I
“STUDY OF AMNIOTIC FLUID INDEX AND FETO
MATERNAL OUTCOME IN TERM PREGNANCY
AT VIMS, BALLARI” By
Dr. VIDYASAGARA M M.B.B.S.
Dissertation Submitted to the Rajiv Gandhi University of Health Sciences,
Bengaluru, Karnataka in partial fulfilment of the requirements for the degree of
MASTER OF SURGERY
IN
OBSTETRICS AND GYNAECOLOGY Under the guidance of
Dr. CHANDRASHEKHAR. T M. D.
PROFESSOR
DEPARTMENT OF OBSTETRICS AND GYNAECOLOGY VIJAYANAGAR INSTITUTE OF MEDICAL SCIENCES
BALLARI, KARNATAKA 2020.
VIII
LIST OF ABBREVIATIONS
ACOG American College of Obstetricians and Gynecologists
AFI Amniotic fluid index
AG Abdominal girth
AFV Amniotic fluid volume
ACE Angiotensin converting Enzyme
ADH Anti diuretic Hormone
BA Birth asphyxia
BP Blood pressure
BMI Body mass index
CPD Cephalo Pelivic Disproportion
CTG Cardio Tocography
2 DP Two diameter deepest vertical pocket
EDD Expected date of delivery
EFW Estimated fetal weight
FHR Fetal heart rate
GA Gestational age
GDM Gestational diabetes Mellitus
Hb Haemoglobin
HIV Human Immuno deficiency Virus
Ht Height
IP No. Inpatient number
IX
IUFD Intra uterine fetal demise
IUGR Intra uterine growth restriction
IgM Immunoglobulin M
IgG Immunoglobulin G
LMP Last menstrual period
LSCS Lower segment caesarean section
MSAF Meconium stained amniotic fluid
ML Millilitre
MVP Maximum vertical pocket
NICU Neonatal intensive care unit
NS Normal Saline
NST Non stress test
PG Prostaglandin
PROM Premature rupture of membranes
RBS Random Blood Sugar
Rh Rhesus antigen
SD Standard deviation
SDVP Single deepest Vertical pocket
SFH Symphysio fundal height
TTTS Twin to Twin transfusion syndrome
USG Ultrasonography
Wt Weight
X
LIST OF TABLES
Table no. Title Page no.
1 Categories based on Amniotic Fluid Volume 2
2 Pathways for Amniotic Fluid 8
3 Correlation of AFV with Fetal and Placental weight in
grams
9
4 Definitions of Oligohydramnios based on USG
Measurements
16
5 Definitions of Polyhydramnios according to various study 28
6 Classification of Polyhydramnios 28
7 Distribution of the study subjects based on amniotic fluid
index
40
8 Age wise distribution of the study subjects among the
groups
41
9 BMI wise distribution of the study subjects among the
groups
42
10 Status wise distribution of the study subjects among the
groups
43
11 Gestation wise distribution of the study subjects among the
groups
44
12 Obstetric profile of the study subjects among the groups 45
13 Distribution of the study subjects based on mode of
delivery among the groups
47
XI
14 Distribution of the study subjects based on mode of
delivery among the groups
48
15 Indication of LSCS in the study subjects among the groups 50
16 Distribution of the study subjects based on oxytocin
augmentation among the groups
52
17 Co-morbid conditions in study subjects among the groups 53
18 Distribution of the study subjects based on colour of liquor
among the groups
55
19 Birth weight of the newborns among the groups 56
20 APGAR scores in the newborns among the groups 57
21 NICU admission of newborns among the groups 59
22 Neonatal complications among the study groups 60
23 Neonatal complications in study subjects among the groups 61
24 Neonatal mortality among the groups 63
25 Causes of Perinatal deaths among the groups 64
XII
LIST OF FIGURES
Fig. Title Page no.
1 Amniotic Fluid Index Measurement of four quadrants showing Normal AFI
3
2 Amniotic Fluid Index Measurement of four quadrants showing oligohydramnios
3
3 Amniotic Fluid Index Measurement of four quadrants showing Polyhydramnios
4
4 Regulation of amniotic fluid formation 6
5 Amniotic Fluid Pathways 7
6 AFV in relation with Gestational Age 9
7 Measurment of SDVP 14
8 Four quadrant method for AFI estimation 15
9 Amniotic band syndrome 20
10 Potter’s syndrome 21
11 Transabdominal amnioinfusion 25
12 Trans vaginal amnioinfusion 25
XIII
LIST OF GRAPHS
Graph. Title Page no.
1 Distribution of the study subjects based on amniotic fluid index
40
2 Age wise distribution of the study subjects among the groups
41
3 BMI wise distribution of the study subjects among the groups
42
4 Status wise distribution of the study subjects among the groups
43
5 Gestation wise distribution of the study subjects among the groups
44
6 Obstetric profile of the study subjects among the groups 46
7 Distribution of the study subjects based on mode of delivery among the groups
47
8 Distribution of the study subjects based on mode of delivery among the groups
49
9 Indication of LSCS in the study subjects among the groups 51
10 Distribution of the study subjects based on oxytocin augmentation among the groups
52
11 Co-morbid conditions in study subjects among the groups 54
12 Distribution of the study subjects based on color of liquor among the groups
55
13 Birth weight of the newborns among the groups 56
14 APGAR scores in the newborns among the groups 58
15 NICU admission of newborns among the groups 59
16 Neonatal complications among the study groups 60
XIV
17 Neonatal complications in study subjects among the groups 62
18 Neonatal mortality among the groups 63
19 Causes of Perinatal deaths among the groups 64
XVI
ABSTRACT
Background
Amniotic fluid performs several functions during the intrauterine life ,A simple
inexpensive, clinically useful test that will accurately determine amniotic fluid
volume is needed. Ultrasonography is noninvasive and clinically can quantitate the
amniotic fluid volume. It can be used to evaluate amniotic fluid volume by
measurement of a single pocket of amniotic fluid or by means of a semiquantitative
four-quadrant technique. Volume assessment by these techniques can be performed
quickly, is easily taught, and is reproducible.
Documentation of abnormalities of amniotic fluid volume may provide valuable
information to enhance fetal health assessment. Decreased amounts of amniotic fluid,
particularly in the third trimester, have been associated with multiple fetal risks,
including death, pulmonary hypoplasia, growth retardation, and other complications.
In contrast increased amounts of amniotic
fluid are correlated with fetal anomalies, twins, and insulin-dependent diabetes.
Our purpose was to determine the value of routine intrapartum amniotic fluid volume
assessment on perinatal outcome.
Objective
1. To study the Amniotic Fluid Index in term pregnancies
2.To Evaluate Fetomaternal outcome in different volumes of Amniotic Fluid
XVII
Methods
This is a prospective observational comparative study conducted at in Department of
Obstetrics and Gynecology, Vijayanagara Institute Of Medical Sciences,[VIMS]
Ballari from 1st January 2018 to 31st December 2018.
In this study, All pregnant women with term pregnancy admitted to labour room who
fulfill’s the inclusion criteria and willing to participate will be selected for the study .
patients will be subjected for ultrasound examination to study Amniotic Fluid index.
Fetomaternal outcome will be studied in different volumes of Amniotic Fluid.
Results
Among 300 subjects , 221 had Normal AFI, 64 had Oligohydramnios and 15 had
Polyhydramnios, majority of subjects in all three groups were in age group of 21-25
years,with normal BMI and booked status, majority of subjects of
Oligohydramnios(42.2%) and normal AFI(34.4%) had gestational age between 39-
39.6 weeks and Polyhdramnios (53.3%) had gestational age 37-37.6 weeks, and are
primigravida in all three groups. Incidence of , Cesarean section(70.3%), Fetal
distress(95.6%), Meconium stained liquor(34.4%),low 1 minutes APGAR, low birth
weight(32.8%), IUGR(29.7%) and NICU admission(35.9%) were common in
Oligohydramnios group.Incidence of Cesarean section(73.3%), Fetal
distress(54.5%),low 1 minutes APGAR, Macrosomia(32.8%), Gestational diabetes
mellitus(26.7%) and NICU admission(33.3%) were common in Polyhydramnios
group.
XVIII
Conclusion
Liquor assessment at term is necessary, as it indicates fetal well being & Abnormal
liquor
volumes at term are associated with increased maternal morbidity and adverse
perinatal outcome.
A detailed history, clinical examination and relevant investigations should be done to
identify the various etiological factors in all cases of abnormal liquor volume, to get
better fetal outcome as well as to avoid the maternal complications.
Keywords: Amniotic fluid index; AFI; Oligohydramnios; Polyhydramnios; Perinatal
outcome; Ultrasonography; Liquor assessment.
~ 1 ~
“STUDY OF AMNIOTIC FLUID INDEX AND FETO MATERNAL
OUTCOME IN TERM PREGNANCY AT VIMS, BALLARI”
INTRODUCTION
Amniotic fluid, once thought to merely provide protection and room for necessary
movement and growth for the fetus, is now understood to be a highly complex and
dynamic system that is studied as a data point to interpret fetal wellbeing. The Amniotic
fluid starts its origin from the maternal plasma by transudation as early as from the
seventh week of gestation. Its amount varies throughout the pregnancy. The Amniotic
fluid performs several functions during the intrauterine life. It helps to shape the fetal
skeleton normally by creating the physical space, promotes fetal lung maturation and
protects the umbilical cord from the compression during labour. Too much or too little
amount of amniotic fluid is the most common clinically detectable intrinsic abnormality1.
Before the era of the invent of ultrasound use in obstetrics, the amniotic fluid
volume was assessed clinically by the bimanual palpation and symphysio-fundal height
which was found to be unreliable subsequently. In 1950, Prof. Sir. Ian Donald was the
first to demonstrate and document the application of ultrasound to medical diagnosis2. In
modern obstetrics, ultrasound is an integral part of the obstetrician’s armamentarium-
almost an extension of the examining finger, because of its non invasive nature, accuracy
and repeatability.
The Amniotic fluid volume assessment is an integral part of the antepartum fetal
surveillance because of its abnormality is an indicator of poor perinatal outcome. Various
ultrasound methods has been proposed for the detection of amniotic fluid, among which
the amniotic fluid
~ 1 ~
“STUDY OF AMNIOTIC FLUID INDEX AND FETO MATERNAL
OUTCOME IN TERM PREGNANCY AT VIMS, BALLARI”
INTRODUCTION
Amniotic fluid, once thought to merely provide protection and room for necessary
movement and growth for the fetus, is now understood to be a highly complex and
dynamic system that is studied as a data point to interpret fetal wellbeing. The Amniotic
fluid starts its origin from the maternal plasma by transudation as early as from the
seventh week of gestation. Its amount varies throughout the pregnancy. The Amniotic
fluid performs several functions during the intrauterine life. It helps to shape the fetal
skeleton normally by creating the physical space, promotes fetal lung maturation and
protects the umbilical cord from the compression during labour. Too much or too little
amount of amniotic fluid is the most common clinically detectable intrinsic abnormality1.
Before the era of the invent of ultrasound use in obstetrics, the amniotic fluid
volume was assessed clinically by the bimanual palpation and symphysio-fundal height
which was found to be unreliable subsequently. In 1950, Prof. Sir. Ian Donald was the
first to demonstrate and document the application of ultrasound to medical diagnosis2. In
modern obstetrics, ultrasound is an integral part of the obstetrician’s armamentarium-
almost an extension of the examining finger, because of its non invasive nature, accuracy
and repeatability.
The Amniotic fluid volume assessment is an integral part of the antepartum fetal
surveillance because of its abnormality is an indicator of poor perinatal outcome. Various
ultrasound methods has been proposed for the detection of amniotic fluid, among which
the amniotic fluid
~ 2 ~
index(AFI) is the most widely used method. Phelan JP and colleagues in 1987
proposed this method3. According to him, the amniotic fluid volume was categorized as
follows,
Table no:1 Categories based on Amniotic Fluid Volume
Normal 8-24 cm
Borderline 5-8 cm
Oligohydramnios <5
Polyhydramnios >25
Oligohydramnios is recently defined as AFI below 5th percentile for the
gestational age. Post dated pregnancy, uteroplacental insufficiency, congenital anomalies
especially renal abnormalities, meconium passage, fetal heart rate abnormalities, low 5
minute APGAR and increased NICU admission are associated with Oligohydramnios4.
Other studies are also shown that it is associated with increased perinatal
morbidity and mortality. Hence antepartum fetal surveillance is mandatory in pregnant
women with Oligohydramnios. Hence Oligohydramnios in term is considered as an
indication for termination of pregnancy.
Polyhydramnios is defined as AFI > 95th percentile for gestational age. More than
fifty percent of women with Polyhydramnios, the etiology was unknown. Congenital fetal
anomalies accounts for 20%, among which Anencephaly occurs in 50% of the cases.
Gestational diabetes, congenital
infections also leads to the development of Polyhydramnios. An increased risk of
congenital abnormalities and perinatal mortality are associated with increasing severity of
Polyhydramnios5. Severe Polyhydramnios (AFI >35 cm) is commonly associated with
major congenital anomaly in 31% of cases.
~ 3 ~
Fig No:1 Amniotic Fluid Index Measurement of four quadrants
showing Normal AFI
Fig No:2 Amniotic Fluid Index Measurement of four quadrants
showing Oligohydramnios
~ 4 ~
Fig No:3 Amniotic Fluid Index Measurement of four quadrants
showing Polyhydramnios
So amniotic fluid volume assessment is an useful method to identify the fetus at risk for
adverse obstetric and perinatal outcome.
Therefore the present study was conducted to find out the maternal and perinatal outcome
and to identify the possible causes of Abnormal liquor volume.
~ 5 ~
OBJECTIVES
1. To study the Amniotic Fluid Index in term pregnancies
2.To Evaluate Fetomaternal outcome in different volumes of Amniotic Fluid
~ 6 ~
REVIEW OF LITREATURE
AMNIOTIC FLUID:
FORMATION:
In first trimester inward transfer of solutes along with passive diffusion of water from
extracellular fluid through the amnion and the permeable skin of the fetus is the likely
source of amniotic fluid. After 20th week, increasing stratification and cornification of the
skin prevents diffusion, the fetal urine becomes the main source of amniotic fluid
thereafter. During 4th- 5th weeks of gestation, fetal kidneys start to develop, by 8th to 11th
weeks it begin to excrete urine and by 20th week produces most of the amniotic fluid.
Daily urine production depends upon the weight of the fetus, approximately 30% of fetal
weight. The excreted urine via the amniotic fluid is recycled back to the fetus by
swallowing, it is approximately 25% of fetal weight, hence it will not serve real excretory
or homeostatic function. Therefore fetal urine output should be adequate to maintain
amniotic fluid volume. An another important contributor of AFV is fetal lung fluid8.
Fig no:4 Regulation of Amniotic fluid formation
~ 7 ~
Sources and Circulation:
During the intrauterine development, the fetus is surrounded by the amniotic fluid . The
precise site of origin of amniotic fluid is not well understood till now. Both maternal and
fetal factors contributes to the development of liquor amnii6,7. It is produced from the
sources listed below
1. Transudation of maternal plasma across the amnion and chorion
2. Transudation from fetal circulation through umbilical cord and placental membranes
3. Transudation of fetal serum through the permeable fetal skin before keratinization
4. Secretion from the amniotic epithelium
5. Fetal urine is the major source after 20 weeks of pregnancy
6. Fetal lung fluid that enters amniotic cavity
7. Secretions from fetal oral-nasal cavities also contributes to small extent
Fig no:5 Amniotic Fluid Pathways ( measurements are in ml/day)
~ 8 ~
Table no :2 Pathways for Amniotic Fluid
6 proposed pathways for fluid movement into and out of amniotic cavity by Brace RA 9
1997:
PATHWAYS ML/DAY TO
FETUS
ML/DAY TO
AMNIOTIC FLUID
Swallowing by the fetus 500-1000 -
Oral secretions - 25
Respiratory tract secretions 170 170
Fetal urine - 800-1200
Intramembranous flow between
placenta, umbilical cords and fetus
400 200-500
Transmembranous flow from
amniotic cavity in to uterine
circulation
- 10
Volume of Amniotic Fluid:
Amount of AFV varies throughout the pregnancy. It increases from 1ml at seven weeks to
25ml at ten weeks, 400ml at 20 weeks reaches about 1 litre at 36 weeks . Thereafter it
decreases progressively to about 800ml at term, as the pregnancy continues post term,
further reduction occurs to the extent of 200ml at 42 weeks8.
AFV changes in pregnancy were studied by Brace RA and Wolf EJ 19899 and their
observations were
1) AFV rises progressively during gestation until 32 weeks.
2) From 32 weeks to term, mean AFV is relatively constant (700-800ml)
~ 9 ~
3)After 40 weeks progressive decline in AFV at a rate 8% per week, with amniotic fluid
volume averaging only 400ml at 42 weeks9.
Queenan et al 1991 also described the correlation of AFV with fetal and placental weight
in grams10.
Table no: 3 Correlation of AFV with Fetal and Placental weight in
grams
Gestation age in weeks 16 28 36 40
Amniotic fluid in ml 200 1000 900 800
Fetal weight in grams 100 200 2500 3300
Placenta in grams 100 200 400 500
Fig no:6 AFV in relation with Gestational Age
~ 10 ~
FUNCTIONS:
Amniotic fluid has number of important roles in embryo and fetal development.
It provides several important functions to the fetus,the important roles of amniotic fluid
are:
Amniotic fluid volume maintains amniotic fluid pressure thereby reducing the
loss of lung liquid, an essential component to lung development. (Nicolini U,
1989)11
Permitting the movement of fetus and musculoskeletal development.
Protect fetus from trauma
Prevent cord compression
Has bacteriostatic properties and prevents infection
Maintains fetal body temperature
Provide nutrition to fetus
Swallowing the fluid leading to gastrointestinal development.
Physical Features of Amniotic Fluid:
Amniotic fluid is slightly alkaline in nature with pH of 7-7.5. Lower electrolyte
concentration of fetal urine makes it hypotonic and it contains more urea, creatinine and
uric acid compared to maternal serum.
With increasing gestational age, fetal urine osmolality decreases. Specific gravity of
liquor amnii is low6,7
The colour of the amniotic fluid changes during the normal course of pregnancy. Before
20 weeks it ranges from a pale straw colour to deep yellow depending upon the amount of
bilirubin. Before 20 weeks bilirubin is the normal constituent of amniotic fluid and does
not indicate the rhesus hemolytic disease in the fetus. After that the bilirubin
~ 11 ~
concentration decreases. Normal amniotic fluid is colourless by 36 weeks of gestation.
White floccules sometimes appear in the fluid during the last 4-5 weeks due to the
presence of desquamated fetal cells and free lipid
material( vernix caseosa)6.
