SOMANZ 2009 ANNUAL CLINICAL AND SCIENTIFIC MEETINGLANGHAM HOTEL, AUCKLAND, NEW ZEALAND30TH OCTOBER – 1ST NOVEMBER 2009

www.somanz.org

MEETING HANDBOOK

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WELCOME – CLAIRE MCLINTOCK It is with enormous pleasure, on behalf of SOMANZ and the organising committee, that I welcome you to Auckland, for the 2009 Annual Scientific Meeting. It has been fun developing a programme – clinical, scientific and social – for you to enjoy this weekend. I would like to thank our sponsors for supporting the meeting and also the Conference Company for their help with the meeting. I hope that you have a wonderful time!

Best wishes

Claire McLintockSOMANZ President

ORGANISING COMMITTEEClaire McLintock – SOMANZ President

Associate Professor Lesley McCowan

Thanks to Robyn North for help organising the session on preeclampsia and small-for-gestational age pregnancies.

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Friday 30th October – Teaching day

8.30am – 8.50am Registration & coffee

8.50am – 9.00am Welcome

9.00am – 9.45am Thromboprophylaxis in pregnancy: update of RCOG guidelines

Review of UK RCOG updated guidelines: comparison with Australia andNew Zealand guidelinesCathy Nelson-Piercy, Obstetric Physician, Guy’s and St Thomas’s Hospital, London, UK

Chair: Claire McLintock

9.45am – 10.30am Special Issues relating to venous thromboembolism in pregnancy

Indications for thrombolysisDr Sanjeev Chunilal, Haematologist, North Shore Hospital, Auckland

IVC filters in pregnancyDr Laura Young, Haematologist, Auckland City Hospital

Chair: Claire McLintock

10.30am – 11.00am Epilepsy in pregnancy – treating for two!Elizabeth Walker, Neurologist, Auckland City Hospital

Chair: Lucille Wilkinson

11.00am – 11.30am Morning tea

11.40am – 1.00pm Cancer in pregnancy

Management of women diagnosed with breast cancer during pregnancy andpre-pregnancy counseling for women with previous breast cancerDr Rita Sasidharan, Oncologist, Auckland City Hospital

How to manage women diagnosed with lymphoma in pregnancyDr Leanne Berkahn, Haematologist, Auckland City Hospital

Chair: Karin Lust

1.00pm – 2.00pm Lunch

2.00pm – 3.30pm CSL special symposium

Pregnancy issues in women with inherited bleeding disorders: comment on recently published international consensus guidelines and presentation of clinical cases

Dr Julia Phillips, Haematologist, Wellington City HospitalDr Shannon Emmet, Haematology Advanced Trainee, Auckland City Hospital

Chair: Denise Aitken

3.30pm – 4.00pm Afternoon tea

4.00pm – 5.30pm Workshop on maternal mental health:

Overview of clinical issues: which women should see a maternal mental health specialistApproach to management of mental illness in pregnancySafety of SSRIs in pregnancyDr Sara Weeks, Psychiatrist Lotofale, AucklandDr Cathy Hapgood, Psychiatrist in Maternal Mental Health, North Shore Hospital, Auckland

Chair: Lesley McCowan

5.30pm – 6.30pm Welcome drinksLangham Hotel

6.30pm Council meeting & dinner

PROGRAMME

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Saturday 31st October – SOMANZ

8.30am – 8.50am Registration & coffee

8.50am – 9.00am Welcome

Saturday morning symposium: Preeclampsia and small-for-gestational age pregnancies

9.00am – 9.15am Overview SCOPE study and screening principlesProfessor Robyn North

9.15am – 9.30am Cessation of smoking early in pregnancy prevents spontaneous preterm birth and small for gestational age infants Associate Professor Lesley McCowan

9.30am – 10.00am Risk factors for customised SGA, normotensive and hypertensive SGA in SCOPEAssociate Professor Lesley McCowan

10.00am – 10.30am Risk factors and prediction of preeclampsia in SCOPE Professor Robyn North

Chair: Jonathan Morris

10.30am – 11.00am Morning tea

11.00am – 11.30am Biomarker discovery in the SCOPE study: proteomic and metabolomic studies Professor Robyn North

11.30am – 12.00pm Mechanisms of sFLT-1 elevation in primate pregnancyProfessor Anne-Marie Hennessey

Chair: Jonathan Morris

Free communications

12.00pm – 12.15pm The effect of cuff size on blood pressure measurement in pregnancyJL Ram, St George Clinical School, University of New South Wales

12.15pm – 12.30pm Comparison of the fetal thymus size between normal and pre-eclamptic pregnanciesNA Mohamed, Sydney Medical School – Nepean, The University of Sydney

12.30pm – 12.45pm The Role of T regulatory and Th17 cells in healthy pregnancy and in preeclampsiaBrigitte Santner-Nanan, Nepean Clinical School, The University of Sydney

12.45pm – 1.00pm Endothelial function is different in women with preeclampsia compared to women with gestational hypertensionAnn E Quinton, Discipline of Obstetrics & Gynaecology, Sydney Medical School, Nepean, University of Sydney

1.00pm – 1.15pm Overview CHIPs study meeting on SundayLaura McGee

Chair: Katie Groom

1.15pm – 2.15pm Lunch & AGM

2.15pm – 3.15pm The ‘swine’ flu epidemic: implications and management of pregnant womenDr Sally Roberts, Infectious Disease Consultant and Microbiologist, Auckland City Hospital

Auckland experience of novel influenza (‘swine’flu) in pregnant womenDr May Chin Soh, Obstetric Medicine Registrar, National Women’s Health, Auckland City Hospital

Chair: Al Haslam

3.15pm – 3.45pm Afternoon tea

Case presentations

3.45pm – 4.00pm Illicit substance use in pregnancy – ‘ecstasy’ and agonyDr Katherine Scott, Royal Brisbane and Women’s Hospital

4.00pm – 4.15pm The other cardiomyopathy of pregnancyDr Anna Antonas, Pro Stephen Gatt, Dr Robert Buist, Dr Sandra Lowe

4.15pm – 4.30pm Does routine assessment of thyroid function in hyperememsis gravidarum add valuable information?Nicholas Bedford, Wellington Hospital

Chair: Eileen Bass

4.30pm – 5.30pm The annual SOMANZ debate. The motion before the meeting:‘life-style modification clinics are better than diabetes clinics to improve pregnancy outcomes in women with high bmi’

For: Leone Callaway Against: Janet Rowan

Chair: Bill Hague

7.00pm – the witching hour Conference dinnerHalloween party with music from The Mermaids

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Sunday 1st November – SOMANZ

8.30am – 8.45am Registration & coffee

8.45am – 10.00am Clinicopathological case conferenceInvited panel and audience

Cathy Nelson-PiercySandra LoweJonathon Morris

CPC Facilitator: Claire McLintock

10.00am – 10.30am Morning tea

Free communications / cases

10.30am – 10.45am Investigation for suspected pulmonary embolism in pregnancyKatherine Scott, Royal Brisbane and Women’s Hospital, Brisbane

10.45am – 11.00am Perinatal risk factors for the neonatal abstinence syndrome in infants born to women on methadone maintenance therapyRalph Nanan, Sydney Medical School – Nepean, The University of Sydney

11.00am – 11.15am Growth restriction in pregnancies of opioid-dependent mothersAnthony JW Liu, Sydney Medical School – Nepean, The University of Sydney

11.15am – 11.30am Population trends in pulmonary embolism following childbirthJonathan Morris, Perinatal Research, Kolling Institute, University of Sydney

Chair Michael Peek

11.30am – 12.30pm Plenary lecture: measuring maternal morbidity – what can we learn?

UKOSS (UK Obstetric Surveillance System): results from the first years and what to expect from AMOSS (the Australasian Maternal Outcomes Surveillance System)

Cathy Nelson-Piercy, Obstetric Physician, Guy’s and St Thomas’s Hospital, London, UK

Chair David Ellwood

12.30pm – 12.45pm Closing remarks & lunch

* Please note this programme is subject to change

SOCIAL PROGRAMME

Welcome cocktail functionFriday 30th OctoberTime: 5.00pm – 7.00pm Langham HotelIncluded with full registration

Hallowe’en partySaturday 31st OctoberTime: 7.00pm – midnightLangham HotelTickets: NZ$100

PROGRAMME Continued

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INTERNATIONAL KEYNOTE SPEAKER

Cathy Nelson-Piercy, Obstetric Physician, Guy’s and St Thomas’sHospital, London, UK Catherine Nelson-Piercy is a Consultant Obstetric Physician at Guy’s and St. Thomas’ Hospitals Trust and Queen Charlotte’s Hospital in London. Her undergraduate studies were at King’s College, Cambridge University and St Bartholomew’s Hospital. She trained as a physician, and was taught Obstetric Medicine by Professor Michael de Swiet. She specialises in the care of women with medical problems in pregnancy. Dr Nelson-Piercy runs special joint clinics for women with renal disease, cardiac, and rheumatic disorders in pregnancy. She offers pre-pregnancy counselling for women with pre-existing medical problems and those with problems in previous pregnancies.

