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PubMed1991

Cocaine: a risk factor for necrotizing enterocolitis.

Necrotizing enterocolitis occurs most often in the small preterm infant, usually with birthweight less than 1.5 kg. Necrotizing enterocolitis has also been described in more mature infants, however, often the result of reduced gastrointestinal blood flow. We describe four relatively large infants from our nursery with varying severity of necrotizing enterocolitis. None had any of the known risk factors; all had a history of maternal cocaine use. Two were initially cared for in the term nursery. All four presented with abdominal distention, bloody stools, vomiting, or residuals. One infant presented with fulminant deterioration and subsequently died; the other three infants were treated medically and survived. It is suggested that a high index of suspicion be maintained for the possibility of necrotizing enterocolitis and feeding intolerance in term and near-term infants exposed in utero to cocaine.

Cocaine↗

PubMed2001

New concepts in necrotizing enterocolitis.

Necrotizing enterocolitis is an overwhelming gastrointestinal emergency that primarily afflicts premature infants born weighing less than 1500 g. Despite years of investigation, the etiology remains unclear, and accepted prevention and treatment strategies are lacking. Studies published over the last year have provided new insight into several aspects of this complex disease. In this review, novel information is presented on (1) the epidemiology; (2) methods of early diagnosis, such as abdominal magnetic resonance imaging; (3) the importance of risk factors, including assessment of feeding strategies and role of bacterial colonization; (4) the pathophysiology, highlighting experimental and clinical trials evaluating the role of inflammatory mediators and growth factors on the disease; (5) preventive strategies, such as anaerobic bacterial supplementation; and (6) surgical interventions, including peritoneal drainage. Understanding some of these important aspects of necrotizing enterocolitis may help improve the outlook of patients with this dreaded disease. Although the incidence of neonatal necrotizing enterocolitis (NEC) and the mortality stemming from this disease have not significantly improved over the last 30 years, there is exciting new information that may significantly improve the outlook of patients with this overwhelming intestinal emergency in the near future.

Enterocolitis, Necrotizing↗

PubMed1998

Necrotizing enterocolitis.

Necrotizing enterocolitis is a relatively common disorder of unknown etiology that primarily affects premature newborns. The majority of babies with necrotizing enterocolitis respond to nonsurgical management, and, despite an increase in the number of premature infants, the surgical mortality rate has improved. This review provides an overview of the current literature covering new developments in etiology, risk factors, pathogenesis, diagnosis, therapy, outcome, and preventable measures related to necrotizing enterocolitis.

Animals↗

PubMed2004

Necrotizing enterocolitis.

Necrotizing enterocolitis is the principal cause of surgical referral in preterm neonates and the most common gastrointestinal emergency among infants. Its pathophysiology is unclear and it carries high levels of mortality and morbidity. This article provides an overview of necrotizing enterocolitis including risk factors, preventative strategies and medical and surgical management.

Enterocolitis, Necrotizing↗

PubMed2004

Concomitant involvement of the small intestine and the distal esophagus in an infant with massive necrotizing enterocolitis.

Necrotizing enterocolitis is a disease of the newborn that may involve the small intestine and/or the colon, and the stomach. To our knowledge, massive necrosis of the small intestine with concomitant involvement of the esophagus has never been reported. A case of a 6-month-old boy with necrotizing enterocolitis and pan-necrosis of the small intestine, cecum, and the lower third of the esophagus is presented. After 70 days of treatment, intestinal transit was established by an anastomosis between the first centimeter of jejunum and the ascending colon. Finally, esophageal transit was established by a total gastric transposition with cervical esophagogastric anastomosis. The patient was maintained under total parenteral nutrition, and after 19 months he developed fulminant hepatic failure due to parenteral nutrition; he then underwent combined liver and small bowel transplantation. After 2 months, the patient died due to undefined neurologic complications, probably related to infection or immunosuppressive therapy.

Anastomosis, Surgical↗

PubMed2000

Inflammation in the developing human intestine: A possible pathophysiologic contribution to necrotizing enterocolitis.

Necrotizing enterocolitis (NEC), a major cause of morbidity and mortality in premature infants, occurs after the introduction of oral feedings in conjunction with initial bacterial colonization of the gut and is hypothesized to be due to an immature (inappropriate) enterocyte response to bacterial stimuli. To test this hypothesis, we compared the enterocyte IL-8 response to inflammatory stimuli [lipopolysaccharide (LPS) and IL-1beta] in immature vs. mature human small intestine. Initial in vitro studies comparing confluent Caco-2 cells, a model for mature human enterocytes, with a primary human fetal intestinal cell line (H4 cells) demonstrated that after inflammatory stimulation fetal cells secreted more IL-8 (LPS, 8-fold; IL-1beta, 20-fold) than Caco-2 cells. IL-8 mRNA activity in fetal compared to Caco-2 cells was proportionately increased by the same magnitude with both stimuli. To validate the in vitro observations, small intestinal organ cultures from fetuses vs. older children were exposed to LPS and IL-1beta. Again in human organ cultures from fetuses compared to older children, IL-8 secretion was greater (LPS, 2.5-fold; IL-1beta, 200-fold) and mRNA activity after stimulation was comparably higher, suggesting that increased transcription of the IL-8 gene may account for the excessive response. Using immunohistochemical staining to identify the cellular source of IL-8, activity was noted predominantly in villous and crypt epithelium but also in a few immunoresponsive lymphoid cells. The observation that immature human enterocytes react with excessive pro-inflammatory cytokine production after inflammatory stimulation may help in part explain why prematures exposed to initial colonizing bacteria develop necrotizing enterocolitis.

Adenocarcinoma↗

PubMed2005

Nitrosative stress in an animal model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a disease of newborns characterized by gut barrier failure. We reasoned that upregulation of inducible nitric oxide synthase (iNOS) may result in nitrosative stress and accumulation of nitroso species in the intestine. Newborn rats were either breast-fed (BF), or formula-fed and additionally subjected to hypoxia (FFH). At Day 4 after birth, the distal ilea were harvested and processed for Western blot analysis and measurement of NO-related metabolites. While BF neonates showed normal morphology, FFH neonates developed signs of NEC by Day 4. These pathological changes correlated with upregulation of iNOS and increases in tissue nitrite, nitrosothiol, and nitrosamine concentrations. Enhanced nitroso levels were most prominent in the mucosal layers of the ileum and iNOS inhibition resulted in a significant decrease in both nitroso species and incidence of NEC. In contrast, increased nitrite levels were distributed evenly throughout the ileum and remained unchanged following iNOS inhibition. Similarly, specimens from NEC patients had higher intestinal levels of NO-related metabolites compared to non-NEC controls. This is the first report of tissue levels of nitroso species in the gut of an animal model of NEC and of human specimens. The results suggest that local nitrosative stress contributes to the pathology associated with NEC. Unexpectedly, the NO breakdown product nitrite, previously considered biologically inert, was found to be present throughout the ileal wall, suggesting that cellular NO metabolism is altered significantly in NEC. Whether nitrite plays a protective or deleterious role remains to be investigated.

Animals↗

PubMed2005

Necrotizing fasciitis: a rare complication of neonatal necrotizing enterocolitis.

Necrotizing fasciitis is a rapidly spreading soft tissue infection affecting the subcutaneous tissue and underlying fascial layers. Although this infection pattern is commonly seen in adults, it is rarely seen in the neonatal population. Herein, we describe a patient who developed extensive necrotizing fasciitis of the abdominal wall after intestinal resection for necrotizing enterocolitis (NEC).

Abdominal Wall↗

PubMed2003

Treatment and prevention of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common serious, acquired gastrointestinal disorder in the newborn infant. Although many variables are associated with development of NEC, only prematurity has been consistently identified in case-controlled studies. Traditionally, the diving seal reflex has been invoked as the mechanism responsible for ischaemic injury and necrosis. Intestinal ischaemia is likely to be the final common pathway in NEC; however, it is due to the release of vasoconstricting substances, such as platelet activating factor, rather than perinatal asphyxia. Bacteria and/or bacterial toxins are likely to have a key role in the pathogenesis of NEC by fostering production of inflammatory mediators. The role of feeding practices in the pathogenesis of NEC remains controversial. Treatment of infants with NEC generally includes a regimen of bowel rest, gastric decompression, systemic antibiotics and parenteral nutrition. Infants with perforation are generally operated upon; however, there has been recent interest in primary peritoneal drainage as an alternative. Prevention of NEC still remains elusive. Avoidance of preterm birth, use of antenatal steroids and breast-milk feeding are practices that offer the greatest potential benefits. Use of any other strategy should await further trials.

Clinical Trials as Topic↗

PubMed2005

Disordered enterocyte signaling and intestinal barrier dysfunction in the pathogenesis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in neonates, and is characterized by the development of diffuse intestinal necrosis in the stressed, pre-term infant. Systemic stress causes a breakdown in the intestinal mucosal barrier, which leads to translocation of bacteria and endotoxin and the initiation of a signaling response within the enterocyte. This review summarizes recent evidence defining a clear role that defective enterocyte signaling plays in the pathogenesis of NEC through the following mechanisms: 1) The localized production of nitric oxide by villus enterocytes results in an increase in enterocyte apoptosis and impaired proliferation; 2) The translocation of endotoxin results in a PI3K-dependent activation of RhoA-GTPase within the enterocyte leading to decreased enterocyte migration and impaired restitution; 3) Dysregulated sodium-proton exchange within the enterocyte by endotoxin renders the enterocyte monolayer more susceptible to damage in the face of the acidic microenvironment characteristic of systemic sepsis; and 4) Endotoxin causes a p38-dependent release of the pro-inflammatory molecule COX-2 by the enterocyte, which potentiates the systemic inflammatory response. An understanding of the mechanisms by which disordered enterocyte signaling contributes to the pathogenesis of barrier failure and NEC--through these and other mechanisms--may lead to the identification of novel therapeutic approaches for this devastating disease.

Bacterial Translocation↗

PubMed2005

Mechanisms of nitric oxide-mediated intestinal barrier failure in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading intestinal emergency in premature infants. The underlying etiology of NEC remains elusive, but hypoxic conditions and early enteral feeding are consistently implicated as the main risk factors in the pathogenesis of NEC. We postulate that nitric oxide (NO) plays a key role as a molecular signaling "hub" in the generation of gut barrier failure in NEC. Clinical studies suggest that inflammatory cytokines and excessive NO production may contribute to the pathogenesis of NEC. One of the major challenges in defining the critical signaling pathways that lead to the development of NEC is the lack of specific biochemical markers that consistently delineate the early stages of NEC. Intestinal pathology and molecular markers derived from late-stage NEC represent end-stage findings and thus provide little insight into the early events that led to intestinal inflammation. Such markers may not represent viable therapeutic targets for the treatment or prevention of NEC. Therefore, novel strategies are needed to identify the patients at risk for NEC and define the clinically relevant molecules that characterize the early stages of NEC. This review will examine the mechanisms of NO-mediated gut barrier failure and propose novel genetic-based approaches for elucidating the critical molecular pathways in NEC.

Enterocolitis, Necrotizing↗

PubMed2005

Heparin-binding EGF-like growth factor (HB-EGF) and necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease that occurs predominantly in premature infants. Despite various advances in management, the mortality of this disease remains high. During the last decade, studies from our laboratory have shown that heparin-binding epidermal growth factor-like growth factor (HB-EGF), a member of the epidermal growth factor (EGF) family, can protect intestinal epithelial cells (IEC) from various forms of injury in vitro. Furthermore, we have used both an intestinal I/R injury model in adult rats, and a neonatal rat pup model of NEC, to show that HB-EGF can protect the intestines from injury. On administration of HB-EGF in the neonatal rat model, the incidence of NEC is reduced from 65% to 27.3% (P < 0.05), and the histological injury score is decreased from 2 to 1.1 (P < 0.05). In addition, the survival rate is increased from 25% to 63.6% and the survival time extended from 59 hours to 73 hours (P < 0.05). In addition, using human specimens from newborns undergoing bowel resection for NEC, we found that the expression of endogenous HB-EGF mRNA in normal areas of the intestine at the resection margins was higher than that of the intestine afflicted with acute NEC. Endogenous HB-EGF may be involved in epithelial cell repair, proliferation, and regeneration during recovery from injury. Exogenous administration of HB-EGF potentiates recovery from intestinal injury in vitro and in vivo. Taken together, these results support a potential therapeutic role for HB-EGF in the treatment of NEC in the future.

