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This is a retrospective review to study the incidence of shoulder dystocia in Malaysian tertiary hospitals. Data was obtained from the National Obstetrics Registry and the study period was from 1st January 2011 to 31st December 2012. Women at risk of Shoulder Dystocia are those in their thirties, overweight, obese with underlying GDM and Gest Hypertension.
We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. Background: Despite the interest in the impact of overweight and obesity on public health, little is known about the social and economic impact of being born large for gestational age or macrosomic. Objective: Provide insight in the short-term health-economic impact of maternal overweight, GDM, and related macrosomia.
Results: The estimation of the direct health-economic burden of maternal overweight, GDM and related macrosomia indicates that associated healthcare expenditures are substantial.
Conclusion: Although overweight and obesity are a recognized concern worldwide, less attention has been given to the health economic consequences of these conditions in women of child-bearing age and their offspring. The foundations of health throughout life are laid during the peri-conceptional period, from conception until birth, and after birth in early childhood.
In contrast, despite the general high interest in the public health burden of overweight and obesity, far less is known about the potential clinical and economic consequences of maternal conditions leading to high birth weight (large for gestational age; LGA) or macrosomia. Maternal overweight, excessive gestational weight gain (GWG) by itself, gestational diabetes mellitus (GDM), defined as mild to moderate hyperglycemia leading to diabetes first diagnosed during pregnancy which disappears after giving birth, and elevated fasting plasma glucose levels during pregnancy have all been reported to be significant risk factors for macrosomia (Shi et al., 2014). Macrosomia is the main cause of (acute) perinatal complications for both mother and infant. Using a hospital-based delivery database of 18 362 subjects in the USA, overweight, obese and severely obese women showed higher risks for LGA, GDM, and preeclampsia in comparison to their normal-weight counterparts (Bodnar et al., 2010). In a study of 366 886 singleton pregnancies from the Danish Medical Birth Registry from 2004 to 2010, the ratio between abdominal circumference and birth weight decreased with increasing maternal BMI, suggesting that maternal obesity results in a general weight gain of the fetus rather than just fat accumulation around the abdomen (Tanvig et al., 2013).
A model to map the health economic consequences of GDM, overweight pregnancies and macrosomia was developed based on decision analytical techniques, a well-accepted methodology in the field of health-economics (Weinstein and Fineberg, 1980). The model included a study population of women of childbearing age who are overweight or obese prior to pregnancy. An analysis can be conducted from the perspective of the society in a pre-selected study country, while it is also possible to consider the payer’s perspective only. Various data sources were considered for developing the framework in order to maximize its external validity for any local setting.
The incidence rate used for our model was 5.5%, derived from the study outcomes reported by Beischer et al.
Mortality outcomes were based on the study by Mitanchez (2010) who evaluated the risks of perinatal complications in infants born to mothers with treated or untreated GDM, including also risk of death. The base case analysis gives the results for the period including pregnancy and delivery only, without including costs of diagnosis and management of GDM, nor of complications beyond the obstetric period or consequences for mother and child on the longer term. The translation of costs per case (pregnancy and delivery only) to national level, based on pregnancy rate and the incidence of GDM, leads to the budget impact. The materials contained on this website are provided for general information purposes only and do not constitute medical, legal, financial or other professional advice on any subject matter. Publications Adams R, Appleton S, Wilson D, Taylor A, Dal Grande E, Chittleborough C, Gill T, Ruffin R.
Almost all cases didn’t have a history of previous shoulder dystocia and 75% of cases were handled by doctors. One third of women in this study, however were not overweight but complicated with shoulder dystocia. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. The calculation of a budget impact of GDM, based on a conservative approach of our model, using USA costing data, indicates an annual cost of more than $1,8 billion without taking into account long-term consequences. The presented outcomes underline the need for preventive management strategies and public health interventions on life style, diet and physical activity. In developing countries maternal short statue, high body mass index (BMI), and T2DM are strong risk factors for macrosomia (Koyanagi et al., 2013). These normal physiological adaptations serve to shuttle sufficient nutrients to the growing fetus, especially during the last trimester of pregnancy. Finally, an observational study at five antenatal centers in Ireland reported that excessive GWG resulted in higher odds for LGA and macrosomia, as well as increased odds for gestational hypertension in women with GDM.
