“MATERNAL FETAL OUTCOME IN PLACENTA PRAEVIA”

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“MATERNAL FETAL OUTCOME INPLACENTA PRAEVIA”

ByDr. NAGAMANI S.D

Dissertation Submitted to theRajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment of the requirements for the degree of

MASTER OF SURGERYIN

OBSTETRICS AND GYNAECOLOGY

Under the guidance ofDr.R.C.PRAMEELA, M.D (OBG)

Associate Professor

DEPARTMENT OF OBSTETRICS AND GYNAECOLOGYMYSORE MEDICAL COLLEGE AND RESEARCH INSTITUTE,

MYSORE2013

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ByDr. NAGAMANI S.D



MASTER OF SURGERYIN



Associate Professor


MYSORE2013

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ByDr. NAGAMANI S.D



MASTER OF SURGERYIN



Associate Professor


MYSORE2013

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CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “MATERNAL FETAL

OUTCOME IN PLACENTA PRAEVIA” is a bonafide research work done by

Dr. NAGAMANI S.D in partial fulfillment of the requirement for the degree of

Master of Surgery (Obstetrics and Gynaecology).

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ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE INSTITUTION

This is to certify that the dissertation entitled “MATERNAL FETAL OUTCOME

IN PLACENTA PRAEVIA” is a bonafide research work done by

Dr. NAGAMANI S.D under the guidance of Dr.R.C.PRAMEELA, Associate

Professor, Department of Obstetrics and Gynaecology, Mysore Medical College

And Research Institute, Mysore.

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COPYRIGHT

Declaration by the Candidate

I hereby declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall have the rights to preserve, use and disseminate this dissertation /

thesis in print or electronic format for academic / research purpose.

© Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.

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ACKNOWLEDGEMENT

First, I thank the Almighty God for the grace bestowed upon me. This

dissertation is the culmination of the help, encouragement and guidance from a

number of people. I would like to thank them all.

I would like to acknowledge my deep sense of gratitude to Associate Professor

Dr. R.C.PRAMEELA under whose guidance and inspiration this work was carried

out.

I am indebted to Dr.Lokesh Chandra H.C, Professor and Head, Dept of

Obstetrics and Gynaecology, Dr.Radhamani, Dr.Prameela, Dr.Chinniwar, Professor

and Unit Chief for their encouragement and support throughout my post graduation.

I wish to thank Assistant Professors Dr.Sunanda, Dr.Mamata,

r.Sudha, Dr.Sushma, Dr.Lakshmikanth for inspiring me about the subject who has

immensely inspired this study.

I also thank Dr.Manjunath, Dr.Sangeetha, Dr.Vijayalakshmi, Dr.Supriya,

Dr.Shwetha Nayak.

I wish thank Dr. Geetha K Avdhani, Dean and Director, MMC & RI for

permitting me to conduct this study in this hospital.

I express my thanks to all my colleagues and staff members of Cheluvamba

Hospital, Mysore for their help and co-operation during my study.

I am thankful to Dr.Lancy D’ Souza, Statistician, for his excellent statistical

analysis.

I would like to thank my parents and for their moral support and finally I am

grateful to all patients who inspite of all their sufferings have helped me to improve

my knowledge and complete the thesis work.

I dedicate this work to my parents, sisters, friend my loving husband and all

my family members for making my life worth living.

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LIST OF ABBREVIATIONS

APH - Antepartum haemorrhage

NICU - Neonatal intensive care unit

FFP - Fresh frozen plasma

PRBC - Packed red blood cells

PNM - Perinatal mortality

MMR - Maternal mortality rate

IVF - Invitro fertilization

TAS - Trans abdominal ultra sound

TVS - Trans vaginal ultras sound

MRI - Magnetic resonance imaging

LSCS - Low segment caesarean section

PP - Placenta previa

PIH - Pregnancy induced hypertension

PPH - Post partum haemorrhage

CD - Caesarean delivery

IUGR - Intra uterine growth retardation

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CONTENTSPART – I

Page No:

1. Introduction 2

2. Aim of study 5

3. Historical Aspects 6

4. Diagnosis and Management 7

5. Review of Literature 10

6. Placenta Previa

a. Anatomy 24

b. Definition 40

c. Incidence 41

d. Classification 42

e. Aetiology 50

f. Patho – Physiology 52

g. Diagnosis 69

h. Management 90

i. Maternal Outcome 120

j. Fetal Outcome 124

k. Placenta Accreta 131

PART – II

7. Materials and Methods 141

8. Observations and Discussions 150

9. Summary and Conclusion 198

10. Bibliography 202

11. Proforma 212

12. Master chart 221

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LIST OF TABLES

Sl.no. Tables Page no.

1. Incidence of placenta previa 151

2. Incidence of placenta previa by different authors 152

3. Incidence of placenta previa according to various studies 154

4. Incidence of placenta previa in cheluvamba hospital 155

5. Correlation of maternal age and placenta previa 156

6. Comparative studies of age distribution in placenta previa. 158

7. Correlation of parity and placenta previa 159

8. Comparitive study of distribution of parity in placenta previa 161

9. Presence /absence of pain abdomen in placenta previa 162

10. Risk factors for placenta previa 163

11. The relative risk of placenta previa associated with previousceasarean section

166

12. Antenatal complications in the present study 169

13. Degree of placenta previa 172

14. Ultra sound of different types of placenta previa 173

15. Management protocol 175

16. Route of delivery: abdominal 175

17. Cesareans section in placenta previa in different study 175

18. Route of delivery: vaginal 176

19. Vaginal delivery in placenta previa in different study 176

20. Intra and post operative complications 177

21. Blood components 178

22. Perinatal morbidity in the present study 181

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23. The prenatal mortality rate according to various authors 183

24. Causes of perinatal mortality in this study 184

25. Correlation between perinatal mortality and type of placentaprevia

186

26. Correlation between perinatal mortality and mode of delivery inplacenta previa

188

27. Correlation between perinatal mortality and gestational age, inplacenta previa

189

28. Correlation between perinatal mortality and birth weight ofinfants

192

29. Maternal mortality in placenta previa by different author 194

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LIST OF FIGURES

Sl.no. FIGURES Page no.

1. Placenta Previa 1

2. Normal placenta 33

3. Fetal and maternal surface 36

4. Normal and placenta previa 40

5. Placenta Previa – Classifications 42

6. Different Classification 43

7. Types of placenta previa 45

8. Vasaprevia 65

9. Colour Dopler of Vasaprevia 67

10. Transabdominal localization of placenta previa 70

11. Transabdominal sonography 73

12. Early placenta previa VS threatened abortion 73

13. Anterior placenta previea 74

14. Marginal placenta previa 74

15. Placenta previa with abruption 79

16. Placenta in minor degree placenta previa 92

17. Placenta in major degree placenta previa 101

18. A case of placenta acreta peripartum hysterectomy 109

19. Hysterectomy Specimen of Placenta Accreta 130

20. Gross specimen of uterus (placenta accrete) 132

21. Colour Doppler study of placenta accreta 136

22. MRI Scan of Placenta Accreta 136

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LIST OF GRAPHS

Sl.no. GRAPHS Page no.

1. Correlation of maternal age and placenta previa 156

2. Correlation of parity and placenta previa 160

3. Risk factors for placenta previa 163

4. Antenatal complications in the present study 170

5. Ultra sound of different types of placenta previa 173

6. Intra and post operative complications 178

7. Perinatal morbidity in the present study 181

8. Causes of perinatal mortality in this study 184

9. Correlation between perinatal mortality and type of placentaprevia

187

10. Correlation between perinatal mortality and mode of delivery inplacenta previa

188

11. Correlation between perinatal mortality and gestational age, inplacenta previa

190

12. Correlation between perinatal mortality and birth weight ofinfants

192

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PART - I

PLACENTA PREVIA

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INTRODUCTION

Haemorrhage in obstetrics is almost life threatening emergency especially in

the last trimester. In placenta previa, the bleeding occurs from the placental site,

which is unfortunately situated in the lower uterine segment, which stretches during

the later half of pregnancy.

There has been substantial reduction in maternal death in placenta previa

throughout globe because of early diagnosis even prior to the bleeding, omission of

internal examination outside the hospital, free availability of blood transfusion

facilities, wider use of caesarean section with expert anaesthesiology, skill and

judgement. All these factors reduced of maternal death of from placenta praevia <1%

or even to zero in some centers.

But in developing countries because of wide gap of the extension of medical

facilities and also the difference in the patients profile between urban and rural

population maternal mortality from placenta praevia in hospital statistics ranges from

less than 1% to as high as 5%.

Patient are rushed in referral hospital after repeated bouts of hemorrhage often

with the history of vaginal examination, inadequate antenatal care, delay in referral

road and transport difficulties contribute to the poor outcome. The ultimate cause of

death was hemorrhage and shock. The morbidity is some what ranged due to

hemorrhage and operative delivery.

So it is very important to recognize placenta previa early and transport them to

the major referral hospital, thereby decreasing the maternal and fetal morbidity and

mortality.