Animals↗

PubMed2004

Current issues in the management of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common surgical emergency in the neonatal intensive care unit and remains a major cause of death in neonates. Although the pathophysiology of NEC has not been completely elucidated, progress has been made in the characterization of the molecular events which may take place during an episode of ischemia. This possible initiating event is followed by a complex cascade of inflammatory mediators active in NEC: epidermal growth factor, platelet-activating factor, and, nitric oxide. Additionally, unique characteristics of the premature gut are thought to be crucial to the development of NEC. The diagnosis of NEC continues to be based on clinical and radiographic features. Several new laboratory tests are under investigation for the purposes of earlier diagnosis, but none have prevailed at this time. Both exploratory laparotomy, with intestinal resection and peritoneal drainage are widely practiced. Mortality rates remain high and have improved little over the last couple of decades. Therefore, prevention remains crucial in order to decrease the incidence of NEC. Cautious feeding regimens, the use of maternal breast milk, passive immunization, and the use of probiotics have all been suggested but not proven as possible preventive methods. Although many advances have been made, significant opportunity remains to improve our understanding of the disease process and to develop better strategies for prevention and treatment.

Enterocolitis, Necrotizing↗

PubMed2000

Inflammatory polyps after necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal period. NEC causes ulceration of the intestinal mucosa and may lead to perforation or a stricture. To the best of the authors' knowledge intestinal inflammatory polyps after NEC have not been described previously. The authors report on a 17-week-old boy with pseudopolyps at the site of a colonic stricture after NEC.

Colonic Polyps↗

PubMed2001

An unusual late complication of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) now is managed frequently successfully without surgical intervention. NEC may result in strictures, which present after the acute inflammatory process has resolved. Strictures usually present as obstruction in the first year or two of life. A case report is presented of an 11-year-old child who had symptoms from a previously undiagnosed NEC stricture as a result of pica when coins obstructed the stricture. As treatment of NEC continues to improve, more and later complications of this disease can be expected. J Pediatr Surg 36:1853-1854.

Child↗

PubMed1999

Necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most serious and frequently acquired gastrointestinal disorder in neonates. The pathogenesis of NEC is unknown, but it may result from a disturbance of the delicate balance among gastrointestinal perfusion, enteric organisms, and enteral feeding. Risk factors for NEC include prematurity, hypoxic-ischemic insult, and formula or breast milk feedings. The clinical spectrum of NEC is multifactoral and ranges from temperature instability, apnea, lethargy, abdominal distention, bilious residuals, and guaiac-positive stools to septic shock, disseminated intravascular coagulation, and death. Medical management is usually adequate treatment for NEC. Surgical treatment is considered if medical management is inadequate to control the spread of the disease. Health care team members must be constantly alert to the presentation of NEC. Expeditious treatment will positively influence the outcome of the disease.

Colectomy↗

PubMed2006

Cytokines in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a devastating intra-abdominal emergency in the newborn period. The disease involves bowel wall inflammation, ischemic necrosis, eventual perforation, and the need for urgent surgical intervention. Unrecognized or left untreated, the neonate can decompensate quickly, often progressing to shock, multisystem organ failure, and eventual death. During the past several years, a number of basic science and clinical trials have been established in an attempt to understand the pathophysiology of NEC. As many researchers feel that NEC develops as an uncontrolled inflammatory response that leads to intestinal ischemia, a large number of studies have been focused on the inflammatory cascade and the role that cytokines play within that cascade. Although a large amount of data has been generated from these studies, the events leading to the ischemic injury of the intestine are still not fully understood. This article will therefore focus on the key cytokines involved with NEC, in an attempt to present the current literature and studies that support their involvement.

Cytokines↗

PubMed2007

The role of the intestinal barrier in the pathogenesis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in neonates and is increasing in frequency because of recent advances in neonatal care. NEC develops in a stressed preterm infant in the setting of intestinal barrier disruption, systemic inflammation, and leads to, multisystem organ failure. The intestinal barrier lies at the interface between microbes within the intestinal lumen and the immune system of the host, and has both immunological and mechanical components. These components serve to protect the host from invading pathogens and, at the same time, provide a surface area for nutrient absorption. Factors that lead to impairments in the function of the intestinal barrier may predispose the host to the invasion of gut-derived microbes and to the development of systemic inflammatory disease. This process, termed "bacterial translocation," may be compounded during instances in which the mechanisms that regulate the repair of the intestinal barrier are disrupted. Bacterial translocation is of particular concern to the newborn patient, in which immaturity of the mechanical barrier and incomplete development of the host immune system combine to render the host at particular risk for the development of intestinal inflammation. This review will serve to provide an overview of recent evidence regarding the components of the intestinal barrier, and the mechanisms by which disruptions in barrier function may contribute to the pathogenesis of NEC.

Animals↗