Maternity Healthcare for Patients with Gestational Diabetes

MATERNITY HEALTH CARE FOR PATIENTS

WITH GESTATIONAL DIABETES

dissertation submitted to

Indira Gandhi National Open UniversityNew Delhi

by

Dr.D.Bharani Kanchana, B.Sc., M.B.B.S

(Reg.No.042743245)

towards partial requirement for the award of the

POST GRADUATE DIPLOMA IN MATERNITY & CHILD HEALTH

SEPTEMBER, 2004

Dedicated to our beloved mentor

Arul Selvar Dr.N.Mahalingam Avl.

Childhood shows the man,

as the morning shows the day

- Milton in Paradise Lost

CERTIFICATE

This is to certify that the dissertation entitled Maternity Health Care for Patients with

Gestational Diabetes, submitted for the award of the Post Graduate Diploma in Maternity

& Child Health to the Indira Gandhi National Open University, New Delhi, is an original work

of Dr.D.Bharani Kanchana, B.Sc., M.B.B.S., carried out at the Kovai Medical Centre &

Hospital, Coimbatore, during the period January 2004 to December 2004, under my guidance

and supervision. This work has not formed the basis for the award of any degree, diploma,

associateship, fellowship or other titles in this University or, any other University or

Institution of Higher Learning.

Dr.Vasantha Elango, M.D. Dr.Raghupathi, M.D.

Associate Professor & Research Supervisor Professor & Head of the Department

Social & Preventive Medicine Social & Preventive Medicine

Coimbatore Medical College Coimbatore Medical College

Coimbatore Coimbatore

DECLARATION

I declare that the thesis entitled Maternity Health Care for Patients with Gestational

Diabetes, submitted by me for the Post Graduate Diploma in Maternity & Child Health to the

Indira Gandhi National Open University, New Delhi, is the record of work carried out by me

during the period from January 2004 to December 2004, under the guidance of Dr.Vasantha

Elango, M.D., Associate Professor, Department of Social & Preventive Medicine,

Coimbatore Medical College, Coimbatore, and has not formed the basis for the award of any

degree, diploma, associateship, fellowship or other titles in this or any other University or

other similar institution of Higher Learning.

Date: Signature of the Candidate

Place:

CONTENTS

Acknowledgement ......................................................................................... i

Abstract........................................................................................................ iv

Preface .......................................................................................................... vi

CHAPTER-1: INTRODUCTION

1.1 Reasons for the development of gestational diabetes ................... 1

1.2 Effects of gestational diabetes ..................................................... 2

1.2.1 Effect of gestational diabetes on the foetus during pregnancy ...... 3

1.2.2 Effect of gestational diabetes on the baby after birth .................... 3

1.2.3 Effect of gestational diabetes on mother ...................................... 4

1.3 Diagnosis for gestational diabetes ................................................ 5

1.4 Treatment for gestational diabetes ............................................... 6

1.4.1 Keeping diet under control .......................................................... 6

1.4.2 Regular physical exercise ............................................................ 7

1.4.3 Taking proper medicines ............................................................. 7

1.4.4 Regular monitoring of blood glucose levels ................................. 7

1.4.5 Checking blood sugar after the birth of baby ............................... 8

1.5 Objectives of the study ................................................................ 8

CHAPTER-2: METHODOLOGY

2.1 Basis for the methodology adopted in this study .......................... 9

2.2 Rationale for choosing the sample group ..................................... 11

2.3 Methods adopted for the diagnosis of gestational diabetes ........... 11

2.3.1 Glucose tolerance test for gestational diabetes ............................. 11

2.4 Expected outcome ...................................................................... 12

CHAPTER-3: RESULTS & DISCUSSION

3.1 Initial assessment ........................................................................ 16

3.2 Statistical analysis & inferences ................................................... 17

3.2.1 Clustering by factors ................................................................... 18

3.2.2 Clustering by patients .................................................................. 25

CHAPTER-4: CONCLUSIONS

4.1 Synthesis of the results and conclusions ....................................... 26

4.2 Recommendations and scope for future study .............................. 29

REFERENCES

List of references .................................................................................. i - ii

i

ACKNOWLEDGEMENT

I place on record my great honour to my research supervisor Dr.Vasantha Elango, M.D.,

Associate Professor, Department of Social & Preventive Medicine, Coimbatore Medical

College (CMC), Coimbatore, for her efficient guidance and assistance throughout this work

on gestational diabetes. I had several occasions of fruitful discussions and debates with my

research supervisor, all of which has resulted in a successful completion of this work. I am

also very much thankful to my research supervisor for a through review of this dissertation,

which has resulted in its significant improvement.

I am indebted to Dr.Raghupathi M.D., Head of the Department, Department of Social &

Preventive Medicine, Coimbatore Medical College (CMC), for providing his fruitful and

timely comments and suggestions towards improvement of this work.

I would always remember the kind co-operation and feed back extended by Dr.Geetha

Christopher, M.D., Dr.Chellammal, M.D., Dr.Vijayalakshmi, M.D.. at the Department

of Obstetrics & Gynaecology, Coimbatore Medical College (CMC), which were very much

thoughtful and beneficial during the synthesis of this dissertation.

The memorable teachings, great help, and knowledge input form Dr.Gandhimadhi, M.D.,

(Paediatrics), and Dr.Nirmala Perumal, M.D. (Obstetrics & Gynaecology), Employee's

State Insurance Corporation's Hospital (ESI), Coimbatore, were very much helpful while

I had been under training at this hospital. It is their memorable concern and care, which have

provided me a comprehensive practical knowledge in maternity and child health care.

ii

I am indebted to Dr.Nalla G. Palaniswamy M.D. (Endocrinology), Chairman, Kovai

Medical Centre & Hospital (KMCH), Coimbatore, for providing a robust platform for

carrying out this research work on gestational diabetes.

Words are inadequate to express my sincere gratitude to Dr.Athima Pathak, M.S.

(Obstetrics & Gynaecology), KMCH, for helping me in various ways to acquire necessary

background practical knowledge and timely support on the issues of maternity and child

health care.

A great sense of appreciation goes to Dr.Kannaki Uthiraraj, M.D, D.G.O., Infertility

Centre, KMCH, for being a good friend, dedicated advisor, and patron in matters relevant

to women's infertility issues. I am thankful to Dr.Kannaki for providing necessary input to this

dissertation from time to time, and helping me in the formulation of this dissertation.

I am thankful to Dr.Babu Rani, D.G.O., M.R.C.O.G., at the KMCH, for having associated

with me from time to time and offering necessary help in my work.

The vital and timely help offered by Dr.Vasanth, M.S., KMCH, has benefited me in my

career, and I express my sincere thanks to him for the same.

I gratefully acknowledge Dr.Uthiraraj, M.D. (Paediatrics), Siva Clinic, Pollachi, for

offering necessary suggestions and promulgating advocacies on maternity and child health,

which were very much helpful in the acquisition of sufficient knowledge.

iii

The great care, mindful attention, and moral support provided my husband Dr.K.Dhanapal,

Ph.D. (Environmental Sciences), Jawaharlal Nehru University, New Delhi, has been very

much instrumental in the successful completion of this dissertation work. His multi-facet

personality, wide knowledge, rich experience in science and social issues, balanced approach,

and timely care for our children Sri Hari and Keshav, have all given me an impetus to carry

out this dissertation work on gestational diabetes. He was also responsible for making me to

get involved in social issues through EPIC-In (Environment With People's Involvement &

Co-ordination in India), a non-governmental organisation addressing local environmental,

socio-economic and ethical issues. His delightful company has always made me charm, and

I would proudly say that "a man exists behind every successful women".

I am thankful to Dr.S.Eswaramoorthi, Ph.D., Environmental Scientist, EPIC-In, for helping

me with statistical analysis of the data and interpretation of results.

"An opportunity is a door to success" and, I am delightful that I had such an opening from

the Indira Gandhi National Open University, New Delhi. I thankfully put on record my

faithful expression of appreciation to them for giving me this rare opportunity to pursue a

Post Graduate Diploma in Maternity & Child Health (PGDMCH). I am sure that, through this

opportunity I will certainly benefit from my career advancement, and enhance my services to

our society especially, to the rural poor Indian women.

iv

ABSTRACT

Gestational diabetes mellitus (GDM) affects a large population of pregnant women. It is

caused by an imbalance between the capacity of the pancreatic ß-cells and the increased

demands for insulin due to decreased insulin sensitivity during pregnancy. Poly cystic ovary

syndrome (PCOS) is also another cause for gestational diabetes. Gestational diabetes results

in macrosomia, difficulty during delivery, intra uterine death (IUD), and may manifest in to

the development of type-2 diabetes.