The fact that some studies do not report increased rates of macrosomia despite the increasing prevalence of obese pregnancies, may be explained by, for instance, changes in obstetric practice such as cesarean section before weeks 40 of pregnancy (Poston et al., 2011). The secondary goal is to lay a basis for fostering interest in the development of targeted preventive approaches in an effort to reduce the related total costs. To estimate the health economic impact of management of macrosomia, the short-term consequences of GDM, obesity and macrosomia were taken into account.
The model consists of two sub-models: (1) development of maternal GDM, (2) maternal obesity, accompanied or not with the development of GDM. Using conventional principles of clinical decision analysis, expected clinical, and economic outcomes are determined as a probability-weighted sum of costs and outcomes further to the initial treatment decisions. Women with (preexisting) diabetes mellitus, both type I and type II, or related morbidity before pregnancy were excluded. The choice of the perspective will depend on the country-specific health economic guidelines.
A narrative review of the scientific literature from several electronic databases was conducted to find studies published between 1994 to July 2014 with the following keywords: birth weight, (rapid) weight gain, growth trajectories, body composition, overweight, obesity, metabolic health, cohort, observational studies, Asia, Australia, and Europe. To illustrate this, the budget impact of GDM for the USA was calculated, since most of the costing data available are provided by USA studies. Population comparison of two clinical approaches to the metabolic syndrome: Implications of the new International Diabetes Federation Consensus Definition. Statistical analysis was performed using IBM SPSS statistics version 20 and variables were assessed by simple logistics regression.
This pilot study also aims to encourage further health technology assessments, based on country- and population-specific data.


Also, the predisposition in people of Asian ethnicity to develop diabetes emphasizes the urgent need to collect more country-specific data on the incidence of macrosomic births and health outcomes. The link between compromised nutritional status of the baby’s mother and low birth weight on one hand, and impaired health of the child in later life on the other hand has now been clearly established. Poorly controlled diabetes, maternal obesity, and excessive maternal weight gain during pregnancy are associated with intermittent, non-physiological periods of fetal hyperglycemia, and subsequent hyperinsulinemia from the start of pregnancy and onward. The need for treatment with insulin further increased the odds for LGA and macrosomia (Egan et al., 2014). Direct comparison between countries is difficult due to different diagnostic strategies and population groups. The subject is closely related to the problem of rising NCD prevalence and the related disease outcomes, and will be of interest for both developing and industrialized countries (Henriksen, 2008; Ma and Chan, 2013). As both mother and child may be subject to various clinical events and disease progression after delivery, the number of possible health states is finite. The model considers thus a cohort of otherwise healthy women with a probability of getting pregnant. The current cost assessment, performed as a pilot, is based only on short-term costs caused by the management of the complications as reported in literature, from the national health care perspective.
Using decision analysis techniques, the authors compared three strategies for an infant with an estimated fetal weight of 4500 g: labor induction, elective cesarean delivery, and expectant treatment (Table 3).
In case of lack of information on direct data, the costs were based on treatment practice derived from guidelines or assumptions based on similarities in treatment (Table 4). All tips, guides and recommendations are followed at your own risk and should be followed up with your own research.
More than 90% of women who had shoulder dystocia had Gestational Diabetes Mellitus (GDM) and more than 80% had Gestational hypertension in 2012.
All categories of staff handling women in labour must be adequately trained to anticipate, diagnose and manage this obstetric emergency.
Macrosomia is associated with an increased risk of developing obesity and type 2 diabetes mellitus later in life. In addition, it would be of interest to further explore the long-term health economic consequences of macrosomia and related risk factors.
The far-reaching relationships with multiple health-related outcomes affecting human capital and productivity have been clearly corroborated (Johnson and Schoeni, 2011).
In addition, the threshold for macrosomia might need to be reconsidered for Asian countries, where average birth weight is in general lower compared to European countries and consequently the cut off weight for LGA (>95th percentile) would be lower. Furthermore, macrosomic infants are more likely to have low 5-min Apgar scores, an index of hypoxia (Johnson and Schoeni, 2011).
The resulting maternal insulin resistance and hormonal responses related to high blood glucose, such as insulin-like growth factors, and growth hormone, lead to greater deposition of body fat and glycogen in muscle and liver in the fetus. Many countries do not perform systematic screening for GDM, and practices often diverge from guidelines.
