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G33 SEVERE METABOLIC DECOMPENSATION AT PRESENTATION OF DIABETES MELLITUS IN CHILDREN AGED <2 YEARS
P. Paul, A. Ghatak, S. Kerr, C. Smith, M. Didi, J. C. Blair.Royal Liverpool Children’s hospital, Alder Hey, Liverpool, Liverpool, UK
Introduction: The incidence of cerebral oedema at presentation of diabetes mellitus is increased in children aged <2 years and those with severe diabetic ketoacidosis. Here we present a 10 year review of the metabolic profile of children aged <2 years at presentation of diabetes mellitus and report increased incidence of diabetic ketoacidosis and more profound metabolic decompensation than in older prepubertal children.
Patients and Methods: Blood pH, base deficit (BD), serum glucose (Glu), sodium (Na), osmolality, and urea at presentation of diabetes mellitus was studied in 21 children (11 female, age (mean (1 SD)) 1.39 (0.30) year) diagnosed between 1994 and 2003. Each child was matched to one or more pre-pubertal control subjects (25 male:19 female, age 8.05 (1.73) year) diagnosed with diabetes mellitus during the same week.
Results: 17/21 (84.8%) children aged <2 years presented in diabetic ketoacidosis compared with 10/44 (22.79%) children aged >2 years. Blood pH was significantly lower in children aged <2 years (7.17 (0.16)) than children aged >2 years (7.3 (0.14)), p 0.004 and BD was significantly higher (19.8 (7.6) mmol/l v 7.29 (11.4) mmol/l), p 0.003. There was no significant difference in serum Glu (30.05 (8.39) mmol/l v 28.43 (9.44) mmol/l), Na (135.3 (4.29) mmol/l v 132.74 (3.41) mmol/l), osmolality (307.96 (11.96) mmol/kg v 299.6 (12.04) mmol/kg), or urea (7.32 (3.41) mmol/l v 5.42 (1.88) mmol/l).
Conclusion: Diabetic ketoacidosis with severe metabolic decompensation is more frequent at presentation of diabetes mellitus in children aged <2 years. This may result from earlier ketogenesis reflecting lower glycogen stores in these young children and account for the excess of cerebral oedema observed in this age group.
G34 IS THERE A ROLE FOR SMALLER DOSES OF INSULIN IN EARLY MANAGEMENT OF DIABETIC KETOACIDOSIS
R. Puttha1, D. Schapira2.1 …