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390 Cerebral Palsy and Neonatal Death in Singletons Born small for Gestational Age at Term
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  1. M Stoknes1,2,
  2. GL Andersen1,3,
  3. MO Dahlseng1,
  4. J Skranes1,
  5. KÅ Salvesen1,4,
  6. LM Irgens5,6,
  7. JJ Kurinczuk7,
  8. T Vik1,2
  1. 1Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology
  2. 2Department of Pediatrics, St. Olavs Hospital, Trondheim University Hospital, Trondheim
  3. 3The Cerebral Palsy Registry of Norway, Habilitation Center, Vestfold Hospital, Tønsberg
  4. 4National Center for Fetal Medicine, Department of Obstetrics and Gynecology, St. Olavs Hospital, Trondheim University Hospital, Trondheim
  5. 5Medical Birth Registry of Norway, Locus of Registry-Based Epidemiological Research, Norwegian Institute of Public Health
  6. 6Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway
  7. 7National Perinatal Epidemiology Unit (NPEU), University of Oxford, Oxford, UK

Abstract

Background and Aims To investigate the role of antenatal versus intrapartum causes in the pathway leading to cerebral palsy (CP) in children born small for gestational age (SGA) at term.

Methods Data on 400488 singleton term live births during 1996–2003 recorded in the Medical Birth Registry of Norway were linked with clinical data for 342 children diagnosed with CP recorded in the CP Registry of Norway. ‘Low’ Apgar score, defined as Apgar score < 4 at five minutes, MRI-findings and subtype of CP were used to assess the timing of the brain injuries leading to CP.

Results In the group of 69 SGA children with CP, six (9%; CI: 4–18) had ‘low’ Apgar scores, and five of these were considered to be of intrapartum origin (7%; CI: 3–16). In the group of 263 non-SGA children with CP, 26 (10%; CI: 7–14) had ‘low’ scores, and 18 of these probably had an intrapartum cause. In addition, an intrapartum cause was assessed as probable in 13 cases among children with Apgar scores > 3. Thus, an intrapartum cause was considered likely in 31 non-SGA children (12%; CI: 8–16), not different from the SGA group (p=0.31).

Conclusions Despite increased odds of both low Apgar score and CP among children born SGA, our findings suggest that that the role of intrapartum causes in the causal chain leading to CP in these children is limited. Instead the results suggest that the majority of children with CP born SGA have antenatal brain injuries, also supported by MRI-findings.

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