This study is based on methodological guidance derived from cost-effectiveness studies in nutrition economics (Lenoir-Wijnkoop et al., 2011). Probabilities of clinical events and utilities are usually accepted as not country-specific and are considered to be transferable beyond their original production location. Maternal short-term costs are related to cesarean section, pre-eclampsia, or gestational hypertension, induction of labor, maternal death. Australian Diabetes Society Gold Coast, Aug 2006Cumulative diabetes incidence: ten-fold risk among those with impaired fasting glucose.
Infants with very severe macrosomia (birth weight >5000 g) are at increased risk of neonatal, post-neonatal and infant death (Boulet et al., 2003).
The greater and more rapid fetal growth (in particular of adipose tissue) subsequently results in increased birth weight. Interestingly, the hyperglycemia and pregnancy outcome (HAPO) study results clearly indicate that relatively mild hyperglycemia was already associated with a significant increase in macrosomia (Zawiejska et al., 2014).
An advantage of applying a Markov process is that it allows long-term modeling of GDM and obesity for the mother and its complications for both mother and child (complicated delivery, macrosomia, and related morbidity).
They can therefore be derived from international studies, while economic measures and information on therapeutic choices depend on a particular region, country or healthcare system (Lampe et al., 2009). In this model we assume that in case of normal pregnancy and vaginal delivery, there is a routine cost of $ 7 790 (Ohno et al., 2011).
Macrosomia also significantly increases the risk for developing obesity in childhood, and non-communicable diseases (NCD) later in life (Morton, 2006). This assumption is, however, based on the 2011 situation in the USA only, and outcomes may be considerably different in case specific costing data of other countries or at other time points would be used. Although these outcomes cannot be extrapolated to other countries because of differences in costs as well as in the organization of national health structures, the principle of calculation remains similar for any part of the world, and will be of use as soon as reliable information becomes available. Health status assessed by the SF-36 along the diabetes continuum in an Australian population.
Because of the lack of costing data from other countries, we performed an extreme sensitivity analysis on the costs by varying ±20%. Psychological Distress Associated with Arthritis, Diabetes, Asthma, Cardiovascular Disease and Mental Health Conditions. How do we become resistant to insulin and what causes our beta cells to fail?Insulin resistance can develop as a result of fat cells releasing more pro-inflammatory chemicals such as IL-6, and fewer anti-inflammatory chemicals such as adiponectin.
The increasing prevalence of diabetes in South Australia: the relationship with population ageing and obesity.
That is not what some of my textbooks say, which claim that type 2 diabetes has a stronger genetic component than type 1 diabetes. Unfortunately their authors have been lazy and taken the fact that type 2 diabetes runs in families as evidence of a genetic link.
It is all to do with the fact that people in the same family follow a similar dietary pattern, and often a similar exercise pattern as well. In fact type 1 diabetes has a much stronger genetic component with a few genes on chromosome 6 being responsible for much of the susceptability. Diabetes Clearing House, Population Research and Outcome Studies, Department of Health, Adelaide, South Australia, June 2005. In type 2 diabetes a large number of genes are associated with risk and none particularly strongly.What happens in the diabeticThere are some tissues in our body that let glucose in without insulin.


Fat and muscle cells contain GLUT-4 transporters, which don't allow much glucose in without insulin being present. Diabetes Clearing House, Population Research and Outcome Studies, Department of Health, Adelaide, South Australia, 2003. The brain on the other hand has a lot of GLUT-3 transporters, which allow appreciable amounts of glucose in without insulin being present.Tissues which let in glucose without insulin are found in the eye, kidneys, peripheral nervous system as well as the liver, ovaries and seminal vesicles.
The unfortunate result for these cells is that they can accumulate too much glucose over time. Diabetes Clearing House, Centre for Population Studies in Epidemiology, Department of Health, Adelaide, South Australia, 2002. However, those cells in the eyes, kidneys and in our peripheral circulation accumulate sorbitol, which causes swelling of the cells due to osmotic pressure. Diabetes and Health Risk Factors 1997 & 1998 - South Australian Health Goals and Targets Health Priority Areas. Most of these complications result from raised levels of glucose in cells which do not rely on insulin to obtain it. In particular some cells lining capillaries and nerves in the kidneys, eyes and limbs are vulnerable.
As a result they leak proteins which ultimately result in constriction of the blood vessels supplying the kidney. Since the brain uses sugar as its main energy source it goes to plan B which is creating ketones, which can provide energy also. Too many ketones acidify our blood and cause excess urination, thirst, vomiting and tummy pain. Ultimately severe dehydration, swelling of the brain and coma can occur, which is why hospitalisation is often needed. This is a serious complication of type 1 diabetes.
