Summer meeting of the Neonatal Society, 2004

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<ul><li><p>Abstract</p><p>Summer meeting of the Neonatal Society, 2004</p><p>1st2nd July, 2004</p><p>St Johns College, Cambridge, UK</p><p>This meeting has been approved by the RCPCH for 7 CPD Credits</p><p>Thursday 1st July</p><p>12.0013.35 Registration and lunch</p><p>13.35 Welcome</p><p>Chair: Dr Andrew Lyon</p><p>13.45 Dr Mark Herbert, John Radcliffe Hospital</p><p>Group B Streptococcus gene expression in nutrient limited environments</p><p>14.00 Dr S Broughton, Kings College Hospital</p><p>Prospective study of risk factors for healthcare utilisation and RSV infection in prematurely</p><p>born infants</p><p>14.15 Dr A Thakor, University of Cambridge</p><p>The role of calcitonin gene related peptide (CGRP) in the umbilical vascular bed</p><p>14.30 Mr J Cockerill, Imperial College London</p><p>Breast milk attenuates poor postnatal growth in male preterm infants</p><p>14.45 Miss R Slater, University College London</p><p>Early Human Development 80 (2004) 169192</p><p> Dr A Lall, Hammersmith Hospital</p><p>T regulatory lymphocytes are found in fetal blood at 29 weeks gestation, but do notNoxious Stimulation Causes Functional Activation of the Somatosensory Cortex in</p><p>Newborn Infants</p><p>15.00 Young Investigator Prize Lecture-Dr David Gardner</p><p>Fetal adaptation to the intrauterine environment: short and longer term consequences for</p><p>physiological development</p><p>15.40 Tea</p><p>Chair: Dr Howard Clark (Young Investigator Prize Winner 2001)doi:10.1016/ FOXP3earlhumdev.2004.07.002</p></li><li><p>16.15 Dr F McCrosson, Royal Infirmary of Edinburgh</p><p>Changes in Body Temperature Immediately After Birth in Preterm Infants Resuscitated in</p><p>Polythene bags</p><p>16.30 Professor C Morley, Royal Womens Hospital, Melbourne</p><p>Resuscitating very premature lambs with a Laerdal bag without PEEP or set tidal volumes</p><p>with PEEP: the effect on carbon dioxide and oxygenation</p><p>16.45 Dr E Johnson, University of Cambridge</p><p>Effect of maternal dexamethasone treatment on circulating and tissue angiotensin-converting</p><p>enzyme concentration in fetal sheep</p><p>Chairman: The President, Professor Andrew Wilkinson</p><p>17.0018.00 The Tizard Lecture-Sir Iain Chalmers</p><p>Confronting therapeutic uncertainties in neonatal care</p><p>From 18.30 Drinks and Jazz band on lawn/patio</p><p>20.00 Conference Dinner/Entertainment (more musicbarCambridge walkPunting)</p><p>Friday 2nd July</p><p>08.0008.45 Breakfast</p><p>Chair: Dr Nicola Robertson</p><p>08.45 Dr L E Dyet, Hammersmith Hospital</p><p>Diffuse White Matter Abnormalities on Magnetic Resonance Imaging of the Brain in</p><p>Preterm Infants at Term and Neurodevelopmental Outcome</p><p>09.00 Dr K Thorngren-Jerneck, Lund University Hospital</p><p>Cerebral glucose metabolism measure by Positron Emission Tomography (PET) Magnetic</p><p>Resonance Imaging (MRI), diffusion weighted imaging (DWI) and 1H Spectroscopy in</p><p>term newborn infants with Hypoxic Ischemic Encephalopathy (HIE) after birth asphyxia</p><p>09.15 Dr O Iwata, University College London</p><p>Delayed hypothermia is neuroprotective in moderate, but not severe, perinatal</p><p>hypoxic-ischaemic injury</p><p>09.30 Dr N Kennea, Hammersmith Hospital</p><p>Functional Extrinsic and Intrinsic Apoptotic Pathways in Human Fetal Mesenchymal Stem Cells</p><p>09.45 Dr D Todd, Westmead Hospital, Australia</p><p>Retinopathy of prematurity in infants b30 weeks gestation in NSW and the ACT from1992 to 2002</p><p>10.00 Dr L Dabydeen, University of Newcastle</p><p>Additional nutrition significantly increases brain growth in babies with perinatal brain damage</p><p>10.15 Keynote LectureDr Robert Tasker</p><p>Hippocampal vulnerability, developmental amnesia, and what else?