Dr Nelson-Piercy has been involved in the development of several evidence-based National Guidelines notably for ‘Contraception in Women with Heart Disease’, BTS / SIGN ‘Asthma in Pregnancy’ and RCOG Green top guideline on ‘Reducing the risk of thromboembolism during pregnancy, birth & the puerperium’. She has over 170 publications and has edited four books and written the successful Handbook of Obstetric Medicine, now in its third edition. She is also one of the central assessors for maternal deaths and chapter author for Heart Disease in ‘Saving Mothers Lives’, CEMACH (Confidential Enquiry into Maternal and Child Health) 2000–02 and 2003–05.

Dr Nelson-Piercy is the vice president and UK representative of the International Society of Obstetric Medicine (ISOM), sits on the Education Committee of the British Maternal and Fetal Medicine Society (BMFMS) and was the first Flexible Working Officer for the Royal College of Physicians of London, with responsibility for flexible / part-time training and working. She is editor in chief of a new journal ‘Obstetric Medicine: the medicine of pregnancy’.Dr Nelson-Piercy was awarded the FRCOG ad eundum in 2007 and is the youngest ever recipient of this honour.

CONFERENCE SPEAKERSLeanne Berkahn, Haematolgist, Auckland City Hospital

Leone Callaway, Obstetric Physician, Brisbane

Shannon Emmett, Haematology advanced trainee, Auckland City Hospital

Lesley McCowan, Obstetrician, National Women’s Health, Auckland City Hospital

Robyn North, Obstetric Physician, University of Adelaide

Julia Phillips, Haematologist, Wellington Hospital

Sally Roberts, Infectious Disease Physician and Microbiologist, Auckland City Hospital

Janet Rowan, Obstetric Physician, National Women’s Health, Auckland City Hospital

Rita Sasidharan, Oncologist, Auckland City Hospital

May Ching Soh, Obstetric Medicine Registrar, National Women’s Health, Auckland City Hospital

Elizabeth Walker, Neurologist, Auckland City Hospital

Sara Weeks, Psychiatrist, Auckland District Health Board

Cathy Hapgood, Psychiatrist, Waitemata District Health Board, Auckland

Laura Young, Haematologist, Auckland City Hospital

Sanjeev Chunilal, Haematologist, North Shore Hospital, Auckland

Sandra Lowe, Obstetric Physician, St George’s Hospital, Sydney

Jonathan Morris, Obstetrician, Royal North Shore Hospital, Sydney

Anne-Marie Hennessey, University of Western Sydney

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CONFERENCE ABSTRACTS

Indications for thrombolysisSanjeev Chunilal

Pulmonary embolism (PE) during pregnancy is associated with a 1 in 40 chance of dying. Although this mortality is lower than 8 – 27% mortality in stable and unstable nonpregnant patients, the latter tend to be significantly older and have associated co-morbidities. As pregnant women have been systematically excluded from studies which have used thrombolytic therapy for PE there remains a paucity of controlled data in the area. We will explore stratification of nonpregnant patients with PE into low and high risk for mortality using echocardiogram and biomarker criterion (Troponin and atrial natriuretic peptide). These data will then be considered in the context of pregnancy. Their validity will be examined focusing on the normal physiological changes during pregnancy. Finally, we will explore the efficacy and safety of thrombolytic therapy for PE outside of pregnancy and how this translates to pregnancy.

Inferior vena cava filters during pregnancy – indications, risks and local experienceLaura Young

Risk of venous thromboembolism (VTE) is increased 5 fold during pregnancy. Up to half of antepartum VTE will occur in the third trimester: IVC filters are a useful adjunct to anticoagulation in the management of VTE which occurs near delivery. Heparin therapy is discontinued during labour due to haemorrhagic risk and IVC filters prevent potential pulmonary emboli (PE) from recent leg or pelvic deep vein thromboses (DVT) during this period. There are no clear guidelines in the literature, but a review of case reports/small series suggests filters are generally considered when acute proximal DVT has occurred ≥36 weeks, or earlier in pregnancy if bleeding complications prevent anticoagulant use.

IVC filters are inserted via jugular or femoral approaches and in the peripartum setting will be retrievable models which can also be extracted percutaneously. Published experience is predominantly in the non-pregnant VTE population and short term. Insertion and removal procedures are safe with few immediate complications. Success rates for removal in the literature are as high as 91% however in Australasian audits are about 60%; consent for IVC filter use must include the risk of failed retrieval.

Complications of longterm filter use include filter thrombosis, DVT and PE. In the one randomised trial of filter use in nonpregnant VTE patients the risk of DVT was increased with indwelling filters.

In summary IVC filters are useful for women with recent VTE and impending labour but the risks of these devices must also be considered in clinical decision making. Three case studies will be presented for further discussion.

Epilepsy in pregnancy – treating for twoElizabeth Walker

The issue of managing epilepsy in pregnancy is currently under scrutiny in the neurology world. There are a number of large prospective databases as well as data from compulsory medical records in Norway on pregnancy outcome. Recently, the American Academy of Neurology has issued guidelines based on extensive review of the literature on management of a number of issues in pregnancy. An overview of the data for pregnancy outcome will be presented. The rate of MCM with drug monotherapy is 3.5% but up to 6% with polytherapy.

The evidence available suggests that the women in pregnancy are not at risk of significant obstetric complications and do not have a higher risk of SGA or severe infection. Some recent studies have suggested that frequent convulsions during pregnancy might be associated with poor neuro-developmental outcome of the offspring.

The risk of valproate has been well established to be associated with a higher risk of major foetal malformation (5 – 6%) compared with other anti-convulsants (3.5%) and especially when it is used in poly-therapy. The recommendation remains that of using monotherapy with the drug most appropriate for the seizure syndrome,

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avoiding valproate if possible, and avoiding poly-therapy if possible. An overview of epilepsy syndromes and drug management will be given.

Therapeutic drug monitoring during pregnancy is critical for lamotrigine where there is a major change in metabolism in the second trimester leading to observation of the reappearance of generalised seizures during the second trimester.

Breast cancer and pregnancyRita Sasidharan

Breast cancer is one of the most commonly diagnosed malignancy during pregnancy. Pregnancy associated breast cancer presents a challenging clinical situation. Trend toward later age at first child birth has resulted in increase in the number of breast cancer cases co existent with pregnancy. Delay in diagnosis remains a problem in pregnancy associated breast cancer. Imaging modalities for staging need to be tailored because of concerns about radiation exposure to the fetus. There is no evidence that pregnancy termination changes overall survival. Management of breast cancer during pregnancy requires a multidisciplinary team approach.

Breast surgery can be safely performed during any trimester of pregnancy. Radiation therapy if required must be delayed until after delivery. Evidence from one prospective cohort and some case control studies and case series support the view that adjuvant chemotherapy can be administered safely during second and third trimester. An anthracycline based regimen is the preferred adjuvant chemotherapy. Currently there is insufficient data regarding safety of Taxanes and Trastuzumab in pregnancy. Endocrine therapy such as Tamoxifen should be withheld until after delivery. Timing of delivery in relation to chemotherapy administration should be carefully considered.

There is no clear evidence so far that subsequent pregnancy after breast cancer is associated with worse maternal survival. There is suggestion that subsequent pregnancy may in fact correspond with an improved survival, however the available studies are limited by potential biases.

Pregnancy issues in women with inherited bleeding disorders: presentation of three individual cases and presentation of a retrospective case series of the use of FVIII/VWF concentrate (biostate) in the management of obstetric patients with severe bleeding disorders in New ZealandShannon Emmett

For women with severe bleeding disorders, pregnancy and particularly delivery can be a time of significant risk to both them and their infants.

The cases of three individual women with different bleeding disorders (severe Type 1 VWD, Type 2B VWD and FIX deficiency) will be discussed. This will include the management of their pregnancies and deliveries.

The retrospective case series, which will be presented, includes all women treated in New Zealand since the introduction of Biostate 4 years ago.

Pregnancy issues in women with inherited bleeding disordersJulia Phillips

Inherited bleeding disorders are common, occurring in approximately 1% of the population. They are associated with an increased risk of post-partum haemorrhage (PPH) and may increase the risk of bleeding in association with interventions during pregnancy and spinal haematoma in association with epidural anaesthesia. A personal or family history of abnormal bleeding should raise suspicion that an inherited bleeding disorder is present.

