Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 285e288

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The rising prevalence of obesity is a pandemic of public concern affecting all age groups. Obesity is not only confined to the well-resourced developed countries but also seen in the lesser-resourced countries as well. The well-to-do overeat and the less-well-to-do consume large amounts of carbohydrates and fat due to limited resources for a balanced diet. It has been reported that, for every increase in body mass index of 5 kg/m2, there was a 30% overall higher mortality with a 40% increase in vascular mortality, a >50% increase in diabetic, renal and hepatic mortality, a 10% increase in neoplastic mortality and 20% increase in respiratory and other mortalities. In addition, being overweight and obese increases the risk of many other conditions including cerebrovascular disease, gall stones, osteoarthritis, sleep apnoea, impaired physical functioning, psychological illness and social discrimination [1]. Obesity is a significant risk factor for maternal morbidity and mortality during pregnancy as well [2]. In this volume, Mitchell and Shaw point out that global obesity has doubled in the period between 1980 and 2008. It has been estimated that, by 2015 there will be 1.5 billion adults classified as overweight and of these 300 million categorised as obese. The authors also provide a worrying assessment of the economic burden of obesity-related diseases globally, which will have a huge impact on the provision of health services. The aetiology of obesity is multifactorial. There is a complex interplay of genetic, environmental and psychological factors that underpin the eating habits of the human race. Savona-Ventura in this volume points out that genetic defects and DNA variants account for a very small proportion of cases. A stronger association has been found between the intrauterine and early childhood nutritional environments, which include both a situation of nutritional deprivation or excess working through the interplay of epigenetic changes and pancreatic and hypothalamic development. It has been postulated that intrauterine metabolic programming may be linked to direct developmental permanent loss in the structural and functional capacity within the b-cell mass of the pancreas. There is a strong relationship between macrosomia and the eventual increased predisposition to childhood and adulthood obesity, a theme that has been further explored in later chapters. Eating behaviour is also influenced by psychological factors. There is a bidirectional relationship between depression, anxiety and obesity, although certain moderators such as gender and age may modify the relationship between psycho-pathology and obesity. Both early relational traumas such as abuse and neglect and personality traits such as high neuroticism and low conscientiousness are related to an increased risk of obesity [1]. Lim and Mahmood provide an overview of serious adverse outcomes associated with obesity in pregnancy, including an increased risk of early pregnancy loss, recurrent miscarriage, foetal developmental abnormalities, thromboembolism, gestational diabetes, pre-eclampsia, dysfunctional labour, post-partum haemorrhage, stillbirths and neonatal deaths. There is a higher caesarean section rate, lower breastfeeding rate and wound infection as compared to women with a healthy body mass 1521-6934/© 2014 Elsevier Ltd. All rights reserved.