A clear knowledge on the development of gestational diabetes, and its relation to other

abnormalities such as irregular menstrual cycle, poly cystic ovary syndrome, macrosomia,

family history of diabetes, etc. is lacking.

Thus, a study with 101 patients has been undertaken at the Kovai Medical Centre & Hospital

(KMCH), Coimbatore. Among the 101 patients, 16 were found to be affected with gestational

diabetes. Of this 16 patients, 8 were given insulin treatment, 6 were put under diet control,

(of this 14 women, one was treated with both insulin and diet control), and two of them were

not treated. The patients who were treated either by insulin or, by diet control had a normal

baby (baby weight�

3 kg). The patient who was administered with insulin, and put under diet

control as well, delivered a baby with a weight of 3.4 kg. One woman in this group had twin

babies, one with a weight of 1.7 kg and another one with 1.9 kg. Among two of the patients

who had not been treated for GDM, one had a 3.3 kg baby born with congenital abnormality,

and for another woman it was her first pregnancy, and so far she has not delivered a baby.

Two mothers had a history of still-born babies, of which one patient had no bad obstetric

v

history (BOH), and afflicted by intra uterine death (IUD) of the baby. It is noteworthy that

this patient had been administered with insulin for the control of gestational diabetes. The

failure of insulin treatment with this patient is attributed to her inability to respond positively

to the administration of insulin due to the development of insulin resistance in patients with

gestational diabetes, and artificially induced hyperinsulinemia. Therefore, a best treatment

procedure for this patient would be the administration of insulin sensitizing agents such as

metformin, thiazolidinediones, and D-chiro-inositol, with necessary follow-up action.

Cluster analysis of the data showed that gestational diabetes is more related to irregular

menstrual cycle than diabetes mellitus, sibling history of diabetes, polyhydramnios, history of

macrosomia, history of still birth babies, history of congenital abnormalities in the baby, and

bad obstetric history. Further, this study showed that, family history of diabetes mellitus is not

closely related with gestational diabetes when compared with other disorders mentioned

above, illustrating the fact that the development of gestational diabetes may be due to external

influences rather than hereditary one. This study further demonstrated the presence of two

groups of patients among the sample population. Such a grouping of patients is expected to

be helpful in further diagnosis and administration of proper medicines, since patients in the

same group are expected to respond similarly to the administered drug.

This study concludes that, before administering insulin for the treatment of gestational

diabetes, the balance between patient's insulin secretion and insulin resistance should be

thoroughly studied in order to avoid intra uterine death (IUD), and improve the treatment for

gestational diabetes.

vi

PREFACE

Women play an important and critical role in shaping our country, family, children's health and

development. Maternity and motherhood is the virtue of women that put them in a pristine

position on par with God in our epics. Women bears the origin of human life, it's sustenance

on Earth, and a meaningful destination for everyone.

In every corner of life, women play a meaningful role, either directly or indirectly, that forms

the basis of every Indian family. However, while considering women themselves, a lot of

intricacies are involved, both physiological and psychological, which affects them from day

to day life, and put them in an irrevocable and painful position in the family structure. Being

on the Board of Directors with EPIC-In (Environment With People's Involvement & Co-

ordination in India - a non-governmental organisation addressing local environmental, social,

and ethical issues in Coimbatore), and having a concern for rural poor women, I have been

thinking on a variety of topics that are most relevant to address the present day issues of

women health. I thought that it would be most beneficial to many educated and uneducated

women, if one of the vital health problems of a family women is sincerely addressed. The

result of such a thinking formed the basis for the present work on gestational diabetes.

Gestational diabetes is an important health problem, which largely influences the social and

health status of an Indian woman, and the health of her noble child. I hope that this work will

benefit the women community of our country, which only can make me pleased.

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1

CHAPTER-1: INTRODUCTION

Gestational diabetes mellitus (GDM) is a condition whereby a pregnant women, who had

no diabetes before, develops such a condition temporarily. The diabetic condition normally

develops in the second half of pregnancy and disappears after the birth of the baby.

Though the general cause for the onset of gestational diabetes is unknown, it is generally

believed that hormones produced during pregnancy blocks the activity of insulin, which in

turn causes glucose intolerance. The pathogenetic mechanisms underlying GDM involve

an imbalance between the capacity of the pancreatic ß-cells and the increased demands for

insulin due to decreased insulin sensitivity during pregnancy (Ryan et al., 1985; Buchanan

et al., 1990; Catalano et al., 1991; Damm et al., 1992; Ryan et al., 1995). Women with

reduced insulin sensitivity or impaired ß-cell function in the non-pregnant state are thus

highly susceptible to develop GDM (Holte et al., 1998). Thus, pregnant mother’s body

should be able to produce more amount of insulin to overcome the blocking effect of

pregnancy hormones.

1.1 Reasons for the Development of Gestational Diabetes:

The causes for the onset of gestational diabetes is still uncertain. Normally, 2 to 5 percent

of women are affected by gestational diabetes. Pregnant women are more likely to develop

gestational diabetes if they meet the following criteria:

Have a family history of type-2 (adult-onset) diabetes.

With an age of 25 and above.

Have obesity.

2

Have previously given birth to a large baby or, with an abnormality.

Previously had a stillbirth, late in pregnancy.

Have a history of gestational diabetes in the past pregnancy.

Though gestational diabetes usually does not cause any symptoms, increase in blood sugar

levels, increased thirst and hunger, and frequent urination, are some of the symptoms,

which are also common late in the pregnancy. Thus, it is difficult to easily figure out the

patient having gestational diabetes without going for a glucose tolerance test.

Also, women are susceptible to gestational diabetes if they had the same in their past

pregnancy. However, it should be noted that every pregnancy is different. Previous history

of gestational diabetes does not necessarily result in its manifestation in subsequent

pregnancy. Similarly, gestational diabetes may appear in subsequent pregnancies, but

could not have shown up in the earlier pregnancy. Thus, during every pregnancy, mother

should be tested for gestational diabetes, irrespective of their past medical history.

1.2 Effects of Gestational Diabetes:

Since the changes in mother’s body that cause gestational diabetes normally occur only

during pregnancy, most of the time, gestational diabetes disappears after the birth of the

baby. After the baby is born, mother’s body goes back to normal function, and the

condition of gestational diabetes goes away. Moreover, gestational diabetes is treatable,

especially if it is found in early stages of pregnancy. If gestational diabetes is found in the

early stage, necessary and adequate treatment can be given to safeguard both the mother

and the child from its detrimental effects. If it is not detected in the early stages, then it can

3

cause several problems to the mother during delivery of the child, and to the child both

during pregnancy and after the birth.

In general, the effect of gestational diabetes can be classified into three groups based on

whether it affects baby or mother, and at what stage, viz.,

1. Effect of gestational diabetes on the foetus during pregnancy.

2. Effect of gestational diabetes on the baby after birth.

3. Effect of gestational diabetes on the mother.

Detailed discussion is presented below.

1.2.1 Effect of Gestational Diabetes on the Foetus During Pregnancy:

Due to increased blood glucose levels in mother’s blood, the baby grows larger. This

makes delivery of the baby injurious and difficult. In some cases, this condition leads to

caesarean. If untreated, gestational diabetes can result in still birth babies.

1.2.2 Effect of Gestational Diabetes on the Baby after Birth:

The offspring of gestational diabetes mother can face any one or, combination of the

following problems:

1. In order to tolerate the increased blood glucose levels of mother, the pancreas of

the baby secretes more amount of insulin while the foetus is growing. This

condition continues even after birth, while higher blood glucose levels no longer

4

exists. Thus, after birth, the baby develops hypoglycaemia (low blood glucose

level). This condition can be overcome by administering glucose through drip.

2. It is highly probable that the newborn baby will develop jaundice (yellowing of

the skin and whites of the eyes). This condition fades away over a few weeks

without the need for a medical treatment.

3. There is an increased risk for the baby to be born with congenital problems, such

as a heart defect. At times, infants can be born with respiratory distress syndrome

(RDS), in which the baby has breathing problems since the lungs have not

matured as normal. But, this condition usually clears up with time.

4. The babies are more likely to be obese (overweight) as children or adults, which

can lead to other health problems later in their life.

5. There is an increased risk for the child to develop type-2 diabetes (development

of diabetes during adult stage).

