ABRUPTIO PLACENTA-AN OBSTETRIC

ENDANGERMENT

Dissertation submitted to

THE TAMILNADU DR. M.G.R. MEDICAL

UNIVERSITY

In partial fulfillment of the regulations

For the award of the degree of

M.S. BRANCH-II

OBSTETRICS AND GYNECOLOGY

KILPAUK MEDICAL COLLEGE

CHENNAI

MAY 2019

CERTIFICATE

This is to certify that the dissertation entitled “Abruptio placenta-an

obstetric endangerment.” is a bonafide record of work done by

Dr.SWETHA.S in Kilpauk Medical college, Chennai during the

period January 2018 to August 2018 under the guidance of

Prof.Dr.K.L.MALARVIZHI.,MD.,DGO.,DNB HOD &Professor

of Obstetrics and Gynaecology,Government Kilpauk Medical

College in partial fulfilment of requirement of MS degree in

Obstetrics and Gynaecology degree examination of The Tamilnadu

Dr. M.G.R Medical University to be held in May 2019.

Dr.P.VASANTHAMANI

MD.,DGO.,MNAMS.,DCPSY.,MBA

Dean

Government Kilpauk Medical College&

Hospital,

Chennai – 600 010

Dr.K.L.MALARVIZHI

MD.,DGO.,DNB

Prof & HOD,Dept. Of Obstertrics &

Gynaecology

Government Kilpauk Medical College&

Hospital,

Chennai – 600 010

DECLARATION

I Dr.SWETHA.S, Post graduate, Department of Obstetrics and

Gynaecology,Government Kilpauk Medical college, solemnly declare

that this dissertation entitled“Abruptio Placenta-an obstetric

endangerment” was done by me at Government Kilpauk Medical College

during 2016-2019 under the guidance and supervision of

Prof.Dr.K.L.MALARVIZHI.,MD.,DGO.,DNB,Professor&Head,

Department of Obstetrics and Gynaecology,Government Kilpauk

Medical College. This dissertation is submitted to the Tamil Nadu

Dr. M.G.R. Medical University towards the partial fulfilment of

requirements for the award of M.S. Degree in Obstetrics and

Gynaecology (Branch-II).

Place: Chennai-10

Date: Dr.SWETHA.S,

Postgraduate student

Dept. Of Obstetrics & Gynaecology

Govt. Kilpauk Medical College

Chennai-10

Prof.DR.K.L.MALARVIZHI,MD.,DGO.,DNB

Professor&HOD

Dept.of Obstetrics and Gynaecology

Guide

Govt.Kilpauk Medical College

Chennai-10

ACKNOWLEDGEMENT

I am thankful to our Dean , Dr.P.VASANTHAMANI, MD.,DGO.,MNAMS.,

DCPSY, MBA,Government Kilpauk Medical College, Chennai for allowing

me to conduct the study and use the facilities and clinical materials available

in the hospital.

It is my greatest pleasure to express my gratitude and thank

Prof.Dr.K.L.MALARVIZHI,MD.,D.G.O.,DNB,Professor&Head,

Department of Obstetrics and Gynaecology,Government Kilpauk Medical

College& Hospital for her valuable guidance, interest, encouragement and the

constructive ideas which she provided for this study.

I take this opportunity to express my deep sense of gratitude and humble

regards to my beloved teacher Prof.Dr.S.USHARANI,M.D.,DGO.,DNB for

being a constant source of inspiration and support.

I thank all my other Professors,Assistant Professors and paramedical Staffs of

this Department of Obstetrics and Gynaceology, Kilpauk Medical College,

Chennai-600010,without whom this would not have been possible.

I sincerely thank Dr.Padmanabhan,PhD, for his constant support during this

study and for his help in the statistical analysis of data and results.

I would like to thank all my fellow post graduates for helping me accomplish

this.

I sincerely thank all my patients for their cooperation .

Last, but not the least,I thank my family and God Almighty for the blessings

showered onto me.

CONTENTS

1. INTRODUCTION 1

2. AIMS OF STUDY 3

3. REVIEW OF LITERATURE 4

4. MATERIALS AND METHODS 38

5. RESULTS & DISCUSSION 40

6. SUMMARY 76

7. CONCLUSION 79

8. BIBLIOGRAPHY 80

9. ANNEXURES 82

Page | 1

INTRODUCTION

• Abruptio placentae is the premature separation of a normally implanted

placenta from the uterus, usually after 20 wk gestation.

• The Royal College of Obstetricians and Gynaecologists (RCOG)

defines antepartum haemorrhage (APH) as bleeding from or in to the

genital tract after 24+0 weeks till the birth of the baby, and recognizes

abruptio placenta (AP) as an important cause of APH.

• It can be an obstetric emergency as it can be a cause of maternal and

fetal mortality and morbidity.

• 50 patients admitted with clinical presentation of abruptio placenta –

vaginal bleeding, pain abdomen or uterine tenderness after 24 weeks of

gestation (gestational age from dating scan was considered ) were

included in the study and the diagnosis of abruptio placenta was

confirmed later on by placental examination.

• All the patients in the study population were clinically evaluated and

worked up immediately with ultrasonogram,complete hemogram,renal

function test,liver function test, serum electrolytes and coagulation

profile and followed up for 4 weeks.

• Maternal outcome like shock,post partum hemorrhage,acute renal

failure, need for mechanical ventilation,Disseminated Intra Vascular

Coagulation,etc will be recorded.

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• The fetal/neonatal outcome like intrauterine demise, birth weights, and

an Apgar score at 1 min and 5 min were recorded and compared.

• The abruption – delivery interval will be correlated with the maternal

and perinatal outcome.

• The data obtained from this study would help in improving maternal

and fetal morbidity and mortality by planning appropriate and timely

management of placental abruption.

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AIMS AND OBJECTIVES

AIMS :

To study the maternal and perinatal outcomes of abruptio placenta in the

Department of Obstetrics and Gynaecology ,KMCH and to see if early

intervention reduces the perinatal mortality and morbidity,thereby improving

the maternal-fetal outcome.

OBJECTIVES:

1)To assess the maternal outcome in the form of maternal mortality/ morbidity.

2)To assess the perinatal outcome in the form of APGAR,Birth

weight&perinatal mortality/morbidity.

3) To discuss future management options and see if early intervention has a

better maternal-fetal outcome.

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REVIEW OF LITERATURE

NORMAL PLACENTATION

• The placenta is a remarkable organ performing many diverse functions

including transport of gases and metabolites, immunological protection

and production of steroid and protein hormones.

• The zygote after repeated mitotic divisions gets converted in to a

blastocyst.The outer layer of the blastocyst is known as the trophoblast

and the inner cell mass is known as the embryoblast.

• The blastocyst after getting embedded into the endometrium, the

trophoblast rapidly proliferates and differentiates into an outer

syncitiotrophoblast and an inner cytotrophoblast.

• The primary, secondary and tertiary villi are formed by the

syncitiotrophoblasts and the intervillous space is formed by the

cytotrophoblasts.

• Until the end of sixteenth week the placenta grows in thickness and

circumference due to the growth of the chorionic villi and expansion of

the inter-villous space.

• After that there is little increase in thickness but it increases

circumferentially until term.

• The implanted placenta by nature separates during the third stage of

labor by a multiphasic process.

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Page | 6

DEFINITION OF ABRUPTIO PLACENTAE

• The Royal College of Obstetricians and Gynaecologists (RCOG)

defines antepartum haemorrhage (APH) as bleeding from or in to the

genital tract after 24+0 weeks till the birth of the baby.

• According to FOGSI , APH is bleeding occurring beyond 20 weeks of

gestation prior to the onset of labour.

CAUSES OF APH

OBSTETRIC CAUSES NON OBSTETRIC CAUSES

Placenta previa Cervical polyp

Abruptio placenta Cervicitis,Cervical ectropion

Vasa previa Cervical or vaginal malignancies

Excessive show Cervical or vaginal lacerations

Uterine rupture Coagulation defects

• Placenta previa and Abruption constitute about 50% of APH.

• Placental abruption is defined as complete or partial separation of

normally located placenta prior to delivery.

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• It can present anytime after the 20 week of gestation till term either as

an ante-partum or an intra-partum event.

• Abruptio placenta is known by several names such as accidental

haemorrhage, ablation placenta and premature separation of placenta.

• AP is classified into concealed and revealed types. In concealed type

the blood collects behind the placenta and there is no evidence of

vaginal bleed whereas in the revealed variety the blood tracks down

between the membranes and the uterine wall to present through the

vagina.

• The primary cause of Abruptio Placenta in majority of the cases

remains unknown but the RCOG recognizes hypertensive disorders of

pregnancy(previously called as pregnancy induced hypertension ),

advanced maternal age, multiparity, premature rupture of membranes

(PROM), smoking, polyhydramnios, abdominal trauma, fetal growth

restriction, intrauterine infections and past history of abruption as

predisposing risk factors.

HISTORICAL PERSPECTIVE OF ABRUPTIO PLACENTA

• In Latin, abruption placenta means “rending asunder of the placenta”

which means separation or splitting of the placenta.

• In 1609 Louis Bourgeois 1st identified the premature separation of

placenta.

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• The term accidental haemorrhage was 1st introduced by Rigby in the

year 1776. He was the one who differentiated between placenta previa

and placental abrution.Hence, he called abrutio placenta an accidental

hemorrhage.

• DeLee and Coole coined the term ABRUPTIO PLACENTAE in the

year 1848 to denote sudden separation of placenta from its normal

attachment site.

EPIDEMIOLOGY OF ABRUPTIO PLACENTA

• The incidence is up to 1.5% in overall pregnancies and 0.3% in

pregnancies at term.

• 14% abruptions occur before 32 weeks of gestation.

