Metabolic adaptation in small for gestational age infants. Issue 3 (March 1993)

• Record Type: Journal Article
• Authors: Hawdon, J M; Ward Platt, M P
• Is Part Of: Archives of disease in childhood. Volume 68:Issue 3(1993)Spec No
• Page Start: 262
• Page End: 268
• Publication Date: 1993-03
• Subjects: Children -- Diseases -- Periodicals; Infants -- Diseases -- Periodicals; 618.920005
• DOI: 10.1136/adc.68.3_Spec_No.262
• Languages: English
• ISSNs: 0003-9888

Abstract

Abstract : Hypoglycaemia has long been recognised as a feature of the failure of metabolic adaptation in infants who are small for gestational age (SGA). This study examined the process of metabolic adaptation by measuring, longitudinally, the concentrations of metabolic fuels and substrates in 33 SGA infants in the first postnatal week, and relating these to cross sectional data in 218 infants of appropriate weight for gestational age (AGA). SGA term infants had higher mean blood lactate concentrations than AGA term infants at delivery (2.98 v 2.10 mmol/l) and in the first few postnatal hours (3.05 v 1.91 mmol/l). Subsequently, although there were no differences in blood glucose concentrations, SGA term infants had lower mean ketone body concentrations (for example day 2: 0.07 v 0.41 mmol/l), and failed to mount a ketogenic response to low blood glucose concentrations. At birth, SGA preterm infants had lower mean blood glucose concentrations than AGA preterm infants (3.17 v 4.16 mmol/l), but there were few postnatal metabolic differences between the two groups. Mean blood glucose concentrations did not differ between AGA and SGA preterm infants. For variables that differed between the groups, multiple regression analysis suggested that both the degree and asymmetry of growth retardation were related to the severity of the metabolic abnormalities. These data suggest that, although there are early metabolic differences between SGA and AGA infants, it is possible that current clinical management is effective in preventing subsequent hypoglycaemia. This is important because of the failure of SGA infants to mount a ketogenic response.