6. There is also a slightly higher chance of stillbirth or death as a newborn. This can

be avoided if the problem is detected earlier, and the glucose levels were well

managed so as to avoid infant death.

1.2.3 Effect of Gestational Diabetes on Mother:

Normally, gestational diabetes does not affect the mother. However, the mother who

developed gestational diabetes during first pregnancy is highly likely to develop the same

5

at the second pregnancy. They are also likely to develop type-2 diabetes. In some mothers,

gestational diabetes leads to high blood pressure. It is also found to be associated with

poly cystic ovary syndrome (PCOS; Bloomgarden, 2003), which leads to infertility.

If mothers control their condition after detection of gestational diabetes, most of them

have healthy pregnancies and healthy babies. If treatment is not taken, mothers with this

condition could have very large babies. Since very large babies are difficult to deliver

through natural delivery (delivery through the vagina), some mothers may need surgery to

deliver their bigger babies. Surgery done towards this end can increase the mother's

chances of getting an infection. Moreover, mothers who have their babies by surgery also

take a longer time to recover.

1.3 Diagnosis for Gestational Diabetes:

Normally it is difficult to detect gestational diabetes unless the doctor has a medical

history of the patient, and ascertain that the patient is likely to develop it. Under this

circumstance, the blood glucose level of pregnant mother is monitored regularly during the

entire pregnancy period through urine test. If pregnant mother develops high blood

glucose levels between 24 – 28 weeks of pregnancy, then she is said to have gestational

diabetes. In order to confirm that the mother has gestational diabetes, glucose tolerance

test is conducted. During this test, the pregnant mother is given a 100 g of glucose

solution to drink after fasting for 8 hours. Then, blood samples are taken at regular

intervals and glucose level is estimated. This is the only way to ascertain the condition of

gestational diabetes in the pregnant mother.

6

1.4 Treatment for Gestational Diabetes

The most important part of treatment is to control blood sugar levels. This can be

achieved by:

1. A carefully planned diet.

2. Regular exercise.

3. Taking proper medicines.

4. Monitoring the blood sugar at regular intervals.

5. Checking blood sugar after the birth.

1.4.1 Keeping Diet Under Control

Keeping the diet under control is another important factor for the patients affected by

gestational diabetes. Taking a balanced diet is important in order to keep the blood sugar

at the optimum level. Normally the diet should consist of a variety of foods including

plenty of starchy fillers such as bread, pasta, rice and potatoes, and at least five portions of

fruit and vegetables each day. Moreover, it is important to limit consumption of sugary

foods like cakes, biscuits and soft drinks. A diet that is low in fat, is also desirable. This

can be achieved by avoiding full-fat dairy products such as butter and cream, and limiting

fatty meat, pies, sausages and burgers. Grilling, steaming or, microwaving food, rather

than frying or roasting means, less fat is added during cooking.

7

1.4.2 Regular Physical Exercise

Apart from diet control and proper medication, gentle and regular exercise, such as

walking, can help reduce blood sugar levels and promote the body condition of the

mother. However, the doctor should be consulted before choosing proper body exercises.

1.4.3 Taking Proper Medicines

Despite making the above lifestyle changes, a few women's blood sugar levels remain too

high, and they may need daily injections of insulin. The extra insulin will not cross the

placenta and will not affect the baby. Any woman who needs to take insulin will be taught

how to take it by her doctor or nurse. Sometimes, it is possible to have too much insulin

and this can cause low blood sugar (hypoglycaemia). Common symptoms of this are

weakness, shaking, hunger and sweating. Thus, for people taking insulin, it is a good idea

to keep a snack handy at all times in case low blood sugar develops.

1.4.4 Regular Monitoring of Blood Glucose Levels

Normally, the blood glucose level should be tested once a week. For some women,

frequent testing may be needed, and a good doctor should be consulted to keep the

gestational diabetes under control. For those who need frequent testing, blood glucose

level needs to be measured in the morning, before breakfast, and again two hours after

breakfast. Sometimes, it may be necessary to test blood glucose levels in the mid-

afternoon.

8

1.4.5 Checking Blood Sugar After the Birth of baby

In almost every case, gestational diabetes disappears after the delivery of the baby.

However, to be sure that the blood glucose levels have become normal, it is necessary to

check the mother's blood sugar levels a few times after the birth.

1.5 Objectives of the study

A clear knowledge on gestational diabetes, its relationship with other disorders in women,

and its effect on their baby is lacking. Further, a definite knowledge on the consequences

of treatment procedures on the patient, as well as on their child, is deficient. Thus, the

main objectives of this study are:

1. To undertstand the relationship between gestational diabetes mellitus (GDM) and other

related disorders viz., diabetes, irregular periods, obesity, poly cystic ovary syndrom

(PCOS), family history of diabetes, macrosomia, still birth, congenital abnormality in

the baby, etc.

2. To study the outcome of treatment procedures (insulin and diet control) adopted for

gestational diabetes, and suggest suitable remedial measures.

In the following chapters, this study has made an attempt towards addressing these issues.

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9

CHAPTER-2: METHODOLOGY

2.1 Basis for the Methodology Adopted in this Study:

The sample group for this study was chosen from the records of the Kovai Medical Centre

& Hospital, Coimbatore (KMCH), which has a devoted section for Obstetrics and

Gynaecology and an Infertility Centre. Many women from different regions, origins and

communities regularly make a visit to this hospital, which makes this hospital a best

repository of records on a diverse group of patients. This diversity in the sample

population is essential in order to have an appraisal of the several factors responsible for

the onset of gestational diabetes in diverse groups of the people.

Once the sample group has been chosen, the development of a suitable methodology

requires a thorough understanding of the problem at hand. This will enable us to plan the

data collection accordingly. Thus, an insight has been made into the possible factors that

might have significant impact on the development of gestational diabetes. Though the

causes for gestational diabetes are still not clearly known, the following factors are said to

be important in inducing women with gestational diabetes:

1. Have a family history of type-2 (adult-onset) diabetes.

2. Age over 25 years.

3. Obesity.

4. Previously given birth to a large baby (macrosomia).

5. Previously given birth to a baby with congenital abnormality.

6. Previously had a stillbirth, late in pregnancy.

10

Thus, in this study all the patients were screened for the following critical parameters viz.,

�Age.

�GRA/PARA.

�Weight.

�History of diabetes mellitus (DM).

�History of gestational diabetes mellitus (GDM).

�Whether treatment has been taken for the patients with the gestational diabetes.

�Family history of diabetes mellitus.

�Past history of still-birth babies.

�Past history of babies with congenital abnormalities.

�Past history of irregular periods.

�Sibling history of diabetes mellitus (DM).

�Past history of big baby (macrosomia).

�History of polyhydramnios.

�History of bad obstetric history (BOH).

�Birth weight of the baby.

These parameters were chosen for this study so as to answer questions on whether

gestational diabetes:

Correlates with obesity?

Does exhibit any pattern with the age?

Prevalent with patients having previous history of large baby?

Have any effect on congenital anomaly in baby?

Whether gestational diabetes is hereditary?

Correlates with dieting pattern of the patients?

Responds positively to medication in reducing its detrimental effect both on the child

and on the mother?

Have drugs administered for gestational diabetes inflict any effect on the health of

foetus and mother?

11

To what extend the foetus is affected by gestational diabetes?

Whether women are more likely to develop gestational diabetes in the first

pregnancy or, in the subsequent pregnancies?

2.2 Rationale for Choosing the Sample Group:

The sample group was chosen based on the earlier conceptions about gestational diabetes.

Since pregnant mothers over an age of 25 years are likely to have gestational diabetes, the

patients selected for screening of gestational diabetes included those who were below the

age of 25 as well those above the age of 25. Thus, by analysing the pattern of occurrence

of gestational diabetes with age, vital clues necessary for linking the age factor with

gestational diabetes could be obtained. Similarly, other related factors were also taken into

account.

2.3 Methods Adopted for the Diagnosis of Gestational Diabetes:

The patients were asked a series of questions relevant to address the current problem. The

necessary particulars obtained from the patients and the results of medical diagnosis of

respective patients are presented in Table 1. The medical diagnosis for gestational diabetes

was carried out as described below:

2.3.1 Glucose Tolerance Test for Gestational Diabetes:

The patients’ urine was routinely tested for sugar throughout pregnancy. If high blood

sugar was detected between 24 and 28 weeks of pregnancy, then they were supposed to

have gestational diabetes.

