“A STUDY OF PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE

“ A STUDY OF PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE OF

The Tamil Nadu Dr. M.G.R Medical University

In partial fulfilment of the requirement for the award of the Degree of

M.S. OBSTETRICS AND GYNAECOLOGY

THE TAMIL NADU Dr. M.G.R MEDICAL UNIVERSITY

INSTITUTE OF OBSTETRICS AND GYNAECOLOGY,

GOVERNMENT HOSPITAL FOR WOMEN & CHILDREN,

MADRAS MEDICAL COLLEGE.

A STUDY OF PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE OF

MEMBRANES” Dissertation submitted to




BRANCH II





APRIL-2018

A STUDY OF PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE OF








BONAFIDE CERTIFICATE

This is to certify that this dissertation entitled “A STUDY OF

PERINATAL OUTCOME IN PRETERM PREMATURE

RUPTURE OF MEMBRANES” is the bonafide original work done by

Dr.S.YOGALAKSHMI , post graduate in the Department of Obstetrics

and Gynaecology, under the guidance of Dr.ARASI SRIVATHSAN,

MD, OG., Professor, Institute of Social Obstetrics and Gynaecology,

Kasturba Gandhi Hospital, Madras Medical College, Chennai, towards

partial fulfilment of the requirement of the Tamil Nadu Dr. M.G.R

Medical University for the award of M.S Degree in Obstetrics and

Gynaecology, March 2018. The period of post graduate study is from

June 2015 to June 2018.

Prof.Dr.ArasiSrivathsan MD, OG Prof Dr.T.K.ShanthyG unasinghMD, DGO

Professor, Director and Superindent,

ISO-KGH IOG

Prof R. NARAYANABABU MD, DCH

Dean.

Madras Medical College.

DECLARATION

I solemnly declare that this dissertation “A STUDY OF

PERINATAL OUTCOME IN PRETERM PREMATURE

RUPTURE OF MEMBRANES” was prepared by me under the

guidance and supervision of Dr.Arasi Srivathsan, MD, OG., Professor,

Institute of Social Obstetrics and Gynaecology, Kasturba Gandhi

Hospital, Madras Medical College, Triplicane, Chennai.

This dissertation is submitted to The Tamil Nadu Dr. M.G.R.

Medical University, Chennai in partial fulfilment of the University

regulations for the award of the degree of M.S. (Obstetrics and

Gynaecology).

Place: Chennai Date: Dr.S.YOGALAKSHMI

ACKNOWLEDGEMENTS

I gratefully acknowledge and sincerely thank Dr.R.Narayana Babu,

MD, DCH., Dean, Madras Medical College, for allowing me to use

thefacilities and clinical materials available in the hospital.

I extend my sincere thanks and gratitude to Dr.T.K.Shanthy

Gunasingh, MD, DGO., Director and Superintendent, IOG, for granting me

permission to utilize the facilities of the institute for my study.

I am extremely grateful to our beloved Professor, Dr.Arasi Srivathsan,

MD, OG., Professor of Obstetrics &Gynaecology, ISO-KGH, for her valuable

guidance, motivation and encouragement given during the study.

I humbly thank all the Professors and Assistant Professors of IOG,

Egmore and Government Kasturba Gandhi Hospital, Triplicane for all their

help during the course of the study.

My sincere thanks to my statistician Mr.Padmanabhan who patiently

helped me in analysing the results of this study.

My special thanks to my family and friends for their physical help and

moral support without which nothing would have been possible.

I am immensely grateful to all the patients who took part in the study.

CONTENTS

SL.NO TITLE PAGE NO.

1 INTRODUCTION 1

2 AIM AND OBJECTIVES 3

3 MATERIALS AND METHODS 4

4 REVIEW OF LITERATURE 7

5 OBSERVATION AND RESULTS 24

6 DISCUSSION 81

7 CONCLUSION 83

8 BIBLIOGRAPHY 84

9 INFORMED CONSENT FORM 88

10 PROFORMA 90

MASTER CHART

ABBREVIATION

ROM - Rupture of membranes

PPROM - Preterm premature Rupture of membranes

MMPs - matrix metallo proteinase

fFN - Fetal fibronectin

HMD - Hyaline membrane disease

RDS - Respiratory Distress syndrome

ACOG - American college of obstetrics and gynaecology

NICE - National institute of clinical Excellence

H/O - History of

MOD - Mode of delivery

LSCS - Lower segment cesarean section

B - booked

UB - unbooked

AFI - amniotic fluid index

NICU - neonatal intensive care unit

BMI - body mass index

NEC - necrotizing Enterocolitis

INTRODUCTION

1

INTRODUCTION

Preterm premature rupture rupture of membranes is defined as

rupture of fetal membrane before onset of labour at less than

37 completed weeks of gestation and after 28 weeks of gestation.

Incidence ranges from 3-10% of all deliveries. Preterm premature rupture

of membrane is one of the important causes of preterm birth can result in

high perinatal morbidity and mortality.

Preterm premature rupture of membranes complicates 3% of

pregnancies and leads to one third of preterm birth. Preterm delivery

affects one in 10 birth in USA and even greater birth in developing

continues and causes 40-75% neonatal death.

There are numerous risk factors for preterm premature rupture of

membrane such as maternal, socioeconomic class, infection at early

gestational age and associated co-morbid condition. Both mother and

fetus are at greater risk of infection after preterm premature rupture of

membrane.

The fetal and neonatal morbidity and mortality risks are

significantly affected by severity of oligohydrominos, duration of latency

and gestation at preterm premature rupture of membrane .

Complication of preterm premature rupture of membrane for the

fetus and newborn consist of prematurity, fetal distress, altered

2

pulmonary development leading to pulmonary hypoplasia, pulmonary

hypertension, necrotizing enterocolitis and neurological disorder.

The treatment relies on accurate diagnosis and gestational age is

dependent. The diagnosis of preterm premature rupture of membrane is

made by a combination of clinical suspicious, patient history and some

simple test.

Any evidence of infection , fetal distress and cord accidents is an

indication for delivery. A gestational age approach to therapy is important

and should be adjusted to each hospitals neonatal care unit. Antenatal

antibiotics and steroids have clear benefits and should be offered to all

women without complication.

The management of patients with preterm premature rupture of

membrane has changed markedly in the past several years. The basis for

this is a combination of better understanding of newborn physiology,

improved neonatal care and the widespread use of fetal monitoring.

An important recent advance is the recognition that an active

observation of program is associated with less morbidity and mortality.

Moreover advances in perinatal and antenatal care will continue to

improve the outcomes of these of these women and their children.

AIMS AND OBJECTIVES

3

AIM & OBJECTIVES

AIM:

To study perinatal outcome in preterm premature rupture of

membrane.

OBJECTIVE:

1. To study risk factors associated with preterm premature

rupture of membrane.

2. To study perinatal morbidity and mortality associated with

preterm premature rupture of membrane.

3. To study the outcome of labour in preterm premature rupture

of membrane.

MATERIALS ANDMETHODS

4

MATERIALS AND METHODS

This study was conducted in ISO-KGH from may 2016-may 2017

under Madras Medical College. Institutional Ethical committee clearance

was obtained from Madras Medical College.

SAMPLE SIZE:

200 patients

STUDY DESIGN:

Prospective observational study

DURATION OF STUDY:

One year

STUDY CENTRE:

Department of obstetrics and gynaecology in ISO KGH, Chennai.

INCLUSION CRITERIA:

All pregnant women with a singleton pregnancy between 28-37

weeks of gestation admitted in labour room were shifted after considering

inclusion and exclusion criteria.

5

EXCLUSION CRITERIA:

1. Multiple pregnancy

2. Fetal growth restriction

3. Uterine anomalies

4. Foetal anomalies

5. Hypertensive disorder complicating pregnancy

6. Gestational diabetes

7. Antepartum haemarrhage ( Placenta praevia, Abruption )

8. Class 2-4 cardiac disease

9. Tumour complicating pregnancy ( Fibroid, Ovarian tumour )

10. Medical disorder complicating pregnancy ( Chronic hypertension,

Chronic renal disease and SLE

STUDY METHOD:

This was prospective observational study which was carried out

those pregnant women admitted with preterm premature rupture of

membranes between 28-36 weeks of gestation. The gestational age was

calculated from LMP, if there is discrepancy of more than seven days

6

between LMP and early weeks USG and consecutive two coincide then

USG EDD should be taken.

For above mentioned patients we will do baseline investigation like

Hb, pcv, Blood grouping and Typing and High vaginal swab. Per

speculum examination should be done to confirm the diagnosis of

preterm premature rupture of membranes. Digital examination only be

done only when the patient is in the active labour.

The above mentioned patients are closely monitored throughout

labour. Immediately after delivery paediatrician was called over and look

sign of infection and Respiratory distress syndrome.

All the information was attached in pretested questionare. In study

all patients are observed until discharge from hospital. The study was

conducted after getting consent from patient. Close monitoring of all

patients of preterm premature rupture of membrane during labour and

baby immediately after delivery and upto discharge.

REVIEW OF LITERATURE

7

REVIEW OF LITERATURE

ROM:

Rupture of membrane or amniorrhexis is a term said during

pregnancy to describe a rupture of the amniotic sac. Normally it occurs

spontaneously at full term either during or at the beginning of lobour.

PPROM:

Preterm premature rupture of membrane defined as rupture of

membrane before 37 completed weeks of gestation.