Abnormal colouring usually results from contamination with meconium or blood, but it
may also be due to bilirubin. High bilirubin levels after 30 weeks is considered as
abnormal6.
Chemical Composition of Amniotic Fluid6,7:
The chemical composition of amniotic fluid is identical to maternal plasma in first half of
pregnancy, as pregnancy advances it is changed markedly due to the addition of fetal
urinary metabolites.
The main content of amniotic fluid is water constitute 98.1-99%, the solid part forms the
minor component of about 1-2 %. Solid component includes organic, inorganic and other
suspended particles
Organic Components:
Protein -0.5mg,
Non protein nitrogen-24mg
Uric acid-4-5 mg,
Sugar 19 mg,
Creatinine 2.2mg/ 100ml of amniotic fluid,
Urea-30 mg,
Total lipids- 50 mg,
Bilirubin,
Enzymes
~ 12 ~
Hormones-Cortisone, human chorionic gonodotrophin, human placental lactogen,
pregnanediol, 17-OH corticosteroids, estriol.
Inorganic Components:
Sodium, potassium, chloride and calcium. Sodium and chloride concentration decreases
as pregnancy advances but potassium remains unchanged.
Others:
Cells from bladder, vagina and respiratory tract
Vernix caseosa
Exfoliated squamous epithelial cell from fetal skin and lanugo hair
Amniotic cells
Evaluation of Amniotic Fluid Volume:
Evaluation of amniotic fluid volume can be done by -
(1) Clinical evaluation
(2) Invasive—dye dilution technique
(3) Ultrasonography(non invasive )
● Single deepest pocket
● Amniotic fluid index (AFI)
● Two diameter fluid pocket
Clinical assessment of amniotic fluid :It requires experienced hands and skills to
diagnose abnormalities in amniotic fluid volume by palpation of the abdomen. In cases of
Oligohydramnios, the clinical findings usually obtained are12 :
(1) Uterine size is much smaller than the period of amenorrhea.
(2) Perception of less fetal movements.
(3) The uterus is “full of fetus” because of scanty liquor.
~ 13 ~
(4) Malpresentations are common.
(5) Evidence of IUGR of the fetus..
Ultrasound evaluation is widely used technique among the various tests available to
detect AFV. Being a non invasive method, makes it ideal for large scale use and repeat
AFV determination in suspected amniotic fluid abnormalities. AFV by USG is done
either by simple visual estimation or by biometric assessment. It is a semiquantitative
method, never represent a true quantitative method13,14
Dye dilution test: It is considered as gold standard for assessment of amniotic fluid
volume. However this is an invasive technique requiring amniocentesis and therefore not
suitable for clinical practice which often needs repeated evaluation. In this technique a
known volume of dye like aminohippurate sodium is injected into the amniotic cavity
through amniocentesis. A sample of dye is taken after 20 minutes which is analysed with
spectrometry for degree of dilution. It reflects the actual AFV but invivo dye
concentrations may undergo rapid changes15.
Ultrasound evaluation of the amniotic fluid
Subjective method: It is based on the visualization of AF pockets without
measurements. The results are reported as either normal, low or high16. Examination by
an experienced sonographer is necessary to reduce the intraobserver variation which is
common in this method17. The results of this method is comparable with objective
methods like AFI, SDVP, 2DP and Dye dilution method.
Single deepest vertical pocket(SDVP): Manning FA et al 18 in 1981described the
concept of measuring the depth of maximum vertical pocket(MVP).They defined Severe
Oligohydramnios as MVP <1cm, reduced liquor as MVP 1-2 cm. In 1984 Chamberlain
~ 14 ~
PF et al19 defined the normal amount of amniotic fluid as the largest vertical pocket
measuring 2-8cm, Oligohydramnios as SDVP <2cm and Polyhydramnios as SDVP >8
cm. While measuring SDVP ultrasound transducer probe should be right angle to the
uterine contour without loops of cord structures and fetal parts.
Fig no:7 Measurment of SDVP
Amniotic fluid index (AFI): This method was proposed by Phelan JP et al3 in 1987.
It is a more objective and reproducible method as it estimates the amniotic fluid in four
quadrants. The uterus is arbitrarily divided into four quadrants by the umbilicus
transversely and linea nigra vertically. The deepest vertical pocket with no loops of cord
and free of fetal parts in each quadrant is measured and it is summed up to give the AFI.
Pockets are measured perpendicular to the floor with the patient in supine position. An
AFI of 5-18 cm is considered normal, AFI of 18cm or greater is Polyhydramnios or less
than 5cm is Oligohydramnios. Recently Oligohydramnios has been defined as less than
3rd and 5th percentile and hydramnios more than 95thand 97th percentile for gestational
~ 15 ~
age20. The reliability of correctly identifying Oligohydramnios or Polyhydramnios using
the percentiles is similar to SDVP(2-8) and AFI (5-18).
Fig no:8 Four quadrant method for AFI estimation
Two diameter pocket method (2-DP): It is an another semiquantitative method to
assess the AFV which was described by Magnan EF et al21 in 1992. He multiplied the
depth of largest vertical pocket to its transverse diameter. According to this method
normal AFV is 2-DP 15.1-50cm2, 2-DP <15cm2 defined as Oligohydramnios and 2DP >
50cm2 defined as hydramnios.
Though the accuracy of ultrasound indices is good to diagnose normal amount liquor
amnii, the sensitivity for both Oligohydramnios and Polyhydramnios remains poor22. All
these measurements suffer from methodological limitations of two dimensional
ultrasound and interference from fetal movements and loops of cord.
Clinical Importance of Amniotic Fluid6,7:
Amniocentesis has to be done to collect amniotic fluid for the following clinical purposes,
~ 16 ~
For the detection of developmental abnormalities and genetic diseases in the fetus
To assess the fetal lung maturity
To check fetal renal maturity
Hyaluronic acid which is rich in AF promotes bone healing
Prostaglandins and hypertonic saline are injected in the amniotic cavity for the induction
of abortion
Artificial rupture of membranes is a one of the method for the induction and
augmentation of labour
Detection of abnormal liquor volume either excess or low by AFI, helps in identifying a
fetus at risk
OLIGOHYDRAMNIOS:
Oligohydramnios is the condition in which the amount amniotic fluid is reduced to <200
ml at term.
Incidence vary between 0.5 - 5%.
Table no :4 Definitions of Oligohydramnios based on USG
Measurements
Manning 18et al MVP < 1cm
Chamberline 19et al SDVP <2cm
Phelan3 et al AFI <5cm
CAUSES OF OLIGOHYDRAMNIOS:
Decrease in amniotic fluid volume in second or third trimester is likely to be associated
with fetal growth restriction, placental abnormality or maternal preeclampsia. The
Jeng 23et al AFI <8cm
~ 17 ~
underlying etiology is uteroplacental insufficiency which can impair fetal growth and
reduce fetal urine output.
Conditions Associated with Oligohyadramnios1,6,24:
Maternal Causes:
1. Preterm premature rupture of membranes- 3-17 %
2. Uteroplacental insufficiency
3. Preeclampsia
4. Postdated pregnancy
5. Autoimmune disorders
6. Drugs like ACE inhibitors, PG synthesis inhibitors
Fetal Causes:
1. Chromosomal abnormalities- triploidy, turner syndrome, trisomy 18 - 4.4-30.7%
2. Intrauterine growth restriction
3. Intrauterine fetal demise
4. Fetal infections
5. Congenital anomalies- 7-37%
Bilateral renal agenesis
Multicystic dysplastic kidneys
Bladder outflow tract obstruction
Infantile polycystic kidney disease
Musculoskeletal
Cardiac
Digestive tract anomalies.
~ 18 ~
Placental Causes:
1. Abruptio placentae
2. TTTS
Idiopathic: Failure of secretion from amnion cells
INTRA UTERINE GROWTH RESTRICTION AND
OLIGOHYDRAMNIOS:
IUGR results in Oligohydramnios due to decreased urine production secondary to
decreased uteroplacental perfusion. Recent studies show the cause to reversal of
intramembranous flow . When single pocket of amniotic fluid is >2cm, between 1&2cm,
<1cm, prevalence of IUGR is %, 20%, and 37%.(Chamberlain PF, 1984)19
PRETERM RUPTURE OF MEMBRANES AND
OLIGOHYDRAMNIOS:
Rupture of membranes prior to 37 weeks of gestation is called as premature rupture of
membranes. It has an incidence of 1.7% between 24-34 weeks of gestation. Survival in
such second trimester Oligohydramnios is approximately 10%. (Shipp TD, 1996)25
FETAL HYPOXIA AND OLIGOHYDRAMNIOS:
In maternal diseases like chronic hypertension, Severe Pre eclampsia, connective tissue
disorders, chronic renal disease fatal hypoxia occurs due to uteroplacental insufficiency.
(Deutinger J, 1987)26
~ 19 ~
Experimental hypoxia results in a reflex redistribution of fetal cardiac output, a decrease
in renal and pulmonary flow, hence urinary output and production of fluid by lung
decreases and the amount of amniotic fluid declines.
But under long term conditions, hypoxia can induce suppression of fetal swallowing
resulting in increase in AFV. Oligohydramnios in fetal hypoxia is caused by placental
dysfunction in addition to hypoxia.
MATERNAL HYPOVOLEMIA AND OLIGOHYDRAMNIOS:
Acute maternal hypovolemia has been found to be the cause of Oligohydramnios. (Sherer
DM, 1990)27 The changes in amniotic fluid volume may be mediated by the changes in
intramembranous flow because the water induced reduction in fetal osmolality would be
expected to reduce intramembranous absorption. (Flack NJ, 1995)28
FETAL EFFECTS OF OLIGOHYDRAMNIOS:
In severe early onset Oligohydramnios, as in renal agenesis, there are several problems
and the fetal outcome is poor.(Garmel SH 1997)29
These problems may not be seen in late onset Oligohydramnios which accompany
intrauterine growth restriction. They are
Pulmonary hypoplasia
Amniotic adhesions or bands causing deformities like amputation
of digits( amniotic band syndrome)
~ 20 ~
Fig no:9 Amniotic band syndrome
Limb deformities like talipes
Potters facies (Low set ears, epicanthic fold, receding mandible ,flattened nose)
~ 21 ~
Fig no: 10 Potter’s syndrome
~ 22 ~
Incidence of Pulmonary hypoplasia is higher with Oligohydramnios (Moessinger AC
1989)30
According to (Fox HE 1994)31 and ( Laura MR 1995 )321995, there are three
possibilities that account for Pulmonary hypoplasia
1. Thoracic compression prevents chest wall excursion and lung expansion
2. Lack of breathing movements decreases lung inflow
3. Failure to retain amniotic fluid leading to impaired lung growth and development
Third trimester Oligohydramnios causes malpresentation, umbilical cord compression,
concentration of meconium in liquor, difficult or externalcephalic version. (Hofmeyr GJ,
1991)33
(Baron C 1995)34 reported 50% increase in variable decelerations during labour and
seven fold increase in cesarean delivery.
(Sarno AP 1989-1990)35 reported that AFI 5 was associated with fivefold increase in
cesarean delivery rates.
Intrapartum complications:
1. Cord compression in labour causing variable deceleration
2. Meconium aspiration syndrome
FETAL DISTRESS AND OLIGOHYDRAMNIOS:
(Leveno KJ 1984)36 described the risks to post term fetuses. Antepartum and intrapartum
fetal distress were found to be a consequence of cord compression due to
Oligohydramnios. The volume of amniotic fluid decreases after 38 weeks and passing
meconium into a reduced amniotic fluid results in thick viscous meconium which may be
swallowed by the fetus resulting in meconium aspiration syndrome.
~ 23 ~
OLIGOHYDRAMNIOS AND NON REACTIVE NST:
Spontaneous deceleration in no stress test with AFI<5cm may predict fetal compromise.
Hoskins IA et al37 showed in a study of 3150 patients of >34 weeks,that fetuses with
antepartum decelerations had statistically significant increased incidences of intrapartum
distress regardless of AFI. They also had significantly increased rates of neonatal acidosis
and low APGAR scores when there were severe decelerations and AFI5cm in the
antepartum period.
The incidence of clinical Oligohydramnios and NST revealing fetal heart decelerations or
bradycardia and an increase in the association with neonatal acidosis and low APGAR
scores was found to increase as the sonographic estimates of amniotic fluid volume were
decreased. So it is suggested that the postdated pregnancy with evidence of reduced AFV
should be considered for a trial of labour with cardiotocogram continuously. In contrast
an AFI>5cm coupled with normal NST has been correlated with a low incidence of fetal
death (<1/1000) within a week.
MANAGEMENT OF OLIGOHYDRAMNIOS:
Managing Oligohydramnios requires proper assessment of mother and fetus to find the
underlying etiology and correct it so the amniotic fluid returns back to normal. Eg.
Discontinuing prostaglandin inhibitor Intrauterine growth restriction needs testing, and
optimal time for delivery. In preterm premature rupture of membranes, need to
administer antibiotic and corticosteroids till gestational age of 32 weeks. (Vermillion ST,
2000)38
~ 24 ~
Isolated third trimester Oligohydramnios may not always be associated with poor
outcome for the baby. (Magann EF, 1999)39
AMNIOINFUSION:
In women with Oligohydramnios, amnioinfusion can be tried prophylactically to avoid
intrapartum fetal heart rate abnormalities due to cord compressions. .
In a randomized trial, (Macri CJ 1992)40, studied prophylactic amnioinfusion in 170 term
and post term pregnancies complicated by both thick meconium and Oligohydramnios.
Amnioinfusion significantly reduced the cesarean delivery rates for fetal distress and
meconium aspiration syndrome.
TRANSABDOMINAL AMNIOINFUSION:
Transabdominal amnioinfusion can be tried for diagnostic and therapeutic purpose for
second trimester oligohydramnios. (Quetel TA, 1992)41 400-600ml Normal saline instilled
transabdominally resulted in better ultrasound visualization. Adding indigo carmine and
detecting it vaginally, helped identifying preterm premature rupture of membranes. (Fisk
NM 1991)42.
(Miyazaki FS 1985)43 noted that various deceleration due to cord compression are
reduced by transabdominal amnioinfusion.
~ 25 ~
Fig no :11 Transabdominal amnioinfusion
TRANSVAGINAL AMNIOINFUSION:
Fig no: 12 Transvaginal amnioinfusion
Predominant indications are:
1.Meconium stained amniotic fluid
2.Variable deceleration
3.Prophylactically for Oligohydramnios 500-800ml bolus of warmed normal saline
followed by a continuous infusion of approximately 3ml/min (Pressman EK, 1998)44
~ 26 ~
In another study (Rinehart BK 2000)45 randomly gave a 500ml bolus of NS at room
temperature alone or 500ml bolus plus continuous infusion of 3ml/min.
AMNIOINFUSION IN VARIABLE DECELERATION:
(Hofmeyer GJ 2012)46 used the Cochrane Database to specifically analyse the effects of
amnioinfusion in management of variable deceleration in fetal heart rate patterns
associated with umbilical cord compression. They used 19 studies, most of them having
less than 200 subjects. The conclusion was that amnioinfusion was useful in reducing
occurrence of variable deceleration, reducing caesarean deliveries incidence, improving
neonatal outcome. The American College of Obstertricians and Gynaecologists (ACOG)
(2013) recommends using amnioinfusion in cases with persistent variable deceleration.
AMNIOINFUSION FOR MECONIUM STAINED AMNIOTIC FLUID:
(John Pierce 2000)47 analysed 13 prospective trials regarding intrapartum amnioinfusion
in 1924 women with moderate to thick meconium stained amniotic fluid. They found that
infants of mothers treated with amnioinfusion had lesser chance of having meconium
below the vocal cords and less likely to have meconium aspiration syndrome as compared
to infants of mothers who were not given amnioinfusion. The caesarean incidence was
also
significantly lower in mothers treated with amnioinfusion. (A M Rathore 2002)48 also
found similar results in a separate study.
( Fraser WD 2005)49 did amnioinfusion in women having thick meconium stained
amniotic fluid in labour and concluded it has no significant benefits.
Because of these findings, ACOG (2006)50 does not recommend amnioinfusion to
dilute meconium stained amniotic fluid.
~ 27 ~
According to (Xu H 2007)51 where continuous monitoring is not possible, amnioinfusion
may be used to lower incidence of meconium aspiration syndrome.
COMPLICATIONS OF AMNIOINFUSION:
Uterine hypertension
Chorioamnionitis
Cord prolapse
Abnormal fetal heart tracing
Uterine rupture
Maternal cardiac or respiratory compromise
Placental abruption
MATERNAL HYDRATION:
Intravenous hydration with 6500ml of an isotonic increased amniotic fluid volume in
markedly dehydrated women. (Sherer DM, 1990)52
(Brace RA 1989)9 showed that changes in maternal intravascular volume can alter fetal
urine output, amniotic fluid volume and to a lesser extent intravascular volume.
(Kilpatrick SJ 1991)53 oral maternal hydration with two litres of water was associated
with an increase in AFI by approximately 30% in women with decreased AFI and normal
AFI.
POLYHYDRAMNIOS:
Excessive amniotic fluid of more than 2000-2200ml is defined as Polyhydramnios1,6,7.
The incidence of Polyhydramnios is 1%-2%, independant of race and ethnicity20.
Multiparous women has increased risk to develop Polyhydramnios than primi.
~ 28 ~
Table no:5 Definitions of Polyhydramnios according to various study
Chamberlin et al19 SDVP > 8 cm
Phelan et al3 AFI > 25 cm
Carlson et al54 AFI > 2SD of the mean for late 2nd and 3rd
trimester (24cm)
Moore et al20 > 95th to 97th percentile for
gestational age
Classification:
Based on the severity, Hill 55, Biggio56 and Golan57 classified the Polyhydramnios as
mild, moderate and severe. Harman CR58 et al studied the perinatal mortality and
anomalies associated with different types of Polyhydramnios.
Table no:6 Classification of Polyhydramnios
Types SDVP
incm
AFI in
cm
% PerinatalMortality in
1000
Anomalies(%)
Mild 8-11 25-30 80 50 ≤ 6
Moderate 12-15 30-35 15 190 ≤ 45
Severe >16 >35 5 540 ≤ 65
Based on the onset, it is further classified as acute and chronic1,6
Acute polyhydramnios: It is a rare condition with acute onset and the accumulation
of fluid within a few days. It often manifests before 20 weeks, associated with
monozygotic twins and chorioangioma of the placenta. Usually spontaneous abortion
occurs, slow amnioreduction can be done for maternal distress. It often needs repeated
amniocentesis.
~ 29 ~
Chronic polyhydramnios: It is the most common type with gradual increase in fluid
over few weeks. It usually occurs after 32 weeks.
Causes of hydramnios:
Polyhydramnios can be due to excessive production of liquor amni or due to defective
absorption. The degree of hydramnios as well as its prognosis is often related the cause.