The majority of women with inherited bleeding disorders have von Willebrand disease. In contrast to PPH in the general population, PPH in women with von Willebrand disease is often delayed, the average time of

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presentation with bleeding being 15 days after delivery. Therapeutic options for prevention and treatment of bleeding in women with von Willebrand disease include plasma-derived factor VIII concentrates, DDAVP and tranexamic acid.

The rarer inherited bleeding disorders include symptomatic carriage of haemophilia A and B, deficiencies of factor I, II, V, VII, X, XI, XIII and platelet function defects. Few data are available to inform the obstetric management of women with these conditions. DDAVP is effective in FVIII deficiency. Other treatment options include tranexamic acid and appropriate coagulation factor concentrates where these are available. Some patients may require fresh frozen plasma or platelet concentrates.

Close collaboration between obstetricians and haematologists is advised to ensure optimal management of women with inherited bleeding disorders during pregnancy, delivery and in the post-partum period.

Consensus expert guidelines on the diagnosis and management of women with von Willebrand andother bleeding disorders have been published recently1. These guidelines and their supporting evidencewill be reviewed.1 James AH, Kouides PA, Abdul-Kadir R, et al. Von Willebrand disease and other bleeding disorders in women:

consensus on diagnosis and management from an international expert panel. Am J Obstet Gynecol 2009;201e1–8.

Maternal mental healthSara Weeks

The management of depression during pregnancy: a report from the American Psychiatric Association and the American College of Obstetricians and Gynecologists, by Yonkers et al gives an excellent review of current thinking around this subject, though of course new literature is being published all the time. A copy of this paper will be provided to attendees.

Bipolar disorder has an extremely high post partum relapse rate, which is further worsened by clinical roughening during pregnancy – however unfortunately the medications used to manage bipolar disorder are challenging to use during pregnancy and breast feeding. In our workshop we intend to use this paper and clinical experience to discuss a number of cases and their management – during pregnancy and post partum. We hope that this workshop will be interactive and welcome questions and discussion.

Overview SCOPE study and screening principles riskfactors and prediction of preeclampsia in SCOPERobyn North

R.A. North1, L.M.E. McCowan2, G.Dekker3, C. Roberts3, L. Poston1, L. Kenny4, P. Baker5, R.Taylor2, J.J. Walker6 on behalf of the SCOPE Consortium.1King’s College London, United Kingdom; 2University of Auckland, New Zealand; 3 University of Adelaide, Australia; 4University College Cork, Ireland; 5The University of Manchester, United Kingdom; 6University of Leeds, United Kingdom.

The main aim of the Screening for Pregnancy Endpoints (SCOPE) project is to develop early pregnancy screening tests that predict preeclampsia, small for gestational age infants (SGA) and spontaneous preterm birth amongst nulliparous women. The SCOPE study is a prospective cohort study of nulliparous women (target n=7,500) to establish a pregnancy biobank with well characterised phenotypes and a comprehensive range of quality specimens, processed according to stringent protocols. Participants are interviewed at 15±1 and 20+1 weeks’ gestation and data collected on demographics, risk factors, medical and family history, current pregnancy, lifestyle and psychological parameters, maternal blood pressure and anthropomorphic measurements. Ultrasound examination at 20 weeks includes fetal measurements and umbilical and uterine artery Doppler waveforms. Data are entered into an internet accessed, auditable database (Medscinet AB,

CONFERENCE ABSTRACTS Continued

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Sweden). Participants are followed prospectively and pregnancy outcome data recorded. To date, there are 4500 participants in SCOPE, with more than 600,000 specimens stored in the biobank. The specimens have been used to discover and validate novel biomarkers, using proteomic, metabolomic and genomic technologies. Clinical risk profiling for each of the main endpoints has been performed in the first 3500 recruits. Results for preeclampsia will be reported. In the future, the screening performance of novel combinations of clinical risk factors, ultrasound measurements and biomarkers will be evaluated in the cohort.

Biomarker discovery in the SCOPE project: proteomic and metabolomic studiesRobyn North

M. Blumenstein, PhD1, L.C. Kenny, PhD MRCOG2, D.I. Broadhurst, PhD3, M.T. McMaster, PhD4, M.A. Black, PhD5, S. Wu, MSc1, R. Prakash BSc1, J. Cooney, PhD6, L.M.E. McCowan, MD FRANZCOG1, G.J.S. Cooper, DPhil FRCPA, FRSNZ1, 7, W. Dunn, PhD3, M. Brown, PhD3, D. B. Kell, PhD3, P.N. Baker, FRCOG, FMedSci3 and R.A North PhD, FRACP8,9

1University of Auckland, New Zealand; 2University College Cork, Ireland; 3The University of Manchester, United Kingdom 4University of California San Francisco, USA, 5University of Otago, New Zealand, 6HortResearch, New Zealand, 7University of Oxford, United Kingdom; 8University of Adelaide, Australia; 9King’s College London, United Kingdom and the SCOPE Consortium

The complex aetiology of preeclampsia involves release of placental factors into the maternal circulation and a maternal predisposition to vascular dysfunction, inflammation and coagulation. We hypothesised that placental-derived proteins and the maternal predisposition may be evident in the plasma proteome and metabolome prior to preeclampsia.

Proteomic Approach. In seven differential gel electrophoresis (DIGE) experiments, we compared the plasma proteome at 20 weeks preceding preeclampsia (n=39) to controls (n=57). Forty-nine spots on the gels were significant (p<0.05, false discovery rate corrected) in repeated experiments, of which 39 were identified by LC-MS/MS. The proteins identified are involved in lipid metabolism, coagulation, complement regulation, extracellular matrix remodelling, protease inhibitor activity and acute-phase responses, indicating novel synergism between pathogenic pathways culminating preeclampsia. Our findings were remarkably similar to proteins complexed to high-density lipoprotein and linked to cardiovascular disease.

Metabolomic Approach. We used metabolomic profiling technology to search for biomarkers in early pregnancy (15 weeks) plasma. A two phase approach was used, with a discovery study (n=60 preeclampsia cases, 60 controls) and validation study (n=39 cases, 40 controls). We identified the presence of a complex metabolic disorder, consistent with impaired mitochondrial fatty acid uptake and utilisation, evident on average 20 weeks prior to the onset of preeclampsia. Of the 45 metabolites that were significantly different prior to preeclampsia, 34 were identified in the validation study. A multivariate predictive model combining 14 metabolites gave an area under the Receiver Operator Characteristic curve of 0.90 with an odds ratios of 17 (95%CI 7–40) and 39 (95%CI 8–189) for discovery and validation data, respectively. This is the first description of the predictive value of metabolomic biomarkers in preeclampsia.

Conclusions: Our findings indicate novel synergism between pathways involved in the pathogenesis of preeclampsia. Ultimately, this protein and metabolite derangement may form the basis of a screening testfor preeclampsia.

Mechanisms of sFLT-1 elevation in primate pregnancyAnne-Marie Hennessy

University of Western Sydney and the Heart Research Institute, Sydney, Australia

The core effects of hypertension and proteinuria are targets in creating animal models of preeclampsia. The additional features of haematological, renal and hepatic changes are rarely seen, and the ‘clinical’ feature of seizure almost never occurs. Given that the pattern of blood pressure adaptation in pregnancy is unique

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to humans and baboons in this arena, the effect of manoeuvres which elevate blood pressure may be highly

relevant to human pregnancy. Similarly, common placental anatomy (haemomonochorial, single disc with

blood flow to the maternal surface of the disc) makes it possible to study likely modulators of placental blood

flow and trophoblast cell function. The recently identified toxin, sFLT-1 (a soluble vascular endothelial growth

factor receptor) can be studied within the context of hypertension and proteinuria and potentially linked to

placental dysfunction. Recent work in our laboratory has identified that acute placental ischaemia is closely

linked with a sustained and dramatic increase in circulating sFLT-1. This increase times directly with an increase

in blood pressure and the eventual development of proteinuria via a renal lesion which closely resembles

human endothelial damage. Further to this, a more recent study has identified that the balance of circulating

cytokines has a similar effect on the eventual and sustained release of sFLT-1 and changes in maternal blood

pressure and proteinuria. The potential to identify whether the sFLT-1 is purely detrimental exists. A pattern

of cause and effect between immune regulators, placental blood flow and hypertension has been made

possible by this approach. The acute nature of these interventions means that interpretation of these events

as relevant to human preeclampsia needs to be made with some caution. However, identifying patterns and

links to hypertension per se has allowed us to link recently discovered placentally-derived toxins with a whole

animal response, and thus the possibility of controlling blood pressure safely with treatments targeted directly

at endothelial cell toxins.