TYPES OF PPROM

Early preterm: 28-32 weeks

Moderate preterm: 32-34 weeks

Late preterm: 34-36 weeks

INCIDENCE:

Incidence of PPROM ranges from 3.0-10.0% of all deliveries.

PPROM complicates approximately 3% of pregnancies and leads to one

third of preterm birth.

8

STRUCTURE OF FETAL MEMBRANES:

These are the membrane that develop outside the embryo but in

close association with it and they carry out certain specific functions.

Fetal membrane consist of amnion, chorion, allantois and yolk sac. The

amnion was innermost membrane of fetus and forms amniotic cavity that

contains amniotic fluid. The chorion was between amnion and decidua.

AMNION:

The amnion is the membrane that closely covers the embryo.

Pregnancy is the period of time during which a child matures with in the

womb of the mother. The period is important for the development of the

fetus. During this time the fetus must be protected from internal

environment of the mothers body and this is achieved in many ways. One

of the primary form of protection is the amniotic sac which is the

protective sac and fluid that surrounds the fetus and prevents damage.

The membrane that forms this sac is known as amnion. The amniotic

fluid provides a shock absorbing effect to the embryo against womb

infections etc. The watery fluid around the embryo helps in maintaining

constant temperature and pressure and protects the embryo in case the

mother has a fall. The amniotic fluid is derived from the mothers blood

and contains foetal cells. This is made use of in the prenatal sex test for

the fetus- known as amniocentesis. In amniocentesis the amniotic fluid is

9

drawn out with a syringe and the cells are tested for the presence of sex

chromosomes.

CHORION:

Chorion is a membrane that develops at the beginning of a

pregnancy between the developing fetus and the mother and continuous

to grow through out the pregnancy. It is formed by two layers the

embryonic mesoderm and double layers of trophoblasts. Chorion protects

the embryo and forms placenta for metabolic exchange between mother

and fetus.

YOLK SAC:

This is the formed below the embryo. In human beings this contains

a fluid but no yolk. It is vestigial organ. Its wall is made of trophoblast

and endoderm. The yolk sac functions as the region of the formation of

blood cells upto about 6th week of development when liver of fetus takes

up this function.

ALLANTOIS:

This is a small bag like structure that develops from the gut of the

embryo and near the yolk sac. This membrane develops around the third

week of development. Gradually the allantois shrinks in size and get

10

enclosed in umbilical cord. Allantois helps in the formation of umbilical

arteries and veins. The allantois also forms blood cells.

ETIOPATHOGENESIS:

WEAKENED FETAL MEMBRANE:

Fetal membrane likely break because they become fragile and

weak. This weakening is a normal process that typically happens at term

as the body prepares for labor and delivery. But, this can be a problem

when it occurs preterm (preterm). The natural weakening of fetal

membrane is thought to be due to one or combination of the following. In

preterm premature rupture rupture of membranes, these process are

activated too early;

CELL DEATH;

When cells undergoes programmed cell death, they release

chemical markers that are detected in high concentration in cases of

preterm premature rupture of membrane

Poor assembly of collagen:

Collagen is a molecule that gives fetal membrane their strength. In

cases of preterm premature rupture of membranes proteins that bind and

cross link collagen to increase its tensile strength are altered.

11

BREAKDOWN OF COLLAGEN:

Collagen is broken down by enzymes called matrix

metalloproteinases (MMPs), which are found at higher level in PPROM

amniotic fluid, this MMPs will break down the strength- bearing

collagen, so prostaglandin production will be synthesized in high amount

to prompt the uterine contraction and cervical ripening. MMPs are

inhibited by tissue inhibitors of MMPs which are found lower levels in

PPROM amniotic fluid.

INFECTION:

Infection and inflammation likely explains why membrane break

earlier than they are supposed to. In studies bacteria have been found in

the amniotic fluid one third of cases of PPROM. Often, testing of

amniotic fluid is normal, but a subclinical infection (too small to detect)

or infection of maternal tissues next to the amniotic fluid, may still be

contributing. In response to infection, the body creates inflammation by

making chemicals (ex: cytokines) that weaken the fetal membrane and

put them at risk for rupture. PPROM is also risk factor in the

development of neonatal infection.

12

GENETICS:

Many genes play role in inflammation and collagen production,

therefore inherited genes may play a role in predisposing a person to

PPROM.

RISK FACTORS:

The cause of PPROM is not clearly understood, but the following

are risk factors that have been shown to increase the chance of it

happening. In many cases however no risk factors is identified.

1.Infectins: urinary tract infection, sexually transmitted diseases, lower

genital infections ( ex: Bacterial vaginosis)

2. Cigarette smoking during pregnancy

3. Illicit drug use during pregnancy

4. Having had PPROM in previous pregnancies

5. Hydrominos: too much amniotic fluid

6. Multiple gestation: being pregnant with two or more fetuses at one

time

7. Having had episodes of bleeding anytime during pregnancy

8. Invasive procedure like amniocentesis and chorionic villous sampling

13

9. Nutritional deficits

10. Cervical insufficiency: having short or prematurely dilated cervix

during pregnancy

11. Low socio economic status

12. Being overweight

DIAGNOSIS OF PPROM:

To know for sure if a women has experienced PPROM a health

care clinician must prove that the fluid leaking from the vagina is

amniotic fluid, and the lobor has not yet started. To do this, a health care

clinician will take a medical history, do a gynecological exam using a

sterile speculum and ultrasound.

HISTORY:

A person with PPROM typically recalls a sudden gush of fluid loss

from the vagina, or steady loss of small amount of fluid.

SPECLUM EXAMINATION:

A health care clinician will insert a sterile speculum into the vagina

in order to see inside and perform the following evaluation. Digital

cervical exams, in which gloved fingers are inserted into the vagina to

14

measure the cervix, are avoided until the women is in active labor to

reduce the risk of infection.

POOLING TEST;

Pooling is when a collection of amniotic fluid can be seen in the

back of vagina (vaginal fornix). Sometimes leakage of fluid from the

cervical opening can be seen when the person coughs or does a valsalva

maneuver.

NITRAZINE TEST:

A sterile cotton swab is used to collect fluid from the vagina and

place it on nitrazine paper (phenaphthazne). Amniotic fluid is mildly

basic (ph 7.1-7.3) compared to normal vaginal secretion which are acidic

( ph 4.5-6 ). Basic flid, like amniotic fluid, will turn the nitrazine paper

from orange to dark blue.

FERN TEST:

A sterile cotton swab is used to collect fluid from vagina and place it

on a microscope slide. After drying, amniotic fluid will form a

crystallization pattern called arborization which resembles leaves of a

fern plant when viewed under a microscope.

15

FETAL FIBRONECTIN :( fFN )

It is the protein produced in pregnancy that determine the risk of

preterm delivery. The fFN test measures the amount of fetal fibronectin in

vaginal secretion and is performed like a pap smear test. A negative test is

a predictor that delivery will not occur in the next two weeks, but a

positive test does not necessarily indicate that preterm delivery is

imminent,

IMMUNOLOGICAL TEST:

Immune- chromatological tests ( Amnisure, Actim PPROM test,

Biosynex Amnioquick ). These are commercially available test kits that

detect chemicals present in amniotic fluid; placental alpha microglobulin-

1 (AmniSure ) and insulin like growth factor binding protein-1 ( Actim

PPROM test ). These are helpful if negative to rule out PPROM, but are

not that helpful if positive because the false positive rate is 19-30%.

DYE TEST

In this test a needle is used to inject indigo carmine dye (blue) into

the amniotic fluid that remains in the uterus through the abdominal wall.

In the case of PPROM, blue dye can be seen on a stained tampon or pad

after about 15-30 minutes. This method can be used to definitively make

a diagnosis, but is rarely done because it is invasive and increase risk of

16

infection. But, can be helpful if the diagnosis is still unclear after the

above evaluations have been done.

ULTRASOUND:

Ultrasound can measure the amount of amniotic fluid still in the

uterus surrounding the fetus. If the fluid levels are low, PPROM is more

likely. This is helpfl in cases when diagnosis is not certain, but is not, by

itself, definitive.

OTHER TESTS:

1. Detection of fetal cells in amniotic fluid

2. Detection of vernix and lanugo hair in amniotic fluid

FALSE POSITIVES:

Like amniotic fluid, blood, semen, vaginal secretion, antiseptics,

basic urine and cervical mucus also have a basic ph and also turn

nitrazine paper blue, Cervical mucus can also make a pattern similar to

ferning on a microscope slide, but it is usually patchy and less branching.

DIFFERENTIALDIAGNOSIS:

Other things to keep in mind that may present similarly to PPROM

are the following:

17

• Urinary incontinence: Leakage of small amounts of urine is

common in the last part of pregnancy

• Normal vaginal secretion of pregnancy

• Increased cervical discharge: this can happen when there is a

genital tract infection

• Semen

• Douching

• Vesicovaginal fistula: an abnormal connection between the bladder

and the vagina

• Loss of the mucus plug

COMPLICATION OF PPROM

COMPLICATIONS INCIDENCE (%)

1. Cord compression 32 to 76

2. Chorioamnionitis 13 to 60

3. Abruptio placentae 4 to 12

4. Antepartum fetal death 1 to 2

5. Respiratory distress syndrome 35

18

MATERNAL

1. Choriomnionitis (acute and subclinical)

This was most common complication occurring in PPROM .Clinical

chorioamnionitis is Diagnosed solely based on clinical signs since access

to uncontaminated amniotic fluid or placenta for culture is invasive and

usually avoided. Typically, the presence of fever with in addition two

other signs like uterine tenderness, maternal or fetal tachycardia and foul

or purulent amniotic fluid. Chorioamnionitis is an indication for

termination of pregnancy not cesarean section the latter was indicated in

obstetric indication only.

