Presented at the Neonatal Society 2003 Autumn Meeting.
Snowdon DM, Ahmed T, Fell JM (introduced by N. Modi)
Chelsea and Westminster Hospital, Fulham Road, London. SW10 9NH. United Kingdom
Aim: Successful early enteral nutrition of preterm infants remains a major challenge. It has been suggested that a major factor in poor tolerance of feeding is immature foregut motility (1) and it has been shown that reduced regular gastric slow wave activity in premature infants is associated with gastric motor abnormalities (2). This study uses cutaneous electrogastrography (EGG) to measure gastric electrical activity non-invasively in preterm infants, in the context of symptoms of feed intolerance.
Subjects: 40 consecutively born preterm infants, whose parents consented, were studied. 13 were born at 25-28 weeks gestation (birth weight 710-1050 grams), 19 at 29-32 weeks gestation (1250-2075g) and 8 at 32-34 weeks gestation (1705-2810g). Infants were excluded if they had a congenital gastrointestinal malformation, other major congenital malformation, intra-uterine growth restriction or were receiving prokinetic treatment.
Method: Infants were fed according to a set enteral feeding protocol. They were defined as having feeding difficulty if they were unable to tolerate full enteral feeds by 2 weeks of age, had large preprandial gastric aspirates, recurrent vomiting or suspicion of aspiration. Gastric electrical activity was measured using cutaneous EGG for 30 minutes immediately before and after a feed, at age 1 week, 2 weeks and 2 weekly intervals until term or discharge.
Results: 14 of the infants (35%) had feeding difficulty episodes. The mean percentage of normal slow wave activity (normogastria) during preprandial recording was 53.2(SD 20.5 ) in the infants with feeding difficulty at the time of recording (FD), 73.1(10.0) in the same infants with no current feeding difficulty (FD-not current) and 69.5(11.1) in the infants who had never had feeding difficulty (Never-FD). A significant difference was seen between the FD group and the Never FD group (p<0.01) but not between the FD-not current and the Never FD infants. A similar pattern was seen in the postprandial period (p=0.01). The post/pre prandial power ratio showed a downward trend when comparing both the FD group and the FD-not current group with the Never-FD infants, but this did not reach statistical significance.
Conclusion: Clinical feed intolerance is associated with significantly reduced normal gastric slow wave activity in preterm infants when compared with those preterm infants who have never had feeding difficulty. However this difference is seen only during the episodes of feeding difficulty and not when the infants are clinically well, thus limiting any predictive value. The rise in amplitude (power), of the slow wave, following feeding appeared to be dampened in those infants with feeding difficulty even when no evidence of feeding difficulty was present at the time of the recording. This may be of use in clinical practice to monitoring progress of infants who are slow to establish feeds and to plan advancement of enteral feeds.
References
1. Bisset WM, Watt JB, Rivers RPA, Milla PJ. Gut 1988; 29: 483-8
2. Reizzo G, Indrio F, Montagna O, Tripaldi C, Laforgia N, Chiloiro M, Mauntone A. Neurogastroenterol. Mot. (2000) 12, 223-229