Cessation of smoking early in pregnancy prevents spontaneouspreterm birth and small for gestational age infantsLesley McCowan1L.M.E. McCowan, 2G.A. Dekker, 1E. Chan, 1A. Stewart, 3L.C. Chappell, 1M. Hunter, 4R. Moss-Morriss, 3R.A. North

on behalf of the SCOPE Consortium.

1University of Auckland, New Zealand; 2University of Adelaide, Australia; 3King’s College London, United

Kingdom, 4University of Southampton, United Kingdom

Objectives: To compare pregnancy outcomes between women who ceased smoking in early pregnancy and

those who either did not smoke in pregnancy or continued to smoke.

Design: Prospective cohort study.

Setting: Auckland, New Zealand and Adelaide, Australia.

Participants: 2504 nulliparous women participating in the Screening for Pregnancy Endpoints (SCOPE) study

grouped by maternal smoking status at 15 ±1 weeks’ gestation.

Main outcome measures: Spontaneous preterm birth and small for gestational age infants (birth weight <10th

customised centile). We compared odds of these outcomes between ceased smokers and non-smokers,

and between current smokers and ceased smokers, using logistic regression, adjusting for demographic and

clinical risk factors.

Results: 80% (n=1992) of women were non-smokers, 10% (n=261) ceased smokers, and 10% (n=251) current

smokers. We noted no differences in rates of spontaneous preterm birth (4%, n=88 v 4%, n=10; adjusted odds

ratio 1.03, 95% CI (0.49 to 2.18; P=0.66) or small for gestational age infants (10%, n=195 v 10%, n=27; 1.06, 0.67

to 1.68; P=0.8) between non-smokers and ceased smokers. Current smokers had higher rates of spontaneous

preterm birth (10%, n=25 v 4%, n=10; 3.21, 1.42 to 7.23; P=0.006) and small for gestational age infants (17%, n=42

v 10%, n=27; 1.76, 1.03 to 3.02; P=0.03) than ceased smokers.

Conclusion: In women who ceased smoking before 15 ±1 weeks’ gestation, rates of spontaneous preterm

birth and small for gestational age infants did not differ from those in non smokers, indicating that these severe

adverse effects of smoking may be reversible if smoking is ceased early in pregnancy.

CONFERENCE ABSTRACTS Continued

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Risk factors for customised, normotensive and hypertensive SGA in SCOPE

Lesley McCowan1L.M.E. McCowan, 2C.T. Roberts, 2G.A. Dekker, 1R.S. Taylor, 1E.H.Y. Chan, 3L.C. Kenny, 4L.C.Chappell, 4R.A. North on behalf of the SCOPE Consortium.1University of Auckland, New Zealand; 2University of Adelaide, Australia; 3University College Cork, Ireland, 4King’s College London, United Kingdom

Objective: To identify clinical risk factors and ultrasound variables associated with the birth of infants who are SGA by customised centiles. We hypothesised that risk factors for SGA would differ if the mother was normotensive or had hypertensive complications.

Methods: 2459 nulliparous participants in the SCOPE (Screening for Pregnancy Endpoints) study were interviewed at 15±1 weeks and had ultrasound growth measurements, umbilical and uterine Dopplers at 20±1 weeks. Variables independently associated with SGA (birthweight <10th customised centile), Normotensive-SGA and Hypertensive-SGA were identifed using logistic regression.

Results: Among 255 (10.4%) SGA infants, 190 (7.7%) were Normotensive-SGA and 65 (2.7%) Hypertensive-SGA. Risk factors associated with SGA and/or Normotensive-SGA (underlined) included older age, lower maternal birthweight, cigarettes, marijuana, current tertiary student, no computer use, termination≤10wks with same partner, >12 months to conceive, asthma, chronic hypertension, family history of preeclampsia, preterm birth or chronic hypertension, vegetarian, low fruit intake pre-pregnancy, small fetal head circumference, and increasing uterine Doppler. High pre-pregnancy green leafy vegetable intake and larger maternal head circumference was protective. Hypertensive-SGA risk factors included increasing socio-economic index, watching >5h television/day, no computer use, fertility treatment, miscarriage >10 wks or termination <10 wks with same partner, family history of preterm birth, moderate-heavy vaginal bleeding, increasing diastolic BP, larger arm circumference, exhausted after work and increasing uterine and umbilical Doppler resistance index. Curtailing activities was protective.

Conclusions: Novel risk factors for infants SGA by customised centiles are identified. Differences in risk factor profiles for Normotensive-SGA and Hypertensive-SGA pregnancies may reflect differences in their pathophysiology.

The Influenza A (H1N1) pandemic: implications or and the management of pregnant womenSally Roberts

Since late April 2009 a new strain on influenza virus has spread worldwide resulting in WHO declaring a pandemic on 11th June. Up until early October there had been 3233 confirmed cases in New Zealand with 1001 hospitalisations and 36,910 confirmed cases in Australia with 4,830 hospitalisations.

During seasonal influenza epidemics and previous influenza pandemics pregnant women have increased morbidity and mortality compared to non-pregnant women. A number of reports from early on in this current pandemic have shown an increased risk for complications, including admission to intensive care, in pregnant women. The USA Novel Influenza A (H1N1) Pregnancy Working Group1 reported that the admission rate for pregnant women exceeded that of the general population. Subsequent reports on the first 272 hospitalised patients in the USA reported 18 (7%) to be pregnant, of whom 6 (33%) had another underlying medical condition such as asthma or diabetes.2 From June 1 to August 31, 2009, 722 patients with Influenza A (H1N1) were admitted New Zealand and Australian Intensive Care Units and 66 (9.1%) were pregnant.3

Pregnant women appear to be at risk of more severe disease and the prompt initiation of antivirals should occur. The current Influenza A (H1N1) strain has been incorporated in the Southern Hemisphere 2010 Influenza vaccine and the use of vaccination should be recommended to all pregnant women.

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1 Jamieson DJ, Hanein MA, Rasmussen SA et al H1N1 2009 influenza virus infection during pregnancy in the USA. Lancet July 29, 2009 DOI:10.1016/S0140-6736(09)61304-0

2 Jain S, Kamimoto L, Bramley AM et al Hospitalised patients with 2009 H1N1 Influenza in the United States, April – June 2009. NEJM 2009; 361

3 The ANZAC Influenza Investigators Critical care Services and 20089 H1N1 Influenza in Australia and New Zealand. NEJM 2009; 361

Biography: Dr Sally Roberts is a graduate of the University of Auckland School of Medicine graduating in 1989. She is a Clinical Microbiologist and Infectious Diseases Physician at Auckland City Hospital and is the Clinical Head of Microbiology at LabPlus, Auckland District Health Board. She was appointed as an Honorary Clinical Senior Lecturer in Department of Medicine, Faculty of Medicine & Health Sciences

Dr Roberts has been on a number of New Zealand Ministry of Health working groups including the MRSA Guidelines Working Group (2002), Scientific Advisory Group for the National Health Committee on antenatal HIV screening (2003), Chair of the National Antenatal HIV Screening Implementation Advisory Group (2005 onwards), Pandemic Influenza Technical Advisory Group, and Tuberculosis Working Group. She provided advice to the Ministry of Health during the recent influenza pandemic and has recently presented the New Zealand data at the 5th Australian Influenza Symposium.

Debate: “Obesity should be managed like diabetes during pregnancy”Janet Rowan

Obese women have higher postprandial glucoses levels compared with lean women and have increased pregnancy risks similar to women with GDM. Lifestyle is a logical cornerstone of treatment for obesity, but I am going to argue that more is required.

In women with GDM, outcomes are improved by lifestyle intervention, pharmacotherapy when required, careful monitoring of the pregnancy and timely delivery. In obese women with GDM compared to lean women with GDM, adverse outcomes are increased if a woman is managed by lifestyle measures but not if managed with insulin. Does pharmacotherapy provide additional advantages over lifestyle? Is it more effective at improving fetal nutrient supply? Are women more accurate about their glucose measurements once they are taking insulin? Is there a role for metformin?

The MiG trial, as well as comparing insulin with metformin for treatment of GDM, had a prespecified aim to examine the impact of glucose control and obesity on outcomes. These data will be shown to strengthen the case for managing obese women in a diabetes clinic….. but cannot be revealed before the debate!

Novel influenza A (H1N1) 09: Clinical outcomes in pregnantwomen from National Women’s Health and Auckland City HospitalMay Ching Soh

Authors: May Ching Soh1, Claire McLintock1, Sally Roberts2, Ngaire Bates2, Eileen Bass1, Matthew Hogg1, Margaret Croxson2 and Lucille Wilkinson1.1 National Women’s Health, Auckland City Hospital, Auckland, New Zealand.2 Auckland City Hospital, Auckland, New Zealand.

Objective: To determine maternal and fetal morbidity and mortality in women with Novel Influenza A (H1N1) 09 who presented to Auckland City Hospital during the 2009 Antipodean winter.