2. Postpartum endometritis

This was another maternal complication of PPROM. Endometritis

was usually associated with chrioamnionitis. The duration of antibiotic

therapy after preterm premature rupture of membrane does not affect the

neonatal morbidity and maternal morbidity.

FETAL

1. Prematurity

2. Hyaline membrane disease

3. Infection

4. Neurological damage

5. Pulmonary hypoplasia

19

6. Cerebral palsy

7. Musculoskeletal deformity

THE ROLE OF CORTICOSTEROIDS:

Corticosteroids decrease perinatal morbidity and mortality after

PPROM. A recent meta-analysis found that corticosteroids after PPROM,

versus no administration, reduced the risk of respiratory distress

syndrome (20 versus 35.4%) intraventricular hemorrhage (7.5 versus

15.9%) and necrotizing enterocolitis (0.8 versus 4.6%) without an

increase in the risk of maternal and fetal infection. The most widely used

and recommended regimens include intramuscular betamethasone 12mg

every 24 hours for two days, or intramuscular dexamethasone 6mg every

12 hours for two days. The National institutes of Health recommends

administration of corticosteroids nefore 30-32 weeks gestation, assuming

fetal viability and no evidence of intra-amniotic infection. Use of

corticosteroids between 32-34 weeks is controversial. Adminstration of

corticosteroids after 34 weeks gestation is not recommended unless there

is evidence of fetal lung immaturity by amniocentesis. Multiple courses

are not recommended because studies have shown that two or more

courses can result in cerebral palsy.

20

ROLE OF ANTIBIOTICS IN PPROM:

Giving antibiotics to patients with PPROM can reduce neonatal

infection and the latent period. A meta- analysis showed that a patient

receiving antibiotics after PPROM, compared those not receiving

antibiotics experienced reduced postpartum endometritis,

chorioamnionitis, neonatal sepsis, neonatal pneumonia and

intraventricular hemorrhage. Another meta-analysis found a decrease in

neonatal intraventricular hemorrhage and sepsis. The regimen studied by

the National institute of Child Health and Human Development trial uses

an intravenous combination of 2 gms of ampicilin and 250 mg of

erythromycin every 6 hours for 48 hours, followed by 250 mg of

amoxicillin and 333 mg of erythromycin every 8 hours for 5 days.

TOCOLYTIC THERAPY:

Limited data are available to help determine whether tocolytic

therapy is indicated after PPROM. As described above, corticosteroids

and antibiotics are beneficial when administered to patients with PPROM,

but no studies of these therapies combined with tocolysis are available.

Tocolytic therapy is not improve neonatal outcome. Long term tocolytic

therapy in patients with PPROM is not recommended; consideration of

this should await further research. ACOG guideline, there is no clear

evidence that tocolytic drug improve outcome and therefore it is

21

reasonable not to use them. However tocolysis should be considered if the

few days gained would be put to good use, such as completing a course of

corticosteroids or in utero transfer.

ACOG GUIDELINE:

There is no clear evidence that tocolytic drugs improve outcome

and therefore it is reasonable not to use them. However, tocolysis should

be considered if the few days gained would be put to good use, such as

completing course of corticosteroids or in utero transfer.

MANAGEMENT OF PPROM

1. 28-31 WEEKS

Delivery before 32 weeks gestation may lead to severe neonatal

morbidity and mortality. In the absence of intra-amniotic infection

pregnancy may be prolonged under antibiotics and corticosteroids until

34 weeks of gestation. Contraindication for conservative management is

chorioamnionitis, abruption and non reassuring fetal heart patterns.

Despite these measures many patients will deliver with in two weeks of

PPROM. During conservative treatment should watch for maternal

temperature, uterine contractions, uterine tenderness and laboratory

evidence of infection like leucocytosis or elevated ESR. Evidence

22

suggests that prolonged latency lead to increased incidence of intra-

amniotic infection.

2. 32-33 WEEKS

PPROM between 32-33 weeks of gestation should be induction of

labor after transport of patients to intensive neonatal care should be

considered. Prolonging pregnancy after documentation of pulmonary

maturity unnecessarily increases the likelihood of maternal infection,

umbilical cord compression and neonatal infection. There are few data to

guide the care of patients without documented pulmonary maturity.

Physicians must balance the risk of respiratory distress syndrome and

other sequelae of premature delivery with the risk of pregnancy

prolongation, such as neonatal sepsis and core accidents. Physician

should administer a course of corticosteroids and antibiotics to patients

without documented lung maturity consider delivery 48 hrs later or

perform careful assessment of fetal well being, observe for intra amniotic

infection, and deliver at 34 weeks.

3. 34-36 WEEKS

When PPROM occurs between 34-36 weeks gestation, physician

should avoid to urge to prolong the pregnancy. Studies shown that labor

induction clearly is beneficial at or after 34 weeks of gestation. One study

showed that Conservative management between 34-36 weeks of

gestational age resulted in an increased risk of chorio amnionitis and a

23

lower average umbilical cord ph. PPROM is not a contraindication to

vaginal delivery.

PREVENTION:

Both intravaginal progesterone and cervical cerclage are used

prophylactically to prevent PPROM in different circumstances, although

evidence is lacking on which is more effective and the relative costs and

benefits of each. In the UK, NICE has the following recommendations for

women who, on a transvaginal ultrasound scan between 16 and 34 weeks,

have a cervical length of <25mm. Women who have previously had a

preterm birth or pregnancy loss between 16 and 34 weeks, should be

offered either intravaginal progesterone or cervical cerclage. Women with

no history of a preterm birth or pregnancy loss between 16 and 34 weeks,

should be offered intravaginal progesterone. Women who have had

PPROM in a previous pregnancy or have a history of cervical trauma,

should be offered cervical cerclage. ACOG does not recommend

intravaginal progesterone or cervical cerclage and either of which not

improve maternal and perinatal outcome.

OBSERVATION AND RESULTS

24

OBSERVATION AND RESULTS

AGE GROUP Vs PPROMGROUP

TABLE 1

PPROMGROUP (GA in weeks) Total

28-32 33-34 <37

AG

E G

RO

UP

UPTO 25

Count 20 16 72 108

% within AGE GROUP

18.5% 14.8% 66.7% 100.0%

% within PPROMGROUP

45.5% 30.8% 69.2% 54.0%

% of Total 10.0% 8.0% 36.0% 54.0%

26-30

Count 20 28 24 72

% within AGE GROUP

27.8% 38.9% 33.3% 100.0%

% within PPROMGROUP

45.5% 53.8% 23.1% 36.0%

% of Total 10.0% 14.0% 12.0% 36.0%

>30

Count 4 8 8 20

% within AGE GROUP

20.0% 40.0% 40.0% 100.0%

% within PPROMGROUP

9.1% 15.4% 7.7% 10.0%

% of Total 2.0% 4.0% 4.0% 10.0%

Total

Count 44 52 104 200

% within AGE GROUP

22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

25

Chi-Square Tests

Value df Asymp. Sig.

(2-sided)

Pearson Chi-Square 22.875a 4 .000

Likelihood Ratio 23.350 4 .000

Linear-by-Linear

Association 8.000 1 .005

N of Valid Cases 200

Patients with Preterm premature rupture of membrane occur in all

age group. 54% belong to age group 22<20 years.36% belongs to age

group 20-25 years. 10% belong to age group >30 years. But it was more

common in age group of < 25 years.

a. 1 cells (11.1%) have expected count less than 5. The minimum

expected count is 4.40.

The distribution of age classification among PPROM group is

statistically significant. Chi =22.8 P=0.005

26

27

TABLE 2

SOCIOECONOMIC CLASS VS PPROMGROUP

PPROMGROUP (GA in weeks ) Total

28-32 33-34 <37

SO

CIO

EC

ON

OM

IC C

LAS

S

3

Count 8 4 16 28

% within SE CLASS 28.6% 14.3% 57.1% 100.0%

% within PPROMGROUP 18.2% 7.7% 15.4% 14.0%

% of Total 4.0% 2.0% 8.0% 14.0%

4

Count 32 48 84 164

% within SE CLASS 19.5% 29.3% 51.2% 100.0%


% of Total 16.0% 24.0% 42.0% 82.0%

5

Count 4 0 4 8

% within SE CLASS 50.0% 0.0% 50.0% 100.0%


% of Total 2.0% 0.0% 2.0% 4.0%

Total

Count 44 52 104 200

% within SE CLASS 22.0% 26.0% 52.0% 100.0%


% of Total 22.0% 26.0% 52.0% 100.0%

28

Chi-Square Tests

Value Df

Asymp. Sig.

(2-sided)



Linear-by-Linear

Association .180 1 .671




Socio economic class distribution among PPROM is statistically

significant Chi=8.26 P=0.81

82% of patient of preterm premature rupture of membrane belongs

to class 4 socioeconomic class as per modified Kuppusamy classification.

