“ANTHROPOMETRY,
MORBIDITY AND MORTALITY AMONG THE
INFANTS OF DIABETIC MOTHERS IN A
TERTIARY CARE CENTRE”
Dissertation submitted to
THE TAMIL NADU DR. M.G.R. MEDICAL UNIVERSITY
In partial fulfillment for the award of the degree of
DOCTOR OF MEDICINE
IN
PAEDIATRICS
BRANCH VII
GOVERNMENT THENI MEDICAL COLLEGE AND HOSPITAL
THENI
APRIL 2016
CERTIFICATE
This is to certify that the dissertation entitled
“ANTHROPOMETRY, MORBIDITY AND MORTALITY AMONG
THE INFANTS OF DIABETIC MOTHERS IN A TERTIARY
CARE CENTRE” submitted by Dr.P.KAMALANATHAN to the
Faculty of Paediatrics, The Tamil Nadu Dr. M.G.R. Medical University,
Chennai in partial fulfillment of the requirement for the award of M.D.
Degree Branch VII (Paediatrics) is a bonafide research work carried out
by him under our direct supervision and guidance.
PROF.DR.M.BALASUBRAMANIAN., PROF.DR.NANDINI KUPPUSAMY., M.D.,DCH., M.D.,DCH., Unit Chief, Professor and Head, Department of Paediatrics, Department of Paediatrics, Government Theni Medical College Government Theni Medical College & Hospital, Theni. & Hospital, Theni.
PROF.DR.K.KATHIRKAMU.,M.S,.
DEAN
GOVERNMENT THENI MEDICAL COLLEGE AND HOSPITAL
THENI
DECLARATION I,Dr.P.KAMALANATHAN solemnly declare that the dissertation
titled “ANTHROPOMETRY, MORBIDITY AND MORTALITY
AMONG THE INFANTS OF DIABETIC MOTHERS IN A
TERTIARY CARE CENTRE” has been prepared by me. This is
submitted to The Tamilnadu Dr.M.G.R. Medical University, Chennai
in partial fulfillment of the rules and regulations for the M.D.Degree
Examination in Paediatrics.
Place : Theni
Date :
DR.P.KAMALANATHAN
ACKNOWLEDGEMENT
It is with immense pleasure and privilege that I express my heartful
gratitude, admiration and sincere thanks to Prof. Dr.NANDINI
KUPPUSAMY, Professor and Head of the Department of Pediatrics, for
her guidance and support during this study.
I am greatly indebted to my guide and teacher, Prof.
Dr.M.BALASUBRAMANIAN, Professor of Pediatrics, for his
supervision, guidance and encouragement while undertaking this study..
I express my sincere thanks and gratitude to Prof. Dr.M.RAJA
RAJESWARAN for his support and for his guidance, supervision,
constant encouragement and support throughout this study.
I wish to express my sincere thanks to Professor
Dr.S.NATARAJA RATHINAM for his valuable suggestions and
support.
I would like to thank Prof. Dr.C.SHANTHA DEVI,
Prof. Dr.M.THANGAMANI, Asst. Professors Dr.SHANTI RANI,
Dr.SHANTAVIBALA, Department of Obstetrics for their kind co-
operation.
I also thank all the members of the Dissertation Committee for
their valuable suggestions.
I gratefully acknowledge the help and guidance received from
Sr.Asst.Professor Dr.D.SIVAKUMARAN and Asst. Professors
Dr.S.SANGEETH, Dr.P.RAGUPATHY, Dr.R.ELANGOVAN,
Dr.A.VIDHYA DEVI, Dr.P.PERIYASAMY, Dr.M. KRITHIKA, and
Dr.R.JEGADHESH for their constant support and suggestions during
this study.
I thank the Dean and the members of Ethical Committee,
Government Theni Medical College and Hospital, Theni for permitting
me to perform this study.
I thank all the parents and children who have ungrudgingly lent
themselves to undergo this study without whom this study would not
have seen the light of the day.
ABBREVIATIONS
AACE - American Association of Clinical Endocrinologists
ACOG - American College of Obstetrics and Gynaecologists
ADA - American Diabetic Association
AGA - Appropriate for gestational age.
ASH - Asymmetric septal hypertrophy
CBG - Capillary blood glucose
CCHD - Complex cyanotic congenital heart disease
CNS - Central nervous system.
COA - Coarctation of aorta.
5% D - 5 % dextrose.
DM - Diabetes mellitus.
EBM - Expressed Breast Milk
ECG - Electrocardiography.
(eg) - Example.
Etc - Et cetera.
FBS - Fasting blood sugar.
GCT - Glucose challenge test.
GDM - Gestational diabetes mellitus.
GIR - Glucose infusion rate
GIT - Gastrointestinal tract.
HbA1C - Glycosylated haemoglobin.
HCT - Hematocrit.
HOCM - Hypertrophic cardiomyopathy.
Hr - Hour
IDDM - Insulin dependent diabetes mellitus.
IUD - Intrauterine death.
IV - Intravenous
IVASH - Interventricular asymmetric septal hypertrophy
LGA - Large for gestational age.
LN - Labour naturalis.
LSCS - Lower segment caesarean section
MAC:HC ratio - Midarm circumference:Head circumference ratio
MgSO4 - Magnesium sulphate
MSAFP - Maternal serum Alpha Feto protein
NICU - Neonatal intensive care unit.
OGTT - Oral glucose tolerance test
PCR - Protein Creatinine Ratio
PCV - Packed cell volume.
PDA - Patent ductus arteriosus
PGDM - Pregestational Diabetes Mellitus
PET - Partial exchange transfusion
PI - Ponderal index
PPBS - Post prandial blood sugar.
RBS - Random blood sugar
RD - Respiratory Distress
SBR - Serum bilirubin
SGA - Small for gestational age.
T3, T4 - Triiodothyronine, Thyroxine
TAPVC - Total anomalous pulmonary venous connection
TSH - Thyroid stimulating hormone
TTN - Transient tachypnoea of newborn
USG - Ultrasonogram
Wks - Weeks.
CONTENTS
S. NO. CONTENTS PAGE NO.
1 INTRODUCTION 1
2 REVIEW OF LITERATURE 2
3 TITLE OF THE STUDY 43
4 AIM OF THE STUDY 44
5 MATERIALS AND METHODS 45
6 RESULTS AND OBSERVATION 50
7 DISCUSSION 79
8 CONCLUSION 86
9 LIMITATIONS 87
10 FUTURE IMPLICATIONS 88
11 ANNEXURES
Bibliography
Master Chart
Proforma
1
INTRODUCTION
Diabetes mellitus is one of the medical complications commonly
associated with pregnancy. It increases fetal and maternal complications
in pregnancy. Improved health care and advances in the management of
diabetes have reduced the incidence of adverse perinatal outcome in
IDM. However rise in the prevalence of gestational diabetes worldwide
could have enormous implications for the babies born to these mothers1
Prevalence of gestational diabetes mellitus varies worldwide and
within racial and ethnic groups. In India the prevalence of gestational
diabetes is high (16.55%) when compared to western countries2 (6-7%).
Around 85% of the diabetes mellitus in pregnancy are found to be
gestational diabetes. Out of overtly diabetic cases 35% are Type 1 DM
and remaining 65% are of Type 2 DM.
2
REVIEW OF LITERATURE
Diabetes mellitus is following a secular trend and is becoming a
global pandemic. As a corollary, the incidence of gestational diabetes is
also on the rise worldwide with majority of cases being reported in Indian
subcontinent. Diabetes during pregnancy is associated with various
maternal and fetal complications. With advent of insulin and various tests
available for screening of diabetes and assessment of fetal well being,
management of gestational diabetes has improved over past decades.
Well controlled maternal diabetes is associated with reduction in maternal
and fetal morbidity and mortality. Various studies have been performed
worldwide comparing clinical profile of mother, clinical profile of infant
and the occurrence of various complications to find the association of
various factors affecting the outcome of newborn thereby intervening at
that level to improve neonatal morbidity.
In Ranade et al study of “Infant of diabetic mothers – An analysis
of 50 cases” 64% of mothers had gestational diabetes and 36% had
pregestational diabetes. Hypoglycemia was the most common
complication and was observed in 50% of infants. 40% babies were
macrosomic, 36% were preterm, 20% had polycythemia, 18% had birth
injury, 14% had hypocalcaemia, 14% had RDS, 8% had
3
hyperbilirubinemia, 4% had congenital anomalies.58% babies were
delivered by cesarean section and mortality rate was observed to be 20%.
In YangJ et al study of “Fetal and neonatal outcome in diabetic
pregnancy" comparing mothers with gestational diabetes to non diabetic
mothers, 45.2% of IDM babies were macrosomic whereas only 12.6%
were macrosomic in non diabetic group. Incidence of congenital
anomalies were 9.1% in IDM compared to 3.1% in non diabetic
group.17.4% mortality rate was observed in diabetics compared to only
5.9 % in non diabetics.
In Mohammed Hussain et al study of “Frequency of various
complications in neonates” born to mothers with gestational diabetes and
pregestational diabetes 40.4% were macrosomic with 23.8% in mothers
with gestational diabetes and 16.6% in mothers with pregestational
diabetes. Birth injury was observed in 19% babies born to diabetic
mothers compared to 14% babies born to mothers with pregestational
diabetes. Hypoglycemia was observed in 23.8%, hyperbilirubinemia in
19%, hypocalcaemia in 16.6%, RDS in 15%, polycythemia in 12% and
congenital heart disease in 4.7%.