Methods: Pregnant women who had presented to our centre with confirmed or probable novel Influenza A (H1N1) 09 detected via RT-PCR on nasopharyngeal swabs between 1 June – 1 Sept, 2009 were included.

Women who were not pregnant, or were transferred to our hospital from other centres specifically for ventilatory support were excluded.

CONFERENCE ABSTRACTS Continued

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Main outcome measures: Maternal outcomes included admission to intensive care unit (ICU), duration of hospital admission, rate of preterm delivery and indication, mode of delivery. Fetal outcomes included rate of infection, gestation at delivery, mode of delivery, admission to NICU.

Results: Twenty-six women were included. 22 women had confirmed infection, and four had Influenza A, not further subtyped in their nasopharyngeal swabs. Thirteen (50%) were Pacific Island or Maori, seven (27%) European and four (15%) Southeast Asian, and two women were from other ethnic groups. Thirteen women (50%) presented in the 3rd trimester. Median body mass index was 29.4 kg/m2 (range 19.8 – 59.2). Of the 17 women who had a chest X-ray on presentation, it was abnormal in ten. Two women were admitted to ICU due to severe maternal hypoxia. There were no maternal or neonatal deaths. Average duration of stay was 3.9 days (range 0 – 52 days). To date, 12 women have delivered, one woman had an ectopic pregnancy at six weeks. Median gestation at delivery was 39+2 weeks (range 32+0 – 40+5 weeks). No adverse neonatal outcomes were reported.

Conclusion: In this cohort of pregnant and postpartum women with novel Influenza A (H1N1) 09 a majority presented in the third trimester, had a high BMI or were of Polynesian ethnicity. Delayed presentation to hospital and radiologic evidence of multilobar consolidation were markers of poor outcome. There were no adverse neonatal outcomes reported as a result of maternal H1N1 infection.

FREE COMMUNICATIONS – SATURDAY

Preeclampsia and SGA session

1. The effect of cuff size on blood pressure measurement in pregnancyJL Ram, CL Ko, MA Brown, S Ong and GJ Mangos. Departments of Medicine and Renal Medicine, St George Clinical School, University of New South Wales, Kogarah, NSW 2217

Introduction: International guidelines and consensus recommend the use of a large cuff when arm circumference (AC) exceeds 33cm for mercury sphygmomanometry, and 32cm for automated BP measurement, yet there have been no studies in pregnancy comparing the effect of cuff size on BP measurement. We measured BP using standard and large cuffs in two studies. In Study 1, we used mercury sphygmomanometry, and in Study 2, an Omron IA2 automated device, in pregnant women with a range of arm sizes and BPs.

Methods: Study 1: A random zero sphygmomanometer was used by a trained observer to measure BP in 219 pregnant women. Six BP readings were taken, three with a standard ‘adult’ and 3 with a ‘large’ cuff, in random order. Study 2: We repeated the study using an automated Omron IA2 blood pressure monitor. We measured BP on 220 pregnant women using a standard size cuff and using a large cuff, in random order.

Results: Study 1: Women with larger arms (AC > 33 cm) were similar in age, gestation (in weeks) and parity but were heavier and were more likely to be hypertensive than those with smaller arms (AC ≤ 33 cm). BP measurements with a standard cuff were generally higher than those with a large cuff (87%/92%, sys/dias, standard cuff ≥ large cuff BP, p<0.05). Using mercury sphygmomanometry, there was a mean difference between the standard and large cuff of 6±6/6±5 mmHg (standard cuff > large cuff BP) with little effect (2%/4%, sys/dias, p<0.05) due to AC. Compared with a large cuff, a standard cuff will diagnose HT in an extra 5% of women with AC ≤ 33 cm and an extra 7% of women with AC > 33 cm. Study 2: Using automated BP measurement, we demonstrated a mean difference of 5±6/2±5 mmHg (standard cuff BP > large cuff), with no effect (0.6%/0.4%, sys/dias, p=ns) due to AC. In both studies, we were unable to demonstrate any clinically meaningful relationship between the difference in measured BP (standard-large cuff) and AC.

Conclusions: Measured BP appears to be more dependent on the cuff size used than AC. Our studies challenge the practice of using a large cuff for large arms in pregnancy, and do not support the arbitrary AC cut-offs recommended in clinical guidelines.

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2. Comparison of the fetal thymus size between normal and pre-eclamptic pregnancies

NA Mohamed*, MJ Peek, A Kirby, R NananSydney Medical School – Nepean. The University of Sydney

Background: It has been suggested that preeclampsia involves the rejection of the fetus by the maternal

immune system, mediated by thymus derived T lymphocytes. Whether this immune process involves size

changes of the fetal thymus is unknown.

Objective: The purpose of this study was to determine whether the fetal thymus is decreased in size in

preeclampsia affected pregnancies compared to normal pregnancies.

Study design: This was a cross-sectional, prospective, comparative study of fetal thymus in 39 women

diagnosed with preeclampsia and 72 healthy pregnant controls. Fetal thymus was measured during ultrasound

fetal growth assessment in fetuses of those patients. The thymus size was determined sonographically in

singleton pregnancies at weeks’ gestation.

Results: There was strong evidence that both the diameter and the perimeter of the fetal thymus are smaller

in women with preeclampsia than in women with normal pregnancies. The means and standard deviations of

thymus diameter were 32.68(±4.68) and 28.60(±5.94) for normal and pre-eclamptic pregnancies respectively

(p<001).The means and standard deviations of thymus perimeter were 92.39(±16.8) and 80.67(±16) for normal

and pre-eclamptic pregnancies respectively (p<001).

Conclusion: Thymic involution appears to be a fetal response to preeclampsia in pregnancy, strengthening

the evidence for the involvement of the immune system in the disease. Future studies will be needed to show

whether the fetal thymus size can be used in the management of preeclampsia or to predict fetal well-being.

3. Growth restriction in pregnancies of opioid-dependent mothers

Anthony JW Liu1, Sinthu Sithamparanathan1, Michael P Jones2, Colleen-Maree Cook1, Ralph Nanan1

1 Sydney Medical School – Nepean, The University of Sydney, Penrith, New South Wales, Australia

2 Psychology Department, Macquarie University, North Ryde, New South Wales, Australia

Background and aims: Intrauterine growth restriction (IUGR) can lead to significant intellectual and

behavioural problems in later life. IUGR represents a frequent feature of pregnancies of opioid-dependent

mothers (ODMs), the causes of which are largely unknown. The objective of this study was to determine the

independent risk factors for IUGR in ODMs.

Design and subjects: We performed a retrospective study analysing maternal and neonatal parameters from

pregnancies of ODM maintained on methadone (n=215). These were compared to smoking non-ODM and

non-smoking non-ODM control groups matched for maternal age, gestational age at delivery, infant birth

date and gender. Logistic regression analysis was performed on all parameters with the outcome of IUGR.

Results: Fifty-seven infants (27%) of ODMs showed symmetrical IUGR. Compared to non-smoking non-ODMs,

the risk of IUGR in non-smoking ODMs was almost 4 times higher (RR 3.48, 95% CI:1.70 – 7.14). Growth restriction

was independent of the last maternal methadone dose and the cumulative methadone dose during

pregnancy. In addition, whereas nicotine and female gender impacted on IUGR in non-ODMs (ORnicotine 3.45,

95% CI:1.82 – 6.67, ORgender 2.37, 95% CI:1.25 – 4.50), these parameters had no influence on IUGR in ODMs.

Maternal body mass index (BMI) was identified as the only independent risk factor for IUGR in infants of ODMs

(OR 1.15, 95% CI:1.03 – 1.28).

Conclusions: Intrauterine growth restriction in pregnancies of ODM is related to maternal BMI rather than to

opiate dosing, nicotine use or infant gender. BMI may itself be an indirect marker of several other genetic,

nutritional and/or social determinants of IUGR.

FREE COMMUNICATIONS – SATURDAY Continued

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4. The role of T regulatory and TH17 cells in healthy pregnancy and in preeclampsiaBrigitte Santner-Nanan*, Michael John Peek*, Roma Khanam*, Luise Richarts*, Erhua Zhu‡, Barbara Fazekas de St Groth‡ and Ralph Nanan*

*Nepean Clinical School, The University of Sydney NSW 2751, Australia. ‡Centenary Institute, The University of Sydney, NSW 2042, Australia.