29

SOCIO ECONOMIC CLASS

30

BMI GROUP vs PPROMGROUP

TABLE 3

PPROMGROUP

(GA in weeks)

28-32 33-34 <37

BM

I GR

OU

P

NORMAL

Count 8 8 16

% within BMI GROUP

25.0% 25.0% 50.0%

% within PPROMGROUP

18.2% 15.4% 15.4%

% of Total 4.0% 4.0% 8.0%

OVERWEIGHT

Count 28 36 56

% within BMI GROUP

23.3% 30.0% 46.7%

% within PPROM

GROUP 63.6% 69.2% 53.8%

% of Total 14.0% 18.0% 28.0%

OBESE

Count 8 8 32

% within BMI GROUP

16.7% 16.7% 66.7%

% within PPROMGROUP

18.2% 15.4% 30.8%

% of Total 4.0% 4.0% 16.0%

Total

Count 44 52 104

% within BMI GROUP

22.0% 26.0% 52.0%

% within PPROMGROUP

100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0%

31

Chi-Square Tests

Value df Asymp. Sig. (2-sided)



Linear-by-Linear Association

2.439 1 .118


a. 0 cells (0.0%) have expected count less than 5. The minimum expected

count is 7.04.

BMI distribution among PPROM is statistically not significant. Chi=5.8

P=0.209

Preterm premature rupture of membrane was more common in obese

patients with 53.8%

32

33

GRAVIDA vs PPROMGROUP

TABLE 4

PPROMGROUP (GA in weeks) Total

28-32 33-34 <37

GR

AV

IDA

1

Count 24 32 52 108 % within GRAVIDA 22.2% 29.6% 48.1% 100.0%

% within PPROMGROUP

54.5% 61.5% 50.0% 54.0%

% of Total 12.0% 16.0% 26.0% 54.0%

2


% within PPROMGROUP

27.3% 30.8% 46.2% 38.0%

% of Total 6.0% 8.0% 24.0% 38.0%

3


% within PPROMGROUP

9.1% 7.7% 0.0% 4.0%

% of Total 2.0% 2.0% 0.0% 4.0%

4


% within PPROMGROUP

9.1% 0.0% 0.0% 2.0%

% of Total 2.0% 0.0% 0.0% 2.0%

5


% within PPROMGROUP

0.0% 0.0% 3.8% 2.0%

% of Total 0.0% 0.0% 2.0% 2.0%

Total


% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

34

Chi-Square Tests


(2-sided)



Linear-by-Linear

Association .180 1 .671



expected count is .88.

Gravidae distribution among PPROM is statistically significant.

Chi=31.38 P=0.000

The preterm premature rupture of membrane was more common in

primigravidae with 54% incidence.

35

36

ABORTION VS PPROMGROUP

TABLE 5

PPROMGROUP

(GA in weeks) Total 28-32 33-34 <37

AB

OR

TIO

N

0

Count 40 48 84 172

% within ABORTIO 23.3% 27.9% 48.8% 100.0%

% within

PPROMGROUP 90.9% 92.3% 80.8% 86.0%

% of Total 20.0% 24.0% 42.0% 86.0%

1

Count 4 4 16 24

% within ABORTIO 16.7% 16.7% 66.7% 100.0%

% within

PPROMGROUP 9.1% 7.7% 15.4% 12.0%

% of Total 2.0% 2.0% 8.0% 12.0%

2

Count 0 0 4 4

% within ABORTIO 0.0% 0.0% 100.0% 100.0%

% within

PPROMGROUP 0.0% 0.0% 3.8% 2.0%

% of Total 0.0% 0.0% 2.0% 2.0%

Total

Count 44 52 104 200

% within ABORTIO 22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

37

Chi-Square Tests


(2-sided)



Linear-by-Linear Association 4.747 1 .029




Previous abortion distribution among PPROM group is statistically

not significant. Chi=6.4 P=0.16

82% of patients with preterm premature rupture of membrane with

previous history of abortion.

38

ABORTION

39

PREVIOUS H/O PPROM VS PPROMGROUP

TABLE 6

PPROMGROUP

(GA in weeks )

Total 28-32 33-34 <37

PR

EV

IOU

S H

/O P

PR

OM

NO

Count 40 52 104 196

% within PREV H/O 20.4% 26.5% 53.1% 100.0%

% within

PPROMGROUP 90.9% 100.0% 100.0% 98.0%

% of Total 20.0% 26.0% 52.0% 98.0%

YES

Count 4 0 0 4

% within PREV H/O 100.0% 0.0% 0.0% 100.0%

% within

PPROMGROUP 9.1% 0.0% 0.0% 2.0%

% of Total 2.0% 0.0% 0.0% 2.0%

Total

Count 44 52 104 200

% within PREV H/O 22.0% 26.0% 52.0% 100.0%

% within

PPROMGROUP 100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

40

Chi-Square Tests


(2-sided)



Linear-by-Linear





Previous history distribution among PPROM is statistically not

significant. Chi=14.4 P= 0.001

98% of patients with PPROM have no previous history.

41

PREVIOUS H/O PPROM

42

MODE OF DELIVERY VS PPROMGROUP

TABLE 7

PPROMGROUP

(GA in weeks )

Total 28-32 33-34 <37

MO

DE

OF

DE

LIV

ER

Y

NORM

AL

Count 40 40 48 128

% within MOD 31.3% 31.3% 37.5% 100.0%

% within PPROM

GROUP 90.9% 76.9% 46.2% 64.0%

% of Total 20.0% 20.0% 24.0% 64.0%

LSCS

Count 4 12 56 72

% within MOD 5.6% 16.7% 77.8% 100.0%

% within PPROM

GROUP 9.1% 23.1% 53.8% 36.0%

% of Total 2.0% 6.0% 28.0% 36.0%

Total

Count 44 52 104 200

% within MOD 22.0% 26.0% 52.0% 100.0%

% within PPROM

GROUP

100.0

% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

43

Chi-Square Tests

Value df

Asymp. Sig.

(2-sided)



Linear-by-Linear





Mode of delivery among PPROM distribution is statistically

significant, Chi=31.9 P=0.00

64% of patients among present study PPROM delivered vaginally.

44

MODE OF DELIVERY

45

BOOKED CASE VS PPROMGROUP

TABLE 8

PPROMGROUP

(GA in weeks ) Total

28-32 33-34 <37

BO

OK

ED

CA

SE

Count 44 52 104 200

% within B /UB 22.0% 26.0% 52.0% 100.0%


% of Total 22.0% 26.0% 52.0% 100.0%

Total

Count 44 52 104 200

% within B /UB 22.0% 26.0% 52.0% 100.0%


% of Total 22.0% 26.0% 52.0% 100.0%

46

BOOKED CASES

a. No statistics are computed because B /UB is a constant.

Booked and Unbooked among PPROM distribution is statistically not

significant.

All patients with PPROM in present study is booked case.

47

ANEMIA VS PPROMGROUP

TABLE 9

PPROMGROUP

(GA in weeks )

Total 28-32 33-34 <37

AN

EM

IA

NO

Count 32 40 92 164

% within ANEMIA 19.5% 24.4% 56.1% 100.0%

% within

PPROMGROUP 72.7% 76.9% 88.5% 82.0%

% of Total 16.0% 20.0% 46.0% 82.0%

YES

Count 12 12 12 36

% within ANEMIA 33.3% 33.3% 33.3% 100.0%

% within

PPROMGROUP 27.3% 23.1% 11.5% 18.0%

% of Total 6.0% 6.0% 6.0% 18.0%

Total

Count 44 52 104 200

% within ANEMIA 22.0% 26.0% 52.0% 100.0%

% within

PPROMGROUP 100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

48

Chi-Square Tests


(2-sided)







Anaemia distribution among PPROM group is statistically not

signicant. Chi=6.4 P=0.04

The above table illustrates that PPROM has no correlation with

preexisting anemia in mother (n=164 ) with a incidence of 64% without

anemia.

49

50

INFECTION vs PPROMGROUP

TABLE 10

PPROMGROUP


28-32 33-34 <37

INF

EC

TIO

N

NO

Count 36 52 100 188

% within INFECTION 19.1% 27.7% 53.2% 100.0%

% within

PPROMGROUP 81.8% 100.0% 96.2% 94.0%

% of Total 18.0% 26.0% 50.0% 94.0%

YES

Count 8 0 4 12

% within INFECTION 66.7% 0.0% 33.3% 100.0%

% within

PPROMGROUP 18.2% 0.0% 3.8% 6.0%

% of Total 4.0% 0.0% 2.0% 6.0%

Total

Count 44 52 104 200

% within INFECTIO 22.0% 26.0% 52.0% 100.0%

% within

PPROMGROUP 100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

51

Chi-Square Tests


(2-sided)







Infection distribution among PPROM group is statistically not

significant.

The above table illustrates that PPROM has no correlation with

history of maternal infection ( n= 188) with a incidence of 84% without

maternal infection and 6% of patients with anemia have PPROM.

52

INFECTION

53

LIQUOR VS PPROMGROUP

TABLE 11

PPROMGROUP


28-32 33-34 <37

LIQ

UO

R (

AF

I)

>8

Count 40 28 68 136

% within LIQUOR 29.4% 20.6% 50.0% 100.0%

% within

PPROMGROUP 90.9% 53.8% 65.4% 68.0%

% of Total 20.0% 14.0% 34.0% 68.0%

5-8

Count 0 12 4 16

% within LIQUOR 0.0% 75.0% 25.0% 100.0%

% within

PPROMGROUP 0.0% 23.1% 3.8% 8.0%

% of Total 0.0% 6.0% 2.0% 8.0%

<5

Count 4 12 32 48

% within LIQUOR 8.3% 25.0% 66.7% 100.0%

% within

PPROMGROUP 9.1% 23.1% 30.8% 24.0%

% of Total 2.0% 6.0% 16.0% 24.0%

Total

Count 44 52 104 200

% within LIQUOR 22.0% 26.0% 52.0% 100.0%

% within

PPROMGROUP 100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

54

Chi-Square Tests

Value df

Asymp. Sig.