However, it is uncommon with type 2 as some insulin is normally available.Curing diabetes naturallyExercising more and consuming foods that do not raise blood sugar levels is the key to reversing diabetes. While it becomes harder to regain full health the longer you have had diabetes, when first diagnosed, the vast majority of people have the potential to completely cure themselves of the condition.The correct dietThe modern western diet is the main cause of diabetes.
For instance on one of my GI lists I have a baked potato with a GI of 111, greater than pure glucose while peanuts are listed with a GI of just 7, which implies that foods containing the East Asian sauce, satay would be very low GI. So in other words the GI is not an absolute value, but just a guideline. Sometimes it is more realistic to consider the glycaemic load or GL of a food, which takes account of the amount of a food you eat. Obviously one Cornflake (GI=93) is not going to raise blood sugar as much as a whole can of baked beans (GI=40), but a small bowl of them probably will.Foods that are normally low GI can be eaten as the main part of a diet for someone with diabetes. These include meat, fish, eggs, dairy as well as nuts, seeds, most vegetables and some fruits. The one vegetable that has a high GI is the potato (this includes the sweet potato), and the fruits with a high GI include ripe bananas, dates and raisins.
Generally speaking fruits from warm climates have a higher GI than those from more temperate climates.
For instance if you exercise soon after consuming the food then some of the blood sugar it creates will be taken up by your muscle cells. If you combine it with other foods of much lower GI or eat a small portion of it you will also find your blood sugar does not rise as far.Timing foodsIn general if you exercise then you will reduce your blood sugar level. A 30 minute exercise stint before food will allow you to get away with a higher overall glycaemic load.
Equally if you do some light exercise soon after a large meal you can lower the peak which your blood sugar will reach.In general it is best to leave some time between any meal and completely sedentary activity such as bed or watching the TV. Kids get it about right when they automatically rush about after a meal, often to the frustration of their bloated parents. A bit of housework, gardening or short walk are often quite effective at making a real dent in your blood sugar readings.Treating diabetes with drugsIt really is best to avoid the need for drugs. I would always advise making concerted efforts to control blood sugar levels with increases in exercise and changes to the diet.
Many people find they can come off drugs completely when they do this properly.For those who cannot control their blood sugar levels without drugs then it is sensible to take them. The cumulative effect over time of high blood sugar levels is extremely damaging, and this is why so many diabetics suffer from amputations, blindness, heart attacks and strokes.Blood sugar lowering agentsThe main one is perhaps Metformin which lowers the amount of sugar your liver produces. Thiazilienediones such as Rosiglitazone increase insulin sensitivity of the tissues and glucosidase inhibitors such as Acarbose reduce absorption of glucose from the gut. All these drugs will be more or less effective in different people depending on how their diabetes is affecting them. Measuring blood sugar levelsDiabetes is diagnosed using criteria that are arbitrary.
There are several ways that are used to measure blood sugar problems:Fasted blood sugar level - FBGThis measures blood sugar levels after not eating anything for at least 8 hours. However, this value will vary depending on factors such as stress, recent exercise and illness.
Secondly their muscles get used to using fat as a fuel place of glucose and so more glucose is left in the blood. If you come into this category the measure below could be more useful to you.Long term blood sugar controlTo assess this we measure the amount of glycosylated haemoglobin - HbA1c, in your red blood cells. Haemoglobin - Hb, is the protein found in red blood cells that is responsible for carrying oxygen to your tissues. In good health somewhere between 3-5% of our haemoglobin is in the HbA1c form.Red blood cells live for an average of 120 days. There are a number of factors that can skew the measurement:People with healthy low blood sugar have longer lived red blood cells that may survive for an average of 150 days. In this case a high end reading for HbA1c does not imply bad blood sugar control.Diabetics with high blood sugar levels have red blood cells that live shorter lives than average, typically around 90days. It may be a better measure than HbA1c, and gives an indication of blood sugar levels over the previous 2-3 weeks(5).Glucose challenge or OGTTThe oral glucose tolerance test - OGTT is a measure of our response to consuming 75g of glucose in one hit.
It is unrealistic as most people never consume such a large and purified amount of glucose.
For most people achieving the low GI meal involves limiting the amount of starchy carbohydrates they eat.



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