• Incidence of abruptio placenta in India varies anywhere between 1:50 to

1:500.This wide variation is because of various modes of presentation

and the inaccurate documentation. It may be a very asymptomatic case

where the diagnosis is retrospectively done by the presence of a retro-

placental clot after delivery (4.5%) or a classical case presenting with

sudden painful bout of bleeding or collapse of a pregnant woman

associated with either overt or covert bleeding along with fetal

compromise.

• The perinatal mortality rate is approximately 20-fold higher in

comparison to pregnancies without abruption (12 percent versus 0.6

percent, respectively) .

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• The majority of perinatal deaths (up to 77 percent) occur in utero;

deaths in the postnatal period are primarily related to preterm delivery.

• A very high index of clinical suspicion is required to diagnose a case of

placental abruption.

BASIC PATHOLOGY INVOLVED IN ABRUPTIO PLACENTA

• The very first event that is thought to occur is the formation of a retro-

placental clot.

• But the event that triggers this clot formation is a matter of question .

• It was postulated that there was an uterine spasm/contraction followed

by relaxation which lead on to venous engorgement that in turn

triggered the rupture of arterioles,which lead to bleeding into the

deciduas basalis.

• This blood can either get collected and form a clot behind the

placenta(concealed) or can dissect between the fetal membranes and

decidua,leading on to a vaginal bleeding(revealed).

• Or, it may disrupt the membranes and enter into the amniotic

cavity,which presents as a blood stained liquor or a port-wine colored

liquor.

• In more severe instances,it may extravasate into the myometrium,

reaches the serosa and may cause bleeding into the peritoneum –a

condition which is known as COUVEILAIRE UTERUS OR

UTEROPLACENTAL APOPLEXY.

Page | 10

• The bleed may be small and self-limited, or may continue to dissect

through the placental-decidual interface, leading to complete or near

complete placental separation.

• The detached portion of the placenta is unable to exchange gases and

nutrients; when the remaining fetoplacental unit is unable to

compensate for this loss of function, the fetus becomes compromised.

• From the diagnostic standpoint, abruption placenta is diagnosed by the

classical triad of : abdominal pain of sudden onset, vaginal bleeding and

a tense,tender uterus.

• It may just be asymptomatic in the early stages or may present with

deadly complications like maternal collapse or fetal distress or even an

intrauterine fetal demise.

RISK FACTORS FOR ABRUPTIO PLACENTA

1)MATERNAL AGE:

The incidence of abruption increases with maternal age.Maternal age >35 yrs

and < 18 yrs is a significant risk factor. In the FASTER TRIAL-First and

Second Trimester Evaluation of Risk trial, women who were older than 40

years of age were 2.3 times at an increased risk of developing abruption than

those who were 35 years or younger. In another study,there is an increased

incidence with maternal age and patients who are over 35 years are twice as

prone to develop abruption .

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The risk of abruptio placentae for women over the age of 35 years was 2.2

times the risk for women aged 19-34 years.

2)PARITY:

A study by Pritchard and colleagues (1991) reported that the incidence of

abruption is higher in women with increased parity.In another study, Toohey

and associates (1995) did not find this association.

But overall, majority of the studies report the incidence of abruption to be

higher in multiparous women.

3)HYPERTENSIVE DISORDERS OF PREGNANCY:

The most common condition associated with abruption seems to be some form

of hypertension (gestational hypertension, chronic hypertension,

preeclampsia).

Hypertensive disorders of pregnancy(mainly gestational hypertension and pre

eclampsia) is associated with 2.1-4% of the abruption cases whereas chronic

hypertension is associated with 1.8-3% of abruptions.(Sibai and coworkers in

1998).

Ananth and associates in2007 reported a 2.4fold increase in the incidence of

placental abruption with chronic hypertension and this incidence was further

increased if there was superimposed preeclampsia or IUGR.

Page | 12

4)NUTRITION AND ANEMIA:

Folic acid deficiency is one of the important factors in the etiology of

abruptio placentae. The possible mechanism between folic acid deficiency and

development of abruption is proved by bone marrow biopsy studies showing

megaloblastic erythropoiesis.

5)PREMATURE RUPTURE OF MEMBRANES:

There is an increased occurence of placental abruption in patients with

premature rupture of membranes,especially if duration was >24hours. The

incidence was 13% when premature rupture of membranes occured between

gestational age 29-32 weeks.

Histological chorioamnionitis is associated with increased incidence of

placental abruption and this association is dependent on its severity of

chorioamnionitis.

6)SMOKING AND COCAINE ABUSE:

Smoking tends to increase the overall risk of abruption placentae. According to

the results of a prospective cohort study the increase in incidence is by 40% for

each year of smoking prior to pregnancy.

Page | 13

The rate of abruption has been reported to be about 13-35% in patients who

use cocaine and the effect seems to be dose dependent.

7)BLUNT ABDOMINAL TRAUMA:

The incidence of abruption in blunt abdominal trauma is somewhere between

1.5-9.4%.Blunt abdominal trauma or rapid decompression of uterus may result

in shearing of placenta due to the sudden stretching or contraction of the

uterine wall. Maternal trauma has been associated with a six fold increase in

the risk of abruption.

8)EXTERNAL CEPHALIC VERSION:

External cephalic version is not a very popular common practice

nowadays,especially in India ,but however,abruption is a well known

Page | 14

complication of ECV, especially when the version was performed under

anaesthesia.

The incidence of abruption is said to be 2 to 9 % according to one study

9)THROMBOPHILIAS:

The association between placental abruption and the maternal thrombophilias

supports the fact that abruption is a final acute clinical presentation of a

chronic placental disease.

10)MULTIPLE PREGNANCY

The risk of placental abruption is increased 2-3 times in multi fetal gestations

and in such patients , subsequently the risk of preterm delivery tends to be on

the higher side and there by adding to the perinatal mortality and morbidity.

In multiple pregnancies there can be a sudden decompression and abruption

after delivery of the first baby.

11)PLACENTA PREVIA:

About 10% women with placenta previa may have placenta previa

concurrently. The bleeding from the placenta previa may collect behind the

placenta and may trigger further separation of the placenta,causing abruption.

12)ABRUPTIO PLACENTA IN PREVIOUS PREGNANCY

Recuurence of severe abruption was noted in about 1 in 8 cases by a study by

Pritchard and co workers.

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13)INVASIVE PROCEDURES:

Invasive procedures like amniocentesis can cause bleeding from the puncture

site which may collect behind the placenta and trigger abruption.

14)OTHERS:

• First trimester ultrasound examination showing a subchorionic or

retroplacental haematoma increases the subsequent risk of placental

abruption by 6-7 fold.

• Uterine tachysystole (> 5 contractions in a 10 minute period) can cause

abruption.

• Unexplained elevation of plasma alpha feto protein is associated with a

5% increase in the incidence of abruption.

• When the membranes rupture as in the case of polyhydramnios there is

sudden decompression of the uterus which leads to the reduction in

uterine volume and a corresponding loss of surface area and as a result

the placenta sheers off.

• Uterine malformations may lead to poor decidualisation and

placentation. The contractility of a malformed uterus may lead to

uncoordinated uterine action resulting in increased risk of placental

Abruption.

Page | 16

RECURRENCE OF ABRUPTION IN SUBSEQUENT PREGNANCIES.

• An antenatal woman with a history of abruptio placentae in previous

pregnancy should be monitored with caution.

• The incidence of recurrent abruption was quite high ,approximately a

20-fold to 30-fold increased chances of abruption in subsequent

pregnancies when the previous pregnancy was complicated by placental

abruption.

PATHOLOGY IN ABRUPTIO PLACENTA

GROSS

• The hallmark of clinical diagnosis of placental abruption is the

presence of retroplacental clots or any adherent clots or hematoma or

hemorrhage of variable size into the placenta or membranes with or

without depression or disruption of the maternal surface of the placenta

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• The retroplacental clots are usually dark, firm, and adherent when

compared to the red, soft, non adherent clots formed during physiologic

placental separation which occurs in the third stage of labor.

MICROSCOPIC

• Upon microscopic examination of the placenta & the uterus in cases

where it has been removed, there were variable structural changes in the

decidua basalis, muscularis of the uterus, chorionic plate; and the

intervillous architecture.

• In low risk pregnancy, the spiral arteries of the uterus will undergo a

transformation from the high resistance muscular arterioles to low-

resistance capacitance vessels.

• Such changes occur due to trophoblastic invasion which occurs in 2

spells, the first (10–16 weeks) and second (16–20 weeks) trimesters.

• In patients with placental abruption, however,the microscopic

pathological changes in the placental bed show a high incidence of

vascular abnormalities with the most common finding (60%) being the

absence of any evidence of the physiologic transformation of

uteroplacental arteries.

• This leads to a decrease in the utero-placental blood flow and

dysfunctional endothelial responses to vasoactive substances.

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• These abnormal placental vessels are prone to ischemia and rupture of

involved vessels, there by causing placental abruption.

• Evidence of vasculopathy may be seen in the placental vessels- such as

atherosis, narrowing of vessels, necrosis, and thrombosis.

• Vessels deep in the myometrium may show changes like vessel

occlusion with surrounding myometrial hemorrhage, which are seen in

about 33% of the cases.

• Decidual hematomas, thrombosis of the vessels, and focal necrosis are

common, together with recent infarcts and these changes may be

extensive enough to involve large areas of the chorionic plate.

• Congestion of the capillaries in the chorionic villi is often present.

Placental abruption usually develops simultaneously with placental

infarction, which is also a major risk factor for fetal or neonatal death.

• Placental infarcts are predominantly caused by spiral artery occlusion in

the myometrium or decidua.

• Organized or old infarcts and hemosiderin granules in the decidua and

chorion are seen in patients with chronic abruption.

Page | 19

Extensive hemorrhage at the top of the image, at the decidual plate, with

placental villi below.(microscopic image of abruption placenta)

TYPES OF ABRUPTIO PLACENTA:

There are two major types of placental abruption:

1) The concealed variety: where the blood gets accumulated behind the

placenta and is not evident outside- may be partial or complete.