(2-sided)



Linear-by-Linear





The amount of liquor distribution among PPROM group is

statistically not significant.

The above table illustrates that that PPROM patients have adequate

liquor (n=136) with a incidence of 68% and ( n=48) 48 patients have

severe oligohydrominos with a incidence of 24%.

55

56

APGAR GROUP vs PPROMGROUP

TABLE 12

PPROMGROUP

(GA in weeks)

28-32 33-34 <37

AP

GA

RG

RO

UP

7 & above

Count 40 48 100

% within

APGARGROUP 21.3% 25.5% 53.2%

% within

PPROMGROUP 90.9% 92.3% 96.2%

% of Total 20.0% 24.0% 50.0%

<7

Count 4 4 4

% within

APGARGROUP 33.3% 33.3% 33.3%

% within

PPROMGROUP 9.1% 7.7% 3.8%

% of Total 2.0% 2.0% 2.0%

Total

Count 44 52 104

% within

APGARGROUP 22.0% 26.0% 52.0%

% within

PPROMGROUP 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0%

57

APGAR GROUP vs PPROMGROUP

Total

AP

GA

RG

RO

UP

7 & above

Count 188

% within APGARGROUP 100.0%

% within PPROMGROUP 94.0%

% of Total 94.0%

<7

Count 12



% of Total 6.0%

Total

Count 200



% of Total 100.0%

58

Chi-Square Tests

Value df Asymp. Sig. (2-sided)




1.759 1 .185




Apgar distribution among PPROM group is statistically significant.

Chi=1.8 P=0.3

The above table illustrates that (n=188) newborn have agar of more

than seven with a incidence of 94% out of which 100 newborn were

belong to late preterm group with a incidence of 50%.

59

60

NICU vs PPROMGROUP

TABLE 13

PPROMGROUP( GA in

weeks ) Total 28-32 33-34 <37

NIC

U

NO

Count 0 4 32 36

% within NICU 0.0% 11.1% 88.9% 100.0%

% within PPROMGROUP

0.0% 7.7% 30.8% 18.0%

% of Total 0.0% 2.0% 16.0% 18.0%

YES

Count 44 48 72 164

% within NICU 26.8% 29.3% 43.9% 100.0%

% within PPROMGROUP

100.0% 92.3% 69.2% 82.0%

% of Total 22.0% 24.0% 36.0% 82.0%

Total

Count 44 52 104 200

% within NICU 22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

Chi-Square Tests


(2-sided)




23.306 1 .000


61



The NICU admission among PPROM group is statistically

significant. Chi =24.8 P =0.0

The above table illustrates that (n=164) 82% of newborn was

admitted in NICU out of which all early PPROM newborn got admitted

in NICU.

62

RESPIRATORY DISTRESS VS PPROMGROUP

TABLE 14

PPROMGROUP( GA in

weeks ) Total 28-32 33-34 <37

RE

SP

IRA

TO

RY

IST

RE

SS

NO

Count 0 8 34 42 % within RD 0.0% 19.0% 81.0% 100.0%

% within PPROMGROUP

0.0% 15.4% 32.7% 21.0%

% of Total 0.0% 4.0% 17.0% 21.0%

YES

Count 44 44 70 158 % within RD 27.8% 27.8% 44.3% 100.0%

% within PPROMGROUP

100.0% 84.6% 67.3% 79.0%

% of Total 22.0% 22.0% 35.0% 79.0%

Total

Count 44 52 104 200 % within RD 22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

Chi-Square Tests


(2-sided)



Linear-by-Linear



63

RESPIRATORY DISTRESS



The above table illustrates that (n=158) 79% of newborn have got RD out

of which all early PPROM newborn have got RD.

64

PHOTOTHERAPY vs PPROMGROUP

TABLE 15


28-32 33-34 <37

PH

OT

OT

HE

RA

PY

NO

Count 8 36 76 120

% within PHOTO 6.7% 30.0% 63.3% 100.0%

% within PPROMGROUP

18.2% 69.2% 73.1% 60.0%

% of Total 4.0% 18.0% 38.0% 60.0%

YES

Count 36 16 28 80

% within PHOTO 45.0% 20.0% 35.0% 100.0%

% within PPROMGROUP

81.8% 30.8% 26.9% 40.0%

% of Total 18.0% 8.0% 14.0% 40.0%

Total

Count 44 52 104 200

% within PHOTO 22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

Chi-Square Tests

Value df

Asymp. Sig.

(2-sided)



Linear-by-Linear



65



The above table illustrates that 40% (n=80) of newborn have

undergone phototherapy out of which 81.8% (n=36) belongs to early

PPROM group.

PHOTOTHERAPY

66

FETAL INFECTION vs PPROMGROUP

TABLE 16

PPROM GROUP (GA in weeks ) Total

28-32 33-34 <37

FE

TA

L IN

FE

CT

ION

NO

Count 32 52 100 184

% within FET INFEC 17.4% 28.3% 54.3% 100.0%

% within PPROMGROUP

72.7% 100.0% 96.2% 92.0%

% of Total 16.0% 26.0% 50.0% 92.0%

YES

Count 12 0 4 16

% within FET INFEC 75.0% 0.0% 25.0% 100.0%

% within PPROMGROUP

27.3% 0.0% 3.8% 8.0%

% of Total 6.0% 0.0% 2.0% 8.0%

Total

Count 44 52 104 200

% within FET INFEC 22.0% 26.0% 52.0% 100.0%

% within PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

Chi-Square Tests


(2-sided)




17.038 1 .000


67

FETAL INFECTION



The above table illustrates that 8% (n=16) of newborn have

clinically obvious infection out of which 6% ( n=12 ) belongs to early

PPROM group.

68

DEATH vs PPROMGROUP

TABLE 17


28-32 33-34 <37

DE

AT

H

NO

Count 32 48 100 180

% within DEATH 17.8% 26.7% 55.6% 100.0%

% within PPROMGROUP

72.7% 92.3% 96.2% 90.0%

% of Total 16.0% 24.0% 50.0% 90.0%

YES

Count 12 4 4 20

% within DEATH 60.0% 20.0% 20.0% 100.0%

% within PPROMGROUP

27.3% 7.7% 3.8% 10.0%

% of Total 6.0% 2.0% 2.0% 10.0%

Total

Count 44 52 104 200

% within DEATH 22.0% 26.0% 52.0% 100.0%

% wiSthin PPROMGROUP

100.0% 100.0% 100.0% 100.0%

% of Total 22.0% 26.0% 52.0% 100.0%

69

Chi-Square Tests

Value df Asymp. Sig. (2-

sided)



Linear-by-Linear





The above table illustrates that 10% (n=16)of newborn have died of

complication out of which 6% (n=6%) in the early PPROM group.

70

71

GA

0 20 40 60 80 1000

20

40

60

80

100

100-Specificity

Sen

sitiv

ity

Sensitivity: 45.0 Specificity: 93.3 Criterion : ≤32

ROC curve

Variable GA

Classification variable PHOTO

Sample size 200

Positive group : PHOTO = 1 80

Negative group : PHOTO = 0 120

Disease prevalence (%) unknown

72

Area under the ROC curve (AUC)

Area under the ROC curve (AUC) 0.690

Standard Errora 0.0392

95% Confidence intervalb 0.621 to 0.753

z statistic 4.850

Significance level P (Area=0.5) <0.0001 a DeLong et al., 1988

b Binomial exact

Youden index

Youden index J 0.3833

Associated criterion ≤32

Sensitivity 45.00

Specificity 93.33

Criterion values and coordinates of the ROC curve [Hide]

Criterion Sensitivity 95% CI Specificity 95% CI +LR -LR

<29 0.00 0.0 - 4.5 100.00 97.0 -

100.0

1.00

≤29 5.00 1.4 - 12.3 96.67 91.7 - 99.1 1.50 0.98

≤30 20.00 11.9 - 30.4 93.33 87.3 - 97.1 3.00 0.86

≤32 45.00 33.8 - 56.5 93.33 87.3 - 97.1 6.75 0.59

≤33 50.00 38.6 - 61.4 86.67 79.3 - 92.2 3.75 0.58

≤34 65.00 53.5 - 75.3 63.33 54.1 - 71.9 1.77 0.55

≤35 75.00 64.1 - 84.0 43.33 34.3 - 52.7 1.32 0.58

≤36 100.00 95.5 -

100.0

0.00 0.0 - 3.0 1.00

73

The above ROC curve implies that less than 32 weeks of gestation

newborn had phototherapy has sensitivity of 45% and specificity of

93.3%.

GA

0 20 40 60 80 1000

20

40

60

80

100

100-Specificity

Sen

sitiv

ity


ROC curve

Variable GA

Classification variable NICU

Sample size 200

Positive group : NICU = 1 164

Negative group : NICU = 0 36


74





z statistic 7.604

Significance level P (Area=0.5) <0.0001 a DeLong et al., 1988 b Binomial exact

Youden index



Sensitivity 73.17

Specificity 77.78



<29 0.00 0.0 - 2.2 100.00 90.3 -

100.0

1.00

≤32 26.83 20.2 - 34.3 100.00 90.3 -

100.0

0.73

≤33 31.71 24.7 - 39.4 88.89 73.9 - 96.9 2.85 0.77

≤34 56.10 48.1 - 63.8 88.89 73.9 - 96.9 5.05 0.49

≤35 73.17 65.7 - 79.8 77.78 60.8 - 89.9 3.29 0.34

≤36 100.00 97.8 -

100.0

0.00 0.0 - 9.7 1.00

75


new born had NICU admission which had 73.2% sensitivity and 77.8%

specificity.