Preeclampsia is the leading cause of morbidity and mortality in pregnancy. Although the aetiology of preeclampsia is still unclear, it is believed to involve maternal rejection of the fetus, possibly due to a suboptimal maternal regulatory T cell (Treg) response. To test whether preeclampsia is associated with an imbalance between maternal Treg cells and effector T cells, we compared the frequencies of circulating Treg, Th1 and Th17 cells at the end of the third trimester of healthy and pre-eclamptic pregnancies. The size of the Treg cell compartment, defined by the frequency of CD4+CD25hi, CD4+CD127loCD25+ and CD4+Foxp3+ cells was significantly higher in normal compared with pre-eclamptic pregnancies. CD4+CD25hi and CD4+CD127loCD25+ populations in preeclampsia were not significantly different from those in non-pregnant controls, while CD4+Foxp3+ cells numbers were slightly lower in preeclampsia. The suppressive activity of ex vivo sorted CD4+CD127loCD25+ Treg cells was not significantly different between the 3 study groups. The percentage of CD4+IL-17-producing cells decreased significantly in healthy compared with pre-eclamptic pregnancies and non-pregnant controls, whereas CD4+IL-10- and CD4+IFNγ-producing cells remained unchanged. Consequently, the ratio of Treg to Th17 cells was significantly increased in healthy but not in pre-eclamptic pregnancies. Thus, preeclampsia is associated with the absence of normal systemic skewing from Th17 to Treg. Finally, pre-eclamptic women had significantly higher levels of soluble endoglin, an inhibitor of TGF-β receptor signalling, which may bias towards IL-17 production. These results suggest that Treg/Th17 homeostasis might be pivotal for the semi-allogeneic fetus to be tolerated within the maternal environment.

5. Endothelial function is different in women with preeclampsiacompared to women with gestational hypertension

Ann E Quinton, Michael J Peek, Colleen-Maree Cook. Discipline of Obstetrics & Gynaecology, Sydney Medical School, Nepean, University of Sydney. Sydney, Australia

Objective: To assess endothelial function using the ultrasound technique of flow mediated dilatation (FMD) in women with preeclampsia (PE) versus gestational hypertension (GH).

Method: Pregnant women were recruited on admission to hospital with hypertension (BP ≥140/90mmHg). Women who also had proteinuria ≥300mg/24 hours were defined as PE, the non-proteinuric group as GH.

Pregnant women were recruited on admission to hospital with hypertension (BP ≥140/90mmHg). Women who also had proteinuria ≥300mg/24 hours were defined as PE, the non-proteinuric group as GH. Ultrasound measurements of the brachial artery diameter pre and post induced reactive hyperaemia were used to calculate FMD, a marker of stimulated endothelial function. Basal volumetric flow (BVF) was calculated from basal arterial diameter and arterial Doppler waveform.

Results: The participants in the two groups were evenly matched in baseline characteristics, except for proteinuria. FMD (m ± SD) was significantly reduced in the GH group (4.4 ± 3.1) compared to the PE group (8.2 ± 4.4) (P<0.0001). There was evidence of a significant interaction between PE and GH (P=0.037) so the diseases were compared separately in the medication and no medication groups. A significant difference between PE (8.9 ± 4.3) and GH (3.7 ± 2.9) when treated with hypertensive medication was found (P<0.0001). There was no difference in FMD between PE and GH when the women were not on medication (P=0.47). The FMD of the PE women was similar to our previously published normal range (9.3 ± 5.0). BVF was significantly decreased in the PE group (399 ± 197) compared to the GH group (509 ± 241) (P=0.04).

Conclusion: In women with GH, endothelial dysfunction was detected whereas the PE group was similar to our normal range in pregnancy. This increase in FMD and decrease in BVF in the PE group may be due to the pathophysiology of PE and be indicative of a compensatory response of the endothelium in PE resulting

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in near normalisation of endothelial function as a rescue mechanism. Interestingly, hypertension has been associated with endothelial dysfunction in non-pregnant adults. From a physiological viewpoint we have shown that PE and GH are different and we hypothesise that PE may therefore be a different disease to GH.

CASES

The other cardiomyopathy of pregnancyDr Anna Antonas, Pro Stephen Gatt, Dr Robert Buist, Dr Sandra Lowe

A 39 year old primigravida presented at 1 week postpartum with acute cardiac failure associated with significant hypertension. She was managed with diuretics, inotropic therapy and ACE Inhibitors. Her left ventricular dysfunction and hypertension returned to normal over one month and she was able to cease all therapy. An exercise stress ECHO performed 3 months later was completely normal.

More than 2 years later she had a further pregnancy. She was monitored with regular cardiac ECHOs and remained well until 34+ weeks gestation. At that time she was admitted to hospital with preeclampsia characterised by moderate hypertension, a slowly falling platelet count and low level proteinuria. She was commenced on a small dose of labetalol which controlled her hypertension. The planned electiveCaesarean section was brought forward but two days prior at 36+ weeks gestation she developed an intercurrent illness with headache, rhinorrhoea and slight sore throat. That evening she became acutely unwell with worsening hypertension refractory to antihypertensive therapy. Over a period of hours she developed pulmonary oedema and an urgent cardiac ECHO demonstrated mild-moderate LV impairment with pulmonary hypertension.

The management of her subsequent delivery and recovery will be discussed.

Illicit substance use in pregnancy – ‘ecstasy’ and agonyKatherine Scott, Karin Lust, Narelle Fagermo, Royal Brisbane and Women’s Hospital

We present the case of a 20 year old university student with an undiagnosed pregnancy who had taken Ecstasy and LSD during end of semester celebrations. Within 24 hours she delivered a still-born term male infant, and subsequently went on to develop eclampsia with seizures, hypertension and proteinuria.

Illicit drug use is not uncommon (up to 22%1) in women of childbearing age and is a significant risk factor for adverse obstetric outcomes. There are 2 case reports of amphetamine use in the peripartum period presenting as an eclamptic syndrome2,3, however no reports of this occurring for Ecstasy or LSD.

Ecstasy (MDMA) is a sympathomimetic amine, similar to amphetamine in its cardiovascular effects, although its structural similarity to serotonin causes the most significant adverse effects of hyperthermia and neurotoxicity. Effects on the cardiovascular system and placental vasculature have not been well described.

LSD was widely studied in animal models during the 1970s and has been shown to cross the placenta, and to cause vasoconstriction of both the uterine and umbilical arteries, with potential for significant compromise of placental blood flow. LSD and its metabolites have also been shown to have a mild oxytocic effect.

We postulate that the combined vasoconstrictive effects of MDMA and LSD resulted in an eclamptic syndrome in this patient, and briefly discuss the literature regarding effects of illicit substance use on pregnancy. 1 National Drug Strategy Household Survey 2007 www.aihw.com.au2 Kuczkowski K. Postpartum convulsions with acute haemodynamic instability in the parturient with recent

amphetamine intake. Arch Gyn Obstet online Jan 23 20093 Elliot R. Amphetamine ingestion presenting as eclampsia. Can J Anaes 1990:31:130–3

FREE COMMUNICATIONS – SATURDAY Continued

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FREE COMMUNICATIONS – SUNDAY

Investigation for suspected pulmonary embolism in pregnancyKatherine Scott, Natalie Rutherford, Karin Lust, Royal Brisbane and Women’s Hospital Brisbane

Pulmonary embolism (PE) is recognised as a leading cause of maternal mortality in the developed world, yet it is a very difficult diagnosis to make on clinical grounds. Supplementary investigations including D-dimer and arterial blood gases (ABGs) are often used to support or exclude the diagnosis, however in most cases imaging is required, despite concerns regarding the risk of ionising radiation to mother and fetus

An audit of all CTPA and VQ/Nuclear Medicine (NM) scans performed at our hospital during pregnancy or postpartum, over a six year period, found 393 scans were done to investigate 382 cases of suspected PE. PE was diagnosed in 15 cases, giving an incidence of 1:2000 confinements, half ante-partum and half post-partum, consistent with reported rates. There were no fatal episodes of PE in the period studied.

Clinical indicators and risk factors were not different enough to discriminate between those with and without PE. Mean D-dimer was statistically different between the groups although not to a clinically useful degree, and ABG was neither clinically nor statistically different. The rate of non-diagnostic imaging was very low (CTPA 8.3%, VQ/NM 1.5%)

We conclude that currently available clinical and laboratory tools are not able to adequately diagnose PE in pregnancy, therefore imaging is indicated. Given the high rate of negative imaging there is a pressing need for further prospective research to develop more reliable clinical algorithms and non-invasive tools for diagnosis of PE.

Perinatal risk factors for the neonatal abstinence syndrome ininfants born to women on methadone maintenance therapyAnthony JW Liu1, Michael P Jones2, Henry Murray1, Colleen-Maree Cook1, Ralph Nanan1

1 Sydney Medical School – Nepean, The University of Sydney, Penrith, New South Wales, Australia2 Psychology Department, Macquarie University, North Ryde, New South Wales, Australia

Background: Following intrauterine opiate exposure neonatal withdrawal occurs in more than 50% of infants. Maternal methadone dosing has been investigated with conflicting results.