Preface / Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 285e288

index (BMI). Having identified risks associated with such pregnancies, a proactive approach to care during pregnancy is desired. Stacey Tsai and colleagues point out that the increased depth of abdominal adipose tissue significantly affects the accuracy of ultrasound scanning due to increased distance of insonation and suboptimal visualisation. Ultrasound scanning during early pregnancy is important as most of these women tend to have irregular cycles and also have increased rates of dizygotic twinning even without the influence of fertility drugs. Screening for congenital anomalies, although possibly challenging, is also important, as these women have higher rates of congenital anomalies when compared to normal-weight women. The sensitivity of certain aneuploidy soft markers decreases as BMI increases, thus resulting in a higher residual missed diagnostic rate. The authors recommend various modifications in routine practice to achieve optimal images of the foetus. Obesity is associated with progressive insulin resistance during pregnancy. Salzer and colleagues propose that insulin resistance and hyperinsulinaemia may be the basic common ground for the metabolic syndrome during pregnancy e elevated blood pressure and diabetes mellitus. Metabolic syndrome is associated with endothelial dysfunction, oxidative stress and attenuated inflammatory responses. They have explored this theme at length in their chapter describing the role of newly discovered factors associated with insulin resistance, secretin and lipid metabolism. All these complex changes explain the pathogenesis of elevated blood pressure and development of diabetes during pregnancy. Benhalima and colleagues reiterate that female babies born to obese mothers are also at an increased risk of developing gestational diabetes mellitus (GDM) in their pregnancies in future. Women with GDM have a sevenfold increased risk of developing type 2 diabetes following pregnancy. History of GDM is also a marker for raised cardiovascular risk and early atherosclerosis. Having recognised these trans-generational risks, it is disheartening to note that there is still a lack of international uniformity in the approach to the screening and diagnosis of GDM. There are continuing controversies: universal versus selective screening, the optimal time for screening, appropriate tests and cut-off values and whether tests should be conducted in one or two steps. It is important that the International Association of Diabetes and Pregnancy Study Group (IADPSG) should decide the most effective screening strategies for the low- and high-resource settings. Jeve and colleagues point out that obesity induces exaggerated low-grade inflammatory response in placenta as well. The low-grade inflammation expressed by higher levels of cytokines contributes to cellular dysfunction promoting metabolic disease. Placenta exhibits a lipotoxic environment that is associated with decreased regulators of angiogenesis and increased markers of inflammation and oxidative stress. This inflammatory milieu in which the foetus develops may have critical consequences for short- and long-term programming of obesity. Drife points out that between 1991 and 2005 venous thromboembolism (VTE) was the leading cause of direct maternal deaths in the UK [2]. In pregnancy, the risk is increased fourfold, and in the post-partum period, it is increased 20-fold. The period of highest risk is around delivery (from 2 days before to 1 day after parturition). The increased risk of VTE continues for at least 6 weeks after delivery. The recent increase in the risk of VTE is related to the rising incidence of obesity. Metabolic syndrome of pregnancy is associated with prothrombotic milieu manifested by platelet hyperactivity, hypercoagulability, reduced fibrinolysis and endothelial dysfunction. It is important for each maternity unit to have evidence-based protocols to identify women at a risk of developing VTE during pregnancy. Evidence from the UK demonstrates that it is possible to reduce deep vein thrombosis (DVT)-related maternal mortality by implementing guidelines at the unit level. Orr and Chien then remind us that sepsis is an important cause of direct maternal deaths [2] and obesity was a risk factor. Obesity during pregnancy increases susceptibility to bacterial, viral, hospital-acquired and parasitic infections. Immunological changes in obesity are poorly understood. The mechanism of immunosuppression in obesity may be caused by suppressed functionality of CD4 T cells and CD8 T cells, T cell diversity, impaired natural killer (NK) cells and decreased cytokine production. It is plausible that the chronic inflammatory milieu of obesity may desensitise the response of the immune system to infection and reduce the body's ability to mount an acute response to infection. Kobayashi and Lim point out that obese pregnant woman are at an increased risk of post-dates pregnancies and hence they are in need of induction of labour. They have a high risk of caesarean delivery, post-partum haemorrhage, infections, prolonged hospital stay and higher perinatal