GA

0 20 40 60 80 1000

20

40

60

80

100

100-Specificity

Sen

sitiv

ity


ROC curve

Variable GA

Classification variable RD

Sample size 200

Positive group : RD = 1 158

Negative group : RD = 0 42


76





z statistic 6.370


Youden index



Sensitivity 72.78

Specificity 69.05



<29 0.00 0.0 - 2.3 100.00 91.6 -

100.0

1.00

≤32 27.85 21.0 - 35.5 100.00 91.6 -

100.0

0.72

≤33 32.28 25.1 - 40.2 88.10 74.4 - 96.0 2.71 0.77

≤34 55.70 47.6 - 63.6 80.95 65.9 - 91.4 2.92 0.55

≤35 72.78 65.1 - 79.6 69.05 52.9 - 82.4 2.35 0.39

≤36 100.00 97.7 -

100.0

0.00 0.0 - 8.4 1.00

77


of newborn had RD and has sensitivity of 72.8% and specificity of 69%.

GA

0 20 40 60 80 1000

20

40

60

80

100

100-Specificity

Sen

sitiv

ity Sensitivity: 66.7 Specificity: 89.4 Criterion : ≤31

ROC curve

Variable GA

Classification variable INFECTIO

Sample size 200

Positive group : INFECTIO = 1 12

Negative group : INFECTIO = 0 188


78





z statistic 3.844

Significance level P (Area=0.5) 0.0001 a DeLong et al., 1988 b Binomial exact

Youden index



Sensitivity 66.67

Specificity 89.36



<29 0.00 0.0 - 26.5 100.00 98.1 -

100.0

1.00

≤29 0.00 0.0 - 26.5 95.74 91.8 - 98.1 0.00 1.04

≤30 33.33 9.9 - 65.1 89.36 84.0 - 93.4 3.13 0.75

≤31 66.67 34.9 - 90.1 89.36 84.0 - 93.4 6.27 0.37

≤34 66.67 34.9 - 90.1 53.19 45.8 - 60.5 1.42 0.63

≤35 100.00 73.5 -

100.0

38.30 31.3 - 45.7 1.62 0.00

≤36 100.00 73.5 -

100.0

0.00 0.0 - 1.9 1.00

79


of newborn had infection with 66.7% sensitivity and 89.4% specificity.

GA

0 20 40 60 80 1000

20

40

60

80

100

100-Specificity

Sen

sitiv

ity


ROC curve

Variable GA

Classification variable DEATH

Sample size 200

Positive group : DEATH = 1 20

Negative group : DEATH = 0 180


80





z statistic 6.203


Youden index



Sensitivity 60.00

Specificity 93.33



<29 0.00 0.0 - 16.8 100.00 98.0 - 100.0 1.00

≤29 20.00 5.7 - 43.7 97.78 94.4 - 99.4 9.00 0.82

≤30 60.00 36.1 - 80.9 93.33 88.6 - 96.5 9.00 0.43

≤33 60.00 36.1 - 80.9 75.56 68.6 - 81.6 2.45 0.53

≤34 80.00 56.3 - 94.3 55.56 48.0 - 62.9 1.80 0.36

≤35 100.00 83.2 - 100.0 40.00 32.8 - 47.6 1.67 0.00

≤36 100.00 83.2 - 100.0 0.00 0.0 - 2.0 1.00


had died with 60% sensitivity and 93.3% specificity.

DISCUSSION

81

DISCUSSION

PPROM was more common in age group of less than 25 years with

a incidence of 54% out of which 36% late PPROM and 10% early

PPROM. Ina study by Noor et al in Ayub medical college in 2006

demonstrated that ( 58.8% ) higher incidence among younger age group.

PPROM was more common in low socio economic class with a

incidence of 82%. In a study done by Sheela et al demonstrated that

62.8% were belongs to low socio economic class.PPROM was more

common in primigravidae with a incidence of 54%. In a study conducted

by Ghandhi M et al majority were primigravidae 42.3% and another study

by Dkeke et al majority were primigravidae 29.1%.

PPROM was not associated with previous history of PPROM and

abortion with a incidence of 2% and 12% respectively. In a syudy by

Revathy et al 17% had previous abortion and 10% had previous history of

PPROM.

In our study 64% of patients had delivered vaginally and 36% had

delivered by LSCS. In a study by Sheela at al 65% had vaginal delivery

compared to 16% by LSCS.

Majority of neonatal morbidity noted in our study was Respiratory

distress contributing to 79% followed by hyperbilirubinaemia by 40%

and followed by sepsis by 8%. Respiratory distress was common in early

PPROM and hyper bilirubinaemia common in late preterm.

82

A study by Emeche et al showed 61% RDS Singel S et al obtained

92% in early PPROM. A study by Emeche et al showed 22% RDS,

17.8% hyper bilirubinaemia and 16% sepsis. Similar study by Signel S et

al in late PPROM showed 6.6% RDS and 16% sepsis. In present study

79% had RDS, 40% had hyper bilirubinaemia and 8% had sepsis.

CONCLUSION

83

CONCLUSION

PPROM was more common in younger age group, low socio

economic class and pimigravidae in present study.

PPROM was not associated with previous history ,booked or un

booked and previous abortion.

In present study most of newborn had better 5min apgar especially

late preterm group.

Majority of neonatal morbidity was due to RDS followed by hyper

bilirubinaemia then followed by sepsis.

In present study RDS was common in early preterm group and

hyper bilirubinaemia common in late preterm group.

In current study most of patients delivered vaginally compared to

36% of LSCS.

BIBL IOGRAPHY

84

BIBLIOGRAPHY

1. Bartfield MC , Carlan SJ, The home management ofpreterm

premature ruptured membranes. Clini Obstet Gynecol.

1998;41(3); 503-14.

2. Goldenberg RL, Rouse DJ, Prevention of premature birth. N

Eng J Med, 1998;339(5);313-20.

3. Jayaram VK, Sudha S. A study of PPROM management and

outcome . J Obstet Gynecol India. 2001;51;58-60.

4. Khuppel Ka, Curtis C, Robert LK Premature rupture of

membranes. Am J Obstet Gynecol.1979;134(6);655-61.

5. Noor S, Nazar AF, Bashir R, Sulthana R. Prevalenceof

PPROM AND ITS OUTCOME. J Ayub Med Coll

Abbottabad.2007;19(4);14-7.

6. Gandhi M, Shah F, Panchal C, Obstetric outcome in premature

rupture of membrane. Internet JGynecol Obstet. 2012;

16(2);1-5.

7. Okeke TC, Enwereji JO, Okoro OS, Airi CO, Ezugwu EC, Agu

PU. The incidence and management outcome of preterm

premature rupture of membrane in a tertiary hospitalin Nigeria.

Am J Clini Med RES, 2014;2910;14-7.

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8. Revathi V, Sowjanya R, Lavanya S Maternal and perinatal

outcome in preterm premature rupture of membranre at term.

IOSR-JDMS.2015;14;12-5.

9. Singhal S Puri M, Gami N. An analysis of factors affecting the

duration of latency period and its impacton neonatal outcome

in patients with PPROM. Arch Gynecol Obstet,

2011;284(6);1339-43.

10. Allens. Epidemiology of preterm premature of membranes.

Clinic Obst Gynecol 1991; 19; 339-51.

11. French JI Mc Gregor JA.The patho-biology of preterm

premature rupture of membranes.Semin perinatal 1966;20;

344-68.

12. Wingfield M, Turner J,Stronge M. Significance of absent

amniotic fluid in labor follow rupture of membrane.J Obs

Gynecol 1993;13; 12-15.

13. Novak-antolic Z, Panzntar M, Verdenik I.Preterm premature

ruptre of membranes and postpartum infection.Eur J Obs Gyn

14. DepartmentofObetetrics and Gyneacology, Women’s Health

Research Centre, Imam Reza Hospital, Mashhad, University of

Medical Sciences, Mashhad, Iran.

86

15. Saira Dars, MS Obstetrics and Gynaecology, Department of

Obstetrics and Gynaecology, Liaquat UniversityHospital,

Hyderabad, Singh,Pakistan.

16. Maxwell GL. Preterm premature rupture of membranes. Obstet

Gynecol Surv 1993;48:576-83.

17. Merenstein GB, Weisman LE. Premature rupture of the

membranes: neonatal cnnsequences. Semin Perinatol

1996;20:375-80.

18. Douvas SG, Brewer JM, McKayML, Rhodes PG, Kahlstorf JH,

Morrison JC. Treatment of premature rupture of the

membranes. J Reprod Med 1984;29:741-4.

19. Cotton DB, Hill, Strassner HT, Platt LD, Ledger WJ. Use of

amniocentesis in preterm gestation wiyh ruptured membranes.

Obstet Gynecol 1984;63:38-43.

20. CarrollSG, Sebire NJ, Nicolaides KH. Preterm prelabour

amniorrhexis. New York/ London:Parthenon;1996.

21. Broekhuizen FF, Gliman M, Hamilton PR. Amniocentesisfor

gram stain and culture in preterm premature rupture of

membranes. Obstet Gynecol 1985;66:316-21.

