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      Necrotizing enterocolitis: treatment based on staging criteria.

      Pediatric Clinics of North America
      Anti-Bacterial Agents, therapeutic use, Bacterial Infections, diagnosis, Digestive System, embryology, Enteral Nutrition, adverse effects, Enterocolitis, Pseudomembranous, epidemiology, therapy, Fetal Organ Maturity, Fluid Therapy, Humans, Infant, Newborn, Infant, Premature, Diseases

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          Abstract

          Neonatal necrotizing enterocolitis is the most important cause of acquired gastrointestinal morbidity or mortality among low birthweight infants. Prematurity alone is probably the only identifiable risk factor. Although the etiology is unknown NEC has many similarities to an infectious disease. Proper staging helps improve reporting and the management of NEC.

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          Clostridium difficile toxin in asymptomatic neonates.

          Clostridium difficile toxin was detected in the feces of 10.5% of normal newborn infants and 55% of neonates in the intensive care unit. None of the normal infants and less than one-third of those in the NICU had any signs of enteric illness. Vaginal delivery and breast-feeding were associated with increased rates of toxin carriage. Although toxin was not detected during antibiotic therapy, it could be found in 85% of infants two weeks or more, and for at least an additional two months, following exposure to antibiotics.
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            Epidemiology of necrotizing enterocolitis: a case control study.

            All neonates with necrotizing enterocoltis cared for at Grady Memorial Hospital from July, 1977, through February, 1979, were compared with controls matched for birth weight and time of admission to the nursery, to examine risk factors which have been implicated in the etiology of the disease. Data on maternal history, birth history, and hospital course were uniformly collected and contrasted for 35 cases and 98 controls. Low birth weight was associated with an increased incidence of NEC and an increased case fatality rate. All babies 36 weeks or more at birth were diagnosed by seven days. More immature infants developed the disease later in their hospital course. In addition, preterm babies who developed NEC after 2 weeks of age appear to be smaller and sicker. Factors previously thought to predispose an infant to the development of the disease, such as prolonged rupture of membranes, infectious complications of pregnancy, low Apgar scores, patent ductus arteriosus, and use of umbilical catheters, were found with equal frequency in cases and controls and may simply represent the descriptive characteristics of a population of sick premature infants. Feeding history and antibiotic use were examined in depth and were not correlated with the development of NEC.
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              Enterocolitis in low-birth-weight infants associated with milk and soy protein intolerance.

              Two low-birth-weight infants developed a syndrome of vomitting, distension, septic appearance, and bloody diarrhea. Both infants developed symptoms after ingestion of cow milk-based formula initially, and, later, soy-based formulas. These symptoms resolved with intravenous fluids and alimentation. Vomiting, diarrhea, melena, and polymorphonuclear leukocytosis recurred with reintroduction of either milk- or soy-based formulas. This sensitivity persisted throughout the neonatal period and was still present at seven to eight months of age. It appears from these data that intolerance to whole protein formulas can cause a syndrome similar clinically to neonatal necrotizing enterocolitis.
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