12

However, a confirmation for gestational diabetes was ascertained only after a test for

glucose tolerance was undertaken. This glucose tolerance test was carried out after eight

hours without food – i.e., the patients were advised to come to the hospital in the morning

without taking any food – including tea/coffee/milk or, other drinks. At the hospital the

patient was given a solution of 100 g of glucose to drink, and then blood samples were

taken at every half-an hour intervals and analysed to see how their body deals with the

glucose, over time (O'Sullivan and Mahan, 1964). If higher glucose levels were detected

during glucose tolerance test, then the patient was classified as having gestational diabetes.

2.4 Expected Outcome:

The results from this study is expected to reveal the following facts:

1. Does gestational diabetes shows any pattern with age, as previous studies

indicate?

2. Whether body weight contributes in any way to the promulgation of gestational

diabetes? This is most important question since body weight directly relates with

both hereditary and dieting pattern of the patient.

3. Whether hereditary complications contribute to the onset of gestational diabetes

in women? Questioned the other way, whether family history of diabetes mellitus

or, gestational diabetes has any correlation with the onset of gestational diabetes

to a mother?

13

4. Whether administration of insulin or, diet control or, both, has in any way be

helpful in getting rid of the detrimental effects of gestational diabetes? If yes,

which one is exercising dominant control?

5. Whether history of birth of a big baby (macrosomia) to a mother is directly

related with gestational diabetes? More precisely, whether all the instances where

the birth of a big baby has taken places certainly points to the susceptibility of the

mother to gestational diabetes?

6. Whether history of still birth baby/babies closely relates with the gestational

diabetes?

7. Whether polyhydramnios ovary indicates or, directly correlates with gestational

diabetes?

8. Whether gestational diabetes dominantly results in the infliction of congenital

abnormalities in the baby?

9. Whether bad obstetric history (BOH) is related with gestational diabetes?

Apart from answering all these questions, this dissertation also makes an attempt to

addresses the level to which these factors are important, both in prediction as well as in

the treatment of gestational diabetes in women.

14

The outcome of this work will benefit doctors:

In the early identification and segregation of patients susceptible to gestational

diabetes, based on the results obtained from related health risk factors.

Identify the risk level of the patient to gestational diabetes in the current pregnancy.

In choosing the best treatment procedure to be adopted for the treatment of the

pregnant mother for gestational diabetes.

To undertake enough precautionary measures to prevent still birth babies.

To prevent or, at least, reduce the risk of birth of babies with congenital

abnormalities to the mothers affected by gestational diabetes.

To safe-guard pregnant mothers with a history of infertility problems from the

dreadful abortions due to the detrimental effects of gestational diabetes.

In addition, the results of this study will benefit social workers, non-governmental

organisations, and interest groups:

To properly identify the group of people susceptible to gestational diabetes.

To rightfully educate best practices to be adopted to overcome the problems posed

by gestational diabetes.

15

To select places or, group of people, for conducting free health camps and

administer necessary medications.

The outcome of this work will also benefit the government:

In preventing further proliferation of gestational diabetes among the people.

In developing necessary infrastructure (such as, supply of healthy food to people

below poverty line, manufacturing and supply facilities for necessary medicines,

providing necessary fund to fuel awareness programmes, etc.) to address the issue

of gestational diabetes.

To make a policy decision on the supply of necessary medicines to the public

health centres. If treatment of gestational diabetes requires only proper food or,

maintenance of health by exercising, then supply of free medicine can be minimized

to target the most-affected patients, and money can be saved. Thus, a policy

decision on the supply and quantity of free medicine can only be made after

thoroughly studying various factors involved in the onset of gestational diabetes in

pregnant women.

Above all, the results are expected to fuel further research in gestational diabetes, and help

to find innovative ways to solve the associated problems in women.

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16

CHAPTER-3: RESULTS AND DISCUSSION

3.1 Initial Assessment

The data collected during this study is presented in Table 1. As a first step in the analysis

of data, the number of patients affected by various disorders was considered. This initial

approach is expected to provide some coarse thought about the reasons for the

development of gestational diabetes and its manifestation.

Of the 101 patients studied, no one was having a history of diabetes mellitus (DM). In the

total sample group, 16 women were having a history of gestational diabetes mellitus

(GDM). This indicates that diabetes mellitus and gestational diabetes have basically

different origins, thus they are differently manifested. This also supports the earlier

conceptions that, development of insulin resistance during pregnancy due to hormonal

changes results in the onset of gestational diabetes in mother due to the failure of the � -

cell compensation (Cavaghan et al., 2000; Homko et al., 2001; Khan, 2001); after delivery

this leads to the development of type-2 diabetes (Catherine et al., 2002).

In the present study, of the 16 patients affected by GDM, 6 patients were put under diet

control, and 8 patients were treated with insulin (of this 14 women, one was treated with

both insulin and diet control). Two patients were not at all treated either by diet control

or, by insulin. The patients who were treated either by insulin or, by diet control had a

normal baby (baby weight� 3 kg). The patient who was administered with insulin, and put

under diet control as well, delivered a baby with a weight of 3.4 kg. Further, one woman

17

in this group had twin babies one with a weight of 1.7 kg and another one with 1.9 kg.

Among two of the patients who had not been treated for GDM, one had a 3.3 kg baby

born with congenital abnormality, and for another woman it was her first pregnancy, and

so far she has not delivered a baby.

Two mothers had a history of still-born babies, of which one was a intra uterine death

(IUD) with no bad obstetric history (BOH). It is noteworthy that the patient who had

suffered from IUD, had been administered with insulin for the control of gestational

diabetes. Another patient who had received insulin treatment, had a previous history of

poly cystic ovary syndrome (PCOS) but, had no bad obstetric history (BOH), and

delivered a baby with a weight of 3 kg. Similarly among two of the patients, who had not

been treated for GDM, one had a 3.3 kg baby born with cardiac problem.

In the sample group, thirty four women were found to be having a family history of

diabetes mellitus; 7 women were having irregular periods, of which one was having poly

cystic ovary syndrome (PCOS); 2 women were having polyhydramnios ovary; 3 women

had a history of bad obstetric history (BOH). One patient was having a sibling history of

diabetes mellitus. Three babies had congenital heart abnormalities, of which one baby had

PDA cardiac disease; only one case of macrosomia was observed.

3.2 Statistical Analysis & Inferences:

In order to further understand the factors responsible for the onset of gestational diabetes,

cluster analysis of the data was carried out. Patients with missing data were omitted from

18

the statistical analysis. Further, age and weight (both that of baby and mother) were not

included for the reason that age and weight are the variables that represent measurements

while, the other data included in the analysis are variables that represent the presence or,

absence of a particular characteristic. Thus, both of these different types of data can not be

mixed together in the cluster analysis procedure employed here. Binary clustering method

was applied to the data after representing absence of a particular property (for example,

poly cystic ovary syndrome) by “zero”, and presence of a property (for example,

gestational diabetes) by “one”. Further, clustering was carried out “by variable” and “by

case” where, “variable” represents the parameters that are thought to be related to GDM,

while the “case” represents the “patients”. Thus, it was made possible to group the factors

related to GDM, as well as to group the patients with similar characteristics.

3.2.1 Clustering by Factors

While clustering by factors that are related to GDM, the following groups were obtained.

This is illustrated in Fig.1

Group-1:

GDM

Insulin

o Irregular period.

�Diet

Group-2:

Congenital heart disease in child.

Polyhydramnios.

o Bad obstetric history (BOH).

19

o Still birth of the baby.

�Sibling history of diabetes mellitus.

�Big baby.

�Diabetes mellitus.

Group-3:

Family history of diabetes mellitus.

This clustering clearly indicates that family history of diabetes mellitus has not related to

the incidence of gestational diabetes. However, other factors are related, but at different

levels.

Group-1 indicates clustering of GDM with insulin, irregular period, and diet control. Since

insulin and diet control were administered factors on to the patients who have suffered

from GDM, rather than observed factors, their clustering can not be taken as to represent

a close relationship between GDM and insulin and/or, diet control. However, these two

factors (insulin and diet control) could not be removed from the statistical model before

carrying out the cluster analysis – since their association (or, non-association) with other

factors such as still born baby or, big baby (which are expected to be controlled by the

insulin administration or diet control) can not be ascertained in the first. The absence of

clustering of insulin administration and diet control, with congenital heart disease in child,

still birth and macrosomia clearly indicates that treatment procedures have succeeded in

regulating the consequence of gestational diabetes. This is understandable if we could

remember that insulin act against the development of congenital abnormalities in child,

prevents still birth, and reduces the chances of having a big baby.

