Morbidity and mortality associated with infant enterostomy and its closure. RESULTS: Thirty-nine infants underwent ileostomy with mucous fistula, 16 underwent ileostomy with a Hartmann pouch, 7 had jejunostomy with mucous fistula, 2 had colostomy with mucous fistula, and 4 had colostomy with a Hartmann pouch. Eighteen (26%) of the 68 infants died in the postoperative period of sepsis (n = 10), continuing necrotizing enterocolitis (n = 5), or respiratory distress (n = 3). Of the remaining 50 infants, complications developed in 34 (68%). These complications included strictures requiring further resection at the time of enterostomy closure in 20 infants; stricture of the enterostomy requiring surgical revision in 6; incisional hernia in 3; parastomal hernia in 4; enterostomal prolapse or intussusception in 6 and 1, respectively; wound dehiscence in 4; wound infection in 8; small-bowel obstruction requiring laparotomy in 2; and anastomotic complications in 2. Only 16 enterostomies were closed uneventfully, with 3 of these infants subsequently dying of sudden infant death syndrome between 6 and 8 months after the operation. Of the surviving infants, 3 (6%) continue to require home hyperalimentation. CONCLUSIONS: Although enterostomy in infants with low birth weight with necrotizing enterocolitis may be lifesaving, it is also a major cause of morbidity. These data suggest the feasibility of a prospective study comparing resection and primary anastomosis with resection and enterostomy.

Enterocolitis, Pseudomembranous↗
PubMed1977

Heat-stable enterotoxigenic Escherichia coli and necrotizing enterocolitis: lack of an association.

During an outbreak of diarrhea in a special care nursery caused by heat-stable enterotoxigenic Escherichia coli (serotype 078:H11:K80), nine (4.3%) of the 205 infants in the nursery developed necrotizing enterocolitis. Cases of necrotizing enterocolitis were not significantly more common in infants colonized or infected with these organisms; heat-stable enterotoxigenic E. coli was isolated from 5(56%) of nine cases of necrotizing ecterocolitis and from 27(38%) of the 71 infants without necrotizing enterocolitis who were also cultured. Our findings suggest that caution should be taken in implicating enterotoxigenic E. coli as a cause of necrotizing enterocolitis.

Animals↗
PubMed2005

Increased incidence of necrotizing enterocolitis in premature infants born to HIV-positive mothers.

OBJECTIVE: To examine if being born to an HIV-positive mother may increase the risk of necrotizing enterocolitis in premature infants. DESIGN: Case-control study. SETTING: Neonatal unit of a level 3 perinatal centre. METHODS: : Over a period of 8.5 years, all cases of necrotizing enterocolitis occurring in premature infants admitted to the neonatal unit were identified. For each case, two controls were retrospectively chosen that matched for postmenstrual age at birth, intrauterine growth and year of birth. Perinatal characteristics were studied in all infants. MAIN RESULTS: There were 79 cases of necrotizing enterocolitis, which were compared with 158 controls. Using multivariate analysis, multiple pregnancy [odds ratio (OR), 2.29; 95% confidence interval (CI), 1.23-4.25; P = 0.009], abnormal umbilical artery velocity (OR, 2.21; 95% CI, 1.08-4.54; P = 0.030), abnormal fetal heart rate (OR, 2.14; 95% CI, 1.05-4.36; P = 0.036) and HIV-positive mother (OR, 6.63; 95% CI, 1.26-34.8; P = 0.025) were significantly more frequent in fetuses who subsequently developed necrotizing enterocolitis. CONCLUSIONS: This preliminary report suggests an association, not previously reported, between maternal HIV-positive status and an increased risk of necrotizing enterocolitis in premature infants. Despite the limitations of this study, we suggest that premature newborn infants of HIV-positive mothers should be monitored very carefully for a possible increased risk of necrotizing enterocolitis.

Adult↗
PubMed1984

Necrotizing enterocolitis can be caused by polycythemic hyperviscosity in the newborn dog.