2) The revealed variety: where the blood tracks between membranes and

escapes through the vagina as bleeding.

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CLASSIFICATION OF ABRUPTIO PLACENTA:

PAGE CLASSIFICATION:

CLASS MATERNAL FETAL

0 asymptomatic,discovered retrospectively

after delivery

usually none

1 Mild/no vaginal bleeding

Uterine tenderness

Maternal vitals are stable

Usually none

2 Moderate vaginal bleeding

Moderate to severe uterine contractions,

titanic contractions

Maternal tachycardia

Fetal distress

Fetal bradycardia

3 Severe vaginal bleeding

Tetanic uterine contractions

Maternal shock

Coagulopathy

Intra uterine fetal death

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SHER & STUDLAND(1985) CLASSIFICATION

CLASS 1- clinically not recognized until delivery.

CLASS 2- the classical signs of abruption is present but the fetus is still alive

CLASS 3- Severe-the fetus is dead

A) Without coagulopathy

B) With coagulopathy

DIAGNOSIS

• Abruptio placenta most commonly present with the classical triad of

abdominal pain, abnormal uterine tenderness and vaginal bleeding

after 20 weeks of gestation.

• However, pain abdomen may be present in only upto 50% of cases

and it is most probably caused due to the hypertonic contractions or

extravasation of blood into the myometrium and it is said that

abruption placenta of a posteriorly situated placenta does not usually

present with pain.

• The classical clinical hallmark of abruption placenta is bleeding per

vaginum ,which may be present in about 80% to 90% of cases.

• The abruption may be concealed in the remaining 10% to 20% of

the cases.

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• One study involving 198 women with a diagnosis of placental

abruption determined that the most common manifestations in their

frequency of occurrence were:

Bleeding per vaginum (70%)

Abdominal pain (50%)

Blood stained amniotic fluid (50%)

Fetal heart rate abnormalities (69%).

• It is also important to note that in 19% of cases, there was neither

bleeding nor pain . Hence,it is important to keep in mind that these

signs and symptoms are not always present and the absence of such

symptoms cannot exclude the diagnosis of an abruption.

• The presentation of the various above mentioned symptoms and their

severity is directly related to the magnitude of placental separation.

• The 1st symptom may be a sudden onset, sharp and severe pain that

either persists or becomes a poorly localized,dull aching pain in the

lower abdomen and/or sacral areas.

• The uterus usually does not relax completely in between

contractions,otherwise called as a tense uterus.

• The occurrence of high-frequency low-amplitude contractions and an

increased baseline uterine tone often is seen in those with placental

abruption.

• It should be remembered that abruptio placentae can also present as

preterm pains/preterm labor. And that appears to be idiopathic. About

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10% of the idiopathic preterm labor cases may be caused by concealed

abruptio placentae and about 60% of the placental abruption cases is

associated with preterm labor.

DIFFERENTIAL DIAGNOSIS OF CONCEALED/MIXED ABRUPTION

Preterm labor

Torsion ovarian cyst

Red degeneration of fibroid

Rupture uterus

Acute hydramnios

FINDINGS THAT FAVOR DIAGNOSIS OF ABRUPTION:

1. level of shock that is out of proportion to the amount of external bleeding.

2. Unexplained anemia and a tense uterus.

3. Association with severe pre eclampsia.

4. uterus might be tense and tender .

5. absent fetal heart rate

6. reduced urine output/oliguria

7. associated with coagulopathy.

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IMAGING IN ABRUPTIO PLACENTA

Historically,ultrasonogram has been a little less helpful in the diagnosis of

placental abruption, with the classical sonographic evidence being rarely seen

or has been difficult to identify.

As a result, the role of sonographic diagnosis in abruptio placentae classically

has been used as a diagnosis of exclusion when the ultrasound has failed to

show the presence of a placenta previa and after ruling out other causes of

vaginal bleeding .

The detection rate of abruptio placenta in ultrasound is somewhere between

5% to 50%.

Only a few patients with the clinical evidence of placental separation have

displayed the classic ultrasound abnormalities of a retroplacental hypoechoic

area or the dissection of blood between the fetal membranes when there is

fresh blood collected in the retroplacental area.

Once an haematoma appears,it is hyperechoic to isoechoic when compared to

the normal placenta and resolution the haematoma again becomes hypoechoic

within 1 week and sonoluscent within 2 weeks.

In recent times,because of the advances in ultrasound resolution, imaging, and

interpretation, there is an improvement in the diagnostic accuracy of targeted

sonography in detecting abruptio placentae in patients who present with

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vaginal bleeding. The ultrasound examination is aimed for the following 7

sonographic features which points towards abruption:

1. Preplacental collection.,under the chorionic plate (between placenta

and amniotic fluid) (Fig.1)

Fig.1. pre placental collection P-placenta, C- collection

2. JELLO sign.: The placenta will show a jello like movement or jiggle

when sudden pressure is applied with the transducer probe

3. Retro placental collection (between the placenta and the myometrium)

(Fig. 2)

fig 2 retroplacental collection P-placenta, R- retroplacental collection

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4. Marginal collection (at the placental margin) (Fig. 3)

(fig 3) Sonographic blood collection at the placental margin (arrow). P,

placenta.

5. Subchorionic membranous collection (between the membranes and the

uterine wall) (Fig. 4)

(fig 4) subchorionic membranous collection between the placental

membranes and the uterine wall on ultrasound. S, subchorionic

collection; F, fetus; P, placenta.

Page | 27

6. Increased placental thickness or echogenicities (defined as thickness

greater than 4 cm perpendicular to the plane of the placenta (Fig.5)

(Fig 5)showing a thickened placenta with heterogenic foci,later

macroscopically confirmed to be an abruption.

7. Intra-amniotic hematoma or collection within the amniotic fluid) (Fig.

6).

Fig 6- inta amniotic hematoma(IA) ; F- fetus.

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CARDIOTOCOGRAPHY IN ABRUPTIO PLACENTA

According to RCOG, there was some sort of a CTG abnormality in

about 69% of the cases of placental abruption.

Hence, continuous electronic fetal heart rate monitoring and the uterine

activity may help the obstetrician in the assessment of the severity of

placental abruption. Even if the uterine contractions are irregular, their

amplitude and frequency usually exceeds that of a normal labor

contraction, and the baseline tone of the uterus is often increased.

Fetal heart rate monitoring might display various FHR abnormalities,

including fetal tachycardia, loss of baseline variability, sinusoidal

pattern , pseudosinusoidal pattern or late decelerations.

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PREDICTORS OF ABRUPTIO PLACENTA

BIOCHEMICAL MARKERS:

MSAFP- Second trimester elevation of MSAFP may be a biochemcial

marker that is related to certain adverse obstetric outcome including

placental abruption. There is chronic villitis and vascular thromboses or

infarction which is thought to cause this elevation.AFP levels

>2.0MoM was found in 17% of pregnancies with placental abruption.

But however, MSAFP is not routinely used for this purpose in practise.

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Beta HCG Increased levels of maternal serum beta hcg has been linked

to an increased chance of developing placental abruption.

PAPP-A Low levels of PAPP-A in the first trimester has been linked

with placental abruption .

Proangiogenic placental growth factor (PIGF) and antiangiogenic

soluble - fms like tyrosine kinase-1(sflt-1) are angiogenic regulators in

pregnancy. Increased ratio of sflt1/PIG F at 21-32 weeks of gestation

puts a woman at risk of placental abrubtion ,in those who have

developed preeclampsia or gestational hytpertension.

Fibronectin produced by the endothelial cell is increased in cases of

placental abruption .

Thrombomodulin ,a marker of endothelial cell damage may be elevated

in placental abruption .

Uterine artery flow measurement:

Increased uterine artery pulsatility index at 11-14 weeks or notching of

the uterine artery waveform at 20-24 weeks also may predict

subsequent placental abruption.

But none of these are accepted as standard methods to diagnose

abruption.

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COMPLICATIONS OF ABRUPTIO PLACENTA

The principal maternal complications associated with abruption placenta are:

• Hemorrhagic shock resulting from acute blood loss which causes a

contraction of the intravascular compartment

• generalized coagulopathy due to active consumption of clotting factors

within the vascular tree and consequent secondary fibrinolysis

• ischemic necrosis of distant organs. The organs most frequently

involved are the kidneys and the anterior pituitary gland.

• Acute renal failure is a serious complication and may lead to maternal

death

• preterm PROM resulting from decidual hemorrhage.

HEMORRHAGIC SHOCK

• Hemorrhagic shock is caused by an absolute reduction in peripheral

circulating blood volume along with subsequent tissue hypo perfusion.

The shock that occurs in patients with abruptio placentae is usually out

of proportion to the observed blood loss.

• The end point of persistent hypotension is asphyxia of both the fetus

and mother; therefore, the immediate treatment is replacement of the

intravascular volume deficit as rapidly as possible and restoring

effective perfusion.

Page | 32

• Crystalloids should be infused until cross matched blood is available.

Crystalloid therapy initially should involve volumes two- to three-times

in excess of the actual hemorrhage, because shock often is associated

with major fluid shifts from the intravascular to the extravascular

compartments.

COAGULOPATHY

• The inciting event leading to DIC with placental abruption is thought to

be entry of thromboplastins from the placental injury site into the

circulation. The thromboplastins cause widespread intravascular

activation of the clotting cascade. There is widespread activation of the

coagulation system within the vascular compartment which produces a

consequent depletion of various clotting factors and a resultant

hemorrhagic state.

• The extensive conversion of fibrinogen to fibrin results in a decrease in

the concentration of fibrinogen.

• Secondary fibrinolysis leads to the formation of fibrin degradation

products (FDP), which, by their anticoagulant effect, further

compromise the hemostatic system.

• Levels of prothrombin, factor V, factor VIII, and platelets also are

decreased.