Objectives: To correlate maternal methadone dose and other risk factors with the development of the neonatal abstinence syndrome (NAS). The aim was to use parameters, which are easily accessible to clinicians managing these patients.

Risk Factor No PE PE p-value

Past History 5.1% 6.6% 0.79

Family History 8.6% 14.3% 0.47

Smoking 23.4% 53.9% 0.012

CS (postpartum PE) 56.6% 75% 0.31

Thrombophilia 24.6% 33.3% 0.53

> 1 Risk Factor 20.5% 46.7% 0.016

Heart rate <100 66.2% 53.3% 0.56

D-dimer <0.15 1.6% 0% N/A

A-a gradient <12 41.8% 20% 0.64

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Methods: Retrospective medical record review of data from 228 cases of opioid dependent pregnant women who delivered 232 live-born infants. Logistic regression analysis was performed on maternal, perinatal and neonatal parameters to identify risk factors for NAS. A prediction model was developed and validated on a separate independent cohort of 188 cases.

Results: Of the 232 infants, 172 (74%) infants were treated for NAS. The risk of withdrawal increased by 17% per 5mg increment of the last maternal methadone dose. The risk was lower for younger gestational ages and for those delivered by Caesarean section compared to those delivered by normal vaginal delivery. Through predictive modeling, gestational age, mode of delivery and last methadone dose were established as risk factors for withdrawal. The model was validated by other statistical measures and its diagnostic performance confirmed on the separate independent cohort.

Conclusions: Our data suggests that timing and mode of delivery as well as last maternal methadone dose are significant risk factors for the development of NAS. Based on these clinical parameters, risk stratification for perinatal management of pregnancies associated with opioid dependency and risk prediction for the neonate might now be possible.

Does routine assessment of thyroid function inhyperemesis gravidarum add valuable information?Nicholas Bedford, (Senior Registrar O&G, Wellington Hospital); Maria Kladnitskia MbChB (Registrar O&G, Wellington Hospital); Michel Sangalli, (MFM Sub-specialist, Wellington Hospital)

Introduction: Nausea and vomiting affects 50-70% of pregnant women1, and hyperemesis gravidarum (HG) occurs in 5%2. HG may be associated with a transient biochemical hyperthyroidism3,4, and previous research has shown resolution without need for treatment5. We hypothesised that there would be no difference in clinical outcomes regardless of thyroid function test (TFT) results, including women who were not tested.

Methods: All cases presenting to the Women’s Health Service at Wellington Hospital between January 2005 and December 2007 with nausea and vomiting in pregnancy were reviewed. 147 first presentations were identified. Data were gathered including demographics, clinical evidence of degree of illness, inpatient management parameters, and results of TFTs. Recurrent admissions were also reviewed.

Results: TFTs were performed in 90/147 (63%) patients, and were abnormal (T4>20.4mmol/L and/or TSH <0.4mmol/L) in 50/90 (56%). Patients who had TFTs performed were more likely (p<0.05) to have clinical evidence of dehydration and significant ketosis. There was also a significant difference (p<0.05) in volume of fluids given, but no difference in duration of stay, requirement for repeat admissions or cumulative days spent in hospital when compared to the untested group. When the group tested were divided into normal and abnormal results, there were significant differences in volume of fluids administered and proportion with electrolyte disturbance, but number of presentations, duration of stay at first admission, or total days in hospital did not reach significance.

Comment: The group who had TFTs performed were clinically more dehydrated and required more fluid management at initial presentation. However outcome measures including duration of stay, total inpatient days, and need for recurrent admissions did not differ between the three groups. Abnormal TFTs may therefore be a proxy for more marked clinical findings, but do not add to normal management. TFTs can therefore be omitted in the routine assessment of hyperemesis, in the absence of other markers of thyroid disease.

References:1 Thyroid disease in pregnancy. ACOG Practice Bulletin No. 37. American College of Obstetricians and

Gynecologists. Obstet Gynecol 2002;100:387–396.2 Nelson-Piercy, C. Handbook of Obstetric Medicine. 3rd Ed., 2006, Informa Healthcare. Pp241–249.3 Goodwin TM, Montoro M, Mestman JH, et al. The role of chorionic gonadotropin in transient hyperthyroidism

of hyperemesis gravidarum. J Clin Endocrinol Metab 1992;75:1333–7.

FREE COMMUNICATIONS – SUNDAY Continued

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4 Fantz CR, Dagogo-Jack S, Ladensen JH, Gronowski AM. Thyroid function during pregnancy. Clin Chem 1999;45:2250–2258

5 Tan JYL, Loh KC, Yeo GSH, Chee YC. Transient hyperthyroidism of hyperemesis gravidarum. BJOG 2002;109:683–688.

Population trends in pulmonary embolism following childbirthJonathan Morris, Charles Algert, Jane Ford, Christine Roberts, Perinatal Research, Kolling Institute,University of Sydney

Background: Pulmonary embolism is the leading cause of maternal death in developed countries. Surgery is a risk factor for pulmonary embolism, and the rate of pulmonary embolism is higher in women who have been delivered by Caesarean section. The incidence of maternal pulmonary embolism has risen in the US in parallel with an increasing rate of Caesarean delivery. There are no Australian data describing trends in puerperal pulmonary embolism at a time when risk factors such as operative delivery, maternal age and maternal BMI are increasing.

Aim: To determine trends and predictive factors for puerperal pulmonary embolism without a known antenatal venous thrombotic event.

Methods: The study population included all maternities in New South Wales (NSW) during 2001 – 2006. Linked birth and hospital admissions records were utilised . The Midwives Data Collection (MDC) collects information on all births ≥20 weeks gestation in NSW. Venous thromboembolism (VTE) events were identified by searching the first five ICD10 diagnosis fields in each hospital discharge record. As well as antenatal and delivery records, admission records up to 12 weeks postpartum were included.

Results: There were 510,916 maternities, to 340,041 women, during 2001 – 2006 that could be linked to both a birth record (MDC) and a hospital admission (APDC). This was 98.5% of all births recorded in the MDC for the period. Among these were 399 maternities where a pulmonary embolism was recorded (0.79 per 1000). There were 259 maternities where a puerperal pulmonary embolism occurred with no antenatal VTE (0.51 per 1000). The rate of Caesarean section rose steadily over the period, from 23.6% of all deliveries in 2001 to 28.9% of deliveries in 2006. The rate of puerperal pulmonary embolism following caesarean rose from 2001 to 2002 but declined gradually each year thereafter. The rate following caesarean section was 2.6 times the rate following vaginal delivery in 2001 and this ratio had declined to 2.2 by 2006. A stillbirth at the current pregnancy represented the largest increase in risk for pulmonary embolism, followed by a history of VTE in a prior pregnancy.

Conclusion: Despite an increase in the rate of Caesarean Section the incidence of puerperal pulmonary embolism is not increasing.

Supported by Funding from National Health and Medical Research Council.

SOMANZ TRAVEL GRANTS AND AWARDSSOMANZ President’s AwardBest clinical presentation by a SOMANZ member at the meeting. AUS$1000.00 – judged by an expert panel at the meeting and is awarded on the last day. Award is provided through an educational grant from Novo Nordisk.

SOMANZ Andrew Phippard Memorial AwardBest oral scientific presentation by a junior member during the meeting. AUS$1000.00 and willbe judged by an expert panel at the meeting and is awarded on the last day.

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SPONSORSThe support of the Meeting sponsors is gratefully acknowledged

Major sponsorCSL Bioplasma189 – 209 Camp RoadBroadmeadows, Vic 3047Australia

Tel: +61 3 9246 5200Fax: +61 3 9246 5299

Contact: Chris FryEmail: christopher.fry@csl.com.auWebsite: csl.com.au, www.cslbiotherapies.co.nz

CSL Bioplasma is and has been the chosen national plasma fractionator of Australia and New Zealand since 1953 and 1962 respectively. Today from voluntary and non-remunerated donations collected in Australia and New Zealand, CSL Bioplasma fractionates a near complete range of plasma-derived therapeutics including coagulation factors, immunoglobulins and albumin.

We are also the chosen national fractionator of Hong Kong, Malaysia, Singapore and Taiwan. Working closely with government health authorities and blood services in each of these countries CSL Bioplasma delivers the benefits that self-sufficiency provides – a sustainable, reliable and high quality source of plasma-derived therapeutics designed specifically to meet each country’s needs. Self-sufficiency protects countries from international supply fluctuations that can lead, and have in the past, to global shortages of these essential products.

CSL has also manufactured blood grouping reagents since the 1930s, and today CSL Bioplasma Immunohaematology provides reagent red blood cells, monoclonal antibodies and associated reagents for immunohaematology testing used to detect and prevent haemolytic transfusion reactions and haemolytic disease of the foetus and newborn.

CSL Bioplasma manufactures plasma products at its purpose built, state of the art plasma fractionation facility at Broadmeadows, near Melbourne, Australia.1,2 Commissioned in 1994, it is one of the most sophisticated plasma fractionation facilities in the world, and was the first commercial scale plasma fractionation facility to use chromatography as its core plasma fractionation technology to separate the individual proteins present in plasma. Chromatography is a gentle and predictable process that produces higher yielding and higher purity plasma-derived products compared to traditional plasma fractionation processes.2

CSL Bioplasma manufactures its entire portfolio of plasma-derived therapeutics using two dedicated and complementary pathogen reduction steps.1 These two steps are included in the manufacturing process of each product solely for the purpose of inactivating or removing pathogens, allowing CSL Bioplasma to maximise product safety.

As a result of its ongoing pioneering work in plasma purification and pathogen safety, CSL Bioplasma offers a portfolio of world class plasma-derived therapeutics.

CSL 1231

References:1 Flood P et al Review of Australia’s Plasma Fractionation Arrangements, Commonwealth of Australia, 20062 Johnston A, Adcock W. The use of chromatography to manufacture purer and safer plasma products.

Biotechnology & Genetic Engineering Reviews. 2000; 17:37–70.

CSL Biotherapies (NZ) Limited666 Great South Road Penrose, AucklandNew Zealand

Tel: +64 9 579 8105Fax: +64 9 579 8106

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International speaker sponsorsanofi-aventis New Zealand limitedLevel 8 James & Wells Tower 56 Cawley StreetEllerslie, Auckland, New Zealand

Tel: +64 9 580 1810 Fax: +64 9 580 1811

Contact: Chet Wiese, Hospital Product Manager NZEmail: chet.wiese@sanofi-aventis.comWebsite: www.sanofi-aventis.com

sanofi-aventis, a leading global pharmaceutical company, discovers, develops and distributes therapeutic solutions to improve the lives of everyone. As a world-class R&D organisation, sanofi-aventis is developing leading positions in six major therapeutic areas: cardiometabolic diseases, thrombosis, oncology, central nervous system, internal medicine and vaccines.

With the recent acquisition of Australia’s leading nutraceutical brands including Nature’s Own and Cenovis, sanofi-aventis ANZ is now a horizontally integrated healthcare provider from complementary medicines, through to patented medicines, generics, over the counter medicines, and vaccines.

With one of the richest and most innovative portfolios in the pharmaceutical industry today, sanofi-aventis currently have 113 compounds in development. In Australia, we are conducting 104 separate trials of both registered products and new compounds.

For many years, sanofi-aventis has also recognised its corporate social responsibilities. Internationally, through our Access to Medicines division, we help fight to eradicate diseases such as: Malaria, African Sleeping Sickness, Leishmaniasis and Tuberculosis. Locally, we support: Angel Flight Australia who co-ordinate non-emergency flights for financially disadvantage people who need medical attention; a number of indigenous health programs across Australia; an East Timorese project to help diagnose and treat epilepsy; and donate our products to those in need through World Vision.

At sanofi-aventis, we are committed to our customers, our employees and even more importantly to the people who rely daily on our medicines.

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Aspen Pharmacare Australia is a subsidiary of Aspen Pharmacare Holdings Limited, the largest listed pharmaceutical company in South Africa. Aspen Pharmacare Australia commenced operations in May 2001. Current annualised sales are $135 million and growing. Besides marketing and distributing products owned by the Aspen Group, we license in products from other companies, and are focused on meeting the needs of our licensors. Aspen Pharmacare Australia is an entrepreneurial driven company which seeks to identify and bring to market drugs in specialist areas that are overlooked by the multinational pharmaceutical industry. We often work in partnership with other companies, including the multinationals.

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As a world-class R&D organisation, sanofi-aventis is developing leading positions in six major therapeutic areas: cardiometabolic diseases, thrombosis, oncology, central nervous system, internal medicine and vaccines.

Sanofi-aventis is proud to be associated with this established and prominent annual meeting of the “cream” of the Australasian obstetric medicine community.

If you would like further information regarding sanofi-aventis products, please contact the medical information department on 0800 119 519 or medinfo.australia@sanofi-aventis.com

Sanofi-aventisresearches and developsmedicines and vaccinesto improve the livesof the greatest numberof people.

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GENERAL INFORMATIONThe following information is offered to make your attendance at the Meeting as pleasant and astrouble-free as possible. If you require help, please call at the registration desk and we will do everythingwe can to assist you.

Accommodation For those registrants who have reserved hotel accommodation through The Conference Company, please ensure that accounts are settled in full prior to your departure and that the appropriate deposit has been deducted from your account.

Badges As a security requirement, we request that participants wear their Meeting name badges at to all sessions.

Car parking Liverpool Street Car Park (Tournament Parking)Corner of Karangahape Road & Liverpool Streets. Enter via Liverpool Street (off City Road).Rates are as follows: NZ$4.00 per half hourMaximum NZ$36.00Early-bird rate NZ$12.00 (entry and pay before 10.00am)Evening rate NZ$12.00 from 6pm (12 hours maximum)

Coat check Please see the registration desk for assistance.

Dress Dress for all sessions is smart casual.

Facsimiles If you wish to send a facsimile, please contact the Meeting registration desk.

Medical servicesEmergency medical services are available on a 24 hour, 7 day basis at the Ascot Accident and Medical Clinic, Greenlane Road, East Remuera, Auckland, telephone (09) 520 9555.

In an emergency dial 111 for an ambulance, the police or the fire department.

MessagesMessages will be displayed on the message and information board located by the Meeting registration desk.

PharmaciesUptown Pharmacy178 Karangahape Road, AucklandTelephone: 09 373 3552

Hours:Monday – Wednesday/Friday 8.30am – 5.30pmThursday 8.30am – 7.00pmSaturday 10.00am – 2.00pm

RefreshmentsMorning tea, lunch and afternoon tea are included in your full meeting registration fee and are provided during the programmed breaks in the exhibition area.

After hours pharmacyNewmarket Day Night Pharmacy60 Broadway, NewmarketTelephone: 09 520 6634

Hours:Monday – Sunday 9.00am – 11.30pm

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Registration deskThe registration desk is located in the pre-function area of the Great Halls of The Langham Hotel. The desk will be open at the following times:

Friday 30th October 7.30am – 6.00pmSaturday 31st October 7.00am – 5.30pmSunday 1st November 7.30am – 1.00pm

Rental carsAvis Rent-a-Car Ltd is offering its corporate rates to conference delegates. Call the Avis office (09 525 1982) and quote the booking reference number AWD: Z994400.

SmokingThe Langham is a smoke free building. Delegates are requested to observe this policy.

Special dietary requirementsIf you have advised any special dietary requirements on your registration requirements, these will have been forwarded to the caterers to prepare special meals for lunches and the social functions.

TaxisTaxis are available from the entrance of The Langham.

TELEPHONE DIRECTORY Emergency services 111(fire/police/ambulance)

Registration desk 09 300 2926

AccommodationLangham Hotel 09 379 5132

Accident & medical clinicQuay Med 68 Beach Road 09 919 2555Monday – Friday 8.00am – 7.00pmSaturday 10.00am – 2.00pm

After hours pharmacy 09 520 6634

Auckland visitors centre 09 366 6888

Taxi servicesRegency Cabs 09 377 8844Co-op Taxis 09 300 3000Super Shuttle 09 522 5100

Airlines Reservations Arrival/Departure InformationAir New Zealand 09 357 3000 09 306 5560Qantas 09 357 8900 09 306 5564

Meeting managers

T H Econference C O M P A N Y

Postal address

PO Box 90-040Auckland 1142New Zealand

Telephone: +64 9 360 1240Facsimile: +64 9 360 1242E-mail: somanz@tcc.co.nz

Street address

31c Normanby RoadMt Eden, AucklandNew Zealand

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is proud to be the national plasma fractionator of Australia and

New Zealand working together with the Australian Red Cross

Blood Service and the New Zealand Blood Service

CSL Limited, Bioplasma Division, 189 - 209 Camp Road, Broadmeadows, Victoria, Australia 3047. ABN: 99 051 588 348 For Medical/Technical Inquiries: Ph: + 61 3 9246 5900 Fax: + 61 3 9246 5801 E-mail: medicalaffairs_bioplasma@csl.com.au

For Customer Service Inquiries: Ph: + 61 3 9246 5231 E-mail: bioplasma.customerservice@csl.com.au Internet: www.cslbioplasma.com.auor

New Zealand Blood Service, 71 Great South Road, Epsom, Auckland, New ZealandPhone: 09 523 5744 Internet: www.nzblood.co.nz

CSL 1213

Photograph – Patrick Reynolds