Although necrotizing enterocolitis has been associated with polycythemia in human infants, a causal relationship has not been established. Forty-six unanesthetized puppies were studied (age 6 to 14 days). Normovolemic polycythemia (Hct 0.70) was induced in 19 pups by exchange transfusion with 75 ml/kg packed red blood cells. Hypervolemic polycythemia (Hct 0.70) was induced in 14 pups by transfusion with 50 ml/kg RBC. Thirteen pups received exchange transfusion with whole blood and served as controls (Hct 0.40). Gross autopsy was performed on all pups 24 hours after transfusion or at death. Necrotizing enterocolitis was defined as areas of violaceous discoloration of the bowel associated with blood in the intestinal lumen. Although lesions appeared throughout the bowel in some pups, involvement of the distal small bowel was most common. Diagnosis was confirmed by microscopic examination. Both gross and microscopic lesions appeared similar to those in necrotizing enterocolitis in human infants. The disorder was seen in 11 of 19 pups with normovolemic polycythemia, eight of 14 pups with hypervolemic polycythemia, and only one of 13 control animals (P less than 0.01). Polycythemia can cause necrotizing enterocolitis in the newborn dog.

Animals↗
PubMed1990

Role of platelet activating factor and tumor necrosis factor-alpha in neonatal necrotizing enterocolitis.

Because previous investigations have suggested that platelet activating factor and tumor necrosis factor-alpha (TNF-alpha) are important mediators of experimental necrotizing enterocolitis in the rat, we measured platelet activating factor, acetylhydrolase (the platelet activating factor breakdown enzyme), and TNF-alpha in the plasma of 12 human neonates with necrotizing enterocolitis and eight age-matched control subjects with similar gestational ages, postnatal ages, and weights. Almost all patients with necrotizing enterocolitis had elevated plasma platelet activating factor values (18.1 +/- 3.6 ng/ml vs. 3.1 +/- 0.9 ng/ml in control subjects, p less than 0.01). Plasma acetylhydrolase activity was lower in patients than in control subjects (10.6 +/- 0.7 nmol/ml/min vs 23.0 +/- 1.4 nmol/ml/min, p less than 0.01). Plasma TNF-alpha concentration was significantly elevated in patients with necrotizing enterocolitis (136 +/- 75 U/ml vs 1.5 +/- 0.8 U/ml, p less than 0.05), although the individual variation was high. There was no correlation between individual TNF-alpha and platelet activating factor levels. We conclude that platelet activating factor and TNF-alpha are elevated in patients with necrotizing enterocolitis and that suppressed platelet activating factor degradation contributes to the increased platelet activating factor levels; platelet activating factor and TNF-alpha may contribute to the pathophysiology of necrotizing enterocolitis.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1979

Transcutaneous oxygen (tcPO2) measurements as an aid to fluid therapy in necrotizing enterocolitis.

Impaired peripheral perfusion is a major problem in necrotizing enterocolitis with delayed recognition and definite documentation being primary factors. While blood pressure and other clinical measurements may improperly estimate the severity of the problem, changes in transcutaneous oxygen measurements and their relationship to arterial oxygen (the tcPO2/PaO2 ratio) potentially afford a sensitive measurement of peripheral perfusion. Experience in our unit confirms a close relationship between tcPO2/ and PaO2 being 0.97 +/- 0.04 (SE). Ten infants with birth weights of 640 to 1380 g, who subsequently developed necrotizing enterocolitis, had strikingly lower ratios initially (0.00, 0.00, 0.00, 0.17, 0.21, 0.43, 0.44, 0.48, and 0.56). Use of the tcPO2/PaO2 ratio to monitor fluid therapy was related to outcome, suggesting that this ratio is important in managing necrotizing enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed1983

An outbreak of Clostridium difficile necrotizing enterocolitis: a case for oral vancomycin therapy?

