{"title":"Comparison of feeding intolerance between very preterm and moderate preterm neonates – a prospective cohort study","authors":"F. Ahammad, T. Begum, JesminAkter, Evana Nasrin","doi":"10.15406/jpnc.2018.08.00339","DOIUrl":null,"url":null,"abstract":"Neonatal death is high in our country and it comprises 60% of total Under-5 mortality.1 So to achieve MDG-4 we have to reduce neonatal death. The Lancet series on neonatal health reported that preterm birth directly causes 28% of neonatal deaths.2 Prematurity and its complication is the major cause of neonatal death in our country and shares around 45% of neonatal death. Premature babies are prone to develop many complications. One of the common complications is Feeding Intolerance (FI). Feeding intolerance can be attributed to the immaturity of gastrointestinal motility,3, 4 as small intestinal motility and phase-3 activity of the migrating motor complex (MMC) are more immature in preterm infants, especially those with a gestational age of less than 32 weeks.3,5 Gastrointestinal motility is influenced by motilin, a 22 amino-acid peptide produced by the enterochromaffin cells of the duodenal and jejunal mucosa.6 Gastric emptying, in particular, is dependent on co-ordination between the motor activities of the gastric antrum and duodenum. Preterm infants often have difficulty in tolerating oral feeds due to immaturity of mechanical and hormonal control of their gastrointestinal system.3 Feed tolerance requires co-ordinated caudal intestinal transit of food. The clusters of phase 3 migrating motor complexes (MMC) that propagate food are associated with a twoto fourfold increase in plasma motilin levels.7 But the association between motilin, MMCs and feed tolerance, however, is unclear in preterm infants. Even though the numbers of MMCs are reduced in preterm infants of less than 32 wk gestation8 fetuses by week 20 of gestation, demonstrate intestinal distribution of motilin similar to that in adults. Motilin levels of fasting preterm infants are also similar to those of term infants, who rarely exhibit the degrees of feeding intolerance characteristic of premature infants.5 It is also noted that fetal intestine is structurally mature by 25 weeks of gestation and capable of digesting and absorbing milk feeds, motor activity develops more slowly and may limit the tolerance to enteral feeds.9 FI often needs prolong parenteral nutrition which predisposes nosocomial infections, hepatic dysfunction and prolong hospitalization.10,11 Though FI is a common problem, literature contain little information about the influence of prematurity on feeding intolerance. There is also scarcity of information regarding the prevalence of feeding intolerance among preterm babiesand whereas the more preterm babies develop more frequent feeding intolerance yet to be determined.","PeriodicalId":92678,"journal":{"name":"Journal of pediatrics & neonatal care","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of pediatrics & neonatal care","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/jpnc.2018.08.00339","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
Neonatal death is high in our country and it comprises 60% of total Under-5 mortality.1 So to achieve MDG-4 we have to reduce neonatal death. The Lancet series on neonatal health reported that preterm birth directly causes 28% of neonatal deaths.2 Prematurity and its complication is the major cause of neonatal death in our country and shares around 45% of neonatal death. Premature babies are prone to develop many complications. One of the common complications is Feeding Intolerance (FI). Feeding intolerance can be attributed to the immaturity of gastrointestinal motility,3, 4 as small intestinal motility and phase-3 activity of the migrating motor complex (MMC) are more immature in preterm infants, especially those with a gestational age of less than 32 weeks.3,5 Gastrointestinal motility is influenced by motilin, a 22 amino-acid peptide produced by the enterochromaffin cells of the duodenal and jejunal mucosa.6 Gastric emptying, in particular, is dependent on co-ordination between the motor activities of the gastric antrum and duodenum. Preterm infants often have difficulty in tolerating oral feeds due to immaturity of mechanical and hormonal control of their gastrointestinal system.3 Feed tolerance requires co-ordinated caudal intestinal transit of food. The clusters of phase 3 migrating motor complexes (MMC) that propagate food are associated with a twoto fourfold increase in plasma motilin levels.7 But the association between motilin, MMCs and feed tolerance, however, is unclear in preterm infants. Even though the numbers of MMCs are reduced in preterm infants of less than 32 wk gestation8 fetuses by week 20 of gestation, demonstrate intestinal distribution of motilin similar to that in adults. Motilin levels of fasting preterm infants are also similar to those of term infants, who rarely exhibit the degrees of feeding intolerance characteristic of premature infants.5 It is also noted that fetal intestine is structurally mature by 25 weeks of gestation and capable of digesting and absorbing milk feeds, motor activity develops more slowly and may limit the tolerance to enteral feeds.9 FI often needs prolong parenteral nutrition which predisposes nosocomial infections, hepatic dysfunction and prolong hospitalization.10,11 Though FI is a common problem, literature contain little information about the influence of prematurity on feeding intolerance. There is also scarcity of information regarding the prevalence of feeding intolerance among preterm babiesand whereas the more preterm babies develop more frequent feeding intolerance yet to be determined.