Both maternal and fetal causes leads to the development of Polyhydramnios.
Its various causes are as follows:
1. Idiopathic: In 66% of cases, cause is unknown
2. Fetal causes:
Congenital anomalies59 -
1.Anencephaly (50%) –It is a most common fetal congenital anomaly causing
polyhydramnios. Increased urination caused by impaired ADH secretion, decreased
swallowing reflex and increased transudation from the exposed meninges are the possible
causes of hydramnios.
Open spina bifida- Increased transudation from the exposed meninges
Esophageal and duodenal atresia (15%) - Decreased swallowing of the liquor
Facial clefts and neck masses- by interfering with normal swallowing
Congenital diaphragmatic hernia
Fetal bartter syndrome
Fetal muscular dystrophy
Fetal sacrococcygeal teratoma
Fetal vein of galen aneurysm
Fetal infections
Hydrops fetalis due to Rh isoimmunisation,
~ 30 ~
cardiothoracic anomalies and fetal cirrhosis
Multiple pregnancy due to large placenta- 10 times the incidence, It is more common in
monoamniotic twins affecting the second sac .
3. Placental causes:
Placental chorioangioma due to increased transudation
4. Maternal causes:
Diabetes (30%)- Due to fetal hyperglycemia causing fetal diuresis and hydramnios
Cardiac or renal diseases due to increased transudation from edematous placenta
Clinical Presentation:
Symptoms1,6,7:
Depending upon the rapidity of its onset and degree of hydramnios, the clinical
presentations will vary. Acute polyhydramnios will manifest like acute abdominal
catastrophe like pain abdomen, nausea, vomiting. In gradual onset, the patient may
present with increased abdominal girth, breathlessness on supine posture, digestive
discomfort, swelling of the legs, varicosities in lower limb, occasionaly it can cause
hyperemesis.Mirror syndrome or ballantyne syndrome occurs in hydrops foetalis with
hydramnios.
Signs1,6,7:
Dyspnoea on supine position
Signs of preeclampsia –hypertension, albuminuria, edema.
The foetus is freely ballottable
Fluid thrill is present
Foetal parts are difficult to palpate, foetal heart sounds are not
easily audible
Malpresentations are common
~ 31 ~
Evaluation60:
Ultrasonography :
It is helpful in the diagnosis of hydramnios
To exclude the other causes of hydramnios.
To detect associated congenital anomalies
To know the lie and presentation of the foetus
Blood Investigations:
Glucose tolerance test should be done to all women to exclude gestational diabetes.
Blood grouping and typing. If USG shows foetal hydrops, maternal antibody screen for
D, C, Kell and Duffy antigen should be done to exclude alloimmunisation. Further
evaluation for non immune hydrops can be done if antibody testing is negative. These
include serology testing for syphilis, IgG and IgM for rubella, toxoplasma, parvovirus and
cytomegalovirus. Invasive testing like amniocentesis can be performed for foetal
karyotyping
Differential Diagnosis6,7:
1. Multiple pregnancy – it can be excluded from polyhydramnios
By
a. Fundal height is more than the period of gestation
b. Too many foetal parts 3. Fluid thrill absent 4. USG will confirm
the diagnosis
2. Large ovarian cyst complicating pregnancy – a. The gravid uterus is felt separately
from the cyst b. The cervix is pushed down into the pelvis but in hydramnios the cervix is
drawn up
3. Maternal ascites- a. Presence of shifting dullness b. Resonance in the midline due to
floating gut whereas in hydramnios it is dull c.Size of the uterus will be normal
~ 32 ~
4. Retroverted gravid uterus with full bladder
5. Hydatiform mole
6. Concealed abruption
Complications1,6,7:
Fetal Complications:
Perinatal morbidity and mortality is increased in polyhydramnios. Most cases of mild
hydramnios are idiopathic and carry a low risk for undiagnosed anomalies compared to
severe hydramnios. Premature delivery and congenital anomalies are the main factors
responsible for morbidity and mortality. Other factors are cord prolapse, hydrops foetalis,
operative delivery and abruption
Maternal Complications:
During Pregnancy:
1. Abruptio placentae is most dreadly complication of hydramnios
2. Gestational hypertension
3. Abnormal foetal presentation
4. PROM
5. Premature delivery either spontaneous or induced
6. Cardio respiratory embarrassment
During Labour:
1. Increased incidence of cord prolapse
2. Dysfunctional labour
3. Uterine inertia sss
4. Increased operative delivery
5. Increased cesarean delivery
6. Postpartum hemorrhage
~ 33 ~
7. Retained placenta
Postpartum Period:
1. Subinvolution is common
2. Puerperal sepsis due to increased operative interference and blood loss
Management :
Conservative Management with close observation will suffice in most of the cases
of minor degree of Polyhydramnios
Moderate type of Polyhydramnios can be managed until labour starts.
Severe type often requires hospitalization, due to maternal respiratory distress,
significant abdominal pain or premature uterine contractions. In this condition
therapeutic amniocentesis is required.
Serial amnioreduction is required in conditions with fetal abnormality or twin-
twin transfusion syndrome with severe polyhydramnios.
Amniocentesis: During amniocentesis 500 ml per hour (1500 to 2000ml per day)
can be removed in single setting . Before the procedure placental localization
should be done with ultra sound.
Risks of Amniocentesis are fetal loss (1.2%), preterm labour, premature rupture of
membranes, placental abruption, chorioamnionitis, Rh isoimmunisation and fetal
pneumothorax.
Prostaglandin synthetase inhibitors: Among the PG synthetase inhibitors,
indomethacin is the most commonly used drug. It reduces the amniotic fluid
volume by decreasing the urine production from the fetal kidneys, decreasing the
production of lung fluid and increased removal of fluid from the lungs as well as
increased movement across fetal membranes. Dose is 1.4-3 mg/kg daily. (25mg 4-
6 hourly to 75 mg 12 hourly). Maternal side effects are GIT disturbances, rectal
irritation, transient prenal insufficiency and cholestatic jaundice.
~ 34 ~
Sulindac is another prostaglandin inhibitor used in the treatment of
polyhydramnios.
If it is decided to induce labour, liquor should be drained carefully in a controlled
manner, either by amniocentesis or by a needle inserted into the forewater to
prevent cord prolapse and abruption.
~ 35 ~
METHODOLOGY
This is prospective observational comparative study conducted at Department of
Obstetrics and Gynaecology, Vijayanagar Institute of Medical Sciences, Ballari from 1st
January 2018 to 31st December 2018.
Institutional ethical clearance was obtained before starting the study.
Written informed consent was taken from the subjects, Form F and Proforma was filled
accordingly. Study was conducted in patients who fulfilled inclusion criteria.
All cases were subjected to detailed history and examination. The assessment of
gestational age was made based on menstrual history, 1st trimester Ultrasonography and
clinical examination.
Inclusion criteria
1.Single live intrauterine gestation
2.Gestational age 37 to 40 weeks of gestation
3.Intact membrane.
Exclusion criteria
1. Gestational age <37 completed weeks
2. Postdated pregnancy
3. Ruptured membranes
4.Uterine scar due to previous lower segment caesarean section(LSCS), myomectomy,
hysterotomy.
5.Multiple Gestation
6.Congenital anamoly
~ 36 ~
The study includes pregnant women with gestational age 37 to 40 weeks who fulfilled
inclusion criteria were enrolled into our study
Study setting: Department of Obstetrics and Gynaecology, Vijayanagar Institute of
Medical Sciences, Ballari.
Study period: One year (12 months) study period. Study was conducted from 1st
January 2018 to 31st December 2018.
Sampling method
All pregnant women with term pregnancy admitted to labour room who fulfilled the
inclusion criteria was selected for the study . All patients was subjected for ultrasound
examination to study Amniotic Fluid index. Fetomaternal outcome was studied in
different volumes of Amniotic Fluid.
Sample size
During the study period of 1 year from 1st January 2018 to 31st December 2018, a total
of 300 cases were enrolled as per inclusion criteria out of which 221 cases were with
normal AFI, 64 cases of Oligohydramnios and 15 cases of Polyhydramnios.
Objective of study
1. To study the Amniotic Fluid Index in term pregnancies
2.To Evaluate Fetomaternal outcome in different volumes of Amniotic Fluid
Method of data collection
The study includes pregnant women with gestational age 37to 40 weeks admitted in
labour room at department of OBG, VIMS , BALLARI.
Written informed consent was taken from the subjects, Form F was filled accordingly.
~ 37 ~
Data was collected using a pretested Proforma meeting the objectives of the study by
convenience sampling method. Detailed history, physical examination and necessary
investigations was undertaken.
Amniotic Fluid index(AFI) to be measured using Phelan’s four quadrant ultrasound
technique. The uterus is arbitrarily divided into four quadrants by the umbilicus
transversely and the linea nigra vertically. The largest vertical pocket free of fetal parts
and umbilical cord loops in each quadrant is measured and sum of these measurements
will give AFI in cm.
An AFI of 6-24cm is normal. AFI of ≤5cm or single deepest vertical pocket ≤2cm is
considered as Oligohydramnios and ≥ 25cm or single deepest vertical pocket ≥8cm is
considered as Polyhydramnios ..
Maternal outcome i.e.mode of delivery ,Indication for LSCS and other associated
complications are studied.
Perinatal outcome i.e. Meconium staining of liquor, APGAR at 1 minute,5 minutes,Birth
weight, NICU admission , reason for NICU admission and perinatal death and its cause
to be assessed.
Pulse rate, BP, FHR, uterine activity, and Partographic monitoring for progress of labour
was done. If any FHR variability, Meconium stained liquor, arrest of descent or maternal
conditions like uterine hyperstimulation was encountered operative delivery was opted.
The data like maternal age ,parity, BMI, pre induction Bishop score, post induction
Bishop score, mode of delivery, induction to delivery interval, indications for LSCS,
NICU admission and maternal complications were analysed using standard statistical
analysis(chi square test).
~ 38 ~
Does the study require any investigations or interventions to be conducted on
patients or animals? If so describe briefly.
Yes, following investigations were done in each patient.
Haemoglobin percentage
Blood grouping and Rh typing
RBS
HIV
HBsAg
Obstetric term scan
~ 39 ~
SAMPLE SIZE ESTIMATION :
The Average admission rate in our labour room for my unit was 2000 cases per year,
based on that we intended to study minimum of 300 cases.
During the study period of 1 year from 1st January 2018 to 31st December 2018, a total of
300 cases were enrolled as per inclusion criteria out of which 221 cases were with
Normal AFI , 64 cases of Oligohydramnios and 15 cases of Polyhydramnios.
~ 40 ~
RESULTS:
Table no. 7: Distribution of the study subjects based on amniotic fluid
index
Of the 300 subjects ,Ultrasonographically 221 subjects had normal AFI(73.7%), 64
subjects had Oligohydramnios(21.3%) and 15 subjects had Polyhydramnios (5%)
Graph no1: Distribution of the study subjects based on amniotic fluid
index
73.7%
21.3%
5.0%
Distribution of the study subjects based on amniotic fluid index
Normal AFI
Oligohydramnios
Polyhydramnios
Distribution of the study subjects based on amniotic fluid index
Category Frequency Percentage
Normal AFI 221 73.7
Oligohydromios 64 21.3
Polyhydromios 15 5.0
Total 300 100.0
~ 41 ~
Table no. 08: Age wise distribution of the study subjects among the
groups
Age wise distribution of the study subjects among the groups Age group Normal Oligohydramios Polyhydramnios P value
n (%) n (%) n (%)
≤ 20 yrs 80 (36.2) 21 (32.8) 3 (20.0) 0.547
21 - 25 yrs 107 (48.4) 34 (53.1) 7 (46.7)
26 - 30 yrs 30 (13.6) 8 (12.5) 4 (26.7)
> 30 yrs 4 (1.8) 1 (1.6) 1 (6.7)
Total 221 (100) 64 (100) 15 (100)
Mean ± SD 22.51 ± 3.17 22.69 ± 3.12 24.47 ± 3.76 0.071
Majority of the subjects that is 48.4%, of normal AFI , 53.1% of Oligohydramnios and
46.7% of Polyhydramnios belongs to age group of 21-25 years ,
The Mean age is 22.51±3.17 in normal AFI,22.69± 3.12 in Oligohydraminos &24.47 ±
3.76 in Polyhydramnios , which is statistically not significant.
Graph no 02: Age wise distribution of the study subjects among the
groups
0.0
10.0
20.0
30.0
40.0
50.0
60.0
≤ 20 yrs 21 - 25 yrs 26 - 30 yrs > 30 yrs
36.2
48.4
13.6
1.8
32.8
53.1
12.5
1.6
20.0
46.7
26.7
6.7
Perc
enta
ge
Age wise distribution of the study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 42 ~
Table no. 09: BMI wise distribution of the study subjects among the
groups
BMI wise distribution of the study subjects among the groups
BMI Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Underweight 5 (2.2) 2 (3.1) 1 (6.6) <0.001
Normal 127 (57.5) 44 (68.8) 4 (26.7)
Over weight 88 (39.8) 18 (28.1) 8 (53.3)
Obese 1 (0.5) 0 (0.0) 2 (13.3)
Total 221 (100) 64 (100) 15 (100)
Mean ± SD 23.85 ± 2.66 23.31 ± 2.41 25.52 ± 3.55 0.015
This table and graph shows majority of subjects that is 57.7% of Normal AFI, 68.8% of
Oligohydramnios & 26.7% of Polyhydramnios had normal BMI with
P value of < 0.001, which is statistically significant.
60% of the Polyhydramnios were overweight & 13.3% were obese which is statistically
significant
Graph no. 03: BMI wise distribution of the study subjects among the groups
0
20
40
60
80
2.2
57.5
39.8
0.5 3.1
68.8
28.1
0.0 6.6
26.7
53.3
13.3
Perc
enta
ge
BMI wise distribution of the study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 43 ~
Table no. 10: Status wise distribution of the study subjects among the
groups
Status wise distribution of the study subjects among the groups
Status Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Booked 214 (96.8) 63 (98.4) 15 (100) 0.63
Unbooked 7 (3.2) 1 (1.6) 0 (0.0)
Total 221 (100) 64 (100) 15 (100)
Majority of the subjects that is 96.8% of normal AFI, 98.4% of Oligohydramnios, 100%
of Polyhydramnios are booked , thus subjects in all three groups are similar in terms of
their booking status.
Graph no. 04: Status wise distribution of the study subjects among the
groups
0.0
20.0
40.0
60.0
80.0
100.0
Booked Unbooked
96.8
3.2
98.4
1.6
100.0
0.0
Perc
enta
ge
Status wise distribution of the study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 44 ~
Table no. 11: Gestation wise distribution of the study subjects among
the groups
Gestation wise distribution of the study subjects among the groups
Gestation age Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
37 – 37.6wks 65 (29.4) 20 (31.3) 8 (53.3) 0.312
38 – 38.6wks 76 (34.4) 15 (23.4) 3 (20.0)
39 – 40wks 80 (36.2) 29 (45.3) 4 (26.7)
Total 221 (100) 64 (100) 15 (100)
Mean ±SD 38.93 ± 0.96 38.96 ± 1.18 38.39 ± 1.14 0.127
In our study majority of the subjects that is 36.2% of normal AFI, 45.3% of
Oligohydramnios, were between 39 to 40 weeks of gestation and 53.3 % of
Polyhydramnios were between 37 to 37.6 weeks of gestation
The mean gestational age is 38.93± 0.96 in normal, 38.96 ± 1.18 in Oligohydramnios
and 38.39 ± 1.14 in Polyhydramnios which was statistically not significant
Graph no. 05: Gestation wise distribution of the study subjects among
the groups
0.0
10.0
20.0
30.0
40.0
50.0
60.0
37 – 37.6 wks
38 – 38.6 wks
39 – 40 wks
29.4 34.4 36.2
31.3
23.4
45.3
53.3
20.0 26.7
Perc
enta
ge
Gestation wise distribution of the study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 45 ~
Table no. 12: Obstetric profile of the study subjects among the groups
Obstetric profile of the study subjects among the groups Variable Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Gravida 1 132 (59.7) 46 (71.9) 7 (46.7) 0.043
Gravida 2 44 (19.9) 10 (15.6) 7 (46.7)
Gravida 3 33 (14.9) 5 (7.8) 0 (0.0)
Gravida 4 10 (4.5) 2 (3.1) 0 (0.0)
Gravida 5 2 (0.9) 1 (1.6) 1 (6.7)
Total 221 (100) 64 (100) 15 (100)
Para 1 37 (16.7) 8 (12.5) 4 (26.7) 0.01
Para 2 32 (14.5) 2 (3.1) 0 (0.0)
Para 3 5 (2.3) 1 (1.6) 0 (0.0)
Para 4 1 (0.5) 0 (0.0) 1 (6.7)
NA 146 (66.1) 53 (82.3) 10 (66.7)
Total 221 (100) 64 (100) 15 (100)
Living 0 1 (0.5) 1 (1.6) 2 (13.3) 0.001
Living 1 38 (17.2) 6 (9.4) 2 (13.3)
Living 2 29 (13.1) 2 (3.1) 0 (0.0)
Living 3 4 (1.8) 1 (1.6) 1 (6.7)
Living 4 1 (0.5) 0 (0.0) 0 (0.0)
NA 148 (67.0) 54 (84.4) 10 (66.7)
Total 221 (100) 64 (100) 15 (100)
Abortion 1 21 (9.5) 6 (9.4) 3 (20.0) 0.311
Abortion 2 4 (1.8) 1 (1.6) 0 (0.0)
Abortion 3 0 (0.0) 1 (1.6) 0 (0.0)
Abortion 4 0 (0.0) 1 (1.6) 0 (0.0)
Nil 196 (88.7) 55 (85.9) 12 (80.0)
Total 221 (100) 64 (100) 15 (100)
~ 46 ~
Above table shows that maximum number of the subjects that is 59.7% of normal AFI,
71.9% of Oligohydramnios, 46.7% of Polyhydramnios are primigravida Which is
statistically not significant.