In a study by Mahmood CB et al titled “Problems and immediate
outcome of infant of diabetic mothers” comparing women with
gestational diabetes and mothers with overt diabetes, hypoglycemia
4
occurred in 23% of pregnancies, with higher incidence in pregestational
group (38.09%) compared to 12.9 % with gestational diabetes. Incidence
of polycythemia was also higher in pregestational diabetes (25.8%)
compared to 9.5% in gestational diabetes.82.6% babies were delivered by
cesarean section, 21% were macrosomic, 19.2% had hypocalcaemia, 5.7
% had congenital anomalies. Mortality rate was found to be 5.7%.
In AK Deorari et al study “Perinatal outcome of infants born to
DM” comparing GDM and PDGM, hypoglycemia was the commonest
complication (43%) and had a higher incidence in infants born to women
with PDGM (21%) than infants born to women with GDM(16%).39.5%
were macrosomic in pregestational group compared to 17.5% in
gestational diabetes. Incidence of birth asphyxia(18% vs. 8%),
polycythemia(11%vs 8%), RDS(5.2% vs. 3.5%) were all higher in infants
born to women with PDGM than those born to women with GDM. 5%
babies were born by cesarean section to overtly diabetic mothers
compared to 4% babies born to gestational diabetes mothers.
In Aklagi et al study comparing women with PDGM and GDM
incidence of cesarean section was more in PDGM. Macrosomia was more
associated with gestational diabetes 14.8% vs 6.8% in pregestational
diabetes. Occurrence of other fetal complications like hypoglycemia
5
(21.9% vs. 18.5%), RDS (13.6% vs. 3.7%) and congenital anomalies
(12.3% vs. 3.7%) were more in women with pregestational diabetes.
In AK Shefali et al study also macrosomia was observed more in
gestational diabetes (27.6 %) than in those with pregestational diabetes
(19.2%). Incidence of congenital anomalies was higher in pregestational
group (3.8%vs1.4%).
In Nili Firouzeh et al study prevalence of diabetes was 2.39% with
69% GDM and 31% PGDM. Out of complications hypoglycemia had the
highest incidence of 31% with the incidence of other complications being
34% for hyperbilirubinemia, 13% for hypocalcaemia, 8.2% for birth
asphyxia, 6.8% polycythemia . 28.6% babies were found to be LGA. The
incidence of morbidities was higher in infants born to mothers with
PGDM. The incidence of hypoglycemia, hypocalcemia and birth
asphyxia babies were significantly higher in GDM babies compared to
PGDM. There was also a significant correlation between the incidence of
hypoglycemia and birth weight of infants (p< 0.05).
6
CLASSIFICATION OF DIABETESMELLITUS IN PREGNANCY:
Diabetes mellitus in pregnancy is classified into 2 types. They are
1. PREGESTATIONAL DIABETES OR OVERT DIABETES:
i.Type–1 (IDDM) is characterized by young age onset (Juvenile)
and absolute insulinopenia. They have genetic predisposition with
presence of autoantibodies. It is rarely diagnosed during pregnancy. It
most often presents with unexpected coma if diagnosed for the first time
during pregnancy.
ii.Type–2 (NIDDM) is characterized by late age of onset,
overweight woman and peripheral tissue (skeletal muscle, liver) insulin
resistance (hyper insulinemia). Genetic predisposition is also observed.
2. GESTATIONAL DIABETES:
Gestational Diabetes Mellitus (GDM) is defined as ‘carbohydrate
intolerance with recognition or onset during pregnancy’, irrespective of
the treatment with diet or insulin. (ACOG, 2013). This definition also
includes some women with previously unrecognized overt diabetes.
GDM poses risk of developing diabetes in 2 subsequent generations.
Women with gestational diabetes have risk of developing Type 2 DM.
7
In 1949, Dr. Priscilla White developed the system of classification of
diabetes complicating pregnancy. Although less important now to guide
the treatment, her classification system is still useful and widely used3.
Table: WHITE’S CLASSIFICATION OF MATERNAL DIABETES
(REVISED)
Gestational diabetes Diabetes not known to be present before pregnancy
Abnormal glucose tolerance test in pregnancy
GD diet Euglycemia maintained by diet alone
GD insulin Diet alone insufficient; insulin required
Class A Chemical diabetes; glucose intolerance before pregnancy, treated by diet alone, rarely seen
Prediabetes; history of large babies >4 kg or unexplained stillbirths after 28 weeks
Class B Insulin dependent; onset after 20 years of age, duration<10 years
Class C C1:onset at 10-19 years of age
C2:duration 10-19 years
Class D D1:onset before 10 years of age
D2:duaration 20 years
8
The potential candidates for GDM are:
(a) Unexplained perinatal loss
(b) Ethnicity (East Asian, Pacific island ancestry)
(c) Overweight baby in previous pregnancies (>=4kg)
(d) Hyperplasia of pancreatic islets in previous stillborn.
(e) Positive family history of diabetes (parents, grandparents,
siblings, uncles and aunts)
(f) Current pregnancy being complicated by polyhydramnios or
D3:calcification of vessels of leg
D4:benign retinopathy
D5:hypertension(not preeclampsia
Class F Nephropathy with >500 mg proteinuria
Class R Progressive retinopathy or vitreous haemorrhage
Class RF Criteria for F and R coexist
Class G Many reproductive failures
Class H
Clinical evidence of arteriosclerotic heart disease
Class T Prior renal transplantation
9
vaginal candidiasis
(g) Persistent glycosuria
(h) 30yrs and above
(i) Obese mothers
PATHOPHYSIOLOGY IN DIABETIC PREGNANCY:
Metabolic changes in normal pregnancy:
Following each meal there occurs several changes in hormones in
pregnancy. With intake of meal, blood sugar level rises followed by
secretion of hormones like glucagon, somatomedin, catecholamine and
insulin, leading to adequate supply of glucose.
The pregnant women tend to develop hypoglycemia between meals
and during sleep compared with non pregnant women. Both during meal
intake and fasting, fetus derives its glucose from mother by facilitated
diffusion across placenta. As pregnancy advances with fetal growth, fetal
nutritional (glucose) needs increases resulting in increased maternal
hypoglycemia in-between meals.
During 2nd and 3rd trimesters, levels of placental hormones like
progesterone, estrogen etc . increase, which increases insulin resistance.
10
So the need for insulin secretion with meals increases in the mother
progressively in the pregnancy.
Table: Diabetogenic hormones in pregnancy4
Hormone Peak level Diabetogenic Potency
Prolactin 10 Weak
Estradiol 26 Very weak
Cortisol 26 Very strong
Progesterone 32 Strong
Metabolic changes in diabetic pregnancy:
In Diabetes, because of inadequate insulin secretion or insulin
resistance hyperglycemia occurs, which is more pronounced following
meals. This maternal hyperglycemia is accompanied by fetal
hyperglycemia which stimulates beta cells of pancreas resulting in
increased insulin levels in fetus. Insulin being anabolic hormone causes
increased fetal growth and deposition of fat. Since oxygen is needed in
the process of conversion of glucose to fat, there is increased oxygen
demand resulting in hypoxia. Hypoxia in turn stimulates catecholamine
synthesis resulting in hypertension, increased erythropoietin synthesis,
raised hematocrit and hypertrophy of myocardium.
11
EFFECTS OF DIABETES ON PREGNANCY
• Maternal • Fetal and Neonatal
MATERNAL
During pregnancy:
Abortion: Recurrent spontaneous abortion may be associated with
uncontrolled diabetes.
Preterm labor (20%) may be due to infection or polyhydramnios.
Infection: Urinary tract infection and vulvo vaginitis.
Increased incidence of pre-eclampsia (25%): More common in
PGDM; occurring 2-3 times more frequently than in non diabetic
women ; dependent upon duration and severity of diabetes
Polyhydramnios (25–50%): increased blood sugar levels in fetus
increases the osmolality resulting in diuresis.
Maternal distress may be due to the combined effects of the large
baby and increased amniotic fluid.
Diabetic retinopathy, micro aneurysms, hemorrhages and
proliferative retinopathy. Laser photocoagulation is the preferred
treatment.
Diabetic nephropathy—may lead to renal failure.
Ketoacidosis
12
During labor:
There is increased incidence of:
Shoulder dystocia: due to disproportionate growth with increased
shoulder/head ratio.
Prolongation of labor due to macrosomia.
Perineal injuries.
Postpartum hemorrhage.
Operative interference.
During Puerperium:
Puerperal sepsis.
Lactation failure
SCREENING FOR DIABETES IN PREGNANCY:
Universal screening is more advantageous over selective screening
since it improves outcome of mother and baby5.A 11fold higher risk of
developing diabetes in pregnancy is noted in Indian Women compared to
Caucasian women.6 Prevalence of gestational diabetes in India7 is 16.5%.
So screening is essential for all pregnant women in India. Screening is
routinely done between 24-28wks of pregnancy.
13
*The Diabetes In Pregnancy Study group India (DIPSI) Guidelines:
The current guidelines say that screening for Diabetes should be
done in 1st trimester since fetal response to maternal hyperglycemia by
insulin secretion starts at 16 wks of pregnancy. If the test results are
negative then repeat testing is indicated at around 24-28wks and then at
around 32-34wks. The method employed is Oral Glucose Challenge Test
(50gm) without any consideration to time of day or last feed. A 140 mg/dl
of plasma glucose or 130 mg/dl of whole blood at 1 hour is considered as
cut off point for consideration of a 100 gm (WHO 75gm) glucose
tolerance test.
* Screening Strategy Based on Risk Assessment: (Recommended by
Fifth International Workshop-Conference on Gestational Diabetes)
Categorization of diabetic women into low, average and high risk
should be done at 1st visit.
Low Risk:
Blood sugar monitoring is not routinely recommended if all of the
following criteria are met:
Ethnicity having low prevalence rate
Absence of diabetes in 1st-degree relatives
Below 25 years of age
Normal prepregnancy weight
14
Normal birth weight
Good obstetric history
Average Risk:
Blood sugar monitoring at 24 to 28 wks by:
Two-step procedure: 50-g GCT, followed by a 100-g OGTT for
those meeting the threshold value in the GCT
One-step procedure: 100-g OGTT for all women having average
risk
High Risk:
Blood sugar monitoring done as soon as possible, by either of the above
mentioned methods, if one or more of the following criteria are met:
Morbidly obese
Strong h/o type 2 DM in the family
history of Gestational diabetes , impaired glucose tolerance test, or
glucosuria in previous pregnancies.
If tests are negative then repeat testing is done at 24 – 28wks or if
signs and symptoms of GDM occur.
15
DIAGNOSIS OF DIABETES MELLITUS IN PREGNANCY:
Criteria for diagnosis of impaired glucose tolerance and diabetes with
75 gm oral glucose
(American Diabetic Association)
Plasma (mg %)
Time Normal
tolerance
Impaired glucose
tolerance Diabetes
Fasting <100 ≥100 and <126 ≥126
2 hours Post
glucose <140 ≥140 and <200 ≥200
• Venous whole blood values are 15% less than the plasma
Criteria for diagnosis of GDM
(Fifth International Workshop Conference on Gestational Diabetes)
Oral Glucose Load
Time 100 g Glucose 75 g Glucose
Fasting 95 mg/dl 95 mg/dl
1-hr 180 mg/dl 180 mg/dl
2-hr 155 mg/dl 155 mg/dl
3-hr 140 mg/dl -
Two or more of the venous plasma glucose concentrations listed must be
met or exceeded for a positive diagnosis.
16
ANTENATAL FOLLOW UP:
Following diagnosis of diabetes pregnant women should be followed up
throughout pregnancy for sugar control and fetal well being:
TESTS TO BE DONE IN FIRST TRIMESTER
Capillary blood sugar levels
Blood urea and Sr.creatinine levels
Glycated hemoglobin
TSH
Free T3 and T4
Spot PCR
Ultrasonographic assessment for pregnancy dating and viability
TESTS TO BE DONE IN SECOND TRIMESTER
Spot urine PCR study in women with elevated value in first
trimester
Repeat HbA1C
Capillary blood sugar levels
Ultrasonography- Detailed anatomic ultrasonogram at 18-20 weeks
Fetal echocardiography: It is an important because the incidence of
congenital cardiac anomalies is five times greater in infants of
mothers with diabetes.
17
MSAFP determination: at 16 to 20 weeks with targeted
sonographic examination at 18 to 20 weeks to identify neural-tube
anomalies.
TESTS TO BE DONE IN THIRD TRIMESTER:
Fetal growth assessment by USG:
In PGDM cases starting at 26 wks should be done once in 4 wks.
In GDM cases must be done at 36-37 wks.
ECG:
In overtly diabetic cases of long duration or in presence of
microvascular complications ECG and echo should be done.
MANAGEMENT OF DIABETES IN PREGNANCY:
PRECONCEPTIONAL COUNSELLING:
The goal of management in preconceptional period is to counsel
the mother and plan the diet and treatment for her to achieve glycemic
control before pregnancy. The incidence of fetal congenital
malformations are lowered significantly (0.8-2%) in women with strict
sugar control in antenatal period. This should be emphasized in the
counseling and self glucose monitoring should be taught. Advice should
be given regarding diet and insulin. She should also be instructed about
complications like diabetic retinopathy and nephropathy and potential
fetal complications.
18
Table: Preconceptional sugar values as recommended by ADA
Time Values(mg/dl)
Pre-prandial 70-100
Postprandial 100-129
Mean <110
HbA1c levels indicate glycemic control over past 4 to 8 wks and it
can be used for assessment of early metabolic control and should be kept
below 7%.
ANTENATAL MANAGEMENT OF DIABETES:
Insulin is indicated for overtly diabetic cases. Gestational diabetes
can be treated with diet alone in milder cases and insulin is indicated in
complicated cases with poor glycemic control.
DIET:
According to ACOG guidelines it should be given as 40%
carbohydrate, 20% protein and 40% fat.
Table: Calorie requirement in diabetic women according to weight
WEIGHT CALORIE (Kcal/Kg)
Normal 30
Overweight 24
Morbid 12
19
EXERCISE:
As per ACOG guidelines moderate exercise should be practiced by
all women with gestational diabetes as a part of treatment.
ORAL HYPOGLYCEMIC AGENTS:
As per ACOG guidelines glyburide and metformin can be used as
first line agents as insulin in women with gestational diabetes
INSULIN:
Table: Indications for Initiation of Insulin in Gestational Diabetes
Time of measurement ADA guidelines8
(mg/dl)
ACOG guidelines
(mg/dl)
Fasting plasma glucose >105 >95
1 hr postprandial plasma glucose >155 >140
2 hr postprandial plasma glucose >130 >120
Insulin is initiated at a dose of 0.7-1U/kg/day in divided doses as a
mixture of short and intermediate acting insulin. The dose is then adjusted
based on blood sugar monitoring.
20
Table: Insulin Options Safe during Pregnancy9
Name Type Onset Peak
effect Duration Dosing
interval
Aspart Rapid 15min 60min 2hrs Start of each meal
Lispro Rapid 15min 60min 2hrs Start of each meal
Regular Intermediate 60min 2-4hrs 6hrs 60-90mins before meal
NPH Intermediate 2hrs 4-6hrs 8hrs Every 8hrs
Detemir Long 2hrs n/a 12hrs Every 12 hrs
Table: Glycemic target during pregnancy as set by AACE10 & ADA11 guidelines
Glucose Increment Patients with GDM (mg/dl)
Patients with T1 or T2 DM
(mg/dl)
Pre-prandial <95 Premeal, bedtime and
overnight glucose 60-99
Postprandial 1 hr postmeal<140
2 hr postmeal<120
Peak postprandial
glucose
100-129
21
MANAGEMENT DURING LABOUR:
In case of well controlled diabetes admission is done at 34 to 36
wks. Earlier admission is indicated in case of poorly controlled diabetes
and in presence of obstetric complications. Earlier admission has the
advantages of
i. achieving good glycemic control
ii. controlling other co-morbid conditions like pre-eclampsia and
polyhydramnios
iii. planning mode and time of delivery.
All such cases should be monitored for fetal well being by daily
fetal movement count and fetal heart rate monitoring done three times a
week.
Wait and watch can be followed till term and no pregnancy should
be allowed to progress beyond the expected date of delivery. Continuous
fetal monitoring is essential during labor and is done by CTG using a
scalp electrode. An arbitrary time of 12 hours is allowed for progression
of labour beyond which augmentation is done using rupture of
membranes or oxytocin drip or pregnancy is terminated by cesarean
section.
22
In well controlled cases induction is done at 38 weeks and in those
with vascular complications (PIH and IUGR) induction is done at 37
weeks, after ruling out obstetric contraindications for normal delivery.
Method of induction is by low rupture of membranes.
Watchful expectancy for spontaneous onset and progression of
labour can be followed in cases of:
i. young primigravida
ii .multigravida with good obstetric history
iii. well controlled diabetes
iv. absence of obstetric contraindications for normal delivery.
Cesarean section is indicated in cases of:
i. elderly primi
ii. multigravida with a bad obstetric history
iii. poorly controlled maternal diabetes
iv. diabetes with obstetric complications like polyhydramnios, pre-
eclampsia and malpresentation.
v. fetal macrosomia.
23
Insulin should be continued till the day before induction or
cesarean section. On the day on induction or cesarean, insulin is stopped
and a meal is skipped. Intravenous normal saline infusion is started and
continued till the time before onset of labour in case of induction. An
oxytocin drip can be started simultaneously. Sugar control can be
achieved by either
1. subcutaneous insulin drip to deliver insulin at a rate of
0.25 to 2 U/hr
(or)
2. by adding 10 units of soluble insulin to 1 litre of 5% intravenous
dextrose and setting the drip at an infusion rate of 100 to 125 ml/hr
to deliver insulin at a rate of 1 to 1.25 U/hr12
Blood glucose monitoring is done hourly and insulin is titrated
accordingly to maintain sugar levels between 80-100mg/dl.
Table: General guidelines for achieving blood glucose control using
insulin drip:
Rate Of Insulin (Units/hr)
Level Of Blood Glucose (mg/dl)
1 100-140
2 141-180
3 181-220
24
MANAGEMENT DURING PUERPERIUM:
Immediately following delivery insulin resistance falls and
requirement of insulin drops dramatically to an extent that insulin may
not be needed in the initial 24 hours, following which insulin requirement
fluctuates. Once the capillary blood glucose starts to rise insulin is started
at one half to two thirds of the antenatal dose and titrated according to the
sugar values.
Prophylactic antibiotics are indicated to control infection.
Breast feeding is encouraged and started early.
Counseling regarding birth control and importance of
preconceptional sugar control should be given to minimize complications
in forthcoming pregnancies.
25
EFFECT OF DIABETES ON FETUS AND NEW BORN:
Infants of diabetic mothers are at increased risk of developing
various complications like congenital malformation, unexplained fetal
loss (abortion and IUD) and perinatal morbidity. Before advances in
management of diabetic care in pregnancy there was very high fetal and
neonatal mortality. With improvement in health care and strict control of
sugar levels, rate of complications decrease and many women may give
birth to normal babies. However these infants have greater risk for
periconceptional, fetal, neonatal, and long-term complications compared
to infants of non-diabetic mothers13
THE PEDERSEN HYPOTHESIS:
Outcome of fetus and neonate is greatly influenced by maternal
sugar control. The Pedersen hypothesised that maternal hyperglycemia
produces increased blood glucose level in fetus because glucose crosses
the placenta readily14.The fetus cannot secrete adequate insulin before 20
weeks of gestation, and hence the embryo and early fetus are subjected to
hyperglycemia. The fetus has a functioning pancreas after 20 weeks of
gestation and can regulate its own glucose metabolism, but, at the same
time diffusion of maternal insulin across placenta decreases. Uncontrolled
sugar levels in mother leads to hyperglycemia in the fetus which in turn
stimulates the fetal pancreas resulting in fetal hyperinsulinemia.
26
The hyperglycemia and hyperinsulinemia either alone or together
increases the growth of the fetus resulting in various complications in late
pregnancy and neonatal period.
27
GROWTH IN INFANTS OF DIABETIC MOTHERS:
In first half of pregnancy insulin secretion from fetal pancreas in
response to hyperglycemia is not adequate to produce macrosomia15.
Whereas after 20wks response of insulin synthesis to hyperglycemia
increases culminating in hyperinsulinemia. This alone or together with
hyperglycemia result in increased fat deposition in interscapular and
abdominal areas by its anabolic effects16.As a result most of the weight
gain occurs in third trimester. Hypertrophy of viscera especially liver ,
spleen and heart occurs with head sparing.
The definition of macrosomia goes by a value of either birth
weight>90th centile for age or more than 4kg. Fat deposition occurs
asymmetrically predominantly around shoulders and interscapular area
resulting in overweight baby without increase in linear growth and HC17.
This differential growth pattern is assessed by parameters like PI,
MAC/HC ratio which act as predictors of neonatal metabolic
complications17. Macrosomia acts as a predictor of metabolic and other
complications like iron deficiency, polycythemia, ASH.[18,19,20]
Macrosomia may be linked with an increased number of primary
cesarean section and obstetric trauma.
Ackler et al found that the incidence of shoulder dystocia to be
around 3% in infants with BW >4kg, whereas the same is 16% in IDMs
weighing >4000g.21
28
CONGENITAL ANOMALIES:
Congenital anomalies are common in newborns of DM mothers
since the risk is high when maternal hyperglycemia exists during
conception or early gestation.22 The prevalence rate is related to the type,
severity and level of control of diabetes. Infants born to PGDM mothers
are more likely to have congenital anomalies than infants born to GDM
mothers because the fetus is spared during the period of organogenesis in
case of gestational diabetes.
In a study by Miller et al incidence of congenital anomalies
correlated well with maternal HbA1c levels. With incidence being 3.4 %
if HbA1c is <8.5% and increasing dramatically to 22.4% if HbA1c is
>8.5 23. Study by Lucas et al also gave similar results for malformations
with overall prevalence rate of 13.3%.
The pathophysiology of increased sugar levels leading to
congenital anomalies is unclear. Studies in animals showed decreased
amount of myoinositol and arachidonic acid and increased amount of
trace metals and sorbitol in embryos24. Production of reactive oxygen
species in mitochondria of vulnerable tissues is increased by
hyperglycemia. These reactive oxygen species disrupt vascularisation of
developing tissues by inhibiting prostacyclin via hydrogen peroxide
production. Overall risk for congenital anomalies in infants of diabetic
mothers (IDM) is 5-6% 25 and contributed mainly (66%) by central
29
nervous system and cardiovascular anomalies26 . Notable anomalies of the
cardiovascular system include ventricular septal defect, transposition of
the great arteries, truncus arteriosus, tricuspid atresia, double outlet right
ventricle and patent ductus arteriosus27. Neurological abnormalities like
anencephaly, encephalocele and myelomeningocele occur due to failure
of closure of neural tube. Skeletal abnormalities include caudal regression
syndrome and spinal anomalies. Gastrointestinal system is affected in the
form of atresias of duodenum and rectum. Other congenital anomalies in
IDM include small left colon syndrome, renal anomalies and limb
anomalies. Neonatal small left colon syndrome is a rare condition in
which the size of the lumen decreases uniformly in rectum and sigmoid
colon and usually presents as feeding intolerance, vomiting, and
abdominal distention. Meglumine diatrizoate (Gastrograffin) enema
makes the diagnosis and often results in evacuation of the colon.
EVALUATION OF IDM AT BIRTH:
GENERAL PRINCIPLES:
As soon as the infant is born, assessment of gestation, breathing
efforts and muscle tone is done as for all newborns and routine care is
given by drying, warmth and suctioning. Vital signs are checked, O2 and
other resuscitative measures are provided if indicated. Then physical
30
examination is done to screen for presence of congenital malformations.
Presence of cyanosis should raise the possibility of cyanotic congenital
heart disease, respiratory distress syndrome, TTN or polycythemia.
Cord blood pH and glucose level may be measured.
Blood glucose estimation is done at 1,2,3,6,12,24,36 and 48 hrs
Hematocrit levels are checked at 1 and 24 hrs.
Calcium levels are checked if there is any symptom of
hypocalcaemia like jitteriness or if the infant is sick.
Bilirubin levels are checked if the infants appear jaundiced.
METABOLIC ABNORMALITIES:
HYPOGLYCEMIA:
Newborn period is a transitional state in glucose homeostasis and
hypoglycemia occurs as the most common metabolic abnormality. The
screening is generally done to identify decrease in sugar values and its
course . The trough in neonatal sugar level is between 1st and 3rd hr of
neonatal life. Since there is no consensus for definition of hypoglycaemia,
screening of all IDM babies is done and a BG value<40mg/dl [28, 29] is
kept as "operational threshold", for treatment based on the available data
at present. As the glucose is transported to the fetus from the mother by
31
facilitated diffusion and there is limited crossing of insulin across the
placenta, maternal hyperglycemic episodes in uncontrolled diabetics
cause episodes of fetal hyperglycemia which in turn cause hyperplasia of
pancreatic islet producing fetal hyperinsulinemia[30,31] .Till delivery the
fetus is dependent on its mother for glucose .Immediately following
delivery , maternal supply of glucose is cut off resulting in hypoglycemia
in initial hrs even in normal newborn. This response is augmented in IDM
as a result of hyperinsulinemia Insulin antagonises the effect of catabolic
hormones and decreases glycogenolysis and gluconeogenesis. As a result
blood glucose recovery to normal level is prolonged in IDM. Incidence of
hypoglycaemia in infants born to diabetic mothers is as high as 50% and
that too is more common in LGA or IUGR babies than in AGA babies32.
Perinatal stress results in release of catecholamines and other catabolic
hormones depleting the glycogen stores leading to further
hypoglycemia33. Neonatal hypoglycemia seen in growth-retarded Infants,
born to diabetic mothers with advanced vascular disease is caused by
decreased hepatic glycogen stores rather than hyperinsulinemia .
Reactive hypoglycemia in infants born to diabetic mother starts as early
as 2 hrs and may persist upto 7 days 34. Symptoms of hypoglycemia
include respiratory distress, sweating, jitteriness, tachypnea, agitation and
seizures. Indices like PI and MAC:HC ratio have more sensitivity and
32
specificity compared to weight for age index to identify the babies more
prone for hypoglycaemia.
Hypoglycemia is usually prevented by supporting early (within 1–2
hours after birth) and frequent breastfeeding, as it has been shown that a
feed of 10 ml/kg breast milk can elevate blood sugar by 18 mg/dl at this
time. Sick neonates who cannot withstand oral feeds or the neonates who
are hypoglycemic in spite of full volume feeds, must be started on iv
glucose infusion at 6mg/kg/min. Rarely, babies with severe and persistent
hyperinsulinism require glucose infusions at a rate more than 10
mg/kg/min.
Management of asymptomatic hypoglycemia:
For blood sugar values between 20 and 40 mg/dl, EBM trial is
given and sugar level repeated after one hour.
1. If repeat blood sugar level is greater than 45mg/dl, feeding is
encouraged 2nd hourly with monitoring of blood sugar level
6th hrly for a period of 48 hrs
2. If repeat blood sugar is <45 mg/dl, IV dextrose is started and
further management is as for symptomatic hypoglycemia.
For blood sugar levels less than 20mg/dl, IV dextrose is started at 6
mg/kg/min and subsequently managed as symptomatic hypoglycemia.
33
Management of symptomatic hypoglycemia:
Any newborn who has neurological manifestation of hypoglycemia
must receive a bolus of 2ml/kg of 10% dextrose followed by glucose
infusion started immediately at the rate of 6 mg/kg/min to avoid occipital
cerebral injury and long-term disability.35 In other circumstances, boluses
should be avoided as increased insulin secretion and rebound
hypoglycaemia will result .Glucose should not be administered at a rate
higher than that required to maintain normoglycaemia, in order to avoid
continued stimulation of insulin secretion.Glucose infusion rate can be
stepped up to 12 mg/kg/min if blood sugar levels fall in the
hypoglycemic range. If 2 or more continous blood glucose levels above
50mg/dl with parenteral therapy for 24 hrs, the GIR is decreased @ 2
mg/kg/min 6th hourly, carefully watching blood sugar level. While
reducing GIR, escalate oral feeds simultaneously. When GIR reaches 4
mg/kg/min and if oral feeding is satisfactory and glucose values are
above 50 mg/dl consistently, GIR could be terminated abruptly.
Recurrent / resistant hypoglycemia:
Defined as a failure to maintain normal blood glucose levels inspite
of glucose infusion at the rate of 12 mg/kg/min or when blood glucose is
not stabilised by 1 week of life.
34
Drugs that are used include:
(1) Diazoxide @ 10-25mg/kg/day in 3 divided doses orally
(2) Hydrocortisone @ 5mg/kg/day in 2 divided doses orally or
intravenously
(3) Glucagon @ 100 mg/kg subcutaneous or intramuscular; 3
doses can be given
(4) Octreotide (synthetic somatostatin) @ of 2-10 µg/kg/day given
subcutaneously thrice daily.
HYPOCALCEMIA AND HYPOMAGNESEMIA:
Neonatal hypocalcaemia (defined by a total serum calcium level of
< 7 mg/dl) is seen in 20-50% of infants born to DM mothers36 . The
nadir in calcium levels occurs between 24 and 72 hours. Its incidence and
severity appear to be related to control of diabetes in pregnancy37. The
etiology is not entirely clear. It could be due to
a. The antagonism of vitamin D in the intestines due to raised
cortisol level and hyperphosphatemia which inturn is due to
tissue catabolism or
b. The delayed rise of parathormone postnatally due to inactive
parathyroids or
c. The increased calcium demands of a macrosomic baby38
35
There is no evidence suggestive of elevated serum calcitonin
concentrations in these infants in the absence of prematurity or
asphyxia. Presentation of hypocalcemia is not specific and its symptoms
resemble that of hypoglycemia. Most dreaded complication is seizure.
Symptomatic hypocalcemia should be treated by injecting 10% calcium
gluconate 2 ml/kg, under cardiac monitoring because rapid intravenous
calcium can cause heart block, refractory bradycardia, and hypotension.
Hypomagnesemia may occur in combination with hypocalcemia
and is characterised by a serum value of <1.5mg/dl. The cause is again
due to parathyroid issues and due to maternal cause, in cases of chronic
diabetic mothers with deranged renal function leading to increased loss of
magnesium in urine, resulting decreased magnesium supply across
placenta to the fetus39. Hypomagnesemia is treated by the slow i.v.
infusion of 5% MgSO4 solution over one hour.
POLYCYTHEMIA:
Incidence of polycythemia is around 20-30% in infants of diabetic
mothers at birth40 and has a correlation with maternal sugar control.
Polycythemia is defined by the Hct more than 65% (or) central venous
Hb greater than 20 mg/dl.
Widness et al described increased erythropoiesis in response to
hyperglycemia. This may be due to fetal hypoxia, secondary to elevated
36
HbA 1 in both maternal and fetal blood. In SGA infants, polycythemia
may be related to placental insufficiency, causing fetal hypoxia and
increased erythropoietin. Symptoms of polycythemia are manifestations
of blood hyperviscosity. If left without treatment polycythemia results in
increased viscosity of blood leading to stasis which causes infarction of
vital organs.
Sludging in cerebral vessels cause jitteriness, irritability and high-
pitched cry and warrant treatment with PET, even when neuroimaging
studies are normal.
PPHN is seen as a result of sludging of pulmonary vasculature.
NEC and intolerance to feeds occur sludging of intestine.
Renal vein thrombosis can occur with increased viscosity which
manifest as hypertension, flank mass, hematuria and thrombocytopenia.
An initial HCT and Plt count is done soon after the baby is born
and repeated daily. A fall in plt count indicates thrombotic complication
in renal, pulmonary or intestinal vasculature.
Treatment is dictated by presence or absence of symptoms and Hct
values.
i. Hydration with .I.V fluids is indicated for asymptomatic babies
whose Hct values fall between 65-70%
ii. PET is done if the baby is symptomatic or Hct value >70%
37
HYPERBILIRUBINEMIA:
Risk for hyperbilirubinemia is more in infants on diabetic mothers
because of polycythemia, ineffective erythropoiesis, and relative
immaturity of hepatic bilirubin conjugation and excretion. Inefficient
conjugation is due to immature glucuronosyltransferase enzyme system.
Circulating red cell precursors are trapped and removed in the spleen
which contributes an additional bilirubin load.SBR measurement should
be started on 1st day and continued upto 5 days. Hyperbilirubinemia is
mostly mild and can be managed by phototherapy, seldom requiring
exchange transfusion.
RESPIRATORY COMPLICATIONS:
Respiratory distress syndrome and transient tachypnoea of
newborn are more common in IDMs compared to normal newborns. [41, 42]
Increased incidence of RDS in IDM is due to the delayed maturation of
type 2 alveolar cells and higher incidence of preterm delivery in mothers
with gestational diabetes mellitus. Cortisol is necessary for maturation of
type 2 alveolar cells. Hyperinsulinemia in IDMs interfere with this action
and cause surfactant deficiency [43, 44, 45]. Studies have demonstrated the
reduction in the incidence of this complication with good glycemic
control during pregnancy [44, 46].
38
FETAL HYPOXIA
High concentrations of insulin and glucose in fetal circulation lead
to elevated basal metabolic rate in the fetus. This might increase fetal
oxygen consumption47 . But the placenta has limited ability to increase
oxygen transport as per demand. Hence fetus compensates for hypoxemia
by increasing oxygen carrying capacity48. Studies have showed that there
is increase in erythropoietin concentration, polycythemia and altered iron
distribution in response to fetal hypoxia 49. This fetal hypoxia also
contributes to increased incidence of metabolic acidosis and fetal death in
IDM.
NEUROLOGIC FUNCTION
Infants of diabetic mothers are at an increased risk for both acute
and long term adverse neurological events.CNS changes occur due to
hypoglycaemia, metabolic complications, birth injuries, birth asphyxia
and polycythemia50.
Onset of symptoms in the first 24 hours postpartum is due to
perinatal depression or hypoglycaemia while symptoms between 1st to 3rd
day of life are due to hypomagnesemia and hypocalcemia. Seizures,
lethargy, jitteriness, changes in tone and movement disorders are usual
39
symptoms.LGA babies are more prone to neurological dysfunction
because of
i. Antenatal factors like fetal hypoxemia, decreased iron store and
fetal cardiomyopathy
ii. Perinatal factors like prolongation of labour due to shoulder
dystocia
Stretching of neck during delivery may result in klumpke’s, erb’s,
recurrent laryngeal nerve and diaphragmatic palsies especially in LGA
babies51.
CARDIAC ABNORMALITIES
The anabolic effect of increased sugar levels and increased insulin
levels lead to glycogen deposition in interventricular septum. Most of
such cases are found postnatally by echocardiography but can also be
diagnosed by prenatal USG.
LONGTERM COMPLICATIONS IN INFANTS OF DIABETIC
MOTHERS:
Long term complications are due to perinatal, natal and postnatal
insults. The major long term complications are
1. Obesity
2. Diabetes
40
3. Adverse neurologic outcomes and
4. Iron deficiency
Not all LGA babies will develop obesity and many may follow
normal population growth standards.
The risk of developing diabetic over long-term in infants of
diabetic mother is more with type 2 diabetes than with type 1 diabetes.
In type 1 diabetes the risk of development of diabetes in offspring is:
<1% in general population.
1 to 4% if mother is affected.
10% if father is affected.
20% if both parents are affected.
In type 2 diabetes the risk of development of diabetes in offspring is:
12-18% in general population.
30% if one parent is affected.
50-60% if both parents are affected.
There is increased risk of delayed motor and cognitive
development in infants of diabetic mother which may occur due to:
41
i. Intra-uterine adverse environment with hypo or hyperglycemia,
acidosis, iron deficiency and hypoxia
ii. Perinatal causes like birth injury and birth asphyxia
iii. Postnatal metabolic complications including hypoglycemia,
hypocalcemia, hypomagnesemia, iron deficiency, polycythemia
and neonatal seizures.
The risk of adverse neurological outcome following neonatal
seizure varies with the cause of seizure. Seizures due to metabolic
problems in neonatal period carry 10–50% risk, whereas those due to HIE
carry 80% risk for subsequent development of neurological abnormality.
IRON DEFICIENCY:
According to few studies, 65% of all infants born to diabetic
mothers and 95% of large for gestation babies show iron deficiency. The
degree of iron deficiency depends on fetal hyperglycemia and maternal
sugar control. Apart from anemia, decreased iron stores may also affect
non-heme iron (heart and brain) resulting in myopathy and neurologic
dysfunction. Perinatally iron deficiency increases susceptibitility of
neonatal brain to hypoxia thereby increasing the risk of hypoxic injury.
Iron therapy in neonatal period is not found to be useful, as
replenishment of iron stores is a slow process and redistribution of iron
42
by breakdown of fetal red cells to iron deficient site occurs, resulting in
spontaneous recovery of iron strores.
43
STUDY
TITLE:
ANTHROPOMETRY, MORBIDITY AND MORTALITY
AMONG THE INFANTS OF DIABETIC MOTHERS IN A
TERTIARY CARE CENTRE
JUSTIFICATION OF THE STUDY:
There are a number of western studies that analyze the prevalence
of GDM and its influence on fetal growth, metabolism and the final
anthropometry attained by such babies. But data on the anthropometry of
infants born to diabetic mothers is sparse in this part of the country. Thus
the current study aims to compare the anthropometric measures of
neonates born to mothers with and without diabetes mellitus and analyze
the extent of disproportionate growth in the offspring of GDM mothers as
well as the morbidities and mortalities seen in infants of diabetic mothers.
44
AIM AND OBJECTIVES
AIM: To quantify the disproportionate growth and to determine the
morbidity pattern among infants of diabetic mothers
PRIMARY OBJECTIVE: To compare the Ponderal Index of neonates
born to diabetes mellitus mothers with that of neonates born to healthy
non-diabetic mothers
SECONDARY OBJECTIVE :To determine the range of complications
occurring in infants of diabetic mothers.
45
MATERIALS AND METHODS
STUDY DESIGN: An observational cross-sectional study.
STUDY AREA: Department of Obstetrics and Department of
Paediatrics ( neonatology), Government Theni Medical College Hospital
STUDY DURATION:September 2014 to August 2015
STUDY POPULATION:
Inclusion Criteria:
All live new born babies born to diabetic mothers (Gestational and
Pre Gestational Diabetes Mellitus) in the Department of Obstetrics and
Gynaecology in Government Theni Medical College Hospital are
included.
Exclusion Criteria:
Gestational age <28 weeks
Multiple gestations
Babies who expire within first 24 hours of life
Mothers with co-morbidities like hypothyroidism and hypertension
Control:
Babies born to non-GDM mothers are designated as control
subjects. For every infant of diabetic mother born and included in the
46
study, the next 5th, 10th and 15th babies born to non-diabetic mothers were
added as controls for comparison of anthropometric measurements.
METHODOLOGY:
Neonates of Diabetic Mothers born in GOVERNMENT THENI
MEDICAL COLLEGE HOSPITAL, during the time frame mentioned
above, will be included in the study after getting informed consent from
the parents. At birth, weight is recorded and a detailed physical
examination is performed to detect congenital anomalies.
Maternal data including age, parity, type and duration of diabetes,
treatment received, co morbid conditions, other complications during
pregnancy and mode of delivery will be reviewed retrospectively from
the clinical records.
Birth weight of the neonate, head circumference, chest
circumference, and length of the babies will be recorded after 24 hours by
the examiner by the following methods:
BIRTH WEIGHT:
Measured by using electronic weighing scale to the nearest of 10
grams. The neonates were classified as SGA, AGA and LGA as per the
intrauterine growth charts by Lubchenco.
47
LENGTH:
Crown heel length is measured to the nearest of 0.1 cm using an
infantometer with the baby in supine position and knees fully extended.
HEAD CIRCUMFERENCE:
Measured to the nearest of 0.1cm at the occipital protuberance
level, above supra orbital ridges and ears
CHEST CIRCUMFERENCE:
Measured at the level of the nipple in a plane at right angles to the
spine and recorded in quiet respiration.
PONDERAL INDEX:
Calculated by the following formula
Weight in grams x 100 / (length in centimetre)3
INVESTIGATIONS :
Blood glucose, serum calcium, serum bilirubin, and complete
blood counts and Echocardiography are done for all infants of diabetic
mothers to determine the range of metabolic, hematologic complications
and cardiac malformations in our area.
48
HYPOGLYCAEMIA:
Blood glucose estimations were done at 1,2,3,6,12,24,48 hours of
life and if found hypoglycemic treated accordingly. Hypoglycemia is
defined as blood glucose concentrations <40mg/dl.
POLYCYTHEMIA:
Hematocrit value of blood is done at 1 & 24 hrs of life.
Polycythemia is taken as a venous Hct > 0.65
HYPERBILIRUBINEMIA:
SBR estimation is done on 4th -5th day or before if needed to detect
hyperbilirubinemia which is diagnosed and treated based on the AAP
(American Academy of Pediatrics) charts.
HYPOCALCAEMIA:
Serum calcium level is checked for all IDMs at 24-72 hours which
is usually the trough period. Hypocalcemia is defined by total serum
alcium values lower than 7mg/dl.
ECHOCARDIOGRAPHY:
It is done at 24-72 hours of life for all IDMs to look for cardiac
malformation as they are five times higher than in normal pregnancies.
49
STATISTICAL METHODS:
Results were analysed using SPSS software 16.0. Descriptive
statistical analysis has been carried out in the present study. Results on
continuous measurements are presented as Mean ± SD and results on
categorical measurements are presented in Number (%). Differences in
the quantitative variables between groups were assessed by means of
unpaired t test. Comparison between groups was made by non parametric
Mann-Whitney test. Chi square test was used to analyze categorical
variables and multivariate analysis was done to test dependent variables.
P value of < 0.05 using a two tailed test was taken as statistically
significant.
50
79
237
Total Neonates under study
Infants of DM Mothers Infants of Non-DM Mothers
RESULTS AND OBSERVATION
TABLE1: TOTAL NEONATES UNDER STUDY:
Group Number
Infants of diabetic mothers 79
Infants of non diabetic mothers 237
Total cases 316
Total number of babies studied was 316. Among them 79 babies
were born to mothers with diabetes mellitus and the remaining 237 babies
were born to non diabetic mothers.
Figure1: Total Neonates Under Study
51
TABLE2: DISTRIBUTION OF INFANTS OF DIABETIC
MOTHERS BY MATERNAL DIABETIC STATUS:
Group Frequency Percentage
Infants of PreGestational Diabetes Mothers 13 16.46 %
Infants of Gestational Diabetes Mothers 66 83.54 %
Total 79
Out of 79 diabetic mothers, 66 had gestational diabetes and 13 had
pregestational diabetes.
Figure2: Distribution of Infants of Diabetic Mothers By Maternal
Diabetic Status
16.46%
83.54%
Infants of PreGestational Diabetes Mothers
Infants of Gestational Diabetes Mothers
52
39
12840
109
0
50
100
150
200
250
Infants ofDiabeticMothers
Infants ofNonDiabetic
Mothers
Female
Male
TABLE 3: GENDER DISTRIBUTION OF NEONATES:
Group Male Female p value
Infants of diabetic mothers 39 (49.4%) 40 (50.6%)
0.535 Infants of non-diabetic mothers 128 (54%) 109 (46%)
Among babies born to diabetic mothers 39 were males and 40 were
females. Among babies born to non-diabetic mothers 128 were males and
109 were females. There is no sex predilection (p-value =0.535 ) among
babies born to diabetic and non-diabetic mothers.
Figure 3: Gender Distribution of Neonates:
53
23%
7.60%
2.50%7.60%
1.30%
3.80%
62%
A1 A2 A3 IUD1 IUD2 Neo Deaths No loss
TABLE4: DISTRIBUTION OF FETAL AND NEONATAL LOSS
AMONG DIABETIC MOTHERS:
Category IUD1 IUD2 A1 A2 A3 D1 No Loss
Diabetic Mothers 6 1 18 6 2 3 49
Out of 79 cases of diabetic mothers 15 had only 1 abortion, 4 had
only 2 abortions, 1 had only 3 abortions, 2 had 1 abortion and 1 IUD, 1
had 1 abortion and 1 neonatal death, 1 had 2 abortions and 1 IUD,1 had 2
abortions and 1 neonatal death, 1 had 3 abortions and 1 IUD, 2 had only 1
IUD, 1 had only 2 IUD, 1 had only 1 fetal loss and 49 had no loss.
Figure 4: Distribution of Fetal And Neonatal Loss among Diabetic
Mothers:
54
12.66%
2.50% 0.40% 0%
0%
0.40%
84.40%
A1 A2 A3 IUD1 IUD2 Neo Deaths No loss
TABLE 5: DISTRIBUTION OF FETAL AND NEONATAL LOSS
AMONG NON- DIABETIC MOTHERS:
Category IUD1 IUD2 A1 A2 A3 D1 No Loss
Non Diabetic mothers 0 0 30 6 1 3 200
Out of 237 cases of non-diabetic mothers 28 had only 1 abortion,
5 had only 2 abortions, 1 had only 3 abortions, 2 had 1 abortions and 1
neonatal death ,1 had 2 abortions and 1 neonatal death, none of them had
IUD and 200 had no loss.
Figure 5: Distribution of Fetal And Neonatal Loss among Non-
Diabetic Mothers:
55
11.40%
88.60%
Diabetic Mothers
LN LSCS
46.80%53.20%
NonDiabetic Mothers
LN LSCS
TABLE 6: MODE OF DELIVERY:
Group Caesarean Normal
Diabetic Mothers 70 9
NonDiabetic Mothers 126 111
Among 79 babies born to diabetic mothers 9 were delivered by LN
and 70 were delivered by LSCS. Among 237 babies born to non diabetic
mothers 111 were delivered by LN and 126 were delivered by LSCS.
Incidence of caesarean deliveries was higher amongst diabetic mothers in
comparison with non diabetic mothers.
Figure 6: Mode of Delivery:
56
24
30
14
92
Infants of DM Mothers
1 2 3 4 5
11684
30
3 4
Infants of Non-DM Mothers
1 2 3 4 5
TABLE 7: DISTRIBUTION OF NEONATES ACCORDING TO
THEIR BIRTH ORDER:
Group 1st 2nd 3rd 4th 5th
Infants of diabetic mothers 24 30 14 9 2
Infants of non-diabetic mothers 116 84 30 3 4
Among babies born to diabetic mothers 24 were 1st born, 30 were
2nd born, 14 were 3rd born, 9 was 4th born and 2 were 5th. Among normal
babies 116 were 1st born, 84 were 2nd born, 30 were 3rd born, 3 was 4th
born and 4 was 5th born.
Figure 7: Distribution of Neonates According To Their Birth Order:
57
22.80%
77.20%
Infants of Diabetic Mothers
LGA Non LGA
5.90%
94.60%
Infants of Non Diabetic Mothers
LGA Non-LGA
TABLE 8: DISTRIBUTION OF NEONATES BASED ON
GEASTATIONAL AGE AND BIRTH WEIGHT:
Group LGA Non-LGA Total
Infants of diabetic mothers 18(22.8%) 61(77.2%) 79(100%)
Infants of non-diabetic mothers 14 (5.9%) 223(94.6%%) 237(100%)
The incidence of LGA babies is higher in diabetic mothers
compared to non-diabetic mothers.
Figure 8: Distribution of Neonates Based on Gestational Age and
Birth Weight:
58
ANTHROPOMETRIC OUTCOME: PRIMARY OUTCOME: TABLE 9: PONDERAL INDEX BETWEEN BABIES BORN TO
DIABETIC AND NON-DIABETIC MOTHERS:
Group No. Mean SD P value
Diabetic 79 2.69 0.33 0.003
Significant Non Diabetic 237 2.45 0.25
Mean Ponderal index of babies born to diabetic mothers is higher
(0.24) than born to non GDM mothers with a p-value of 0.003
Figure 9 : Ponderal Index Between Babies Born To Diabetic And
Non-Diabetic Mothers
PI - Ponderal Index
59
TABLE 10: PONDERAL INDEX BETWEEN LGA BABIES BORN
TO DIABETIC AND NON-DIABETIC MOTHERS:
Mean ponderal index in LGA babies born to diabetic mothers is
not significantly higher than LGA babies born to nondiabetic mothers
Group No. Mean SD P value
Diabetic 18 2.97 0.246 0.458 Not
significant Non Diabetic 14 2.89 0.343
Figure 10 : Ponderal Index Between LGA Babies Born To Diabetic
And Non-Diabetic Mothers:
PI - Ponderal Index
60
TABLE 11: BIRTH WEIGHT DIFFERENCE BETWEEN BABIES
BORN TO DIABETIC AND NON-DIABETIC MOTHERS
Group No Mean SD P Value
Diabetic 79 3.09 0.59 0.001 Significant Non -diabetic 237 2.89 0.42
Mean birth weight of babies born to diabetic mothers is higher
(0.20) than the babies born to non-diabetic mothers with a p value
of 0.001
Figure 11: Birth Weight Difference Between Babies Born To Diabetic
And Non-Diabetic Mothers
BW-Birth Weight
61
TABLE 12: CHEST CIRCUMFERENCE BETWEEN BABIES
BORN TO DIABETIC AND NON-DIABETIC MOTHERS :
Group No Mean SD P Value
Diabetic 79 32.28 2.3 0.155 Not
significant Non -diabetic 237 30.63 1.8
There is no significant difference in chest circumference between
the babies born to diabetic and non-diabetic mothers.
Figure 12: Chest Circumference Between Babies Born To Diabetic
And Non-Diabetic Mothers :
CC-Chest Circumference
62
TABLE 13: HEAD CIRCUMFERENCE BETWEEN BABIES
BORN TO DIABETIC AND NON DIABETIC MOTHERS
Group No Mean SD P Value
Diabetic 79 33.01 1.54 0.778 Not
Significant Non -diabetic 237 32.96 1.25
There is no significant difference in head circumference between
the babies born to diabetic and non-diabetic mothers.
Figure 13: Head Circumference between Babies Born To Diabetic
And Non Diabetic Mothers
HC- Head Circumference
63
TABLE 14: LENGTH BETWEEN BABIES BORN TO DIABETIC
AND NON DIABETIC MOTHERS
Group No Mean SD P Value
Diabetic 79 48.22 2.8 0.036
Significant Non -diabetic 237 48.78 1.7
There is a significant difference in mean length between babies
born to diabetic and non diabetic mothers.
Figure 14: Length between Babies Born To Diabetic And Non
Diabetic Mothers
64
TABLE 15: HEAD--CHEST CIRCUMFERENCE DIFFERENCE
BETWEEN BABIES BORN TO DIABETIC AND NON DIABETIC
MOTHERS
Group No Mean SD P Value
Diabetic 79 0.72 1.5 0.001 Significant Non -diabetic 237 2.3 1.5
The head-chest circumference difference is significant in babies
born to diabetic mothers compared to non-diabetic mothers.
Figure 15: Head--Chest Circumference difference between Babies
Born to Diabetic and Non Diabetic Mothers
HC.CC Head Circumference-Chest Circumference difference
65
35.44%
64.56%
Yes No
MORBIDITY PATTERN
TABLE 16: HYPOGLYCEMIA :
Hypoglycemia Frequency Percentage
Yes 28 35.44%
No 51 64.56%
Out of 79 infants of diabetic mothers, hypoglycemia was documented
in 28cases.
Figure 16: Hypoglycemia:
66
820
1041
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
LGA babies Non-LGAbabies
No
Yes
TABLE 17: HYPOGLYCEMIA IN LARGE FOR
GESTATIONAL AGE BABIES:
Hypoglycemia Frequency Percentage
In LGA babies 8 44%
In non LGA babies 20 32%
Out of the 28 cases of hypoglycemia documented, 8 were found in
the LGA babies.
Figure 17: Hypoglycemia in Large for Gestational Age Babies:
67
7.60%
92.40%
Yes No
TABLE 18 : HYPOCALCEMIA:
Hypocalcemia Frequency Percentage
Yes 6 7.6%
No 73 92.4%
Out of 79 infants of diabetic mothers, hypocalcemia was
documented in 6 cases.
Figure 18 : Hypocalcemia:
68
2 4
16 57
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
LGAbabies Non LGAbabies
No
Yes
TABLE 19: HYPOCALCEMIA IN LARGE FOR GESTATIONAL
AGE BABIES:
Hypocalcemia Frequency Percentage
In LGA babies 2 11.11%
In non LGA babies 4 6.5%
Out of the 6 cases of hypocalcemia documented, 2 were found in
the LGA babies and 4 in non LGA babies
Figure 19 : Hypocalcemia In Large For Gestational Age Babies:
69
27.50%
72.50%
Yes No
TABLE 20 : HYPERBILIRUBINEMIA :
Hyperbilirubinemia Frequency Percentage
Yes 22 27.5%
No 57 72.5%
Out of 79 infants of diabetic mothers, hyperbilirubinemia was
documented in 22 cases.
Figure 20: Hyperbilirubinemia :
70
5 17
13 44
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
LGA babies NonLGAbabies
No
Yes
TABLE 21: HYPERBILIRUBINEMIA IN LARGE FOR
GESTATIONAL AGE BABIES:
Hypocalcemia Frequency Percentage
In LGA babies 5 27.8%
In non LGA babies 17 27.9%
Out of the 22 cases of hyperbilirubinemia documented, 5 were
found in the LGA babies and 17 in non-LGA babies.
Figure 21: Hyperbilirubinemia in Large for Gestational Age Babies:
71
3.80%
96.20%
Yes No
TABLE 22 : POLYCYTHEMIA:
Polycythemia Frequency Percentage
Yes 3 3.8 %
No 76 96.2 %
Out of 79 infants of diabetic mothers, polycythemia was
documented in 3 cases and 76 babies had no polycythemia. No
polycythemia was documented in LGA babies.
Figure 22 : Polycythemia:
72
6.40%
93.60%
Yes No
TABLE 23 : BIRTH ASPHYXIA:
Polycythemia Frequency Percentage
Yes 5 6.4 %
No 74 93.6 %
Out of 79 infants of diabetic mothers, birth asphyxia was observed
in 5 cases.
Figure 23 : Birth Asphyxia:
73
TABLE 24: BIRTH ASPHYXIA IN LARGE FOR GESTATIONAL
AGE BABIES:
Hypocalcemia Frequency Percentage
In LGA babies 3 16.67 %
In non LGA babies 2 3.28 %
Out of the 5 cases of birth asphyxia documented, 3 were found in
the LGA babies and 2 in non-LGA babies.
Figure 24 : Birth Asphyxia In Large For Gestational Age Babies:
32
1559
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
LGA babies NonLGAbabies
No
Yes
74
24%
76%
Yes No
TABLE 25: RESPIRATORY DISTRESS :
Hypoglycemia Frequency Percentage
Yes 19 24 %
No 60 76 %
Out of 79 infants of diabetic mothers, respiratory distress was
observed in 19 babies.
Figure 25: Respiratory Distress:
75
7
12
11
49
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
LGA babies Non LGAbabies
No
Yes
TABLE 26: RESPIRATORY DISTRESS IN LARGE FOR
GESTATIONAL AGE BABIES:
Hypocalcemia Frequency Percentage
In LGA babies 7 38.9 %
In non LGA babies 12 19.7 %
Out of the 19 cases of respiratory distress documented, 7 were
found in the LGA babies and 12 in non-LGA babies
Figure 26: Respiratory Distress in Large for Gestational Age Babies:
76
TABLE 27: CONGENITAL HEART DISEASES:
ECHOCARDIOGRAPHY FINDINGS
Frequency Percent
NORMAL STUDY 60 75.9%
MINOR ANOMALIES 12 15.2%
Small ASD 3
Small closing PDA 8
Trivial PFO 1
MAJOR ANOMALIES 7 8.9%
Complex CCHD 1
TAPVC 1
Large PDA 1
Mid muscular VSD 1
ASD OS 3
Total 79 100%
Out of 79 infants of diabetic mothers, 60 babies had normal ECHO
findings, 12 babies had minor anomalies like small closing PDA and 7
babies had major congenital cardiac anomalies.
77
1
78
Yes No
TABLE 28: CONGENITAL ANAMOLIES OTHER THAN
CONGENITAL HEART DISEASE:
Anomaly Frequency Percent Valid Percent
Cumulative Percent
Yes 1 1.3 1.3 1.3
No Anomaly 79 98.8 98.8 100.0
Total 80 100.0 100.0
In this study congenital anomaly was found in only one baby born
to pre gestational diabetic mother. The baby had imperforate anus,
cerebellar hypoplasia and lissencephaly. No anomalies were seen in the
rest of the babies included in the study.
Figure 27: Congenital Anamolies Other Than Congenital Heart
Disease:
78
76
3
Alive Dead
FIGURE 28: MORTALITY IN INFANTS OF DIABETIC
MOTHERS:
Out of 79 babies included in the study, 3 babies died and 76 babies
were alive.
Of the three babies:
-2 were born to gestational diabetes mothers and
- 1 baby was born to pregestational diabetes mother
2 babies died due to cyanotic congenital heart disease and 1 baby died
due to severe birth asphyxia.
79
DISCUSSION
Diabetes mellitus complicating pregnancy is a global problem and
the disease progression is in an increasing trend. The effect of this
maternal illness on the fetal growth is a much discussed topic in the field
of neonatal medicine. Efforts to quantify these effects help us to
determine the need for intervention in order to help such mothers deliver
healthier neonates. Neonatal anthropometry is one such method, a
bedside tool noninvasive in nature that could help to assess and quantify
the degree of influence the maternal illness has had on the neonate.
Various studies are being conducted worldwide on the complications of
diabetic pregnancies, and more changes are being made in the treatment
modalities for fine tuning. Both the treating obstetricians and
pediatricians should be familiar with the newer guidelines in the
management of diabetes complicating pregnancies.
Disproportionate growth in the off springs of GDM mothers has
been researched extensively in order to understand its pathophysiology
and outcome. A number of direct and derived physical parameters have
been employed in various studies to assess this disproportionate growth.
In this study anthropometric measures were used to identify babies
with disproportionate growth born to diabetes mellitus mothers. This was
done keeping in mind that, babies born to mothers with diabetes mellitus
80
are disproportionately larger, represented by a high ponderal index, birth
weight and chest circumference.
Also an attempt was made in this study to describe the pattern of
complications in neonates born to diabetic mothers and emphasize the
need for a strict glycaemic control during pregnancy and careful follow
up of neonates during the neonatal period for early diagnosis and
management of complications.
Totally 316 babies were included in the present study. Out of them
79 were born to diabetic mothers and 237 were born to non-diabetic
mothers. Out of the 79 diabetic mothers, 13 mothers had pregestational
diabetes and 66 mothers had gestational diabetes mellitus.
Table 29: Distribution of Gestational and Pregestational Diabetes
Mellitus:
STUDIES GDM PGDM
Aarumugam et al52 92.7 % 7.3 %
Banerjee et al53 73.3% 26.6%
Kavitha et al54 64.8 % 35.1 %
Present study 83.54 % 16.46 %
In most of the studies the percentage of GDM mothers is greater
than the percentage of DM mothers. In this study too, it is the same.
81
MODE OF DELIVERY:
In this study 89 % of babies were delivered by LSCS and 11 % of
babies were delivered by LN. In Alam et al study 55.0 % of babies were
delivered by LSCS and 45.0 % of babies were delivered by LN. In
Akhlagi et al conducted at Mashad university of medical sciences, Iran
(Jan 2001 – April 2002), 79.8 % of babies were delivered by LSCS and
20.2 % of babies were delivered by LN.
Table 30: Mode of Delivery
STUDIES LN LSCS
Alam et al55 45% 55%
Aklagi et al56 20.2% 79.8%%
Present study 11% 89%
The incidence of caesarean section among diabetic mothers is
higher in present study compared to previous studies.
ANTHROPOMETRIC COMPARISON:
From the present study we found that the ponderal index is
significantly higher in babies born to DM mothers. The mean difference
was 0.24 (at a p-value of 0.003). Similar results have been obtained in the
studies conducted by Armangil et al 58. They had concluded that the
82
ponderal index is higher in LGA babies born to GDM mothers compared
to LGA babies born to non GDM mothers with mean difference of 0.13
between the groups. But in the present study the mean ponderal index of
LGA babies of diabetic mothers is not significantly higher than that of
LGA babies born to non-diabetic mothers.
This study also shows that there is no significant difference in head
circumference and chest circumference between the babies born to DM
mothers and the babies born to non-diabetic mothers.
The mean birth weight of babies born to diabetic mothers is
significantly higher than that of babies of non-diabetic mothers in the
present study. The mean difference was 0.2 at a p-value of 0.001. These
results indicate disproportionate growth in babies born to DM mothers. It
also indirectly suggests increased adiposity as the cause for
disproportionate growth. Similar results were found in the study done by
Anupama et al.
In this study, incidence of caesarean section is higher among
mothers with DM compared to normal mothers. This again can also be
attributed to the disproportionate growth observed among these babies.
83
MORBIDITY PATTERN:
Table 31: Incidence of Hypoglycemia
STUDIES INCIDENCE
Akhlagi et al 50.4%
Alam et al 35%
Present study 35% The results are comparable with previous studies.
Table 32: Incidence of Hyperbilirubinemia
STUDIES INCIDENCE
Mohammed Hussain et al 19%
Nili firouzeh et al 34%
Alam et al 30%
Present study 27.5%
The results are comparable with previous studies.
Table 32: Incidence of Asphyxia
STUDIES INCIDENCE
Nili firouzeh et al 8.2%
AK Deorari et al 8%
Present study 6.25%
This is comparable with previous studies.
84
Table 34 : Incidence of Hypocalcemia
STUDIES INCIDENCE
Ranade et al 14%
Alem et al 15%
Nili firouzeh et al 13%
Present study 7.5%
The incidence of hypocalcemia in this study is less when compared
with previous studies.
Table 33 : Incidence of Respiratory Distress
STUDIES INCIDENCE
Ranade et al 14%
Mohammed Hussain et al 15%
Present study 23.75%
The incidence of respiratory distress in this study is more when
compared with previous studies.
85
Table 35 :Incidence of Polycythemia
STUDIES INCIDENCE
Mohammed Hussain et al 12%
Mahmood CB et al 9.5%
Nili Firouzeh et al 6.8%
AK Deorari et al 8%
Present study 3.75%
The incidence of polycythemia in this study is less when compared
with previous studies.
Table 36: Incidence of Congenital Anomalies
STUDIES INCIDENCE
Ranade et al 4%
Akhlagi et al 3.7%
AK Shefali et al 1.4%
Present study 1.25%
The present study result is comparable to AK Shefali et al study.
86
CONCLUSION
Gestational diabetes is more common than pregestational diabetes.
There is a significant increase in cesarean deliveries among DM
mothers.
Babies born to Diabetes Mellitus mothers have higher birth weight
and ponderal index compared to babies of non-diabetic mothers.
This indicates disproportionate growth in these babies.
Complications like respiratory distress, hypoglycemia and
hypocalcemia are more common among LGA babies of diabetic
mothers compared to non LGA babies of diabetic mothers.
Anthropometric assessment at birth helps to identify these babies
more prone for complications in neonatal period. Hence close
monitoring of LGA babies in the nursery is indicated.
The incidence of major congenital heart diseases is higher among
the infants of diabetic mothers .So screening Echocardiography in
all IDMs will help to diagnose and manage cardiac cases earlier
and better.
Early recognition, precise assessment and appropriate management
of complications as per guidelines would reduce the mortality and
morbidity among babies born to diabetic mothers.
87
LIMITATIONS
Foetal insulin levels in the cord blood sample to confirm
hyperinsulinemia as the cause for the complications in the neonatal
period was not done since it is not available in our institution.
Long term complications like obesity, iron deficiency, diabetes etc.
could not be assessed, since it doesnot come under the purview of
this study.
88
FUTURE IMPLICATIONS
Studies have time and again proven that GDM and LGA at birth
are significant risk factors for developing type 2 diabetes, obesity and
childhood metabolic syndrome . Ponderal index at birth can serve as a
measure to identify those babies who have been affected by the adverse
intrauterine environment in GDM mothers. Conducting similar studies on
a larger population may help us derive a "threshold ponderal index"
above which the offsprings are more likely to develop long term
metabolic complications. High risk newborns thus identified can be
followed up at regular intervals and can be introduced to earlier lifestyle
modifications.
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Key to Master Chart
Sex:
M - Male
F - Female
Growth:
AGA - Appropriate for Gestational Age
LGA - Large for Gestational Age
Diabetes Type:
GDM - Gestational Diabetes Mellitus
PG - Pregestational Diabetes Mellitus
For NICU Admission, Respiratory Distress, Hypoglycemia,
Hypocalcemia, Hyperbilirubinemia, Polycythemia, Birth Asphyxia,
Congenital Anomalies :
Y - Yes
N - No
NA - Not Applicable
ECHO
NL - Normal
PROFORMA
NAME : Baby of……………. IP NO :
SEX : MOTHER’S IP NO :
DOB : DATE/TIME:
ANTENATAL AND BIRTH DETAILS :
PARITY :
MATERNAL ILLNESS : PRE GESTATIONAL DIABETES / GDM
If PreGestational DM :Type1/Type2
If GDM :Time of diagnosis: ________Gestational weeks
Treatment : Diet / Insulin / OHA
Control : Controlled/Uncontrolled
ANY OTHER ILLNESS :
MODE OF DELIVERY : Normal/Instrumental/Caesarean
If Caesarean :Ind:
PREVIOUS FETAL / NEONATAL DEATHS:
BABY DETAILS:
MATURITY : TERM / PRETERM / POST TERM
GESTATIONAL AGE : WEEKS
BABY’S ANTHROPOMETRY:
BIRTH WEIGHT :
LENGTH :
PONDERAL INDEX :
HEAD CIRCUMFERENCE :
CHEST CIRCUMFERENCE :
MORBIDITY AND MANAGEMENT DETAILS:
INVESTIGATIONS AND TREATMENT DETAILS:
TIME OF START OF BREAST FEEDS:
NICU ADMISSION : YES/NO
DURATION OF ADMISSION:
HYPOGLYCEMIA : YES/NO
DEXTROSE INFUSION: YES/NO
GLUCOSE INFUSION RATE
DURATION
RESPIRATORY DISTRESS: YES/NO
OXYGEN THERAPY
HYPERBILIRUBINEMIA:YES/NO
PHOTOTHERAPY/EXCHANGE
TRANSFUSION
DURATION
HYPOCALCEMIA :CALCIUM SUPPLEMENTATION/NOT
POLYCYTHEMIA : YES/NO
BIRTH INJURIES/ ASPHYXIA:
ECHOCARDIOGRAPHY:
CONGENITAL ANOMALIES: YES/NO
DIAGNOSIS:
