histopathological analysis of patients with abruptio...

HISTOPATHOLOGICAL ANALYSIS OF PATIENTS WITH

ABRUPTIO PLACENTA IN A TERTIARY HEALTH CARE CENTRE

Dissertation submitted in

Partial fulfillment of the regulations required for the award of

M.D. Degree

in

PATHOLOGY - BRANCH III

THE TAMILNADU

DR.M.G.R.MEDICAL UNIVERSITY

CHENNAI

MAY 2019

DECLARATION

I hereby declare that the dissertation entitled “HISTOPATHOLOGICAL

ANALYSIS OF PATIENTS WITH ABRUPTIO PLACENTA IN A

TERTIARY HEALTH CARE CENTRE” is a bonafide research work done

by me in the Department of Pathology, Coimbatore Medical College during the

period from JANUARY 2017 TO JUNE 2018 under the guidance and

supervision of Dr.G.S.THIRIVENI BALAJJI, M.D, Associate Professor,

Department of Pathology, Coimbatore Medical College.

This dissertation is submitted to The Tamilnadu Dr.MGR Medical

University, Chennai towards the partial fulfillment of the requirement for the

award of M.D., Degree (Branch III) in Pathology. I have not submitted this

dissertation on any previous occasion to any University for the award of any

Degree.

Place : Coimbatore Dr. A. PETER SAMIDOSS

Date :

CERTIFICATE

This is to certify that dissertation entitled “HISTOPATHOLOGICAL

ANALYSIS OF PATIENTS WITH ABRUPTIO PLACENTA IN A

TERTIARY HEALTH CARE CENTRE” is a bonafide work done by

Dr. A. PETER SAMIDOSS, a postgraduate student in the Department of

Pathology, Coimbatore Medical College, Coimbatore under guidance and

supervision of Dr.G.S.THIRIVENI BALAJJI, M.D, Associate Professor,

Department of Pathology, Coimbatore Medical College, Coimbatore in partial

fulfillment of the regulations of the Tamil Nadu Dr. M. G. R. Medical

University, Chennai towards the award of M.D. Degree (Branch III) in

Pathology.

Guide Head of the Department

Dr.G.S.THIRIVENI BALAJJI, M.D, Prof. Dr. C. LALITHA, M.D.,

Associate Professor, Professor and Head,

Department of Pathology, Department of Pathology,

Coimbatore Medical College, Coimbatore Medical College,

Coimbatore -14. Coimbatore -14.

Prof. Dr. B.ASOKAN, M.S, M.Ch.,

Dean,

Coimbatore Medical College,

Coimbatore -14.

ACKNOWLEDGEMENT

To begin with, I thank the almighty God for bestowing his blessing on me

in this dissertation to be a successful one.

I wish to thank our beloved Dean Prof. Dr.B.ASOKAN,M.S.,M.Ch,

Coimbatore Medical College and Hospital, Coimbatore for permitting me to

conduct this study.

I thank Prof. Dr. C.LALITHA, M.D., Professor and Head of the

Department, Department of Pathology, Coimbatore Medical College,

Coimbatore for her guidance and support.

I wish to express my gratitude and sincere thanks to my guide

Dr.G.S.THIRIVENI BALAJJI, M.D, Associate Professor, Department of

Pathology, Coimbatore Medical College, Coimbatore. This dissertation bears

her valuable suggestions and highly professional advice.

My heartful thanks to Dr.S.YOGALAKSHMI, M.D, Assistant

Professor, Department of Pathology, Coimbatore Medical College, Coimbatore

for her timely advice and suggestion through the course of my work.

I thank all my Associate Professors and Assistant Professors of

Department of Pathology, Coimbatore Medical College, Coimbatore for their

opinion and encouragement.

I thank Department of Obstetrics &Gynecology, Coimbatore Medical

College, Coimbatore, for providing clinical cases, valuable support and

guidance which made this dissertation possible. I thank all my patients for their

co-operation and support.

My deepest and most heart whelming thanks goes to my parents, my

father Mr.P.S.AYYAPILLAI and my mother Mrs.A.PADMAVATHY who

have showered me with lots and lots of love.

My special thanks to my wife Mrs. ANGELIN TISHA B.Tech, whose

love, support and constant patience have taught me so much about sacrifice,

discipline and compromise.

At this juncture, I have a special mention about my elder brother

Dr.A.ARUL KAMALRAJ, Ph.D., and my younger brother Mr.A.ANANDHA

SELVA REUBEN, MBA., without them, I couldn’t have travelled this far.

My heartful thanks to Lab Technicians, Mr. M. SUBRAMANIAN,

Mrs. S.J. MUTHUSELVI, Mrs. K. ARULMANI, Mrs. S. SHARMILA

DEVI, Mrs.SUNDARAMBAL and typist Mrs.SASIKALA for their help in

technical aspects. I thank my junior Dr. D.JENIFER for her help in grossing

the specimens.

I thank all my non-teaching staffs working in Department of Pathology,

Coimbatore Medical College, Coimbatore.

I would like to dedicate this book to my family’s little princess

A.BRINDHA.

I also thank my batch mates and my juniors for their love and support

Dr. A. PETER SAMIDOSS

CERTIFICATE – II

This is to certify that this dissertation work titled

“HISTOPATHOLOGICAL ANALYSIS OF PATIENTS WITH

ABRUPTIO PLACENTA IN A TERTIARY HEALTH CARE CENTRE”

of the candidate Dr. A. PETER SAMIDOSS with registration number

201613255 for the award of M.D Degree in the branch of PATHOLOGY.

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 7% percentage of plagiarism in the

dissertation.

Guide and Supervisor

CONTENTS

S.NO PARTICULARS PAGE NO.

1. INTRODUCTION 1-4

2. AIM OF THE STUDY 5

3. OBJECTIVES OF THE STUDY 6

4. REVIEW OF LITERATURE 7-37

5. MATERIALS AND METHODS 38-45

6. OBSERVATION AND RESULTS 46-68

7. DISCUSSION 69-84

8. SUMMARY 85-92

9. CONCLUSION 93-98

10. BIBLIOGRAPHY 99-108

11. ANNEXURES

I: Proforma and Consent Form 109-110

II: Master Chart 111-112

LIST OF TABLES

S.

NO. TITLE

PAGE

NO.

1. Age Distribution among cases and controls 46

2. Mean age of the study 47

3. Correlation of clinical features among cases and control 48

4. Histopathological features of Acute abruption in the study 49

5. Histopathological features of chronic abruption in the study 50

6. Expression of Histopathological features of acute abruption

in acute abruption cases and in acute abruption with chronic

features cases

51

7. Statistics - Histopathological features of acute abruption 52

8. Expression of Histopathological features of chronic

abruption in acute abruption cases and in cases of Acute

abruption with chronic features

53

9. Statistics - Histopathological features of chronic abruption 55

10. Association of paternal smoking with cases of acute

abruption and acute abruption with chronic features

58

11. Gender distribution of children in Placental Abruption 59

12. Status of children in Placental Abruption 60

13. Correlation between chorioamnionitis and preterm

deliveries among Placental Abruption

61

14. Pregnancy Induced Hypertension 62

15. Analysis of gravida between cases and control 63

16. Histopathological features of acute abruption in Primi

gravida and Multi gravida

64

17. Histopathological features of chronic abruption in Primi


67

LIST OF CHARTS

S.

NO TITLE

PAGE

NO.

1. Age Distribution among Cases and Controls 46

2. Mean age of the study 47

3. Correlation of Clinical features among cases and control 48

4. Histopathological features of Acute abruption in the study 49

5. Histopathological features of chronic abruption in the study 50

6. Expression of Histopathological features of acute abruption

in acute abruption cases and in Acute abruption with chronic

features cases

51

7. Statistics - Histopathological features of acute abruption 52

8. Expression of Histopathological features of chronic

abruption in acute abruption cases and in cases of Acute

abruption with chronic features

54

9. Statistics - Histopathological features of chronic abruption 56

10. Association of Paternal Smoking with cases of acute

abruption and acute abruption with chronic features

58

11. Gender distribution of children in Placental Abruption 59

12. Status of children in Placental Abruption 60

13. Correlation between chorioamnionitis and preterm

deliveries among placental abruption

61

14. Pregnancy Induced Hypertension 62

15. Analysis of gravida between cases and control 63

16. Histopathological features of acute abruption in Primi


65

17. Histopathological Features of Chronic Abruption In Primi


67

LIST OF COLOUR PLATES

S.NO TITLE

1 Gross; Placental Abruption

Dilated tortuous vessels over the membranes

2 Gross; Placental Abruption

Maternal surface- indentation and hemorrhagic areas

3 Gross- Placental Abruption

Placental infarction with congestion

4 Gross – Placental Abruption

Retroplacental blood clot with vessel thrombus

5 Gross- Placental Abruption

Retroplacental hemorrhage

6 Microscopy - Placental Abruption -

funisitis

7 Microscopy - Placental Abruption

Squamous mataplasia with moderate chorioamnionitis


Squamous mataplasia with moderate chorioamnionitis


Mild chorioamnionitis


Moderate chorioamnionitis


Severe chorioamnionitis


moderate chorioamnionitis with haemorrhage


Acute deciduitis with fibrinoid necrosis


Intervillous haemorrhage


Intervillous and intravillous haemorrhage


Intervillous haemorrhage and adjacent area of acute deciduitis with

haemorrhage


Intervillous haemorrhage and acute deciduitis


Intervillous haemorrhage


Villous haemorrhage with large area of haemorrhage


Moderate chorioamnionitis with adjacent area of hemorrhage


Increased syncytiotrophoblastic knotting


Increased syncytiotrophoblastic knotting


Increased syncytiotrophoblastic knotting with multinucleated giant cell


Vasculopathy(vessels with marginal hematoma)


Vessel with thick muscular cuffing and adjacent marginal haematoma


Vessel with thrombus and villous infarction

ABBREVIATIONS

AFP : Alpha Fetoprotein

BP : Blood Pressure

CAOS : Chronic Abruption-Oligohydramnios

Sequence

COPD : Chronic Obstructive Pulmonary Disease

DIC : Disseminated Intravascular Coagulation

DM : Diabetes Mellitus

eNOS : Endothelial Nitric Oxide Synthase

HLA : Human Leukocyte Antigen

IL-1 : Interleukin-1

IUGR : Intra Uterine Growth Retardation

MMP : Matrix Metalloproteinases

NK CELL : Natural Killer Cell

NO : Nitric Oxide

PAPPA-A : Pregnancy Associated Plasma Protein A

RBC : Red Blood Cell

TH 1

LYMPHOCYTES

: T- Helper 1 Lymphocytes

TNF-α : Tumor Necrosis Factor-α

INTRODUCTION

1

INTRODUCTION

BACKROUND OF THE STUDY

Abruptio placenta was first described by E Rigby in 1775 by

publishing an essay on Uterine hemorrhage which precedes the delivery of

the fetus. Placental abruption (also known as abruptio placentae) is a

complication of pregnancy, wherein the placental lining has separated from

the uterus of the mother prior to delivery. It is the most common pathological

cause of late pregnancy bleeding. In humans, it refers to the abnormal

separation after 20 weeks of gestation and prior to birth. It occurs on average

in 0.5% or 1 in 200 deliveries1. In Coimbatore Medical College, the

incidence of patients with placental abruption is about 1 to 2 patients per

month and Intra Uterine death is 0-1 per month. Preterm deliveries

associated with over half of all pregnancies complicated by placental

abruption, and it leads to many adverse maternal and fetal outcomes. The

etiology of placental abruption remains hypothetical but is thought to be the

consequence of abnormal invasion of trophoblast leading to rupture of spiral

arteries and premature separation of the placenta2.

In spite of being an unique obstetrical condition, specific diagnostic

clinical criteria is not available for placental abruption. Histological

evidences supportive to chronic process that often go with placental

2

abruption has led researchers to hypothesize that the condition is the end

result of a chronic process which starts very early in pregnancy, and perhaps

even prolonging to the time of implantation. In the presence of vaginal

bleeding associated with abdominal pain, uterine tenderness or uterine

contractions, placental abruption is first thought to be in the differential

clinical diagnosis. Old or freshly adherent blood clots at delivery is

diagnostic of abruption. Some of these placentas may have histologic

features of placental abruption. Moreover, there have been cases of women

diagnosed with placental abruption based on histological markers that

showed a clinically unremarkable obstetrical course and outcome.

Because of these uncertainties in making the diagnosis of placental

abruption, we try to find the correlation between a clinical and histologic

diagnosis of placental abruption. Furthermore, we have estimated

associations between acute and chronic features with placental abruption.

This is to determine if clinical and pathological findings from the placenta

may perhaps provide some insight as to whether placental abruption is the

result of an acute event or a chronic process.

The causes of placental abruption are multifactorial, defective

mechanism in early vascularization during placentation, immunologically

mediated dysfunction, acute and chronic inflammatory processes might be

playing significant roles in the development of placental abruption3. Many

3

maternal modifiable risk factors during pregnancy such as pregnancy

induced hypertension, polyhydramnios, thrombophilia, preterm premature

rupture of membranes, intrauterine infection are associated with increased

risk of placental abruption.

It has been shown that trophoblast releases a factor that inhibits

platelet aggregation (O'Brien et-al 1987) and it has been postulated that this

factor is needed for normal placental blood flow, when it is decreased,

abruption may take place. Toivonen et a l(2004) found that the low activity

haplotype C-A (His 113-His139) of the microsomal epoxide hydrolase gene

was less frequent in women with abruptio placenta. Tsegaselassie

workalemathu et al (2013, Sep 12) conducted a study by integrating

multiple genomic analytical strategies that provides opportunities for

identifying novel biological pathways for exploring the underlying molecular

mechanisms, for placental abruption4. In addition, genetic risk scores

analyses support the promise of using genetic association studies in placental

abruption risk prediction. Further efforts are needed to understand placental

abruption pathological mechanisms and facilitate the development of

prevention strategies5.

There are only few studies relating to abruptio placenta in

primigravida patients compared to multigravida patients. Present study aims

to study the histomorphological features of abruptio placenta of primigravida

4

compared to multigravida patients and to analyze the features more

associated with Intra Uterine death incidence. This could enlighten us about

the pathway leading to grave prognosis and fatality in such patients, thus

enabling us to prevent maternal and fetal deaths in abruptio placenta.

Also though abruptio placenta is an acute event, it usually has an

underlying chronic etiology like deciduitis and decidual vasculopathy. If the

pathogenesis is unravelled by studying patients with placental abruption,

subsequent pregnancies might be given more attention and preventive

measures may be undertaken.

Thus, present study analyses the incidence, clinical features and

histomorphological features of placenta in abruptio placenta patients. It also

intends to compare the features of abruptio placenta with 50 control patients

of normal delivery; and also differences in histomorphology of abruptio

placenta in primi gravida and multi gravida patients are analysed in present

study.

AIMS AND OBJECTIVES

5

AIM OF THE STUDY

To study the incidence, clinical features and histomorphological

features of abruptio placenta in a tertiary health care Centre. To compare

abruptio placenta with normal placenta and to analyze the differences in

histomorphology of abruptio placenta in primi gravida and multi gravida

patients.

6

OBJECTIVES

1. To analyse the incidence and clinical features of abruptio placenta in a

tertiary health care centre.

2. To study the histopathological features of placenta in abruptio

placenta and compare with normal placenta.

3. To study the morphological difference of abruptio placenta of primi

gravida with that of multi gravida patients.

REVIEW OF LITERATURE

7

ANATOMY OF NORMAL PLACENTA

The only organ with defined end date and which develops in

adulthood is placenta. The demand for fetal nutrition increases in its ninth

week of development, where major role is played by placenta in facilitating

nutrient and gas exchange between the fetal and maternal compartments 6.

The extraembroyonic mesoderm (chorionic plate) and trophoblast

gives rise to the fetal component of the placenta, the uterine endometrium

gives rise to the maternal component7.

As soon as the blastocyst implants, the uterine luminal epithelium and

mucosa begins close and stable interaction with the trophoblast, to

commence the development of the placenta. The inner cell mass (also called

embryoblast, which is composed of larger cells arranged in small groups) is

surrounded by blastocyst cavity (blastocoel), which in turn is surrounded by

the outer wall (the trophoblast), which is the precursor of the placenta. From

these cells, the amnion, embryo and umbilical cord are derived. Placenta

formation is contributed by trophoblast, embryoblast-derived mesenchyme

and embryoblast-derived blood vessels8. In the blastocyst, the orientation is

normally in such a way that the portion which comprises the embryonic pole

attaches to the endometrium.

Six to seven days after fertilization, implantation begins.

8

SHAPE AND SIZE OF PLACENTA:

A developed placenta that measures about 15 to 20 cms in diameter, 3

to 4 cm in thickness and weighs about 500 to 600 grams, is a flattened

discoid mass which is circular or oval in outline8. Fetal surface and Maternal

surface are the two surfaces of an expelled placenta.

Fetal surface –Macroscopically, fetal surface is covered with amnion

and appears smooth, shiny and transparent. Fetal surface is closely applied to

the subjacent chorion which has mottled appearance. Umbilical cord attaches

near the center of this surface, branches of umbilical vessels radiates out

under the amnion from this point. These veins are larger and deeper than the

arteries. Villous chorion forms the fetal part of placenta and chorionic villi

arise from it which in turn projects into the intervillous space which contains

maternal blood9.

Maternal surface -Maternal surface is divided into 15 to 30 lobes by

a series of grooves and is granular in appearance. These lobes are called as

cotyledons. These grooves resemble the bases of incomplete placental

septate which becomes prominent after the third month18

. From maternal

side of intervillous space towards the chorionic plate, these placental septate

extends, but do not reach the chorionic plate. These septate are complex in

structure and consists of components of cytotrophoblastic shell, residual

syncytium and maternally derived material including decidual cells,

9

occasional blood vessels, gland remnants, collagenous and fibrinoid

extracellular matrix10

.

Placental tissues are arranged as chorionic plate, basal plate and

intervillous space.

Chorionic plate -On the fetal aspect it is enclosed by amniotic

epithelium. Stromal side of which has connective tissue layer containing

main branches of umbilical vessels. Near to this is diminishing layer of

cytotrophoblast and inner syncytial wall of intervillous space. The

connective tissue layer is formed by the union between mesenchyme

enclosed surfaces of amnion and chorion forms. Except near the large

vessels, this connective tissue is more fibrous and less cellular than umbilical

cord Wharton’s jelly11

. The large vessels radiate and divide from the cord

attachment till they reach the bases of the trunks of villous stems. These

large vessel branches enter and arborize within the intermediate and terminal

villi.

Basal plate - During second half of pregnancy, the basal plate is

thinned and gradually modified. There is relative decrease in decidual

elements and increase in deposition of fibrin12

.

Intervillous space - Intervillous space is developed from lacunae that

is developed in syncytiotrophoblast and finally coalesce. The maternal blood

10

reaches the intervillous space through different layers of basal plate.

Maternal blood arrives this space from spiral endometrial arteries that opens

through the spaces in cytotrophoblastic shell and release blood in the

intervillous space. At term, the walls of most spiral arteries which contains

fibrinoid matrix in which cytotrophoblast is embedded. This lets expansion

of arterial lumen to give an enhanced blood flow which is privileged in being

not dependent of vasoconstrictors13

. Endometrial veins are draining this large

space. The veins that drain the blood away from the space penetrate the basal

plate and anastomose with the tributaries of uterine veins. Numerous

branches of chorionic villi which arises from stem villi are continuously

immersed with maternal blood that circulates through the intervillous space.

STRUCTURE OF PLACENTA:

Microscopically full term placenta’s cross section shows cut sections

of many chorionic villi. Chorionic villi are important structures that involves

in exchange between mother and fetus. Each stem villus contains its base at

the chorionic plate that progressively branch into intermediate and terminal

villi.

Each villus contains a core of connective tissue having collagen type I,

type III, type V, type VI and fibronectin. Type I collagen is frequently found

as bundles whereas type III collagen fibers are thinner making a meshwork.

Collagen V and VI are seen as fibers that are closely related to type I and III.

11

Collagen type IV and basal lamina related molecules, laminin are present in

stroma in association with basal lamina of trophoblast along with fetal

vessels. Cyto and syncytiotrophoblast covers this matrix and are immersed

by maternal blood in the intervillous space. Numerous desmosomes provides

cohesion in between the cells of cytotrophoblast. Cohesion between Cyto

and syncytiotrophoblast, between their opposed plasma membranes is also

provided by desmosomes14

.

In earlier stages, a continuous layer on the basal lamina is formed by

cytotrophoblast. After the fourth month, it steadily expends itself to form

syncytium. As the cytotrophoblast reduces, the syncytium becomes

progressively thinner and adjacent to the basal lamina over a progressively

large area. Until term, some singly disposed cytotrophoblastic cells persist.

The villous cytotrophoblast cells are pale staining by only slight

basophilia. Electron microscopically, they show very less organelles and

electron translucent cytoplasm. In the cytoplasm, cell organelles like a few

clusters of ribosomes, narrow cisternae of rough endoplasmic reticulum,

Golgi apparatus and large mitochondria are seen. Also, intermediate

filaments particularly related with desmosomes are seen. An intercellular gap

of 20 nm is seen in the membranes of adjacent cells between the

desmosomes15

. These gaps sometimes widen to accommodate microvillous

cell projections from cell surfaces.

12

The syncytial cytoplasm is complex, more electron dense than that of

villous trophoblast cells and are more strongly basophilic. It shows complex

infoldings into the cytoplasm where the plasma membrane joins the basal

lamina. Numerous long microvilli are seen in the surface bordering the

intervillous space. Cytoplasm contains numerous ribosomes, cisternae of

endoplasmic reticulum, scattered Golgi complex, mitochondria, cytoskeleton

of microfilaments, protrusion of vesicles and vacuoles and numerous

lysosomes and phagosomes. It is a highly active layer through which most

transplacental circulation occurs. Also, it is responsible for the secretion of

various placental proteins into the maternal circulation including chorionic

gonadotrophin, chorionic somatomammotropin and others16

.

At all stages, in both layers of trophoblast, glycogen is present. Lipid

droplets are also present in both layers, within the cytoplasm and basal

lamina. These droplets reduce in number when age advances and may

represent fat in transit from maternal to fetus. Membrane bound granular

bodies are present mainly in cytoplasm of syncytiotrophoblast. Some of

these are secretory granules. Lysosomes and phagosomes are related with

degradation of materials phagocytosed from intervillous space.

In the immature placenta syncytial sprouts are found which represent

first stages of development of new terminal villi. These later get invaded by

cytotrophoblast and villous mesenchyme. Syncytial sprouts are also seen in

13

the term placenta but the enclosed nuclei here are largely degenerative.

Syncytial knots represent similar aggregates of degenerative nuclei. This

represents a sequestration phenomenon which involves removal of senescent

nuclear material from adjacent metabolically active areas of syncytium17

.

These sprouts may detach and form maternal syncytial emboli. Daily a

passage of some 1,00,000 such sprouts into the maternal circulation has been

computed.

Fibrinoid deposits are found on villous surface in areas lacking

syncytiotrophoblast which appears to be a repair mechanism in which

fibrinoid forms a wound surface that is subsequently re-epithelialized by

trophoblast. Tenascin is an extracellular matrix glycoprotein that is localized

in the stroma adjacent to these sites.

Large reticulum cells, fibroblasts and large phagocytic Hoffbauer cells

are present in villous core. There is increase in mesenchymal collagen from

network to fine fibers in early mesenchymal villi to densely fibrous stroma

of stem villi of second and third trimester. Stromal channels found in

immature intermediate villi is infilled by collagen after about 14th week to

give the fibrous stroma characteristic of the stem villus.

The fetal vessels include arterioles and capillaries. Their endothelium

contains fine cytoplasmic filaments. Pericytes may be found in close

association with capillary endothelial cells. The vessels are surrounded

14

externally by peri endothelial basal lamina membrane. From second

trimester onwards and later the terminal villi show dilated thin walled

capillaries immediately adjacent to villous trophoblast. The two basal

laminae are apparently fused to produce a vasculosyncytial interface.

Normal placentation contains vascular re-modelling that involves

change from high-resistance spiral arteries into low-resistance blood vessels

in uteroplacental circulation in order to provide a high-flow of blood for

perfusion of the intervillous space. Gradually invading trophoblasts are

replacing a part of the maternal endothelium and tunica media in the arteries

and portion of the smooth muscle is replaced by fibrous tissue, and the spiral

arteries lose their peculiar arterial structure in the wall and the diameter of

lumen enlarges. These changes related with normal implantation are over by

the 23rd week of gestation. These vascular changes range from the

intervillous space into the decidua and to the inner third of the myometrium.

Fetal wellbeing is also dependent on controlled growth and activity of

placental villous development. Budding and maturation of the villi endure

throughout the period of gestation. In Later part of gestation, trophoblast

proliferation is mostly connected with regeneration and repair processes, so

that the boundary between mother and fetus would be thinner and more

effective in diffusive transport. At term, during the third stage of labour,

15

uterine contractions cause separation of the placenta in four consecutive

phases:

1. Latent (wall in the placental site remains thin while placenta-free

wall is thick),

2. Contraction (thickening of wall in the placenta-site),

3. Detachment (actual detachment of the placenta from the adjacent

uterine wall),

4. Expulsion (sliding of the placenta out of the uterine cavity). This

process starts frequently from the lower pole of the placenta and

goes on successively upwards in the uterine cavity.

16

ABRUPTIO PLACENTAE

Placental abruption is a main obstetric complication and an major

cause of both maternal and perinatal morbidity and mortality, with an

incidence of 5.9 to 6.5 per 1000 singleton births and 12.2 per 1000 twin

births18

, Placental abruption has been reported in approximately 1% of all

pregnancies. Bleeding with placental abruption is usually maternal, although

the placental disc disruption with secondary bleeding from villous vessels

can occur. The maternal mortality rate is approximately 1%, primarily

caused by severe hemorrhage and its complications like disseminated

intravascular coagulation (DIC) and renal failure. The perinatal mortality

rate is high, ranging from 4.4% to 6.7% depending on accessibility to

neonatal care facilities and gestational age. Although neonatal outcomes

have improved because of advanced medical management in neonatal care,

surviving children still have an increased risk of long-term complications,

most significantly neurologic impairment.

PLACENTAL ABRUPTION: Clinical diagnosis of complete or partial

detachment of normally implanted placenta from the uterine wall prior to

delivery. Word ‘abruptio’ means ‘rending asunder of placenta’ denotes

sudden accident19

.

17

Retroplacental hematoma:

Hemorrhage or blood clot between basal plate and uterine wall

Etiology

Rupture of decidual artery

impaired placentation

acute or chronic inflammation

CLINICAL ISSUES

Epidemiology

Incidence

Abruption affects - 1% of unselected pregnancies as determined by

clinical recognition.

Incidence of 2-4% when including partial or small retroplacental

hematomas based on pathological examination.

Presentation

Clinical symptoms of abruption

In early stages, there may be no symptoms

Sudden onset of abdominal pain

Uterine tenderness

Uterus may be disproportionately enlarged

18

Painful rigid abdomen with tetanic uterine contraction20

(contractions which don’t stop and might follow one another so

quickly and seem continuous)

Vaginal bleeding

Pallor

Otherwise unexplained preterm birth

No reassuring fetal status (decreased fetal movement, worrisome fetal

heart rate)

Natural History

• Preterm delivery

• Progressive uterine enlargement with interstitial hemorrhage

(Couvelaire uterus)

• Poor uterine contractility with risk of postpartum hemorrhage and

disseminated intravascular coagulopathy

CLASSIFICATION (BASED ON SEVERITY)

CLASS 0: Asymptomatic. Diagnosis is done retrospectively by

noticing a depressed area on a delivered placenta or an organized blood clot.

CLASS 1 - Mild and denotes approximately 48% of all cases.

Characteristics include the following

- No vaginal bleeding to mild vaginal bleeding

- Slightly tender uterus

19

- Normal maternal BP and Heart rate

- No coagulopathy

- No fetal distress

CLASS 2 - Moderate and denotes approximately 27% of all cases.


- No vaginal bleeding to moderate vaginal bleeding

- Uterine tenderness will be moderate to severe along with

possible tetanic contractions

- Orthostatic alterations in BP and heart rate with maternal

tachycardia

- Fetal distress

- Hypofibrinogenemia (50 -250 mg/ dL)

CLASS 3 - Severe and represents approximately 24% of all cases.


- No vaginal bleeding to heavy vaginal bleeding

- Very painful tetanic uterus

- Maternal shock

- Hypofibrinogenemia (<150 mg/dL)

- Coagulopathy

- Fetal death

20

ULTRA SONOGRAPHIC CRITERIA FOR DIAGNOSIS OF

PLACENTAL ABRUPTION21

1. Preplacental collection under the chorionic plate (between the

placenta and amniotic fluid)

2. Jello-like movement of the chorionic plate with fetal activity.

3. Retroplacental collection

4. Marginal hematoma

5. Subchorionic hematoma

6. Increased heterogenous placental thickness (more than 5 cm in a

perpendicular plane)

7. Intra- amniotic hematoma

TYPES OF ABRUPTIO PLACENTA22

1. CONCEALED HAEMORRHAGE(20%)

- Bleeding is confined within the uterine cavity

- Separation may be complete

- Complications are often severe

- Coagulopathies, intrauterine deaths and perinatal deaths are

more likely.

2. EXTERNAL HEMORRHAGE (80%)

- Major form of abruptio placenta, blood comes out of cervix.

- Placental separation is usually incomplete

- Complications are less severe

21

3. RELATIVELY HEMORRHAGE

- Placental separation is usually incomplete and due to

intact membranes, the blood remains concealed.

- Occasionally the placental separation involves only the

rim of placenta. Here the most important complication is

the possibility of premature labour.

GRADES OF PLACENTALABRUPTION23

(BASED ON VOLUME OF

RETROPLACENTAL CLOT)

Grade 1:

Diagnosis of placental abruption is made retrospectively and the

retroplacental clot volume of approximately 150 ml, fetuses are usually not

at risk and favorable perinatal outcome occurs frequently. This is not

recognized clinically before delivery.

Grade 2:

Antepartum hemorrhage is accompanied by the classical features of

abruption and the fetus is alive, and the retroplacental clot volume is about

150-500 ml, 92% of those patient had abnormal fetal heart rate patterns and

perinatal mortality is high if the patient delivered vaginally.

22

Grade 3:

Incorporate the features of grade 2 but fetal demise is confirmed.

Grade 3a – without coagulopathy

Grade 3b – with coagulopathy

Risk Factors based on published studies

Maternal age (35 years or more, younger than 20 years)

Multiparity

Cigarette smoking (Maternal smoking is associated with up to 90%

increased risk, paternal smoking is also a risk factor, dose dependent

association24

)

Cocaine intoxication and drug abuse

Alcohol consumption

Hyperhomocysteinemia25

(strong indicator of folate and vitamin B12

deficiency)

The risk of adverse pregnancy outcome and venous thromboembolism

will be increased by inherited and acquired thrombophilia.

Infertility treatment

Prior abruption

Prior caesarean delivery

Habitual abortions

23

Multiple gestations

Hypertensive disorders (chronic hypertension with superimposed

preeclampsia increased the risk for placental abruption, most common

cause of abruption occurring in approximately 44% of all cases26

.)

Mild and severe preeclampsia

Chronic hypertension with preeclampsia

Sudden decompression of the uterus - Preterm Premature rupture of

membranes27

(PPROM before 37 weeks of gestation develop placental

abruption), delivery of first twin.

Prolonged rupture of membranes (> 24 hours)

Elevated second trimester maternal serum alpha-fetoprotein(AFP) –

associated with up to a tenfold increased risk of abruption28

.

Subchorionic hematoma

Oligohydramnios

Severe Chorioamnionitis

Short umbilical cord

Retroplacental fibromyoma

Diabetes

Low socioeconomic status

Dietary and nutritional deficiency

Male fetus

24

Trauma29

(motor vehicle collision, assault falls) (placental abruption

usually becomes manifest within 6-48 hours after trauma but can

occur up to 5 days later)

PATHOPHYSIOLOGY

An extreme anti-fetal immune response might be playing a major role

in the pathogenesis of abruptio placenta. In normal pregnancy, there is

upregulation of the humoral immune response and downregulation of the

cell-mediated immune response, that protects the pregnancy, where the

fetus signifies a semi-allograft. Syncytiotrophoblasts and Fetal villous

cytotrophoblasts normally express human leukocyte antigens (HLA)-G

and - E which could block the cytotoxic response of maternal natural killer

(NK) cells and thus enable the trophoblastic invasion into the maternal side

during early gestation. The soluble HLA-G levels have been shown to be

decreased strongly in placental abruption. In women with abruptio placenta,

there will be increased cell-mediated immunity with activated NK cells and

T helper-1 (TH1) lymphocytes, leading to abnormal trophoblast invasion

into the spiral arteries as well as unusually decreased levels of soluble

HLA-DR. This might be considered as an exaggerated fetal allograft

rejection.

In addition, significantly increased levels of anti-HLA antibodies have

been found in the circulation of patients with placental abruption. This

25

indicates the presence of an increased humoral immune response of the

mother against the semi-allogenic fetus and this is suggested to have a

pivotal role in the pathogenesis of abruptio placenta.

Hypertension, Trauma or coagulopathy leads to the destruction of

the anchoring placental villi from the expanding lower uterine segment, and

in turn, leads to bleeding in the decidua basalis near its interface with the

shelf of placental cytotrophoblast and anchoring villi. This could push the

placenta away from the uterus and cause more bleeding. The ruptured blood

vessels might be congenitally defective as a result of abnormal placentation

or damage occurred during pregnancy caused by hypoxia, under perfusion of

the uteroplacental circulation. Early placental damage is caused by leakage

of feto-maternal alpha-feto-protein during second trimester, low levels of

first trimester pregnancy associated plasma protein A (PAPP-A) and

elevated levels of beta human chorionic gonadotropin30

. Bleeding through

the vagina, called overt or external bleeding, occurs 80% of the time, though

sometimes the blood will pool behind the placenta, known as concealed or

internal placental abruption.

In smoking, increased homocysteine levels in plasma can induce

endothelial cell injury and dysfunction, leading to local thromboembolism

and defects within the placental vascular bed. Also, nicotine has

vasoconstrictive effects on uterine and umbilical arteries and

26

carboxyhemoglobin interfere with oxygenation. The hypoxic changes caused

by nicotine and carbon monoxide can lead to placental infarcts, suggesting

that increased capillary fragility might result in arterial rupture, leading to

placental abruption. Smokers also have lower concentrations of cellular

fibronectin which connects the trophoblasts to the uterine decidua31

.

The etiology of placental abruption remains speculative, acute and

chronic inflammatory processes had been proposed to cause placental

abruption by activating cytokines such as Interleukin-1 and Tumor Necrosis

Factor-α, these cytokines up regulate the production and activity of matrix

metalloproteinases in the trophoblast32

. The result is destruction of the

extracellular matrix and cell to cell interactions, which may lead to

disruption of the normal placental attachment and to premature separation of

the placenta.

MAJOR COMPLICATIONS OF ABRUPTIO PLACENTA

1. A large loss of blood - Hypovolemic shock – may require

blood transfusions.

2. A severe case of shock may affect other organs, such as

liver, kidney, and pituitary gland. Diffuse cortical necrosis in

the kidney is a serious and often fatal complication33

.

3. If the mother’s blood loss cannot be controlled, an

emergency hysterectomy may become necessary.

27

4. The uterus may not contract properly after delivery so the

mother may need medication to help her uterus to contract

5. Consumptive coagulopathy

6. Renal failure

7. Uterine apoplexy

8. Postpartum haemorrhage

9. Puerperal sepsis

10. Acute Cor-pulmonale

11. Transplacental haemorrhage

12. Transfusion hepatitis

13. Maternal mortality

14. Fetal mortality

FETAL RISKS

1. Intra uterine growth restriction (IUGR)

2. The baby may be born at a Low birth weight.

3. Preterm delivery (prior to 37 weeks of gestation)

4. The fetus may be deprived of oxygen and thus suffer from

Asphyxia.

5. Placental abruption may also result in fetal death, or

Stillbirth.

28

6. The newborn infant may have learning issues at later

developmental stages, often requiring professional

pedagogical aid.

7. Perinatal death

MACROSCOPIC FEATURES

General Features

Normal gross placental examination with isolated sudden acute

abruption

Compressed, nonadherent blood clot submitted with placenta

Placenta with fresh (intrapartum) hematoma

Soft, red clot loosely adherent to basal plate

Concavity or compression of overlying disc

Acute infarct of overlying parenchyma

Placenta with older hematoma

Firm, brown clot adherent to basal plate

Concavity or compression of overlying disc

Pale, firm infarct of overlying parenchyma

29

MICROSCOPIC PATHOLOGY

Histological Features

No alterations in cases of sudden, complete placental separation

Nonadherent blood clot

- Compressed and layered aggregate of red blood cells (RBCs) and

fibrin

- May contain portions of decidua

Placenta with fresh hematoma

Hematoma with predominance of RBCs and few fibrin strands

Dissecting haemorrhage through basal plate may be in direct

continuity with villi

Villous congestion &/or edema with intravillous stromal hemorrhage

Acute villous infarction

Acute inflammation in decidua basalis or admixed with hematoma

Placenta with older hematoma

Hematoma with degenerating RBCs and t fibrin

Basal plate necrosis with acute Inflammation

Hemosiderin-laden macrophages in later stages

Complete villous infarction with avascular and sclerotic stroma

30

Associated changes in maternal vessels of basal plate

Decidual vasculopathy

Thrombosis, fibrinoid necrosis, atherosis

Persistent vascular mural smooth muscle34

Venous thrombosis

Treatment

Expectant or aggressive obstetric management based on clinical

assessment

Transfusion as necessary for maternal &/or fetal haemorrhage

Prognosis

Fetal morbidity dependent on extent of lesion and gestational age

Risk of stillbirth with massive (> 50% of placental surface) abruption

at or near term

Maternal risk of abruption in subsequent pregnancy

CHRONIC ABRUPTION

Definition

Repetitive or persistent hemorrhage with associated placental

separation involving peripheral plate or membranes not associated with

imminent delivery35

.

31

CLINICAL ISSUES

Presentation

May be asymptomatic

Vaginal bleeding

Loss of fluid per vagina

Abdominal pain

False/threatened preterm labor

Evolving oligohydramnios

Premature rupture of membranes

Intrauterine fetal growth restriction

Intrauterine fetal death

Treatment

Increased fetal monitoring

Surveillance of amniotic fluid levels

Serial imaging for detection of resolution versus extension of lesion

Tocolytics and corticosteroids as appropriate for gestational age and

clinical parameters36

Elective delivery in cases of poor fetal growth or fetal distress

32

Prognosis

Larger volume of hematoma related to less favourable outcomes

Related to gestational age and fetal well-being

- Complications of prematurity, including chronic lung disease

- Risk of adverse neurodevelopmental outcome

60% develop chronic abruption-oligohydramnios sequence (CAOS)

IMAGE FINDINGS

Ultrasonographic Findings

Sonolucency at the site of hematoma/clot

Decreased amniotic fluid/oligohydramnios

MACROSCOPIC FEATURES

General Features

Degenerating blood clot ± more recent haemorrhage

Circumvallate membrane insertion with associated degenerating

marginal blood clot

Subchorionic clot

Less Common Features

Brown-green discoloration of fetal surface and membranes

Associated parenchymal lesions, including infarcts

33

MICROSCOPIC PATHOLOGY

Histological Features

Marginal or peripheral Subchorionic hematomas

- Expansion of peripheral corner of placental disc with displacement

of chorionic plate, peripheral membranes, or basal decidua by hematoma

Intermediate hematomas consist of laminated fibrin

Remote hematomas may be dissolved, appearing as lightly

eosinophilic granular or fibrillary material

Adjacent parenchyma is variably affected by increased perivillous

fibrinoid or villous infarction

Diffuse chorioamniotic hemosiderosis37

- Increased chorionic macrophages

- Accumulation of hemosiderin pigment in chorionic

plate and extraplacental membranes

Associated lesions

- Villous infarcts

- Regions of decidual necrosis

- Inflammatory infiltrate associated with hematoma

- Necrotizing chorioamnionitis

Yinka oyelese, MD; and cande V. Anand, PhD, MPH concluded that

placental abruption remains an important cause of perinatal mortality and

34

morbidity. Perinatal mortality is determined by the severity of the abruption

and the gestational age at which it occurs38

.

Minna tikkanen et al studied Finnish population and concluded that

placental abruption is rare in Finland but still an important cause of maternal

death39

.

Minna tikkanen studied the risk factors for placental abruption.

According to his study, abruption occurs more frequently in older women

(≥35 years), but usually this increase has been attributed to multiparity (three

or more deliveries) independent of age. Smoking has a dose dependent

association with placental abruption. Paternal smoking is also a risk factor

and doubles the risk. If both partners smoke, the risk is additive and nearly

fivefold. Chronic hypertension with superimposed preeclampsia increased

risk for placental abruption 2.8 to 7.7fold. Both hyperhomocysteinemia and

thrombophilia increases the risk of placental abruption 3 to 7fold.

Chorioamnionitis was strongly associated with placental abruption in both

term and preterm pregnancies. Cesarean first delivery increases the risk of

placental abruption by 30-40% in the next pregnancy compared with women

having a vaginal first delivery. If the interpregnancy interval is less than a

year, the risk of abruption is increased by 52% in women with vaginal first

delivery and by 111% in women with Caesarean first delivery. Other

pregnancy related risk factors for placental abruption include placenta

35

previa, bleeding during pregnancy, multiple pregnancy, alcohol and cocaine

use. The detection of Subchorionic or retroplacental hematoma in the first

trimester by ultrasound examination increases the risk for subsequent

placental abruption six to eleven fold. In conclusion, the placental abruption

is a complex disease. Even though placental abruption is relatively rare, the

consequences may be severe to the mother and fetus alike. Despite research,

placental abruption is still the ‘big unknown’40

.

Denise A.Elsasser, MPH et al, concludes that,

(1) The concordance between the clinical and pathological diagnosis

of placental abruption is poor.

(2) clinical diagnosis for abruption should include retroplacental clot,

sonographic visualization of abruption, painful vaginal bleeding

accompanied by nonreassuring fetal status or uterine

hypertonicity.

(3) Vast majority of placental abruption cases appears to have a long

standing chronic etiology.

These findings may serve important roles in the diagnosis and

appropriate clinical management of women diagnosed with placental

abruption41

.

36

Gali Pariente et al studied about the critical analysis of risk factors

and perinatal outcomes, in their study placental abruption was significantly

more common among preterm deliveries. At preterm pregnancies, acute

inflammation associated conditions are more common. Indeed Nathan et al

confirmed the association of histologic chorioamnionitis with placental

abruption in both preterm and term pregnancies. In this study maternal sepsis

and PROM were significantly very common in pregnancies with placental

abruption, reflecting conditions associated with acute inflammation42

. Small

for gestational age and hypertensive disorders, reflecting chronic processes

associated with vascular dysfunction, were found to be in strong association

with placental abruption, according to the literature, Ananth et al has

postulated that there are acute and more often chronic disease processes

reflected in the known associated risk factors for placental abruption. They

concluded that placental abruption is an independent risk factor for perinatal

mortality. Since the incidence of placental abruption has increased during the

last decade, risk factors should be carefully evaluated in an attempt to

improve surveillance and outcome43

.

Miami A.Ali, Thaeer Jawad studied the correlation between the

clinical diagnosis and histopathological findings of placental abruption.

According to this study, a common presentation of placental abruption is

with mild vaginal bleeding, no uterine tenderness and no coagulopathy,

37

usually occurring in the last 4weeks of gestation. Preterm placental abruption

is significantly associated with histological diagnosis of chorioamnionitis.

Lockwood et al in 2005 explained this as neutrophils are a rich source of

proteases that can degrade extracellular matrix. Compared to control cases,

placentas of pregnancies complicated by placental abruption are frequently

observed with acute and chronic histological lesions. This may support the

hypothesis that placental abruption is the result of an acute event or a chronic

inflammation and vascular dysfunction44

.

MATERIALS AND METHODS

38

MATERIALS AND METHODS

DESIGN/METHODOLOGY

STUDY POPULATION : Women with clinical diagnosis of abruptio

Placenta attending Coimbatore medical

College hospital.

STUDY DESIGN : Prospective case control study

SAMPLE SIZE : Totally 100 pregnancy cases

50 cases (abruptio placenta)

50 control

DURATION OF STUDY : One and Half years

Prospective case control study was conducted on 100 pregnant women

attending the Obstetrics & Gynaecology Department of Government

Coimbatore Medical College and Hospital, over a period of one and half

years from January 2017 to June 2018. The study was approved by the local

Medical Research Ethics Committee, Government Coimbatore Medical

College and Hospital. Written, understandable, Informed consent was

obtained from all the participants before enrolling in the study. The study

included 50 singleton pregnant women with clinical diagnosis of placental

abruption compared to 50 consecutive normal pregnancies. All were

attending the labour ward. Their gestational age ranged from 24 to 40 weeks

calculated from the last menstural period or early ultrasound.

39

INCLUSION CRITERIA:

All the patients with signs and symptoms of abruptio placenta.

Caesarean section and normal delivery included.

Booked and immunized cases.

Primi gravida and Multi gravida with and without Intra Uterine death.

Women with a confirmed or suspected clinical diagnosis of placental

abruption were eligible for recruitment as potential cases. Placental

abruption cases, or women suspected to have experienced an abruption by

the delivering physician, were regarded as true cases if they satisfied at least

one of the following 3 specific clinical criteria45

.

(1) Patients presenting with clinical signs of painful vaginal

bleeding accompanied by at least one of the following: nonreassuring fetal

status, severe abdominal pain, tetanic uterine contractions, or uterine

hypertonicity.

(2) The freshly delivered placenta showing evidence of clinically

significant retroplacental bleeding or clots, or

(3) Placental abruption diagnosed on prenatal ultrasound67

.

40

EXCLUSION CRITERIA:

Cases with type 2 diabetes mellitus/systemic hypertension.

Cases with Seropositivity

Cases with TORCH infection

Cases with bronchial asthma/COPD

Cases with history of treatment for primary infertility

Abruptio placenta patients ending in maternal death.

Vaginal bleeding was categorized as those who presented with

bleeding upon admission to the hospital, had episodes of bleeding

immediately prior to the onset of labour, or had excessive bleeding during

labour. Nonreassuring fetal status was classified when either bradycardia or

tachycardia was documented, a charted steep decrease in fetal heart rate was

seen on tracings, or otherwise documented by phycisian46

. Bradycardia

defined as baseline heart rate less than 110 and tachycardia defined as

baseline heart rate greater than 160 beats per minute.

Women with pregnancies that were not complicated by placental

abruption were enlisted as controls, and were compared to abruption cases.

Control cases were identified in the absence of the following:

(1) Any clinical documentation of abruption,

(2) Presence of medical illnesses such as Diabetes Mellitus and

hypertensive disorders,

41

(3) Presences of PROM,

(4) Multiple pregnancies,

(5) In cases or controls, women who are diagnosed as placenta previa.

Full history which includes medical, surgical, gynaecological

and obstetrical, social histories were taken. For all cases and controls, both

general & obstetrical clinical examination were done. All the placentas

(cases & controls) were embedded in 10% neutral buffered formalin and

allowed to fix for 24 hours.

Optimal sampling techniques included 3 placental sections, one with

2 sections of umbilical cord and a roll of extraplacental membranes, one

section each of fetal and maternal surfaces. When gross lesions were

identified, additional sections, up to 3 were made. Then the sections were

subjected to tissue processing, section cutting and Haematoxylin & Eosin

staining.

STAGES OF TISSUE PROCESSING:

(1) FIXATION – stabilizes and hardens tissue with minimal

distortion of cells.

(2) DEHYDRATION – removal of water and fixative from the

tissue.

(3) CLEARING – removal of dehydrating solutions, making the

tissue components receptive to the infiltrating medium.

42

(4) INFILTRATING – permeating the tissue with a support

medium.

(5) EMBEDDING – orienting the tissue sample in a support

medium and allowing it to solidify.

TISSUE PROCESSING SCHEDULE:

10% formalin – 4 hours

70% ethyl alcohol – 1 hour






Xylene – 1 hour

Xylene – 1 hour

Xylene – 1 hour

Paraffin – 1 hour

Paraffin – 1 hour

After proper processing, the paraffin blocks were made. Sectioning

was done with Microtome and slides were prepared. Then staining was done

with Ehrlich’s Haematoxylin and Eosin stain.

43

HEMATOXYLIN AND EOSIN STAINING:

Deparaffinisation – xylene 1 - 5 minutes

Xylene 2 - 5 minutes

90% alcohol - 5 minutes

70% alcohol - 5 minutes

Water wash - 10 minutes

Nuclear staining – Ehrlich’s Haematoxylin - 8 minutes


Differentiation with 1% acid alcohol - 1 dip


Bluing in tap water – 10 minutes

Cytoplasmic staining - 1% Eosin - 1 minute

Water - 1 dip

Xylene – mount

Gross examination of the placentas was performed in the fresh state.

Histopathological evaluation included both gross and microscopic findings

of the placenta, umbilical cord, and membranes. A diagnosis of placental

abruption was made by the macroscopic and microscopic examination of the

placenta. Macroscopic evidence of abruption included retroplacental

haemorrhage, indentation or hematoma with or without recent or old

infarctions. On microscopic examination, we looked for villous infarctions

associated with decidual destruction, haemorrhage and adjacent increased

syncytiotrophoblastic knotting. In cases of older abruption (i.e., a few days

44

duration) a search for foci of villous compression due to hematoma and

evidence of bleeding of 2–3 days duration such as pigmented histiocytes

(hemosiderin-laden macrophages), was also performed. It is observed that in

old and small abruptions, the only observations may be minor colour

changes and infarcts. Although approximate estimates can be given

regarding the age of retroplacental clots, exact figures cannot be given.

Villous oedema, although a fairly nonspecific change, is a consistent finding

in cases of placental abruption. Due the nonspecific nature of this histologic

finding, we did not score villous edema47,48

.

Histological lesions evidence from previous studies collectively

suggests that placental abruption is the manifestation of clinical events that

likely have at least 2 distinct causative pathways:

(1) Acute inflammation–associated conditions and

(2) Chronic processes including vascular dysfunction and chronic

inflammation.

Acute histologic lesions included chorioamnionitis, acute deciduitis,

funisitis, villous edema, villous stromal haemorrhage, and meconium stained

membranes associated with amnion necrosis and pigmented macrophages.

Chorioamnionitis was defined by the presence of inflammatory infiltrates of

neutrophils at two or more sites on the chorionic plate and extra-placental

membranes. It was classified into one of four grades: none, mild, moderate

and severe.

45

(1) Mild chorioamnionitis - the presence of few scattered neutrophils

(5–10/high power field) in the Subchorionic space and adjacent

chorion.

(2) Moderate chorioamnionitis- many neutrophils (11–30/high power

field) in the lower half of the chorionic plate.

(3) Severe chorioamnionitis- dense infiltrates of neutrophils

(>30/high power field) throughout the chorionic plate into the

amnion.

Funisitis was defined when neutrophils infiltrated the umbilical cord

stroma (Wharton’s jelly). Villous stromal haemorrhage was identified if

there were erythrocytes within the stroma of chorionic villi49,50

.

Chronic lesions included chronic deciduitis (lymphocytes with or

without plasma cells), maternal floor decidual necrosis, villitis, decidual

vasculopathy (specifically, in the vessels of the extraplacental membrane

roll), placental infarction, intervillous thrombosis, villous maldevelopment,

and hemosiderin deposition. Villous mal-development included the findings

of delayed maturation (increased villous size, increase in stromal cells and

decreased syncytial knotting) and accelerated villous maturation (small and

slender villi with reduced branching, and increased syncytial knotting).

Decidual vasculopathy comprised of muscular thickening, decidual

thrombosis or atherosis occurring within the vessels contained in the

extraplacental membrane roll51

.

OBSERVATION AND RESULTS

46

RESULTS AND OBSERVATION

Table 1: Age Distribution among Cases and Controls

Age Cases

( n=50)

Controls

(n= 50)

15- 20 years 6(54.5%) 5(45.5%)

21-25 years 13(48.1%) 14(51.9%)

26-30 years 17(50.0%) 17(50.0%)

31-35 years 12(50.0%) 12(50.0%)

36-40 years 2(50.0%) 2(50.0%)

Total 50(100%) 50(100%)

CHART 1: Age Distribution among Cases and Controls

15-20 21-25 26-30 31-35 36-40

Years

In present study, the common age group (50%) of occurrence of

placental abruption was 26-30 years.

0

2

4

6

8

10

12

14

16

18

6

13

17

12

2

5

14

17

12

2

Age Distribution

Cases

Controls

47

Table 2:Mean age

GROUPS N Mean Std.

Deviation

AGE

Cases 50 27.22 5.68

Control 50 27.34 5.50

CHART 2: Mean age

In present study, the mean age of occurrence of placental abruption

was 27.2. Median age was 27 years. The youngest age was 16 years and the

oldest age was 37 years.

27.16

27.18

27.2

27.22

27.24

27.26

27.28

27.3

27.32

27.34

Cases Control

27.22

27.34

Mean age

2727

Median Age

Cases Control

48

Table 3: Correlation of Clinical features among cases and control

Clinical features Cases Controls

Acute onset of abdominal pain 100(100.0%) 0(0.0%)

Vaginal bleeding 50(100.0%) 0(0.0%)

Uterine tenderness 46(92.0%) 0(0.0%)

Retroplacental hemorrhage 50(100.0%) 0(0.0%)

Meconium stained membrane 39(78.0%) 0(0.0%)

CHART 3: Correlation of Clinical features among cases and control

In present study, acute onset of abdominal pain, vaginal bleeding

and retroplacental haemorrhage were the predominant clinical features

(100%) followed by uterine tenderness (92%), and meconium stained

membranes (78%).

0102030405060708090

100

Acu

te o

nse

t o

f

abd

om

inal

pai

n

Vag

inal

ble

edin

g

Ute

rine

tend

ernes

s

Ret

rop

lace

nta

l

hem

orr

hag

e

Mec

oniu

m s

tain

ed

mem

bra

ne

100

50 46 5039

0 0 0 0 0

Clinical features

Cases Controls

49

Table 4: - Histopathological features of Acute abruption in the study

Histopathological features of acute

abruption

Cases Controls

Funisitis 20(40%) 1(2.0%)

Intervillous haemorrhage 50(100.0%) 0(0.0%)

Intravillous haemorrhage 50(100.0%) 0(0.0%)

Chorioamnionitis 43(86.0%) 3(6.0%)

Chorioamnionitis with haemorrhage 35(70.0%) 0(0.0%)

Acute deciduitis 20(40%) 0(0.0%)

Decidual hemorrhage 44(88%) 0(0.0%)

Increased syncytio trophoblastic

knotting

50(100.0%) 0(0.0%)

CHART 4: Histopathological features of Acute abruption in the study

In present study, intervillous haemorrhage, intravillous haemorrhage

and increased syncytiotrophoblastic knotting were the predominant (100%)

acute histological features, followed by decidual haemorrhage (88%), and

chorioamnionitis (86%).

01020304050

Funis

itis

inte

rvil

lous

hae

mo

rrhag

e

intr

avil

lous

hae

mo

rrhag

e

Cho

rio

amnio

nit

is

Cho

rio

amnio

nit

is

wit

h …

Acu

te d

ecid

uit

is

Dec

idual

hem

orr

hag

e

incr

ease

d

syncy

tio

tro

pho

bl

asti

c kno

ttin

g

20

50 5043

35

20

4450

1 0 0 3 0 0 0 0


abruption

Cases Controls

50

Table 5: Histopathological features of chronic abruption in the study

Histopathological features of chronic

abruption

Cases

Controls

Villitis 22(44.0%) 0(0.0%)

Villous infarction 17(34.0%) 0(0.0%)

Villous maldevelopment 22(44.0%) 0(0.0%)

Maternal floor decidual necrosis 22(44.0%) 0(0.0%)

Decidual vasculopathy 23(46.0%) 0(0.0%)

CHART 5: Histopathological features of chronic abruption in the study

In present study, Decidual vasculopathy was the predominant chronic

histological feature (46%) of placental abruption, followed by villitis (44%),

villous maldevelopment (44%), and Maternal floor decidual necrosis.

0

5

10

15

20

25

Vil

liti

s

Vil

lous

infa

rcti

on

Vil

lous

mal

dev

elo

pm

ent

Mat

ernal

flo

or

dec

idual

nec

rosi

s

Dec

idual

vas

culo

pat

hy

22

17

22 22 23

0 0 0 0 0


abruption

Cases Controls

51

Table 6: Expression of Histopathological features of acute abruption in

acute abruption cases and in Acute abruption with chronic features

cases

Acute abruption features

acute

abruption

(n=28cases )

Acute abruption with

chronic features

( n=22 cases )

Intervillous haemorrhage 28(56.0%) 22(44.0%)

Intravillous hemorrhage 28(56.0%) 22(44.0%)

chorioamnionitis 27(62.8%) 16(37.2%)

Chorioamnionitis with

haemorrhage

23(65.7%) 12(34.3%)

Acute deciduitis 17(85.0%) 19(63.3%)

Decidual haemorrhage 25(56.8%) 19(43.2%)

Increased syncytiotrophoblastic

knotting

28(56.0%) 22(44.0%)

CHART 6: Expression of Histopathological features of acute abruption

in acute abruption cases and in Acute abruption with chronic feature

cases

0

5

10

15

20

25

30

Funis

itis

Inte

rvil

lous

hae

mo

rrhag

e

Intr

avil

lous

hae

mo

rrhag

e

Cho

rio

amnio

nit

is

Cho

rio

amnio

nit

is w

ith

hae

mo

rrhag

e

Acu

te d

ecid

uit

is

Dec

idual

hem

orr

hag

e

28 28 2723

17

2528

22 22

1612

19 1922

Expression of Histopathological features of acute

abruption in acute abruption cases and in cases of

Acute abruption with chronic feature

Isolated acute abruption Acute abruption with chronic features

52

In present study, Acute deciduitis was the predominant

histopathological feature (85%) in acute abruption cases followed by

chorioamnionitis with haemorrhage (65.7%), and chorioamnionitis (62.8%).

Table 7: Statistics - Histopathological features of acute abruption

Histopathological features of

acute abruption

acute

abruption

Acute abruption

with chronic

features

P

value


haemorrhage

Yes 23(65.7%) 12(34.3%)

.035* No 5(33.3%) 10(67.7%)

Acute deciduitis Yes 17(85.0%) 3(15.0%)

.000* No 11(36.7%) 19(63.3%)

Decidual Haemorrhage Yes 25(56.8%) 19(43.2%)

.752 No 3(50.0%) 3(50.0%)

Increased

syncytiotrophoblastic

knotting

Yes 28(56.0%) 22(44.0%)

NA No 0(0.0%) 0(0.0%)

*-Statistically significant (p<0.05)

CHART 7: Statistics - Histopathological features of acute abruption

In present study, chorioamnionitis with haemorrhage was present in 23

cases (65.7%) of isolated placental abruption. By applying Chi-square test, P

23

5

17

11

25

3

28

0

12 10

3

19 19

3

22

005

1015202530

Yes No Yes No Yes No Yes No


haemorrhage

Acute deciduitis Decidual Haemorrhage Increased


knotting

Histopathological features of acute abruption

acute abruption Acute abruption with chronic features

53

value is 0.035 which is Statistically significant (p<0.05). Thus, it indicates

that chorioamnionitis with haemorrhage was a significant feature of acute

abruption.

Acute deciduitis was present in 17 cases (85%) of acute placental

abruption. By applying Chi-square test, P value is 0.00 which is Statistically

significant (p<0.05). Thus, it indicates that Acute deciduitis was a feature of

acute abruption.

Table 8: Expression of Histopathological features of chronic abruption

in acute abruption cases and in cases of Acute abruption with chronic

features


chronic abruption

acute

abruption

(n=28 cases)

Acute abruption with

chronic features

( n=22 cases )

Placental infarction 0(0%) 22(100%)

Villitis 0(0%) 22(100%)

Villous infarction 0(0%) 17(100%)

Villous maldevelopment 0(0%) 22(100%)

Maternal floor decidual necrosis 0(0%) 22(100%)

Decidual vasculopathy 1(4.3%) 22(100%)

54

CHART 8: Expression of Histopathological features of chronic

abruption in acute abruption cases and in cases of acute abruption with

chronic features

In present study, all the features of chronic abruption were present

in all the cases of acute abruption with chronic features.

0 0 0 0 0 1

22 22

17

22 22 22

0

5

10

15

20

25

Pla

centa

l in

farc

tio

n

Vil

liti

s

Vil

lous

infa

rcti

on

Vil

lous

mal

dev

elo

pm

ent

Mat

ernal

flo

or

dec

idual

nec

rosi

s

Dec

idual

vas

culo

pat

hy

Histopathological correlation between

acute abruption and Acute abruption with

chronic features


55

Table 9: Statistics - Histopathological features of chronic abruption


chronic abruption

acute

abruption

Acute abruption

with chronic

features

P

value

Placental infarction Yes 0(0.0%) 22(100.0%)

.000* No 28(100.0%) 0(0.0%)

Villitis

Yes 0(0.0%) 22(100.0%) .000*

No 28(100.0%) 0(0.0%)

Villous Infarction

Yes 0(0.0%) 17(100.0%)

.000* No 28(84.8%) 5(15.2%)

Villous maldevelopment

Yes 28(56.0%) 22(44.0%)

.000* No 0(0.0%) 0(0.0%)

Maternal floor decidual

necrosis

Yes 0(0.0%) 22(44.0%) .000*

No 28(100.0%) 0(0.0%)

Decidual vasculopathy Yes 1(4.3%) 0(0.0%)

.000* No 27(100.0%) 22(95.7%)


56

CHART 9: Statistics - Histopathological features of chronic abruption

In present study, placental infarction was present in 22 cases (100%)

of acute placental abruption with chronic features. By applying Chi-square

test, P value is 0.000 which is statistically significant (p<0.05). Villitis was

present in 22 cases (100%) of acute placental abruption with chronic

features. By applying Chi-square test, P value is 0.000 which is statistically

significant (p<0.05). Villous Infarction was present in 17 cases (100%) of

0

28

0

28

0

28

28

0

0

28

1

27

22

0

22

0

17

5

22

0

22

0

0

22

0 5 10 15 20 25 30

Yes

No

Yes

No

Yes

No

Yes

No

Yes

No

Yes

No P

lace

nta

l in

farc

tion

Vil

liti

sV

illo

us

Infa

rcti

on

Vil

lou

s

mal

dev

el

op

men

t

Mat

ern

al f

loor

dec

idu

al n

ecro

sis

Dec

idu

al

vas

culo

pat

hy

Acute abruption with chronic features acute abruption

57

acute placental abruption with chronic features. By applying Chi-square test,

P value is 0.000 which is statistically significant (p<0.05). Villous

maldevelopment was present in 22 cases (100%) of acute placental

abruption with chronic features. By applying Chi-square test, P value is

0.000 which is statistically significant (p<0.05). Maternal floor decidual

necrosis was present in 22 cases (100%) of acute placental abruption with

chronic features. By applying Chi-square test, P value is 0.000 which is

statistically significant (p<0.05). Decidual vasculopathy was present in 22

cases (95.7%) of acute placental abruption with chronic features. By

applying Chi-square test, P value is 0.000 which is statistically significant

(p<0.05).

Thus, the overall picture of placental infarction, villitis, villous

maldevelopment, maternal floor decidual necrosis and decidual vasculopathy

were significant features of acute abruption with chronic features cases.

58

Table 10: Association of Paternal Smoking with cases of acute abruption

and acute abruption with chronic features

Paternal

smoking acute abruption

Acute abruption

with chronic

features

P

value

Present 4(15.4%) 22(84.6%) .000*

Absent 24(100.0%) 0(0.0%)


CHART 10: Association of Paternal Smoking with cases of acute

abruption and cases of acute abruption with chronic features

In present study, paternal smoking was present in 4 cases (15.4%) of

isolated acute abruption whereas it was present in 22 cases (84.6%) of acute

abruption with chronic features. By applying Chi-square test, P value is

4

22

24

00

5

10

15

20

25

30


Present Absent

59

0.000 which is statistically significant (p<0.05). Thus paternal smoking can

be considered as a significant independent risk factor associated with acute

abruption with chronic features.

Table 11: Gender Distribution of Children in Placental Abruption

Gender Male Female P value

Abruption cases

(total=50)

30(60.0%) 20(40.0%)

.000*

Control

(total=50)

30(60.0%) 20(40.0%)


CHART 11: Gender Distribution of Children in Placental Abruption

0

5

10

15

20

25

30

Male Female

30

20

30

20

Gender distribution of children in cases

and controls

Cases Controls

60

In present study, both the cases and controls had 30 male babies and

20 female babies. By applying Chi-square test, P value is 0.000 which is

statistically significant (p<0.05). Thus, there was a significant association

between incidence of placental abruption and male babies.

Table 12: Status of Children in Placental Abruption

Status of child male female P value

Alive 4(19.0%) 17(81.0%)

.000* Intra uterine death 26(89.7%) 3(10.3%)


CHART 12: Status of Children in Placental Abruption

In present study, among the 50 placental abruption cases, 26 male

babies (89.7%) had undergone intrauterine death. By applying Chi-square

0

5

10

15

20

25

30

Male Female

4

17

26

3

Fetal outcome in Placental Abruption

Alive IUD

61

test, P value is 0.000 which is statistically significant (p<0.05). Thus, there

was a significant association between placental abruption and intrauterine

death of male babies.

Table 13; Correlation between chorioamnionitis and preterm deliveries

among placental abruption

CHART 13: Correlation between chorioamnionitis and preterm

deliveries among placental abruption

01020304050

Yes No

Preterm deliveries -

42

16

1

Correlation between chorioamnionitis and

preterm deliveries among placental

abruption

chorioamnionitis Yes chorioamnionitis No

Chorioamnionitis Vs

preterm deliveries

Preterm deliveries

P value Yes No

chorioamnionitis

Yes 42(97.7%) 1(2.3%)

.134 No 6(85.7%) 1(14.3%)

62

In present study, 42 placental abruption cases which had preterm

deliveries demonstrated histological features of chorioamnionitis. By

applying Chi-square test, P value is 0.134 which is not statistically

significant.

Table 14: Pregnancy Induced Hypertension

PIH

Cases

(total=50)

Controls

(total=50)

P value

Present 24(100.0%) 0(0.0%)

.000* Absent 26(34.2%) 50(65.8%)


CHART 14: Pregnancy Induced Hypertension

0

10

20

30

40

50

Cases Controls

24

0

26

50

Pregnancy induced hypertension in

placental abruption

Present Absent

63

In present study, 24 placental abruption cases (100%) were associated

with pregnancy induced hypertension. By applying Chi-square test, P value

is 0.000 which is statistically significant (p<0.05). Thus, Pregnancy Induced

Hypertension has a significant association with cases of placental abruption.

Table 15: Analysis of gravida between cases and control

Gravida Primi gravida Multi gravida P value

Cases 17(34%) 33(66%)

.000*

Control 17(34%) 33(66%)


CHART 15: Analysis of gravida between cases and control;

0

10

20

30

40

Primi gravida Multi gravida

17

33

17

33

Analysis of gravida between cases and

controls

Cases Controls

64

In present study, both the cases and controls had 17 primi gravida and

33 multi gravida. By applying Chi-square test, P value is 0.000 which is

statistically significant (p<0.05). Thus, Multi gravida pregnancies were

significantly associated with incidence of placental abruption.

Table 16: Histopathological features of acute abruption in Primi


Histopathological features

of acute abruption

Multi gravida

(33 cases)

Primi gravida

( 17 cases)

P value

Funisitis 12(60.0%) 8(40.0%) .465

Intervillous haemorrhage 33(66.0%) 17(34.0%) NA

Intravillous haemorrhage 33(66.0%) 17(34.0%) NA

Chorioamnionitis 26(60.5%) 17(39.5%) .041


haemorrhage

18(51.4%) 17(48.6%) .001*

Acute deciduitis 3(15.0%) 17(85.0%) .000*

Decidual haemorrhage 27(61.4%) 17(38.6%) .061

Increased


knotting

33(66.0%) 17(34.0%) NA


65

CHART 16: Histopathological features of acute abruption in Primi


In present study, chorioamnionitis with haemorrhage was present in

17 cases (48.6%) of placental abruption in primi gravida. By applying Chi-

square test, P value is 0.001 which is statistically significant (p<0.05).

Acute deciduitis was present in 17 cases (85%) of placental

abruption in primi gravida. By applying Chi-square test, P value is 0.000

which is statistically significant (p<0.05). Thus, chorioamnionitis with

haemorrhage and acute deciduitis were significantly associated with

placental abruption in primi gravida.

0

5

10

15

20

25

30

35

Funis

itis

Inte

rvil

lous

hae

mo

rrhag

e

Intr

avil

lous

hae

mo

rrhag

e

Cho

rio

amnio

nit

is

Cho

rio

amnio

nit

is w

ith

hae

mo

rrhag

e

Acu

te d

ecid

uit

is

Dec

idual

hem

orr

hag

e

Incr

ease

d

syncy

tio

tro

pho

bla

stic

kno

ttin

g

12

33 33

26

18

3

27

33

8

17 17 17 17 17 17 17


abruption in primi and multi gravida

Multi gravida Primi gravida

66

Table 17: Histopathological features of chronic abruption in primi

gravida and multi gravida

Histopathological

features of chronic

abruption

Multi gravida

(33 cases)

Primi gravida

( 17 cases)

P value

Placental infarction 21(95.0%) 1(4.5%) .000*

Villitis 21(95.0%) 1(4.5%) .000*

Villous infarction 16(94.1%) 1(5.9%) .003*

Villous maldevelopment 21(95.0%) 1(4.5%) .000*

Maternal floor decidual

necrosis

21(95.0%) 1(4.5%) .000*

Decidual vasculopathy 22(95.7%) 1(4.3%) .000*


67

CHART 17: Histopathological features of chronic abruption in primi

gravida and multi gravida

In present study, placental infarction, villitis, villous maldevelopment,

and maternal floor decidual necrosis were present in 21 cases (95%) of

placental abruption in Multi gravida. By applying Chi-square test, P value is

0.000 which is statistically significant (p<0.05). Thus, placental infarction,

villitis, villous maldevelopment, and maternal floor decidual necrosis were

0

5

10

15

20

25

Pla

centa

l in

farc

tio

n

Vil

liti

s

Vil

lous

infa

rcti

on

Vil

lous

mal

dev

elo

pm

ent

Mat

ernal

flo

or

dec

idual

nec

rosi

s

Dec

idual

vas

culo

pat

hy

21 21

16

21 2122

1 1 1 1 1 1


abruption in primi and multi gravida

Multi gravida Primi gravida

68

significantly associated with placental abruption in multi gravida. These

were the features of acute abruption with chronic features.

Villous infarction was present in 16 cases (94.1%) of placental

abruption in Multi gravida. By applying Chi-square test, P value is 0.003

which is statistically significant (p<0.05). Thus, villous infarction was a

significant feature of placental abruption in multi gravida which was a

feature associated with acute abruption with chronic features.

COLOUR PLATES

COLOUR PLATES

FIGURE 1: GROSS; PLACENTAL ABRUPTION

Dilated Tortuous Vessels Over The Membranes

FIGURE 2: GROSS; PLACENTAL ABRUPTION

Maternal Surface- Indentation and Hemorrhagic Areas

(A – Hemorrhagic), (B- Indentation)

FIGURE 3: GROSS- PLACENTAL ABRUPTION

RETROPLACENTAL BLOOD CLOT WITH VESSEL THROMBUS

(A-Retro placental Blood Clot), (B-Vessel Thrombus)

FIGURE 4: GROSS – PLACENTAL ABRUPTION

PLACENTAL INFARCTION WITH CONGESTION

(A- Placental Infarction), (B-Grey Necrotic Areas)

FIGURE 5: GROSS- PLACENTAL ABRUPTION

RETROPLACENTAL HEMORRHAGE

FIGURE 6: MICROSCOPY- PLACENTAL ABRUPTION

FUNISITIS

(H&E STAIN - 400X)


SQUAMOUS MATAPLASIA WITH MODERATE CHORIOAMNIONITIS

(H&E STAIN – 400 X)


SQUAMOUS MATAPLASIA WITH MODERATE CHORIOAMNIONITIS



MILD CHORIOAMNIONITIS


FIGURE 10 : MICROSCOPY- PLACENTAL ABRUPTION

MODERATE CHORIOAMNIONITIS


FIGURE 11: MICROSCOPY - PLACENTAL ABRUPTION

SEVERE CHORIOAMNIONITIS



MODERATE CHORIOAMNIONITIS WITH HAEMORRHAGE


(A- Moderate Chorioamnionitis), (B- Haemorrhage Area)


ACUTE DECIDUITIS WITH FIBRINOID NECROSIS


(A-Acute Deciduitis), (B- Layering Of Fibrinoid Necrosis)


INTERVILLOUS HAEMORRHAGE



INTERVILLOUS AND INTRAVILLOUS

HAEMORRHAGE



INTRAVILLOUS HAEMORRHAGE AND ADJACENT AREA OF ACUTE

DECIDUITIS WITH HAEMORRHAGE


(A- Haemorrhage),(B- Acute Deciduitis),(C- Initra Villous Haemorrhage)


INTERVILLOUS HAEMORRHAGE AND ACUTE DECIDUITIS


(A-Acute Deciduitis),(B- Intervillous Haemorrhage)


INTERVILLOUS HAEMORRHAGE WITH VILLOUS INFARCTION


(A- Intervillous Haemorrhage),(B-Villous Infarction)


VILLOUS HAEMORRHAGE WITH LARGE AREA OF HAEMORRHAGE


(A- Villous Haemorrhage),(B- Large Area Of Haemorrhage)


MODERATE CHORIOAMNIONITIS WITH ADJACENT AREA OF HEMORRHAGE


(A- Moderate Chorioamnionitis),(B- Hemorrhage Area)


INCREASED SYNCYTIOTROPHOBLASTIC KNOTTING



INCREASED SYNCYTIOTROPHOBLASTIC KNOTTING WITH MULTINUCLEATED

GIANT CELL


(A- Increased Syncytiotrophoblastic Knotting),(B- Multinucleated Giant Cell)


VASCULOPATHY (VESSELS WITH MARGINAL HEMATOMA)



VESSEL WITH THICK MUSCULAR CUFFING AND ADJACENT MARGINAL

HEMATOMA



VESSEL WITH THROMBUS AND VILLOUS INFARCTION


69

DISCUSSION

The incidence of Abruptio placenta in Coimbatore Medical College

hospital is 40 cases per year. In this study, we have collected placentas from

50 consecutive clinically diagnosed cases of placental abruption attending

Coimbatore medical college hospital for the period of one and half years

(from January 2017 to June 2018). In the same period, we have collected

placentas from 50 consecutive normal deliveries as Control. Being a tertiary

health care centre, many of the placental abruption cases are referred from

Primary Health Centres and Taluk Government Hospitals around

Coimbatore including Nilgiris, Pollachi, Valparai, Dharapuram, Erode, and

Namakkal district. Among the 50 placental abruption cases, 43 cases were

referred from Primary Health Centres and Taluk Government Hospitals, 7

cases were attending the Government Coimbatore medical college itself.

In present study, clinical and histopathological features of placental

abruption were studied and compared with the normal placenta. In addition

to, the clinical and histopathological features of placental abruption in primi

gravida and multi gravida were compared.

70

AGE AND OBSTETRIC HISTORY

In Dr. Vaibhavi et al study, the most common age of occurrence was

20-30 years, only 20% of cases were primi gravida and, 80% were multi

gravida, denoting that the multiparity being a significant risk factor52

. In

Miami A.Ali, Thaeerjawad study, the common age group was 25-35 years.

In Minna Tikkanen study, placental abruption occurs most commonly in

women more than 35 years, but this was attributed to multiparity (≥3

deliveries) independent of age53

. Krohn M etal studied either increased

parity or maternal age increased the risk54

. In Baumann P et al study,

maternal age more than 35 years had high risk of abruption in primi gravida

but not among multi gravida. In many other studies, advancing maternal age

being an important independent risk factor. In few studies, patients less than

20 years of age have also been under the risk of placental abruption55

.

In present study, the most common age of occurrence was 26-30 years

accounting to 32% (16 cases). The age group between 21- 35 years

comprising 84% (42 cases) of placental abruption cases. Two patients were

more than 35 years, 6 patients were ≤20 years. One patient was 16 years old.

Mean age of occurrence of placental abruption was 27.2 years. Among the

50 placental abruption patients, 17 patients were primi gravida, 33 patients

were multi gravida. Among the multi gravida, 6 patients were grand multi

71

gravida (≥4 deliveries). This signifies the multiparity being the common risk

factor for placental abruption.

PATERNAL SMOKING

Minna Tikkanen et al studied that the paternal smoking was a major

risk factor for placental abruption and it doubles the risk. If both partners are

smokers, there will be fivefold increase in the risk of placental abruption.

Among women with previous history of abruption, there is increased risk of

abruption irrespective of the history of smoking56

. Kyrklund-Blomberg et al

studied that the maternal smoking had the dose dependent increase in the risk

of placental abruption57

. In present study, there was no history of maternal

smoking among the cases. But 26 cases had history of paternal smoking

which was accounting for 52% of placental abruption. In acute abruption,

paternal smoking was present in 4 cases (15.4%), whereas in acute abruption

with chronic features, 22 cases had history of paternal smoking (84.6%)

which is statistically significant (P<0.05). Thus, it signifies that paternal

smoking is a significant risk factor for acute abruption with chronic features

and in multi gravida.

In smoking, increased homocysteine levels in plasma could trigger

endothelial cell injury and functional abnormalities, causing local

thromboembolism and abnormal changes within the placental vascular bed.

Also, carboxyhemoglobin interferes with oxygenation, and nicotine has

72

effects of vasoconstriction on uterine and umbilical arteries. The hypoxic

changes developed by nicotine and carbon monoxide could cause placental

infarcts, signifying that capillary fragility is increased and it might result in

arterial rupture, leading to placental abruption58

. Cellular fibronectin levels

are low in smokers which attaches the trophoblasts to the uterine decidua.

Smoking is also related to a dose-dependent increased risk of venous

thrombosis in connection with pregnancy.

ANAEMIA

In Vaibhavi et al study, 30 cases were associated with anaemia which

is accounting to 37.5% of placental abruption cases59

. In present study, 41

cases were associated with clinical findings of anaemia which was

accounting to 82% of placental abruption.

PREGNANCY INDUCED HYPERTENSION

In Vaibhavi et al study, 29 cases had pregnancy induced hypertension

which was accounting to 36.25% of placental abruption. Kramer MS et al

studied that transient hypertension in pregnancy and mild preeclampsia

complicated pregnancies had been associated with the increase in the risk of

placental abruption, even though severe preeclampsia is a strong and major

risk factor for abruptio placenta. In present study, 24 cases are associated

with the pregnancy induced hypertension which was contributing to 48% of

73

placental abruption cases which is statistically significant (P<0.05). Placental

abruption and pre-eclampsia might be sharing the same common aetiology

with failed placentation in early pregnancy. This could lead to the placental

dysfunction and further increases the risk of abruption of placenta in women

with pregnancy induced hypertension.

GESTATIONAL DIABETES MELLITUS

In Vaibhavi et al study, two patients had gestational diabetes which

was accounting to 2.5% of placental abruption. In this study, one patient had

gestational diabetes which was accounting to 2% of the placental abruption.

HYDRAMNIOS

In Vaibhavi et al study, 6 patients were found with hydramnios which

was accounting to 7.5% of the placental abruption cases. In present study,

one patient had hydramnios which was accounting to 2% of the placental

abruption cases.

PREMATURE RUPTURE OF MEMBRANE

In Vaibhavi et al study, 4 patients were associated with premature

rupture of membranes which was accounting to 5% of placental abruption

cases. In present study, 2 patients were associated with premature rupture of

membranes which was accounting to 4% of placental abruption. Usually

74

PROM precedes abruption, and sometimes abruption may cause PROM.

Placental abruption is usually associated with dense infiltration of

neutrophils in decidua which secretes more amount of proteases that could

destroy the cellular matrix, ultimately leads to PROM60

. It is very difficult to

fix whether decidual neutrophil infiltration is secondary to disruption of

vessels or whether it is the primary reason of abruption. Preterm premature

rupture of membrane is frequently associated with ascending intrauterine

infection.

CLINICAL FEATURES

Regarding the clinical features of placental abruption, Miami

A.Ali,Thaeerjawad studied that the most common clinical feature leading to

a diagnosis of placental abruption was retroplacental haemorrhage seen in 33

cases which was accounting to 76% of placental abruption, followed by

vaginal bleeding in 13 cases which was accounting to 26% of placental

abruption. Then uterine hypertonicity was found in 5 cases which was

accounting to 10% of placental abruption. In Vaibhavi et al study,

retroplacental haemorrhage was found in 76 cases which was accounting to

95.5% of placental abruption cases. In Present study, retroplacental

haemorrhage, vaginal bleeding, uterine tenderness and acute onset of

abdominal pain were found in all the 50 cases of placental abruption which

was accounting to 100% of placental abruption. Placental abruption cases are

75

graded by the amount of retroplacental haemorrhage, status of the child and

coagulopathy. Among the 50 patients, 5 patients were under grade 1

category which was accounting to 10% of placental abruption, 15 patients

were under grade 2 which was accounting to 30% of placental abruption, 28

patients were under grade 3a which was accounting to 56% of placental

abruption, 2 patients were under grade 3b which was accounting to 4 % of

placental abruption.

DISSEMINATED INTRAVASCULAR COAGULATION

In Vaibhavi et al study, 27 patients (33.7%) out of 80 patients

developed Disseminated intravascular coagulation. In present study, 2

patients were developed Disseminated intravascular coagulation which was

accounting to 4% of placental abruption. Placental abruption causes massive

bleeding which in turn leads to maternal hypovolemic shock. Blood loss

might be underestimated in abruption because of concealed haemorrhage

into the myometrium which is very difficult to measure. Then the

coagulation cascade is activated. When the detachment of placenta is large

enough to cause intrauterine death of fetus, the risk of getting disseminated

intravascular coagulation is much increased. Haemorrhage associated with

disseminated intravascular coagulation causing further consumption of

clotting factors, sets off a vicious cycle61

. In DIC, fibrinolysis and

coagulation results in extensive clotting and bleeding.

76

MODE OF DELIVERY

In Vaibhavi et al study, 54 patients (67.5%) had vaginal delivery and

26 patients (32.5%) had undergone Caesarean section. First caesarean

delivery increases the risk of abruptio placenta by 30-40% in the next

delivery compared with women who had a first normal vaginal delivery.

According to Finnish study, this risk was 2.4fold in primi gravida and 3.9

fold in multi gravida with first Caesarean delivery62

.

In present study, 4 patients (8%) had the vaginal delivery whereas

46 patients (92%) underwent emergency Caesarean section. Out of 50

placental abruption patients, 15 patients were found with the history of

previous caesarean delivery which was accounting to 30% of placental

abruption.

INTRAUTERINE DEATH

Regarding fetal outcome, Vaibhavi et al studied that 41 patients

(51.5%) had stillborn babies, 39 patients (48.75%) had alive babies. In

present study, 29 patients out of 50 had intrauterine death of fetus which

was accounting to 58% of placental abruption that suggests poor perinatal

outcome. 21 patients (42%) had alive babies. Among the 29 intrauterine

death, 26 patients had male baby (89.7%) which was statistically significant

(P<0.05), and 4 patients had female baby (13.8%). Among the 21 alive

77

babies, 17 babies were female (81%) and 4 babies were male (19%). Acute

placental separation cut off the oxygen supply and nourishment to the fetus,

so that the fetus frequently dies. The significance of male babies more prone

to intrauterine death is yet to be deciphered.

PRETERM DELIVERY

In Minna Tikkanen et al study, 40-60% of new born babies delivered

after placental abruption were preterm. In present study, among the 50

patients, 48 patients had preterm babies which was accounting to 96% of the

placental abruption. Only 2 patients (4%) had term babies. High perinatal

mortality could be explained by a strong association with preterm delivery.

In Ananth CV, Wilcox AJ study, even term babies with normal birth weight

have 25fold increase in mortality with placental abruption, compared with

term babies without abruption63

. In present study, 49 patients delivered

preterm babies which was accounting to 98% of placental abruption. The

risk to the fetus depends on the severity of placental abruption and the

gestational age at which the placental abruption occurs.

SECOND TRIMESTER FETAL LOSS

In Pelle G. Lindqvist, Catharina Happach study, Previous second

trimester and repeated fetal loss had a strong association with increased risk

of placental abruption, and second trimester fetal loss has a strong

78

connection with maternal thrombophilia64

. In present study, one patient of

placental abruption had a history of previous intrauterine death which

occurred in third trimester. This signifies that the previous second and third

trimester fetal loss has been identified as a major risk factor for subsequent

stillbirth.

HISTOPATHOLOGICAL FEATURES

ACUTE ABRUPTION

Regarding the histopathological features of acute abruption, In

Miami A.Ali, Thaeerjawad study, funisitis was found in 3 patients (20%),

chorionic villous haemorrhage was found in 8 patients (16%),

chorioamnionitis in 9 patients (18%), meconium stained membranes in 5

patients (6%), acute deciduitis in 1 patient (2%). In Denise A Elsasser MPH

et al study, 6.1% had funisitis, 53% had chorionic villous haemorrhage,

8.5% had acute deciduitis, 12.2% had meconium stained membranes, 97.8%

had at least one lesion65

.

In present study, funisitis was found in 20 patients (40%), intervillous and

intravilloushaemorrhage were found in all the 50 patients (100%),

chorioamnionitis with haemorrhage was found in 35 patients (70%), acute

deciduitis was found in 20 patients (40%), decidual haemorrhage was found

79

in 44 patients (88%), increased syncytiotrophoblastic knotting was found in

all the 50 patients (100%).

ACUTE ABRUPTION WITH CHRONIC FEATURES

Regarding the histopathological features of chronic abruption, In

Miami A.Ali, Thaeerjawad study, placental infarction was found in 9

patients (60%), villitis was found in 14 patients (93.3%), villous

maldevelopment was found in 14 patients (93.3%), maternal floor decidual

necrosis was found in 1 patient (6.7%), decidual vasculopathy was found in

6 patients (40%). In Denise A Elsasser MPH et al study, placental infarction

was found in 49% of patients, chronic deciduitis was found in 98% of

patients, decidual necrosis was found in 4.1% of patients, villous

maldevelopment was found in 80% of patients, decidual vasculopathy was

found in 30.6% of patients. In present study, villitis is found in 22 patients

(44%), villous infarction is found in 17 patients (34%), villous

maldevelopment is found in 22 patients (44%), maternal floor decidual

necrosis is fond in 22 patients (44%), and decidual vasculopathy is found in

23 patients (46%).

In present study, we didn’t get isolated chronic placental abruption

cases, instead we got cases of acute placental abruption with chronic

features. In 50 cases, 28 cases were acute placental abruption, 22 cases

were acute placental abruption with chronic features. When these two

80

categories were compared, Intervillous haemorrhage was found in 28 cases

(56%) of acute placental abruption, whereas it was found in 12 cases (44%)

of acute abruption with chronic features. Intravilloushaemorrhage was

found in 28 cases (44%) of placental abruption, whereas it was found in 22

cases of acute placental abruption with chronic features. Chorioamnionitis

was present in 27 cases (62.8%) of acute placental abruption, whereas it was

found in 16 cases (37.2%) of acute placental abruption with chronic features.

Chorioamnionitis with haemorrhage was found in 23 cases (65.7%) of

acute placental abruption which is statistically significant (P<0.05), whereas

it was found in 12 cases (34.3%) of acute abruption with chronic features.

Acute deciduitis was found in 17 cases (85%) of acute placental abruption

which is statistically significant (P<0.05), whereas it was found in 3 cases

(63.3%) of acute abruption with chronic features. Decidual haemorrhage

was found in 25 cases (56.8%) of placental abruption, whereas it was found

in 19 cases (43.2%) of acute abruption with chronic features. Increased

syncytiotrophoblastic knotting was found in 28 cases (56%) of placental

abruption, whereas it was found in 22 cases (44%) of acute abruption with

chronic features. Miami A.Ali, Thaeerjawad studied that a significant

connection exists between preterm placental abruption and chorioamnionitis.

In present study, 48 placental abruption cases associated with preterm

deliveries, among that 42 cases are found with the features of

chorioamnionitis which is statistically significant (P<0.05).

81

Placental infarction was not found in 28 cases of acute placental

abruption (0%), whereas it was found in all the 22 cases (100%) of acute

abruption with chronic features which is statistically significant (P<0.05).

Villitis was not found in 28 cases of acute placental abruption (0%), whereas

it was found in all the 22 cases (100%) of acute abruption with chronic

features which is statistically significant (P<0.05). Villous infarction was

not found in 28 cases of acute placental abruption (0%), whereas it was

found in 17 cases (77.3%) of acute abruption with chronic features which is

statistically significant (P<0.05). Villous maldevelopment was not found in

28 cases of acute placental abruption (0%), whereas it was found in all the

22 cases (100%) of acute abruption with chronic features which is

statistically significant (P<0.05). Maternal floor decidual necrosis was not

found in 28 cases of acute placental abruption (0%), whereas it was found in

all the 22 cases (100%) of acute abruption with chronic features which is

statistically significant (P<0.05). Decidual vasculopathy was found in one

case (4.3%) of acute placental abruption, whereas it was found in all the 22

cases (100%) of acute abruption with chronic features which is statistically

significant (P<0.05).

Bleeding at the decidual-placental interface causes abruption. Acute

vasospasm of the small blood vessels might be the event that precedes the

separation of placenta. Lack of adequate invasion of trophoblasts might be

82

the cause of early separation66

. A prospective study has found that at 20-24

weeks of gestation, notching changes in the Doppler waveform of the uterine

artery which is an important marker of impaired uteroplacental circulation,

had a strong association with placental abruption67

. Thus uteroplacental

insufficiency might be playing a critical role in the pathology of abruption.

The acute and chronic inflammatory processes are playing a major role in

causing placental abruption by triggering the activation of cytokines like

Interleukin-1 and Tumor necrosis factor- α. These cytokines are upregulating

the production and activity of trophoblast matrix metalloproteinases. This

leads to extracellular matrix destruction and loss of cell-cell interactions,

which might lead to interruption in the attachment of normal placenta which

leads to premature separation of placenta68

. Ananth et al studied that in cases

of placental abruption, acute inflammatory conditions are more common at

preterm than term pregnancies whereas chronic inflammatory processes are

present throughout the gestation69

.

Furthermore, in this study, we have compared the histopathological

features of placental abruption between primi and multi gravida. In 50 cases

of placental abruption, 17 cases were primi and 33 cases were multi gravida.

Funisitis was present in 8 cases of primi (47%) and 12 cases of multi gravida

(33.4%). Intervillous haemorrhagewas present in 17 cases of primi (100%)

and 33 cases of multi gravida (100%). Intravilloushaemorrhagewas present

83

in 17 cases of primi (100%) and 33 cases of multi gravida (100%).

Chorioamnionitis was present in 17 cases of primi (100%) and 33 cases of

multi gravida (100%). Chorioamnionitis with haemorrhage was present in

17 cases of primi (100%) and 18 cases of multi gravida (54.5%). Acute

deciduitis was present in 17 cases of primi (100%) and 3 cases of multi

gravida (9%). Increased syncytiotrophoblastic knottingwas present in 17

cases of primi (100%) and 33cases of multi gravida (100%). Placental

infarction was present in 1 case of primi (5.8%) and 21 cases of multi

gravida (63.6%). Villitis was present in 1 case of primi (5.8%) and 21 cases

of multi gravida (63.6%). Villous infarction was present in 1 case of primi

(5.8%) and 16 cases of multi gravida (48.5%). Villous malformation was

present in 1 case of primi (5.8%) and 21 cases of multi gravida (63.6%).

Maternal floor decidual necrosis was present in 1 case of primi (5.8%) and

21 cases of multi gravida (63.6%). Decidual vasculopathy was present in 1

case of primi (5.8%) and 22 cases of multi gravida (66.7%). This

comparative study showed that the features of acute placental abruption was

significantly seen in primi gravida when compare to multi gravida, even

though intervillous haemorrhage, intravilloushaemorrhage and increased

syncytiotrophoblastic knotting are seen in both primi and multi gravida. In

addition to that, the features of chronic placental abruption were

significantly seen in multi gravida.

84

In Seven cases of placental abruption, umbilical cord lining showed

squamous metaplasia. Four cases of placental abruption demonstrated

multinucleated giant cells in the decidua. Chronic deciduitis and

Hemosiderin-laden macrophages were not found in placental abruption cases

that we have studied.

One patient in placental abruption cases previously delivered

anomalous baby. One patient had multiple intramural fibroids which

undergone hysterectomy. No maternal death occurred in the placental

abruption cases that we have analysed.

SUMMARY

85

SUMMARY

The present study was a prospective study.

Aim of the study was to analyze the incidence and histomorphological

features of abruptio placenta in a tertiary health care centre, to compare

the histopathological features abruptio placenta with normal placenta and

to analyze the differences in histomorphology of abruptio placenta in

primigravida and multigravida patients.

The study period was 1 and half years from January 2017 to June 2018.

Our study consists of 50 clinically diagnosed cases of placental abruption

(cases) and 50 normal deliveries (control).

INCIDENCE - The incidence of Abruptio placenta in Coimbatore Medical

College Hospital was 35-40 cases per year.

REFERRED CASES - Among the 50 placental abruption cases, 43 cases

were referred cases.

AGE - The common age group of occurrence placental abruption in our

study was 26-30 years. The mean age of occurrence of placental abruption

was 27.2. The median age of occurrence was 27 years. The youngest age was

16 years and the oldest age was 37 years.

86

GRAVIDA - Among the 50 placental abruption cases, 17 cases were primi

gravida, 33 cases were multi gravida. Among the multi gravida, 6 cases were

grand multi gravida (≥4 deliveries).

PATERNAL SMOKING - In acute abruption, paternal smoking was

present in 4 cases, whereas in placental abruption with chronic features, 22

cases had history of paternal smoking which is statistically significant

(P<0.05). Thus, paternal smoking can be considered as a significant

independent risk factor associated with acute abruption with chronic

features.

ANAEMIA - 41 cases were associated with clinical findings of anaemia

which was accounting to 82% of placental abruption.

PREGNANCY INDUCED HYPERTENSION - 24 cases were associated


placental abruption cases which is statistically significant (P<0.05). Thus,

Pregnancy Induced Hypertension has a significant association with cases of


GESTATIONAL DIABETES MELLITUS - One case had gestational

diabetes which was accounting to 2% of the placental abruption.

HYDRAMNIOS - One case had hydramnios which was accounting to 2%

of the placental abruption cases.

87

PROM - 2 cases were associated with premature rupture of membranes


DIC - 2 cases were developed Disseminated intravascular coagulation which

was accounting to 4% of placental abruption.

MODE OF DELIVERY - Among the cases of placental abruption, 4 cases

had vaginal delivery whereas 46 cases underwent emergency Caesarean

section.

PREVIOUS CAESAREAN DELIVERY - Out of 50 placental abruption

cases, 15 cases were found with the history of previous caesarean delivery


INTRAUTERINE DEATH - 29 cases out of 50 had intrauterine death of

fetus. Among the 29 intrauterine death, 26 cases had male babies (89.7%)

which is statistically significant (P<0.05), and 4 cases had female baby

(13.8%). Thus, there was a significant association between placental

abruption and intrauterine death of male babies.

PRETERM DELIVERY - 49 cases delivered preterm babies which was

accounting to 98% of placental abruption. 42 placental abruption cases

which had preterm deliveries were demonstrated histological features of

chorioamnionitis.

88

PREVIOUS HISTORY OF FETAL LOSS - One case of placental

abruption had history of previous intrauterine death which occurred in third

trimester.

CLINICAL FEATURES - Acute onset of abdominal pain, vaginal bleeding

and retroplacental haemorrhage were significantly associated with placental

abruption, followed by uterine tenderness, and meconium stained

membranes.

SIGNIFICANT HISTOPATHOLOGICAL FINDINGS IN

PLACENTAL ABRUPTION

- In present study, intervillous haemorrhage, intravillous

haemorrhage and increased syncytiotrophoblastic knotting were significantly

associated with placental abruption.

- Decidual vasculopathy was significantly associated with acute

placental abruption with chronic features, followed by villitis, villous

maldevelopment, and Maternal floor decidual necrosis.

89

SIGNIFICANT HISTOPATHOLOGICAL FINDINGS IN ACUTE

PLACENTAL ABRUPTION


23 cases (65.7%) of acute placental abruption. By applying Chi-square

test, P value is 0.035 which is statistically significant (p<0.05). Thus,

it indicates that chorioamnionitis with haemorrhage was a

significant feature of acute abruption.


abruption. By applying Chi-square test, P value is 0.00 which is

Statistically significant (p<0.05). Thus, it indicates that Acute

deciduitis was a feature of acute abruption.


ABRUPTION WITH CHRONIC FEATURES


of acute placental abruption with chronic features. By applying Chi-


Villitis was present in 22 cases (100%) of acute placental abruption

with chronic features. By applying Chi-square test, P value is 0.000

which is statistically significant (p<0.05).

90

Villous Infarction was present in 17 cases (100%) of acute placental

abruption with chronic features. By applying Chi-square test, P value

is 0.000 which is statistically significant (p<0.05).

Villous maldevelopment was present in 22 cases (100%) of acute

placental abruption with chronic features. By applying Chi-square test,

P value is 0.000 which is statistically significant (p<0.05).

Maternal floor decidual necrosis was present in 22 cases (100%) of

acute placental abruption with chronic features. By applying Chi-


Decidual vasculopathy was present in 22 cases (95.7%) of acute




maldevelopment, maternal floor decidual necrosis and decidual

vasculopathy were significant features of acute abruption with chronic

features cases.

91

SIGNIFICANT HISTOPATHOLOGICAL FINDINGS OF

PLACENTAL ABRUPTION IN PRIMI GRAVIDA

In present study, chorioamnionitis with haemorrhage was present

in 17 cases (48.6%) of placental abruption in primi gravida. By

applying Chi-square test, P value is 0.001 which is statistically

significant (p<0.05).

Acute deciduitis was present in 17 cases (85%) of placental abruption

in primi gravida. By applying Chi-square test, P value is 0.000 which

is statistically significant (p<0.05).

Thus, chorioamnionitis with haemorrhage and acute deciduitis were

significantly associated with placental abruption in primi gravida.


PLACENTAL ABRUPTION IN MULTI GRAVIDA

In present study, placental infarction, villitis, villous

maldevelopment and maternal floor decidual necrosis were present

in 21 cases (95%) of placental abruption in Multi gravida. By applying

Chi-square test, P value is 0.000 which is statistically significant

(p<0.05). Thus, placental infarction, villitis, villous

maldevelopment, and maternal floor decidual necrosis were

significantly associated with placental abruption in multi gravida.

92

These were the features of acute abruption with chronic features.


abruption in Multi gravida. By applying Chi-square test, P value is

0.003 which is statistically significant (p<0.05). Thus, villous

infarction was a significant feature of placental abruption in multi

gravida which was a feature associated with acute abruption with

chronic features.

CONCLUSION

93

CONCLUSION

This study is the first type of it, which is carried out in Government

Coimbatore Medical College Hospital.

INCIDENCE

The incidence of abruptio placenta in Government Coimbatore

Medical College Hospital is 3 per month.

INTRAUTERINE DEATH

Abruptio placenta is an important cause of perinatal mortality and

morbidity. In this study, out of 50 placental abruption cases, 29 cases

had intrauterine death and these were significantly associated with

male babies.

REFERRED CASE MANAGEMENT

Being a tertiary health care centre, Government Coimbatore Medical

College is playing a vital role in the management of placental

abruption, most of which are referred from Primary Health Centres

and Taluk Government Hospitals.

94

MULTIPARITY AND PLACENTAL ABRUPTION

Multiparity and Grand multiparity are strongly associated with

placental abruption, so that, the proper health education regarding the

complications of multiparity should be given to the mothers through

the Primary health centres and Taluk Government hospitals.

MODIFIABLE RISK FACTORS IN PLACENTAL ABRUPTION

Modifiable risk factors like anaemia, pregnancy induced hypertension,

and multiparity in placental abruption should be early detected and

managed appropriately to reduce the incidence of placental abruption.

Placental abruption and pre-eclampsia might be sharing the same

common etiology with failed placentation in early pregnancy. This

could lead to the placental dysfunction and further increases the risk of

abruption of placenta in women with pregnancy induced hypertension.

CLINICAL FEATURES

Acute onset of abdominal pain, vaginal bleeding and retroplacental

haemorrhage were the predominant clinical features in placental

abruption.

95

PATHOLOGY OF ACUTE ABRUPTION IN PRIMI GRAVIDA

Chorioamnionitis with haemorrhage and acute deciduitis were the

features significantly associated with acute abruption (P<0.05). The

same features were significantly associated with placental abruption in

primi gravida. Thus it indicates that infection followed by acute

inflammation could be the pathogenesis in placental abruption in primi

gravida patients.

PATHOLOGY OF ACUTE ABRUPTION WITH CHRONIC

FEATURES IN MULTI GRAVIDA

Acute inflammatory process was playing a major role in placental

abruption of primi gravida, whereas in multi gravida in addition to the

acute events, chronic inflammatory process was also taking part in

placental abruption. Infection and inflammation causing tissue damage

mediated by IL-1 and TNF-α. These cytokines increases the

production of matrix metalloproteinases (MMPs) which causes the

destruction of extracellular matrix and cell-cell interactions securing

placenta, that leads to premature separation of placenta72

. Thrombin

enhanced interleukin-8 (IL-8) might explain the decidual neutrophil

infiltration, which may activate MMPs, contributing to the degradation

96

of extra cellular matrix involved in fetal membrane rupture, that

causes premature rupture of membranes70

.

Unfortunately, either accurate prediction or prevention of placental

abruption are not possible at present time. Further studies regarding

acute inflammatory process in the placenta of primi gravida are

recommended to predict placental abruption in subsequent

pregnancies. Serological markers like C–Reactive Protein /

homocysteine (indicators of inflammation) to detect acute placental

infarction in primi gravida may be tried in future.

While placental infarction, villitis, villous maldevelopment, maternal

floor decidual necrosis and decidual vasculopathy were significant

features (P<0.05) in cases of acute abruption with chronic features.

The same features were significantly associated with placental

abruption in multi gravida patients. Thus it indicates that, in multi

gravida there was a chronic process, predominantly involving the

vascular channels as etiology for placental abruption. Hypoxia could

be significant factor underlying these vascular changes. Thus, there is

a significant association of chronic features of placental abruption and

multi gravida.

97

PATERNAL SMOKING

Paternal smoking is a major risk factor for chronic inflammatory

processes in placental abruption. In acute abruption, paternal smoking

is present in 4 cases, whereas in placental abruption with chronic

features, 22 cases had the history of paternal smoking which is

statistically significant (P<0.05).

Nakatsuka et al studied that hypoxia and nitric oxide (NO)

metabolites generated by apoptosis might cause cell death and

subsequent placental abruption takes place in chorioamnionitis71

. Kiss

et al studied that inflammation or acute hypoxia would impair

synthesis of nitric oxide synthase from endothelium (eNOS) or

production of NO from trophoblast. This leads to further adhesion of

platelets, aggregation, and formation of thrombus as well as abnormal

placental vascular resistance, resulting in placental abruption72

.

The hypoxic changes developed by nicotine and carbon monoxide

could cause placental infarcts, signifying that capillary fragility is

increased and it might result in arterial rupture, leading to placental

abruption.In this study, chronic vascular changes are predominantly

present in multi gravida.

98

Being a preventable risk factor, cessation of smoking reduces adverse

pregnancy outcomes including placental abruption.

Further studies regarding the serological inflammatory markers and

vascular changes in the placenta of primi gravida would be useful in

predicting placental abruption in subsequent pregnancies.

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85

SUMMARY

The present study was a prospective study.

Aim of the study was to analyze the incidence and histomorphological

features of abruptio placenta in a tertiary health care centre, to compare

the histopathological features abruptio placenta with normal placenta and

to analyze the differences in histomorphology of abruptio placenta in

primigravida and multigravida patients.

The study period was 1 and half years from January 2017 to June 2018.

Our study consists of 50 clinically diagnosed cases of placental abruption

(cases) and 50 normal deliveries (control).

INCIDENCE - The incidence of Abruptio placenta in Coimbatore Medical

College Hospital was 35-40 cases per year.

REFERRED CASES - Among the 50 placental abruption cases, 43 cases

were referred cases.

AGE - The common age group of occurrence placental abruption in our

study was 26-30 years. The mean age of occurrence of placental abruption

was 27.2. The median age of occurrence was 27 years. The youngest age was

16 years and the oldest age was 37 years.

86

GRAVIDA - Among the 50 placental abruption cases, 17 cases were primi

gravida, 33 cases were multi gravida. Among the multi gravida, 6 cases were

grand multi gravida (≥4 deliveries).

PATERNAL SMOKING - In acute abruption, paternal smoking was

present in 4 cases, whereas in placental abruption with chronic features, 22

cases had history of paternal smoking which is statistically significant

(P<0.05). Thus, paternal smoking can be considered as a significant

independent risk factor associated with acute abruption with chronic

features.

ANAEMIA - 41 cases were associated with clinical findings of anaemia


PREGNANCY INDUCED HYPERTENSION - 24 cases were associated


placental abruption cases which is statistically significant (P<0.05). Thus,

Pregnancy Induced Hypertension has a significant association with cases of


GESTATIONAL DIABETES MELLITUS - One case had gestational

diabetes which was accounting to 2% of the placental abruption.

HYDRAMNIOS - One case had hydramnios which was accounting to 2%

of the placental abruption cases.

87

PROM - 2 cases were associated with premature rupture of membranes


DIC - 2 cases were developed Disseminated intravascular coagulation which

was accounting to 4% of placental abruption.

MODE OF DELIVERY - Among the cases of placental abruption, 4 cases

had vaginal delivery whereas 46 cases underwent emergency Caesarean

section.

PREVIOUS CAESAREAN DELIVERY - Out of 50 placental abruption

cases, 15 cases were found with the history of previous caesarean delivery


INTRAUTERINE DEATH - 29 cases out of 50 had intrauterine death of

fetus. Among the 29 intrauterine death, 26 cases had male babies (89.7%)

which is statistically significant (P<0.05), and 4 cases had female baby

(13.8%). Thus, there was a significant association between placental

abruption and intrauterine death of male babies.

PRETERM DELIVERY - 49 cases delivered preterm babies which was

accounting to 98% of placental abruption. 42 placental abruption cases

which had preterm deliveries were demonstrated histological features of

chorioamnionitis.

88

PREVIOUS HISTORY OF FETAL LOSS - One case of placental

abruption had history of previous intrauterine death which occurred in third

trimester.

CLINICAL FEATURES - Acute onset of abdominal pain, vaginal bleeding

and retroplacental haemorrhage were significantly associated with placental

abruption, followed by uterine tenderness, and meconium stained

membranes.

SIGNIFICANT HISTOPATHOLOGICAL FINDINGS IN

PLACENTAL ABRUPTION

- In present study, intervillous haemorrhage, intravillous

haemorrhage and increased syncytiotrophoblastic knotting were significantly

associated with placental abruption.

- Decidual vasculopathy was significantly associated with acute

placental abruption with chronic features, followed by villitis, villous

maldevelopment, and Maternal floor decidual necrosis.

89


PLACENTAL ABRUPTION


23 cases (65.7%) of acute placental abruption. By applying Chi-square

test, P value is 0.035 which is statistically significant (p<0.05). Thus,

it indicates that chorioamnionitis with haemorrhage was a

significant feature of acute abruption.


abruption. By applying Chi-square test, P value is 0.00 which is

Statistically significant (p<0.05). Thus, it indicates that Acute

deciduitis was a feature of acute abruption.


ABRUPTION WITH CHRONIC FEATURES


of acute placental abruption with chronic features. By applying Chi-


Villitis was present in 22 cases (100%) of acute placental abruption

with chronic features. By applying Chi-square test, P value is 0.000

which is statistically significant (p<0.05).

90

Villous Infarction was present in 17 cases (100%) of acute placental

abruption with chronic features. By applying Chi-square test, P value

is 0.000 which is statistically significant (p<0.05).

Villous maldevelopment was present in 22 cases (100%) of acute



Maternal floor decidual necrosis was present in 22 cases (100%) of

acute placental abruption with chronic features. By applying Chi-


Decidual vasculopathy was present in 22 cases (95.7%) of acute




maldevelopment, maternal floor decidual necrosis and decidual

vasculopathy were significant features of acute abruption with chronic

features cases.

91


PLACENTAL ABRUPTION IN PRIMI GRAVIDA

In present study, chorioamnionitis with haemorrhage was present

in 17 cases (48.6%) of placental abruption in primi gravida. By

applying Chi-square test, P value is 0.001 which is statistically

significant (p<0.05).

Acute deciduitis was present in 17 cases (85%) of placental abruption

in primi gravida. By applying Chi-square test, P value is 0.000 which

is statistically significant (p<0.05).

Thus, chorioamnionitis with haemorrhage and acute deciduitis were

significantly associated with placental abruption in primi gravida.


PLACENTAL ABRUPTION IN MULTI GRAVIDA

In present study, placental infarction, villitis, villous

maldevelopment and maternal floor decidual necrosis were present

in 21 cases (95%) of placental abruption in Multi gravida. By applying

Chi-square test, P value is 0.000 which is statistically significant

(p<0.05). Thus, placental infarction, villitis, villous

maldevelopment, and maternal floor decidual necrosis were

significantly associated with placental abruption in multi gravida.

92

These were the features of acute abruption with chronic features.


abruption in Multi gravida. By applying Chi-square test, P value is

0.003 which is statistically significant (p<0.05). Thus, villous

infarction was a significant feature of placental abruption in multi

gravida which was a feature associated with acute abruption with

chronic features.

STUDY PROFORMA

NAME :

AGE/SEX :

DATE OF ADMISSION :

IP NO :

ADDRESS :

CONDITION AT DISCHARGE :

OBSTETRIC HISTORY :

PRIMI/MULTIGRAVIDA :

BOOKED OR NOT :

IMMUNIZED OR NOT :

CAESAREAN SECTION/NORMAL

DELIVERY :

HISTORY OF PREVIOUS

DELIVERY :

HISTORY OF ANY DRUG

INTAKE DURING PREGNANCY :

HISTORY OF DIABETES

MELLITUS :

HISTORY OF HYPERTENSION :

HISTORY SEROPOSITIVITY :

HISTORY OF TORCH INFECTION :

HISTORY OF BRONCHIAL

ASTHMA/COPD :

HISTORY OF TREATMENT FOR

PRIMARY INFERTILITY :

Nehahspapd; xg;Gjy; gbtk;

ngah; :

taJ :

ghypdk; :

Kfthp :

cs;Nehahsp mDkjp vz; :

kUj;Jt Muha;r;rpf;fhf vd;Dila fh;g;gfhy rk;ge;jkhd Nfs;tpfSf;Fg; gjpy;

mspf;fTk; Foe;ij gpwe;j gpd; vLf;fg;gLk; eQ;Rf;nfhbia Muha;r;rpf;fhf toq;Ftjw;Fk;

kdg;g+h;tkhf rk;kjpf;fpd;Nwd;.

Nehahspapd; ifnahg;gk;

,lk; :

Njjp :

II: MASTER CHART

MASTER CHART - Cases (column no 1-44)

S.N

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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

1 83 yes 26/f primi - yes Yes no no no spontaneous

expulsionmale IUD 1.8kg 200 ml preterm 3a no no yes yes

2 96 yes 34/f G3P1L1 Prev FTND yes no no no no emergency LSCS female alive 2 kg 220ml preterm 2 no yes yes yes

3 20123 yes 33/f G2P1L1 prev LSCS no Yes no no no emergency LSCS female alive 2.2kg 150 ml preterm 2 no no yes yes

4 13256 yes 21/f primi - yes no no no nospontaneous

expulsionmale IUD 1.8kg 300 ml preterm 3a no no yes yes

5 20457 yes 20/f primi - yes no no no no emergency LSCS male IUD 1kg 350 ml preterm 3a no no yes yes

6 22152 no 35/f G3P1L1A1 Prev FTND yes no no no no emergency LSCS male IUD 1.2kg 380 ml preterm 3a no yes yes yes

7 23609 yes 34/F G5P2L1A2 Prev 2 LSCS yes no no no no emergency LSCS male IUD 1.9Kg 600 ml preterm 3a no no yes yes

8 24225 no 22/f G2P1P1 prev LSCS yes Yes yes no no emergency LSCS female alive 2kg 250 ml preterm 2 no yes yes yes

9 30208 yes 26/f G3P2L2 prev LSCS no Yes no no no emergency LSCS male alive 1.9 kg 230 ml preterm 3a no yes yes yes

10 32007 yes 23/f G2P1L1 Prev FTND yes no no no no emergency LSCS male IUD 1.6 kg 380 ml preterm 3a no no yes yes

11 37319 no 28/f primi - yes Yes no no no emergency LSCS female alive 1.5 kg 100 ml preterm 1 no no yes yes

12 37683 no 21/f primi - yes Yes no no no emergency LSCS female alive 1.4 kg 80 ml preterm 1 no no yes yes


expulsionmale IUD 0.8 kg 280 ml preterm 3a no yes yes yes


1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20


expulsionmale IUD 1.3 kg 230 ml preterm 3a no no yes yes

15 30933 no 24/f G2P1L1 prev LSCS yes no no no no emergency LSCS male alive 1.5 kg 190 ml preterm 2 no yes yes yes

16 42499 yes 35/f G3P2L2 Prev FTND no no no no no emergency LSCS female IUD 1.5 kg 400 ml preterm 3a no yes yes yes

17 44356 yes 23/f G2P1L1 prev FTND yes no no no no emergency LSCS male IUD 1.7 kg 300 ml preterm 3a no no yes yes

18 44949 yes 30/f G5P3L2A1 pre FTND yes Yes no no no emergency LSCS male IUD 1.5 kg 220 ml preterm 3a no yes yes yes

19 45160 no 27/f G3P2L2 prev FTND yes no no no no emergency LSCS female alive 2.1 kg 100 ml term 1 no yes yes yes

20 41445 yes 36/f G8P5L5A2 prev FTND yes Yes no no no emergency LSCS male IUD 1.8 kg 220 ml preterm 3a no yes yes yes

21 48980 yes 22/f primi yes no no no no emergency LSCS male IUD 1.5 kg 250 ml preterm 3a no yes yes yes

22 51384 yes 30/f G5P4L4 Prev FTND yes Yes no no no emergency LSCS male IUD 2.6 kg 300 ml preterm 3b no yes yes yes

23 79192 yes 34/F G4P2L2A1 prev FTND yes Yes no no no emergency LSCS female alive 1.9Kg 190 ml preterm 2 no yes yes yes

24 83265 yes 29/f G2P1L1 prev LSCS yes no no no no emergency LSCS male IUD 2 kg 420 ml preterm 3a no yes yes yes

25 90164 yes 35/f G3P1L0A1

Pre IUD,

spontaneous

expul

yes Yes no no no emergency LSCS female alive 2 kg 430 ml preterm 2 no yes yes yes

26 91101 yes 27/f G2P1L1 prev LSCS no no no no no emergency LSCS male IUD 1.8 kg 440 ml preterm 3a no no yes yes

27 95654 yes 28/f G3P2L2 prev FTND yes Yes no no yes emergency LSCS female Alive 2.2 kg 300 ml term 2 no yes yes yes

28 100733 yes 19/f primi yes no no no no emergency LSCS male alive 2 kg 140 ml preterm 1 no yes yes yes

29 100739 yes 23/f short primi yes Yes no no no emergency LSCS female alive 2.1 kg 380 ml preterm 2 no no yes yes

30 117205 yes 30/f G4P1L1A2 prev FTND yes no no no no emergency LSCS male IUD 1.5 kg 400 ml preterm 3a no yes yes yes

31 23865 yes 26/f G3P2L2 prev LSCS no no no no no emergency LSCS female alive 2.5 kg 130 ml preterm 1 no yes yes yes

32 131956 yes 22/f primi - yes Yes no no no emergency LSCS male IUD 0.8 kg 380 ml preterm 3a no no yes yes

33 117505 yes 35/f G3P1L1A1 prev LSCS yes no no no no emergency LSCS female alive 2 kg 350 ml preterm 2 no no yes yes


1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

34 3119 yes 30/f G3P2L2 prev FTND yes Yes no no no emergency LSCS male IUD 1.8 kg 430 ml preterm 3a no yes yes yes

35 40417 yes 19/f primi - yes Yes no no no emergency LSCS female alive 2 kg 330 ml preterm 2 no no yes yes

36 4801 yes 32/f G3P1L1A1 prev LSCS yes Yes no no no emergency LSCS female alive 2 kg 300 ml preterm 2 no yes yes yes

37 5376 yes 33/f G3P2L1 prev LSCS no no no no no emergency LSCS female IUD 1.7 kg 700 ml preterm 3a no yes yes yes

38 5434 yes 37/f G3P1L1A1 prev LSCS yes no no no no emergency LSCS female alive 2 kg 500 ml preterm 2 no yes yes yes

39 11607 yes 29/f G2P1L1 Prev FTND yes Yes no no no emergency LSCS male IUD 1.8kg 430 ml preterm 3a no no yes yes

40 175189 yes 19/f primi - yes no no no no emergency LSCS female alive 2 kg 200 ml preterm 2 no no yes yes

41 183889 yes 19/f primi - yes Yes no no no emergency LSCS male IUD 1.9 kg 450 ml preterm 3a no no yes yes

42 185392 yes 21/f primi - yes Yes no no no emergency LSCS female alive 2 kg 400 ml preterm 2 no no yes yes

43 190860 yes 16/fprimi,

unmarried- yes no no no no emergency LSCS male IUD 1.8 kg 460 ml preterm 3a no

un

marriedyes yes

44 191634 no 25/f G2P1L0

prev FTND ,

anomalous

baby

no no no no no emergency LSCS female IUD 1.5 kg 480 ml preterm 3a no yes yes yes

45 194446 yes 27/f G2P1L1 prev FTND yes no no no no emergency LSCS male IUD 1 kg 440 ml preterm 3a no no yes yes

46 193562 yes 26/f G2P1L1 prev FTND yes Yes no no no emergency LSCS male IUD 1.6 kg 420 ml preterm 3a no no yes yes

47 194380 yes 22/f primi - yes no no no no emergency LSCS male alive 2.2 kg 380 ml preterm 2 no yes yes yes

48 196450 yes 35/f G3P2L2 Prev LSCS yes Yes no no yes emergency LSCS male IUD 1.7 kg 400 ml preterm 3a no no yes yes

49 216015 yes 30/f G4P1L1A2 Prev LSCS no Yes no no no emergency LSCS male IUD 1.5 kg 1000 ml preterm 3b no yes yes yes

50 219657 yes 34/f G3P1L1A1 prev LSCS no Yes no no no emergency LSCS male IUD 1.8 kg 530 ml preterm 3a no no yes yes


S.N

O

IP N

O

con

cea

led

/rev

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d h

emo

rrh

ag

e

pla

cen

tal

ind

enta

tio

n

pla

cen

tal

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rcti

on

mec

on

ium

sta

ined

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t

h/o

ute

rin

e te

nd

ern

ess

h/o

pre

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fun

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us

hem

orr

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ge

intr

av

illo

us

hem

orr

ha

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liti

s

vil

lou

s in

farc

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n

vil

lou

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ald

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op

men

t

cho

rio

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nio

nit

is m

ild

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d/s

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dec

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d a

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n

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s

fib

roid

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h/o

hy

ster

ecto

my

h/o

ma

tern

al

dea

th

21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44

1 83revealed

hemorrhage+yes no yes yes no no yes yes no no no

chorioamnionitis+

moderateyes yes yes no yes no yes no no no no

2 96revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild yes yes yes yes yes yes no yes no no no

3 20123revealed

hemorrhage+yes no yes yes no yes yes yes no no no chorioamnionitis+ mild yes no yes no yes yes yes no no no no

4 13256revealed

hemorrhage+yes no no yes no yes yes yes no no no

chorioamnionitis+


5 20457revealed

hemorrhage+yes no yes yes no yes yes yes no no no

chorioamnionitis+


6 22152revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild yes no yes yes yes yes no yes no no no

7 23609revealed

hemorrhage+yes no yes yes no no yes yes no no no chorioamnionitis+ mild yes no yes no yes no yes no no no no

8 24225revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild yes yes yes yes yes yes no yes no no no

9 30208revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild yes no no yes yes yes no yes no no no

10 32007revealed

hemorrhage+yes no yes yes no yes yes yes no no no chorioamnionitis+ mild yes yes yes no yes no yes no no no no

11 37319revealed

hemorrhage+no no no no no yes yes yes no no no

chorioamninitis+


12 37683revealed

hemorrhage+no no no no no yes yes yes no no no

chorioamnionitis+


13 38532revealed

hemorrhage+no no no yes no no yes yes no no no

chorioamnionitis+



21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44

14 30173revealed


chorioamnionitis+


15 30933revealed

hemorrhage+no yes no yes no no yes yes yes yes yes chorioamnionitis+ mild no no yes yes yes yes no yes no no no

16 42499revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild yes no yes yes yes yes no yes no no no

17 44356revealed

hemorrhage+no no no yes no no yes yes no no no chorioamnionitis+ mild yes no no no yes no yes no no no no

18 44949revealed

hemorrhage+yes yes yes yes no yes yes yes yes yes yes chorioamnionitis+ mild yes no yes yes yes yes no yes no no no

19 45160revealed

hemorrhage+no yes no no no yes yes yes yes no yes no chorioamnionitis yes no yes yes yes yes no yes no no no

20 41445revealed

hemorrhage+yes yes yes yes yes yes yes yes yes no yes no chorioamnionitis yes no yes yes yes yes no yes no no no

21 48980revealed


chorioamnionitis+


22 51384revealed

hemorrhage+yes no yes yes no yes yes yes no no no chorioamnionitis+ mild no no yes no yes no yes no no no no

23 79192revealed

hemorrhage+yes yes yes yes no yes yes yes yes yes yes chorioamnionitis+ mild yes no yes yes yes yes no yes no no no

24 83265revealed

hemorrhage+yes yes yes yes no yes yes yes yes yes yes chorioamnionitis+ mild no no yes yes yes yes no yes no no no

25 90164revealed

hemorrhage+yes yes yes yes yes no yes yes yes no yes no chorioamnionitis no no yes yes yes yes no yes no no no

26 91101revealed


chorioamnionnisitis+

mildno no no no yes no yes no no no no

27 95654revealed

hemorrhage+yes yes yes yes no no yes yes yes no yes


mildyes no yes yes yes yes no yes no no no

28 100733revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes


moderateyes yes yes yes yes yes no yes no no no

29 100739revealed

hemorrhage+yes no no yes no no yes yes no no no

chorioamnionnisitis +


30 117205revealed

hemorrhage+yes yes yes yes no no yes yes yes no yes no chorioamnionitis no no no yes yes yes no yes no no no

31 23865revealed

hemorrhage+no yes no no no no yes yes yes yes yes chorioamnionitis+ mild no no yes yes yes yes no yes no no no

32 131956revealed


chorioamnionitis+


33 117505revealed



mildyes no yes no yes no yes no no no no


21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44

34 3119revealed

hemorrhage+yes yes yes yes no yes yes yes yes yes yes chorioamnionitis+ mild no no yes yes yes yes no yes no no no

35 40417revealed




36 4801revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes


mildyes no yes yes yes yes no yes no no no

37 5376revealed

hemorrhage+yes yes no yes no no yes yes yes yes yes


mildno no no yes yes yes no yes no no no

38 5434revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes chorioamnionitis+ mild no no yes yes yes yes no yes no no no

39 11607revealed

hemorrhage+yes no yes yes no yes yes yes no no no no chorioamnionitis no no yes no yes no yes no no no no

40 175189revealed


chorioamnionitis+


41 183889revealed


chorioamnionitis+


42 185392revealed




43 190860revealed


chorioamnionitis+


44 191634revealed

hemorrhage+yes yes yes yes no no yes yes yes yes yes no chorioamnionnisitis no no yes yes yes yes no yes no no no

45 194446revealed

hemorrhage+yes no yes yes no yes yes yes no no no chorioamnionitis+ mild no no no no yes no yes no no no no

46 193562revealed



mildno no yes no yes no yes no no no no

47 194380revealed


choriodramonnisitis+


48 196450revealed

hemorrhage+yes no no yes no no yes yes no no no


mildyes no yes no yes no yes no no no no

49 216015revealed

hemorrhage+yes yes yes yes yes no yes yes yes yes yes no chorioamnionitis no no yes yes yes yes no yes no no no

50 219657revealed

hemorrhage+yes no yes yes no yes yes yes no no no chorioamnionitis+ mild yes no yes no yes no yes no yes yes no

Master chart - Control (Col 1-44)S

NO

IP N

O

refe

rred

/no

t

Ag

e

ob

stet

ric

his

tory

pre

vio

us

del

iver

y

anae

mic

/no

t

h/o

PIH

h/o

GD

M

h/o

hy

dra

mn

ias

h/o

PR

OM

mo

de

of

del

iver

y

mal

e/fe

mal

e

stat

us

of

chil

d

bir

th w

eig

ht

retr

op

lace

nta

l cl

ot

pre

term

/ te

rm

abru

pti

on

h/o

mat

ern

al s

mo

kin

g

h/o

pat

ern

al s

mo

kin

g

h/o

su

dd

en o

nse

t o

f

abd

om

inal

pai

n

h/o

vag

inal

ble

edin

g

con

ceal

ed/r

evea

led

hem

orr

hag

e

h/o

pla

cen

tal

ind

enta

tio

n

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

1 885 no 26/f primi - no no no no no FTND male alive 2.2kg no term no no no no no no no

2 1101 no 34/f G3P2L2 Prev FTND no no no no no FTND female alive 2kg no term no no no no no no no

3 20223 no 33/f G2P1L1 prev LSCS no no no no no LSCS female alive 1.9kg no term no no no no no no no


5 20557 no 20/f primi - no no no no no FTND male alive 2kg no term no no no no no no no

6 22252 no 35/f G3P2L2 Prev FTND no no no no no FTND male alive 1.8kg no preterm no no no no no no no

7 23209 no 34/F G4P3L3 Prev 2 LSCS no no no no no LSCS male alive 2.5kg no term no no no no no no no

8 24925 yes 22/f G2P1P1 prev LSCS no no no no no LSCS female alive 2.5kg no term no no no no no no no

9 30298 no 26/f G3P2L2 prev LSCS no no no no no LSCS male alive 2.1kg no term no no no no no no no

10 32607 no 23/f G2P1L1 Prev FTND no no no no no FTND male alive 2kg no term no no no no no no no

11 39319 no 28/f primi - no no no no no FTND female alive 2kg no term no no yes no no no no

12 37633 no 21/f primi - no no no no no FTND female alive 2.3kg no term no no no no no no no

13 38522 no 28/f primi - no no no no no LSCS male alive 2kg no term no no no no no no no


15 30233 no 24/f G2P1L1 prev LSCS no no no no no LSCS male alive 2kg no term no no yes no no no no

16 42899 yes 35/f G3P2L2 Prev FTND no no no no no FTND female alive 1.9kg no preterm no no no no no no no

17 44856 no 23/f G2P1L1 prev FTND no no no no no FTND male alive 2kg no term no no no no no no no

18 44979 no 30/f G3P2L2 pre FTND no no no no no FTND male alive 2kg no term no no no no no no no

19 45120 no 27/f G3P2L2 prev FTND no no no no no LSCS female alive 2kg no term no no no no no no no

20 41495 no 36/f G4P3L3 prev FTND no no no no no FTND male alive 1.8kg no preterm no no yes no no no no

21 48930 yes 22/f primi - no no no no no FTND male alive 1.9kg no term no no yes no no no no

Master chart - Control (Col 1-44)

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

22 51334 yes 30/f G5P4L4 Prev FTND no no no no no FTND male alive 2.2kg no term no no no no no no no

23 79642 yes 34/F G4P3L3 prev FTND no no no no no FTND female alive 2.3kg no term no no no no no no no

24 83875 no 29/f G2P1L1 prev LSCS no no no no no LSCS male alive 2.5kg no term no no no no no no no

25 90744 no 35/f G3P2L2 Prev LSCS no no no no no LSCS female alive 2kg no term no no no no no no no

26 91701 no 27/f G2P1L1 prev LSCS no no no no no LSCS male alive 2kg no term no no yes no no no no

27 95354 no 28/f G3P2L2 prev FTND no no no no no FTND female alive 2kg no term no no no no no no no


29 100789 no 23/f primi - no no no no no FTND female alive 2kg no term no no no no no no no


31 23855 no 26/f G3P2L2 prev LSCS no no no no no LSCS female alive 1.8kg no preterm no no no no no no no

32 131936 no 22/f primi no no no no no FTND male alive 2.2kg no term no no yes no no no no

33 117545 no 35/f G2P1L1 prev LSCS no no no no no LSCS female alive 2.1kg no term no no yes no no no no

34 31339 yes 30/f G3P2L2 prev FTND no no no no no FTND male alive 2kg no term no no no no no no no


36 4822 no 32/f G3P2L2 prev LSCS no no no no no LSCS female alive 1.9kg no term no no no no no no no

37 5396 no 33/f G3P2L1 prev LSCS no no no no no LSCS female alive 1.9kg no preterm no no no no no no no

38 5494 no 37/f G3P2L2 prev LSCS no no no no no LSCS female alive 2kg no term no no no no no no no

39 11627 no 29/f G2P1L1 Prev FTND no no no no no FTND male alive 2.2kg no term no no yes no no no no

40 175349 no 19/f primi - no no no no no FTND female alive 2.3kg no term no no no no no no no



43 190340 yes 22/f primi - no no no no no FTND male alive 1.5kg no term no no no no no no no

44 191944 yes 25/f G2P1L1 prev FTND no no no no no FTND female alive 1.9kg no preterm no no no no no no no


46 193382 no 26/f G2P1L1 prev FTND no no no no no FTND male alive 1.9kg no term no no no no no no no

47 194980 no 22/f primi - no no no no no FTND male alive 2kg no term no no no no no no no

48 194950 no 35/f G3P2L2 Prev LSCS no no no no no LSCS male alive 2.1kg no term no no no no no no no

49 216765 yes 30/f G3P2L2 Prev LSCS no no no no no LSCS male alive 2kg no term no no yes no no no no

50 214757 no 34/f G3P2L2 prev LSCS no no no no no LSCS male alive 2kg no term no no no no no no no


S N

O

IP N

O

pla

cen

tal

infa

rcti

on

mec

on

ium

sta

ined

mem

bra

ne/

no

t

h/o

ute

rin

e te

nd

ern

ess

h/o

pre

vio

us

abru

pti

on

fun

isit

is

inte

rvil

lou

s h

emo

rrh

age

intr

avil

lou

s h

emo

rrh

age

vil

liti

s

vil

lou

s in

farc

tio

n

vil

lou

s m

ald

evel

op

men

t

cho

rio

amn

ion

itis

cho

rio

amn

ion

itis

wit

h

hem

orr

hag

e

acu

te d

ecid

uit

is

dec

idu

al h

emo

rrh

age

mat

ern

al f

loo

r d

ecid

ual

nec

rosi

s

incr

ease

in

tro

ph

ob

last

ic

kn

ott

ing

dec

idu

al v

ascu

lop

ath

y

iso

late

d a

cute

ab

rup

tio

n

acu

te a

bru

pti

on

wit

h c

hro

nic

feat

ure

s

fib

roid

h/o

hy

ster

ecto

my

h/o

mat

ern

al d

eath

23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44

1 885 no no no no no no no no no no no no no no no no no no no no no no














15 30233 no no no no yes no no no no no no no no no no no no no no no no no





20 41495 no no no no no no no no no no yes no no no no no no no no no no no



23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44






























histopathological analysis of patients with abruptio...

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