Graph no. 06: Obstetric profile of the study subjects among the groups
0.0 20.0 40.0 60.0 80.0 100.0
Gravida 1
Gravida 2
Gravida 3
Gravida 4
Gravida 5
Para 1
Para 2
Para 3
Para 4
NA
Living 0
Living 1
Living 2
Living 3
Living 4
NA
Abortion 1
Abortion 2
Abortion 3
Abortion 4
Nil
59.7
19.9
14.9
4.5
0.9
16.7
14.5
2.3
0.5
66.1
0.5
17.2
13.1
1.8
0.5
67.0
9.5
1.8
0.0
0.0
88.7
71.9
15.6
7.8
3.1
1.6
12.5
3.1
1.6
0.0
82.8
1.6
9.4
3.1
1.6
0.0
84.4
9.4
1.6
1.6
1.6
85.9
46.7
46.7
0.0
0.0
6.7
26.7
0.0
0.0
6.7
66.7
13.3
13.3
0.0
6.7
0.0
66.7
20.0
0.0
0.0
0.0
80.0
Percentage
Obstetric profile of the study subjects among the groups
Polyhydramnios Oligohydramnios Normal
~ 47 ~
Table no. 13: Distribution of the study subjects based on mode of
delivery among the groups Distribution of the study subjects based on mode of delivery among the
groups
Mode of
delivery Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
LSCS 44 (19.9) 45 (70.3) 11 (73.3) <0.001
Vaginal 177 (80.1) 19 (29.7) 4 (26.7)
Total 221 (100) 64 (100) 15 (100)
This table shows that majority of subjects that is 73.3% of Polyhydramnios, 70.3% of
Oligohydramnios had LSCS compared to 19.9% of normal AFI group and maximum
number of subjects that is 80.1% of normal AFI had vaginal delivery compared to 29.7%
of Oligohydramnios, 26.7% Polyhydramnios.
which is statistically significant
Graph no. 07: Distribution of the study subjects based on mode of
delivery among the groups
0.0
20.0
40.0
60.0
80.0
100.0
LSCS Vaginal
19.9
80.1 70.3
29.7
73.3
26.7 Perc
enta
ge
Distribution of the study subjects based on mode of delivery among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 48 ~
Table no. 14: Distribution of the study subjects based on mode of
delivery among the groups Distribution of the study subjects based on mode of delivery among the groups
Mode of delivery Normal
Oligohydramnio
s
Polyhydramnio
s P value
n (%) n (%) n (%)
LSCS 44 (19.9) 45 (70.3) 11 (73.3) <0.001
Spontaneous vaginal
delivery 167 (75.6) 16 (25.0) 3 (30.0) <0.001
Induced vaginal delivery 10 (4.5) 3 (4.7) 1 (6.7) 0.931
Instrumental vaginal delivery 13 (5.9) 4 (6.3) 1 (6.7) 0.987
This table shows that majority of subjects that is 73.3% of Polyhydramnios, 70.3% of
Oligohydramnios had LSCS compared to 19.9% of normal AFI group and maximum
number of subjects that is 80.1% of normal AFI had vaginal delivery compared to 29.7%
of Oligohydramnios, 26.7% Polyhydramnios.
which is statistically significant
4.5% of normal AFI , 4.7% of Olighydramnios , 6.7% of Polydramnios had induced
vaginal delivery and 5.9% of normal AFI, 6.3% of Oligohydramnios, 6.7% of
Polyhydramnios had instrumental vaginal delivery which is statistically not significant
~ 49 ~
Graph no. 08: Distribution of the study subjects based on mode of
delivery among the groups
0.020.040.060.080.0
19.9
75.6
4.5 5.9
70.3
25.0
4.7 6.3
73.3
30.0
6.7 6.7
Distribution of the study subjects based on mode of delivery among the groups
Normal
Oligohydramnios
~ 50 ~
Table no. 15: Indication of LSCS in the study subjects among the groups
Indication of LSCS in the study subjects among the groups
Indication of LSCS Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Arrest of descent 7 (15.9) 0 (0.0) 2 (18.2) <0.001
Breech 1 (2.3) 0 (0.0) 0 (0.0)
Cephalo-pelvic
disproportion 7 (15.9) 1 (2.2) 2 (18.2))
Deep transverse arrest 0 (0.0) 1 (2.2) 0 (0.0)
Fetal distress 27 (61.4) 43 (95.6) 6 (54.5)
Non progression of labour 1 (2.3) 0 (0.0) 1 (9.1)
Second stage arrest 1 (2.3) 0 (0.0) 0 (0.0)
Total 44 (100) 45 (100) 11 (100)
The most common indication for LSCS in all three groups that is 61.4% of normal AFI
95.6% of oligohydramnios and 54.5% of polyhydramnios is fetal distress for which P
value is < 0.001 which is statistically significant.
Second most common indication for LSCS is arrest of descent and CPD in normal
AFI(15.9%), CPD and deep transverse arrest in oligohydramnios(2.2%) and arrest of
descent and CPD in polyhydramnios(18.2%)
~ 51 ~
Graph no. 09: Indication of LSCS in the study subjects among the
groups
0.0
20.0
40.0
60.0
80.0
100.0
AD Breech CPD DTA FD NPL 2ndstagearrest
15.9
2.3
15.9
0.0
61.4
2.3 2.3 0.0 0.0 2.2 2.2
95.6
0.0 0.0
18.2
0.0
18.2
0.0
54.5
9.1
0.0
Perc
enta
ge
Indication of LSCS in the study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 52 ~
Table no. 16: Distribution of the study subjects based on oxytocin
augmentation among the groups
Distribution of the study subjects based on oxytocin augmentation among the groups
Oxytocin Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Yes 99 (55.9) 15 (78.9) 3 (75.0) 0.115
No 79 (44.1) 4 (21.1) 1 (25.0)
Total 177 (100) 19 (100) 4 (100)
In our study 55.9% of normal AFI, 78.9% of Oligohydramnios , 75% of Polyhydramnios
had oxytocin augmentation during vaginal delivery which is statistically not significant
Graph no. 10: Distribution of the study subjects based on oxytocin
augmentation among the groups
0.0
20.0
40.0
60.0
80.0
Yes No
55.9
44.1
78.9
21.1
75.0
25.0
Perc
enta
ge
Distribution of the study subjects based on oxytocin augmentation among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 53 ~
Table no. 17: Co-morbid conditions in study subjects among the groups
Co-morbid conditions in study subjects among the groups
Co-morbid conditions Normal Oligohydramnios Polyhydramnios
n (%) n (%) n (%)
Pre-eclampsia 26 (11.8) 14 (21.9) 2 (13.3)
Gestational HTN 7 (3.2) 1 (1.6) 1 (6.7)
Gestational DM 0 (0.0) 0 (0.0) 4 (26.7)
RH negative pregnancy 11 (5.0) 3 (4.7) 0 (0.0)
HBsAg positive 3 (1.4) 2 (3.1) 0 (0.0)
Hypothyroidism 1 (0.5) 1 (1.6) 1 (6.7)
Severe anaemia 4 (1.8) 0 (0.0) 0 (0.0)
Asthma 0 (0.0) 1 (1.6) 0 (0.0)
In our study 11.8% of Normal AFI , 21.9% of Oligohydramnios subject had preeclampsia
and 26.7% of Polyhydramnios had gestational diabetes mellitus as a most common co
morbid condition, followed by Rh negative pregnancy as co morbid condition in 4.7% of
normalAFI and 5% of Oligohydramnios and preeclampsia(13.3%) in Polyhydramnios
~ 54 ~
Graph no. 11: Co-morbid conditions in study subjects among the groups
0.0
5.0
10.0
15.0
20.0
25.0
30.0
11.8
3.2 0.0
5.0
1.4 0.5 1.8
0.0
21.9
1.6 0.0
4.7 3.1
1.6 0.0
1.6
13.3
6.7
26.7
0.0 0.0
6.7
0.0 0.0
Co-morbid conditions in study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 55 ~
Table no. 18: Distribution of the study subjects based on colour of liquor
among the groups
Distribution of the study subjects based on colour of liquor among the
groups
Liquor color Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Meconium stained 23 (10.4) 22 (34.4) 2 (13.3) <0.001
Clear liquor 198 (89.6) 42 (65.6) 13 (86.7)
Total 221 (100) 64 (100) 15 (100)
This table shows that among the subjects 34.4% in Oligohydramnios , 13.3% in
Polyhydramnios had meconium stained liquor compared 10.4 % in normal AFI group for
which P value is < 0.001 which is statistically significant.
Graph no. 12: Distribution of the study subjects based on color of liquor
among the groups
0.0
20.0
40.0
60.0
80.0
100.0
Meconium stained Clear liquor
10.4
89.6
34.4
65.6
13.3
86.7
Perc
enta
ge
Distribution of the study subjects based on color of liquor among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 56 ~
Table no. 19: Birth weight of the newborns among the groups
Birth weight of the newborns among the groups Birth wt Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Normal (≥2.5Kg) 171 (77.4) 42 (65.6) 10 (66.7)
LBW (1.5-2.4kgs) 41 (18.6) 21 (32.8) 2 (13.3) 0.001
VLBW (<1.5 kgs) 0 (0.0) 1 (1.6) 0 (0.0)
Macrosomia (>3.5kgs) 9 (4.1) 0 (0.0) 3 (20.0)
Total 221 (100) 64 (100) 15 (100)
Mean ± SD 2.76 ± 0.39 2.54 ± 0.47 3.03 ± 0.55 <0.001
Majority of subjects that is 77.4% in normal AFI , 65.6% in Oligohydramnios, 66.7% in
Polyhydramnios had birth weight of the babies in normal range(≥2.5Kg)
32.8% of Oligohydramnios had low birth weight for there babies(1.5-2.4kgs) compared to
18.6% of normal AFI & 13.3% of Polyhydramnios which is statistically significant
The Mean birth weight among normal AFI is 2.76 ±0.39, Oligohydramnios is
2.54±0.47,Polyhydramnios is 3.03±0.55 with p value <0.001 which is statistically
significant
Graph no. 13: Birth weight of the newborns among the groups
0.0
20.0
40.0
60.0
80.077.4
18.6
0.0 4.1
65.6
32.8
1.6 0.0
66.7
13.3
0.0
20.0 Perc
enta
ge
Birth weight of the newborns among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 57 ~
Table no. 20: APGAR scores in the newborns among the groups
APGAR scores in the newborns among the groups
APGAR score Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
APGAR score at 1 min
Normal 196 (88.7) 51 (79.7) 10 (66.7)
Low 25 (11.3) 13 (20.3) 5 (33.3) 0.019
APGAR score at 5 min
Normal 220 (99.5) 64 (100) 15 (100)
Low 1 (0.5) 0 (0.0) 0 (0.0) 0.836
Total 221 (100) 64 (100) 15 (100)
Among the study subjects 20.3% of Oligohydramnios , 33.3% of Polyhydramnios had
low Apgar score at 1 minute compared to 11.3% of normal AFI which is statistically
significant
99.5% in normal AFI, 100% in Oligohydramnios, 15% in Polyhydramnios group had
normal APGAR score at 5 minutes which is statistically not significant .
~ 58 ~
Graph no. 14: APGAR scores in the newborns among the groups
0.0
20.0
40.0
60.0
80.0
100.0
Normal Low Normal Low
APGAR 1min APGAR 5min
88.7
11.3
99.5
0.5
79.7
20.3
100.0
0.0
66.7
33.3
100.0
0.0
Perc
enta
ge
APGAR scores in the newborns among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 59 ~
Table no. 21: NICU admission of newborns among the groups
NICU admission of newborns among the groups
NICU admission Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
No 193 (87.3) 41 (64.1) 10 (66.7) <0.001
Yes 28 (12.7) 23 (35.9) 5 (33.3)
Total 221 (100) 64 (100) 15 (100)
Among the study groups 35.9% of Oligohydramnios
& 33.3% of Polyhydramnios compared to 12.7% of normal AFI newborns born were
admitted in NICU which is statistically significant
Graph no. 15: NICU admission of newborns among the groups
0.0
20.0
40.0
60.0
80.0
100.0
No Yes
87.3
12.7
64.1
35.9
66.7
33.3
Perc
enta
ge
NICU admission of newborns among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 60 ~
Table no. 22: Neonatal complications among the study groups
Neonatal complications among the study groups
Complication Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
Yes 29 (13.1) 22 (34.4) 3 (20.0) 0.00049
No 192 (86.9) 42 (65.6) 12 (80.0)
Total 221 (100) 64 (100) 15 (100)
This table shows that 34.4% of Oligohydramnios & 20% of Polyhydramnios had
neonatal complications compared to 13.1% of normal AFI which is statistically
significant.
Graph no. 16: Neonatal complications among the study groups
0
20
40
60
80
100
Yes No
13.1
86.9
34.4
65.6
20
80
Perc
enta
ge
Neonatal complications among the study groups
Normal
Oligohydramnios
Polyhydramnios
~ 61 ~
Table no. 23: Neonatal complications in study subjects among the
groups
Neonatal complications in study subjects among the groups
Complications Normal Oligohydramnios Polyhydramnios
n (%) n (%) n (%)
IUGR 16 (7.2) 19 (29.7) 0 (0.0)
Meconium aspiration syndrome 8 (3.6) 3 (4.7) 0 (0.0)
Birth asphyxia 3 (1.4) 0 (0.0) 1 (6.7)
Fetal Hypoglycaemia 0 (0.0) 0 (0.0) 2 (13.3)
Cord around the neck 2 (0.9) 0 (0.0) 0 (0.0)
Macrosomia 9 (4.1) 0 (0.0) 3 (20.0)
Sepsis 0 (0.0) 2 (3.1) 0 (0.0)
IUGR is the most common neonatal complication associated with Oligohydramnios
29.7% compared to normal AFI (7.2%) and Polyhydramnios(0%)
Macrosomia is the most common neonatal complication associated with
Polyhydramnios(20%) compared to normal AFI(4.1%) and Oligohydramnios(0%)
13.3% of Polyhydramnios fetus had fetal hypoglycaemia .
~ 62 ~
Graph no. 17: Neonatal complications in study subjects among the
groups
0.0
10.0
20.0
30.0
7.2 3.6 1.4 0.0 0.9
4.1 0.0
29.7
4.7 0.0 0.0 0.0 0.0
3.1 0.0 0.0
6.7 13.3
0.0
20.0
0.0 Perc
enta
ge
Neonatal complications in study subjects among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 63 ~
Table no. 24: Neonatal mortality among the groups
Neonatal mortality among the groups
Mortality Normal Oligohydramnios Polyhydramnios P value
n (%) n (%) n (%)
No 220 (99.5) 60 (93.8) 14 (93.3) <0.006
Yes 1 (0.5) 4 (6.3) 1 (6.7)
Total 221 (100) 64 (100) 15 (100)
Neonatal Mortality was associated with Oligohydramnios(6.3%) and
Polyhydramnios(6.7%) compared to normal AFI(0.5%)
Graph no. 18: Neonatal mortality among the groups
0.0
20.0
40.0
60.0
80.0
100.0
No Yes
99.5
0.5
93.8
6.3
93.3
6.7
Perc
enta
ge
Neonatal mortality among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 64 ~
Table no. 25:Causes of Perinatal deaths among the groups
Causes of Perinatal deaths among the groups
Causes Normal Oligohydramnios Polyhydramnios
Birth asphyxia,Meconium Aspiration Syndrome 0 1 0
Birth asphyxia 0 0 1
Meconium Aspiration Syndrome 1 1 0
Sepsis 0 2 0
Total 1 4 1
Common Cause of perinatal mortality in Oligohydramnios, due to birth asphyxia
meconium aspiration and sepsis
1 baby died in Polyhydramnios due to birth asphyxia
1 baby died in normal AFI due to meconium aspiration syndrome
Graph no. 19: Causes of Perinatal deaths among the groups
0.0
2.0
4.0
6.0
8.0
10.0
BA,MAS BA MAS Sepsis
0.0 0.0 0.5
0.0
1.5
0.0
1.5
3.1
0.0
9.1
0.0 0.0
Perc
enta
ge
Causes of Perinatal deaths among the groups
Normal
Oligohydramnios
Polyhydramnios
~ 65 ~
DISCUSSION
It has been widely accepted that with standard antenatal care and early detection of
abnormal liquor volume has reduced the neonatal complications
Oligohydramnios with AFI ≤ 5cm can lead to an increase in perinatal mortality and
morbidity. Under these conditions, there is increased frequency of meconium stained
liquor, fetal distress, low apgar scores, abnormal Fetal heart rate patterns.
Polyhydramnios with AFI>25 cm can lead to an increased maternal & perinatal morbidity
& mortality.
Various studies have been presented to know the perinatal morbidity and mortality in
pregnancy with Abnormal liquor volume. In the same way our study was tried to reveal
the fetomaternal outcome in Normal liquor volume, Oligohydramnios & Polyhydramnios
in our department of Obstetrics and Gynaecology,Vijayanagara institute of medical
sciences ,Ballari.
In our study total number of cases studied were 300, amongst that 221 were of normal
AFI(73.7%), Oligohydramnios were 64 (21.3%) which is comparable with Umber et al
200361 in which 70% were with normal AFI & 29% were with Oligohydramnios. In
present study Polyhydramnios was 15(5%) compared to Neetu Meena et al62 (1.4%) is
more.
In our study majority of the subjects were between 21-25 yrs , i.e 53.1% of
Oligohydramnios group & 48.4% of normal AFI which is comparable to Shubhadeep et
al63 60% & 58% each .
~ 66 ~
In present study 46.7% of Polyhydramnios group is comparable with Neetu Meena et
al62 i.e 51%.
Age (21-25yrs) Neetu Meena et al
622016
Shubhadeep et al63
2015
Present study
Oligohydramnios - 60% 53.1%
Polyhydramnios 51% - 46.7%
Normal AFI - 58% 48.4%
In our study majority of them were booked cases in all the groups , 98.4% of
Oligohydramnios , 96.8% of Normal AFI were booked cases which is more when
compared to Shubhadeep et al63 i.e 88% in Oligohydramnios& 86% in normal AFI were
booked cases .
The importance of this factor lies in the fact that early detection and management of the
cases can minimise the fetal hazards and maternal morbidity.
Booked cases Shubhadeep et al63 Present study
Oligohydramnios 88% 98.4%
Normal AFI 86% 96.8%
In our study mean age of gestation was >38.9±0.96 weeks in all the groups which is
comparable with Pradeep R Gaikwad et al 2016 64in his study Mean gestational age was
37.95±2.29 weeks …
~ 67 ~
Gestational age(weeks) Pradeep R Gaikwad et al
2016 64
Present study
Mean age 37.95 ±2.29
38.9±0.96
In our study, among the parity distribution, 71.9% of the cases in Oligohydramnios group
were Primigravida, which is comparable to study done by Shubhadeep et al63 i.e 70%,in
the same study 72% had normal AFI but our study had 59.7% of Normal AFI .
In Polyhydramnios group there were equal number of Primigravida & Multigravida
which is 46.7%,which is more when compared to study by Guin G et al65 in which
Polyhydramnios increased with increasing parity.
Primigravida Shubhadeep et al63 Guin G et al65 Present study
Oligohydramnios 70% - 71.9%
Polyhydramnios - 13.2% 46.7%
Normal AFI 72% - 59.7%
In our study, 11.8% were Preeclamsia &3.2% were gestational hypertension in Normal
AFI group, 21.9% were preeclampsia, 1.6% were Gestational hypertension in
Oligohydramnios group, 13.3% were preeclampsia&6.7% were Gestational hypertension
in Polyhydramnios group as compared to Shubhadeep et al63, Pradeep R Gaikwad et al
2016 64 ,Guin G et al study65
~ 68 ~
Hypertensive
disorders in
pregnancy
Shubhadeep et
al63
Pradeep R
Gaikwad et al
2016 64
Guin G et al65 Present study
Oligohydramnios 30% 34.6% 3.5% 23.5%
Polyhydramnios - - 17.7% 20%
Normal AFI 26% 27.4% - 15%
In our study, GDM were present in 26.7% in Polyhydramnios group as compared to Guin
G et al65 study where 20% cases were GDM and 5% cases were GDM in Vaid S et al66
study.
In our study, 5% in Normal AFI & 4.7% in Oligohydramnios group were Rh negative
pregnancy as compared to Guin G et al65 where Rh negative pregnancy were 4.4% &
Shubhadeep et al63 i.e 6% in Oligohydramnios& 2% in NormalAFI group.
In our study, Severe anemia were present in 1.8% in normal AFI group which is
comparable with Pradeep R Gaikwad et al 2016 64 1.9% in normal AFI group.
Mode of delivery:
In our study Normal AFI group had 80.1% of vaginal delivery amongst that 75.6% had
Spontaneous vaginal delivery, 4.5% had Induced vaginal delivery , 5.9% had
Instrumental vaginal delivery, in this 55.9% had Oxytocin augmentation which is
comparable with Pradeep R Gaikwad et al 2016 64, Shubhadeep et al63.( 83%
Spontaneous, 5% Induced vaginal delivery)
~ 69 ~
In Oligohydramnios group 29.7% had vaginal delivery amongst the vaginal deliveries
25% Spontaneous vaginal delivery , 4.7% had Induced vaginal delivery & 6.3% had
Instrumental vaginal delivery .Oxytocin augmentation was done in 78.9% of the cases
which is comparable with Pradeep R Gaikwad et al 2016 64, Shubhadeep et al63 ( 16%
Spontaneous & 22% Induced vaginal delivery)
In Polyhydramnios group 26.7% had vaginal deliveries in that 30.3% were Spontaneous
vaginal deliveries , 6.7% were Induced vaginal delivery & Instrumental vaginal delivery
.75% of vaginal delivery had oxytocin augmentation which is less when compared with
Guin G et al 65( 86.6% spontaneous vaginal& 13.3% induced)
Vaginal delivery Pradeep R Gaikwad
et al 2016 64
Guin G et al65 Present study
Oligohydramnios 26.4% - 29.7%
Polyhydramnios - 86.6% 26.7%
Normal AFI 62.4% - 80.1%
Meconium stained liquor was present in 13.3% in Polyhydramnios group,10.4% of
Normal group &34.4% in Oligohydramnios group which is comparable with Shubhadeep
et al63 & Pradeep R Gaikwad et al 2016 64
~ 70 ~
Meconium stained
liquor
Shubhadeep et al63 Pradeep R Gaikwad
et al 2016 64
Present study
Oligohydramnios 48% 36.7% 34.4%
Polyhydramnios - - 13.3%
NormalAFI 12% 25.4% 10.4%
Caesarean section :
19.9% of normal AFI group had Caesarean section which is less when compared with
Pradeep R Gaikwad et al 2016 64 (37.7%)
The indication for LSCS were ,15.9% had Arrest of descent & Cephalopelvic
disproportion , 61.4% had Fetal distress , non progress of labour & second stage arrest as
the cause for LSCS
70.3% had LSCS in Oligohydramnios group which is comparable with Pradeep R
Gaikwad et al 2016 64 (73.4%) and the indications were fetal distress majority of the
cases had this indication (95.6%) which is comparable with Shubhadeep et al63(70% fetal
distress), Guin G et al65(80% fetal distress). 2.2% had cephalopelvic disproportion & deep
transverse arrest as the indication
73.3% had LSCS in Polyhydramnios which is significantly more when compared with
Neetu Meena et al62(25%) The indications were 54.5% had Fetal distress as the major
causes 18.2% had Arrest of descent & cephalopelvic disproportion , 9.1% had non
progress of labour which is comparable with Neetu Meena et al62 (10%)
~ 71 ~
LSCS Neetu Meena et al62 Pradeep R Gaikwad
et al 2016 64
Present study
Oligohydramnios - 73.4% 70.3%
Polyhydramnios 25% - 73.3%
Normal AFI - 37.2% 19.9%
NEONATAL OUTCOME
In this study majority of the subjects had normal weight babies (>2.5kg),77.4% in normal
AFI, 65.6% in Oligohydramnios which is comparable with Umber A61 study(80.7%
normal AFI, 61% Oligohydramnios) 66.7% in Polyhydramnios group
Low birth weight babies(1.5kg-2.5kg) were 18.6% in normal AFI, 32.8% in
Oligohydramnios, 13.3% in Polyhydramnios group which is comparable with
Shubhadeep et al63 & Chate P et al67
Low birth weight Shubhadeep et al63
Chate P et al67 Present study
Oligohydramnios 42% 62% 32.8%
Normal AFI 12% 28% 18.6%
polyhydramnios - - 13.3%
Macrosomia (>3.5kg) were seen in 20% of Polyhydramnios & 4.1% in normal AFI
group which is comparable with umber A et al61(10%)
Mean birth weight among the study subjects were 2.76±0.39 in normal AFI, 2.54±0.47 in
Oligohydramnios, 3.03±0.55 in Polyhydramnios group which is statistically significant
~ 72 ~
APGAR score at 1 minute were normal in 88.7% of normal AFI, 79.7% in
Oligohydramnios, 66.7% in Polyhydramnios
Low APGAR at 1 minute were 11.3% in normal AFI, 20.3% in oligohydramnios , 33.3%
in Polyhydramnios group which is comparable with Chate P et al67, Pradeep R Gaikwad
et al 2016 64
APGAR 1 min(<7) Chate P etal67 Pradeep R Gaikwad
et al 2016 64
Present study
Oligohydramnios 30% 26.5% 20.3%
Polyhydramnios - - 33.3%
Normal AFI 18%
11.7% 11.3%
After resuscitation APGAR score at 5 minutes were 99.5% normal in normal AFI , 100%
in Oligohydramnios & Polyhydramnios group
NICU admission required in the study subjects were 12.7% in normal AFI, 35.9% in
Oligohydramnios , 33.3% in Polyhydramnios group which is comparable with Chate P et
al67, Pradeep R Gaikwad et al 2016 64.
NICU admission Chate p et al67 Pradeep R Gaikwad
et al 2016 64
Present study
Oligohydramnios 42% 28.5% 35.9%
Polyhydramnios - - 33.3%
Normal AFI 12% 19.6% 12.7%
~ 73 ~
13.1% of Normal AFI, 34.4% of Oligohydramnios , 20% of Polyhydramnios group had
neonatal complications .
IUGR is the most common neonatal complication associated with Oligohydramnios
29.7% compared to normal AFI (7.2%) and Polyhydramnios(0%)
IUGR Guin G et al65 Pradeep R Gaikwad
et al 2016 64
Present study
Oligohydramnios 14.2% 44.8% 29.7%
Normal AFI 11.4% 13.7% 7.2%
Macrosomia is the most common neonatal complication associated with
Polyhydramnios(20%) compared to normal AFI(4.1%) and Oligohydramnios(0%)
Fetal hypoglycaemia was present in 13.3% of Polyhydramnios & none of the babies had
fetal hypoglycemia in normal AFI group &Oligohydramnios .
Neonatal mortality
In our study there were 4 neonatal deaths in Oligohydramnios group which is 6.3% ,
causes for perinatal mortality was due to Birth asphyxia , meconium aspiration , sepsis
which is more compared to study done by Chate P et al67(2%) & less compared to Guin G
et al65(12.6%)
1 baby died in Polyhydramnios group due to birth asphyxia (6.7%)which is less
compared to Guin G et al65(42.2%)
~ 74 ~
1 baby died in normal AFI group due to meconium aspiration syndrome (0.5%) Which is
less compared to Pradeep R Gaikwad et al 2016 64 (3.9%).
The present study showed higher rates of Fetal distress, LSCS rates and NICU admissions
., but the induction rates and the incidence of LBW babies were lower in the present
study.
Since the incidence of diabetes mellitus in Polyhydramnios was found to be high 26.7%
(1.5–6.6% in the literature), there is a need to screen these subjects repeatedly during the
course of pregnancy and establish early euglycemia. Since none of the patients was a
known diabetic and none had a congenital anomaly, it is possible that they were all
gestational diabetics.
These results support the fact that Oligohydramnios & Polyhydramnios are associated
with considerable adverse fetal outcome and maternal morbidity. Early diagnosis, skilful
management of cases and good paediatric backup will go a long way in improving the
obstetric outcome.
~ 75 ~
CONCLUSION
Abnormal liquor volume is being detected more often these days due to increase
in booking status of cases and routinely performed obstetric USG.
Oligohydramnios is one of the indicators of poor perinatal outcome because of its
association with Fetal heart rate abnormalities, Meconium staining of amniotic fluid,
umbilical cord compression, poor tolerance of labour, increased Cesarean rate for fetal
distress, low birth weight and low APGAR score, increased NICU admission and
neonatal mortality.
Polyhydramnios is also the indicators of poor perinatal outcome because of its
association with Fetal heart rate abnormalities,Gestational diabetes mellitus umbilical
cord prolapse, poor tolerance of labour, increased Cesarean rate for fetal distress and
CPD, Macrosomia and low APGAR score, increased NICU admission and neonatal
mortality.
From this study, we conclude that cases with abnormal liquor volume is a high
risk pregnancy which requires proper antepartum care and intensive fetal surveillance in
both antepartum and intrapartum period and good neonatal care necessary for better
perinatal outcome.
~ 76 ~
SUMMARY
This is prospective observational comparative study conducted at Department of
Obstetrics and Gynaecology, Vijayanagar Institute of Medical Sciences, Ballari from 1st
January 2018 to 31st December 2018
1. Among 300 cases , 221 case were with Normal AFI, 64 were Oligohydramnios, 15
were Polyhydramnios.
2. Majority of the Oligohydramnios cases were primigavida(59.1%) and
Polyhydramnios cases were multigravida.(46.7%).
3. Majority of subjects were in age group 21-25 years
4. All the study subjects were comparable based on there BMI and Booked status.
5. 70.3% in Oligohydramnios and 73.3% in Polyhydramnios group. were underwent
Cesarean section compared to 19.9% in Normal AFI
6. Fetal distress was the leading cause of Cesarean in Oligohydramnios(95.6 ) and
Polyhydramnios (54.5%) compared to normal AFI(61.4%).
7. CPD was the second most common indication in Polyhydramnios group (18.2%)
8. There was No significant difference in instrumental delivery in all three groups
9. There was No significant difference in all three groups based on oxytocin
augmentation
10. The most common co morbid condition associated with Oligohydramnios(21.9%)
and normal AFI(11.8%) was Pre eclampsia and with Polyhydramnios (26.7%) was
Gestational diabetes mellitus.
11. The most common cause was found to be idiopathic in both Oligohydramnios and
Polyhydramnios group
~ 77 ~
12. Meconium stained liquor was common in Oligohydramnios group(34.4%) compared
to Polyhydramnios(13.3%) and normal AFI(10.4%) groups
13. Low Birth weight (1.5-2.5 kg) were high in Oligohydramnios group (32.8%)
14. Macrosomia(>3.5kg) were relatively high in Polyhydramnios (20.0%) compared to
other two groups
15. Incidence of Low APGAR at 1 min were relatively high in Polyhydramnios (33.3%)
and Oligohydramnios(20.3%) compared to normal AFI( 11.3%)
16. Number of NICU admissions were high in Oligohydramnios (35.9%) and
Polyhydramnios(33.3%) compared to normal AFI( 12.7%)
17. Association of Neonatal complications was seen with Oligohydramnios (34.4%)
and Polyhydramnios(20%) group
18. IUGR was the most common neonatal complication associated with
Oligohydramnios 29.7%
19. 9.Neonatal Mortality was high in Oligohydramnios(6.3%) and Polyhydramnios
(6.7%) compared to normal AFI(0.5%)
~ 78 ~
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~ 86 ~
CONSENT FORM EMPTY FORM
I _______________________________ have been told in a language that I
understand about the study. I have been told that this is for a research procedure, that my
participation is voluntary and I/he/she reserve the full right to withdraw from the study at
my own initiative at any time, without having to give any reason and that right to
participate or withdraw from the study at any stage will not prejudice my/his/her, rights
and welfare. Confidentiality will be maintained and only be shared for academic
purposes.
I hereby give my consent to participate in the above study. I am also aware that I
can withdraw this consent at any later date if I wish to. This consent form being signed
voluntarily indicating my agreement to participate in the study until I decide otherwise. I
understood that I will receive a signed and dated copy of this form.
I have signed this consent form before my participation in this study.
Signature of the research subject
Date :
Place :
~ 87 ~
~ 88 ~
PROFORMA
CASE NO:
Name Age IP No.
Address Education
Socioeconomic status Booked / Unbooked
Obstetric history
Married
Obstetric score G P L A
Menstrual history – LMP: EDD:
Past history
Family history
Personal history
GENERAL EXAMINATION :
Pulse rate - Blood pressure -
Built - Pallor - Oedema
SYSTEMIC EXAMINATION :
1 )Cardio vascular system 2 )Respiratory system
3 )Per-abdomen
Obstetric examination
Height of fundus -
Presentation -
Fetal heart rate
Liquor clinically - INCREASED/ADEQUATE/DECREASED
4 )Per-vaginum
HT
WT
BMI
~ 89 ~
INVESTIGATIONS
Blood : Hb % - Blood group- HIV- HbsAg - RBS -
Urine : Albumin - Sugar - Microscopy -
NST - Reactive / Non reactive
USG
DATE GESTATIONAL
AGE
EFW
PLACENTA
LIQOUR
EDD
Diagnosis:
Mode of delivery 1)Vaginal a)spontaneous b)induced
2) LSCS a)emergency b)elective Indication:
Mode of induction
Induction to delivery interval:
Oxytocin augmentation done/ not done AFI
Baby details:
Baby cried after birth - Yes /No
Sex - Male /Female
Baby weight -
Apgar score - 1 min
5 min
Baby resuscitated -
Meconium stained amniotic fluid –Yes /No
Associated complication for baby -
Admission in NICU - Yes / No Days-
Follow up
Condition of baby on discharge -
Condition of mother on discharge -
~ 90 ~
KEY TO MASTER CHART
AD Arrest of descent
AN Anemia
AFI Amniotic fluid index
BA Birth asphyxia
BMI Basal metabolic index
D Decreased
DBP Diastolic blood pressure
F Forceps
FD Fetal distress
GDM Gestational diabetes melitius
I Increased
IUGR Intra uterine growth restriction
LSCS Lower segment caesarean section
M Meconium
MSA Meconium Aspiration Syndrome
NST Non stress test
NICU Neonatal intensive care unit
PE Preeclampsia
PND Prenatal death
RBS Random blood sugar
RN Rh negative
SBP Systolic blood pressure
SFH Symphysio fundal height
VD Vaginal delivery
VA Vaccum
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
e d
eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
1 Devamma 55514 21 B 1 _ _ _ 40 25.4 120 80 36 A 8.8 92 NIL R 7 N V S Y NIL A M 2.3 6 8 MSA Y NO
2 Veena 56537 21 B 1 _ _ _ 39+3 26.2 120 80 37 A 12 76 NIL R 10.4 N LSCS * * EM AD NIL A M 3 7 9 NIL N NO
3 Thippamma 53807 19 B 1 _ _ _ 39+6 22.8 120 90 34 D 9.9 83 NIL R 10.6 N V VA S Y NIL A F 2 6 8 NIL N NO
4 Lakshmi 55505 27 B 1 _ _ _ 37 24.2 120 80 35 A 11.3 82 NIL R 10 N V S Y NIL A F 2.1 7 9 NIL N NO
5 Sahibamma 57369 19 B 1 _ _ _ 38+3 21.9 116 72 38 A 10.6 79 NIL R 10.1 N V S Y NIL A M 3.1 7 9 NIL N NO
6 Barathi 57081 28 B 1 _ _ _ 40 23 130 80 35 A 14.8 86 NIL R 8.2 N V S Y NIL A F 2.5 7 9 NIL N NO
7 Rekhamma 57296 25 B 2 1 1 _ 40 20.7 110 70 36 A 9.1 78 NIL R 10.4 N V VA S Y NIL A F 2.6 7 9 NIL N NO
8 Renukamma 58777 22 B 2 _ _ 1 38+5 20.8 100 70 36 A 9.3 78 NIL R 9.8 N LSCS * * Em FD NIL A M 2.5 7 9 NIL N NO
9 Malashree 59322 22 B 2 _ _ 1 39+3 20.7 116 70 37 A 9.1 86 NIL R 12.4 N V S Y NIL A F 3 6 8 BA Y NO
10 Sowmya 59162 20 B 1 _ _ _ 38 23.7 160 100 36 A 12.4 79 2+ R 8.6 N LSCS * * Em Breech MPE A M 2.6 7 9 NIL N NO
11 Akhila 57711 20 B 1 _ _ _ 39+4 21.7 110 70 35 A 11 82 NIL R 7.4 N V S Y NIL A M 2.5 7 9 MSA N NO
12 Sridevi 53471 23 B 2 1 1 _ 37 30.4 110 70 40 I 9.9 74 NIL R 26 P LSCS * * Em FD NIL A F 2.5 6 9 NIL N NO
13 Shamina banu 54678 32 B 2 1 0 _ 37 33.4 130 100 42 I 9.8 117.9 NIL R 26 P LSCS * * EM FD GDM A M 3 6 8 hypogly Y NO
14 Bargavi bai 56631 21 B 1 _ _ _ 38 21.3 110 70 35 D 10.5 80 NIL R 0 O LSCS * * EM FD NIL A F 2.2 7 9 IUGR N NO
15 Nandini 56816 21 B 1 _ _ _ 39 21.6 110 70 36 D 10.9 79 NIL R 2 O LSCS * * EM FD NIL A F 2.8 7 9 NIL N NO
16 Shabana 57157 21 B 1 _ _ _ 38 22.5 118 70 35 D 12.9 70 NIL R 4 O LSCS * * EM FD NIL A F 2.5 7 9 NIL N NO
17 Gayathri 58187 25 B 1 _ _ _ 39 21 116 76 34 D 9.8 76 NIL R 3 O LSCS * * EM FD NIL A F 2.5 7 9 NIL N NO
18 Sulochana bai 58719 20 B 1 _ _ _ 38+3 20.5 120 80 36 A 11.9 83 NIL R 4 O V F S Y NIL A F 2.9 7 9 NIL N NO
19 Tulasi 59425 20 B 1 _ _ _ 37+2 23.8 120 76 36 A 8.5 71 NIL R 3 O LSCS * * EM FD NIL A M 2.6 7 9 NIL N NO
20 Nirmala 59156 30 B 1 _ _ _ 39+3 23 112 86 36 D 9.6 70 NIL R 3 O LSCS * * EM FD NIL A F 2.9 7 9 NIL N NO
21 Gadamma 64092 20 B 1 _ _ _ 38 20.7 116 76 36 D 10 78 NIL R 5 O LSCS * * EM FD NIL A F 2.5 7 9 MSA N NO
22 Malashree 75986 20 B 1 _ _ _ 39+6 25 118 78 37 A 11.1 108 NIL R 13.6 N LSCS * * EM FD NIL A M 2.8 7 9 MSA N NO
23 Shanthamma 73019 30 B 1 _ _ _ 38 25.2 134 100 36 A 11.6 78 Traces R 9.1 N V S Y MPE A F 2.6 7 9 NIL N NO
24 Yashoda 76027 19 B 3 _ _ 2 39+2 26.67 150 90 38 A 12 89 Traces R 8 N V S Y MPE A M 3.1 7 9 NIL N NO
25 Rehana 76024 24 B 2 1 1 _ 38 27.8 112 80 39 A 9.1 75 NIL R 5.3 N LSCS * * EM FD NIL A M 3.4 7 9 NIL N NO
26 Sujatha 75349 20 B 1 _ _ _ 40 20 120 80 39 I 10.7 133 NIL R 27 P LSCS * * EM FD NIL A M 3.6 7 9 NIL N NO
27 Nazefa 75066 21 B 1 _ _ _ 37+6 26.5 150 100 37 A 11.1 79.3 2+ R 8.8 N LSCS * * EM FD MPE A M 2.3 5 8 MSA Y YESMeconium aspiration
28 Jugamma 69694 22 B 3 2 2 _ 39+3 26.6 110 70 36 A 9.7 84 NIL R 15 N V I Y NIL A M 3.2 7 9 NIL N NO
29 Danamma 67757 35 B 3 2 2 _ 39 25.6 110 80 37 A 11.2 82 NIL R 8 N LSCS * * EM nd stage a NIL A F 2.8 7 9 NIL N NO
30 Pallavi 76047 24 B 1 _ _ _ 40 20.9 140 90 38 A 9.7 78 2+ R 13.7 N V VA S Y MPE A M 3.3 7 9 NIL N NO
31 Bhagya bai 60305 21 B 1 _ _ _ 40 24.5 110 70 34 D 11.6 82 NIL R 4 O LSCS * * EM FD NIL A F 2.3 7 9 NIL N NO
32 Bavani 64107 26 B 1 _ _ _ 40 26.5 140 90 42 I 11 70 1+ R 28 P LSCS * * EM AD MPE A F 3.3 7 9 NIL N NO
33 Shanu 63112 30 B 1 _ _ _ 37 22.4 110 70 40 I 10.2 83 NIL R 25 P LSCS * * EM FD NIL A M 2.7 7 9 NIL N NO
34 Shamshad 63531 23 B 1 _ _ _ 38 20.3 146 90 35 D 9.1 78 1+ R 0 O LSCS * * EM FD MPE A M 2.6 7 9 NIL N NO
35 Sunitha 62220 30 B 1 _ _ _ 37+5 21.6 110 70 34 D 9.6 80 NIL R 3 O LSCS * * EM FD NIL A M 2.8 7 9 NIL N NO
36 Shanthakumari 64277 20 B 1 _ _ _ 38+6 26.6 110 70 35 D 10.2 80 NIL R 4 O LSCS * * EM FD NIL A F 2.6 7 9 MSA N NO
37 Lakshmi 75365 21 B 4 _ _ 3 37+1 25 114 78 38 A 11.2 88 NIL R 11.7 O V S Y Hypothyroid A F 2.5 7 9 NIL N NO
38 Jedeshwari 76926 21 B 1 _ _ _ 37+5 20.4 130 80 42 I 12.8 83 NIL R 27 P V S Y NIL A F 2 7 9 NIL N NO
39 Vani 77855 23 B 2 1 0 _ 39+1 21.3 110 70 39 I 12 79 NIL R 26 P V S Y NIL A F 3 7 9 NIL N NO
40 Revathi 73874 20 B 1 _ _ _ 38+4 25.1 130 80 29 D 11.3 70 NIL R 0 O LSCS F * * EM FD HBSAg+ A F 2.1 7 9 IUGR N NO
41 Reddamma 74111 22 B 3 2 2 _ 39+3 28.3 140 90 38 A 9.8 76 Traces R 14.6 N V S Y MPE A F 3.7 7 9 NIL N NO
42 Shameem 75024 30 B 3 2 2 _ 40 26.7 140 90 42 A 11.4 82 3+ R 11.1 N LSCS * * EM AD SPE A M 3.6 7 9 NIL N NO
43 Nagamma 76003 25 B 1 _ _ _ 38+4 28.3 130 80 32 A 10 107 NIL R 8.8 N V S Y NIL A F 2.6 7 9 NIL N NO
44 Mahadevi 76251 23 B 1 _ _ _ 37+6 32.9 150 100 32 A 9.5 116 NIL R 9.5 N V S Y GH A M 3 7 9 NIL N NO
45 Shabeena banu 75825 25 B 1 _ _ _ 38+2 27.1 136 90 29 A 9.8 107 1+ R 5 O V VA S Y MPE A F 2.6 7 9 NIL N NO
46 Rasul bee 75115 18 B 1 _ _ _ 39+4 27.04 120 70 38 A 10.1 79 NIL R 15.8 N V S Y NIL A F 3.7 7 9 NIL N NO
47 Khaderbee 75779 20 B 2 _ _ 2 40 24.1 110 80 32 A 12.2 79 NIL R 12 N V S Y NIL A F 2.7 7 9 NIL N NO
48 Eramma 76181 21 B 2 1 1 _ 39+6 20 126 88 31 A 10 85 NIL R 8.3 N V S Y NIL A M 2.4 7 9 NIL N NO
49 Girijamma 75393 22 B 1 _ _ _ 40 20.2 110 70 34 A 11.6 83 NIL R 7.8 N V F S Y NIL A F 2.6 7 9 NIL N NO
50 Yashoda 72491 21 B 1 _ _ _ 40 23.8 130 90 32 A 10.8 75.9 NIL R 9.3 N LSCS * * EM AD GH A M 3.2 7 9 NIL N NO
51 Asma begum 77745 28 B 2 1 1 _ 40 28.5 110 70 37 A 11.4 78 NIL R 7.8 N LSCS * * FD NIL A M 2.8 7 9 NIL N NO
52 Sahakunthala 77807 25 B 1 _ _ _ 39+5 26.7 116 74 38 A 6.2 85 NIL R 12 N V S Y SA A M 2.7 7 9 NIL N NO
53 Varalakshmi 77774 22 B 2 1 1 _ 37+6 25 118 60 36 A 11.1 86 NIL R 10.5 N LSCS * * EM CPD NIL A M 2.8 7 9 NIL N NO
MASTER CHART
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
e d
eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
MASTER CHART
54 Anusha 77561 32 B 1 _ _ _ 38+1 23.6 130 90 38 A 12.1 113 1+ R 10.4 N V S Y MPE A M 3.2 7 9 NIL N NO
55 Lalitha 77474 23 B 2 1 1 _ 40 22.5 112 68 37 A 10.8 87 NIL R 8.4 N V S Y NIL A M 2.5 7 9 NIL N NO
56 Huligamma 77464 28 B 3 2 2 _ 39+6 24.6 110 76 39 A 9.5 68 NIL R 14.1 N V S Y NIL A F 3.6 7 9 NIL N NO
57 Lakshmi 77887 22 B 3 2 2 _ 39 28.9 110 70 38 A 7.3 90 NIL R 9.2 N V S Y MA A M 3 7 9 NIL N NO
58 Rajamma 77809 22 B 1 _ _ _ 38+5 23.5 112 78 37 A 10.2 78 NIL R 11.6 N V S Y NIL A F 2.7 7 9 NIL N NO
59 Jyothi 76046 21 B 1 _ _ _ 38+6 18.9 126 78 34 A 11.6 92 NIL R 14.1 N V VA S Y NIL A F 2.3 7 9 NIL N NO
60 Shilpa 76072 20 B 1 _ _ _ 38+2 21.3 118 76 34 A 10.3 82 NIL R 12.6 N V S Y NIL A F 2.5 7 9 NIL N NO
61 Jyothi 76726 24 B 1 _ _ _ 39+5 24.9 116 76 35 A 10.9 78 NIL R 4 O V S Y NIL A M 2.6 7 9 NIL N NO
62 Nalini 76760 24 B 1 _ _ _ 38+1 23 116 76 34 A 10.2 82 NIL R 14.7 N V S Y NIL A F 3 7 9 NIL N NO
63 Raziya 76064 20 B 1 _ _ _ 38+3 24.6 112 78 36 A 10.7 86 NIL R 9.7 N V F S Y NIL A F 2.1 7 9 IUGR N NO
64 Wajiya Banu 61051 20 B 1 _ _ _ 39 24.2 122 80 36 A 9 76 NIL R 9.7 N V S Y NIL A F 2.9 5 8 BA Y NO
65 Devamma 55514 21 B 1 _ _ _ 39+2 23.4 116 80 36 A 8.2 92 NIL R 12.2 N V S Y NIL A M 2.3 6 8 MSA Y NO
66 Mani 77469 20 B 1 _ _ _ 39+5 23.83 140 90 38 A 9.2 62 NIL R 13.7 N V S Y GH,MA A M 3.4 7 9 NIL N NO
67 Gousiya 77800 28 B 2 1 1 _ 37+6 26.8 150 90 28 D 7.7 85 3+ R 6.2 N LSCS * * EM FD MA,SPE A F 1.9 7 9 IUGR N NO
68 Huligamma 75216 20 B 1 _ _ _ 39+2 26.4 112 60 37 A 9.8 85 NIL R 9.9 N V S Y NIL A M 2.8 7 9 NIL N NO
69 Rizwana 75206 20 B 1 _ _ _ 39+4 25.2 116 76 35 A 10.8 92 NIL R 10.3 N V S Y NIL A M 2.76 6 8 MSA Y NO
70 Yogeshwari 76068 20 B 1 _ _ _ 38+6 27.2 120 76 35 A 10.8 87 NIL R 10.5 N V S Y NIL A M 2.7 7 9 NIL N NO
71 Mala 78208 20 B 1 _ _ _ 38+3 23.7 130 80 34 A 10 78 NIL R 10.5 N V S Y NIL A M 2.3 6 8 BA Y NO
72 Ranjitha 75005 20 B 1 _ _ _ 37+5 24.2 130 76 35 A 11.2 96 NIL R 13 N V S Y NIL A F 2.6 7 9 NIL N NO
73 Shivamma 78202 20 B 4 3 3 _ 37+3 24.4 126 76 36 A 6.8 79 NIL R 12.2 N V S Y SA A F 2.6 7 9 MSA N NO
74 Janaki 77876 20 B 2 _ _ 1 39+5 24.3 160 100 35 A 9.9 68 3+ R 6.4 N LSCS * * EM FD NIL A F 2.8 7 9 NIL N NO
75 Ummeaisha 76927 20 B 1 _ _ _ 39+5 25.2 120 76 36 A 11.9 90 NIL R 8.1 N LSCS * * EM FD NIL A M 2.9 7 9 NIL N NO
76 Devi 73661 20 B 1 _ _ _ 39 25 112 76 35 A 11.1 96 NIL R 9.3 N V S Y NIL A M 2.6 7 9 NIL N NO
77 Lakshmidevi 76790 26 B 3 2 2 _ 39+2 25.2 122 80 36 A 9.4 86 NIL R 12.9 N V S Y NIL A F 2.4 7 9 NIL N NO
78 Rajamma 77809 22 B 1 _ _ _ 38+5 23.6 112 72 36 A 10.2 89 NIL R 12.3 N V S Y NIL A F 2.5 7 9 NIL N NO
79 Vimala 77849 22 B 1 _ _ _ 39 23.1 120 80 38 A 11.6 63 NIL R 9.3 N LSCS * * EM CPD NIL A M 3.6 7 9 NIL N NO
80 priyanka 2033 21 B 1 _ _ _ 40 24 110 70 36 D 10.5 96 NIL R 4 O V S Y M NIL A M 2.5 6 8 MSA Y NO
81 Renukkamma 4146 30 B 1 _ _ _ 38 25 120 76 32 A 10.8 87 NIL R 10.4 N LSCS * * M EM FD NIL A M 2.6 7 9 MSA Y NO
82 Rangaveni 4097 20 B 1 _ _ _ 38 23.1 116 72 32 A 9.7 86 NIL R 12 N V S Y NIL A F 2.25 7 9 NIL N NO
83 Nagamma 4513 28 B 4 3 3 _ 40 19.9 116 70 32 A 8.6 82 NIL R 11.6 N V S * A,RN A M 2.6 6 8 NIL N NO
84 Indu 3553 25 B 1 _ _ _ 38 26.7 120 80 42 I 9.9 87 NIL R 28 P LSCS * * M EM FD NIL A F 2.7 7 9 NIL N NO
85 Ambadevi 3144 23 B 2 1 0 _ 37 23 110 68 30 D 9 82 NIL R 3.6 O LSCS * * EM CPD NIL A F 2.7 7 9 NIL N NO
86 Hussainamma 3409 22 B 1 _ _ _ 39 20.6 108 74 32 A 10.3 80 NIL R 8.6 N V S Y M A A F 2.2 6 8 NIL N NO
87 Parveen 4301 21 B 1 _ _ _ 40 19.3 102 68 35 A 11.8 86 NIL R 9.2 N V S Y NIL A M 3.3 7 9 NIL N NO
88 Lakshmi 4367 21 B 1 _ _ _ 38 19.2 140 90 34 A 13 94 NIL R 12.6 N V I Y PE A M 2.9 7 9 NIL N NO
89 Neelamma 3679 21 UB 1 _ _ _ 38 24 112 60 34 A 9.6 90 NIL R 14 N V S Y NIL A M 2.6 7 9 NIL N NO
90 Renukkamma 3688 21 B 1 _ _ _ 40 25.9 110 70 32 A 11.8 91 NIL R 3.2 O V S Y M NIL A M 2.6 7 9 IUGR N NO
91 Manjula 2563 20 B 1 _ _ _ 38 25.9 110 74 36 I 10.3 96 NIL R 27 P LSCS * * EM AD A A F 2.4 7 9 NIL N NO
92 Anitha 4457 21 B 1 _ _ _ 38 25.2 106 68 32 A 9.7 82 NIL R 11 N V S Y NIL A F 2.1 6 8 around Y NO
93 Vishalakshi 1403 25 B 5 _ 0 4 39 26 146 92 30 D 14.3 89 1+ R 2.3 O V S Y M GH A M 1.9 6 8 IUGR Y NO
94 Basavarajeshwari 4404 20 UB 1 _ _ _ 37 29.2 110 72 32 A 11.7 82 NIL R 8.4 N V S Y NIL A F 2.5 7 9 NIL N NO
95 Padmavathi 5303 29 B 2 _ _ 1 40 26.6 116 74 40 I 9.4 82.1 NIL R 26 P V F I Y NIL A M 3.2 7 9 NIL N NO
96 Sarawathi 5976 27 B 5 4 3 _ 37 25.2 130 86 47 I 12.5 170 NIL R 28 P LSCS * * GDM A M 3.9 6 8 Hypo+BA Y NO
97 Sumithra 4526 20 B 1 _ _ _ 39 23.5 112 70 32 I 10.8 88 NIL R 10.8 N V S Y NIL A F 2.5 7 9 NIL N NO
98 Grijamma 4543 20 B 1 _ _ _ 40 29.2 110 70 33 A 11.7 86.7 NIL R 9.2 N V S Y NIL A F 2.2 7 9 IUGR N NO
99 Sana 4414 22 B 2 1 1 _ 39 23.5 126 80 35 A 15 91.3 NIL R 12.8 N V S Y NIL A M 3.1 7 9 NIL N NO
100 Lakshmi 2516 25 B 1 _ _ _ 39 26 110 70 30 A 13.6 90 NIL R 8.2 N LSCS * * M EM FD NIL A F 2 7 9 IUGR N NO
101 Lalitha 1536 20 B 1 _ _ _ 37 25.8 108 68 32 A 10.4 96 NIL R 9.1 N LSCS * * EM CPD A A M 2.4 7 9 NIL N NO
102 Shanthamma 2596 26 B 1 _ _ _ 40 26.6 136 92 36 A 8.6 80.3 1+ R 14.4 N LSCS * * EM FD A A M 3.5 7 9 NIL N NO
103 Rathnamma 83884 20 B 1 _ _ _ 39 25.7 110 70 31 D 11.5 92 NIL R 4.8 O V S Y M NIL A F 2.3 7 9 IUGR N NO
104 Chand bee 85515 26 UB 4 2 2 1 39 21.3 120 70 33 A 10.1 91 NIL R 14.1 N V S * NIL A M 2.6 7 9 NIL N NO
105 Hampamma 1627 20 B 1 _ _ _ 37 19.1 126 82 34 A 11.7 89 NIL R 13 N V VA S * NIL A M 2.5 7 9 NIL N NO
106 Anjali 1666 26 UB 3 2 2 _ 39 27.3 120 74 34 D 9.8 81 NIL R 2 O V S * NIL A M 3.1 7 9 NIL N NO
107 jademma 8670 22 B 2 1 1 _ 39 29 108 73 32 A 13 80 NIL R 9.1 N V S Y NIL A M 2.3 7 9 NIL N NO
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
e d
eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
MASTER CHART
108 Saritha 4339 27 B 2 1 1 _ 40 23 136 90 34 A 7.8 90 2+ R 7.6 N V I Y A,PE A M 3.02 7 9 NIL N NO
109 Asma begum 4376 19 B 1 _ _ _ 39 20 124 76 35 A 9.5 87.4 NIL R 10.2 N V S Y NIL A F 3.1 7 9 NIL N NO
110 Ruksana 8510 22 B 3 2 2 _ 39 29.2 130 96 34 A 9.4 103 1+ R 9.4 N V S Y PE,RN A F 2.5 6 8 NIL N NO
111 Gangamma 85628 25 B 3 2 2 _ 37 26 120 70 34 A 9.6 112 NIL R 9.2 N V S * NIL A M 2.4 7 9 NIL N NO
112 Shivagangamma 85560 20 B 1 _ _ _ 40 23 110 70 33 A 10.1 72 NIL R 8.6 N LSCS * * EM FD NIL A M 2.5 7 8 NIL N NO
113 Ashwini 84284 24 B 3 1 _ 1 39 20.5 112 78 36 D 11.3 91 NIL R 3.2 O LSCS * * EM DTA NIL A M 3.5 6 8 NIL Y NO
114 Yasmin 11638 25 B 1 _ _ _ 38 26.6 110 70 35 D 9.5 72 NIL R 4.2 O V S Y NIL A M 3.5 7 9 NIL N NO
115 Sahaya mary 12405 20 B 1 _ _ _ 38 25.8 140 90 35 D 10.5 95 2+ R 5 O LSCS * * EM FD PE A M 2.8 7 9 NIL N NO
116 Anamma 9619 20 B 1 _ _ _ 39 19.1 136 98 34 A 10.8 118 2+ R 13.2 N V S * PE A F 2.7 7 9 NIL N NO
117 Sabhiya 8599 25 B 2 1 1 _ 40 21.3 112 70 34 D 10.8 84 NIL R 3.4 O V S Y HBSAg+ A M 2.8 7 9 NIL N NO
118 Kavitha bai 84761 22 B 1 _ _ _ 40 23 112 70 35 A 11.1 153 NIL R 10 N LSCS * * EM FD NIL A F 2.9 7 9 NIL N NO
119 Karibassama 8109 23 B 1 _ _ _ 39 26.6 146 88 36 A 9.5 90 1+ R 11.6 N V S Y PE A F 2.7 7 9 NIL N NO
120 Lakshmi 85507 20 B 1 _ _ _ 40 25 130 90 33 D 10.4 70.5 NIL R 1 O LSCS * * EM FD PE,RN A F 3 7 9 NIL N NO
121 Sarojamma 9620 23 B 2 1 1 _ 40 25 110 70 35 A 12.6 108 NIL R 9.3 N V S Y HBSAg+ A F 2.6 7 9 NIL N NO
122 Lakshmi 85543 27 B 3 1 1 1 39 26 112 72 36 A 10.9 96 NIL R 9.5 N V S Y NIL A F 3.4 7 9 NIL N NO
123 Kavitha 9571 26 B 3 2 2 _ 39 19.1 140 90 35 A 9 120 1+ R 14 N V S * NIL A M 3 7 9 NIL N NO
124 Koteshwari 8555 22 B 1 _ _ _ 39 21 110 70 36 A 12 70.9 NIL R 12 N V S * NIL A F 2.7 7 9 NIL N NO
125 Gangotri 13964 22 B 1 _ _ _ 38 27 112 76 34 A 10.9 80 NIL R 9.2 N V S * NIL A M 2.5 7 9 NIL N NO
126 Roopa bai 9574 20 B 1 _ _ _ 40 25 130 96 35 A 10.2 102 1+ R 10.5 N V S * PE A F 2.6 7 9 NIL N NO
127 Kavitha 84717 23 B 3 2 2 _ 39 29 128 78 36 A 10 89 NIL R 15 N V S Y RN A F 2.6 7 9 NIL N NO
128 Eramma 85476 20 B 1 _ _ _ 40 27 110 70 34 A 9.5 90 NIL R 16 N V S Y NIL A F 2.6 7 9 NIL N NO
129 Savithri 9627 20 B 2 1 1 _ 40 27 120 76 36 A 12.8 92 NIL R 14 N V VA S * NIL A M 3 7 9 NIL N NO
130 Roja 85480 19 B 1 _ _ _ 40 25.2 140 90 34 A 10.8 99 1+ R 15 N V S Y PE A F 2.4 7 9 NIL N NO
131 Jyothi 83805 22 B 2 _ _ 1 40 23 112 60 35 A 9.4 68 NIL R 12 N V S * NIL A F 2.5 7 9 NIL N NO
132 Yenkamma 85090 20 B 1 _ _ _ 39 21.5 140 90 35 A 10.6 76 2+ R 13.5 N V S Y NIL A M 2.5 7 9 NIL N NO
133 Sunitha 85929 20 B 1 _ _ _ 39 21 110 70 36 A 10.3 89 NIL R 11.8 N V F S Y NIL A F 2.9 7 9 NIL N NO
134 Mahankali 9553 21 B 1 _ _ _ 39 19.1 130 80 34 A 10.2 82 NIL R 10.8 N V S * NIL A M 2.3 7 9 NIL N NO
135 Honnuramma 8548 20 B 1 _ _ _ 37 22.8 110 70 34 A 10.5 105 NIL R 19.6 N V S Y NIL A F 2.33 7 9 NIL N NO
136 Pallavi 84187 25 UB 4 3 3 _ 38 25 110 70 36 A 8.6 74 NIL R 9 N V S * A A M 2.7 7 9 NIL N NO
137 Usha 8463 27 B 3 1 1 1 40 21.3 136 90 37 A 9.1 111 2+ R 14 N V S Y PE A M 2.8 7 9 NIL N NO
138 Mahankali 84475 20 B 1 _ _ _ 37 20.5 130 90 30 D 9.2 77.3 1+ R 2 O LSCS * * EM FD PE A M 2 6 7 IUGR Y YES BA,MAS
139 Neelamma 84973 22 B 3 1 1 _ 39 23 120 70 36 A 11 80 NIL R 12.6 N V S Y NIL A F 2.9 7 9 NIL N NO
140 Rekha 84082 19 B 1 _ _ _ 39 21.3 110 72 36 A 12.9 76 NIL R 15 N V S * NIL A M 2.9 6 8 NIL N NO
141 Banu bee 84434 21 B 3 2 2 _ 40 25.1 160 100 36 A 11.5 83 4+ R 8 N V I Y PE A M 2.5 6 9 NIL N NO
142 Basamma 84697 20 B 4 2 1 1 40 21.3 120 70 36 A 9.2 96 NIL R 10 N V S * NIL A M 3 7 9 NIL N NO
143 Penamma 4370 19 B 1 _ _ _ 39 23.3 116 70 31 D 10.9 90 NIL R 3.5 O V S * M NIL A F 2.3 7 9 IUGR Y NO
144 Renuka 12400 26 B 2 _ _ 1 37 21.3 120 70 36 D 12.6 72 NIL R 4 O LSCS * * M EM FD NIL A M 3 7 9 NIL N NO
145 Roja 84360 25 B 1 _ _ _ 39 22.8 120 68 36 A 11.5 78 NIL R 7 N LSCS * * M EM FD NIL A M 3 7 9 NIL N NO
146 Thayamma 9087 24 B 3 2 2 _ 40 26.7 120 70 37 A 13.5 70 NIL R 16.5 N V S Y NIL A M 3.5 7 9 NIL N NO
147 Ashwini 84957 20 B 1 _ _ _ 40 23.3 110 70 37 A 13.4 86 NIL R 14.5 N V S Y NIL A M 2.7 7 9 NIL N NO
148 Latha 81921 19 B 2 _ _ 1 39 23.3 120 80 37 A 11.2 80 NIL R 7 N LSCS * * M EM FD NIL A M 31 7 9 NIL N NO
149 Aliya 81994 19 B 2 1 _ _ 38 25 150 96 36 A 9.7 74.9 NIL R 9.6 N V S Y NIL A F 2.5 7 9 NIL N NO
150 Honnuramma 81943 28 B 3 2 2 _ 37 25.7 120 80 37 A 13 78 NIL R 12.6 N V S Y NIL A M 3 7 9 NIL N NO
151 Aruna 8550 23 B 2 1 1 _ 38 23.5 120 70 35 A 12.5 76 NIL R 13 N V S Y NIL A M 2.5 7 9 NIL N NO
152 Rekha 81899 21 B 1 _ _ _ 40 23.5 120 70 30 D 10.6 79 NIL R 0.8 O LSCS * * M EM FD RN A M 2.5 6 8 NIL N NO
153 Amrutha 81844 20 B 1 _ _ _ 40 20 110 70 33 D 7.4 96 NIL R 4.8 O LSCS * * M EM FD NIL A M 3 6 8 NIL N NO
154 Shakunthala 83533 18 B 1 _ _ _ 39 25.7 110 70 36 A 10.6 92 NIL R 12 N LSCS * * EM CPD PE A M 3.2 7 9 NIL N NO
155 Vindhya bai 78297 20 B 2 _ _ 1 39 23.5 110 70 37 A 10.4 91 NIL R 11.5 N V S Y NIL A M 3 7 9 NIL N NO
156 Vanjakshi 83501 25 B 2 1 1 _ 39 25 110 70 30 D 12.8 83 NIL R 0.5 O LSCS * * EM FD NIL A M 2 7 9 IUGR Y NO
157 Pavithra 82675 22.5 B 1 _ _ 1 38 22 110 70 37 A 11.2 76 NIL R 18.3 N V S * NIL A M 3.1 7 9 NIL N NO
158 Yariyamma 83052 30 B 3 2 2 _ 38 29.3 120 74 36 A 10.6 92 NIL R 10.6 N V S * NIL A F 2.9 7 9 NIL N NO
159 Renukamma 58777 22 B 2 _ _ 1 40 20.8 110 70 36 A 9.3 91 NIL R 10.5 N LSCS * * EM FD RN A M 2.5 7 9 NIL N NO
160 Malasree 59322 22 B 2 _ _ 1 41 22 116 76 37 A 9.1 76 NIL R 13 N V I Y M NIL A F 3 6 7 NIL Y NO
161 Veena 56537 21 B 1 _ _ _ 39 22.5 120 70 36 A 12.6 92 NIL R 10 N LSCS * * M EM AD NIL A M 3 7 9 NIL Y NO
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
e d
eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
MASTER CHART
162 Akhila 57711 20 B 1 _ _ _ 38 27.3 112 74 36 A 11.8 85 NIL R 14 N V * * M NIL A M 2.5 7 9 NIL N NO
163 Devamma 55514 21 B 1 _ _ _ 40 23.2 120 70 36 A 8.2 92 NIL R 11 N V S Y A A M 2.3 6 9 NIL Y NO
164 Rekhamma 57296 25 B 2 1 1 _ 40 23.2 126 70 37 A 9 73 NIL R 12 N V * * NIL A F 3.1 7 9 NIL N NO
165 Umadevi 83031 20 B 1 _ _ _ 39 25 150 92 34 A 10.1 86 2+ R 9 N LSCS * * M EM FD PE A M 2.5 6 8 NIL Y NO
166 Hameeda banu 83623 20 B 2 1 1 _ 40 22.8 120 70 34 D 10.6 78 NIL R 4.5 O V S Y NIL A F 2.8 7 9 NIL N NO
167 Shankaramma 2941 20 B 1 _ _ _ 40 20.9 140 90 37 A 11.6 102 NIL R 9.8 N V S * PE A M 2.8 7 9 NIL N NO
168 Mabuni 84182 20 B 1 _ _ _ 37 21.3 116 74 28 D 11.7 90 NIL R 2 O V I * M NIL A M 1.5 7 9 IUGR Y YES Sepsis
169 Nagaveni 141679 20 B 1 _ _ _ 40 22.8 140 90 36 D 9.8 105 NIL R 2.8 O LSCS * * EM FD PE A F 3.2 7 9 NIL N NO
170 Vanitha 2631 22 B 1 _ _ _ 39 29.9 120 70 38 A 9.8 101 NIL R 9.2 N V S * NIL A M 3.7 7 9 NIL N NO
171 Nagalakshmi 2369 19 B 1 _ _ _ 40 25.8 112 74 35 D 11.2 92 NIL R 2.4 O LSCS * * EM FD NIL A F 2.7 7 9 NIL N NO
172 Bargavi bai 56631 21 B 1 _ _ _ 40 21.3 110 70 32 D 10.6 101 NIL R 0 O LSCS * * EM FD NIL A F 2.2 7 9 NIL N NO
173 Nandhini 56816 21 B 1 _ _ _ 41 21.3 110 70 33 D 10 72 NIL R 2 O LSCS * * EM FD RN A F 2.8 7 9 NIL N NO
174 Sulochana bai 58719 20 B 1 _ _ _ 30 26.7 120 70 36 A 11.9 92 NIL R 12 N V S * RN A F 2.9 7 9 NIL N NO
175 Nirmala 59156 30 B 1 _ _ _ 40 23.5 120 76 36 D 9.6 71 NIL R 3.8 O LSCS * * EM FD A A F 2.9 7 9 NIL N NO
176 Saibamma 57369 19 B 2 _ _ 1 40 21.3 116 70 36 A 10.6 71 NIL R 11 N V S * NIL A M 3.1 7 9 NIL N NO
177 Barathi 570081 28 B 1 _ _ _ 40 21.3 112 76 36 A 8.8 72 NIL R 12.6 N V S * A A F 2.5 7 9 NIL N NO
178 Hampamma 2964 20 B 4 2 2 1 37 21.3 116 70 33 A 11.6 92.3 NIL R 8 N V S * NIL A M 2.3 7 9 IUGR N NO
179 Rehana 2984 20 B 1 _ _ _ 37 25.1 110 70 35 A 10.9 110 NIL R 10.5 N V S * NIL A M 2.8 7 9 NIL N NO
180 Lakshmi 83749 31 B 1 _ _ _ 40 27.9 160 100 30 D 12.6 102 4+ R 1.8 O LSCS * * M EM FD PE A M 2.1 7 9 IUGR Y NO
181 Shabana 57157 21 B 1 _ _ _ 40 20.5 110 70 34 D 12.9 92 NIL R 0 O LSCS * * EM FD NIL A F 2.5 7 9 NIL N NO
182 Tulsi 59425 20 B 1 _ _ _ 40 25.5 110 70 35 D 8.5 72 NIL R 2 O LSCS * * EM FD A A M 2.6 7 9 NIL N NO
183 Gayatri 58187 25 B 1 _ _ _ 40 22.8 110 70 34 D 10.6 91 NIL R 4 O LSCS * * M EM FD NIL A F 2.5 7 9 NIL Y NO
184 Salma bee 84799 24 B 5 4 4 _ 39 19.1 116 70 36 A 11.8 92 NIL R 12 N V S * NIL A F 2.5 7 9 NIL N NO
185 Akshata 83364 25 B 2 _ _ 1 41 23.4 150 100 35 D 10.6 82 2+ R 2 O LSCS * * EM FD PE A F 2.3 6 9 IUGR Y NO
186 Sumangala 84207 25 B 2 1 1 _ 40 23.1 110 70 37 A 11.2 78 NIL R 9 N V S * NIL A M 3 7 9 NIL N NO
187 Lakshmi 84603 26 B 3 2 2 _ 38 22 110 70 36 A 9.5 86 NIL R 13 N V S * NIL A M 2.9 7 9 NIL N NO
188 Yasmeen 2740 32 UB 5 2 2 2 39 22 120 70 36 A 9.8 82 NIL R 12 N V S * NIL A F 2.8 7 9 NIL N NO
189 Gowri 2820 25 B 3 2 2 _ 39 27.3 116 70 35 a 8.4 86 NIL R 13.2 N V S * NIL A M 3.2 7 9 NIL N NO
190 Jamuna 83057 20 B 1 _ _ _ 39 20.2 164 100 35 A 9.9 92 2+ R 11 N V I * PE A M 2.7 7 9 NIL N NO
191 Janaki 84232 21 B 1 _ _ _ 40 23 122 74 36 A 10.6 78 NIL R 13 N V S * NIL A F 2.6 7 9 NIL N NO
192 Shardamma 84235 21 B 1 _ _ _ 39 20 116 72 36 A 13 86 NIL R 12 N V S * NIL A F 2.4 7 9 NIL N NO
193 Vijayalakshmi 84653 20 B 3 2 2 _ 37 27 140 90 34 D 12.1 82 1+ R 0 O LSCS * * M EM FD PE A F 2.3 6 9 IUGR Y NO
194 Nooramma 83180 25 B 3 _ _ 2 37 22.5 142 90 30 D 11.2 82 2+ R 4 O LSCS * * M EM FD PE A M 2.2 6 9 IUGR Y NO
195 Thipamma 85883 20 B 1 _ _ _ 38 20 120 70 36 A 9.1 95 NIL R 11.5 N V S * M HBSAg+ A M 2.4 7 9 NIL N NO
196 Sowmya 8459 22 B 1 _ _ _ 39 27 110 70 35 A 10.8 86 NIL R 14 N LSCS * * EM FD NIL A M 3.02 7 9 NIL N NO
197 Rekha 83144 20 B 1 _ _ _ 37 22.5 122 70 37 A 13.6 78 NIL R 13 N V S * NIL A M 2.2 5 8 IUGR Y NO
198 Jambakka 9499 25 B 1 _ _ _ 38 27 116 70 37 A 9.2 86 NIL R 14 N LSCS * * M EM FD NIL A M 2.3 7 9 IUGR Y NO
199 Priyanka 1935 22 B 2 1 1 _ 40 20 120 70 36 A 10.9 86 NIL R 14 N V S * NIL A M 3.1 7 9 NIL N NO
200 YAMUNA 84316 20 B 1 _ _ _ 38 23 110 70 34 D 9.2 86 NIL R 2 N V S * NIL A M 2 4 4 IUGR Y NO
201 Mallama 84094 23 B 1 _ _ _ 40 23.5 110 70 36 A 11.5 71 NIL R 14.5 N V S * NIL A F 2.6 7 9 NIL N NO
202 Jettama 82735 21 B 2 _ _ 1 40 23.5 130 70 35 D 10.7 71 NIL R 5 O LSCS * EM FD NIL A M 3 7 9 NIL N NO
203 Yashodha 82783 25 B 1 _ _ _ 38 25 110 70 33 A 9.7 101 NIL R 11 N V S * NIL A F 2.3 7 9 NIL N NO
204 Chandrakala 85727 23 B 2 1 1 _ 40 25 120 70 36 A 14.3 71 NIL R 12 N V S * NIL A M 2.8 7 9 NIL N NO
205 Anitha 856884 20 B 1 _ _ _ 40 26 110 90 33 A 6.6 73 NIL R 7.5 N LSCS * * M EM FD SA,PE A M 3.3 7 9 IUGR Y NO
206 Vanitha 83166 18 B 1 _ _ _ 39 21 110 70 35 A 11.4 82.6 NIL R 8 N V S * NIL A M 2.5 6 8 around Y NO
207 Mahadevi 85512 20 B 1 _ _ _ 39 21 120 72 36 A 12 71 NIL R 15 N V S * NIL A M 2.6 7 9 NIL N NO
208 Pavithra 85116 19 B 1 _ _ _ 38 25 110 70 33 A 12.1 71.3 NIL R 9.3 N LSCS * * EM FD NIL A F 2.3 7 9 IUGR N NO
209 Thipakka 85328 24 B 1 _ _ _ 38 27 142 90 34 A 11.2 85.5 NIL R 8.5 N V S * GHTN A F 2.3 7 9 IUGR Y NO
210 Haseena 85807 30 B 3 2 1 _ 37 21 120 70 38 A 10.8 80 NIL R 12 N V S * NIL A M 3.6 7 9 NIL N NO
211 Sanjana 85740 19 B 1 _ _ _ 39 27 120 76 38 A 11.7 70 NIL R 10.8 N V S * NIL A M 3.3 7 9 NIL N NO
212 Umadevi 82619 20 B 1 _ _ _ 39 21 108 70 37 A 10.8 72.1 NIL R 10.2 N V S * NIL A M 2.8 7 9 NIL N NO
213 Lakshmi 82231 24 B 1 _ _ _ 39 23 130 86 31 A 8 101 NIL R 8 N LSCS * * M EM FD MA A F 2 7 9 IUGR Y NO
214 Parvathi 82620 22 B 1 _ _ _ 40 25 120 68 36 A 11.6 71.3 NIL R 12 N LSCS * * EM CPD NIL A M 3.5 7 9 NIL N NO
215 Mala 85725 20 B 2 1 1 _ 39 27 130 90 39 I 9 173 NIL R 26 P V S * GDM A M 4 5 7 CROSOM Y YES BA
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
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eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
MASTER CHART
216 Neelamma 82769 20 B 1 - _ _ 39 26 110 70 34 A 9.4 72 NIL R 13 N V S * NIL A M 2.3 7 9 NIL N NO
217 Vaishali 83238 22 B 1 _ _ _ 37 27 170 100 37 A 8.8 93.7 4 R 9.6 N LSCS * * EM CPD PE A F 3.7 7 9 NIL N NO
218 Nagalakshmi 82793 22 B 2 1 1 _ 39 25 110 70 37 A 11.2 91 NIL R 15 N V S * NIL A M 2.6 7 9 NIL N NO
219 Yeriamma 83278 24 B 1 _ _ _ 40 20 120 70 31 D 10.8 71.2 NIL R 4 O LSCS * * M EM FD ASTHMA A F 2.1 7 9 NIL Y NO
220 Varalakshmi 82053 25 B 1 _ _ _ 39 25 156 94 36 A 11.1 72 2 R 10 N V S * PE A M 2.5 7 9 NIL N NO
221 Lakshmi 82459 20 B 1 _ _ _ 38 26 116 76 34 A 9.6 72 NIL R 12.6 N V S * NIL A F 2.4 7 9 IUGR N NO
222 Rehamad bee 83204 20 B 4 2 2 1 38 24 120 70 36 A 9.6 69 NIL R 10 N V S * MA A M 2.9 7 9 NIL N NO
223 Shekuma 82262 21 B 2 1 _ _ 39 20 126 74 34 A 7.6 76 NIL R 9.8 N V S * MA A F 2.2 7 9 NIL N NO
224 Boya Madavi 82258 22 B 1 _ _ _ 40 24 108 70 36 A 13.4 99 NIL R 13.5 N V S * NIL A F 2.6 7 9 NIL N NO
225 Shanthamma 83226 20 B 1 _ _ _ 38 27 130 76 36 A 9.8 70 NIL R 13 N V S * NIL A F 2.4 7 9 NIL N NO
226 Sarawathi 82983 26 B 3 2 2 _ 39 23 110 76 36 A 8.6 72 NIL R 9.5 N V S * NIL A M 3 7 9 NIL N NO
227 Nagamma 84076 24 B 2 1 1 _ 39 20 110 76 32 A 12.1 72 NIL R 12 N V S * NIL A M 2.2 7 9 IUGR Y NO
228 Savithri 80733 25 B 1 _ _ _ 39 26 130 80 40 I 10.7 97.4 NIL R 28 P LSCS * * M EM FD GT A F 2.8 6 8 NIL Y NO
229 Chowdamma 81440 30 B 1 _ _ _ 40 21 120 76 37 A 10.8 91 NIL R 12.5 N V S * NIL A M 2.9 7 9 NIL N NO
230 Geetha 80882 24 B 1 _ _ _ 40 22 110 70 36 A 12 72 NIL R 10.5 N V S * M NIL A M 2.5 7 9 NIL N NO
231 Virupamma 81425 20 B 1 _ _ _ 39 26 120 70 37 A 9.9 91 NIL R 9 N V S * NIL A F 3 7 9 NIL N NO
231 Aruna 85026 20 B 2 _ _ 1 40 22 140 90 36 A 11.2 70 2 R 3 O LSCS * * M EM FD PE A M 3 7 8 NIL Y NO
233 Kotramma 81756 21 B 1 _ _ _ 40 26 116 70 36 A 10..2 102 NIL R 10 N V I * NIL A M 2.7 7 9 NIL N NO
234 Bomakka 80485 25 B 3 2 1 _ 38 24 110 70 35 A 7.9 71 NIL R 11.5 N V S Y MA A M 2.5 7 9 NIL N NO
235 Renuka 80605 20 B 2 1 0 _ 40 21 110 70 37 A 13.4 85.2 NIL R 9 N V S * RN,HBSA A M 2.9 7 9 NIL N NO
236 Lakshmi 80602 24 B 3 2 2 _ 38 21 120 68 36 A 9.2 71 NIL R 10.5 N V S Y NIL A F 3.2 7 9 NIL N NO
237 Uma 80693 22 B 3 2 2 _ 40 23.5 136 92 36 A 7.9 81 NIL R 13 N V S GTN A F 2.9 7 9 NIL N NO
238 Radhika 80944 20 B 2 1 1 _ 39 25 130 90 28 D 10.2 76 NIL R 0 O LSCS * * EM FD NIL A M 1.76 7 9 IUGR Y NO
239 Gangamma 80850 25 B 1 _ _ _ 40 25 120 76 37 A 10.2 76 NIL R 13.5 N V S Y NIL A M 3.1 7 9 NIL N NO
240 Jugunu 81494 25 UB 3 2 2 _ 40 27 120 70 35 A 10.6 76 NIL R 10 N LSCS * * EM AD NIL A M 2.8 7 9 NIL N NO
241 Anjali 81746 20 B 1 _ _ _ 38 29 120 70 30 A 11 86 NIL R 8.6 N V S * NIL A F 1.9 7 9 IUGR Y NO
242 Amrutha 81439 22 B 1 _ _ _ 38 21 110 66 35 A 9 65 NIL R 10.2 N V S Y RN A F 2.5 6 8 NIL N NO
243 Sunitha bai 82476 20 B 1 _ _ _ 39 22 140 90 36 A 10.9 101.4 NIL R 11.6 N V S * GHTN A F 2.8 7 9 NIL N NO
244 Govindamma 81370 30 B 4 3 3 _ 40 24 120 70 37 D 10.3 91 NIL R 2.5 O V S Y NIL A M 3.2 6 9 NIL N NO
245 Pallavi 81357 20 B 1 _ _ _ 40 21 120 74 36 D 12.4 91 NIL R 2 O LSCS * * M EM FD NIL A M 2.9 7 9 NIL N NO
246 Balkis 81338 25 B 2 1 1 _ 38 27 120 74 36 A 9.9 82.3 NIL R 13.5 N V S Y NIL A F 3 7 9 NIL N NO
247 Rathnamma 82465 20 B 1 _ _ _ 40 25 120 74 35 A 10.1 81 NIL R 9.6 N V S * NIL A F 2.5 6 8 NIL N NO
248 Rajamma 82593 21 B 1 _ _ _ 40 29 120 70 36 D 10 84 NIL R 3.5 O LSCS * * M EM FD NIL A M 2.8 7 9 NIL Y NO
249 Lakshmi 85482 23 B 2 1 1 _ 39 24 110 70 36 A 10 78 NIL R 12 N V S * NIL A F 2.5 7 9 NIL N NO
250 Sharadha 82794 20 B 1 _ _ _ 39 23 126 80 35 A 9 82 NIL R 11 N V S Y MA A M 3 7 9 NIL N NO
251 Savitha 82036 26 B 1 _ _ _ 40 23.7 170 108 28 D 10.9 74 4 R 3.5 O LSCS * * M EM FD PE A F 1.8 7 9 IUGR Y NO
252 Gangamma 84671 20 B 1 _ _ _ 39 20 120 76 34 A 11.5 126 NIL R 8 N V S Y NIL A M 2.6 7 9 NIL N NO
253 Thriveni bai 84495 19 B 1 _ _ _ 39 20 120 68 38 A 9.7 73.2 NIL R 6 N LSCS * * EM CPD NIL A F 3.3 7 8 NIL Y NO
254 Nethravathi 82393 25 B 1 _ _ _ 39 19 120 72 28 D 9.5 72 NIL R 1 O V S Y NIL A F 1 7 9 IUGR Y NO
255 Kavitha 82657 23 B 2 _ _ 1 39 25 146 92 40 I 12.6 61.3 1 R 28.5 P LSCS * * EM CPD YPOTHY A M 3 7 9 NIL N NO
256 Premalla 82329 20 B 1 _ _ _ 38 23 126 70 35 A 9.8 71 NIL R 12.6 N V S Y NIL A M 2.5 6 8 NIL N NO
257 Hanumanthamma 82456 30 B 3 2 2 _ 39 22 120 74 37 A 9.6 71 NIL R 13 N V S Y NIL A M 3.2 7 9 NIL N NO
258 Shanthi 82438 23 B 1 _ _ _ 40 24 140 96 37 D 10.6 77.5 1 R 1.2 O LSCS * * EM FD NIL A F 3 7 9 NIL N NO
259 Durgamma 12432 19 B 1 _ _ _ 38 22 130 90 36 A 10.1 97 NIL R 13.5 N LSCS * * EM FD GHTN A M 3 7 9 NIL Y NO
260 Lalithamma 12491 26 B 1 _ _ _ 39 25 110 70 36 A 11.3 85 NIL R 14 N V S * NIL A F 3 7 9 NIL N NO
261 Yashoda 82767 22 B 1 _ _ _ 39 23 110 70 37 A 10.9 72 NIL R 1.6 N V S Y RN A F 2.9 7 9 NIL N NO
262 Marema 84600 22 B 1 _ _ _ 39 21 112 74 33 A 11.1 101 NIL R 12 N V S Y NIL A F 2.5 7 9 NIL N NO
263 Kattema 8460 22 B 2 1 1 _ 39 24 130 86 35 A 9.7 103 NIL R 14 N V S * NIL A M 2.7 7 9 NIL N NO
264 Bhagyama 84359 27 B 4 3 2 _ 40 22 120 70 38 A 9.7 70 NIL R 9.2 N V S Y NIL A F 3.2 7 9 NIL N NO
265 Muttamma 81762 20 B 1 _ _ _ 38 25 120 70 37 A 11 91.3 NIL R 9 N LSCS * * EM AD NIL A M 3.2 7 8 NIL Y NO
266 Nethravathi 81704 21 B 1 _ _ _ 37 21 136 96 32 D 10.4 76 NIL R 1.5 O LSCS * * EM FD NIL A M 2.2 7 9 IUGR Y NO
267 Gangamma 81031 23 B 1 _ _ _ 40 22 126 76 35 A 11.4 92 NIL R 8 N LSCS * * M EM FD NIL A F 2.6 7 9 NIL N NO
268 Sabbu 81391 21 B 2 1 1 _ 39 20 120 70 36 A 9.8 71 NIL R 10.5 N V S Y NIL A F 2.7 7 9 NIL N NO
269 Sunitha 80769 22 B 2 1 1 _ 38 25 120 74 36 A 10 72 NIL R 9.8 N V S Y NIL A M 2.5 7 9 NIL N NO
Sl n
o
Nam
e
IP N
O
Age
Boo
ked
/Un
boo
ked
Gra
vid
a
par
a
livin
g
abor
tion
gest
atio
nal
age
(wee
ks)
BM
I
SB
P
DB
P
SF
H(c
ms)
Clin
ical
yliq
uor
(I,A
,D)
Hb
RB
S
Uri
ne
alb
um
in
Ad
mis
sion
NS
T(R
/NR
)
AF
I(cm
s)
Nor
mal
,Olig
o,P
oly
Mod
e of
del
iver
y(V
agin
al/L
SC
S)
oper
ativ
e d
eliv
ery
Ind
uce
d/S
pon
tan
eou
s d
eliv
ery
Oxy
toci
n a
ugm
enta
tion
(yes
/no)
colo
r of
liq
uor
Em
erge
ncy
/Ele
ctiv
e L
SC
S
Ind
icat
ion
of
LS
CS
Mat
ern
al c
omp
licat
ion
s
Bab
y(A
ive/
Dea
d)
SE
X o
f b
aby(
Mal
e/F
emal
e)
bir
th w
eigh
t(K
gs)
AP
GA
R-1
min
Ap
gar-
5 m
in
per
inat
al c
omp
licat
ion
s
Ad
mis
sion
to
NIC
U
PN
ND
cau
se o
f p
erin
atal
dea
th
MASTER CHART
270 Nagaveni 80742 19 B 1 _ _ _ 38 29 126 82 36 A 14.1 96 NIL R 10 N V S Y RN A M 2.6 7 9 NIL N NO
271 Lakshmi bai 81408 23 B 3 2 2 _ 38 19 132 74 36 A 6.2 101 NIL R 18 N V S * SA A M 2.7 7 9 NIL N NO
272 Kavitha 81613 25 B 1 _ _ _ 40 26 110 70 36 D 10.6 71 NIL R 2 O LSCS * * M EM FD NIL A M 2.8 7 9 NIL N NO
273 Lakshmi 81619 20 B 2 1 1 _ 38 21 116 70 36 A 8.9 89 NIL R 10.3 N V S * MA A M 2.8 7 9 NIL N NO
274 Umadevi 82079 25 B 2 1 1 _ 38 21 120 74 37 A 10.5 92 NIL R 7 N V S * RN A M 3.2 7 9 NIL N NO
275 Lakshmi 82629 20 B 1 _ _ _ 40 23 116 76 35 A 9 72 NIL R 10 N LSCS * * M EM FD NIL A F 2.4 7 9 IUGR Y NO
276 Bhuvaneshwari 82328 21 B 1 _ _ _ 40 25 110 70 35 A 13.3 71.3 NIL R 11.5 N LSCS * * M EM FD NIL A F 3.1 7 9 NIL N NO
277 Asha 84199 21 B 2 _ _ 1 40 25 140 90 37 A 9.7 87 NIL R 12.5 N V S Y NIL A F 3.4 7 9 NIL N NO
278 Renuka 81719 24 B 3 1 1 1 39 25 130 82 38 A 11.6 81.9 NIL R 11.5 N V S * RN A M 3.7 7 9 NIL N NO
279 Ambamma 81242 35 UB 4 3 3 _ 38 21 112 76 34 A 9.4 71 NIL R 10.6 N V S * NIL A F 2.5 7 9 NIL N NO
280 Sharadha 81263 26 B 3 2 2 _ 40 25 118 74 36 A 9.6 126 NIL R 16.3 N V S * NIL A F 3.2 7 9 NIL N NO
281 Lakshmi 81139 24 B 2 _ _ 1 40 25 130 74 33 A 11.9 91 NIL R 6.5 N V VA S Y M HYPOTHYRO A M 2.5 7 9 NIL N NO
282 Gethamma 81907 20 B 1 _ _ _ 40 20 110 70 34 D 11.7 98.2 NIL R 0 O LSCS * * EM FD NIL A F 3 7 9 NIL N NO
283 shanthamma 824327 22 B 1 _ _ _ 39 23 120 60 37 A 11 84 NIL R 9 N V S Y NIL A F 2.8 7 9 NIL N NO
284 Nagamma 82134 25 B 2 1 1 _ 38 24 150 90 34 D 10 78 1+ R 3.5 O V I Y M NIL A M 2 6 8 IUGR Y YES MAS
285 Sheela 83251 21 B 1 _ _ _ 41 25 110 70 37 A 11 82 NIL R 10.5 N LSCS I Y M EM NPL NIL A M 3.2 7 9 NIL N NO
286 Salma banu 82316 23 B 4 1 1 2 37 23 117 78 36 A 10 84 NIL R 8 N V S * NIL A F 3 7 9 NIL N NO
287 Rangamma 81672 24 B 2 _ _ 1 38 21 120 70 37 A 8 90 NIL R 6 N V F S Y M A A F 3.1 6 8 NIL Y NO
288 Eramma 81980 27 B 3 1 1 1 38 25 110 80 32 D 9 85 NIL R 4 O V S * M NIL A F 2.2 7 9 NIL Y NO
289 Ayisha begaum 84311 21 B 1 _ _ _ 37 23 160 100 30 D 10 95 3+ R 6 N LSCS * * M EM FD PE A M 2.4 6 8 NIL Y NO
290 Neelamma 85321 23 B 2 _ _ 1 38 26 110 70 42 I 12 190 NIL R 27 P LSCS * * EM NPL GDM A F 3.3 7 9 NIL Y NO
291 Jaya bai 85790 27 B 1 _ _ _ 36 21 112 60 36 A 11 80 NIL R 8 N V VA S Y NIL A M 3 7 9 NIL N NO
292 Yashodamma 85921 24 B 1 _ _ _ 37 26 110 70 37 A 10 87 NIL R 9 N V S Y NIL A M 2.9 7 9 NIL N NO
293 Ruhina 86101 22 B 1 _ _ _ 36 24 150 90 34 D 10 94 2+ R 4 O V VA I Y M PE A F 3 6 8 NIL Y NO
294 Anitha 86123 19 B 1 _ _ _ 39 19 110 60 37 A 9 89 NIL R 10 N V S * NIL A M 2.9 7 9 NIL N NO
295 Ruksar begaum 86243 23 B 2 1 1 _ 41 25 110 70 38 A 11 98 NIL R 11 N V I * NIL A M 3 7 9 NIL N NO
296 Chaitra 86341 24 B 1 _ _ _ 38 23 110 70 36 A 10 87 NIL R 10 N V S Y M NIL A F 2.8 7 9 NIL N NO
297 honnuramma 86458 28 B 3 2 1 _ 37 27 120 80 38 A 11 90 NIL R 9 N LSCS * * EM AD NIL A M 3.5 7 9 NIL N NO
298 Chandramma 87123 21 B 1 _ _ _ 37 18 160 100 30 D 9 85 4+ R 3 O LSCS * * EM FD PE A M 1.6 6 8 IUGR Y YES Sepsis
299 Lakshmi 87231 24 B 2 1 1 _ 39 25 110 70 38 A 12 78 NIL R 10 N V F S Y M NIL A F 3.2 7 9 NIL N NO
300 Nagamma 87346 27 B 3 1 1 1 41 26 120 80 38 A 11 85 NIL R 7 N V I * NIL A M 3 7 9 NIL N NO
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ANNEXURES
Ultrasonography Machine
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Four Quadrant Technique for estimation of Amniotic Fluid Index