</p><p>11.00 Coffee</p><p>Abstract170</p></li><li><p>Abstract 171Noxious stimulation causes functional activation of the somatosensory cortex in</p><p>Chair: Dr Helen Budge (Young Investigator Prize Winner 2002)</p><p>11.20 Young Investigator Prize Lecture-Dr Karen Luyt</p><p>Metabotropic Neurotransmitter</p><p>Receptors in Oligodendrocytes: novel potential players in white matter development,</p><p>injury and repair</p><p>12.00 Dr M Gnanalingham, University Hospital Nottingham</p><p>Impact of delivery temperature on uncoupling protein-1 and -2 abundance on brown</p><p>adipose tissue in the newborn</p><p>12.15 Dr K L Franko, University of Cambridge</p><p>Effect of Maternal Protein Deprivation During</p><p>Pregnancy on Hepatic Gluconeogenic Enzyme in Rat Fetuses at Term</p><p>12.30 Keynote lecture-Dr Dino Giussani</p><p>Oxygen, fetal growth and cardiovascular development</p><p>13.15 Close of meeting and lunch</p><p>Our thanks in particular to Chiesi, and also to Draeger Medical, Fisher Paykel, S.L.E. and Vygon for</p><p>sponsoring this meeting.newborn infants</p><p>Rebeccah Slater1, Shiromi Gallella2, Stewart Boyd3, Judith Meek2, Maria Fitzgerald1</p><p>1Department of Anatomy and Developmental Biology, University College London,</p><p>London, UK2Department of Paediatrics, University College London Hospital, London, UK3Neurosciences Unit, Institute of Child Health, London, UK</p><p>Introduction: Noxious sensations can clearly stimulate the central nervous system,</p><p>producing reflex movements and a biochemical response, at a very early age</p><p>(Fitzgerald, 1999; Smith, 2000). The true experience of pain requires functional</p><p>maturation of higher brain centres, however, it is unclear at what CNS level this</p><p>response is produced. Here we report on the use of near infra red spectroscopy (NIRS)</p><p>to study the maturation of the cortical response to noxious sensation.</p><p>Aim: To use NIRS to investigate cortical pain processing in neonates using the</p><p>haemodynamic response in the somatosensory cortex to noxious stimulation.</p><p>Methods: Eleven preterm infants were studied during routine phlebotomy. All infants</p><p>had normal appearances on cranial ultrasound scans. The haemodynamic response to</p><p>the heel lance was measured using a double channel NIR spectrophotometer. The</p><p>optodes were positioned symmetrically on each side of the head over the</p><p>somatosensory cortex and changes in oxyhaemoglobin (HbO2), deoxyhaemoglobin</p><p>(HHb) and total haemoglobin (HbT) concentrations were measured.</p></li><li><p>Table showing maximum change in HbT in the contralateral and ipsilateral</p><p>somatosensory cortex following painful stimulation and a sample trace of the evoked</p><p>response in one infant.</p><p>Conclusion: Infants between 29 and 42 weeks pma show a large localised</p><p>somatosensory response to painful stimulation. The magnitude of the evoked responses</p><p>is similar to those obtained using visual and olfactory stimuli. This study shows that</p><p>noxious stimulation evokes neural activity in the somatosensory cortex at this age and</p><p>that both preterm and term infants are able to mount a cortical response to painful</p><p>stimuli.</p><p>42+0 10.62 0.63</p><p>Abstract172References</p><p>Smith RP, Gitau R, Glover V, Fisk NM. 2000 Pain and stress in the human fetus. Eur J Obstet</p><p>Gynecol Reprod Biol. 92:1615.</p><p>Fitzgerald M. 1999 The developmental neurobiology of pain. The textbook of pain, 4th edition. EdResults: A haemodynamic response was successfully measured in seven infants with a</p><p>mean post menstrual age (pma) of 36.3 weeks. Four studies were excluded due to</p><p>motion artefact. Following the heel lance there was an increase in HbT in the</p><p>contralateral somatosensory cortex and a decrease in the ipsilateral somatosensory</p><p>cortex.</p><p>Postmenstrual</p><p>age (weeks)</p><p>Maximum change in contralateral HbT</p><p>(Amol/l) during 20 s following heel lanceMaximum change in ipsilateral HbT</p><p>(Amol/l) during 20 s following heel lance</p><p>29+5 8.67 2.0635+5 9.49 6.0530+0 1.53 9.0835+1 2.39 0.5637+5 3.11 3.9743+2 2.11 12.98Wall PD and Melzack R, Churchill Livingstone, pp 235252.</p></li><li><p>Abstract 173Prospective study of risk factors for healthcare utilisation and RSV Infection in</p><p>prematurely born infants</p><p>Authors: Simon Broughton1, Alison Roberts1, Grenville Fox2, Mark Zuckerman3 and</p><p>Anne Greenough1</p><p>1Department of Child Health, Guys Kings and St Thomas Medical School, Kings</p><p>College Hospital, Denmark Hill, London SE5 9RS, UK2Department of Child Health, Guys, Kings and St Thomas Medical School, St</p><p>Thomas Hospital, Lambeth Palace Rd, London SE1 7EH, UK3Department of Microbiology, Guys Kings and St Thomas Medical School, Kings</p><p>College Hospital, Denmark Hill, London SE5 9RS, UK</p><p>Background: Prematurely born infants frequently require readmission or GP contacts</p><p>following NICU discharge, data from retrospective studies suggests this may be increased</p><p>following RSV infection.</p><p>Aims: In a prospective study to determine risk factors for healthcare utilisation and RSV</p><p>infection in babies born prematurely.</p><p>Methods: Babies born b32 weeks of gestation were recruited if they were born withinsix months of the onset of the RSV season. Following discharge from the neonatal</p><p>unit, data were collected regarding subsequent healthcare utilisation; the number and</p><p>length of hospital admissions and GP consultations. The parents were asked to</p><p>contact a member of the research team if their baby had signs of a lower respiratory</p><p>tract infection (LRTI). In addition, all parents were contacted on a fortnightly basis</p><p>by the research team. If either contact indicated the baby had a LRTI, a member of</p><p>the research team visited the baby at home or at hospital and a nasopharyngeal</p><p>aspirate (NPA) was obtained. Healthcare utilisation and RSV infection were then</p><p>related to demographic, social and neonatal data to identify risk factors. Ethical</p><p>approval was obtained from the ethics committee and consent was obtained from the</p><p>parent.</p><p>Results: 119 babies (median gestational age 29, range 2331 weeks) were recruited.</p><p>Eighty-six of the babies had signs of LRTI on 149 occasions and NPAs were</p><p>obtained. Thirty-eight (32% of 119) were RSV positive on 41 occasions. In addition</p><p>eight babies were positive for influenza and five for parainfluenza. Regression analysis</p><p>demonstrated that risk factors increasing for hospital admission were RSV infection</p><p>(odds ratio (OR) 3.21 (95% confidence intervals 1.298.01)) and parental smoking</p><p>(OR 3.59 (1.349.66)). Risk factors for hospital length of stay were gestation out of</p><p>oxygen ( pb0.001), parental smoking ( p=0.012) and RSV infection ( p=0.022).Antenatal infection was protective ( p=0.049). The only risk factor identified for GP</p><p>consultations was RSV infection ( pb0.001). Risk factors identified for RSV infectionwere smoking in pregnancy (OR 3.59(1.059.66)), being male (OR 2.62(1.056.50))</p><p>and the number of siblings (OR 1.65(1.122.14)) and antenatal infection was</p><p>protective (OR 0.35(0.120.97)).</p><p>Conclusion: RSV infection does increase healthcare utilisation in prematurely born infants.</p><p>These results further emphasise the need to counsel women against smoking during andafter pregnancy.</p></li><li><p>Corresponding Author: Prof. Anne Greenough.</p><p>Breast milk attenuates poor postnatal growth in male preterm infants</p><p>Jason Cockerill1, Ian de Vega2, Caroline Dore, Sabita Uthaya1 and Neena Modi1</p><p>1Imperial College London;2Hammersmith Hospitals Trust, London UK</p><p>Background: Extremely preterm birth is an acknowledged risk factor for poor growth.</p><p>Abstract174Current clinical practice aims to promote postnatal weight gain and head growth. Male</p><p>infants are known to achieve less well than females over a range of outcomes, but there has</p><p>been little comparative evaluation of growth.</p><p>Aims: The aim of this study was to compare the pattern of weight gain and head growth to</p><p>age term-equivalent in male and female infants born V32 weeks gestational age (GA) andto relate these to breast milk received and illness severity.</p><p>Methods: This study was approved by the hospital research ethics committee. We</p><p>extracted the following information from the Queen Charlottes and Chelsea Hospital</p><p>neonatal database on all inborn infants V32 weeks GA who remained in the neonatal unitup to z37 weeks postmenstrual age and who had been admitted between 01/01/2002 and31/12/2003: sex, head circumference (HC) and weight (Wt) at birth (B) and discharge (D),</p><p>date of birth and discharge, antenatal and postnatal steroid exposure, number of days any</p><p>breast milk was received and number of days receiving level 1 and 2 intensive care (3). We</p><p>expressed each anthropometric index as standard deviation score (SDS) and growth</p><p>between birth and 6 weeks as SDS gain (SDSG) calculated using commercially available</p><p>software based on the 1990 British growth reference. SDSG is the change in SDS adjusted</p><p>for sex and reference correlations between measurements at two time points. We expressed</p><p>days of level 1 and 2 intensive care (%L1 and 2IC) and the number of days breast milk</p><p>was received (%BM) as a percentage of the number of days from birth to discharge. Data</p><p>were analysed using SPSS version 11.5. Unless otherwise stated, data are presented as</p><p>mean (SD). The independent and paired samples t-test was used for between and within</p><p>group comparisons; equal variances were not assumed. Linear and multiple regression</p><p>analyses were used to compare weight and HC SDSG in male and female infants and to</p><p>investigate the interaction between %BM and sex.</p><p>Results: There were 29 boys and 32 girls. There was no significant difference between</p><p>boys and girls in GA, birth weight and HC, discharge HC, %BM or %L1 and 2IC</p><p>(table). No infant received postnatal steroids and all but 5 (4 boys, 1 girl) received</p><p>antenatal steroids.</p><p>GA</p><p>weeks</p><p>Bwt</p><p>Kg</p><p>BWt</p><p>SDS</p><p>BHC</p><p>cm</p><p>BHC</p><p>SDS</p><p>Dwt</p><p>Kg</p><p>DWt</p><p>SDS</p><p>DHC</p><p>Cm</p><p>DHC</p><p>SDS</p><p>Wt</p><p>SDSG</p><p>HC</p><p>SDSG</p><p>%BM %L1</p><p>and 2IC</p><p>Boys 29.0</p><p>(2.5)</p><p>1.22</p><p>(0.35)</p><p>0.55(0.91)</p><p>27.0</p><p>(2.07)</p><p>0.35(1.16)</p><p>2.59</p><p>(0.45)</p><p>1.83(0.98)</p><p>34.4</p><p>(1.7)</p><p>0.37(1.38)</p><p>1.81(1.08)</p><p>0.02(1.93)</p><p>81.6</p><p>(16.1)</p><p>37.2</p><p>(32.3)</p><p>Girls 28.6</p><p>(1.8)</p><p>1.14</p><p>(0.29)</p><p>0.24(0.99)</p><p>26.0</p><p>(2.2)</p><p>0.56(1.21)</p><p>2.68</p><p>(0.48)</p><p>1.22(0.94)</p><p>34.0</p><p>(3.3)</p><p>0.02</p><p>(2.81</p><p>1.25(0.81)</p><p>0.52</p><p>(3.53)</p><p>78.4</p><p>(23.5)</p><p>39.2</p><p>(27.8)p 0.46 0.38 0.21 0.09 0.50 0.44 0.02 0.59 0.49 0.035 0.47 0.54 0.79</p></li><li><p>Abstract 175There was a highly significant fall in weight SDS between birth and discharge</p><p>in both boys (mean difference 1.28, pb0.0001) and girls (mean difference 0.98,pb0.0001). In contrast, head growth was maintained. No impact of %L1 and 2ICon growth was identified. Though not significantly different between boys and</p><p>girls at birth, by discharge, boys had a significantly lower weight SDS and weight</p><p>SDSG was more negative (table). Multiple regression analysis, allowing for BWt</p><p>SDS, showed a significant positive relationship between weight SDSG and %BM</p><p>in the boys (B=0.031; p=0.01) but not the girls (B=0.009; p=0.23). There was ahighly significant interaction between sex and %BM ( p=0.007). Based on the</p><p>mean BWt SDS for the whole group, and using the regression coefficients</p><p>obtained from the analysis of each sex separately, the mean difference between</p><p>boys and girls was 1.77 SDSG at 50%BM ( pb0.0001), reducing to0.22 SDSG at100%BM ( p=0.35).</p><p>Conclusion: Clinical management appears to have sustained postnatal head growth, in</p><p>contrast to weight gain, in this 2002/2003 cohort of extremely preterm infants. Postnatal</p><p>weight gain in boys is significantly worse than in girls but this difference is substantially</p><p>reduced by breast milk.</p><p>Additional nutrition significantly increases brain growth in babies with perinatal</p><p>brain damage</p><p>Dabydeen L, Thomas JE, Aston TJ, Hartley H, Sinha SK, Eyre JA</p><p>Developmental Neuroscience Group, School of Clinical Medical Sciences, University</p><p>of Newcastle upon Tyne UK NE1 4LP</p><p>Hypothesis: That increased nutrition during the first year in children with significant</p><p>perinatal brain damage will optimi...</p></li></ul>