During a 2-month period, 13 infants in this neonatal intensive care unit developed necrotizing enterocolitis, increasing the prevalence in inborns from 5.2 to 20.5/1,000 live births. Fifty-seven perinatal and neonatal factors, many of which have previously been associated with necrotizing enterocolitis, were compared between the infants with necrotizing enterocolitis and 17 unaffected inborn control infants admitted concurrently. Clostridium difficile cytotoxin was detected in the stools of 12 affected infants (92.3%) in comparison with two control infants (11.8%) (P less than .001), and the organism was isolated in eight affected neonates (61.5%) compared to none of the control infants (P less than .001). The outbreak was terminated upon institution of oral vancomycin therapy in cases and infant contacts, and strict antiinfective measures in the neonatal intensive care unit. This indicates an etiologic role of C difficile in the outbreak. Oral vancomycin in the management of necrotizing enterocolitis was assessed by therapeutic response, drug levels, and occurrence of side effects. Oral vancomycin therapy is indicated in necrotizing enterocolitis outbreaks in units where C difficile is endemic.

Clostridium Infections↗
PubMed2001

Molecular mechanisms contributing to necrotizing enterocolitis.

OBJECTIVE: To examine the cellular mechanisms involved in the pathogenesis of necrotizing enterocolitis (NEC). SUMMARY BACKGROUND DATA: Necrotizing enterocolitis is a major cause of death and complications in neonates; the cellular mechanisms responsible for NEC are unknown. The inducible form of cyclooxygenase (i.e., COX-2) is activated by the transcription factor nuclear factor (NF)-kappaB and is thought to play a role in inflammation. METHODS: Segments of perforated and adjacent uninvolved small intestine from neonates with NEC were analyzed for COX-2 expression by immunohistochemistry. NEC was induced in weanling (18 days old) rats by occlusion of superior mesenteric vessels for 1 hour and intraluminal injection of platelet activating factor (50 micro/kg). Small intestine was harvested for protein extraction. Western immunoblot was performed to determine expression of COX-2. Gel shift assays were performed to assess NF-kappaB binding activity. RESULTS: Immunohistochemical analysis showed increased COX-2 protein expression in the perforated intestinal sections of all 36 neonates but not in adjacent normal intestine. Increased expression of COX-2 protein and NF-kappaB binding activity was noted in the small intestine of weanling rats at 0 and 3 hours after induction of NEC. CONCLUSIONS: Increased COX-2 expression was identified in all neonatal intestinal segments resected for perforated NEC. In addition, a coordinate induction of COX-2 expression and NF-kappaB binding was noted in a rodent model of NEC. These findings suggest that the COX-2/NF-kappaB pathway may play a role in the pathogenesis of NEC. Therapeutic agents that target this pathway may prove useful in the treatment or possible prevention of NEC.

Animals↗
PubMed2004

Epidermal growth factor and necrotizing enterocolitis.

As the number of extremely low-birth-weight infants increases,necrotizing enterocolitis remains a critical eminent problem. Supplementation of enteral feeds with biologically active substances normally present in breast milk, such as epidermal growth factor, seems to be a logical and safe way to reduce the incidence of intestinal inflammation and necrotizing enterocolitis. Continuing basic research and clinical studies are essential before epidermal growth factor can be introduced as an efficient therapeutic approach in the treatment of neonatal necrotizing enterocolitis.

Animals↗
PubMed2002

The changing face of surgical indications for necrotizing enterocolitis.

PURPOSE: The aim of this study was to compare the proportion of operations for acute necrotizing enterocolitis (NEC) and post NEC strictures. METHODS: The authors reviewed 195 charts of children referred to our institution for NEC or post-NEC strictures between 1990 and 1999. Seventy-one children were classified as Bell stage I and were excluded. The remaining 124 patients were classified as either Bell stage II or III and formed the basis of our study. These patients were subdivided into 2 groups: (1) group I (n = 69) comprised patients treated from 1990 until 1994 and (2) group II (n = 55) from 1995 until 1999. Statistical analysis consisted of X(2) and Student's t tests. Significance occurred when P less-than-or-equal 0.05. RESULTS: Both groups were similar with regard to sex, obstetrical history, indomethacin use, umbilical artery catheter use, and enteral feeding. The total operative rate for all patients with either acute NEC or post NEC strictures increased over time from 46% (32 of 69) in group I to 69% (38 of 55) in group II (P <.01). Specifically, post-NEC stricture was the initial operation in 16% (5 of 32) of group I patients versus 37% (14 of 38) of group II patients (P <.05). Subdividing each group by method of treatment of their NEC showed that medically treated patients had an increased incidence of stricture over time (group I, 15% v. group II, 48%; P <.01). Surgically treated children maintained a similar rate of stricture (group I, 36% v. group II, 33%). The mortality rate was comparable in both groups. CONCLUSIONS: At our institution, the total operative rate for necrotizing enterocolitis has increased over the last 10 years. This is because of 2 factors: (1) an increase in the percentage of stage III patients and (2) an increase in referrals for post--necrotizing enterocolitis strictures. No specific criteria could be identified to predict which patients were at risk for post--necrotizing enterocolitis strictures after medical treatment.

