Feeding Practices for Infants Weighing Less Than 1500 G at Birth and the Pathogenesis of Necrotizing Enterocolitis

Gamma, Edmund F. La; Browne, Lyle E.

doi:10.1016/s0095-5108(18)30346-4

Cited by 116 publications

(43 citation statements)

References 113 publications

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“…During their admission, they received either enteral feeding, total parenteral nutrition or a combination; and their caloric intake was maintained X80 kcal kg À1 per day by the end of the first week using our feeding strategy. 22,23 According to the NICU protocol, their weight, blood pressure, glucose, heart rate and ventilator settings including FiO 2 , peak inspiratory pressure (PIP), positive end-expiratory pressure (PEEP), mean airway pressure (MAP) as well as rate were recorded. Ventilator settings, arterial blood gases and other variables were recorded 7 days before, during and after the initiation of glucocorticoid therapy.…”

Section: General Medical Managementmentioning

confidence: 99%

Postnatal betamethasone vs dexamethasone in premature infants with bronchopulmonary dysplasia: a pilot study

et al. 2008

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Objective: As effects of glucocorticoids differ with respect to preparation, dose and duration, we hypothesized that a postnatal regimen of a low-dose, short-course betamethasone treatment had comparable efficacy and a better safety profile compared to the conventional high-dose, dexamethasone.Study Design: To test our hypothesis, we selected premature neonates with a birth weightp1000 g and a gestational age p29 weeks who were ventilated >10 postnatal days with an FiO 2 >0.4 and no ability to wean mechanical support for X3 consecutive days. These neonates either received twice daily dexamethasone 0.25 mg kg À1 per dose intravenously for 3 days tapered to 0.125 mg kg À1 per dose for 4 days (June 1999 to December 2000) or betamethasone 0.125 mg kg À1 per day intramuscularly once per day for 3 days (January 2001 to December 2002). Result:We found a significant reduction in FiO 2 after 3 days in both glucocorticoid treatment groups. There were no significant differences between the two treatment groups in the clinical parameters including decrease in FiO 2 , oxygenation index, mean airway pressure and percent extubation. Duration of ventilation, number of oxygen days and length of hospital stay were comparable in the two groups. Of particular interest, the betamethasone group showed fewer adverse effects, such as poor weight gain and high blood glucose, than the dexamethasone group.Conclusion: A short course of low-dose betamethasone has comparable efficacy and seemingly a better short-term safety profile compared to conventional dexamethasone treatment.

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Section: General Medical Managementmentioning

confidence: 99%

Postnatal betamethasone vs dexamethasone in premature infants with bronchopulmonary dysplasia: a pilot study

et al. 2008

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“…35 Patients were followed by serial radiography every 8 hours until their condition improved, stabilized, or they perforated.…”

Section: Definitionsmentioning

confidence: 99%

Human Granulocyte Colony-stimulating Factor May Improve Outcome Attributable to Neonatal Sepsis Complicated by Neutropenia

Kocherlakota

Gamma

1997

Pediatrics

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ABSTRACT. Objectives. To determine whether adjunctive therapy with recombinant human granulocyte colony-stimulating factor (rhG-CSF) could reverse sepsis-associated neonatal neutropenia and improve neonatal survival compared with conventional therapy in a phase I/II-type trial.Study Design. An intravenous infusion of rhG-CSF (10 g/kg/d ؋ 3 d) was administered to 14 septic neutropenic neonates. Neutrophilic responses and outcome of these neonates were compared with 11 concurrently treated, retrospectively selected, case-matched control septic patients identified by using a search of medical records coded for sepsis with neutropenia ( 24 hours).Results. Seven neonates with early-onset sepsis with neutropenia at birth and seven neonates with late-onset sepsis plus neutropenia (all with necrotizing enterocolitis) were entered in the rhG-CSF treatment group. Results were compared with a conventional therapy control group (five early onset, six late onset). No significant differences existed in the birth weight, gestational age, use of antibiotic therapy, magnitude of respiratory support, severity of metabolic acidosis, use of vasopressors, or other supportive therapy between the two groups. In the rhG-CSF-treated group and in the conventionally treated control group, the absolute neutrophil count (ANC) (mean ؎ SEM) was 585 ؎ 138 and 438 ؎ 152, respectively. The ANC increased to more than baseline in the rhG-CSF-treated group by 10-fold versus 2-fold at 24 hours, 18-fold versus 4-fold at 48 hours, 24-fold versus 5-fold at 72 hours (significant by one-way analysis of variance in the rhG-CSF group only), and 29-fold versus 16-fold at 7 to 10 days when compared with the conventional therapy group. There were no nonresponders in the rhG-CSF group by 24 hours after the first dose of study drug. Monocyte cell counts also increased significantly in both groups by 7 days after entry into this protocol but remained within normal range for age. No clinically significant effect on lymphocytes, erythrocytes, or platelet counts was noted. Thirteen patients in the rhG-CSF-treated group (92%; 13 out of 14) and five in the conventionally treated group (55%; 5 out of 11) survived to 28 days after the onset of the signs of sepsis. No adverse effects were noted in the rhG-CSF-treated group.Conclusions. rhG-CSF can increase the neutrophil count in critically ill septic neutropenic neonates. This finding suggests that rhG-CSF may be effective in a therapeutically useful time frame to treat septic neonates with neonatal neutropenia attributable to bone marrow suppression or neutrophil consumption. Future randomized trials are needed to validate the beneficial effects of rhG-CSF and to determine whether any significant side effects of therapy exist. Pediatrics 1997;100(1). URL: http: //www.pediatrics.org/cgi/content/full/100/1/e6; neonatal sepsis, recombinant human granulocyte colony stimulating factor, bacteremia, cytokines, very low birth weight, neutropenia.

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“…36,37 The majority of the preterm infants who develop NEC have been enterally fed, something not pos- sible in infants whose intestines have suffered an ischemic insult. 38 However, one quarter of all cases of NEC occur beyond one month after birth, primarily in extremely low birth weight babies whose corrected age is less than 34 weeks postconception. 33 Currently there are three logical categories for the etiology of NEC: 1) infection, 2) ischemic reperfusion injury, and 3) intestinal inflammation.…”

Section: Necrotizing Enterocolitismentioning

confidence: 99%

Development of Gastrointestinal Function: Risk Factors for Necrotizing Enterocolitis

Clark

Mitchell

2004

The Journal of Pediatric Pharmacology and Therapeutics

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REVIEW ARTICLEThe intestinal tract of the fetus matures rapidly in the third trimester of the pregnancy. The premature infant has decreased intestinal motility, limited digestion, absorption and excretion, and poor intestinal barrier defense. These limitations place the infant at high risk for acute intestinal injury, necrotizing enterocolitis. This article reviews the development of the gastrointestinal tract in the fetus, the barriers to feeding the high risk, premature infant, and the most serious intestinal disease, necrotizing enterocolitis.

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Feeding Practices for Infants Weighing Less Than 1500 G at Birth and the Pathogenesis of Necrotizing Enterocolitis

Cited by 116 publications

References 113 publications

Postnatal betamethasone vs dexamethasone in premature infants with bronchopulmonary dysplasia: a pilot study

Postnatal betamethasone vs dexamethasone in premature infants with bronchopulmonary dysplasia: a pilot study

Human Granulocyte Colony-stimulating Factor May Improve Outcome Attributable to Neonatal Sepsis Complicated by Neutropenia

Development of Gastrointestinal Function: Risk Factors for Necrotizing Enterocolitis

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