22. Galask RP,Varner MW, Petzold CR, Wilbur SL. Bacterial

attachment to the chorionic membranes. Am J Obstet Gynecol

1984;148:915-28.

87

23. Gyr TN, Malek A, MathezLoic F, Altermatt HJ, Bodmer T,

Nicolaides K, et al. Permeation of human chorionic membranes

by Escherichia coli in vitro. Am j Obstet Gynecol

1994;170:223-7.

24. Royal college of Obstetricians and Gynaecologist. Clinical

Governance Advice 1c; Developing a clinical practice

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RCOG: 2006.

25. Baptisti A, Chemical test for the determination of ruptured

membranes. Am J Obstet Gynecol 1938;35:688-90.

26. Abe T, The detecyion of rupture of the fetal membranes with

nitrazine indicator. Am J Obstet Gynecol 1940;39;400-4.

27. Paavola A, Methods based on the study of crystals and fat

staining; use in diagnosing rupture of membranes. Ann Chir

Gynecol Fenn 1958;47:22-8.

28. Volet B, MorierGenoud J, The crystallization test in amniotic

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29. Brosens I, Gordon H. The cytological diagnosis of ruptured

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Br Commonwealth 1965;72:342-6

INFORMED CONSENT

FORM

88

INFORMATION SHEET

• We are conducting a study on “PERINATAL OUTCOME IN

PRETERM PREMATURE RUPTURE OF MEMBRANES” in

KGH, Chennai. Your participation in the study is very valuable to us.

• The purpose of this study to evaluate the perinatal morbidity and

mortality and outcome of labour in preterm premature rupture of

membranes.

• We will follow those patients admitted to hospital labour ward with

history of draining P/V after 28 weeks and before 37 weeks of

gestation. We will monitor the outcome of labour and neonatal

outcome. Those babies followed upto period of hospitalization and

followed for morbidity and mortality.

• The privacy of the patients in the research will be maintained

throughout the study. In the event of any publication or presentation

resulting from the research, no personally identifiable information will

be shared.

• Taking part in the study is voluntary. You are free to decide whether

to participate in this study or to withdraw at any time, your decision

will not result in any loss of benefits to which you are itherwise

entitled.

• I have been given an information sheet giving details of the study.

• The results of the special study may be intimated to you at end of the

study period or during the study if anything is found abnormal which

may aid in the management or treatment.

Signature of the participant Signature of the investigator

Institution:

Date:

89

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PROFORMA

90

PROFORMA

� NAME

� AGE

� IP NO

� PARITY

� SOCIO ECONOMIC STATUS

� PREVIOUS OBSTETRIC HISTORY

� PREVIOUS H/O ABORTION

� LMP/EDD

� WEIGHT GAIN DURING PREGNANCY (kg)