Acute Disease↗
PubMedDate not supplied

Neonatal necrotizing enterocolitis: diagnosis, management, and pathogenesis.

The diagnosis of neonatal necrotizing enterocolitis is one of great concern to pediatric and neonatal clinicians. Intravenous access remains an integral part of the medical and surgical management of infants with this diagnosis, and the infusion nurse is intimately involved in the care of these patients. This article discusses the definition of necrotizing enterocolitis, presents current knowledge regarding its basic pathophysiology, and identifies common and rare sequelae of this oftentimes devastating disease of premature infants. Medical and surgical management goals of therapy are described. This overview will aid the infusion nurse in caring for these patients.

Colectomy↗
PubMed2001

Necrotizing enterocolitis in the full-term neonate.

Necrotizing enterocolitis (NEC) is a relatively common disorder of multifactorial aetiology that primarily affects preterm newborns, but has been reported to occur in the full-term neonate as well. This review focuses on known and recent developments in the epidemiology, pathogenesis, diagnosis, management and prevention of NEC in the full-term neonate.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed2004

Effects of nitric oxide synthase inhibition on intestinal damage in rats with experimental necrotizing enterocolitis.

In the inflamed intestinal mucosa of necrotizing enterocolitis (NEC), nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) may contribute to the pathogenesis of local intestinal damage. To study the importance of iNOS for the pathogenesis of NEC, the effects of selective (aminoguanidine, AG) and nonselective (L-nitroarginine methyl ester, L-NAME) iNOS inhibitors on intestinal morphologic changes were assessed in neonatal rats with experimental NEC. The neonatal rats were randomized into one of the five treatment groups. The control group consisted of rats that were breast-fed. The NEC group, consisting of neonates separated from their mothers, were gavaged with a special rodent formula to produce NEC. Rats in the sham, the AG, and the L-NAME groups were gavaged in a similar fashion to those in the NEC group; in addition, they were treated with 0.9 % saline, 10 mg/kg/day AG, and 10 mg/kg/day L-NAME, respectively. The rats were sacrificed on day 4, and the last 4 cm of terminal ileum was harvested for morphological studies and detection of nitrite and nitrate levels in tissue. The animals in the NEC and sham groups showed various degrees of intestinal inflammatory changes and increased tissue levels of nitrite and nitrate compared to those in the control group. Both AG and L-NAME treatment decreased the tissue levels of these nitrogen oxides, but the inflammatory changes of the intestine appeared to be attenuated only in the AG treated animals. L-NAME treatment did not improve the intestinal damage and increased mortality. These results may indicate that NO synthesized by iNOS plays a pathogenic role in formula-fed induced NEC and that inhibition of iNOS improves intestinal inflammatory damage.

Animals↗
PubMed2005

Intestinal and hepatic expression of BNIP3 in necrotizing enterocolitis: regulation by nitric oxide and peroxynitrite.

Necrotizing enterocolitis (NEC) is characterized by the upregulation of proinflammatory proteins, nitrosative stress, and increased enterocyte apoptosis. We examined the expression and regulation of the Bcl-2/adenovirus EIB 19-kDa-interacting protein 3 (BNIP3), a pro-apoptotic gene regulated by nitric oxide (NO) in hepatocytes, in NEC. Newborn rats subjected to hypoxia and fed a conventional formula by gavage (FFH) developed NEC and demonstrated elevated expression of BNIP3 mRNA and protein in mucosal scrapings of the ileal samples and in the liver. In contrast, control rats [breast-fed (BF) without hypoxia] did not develop NEC or elevated BNIP3 expression in these tissues. BNIP3 expression paralleled the histological manifestation of NEC. Supplementation of the formula with L-Nomega-(1-iminoethyl)lysine, an inducible NO synthase inhibitor, reduced BNIP3 expression in FFH animals to the levels found in BF animals. Both hypoxia and peroxynitrite upregulated BNIP3 protein expression in human intestinal cells. Finally, ileal samples obtained from infants undergoing surgical resection for acute NEC demonstrated higher levels of BNIP3 protein. Because hypoxia and formation of reactive nitrogen species may promote gut barrier failure, we propose that upregulation of the cell death-related protein BNIP3 is one possible mechanism associated with enterocyte cell death observed in the intestine with NEC.

Animals↗
PubMed2002

[Peritoneal drainage as an alternative to laparotomy in premature infants with complicated necrotizing enterocolitis].

UNLABELLED: The highest mortality due to necrotizing enterocolitis (NEC) in noted among low birth weight infants. Poor general medical condition of those children does not allow for major surgery despite obvious symptoms of perforation that usually require laparotomy. The aim of this study was assessment of the outcome of peritoneal drainage in complicated NEC in low birth weight infants. MATERIAL AND METHODS: Peritoneal drainage was employed in the treatment of fifteen children with perforated NEC between 1995 and 2002. Mean gestational age of studied newborns was 28.2 weeks, mean birth weight 1178 g (670-2540 g). RESULTS: Eight children survived. Their mean gestational age was 26.8 weeks, mean birth weight--876 g. Seven children died 1-15 days after the perforation. Their mean gestational age was 29.9 weeks, mean birth weight 1227 g. CONCLUSIONS: Survival of low birth weight infants with perforated NEC treated by the peritoneal drainage was 53.3%. The result doesn't seem to be very good unless we remember that before introduction of peritoneal drainage those children would probably die during surgery. Taking in account positive opinions about this method we may conclude that the use of peritoneal drainage could be extended to more patients with complications of NEC and should not be reserved for "hopeless" cases only.

Drainage↗
PubMed1975

Necrotizing enterocolitis in low-birth-weight infants fed an elemental formula.

The incidence of necrotizing enterocolitis in the newborn infant has increased within the same time period that increasing emphasis has been placed on oral alimentation of very small infants. A prospective investigation was conducted to determine the nutritional efficacy as well as the incidence of necrotizing enterocolitis of a standard cow milk formula compared with an elemental formula. Sixteen infants who weighed less than 1,200 gm were randomized and fed one of the two formulas. The clinical status of the two groups was similar. Seven of eight (87.5%) infants fed the elemental formula and two of eitht (25%) fed the standard cow milk formula developed necrotizing enterocolitis (p less than 0.02). The hypertonicity of the elemental diet may have contributed to the increased incidence of necrotizing enterocolitis in infants fed this formula.

Animals↗
PubMed1984

Intussusception associated with necrotizing enterocolitis.

Two premature infants whose clinical picture initially was that of necrotizing enterocolitis eventually developed intussusception. The symptomatology of these two conditions is similar, and when they coexist, recognition of a complicating intussusception is difficult. The pathogenic relationship between necrotizing enterocolitis and intussusception remains obscure. The possibility that necrotizing enterocolitis can be a leading point in the development of intussusception is discussed.

Enterocolitis, Pseudomembranous↗
PubMed1993

T-cryptantigen determination affects mortality in necrotizing enterocolitis.

Testing of infants suspected of having necrotizing enterocolitis for evidence of exposure of the Thomsen-Friedenreich cryptantigen (TCA) has been advocated, because patients with TCA exposure can have severe hemolytic reactions when undergoing transfusion with plasma containing blood products. We compared 62 patients who were managed with knowledge of TCA exposure status during a four year period with 66 patients who were not screened during a comparable four year period. Evidence of hemolysis after blood transfusion occurred significantly more frequently in patients who were not screened (42 versus 15 percent, p < 0.05) and there was significantly greater mortality (18.0 versus 4.5 percent, p < 0.05) in the group that was not screened. These findings suggest that screening for TCA exposure is not only of diagnostic and prognostic value in necrotizing enterocolitis, but is important for patient management and outcome.

Antigens, Tumor-Associated, Carbohydrate↗