Preface / Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 285e288


morbidity and mortality. There is a paucity of data on the best method of induction of labour in this group of women. These women tend to have prolonged and dysfunctional labour, leading to the requirements for higher doses of oxytocin. Care of obese women during labour could be challenging and places a significant demand on health-care resources. With the increased risk of intra-partum emergencies, it is essential that delivery be conducted in a facility where senior obstetric staff and access to theatre are immediately available. This is especially relevant for women living in rural and remote communities. In such situations, local protocols should clearly specify transport arrangements. The authors provide a robust framework for the care of obese women during labour and make a case for a multidisciplinary approach to the care of these women throughout pregnancy. Ayres-de-Campos then addresses the issues related to challenging caesarean sections especially for women with morbid obesity. These women are at an increased risk of deep-seated wound infection, haematoma, seroma, abscesses and dehiscence. The review makes a justifiable case for the use of appropriate surgical technique, appropriate prophylactic antibiotics and dosage. He recommends the use of vacuum-assisted devices at the incision site, which lead to faster wound healing and also reduce the risk of surgical site infection. However, the risk of DVT in this group of women should not be overlooked. Woolner and Bhattacharya remind us that, in 2009, there were 2.6 million stillbirths worldwide. Although pregnancy outcomes have improved in the effluent countries, the risk of stillbirth remains high. Furthermore, in utero foetal death is more common in overweight and obese women. They have explored the relationship between maternal obesity and stillbirth. The effect of obesity is dose dependent: the higher the BMI, the higher the risk of stillbirth. The pathophysiology is unclear but it is possibly related to placental dysfunction, placental inflammation, impaired glucose tolerance and excessive hyperlipidaemia. A hyper-inflammatory state in obese women may contribute to adverse foetal outcome. Animal studies have shown that overfed adolescent sheep had reduced placental growth and lower-birthweight lambs. The evidence suggests that diabetes and hypertensive disorders are associated with both obesity and stillbirth, but that obesity poses an independent risk factor for stillbirth. Pre-pregnancy weight appears to affect the risk of stillbirth. Similarly, an inter-pregnancy weight gain of 3 kg/m2 independently increases the risk of stillbirth in a subsequent pregnancy. Santangeli and colleagues have reviewed the long-term effects of maternal obesity on the newborn and their childhood. They point out that it is not the actual weight of the offspring but an increase in percentage fat and fat mass that really matters. This trend continues as early child obesity. It has been postulated that these babies are born in a hyperinsulinaemic state with altered programming of ‘central reward pathways’, and this may exert long-term effects on the body. Childhood obesity in turn increases chances of later-life obesity, type 2 diabetes and cardiovascular disease. Finally, Harper proposes that, as obesity is incrementally rising, we must develop focussed strategies to reduce morbidity and mortality associated with these pregnancies. Her chapter provides a thoughtful evidence-based advice as regards streamlined care of these women during pregnancy. She proposes that, at the booking visit, individualised risk assessment should be carried out for antenatal care, GDM screening, VTE risk assessment, pre-eclampsia and anaesthetic assessment. These women should be well supported to develop a partnership so that nutritional and lifestyle advice can be given not only during pregnancy but postnatally as well. Maternity hospitals looking after these high-risk women should have clearly defined protocols in place, and should have appropriately trained senior staff available to deal with the challenges during labour. Similarly, access to intensive care unit should be readily available. Public health campaigns should focus on periconceptual nutrition and folic acid supplementation. There is a clear message from this publication: that pregnancies among obese women should be treated as high risk and be looked after by a multidisciplinary team. Protocol-based policies for close surveillance starting during the pre-pregnancy phase should be initiated and be continued during pregnancy. Health-care planners should raise public awareness of the dangers of obesity in pregnancy, similar to the public health about smoking in pregnancy. More research is needed regarding epigenetic factors and how they can be influenced as well as the role of thoughtless eating. Given the fact that the prevalence of obesity is rising worldwide and the cost of treating it is soaring, educating young women about a healthy lifestyle is essential in the hope of tackling the vicious cycle obesity is creating.


Preface / Best Practice & Research Clinical Obstetrics and Gynaecology 29 (2015) 285e288

References [1] Mahmood T, Arulkumaran S, editors. Obesity- A ticking time bomb for reproductive health. Elsevier insights; 2013, ISBN 978-0-12-416045-3. [2] Centre for Maternal and Childhood Enquiries. Saving mother’s lives: reviewing maternal deaths to make motherhood safer; 2006-2008. The eighth report on the confidential enquiries into maternal deaths in the United Kingdom. BJOG 2011; 118(suppl. 1). 1-203.

Tahir Mahmood, CBE, MD, FRCPE, FRCPI, FACOG, FRCOG, Consultant Obstetrician & Gynaecologist Victoria Hospital, Kirkcaldy, Scotland, UK President European Board And College of Obstetrics & Gynaecology (EBCOG)


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