20

Under group-II, diabetes mellitus, sibling history of diabetes mellitus, history of big baby,

still birth baby, polyhydramnios, bad obstetric history, and congenital abnormality in child

have clustered. Of these factors, diabetes mellitus, sibling history of diabetes mellitus, and

birth of a big baby are closely related and form a sub-cluster-1. Cases of still birth babies

and bad obstetric history are closely associated and forms sub-cluster-2; Cases of

polyhydramnios and congenital abnormality forms sub-cluster-3.

The observation that gestational diabetes falls under a different group separate from the

factors of sub-cluster-1 (diabetes mellitus, sibling history of diabetes and history of big

baby) indicates that, macrosomia is more due to prevalence of maternal diabetes, rather

than gestational diabetes. This observation is supported by the findings of the earlier study

of Raychaudhuri and Maresh (2000), where growth acceleration among fetuses of diabetic

mothers was reported to start at 22 weeks of gestation and to continue despite

improvements in diabetic control. Such an acceleration in the fetus growth was attributed

to prevailing maternal glucose concentrations in the early trimesters (Wong et al., 2002).

However, in the sample group, a mother who had a over weight baby (4.4 kg) with a

family history of diabetes did not had either diabetes or gestational diabetes. This can be

explained as due to maternal obesity, since this mother had a weight of 81 kg. Previous

studies have indicated that women who had large-for-gestational-age (LGA) babies did

not have higher HbA , but had the mean first-trimester HbA levels of 7.5-8.1%, which isIC IC

higher than normal standards; also, maternal obesity was thought to be a major factor for

LGA babies. (Wong et al., 2002). Secondly, early programming of fetal growth by

21

elevated maternal glucose levels during the periconceptional period may result in

subsequent LGA babies. Whether this was the case with this particular patient could not

be confirmed, as the patient was not screened for glucose intolerance before pregnancy.

Thirdly, HbA might not be a good predictor for LGA babies since episodicIC

hyperglycaemia could be associated with normal HbA results (Kyne-Gizebalski et al.IC

1999), and it is also well known that many women with satisfactory glucose control based

on HbA or sugar profile still had LGA babies. These may be due to episodicIC

hyperglycaemia, which is not reflected by HbA results. Thus, we conclude that thisIC

particular patient was more likely having episodic hyperglycaemia, and could develop

diabetes in the later age.

Similarly, factors of sub-cluster-2 (still birth babies and bad obstetric history, and sub-

cluster-3 (polyhydramnios and congenital abnormality) are not so closely related with

gestational diabetes than irregular periods. Thus, it is suggested that the factors that are

responsible for the onset of gestational diabetes is also responsible for irregular periods

(oligomenorrhoea). Oligomenorrhoea is often associated with disorders in ovulation, the

causes of which are: 1) hypogonodotrophic hypogonadism characterised by a selective

failure of the pituitary gland to produce luteinizing hormone and follicle stimulating

hormone, 2) hyperprolactinaemia, usually caused by a pituitary microadenoma leading to a

reduction in the production of pituitary luteinizing hormone and follicle stimulating

hormone, 3) poly cystic ovary syndrome, resulting mainly from an excess of androgen

production within the ovary that leads to the recruitment of large numbers of small

preovulatory follicles, which fail to respond to normal concentrations of follicle

22

stimulating hormone, 4) premature ovarian failure and, 5) genetic abnormalities, the

commonest of which is Turner's syndrome, in which underdeveloped ovaries result in

primary ovarian failure (premature menopause) (Hamilton-Fairley and Taylor, 2003). The

impact of these disorders on gestational diabetes is uncertain.

From the available data, it was found that, a women who was having both a history of

GDM as well as a family history of diabetes, also had poly cystic ovary syndrome (PCOS).

Earlier study by Holte et al. (1998) have closely linked irregular menstrual cycles with

GDM, and it also pointed out an exceptionally high prevalence of poly cystic ovaries in

women with previous GDM. PCOS is associated with a 40% reduction in insulin

sensitivity (the inverse of insulin resistance; Dunaif, 1997)), and with relative � -cell

dysfunction (Dunaif and Finegood, 1997). Among women with oligomenorrhea (menses�

6/year), 77% have PCOS and 33% have glucose intolerance (Bloomgarden, 2003). Thus,

it is apparent that irregular menstrual cycle and GDM are closely related, as we have

observed in our study. Since PCOS is associated with insulin resistance, women with

PCOS are at an increased risk for developing type-2 diabetes, dyslipidemia, hypertension,

and heart disease (Peppard et al., 2001). The women who had PCOS was treated with

insulin during pregnancy, which helped her to have a normal baby, weighing 3 kg. But,

this women is more likely to be affected by type-2 diabetes.

Previous study by Mills et al. (1988) indicated that there is a close relationship between

hyperglycaemia and the risk of spontaneous abortion. Similarly, hyperinsulinemia and

insulin resistance are often observed in women with PCOS. However, in our study, where

23

a pregnant woman with GDM, having no signs of PCOS, was administered with insulin

towards treatment for gestational diabetes, which subsequently resulted in intra uterine

death (IUD) of the baby. This clearly shows that the patient had not reacted well to the

administration of insulin. The failure of insulin treatment is attributed to the development

of insulin resistance in patients who were having gestational diabetes (Homko et al.,

2001), and the development of hyperinsulinemia. The development of insulin resistance in

GDM cases has two path ways: 1) insulin resistance preceding pregnancy, which is

probably partially inherited and partially acquired and, 2) a physiological increase in insulin

resistance that occurs in all women during the second half of pregnancy, disappears

postpartum, and is believed to be the result of increased blood levels of several gestational

hormones (Catalano et al., 1991; Sivan et al., 1997). Further, there are clear evidences

pointing towards a link between obesity and � -cell dysfunction. An increased body fat

content in the patients with diabetic condition results in the higher levels of production of

free fatty acids through enhanced fat metabolism (lipolysis) towards meeting the energy

needs of the body cells. An increase in free fatty acid levels elevate the insulin secretion

rate, resulting in hyperinsulinemia. Thus, a feedback loop between insulin resistance and

insulin secretion exists (Vrbikova, et al., 2002). Given the fact that hyperinsulinemia is

also a risk factor for miscarriage (Bloomgarden, 2004), and the patient might have already

been affected by insulin resistance, the administration of excess insulin for the treatment of

GDM has resulted in miscarriage. This means that the patient's body was already secreting

normal or, excess levels of insulin (as in the normal women), but due to insulin resistance,

she developed glucose intolerance and identified as GDM patient. The administration of

24

additional insulin by injection caused a temporary hyperinsulinemia, which has led to the

intra uterine death (IUD). Thus, this particular patient should be given insulin sensitizing

agents such as metformin, thiazolidinediones, and D-chiro-inositol, taking into

consideration its side effects. A recent study has also demonstrated that the use of

troglitazone, an insulin sensitizing agent of the thiazolidinedione class, has significantly

improved the hyperinsulinemia (Azziz et al., 2001).

Under group-III, only one factor is observed to fall i.e., the family history of diabetes

mellitus. This implies that the family history of diabetes is not so much related with GDM

as that of other factors viz., irregular period, bad obstetric history, macrosomia, etc. Thus,

the inclusion of no family history of diabetes as one of the criteria among the others (age

< 25 years; not members of an ethnic/radical group with a high prevalence of diabetes,

normal body weight) for selective screening of patients for gestational diabetes, as

recommended by the American Diabetes Association, may not be an effective one to

address the problem of GDM, at the least, in Indian women. Williams et al. (1999) have

also expressed concern over such a selective screening and demonstrated that around 90%

of their obstetric population did not have all the four risk factors (family history of

diabetes, age > 25 years; members of an ethnic/radical group with a high prevalence of

diabetes, abnormal body weight). Since the diabetes population in India is on the rise, it is

suggested that Universal Screening should be adopted for GDM as suggested by Williams

et al. (1999).

25

3.2.2 Clustering by Patients:

The cluster analytical results, grouping patients with similar characters, is given in Fig.2.

In this diagram, the patients are clustered according to their physiological conditions. The

cluster analytical results illustrates two distinct group of patients, with sub-groups,

reflecting the fact that in the sample group ethnicity, regional influences, and genetic

influences may have been present. Since the ethnic, regional and genetic data for these

patients were not made available, it is not possible to decipher the interrelations of such a

grouping of patients. However, this grouping of patients into clusters will be very much

useful in administration of proper medicines, since the patients in the same group are

expected to respond similarly to the administered drug. Thus, before administering all the

patients with insulin or other drugs, a single patient from each cluster (or, sub-cluster) can

be tested for the response. From the analysis of such a response, further progression

towards ailment of other patients could be made. However, more in depth knowledge of

each patient should be acquired, since each individual is unique in their physiological

response to external and internal pressures. Thus, further research is needed in this

direction, which might form an extension of this work in the near future.

� � � � � � � � � �

26

CHAPTER-4: CONCLUSIONS

4.1 Synthesis of the Results and Conclusions

One hundred and one patients were studied for gestational diabetes (GDM) and associated

critical parameters viz., weight, history of diabetes mellitus (DM), family history of

diabetes mellitus (FDM), irregular menstrual cycle, polyhydramnios uterus, bad obstetric

history (BOH), macrosomia, still birth baby, babies born with congenital abnormalities,

and birth weight of the baby. Fig.3 illustrates various abnormalities among patients.

Out of the 101 patients studied, no one was having a history of diabetes mellitus (DM). In

the total sample group, 16 women were having a history of gestational diabetes mellitus

(GDM). This indicates that diabetes mellitus and gestational diabetes have basically

different origins, thus they are differently manifested. Of the 16 patients affected by GDM,

6 patients were put under diet control and 8 patients were treated with insulin (of this 14

women, one was treated with both insulin and diet control). Two patients were not treated

either by diet control or with insulin. The patients who were treated either by insulin or,

by diet control had a normal baby (baby weight� 3 kg). The patient who was

administered with insulin, and put under diet control as well, delivered a baby with a

weight of 3.4 kg. Further, one woman had twin babies one with a weight of 1.7 kg and

another one with 1.9 kg. Among two of the patients who had not been treated for GDM,

one had a 3.3 kg baby born with congenital abnormality, and for another woman it was her

first pregnancy, and so far she has not delivered a baby.

27

Two mothers had a history of still-born babies, of which one patient with no bad obstetric

history (BOH), was afflicted by intra uterine death (IUD) of the baby. It is noteworthy that

the patient who had suffered from IUD, had been administered with insulin for the control

of gestational diabetes. This is attributed to the patient's inability to respond positively to

the administration of insulin due to the development of insulin resistance in patients with

gestational diabetes. Since hyperinsulinemia is one of the risk factors for miscarriage

(Bloomgarden, 2004), and this patient is expected to be already affected by insulin

resistance, the administration of excess insulin for the treatment of GDM might have

resulted in miscarriage. A best treatment procedure for this patient would be

administration of insulin sensitizing agents such as metformin, thiazolidinediones, and D-

chiro-inositol, with necessary follow-up action.

Another patient, who have received insulin treatment, had a previous history of poly cystic

ovary syndrome (PCOS) with no bad obstetric history (BOH), and she delivered a baby

with a weight of 3 kg. Similarly among two of the patients who have not been treated for

GDM, one had a 3.3 kg baby born with cardiac problem. Thus, insulin administration with

sufficient care is essential to yield good results for GDM patients.

The statistical analysis of the data revealed two distinct group of patients, reflecting the

fact that in the sample group ethnicity, regional, and genetic influences may have been

present. Since the ethnic, regional, and genetic data for these patients were not made

available, it is not possible to decipher the interrelations between these two groups.

However, grouping of patients in this manner will be very much useful in advocating a

28

suitable treatment procedure, since the patients in the same group are expected to respond

similarly to a particular drug. Further research in this direction is essential to benefit from

such an analysis.

The clustering by factors clearly indicated that family history of diabetes mellitus has not

related to the incidence of gestational diabetes. This disagrees with the recommendation of

the American Diabetes Association that women with no family history of diabetes mellitus

can be neglected from diagnosis for GDM. Thus, this study is in favour of an Universal

Screening suggested by Williams et al. (1999) to move towards a better maternal health

care.

The statistical analysis also showed that, though GDM clusters with other factors such as

diabetes mellitus, sibling history of diabetes, still birth baby, polyhydramnios and

congenital abnormalities in the baby, irregular menstrual cycle was found to have more

close relationship with GDM, as demonstrated in earlier studies. Thus, women with

irregular periods may be prioritised for the diagnosis of GDM, to take necessary maternal

health care in time.

This study also suggested that, the patients condition with regard to hyperinsulinemia and

insulin resistance should be identified, and necessary precautionary measures should be

taken, before administering insulin so as to avoid miscarriage during pregnancy.

29

4.2 Recommendations and Scope for Future Study:

1. This study was carried out with a small population. In order to clearly understand

the intricacies involved in the development of GDM, and to administer proper

medication in time, a large number of individuals should be studied. Such a study

would be possible only if all the data available from all the hospitals are pooled

together to form a meta database. This meta database might be very much useful

for further research in this direction, apart from helping all the physicians to

understand the multitude of interrelations and interactions among all the

diseases/disorders. Thus, creation of a meta database is suggested with the co-

operation from each and every corner of the medical community.

2. Since GDM is related with type-2 diabetes and cardiac problems, the follow-up

of the affected patient should be carried out in order to take necessary care, and

enhance the livelihood of the women community.

3. Although � -cell dysfunction clearly occurs before the onset of overt diabetes,

abnormal � -cell function in individuals at risk for diabetes but with normal

glucose levels has proved more difficult to demonstrate. This problem can be

solved by administering agents such as glucocorticoids, thiazolidinediones, and

FFAs, which either exacerbate or ameliorate insulin resistance (Cavaghan et al.,

2000). Such treatment might reveal latent, subclinical defects in � -cell function,

and facilitate identification of individuals at high risk of developing diabetes.

30

Whether such a diagnosis can also be applied for early detection of gestational

diabetes can be studied.

4. The GDM patients should also be monitored for � -cell dysfunction as well as

insulin resistance. This is necessary since administration of insulin to compensate

for the adverse effects of GDM might result in miscarriage in hyperinsulinemia

patients.

5. Hypersecretion of maternal serum activin-A is observed in patients with

gestational diabetes, which reverts back to normal after insulin treatment

(Petraglia et al., 1995). Since preterm labour is also associated with increased

concentrations of activin-A, which imposes an increased risk of neonatal

morbidity and death, and a derangement of placental hormonal activity, further

study on the relation between gestational diabetes and activin-A levels would

benefit in the treatment of patients with GDM.

6. The insulin resistance is associated with both PCOS and GDM. Thus, patients

with GDM can be followed-up for preventive medication for PCOS so as to

improve fertility in women. This will greatly enhance fertility related health care.

7. In some cases of GDM, administration of insulin results in pre-eclampsia

(Williams et al., 1999), which is defined as persistent high blood pressure, and

this condition can be diagnosed with proteinuria elevation ( � 300 mg or more of

urinary protein per 24 h, and hypertension, defined as blood pressure of 140/90

31

mm Hg or, higher, and first diagnosed after 20 week of gestation). The causes for

the pre-eclampsis are not yet clearly understood (Reis et al., 2002). Thus, in

future studies, the reasons for the onset of pre-eclampsia in GDM patients could

be studied in order to have a successful pregnancy and a healthy baby.

� � � � � � � � � �

i

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....................................... Every ending has its own beginning .................................

Continued on next page

Table 1: List of Patients Studied for Gestational Diabetes

S.No. IP No. NameAGE (yr) GRA/

PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

Diet Insulin

1 063862 Ms.S.SAVITHA 24 PRIMI NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.3

2 063900 Mrs.BHARATHI 23 PRIMI 65 + - - + NIL NIL NIL NIL NIL NIL NIL

3 063624 Mrs.JANAKI BABU 31 G P L A5 0 0 4 60 + - + NIL NIL NIL NIL + NIL NIL +

Twins

1.7

1.9

4 Mrs.LATHA 29 G2P1L1A0 82 NIL + -- - + NIL NIL NIL NIL

5 062563 Mrs.AKILANDESHWARI 28 G2P1L0 NIL + - + + H/o IUD + NIL NIL NIL NIL NIL NIL Not yet delivered

6 063848 Mrs.FRAZANA 30 PRIMI 66 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL Not yet delivered

7 063669 Mrs.RIPAYA 22 PRIMI 75 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL

Twins

800 g

450 g

8 063740 Mrs.SAKUNTHALA 23 G2P0L0A1 NIL NIL - - + NIL NIL NIL NIL NIL + NIL Not yet delivered

9 064021 Mrs.RADHA 27 G2P1L1P1 82 NIL + + - + NIL NIL NIL NIL NIL NIL NIL Not yet delivered

10 063731 Mrs.MEHARAJ BEGAM 21 PRIMI NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.75

11 055350 Mrs.KAVITHA 28 G7P0A6 NIL + - + NIL NIL NIL + NIL NIL NIL + 2.1

12 063913 Mrs.BHUVANESHWARI 32 G3P1L1A1 64.4 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.985

13 063459 Mrs.JAYANTHI 28 PRIMI 66 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL

14 062429 Mrs.BINDHU 34 PRIMI 75 + - + + NIL NIL

H/o

PCOD

+

NIL NIL NIL NIL 3

15 063533 Mrs.MAHESWARI 26 PRIMI 66 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.65

16 063500 Mrs.HEPSIBHA 22 PRIMI NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.48

Table-1 continued........


S.No. IP No. Name AGE (yr)GRA/

PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

17 063507 Mrs.VASANTHI 33 G2P1L1A0 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.1

18 063543 Mrs.VIJAYALAKSHMI 21 G2P0L0A1 64 NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL 2.8

19 063493 Mrs.DHIVYA SUNDARI 23 PRIMI 83 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.7

20 063178 Mrs.PONMANI 22 G2P0L0A1 68 NIL + - + + NIL NIL NIL NIL NIL + NIL 3

21 063504 Mrs.VIDHYA 24 PRIMI 64 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3

22 063446 Mrs.PARIMALA 29 PRIMI 57 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.3

23 064061 Mrs.RADHI PRIYA 22 PRIMI 62 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.5

24 062695 Mrs.SARANICA 26 PRIMI 50 NIL NIL - - NIL NIL

+ PDA

CARDIA

C

NIL NIL NIL NIL NIL 3.2

25 063447 Mrs.JAYALAKSHMI 30 G2P1L1A0 80 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.025

26 063413 Mrs.VASANTHAMANI 24 G2P1L1A0 63 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.8

27 063301Mrs.CHITRA

SUKUMARAN29 PRIMI NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.4

28 063306 Mrs.HEMA LATHA 28 G2P1L1A0 67 NIL NIL - - + NIL NIL + NIL NIL NIL NIL 3.36

29 063326 Mrs.CHITRA 33 G2P1L1A0 48 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 2.6

30 063347 Mrs.GUNASUNDARI 19 PRIMI 65 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.9

31 063352 Mrs.GANDHIMADHI 25 G2P1L1 76 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.2

32 063366 Mrs.VANITHA DINESH 25 PRIMI 61 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.6

33 063231 Mrs.RAJALAKSHMI 32 G3P2L1A0 68 NIL NIL - - NIL NIL + NIL NIL NIL NIL NIL 3.2

34 063436 Mrs.RATHINAM 30 G4P0L0A3 52 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL + 1.5

35 063239 Mrs.SHANMUGAPRIYA 22 G3P1L1A1 77 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3




PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

36 063229 Mrs.GANGARATHINAM 28 PRIMI 91 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.2

37 063221 Mrs.SUMATHI 28 G3P1L1A1 74.5 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.9

38 063168 Mrs.NANDHINI 22 PRIMI 75.5 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3

39 063163 Mrs.MAHALAKSHMI 25 PRIMI 77 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 2.9

40 060568 Mrs.DEVI 24 PRIMI 66 NIL + + - + NIL NIL + NIL NIL NIL NIL 2.5

41 060566 Mrs.GOMATHI 25 PRIMI 69 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.5

42 060568 Mrs.MUTHULAKSHMI 30 G3P1L1A1 67 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.1

43 Mrs.JAYASHRI 25 PRIMI 80 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.9

44 060548 Mrs.SANGEETHA RAVI 25 G2P1L1 65 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.3

45 060684 Mrs.RAJESWARI 25 PRIMI 60 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.2

46 060632 Mrs.HARIPRIYA 22 PRIMI 64 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.9

47 060630 Mrs.SUDHA 24 PRIMI 70 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3

48 060623 Mrs.SATHYA BAMA 28 G2P1A1 65 NIL + + - + - + + NIL NIL NIL NIL 3.1

49 060621 Mrs.ASHA 31 G3L1A1 66 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.9

50 060610 Mrs.CHITRALEKHA 21 PRIMI 78 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.4

51 060608 Mrs.SATHYA PRIYA 30 G3P1L1A1 74 NIL + + + NIL NIL NIL NIL NIL NIL NIL NIL 3.4

52 060609 Mrs.SHANTHI 25 PRIMI 62 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.8

53 060935 MRS.JAMUNARANI 26 G2P0L0A1 65 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.8

54 060907 MRS.JEPA 24 PRIMI 64 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 1.55

55 060878 MRS.GEETHA 32 PRIMI 96.5 NIL + + - + NIL NIL NIL NIL NIL NIL NIL 3.38




PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

56 060868 MRS.SAVITHA MURALI 25 PRIMI 63 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3

57 060859 MRS.LINDA JOSEPHINE 30 PRIMI 60 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 2.6

58 060840 MRS.KAVITHA 31 G2P0L0A0 68 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.2

59 060829 MRS.PALANIAMMAL 23 PRIMI 74.5 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3.5

60 060810 MRS.BABITHA 27 PRIMI 73.5 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 2.7

61 060809 MRS.SATHY 29 G3P1L1A1 77 NIL + - + + NIL NIL NIL NIL NIL NIL NIL 3.9

62 060807 MRS.KARUNAMBIGAI 23 G2P1L0A0 66 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.3

63 060773 MRS.ANANDHI 26 PRIMI 65 NIL NIL + NIL NIL + NIL NIL NIL NIL NIL NIL 2.8

64 060774 MRS.VISHNUPRIYA 26 PRIMI 81.5 NIL NIL - - - NIL NIL NIL NIL NIL NIL NIL 2.8

65 061240 MRS.JAYASUDHA 26 G2P2L1A0 69 NIL NIL - - - NIL NIL NIL NIL NIL NIL NIL 2.7

66 061216 MRS.KOUSALYA 26 G2P1L1A0 61 NIL NIL - - - NIL NIL + NIL NIL NIL NIL 2.28

67 061345 MRS.UMA MAHESWARI 26 PRIMI 76 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.39

68 061517 MRS.SUBABIJU 26 PRIMI 40.4 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.6

69 061392 MRS.JANAKI 25 PRIMI 57 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 3

70 061259 MRS.VASANTHAMANI 35 PRIMI 71 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.3

71 061245MRS.MEERA

ANANDHAKUMAR27 PRIMI 81 NIL NIL - - + NIL NIL NIL NIL NIL NIL NIL 3.3

72 061060 MRS.GEETHA 21 PRIMI 51 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL NIL 2.1

73 061412 MRS.JAGATHEESWARI 25 PRIMI 68 NIL NIL - - NIL NIL - + NIL NIL NIL NIL 3.1

74 061105 MRS.AGNESPUSPHA 28 PRIMI 71 NIL NIL - - + NIL NIL NIL NIL NIL NIL 2.8

75 061241 MRS.SAMPOORNAM 31 G2P1L1A0 80 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL 3.1




PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

76 061000 MRS.SINDHU 29 PRIMI NIL NIL - - + NIL NIL NIL NIL NIL NIL 2.6

77 061124 MRS.MOHANAPRIYA 24 PRIMI 64 NIL NIL - - - NIL NIL NIL NIL NIL NIL 2.7

78 061141 MRS.SONIBATNA 26 G2P1L1A0 55 NIL NIL - - + - NIL NIL NIL NIL NIL 2.5

80 064167 MRS.CHANDARAKALA 29 G3P2L1A2 81.5 NIL NIL - - + NIL NIL NIL + NIL NIL 4.4

81 064276 MRS.MAHESWARI 31 G2P1L1A0 86 NIL NIL - - NIL NIL NIL NIL NIL NIL NIL 3.4

82MRS.ANGES PUSHPA

PRABA27 PRIMI 71 NIL NIL - - + - NIL NIL - 2.9

83 MRS.MOHANA PRIYA 24 PRIMI 64 NIL NIL - - NIL NIL NIL NIL NIL 2.7

84 MRS.ANITHA 26 PRIMI 77 NIL + - + NIL NIL NIL NIL NIL 1.7

85MRS.MEENAKSHI

MYTHILI23 PRIMI 23 NIL NIL - - NIL NIL NIL NIL NIL 2.9

86 MRS.ANU REKHA 24 G3P1L1A1 NIL NIL - - NIL NIL NIL NIL NIL 2.9

87 MRS.ANJU 29 PRIMI NIL NIL - - + NIL NIL NIL NIL 2.6

88 MRS.RENUKHA DEVI 26 G3P2L1A0 NIL NIL - - NIL NIL NIL NIL NIL 2.5

89 MRS.GEETHA 24 PRIMI NIL NIL - - NIL NIL NIL NIL NIL 2.1

90 MRS.SONI BAFNA 24 PRIMI 55 NIL NIL - - + NIL NIL NIL NIL 2.49

91 MRS.KAVITHA 29 G3P1L1A1 72 NIL NIL - - NIL NIL NIL NIL NIL 3.1

92 MRS.JOTHIMANI 23 PRIMI 65 NIL NIL - - NIL NIL NIL NIL NIL 3.3

93 MRS.VANITHA 30 PRIMI 70.5 NIL NIL - - NIL NIL NIL NIL NIL 2.7

94 MRS.HEMAPRIYA 20 PRIMI 69 NIL NIL - - NIL NIL NIL NIL NIL 3.6

95MRS.DHIVYA

RAJKUMAR25 PRIMI 65 NIL NIL - - NIL NIL NIL NIL NIL 2.3



PARA

W

(kg)

H/o

DM

H/o

GDMTreatment

Family

H/o DM

H/o still

birth baby

H/o

congenetal

abnormalit

y

H/o

irregular

periods

Sibling

H/o DM

H/o big

baby

H/o

polyhydra

mnios

H/o BOHBirth weight

(kg)

96 MRS.KAVITHA 23 PRIMI NIL NIL - - + NIL NIL NIL NIL 3.1

97 060840 MRS.KAVITHA 31 G2P0L0A1 NIL + NIL NIL NIL NIL 3.2

98 060831 MRS.VASANTHI 25 65 NIL + NIL NIL NIL NIL 1.69

99 MRS.SAGUNTHALAI 25 G3P1L1A1 NIL NIL NIL NIL NIL 3.3

100 061093 MRS.RENUKA DEVI 34 G3P2L1A0 84 NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL 2.5

101 061060 MRS.GEETHA 24 51 NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL NIL 2.1

Blank spaces indicate missing data; (+) sign indicates the presence of a particular abnormality; (-) sign indicates the absence of a particular abnormality;

In case of insultin/diet control treatment, (+) sign indicates insulin administration/diet control, and (-) sing indicates no treatment.

GRA/PARA:

G - Number of times pregnancy has taken place.

P - Number of times pregnancy has taken place with successfull delivery.

L - Number of living children before pregnancy.

A - Number of abortions.

H/o DM: History of diabetes mellitus. H/o irregular periods: History of irregular periods.

H/o GDM: History of gestational diabetes mellitus. Sibling H/o DM: Sibling history of diabetes mellitus.

Family H/o DM: Family history of diabetes mellitus. H/o big baby: History of big babies (macrosoma).

H/o still birth baby: History of still birth babies. H/o polyhydramnios: History of polyhydramnios.

H/o congentical abnormality: History of congenetical abnormality in H/o BOH: History of bad obstetric history.

delivered child. Birth weight: Birth weight of the baby.

Fig.1. Grouping by factors

---------------------------

Cluster Membership of Cases using Ward Method

Due to missing data, some cases have been excluded from computations.

Data Information

71 unweighted cases accepted.

29 cases rejected because of missing value.

Absolute Binary Squared Euclidean measure used.

Number of Clusters

Label Case 5

BIGBABY 1 1

BOH 2 1

C_ABNORM 3 1

DIET 4 2

DM 5 1

FDM 6 3

GDM 7 4

I_PERIOD 8 5

INSULIN 9 4

POLY 10 1

S_DM 11 1

SB_BABY 12 1

* * * * * * H I E R A R C H I C A L C L U S T E R A N A L Y S I S * * * * * *

Dendrogram using Ward Method

Rescaled Distance Cluster Combine

C A S E 0 5 10 15 20 25

Label Num +---------+---------+---------+---------+---------+

DM 5

S_DM 11

BIGBABY 1

SB_BABY 12

POLY 10

BOH 2

C_ABNORM 3

GDM 7

INSULIN 9

DIET 4

I_PERIOD 8

FDM 6

Fig-2: Grouping of Patients

Dendrogram using Ward Method

Absolute Binary Squared Euclidean measure used.

Due to missing data, some cases have been excluded.

71 unweighted cases accepted.

29 cases rejected because of missing value.

Rescaled Distance Cluster Combine

C A S E 0 5 10 15 20 25

Label Num +---------+---------+---------+---------+---------+

Mrs.RENUKA DEVI 99

Mrs.GEETHA 100

Ms.S.SAVITHA 1

Mrs.VASANTHAMANI 70

Mrs.GEETHA 72

Mrs.SUBABIJU 68

Mrs.JANAKI 69

Mrs.VISHNUPRIYA 64

Mrs.JAYASUDHA 65

Mrs.PALANIAMMAL 59

Mrs.KARUNAMBIGAI 62

Mrs.SHANTHI 52

Mrs.JAMUNARANI 53

Mrs.SUDHA 47

Mrs.ASHA 49

Mrs.RAJESWARI 45

Mrs.HARIPRIYA 46

Mrs.JAYASHRI 43

Mrs.SANGEETHA RAVI 44

Mrs.GOMATHI 41

Mrs.MUTHULAKSHMI 42

Mrs.GANGARATHINAM 36

Mrs.SUMATHI 37

Mrs.VANITHA DINESH 32

Mrs.SHANMUGAPRIYA 35

Mrs.GUNASUNDARI 30

Mrs.GANDHIMADHI 31

Mrs.JAYALAKSHMI 25

Mrs.VASANTHAMANI 26

Mrs.PARIMALA 22

Mrs.RADHI PRIYA 23

Mrs.VIJAYALAKSHMI 18

Mrs.VIDHYA 21

Mrs.HEPSIBHA 16

Mrs.VASANTHI 17

Mrs.JAYANTHI 13

Mrs.MAHESWARI 15

Mrs.MEHARAJ BEGAM 10

Mrs.BHUVANESHWARI 12

Mrs.RIPAYA 7

Mrs.RATHINAM 34

Mrs.SARANICA 24

Mrs.RAJALAKSHMI 33

Mrs.KOUSALYA 66

Mrs.JAGATHEESWARI 73

Mrs.HEMA LATHA 28

Mrs.KAVITHA 11

Mrs.UMA MAHESWARI 67

Mrs.MEERA ANANDHAKUM 71

Mrs.FRAZANA 6

Mrs.KAVITHA 58

Mrs.BABITHA 60

Mrs.SAVITHA MURALI 56

Mrs.LINDA JOSEPHINE 57

Mrs.CHITRALEKHA 50

Mrs.JEPA 54

Mrs.NANDHINI 38

Mrs.MAHALAKSHMI 39

Mrs.CHITRA SUKUMARAN 27

Mrs.CHITRA 29

Mrs.DHIVYA SUNDARI 19

Mrs.SAKUNTHALA 8

Mrs.PONMANI 20

Mrs.SATHY 61

Mrs.AKILANDESHWARI 5

Mrs.RADHA 9

Mrs.GEETHA 55

Mrs.DEVI 40

Mrs.SATHYA BAMA 48

Mrs.SATHYA PRIYA 51

Mrs.ANANDHI 63

0

10

20

30

40

50

60

70

80

90

Number of

patients

affected

Fig.3: Classification of patients with

respective afflictions

Series1 0 16 6 8 34 2 3 7 1 1 2 3 83

1 2 3 4 5 6 7 8 9 10 11 12 13

The numbers 1, 2, 3, …..13, indicates categories as described below, with corresponding number of patients affected under each category.

1 - Patients with a history of diabetes mellitus.

2 - Patients with a history of gestational diabetes mellitus.

3 - Patients put under diet control.

4 - Patients administered with insulin.

5 - Patients with a family history of diabetes mellitus.

6 - Patients with a history of still borne babies.

7 - Children with congenital abnormalities.

8 - Patients with irregular periods.

9 - Patients with a sibling history of diabetes mellitus.

10 - Patients with a history of big babies.

11 - Patients with polyhydramnios.

12 – Patients with bad obstetric history.

Documents

Maternity Healthcare for Patients with Gestational Diabetes