• DIC is seen in 10% of cases of abruption and is seen mostly in severe

cases of abruption associated with fetal death or massive hemorrhage.

Page | 33

• Steps for immediate delivery of the fetus should be taken that would

help to improve the haemostatic competence

ISCHEMIC NECROSIS OF DISTANT ORGANS

• Ischemic damage to the kidneys is a well known complication of severe

abruptio placentae and takes the form of acute tubular necrosis, bilateral

cortical necrosis, or both.

• The pathological changes are explained on the basis of inadequate

blood supply and hypoxia from hemorrhagic hypovolemia (or)an

obstruction secondary to focal fibrin deposits in the precapillary

arterioles due to DIVC.

• Acute tubular necrosis, the most common cause of anuria in

obstetrics,is generally due to hemorrhagic shock with resultant anoxic

insult to the tubular structures of the renal medulla.

• When extreme oliguria or anuria develops,it is impossible to initially

distinguish between acute tubular necrosis and acute cortical necrosis.

• Acute renal failure with lower nephron damage usually occurs later in

the abruption process and is reversible after a period of time. In

contrast, the pattern of acute cortical necrosis shows involvement early

in the abruption process; if the condition is untreated by dialysis, the

clinical course progresses to death from uremia in 7 to 12 days.

Page | 34

• The key to prevention of renal ischemic damage is vigorous blood and

fluid therapy to combat hypovolemic shock.

PERINATAL COMPLICATIONS

• The perinatal morbidity and mortality rate associated with abruption is

as high as 20% to 40% and accounts for 15% of all perinatal deaths.

The three major causes of perinatal death are fetal anoxia,

exsanguination (because, in rare cases, rupture of fetal placental vessels

can occur), and prematurity.

• The likelihood of a normal neonatal outcome decreases with the

severity of abruption. Poor outcome may be caused by the fact that

perinatal hypoxic–ischemic injury starts in utero, caused by an

interruption in placental blood flow and gas exchange.

MANAGEMENT

GENERAL MANAGEMENT:A proper history and quick cinical

assessment should be done in women presenting with antepartum

haemorrhage and decided whether urgent intervention is required to

manage maternal or fetal compromise. In those women presenting with

massive haemorrhage,iv lifelines should be secured, blood drawn for

crossmatching and resuscitation should be started immediately since

mother is the priority and should be stabilised first. Meanwhile blood

should be collected for investigations to identify complications.

Page | 35

The investigations include:

Blood Hb%

Platelet count

Leucocyte count

Peripheral blood smear

Blood for grouping and typing

Bleeding and clotting time

Clot observation and retraction time

Prothrombin time

Activated partial thromboplastin time

Serum fibrinogen level

Fibrin degradation product levels

D-dimer levels

Liver function tests

Renal function tests

Serum electrolytes

Page | 36

OBSTETRIC MANAGEMENT:

The clinical presentation of placental abruption being variable, the obstetric

management is individualised on individual basis.The presentation,

gestaional age and the degree of maternal and fetal compromise will direct

the management.

In cases of abruption at or near term with a live fetus, prompt delivery is

indicated. If there is fetal compromise, and delivery is not

imminent,Caesarean section should be performed. When the maternal and

fetal conditions are reassuring vaginal delivery may be reasonable.

In patients with severe placental abruption resulting in intrauterine fetal

death, if the mother is stable, it is reasonable to allow for a vaginal delivery

in the absence of any obstetric indications.

Labour usually progresses rapidly because of viguorous uterine

contractions and an amniotomy and oxytocin augmentation may speed up

delivery. The main purose of doing an amniotomy is to hasten the onset of

labour and by encouraging uterine contractions, to reduce uterine bleeding.

Anytime, when the fetal heart rate deteriorates, or the maternal condition

becomes worse or when labor does not progress rapidly or in case of

obstetrical indications like cephalopelvic disproportion, a scarred uterus or

a fetal malpresentation,a caesarean delivery may be performed to avoid

worsening of coagulopathy. But stabilisation of the patient and correction

Page | 37

of any coagulation defects is very much essential during surgery. The

patient should be closely monitored paying attention to vital signs, amount

of blood loss, urine output.

PREVENTION OF ABRUPTIO PLACENTA

• Early diagnoses and appropriate treatment of hypertensive disorders

of pregnancy.

• Avoidance of sudden rupture of membranes.

• Avoidance of trauma especially forceful external cephalic version

• Regular intake of folic acid in early pregnancy

Page | 38

MATERIALS AND METHOD:

TYPE OF STUDY : LONGITUDINAL STUDY(OBSERVATIONAL)

PERIOD OF STUDY : JAN 2018 - AUGUST 2018

PLACE OF STUDY : Dept. Of Obstetrics and Gynaecology

Govt. Kilpauk Medical College,Chennai.

METHODOLOGY:

• Patients admitted with clinical presentation of abruptio placenta –

vaginal bleeding, pain abdomen or uterine tenderness after 24 weeks of

gestation (gestational age from dating scan was considered ) were

included in the study as cases.

The diagnosis of abruption placenta was confirmed later on by placental

examination.

• All the patients in the study population were clinically evaluated and

worked up immediately with ultrasonogram,complete hemogram,renal

function test,liver function test, serum electrolytes and coagulation

profile and were followed for about 4 weeks

• A questionnaire which included the demographic profile and risk

factors of the mothers was used to collect data. This included details

like maternal age, obstetric score,AN visits,and the gestational period at

which abruption occurred ,etc. Details of associated medical problems

(preeclampsia, gestational diabetes mellitus (GDM), hypothyroidism

and infertility) and obstetrical risk factors (previous caesarean, multiple

Page | 39

pregnancies,anemia,polyhydramnios,growth restriction, history of

threatened abortion, previous preeclampsia and PROM) were noted.

• Intra-partum findings were recorded.

• Maternal outcome like shock,post partum hemorrhage,acute renal

failure, need for mechanical ventilation,Disseminated Intra Vascular

Coagulation,etc were recorded.

• The fetal/neonatal outcome like intrauterine demise, birth weights, and

an Apgar score at 1 min and 5 min were recorded and compared.

• The grade of abruption and type of abruption was compared with the

maternal and perinatal outcome.

Page | 40

RESULTS & DISCUSSION

AGE DISTRIBUTION

Of the 51 patients included in the study, the youngest age at which abruption

occurred was 18 years and the oldest age was 33 years.The average age of the

study group was 24.5 years.

AGE GROUP NO. OF PATIENTS PERCENTAGE

30 3 5.8%

It was also noted that in both extremes of age, the severity of abruption was

high.

16%

41%

37%

6%

Age distribution

< 20 yrs 20-25 yrs 26-30 yrs >30 yrs

Page | 41

ABRUPTION AND GESTATIONAL AGE

The average gestational age of occurrence of abruption was 34 weeks,with

least GA being 25 weeks of gestation.

The distribution of abruption based on gestational age is as follows:

GESTATIONAL AGE CASES % OF CASES

24-34 weeks 26 50.98

35-36 weeks 17 33.33

>37 weeks 8 15.68%

50.98

33.33

15.68

gestational age

24-34 weeks

35-36 weeks

>37 weeks

Page | 42

DISTRIBUTION OF CASES BASED ON BOOKING STATUS

Among the 51 participants in the study,96.1%(49) were booked and 3.9% (2)

were unbooked. It was noticed that the unbooked patients invariably presented

with grade 3 abrution when compared to the booked patients(Grade 1- 7.8%,

grade 2- 39.2% and grade 3- 49%).

96.1

3.9

BOOKING

BOOKED

UNBOOKED

Page | 43

Among the booked patients,18(36.7%) had concealed abruptions and

31(63.3%) had revealed abruption.and among those who were unbooked, 50%

had concealed and 50% had revealed abruption.

Page | 44

DISTRIBUTION BASED ON PARITY

PARITY NUMBER OF CASES PERCENTAGE

PRIMI 23 45.1%

MULTI 28 54.9%

Of the multigravidas, 7 (13.7%) were 3rd gravida and above and all of them

presented with grade 3 abruption. Multiparity is hence a risk factor for the

development of abruption. Of all the multigravidas(3 or more), 71.4% of them

presented with revealed abruption and the remaining 28.6% presented with

concealed abruption.

45%

55%

PARITY

PRIMI MULTI

0

100

multiparity

PARITY AND ABRUPTION

revealed abruption concealed abruption

Page | 45

DISTRIBUTION BASED ON THE GRADE AND TYPE OF

ABRUPTON

GRADE(SHER

CLASSIFICATION)

NO. OF CASES % OF CASES

1 4 7.84%

2 20 39.21%

3 27 52.94%

DISTRIBUTION BASED ON TYPE OF ABRUPTION

TYPE OF

ABRUPTION

NO. OF PATIENTS % OF PATIENTS

COCNEALED 19 37.3%

REVEALED 32 62.7%

8%

39%53%

GRADES OF ABRUPTION

GRADE 1 GRADE 2 GRADE 3

37%

63%

TYPE OF ABRUPTIONCONCEALED REVEALED

Page | 46

DISTRIBUTION BASED ON RISK FACTORS

RISK FACTORS NO. OF CASES % OF CASES

PRE ECLAMPSIA 31 60.78

ANEMIA 26 50.98

MULTIPARITY 7 13.72

POLYHYDRAMNIOS 12 23.50

PLACENTA PREVIA 2 3.92

GDM 4 7.84

TWINS 2 3.92

Thus,in our study 60.78% of the patients had pre eclampsia,and 50.98 %

patients had anemia which were considered as the two leading risk factors for

the development of abruption.

Page | 47

ANEMIA AND ABRUPTION DISTRIBUTION

Among all the abruption cases under study, 25 patients (49%) did not have

anemia and 26 patients(51%) had anemia complicating pregnancies.Among all

these cases,4 cases(7.8%) had grade 1 abruption, 20 (39.2%) had grade 2

abruption and 27(60%) had grade 3 abruption.Among those with grade 3

abruption,9(33.3%) were not anemic whereas 18( 66.7%) were anemic.Hence

anemia is a risk factor for severe grades of abruption.

It was also notes that in those patients without anemia,11(21.6%) had

concealed abruption and 14( 27.5%) had revealed abruption, but in those

complicated with anemia,8(15.7%) presented with concealed abruption and

18( 35.3%) presented with revealed abruption.

Page | 48

PRE ECLAMPSIA AND ABRUPTION DISTRIBUTION

Among all the abruption cases,20(39.2%) did not have pre eclampsia, whereas

31(60.8%) cases were complicated by pre eclampsia.In patients with grade 1

abruption, 50 % had pre eclampsia and 50% did not have. In grade 2

abruption,35% did not have and 65% had pre eclampsia and in those with

grade 3 abruption,40.7% did not have pre eclampsia whereas 59.3% had pre

eclampsia. This shows that pre eclampsia is an important risk factor for

development of more severe grades of abruption.

Also 23.5% of cases with concealed abruption and 37.3% of cases with

revealed abruption had pre eclampsia ,whereas only 13.7% of cases with

concealed abruption and 25.5% of cases with revealed abruption did not have

pre eclampsia.

Page | 49

POLYHYRAMNIOS AND ABRUPTION PATTERN

Among all the abruption cases,39(76.5%)did not have polyhydramnios and

only 12 (23.5%) had polyhydramnios.Among those with grade 1 abruption,

only 25% had polyhydramnios. In those with grade 2 abruption, only 35% had

polyhydramnios and among those with grade 3 abruption,only 14.8% had

polyhydramnios.Hence polyhydramnios alone is not a single independent risk

factor for predicting the severity of abruption.

In our study, only 26.3% of those with concealed abruption and 21.9% of those

with revealed abruption. Hence polyhydramnios did not influence the type of

abruption.

Page | 50

PLACENTA PREVIA AND ABRUPTION PATTERN

In our study,49(96.1%) of the patients did not have placenta previa and

2(3.9%) patients had placenta previa and those who had placenta previa

presented with grade 2 or grade 3 abruptions.Among those cases who had

placenta previa, the abruption was revealed in both the cases.

Hence abruption cases complicated by placenta previa usually tend to present

as revealed abruption.

0

20

40

60

80

100

120

abruption

no previa

placenta previa

0

20

40

60

80

100

120

no placentaprevia

placenta previa

revealed

concealed

Page | 51

GDM AND ABRUPTION

Among all the abruption cases,47(92.2%) cases did not have GDM and

4(7.8%) of the cases had GDM.of those patients with grade 1

abruption,nobody had GDM, in grade 2 abruption,2(10%) had GDM and in

grade 3 abruption, 2(7.8%) had GDM.Hence GDM is not an independent risk

factor for determining the severity of abruption.

In our study, among those with GDM, 50% showed revealed abruption and

50% showed concealed abruption,whereas in normal population incidence

revealed abruption was high.

Page | 52

TWIN PREGNANCY AND ABRUPTION PATTERN

In our study,49(96.1)patients had only a singleton pregnancy whereas 2(3.9)

patients had a twin pregnancy.Both the patients presented with grade 2

abruption and both the patients presented as a revealed abruption.

Page | 53

DISTRIBUTION BASED ON PRESENTING SYMPTOMS

PRESENTING

SYMPTOMS/SIGNS

NO. OF CASES % OF CASES

PAIN ABDOMEN

42 82.35%

BLEEDING P/V

32 62.74%

TENSE/TENDER UTERUS 17 33.33%

DECREASED FETAL

MOVEMENTS

5 9.8%

ASYMPTOMATIC

3 5.8%

The leading presenting complaints in cases of abruption placenta was found to

be pain abdomen in 82.35% of cases followed by bleeding p/v in 62.74% of

cases.Tense/ tender uterus was found only in 33.33% of cases and about 5.8 %

of the cases were found to be totally asymptomatic.

Page | 54

PRESENTING SYMPTOMS AND SEVERITY OF ABRUPTION

In our study, 96.3% of cases with grade 3 abruption; 80% of cases with grade

2 abruption and 0% of those with grade 1 abruption presented with pain

abdomen.

In this study,59.3% of cases with grade 3 abruption,80% of cases with grade 2

abruption presented with complaints of bleeding per vaginum.

In this study 35% of cases with grade 2 abruption and 37% of cases with grade

3 abruption presented with a tense/tender uterus.

Page | 55

LEVEL OF SHOCK AND SEVERITY OF ABRUPTION

In our study,of those who presented with level 1 shock, 4(11.1% ) cases had

grade 1 abruption 17(47.2%) cases had grade 2 abruption and15( 41.7% ) cases

had grade 3 abruption.

Among those cases who presented with level 2 shock,3(21.4%) cases had 2

abruption,11( 78.6%) cases had grade 3 abruption.

Among those cases who presented with level 3 shock, 100% of the cases had

grade 3 abruption.

Among those who presented with level 1 shock,47.2% cases presented with

concealed abruption and 52.8% cases presented with revealed abruption. Of

those who presented with 2 shock,14.3% cases had concealed and 85.7% cases

had revealed abruption and 100% of the cases with level 3 shock had revealed

abruption.

Page | 56

DISTRIBUTION OF CASES BY MODE OF DELIVERY

Among all the 51 cases of abruption,37(72.5%) cases underwent cesarean

section,13(25.5%) cases had a normal vaginal delivery and1(2%) case had an

instrumental delivery.

In this study,among those who delivered by labor natural, 7.7% had grade 1

abruption, 7.7% had grade 2 abruption and 84.6% had grade 3 abruption.

Among those who delivered by LSCS, 8.2% cases had grade 1 abruption,

48.6% cases had grade 2 abruption and 43.2% of cases had grade 3 abruption.

Instrumental delivery was done only for 1 case,which was a grade 2 abruption.

72%

26%2%

MODE OF DELIVERY

LSCS NORMAL DELIVERY INSTRUMENTAL DELIVERY

Page | 57

DISTRIBUTION BY COMPLICATIONS

COMPLICATION NO. OF CASES % OF CASES

PPH 10 19.6%

Acute Kidney Injury(AKI) 24 47.05%

NEED FOR DIALYSIS 11 21.56%

MASSIVE BLOOD

TRANSFUSION(>/= 4)

12 23.52%

DIVC 9 17.64%

HELLP 13 25.49%

PULMONARY EDEMA 1 1.96%

VENTILATORY

SUPPORT

3 5.88%

COUVEILAIRE UTERUS 15 29.41%

The average duration of hospital stay was 19.71 days( 9.25 days in grade 1

abruption;18.1 days for grade 2 and 22.44 days for grade 3 abruptions.

There were no maternal deaths due to abruption placenta or its complications

in this study.

Page | 58

GRADES OF ABRUPTION AND POST PARTUM HEMORRHAGE

In our study, of the10 cases(19.6%) which were complicated by PPH, 30% of

the patients had grade 2 abruption and 70 % of the cases had grade 3

abruption.

And among those cases who were complicated by PPH, 50% was a revealed

abruption and 50 % was concealed.

Page | 59

GRADES OF ABRUPTION AND ACUTE KIDNEY INJURY

In our study, of the 24 cases(47.05%) that were complicated by AKI, 25% had

grade 2 abruption and 75% had grade 3 abruption.

Among the cases complicated by AKI,41.7% cases had concealed and 58.3%

cases had revealed abruption.

Page | 60

GRADE OF ABRUPTION AND NEED FOR DIALYSIS

Among all the cases of abruption,11 cases(21.56%) had AKI which required

dialysis, among which,all 11 cases(100%) was due to grade 3 abruption.

Of all these cases,36.4% was concealed and 63.6% was revealed abruption.

Page | 61

ABRUPTION AND MASSIVE BLOOD TRANSFUSION

Of all the cases complicated by abruption, 12 cases (23.52%) required massive

blood transfusion of 4 or more blood units of which all 12(100%) was due to

grade 3 abruption.

And among these cases, 50% had concealed abruption and 50% had revealed

abruption.

Page | 62

GRADES OF ABRUPTION AND DIVC

Among all the cases of abruption, 9 cases(17.64%) had DIVC,of which 11.1%

was due to grade 1 abruption and 88.9% was due to grade 3 abruption; and

11.1% had concealed and 88.9% had revealed abruption.

Page | 63

GRADES OF ABRUPTION AND HELLP SYNDROME

Among all the cases of abruption under study,13cases(25.49%) was

complicated by HELLP syndrome , of which,23.1% was due to grade 2

abruption and 76.9% was grade 3 abruption.Also,38.5% of the cases had

concealed abruption and 61.5% of the cases had revealed abruption.

Page | 64

ABRUPTION AND PULMONARY EDEMA;NEED FOR

VENTILATORY SUPPORT

In our study, of all the cases of abruption,1 case(1.96%) went in for pulmonary

edema and 3 cases(5.88%) needed ventilator support.

Among the cases that required ventilator support, 33.3% had grade 2 abruption

and the remaining 66.7% had grade 3 abruption.

Page | 65

ABRUPTION AND COUVELAIRE UTERUS

Among all the cases of abruption, 15 cases (29.41%)had couvelaire uterus, of

which 6.7% cases had grade 1 abruption ;13.3% cases had grade 2 and 80% of

the cases had grade 3 abruption.

Also, 40% of the cases of couvelaire uterus occurred in concealed abruptions.

Page | 66

In our study,among the 51 patients, a total of 15 cases(29.41%) had couvelaire

uterus,which was detected during a caesarean section. The average amount of

retro placental clots found in these cases was 390 gram. Among these cases

with a couvelaire uterus,the rates of complications are as follows.

About 3 patients(20%) went in for post partum hemorrhage(PPH);10

cases(66.66%) went in for acute kidney injury;6 cases(40%) required

hemodialysis;9 cases(60%) required a blood transfusion of 4 or more units;6

cases(40%) were complicated by DIVC and 3 cases (20%) went in for HELLP

syndrome. This shows that in patients with couvelaire uterus,the complication

rates are quite high,especially post partum hemorrhage and acute kidney

injury.

Among those patients who required hemodialysis;1 case(16.66%) required

only 1 cycle; 2 cases (33.33%) required 2 cycles and 3 cases(50%) required 3

or more cycles or hemodialysis.

0

2

4

6

8

10

12

PPH AKI DIALYSIS MASSIVETRANSFUSION

DIVC HELLP

Page | 67

ABRUPTION- DELIVERY INTERVAL

The average abruption – delivery interval in our study was 3.32 hours, which

was around 2.4 hours in grade 2 abruption and 4 hours in grade 3 abruption.

RETROPLACENTAL CLOTS AND ABRUPTION

In our study, among all the cases of abruption,the average amount of

retroplacental clots was 269.6 grams.

In grade 1 abruption, average retroplacental clots was 50g

In grade 2 abruption, average retroplacental clots was 162.5g

In grade 3 abruption,average retroplacental clots was 381.4g

17%

33%

50%

HEMODIALYSIS

1 CYCLE 2 CYCLES 3 OR MORE CYCLES

Page | 68

In our study, majority of the patients(49.01%) had 100-299 gram of retro

placental clots,27.45% of cases had 300-499 gram retro placental

clots,15.68% cases had retroplacental clots 500 gram or more and only 7.84%

cases had retroplacental clots

Page | 69

DISTRIBUTION OF COMPLICATION BASED ON RETRO

PLACENTAL CLOTS

In our study, among the 10 patients who had post partum hemorrhage, 40 %

had 100-299 gram of retro placental clots and 30% had retro placental clots of

300-499 gram and 30% had 500 gram or more of retro placental clots.

40%

30%

30%

PPH

100-299 gram 300-499 gram 500 gram& above

RETRO

PLACENTA

L CLOTS(g)

PPH AKI DIALYSI

S

BLOOD

TRANSFUSION

(4/MORE)

DIVC HELLP PULMON

ARY

EDEMA

VENTILATOR

SUPPORT

Page | 70

Among the 24 patients who went in for acute kidney injury, 37.5% cases had

RP clots of 300-499 gram, 33.33% had RP clots of 100-299 gram and 29.16%

had RP clots of 500 grams or more.

Among the 11 cases which required dialysis, 9.09% of cases had only 100-299

gram of retro placental clots, 54.54% had 300-499 gram of retro placental clots

and 36.36% had retro placental clots of 500 gram and above.

33%

38%

29%

AKI

100-299gram 300-499gram 500 gram& above

9.09

54.54

36.36

DIALYSIS

100-299gram

300-499gram

500 gram and above

Page | 71

Among the 12 cases that required a blood transfusion of 4 or more units,

58.33% cases had 500 gram or more of retro placental clots,33.33% had 300-

499 gram retro placental clots and 8.33% cases had retro placental clots of

100-299 gram.

Among the 9 cases that were complicated by DIVC, 11.11% cases had retro

placental clots 100-299 grams, 55.55% cases had retro placental clots of 300-

499 gram and 33.33% cases had retro placental clots of 500 gram and above.

8%

33%

59%

BLOOD TRANSFUSION >4 UNITS

100-299gram 300-499gram 500gram & above

11.11

55.55

33.33

DIVC

100-299gram

300-499gram

500 gram& above

Page | 72

Among those who developed HELLP syndrome, 38.46% cases had 100-299

gram retro placental clots, 53.84% cases had 300-499 gram of retro placental

clots and 7.69% cases had retro placental clots of 500 gram and above.

Only one case had pulmonary edema ,in whom retroplacental clots was

Page | 73

FETAL OUTCOME- BIRTH WEIGHT

The average weight of the fetuses delivered was 2.02 kg .The average birth

weight of the babies were 2.47kg in grade 1 abruption, 2.1kg in grade 2

abruptions and 1.89kg in grade 3 abruptions.

This low birth weight is attributed to premature delivery of the fetuses in view

of abruption placenta.

Page | 74

FETAL OUTCOME- APGAR

The average 1 minute APGAR for the babies delivered was 5 and the 5 minute

APGAR was 7. But this APGAR score only denotes the well being of those

babies which were delivered promptly in grade 1/ grade 2 abruptions. Hence

when the diagnosis of an abruption is made and appropriate timely delivery of

the fetus is done, the fetal outcome is usually good.

Page | 75

ABRUPTION AND INTRAUTERINE FETAL DEMISE

In our study, among all 51 cases of abruption,26 cases(50.9%) presented with

an intrauterine fetal demise and the remaining 25 cases (49.1%) cases had live

babies. Among those cases with intrauterine fetal demise,16 cases(61.53%)

underwent a caesarean section and 10 cases(38.46%) delivered by labor

natural. Among the live babies, 21 cases (84%) were delivered by caesarean

section and 3 cases(12%) by labor natural and 1 case(4%) by instrumental

delivery.

0

5

10

15

20

25

30

IUD BABIES LIVE BABIES

INSTRUMENTAL DELIVERY

LSCS

NORMAL DELIVERY

Page | 76

SUMMARY

• Among all the cases of abruption included in this study,the maximum

incidence of abruptio placenta was seen between age group 20-25

years(41.1%). The lowest age of abruptio placenta in this study was 18

years and the highest was 33 years.

• The incidence of abruption was greatest in multipara( 55% ) when

compared to primi.

• Maximum incidence of abruption occurred between 24-34

weeks(51.9%) weeks of gestation.

• Booked antenatal cases constituted the majority because of the

government policies and extended coverage by the primary health care

system produced by our State Government. Only 2 cases were

unbooked in our study.

• The main presenting symptoms were abdominal pain in 82.5%;

followed by vaginal bleeding in 62.74%.9.8% of the cases presented

with reduced perception of fetal movements and 5.8% cases were

asymptomatic.

• The majority of abruptions were Grade 3 abruptions(52.94%) followed

by Grade2 and Grade 1, as per Sher’s classification.

• Majority of the abruptions were revealed abruptions(62.7%).

• The average abruption – delivery interval was 3.32 hours, which

reflects the proper antenatal counselling & the available free transport

Page | 77

facilities,that has enabled the patient to identify the alarming symptoms

and the prompt timely management by the hospital.

• The most common risk factor that was found in our patients was pre

eclampsia of varying severities in 60.78% followed by anemia in

50.98% of the cases.Multiparity of 3rd gravida and above was found in

13.72%, polyhydramnios in 23.5%,placenta previa and multiple

pregnancy in 3.92% and gestational diabetes in 7.84% of the cases.

• 72.5% of the cases in our study were delivered by cesarean section ,

25.5% by normal vaginal delivery and 2% by instrumental delivery.

The most common indication for a cesarean delivery was previous

LSCS/ fetal distress.thought he LSCS rate was high, the maternal

morbidity was lesser and perinatal outcome was better for the live

babies .

• The most common complication observed was acute kidney injury,in

47.05% of the cases and 21.56% of the cases required

dialysis.Couvelaire uterus was found in 29.4% of the cases in cesarean

section. Coagulation abnormalities were present in 17.64% of

patients.25.49% of the cases went in for HELLP syndrome,19.6% of the

cases went in for PPH.23.52% of cases required a blood transfusion of

>4 units. 5.8% of the cases required ventilatory support.

• The average amount of retroplacental clots was 269.6 grams and all the

above mentioned complications was high in patients in whom

retroplacental clots was above 300 grams.

Page | 78

• There was no maternal mortality in our study,which is attributed to the

prompt and timely action in the diagnosis and management of abruption

cases and to the multidisciplinary approach with the availabilty of

expert obstetricians,anaesthesiologists,

paediatricians,nephrologists,physicians and cardiologists.

• 51% of the cases had an intrauterine fetal demise, which was due to the

grade 3 abruption.Among these 61.53% cases had a cesarean delivery

and 38.46% cases had normal delivery.

• Among those live babies delivered,84% were delivered by cesarean

section and the average birth weight of the babies was 2.02 kg and this

low birth weight is attributed to prematurity.

• Among the live babies, the average 1 minute APGAR was 5 and 5

minute APGAR was 7, and these babies did cope up well after delivery.

This is attributed to the timely delivery of these salvageable babies in

cases of abruptio placenta.

Page | 79

CONCLUSION

This study has shown that placental abruption represents a set of potentially

serious obstetric emergency, which has a great impact on maternal and

neonatal mortality and morbidity and is one of the major risk factors for a

preterm delivery.

The chief risk factors identified in this study are pre eclampsia and anaemia

complicating pregnancy. So if these risk factors are identified at an early stage

by adequate antenatal care and treated appropriately, the incidence of

abruption and hence the maternal and perinatal mortality/morbidity can be

reduced in our community.

A major number of patients presented with Grade 3 abruption with a resultant

intrauterine death of fetus. So early identification of the problem and timely

referrals from the peripheral institution would help to bring down the perinatal

and maternal mortality and morbidity.

Page | 80

BIBLIOGRAPHY

1. Konje JC, Taylor DJ. Bleeding in later pregnancy. In: James DK, Steer PJ, Weiner

CP, Gonik B editors. High risk pregnancy 3 rd ed. Philadelphia: Pennsylvania; 2006.

1266-71.

2. Pitaphrom A, Sukcharoen N. Pregnancy outcomes in placental abruption. J Med

Oncolassoc Thai. 2006; 1572-8.

3. Ananth CV, Lavery JA, Vintzileos AM. Severe Placental Abruption:Clinical

definition and associations with maternal complications. Am J Obstet Gynaecol.

2016;214;272.e1-9

4. Kyrklund-Bloomberg BN, Gennser G, Cnattinguis S. Placental abruption and

perinatal death. Paediatr Perinat Epidemiol. 2001;15:290-7.

5. Willium A, Lieberman E, Mittendorf R. Risk factors of abruption placentae. A J of

Epidemiol. 1991; 134(9):965-72.

6. Menom MK, Sokshi SK. Accidental haemorrhage in teaching hospital. J Obstet

Gynaecol Ind. 1961; 11:335-41.

7. Wasnik SN and Naiknaware SV. Antepartum Haemorrhage: Causes and its effects

on Mother Child: An Evaluation. Obstetri Gynaecol Internat J. 2015;3(1):00072.

8. Bibi S, Ghaffer S, Pir MA, Yousfani S. Risk factors and clinical outcome in

placental abruption: a retrospective analysis J Pak Medic Associat. 2009:59(10):672-

4

Page | 81

9.Campbell S, Lee C. Disorders of placentation. In: Obstetrics by ten teacher 17th ed.

Arnold London 2002.p.171-3.

10. Shrivastava V, Kotur P, Jauhari A. Maternal and Fetal outcome among Abruptio

Placentae at a rural tertiary hospital in Karnataka, India: A Retrospective analysis. Int

J Res Med Sci. 2014;2(4):1655-8.

11. Subramaniyan V, Pachamuthu U, Dhanapal M, Abruptio Placentae: A

Retrospective Study. 2016;5:10.

12. Choudhary V. Rathi Somani S, Somani S. Evaluation of Risk factors and

Obstetric and Perinatal Outcome in Abruptio Placentae. 2015;14(5):36-9.

Page | 82

ANNEXURES

STUDY PROFORMA

ABRUPTIO PLACENTA-AN OBSTETRIC ENDANGERMENT

NAME OF THE PATIENT

PATIENT IP NUMBER

DATE & TIME OF ADMISSION

REFERRAL

AGE

HEIGHT(cm)

WEIGHT(Kg)

BMI

VITALS AT THE TIME OF ADMISSION

LEVEL OF SHOCK

OBSTETRIC SCORE WITH PREVIOUS

MODE OF DELIVERY(IF ANY)

LMP

EDD

Page | 83

GESTATIONAL AGE AS PER LMP

GESTATIONAL AGE AS PER DATING

SCAN

PRESENTING COMPLAINTS WITH

DURATION

WHETHER BOOKED AND IMMUNISED*

PREVIOUS OBSTETRIC EVENTS

OTHER OBSTETRIC RISK

FACTORS:(YES/NO)

1)ANEMIA

2)PRE-ECLAMPSIA

3)GDM

4)MULTIFETAL GESTATION

5)CONCEPTION AFTER ARTIFICIAL

REPRODUCTIVE TECHNOLOGY

6)NON VERTEX PRESENTATION

7)PREVIOUS LSCS

8)PROM/PPROM

9)POLYHYDRAMNIOS

10)PREVIOUS HISTORY OF

Page | 84

ABRUPTION

11) MATERNAL TOBACCO

CHEWING/SMOKING

12)HISTORY OF BLUNT ABDOMINAL

TRAUMA/FALL

EXAMINATION FINDINGS

ULTRASONOGRAM

CONCEALED/ REVEALED ABRUPTION

GRADE OF ABRUPTION (TABLE-1)**

LAB INVESTIGATIONS

HEMOGLOBIN

TOTAL COUNT

DIFFERENTIAL COUNT

PLATELETS

PCV

BLEEDING TIME/CLOTTING TIME

BLOOD SUGAR

UREA

Page | 85

CREATININE

Na+/ K+

URINE ALBUMIN/SUGAR

SERUM BILIRUBIN

ASPARTATE AMINO TRANSFERASE

ALANINE AMINO TRANSFERASE

SERUM ALKALINE PHOSPHATASE

SERUM PROTEIN/ALBUMIN/GLOBULIN

PROTHROMBIN TIME

ACTIVATED PARTIAL

THROMBOPLASTIN TIME

INR

SERUM FIBRINOGEN

D-DIMER

ABRUPTION-DELIVERY INTERVAL

DETAILS OF BLOOD AND BLOOD

PRODUCTS TRANSFUSED

MODE OF DELIVERY

RETROPLACENTAL CLOTS(IN GRAM)

COUVELAIRE UTERUS

Page | 86

COMPLICATIONS

DISSEMINATED INTRAVASCULAR

COAGULATION

HYPOVOLEMIC SHOCK

POST PARTUM HEMORRHAGE

PROLONGED HOSPITAL STAY(> 12

DAYS)

ACUTE RENAL FAILURE

VENTILATORY SUPPORT

MATERNAL DEATH

MATERNAL CONDITION AFTER

DELIVERY

BABY DETAILS(ALIVE/DEAD,

SEX,TERM/PRETERM, APGAR, BIRTH

WEIGHT, ANY CONGENITAL

ANOMALIES)

Page | 87

PATIENT INFORMATION SHEET

• We are conducting a study on Abruptio Placenta and its maternal and

perinatal outcomes in patients attending Government Kilpauk Medical

College Hospital, Chennai and for that your participation. may be

valuable to us.

• The purpose of this study is to diagnose placental abruption, analyse its

maternal and fetal outcomes and see if early intervention helps in

improving the maternal and fetal outcome.

• You have been diagnosed with abruption placenta and you are an

eligible candidate for this study.

• 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 this 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 otherwise

entitled.

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

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

which may aid in the management or treatment.

Signature of investigator Signature of participant

Page | 88

PATIENT CONSENT FORM

Title of the project:

Name : Date :

Age : IP No :

Sex : Project Patient No :

• The details of the study have been provided to me in writing and explained to me

in my own language.

• I confirm that I have understood the above study and had the opportunity to ask

questions.

• I understand that my participation in the study is voluntary and that I am free to

withdraw at any time, without giving any reason, without the medical care that

will normally be provided by the hospital being affected.

• I agree not to restrict the use of any data or results that arise from this study

provided such a use is only for scientific purpose(s).

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

• I fully consent to participate in the above study.

Page | 89

A STUDY ON RISK FACTORS AND OUTCOME OF ABRUPTIO PLACENTA

பங்குபபறுபவரின் பபயர் : வயது: எண் :

• மேமேகுறிப்பிட்டுள்ள ேருத்துவ ஆய்வின் விவரங்கள் எனக்கு • விளக்கப்பட்டது. நான் இவ்வாய்வில் தன்னிச்சையாக பங்மகற்கிமறன்.

• எந்த காரணத்தினாமோ எந்த ைட்டைிக்கலுக்கும் உட்படாேல் நான் இவ்வாய்வில் இருந்து விேகிக்பகாள்ளல்ோம் என்றும் அறிந்துபகாண்மடன்.

• இந்த ஆய்வு ைம்பந்தோகமவா, இசத ைார்ந்து மேலும் ஆய்வு • மேற்பகாள்ளும்மபாதும் இந்த ஆய்வில் பங்குபபறும் ேருத்துவர் என்னுசடய ேருத்துவ அறிக்சககசள பார்ப்பதற்கு என் அனுேதி மதசவயில்சே என அறிந்துபகாள்கிமறன்.

• இந்த ஆய்வின் மூேம் கிசடக்கும் தகவசேமயா, • முடிசவமயா பயன்படுத்திக்பகாள்ள ேறுக்கோட்மடன்.

• இந்த ஆய்வில் பங்குபகாள்ள ஒப்புக்பகாள்கிமறன். • இந்த ஆய்சவ மேற்பகாள்ளும் ேருத்துவஅணிக்க உண்சேயுடன் இருப்மபன் என்றும் உறுதியளிக்கிமறன்.

பங்மகற்பவரின்சகபயாப்பம் ஆய்வாளரின்சகபயாப்பம்:

இடம் :

மததி :

Page | 90

Page | 91

PLAGIRSM CERTIFICATE

This is to certify that this dissertation work titled Abruptio placenta-an obstetric

endangerment was done by the candidate Dr.SWETHA.S with registration Number

221616154 for the award of MD degree in the branch of Obstetrics And Gynaecology . I

personally verified the urkund.com website for the purpose of plagiarism Check. I found that the

uploaded thesis file contains from introduction to conclusion pages and result shows 17 %

percentage of plagiarism in the dissertation.

Guide & Supervisor.

Dr.K.L.MALARVIZHI MD.,DGO.,DNB

Professor & Head

Dept. of obstetrics and Gynaecology

Govt.Kilpauk Medical College

Chennai -600010

Page | 92

Page | 93

S.No NAME AGE OBS SCORE GA BOOKING

preeclamps

ia anemia

multiparit

y

polyhydra

mnios

placenta

previa GDM twins pain

bleeding

PV

uterine

tenderness

decrease

d FM FH GRADE

SHOCK

LEVEL

CONCEALED/

REVEALED

MODE OF

DELIVERY

A-D

INTERVA

L RP CLOTS

couvela

ire

APGAR

1

APGAR

5

BIRTH

WT PPH AKI

DIALYS

IS

MASSIVE

TRANSFUSION DIVC HELLP

PUL.

EDEMA

VENTIL

ATOR

HOSPITA

L STAY

MATERNA

L DEATH

1 priya 25 primi 38 B 1 1 0 0 0 0 0 1 0 0 0 A 3 1 1 1 0.75 500 0 0 2.8 1 1 0 0 0 0 0 0 12 nil

2 banupriya 24 G2 A1 31 B 1 0 0 0 0 0 0 1 1 0 0 P 2 1 2 3 0.5 100 A 6 8 1.5 0 0 0 0 0 0 0 0 28 nil

3 jayanthi 33 G6P2L1A3 28 UB 1 1 1 0 0 0 0 1 0 0 0 A 3 1 1 1 12 600 0 0 1.4 1 1 1 1 0 0 0 0 40 nil

4 sathya 24 G2P1L1 28 B 0 1 0 0 0 0 0 0 0 0 1 A 3 1 1 1 3 350 0 0 1 0 0 0 0 0 1 0 0 17 nil

5 chithra 28 G3P2L2 34 B 1 1 1 0 0 0 0 1 0 0 0 A 3 1 1 3 5 500 P 0 0 1.9 0 1 0 1 0 0 0 0 16 nil

6 vani 19 primi 36 B 0 1 0 0 0 0 0 1 1 0 0 P 2 1 2 3 2 200 A 5 7 2.3 0 0 0 0 0 0 0 0 19 nil

7 gnaneswari 25 G2P1L1 34 B 0 1 0 0 0 0 0 1 1 1 0 A 3 2 2 3 4 400 P 0 0 1.9 0 0 0 0 0 0 0 0 10 nil

8 magarajothi 26 G2P1L1 27 B 0 1 0 0 0 0 0 1 1 0 0 A 3 1 2 3 2 500 P 0 0 0.7 1 1 0 1 1 0 0 0 22 nil

9 rajeswari 22 G2P1L1 36 B 1 0 0 0 0 0 0 0 0 0 0 P 1 1 1 3 50 A 6 8 2.3 0 0 0 0 0 0 0 0 10 nil

10 keerthana 18 primi 34 B 1 0 0 0 0 0 0 1 0 0 1 P 2 1 1 3 1 100 A 3 4 2 0 0 0 0 0 0 1 1 47 nil

11 shakila 24 G3P2L2 36 B 0 0 1 0 1 0 0 1 1 1 0 A 3 3 2 3 3 300 A 0 0 2.8 1 0 0 0 0 0 0 0 16 nil

12 devi 24 primi 26 B 1 0 0 0 0 0 0 1 0 0 0 A 3 2 1 3 2 300 P 0 0 0.7 0 1 1 1 1 1 0 1 80 nil

13 renuka 24 primi 25 B 1 0 0 0 0 0 0 0 0 0 0 P 1 1 1 3 50 P 5 7 2.2 0 0 0 0 0 0 0 0 12 nil

14 sharmila 28 G2P1L1 36 B 1 1 0 0 0 0 0 1 1 0 0 A 3 2 2 3 4 500 P 0 0 2.4 0 1 1 1 1 1 0 1 27 nil

15 nandhini 23 primi 28 B 1 0 0 1 0 0 0 1 0 0 1 A 3 1 1 1 2 100 0 0 0.7 0 0 0 0 0 1 0 0 17 nil

16 dhivya 18 primi 32 B 0 1 0 1 0 0 0 1 1 1 0 A 3 1 2 3 4 450 A 0 0 2 0 0 0 1 0 0 0 0 16 nil

17 shyamala 20 primi 36 B 1 0 0 0 0 0 0 1 0 0 1 A 3 2 1 3 6 300 P 0 0 2.4 0 1 1 1 0 1 0 0 29 nil

18 priya 23 G2P1L1 37 B 0 0 0 1 0 0 0 1 1 1 0 A 3 2 2 3 7 750 P 0 0 2.3 0 0 0 1 1 0 0 0 12 nil

19 hemalatha 26 G2P1L1 30 B 1 0 0 0 0 0 0 1 0 0 0 P 2 1 1 3 3 100 A 5 7 1.1 0 1 0 0 0 1 0 0 27 nil

20 bhuvaneshwari 18 primi 36 B 0 0 0 1 0 1 0 1 0 0 0 A 3 1 1 1 4 250 0 0 2 0 0 0 0 0 0 0 0 11 nil

21 akhila 21 primi 37 B 0 0 0 1 0 0 0 0 0 0 0 P 1 1 1 3 50 A 5 7 3 0 0 0 0 0 0 0 0 9 nil

22 krishnaveni 29 G2A1 38 B 1 0 0 0 0 0 0 1 1 0 0 P 2 1 2 3 2 100 A 5 8 2 0 0 0 0 0 0 0 0 10 nil

23 prabhavathy 28 G2P1L1 31 B 1 0 0 0 0 0 0 1 1 1 0 A 3 2 2 1 3 200 0 0 1.4 0 0 0 0 0 0 0 0 9 nil

24 dhanalakshmi 18 G2P1L1 34 B 1 0 0 0 0 0 0 1 1 1 0 A 3 2 2 3 4 300 A 0 0 2.1 0 1 1 0 0 1 0 0 24 nil

25 dhanalakshmi 21 primi 33 B 0 1 0 1 0 0 0 1 1 0 0 P 2 1 2 3 2 200 P 4 6 1.8 0 0 0 0 1 0 0 0 27 nil

26 priyanka 25 G2P1L1 32 B 1 1 0 0 0 0 0 1 0 0 0 A 3 1 1 3 3 300 P 0 0 1.6 1 1 0 0 0 0 0 0 16 nil

27 meena 28 G2P1L1 34 B 0 0 0 1 0 1 0 1 0 0 0 P 2 1 1 3 2 150 A 5 8 2.1 1 0 0 0 0 0 0 0 12 nil

28 thendral 32 G4P2L2A1 36 B 1 1 1 0 0 0 0 1 1 0 0 A 3 2 2 3 5 250 A 0 0 2.2 0 1 0 0 0 1 0 0 21 nil

29 ramya 18 primi 32 B 1 1 0 0 0 0 0 1 0 0 0 A 3 1 1 3 3 500 P 0 0 1.9 0 1 1 1 0 0 0 0 27 nil

30 vidhya 26 primi 34 B 0 0 0 1 0 0 0 0 1 0 0 P 2 1 2 2 4 200 A 4 6 2 0 1 0 0 0 0 0 0 15 nil

31 rajeswari 26 primi 38 B 1 1 0 0 0 0 0 1 1 1 0 P 2 1 2 3 4 150 A 6 8 3 0 0 0 0 0 0 0 0 10 nil

32 latha 18 primi 36 B 0 1 0 0 0 0 0 0 1 0 0 P 2 1 2 3 2 250 P 5 7 2.6 0 0 0 0 0 0 0 0 12 nil

33 valli 29 primi 38 B 1 0 0 0 0 0 0 0 1 0 0 P 2 1 2 3 4 150 A 6 8 2.7 0 0 0 0 0 0 0 0 10 nil

34 pushpa 24 G3P2L2 36 B 0 1 1 0 0 0 0 1 1 1 0 A 3 2 2 3 6 550 P 0 0 2.2 0 1 1 1 0 0 0 0 26 nil

35 shantha 28 G2P1L1 32 B 1 1 0 0 0 0 0 1 1 1 0 A 3 1 2 1 4 400 0 0 1.8 1 0 0 0 1 1 0 0 22 nil

36 devi 27 G2P1L1 35 B 0 1 0 1 0 0 0 1 0 0 0 P 2 1 1 3 2 200 A 4 7 2.2 1 1 0 0 0 0 0 0 12 nil

37 minnal 25 primi 32 B 1 1 0 0 0 0 0 1 1 0 0 A 3 1 2 1 4 350 0 0 1.9 0 1 1 0 1 0 0 0 28 nil

38 jayalakshmi 28 G2A1 34 B 1 0 0 0 0 0 0 1 1 1 0 P 2 2 2 3 3 150 A 5 8 2 0 0 0 0 0 0 0 0 14 nil

MASTER CHART

39 amudha 18 primi 38 B 0 1 0 0 0 0 0 1 0 0 0 A 3 1 1 1 4 300 0 0 2.9 0 1 0 1 0 0 0 0 16 nil

40 gowri 21 primi 36 B 1 1 0 0 0 0 0 1 1 1 0 P 2 2 2 3 2 100 A 6 7 2.6 0 0 0 0 0 0 0 0 10 nil

41 sneha 25 primi 38 B 1 0 0 1 0 1 0 1 1 1 0 P 2 1 2 1 2 150 6 8 2.5 1 1 0 0 0 0 0 0 11 nil

42 muthumari 23 G4P3L3 30 UB 0 1 1 0 0 0 0 1 1 0 0 A 3 2 2 1 1 250 0 0 1.4 1 1 1 1 0 0 0 0 26 nil

43 priya 28 primi 35 B 1 0 0 1 0 0 1 1 1 1 0 P 2 1 2 3 2 200 A 6 8 1.5 0 0 0 0 0 1 0 0 29 nil

44 priya 28 primi 35 B 1 0 0 1 0 0 1 1 1 1 0 P 2 1 2 3 2 200 A 5 7 1.8 0 0 0 0 0 1 0 0 29 nil

45 vinodhini 30 G3P2L2 34 B 1 1 0 0 0 0 0 1 1 1 0 A 3 2 2 1 4 350 0 0 2 0 1 0 0 1 1 0 0 20 nil

46 manimegalai 26 G2P1L1 36 B 0 0 0 0 1 0 0 0 1 0 0 P 2 1 2 3 1 150 A 7 8 2.2 0 0 0 0 0 0 0 0 10 nil

47 valli 23 G2A1 34 B 1 1 0 0 0 0 0 1 1 0 0 P 2 2 2 3 3 200 A 6 8 2.1 0 1 0 0 0 0 0 0 13 nil

48 selvi 26 G2P1L1 36 B 0 0 0 0 0 0 0 0 0 0 1 P 1 1 1 1 50 7 8 2.4 0 0 0 0 0 0 0 0 6 nil

49 muthulakshmi 32 G3P2L2 35 B 0 0 1 0 0 0 0 1 1 0 0 A 3 1 2 3 5 350 P 0 0 2.1 0 1 1 0 0 0 0 0 20 nil

50 saradha 26 G2A1 34 B 1 1 0 0 0 0 0 1 1 1 0 P 2 1 2 3 4 200 A 2 0 1 0 0 0 0 0 0 17 nil

51 kanimozhi 22 primi 36 B 1 1 0 0 0 1 0 1 1 1 0 A 3 1 2 3 3 400 P 0 0 2.6 0 1 1 0 1 1 0 0 26 nil