Abstract
1
1. Royal Hobart Hospital, NEW TOWN, TAS, Australia
The Lancet described climate change as the greatest global health threat of the twenty-first century. This talk will focus on the effects of heat and poor air quality on pregnancy outcomes, and strategies to minimise harm. Climate change magnifies existing inequalities, and on a global and national scale women are especially vulnerable to the effects of climate change. Reversing gender inequalities is associated with benefits for climate mitigation and adaptation.
2
1. Australian Women and Girls Health Research Centre, The University of Queensland, Herston, QLD, Australia
Natural disasters, like floods, can have widespread impacts on communities, including babies in utero. The QF2011 Study worked with women who were pregnant during the 2011 Queensland floods and assessed stress during pregnancy and child development throughout early childhood. Dr Moss built on this work after joining the Australian Longitudinal Study on Women's Health (ALSWH), investigating links between maternal depression during the child's early life course (pre-conception, pregnancy and early childhood) and childhood development. Prenatal maternal stress was linked with a range of adverse outcomes in children, including difficult temperament, lower social skills, poorer cognitive and motor development, and a higher likelihood of behaviour, sleep and interpersonal problems. Chronic or ongoing stress was also important, with longer exposure linked with poorer outcomes for children. However, these negative consequences are not inevitable: five key strategies can make a difference. 1) Minimise diet changes, which includes keeping up multivitamins and not skipping meals. 2) See the same midwife (midwifery group care was associated with less stress in mothers and better development in children). 3) Use emotionally-available parenting strategies such as sensitivity and structuring, which can buffer the effects of high prenatal stress on child development. 4) Match coping strategies to the situation, using emotional focused strategies (e.g., reframing, acceptance, emotional support) for stressors that are uncontrollable and problem-focused strategies (e.g., planning, instrumental support) for stressors where actions can make a difference. Limit the use of dysfunctional strategies such as denial, self-blame and venting. 5) Screen for perinatal mental health problems, including post-traumatic stress symptoms. Screening should occur during pregnancy and in the first postnatal year but 20% of Australian women do not receive the recommended screening. This is particularly important following natural disasters. Natural disasters can be devastating and effects can linger long after flood waters subside. Working together though, we can make a difference for mothers and babies caught up in these events.
3
1. Faculty of Health, University of Technology Sydney, Sydney, NSW, Australia
2. St George and Sutherland Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW, Australia
3. School of Clinical Medicine, UNSW Medicine & Health, University of NSW, Sydney, NSW, Australia
4. Maternal and Child Health, Burnet Institute, Melboure, VIC, Australia
Hypertensive disorders of pregnancy, (HDP) including chronic hypertension, preeclampsia and gestational hypertension, complicate 5–10% of pregnancies and are associated with long-term cardiovascular and other chronic disease sequelae, including Type 2 diabetes mellitus and chronic renal disease. For women who have experienced HDP, cardiovascular disease (CVD) rates are 2–3 times higher compared with those who did not. This risk of premature disease and death is present within 10 years after the affected pregnancy, remains after adjusting for the presence of other cardiovascular risk factors, and is further increased in early-onset and recurrent HDP.
The link between preeclampsia and CVD has been known for many years, with the first meta-analysis published in 2007. Both Australian and international societies, including SOMANZ and the International Society for the Study of Hypertension in Pregnancy (ISSHP), recommend that women and healthcare providers are provided with information about HDP and later CVD.
Despite the length of time that this topic has been addressed in research, knowledge has not translated into practice. Research conducted by our team in Australia has identified knowledge gaps around health after HDP. Whilst overall healthcare providers were aware that there is increased cardiovascular risk after preeclampsia, they were less aware of risks after gestational hypertension and some specific risks including diabetes. Only one third of participants were aware about the risks starting to manifest within 10 years after HDP. Regarding how to close the knowledge to practice gap, we identified that both women and HCPs wanted more information about long-term and modifiable risk factors post-HDP, and a more structured transition from hospital to community health post-HDP, including automated alerts to remind women about key follow-up appointments.
Our research team is now seeking to implement these findings, evaluating a program for women, general practitioners, and other primary healthcare providers. Ultimately, we aim to improve care of women following HDP, and contribute to improving women's health trajectories. This talk will summarise work to date including progress on implementation studies.
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1. Department of Obstetrics and Gynaecology, University of Melbourne, Carlton, VIC, Australia
2. Mercy Perinatal, Mercy Hospital for Women, Melbourne, Victoria, Australia
3. Liggins Institute, University of Auckland, Auckland, New Zealand
4. Centre for Maternal Fetal Medicine, Mater Mothers’ Hospital, Brisbane, Queensland, Australia
5. School of Women's and Children's Health, UNSW Health, University of New South Wales, Sydney, New South Wales, Australia
6. Maternal Fetal Medicine, Joan Kirner Women's & Children's Sunshine Hospital, Melbourne, Victoria, Australia
7. The University of Sydney Northern Clinical School, Women and Babies Research, Sydney, New South Wales, Australia
8. Department of Maternal Fetal Medicine, Royal Women's Hospital, Melbourne, Victoria, Australia
5
1. The Northern Hospital, Epping, VIC, Australia
2. The University of Melbourne, Parkville, VIC, Australia
To develop a model identifying women at risk of hypertension representation.
International Classification of Diseases 10th ed (ICD-10) codes combined with a manual medical records search identified all deliveries that resulted in representation to hospital with hypertension.
A structured manual medical records search combined with coding data compared a randomised sample of all deliveries who were not readmitted with hypertension, to all patients who were. A multivariable analysis identified independent risk factors for readmission.
Bootstrapping was used to rank factors based on probability of inclusion. The area under the receiving operator characteristic (ROC) curve or C-stat was used to test the final model's discriminative ability.
The women who represented were of greater mean age (32, 30), with higher median BMI (31, 26), they had higher median peak systolic blood pressure in the delivery admission (150 mmHg v 131 mmHg) and only 48.6% had a previous diagnosis of hypertension.
The highest performing risk model had 6 factors: gestational hypertension, pre-eclampsia, peak systolic blood pressure, 3 or more hypertensive blood pressure readings, elective caesarean and antenatal aspirin prescription with a C-stat of 0.90.
This study is limited by being retrospective. The use of aspirin and pre-eclampsia may limit reliability over time as guidelines and trends in prescription and diagnosis change.
Once verified, our model could identify patients for programs aimed at preventing post-partum representation as well as the short and long term complications of post-partum hypertension.
6
1. UNSW Medicine, University of New South Wales, Sydney, NSW
2. School of Women's and Children's Health, UNSW Medicine, University of New South Wales, Sydney, NSW
3. Department of Women's and Children's Health, St George Hospital, Sydney, NSW
4. Obstetrics and Gynaecology, Endocrinology, Royal Hospital for Women, Sydney, NSW
5. Obstetrics Medicine Research Group, St George Hospital, Sydney, NSW
6. Royal Hospital for Women, Sydney, NSW
7
1. UNSW Medicine, UNSW, Kensington
2. School of Clinical Medicine, St George and Sutherland Clinical Campus, Sydney
Baseline (6 M postpartum) BP averaged 123 ± 13/ 81 ± 10 mmHg; 12 M average was 122 ± 12/ 80 ± 10 mmHg, with a mean difference in systolic BP of 1.4 ± 10.1 mmHg (p = 0.04) and diastolic BP of 1.4 ± 8.3 mmHg (p = 0.01). Weight at 6 M and 12 M averaged 75.7 kg ± 18.2 kg and 75.2 kg ± 18.6 kg respectively (p = 0.036), waist circumference 92.6 ± 16.0 cm and 91.9 ± 17.0 cm (NS), and BMI 27.9 ± 6.3 and 27.7 ± 6.5 (NS).
8
1. Therapeutics Discovery and Vascular Function Group, Heidelberg, Victoria, Australia
2. Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria, Australia
3. Queen Mary University of London, London, England
4. Mercy Hospital for Women, Heidelberg, Victoria, Australia
5. Department of Physiology, Monash University, Clayton, Victoria, Australia
9
1. The University of Newcastle, Callaghan, NSW, Australia
2. University of Groningen, Groningen, The Netherlands
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1. Discipline of Women's Health, School of Clinical Medicine, UNSW Medicine and Health, Sydney, NSW, Australia
2. St George and Sutherland Clinical Campus, School of Clinical Medicine, UNSW Medicine and Health, Sydney, NSW, Australia
3. Department of Women and Children's Health, St George Hospital, Sydney, NSW, Australia
4. The University of Sydney Children's Hospital Westmead Clinical School, The University of Sydney, Sydney, NSW, Australia
5. Department of Renal Medicine, St George Hospital, Sydney, NSW, Australia
6. Department of Endocrinology, St George Hospital, Sydney, NSW, Australia
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1. Royal Hobart Hospital, Mount Stuart, TAS, Australia
Until 30 years ago, the expectation for a patient with cystic fibrosis was for them to struggle into late adolescence or early adulthood. Females were particularly prone to an accelerated decline and early death. Since then, however, advances in CF care have resulted in a dramatic improvement in life expectancy. Contraception and family planning have already become a routine part of CF care and we are seeing increasing numbers of pregnancies with successful outcomes for both mother and child, a trend which is likely to continue into the future, especially with the relatively recent advent of CFTR modulator therapy, which promises long-term disease modification with further reductions in morbidity and mortality. Establishing links between CF units and local obstetric services is, therefore, an important part of modern multidisciplinary care.
I will present an update on cystic fibrosis management, referencing opportunities and challenges in the field of feto-maternal medicine
12
1. Department of Diabetes and Endocrinology, Royal Hobart Hospital, Hobart
2. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia
3. School of Medicine, University of Tasmania, Hobart
Multiple Endocrine Neoplasia type 1 (MEN 1) is an autosomal dominant condition characterised by the development of multiple endocrinopathies. These include primary hyperparathyroidism, pituitary adenomas and gastroenteropancreatic neuroendocrine tumours, among others. These neoplasms often develop prior to reproductive years and may impact reproductive health. The data regarding the impact MEN 1 on reproductive outcomes was limited to two case reports prior to our work. The Tasman 1 MEN 1 kindred is the largest MEN 1 kindred globally with over 2500 descendants of a common ancestor across 9 generations. We examined the impact of MEN 1 on (1) fertility, (2) pregnancy and peripartum outcomes and (3) neonatal outcomes within the Tasman 1 kindred. We additionally present data on MEN 1-associated primary hyperparathyroidism, the evolution of hypercalcemia across pregnancy and its impact.
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1. The University of Melbourne, Parkville, VIC, Australia
A brief presentation of the Replanting the Birthing Trees project which combines Indigenous ways of knowing, being and doing with rigorous Indigenous-led research and practice evidence to implement and evaluate community-led continuity-of-care for the first 2000 days with seven perinatal services in two jurisdictions (Western Australia and Victoria), and concurrently build infrastructure for sustainable service delivery.
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1. University Of Tasmania, Hobart, TAS, Australia
This presentation focuses on the Australian context, exploring the topics of Indigenous Data Sovereignty and Indigenous Data Governance and challenges field of Obstetric Medicine to operationalise these concepts within their research. Globally the Indigenous Data Sovereignty movement is a powerful force positively reshaping the Indigenous research landscape. A central ambition of the movement is the centring of Indigenous priorities and needs over the usual practice of prioritising the wants of non-Indigenous institutions, policy entities, and researchers. The sought result is a reduction of BADDR data-based research1: that is data that leads to blaming, is aggregated, is decontextualised, has a deficit focused, and is restricted for Indigenous analysis and publications. Yet while the Indigenous Data Sovereignty movement has been remarkably successful in raising awareness of Indigenous data rights, enactment of those rights within research has been harder to achieve. This presentation gives an overview of the Australian Indigenous Data Sovereignty movement and details Australia's obsession with BADDR data. I then provide a case study example of Indigenous Data Sovereignty and Indigenous Data Governance being operationalised in Australian research.
1. Walter, Maggie. “The Voice of Indigenous Data: Beyond the Markers of Disadvantage.” Griffith Review 60 (2018): 256–63.
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1. Royal Brisbane and Women's underline Hospital, Herston, QLD, Australia
In 2016, the WHO estimated that 1 million pregnant women were infected with syphilis. Syphilis in pregnancy is the second leading cause of stillbirth and is associated with a multitude of adverse pregnancy and neonatal outcomes. Australia has seen a rapid, and continued, rise in syphilis among women of reproductive age and during pregnancy since around 2015 which has resulted in an associated rise in cases of congenital syphilis. And yet, syphilis is easily diagnosed on serology, treatment with benzathine penicillin is safe and highly effective in pregnancy and treatment prior to delivery can prevent congenital syphilis. However, the ongoing challenges to identifying, diagnosing, engaging women in treatment and contact tracing their partners reflect the ongoing increase in cases of syphilis in pregnancy.
This talk will highlight some of the epidemiological features associated with syphilis in pregnancy, provide an update on criteria for testing and an overview of the essential features and challenges in the management of women with syphilis in pregnancy.
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1. Pregnancy Research Centre, The Royal Women's Hospital, Parkville, Victoria, Australia
2. Maternal Fetal Medicine, The Royal Women's Hospital, Parkville, Victoria, Australia
3. Obstetrics & Gynaecology, The University of Melbourne, Parkville, Victoria, Australia
In her sixth pregnancy, the patient was referred for pregnancy care at 8 weeks gestation. She had no pre-existing hypertension or proteinuria, and no history of chronic kidney disease, anti-phospholipid syndrome or systemic lupus erythematosus.
She was commenced on low dose aspirin (150 mg nocte) with planned fortnightly outpatient review. At 13 weeks’ gestation, she had a Fetal Medicine Foundation (UK) preeclampsia risk evaluation, with a 1 in 2 high-risk result for the development of subsequent preeclampsia in her current pregnancy.
The sFlt-1:PlGF testing commenced at 21 weeks. Although the patient remained normotensive with no proteinuria, the sFlt-1:PlGF test results steadily increased from 27 at 21 weeks (normal <38) to 141 at 25 weeks. The patient was admitted with a diagnosis of preeclampsia at 25 weeks and 3 days. A growth and wellbeing fetal ultrasound was initially normal. Because of her poor obstetric history and evolving preeclampsia, corticosteroid loading for fetal lung maturation was administered and anti-hypertensive medication commenced. FGR was diagnosed at 26 weeks and 5 days, maternal blood pressure deteriorated, and booster corticosteroid dose was administered.
At 27 weeks, magnesium sulphate for fetal neuroprotection was administered and the patient underwent an emergency caesarean section for developing fetal compromise, delivering a baby girl weighing 718 grams. The mother progressed well postnatally. After 11 weeks of neonatal intensive care, the baby was discharged home weighing 2.27 kilograms.
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Michelle MO O'Connor1,
1. Metro North Hospital and Health Service - Royal Brisbane and Women's Hospitals, Brisbane, QUEENSLAND, Australia
2. Office of the Chief Nursing and Midwifery Officer, Department of Health, Bracken Ridge, Queensland, Australia
The Ngarrama midwifery group practice at the Royal Brisbane Women's Hospital commenced in 2012, after extensive community consultation, support and intentional co-design process. Metro North Elders named the service ‘Ngarrama’ which means ‘Calling the protective forces, the Birth Spirit which will protect the hopes, dreams and guardianship of our mothers and babies.” Ngarrama Maternity Services has grown, and collectively provided care for more than 3000 Aboriginal and / or Torres Strait Islander women and their babies over the past decade. A Ngarrama Elder has described the services as ‘Ngarrama Angels - as you are supporting our women and future generations by supporting traditional ways and importance of country”.
This presentation will share the principles and model which the Ngarrama service is founded within and also clinical outcome data from the Ngarrama service, showing closing the gap outcomes achieved, such as preterm birth, mode of birth and consumer perspective insight.