� BMI

� MANAGEMENT BASED ON GESTATIONAL AGE

� HIGH RISKS DURING PREGNANCY AND DELIVERY

� BABY DETAILS

• Mode of delivery

• Preterm neonatal complication

• Birth weight

• Apgar

• Mother side/ admitted

� POST PARTUM NEONATAL FOLLOW UP

MASTER CHART

S.no

NAME

AGE

SE CLASS

BMI

GRAVIDA

ABORTIO

GA

PREV H/O

MOD

B /UB

ANEMIA

INFECTIO

LIQUOR

5min APG

NICU

RD

PHOTO

FET INFEC

DEATH

1N

ith

ya

27

42

32

03

20

1B

00

07

11

10

0

2S

ug

an

ya

22

32

11

03

60

1B

00

08

00

00

0

3A

nit

ha

22

42

51

03

60

1B

00

08

00

00

0

4Is

hw

ary

a2

84

25

10

30

01

B0

00

81

11

00

5O

ma

tha

l2

33

27

10

32

01

B0

00

91

11

00

6K

art

hik

a1

95

28

10

35

01

B1

10

90

01

00

7T

am

ilse

lvi

27

43

35

23

50

1B

00

08

11

00

0

8Je

nn

ath

ma

ry

23

32

52

03

40

1B

00

08

11

10

0

9Je

ya

sri

23

32

62

03

60

1B

00

08

00

00

0

10

Na

nd

hin

i2

64

28

10

34

01

B0

00

81

00

00

11

Pra

bh

a3

24

29

10

33

01

B0

00

91

01

00

12

Lath

ara

ja2

64

30

10

36

01

B0

00

51

01

00

13

Re

va

thy

29

43

21

03

50

2B

10

09

10

00

0

14

De

vi

30

42

73

13

40

1B

00

19

10

00

0

15

Ila

kiy

a2

64

22

20

34

01

B0

01

91

00

00

16

Ve

nu

ma

dh

av

i2

74

25

20

34

01

B0

01

91

11

00

17

Sh

ali

ni

22

43

22

13

60

2B

00

28

11

10

0

18

De

vi

20

43

02

13

60

2B

10

21

01

10

00

19

Sri

na

nd

hin

i2

04

29

20

36

02

B0

02

91

10

00

20

Joth

i2

44

28

10

35

02

B0

02

91

10

00

21

Ma

lath

i2

34

36

10

36

02

B0

02

80

01

00

22

Ay

sha

20

43

32

03

60

2B

00

29

11

00

0

23

Inb

av

all

i3

04

25

41

32

01

B0

00

91

11

10

24

Am

ud

ha

20

42

61

03

40

2B

00

28

11

00

0

25

Lax

mi

21

42

81

03

50

1B

00

09

11

10

1

26

Me

racu

lin

23

42

32

03

60

1B

00

09

00

00

0

27

Sa

ran

ya

25

42

51

03

40

1B

00

09

11

00

0

28

Sa

ran

ya

26

43

71

03

30

1B

00

09

11

00

0

29

Pri

ya

24

52

83

03

21

1B

10

08

11

10

0

30

Lali

tha

27

42

62

03

50

1B

00

08

11

00

0

31

Ra

va

na

mm

al

18

43

22

13

60

1B

00

09

11

00

0

32

Ela

kiy

a3

24

30

20

31

01

B1

10

81

11

00

33

Ary

a1

84

22

10

29

01

B0

00

71

11

00

34

Go

ma

thy

24

32

21

03

60

1B

00

09

00

00

0

35

Re

shm

a2

54

28

10

33

01

B1

00

70

00

00

36

Pa

thch

iya

mm

al

37

42

72

03

50

2B

00

08

11

00

0

37

No

orj

ah

an

22

42

71

03

60

2B

00

08

11

10

0

38

Sh

ali

ni

25

42

51

03

60

2B

00

09

11

00

0

39

Su

mit

hra

28

42

82

03

60

2B

00

08

00

00

0

40

Ch

itra

31

42

72

03

60

2B

00

17

11

10

0

41

Pa

tta

mm

al

29

42

32

13

50

2B

00

27

11

00

0

42

Jen

ife

r2

13

29

10

36

02

B0

02

91

10

00

43

Jey

ara

ni

25

42

81

03

60

1B

00

08

11

01

0

44

Ma

ha

lax

mi

21

42

81

03

00

1B

00

08

11

11

0

45

Ga

jap

riy

a3

04

27

10

34

01

B0

00

91

11

00

46

Um

a2

64

24

10

34

02

B1

02

91

10

00

47

Re

va

thy

23

42

92

03

00

2B

00

08

11

00

1

48

An

ge

l3

04

26

10

29

01

B0

02

81

10

01

49

Pri

ya

29

33

01

03

00

1B

11

05

11

11

1

50

Lax

mi

32

43

02

03

40

2B

10

22

11

00

1

51

Ind

ira

ni

27

42

32

03

20

1B

00

07

11

10

0

52

Ma

ri2

23

21

10

36

01

B0

00

80

00

00

53

Ka

ma

tch

i2

44

25

10

36

01

B0

00

80

00

00

54

Re

nu

ka

28

42

51

03

00

1B

00

08

11

10

0

55

Aji

tha

23

32

71

03

20

1B

00

09

11

10

0

56

Sa

rojo

19

52

81

03

50

1B

11

09

00

10

0

57

Ka

dh

arb

ee

27

43

35

23

50

1B

00

08

11

00

0

58

Jey

ala

xm

i2

53

25

20

34

01

B0

00

81

11

00

59

Pa

lan

iya

mm

al

23

32

62

03

60

1B

00

08

00

00

0

60

Pa

ttu

26

42

81

03

40

1B

00

08

11

00

0

61

Kri

shn

av

en

i3

24

29

10

33

01

B0

00

91

11

00

62

Me

ga

bu

26

43

01

03

60

1B

00

05

11

10

0

63

Su

nd

ari

29

43

21

03

50

2B

10

09

11

00

0

64

Ra

dh

ab

ai

30

42

73

13

40

1B

00

19

11

00

0

65

Ma

ry2

64

22

20

34

01

B0

01

91

10

00

66

Ush

a2

74

25

20

34

01

B0

01

91

11

00

67

Mu

rug

am

ma

l2

24

32

21

36

02

B0

02

81

11

00

68

Gn

an

ap

ush

pa

m2

04

30

21

36

02

B1

02

10

11

00

0

69

Sa

ray

a2

04

29

20

36

02

B0

02

91

10

00

70

An

ura

dh

a2

44

28

10

35

02

B0

02

91

10

00

71

Pa

ttu

23

43

61

03

60

2B

00

28

00

10

0

72

Mu

niy

am

ma

l2

04

33

20

36

02

B0

02

91

10

00

73

Ma

rgre

t3

04

25

41

32

01

B0

00

91

11

10

74

Va

div

am

mig

ai

20

42

61

03

40

2B

00

28

11

00

0

75

Ch

inn

ap

on

nu

21

42

81

03

50

1B

00

09

11

10

1

76

Ra

jala

xm

i2

34

23

20

36

01

B0

00

90

00

00

77

Re

nu

ka

25

42

51

03

40

1B

00

09

11

00

0

78

Am

ud

ha

26

43

71

03

30

1B

00

09

11

00

0

79

Pit

cha

iya

mm

al

24

52

83

03

21

1B

10

08

11

10

0

80

Ga

ng

a2

74

26

20

35

01

B0

00

81

10

00

81

Se

lvi

18

43

22

13

60

1B

00

09

11

00

0

82

Pre

ma

32

43

02

03

10

1B

11

08

11

10

0

83

Ra

ni

18

42

21

02

90

1B

00

07

11

10

0

84

Ba

ckia

m2

43

22

10

36

01

B0

00

90

00

00

85

Ch

inn

ath

ai

25

42

81

03

30

1B

10

07

00

00

0

86

Pa

ram

esh

wa

ri3

74

27

20

35

02

B0

00

81

10

00

87

Ko

kil

a2

24

27

10

36

02

B0

00

81

11

00

88

Bh

av

an

i2

54

25

10

36

02

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00

91

10

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89

Pa

vit

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28

42

82

03

60

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00

08

00

00

0

90

Pa

dm

ap

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a3

14

27

20

36

02

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01

71

11

00

91

Dh

ara

ni

29

42

32

13

50

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00

27

11

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92

Ma

nu

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21

32

91

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60

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00

29

11

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0

93

Ka

laiv

an

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54

28

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81

10

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94

He

ma

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14

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81

11

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95

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lli

30

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71

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96

Sa

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64

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91

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97

Ka

na

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23

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92

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98

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30

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32

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42

22

03

40

1B

00

19

11

00

0

11

6La

xm

i2

74

25

20

34

01

B0

01

91

11

00

11

7M

ala

rko

di

22

43

22

13

60

2B

00

28

11

10

0

11

8M

ala

thy

20

43

02

13

60

2B

10

21

01

10

00

11

9S

ug

an

thi

20

42

92

03

60

2B

00

29

11

00

0

12

0S

elv

i2

44

28

10

35

02

B0

02

91

10

00

12

1R

en

uk

a2

34

36

10

36

02

B0

02

80

01

00

12

2P

ari

ma

la2

04

33

20

36

02

B0

02

91

10

00

12

3M

oh

an

a3

04

25

41

32

01

B0

00

91

11

10

12

4B

ha

va

ni

20

42

61

03

40

2B

00

28

11

00

0

12

5S

ha

ny

hi

21

42

81

03

50

1B

00

09

11

10

1

12

6S

ath

ya

23

42

32

03

60

1B

00

09

00

00

0

12

7Lx

mi

25

42

51

03

40

1B

00

09

11

00

0

12

8D

ev

i2

64

37

10

33

01

B0

00

91

10

00

12

9S

use

ela

24

52

83

03

21

1B

10

08

11

10

0

13

0K

ott

esw

ari

27

42

62

03

50

1B

00

08

11

00

0

13

1In

dir

an

i1

84

32

21

36

01

B0

00

91

10

00

13

2S

ug

un

a3

24

30

20

31

01

B1

10

81

11

00

13

3M

un

iya

mm

al

18

42

21

02

90

1B

00

07

11

10

0

13

4P

arv

ee

nb

an

u2

43

22

10

36

01

B0

00

90

00

00

13

5S

ud

ha

25

42

81

03

30

1B

10

07

00

00

0

13

6P

ree

thi

37

42

72

03

50

2B

00

08

11

00

0

13

7M

an

ka

ya

rsi

22

42

71

03

60

2B

00

08

11

10

0

13

8G

ow

ri2

54

25

10

36

02

B0

00

91

10

00

13

9A

nis

ha

28

42

82

03

60

2B

00

08

00

00

0

14

0G

ee

tha

31

42

72

03

60

2B

00

17

11

10

0

14

1P

ala

ya

m2

94

23

21

35

02

B0

02

71

10

00

14

2B

an

um

ath

y2

13

29

10

36

02

B0

02

91

10

00

14

3S

ulo

cha

na

25

42

81

03

60

1B

00

08

11

01

0

14

4B

hu

va

ne

shw

ari

21

42

81

03

00

1B

00

08

11

11

0

14

5S

um

ath

y3

04

27

10

34

01

B0

00

91

11

00

14

6U

ma

ma

he

swa

ri2

64

24

10

34

02

B1

02

91

10

00

14

7P

ush

pa

m2

34

29

20

30

02

B0

00

81

10

01

14

8S

aro

ja3

04

26

10

29

01

B0

02

81

10

01

14

9P

rab

ha

va

thy

29

33

01

03

00

1B

11

05

11

11

1

15

0Lo

ga

mm

al

32

43

02

03

40

2B

10

22

11

00

1

15

1V

asa

nth

a2

74

23

20

32

01

B0

00

71

11

00

15

2P

riy

a2

23

21

10

36

01

B0

00

80

00

00

15

3G

ow

ri2

44

25

10

36

01

B0

00

80

00

00

15

4S

ara

ny

a2

84

25

10

30

01

B0

00

81

11

00

15

5S

rala

23

32

71

03

20

1B

00

09

11

10

0

15

6S

he

eja

19

52

81

03

50

1B

11

09

00

10

0

15

7V

ija

ya

27

43

35

23

50

1B

00

08

11

00

0

15

8K

um

ari

25

32

52

03

40

1B

00

08

11

10

0

15

9C

hin

na

po

nn

u2

33

26

20

36

01

B0

00

80

00

00

16

0A

lam

elu

26

42

81

03

40

1B

00

08

11

00

0

16

1U

sain

ab

an

u3

24

29

10

33

01

B0

00

91

11

00

16

2V

ara

lax

mi

26

43

01

03

60

1B

00

05

11

10

0

16

3S

um

ath

y2

94

32

10

35

02

B1

00

91

10

00

16

4P

ush

ph

ala

tha

30

42

73

13

40

1B

00

19

11

00

0

16

5La

tha

raja

26

42

22

03

40

1B

00

19

11

00

0

16

6K

am

atc

hi

27

42

52

03

40

1B

00

19

11

10

0

16

7M

all

iga

22

43

22

13

60

2B

00

28

11

10

0

16

8M

ah

ala

xm

i2

04

30

21

36

02

B1

02

10

11

00

0

16

9R

aji

na

ma

la2

04

29

20

36

02

B0

02

91

10

00

17

0M

ala

rko

di

24

42

81

03

50

2B

00

29

11

00

0

17

1M

all

iga

23

43

61

03

60

2B

00

28

00

10

0

17

2V

asa

nth

i2

04

33

20

36

02

B0

02

91

10

00

17

3A

nja

lam

30

42

54

13

20

1B

00

09

11

11

0

17

4S

um

ith

ra2

04

26

10

34

02

B0

02

81

10

00

17

5S

ha

nth

i2

14

28

10

35

01

B0

00

91

11

01

17

6S

un

da

ri2

34

23

20

36

01

B0

00

90

00

00

17

7K

av

ith

a2

54

25

10

34

01

B0

00

91

10

00

17

8M

ala

26

43

71

03

30

1B

00

09

11

00

0

17

9B

rin

dh

a2

45

28

30

32

11

B1

00

81

11

00

18

0M

all

iga

27

42

62

03

50

1B

00

08

11

00

0

18

1S

ara

la1

84

32

21

36

01

B0

00

91

10

00

18

2S

ha

lin

i3

24

30

20

31

01

B1

10

81

11

00

18

3B

ha

va

ni

18

42

21

02

90

1B

00

07

11

10

0

18

4A

lam

elu

24

32

21

03

60

1B

00

09

00

00

0

18

5P

usp

ha

25

42

81

03

30

1B

10

07

00

00

0

18

6V

ara

lax

mi

37

42

72

03

50

2B

00

08

11

00

0

18

7A

na

nd

hi

22

42

71

03

60

2B

00

08

11

10

0

18

8S

ub

bu

lax

mi

25

42

51

03

60

2B

00

09

11

00

0

18

9C

hit

ra2

84

28

20

36

02

B0

00

80

00

00

19

0D

ee

pa

31

42

72

03

60

2B

00

17

11

10

0

19

1P

an

jav

arn

am

29

42

32

13

50

2B

00

27

11

00

0

19

2S

iva

ran

jin

i2

13

29

10

36

02

B0

02

91

10

00

19

3N

ad

hiy

a2

54

28

10

36

01

B0

00

81

10

10

19

4K

an

ag

a2

14

28

10

30

01

B0

00

81

11

10

19

5M

an

ime

ga

lai

30

42

71

03

40

1B

00

09

11

10

0

19

6N

ag

am

ax

mi

26

42

41

03

40

2B

10

29

11

00

0

19

7S

ow

miy

a2

34

29

20

30

02

B0

00

81

10

01

19

8R

an

i3

04

26

10

29

01

B0

02

81

10

01

19

9P

ad

ma

pri

ya

29

33

01

03

00

1B

11

05

11

11

1

20

0B

ab

y3

24

30

20

34

02

B1

02

21

10

01

Documents

“A STUDY OF PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE