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JOURNAL ARTICLE
REVIEW
Pathogenesis and prevention of necrotizing enterocolitis.
Current Opinion in Infectious Diseases 2011 June
PURPOSE OF REVIEW: Necrotizing enterocolitis (NEC) remains the most common serious acquired gastrointestinal disorder affecting preterm infants. Here we review recent advances in our understanding of the pathogenesis of this multifactorial condition and consider the implications for practice and research.
RECENT FINDINGS: NEC is an important cause of mortality and serious morbidity in preterm infants. The risk is inversely proportional to gestational age and weight at birth. Fetal growth restriction and compromise may be additional specific risk factors. NEC, particularly severe NEC requiring surgical intervention and NEC with invasive infection, is associated with acute morbidity and mortality and adverse neurodevelopmental outcomes. The principal modifiable postnatal risk factors for NEC in preterm infants relate to enteral feeding practices including formula milk feeding, early and rapid advancement of enteral feed volumes, and exposure to H2-receptor antagonists.
SUMMARY: Our understanding of the pathogenesis of this condition remains incomplete. With the exception of feeding with human milk, only limited evidence is currently available to support interventions to prevent NEC. Promising strategies that merit further evaluation in randomized controlled trials include the use of prebiotics and probiotics and the avoidance of exposure to H2-receptor antagonists.
RECENT FINDINGS: NEC is an important cause of mortality and serious morbidity in preterm infants. The risk is inversely proportional to gestational age and weight at birth. Fetal growth restriction and compromise may be additional specific risk factors. NEC, particularly severe NEC requiring surgical intervention and NEC with invasive infection, is associated with acute morbidity and mortality and adverse neurodevelopmental outcomes. The principal modifiable postnatal risk factors for NEC in preterm infants relate to enteral feeding practices including formula milk feeding, early and rapid advancement of enteral feed volumes, and exposure to H2-receptor antagonists.
SUMMARY: Our understanding of the pathogenesis of this condition remains incomplete. With the exception of feeding with human milk, only limited evidence is currently available to support interventions to prevent NEC. Promising strategies that merit further evaluation in randomized controlled trials include the use of prebiotics and probiotics and the avoidance of exposure to H2-receptor antagonists.
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