Michelle O'Connor
Midwifery Unit Manger
michelle.oconnor@health.qld.gov.au
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1. Discipline of Women's Health, School of Clinical Medicine, UNSW Medicine and Health, Sydney, NSW, Australia
2. Department of Women's and Children's Health, St George Hospital, Sydney, NSW, Australia
3. Department of Renal Medicine, Liverpool Hospital, Sydney, NSW, Australia
4. The George Institute for Global Health, Sydney, NSW, Australia
5. Nepean and Blue Mountains Local Health District, Sydney, NSW, Australia
1. World Health Organisation. Statement on maternal sepsis https://www.who.int/reproductivehealth/publications/maternal_perinatal_health/matern alsepsis-statement/en/ (2017).
2. Rudd, K.E., et al. The global burden of sepsis: barriers and potential solutions. Critical Care 22, 232 (2018).
3. Bonet, M., et al. Frequency and management of maternal infection in health facilities in 52 countries (GLOSS): a 1-week inception cohort study. The Lancet Global Health https://doi.org/10.1016/S2214-109X(20)30109-1 (2020).
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Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract affecting both males and females, with a typical onset in young adulthood. This disease onset often coincides with the prime reproductive years of patients. Over the last several years, new treatments called biologics and small molecule therapies have become available for the treatment of inflammatory bowel disease (IBD) and other inflammatory diseases.These therapies are very effective at inducing and maintaining clinical remission in patients with IBD however many patients may be anxious about the effects of these medications on fertility and the safety of these medications during pregnancy and in breastfeeding. It is therefore imperative that both gastroenterologists and obstetricians are up to date regarding the safety of these medications in the pre- and post-conception stage and during breastfeeding. This talk will summarise the safety of current medications commonly used to treat IBD and discuss the role of disease monitoring, obstetrician and gastroenterology collaboration and the importance of maintaining disease remission to neonatal outcomes.
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1. Department of Maternal Fetal Medicine, Royal Women's Hospital, Parkville, VIC, Australia
2. Department of Nephrology, Royal Melbourne Hospital, Parkville, VIC, Australia
3. Department of Medicine, University of Melbourne, Parkville, VIC, Australia
4. Department of Obstetrics & Gynaecology, University of Melbourne, Parkville, VIC, Australia
The mean maternal age was 32.9 years (range 28–41); 18 women (78%) had pre-existing hypertension and 2 women had pre-existing type 1 diabetes. The mean interval from transplantation to delivery was 8.8 years (range 2–19). Pre-eclampsia complicated over half (55%) of all pregnancies. Seventeen women (17/31; 55%) had an attempt at vaginal birth; 14 women had a pre-labour Caesarean delivery. The overall CS rate was 61% (n = 19) with 2 renal transplant injuries occurring at the time of birth. Mean gestational age at delivery was 34.2 weeks (range 20.0–40.4) with 69% (22/32) delivering prior to 37 weeks. The mean birth weight was 2140 g (range 456–3754) with over half of infants requiring admission to special or neonatal intensive care. The perinatal mortality rate was 125 per 1000 births including 2 stillbirths, and 2 neonatal deaths (MCDA twins).
There was a significant rise in creatinine levels pre-pregnancy and 3 months postpartum (102.10 vs 117.50umol/L). Graft loss, defined as either returning to dialysis or requiring transplantation, was not observed within a year of delivery; however, at time of follow-up, 2 women required a second transplant 3 and 9 years postpartum, respectively.
21
1. University of New South Wales, Sydney, NSW
2. Royal Hospital for Women, Randwick, NSW, Australia
3. Children's Hospital and Westmead Clinical School, University of Sydney, Sydney, NSW
4. Prince of Wales Hospital and Community Health Services, Sydney, NSW
22
1. Obstetrics and Gynaecology, Liverpool Hospital, Liverpool, NSW, Australia
2. Women's Health Initiative Translational Unit, Ingham Institute, Liverpool, NSW, Australia
3. School of Medicine, Western Sydney University, Penrith, NSW, Australia
1. Allotey, J., et al., Clinical manifestations, risk factors, and maternal and perinatal outcomes of coronavirus disease 2019 in pregnancy: living systematic review and meta-analysis. BMJ, 2020. 370: p. m3320.
2. Villar, J., et al., Maternal and Neonatal Morbidity and Mortality Among Pregnant Women With and Without COVID-19 Infection: The INTERCOVID Multinational Cohort Study. JAMA Pediatr, 2021. 175(8): p. 817–826.
3. Wei, S.Q., et al., The impact of COVID-19 on pregnancy outcomes: a systematic review and meta-analysis. Cmaj, 2021. 193(16): p. E540-e548.
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1. The George Institute for Global Health, UNSW, Sydney, Australia
2. Discipline of Women's Health, School of Clinical Medicine, UNSW Medicine and Health, Sydney, Australia
3. Department of Women's and Children's Health, St George Hospital, Sydney, Australia
4. St George and Sutherland Clinical School, UNSW Medicine, Sydney, Australia
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1. Maternal-Fetal Medicine, Royal Women's Hospital, Parkville, Victoria, Australia
Human pregnancy disorders secondary to chronic placental dysfunction (CPD), such as preeclampsia (PE) and many cases of fetal growth restriction (FGR), are major causes of perinatal and maternal morbidity and mortality throughout the world.
The discovery of placenta-derived proteins, such as soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF), that reflect CPD and which circulate and are measurable in the maternal blood has been a major advance in facilitating the diagnosis and prognosis of CPD disorders.
In particular, circulating levels of sFlt-1 (which is increased in PE) and of PlGF (which is decreased in PE), when expressed as a ratio sFlt-1/PlGF, have been to shown to reflect the onset and severity of PE.
However, exploring the full extent of the clinical utility of the sFlt-1/PlGF blood test in human pregnancy care remains an area of current interest.
To this end, since introducing the test into routine clinical practice in 2016, the Department of Maternal-Fetal Medicine at the Royal Women's Hospital in Melbourne has maintained a database of sFlt-1/PlGF test results (now in excess of 8000) with associated clinical, laboratory and ultrasound information.
Based on analyses of the information in this database, it is becoming increasingly clear the sFlt-1/PlGF blood test has clinical utility in broad range of pregnancy care scenarios, in addition to monitoring the onset and severity of PE. These scenarios include monitoring the rate of deterioration in cases of PE, optimising maternal mental health in women with a poor past pregnancy outcome history, clarifying the differential diagnosis in PE-like conditions, diagnosing and managing idiopathic FGR, assessing for impending CPD at term with relevance to the associated timing and mode of delivery, and triaging women with suspected PE in terms of their requirement for ongoing inpatient versus outpatient care.
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1. Women's and Children's Hospital, North Adelaide, Hackney, South Australia, Australia
2. Central Northern Adelaide Renal and Transplantation Services (CNARTS), Royal Adelaide Hospital, Adelaide, South Australia, Australia
3. Australia and New Zealand Dialysis and Transplant Registry (ANZDATA), South Australian Health & Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia
4. Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia
5. Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia
1. Hewawasam E, Davies CE, Gulyani A, Li Z, Clayton PA, Sullivan E, McDonald SP, Jesudason S. Factors influencing fertility rates in Australian women receiving kidney replacement therapy: analysis of linked Australia and New Zealand Dialysis and Transplant Registry and perinatal data over 22 years, Nephrology Dialysis Transplantation, 2021; 37(6): 1–10.
2. Hewawasam E, Gulyani A, Davies CE, Sullivan E, Wark S, Clayton PA, McDonald SP, Jesudason S. Parenthood and pregnancy for end stage renal disease: protocol of national study of perinatal and parental outcomes through population record linkage. BMJ Open, 2020; 10(5): 1–7.
3. Hewawasam, E., Davies, C. E., Li, Z., Clayton, P., Sullivan, E., McDonald, S. P., & Jesudason, S. (2022). Determinants of Perinatal Outcomes in Dialyzed and Transplanted Women in Australia. Kidney International Reports, 7(6), 1318–1331.
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1. Faculty of Medicine, Monash University, Clayton, Victoria, Australia
2. Faculty of Medicine, Duke-NUS Medical School, Singapore
3. Monash University, Clayton, Victoria, Australia
4. Monash Centre for Health Research and Implementation, Monash University, Clayton, Victoria, Australia
1. Parikh NI, Gonzalez JM, Anderson CAM, Judd SE, Rexrode KM, Hlatky MA, et al. Adverse Pregnancy Outcomes and Cardiovascular Disease Risk: Unique Opportunities for Cardiovascular Disease Prevention in Women: A Scientific Statement From the American Heart Association. Circulation. 2021;143(18):e902-e16.
27
1. University of Sydney, St Leonards, NSW, Australia
2. Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
3. ARC Centre in Data Analytics for Resources and Environments (DARE), St Leonards, New South Wales, Australia
4. Women and Babies Research, Kolling Institute The University of Sydney Northern Clinical School Faculty of Medicine and Health, St Leonards, New South Wales, Australia
Figure 1: Mixed effects model. Estimated probability of birth weight > P90 by plasma glucose measures and BMI class
1. O'Sullivan EP, Avalos G, O'Reilly M, et al. Atlantic Diabetes in Pregnancy (DIP): The prevalence and outcomes of gestational diabetes mellitus using new diagnostic criteria. Diabetologia. 2011;54(7):1670–1675.
2. HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, et al. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008;358(19):1991–2002. doi:10.1056/NEJMoa0707943
28
1. Western Health, Melbourne
2. University of Melbourne, Melbourne, Victoria, Australia
3. St Vincent's Research Institute, Fitzroy, Victoria, Australia
4. Monash Health, Melbourne, Victoria, Australia
29
1. Central Coast Haematology, North Gosford, NSW, Australia
Myeloproliferative neoplasms (MPN) are a group of hematopoietic stem cell-derived clonal disorders associated with an increased risk of thrombotic and haemorrhagic complications. Approximately 20% of patients with myeloproliferative neoplasma are under 40 years of age at diagnosis. Pregnant women with MPN are at increased risk of maternal thrombosis and haemorrhage and also of placental dysfunction resulting in pre-eclampsia, foetal growth restriction, pre-term delivery and foetal loss. The risks of pregnancy and the strategies used to improve outcomes will be discussed.
30
1. University of NSW, Sydney, NSW
2. Department of Haematology, NSW Health Pathology, Randwick, NSW
3. Prince of Wales Hospital, Royal Hospital for Women, Randwick, NSW, Australia
Patients with transfusion-dependent thalassaemia require lifelong red cell transfusions for survival. This leads to iron overload, and further complications including cardiac disease, diabetes, hypopituitarism, hypothyroidism, osteoporosis and red cell antibodies. Many women with transfusion-dependent thalassaemia now conceive. The optimal management involves a multi-disciplinary team from pre-conception until post-partum. Current knowledge, local data and best practice of management of transfusion-dependent thalassaemia in pregnancy will be presented.
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1. Counties Manukau DHB, Manukau, AUCKLAND, New Zealand
Counties Manukau Health (CMH) is one of New Zealand's fastest growing DHB populations with approximately 7400 births occurring in a Counties Manukau facility during 2020. It is home to New Zealand's second largest Maaori population and largest population of Pacific people, as well as a fast-growing Asian community. Our population is diverse and vibrant with strong cultural values.
During 2021 CMH provided for @620 women experiencing perinatal loss from 12 weeks onwards. In late 2021, CMH had the opportunity to look at developing a new way to provide support to women and whanau experiencing perinatal loss within our service.
It hoped to change from the previously separate services which provided support for women dependant on gestation and to move towards developing a team with the remit to encompass support for all pregnancy loss from the second trimester onwards into one cohesive service.
This new team consists of two Specialist Perinatal Loss Midwives who provide support for all women and whanau experiencing pregnancy loss from 12 weeks gestation, whether through termination of pregnancy, miscarriage or stillbirth, as well as neonatal deaths up to 28 days of life. The team is supported by Obstetrics and Gynaecology Consultants and works closely with the associated Maternal and Fetal Medicine Team.
Key responsibilities of the team include, working in partnership with women, their whanau, and other health professionals to plan and co-ordinate care. Planning of any follow up postnatal care and review for women and their whanau who have experienced perinatal loss. Support staff with individual professional development needs as well as providing opportunities for staff debrief. Developing and facilitating multi-disciplinary training and education for staff relating to the care of women and whanau and perinatal loss. Planning, preparing and coordinating Women's Health Perinatal Mortality Meetings as well as the completing of PMMRC documentation acting as PMMRC Local Coordinators. The team in the future hope to also expand into the provision of post natal contraception for women prior to discharge from hospital.
This newly developed team hope to ensure that, whether a pregnancy loss is planned, or spontaneous and unexpected, women and their whanau feel that their individual values, beliefs and needs are met. That all women experience equitable and non-judgemental care and that they feel supported and respected and that their voices are heard.
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1. University of Queensland, Brisbane, Queensland, Australia
2. Department of Nephrology, Mater Hospital Brisbane, South Brisbane, Queensland, Australia
1. Wiles, K., Chappell, L., Clark, K. et al. Clinical practice guideline on pregnancy and renal disease. BMC Nephrol 20, 401 (2019). https://doi.org/10.1186/s12882-019-1560-2.
2. Rudland, V.L., Price, S.A., Hughes, R., Barrett, H.L., Lagstrom, J., Porter, C., Britten, F.L., Glastras, S., Fulcher, I., Wein, P., Simmons, D., McIntyre, H.D. and Callaway, L. (2020), ADIPS 2020 guideline for pre-existing diabetes and pregnancy. Aust N Z J Obstet Gynaecol, 60: E18-E52. https://doi.org/10.1111/ajo.13265.
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1. University of New South Wales, Sydney
2. Women and Children's Health, St George Hospital, Sydney
3. School of Women's and Children's Health, University of New South Wales, Sydney
4. Westmead Children's Hospital Clinical School, The University of Sydney, Sydney
5. Institute of Endocrinology and Diabetes, Westmead Children's Hospital, Sydney
34
1. The University of New South Wales, Sydney
35
1. Department of Obstetric Medicine, Royal Brisbane & Women's Hospital, Brisbane, Qld, Australia
2. Department of Thoracic Medicine, Royal Brisbane & Women's Hospital, Brisbane, Qld, Australia
3. Department of Radiology, Royal Brisbane & Women's Hospital, Brisbane, Qld, Australia
4. Queensland Xray, Brisbane, Qld, Australia
5. The Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Qld, Australia
6. Department of Obstetrics, Royal Brisbane & Women's Hospital, Brisbane, Qld, Australia
Anomalous systemic arterial supply to the basal segment of the lung (ABLL) is a rare congenital malformation. It is characterised by aberrant systemic arterial supply to the basal segment of the lung, with normal venous drainage to the pulmonary veins and normal bronchial branching. (1) ABLL may be complicated by massive haemoptysis, heart failure from left-to-right shunt, and infection. (2, 3) We describe a case of this condition presenting in the third trimester of pregnancy. To our knowledge this is the first case of a pregnant woman presenting with haemoptysis due to ABLL, managed post-partum with transarterial embolisation.
A 36-year-old woman in her first pregnancy presented at 35 weeks’ gestation to the emergency department of a tertiary obstetric centre with a four-day history of low-volume frank haemoptysis. CT chest angiogram demonstrated a wedge-shaped focus of consolidation in the posteromedial right lower lobe suggestive of pulmonary infarction. This pulmonary segment was supplied by a systemic artery arising from the aorta. There was a small rounded arterially-enhancing focus in the right lower lobe possibly representing an aneurysm in the systemic feeder artery. A multidisciplinary approach was necessary to determine treatment options, which ultimately consisted of elective caesarean section at 36 weeks and 4 days gestation, followed by a successful post-partum transarterial embolisation.
Changes to cardiac output and elevation of the diaphragm may be relevant to the presentation of this condition in pregnancy. Most published cases of related conditions presenting for the first time during pregnancy coincided with development of peak cardiac output in the second trimester, likely causing increased blood flow via the aberrant artery. (4–6) In our patient's case there was no haemoptysis until the 35th week, making this mechanism unlikely the sole factor. In our patient the systemic arterial supply arose from the thoracic aorta at the level of the diaphragmatic crus. This may have resulted in mechanical compression of the arterial supply to the involved pulmonary tissue, leading to infarction and haemoptysis.
Regarding the mode of delivery, vaginal delivery with an unsecured aberrant arterial supply to the lungs has not been described. In our patient, the risks of labour, and the significant potential for an unsuccessful vaginal delivery requiring emergency caesarean section, prompted a decision to proceed with elective caesarean section.
While surgical resection has traditionally been the management modality of choice for ABLL, transarterial embolisation has been used in recent years in selected cases. (7)
1. Campbell DC, Jr., Murney JA, Dominy DE. Systemic arterial blood supply to a normal lung. JAMA : the journal of the American Medical Association. 1962;182:497–9.
2. Currarino G, Willis K, Miller W. Congenital fistula between an aberrant systemic artery and a pulmonary vein without sequestration. A report of three cases. The Journal of pediatrics. 1975;87(4):554–7.
3. Yabek SM, Burstein J, Berman W, Jr., Dillon T. Aberrant systemic arterial supply to the left lung with congestive heart failure. Chest. 1981;80(5):636–7.
4. Shaikh S, Saad RA, Christie G, Kerr KM, Remmen H. Spontaneous dissection of an anomalous systemic artery in the lung during pregnancy: a rare cause of hemoptysis. Ann Thorac Surg. 2006;82(2):725–6.
5. Freeman RK, Maxwell JM. Intralobar bronchopulmonary sequestration presenting as hemoptysis: evidence for an acquired cause. Mil Med. 1998;163(7):502–3.
6. Sayegh L, Greer M, Rabih F, Marts L. Pulmonary Sequestration Presenting as Hemoptysis in Pregnancy. American Journal of Respiratory and Critical Care Medicine. 2020;201:A3744.
7. Saida T, Ninomiya H, Hojo F, Nakayama M, Yamauchi T, Saida Y. Systemic arterial supply to the normal basal segments of the left lower lobe treated by coil embolization, with long-term follow-up. Radiat Med. 2006;24(5):365–8.
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1. Obstetrics and Gynaecology, Liverpool Hospital, Liverpool, NSW, Australia
2. Neurosurgery, Liverpool Hospital, Liverpool, NSW, Australia
This report describes a case of spinal meningioma in a twin pregnancy causing severe neurological impairment, poor mobility and recurrent falls requiring premature delivery and urgent surgical management.
She represented with progressive deterioration in neurological function including urinary incontinence and was wheel chair bound due to significant lower limb weakness causing recurrent falls. An MRI spine revealed a 10 × 10 × 20 mm, homogenous well defined extramedullary lesion at the T7 level, with associated cord compression. Differential diagnoses included meningioma and schwannoma. She underwent an uncomplicated elective caesarean section at 33 weeks gestation followed by T6 to T8 laminectomies and resection of the extramedullary lesion 48 h later. Her post-natal course was uncomplicated and her lower limb weakness gradually improved post operatively. Histopathology confirmed a meningioma (World Health Organisation Grade 1). Repeat MRI of the spine showed full resection of the lesion and she is currently undergoing rehabilitation as an inpatient.
1. Wiemels J, Wrensch M, Claus EB. Epidemiology and etiology of meningioma. Journal of neurooncology. 2010, 99(3):307–14. doi: 10.1007/s11060-010-0386-3
2. Dumitrescu BC, Tataranu L.G., Gorgan M.R. Pregnant woman with an intracranial meningioma – case report and review of the literature. Rom. Neurosurg. 2014, 21: 489–496
3. Giraldi L, Lauridsen EK, Maier AD, Hansen JV, Broholm H, Fugleholm K, Scheie D, Munch TN. Pathologic characteristics of pregnancy-related meningiomas. Cancers 2021, 13, 3879. https://doi.org/10.3390/cancers13153879
4. Maiuri F, Montagnani S, Gallicchio B. Estrogen and progesterone receptors in meningiomas. Surgical Neurology 1986, 26: 435–440.
5. Molina-Botello D, Rodriguez-Sanchez JR, Cuevas-Garcia J, Cardenas-Almaraz BV, Morales-Acevedo A, Mejoia-Perez SI, Ochoa-Martinez E. Pregnancy and brain tumors; a systematic review of the literature. Journal of clinical neuroscience. 2021, 86: 211–216. doi: 10.1016/j.jocn.2021.01.048
37
Katherine J Creeper1,
1. King Edward Memorial Hospital, Subiaco, WA, Australia
2. University of Western Australia, Perth, WA, Australia
38
1. King Edward Memorial Hospital, Subiaco, Western Australia, Australia
Hydroxychloroquine (HCQ) use is associated with a reduced risk of flare in pregnant patients with SLE.1,2 A recent meta-analysis of 1132 pregnancies reported a reduction in pre-eclampsia risk for patients taking HCQ, however this has never been examined in an Australian cohort.3
We aimed to investigate the association between HCQ use, risk of pre-eclampsia and neonatal outcomes in Australian women with SLE.
11.8% of HCQ exposed pregnancies were complicated by pre-eclampsia, compared to 25% of pregnancies not exposed to HCQ (unadjusted OR 0.40, 95% CI 0.14–1.15). When adjusted for aspirin use, BMI, lupus nephritis, lupus flare in pregnancy and presence of antiphospholipid antibodies, HCQ use was associated with a significantly lower risk of pre-eclampsia (aOR 0.16, 95% CI 0.04–0.64) compared with non-HCQ use. There was no association between HCQ use and the neonatal outcome of gestation at delivery, special care nursery admission or birthweight in this cohort. Aspirin use was not associated with a decreased risk of pre-eclampsia, regardless of HCQ exposure.
1. Knight C, Nelson-Piercy C. Management of systemic lupus erythematosus during pregnancy: challenges and solutions. Open Access Rheumatology: Research and Reviews 2017:9 37–53.
2. Marder W. Update on pregnancy complications in systemic lupus erythematosus. Current Opinion Rheumatology 2019, 31:650–658.
3. Duan J, Ma D, Wen X et al. Hydroxychloroquine prophylaxis for preeclampsia, hypertension and prematurity in pregnant patients with systemic lupus erythematosus: A meta-analysis. Lupus 2021, Vol 30(7) 1163–1174.
39
1. The University of Melbourne, Parkville, VIC, Australia
2. The Northern Hospital, Epping, VIC, Australia
1. To establish the rate of HDP at Northern Health.
2. To describe the characteristics of patients with HDP.
Of the 17746 patients, 827 had a HDP diagnosis. HDP patients were on average 31.0 years old, had a BMI of 30.7 kg/m2 and 27.4% (227/827) had GDM. Non-HDP patients were younger (29.8 years old, p < 0.001), had a lower BMI (26.8 kg/m2, p < 0.001) and a lower proportion of GDM (21.0%, p < 0.001). The two populations had a similar distribution of Socioeconomic Indexes for Areas (SEIFA).
40
1. Department of Obstetric Medicine, Royal Women's Hospital, Parkville, VIC, Australia
2. Department of Nephrology, Royal Melbourne Hospital, Parkville, VIC, Australia
3. Department of Medicine, University of Melbourne, Parkville, VIC, Australia
4. Department of Maternal Fetal Medicine, Royal Women's Hospital, Parkville, VIC, Australia
5. Department of Obstetrics & Gynaecology, University of Melbourne, Parkville, VIC, Australia
A 32yo G2P1−1 kidney transplant recipient presented for maternity care. She had a history of end-stage kidney disease due to reflux nephropathy and had received a living-related kidney transplant in 2019. Three months pre-conception, acute T-cell mediated rejection was treated with pulsed steroids, with resolution of changes confirmed on follow-up biopsy. Her first pregnancy prior to transplant was complicated by severe pre-eclampsia (PET) and fetal growth restriction (FGR) resulting in a termination of pregnancy and subsequent neonatal death at 22 + 1 weeks’ gestation.
Early antenatal history was unremarkable. Baseline blood pressure was 120/70 mmHg, creatinine 130umol/L. Medication included aspirin 100 mg d, azathioprine 100 mg mane, prednisolone 5 mg d, tacrolimus 6.5/6 mg bd.
At 20 + 1 weeks, creatinine was rising (200umol/L); obvious precipitants (infection, obstruction) were excluded. Tacrolimus trough level was 5.8ug/L. Transplant biopsy showed new acute thrombotic microangiopathy (TMA) changes in one glomerulus and an arteriole. The sFlt-1/ PlGF ratio (PERT) was elevated at 90 suggestive of evolving early-onset PET. The tacrolimus dose was reduced and Labetalol 100 mg bd was commenced. Creatinine improved to 159umol/L.
At 22 + 3 weeks, she was admitted for presumed HELLP. Blood pressure was 135/95 mmHg with sustained clonus. Investigations showed haemoglobin 86 g/L, platelets 131 × 109, creatinine 180umol/L, haptoglobin <0.1 g/L and LDH 370U/L. However, the clinical picture was not entirely consistent hence alternative diagnoses were considered including TMA due to tacrolimus, atypical haemolytic uraemic syndrome (aHUS) and atypical PET.
At 22 + 5 weeks, progressive hypertension (160/110 mmHg), thrombocytopenia (platelets 93 × 109) and renal impairment were noted (creatinine 206umol/L). ADAMTS13 was normal. Antiphospholipid antibodies were negative. At his gestation, every effort was made to prolong the pregnancy. Following MDT discussion, treatment with eculizumab and high dose prednisolone was commenced, and tacrolimus was ceased.
Nocturnal hypertension remained problematic despite anti-hypertensive therapy. Renal impairment (peak urea 20.5 mmol/L, creatinine 235umol/L, urine protein-creatinine-ratio 163 mg/mmol) was progressive. Dialysis was commenced at 24 + 1 weeks for fetal well-being.
At 24 + 4 weeks, uncontrolled hypertension, progressive anaemia (60 g/L) and thrombocytopenia (36 × 109) prompted delivery by classical caesarean section, resulting in the livebirth of a female infant weighing 538 g. At 4 weeks postpartum, infant and mother are well. Creatinine remains elevated at 180umol/L however she is not dialysis dependent.
This clinical conundrum explores the overlapping diagnostic features of pregnancy-associated TMA, aHUS and PET, and the options for therapeutic intervention in an attempt to prolong the pregnancy at a peri-viable gestation and balancing the risks of graft loss.
41
1. Royal Hospital for Women, Randwick, NSW, Australia
2. Conjoint Clinical Lecturer, University of New South Wales, Kensington, NSW, Australia
Hyponatraemia is predominantly a disorder of water balance in which there is a relative excess of body water compared to total body sodium and potassium. Anti-diuretic hormone (ADH) is one of the main hormones responsible for maintaining water homeostasis in the body. ADH acts on the AVPR2 receptor in the collecting ducts of the nephrons of the kidneys leading to an increase in water reabsorption. An increase in osmolality, volume depletion, emotional stress, nausea, vomiting, and pain all stimulate the release of ADH. Oxytocin is structurally similar to ADH and mimics activity on the AVPR2 receptor.
Pregnancy is a state manifested by plasma volume expansion and sodium retention. Oestrogen and relaxin naturally released in pregnancy stimulate systemic vasodilation leading to a systemic arterial blood pressure decrease. This triggers the release of ADH causing water retention.
During labour, common symptoms of nausea, stress and pain stimulate the release of ADH. The natural release of oxytocin and administration of synthetic oxytocin also mimics the activity of ADH. This in addition to water intoxication through polydipsia and administration of intravenous fluids predispose the woman to hyponatraemia.
In recent years, there has been an increase in diagnosis of hyponatraemia in labour. This may be attributed to the above mechanisms as well as social encouragement of hydration in pregnancy and labour. We present the cases of five women who delivered in our tertiary unit and were diagnosed with hyponatraemia during labour or postnatally secondary to water intoxication. We review the acute management of these cases, along with the maternal and fetal outcomes.
42
1. Royal Adelaide Hospital, Adelaide, SA, Australia
2. Department of Obstetrics and Gynaecology, St Vincent's Hospital, Sydney, NSW, Australia
3. Pregnancy Outcomes Unit (retired), SA Health, Adelaide, SA, Australia
4. Department of Obstetrics and Gynaecology, Northern Adelaide Local Health Network, Adelaide, SA, Australia
5. Robinson Research Institute, University of Adelaide, Adelaide, SA, Australia
1. Marathe JA, Lim WH, Metz MP, Scheil W, Dekker GA, Hague WM. A retrospective cohort review of intrahepatic cholestasis of pregnancy in a South Australian population. Eur J Obstet Gynecol Reprod Biol. 2017;218:33–8.
43
1. Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
2. Western Health, St Albans, Victoria, Australia
44
1. Tan tock seng hospital, Singapore, SINGAPORE
2. Yong Loo Lin School of Medicine, Singapore, SINGAPORE
3. Maternal fetal medicine, KK women's and children's hospital Singapore, Singapore
Subsequently she had 2 more pregnancies at 2-year intervals. Her platelet counts ranged from 1079–1260 x109/L with occasional myelocytes on peripheral blood film. She had mild Anemia Hb:10 gm/dl, with variable leucocyte counts 10 −17 × 109/L. She had intermittent headaches and peripheral numbness with rising platelet counts. Although based on her revised IPSET-thrombosis risk stratification she was considered low risk for thrombosis, she was offered cytoreduction with Interferon due to her symptoms and rising platelet counts which she declined. Hence, she was only on Aspirin for both her pregnancies and was advised Clexane postpartum for 6 weeks. She had uncomplicated pregnancies with induction of labor at full term with normal vaginal deliveries.
1. Gangat Naseema, Tefferi Ayalew. Myeloproliferative neoplasms and pregnancy: Overview and practice recommendations.Am J Hematol. 2021;96:354–366.
45
1. The Northern Hospital, Epping, VIC, Australia
2. University of Melbourne, Melbourne, VIC, Australia
There is emerging evidence that the breakdown product of prolactin plays a role in the pathophysiology of peripartum cardiomyopathy (3). Studies inhibiting prolactin secretion with the dopamine agonist bromocriptine have demonstrated efficacy in reducing mortality, morbidity and assisting left ventricular ejection fraction (LVEF) recovery in women with peripartum cardiomyopathy (3). Risk of recurrent cardiomyopathy can be as high as 20% in women with subsequent LVEF normalisation, and 50% in women with a persisting impairment (3). As such, optimising therapeutic strategies is imperative in managing women with this condition.
Following a late referral, she was first reviewed at 22 weeks gestation whilst on perindopril, apixaban, ivabradine, spironolactone and frusemide (although with probable suboptimal compliance). Medications were adjusted following urgent cardiological review and she continued pregnancy on carvedilol with active surveillance including planned echocardiogram and NT-proBNP levels.
At 36 weeks gestation her NT-pro BNP rose >300 pg/mL and transthoracic echocardiogram (TTE) demonstrated a mildly dilated LV with moderate systolic dysfunction, LVEF 35–40%.
Delivery was brought forward, and she underwent a caesarean section at 36 + 4 gestation with concurrent tubal ligation. She was not breastfeeding due to other factors, so was treated with seven days of bromocriptine postpartum with subsequent normalisation of her NT-pro BNP and LVEF.
1. Isezuo, S.A. and Abubakar, S.A. (2007) Epidemiologic Profile of Peripartum Cardiomyopathy in a Tertiary Care Hospital: Ethnicity and Disease, 17(2): 228–233.
2. Kamiya, C.A. et al. (2011). Different characteristics of peripartum cardiomyopathy between patients complicated with and without hypertensive disorders. Results from the Japanese Nationwide survey of peripartum cardiomyopathy: Circulation Journal 75(8): 1975–1981
3. Davis, M. et al. 2020: Peripartum Cardiomyopathy: JACC State-Of-the-Art-Review, Journal of the American College of Cardiology.
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Alexandra Fullerton1, Richard Skoien2,3,
1. Obstetric Medicine, Women's and Newborn Services, Royal Brisbane and Women's Hospital, Brisbane, QLD, Australia
2. Gastroenterology and Hepatology, Royal Brisbane and Women's Hospital, Brisbane, QLD, Australia
3. School of Medicine, University of Queensland, Brisbane, QLD, Australia
47
1. Redcliffe Hospital, Redcliffe, Queensland
A 35 year old G4P2M1 presented to the Emergency Department with severe abdominal pain and vomiting and was diagnosed with pancreatitis. Her serum was noted to be lipaemic and a lipid profile was performed revealing triglycerides of 172.5 mmol/L.
Medical background was significant for well-controlled type 2 diabetes (with a recent HbA1c of 6.5%), polycystic ovarian syndrome, subclinical hypothyroidism and dyslipidaemia. Regular medications included fenofibrate 145 mg daily, metformin XR 2 g daily, atorvastatin 80 mg nocte, thyroxine 75 mcg daily, Optisulin 50 units nocte and Novorapid 20 units TDS. Prior to planning pregnancy the patient's diabetes was controlled with semaglutide and metformin. The patient lived with her husband and 2 children and was a non-smoker. She drink minimal alcohol of less than 1 standard drink per week.
The patient had undergone an unsuccessful cycle of in vitro fertilisation (IVF) around 2 weeks prior to her presentation involving oestrodiol 6 mg, with a negative beta HCG a week prior to presentation. Of note, her triglycerides completed 2 months prior to her IVF cycle were normal at 1.1 mmol/L. Review of previous investigations demonstrated elevated triglycerides on external pathology in 2017, 2018 and 2019 correlating with previous pregnancies and IVF.
The patient was managed initially with an insulin infusion and was kept nil by mouth, with fenofibrate 145 mg continued. The insulin infusion was ceased when triglycerides fell below 10 mmol/L, and subcutaneous insulin was resumed. Fish oil 2 g BD was added to her therapy. Repeat triglycerides a month following her presentation were 2.8 mmol/L.
Hypertriglyceridaemia induced by high dose oestrogen therapy is a rare but recognised complication of in vitro fertilisation. Although the patient had a background of diabetes this was well controlled, and the significant and rapid elevation in triglyceride levels after her IVF cycle were highly suggestive that this was the acute precipitant. Proposed mechanisms include oestrogen-induced inhibition of lipoprotein lipase and increased hepatic triglyceride synthesis.
Future cycles of IVF and pregnancy would pose risk of recurrent severe hypertriglyceridaemia for this patient. She currently remains ambivalent about pursuing future pregnancy, but further IVF attempts would need to avoid high dose oestrodiol and close monitoring during pregnancy would be required. Further adjunctive therapies such as gemfibrozil may be required during pregnancy, and plasmapheresis could be considered in severe hypertriglyceridaemia.
48
1. School of Medicine, University of Wollongong, Wollongong, NSW, Australia
2. Illawarra Health and Medical Research Institute, Wollongong, NSW, Australia
This project aimed to develop, implement, and evaluate the Beyond the Bump (BtB) postpartum pilot program to improve access to expert education on health and wellbeing, and support women to be more physically active in their first year postpartum. A three-stage mixed-methods design was used: (1) needs assessment through online focus groups and phone interviews to inform the design of the BtB program, (2) pilot study to implement the program (a ten-week series of live webinars) and assessment of health behaviours through a pre- and post-program survey, and (3) evaluation to seek feedback on the program through surveys or phone interviews of women who attended stage 2. Women in their first year postpartum participated in all three stages and postpartum primary care health professionals participated in only stage one. The needs assessment with 12 women and 16 health practitioners identified a strong need for an online postpartum program during COVID-19 that included access to postpartum professionals. Topics suggested for live webinars included support for returning to fitness and work, pelvic floor, babies first aid and sleep among others. The BtB online ‘live’ program was developed based on suggested needs and time-of-day ‘morning’, however, attendance to all ten sessions in the program was poor (23% of eligible women (n = 162) participated in first session and 5% in the last session). Barriers to attendance included ‘too busy’, ‘forgot’, and ‘topic not relevant for age of child’. 88% of women reported education as the most enjoyable part of the program, with 19% reporting physical activity as the most liked portion of the program. 100% of women interviewed would recommend the program to a friend. Cited barriers for non-attendance were factors that may be easily addressed in the future reiterations of BtB programs. More research is needed to improve the uptake and value placed on mothers’ level of physical activity and fitness. Future postpartum programs may benefit from integrating online platforms that are more flexible than a live webinar to improve attendance and separating 0–6- and 6–12-months postpartum topics to improve relevance.
49
Emily Aldridge1,2,
1. Robinson Research Institute, The University of Adelaide, Adelaide, SA, Australia
2. Department of Cardiology, Lyell McEwin Hospital, Elizabeth Vale, SA, Australia
3. Adelaide Medical School, The University of Adelaide, Adelaide, SA, Australia
4. Flinders Health and Medical Research Institute, Flinders University, Bedford Park, SA, 5042
5. Division of Women's Health, Lyell McEwin Hospital, Elizabeth Vale, SA, Australia
50
1. Monash Health, Clayton South, VIC, Australia
Transparency, one of the usefulness criteria, was also a concern; four studies (16.7% CI95% [1.7–31.6]) were registered in a trial database (only one study registered prospectively), and no published protocols. Seven studies (29.2% CI95% [11–47.4]) disclosed funding disclosure, four studies (16.7% CI95% [1.7–31.6]) included comments on conflicts of interest, while none mentioned availability of raw data.
Trustworthiness assessment revealed the following concerns: two studies had a short time between last participant recruited to publication (≤6 months), in six additional studies this time could not be calculated. External validity was inconsistent between the studies, many excluding key demographics (ie. multiple pregnancies, rupture of membranes) or failing to report on important patient characteristics (ie. previous pre-term pregnancies, cervix status).
51
1. King Edward Memorial Hospital, Subiaco, Western Australia, Australia
Upon arrival, she underwent augmentation of labour and had a spontaneous vaginal delivery. During labour she became hypoxic and repeat chest x-ray post-partum showed the left lower zone opacity, now also containing an air fluid level consistent with an intrathoracic stomach. Computed tomography confirmed a defect in the central left hemidiaphragm, with herniation of the gastric body and a section of the transverse colon through the defect. There was collapse of the left lung and associated mediastinal shift.
She underwent endoscopic decompression and laparoscopic mesh repair of a 5 cm left sided diaphragmatic hernia and had an uneventful post-operative recovery. She was discharged with her baby after six days.
MDH is rare and presents with non-specific respiratory and gastrointestinal symptomology. These symptoms have significant overlap with more benign complaints of pregnancy, making MDH hard to diagnose.
In the contemporaneous literature (case reports from 2000 onwards); 28 of 46 cases of MDH had a documented alternative diagnosis, treatment plan or presented for medical review more than once before receiving a correct diagnosis.1−41 The majority of these presented with typical symptoms: 79% with chest or epigastric pain, 50% with nausea and vomiting and 18% with dyspnoea.8, 15−41 Overall, MDH was associated with high maternal (9%) and fetal (15%) mortality. Preterm birth was also common, occurring in 46%.1−41
Our case and literature review suggest that it is important to maintain an index of suspicion for MDH in women who present with any combination of chest or epigastric pain, dyspnoea or nausea and vomiting. Prompt diagnosis is essential to ensure maternal wellbeing and a successful pregnancy outcome.
52
1. Department of Obstetric Medicine, Joan Kirner Women's and Children's at Sunshine Hospital, St Albans, VIC, Australia
2. Department of General Internal Medicine, Western Health, St Albans, VIC, Australia
3. Department of Obstetrics, Royal Women's Hospital, Parkville, VIC, Australia
Case B – IVIG (2 mg/kg), prednisolone (50 mg daily) and a pool of platelets was administered acutely for a platelet count of 2 at 24 weeks gestation. On maintenance treatment of hydroxychloroquine 400 mg daily and prednisolone 25 mg daily, the platelet count was 108 at 8 weeks and 253 at 4 months of treatment, demonstrating complete and sustained treatment response. She delivered at 31 weeks gestation by ELCS with spinal anaesthesia, due to intermittent absent end diastolic flow (type 3 selective intrauterine growth restriction) in Twin B, with post-partum haemorrhage of 1.5 L. Twin A and Twin B had an uncomplicated course in neonatal intensive care for prematurity care. There was no neonatal thrombocytopenia.
53
1. Adelaide Medical School, University of Adelaide, Flinders Park, SA, Australia
Previous studies have outlined the importance of effective early post-partum interventions at reducing cardiovascular disease risk in women who have experienced a pregnancy complication. This led to the emergence of the COFFEE clinic, an early post-partum cardiovascular education and intervention service at the Lyell McEwin Hospital. The major problem facing the COFFEE clinic is only 50% of referred women attend their appointments. The aim of this retrospective study is to compare socioeconomic factors between women who attend their scheduled COFFEE clinic appointment and those who do not attend their appointment. This study analysed medical records of a preliminary sample of 696 women referred to the COFFEE clinic between the 1st of January 2018 to the 31st of December 2021. Differences in patient demographics and socioeconomic variables between women who attended and those who did not were completed using independent sample t-test, Fisher's exact test, chi-square tests and multivariate linear or logistic regressions. The preliminary results showed mean age of the cohort was 32 years, the majority were English speaking, and the majority were employed. Two-thirds of the cohort were referred for Gestational Diabetes Mellitus (69.1%) and one-third were referred for hypertensive disorders of pregnancy (34.3%). There were no statistically significant differences between women who attended and those who did not for any of the socioeconomic variable. The results of this study reveal a vulnerable group within this cohort of women who can be targeted for addition engagement.
54
1. Endocrinology, Singapore General Hospital, Singapore
A 35-year-old Chinese lady was on follow up for gestational diabetes mellitus (GDM) that was well controlled on metformin therapy. At around 32 weeks of gestation, she developed significant polyuria and polydipsia and reports having to drink and pee up to ten litres per day. She had cravings for cold, sugar-sweetened beverages. She denied headache, visual disturbance, and did not have symptoms suggestive of hypocortisolism and hypothyroidism.
Her biochemistry evaluation revealed serum sodium of 138 mmol/L, serum osmolality of 285 mmol/kg, and urine osmolality of 66 mmol/kg. Her liver function test was normal. Her thyroid function test showed fT4 of 8.0pmol/L, TT4 125 nmol/L, TSH 2.61 mu/L, which was appropriate for gestation.
She was started on nasal desmopressin at bedtime with improvement of symptoms. Her urine osmolality also increased to 669 mmol/kg. A magnetic resonance imaging (MRI) pituitary (non-contrast) which was performed prior to delivery showed normal sized pituitary gland with poorly visualised posterior pituitary bright spot, and central pituitary stalk. A provisional diagnosis of gestational diabetes insipidus was made.
She delivered via normal vaginal delivery uneventfully. She was reviewed at 2 and 5 weeks post-partum, but her symptoms were still persistent, suggesting the possibility of an alternative diagnosis, as most cases of gestational diabetes insipidus should resolve by 6 weeks post-partum.
At 3 months post-partum, her fT4 was low at 7.1pmol/l (Reference:8.8- 14.4), TSH 3.44 mu/L, serum sodium 140 mmol/L, serum osmolality 291 mmol/Kg, urine osmolality was 84 mmol/kg, and her 1 mcg Synacthen stimulation test showed appropriate peak cortisol response of 596 nmol/L. Repeat MRI pituitary scan (contrasted) showed that the pituitary gland appears prominent and showed prominent contrast enhancement. Normal high T1 signal intensity was noted in the posterior pituitary gland. There were no discrete nodules noted in the pituitary glands. As such, a diagnosis of hypophysiitis was considered.
In view of the risks associated with biopsy as the gold standard for determining the underlying aetiology, ancillary tests were performed instead. TB Quantiferon test, Syphyllis serology, Anti-nuclear antibody (ANA), Anti-neutrophil cytoplasmic antibody (ANCA), ENA screen were performed and returned unremarkable. She was started on levothyroxine 25 mcg om and continued on nasal ddAVP at bedtime.
55
1. Mater Health, Brisbane
Cardiac disease represents the largest single cause of indirect maternal death, arrhythmias being the immediate or underlying cause in 10.7% of maternal cardiovascular deaths.1, 2 Physiological changes predispose to cardiovascular symptoms in pregnancy. Palpitations, dyspnoea, and syncope have been described in 11.5%, 37.5% and 1% of healthy pregnant women respectively. Holter monitoring in healthy asymptomatic pregnant women found supraventricular ectopic beats (SVEs) and ventricular ectopic beats (VEBs) in 58% and 52% of women. More than 100 SVEs per hour occurred in 4% of women, and more than 50 VEBs per hour occurred in 2% of women.3 A study of Holter monitoring in symptomatic pregnant women demonstrated that only 10% of symptomatic episodes were accompanied by arrhythmias.3 A retrospective review of the diagnostic yield of 24-h Holter monitoring, echocardiography, thyroid function and full blood count in previously healthy woman presenting with palpitations (66%), presyncope/syncope (32%), dyspnoea (23%) and chest tightness (8%) over a 3-year period was performed. 24-h Holter monitoring was performed on 183 women, mean age 30 years, mean BMI 27.6 kg/m2. 24-h Holter monitoring revealed no significant arrhythmia in 141 women (77%), sinus tachycardia > 100bpm for > 10% recording in 26 women (14%), and significant arrhythmia in 16 women (8.7%) (13 > 1% VEBs, 2 with runs VT; 5 > 1% SVEs). Holter monitoring resulted in a change in therapy in 5 women (2.7%). Cardiovascular symptom type, maternal age, obesity, parity, or anaemia were not predictive of tachycardia or arrhythmia. Forty-five per cent of women recorded no symptomatic events during the 24-h recording. Ninety-two per cent of events recorded correlated with sinus rhythm, sinus tachycardia or sinus rhythm with isolated VEBs. Echocardiography revealed abnormalities in 2 women (1.8%), 1 woman with mitral valve prolapse, and another woman with dilated cardiomyopathy in setting 32% ventricular ectopic beats. Thyroid function was normal in 122/122 patients, 12/183 (6.6%) had Hb < 105 g/dL. No adverse clinical cardiac events occurred during pregnancy. 24-h Holter monitoring, and echocardiography have a relatively low diagnostic yield in investigating women without underlying cardiovascular disease who develop cardiovascular symptoms in pregnancy. Further studies examining monitoring with longer periods with Holter monitoring, 14-day adhesive patch electrocardiographic monitoring, event loop recording, Smart Watch devices or the Kardiamobile smartphone monitor increases detection of arrhythmias resulting in change in management and outcome in this low-risk population may be worthwhile.
Most women can be reassured that their symptoms are likely to be benign.
1. Knight M, Bunch K, Kenyon S, et al. A national population-based cohort study to investigate inequalities in maternal mortality in the United Kingdom, 2009–17. Paediatr Perinat Epidemiol 2020; 34: 392–398. 2020/02/06. DOI: 10.1111/ppe.12640.
2. Briller J, Koch AR, Geller SE, et al. Maternal Cardiovascular Mortality in Illinois, 2002–2011. Obstet Gynecol 2017; 129: 819–826. 2017/04/07. DOI: 10.1097/AOG.0000000000001981.
3. Shotan A, Ostrzega E, Mehra A, et al. Incidence of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. Am J Cardiol 1997; 79: 1061–1064. 1997/04/15. DOI: 10.1016/s0002-9149(97)00047-7.
56
1. Mater Health, Brisbane
Gordon's syndrome, also known as pseudohypoaldosteronsim type II and familial hyperkalaemic hypertension, is a rare inherited condition characterised by familial hyperkalaemia, normal anion gap hyperchloraemic metabolic acidosis and low renin with normal glomerular filtration rate. Variable features include hypertension, hypercalciuria, short stature, low aldosterone, and dental anomalies. Gordon syndrome is caused by gain of function mutations in the genes regulating the thiazide-sensitive sodium-chloride transporter channel located on the distal convoluted tubules of renal nephrons.1 Four genes have been implicated - WNK1 on chromosome 12, WNK4 on chromosome 17, CUL3 on chromosome 2 and KLHL3 on chromosome 5.2 Gordon syndrome is usually inherited as an autosomal dominant condition with high penetrance although autosomal recessive inheritance has been described with KLHL3, and de novo mutations have been reported.3
Individuals with a CUL3 variant have more severe hyperkalaemia and metabolic acidosis, earlier and more severe hypertension, and greater likelihood of growth impairment compared to those harbouring KLHL3, WNK1, or WNK4 alterations.4
Thirteen pregnancies in 7 women with Gordon's syndrome have been described previously. A further 11 pregnancies in 3 women with Gordon's syndrome have been combined and the outcomes reviewed.
Eleven pregnancies occurred in 5 women who had hypertension preconception. Pregnancy complications were eclampsia and fetal death in one pregnancy, preeclampsia (4 cases), fetal growth restriction (FGR) (3), hypertension at term (3), and delivery prior to 37 weeks gestation in 4 pregnancies.
Thirteen pregnancies occurred in 5 women with normal blood pressure pre-conception. These pregnancies were complicated by preeclampsia (1 case), FGR (1), placental abruption (1), delivery prior to 37 weeks (3), fetal symbrachydactyly (1)l, fetal echogenic bowel and short long bones. (1)
Eleven pregnancies were to women taking thiazide diuretics pre-conception. Thiazides were continued during 6 pregnancies. These 6 pregnancies were complicated by PET (4 cases) and FGR (4). No congenital anomalies occurred.
Maternal serum potassium varied but did not provide management issues.
The results for genetic testing were available for only 4 women. One woman had WNK4 and another KLHL3 mutation. Two sisters tested negative for WNK1 and WNK4 – KLHL3 and CUL3 testing were not performed. Pregnancies in these 4 women were uncomplicated other than one case of PPROM and three cases of hypertension at term.
Gordon's syndrome appears to be associated with a high risk of pregnancy complications, especially in women with preconception hypertension. Assessing whether specific mutations predict adverse pregnancy outcomes would be valuable.
1. Proctor G and Linas S. Type 2 pseudohypoaldosteronism: new insights into renal potassium, sodium, and chloride handling. Am J Kidney Dis 2006; 48: 674–693. 2006/09/26. DOI: 10.1053/j.ajkd.2006.06.014.
2. Glover M, Ware JS, Henry A, et al. Detection of mutations in KLHL3 and CUL3 in families with FHHt (familial hyperkalaemic hypertension or Gordon's syndrome). Clin Sci (Lond) 2014; 126: 721–726. 2013/11/26. DOI: 10.1042/CS20130326.
3. O'Shaughnessy KM. Gordon Syndrome: a continuing story. Pediatr Nephrol 2015; 30: 1903–1908. 2014/12/17. DOI: 10.1007/s00467-014-2956-7.
4. Boyden LM, Choi M, Choate KA, et al. Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities. Nature 2012; 482: 98–102. 2012/01/24. DOI: 10.1038/nature10814.
57
1. Mater Health, Brisbane
Hyperemesis gravidarum (HG) complicates 0.5–2% of pregnancies. Anti-emetic therapy (AET) may cause extrapyramidal side-effects (EPS). Cognitive dysfunction, hallucinations and severe agitation with akathisia may lead to self-harm.1 Akathisia may be overlooked or incorrectly attributed to a primary mental health disorder, hysteria, or a functional disorder. A case of akathisia and oculogyric crisis due to AET for HG is presented. The treatment options for EPS and ongoing treatment of HG are discussed.
A 20-year primigravid presented at 8 weeks’ gestation with a 3-week history of HG despite taking ondansetron, metoclopramide, pyridoxine-doxylamine, and omeprazole. Intravenous fluids were commenced, and 2 doses of intravenous prochlorperazine administered in addition to existing medications. The woman subsequently complained of extreme agitation, restlessness, and anxiety. She manifested a hyperextended neck and fixed conjugate upward gaze consistent with akathisia and oculogyric crisis. Prochlorperazine, metoclopramide and ondansetron treatment were ceased, and antihistamines, intravenous hydrocortisone and thiamine were administered. The EPS and vomiting resolved overnight.
One case of oculogyric crisis and two cases of acute dystonia have been reported following prochlorperazine therapy for HG.234
Oculogyric crises have been described following metoclopramide and ondansetron therapy in non-pregnant individuals.5, 6 Akathisia has been reported in 9–44%, 5–32% and 0.8–3% of non-pregnant individuals treated with prochlorperazine, metoclopramide and ondansetron respectively.7, 8
Cytochrome P450 2D6 genetic polymorphisms may predispose to acute dystonic reactions with metoclopramide, prochlorperazine and ondansetron due to slowing of drug metabolism.9
EPS usually resolve within 24–48 h of drug cessation. Anticholinergic and antihistamine medications may be used for severe symptoms. Intravenous diphenhydramine is the drug of choice in pregnancy. Ondansetron may not be reversed by diphenhydramine, and short-term benzodiazepines may be preferable.10
Drug-induced EPS affects the management of HG. Akathisia and dystonia have been reported following the use of mirtazapine, promethazine, cyclizine, droperidol and gabapentin. Doxylamine, diphenhydramine and glucocorticoids may be used safely. EPS has not been described with granisetron . Benzodiazepines may be therapeutic in HG and EPS though with a potential risk of prematurity and low birth weight. Transdermal scopolamine and clonidine may be effective in the management of HG and EPS.
Oculogyric crises are rare though easily recognised. The incidence of akathisia is unknown, and it may be overlooked. Obstetric physician's awareness of the potential for akathisia with anti-emetic s for HG is important.1, 11
1. Cheng HM, Park JH and Hernstadt D. Akathisia: a life-threatening side effect of a common medication. BMJ Case Rep 2013; 2013 2013/05/24. DOI: 10.1136/bcr-2012–007713.
2. Williams P AH. Akathisia preceding an oculogyric crisis in a patient treated with prochlorperazine for hyperemesis gravidarum. Case Rep Perinat Med 2014; 3: 15–17.
3. Beirne M and Fenton J. Acute dystonic reaction secondary to prochlorperazine use in the treatment of hyperemesis gravidarum. Ir J Med Sci 2007; 176: 53–54. 2007/09/13. DOI: 10.1007/s11845–007-0005-2.
4. Coralic Z, Kim AS and Vinson DR. Prochlorperazine-Induced Hemidystonia Mimicking Acute Stroke. West J Emerg Med 2015; 16: 572–574. 2015/08/13. DOI: 10.5811/westjem.2015.4.26003.
5. Macachor JD, Kurniawan M and Loganathan SB. Ondansetron-induced oculogyric crisis. Eur J Anaesthesiol 2014; 31: 712–713. 2014/10/12. DOI: 10.1097/EJA.0000000000000169.
6. Koban Y, Ekinci M, Cagatay HH, et al. Oculogyric crisis in a patient taking metoclopramide. Clin Ophthalmol 2014; 8: 567–569. 2014/03/29. DOI: 10.2147/OPTH.S60041.
7. Patka J, Wu DT, Abraham P, et al. Randomized Controlled Trial of Ondansetron vs. Prochlorperazine in Adults in the Emergency Department. West J Emerg Med 2011; 12: 1–5. 2011/06/22.
8. Miller LG and Jankovic J. Metoclopramide-induced movement disorders. Clinical findings with a review of the literature. Arch Intern Med 1989; 149: 2486–2492. 1989/11/01. DOI: 10.1001/archinte.149.11.2486.
9. Wong DY and Fogel BL. Acute pharmacogenetic dystonic reactions in a family with the CYP2D6 *41 allele: a case report. J Med Case Rep 2021; 15: 432. 2021/08/20. DOI: 10.1186/s13256-021-03022-x.
10. Spiegel JE, Kang V, Kunze L, et al. Ondansetron-induced extrapyramidal symptoms during cesarean section. Int J Obstet Anesth 2005; 14: 368–369. 2005/09/13. DOI: 10.1016/j.ijoa.2005.06.001.
11. Wright MT. Antiemetics, akathisia, and pregnancy. Psychosomatics 2007; 48: 461–466. 2007/12/12. DOI: 10.1176/appi.psy.48.6.461.
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1. Mater Health, Brisbane
Postpartum seizures have a broad differential diagnosis. Common causes include eclampsia, cerebral vein sinus thrombosis (CVST), posterior reversible encephalopathy (PRES), cerebral haemorrhage, drug withdrawal and metabolic abnormalities. Correct diagnosis is crucial to acute management and the risk of recurrence in subsequent pregnancy.
A 22-year-old primigravida with no significant history was induced post-dates with epidural anaesthesia. Sixteen hours after rupture of membranes emergency caesarean section was performed for obstructed labour and abnormal cardiotocogram. A live female birthweight 5270 g was delivered. The woman re-presented 5 days postpartum because of hypogastric pain. Upon sitting up abruptly following a pelvic ultrasound she manifested 2 episodes of tonic-clonic convulsions each lasting 5–10 min followed by post-ictal confusion. Physical examination revealed temperature 36.8o, BP 130/80 mmHg, no proteinuria, no neck stiffness, mild hyperreflexia but no clonus. The woman was treated with intravenous midazolam and magnesium sulphate infusion, acyclovir, and ceftriaxone. Biochemistry and haematology tests were normal, magnetic resonance (MRI) venography showed diffuse pachymeningeal enhancement with distended dural venous sinuses consistent with intracranial hypotension. Electroencephalogram was unremarkable. The woman complained of 6/10 headache, tinnitus, and shoulder stiffness. She declined an epidural blood patch.
MRI in 136 women with postpartum convulsions revealed no abnormality in 36%, CVST in 24%, PRES in 21%, intracerebral haemorrhage in 7% and subarachnoid haemorrhage in 4%.1, 2
Unintentional dural puncture complicates 0.6–2.7% of labour epidural catheter placement, with this being unrecognised at time of anaesthesia in 16–38% of cases.3 Eighteen previous cases of seizures following epidural anaesthesia in pregnancy in the setting of headache and radiological signs of intracranial hypotension and in the absence of an alternative cause have been reported. Seizures occurred between 2–7 days postpartum Dural puncture and intracranial hypotension may also be complicated by subdural, subarachnoid, and cerebral haemorrhage, CVST, PRES, Horner's syndrome, cranial nerve palsies, auditory loss, and infection. Post-dural puncture headache with intracranial hypotension may be atypical without a positional component in 5.6% of cases.4
Seizures and other neurological complications postpartum result in significant maternal (and physician) anxiety particularly when unexplained. Awareness of the broad range of potential complications with intracranial hypotension following dural puncture is important for reassuring women developing these complications both immediately and with regard to future pregnancy.
1. El Ameen N AM, Kotb A. MRI of the brain in postpartum convulsions; pose diagnostic dilemnas. The Egyptian Journal of Radiology and Nuclear Medicine 2017; 48: 999–1004.
2. Hiremath R, Mundaganur P, Sonwalkar P, et al. Cross sectional imaging of post partum headache and seizures. J Clin Diagn Res 2014; 8: RC01-05. 2015/02/06. DOI: 10.7860/JCDR/2014/8783.5234.
3. Richardson MG, Lee AC and Wissler RN. High spinal anesthesia after epidural test dose administration in five obstetric patients. Reg Anesth 1996; 21: 119–123. 1996/03/01.
4. Loures V, Savoldelli G, Kern K, et al. Atypical headache following dural puncture in obstetrics. Int J Obstet Anesth 2014; 23: 246–252. 2014/06/18. DOI: 10.1016/j.ijoa.2014.04.005.
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1. Medical Obstetrics, Northern Health, Melbourne, Victoria, Australia
2. Obstetrics and Gynaecology Resident, Northern Health, Melbourne, Victoria, Australia
3. Advanced Trainee in General Medicine, Northern Health, Melbourne, Victoria, Australia
4. Faculty of Medicine Dentistry and Health Sciences, University of Melbourne, Melbourne, Victoria, Australia
5. Biostatistics, Northern Health, Melbourne, Victoria, Australia
6. Head of Medical Obstetrics and Nephrologist, Northern Health, Melbourne, Victoria, Australia
Tests for statistical significance (Chi-square, Mann-Whitney) were conducted when relevant.
A number of similarities were observed between the patients with HDP and the dnHDP group, including socioeconomic status, maternal age at delivery (32.4 ± 4.9, 31.9 ± 5.6 years), BMI (32 (25–38), 31 (24–41) kg/m2) nulliparity (48.6%, 40.5%) and antenatal aspirin prescription (28.6%, 27%).
The median birthweight of the HDP group was less (3130 (2790–3410) grams) compared to the dnHDP (3290 (3020–3800) grams). There was less gestational diabetes mellitus (GDM) in the HDP versus group (20% versus 40.5%) (p = 0.08).
Differences were observed in the urine protein to creatinine ratio (uPCR) antenatally. The HDP group had 48.6% with a uPCR >30 mg/mmol compared to 2.7% in the dnHDP group within 4 weeks of delivery (p < 0.001).
Antenatally, the median blood pressure readings for the HDP were higher than the dnHDP group, who had normal antenatal blood pressure readings. Postpartum, the median blood pressure readings were elevated in both groups (174/107 mmHg – HDP, 160/100 mmHg – dnHDP), however the HDP were significantly more elevated (SBP p = 0.031, DBP <0.001).
1. De Zoysa M, Chung JH, Adkins K, Steller J. Factors associated with postpartum readmission for hypertensive disorders of pregnancy. American Journal of Obstetrics & Gynecology. 2022;226(1):S462-S3.
2. Al-Safi Z, Imudia AN, Filetti LC, Hobson DT, Bahado-Singh RO, Awonuga AO. Delayed Postpartum Preeclampsia and Eclampsia: Demographics, Clinical Course, and Complications. Obstetrics & Gynecology. 2011;118(5).
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1. School of Medicine, University of Queensland, Brisbane, Queensland, Australia
2. Queensland Diabetes and Endocrine Centre, Mater Hospital Brisbane, Brisbane, QLD, Australia
JM, a 34-year-old woman, G3P1, presented with hypertension at 32 weeks’ gestation. She had Type 1 Diabetes Mellitus and was experiencing hypoglycaemic episodes despite reducing her insulin. TFTs revealed a TSH of 2.55 mIU/L and T4 of <5.2pmol/L whilst on Thyroxine 75micrograms daily for Hashimoto's thyroiditis.
She naturally conceived in 2015, however could not breastfeed and experienced long-term fatigue post-delivery. She had a miscarriage in 2020 following ovarian induction with clomiphene for presumed polycystic ovarian syndrome. Her current pregnancy was via IVF.
An anterior pituitary hormone panel revealed secondary adrenal insufficiency (Table 1). A non-contrast MRI pituitary showed only a partial empty sella with no pituitary lesion (Figure 1). Retrospectively, a low TSH was present 3-months post-delivery of her first child (Figure 2). Whilst the aetiology of her panhypopituitarism remained unclear, it was thought likely to have occurred between her first two pregnancies.
Hydrocortisone replacement was commenced (12miligrams mane, 8miligrams midi), and her Thyroxine was increased to 150micrograms daily with symptomatic improvement. Her hypoglycaemic events resolved. She underwent a caesarean section with hydrocortisone stress dosing at 36 weeks’ gestation for foetal indications.
Now 6 weeks post-partum, JM has had one menstrual cycle. She is euthyroid (TSH 0.6 mIU/L [0.3–3.5 mIU/L], T4 12.6pmol/L [9.0–19.0pmol/L]) on Thyroxine 150micrograms daily. A repeat anterior pituitary screen remains concerning for panhypopituitarism –IGF-1 6 nmol/L (11–38 nmol/L), Prolactin 163 mIU/L (<500 mIU/L), FSH 8IU/L, LH 3IU/L, Oestradiol 148pmol/L. An overnight Metyrapone test suggests persistent central adrenal insufficiency with an ACTH 28 ng/L (9–51 ng/L), cortisol <50 nmol/L (100–535 nmol/L) and a 11-deoxycortisol of 104.4 nmol/L (>200 nmol/L).
Panhypopituitarism is rare and associated with miscarriage, gestational hypertension, placental abruption, and post-partum haemorrhage.1 Pregnancy-related conditions resulting in panhypopituitarism include Sheehan's syndrome and lymphocytic hypophysitis.2 Non-pregnancy conditions include lesions with mass effect on the pituitary and/or stalk, Empty Sella syndrome, infiltrative disease, head injury and iatrogenicity (Table 2).3
Symptoms are often non-specific and dependent on the degree of hormones affected. An intact hypothalamic-gonadal-axis is required to achieve a successful pregnancy and the diagnosis is often made when investigating infertility.4 Failure of lactation postpartum holds high specificity.5
Furthermore, prolactin, cortisol and thyroid levels have trimester-specific cut offs, and dynamic testing should be cautiously interpreted due unclear reference ranges. IGF-1 levels are affected by oestrogen, and current assays cannot distinguish placental from maternal growth hormone.6 MRI has limited value given the inability to use gadolinium contrast during pregnancy. Therefore, a high clinical suspicion is often required when investigating pregnant women for hypopituitarism.
1. Du X, Yuan Q, Yao Y, Li Z, Zhang H. Hypopituitarism and successful pregnancy. Int J Clin Exp Med. 2014 Dec 15;7(12):4660–5. PMID: 25663963; PMCID: PMC4307410.
2. Karaca Z, Tanriverdi F, Unluhizarci K, Kelestimur F. Pregnancy and pituitary disorders. Eur J Endocrinol. 2010 Mar;162(3):453–75. doi: 10.1530/EJE-09-0923. Epub 2009 Nov 24. Erratum in: Eur J Endocrinol. 2010 Jun;162(6):1167. PMID: 19934270.
3. Kim SY. Diagnosis and Treatment of Hypopituitarism. Endocrinol Metab (Seoul). 2015 Dec;30(4):443–55. doi: 10.3803/EnM.2015.30.4.443. PMID: 26790380; PMCID: PMC4722397.
4. Vila G, Fleseriu M. Fertility and Pregnancy in Women With Hypopituitarism: A Systematic Literature Review. J Clin Endocrinol Metab. 2020 Mar 1;105(3):dgz112. doi: 10.1210/clinem/dgz112. PMID: 31652320
5. Bhushan D, Agarwal M, Shukla RK. Hypopituitarism: A Rare but Often Neglected Condition. Indian J Crit Care Med. 2020 May;24(5):350–352. doi: 10.5005/jp-journals-10071–23422. PMID: 32728328; PMCID: PMC7358872.
6. Morton A, Teasdale S. Physiological changes in pregnancy and their influence on the endocrine investigation. Clin Endocrinol (Oxf). 2022 Jan;96(1):3–11. doi: 10.1111/cen.14624. Epub 2021 Nov 1. PMID: 34724247.
7. Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a reference table for clinicians. Obstet Gynecol. 2009 Dec;114(6):1326–1331. doi: 10.1097/AOG.0b013e3181c2bde8. Erratum in: Obstet Gynecol. 2010 Feb;115(2 Pt 1):387. PMID: 19935037.
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1. The Royal Brisbane and Women's Hospital, Herston, QLD, Australia
2. School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, Queensland, Australia
3. Mater Research Institute, University of Queensland, Brisbane, Queensland, Australia
4. Royal Hospital for Women, Randwick, NSW
62
1. Mater Hospital, South Brisbane, QLD, Australia
2. University of Queensland, Brisbane
Alagille syndrome (ALGS) is a complex multisystem condition caused by mutations in JAG1 or NOTCH2genes.(1) The incidence is estimated to be 1:35000 individuals.(2) The mutation occurs de novo in 60% of affected individuals, the remainder being autosomal dominant.(3) Characteristic features include bile duct paucity, cholestasis, cardiac malformations, ocular disorders, renal anomalies, renovascular disease and cerebrovascular abnormalities, hypertension, abnormal facies and short stature.(2) ALGS may manifest significant intrafamilial variability in manifestations.(4)
A 38-year-old primigravid was admitted at 21 weeks’ gestation with new hypertension and headache. ALGS was diagnosed in childhood after her sister presented with cholestasis, ultimately requiring liver transplantation. Her father and paternal cousin were also affected. Manifestations of ALGS included typical facies, mild-moderate pulmonary stenosis (peak/mean gradient 36/17 mmHg) and pigmentary retinopathy. At 8 weeks’ gestation serum creatinine had been 79umol/L (normal < 78), urine protein:creatinine and liver function tests normal. On examination, blood pressure was 169/73 mmHg with bilateral ankle oedema. Urine protein-creatinine ratio was now elevated at 46 mg/mmol (normal <30). There were no other clinical or biochemical features of pre-eclampsia. Labetalol was commenced with good effect. Autoimmune, vasculitis and antiphospholipid screens were negative. Phaeochromocytoma, primary aldosteronism, renal artery stenosis and hyperthyroidism were excluded.
The woman's blood pressure was well controlled on twice-weekly outpatient visits until she re-presented at 26 weeks’ gestation with hypertension and a severe retroorbital headache. Urine protein-creatinine ratio had increased to 178 mg/mmol. Satisfactory growth and normal dopplers was seen on fetal ultrasound. CT head venogram excluded dural venous sinus thrombosis and intracranial haemorrhage. Antihypertensives were uptitrated initially with good effect. She developed episodes of severe hypertension over the subsequent 48 h requiring oral nifedipine and intravenous hydralazine. Delivery was indicated given her severe hypertension in the setting of pre-eclampsia. She underwent emergency classical caesarean section and delivered an 878 gram boy at 26 weeks and 3 days gestation.
Including this case, 12 successful pregnancies have been described in women with ALGS.(5) Complications included fetal growth restriction (FGR-7cases), pre-eclampsia (2), maternal cholestasis (2), HELLP syndrome (1) and postpartum maternal pulmonary oedema (1).(5) Miscarriage rates of 27% have been reported after 10 weeks’ gestation.(4) ALGS represent high risk pregnancies. Specific management considerations include assessment of the severity of cardiac disease, monitoring for liver dysfunction, cholestasis, renal dysfunction and pre-eclampsia as well as monitoring for FGR.(5) DNA-based pre-implantation and prenatal diagnosis of ALGS may be performed.(6)
1. Mitchell E, Gilbert M, Loomes KM. Alagille Syndrome. Clin Liver Dis. 2018;22(4):625–41.
2. Kamath BM, Baker A, Houwen R, Todorova L, Kerkar N. Systematic Review: The Epidemiology, Natural History, and Burden of Alagille Syndrome. J Pediatr Gastroenterol Nutr. 2018;67(2):148–56.
3. Hannoush ZC, Puerta H, Bauer MS, Goldberg RB. New JAG1 Mutation Causing Alagille Syndrome Presenting With Severe Hypercholesterolemia: Case Report With Emphasis on Genetics and Lipid Abnormalities. J Clin Endocrinol Metab. 2017;102(2):350–3.
4. Elmslie FV, Vivian AJ, Gardiner H, Hall C, Mowat AP, Winter RM. Alagille syndrome: family studies. J Med Genet. 1995;32(4):264–8.
5. Morton A, Kumar S. Alagille syndrome and pregnancy. Obstet Med. 2021;14(1):39–41.
6. Renbaum P, Brooks B, Kaplan Y, Eldar-Geva T, Margalioth EJ, Levy-Lahad E, et al. Advantages of multiple markers and polar body analysis in preimplantation genetic diagnosis for Alagille disease. Prenat Diagn. 2007;27(4):317–21.
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Corey Markus1, Suzette Coat2, Hanns-Ulrich Marschall3, Susan Matthews1, Wayne Rankin4,5,6,
1. Flinders University International Centre for Point-of-Care Testing, Adelaide, Australia
2. Robinson Research Institute, The University of Adelaide, Adelaide, Australia
3. University of Gothenburg, Gothenburg, Sweden
4. Chemical Pathology Directorate, SA Pathology, Adelaide, South Australia
5. Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA
6. Adelaide Medical School, The University of Adelaide, Adelaide, SA
Assay standardisation is an underappreciated aspect in the setting of large-scale international clinical trials, particularly those combining patient results from different laboratory services. Assay standardisation has been gaining increasing attention, especially for frequently ordered analytes, e.g., Creatinine and HbA1c, which have clearly defined medical decision points derived from strong outcome studies. In the case of bile acid (BA) measurements, this situation is less certain and results from quality assurance programs demonstrate significant methodological variations. Furthermore, these methodical variations may be reflected in results for patient samples.
In recognition of the between-laboratory heterogeneity in BA results, the Bile Acid Comparison and Harmonisation (BACH) study was established as a sub-study of the international randomised ‘Trial of URsodeoxycholic acid vs. RIFampicin in severe early-onset Intrahepatic Cholestasis of pregnancy’ (TURRIFIC). We here show results from the BACH project with respect to methodology questionnaires, between-laboratory variability in results and the potential for mathematical recalibration and harmonisation for Australian laboratories servicing TURRIFIC recruitment sites.
Laboratories providing BA measurements for TURRIFIC in Australia were invited to participate in the BACH project, with participation considered as an in-kind contribution. Pooled serum comparison samples were prepared from remainder clinical samples and, to obtain pools with higher BA values, some were spiked with bile or discrete BA species. Commutability — the relationship of spiked serum samples with native clinical samples — was assessed in a manner consistent with international guidelines. Mathematical recalibration and harmonisation were investigated via a consensus value approach using the median value of each sample from all participating laboratories.
Nine laboratories were recruited into BACH, all of which responded to the methodological questionnaire, and all assayed the full comparison sample set. Participants represented the commonly used commercial enzymatic reagents: four sites using Randox, three Diazyme and two Abbott reagents. One reagent manufacturer displayed minor assay non-linearity. Sixty pooled serum comparison samples were produced, including eleven spiked with bile fluid or BA species. Glycodeoxycholic and cholic acids demonstrated potential commutability as reference materials. Recalibration and harmonisation decreased the between-laboratory variability from 8.8% to 2.5% pre- and post-harmonisation respectively: a reduction of 72%.
We have presented an overview of the current situation for BA measurements in Australia and successfully demonstrated harmonisation of BA results, allowing pooling of results for statistical analysis. We aim to extend this study to the European sites, using the same reference samples and including mass spectrometry reference methods.
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1. Royal Hospital for Women, Randwick, NSW, Australia
2. Child population and Translational Health Research, Children's Hospital at Westmead Clinical School and Menzies Centre for Health Policy and Economics, University of Sydney, Camperdown, NSW, Australia
3. School of Population Health, University of New South Wales, Kensington, NSW, Australia
4. University of New South Wales, Darlinghurst, NSW, Australia
5. St Vincent's Hospital, Darlinghurst, NSW, Australia
6. co-last authors,
7. Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Iceland
1. Skiba MA, Islam RM, Bell RJ, Davis SR. Hormonal contraceptive use in Australian women: Who is using what?. Australian and New Zealand Journal of Obstetrics and Gynaecology. 2019 Oct;59(5):717–24.
65
1. Division of Medicine, Ipswich Hospital, Queensland Health
KH, a 38 year old female presented 9 days postpartum with left upper quadrant abdominal pain. Her pregnancy was complicated by gestational thrombocytopaenia and shoulder dystocia during vaginal delivery.
She had a background of attention deficit hyperactivity disorder. Her obstetric history was G7P4T2M1 with a previous postpartum haemorrhage in 2017. Her medications included lisdexamfetamine 50 mg mane, clexane 60 mg mane and ferrous sulphate 325 mg mane.
KH had been incarcerated since her second trimester and was an ex-smoker. She denied alcohol or recreational drug use. There was no family history of autoimmune or thrombophilic disorders.
KH reported fluctuating left abdominal pain one month prepartum but had not notified staff. At day 9 postpartum, she felt a sudden onset of shooting pain in the left upper abdomen associated with vomiting. There was no history of trauma or vaginal bleeding.
She had a blood pressure of 159/107 mmHg and a low-grade temperature of 37.8 degrees Celsius. On palpation, her abdomen was soft but tender at the left upper quadrant with guarding. Her cardiovascular examination was unremarkable. She was hyperreflexic with no clonus.
Investigations included a haemoglobin of 148 g/L and platelets of 228 10^9 /L with a normal blood film and coagulation profile. Her urine protein creatinine ratio was 26 g/mol. Computed tomography (CT) of her abdomen showed multiple hypodense regions within the spleen, suspicious of splenic infarcts. Autoimmune, infectious and antiphospholipid screens were negative. She had a normal echocardiogram with no evidence of atrial fibrillation on telemetry. CT angiogram demonstrated dissection of the splenic artery and luminal narrowing of the left vertebral artery at the level of C2/3.
Multidisciplinary input was sought with advice from vascular medicine and surgery. KH was commenced on warfarin. Blood pressure control in the setting of pre-eclampsia was also prioritised. She is planned for follow-up six week progress imaging.
Splenic infarcts are rare events and generally occur in embolic or hypercoagulable states1. There is no consensus as to the diagnostic workup or therapeutic approach1. Previous reported cases of postpartum splenic infarcts have been associated with infection such as bacterial endocarditis2 or in the setting of rheumatological3 or haematological conditions. Preeclampsia is associated with vascular dissections and aneurysms4. We present this rare case of splenic infarcts associated with a splenic artery dissection in a patient with pre-eclampsia and no history of pre-existing thrombophilia, connective tissue or autoimmune disorder.
1. O'Donnell M, Shatzel JJ, Olson SR, et al. Arterial thrombosis in unusual sites: A practical review. Eur J Haematol. 2018;101(6):728–736. doi:10.1111/ejh.13165
2. Siva S, Smoleniec J. Splenic infarction in pregnancy. Aust N Z J Obstet Gynaecol. 1999;39(2):252–254. doi:10.1111/j.1479-828x.1999.tb03385.x
3. Soy M, Sayin NC, Unlü E. Splenic infarction in a pregnant woman with systemic lupus erythematosus. Clin Rheumatol. 2005;24(6):663–664. doi:10.1007/s10067-004-1069-2
4. Hunsaker DM, Turner S, Hunsaker JC 3rd. Sudden and unexpected death resulting from splenic artery aneurysm rupture: two case reports of pregnancy-related fatal rupture of splenic artery aneurysm. Am J Forensic Med Pathol. 2002;23(4):338–341. doi:10.1097/00000433-200212000-00007
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1. Liverpool Hospital SWSLHD, Smithfield, NSW, Australia
Dr Sehrish Qureshi , Dr Gauthami Bhagwanani Professor Jon Hyett Dr Luiza Peculis Department of Obstetrics and Gynaecology Liverpool Hospital Australia
Dr Renuka Shanmugalingam Department of Renal Medicine Liverpool Hospital Australia
Dr Penny Motum, Danny Hsu Department of Haematology Liverpool Hospital Australia
APLS in pregnancy is characterized by the presence of autoantibodies that are directed against phospholipid-binding proteins. The hallmark of APLS comprises the presence of persistent antiphospholipid antibodies (APLA) in the setting of arterial and venous thrombus and/or pregnancy loss.
Diagnosis of catastrophic APLS is based on the clinical involvement of at least three organ systems over a period of less than 1 week, with histopathological evidence of small-vessel occlusion and serological confirmation of the presence of APLS or lupus anticoagulant with high titre levels
The most common complications of APLS in pregnancy include recurrent miscarriages, pre-eclampsia/eclampsia, HELLP syndrome, placental insufficiency, prematurity, intrauterine growth restriction, fetal distress, fetal or neonatal thrombosis and arterial or venous thrombosis.
A Computed tomography pulmonary angiogram (CTPA) was negative for PE, but revealed the presence of hepatic infarcts. She also incidentally was found to be positive for Covid-19 at the time of admission. She had significantly impaired sflt1/plgf ratio which suggested placental dysfunction. Her liver function tests were also deranged. An ultrasound showed evidence of fetal growth restriction, with an estimated fetal weight less than 5%.
Ms C was managed with plasmapheresis, intravenous immunoglobulins and prednisone.
Following extensive counselling, a surgical termination of pregnancy was decided on based on the severity of her illness and the anticipated poor obstetric outcome.
1. Catastrophic antiphospholipid syndrome in pregnancy: a life-threatening condition | BMJ Case Reports
2. Catastrophic antiphospholipid syndrome and pregnancy. Clinical report - PubMed (nih.gov)
67
1. Department of Maternal Fetal Medicine, Royal Women's Hospital, Parkville, VIC, Australia
2. Department of Clinical Haematology, Peter MacCallum Cancer Center/Royal Melbourne Hospital, Melbourne, VIC, Australia
3. Department of Obstetrics & Gynaecology, University of Melbourne, Parkville, VIC, Australia
Fetal chromosomal aneuploidy screening with non-invasive techniques identifying cell-free DNA in the maternal circulation from as early as 10 weeks’ gestation is increasingly utilised as a primary screening modality in obstetric practice. While the purpose of the test is aimed at the identification of placental-derived DNA to inform the fetal risk of aneuploidy, it is estimated that 1 in 12,500 NIPT tests will detect circulating tumour DNA allowing for the early detection of occult maternal malignancies.
We present the case of a 25 year-old G2P1 who undertook aneuploidy screening with primary non-invasive prenatal testing (NIPT; percept) at 11 + 2 weeks gestation. Results were consistent with the presence of several segmental and whole chromosome changes and a referral to oncology was made to assess the patient for occult maternal malignancy. A breast and abdominal sonogram were unremarkable; a maternal transthoracic echo confirmed normal systolic function. A low dose FDG PET scan demonstrated FDG-avid left cervical and mediastinal lymphadenopathy, concerning for lymphoma. At 14 + 2 weeks’ gestation, cervical lymph node biopsy confirmed nodular sclerosis classical Hodgkin lymphoma. Her disease was stage 2A, with Hasenclever International Prognostic Score = 1. ABVD chemotherapy was commenced at 17 weeks with intent of treating to 6 cycles. Interim re-staging by shielded CT after cycle 2 showed a good mediastinal but lesser cervical structural response. Three more cycle of AVD chemotherapy were administered during pregnancy. The pregnancy was complicated by a SARS-CoV-2 infection at 34 weeks with a mild course. Serial ultrasound scans confirmed fetal well-being and an induction of labour was planned in a timed manner at 38 + 1 weeks; a female infant weighing 3390 g was delivered in good condition by vaginal birth. The patient chose to formula feed. A restaging PET scan 2 weeks postpartum demonstrated significant residual cervical disease with minimal response to treatment. Following oncology MDT discussion, the consensus was for second line treatment comprising salvage chemotherapy (ICE), autograft following response, and consideration of radiation therapy to the cervical mass. The risks of treatment including premature ovarian failure and infertility, and options for fertility preservation including Zoladex (GnRH agonist) injection, egg/embryo freezing or ovarian tissue cryopreservation were discussed. The patient chose the latter option. At time of abstract submission, the patient had received her first cycle of salvage chemotherapy.
68
1. Department of Maternal Fetal Medicine, Royal Women's Hospital, Parkville, VIC, Australia
2. Department of Diabetes and Endocrinology, Royal Melbourne Hospital, Parkville, VIC, Australia
3. Department of Obstetrics & Gynaecology, University of Melbourne, Parkville, VIC, Australia
4. Department of Obstetric Medicine, Royal Women's Hospital, Parkville, VIC, Australia
5. Department of Medicine, University of Melbourne, Parkville, VIC, Australia
We present the case of a 24 year-old G3P2 + 1−1 Afghan refugee who booked in at 28 weeks’ gestation for antenatal care after recent immigration to Australia. She had a previous Caesarean section for twins in 2018, with death of twin 1 in the neonatal period secondary to a presumed cardiac arrhythmia. A subsequent vaginal birth in 2021 was uneventful. Her only medical history was hypertension in her previous pregnancies. Early antenatal history is uncertain but she reports methyldopa use until she arrived in Australia.
At 31 weeks’ gestation, she presented to the emergency department with headache. She was normotensive and investigations excluded pre-eclampsia. At 38 + 4 weeks gestation she presented in spontaneous labour. After eight hours, she was noted to be clammy, sweaty and complained of abdominal pain. Prolonged fetal bradycardia prompted an emergency Caesarean section under general anaesthetic for suspected scar rupture.
Intra-operatively, she was profoundly hypertensive with 10 min of narrow complex tachyarrhythmia and a short run of ventricular tachycardia that was not concordant with surgical stimulus. The tachyarrhythmia and hypertension responded briskly to intravenous labetalol and the response was sustained. A live female infant weighing 3.93 kg was delivered in good condition. Delivery was complicated by a 2-litre postpartum haemorrhage.
Day 1 post-partum blood pressure remained in the low-normal range (110/65 mmHg). Heart rate and rhythm were unremarkable (81bpm sinus rhythm). However, she was intermittently sweaty and flushed. A secondary hypertension screen was performed. Troponin was acutely elevated (2 > 1596 > 93 ng/L) and transthoracic echocardiogram showed mild to moderate segmental systolic dysfunction and akinesis of inferoseptal and anteroseptal wall segments consistent with Takotsubo cardiomyopathy. CT coronary angiogram showed entirely normal coronary vessels. Metoprolol was commenced.
Day 4 post-partum, secondary hypertension was returned showing markedly elevated plasma metanephrines (normetanephrine >26,093 pmol/L (N < 900); metanephrine 70pmol/L (N < 500); 3-methoxytyramine >1,609pmol/L (N < 110)). CT CAP revealed a 45 mm left adrenal mass and 15 mm right aortocaval lesion suggestive of either paraganglioma or phaeochromocytoma with metastases. Solid pulmonary nodules were noted through-out bilateral lungs. Gatate PET scan was arranged. At the time of abstract submission, the result of this study was pending. Metoprolol was discontinued and prazosin commenced to achieve alpha blockade in preparation for potential surgery on the adrenal mass. Genetic testing was arranged.
This case demonstrates the diagnostic challenge of catecholamine secreting neuroendocrine tumours in pregnancy. It presents an opportunity for discussion around management in pregnancy and the early post-partum period.
69
1. Christian Medical College, Vellore, Vellore, TAMIL NADU, India
1. Arachchi, N.S.M., Ganegama, R., Husna, A.W.F. et al. Suicidal ideation and intentional self-harm in pregnancy as a neglected agenda in maternal health; an experience from rural Sri Lanka. Reprod Health 16, 166 (2019). https://doi.org/10.1186/s12978-019-0823-5
2. Catherine MacLeod Hall, Emma Molyneaux, Hannah Gordon, Kylee Trevillion, Paul Moran, Louise M. Howard, The association between a history of self-harm and mental disorders in pregnancy, Journal of Affective Disorders. https://doi.org/10.1016/j.jad.2019.06.062.
70
1. Christian Medical College, Vellore, Vellore, TAMIL NADU, India
Antenatal depression is a common health problem that is neglected in developing countries. The aim was to estimate the prevalence, risk factors and implications of antenatal depression among those with and without medical comorbid illnesses, as that has not been studied much in the developing countries. The stigma with mental health problems precludes referral to available mental health professionals. We aimed to develop a screening system for appropriate referral.
This cross-sectional study was done among women attending the Obstetric Medicine Clinic and the regular antenatal clinic at a tertiary care university teaching hospital. 291 patients were consecutively recruited from the Obstetric Medicine Clinic (148) and from the Antenatal clinics (143) after informed consent if they were more than 18 years and were able to read and write the vernacular or English language. Sample size was calculated based on a pilot study that found 20% prevalence of depression among women with medical comorbidities, assuming 10% among those without comorbidities with power at 80% and alpha error at 5% for a two-sided test to be 199 in each group. The Edinburgh Postnatal Depression Scale (EPDS) was used to screen for depression and the Beck's Depression Inventory to assess severity. The maternal and foetal outcomes were obtained from hospital electronic records. Epi data form was used for data entry and SPSS version 21 for analysis. The study was approved by the institutional review board in August 2019. IRB Min No: 10161 dated 06.08.2019
24.3% had scored 11 or higher on the EPDS, reflecting a high likelihood of depression. 10.5% had a score >20 on Beck`s depression inventory suggestive of moderate to severe depression. Domestic violence [OR 4.4171(95%CI 1.58–12.34)], Marital conflict [OR – 2.977 (95%CI 1.103–8.037)], smoking in the partner or a family member [OR- 3.328 (95%CI 1.125–9.842)], family expectations regarding the gender of the baby [ OR – 2.071 (95% CI 1.075–3.990)] and unplanned pregnancy[OR 2.0540 (95%CI 1.19–3.55)(p = 0.009)] were associated with a higher risk for depression in both groups. On multivariate regression, spouse staying with the woman was protective OR 0.284 (95% CI 0.20–0.4) (p < 0.001) and domestic violence, an independent risk factor OR 3.475(95% CI 1.208–9.998) (p = 0.021)for depression.
Social factors play a crucial role in maternal mental health. Social history is essential to identify those at risk and to provide adequate management of antenatal depression.
71
1. Diabetes and Endocrinology, Royal Melbourne Hospital, Parkville, VIC, Australia
2. Obstetric Medicine, Royal Women's Hospital, Parkville, Victoria, Australia
Differentials for hypercalcemia include PTH dependant and PTH independent causes. Appropriate work-up of hypercalcemia includes reviewing causative medications (i.e. in this patient including elevit, cholecalciferol), biochemistry, urinary calcium to assess for familial hypocalcuric hypercalemia and radiology if indication. Imaging choice to localise a possible parathyroid adenoma need so be rationalised against radiation exposure in these young females; with radiological options include of US, nuclear medicine sestimibi, standard CT neck and newer 4DCT carrying radiation exposure of 0 mGy, 11 mGy, 60–75 mGy and 150 mGy respectively (4).
No formal guidelines exist regarding that management of primary hyperparathyroidism. Management options including medical management include cessation of causative medications, intravenous fluid therapy, frusemide and calcitonin (1). Operative management remains the definitive treatment option when a parathyroid adenoma is suspected. Operative timing in second trimester is preferred, however abnormal PERT test may require surgical intervention in third trimester (1). Meta-analysis revealed no major adverse outcomes in 15 individuals who underwent parathyroidectomy in third trimester (5).
1. Dandurand K, Khan AA. Hypercalcemia in pregnancy. Endocrinol Metab Clin N Am 50 (2021) 753–768. 3–768 https://doi.org/10.1016/j.ecl.2021.07.009
2. Cetani F, Saponaro F, Marcocci C. Non-surgical management of primary hyperparathyroidism. Best Pract Res Clin Endocrinol Metab. 2018;32(6):821–835
3. Hultin H, Hellman P, Lundgren E, et al. Association of parathyroid adenoma and pregnancy with preeclampsia. J Clin Endocrinol Metab 2009;94(9):3394–9.
4. Hubbard P., Callahn J., Cramb J., Budd R., Kron T. Audit of radiation dose delivered in time-resolved four-dimensional computed tomography in a radiotherapy department. J Med Imag Radiat Oncol. 2015;59:346–352
5. Constantinos Nastos, Anna Paspala et al. (2021) Surgical management of primary hyperparathyroidism during pregnancy: a systematic review of the literature, Gynecological Endocrinology, 37:12, 1086–1095, DOI: 10.1080/09513590.2021.1932801
72
1. Obstetrics and Gynaecology, Royal Hobart Hospital, Hobart, Tasmania, Australia
Pulmonary hypertension (PH) is considered a contraindication to pregnancy (1). The maternal mortality rate with PH has been reported up to 30–56% (2). Below, we discuss the new diagnosis of PH, likely secondary to rheumatic heart disease, in a concealed pregnancy.
A 23-year-old multigravida Tongan woman presented with a one week history of shortness of breath, haemoptysis and bilateral lower limb oedema. She was covid positive and incidentally found to have a gravid uterus confirmed on USS to be approximately 36 weeks gestation. There was no significant past medical history. On examination she was tachycardic and tachypnoeic with increased work of breathing, diffuse crepitations and pitting oedema to mid shins.
A Chest x-ray showed massive cardiomegaly and bilateral consolidation. An echocardiogram showed global dilatation, with significant mitral regurgitation, a severely thickened mitral valve with stenosis, severe tricuspid regurgitation and a pulmonary pressure of 63 mmHg. She was treated with dexamethasone, diuretics, remdesivir and benzyl penicillin/azithromycin for associated COVID pneumonia.
She had spontaneous rupture of membranes at 36 + weeks and she was transferred to a tertiary centre. Her case was discussed with Maternal Fetal medicine specialists and a cardiac obstetric anaesthetist. The intensive care team, paediatrics, anaesthetics, cardiology and the infectious diseases team were all notified of her impending arrival. A plan was made for a vaginal delivery with regional anaesthetic, given the advantage of vasodilation, and a short second stage with instrumental delivery if needed. Avoid oxytocics due to risk of pulmonary vasoconstriction.
She started contracting at 0400 the following day. She had an early epidural and insertion of an arterial line. Her contractions became 1 in 10 min. it was thought important to encourage delivery rather than expectant management with the hope for delivery during daytime hours. She was given misoprostal 50 mcg at 1330 for augmentation.
Her labour then progressed well, she pushed with good decent and a 15 min second stage without assistance. Baby was born in good condition, there was brisk loss at birth. Bleeding was managed with 2 units of IM syntocinon and 1 g IV tranexamic acid. Her post partum course was fortunately uneventful with ICU and cardiology input. She was referred for cardiac valve surgery.
The cardiovascular demands of pregnancy are often not met by women with PH (3). This can present with shortness of breath and oedema but can lead to devasting outcomes if not appropriately managed by a multidisciplinary team.
1. Pieper, P G, and E S Hoendermis. “Pregnancy in women with pulmonary hypertension.” Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation vol. 19,12 (2011): 504–8. doi:10.1007/s12471-011-0219-9
2. Hemnes, Anna R., et al. “Statement on Pregnancy in Pulmonary Hypertension from the Pulmonary Vascular Research Institute.” Pulmonary Circulation, vol. 5, no. 3, 2015, pp. 435–65. JSTOR, https://doi.org/10.1086/682230. Accessed 16 Jun. 2022.
3. Kiely, David G et al. “Pregnancy and pulmonary hypertension: a practical approach to management.” Obstetric medicine vol. 6,4 (2013): 144–54. doi:10.1177/1753495X13495193
73
1. Department of O&G, Bankstown Hospital, Bankstown, NSW, Australia
2. School of Medicine, University of New South Wales, Kensington, NSW, Australia
1. Berghella V, Hughes BL, 2022, UpToDate - COVID-19: Overview of pregnancy issues, Last updated 8 June 2022, From: https://www.uptodate.com/contents/covid-19-overview-of-pregnancy-issues
2. Zaigham M, Andersson O, 2020, Maternal and perinatal outcomes with COVID-19: A systematic review of 108 pregnancies, Acta Obstet Gynecol Scand, 99:823–829
74
Catherine E Leggett1, Usha Ritchie2, Lynn Costi1, David Elliot3, Arduino A Mangoni3,4,
1. Women's and Children's Health Network, SA Pharmacy, North Adelaide, South Australia, Australia
2. Central Adelaide Local Health Network, SA Pharmacy, Adelaide, South Australia, Australia
3. Department of Clinical Pharmacology, Flinders Medical Centre, Bedford Park, South Australia, Australia
4. Discipline of Clinical Pharmacology, College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, Australia
5. Robinson Research Institute, University of Adelaide, North Adelaide, South Australia, Australia
1. Hale, T. W. (2020). Hale's Medications & Mothers’ Milk 2021: A Manual of Lactational Pharmacology. Springer Publishing Company.
75
Jonathan JS Sen1,
1. Baker Heart and Diabetes Institute, Melbourne
2. Western Health, St Albans, VICTORIA, Australia
76
1. Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia
2. Women's and Newborn Services, Royal Brisbane and Women's Hospital, Brisbane, QLD, Australia
3. Department of Obstetrics and Gynaecology, Sunshine Coast University Hospital, Birtinya, QLD, Australia
4. School of Medicine and Dentistry, Griffith University, Sunshine Coast, QLD, Australia
Maternal mortality, the most severe adverse outcome for a woman related to pregnancy, has traditionally been used as a marker of the quality and safety of maternity health care. Throughout Australia, there is a systematic approach to examining and reporting maternal mortality. This enables identification of contributing factors to improve outcomes. In developed countries where maternal mortality rates are low, maternal morbidity may be a more important indicator of quality health care (1).
However, there is no consistent, systematic approach to examining maternal morbidity. Worldwide, short and long term impairment as a result of pregnancy, and the ensuing impact this has on women and their families is largely unknown. It is commonly quoted that for every maternal death there are 20–30 cases of acute or chronic maternal morbidity, but the validity of this is unclear (12,3).
In Australia, maternal morbidity burden is inconsistently recorded in each state, contributing to limited national data. Thus, we do not know the extent to which maternal morbidity impacts the physical and mental health of women, maternity care providers and the health care system in Australia. This is an important gap in our quality assurance systems.
As part of the work of the Queensland Maternal and Perinatal Quality Council, we are working towards a better understanding of maternal morbidity. However, we have discovered that a key challenge in collecting data regarding maternal morbidity is that it is difficult to define.
In this presentation, we will explore the various ways of defining maternal morbidity and consider the advantages and disadvantages of each definition. Standardisation of the definition of maternal morbidity is an essential first step if we wish to systematically examine maternal morbidity, to improve the care we provide to Australian women and their families.
1. Firoz T, Chou D, von Dadelszen P, Agrawal P, Vanderkruik R, Tunçalp O, et al. Measuring maternal health: focus on maternal morbidity. Bulletin of the World Health Organization. 2013;91(10):794–6.
2. Chou D, Tunçalp Ö, Firoz T, Barreix M, Filippi V, von Dadelszen P, et al. Constructing maternal morbidity – towards a standard tool to measure and monitor maternal health beyond mortality. BMC Pregnancy Childbirth. 2016;16(1):45.
3. Vanderkruik RC, Tunçalp Ö, Chou D, Say L. Framing maternal morbidity: WHO scoping exercise. BMC Pregnancy Childbirth. 2013;13:213.
77
1. Hunter New England Local Health District, Kotara, NSW, Australia
78
1. Western Health, Footscray, VIC, Australia
2. University of Melbourne, Melbourne, Victoria, Australia
1. WAPM (World Association of Perinatal Medicine) Working Group on COVID-19. Maternal and perinatal outcomes of pregnant women with SARS-CoV-2 infection. Ultrasound Obstet. Gynecol. 2021, 57, 232–241. Accessed 23 Jun 22. Available from: https://doi.org/10.1002/uog.23107
2. Pathirathna, M.L.; Samarasekara, B.P.P.; Dasanayake, T.S.; Saravanakumar, P.; Weerasekara, I. Adverse Perinatal Outcomes in COVID-19 Infected Pregnant Women: A Systematic Review and Meta-Analysis. Healthcare 2022, 10, 203. Accessed 23 Jun 22. Available from: https://doi.org/10.3390/healthcare10020203
3. Skjefte M, Ngirbabul M, Akeju O, Escudero D, Hernandez-Diaz S, Wyszynski D, Wu J. Covid-19 vaccine acceptance among pregnant women and mothers of young children: results of a survey in 16 countries. Eur J Epidemiol. 2021 Feb;36(2):197–211. Accessed 23 Jun 22. Doi: 10.1007/s10654-021-00728-6.
79
1. Ballarat Health Services, Ballarat, VIC, Australia
Her haemoglobin decreased from 134 g/L to 63 g/L over three days, causing dizziness, shortness of breath and fetal distress with tachycardia. The patient's advanced care directive was reviewed but the patient did not agree to blood products. Multidisciplinary discussions were held with obstetricians, ENT surgeons, haematologists, nephrologists, anaesthetics and paediatricians.
Two cauterisations were performed and rapid rhino inserted. Tranexamic acid and labetalol were prescribed.
The first issue was the patient's life-threatening anaemia. There was fetal distress but delivery would significantly risk maternal death. The anaemia was managed medically using intravenous iron (ferric carboxymaltose) and fortnightly erythropoietin.
The second issue was planning delivery. Generally, JW patients are recommended less invasive surgery, to minimise bleeding. However, there was concern that second stage of labour valsalva and hypertension may result in further nasal bleeds, and caesarean would be safer.
At 36 weeks an ultrasound showed normal growth but raised Umbilical artery doppler.
The patient had an elective Caesar at 37 + 3 with two obstetricians and cell saver. Her pre-operative haemoglobin was 114 g/L. The weighed blood loss was 312 mls.
Our case had the added complexity of Jehovah's witness status. Risk of maternal death rises significantly at haemoglobin levels below 60 g/L in JW.(2) In these patients, clear communication of the medical, ethical and legal implications of decisions is paramount. In patients who refuse blood products, the fastest method to optimise haemoglobin is intravenous iron alongside erythropoietin.(3) Cell saver is often acceptable to patients with JW and should be utilised where possible.(4)
1. Piccioni MG, Derme M, Salerno L, et al. Management of Severe Epistaxis during pregnancy: A Case Report and Review of Literature. Case Rep Obstetric Gynaecology. 2019;2019:5825309. Published 2019 Jan 20. dot: 10.1155/2019/5825309
2. Herbert PC, Biro GP. Review of physiological mechanisms in response to anaemia. Can Med Assoc J. 1997;156:27–40
3. Tanaka M, Matsuzaki S, Endo M, et al. Obstetric Outcomes and acceptance of alternative therapies to blood transfusion by Jehovah's Witnesses in Japan: a single-centre study. International Journal of Haematology. 2018; 108:432–437
4. Waters JH. Intraoperativr blood recovery. ASAIO J. 2013;59:11–17
80
1. Mater Health, Brisbane
Ursodeoxycholic acid, currently the mainstay of treatment for intrahepatic cholestasis of pregnancy (ICP), has no significant effect on stillbirth and neonatal unit admission. 1, 23
Hague et al. recently described the protocol for a randomised superiority trial (TURRIFIC trial) comparing the efficacy of ursodeoxycholic acid with rifampicin in women with severe early onset ICP.4
Hepatotoxicity with rifampicin monotherapy has been reported in approximately 2% of patients with latent tuberculosis and 4.8% of patients with cholestatic pruritus.5, 6 Hepatoxicity is usually self-limiting and resolves despite continuation of treatment.5 Grade 3 or grade 4 hepatic failure leading to drug discontinuation was reported in 0–0.7% of individuals who received 4 months of rifampicin monotherapy for latent tuberculosis.7
Two small case series of rifampicin therapy in primary biliary cirrhosis however found that 5 of 57 (8.8%) patients developed significant hepatitis, onset 4–8 weeks after commencing therapy. 8, 9 Two patients had coagulopathy, one patient requiring liver transplantation.
Acute kidney injury has been reported in 0.1% of individuals treated with rifampicin, mechanisms including interstitial nephritis, acute tubular nephritis and proliferative crescentic glomerulonephritis.10
Fourteen cases of disseminated intravascular coagulation (DIC), including 4 deaths, have been described following ingestion of rifampicin.11 Symptoms occurred within hours of rifampicin ingestion, typically in the setting of previous exposure. DIC is induced by immunoallergic reactions mediated by IgG and IgM antibodies against target cells expressing blood antigen I.
Anaphylaxis, serum sickness, autoimmune haemolytic anaemia, thrombocytopaenia and hypotension may rarely occur due to hypersensitivity reactions to rifampicin, with causation established by positive skin testing.12 Rifampicin may also precipitate coagulopathy in the setting of vitamin K deficiency.13
Rifampicin has a low incidence of serious adverse effects, though close monitoring of liver function, renal function, full blood count and prothrombin time will be important for early detection. While DIC with rifampicin is extremely rare, awareness of this possibility will be important, particularly in women who have been previously exposed, given the rapidity of onset, and the risk of recurrence of ICP in subsequent pregnancies.
1. Parizek A, Simjak P, Cerny A, et al. Efficacy and safety of ursodeoxycholic acid in patients with intrahepatic cholestasis of pregnancy. Ann Hepatol 2016; 15: 757–761. 2016/08/06. DOI: 10.5604/16652681.1212562.
2. Chappell LC, Bell JL, Smith A, et al. Ursodeoxycholic acid versus placebo in women with intrahepatic cholestasis of pregnancy (PITCHES): a randomised controlled trial. Lancet 2019; 394: 849–860. 2019/08/06. DOI: 10.1016/S0140-6736(19)31270-X.
3. Ovadia C, Sajous J, Seed PT, et al. Ursodeoxycholic acid in intrahepatic cholestasis of pregnancy: a systematic review and individual participant data meta-analysis. Lancet Gastroenterol Hepatol 2021; 6: 547–558. 2021/04/30. DOI: 10.1016/S2468-1253(21)00074-1.
4. Hague WM, Callaway L, Chambers J, et al. A multi-centre, open label, randomised, parallel-group, superiority Trial to compare the efficacy of URsodeoxycholic acid with RIFampicin in the management of women with severe early onset Intrahepatic Cholestasis of pregnancy: the TURRIFIC randomised trial. BMC Pregnancy Childbirth 2021; 21: 51. 2021/01/14. DOI: 10.1186/s12884-020-03481-y.
5. Senousy BE, Belal SI and Draganov PV. Hepatotoxic effects of therapies for tuberculosis. Nat Rev Gastroenterol Hepatol 2010; 7: 543–556. 2010/09/03. DOI: 10.1038/nrgastro.2010.134.
6. Webb GJ, Rahman SR, Levy C, et al. Low risk of hepatotoxicity from rifampicin when used for cholestatic pruritus: a cross-disease cohort study. Aliment Pharmacol Ther 2018; 47: 1213–1219. 2018/02/23. DOI: 10.1111/apt.14579.
7. Ziakas PD and Mylonakis E. 4 months of rifampin compared with 9 months of isoniazid for the management of latent tuberculosis infection: a meta-analysis and cost-effectiveness study that focuses on compliance and liver toxicity. Clin Infect Dis 2009; 49: 1883–1889. 2009/11/17. DOI: 10.1086/647944.
8. Bachs L, Pares A, Elena M, et al. Comparison of rifampicin with phenobarbitone for treatment of pruritus in biliary cirrhosis. Lancet 1989; 1: 574–576. 1989/03/18. DOI: 10.1016/s0140–6736(89)91608-5.
9. Prince MI, Burt AD and Jones DE. Hepatitis and liver dysfunction with rifampicin therapy for pruritus in primary biliary cirrhosis. Gut 2002; 50: 436–439. 2002/02/13. DOI: 10.1136/gut.50.3.436.
10. Blajchman MA, Lowry RC, Pettit JE, et al. Rifampicin-induced immune thrombocytopenia. Br Med J 1970; 3: 24–26. 1970/07/04. DOI: 10.1136/bmj.3.5713.24.
11. Sousa G, Carreiro A and Duarte P. Rifampicin-induced disseminated intravascular coagulation: An antibody-mediated side effect. Pulmonology 2020 2020/05/23. DOI: 10.1016/j.pulmoe.2020.04.006.
12. Sveroni D, Stefos A, Rigopoulou EI, et al. Rifampicin: not always an innocent drug. BMJ Case Rep 2018; 11 2018/12/21. DOI: 10.1136/bcr-2018-227356.
13. Van Steenbergen W and Vermylen J. Reversible hypoprothrombinemia in a patient with primary biliary cirrhosis treated with rifampicin. Am J Gastroenterol 1995; 90: 1526–1528. 1995/09/01.
81
1. Department of Renal Medicine, Box Hill Hospital, Eastern Health, Melbourne, VIC, Australia
2. Eastern Health Clinical School, Monash University, Melbourne, Vic, Australia
Author Index
Adno, Alan (36)
Aldridge, Emily (49)
Alwis, Natasha de (4,8)
Andrews, Shawana (13)
Archer, Dimity (78)
Arstall, Margaret A (49)
Baines, Katherine J (9)
Banks, Sam (43)
Banks, Sam SB (75)
Bardin, Michele (45)
Barnden, Kristine (1)
Barrett, Helen (61)
Beard, Sally (4,8)
Beech, Amanda (6,41)
Bhagwanani, Gauthami (22,36,66)
Bijoy, PhebyMercy (70)
Binder, Natalie K (4)
Brennecke, Shaun (16,24)
Britton, Sumudu (15)
Brown, Mark A (10)
Brumby, Catherine (81)
Bubb, Kristen J (8)
Burgess, John (12)
Callaway, Leonie (61,76)
Calvert, Harriet L (77)
Canty, Alison (22)
Christensen, Britt (19)
Christie, Hannah E (48)
Coat, Suzette (63)
Cobden, Elizabeth (79)
Cole, Michelle (65)
Cosgrave, Madeleine (81)
Costi, Lynn (74)
Cowan, Stephanie (26)
Craig, Maria E (33)
Creeper, Katherine J (37)
Crespigny, Paul Champion de (20,40)
Cutts, Briony (52)
Davies, Chris (25)
Davis, Gregory K (10)
Deitch, Jessica (28)
Dekker, Gustaaf (49)
Dekker, Gustaaf A (42)
Dixon, Jordan (43)
Dixon, Jordan JD (75)
Duncan, Petrina (35)
Elaine Osei-Safo (26)
El-Hamawi, Zaynab (21)
Elise Regan- Gomm (78)
Elliot, David (74)
Esber, Yamema (10)
Fato, Bianca R (8)
Fergusson, Emily K (6)
Forsyth, Cecily (29)
Foster, Ailsa Borbolla (77)
Francois, Monique E (48)
Frawley, Natasha (79)
Frost, Joanne (76)
Fulcher, Ian (36)
Fullerton, Alexandra (46)
Gebara, Sarah A (41)
George, Julie (44)
Gerhardy, Laura (64)
Gibson, Peter G (9)
Gillies, Malcolm (64)
Giudice, Sonita (17)
Glastras, Sarah (27)
Gow, Megan L (10,33)
Graham, Dorothy F (37)
Graham, Dorothy (38)
Groom, Katie (4)
Hackett, Maree (23)
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