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Placenta previa involves bleeding from placental site completely, which is

located in the lower uterine segment either partially or completely and as the lower

uterine segment stretches near term or in labour the associated bleeding is inevitable.

The fact that placenta attached to the developing and stretching lower uterine

segment would ultimately result in bleeding, if only during labour, led to the original

classification of placenta previa as ‘unavoidable’ or ’ inevitable’ antepartum

hemorrhage.

Antepartum hemorrhage forms one of the most dangerous and devastating

group of disorders in obstetrics. Placenta previa contributes to 1/5th of the cases of

antepartum hemorrhage.

This catastrophic complication not only poses a risk to the fetus but also

endangers the mother’s life. Developed countries have a near zero maternal mortality

rate for placenta previa but even with today’s better medical facilities and awareness

India lags way behind.

The maternal and neonatal outcome can be definitely improved in placenta

previa as it can be diagnosed by antenatal USG even before the first episode of

bleeding. Once the condition is diagnosed, the case should be judiciously managed

and all steps required should be taken to treat the complications associated with such

cases. These cases are to be managed only in centers where there are facilities for

blood transfusion, immediate operative intervention and NICU facilities round the

clock to attend to the usually preterm babies. Even better ANC and thorough

screening of the patient with second trimester scan, better referral system, transport

and more hospitals with 24 hours blood bank facility are the need of the hour. All

these measures can probably bring down the maternal and perinatal mortality and

morbidity rate and achieve the standards of developed countries.

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Most studies done on this subject were conducted about a span of a decade

ago. So, I was interested in knowing whether we are any better in managing this

obstetric emergency; so as to achieve our ultimate goal of healthy mother and healthy

baby at the end of every pregnancy.

We must re-assimilate our resources and plan a strategy to filling the above

mentioned lacuna for the prosperous future of our action.

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AIM OF STUDY

This study was undertaken to study in detail, the incidence, clinical aspects

regarding the course of pregnancy and to know the effectiveness of our management

inspite of the patient being referred late and its maternal and perinatal outcome.

To study the distribution of the etiology and predisposing risk factors.

To find out the maternal morbidity and mortality.

To analyze the perinatal outcome.

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HISTORICAL ASPECTS

In 1709, Schancher described the Implantation in placenta previa at autopsy

and in 1758 Vonwaibaum used an animal, bladder distended with air as vaginal

tampon to control the hemorrhage. Neumann abd luh (1834) advocated the idea of

secondary isthmial implantation. Robert Raruer- 1858, a great teacher of that time

described the modes of implantation of fertilized ovum in the cavity of the uterus.

Primary and secondary isthimal implantation’s been thought of and extension of the

placental tissue from its normal situation into the lower uterine segment as a tongue

shaped process was described.

Mauriceau advocated rupturing the membranes to induce the labour and

control the bleeding. In 1860, Braxton Hicks described the technique of combined

internal and external bipolar version to use the fetus as a “plug till the danger is over”.

In the early part of the twentieth century, Voorhees placed a 10 cm bag filled with

water in the cervix to compress the placenta and willet attached a T clamp with

weights of 1-2 pounds the fetal scalp for tamponade of the bleeding pacental site by

the fetal head.

The most significant advance in the management of placenta previa occurred

in 197 when Bill noting the high maternal mortality ( 10% in all cases and 25% in

total placenta previa) advocated liberal use of blood transfusion and more frequent

performance of caesarean section.

In 1945 Johnson and Macafee independently advocated “Conservative”

management of placenta previa for the sole purpose of improving perinatal mortality.

Which had 2 things in the preview.

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1. Prolonging the intrauterine life of the fetus up to the period of maturity,

with the best of attention to the mother and her general condition.

2. To keep an open mind to the mode of management with respect to each

case and not on an standard lines. A vigilant attitude with all responsibility

to tide over a grave situation. Macafee presented a paper in 1945, Aug

from the Royal hospital Belfast, with a study of 174 cases of placenta

previa when an antepartum hemorrhage ranked 4th as the cause of maternal

mortality.

Diagnosis and management

An important mile-stone in the diagnosis of placenta previa is the work of

Meena, Mller and holly (1930), where they injected a radio opaque dye within the

amniotic Cavity (Strontium Iodine) and noticed a filling defect in the region of the

placenta on radiography, Ude and Urner, 1934 thought of another method called

cystography, which consist of injecting a radio opaque dye into the bladder per

urethra and delineating its confines in relation to the lower uterine segment. Placenta

being implanted in the lower segment could be easily visualized as a soft- tissue

between the fetal head and the bladder wall.

Francis Burker (1935) from Liver- pool hospital again emphasized the need of

placental localization and tried the technique of amniography. Snow and Powell

(1934) claimed to be able to demonstrate the placenta in the ordinary films without

using any special technique especially in a lateral radiograph.

In 1941, Ball and Golden were experiencing on the fact that a positive

diagnosis of placenta previa could be made by observing the displacement of

presenting parts from mid coronal and mid sagittal panes of pelvic brim. Moir J.C

(1944) from USA carried out a series of experiments and convincingly demonstrated

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that uterine wall, placenta and amniotic fluid threw shadows of indistinguishable

density, so that they merge imperceptibly into one another and an asymmetrical

distribution of amniotic fluid could falsely indicate placental position.

Reid (1949), working at Oxford drew attention to the importance of persisting

fetal displacement. Positioning of a lateral direction settled many problems and the

probable fallacies regarding the thickness of shadow in the anterior and posterior

walls due to asymmetrical distribution of liquor were avoided. Blaire Hartly of

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Manchester (1954) thought of demonstrating calcareous deposits in the placenta

identified after 32 weeks of pregnancy.

Various views regarding a pelvic examination at the time of admission were

put forth. Delee stated that a mere speculum examination in daylight could do.

Marshell stated that the patients who are decided for caesareans section should have

vaginal examination.

Radio Necletide localization of placenta started gaining favor in 1969- 1970,

as reported from Houston(Texas), Angelweich and John Burdine had Iodine 131,

tagged human albumin technetium and indium for this purpose and gave comparative

results.

A major breakthrough in the management of placenta previa came when ultra

sound (1958) was used as diagnostic aid while all others invasive technique had

several disadvantages, ultra sound had the unique merit of being non- invasive and

easier to adopt with a high degree of accuracy. Several workers at various part of the

world started identifying the placental localization, using sooner from 1960 onwards.

Gotterfield (1966) Denver. Donald and Abdullah(Glasgow 1968) Campbell

and Kohorn ( London 1978) Kabayashi et al ( Booklyn 1970), Suden (Sweden 1970)

Santer et al (Dollas 1978) bowce et al (Chicago, 1978) are the pioneers in this field

and have reported an accuracy of more than 95% in their studies in placental

localization.

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REVIEW OF LITERATURE

Harvey (1971) reviewed 89 patients retrospectively who were diagnosed with

placenta previa and fetal weight was plotted on graph using 1 to 2 standard deviation

from normal. All but 3 infants weights were normal for gestational age. There was no

evidence of fetal growth retardation in women diagnosed with placenta previa.

McShane PM, Heyl PS and Epstein MF (1985) studied 147 cases with partial

or complete placenta previa from 1975-1982 and concluded that a history of prior

cesarean section was associated with significant increase in maternal morbidity,

including massive hemorrhage ,placenta accrete and hysterectomy. Despite the use of

tocolysis, 2/3rd of patients delivered before 36 weeks of gestation and perinatal

mortality was 81/1000. Significant correlation was detected between severity of APH

in mothers and neonatal transfusion required.

Tariq Khashoggi, Arab Board (1995) from 1988-1991 reviewed 96 cases of

major placenta previa with expectant management, confinement in hospital and blood

transfusions in ANC. Expectant management was carried out by doing an LSCS at 37

completed weeks. The results were, no maternal mortality and fetal mortality of

41.8/1000, where prematurity remain the prime factor of mortality.

Taylor YM (1995) investigated 810 women of Asian origin living in

Washington and took 2917 white women randomly as control. They concluded that

women of Asian origin had 86% increased chance for placenta previa than compared

to control with OR of 1.86.

Hemmadi (1995) from Wadia Hospital, Bombay, reviewed 318000 deliveries

over 3 years, of which 132 cases of placenta previa with an incidence of 0.4%. Author

observed that caesarean section is the mainstay of treatment in cases of placenta

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previa. This has resulted in decrease in perinatal mortality from 514 to 166/1000 and

maternal mortality from 3.76% to 0.75%. Author concluded that all the patients

treated with conservative means should undergo an elective caesarean section as soon

as fetal maturity can be documented to further minimize the maternal mortality

resulting from hemorrhage and its associated complications.

Edward T Wolf (1996) conducted a study over a decade ( 1980-1990) and

studied 54969 deliveries of which 171 were singleton pregnancy with placenta previa.

Small for gestational age in study group versus control group were 4.1% (7/171) and

5.81% (10/171). Mean birth weight was 2259 grams and 2476 grams in study and

control groups. This was not statistically significant. Hence, placenta previa per se

must not be attributed for small for gestation age infants.

(Catanzarite et al., 1996). The leading indication for cesarean hysterectomy is

placenta accrete.

(Miller et al., 1997).Placenta previa complicates approximately 5 of 1,000

deliveries and has a mortality rate of 0.03% (Ananth et al., 2003). Among women

with placenta previa, the incidence of placenta accreta is almost 10%.

Ananth CV(1997) studied the risk of uteroplacental bleeding disorders in

pregnancy with increasing parity, smoking , history of PIH and sex of the off-spring

in 123941 singleton women (1980-1993). His results showed that placenta previa

increased with maternal age by 9 times when age was >40 years (control 20 years old

pregnant women) and there was no relation of sex of the offspring with incidence of

placenta previa.

Placenta previa in pregnancy apparently appears as protective factor against

PIH but this deduction is probably due to increase in premature deliveries, hence less

chance for PIH at term.

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Reddi Rani P. and Latha (1999) from JIPMER, Pondicherry.100 patients with

placenta previa over a 4 year were reviewed. Incidence was 0.57%. Previous

caesarean section/ abortion was associated in 20% of cases. Most of women were

multiparous in the age group of 20-29 years, while 48% of the patients had major

degree of placenta previa and 33% had preterm deliveries and caesarean section rate

was 64%. Perinatal mortality was 240/1000. However there was no maternal death.

Author concludes that placenta previa account for approximately 0.5% of all

deliveries but still remains a major cause of perinatal morbidity and mortality.

Women with placenta previa stayed longer in hospital and had higher rate of

caesarean section but perinatal mortality remained high and the principal cause was

prematurity. Improvement in ultrasound, blood transfusion facilities, early detection

of placenta previa and conservative management will help to decrease the perinatal

mortality.

Joan MG Crane (1999) – carried out a population bases retrospective cohort

from 1988-1995 in Nova Scotia. Among 92984 pregnancies, 305 cases were placenta

previa (incidence 0.33%). Outcome was studied and it was observed that the

incidence of prematurity in placenta previa was 46.5% versus 7.27% in term

pregnancies (OR=2.65). The odd ratio of Major congenital anomalies and RDS was

2.48 and 4.94 in cases of placenta previa. There was no increase in fetal growth

restriction and perinatal mortality (2.3% Vs 0.78).

Mahesh R (2000) carried out study in Cheluvamba hospital , Mysore during

the period 15th February 1997 to 14th February 1999(2 years study).During this period

13351 cases were delivered of these 107 cases were placenta previa, with a incidence

of 1:125 (0.80%) which was compared with other studies which varies from 0.47% to

0.84%, but still remains a major cause of perinatal morbidity and mortality.

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Retrospective analysis of incidence of placenta previa for the past 2 years in our

institute showed 1:126. Hence, there is no change in incidence of placenta previa in

last 4 years in our insititute.at present incidence decreased to 0.41%. Majority of the

placenta previa cases belongs to the age group 21-25 years, (42.06%) . According to

Macafee maximum age group was 25-30 years. In B. Das series mean age was 29.6

years. Advancing maternal age appears to increase the risk of placenta previa

independent of other factors. Majority of the placenta previa cases belongs to the

parity 2-3 (65.42%). As it has been noted in other studies, the incidence of placenta

previa is higher in women with higher parity and women who are well into

reproductive span of life.

Kondur Pallavi (2001) In her study of 60 cases of placenta previa incidence

was 0.70%, highest in the maternal age group 20-29, 63.4% and highest in the

multiparous 78.4%. It was 18.3% in primi and 3.3in grand multi. The incidence of

preior cesearean section was 21.7%, prior abortion was 18.3% twin gestation was

1.7%. severe amemia less than seven contributed to 28.3%. malpresantions

contributed to 23.3%. Ist trimester bleeding 15% of cases II nd trimester bleeding

1.7% and PIH in 3.3%. 56.7% cases required blood trasfusions 18.3% were presented

with shock /hipotetion. PPH was noticed in 8.3% adherent placenta in 3.3%. one of

the case of placenta accrete required cesearean hysterectomy. Perinatal morbidity

requiring resuscitation and NICU admission 43.4%. Pernatal death was 36.6%.

Perinatal mortality was same in both the clical type of placenta previa. The perinatal

death were more in the case delivered vaginaly that is 63.1% than those delivered

abdominaly 24.3% . Perinatal mortality was more in 28 to 33 weeks gestational group

that is 59.3% and infants with birth weight less than 1000gm had very poor survival

rate.

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Buttler (2001) studied the association between maternal serum alpha feto

protein and adverse outcome in pregnancy with placenta previa. He evaluated 107

pregnancies with placenta previa and found that 14/107 cases (13%)(95% CI: 7%,

21%) had MSAFP at least twice the multiple of median. He also found that there was

an increased incidence in hospitalization for APH at gestational age <30 weeks (50%

versus 15%), Delivery at gestational age <30 weeks (29% versus 5%) and preterm

delivery at <34 weeks (14% versus 1%) when compared with control of women who

had MSAFP <2 MOM.

Sheiner (2001) studied deliveries at institutions between 1990-1998

complicated with placenta previa for the incidence, observed risk factors and maternal

and perinatal outcome. He concluded that abnormal placentation per se was not an

independent risk factor for possible obstetric complications. Placenta previa detection

should encourage careful evaluation with timely delivery to reduce maternal and

perinatal mortality.

Gillian(2002) studied the association between previous LSCS and placenta

previa and demonstrated that the joint effect of parity and previous LSCS had higher

chance of placenta previa in prime’s versus previous LSCS had an increased OR of

1.72 and G9 pregnancies with previous LSCS had an OR of 8.76 for placenta previa.

Gilliam et al., (2002).Numerous studies have confirmed the increased risk of

placenta previa following cesarean section. Women who had four or more deliveries

with a single cesarean section had a 1.7 fold increased risk of placenta previa whereas

women with parity greater than four and four or more prior cesarean section had

almost a nine-fold increased risk of placenta previa. This was reported in Europe and

India.

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The maternal mortality rate secondary to placenta previa is approximately

0.03%. The great majority of deaths are related to uterine bleeding and the

complication of disseminated intravascular coagulopathy. In early pregnancy, a partial

previa can often self-correct as the uterus enlarges and the placental site moves

cephalad. Women older than 30 years are 3 times more likely to have placenta previa

than women younger than 20 years. Babies born to women-with placenta previa tend

to weigh less than babies born to women without placenta previa.

A. S. Faiz (2003).Our results showed that the overall prevalence rate of

placenta previa was 4.0 per 1000 births, with the rate being higher among cohort

studies (4.6 per 1000 births), USA-based studies (4.5 per 1000 births) and hospital-

based studies (4.4 per 1000 births) than among case-control studies (3.5 per 1000

births), foreign-based studies (3.7 per 1000 births) and population-based studies (3.7

per 1000 births), respectively. Advancing maternal age, multiparity, previous

Cesarean delivery and abortion, smoking and cocaine use during pregnancy, and male

fetuses all conferred increased risk for placenta previa. Strong heterogeneity in the

associations between risk factors and placenta previa were noted by study design,

accuracy in the diagnosis of placenta previa and population-based versus hospital-

based studies.

Ananth CV (2003) concluded after studying 22368335 singleton pregnancies,

that maternal mortality was 10.7 per 1000 live births with placenta previa and 2.5 per

1000 live births in singleton pregnancies without placenta previa.

Tuzovic (2003) assessed the risk factor of placenta previa in 202 patients over

10 years. He included 1004 random simple singleton pregnancies as controls .He

reached to a conclusion that advanced maternal age, especially >34 years; 3 or more

previous pregnancies, parity of 2 and more ,rising number of previous abortions and

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history of previous cesarean section. He also studied the increasing chance for

placenta previa with history of alcohol and cocaine abuse. History of placenta previa

in previous pregnancies was associated with increased risk for placenta previa. There

was no statistical association with sex of the baby and incidence of placenta previa.

Razia (2003) studied the fetal outcome in major degree of placenta previa in

52 patients out of 1230 deliveries. She concluded that the neonatal mortality due to

prematurity was 40% due to low APGAR score was 70%, due to RDS was 14 babies

(42.42%), anemia was responsible for 3.9% (Hb<13.5g/dl) and 6% (2 babies) had

hyperbilirubenemia. She summarized that regular ANC was a must and antenatal

steroids given in premature pregnancy and neonatal unit must be equipped to come

prepared for premature babies.

Sharma A (2004) studied tocolysis therapy and evaluated the role of ritodrine

in symptomatic placenta previa. Total of 60 women of placenta previa with

gestational age between 28 to 34 weeks were studied, 30 women were given ritodrine

and 30 women were treated symptomatically. They observed that in the study group,

pregnancies were prolonged when compared to the control group (2270 grams versus

1950 grams) (p<0.05). the drug had no adverse effect on mother and fetus.

Jackson RA (2004)- aim of study was to analyze whether pregnancies

following IVF had higher risk of perinatal mortality, preterm delivery and increased

chances of placenta previa. They studied 15 studies from 1978-2002, encompassing a

total of 12283 IVF and 1.9 million spontaneously conceived pregnancies and

concluded significantly higher odds ratio for IVF of each as follows: perinatal

mortality ( OR 2.2; 95% CI 1.6,3.0 ), Prematurity (OR 2.0; 95%, CI 1.7, 2.2) , LBW

( OR 1.8, 95%; CI 1.42,2.2) , Very LBW ( OR 2.7; 95%, CI 2.3, 3.1) and small for

gestational age ( OR 1.6; 95%, CI 1.3,2) . Placenta previa were also significantly

17

more prevalent in IVF group. Hence, IVF patients are required to be treated as high

risk patients and need utmost detailed care and management.

Emily C. Olive (2005) studied 1612 (4.3/1000) women of 375790 women

having significant placenta previa tend to be older, had a previous cesarean section,

required general anesthetic and had preterm delivery only 61% of them delivered in

hospital with 24 hours onsite blood bank; 33% in hospitals with on call blood bank

services after hours and 6% in hospitals with no blood banks. 233 (14%) women had

major morbidity (OR = 15, 95% CI, 12.9- 17.4). Morbidity at term and women

undergoing elective section or deliveries in hospitals with 24 hours blood bank

facilities versus hospitals without it was 40% versus 55%(p=0.06). Hence even today,

guidelines on appropriate level of care for women with placenta previa are needed.

Richard L. Naeye (2005) studied 1006 women and concluded that women who

smoked >20 cigarettes per day had 50% increase in fetal and neonatal death

associated with abruption placenta and placenta previa. He also concluded that a

mother who stops smoking decreases her chance of perinatal mortality by 23% in

abruption and 33% in placenta previa. Maximum benefits were seen in women > 30

years and old.

Oyelue (2006) conducted a study on women with placenta previa and

observed that when placenta is at a distance of >2cm from cervical os, women had

more chances of having a safe vaginal delivery. They also concluded that regional

anesthetic for LSCS is safe and rate of placenta accreta increased due to increase in

rate of primary LSCS.

Ananth (2006) concluded that along with increase in age and parity (3+) the

decrease in spacing between pregnancies is also taken as a separate confounding

factor for placenta previa.

18

Allen VM (2006) searched article in Cochrane Library and Medline from

1990-2005 related to ICSI, IVF, GIFT, ZIFT was excluded. Observed that the

perinatal mortality was significantly higher in the study group, than in spontaneous

conception. He also mentioned the risk for prematurity, low birth weight, gestational

hypertension and placenta previa. In the study group, perinatal mortality in assisted

conception, twin pregnancies appear to be lowest than in spontaneously conceived

twin pregnancies .Due to the above mentioned factors closed surveillance is

mandatory.

Jaswal A Manakatla (2006) concluded that there is an increase in duration of

prolongation of pregnancy with encirclage and perinatal outcome better with

increased weight at birth and better Apgar. Jaswal has encouraged further work in

order to prove it value in women of placenta previa.

Oppenheimer I (2007).Placenta previa is an obstetric complication that occurs

in the second and third trimesters of pregnancy. It may cause serious morbidity and

mortality to both the fetus and the mother. It is one of the leading causes of vaginal

bleeding in the second and third trimesters.

Zlatnik MG (2007).Among the 38 540 women, 230 women had previas

(0.6%). Compared to controls, pregnancies with previa were significantly associated

with preterm delivery prior to 28 weeks (3.5% vs. 1.3%; p = 0.003), 32 weeks (11.7%

vs. 2.5%; p < 0.001), and 34 weeks (16.1% vs. 3.0%; p < 0.001) of gestation. Patients

with previa were more likely to be diagnosed with postpartum hemorrhage (59.7% vs.

17.3%; p < 0.001) and to receive a blood transfusion (11.8% vs. 1.1%; p < 0.001).

Survival curves demonstrate the risk of preterm delivery at each week and showed an

overall higher rate of preterm delivery for patients with a placenta previa.

19

Gobman (2007) analyzed the pregnancy outcome in women with placenta

previa in relation to the number of previous sections in 19 academic centers over 4

years. His study consisted of 868 women, of which 488 cases had no previous

sections, 252 cases with 1 previous section, 76 cases with 2 previous sections and 52

cases with 3 or more previous sections. he concluded that women with increasing

number of previous sections were associated with increased maternal morbidity but

not with increased perinatal morbidity.

Quiying Yang (2008) conducted a retrospective cohort study of 167512627

pregnancies in the US over 5 years (1995-2000). They derived the following results.

The incidences of placenta previa in various races were:

White women- 3.3/1000 pregnancies ( OR- 1.39 to 2.15)

Black women- 3.0/1000 pregnancies

Other races- 4.5/1000 pregnancies

Chinese - 5.6/1000 pregnancies

Japanese – 5.1/1000 pregnancies

Filipinos – 7.6/1000 pregnancies

Asian Indian – 4.5/1000 pregnancies

Korean – 5.9/1000 pregnancies

Vietnamese – 4.4/1000 pregnancies

Other Asian or Pacific islanders – 4.4/1000 pregnancies

The study concluded that the Asian women had excess risk of placenta previa

when compared with white women with an OR of 1.39 to 2.15.

Among the Asians, the Vietnamese had the lowest risk whereas the Filipinos

women had the highest risk for placenta previa. Hence, meticulous USG evaluation

must be carried out, to rule out placenta previa in Asian American pregnant women.

20

Savita Rani Singhal (2008) studied 7510 deliveries. She foun that 226 women

had APH(3.01%). Placenta previa was responsible for 52.64%APH cases. She

concluded a high morbidity and perinatal mortality of 61.5% and 53.5% respectively.

Associated with placenta previa there was high maternal morbidity in terms of

increased anemia. APH and PPH, blood transfusion and cesarean rates and puerperal

pyrexia, associated with placenta previa.

Suk-Joo Choi (2008).The objective of this study was to identify antepartum

risk factors for peripartum hysterectomy in women with placenta previa. The medical

records of women with placenta previa who underwent cesarean section (C/S) were

reviewed retrospectively. Data regarding the reproductive history and peripartum

outcomes were analyzed. Multivariable analysis was used to identify factors

independently associated with hysterectomy. During an 8.5-year period, 346 cases of

placenta previa were identified in 24,987 deliveries (1.4%). An emergent

hysterectomy was performed in 31 patients (9.0%). Multiparity, total previa, history

of abortion, C/S, and placenta previa was more common in the hysterectomy group.

An increasing number of abortions and C/S were associated with a higher frequency

of hysterectomy. By the multivariable analysis, previous abortion, previous C/S, and

total previa were significant risk factors for hysterectomy. We concluded that in

women with placenta previa, history of abortion as well as prior C/S, and a total

previa are strong antepartum risk factors for peripartum hysterectomy.

In Egypt, El Sherbiny, (2008) reported that the risk of placenta accreta is about

15% after one cesarean section and 60% after previous four cesarean section.

Shonali Mayekar (2008) Sthe study concluded that the factors significantly

associated with development of placenta previa were advanced maternal age, number

of previous cesarean sections, number of previous abortions and multiparity; and the

21

incidence of placenta previa was 1.8%. During the period of 2 years (2006 - 2008) she

studied 4759 deliveries. The complications seen most commonly in the neonatal

outcome was prematurity at birth (42.85%) followed by RDS (28.5%) and aspiration

(14.2%). 48% of the babies required resuscitation, out of which 24% required further

NICU admission. The neonatal mortality calculated was 280/1000 live births.

Vergani et al.,( 2009).A recent study concluded that more than two thirds of

women with a distance of more than 10 mm from the placental edge to cervical os

have vaginal delivery without an increased risk of hemorrhage.

Milosevic et al., (2009).A recent study concluded that more than two thirds of

women The exact etiology of placenta previa is unknown. The condition may be

multifactorial and is postulated to be related to multiparity, multiple gestations,

advanced maternal age, previous cesarean delivery, previous. abortion and possibly,

smoking. Unlike first trimester bleeding, second and third trimester bleeding is

usually secondary to abnormal placental implantation.

RCOG (2011).The risk of neonatal mortality is higher for placenta previa

babies compared with pregnancies without placenta previa.

Gorodeski IG The present study evaluated the association between maternal

and fetal-neonatal outcome in women with placenta previa (PP) and the site of

Plaacenta Previa, i.e. low lying, marginal, partial or total. The study group was

composed of 154 women (159 newborns) and the control group of 300 woman (305

newborns). Of the various parameters examined, the following 3 were associated with

Placenta Previa localization: advanced maternal age was associated with major types

of Placenta Previa, while focal accretion of the placenta and neonatal mortality in

cases of vaginal delivery were associated with minor types of Placenta Previa. No

connection was found between antepartum, intrapartum or postpartum blood loss and

22

any specific type of Placenta Previa. A review of the literature and the results of the

present study revealed that the use of the modern aggressive (conservative-active)

management protocol in women with Placenta Previa has resulted in a significant

reduction in the maternal and perinatal complication rates, as well as a relative

decrease in the importance of major types of Placenta Previa and a relative increase of

that of the minor types.

Sheiner E. Placenta previa complicated 0.38% (n = 298) of all singleton

deliveries (n = 78 524). A back-step multiple logistic regression model found the

following factors to be independently correlated with the occurrence of placenta

previa: maternal age above 40 years (OR 3.1, 95% CI 2.0-4.9), infertility treatments

(OR 3.1, 95% CI 1.8-5.6), a previous Cesarean section (OR 1.8, 95% CI 1.4-2.4), a

history of habitual abortions (OR 1.3, 95% CI 1.3-2.7) and Jewish ethnicity (OR 1.3,

95% CI 1.1-1.8). Pregnancies complicated with placenta previa had significantly

higher rates of second-trimester bleeding (OR 156.0, 95% CI 87.2-277.5),

pathological presentations (OR 7.6, 95% CI 5.7-10.1), abruptio placentae (OR 13.1,

95% CI 8.2-20.7), congenital malformations (OR 2.6, 95% CI 1.5-4.2), perinatal

mortality (OR 2.6, 95% CI 1.1-5.6), Cesarean delivery (OR 57.4, 95% CI 40.7-81.4),

Apgar scores at 5 min lower than 7 (OR 4.4, 95% CI 2.3-8.3), placenta accreta (OR

3.6, 95% CI 1.1-9.9) postpartum hemorrhage (OR 3.8, 95% CI 1.2-10.5), postpartum

anemia (OR 5.5, 95% CI 4.4-6.9) and delayed maternal and infant discharge from the

hospital (OR 10.9, 95% CI 7.3-16.1) as compared to pregnancies without placenta

previa. In a multivariable analysis investigating risk factors for perinatal mortality, the

following were found to be independent significant factors: congenital malformations,

placental abruption, pathological presentations and preterm delivery. In contrast,

23

placenta previa and Cesarean section were found to be protective factors against the

occurrence of perinatal mortality while controlling for confounders.

Richard E. Besinger. The clinical use of tocolysis in symptomatic placenta

previa was associated with a clinically significant delay of preterm delivery.

Significant improvement in clinical parameters such as interval from admission to

delivery (39.2 vs 26.9 days, p < 0.02) and birth weight (2520 vs 2124 gm, p < 0.03)

was observed in the tocolysis group. There was no observed statistical difference

between the two treatment groups with regard to incidence of recurrent bleeding,

interval from admission to first recurrent bleeding, and need for transfusion. There

was a trend for patients with multiple bleeding episodes to have been receiving

tocolytic therapy (p < 0.10). A trend for requiring a postpartum transfusion was also

noted in the tocolysis group (p < 0.09). Treated pregnancies receiving long-term

maintenance tocolysis with oral or subcutaneous terbutaline exhibited a greater degree

of pregnancy prolongation than those treated with short-term intravenous magnesium

alone (43.7 vs 15.3 days, p < 0.02).

24

ANATOMY

Placental Organization

The term hemochorial is used to describe human placentation. It derives from

hemo referring to maternal blood, which directly bathes the syncytiotrophoblast, and

chorio for chorion (placenta). The older term hemochorioendothelial takes into

consideration that chorionic tissue is separated from fetal blood by the endothelial

wall of the fetal capillaries that traverse the villous core.

Chorionic Villi

Beginning on approximately the 12th day after fertilization, chorionic villi can

first be distinguished. Mesenchymal cords derived from extraembryonic mesoderm

invade the solid trophoblast columns. These form secondary villi. After angiogenesis

begins in the mesenchymal cores, the resulting villi are termed tertiary. Although

maternal venous sinuses are tapped early in implantation, maternal arterial blood does

not enter the intervillous space until around day 15. By approximately the 17th day,

however, fetal blood vessels are functional, and a placental circulation is established.

The fetal-placental circulation is completed when embryonic blood vessels are

connected with chorionic vessels. In some villi, there is failure of angiogenesis from

lack of circulation. They can be seen normally, but the most striking exaggeration of

this process is seen with hydatidiform mole.

Villi are covered by the outer layer of syncytium and inner layer of

cytotrophoblasts, which are also known as Langhans cells. Cytotrophoblast

proliferation at the villous tips produce the trophoblastic cell columns that form

anchoring villi. They are not invaded by fetal mesenchyme, and they are anchored to

the decidua at the basal plate. Thus, the base of the intervillous space faces the

maternal side and consists of cytotrophoblasts from cell columns, the covering shell

25

of syncytiotrophoblast, and maternal decidua of the basal plate. The base of the

chorionic plate forms the roof of the intervillous space and consists of two layers of

trophoblasts externally and fibrous mesoderm internally. The “definitive” chorionic

plate is formed by 8 to 10 weeks as the amnionic and primary chorionic plate

mesenchyme fuse together. This formation is accomplished by expansion of the

amnionic sac, which also surrounds the connective stalk and the allantois and joins

these structures to form the umbilical cord (Kaufmann and Scheffen, 1992).

The human hemochorial placenta can be subdivided into hemodichorial or

hemomonochorial (Enders, 1965). The dichorial type is more prominent during the

first trimester of gestation. It consists of the inner layer of the cytotrophoblasts with

the associated basal lamina, covered by a layer of syncytiotrophoblasts. Later in

gestation the inner layer of cytotrophoblasts is no longer continuous, and by term

there are only scattered cells present. These create a narrowest hemomonochorial

barrier that aids nutrient and oxygen transport to the fetus.

Placental Development

Development of the chorion and Decidua

In early pregnancy, the villi are distributed over the entire periphery of the

chorionic membrane. A blastocyst dislodged from endometrium at this stage of

development appears shaggy. As the blastocyst with its surrounding trophoblasts

grows and expands into the decidua, one pole extends outward toward the endometrial

cavity. The opposite pole will form the placenta from villous trophoblasts and

anchoring cytotrophoblasts. Chorionic villi in contact with the decidua basalis

proliferate to form the chorion frondosum – or leafy chorion which is the fetal

component of the placenta. As growth of embryonic and extraembryonic tissues

26

continues, the blood supply of the chorion facing the endometrial cavity is restricted.

Because of this, villi in contact with the deciduas capsularis cease to grow and

degenerate. This portion of the chorion becomes the avascular fetal membrane that

abuts the deciduas parietalis, that is, thechorion leave – or smooth chorion. The

chorion laeve is generally more translucent than the amnion and rarely exceeds 1-mm

thickness. The chorion is composed of cytotrophoblasts and fetal mesodermal

mesenchyme that survives in a relatively low-oxygen atmosphere.

Until near the end of the third month, the chorion laeve is separated from the

amnion by the exocoelomic cavity. Thereafter, they are in intimate contact to form an

avascular amniochorion. These two structures are important sites of molecular

transfer and metabolic activity. Moreover, they constitute an important paracrine arm

of the fetal-maternal communication system.

With continued expansion of the embryo-fetus, the uterine lumen is

obliterated, and the chorion laeve becomes contiguous with the entire maternal

decidua parietalis that is not occupied by the placenta. As the fetus grows, the decidua

capsularis merges with the parietalis. The capsular is then is largely lost by pressure

and the attendant loss of blood supply. The area of decidua where deciduas capsularis

and decidua parietalis merge is referred to as the decidua vera.

Maternal Regulation of Trophoblast Invasion and Vascular Growth

Decidual natural killer cells (dNK) accumulate in the deciduas during the first

half of pregnancy and are found in direct contact with trophoblasts. These cells lack

cytotoxic functions as well as other unique properties that distinguish them from

circulating natural killer cells and from natural killer cells in the endometrium prior to

pregnancy (Manaster and co-workers, 2008). This is important because it prevents

27

them from recognizing and destroying fetal cells as “foreign”. Hanna and associates

(2006) have elucidated the ability of dNK cells to attract and promote invasion of

trophoblast into the decidua and promote vascular growth. Decidual NK cells express

both interleukin-S and interferon-inducible protein-IO, which bind to receptors on

invasive trophoblast cells to promote their invasion into the decidua toward the spiral

arteries. Decidual NK cells also produce proangiogenic factors, including VEGF and

placental growth factor (PIGF), which promote vascular growth in the decidua. In

addition, trophoblasts secrete specific chemokines that attract the dNK cells to the

maternal-fetal interface. Thus, both cell types simultaneously attract each other to

promote decidual population.

Trophoblast Invasion of the Endometrium

The extravillous trophoblast of the first-trimester placenta are highly invasive.

They form columns of cells that extend from the endometrium to the inner third of the

myometrium. Recall that hemochorial placental development requires invasion of en-

dometrium and spiral arteries. The invasive ability of trophoblasts results from their

ability to secrete numerous proteolytic enzymes capable of digesting the extracellular

matrix as well as activating proteinases already present in the endometrium.

Trophoblasts produce urokinase-type plasminogen activator, which converts

plasminogen into the broadly acting serine protease plasmin. This in turn both

degrades matrix proteins and activates matrix metalloproteinases (MMPs), which are

a family of structurally similar enzymes. One member of the family, matrix

metalloproteinase-9 (MMP-9), appears to be critical for human trophoblast invasion.

MMP-9 production is increased by trophoblast factors such as ILl and heG as well as

paracrine uterine factors such as leukemia inhibiting factor and colony-stimulating

28

factor-1 (Bischof, 2002; Fitzgerald, 200S; Librach, 1991, and all their colleagues).

The relative ability to invade maternal tissue in early pregnancy compared

with limited invasiveness in late pregnancy is controlled by autocrine and paracrine

trophoblastic and endometrial factors. Trophoblasts secrete insulin-like growth factor

II, which acts in an autocrine manner. It promotes invasion into the endometrium,

whereas decidual cells secrete insulin like growth factor binding protein type 4, which

blocks this autocrine loop. Thus, the degree of trophoblast invasion is controlled by

regulation of matrix degradation as well as by factors that cause trophoblast

migration.

Integrin subunit expression also appears important to control trophoblast

invasion and adhesive interactions between trophoblast cells during column

formation. Recall that the decidual cell becomes completely encased by a pericellular

extracellular matrix membrane. This “wall” around the decidual cell provides

scaffolding for attachment of the cytotrophoblasts of the anchoring villi. The

cytotrophoblast first elaborate selected proteinases that degrade decidual extracellular

matrix. Thereafter, expression of a specific group of integrins enables the docking of

these cells. There are also integrin-mediated adhesive interactions of trophoblast cells

with each other. In particular, the interaction of L-selectin with its carbohydrate

ligands in the cytotrophoblast is important in formation and maintenance of cell

columns (Prakobphol and colleagues, 2006). Trophoblasts are further secured by fetal

fibronectin (Feinberg and colleagues, 1991). Fetal-specific fibronectin (fFN).is a

unique glycopeptide of the fibronectin molecule. It is also called trophoblast glue to

describe a critical role in the migration and attachment of trophoblasts to maternal

decidua. And related, presence of fFN in cervical or vaginal fluid is used as a

prognostic indicator for preterm labor.

29

Invasion of Spiral Arteries

One of the most remarkable features of human placental development is the

extensive modification of maternal vasculature by trophoblasts, which are by

definition of fetal origin. These events occur in the first half of pregnancy and are

considered in detail because of their importance to uteroplacental blood flow. They

are also integral to some pathological conditions such as preeclampsia and fetal-

growth restriction. Modifications of spiral arteries are carried out by two populations

of extravillous trophoblast-interstitial trophoblast, which surrounds the arteries, and

endovascular trophoblast, which penetrates the spiral artery lumen.. The role of the

endovascular trophoblast, function of the interstitial trophoblast has more recently

been investigated (Benirschke and Kaufmann, 2000; Pijnenborg and colleagues,

1983). These interstitial cells are now recognized to constitute a major portion of the

placental bed, penetrating the decidua and adjacent myometrium. They aggregate

around spiral arteries, and their functions may include vessel preparation for

endovascular trophoblast invasion.

Endovascular trophoblast enters the lumen of the spiral arteries and initially

forms cellular plugs. It then destroys vascular endothelium via an apoptosis

mechanism and invades and modifies vascular media. Thus, fibrinoid material

replaces smooth muscle and connective tissue of the vessel media. Spiral arteries later

regenerate endothelium. Hamilton and Boyd (1966) report that Friedlander in 1870

first described structural changes in spiral arteries. Invading endovascular trophoblast

can extend several centimeters along the vessel lumen, and they must migrate against

arterial flow. These vascular changes are not observed in the decidua parietalis, which

is, in decidual sites removed from the invading cytotrophoblasts. Of note, invasion by

trophoblasts involves only the decidual spiral arteries and not decidual veins.

30

Ramsey and Donner (1980) described that development of these utero

placental vessels proceeds in two waves or stages. The first wave occurs before 12

weeks post fertilization and consists of invasion and modification of spiral arteries up

to the border between deciduas and myometrium. The second wave is between

12 and 16 weeks and involves some invasion of the intramyometrial segments of

spiral arteries. The remodeling by this two-phase invasion converts narrow-lumen,

muscular spiral arteries into dilated, low-resistance uteroplacental vessels. Molecular

mechanisms of these crucial events, and their significance in the pathogenesis of

preeclampsia and fetal-growth restriction, have been reviewed by Kaufmann (2003)

and RedHorse (2006) and their associates.

Establishment of Maternal Blood FlowAbout 1 month after conception, maternal blood enters the intervillous space

in fountain-like bursts from the spiral arteries. Blood is propelled outside of the

maternal vessels and sweeps over and directly bathes the syncytiotrophoblast. The

apical surface of the syncytiotrophoblast consists of a complex microvillous structure

that undergoes continual shedding and reformation during pregnancy.

Villus BranchingAlthough certain villi of the chorion frondosum extend from the chorionic

plate to the decidua to serve as anchoring villi, most arborize and end freely in the

intervillous space. As gestation proceeds, the short, thick, early stem villi branch to

form progressively finer subdivisions and greater numbers of increasing smaller villi.

Each of the truncal or main stem villi and their ramifications (rami) constitute a

placental lobule, or cotyledon. Each lobule is supplied with a single truncal branch of

the chorionic artery. And each lobule has a single vein so that lobules constitute

31

functional units of placental architecture.

Placental Growth and MaturationPlacental Growth

In the first trimester, placental growth is more rapid than that of the fetus. But

by approximately 17 postmenstrual weeks, placental and fetal weights are

approximately equal. By term, placental weight is approximately one sixth of fetal

weight. According to Boyd and Hamilton (1970), the average placenta at term is 185

mm in diameter and 23 mm in thickness, with a volume of 497 mL and a weight of

508 g. These measurements vary widely, and there are multiple variant placental

forms and several types of umbilical cord insertions.

Viewed from the maternal surface, the number of slightly elevated convex

areas, called lobes, varies from 10 to 38. Lobes are incompletely separated by grooves

of variable depth that overlie placental septa, which arise from folding of the basal

plate. Although grossly visible lobes are commonly referred to as cotyledons, this is

not accurate. Correctly used, lobules or cotyledons are the functional units supplied by

each primary villus.

The total number of placental lobes remains the same throughout gestation,

and individual lobes continue to grow – although less actively in the final weeks

(Crawford, 1959).

Placental Maturation

As villi continue to branch and the terminal ramifications become more

numerous and smaller, the volume and prominence of cytotrophoblasts decrease. As

the syncytium thins, the fetal vessels become more prominent and lie closer to the

surface. The villous stroma also exhibits changes as gestation progresses. In early

32

pregnancy, the branching connective-tissue cells are separated by an abundant loose

intercellular matrix. Later, the stroma becomes denser and the cells more spindly and

more closely packed.

Another change in the stroma involves the infiltration of Hofbauer cells,

which are fetal macro phages. These are nearly round with vesicular, often eccentric

nuclei and very granular or vacuolated cytoplasm. Hofbauer cells are characterized

histochemically by intracytoplasmic lipid and by phenotypic markers specific for

macrophages. They increase in numbers and maturation state throughout pregnancy.

These macrophages are phagocytic, have an immunosuppressive phenotype, can pro-

duce a variety of cytokines, and are capable of paracrine regulation of trophoblast -

functions (Cervar and colleagues, 1999; Vince and Johnson, 1996).

Some of the histological changes that accompany placental growth and

maturation provide an increased efficiency of transport and exchange to meet

increasing fetal metabolic requirements. Among these changes are decreased

syncytiotrophoblastic thicknesses, significant cytotrophoblast reduction, decreased

stroma, and increased number of capillaries with their approximation to the syncytial

surface. By 16 weeks the apparent continuity of the cytotrophoblasts is lost. At term,

the covering of the villi may be focally reduced to a thin layer of syncytium with

minimal connective tissue in which thin-walled fetal capillaries abut the trophoblast

and dominate the villi.

There are some changes in placental architecture that can cause decreased

efficiency of placental exchange if they are substantive. These include thickening of

basal lamina of trophoblast or capillaries, obliteration of certain fetal vessels, and

fibrin deposition on the villi surface.

33

.

Fig 2

34

Summary of development of placenta

Chorion frondosum and decidua basalis

In the early week of development chorionic villi cover the entire surface of the

chorion. As pregnancy advances villi on the embryonic pole continue to grow and

expand, thus giving rise to the chorion frondosum, villi on the abembryonic pole

degenerate, and by the 3rd month this side of chorion is smooth known as the chorion

leave.

The difference in embryonic and abembryonic poles of the chorion is reflected

in the structure of the decidua, which is the functional layer the endometrium and is

shed during parturition. The deciduas over the chorion frondosum, the deciduas

basalis, consist of compact layer of large cells, decidual cells, with abundant amounts

of lipid and glycogen. This layer, the decidual plate is tightly connected to the

chorion. The decidual layer over the abembryonic pole is known as the decidua

capsularis. With increase in the size of the chorionic vesicle, this layer becomes

stretched and degenerates subsequently, the chorion leave comes into contact with

uterine wall (deciduas parietals) on the opposite side of the uterus, and two fuse

obliterating the uterine lumen. Hence the only portion of chorion participating in the

exchange process is the chorion frondosum, which together with the deciduas basalis,

makes the placenta. Similarly fusion of the amnion and chorion to form the amnio-

chorionic membrane obliterates the chorionic cavity; it is this membrane that ruptures

during labour.

Structure of the placenta

By the beginning of the 4th month the placenta has two components

a. Fetal portion formed by the chorion frondosum

35

b. Maternal portion formed by the deciduas basalis.

On the fetal side chorionic plate borders the placenta.

On the maternal side, it is bordered by the deciduas basalis.

In the junctional zone trophoblast and decidua cell intermingle. The zone is

characterized by decidual and syncytial giant cells rich in amorphous extracellular

material. By this time most cytotrophoblast cells have degenerated, between chorionic

and decidual plates are the intervillous that are filled with maternal blood. They are

derived from lacunae in the syncytiotrophblast and are lined with syncytium of fetal

origin. The villous trees grow into the intervillous blood lakes.

During 4th and 5th month the decidua forms a number of decidua septa which

project into intervillous spaces but do not reach the chorionic plate. These septa have

core of maternal tissue but their surface is covered by a layer of syncytial cells, so that

at all times syncytial layer separates maternal blood in intervillous lakes from fetal

tissue of the villi. As a result of this septum formation, the placenta is divided into a

number of compartments of cotyledons. Since the decidual septa do not reach the

chorionic plate, contact between intervillous spaces in the various cotyledons is

maintained.

As a result of the continuous growth of the fetus and expansion of the uterus

the placenta also enlarges. It increase in the surface are roughly parallels that of the

expanding uterus, and throughout pregnancy it covers approximately 15-30% of the

internal surface of the uterus. The increase in the thickness of the placenta results

from arborization of existing villi and is not caused by further penetration into

maternal tissues.

36

Fig.3

36

Fig.3

36

Fig.3

37

Full term placenta

At full term placenta is discoid shape a diameter of 15-25 cm, 3 cm thick

weight of 500-600 gm. At birth it is torn from the uterine wall and approximately 30

minutes after birth of the child, is expelled from the uterine cavity.

Mechanism of separation of Placenta.

Marked retraction reduces effectively the surface area at placental site to half.

But as placenta is inelastic it cannot pace with extent of diminution resulting in

buckling. The plane of separation runs through deep spongy layer of decidua basalis.

Central separation (Schlutze)

The detachment of placenta from its uterine attachment starts at the center

resulting in opening of few uterine sinuses and accumulation of blood behind placenta

with increasing contraction detachment occurs facilitated by weight of placenta and

retro placental blood whole of the placenta get detached.

Marginal Separation (Mathews Duncan)

The separation starts at the margin as it is unsupported, with increasing

contraction more placenta get separated, more frequently seen.

Separation of membranes.

The membranes which are attached loosely in the active part are throne in to

multiple folds. Those attached to lower segment are already separated during its

stretching, this separation is facilitated by uterine contraction and mostly by weight of

the placenta. The membranes so separated, carry with them remnants of decidua vera.

38

Mechanism of control of bleeding.

After placental separation innumerable torn sinuses which have circulation of

blood from uterine and ovarian vessels have to be obliterated. The occlusion is

affected by complete retraction whereby the arteries as they pass tortuously through

the interlacing intermediate layer of myometrium are literally clamped. This living

ligature is the principle mechanism of hemostasis. Thrombosis occurs to occlude the

torn sinuses facilitated by hyper coagulable state of pregnancy.

Apposition of the wall of uterus following expulsion of the placenta myo-

tamponade.

When after birth the placenta is viewed from the maternal side 15-20 bulging

areas the cotyledons covered by a thin layer of decidua basalis are seen. Groves

between the cotyledons formed by decidual septa much of the deciduas remains

temporarily in the uterus and is expelled with subsequent uterine bleeds.

The fetal surface of the placenta is covered entirely by the chorionic plate, a

number of large arteries and veins, the chorionic vessels converge towards the

umbilical cord. The chorion, in turn in covered by the amnion. Attachment of the

umbilical cord is usually eccentric and occasionally margin. Rarely does it insert into

the chorionic membranes outside the placenta.

Lower uterine segment

Anatomically:-

That part of the uterus, which lies between anatomical and histological internal

os or that portion of the uterus where the uterovesical fold of peritoneum is loosely

adherent. This definition only serves at laparotomy.

39

Physiologically:–

It is that position which passively stretches during labour and takes hardly any

active contractile part in expulsion of placenta.

In metric terms: –

It is that portion which lies within 3 inches, 5-7.5 cms of the internal os. This

definition is most practical value in diagnosis because it represents the distance over

which the uterine cavity can be explored by examining finger passed through the

cervix.

Lower uterine segment starts developing as early as 8th week of gestations, at

20th week of gestation, it measures about 0.5 cm, gradually increases in length more

slow nearing terms, it measures about 5-7.5 cm in length nearing term.

40

DEFINITION:11

Placenta previa refers to a placenta that is situated wholly or partially

within the lower uterine segment at or after 28 weeks gestation.

Prior to 28 weeks placenta may be situated in or close to the developing

lower uterine segment and is described as low lying placenta, most low lying

placenta will not become placenta previa.The term previa (L in front of) denotes

the position of the placenta in relation to the presenting part.

Fig 4. Normal and placenta previa

41

INCIDENCE:12,13

One third of antepartum hemorrhage belongs to placenta previa.

At term incidence 0.4-0.8% of all pregnancies it is common incidental

finding in 2nd trimester accounting for 4% at 20-24 weeks. But at term only 0.4%

because of differential growth of uterus and placenta. 80% of cases found in

multiparous, incidence increase beyond age 35 with high birth order pregnancy

and in multiple pregnancies.

Increase in family planning acceptance with limitation and spacing of birth

lowered the incidence of placenta previa.

The incidence of placenta previa quoted by different authors

Total placenta previa – 23.0% to 31.3%Partial placental previa – 20.6% to 33.0%Low lying placenta – 27.0% to 54.9%

Placenta previa is significant cause of premature delivery and maternal

morbidity perinatal mortality rates are high as 81/1000 were reported earlier days

an overall incidence of 22% of RDS have been reported. In present day placenta

previa is seldom responsible for maternal mortality but the maternal morbidity in

striking especially in patients who had one or more prior cesarean section.

The rate of primary caesarean delivery has been steadily increasing as the

population attributable risk for prior caesarean delivery, subsequent risk of

placenta previa is 14%.This implies that by reducing primary and repeat cesarean

delivery rates by half, the risk for placenta previa could be reduced by14%

similarly the rate of spontaneous and induced abortions are 20% and 5%. If this

rates are reduced by 50% then, 6.5% and 1.5% of placenta previa cases could

potentially be averted.

42

Fig 5. Placenta Previa – Classifications17,46,48

43

Fig. 6 Different Classification

The placental encroachment is graded according to the area occupied with respect

to internal os.

1. William’s ClassificationA. Total placental previa: The internal cervical os is covered completely

by the placenta.

B. Partial placenta previa: The internal os is partially covered by the

placenta.

C. Marginal placenta previa: The edge of the placenta is at the margin of

the internal os.

D. Low lying placenta: The placenta is implanted in the lower uterine

segment such that the placental edge does not reach the internal os but

is in close proximity to it.

44

2. Newman White (1929)a. Central : As the placental cover the entire internal os

b. Marginal : placental reaches upto margin of internal os

c. Lateral : placenta merely dips into the lower segment and is

just within the reach of the examining finger.

3. According to F.J. BrownI degree – Type I – where placenta dips into lower uterine segment by its

lower margin, the greater part of it being in the upper segment.

II degree – Type II – when edge of the placenta reaches the internal os

III degree – Type III – when placenta overlaps / covers the internal os when

it is closed but does not cover it entirely when fully dilated.

IV degree – Type IV placenta covers the whole internal os when it fully

dilated.

45

Fig 7. Types of placenta previa

4. Cavanagh and Woods classification (1987)

Type 1 – Low placenta implantation but the lower edges does not reach the

internal os.

Type II – The lower placenta edge reaches the internal os but does not

covers it.

46

Type III – The placenta completely covers the internal os when the cervix

is closed but only partially covers the internal os when the cervix is dilated.

Type IV – The placenta covers the internal os when cervix is closed or

dilated.

5. Ultrasound classification Jauniaux and Campbell

Type I – Low lying placenta positioned close to the internalos (within 5

cms)

Type II – when edge of the placenta reaches internal os

Type III – when it covers internal os when it is closed.

Type IV – the placenta covers the internal os when cervix is dilated.

In the majority placenta lies in the anterior or posterior wall the latter being

more common.

6. Placental overlay method by Curtis J. (1947)

Based on estimation of an area of cervical canal which would be covered

by placenta if the cervix is completely dilated.

In this cervical dilatation is considered from 0-10 cm in diameter which is

maximum dilatation. The average diameter of placenta is 20 cm at term.

a. Normal placenta is one which is not palpable even after full dilatation

of cervix 10 cms.

b. Low implantation (upto 30%) where placental edge can be palpated

through the dilated os 4 cms.

47

c. Partial placenta previa (30-40%) when placental edge palpated through

cervical os with more than 4 cm dilated.

d. Central placenta previa when more than 50% of the placental tissue is

covering the internal os.

7. Dewhurt’s Classification

Grade I Placenta extends to the lower segment

Grade II Placenta extends to os

Grade III Placenta covers os eccentrically

Grade IV Placenta covers os centrally

Clinically placenta previa is classified as:

Minor: – encompassing type I and type II anterior

Major: – encompassing type II posterior type III and type V.

8. Radiological method by V.B. Athmaran and Banerji (1976) by single

film angioplacentography.

Grade 0 No placenta praevia

Grade I Include Types I and II

(In Type I, placental edge extends down to the level of

inferior edge of the sacroiliac joint. In Type II, placental

edge extends down to the level of ischial spine.)

Grade II Includes Types III and IV.

(In Type III, placental edge extends below the level of ischial

spine. In Type IV, placental edge is above the level of

48

symphysis pubis on both sides of pelvis.) In this method, the

overall accuracy in diagnosing and excluding placenta previa

is 100%.

Oppenheimer et al. (1991) performed transvaginalsonography and measured

distance between the lower edge of placenta and internal os. The measurement less

than or equal to 2 cms underwent caesarean section and they made traditional

classification obsolete.

9. Oppenheimer a classification of Placenta previa AMJ Obstetricgynecal

2009

New classification could describe the distance on transvaginalsonography

that is performed within 28 days of term in the following way.

1. >20 mm away from internal os caesarean section delivery for previa not

indicated.

2. 11-20 mm lower likelihood of bleeding and need for caesarean section

delivery.

3. 0-10 mm higher likelihood of bleeding and need for caesarean section delivery.

4. Overlap of internal os by any distance caesarean section delivery indicated.

Vergani et al. provoke that the time honoured classification of placenta previa

should be abandoned. Treatment decision should be based on the measured

distance of placental edge to internal cervical os by transvaginalsonography

wherever possible.

49

The classification of placental previa is important as there is an increasing

incidence of morbidity and mortality in the mother and fetus as the grade of

placenta previa increases, regardless of type of classification used, also

classification assists in management decision.

These definitions of different types of placenta previa are based on findings during

vaginal examinations performed at time of delivery (obsolete now) or on visual

observation of placenta and cervix relationship at the time of caesarean section.

Despite the apparent precision of their definitions prenatal and intrapartum

differentiation between marginal, partial and low lying placenta is difficult.

By one of the transperinealendovaginal ultrasound it is possible now-a-

days to define precisely the relation of the lower border of the placenta to the

internal cervical os.

Incidence of spontaneous abortions are more frequent in pregnancies with

low placental implantation (0.4 to 0.6 of all live births).

The risk of placenta previa in grand multipara is 5%, whereas in nullipara

is 0.2% with a recurrence rate of about 4-8%.

50

ETIOLOGY

The etiology of placenta previa is unclear however damage to endometrial

and myometrium or any process that interferes with placental migration increase

the risk of placenta previa.

Placenta previa result from implantation of zygote low in the cavity of the

uterus, the actual implantation site being in the isthmus or in the immediate

neighborhood of the isthmus, Robert Barnes 1853 described this primary isthmal

implantation.

Newman &Luh 1934 described secondary isthmal implantation – placenta

in its development comes to extend into the isthmus.

Abnormalities of the size, site of placenta and site of cord insertion have been

noticed in placenta previa.

Before going further there is rare nidation cervical pregnancy, in which the

zygote becomes implanted and develops in the cervical canal.

Dropping down theoryThe fertilized ovum drops down and is implanted in the lower segment.

Poor decidual reaction in the upper segment may be the cause. Failure of the

zonapellucida to disappear in time, This explain the formation of central placenta

previa.

Persistence of Chorionic activity:Persistence of Chorionic activity in the decidua capsularis and its

subsequent development into capsular placenta which comes in contact with

decidua Vera of the lower segment can explain the formation of lesser degrees of

Placenta previa.

51

Defective decidua:Defective decidua results in spreading of chorionic villi over wide area on

uterine surface to get nourishment. During this process not only Placenta become

membranous but encroaches on to the lower segment. Such a placenta previa may

invade underlying decidua or myometrium to cause placenta accreta, increta,

percreta.

Large placental surface:Large placental surface in multiple pregnancies and Rh iso-

immunisationcould predispose to lower implantation.

A delayed implantation of fertilized ovum could be another cause.

Normal physiologyThe blastocyst usually implants into upper anterior portion of uterus with a

rich vascular supply. After the implantation, the chorionic villi grow into deciduas.

At first these chorionic villi surround the blast cyst soon after the portion of

chorionic villi in contact with deciduasbasalis proliferates into placenta and

remaining atrophies.

The chorionic villi are 2 types one opens into intervillous space and other

in the anchoring villi to stabilize the embryo and placenta and is normally

confined to endometrium.

Functional villi have two invasions.

Primary invasion into endometrium.

Secondary invasion into 1/3 of myometrium.

The nitabuchs membrane limits the invasion of anchoring villi.

52

PATHOPHYSIOLOGY

It is probable that as a result of some local aberration in uterine blood

supply the distinction between the areas of chorionf rondusum and chorionic leave

does not occur and the developing ovum comes to derive its nourishment from

lower region of uterus than in customary. With placenta praevia blastocyst

implants itself in the lower segment over or near the internal os.49,50

Decidual reaction in lower uterine segment is often inadequate so abortion

occurs, also because of local inadequacy of decidua, patchy areas of morbid

adhesion may occur

A large percentage about 90% migrates upward. In the presence of more

than 2 cm placental cervical overlaps migration is rare. (Oppenheimer & others

2001).

There are 2 current theories.

1. The growth of lower uterine segment form 0.5cm -5 cm causes movement of

placenta away from the internal os( Clark et al,2004).50

2. Second theory postulates that the chorionic villi have the ability to grow in one

areas and to remain dormant in other. (Bhide&Thilaganathan).11,51

The deciduasbasalis is less developed in lower segment of uterus. The

fibrinoid layer of nitabach which stops further invasion of chorionic villi may be

absent. Therefore placenta tissue may come into direct contact with the

myometrium and placenta accreta, Increta and per creta can develop.

Millon (1959) showed relatively high incidence of placenta accreta.

In multipara hysterectomy is probable safe mode of delivery.

53

It was later proposed that placenta previa could develop after implantation

in poorly vascularized upper uterine segment. The placenta thus spread over a

larger area in order to function normally, on occasion extending into the lower

segment.

Due to increase vascularity, lower uterine segment and cervix becomes soft

and more friable. Certainly in some cases of placenta previa the placenta is found

to be thin and have large surface area. There is often tongue shaped extension

from main placental mass. Extensive areas of degeneration with infarction and

calcification may be evident, Succinturate lobes are not uncommon. The

association with high parity might indicate that a highly fertile patient is more

likely to retain, the ovum when its implants low within the uterus.

Abnormalities in placenta formation, cord insertion and vessel distribution

more common with placenta previa. All varieties of placental malformation are

seen: Ex: Bipartite, SuccenturateMembranacea. Fenestrate and Accreta. Equally

varied are the insertion of umbilical cord and distribution of the umbilical blood

vessels. Eg; Battledore insertion and velamentous distribution of the vessels.

Risk factors:

1. Advanced maternal age11,50,56

The risk increases with increasing maternal age. Ananth et al. 1996 has

shown that women older than 35 years have nearly 9 fold increased risk of

developing placenta previa than women in younger age group. One in 100 for

women >35 years of age. As women age collagen progressively replaces normal

54

muscle in the wall of myometrial arteries. These lesions may restrict the luminal

expansion of the arteries and consequently restrict the blood flow to placenta.

The atrophic changes in older women may also result in defective

vascularization of deciduas. Both under perfusion and under vascularization have

been postulated in development of placenta previa.

2. Parity12,50,56

Higher the parity higher the incidence of placenta previa.

1.2 times following one delivery

1.5 following 2 deliveries

0.2% in nulliparous 5% grand multi

2.2% of incidence in multiparity compared to 0.3% in general population

In nulliparous women lower segment formation occur mostly in weeks

leading uptolabour.

In multiparous women this development in less pronounced and may occur

at part of the labour process. This may explains the large observed difference in

incidence of placenta previa between nulliparous and multiparous.

3. Smoking and cocaine abuse50,57

Probably due to defective decidualization leads to increased risk of

placenta previa.

Williams and colleagues 1991 have shown that 2 fold increase risk and is

confirmed by other studies of Ananth (2003) carbon monoxide hypoxemia causing

compensatory placental hypertrophy and also related defective decidual

vascularization.

55

The women smoking more than 20 cigarettes per day had risk of 2.6 to 4.4

times of placenta previa and in those who stop smoking, perinatal mortality

decreased by 33%.

4. Multiple pregnancy/Placental size50,56

Ananth et al 2003 has shown 40% higher among twins in comparison to

singleton pregnancies because the placenta due its bigger size has a greater chance

of encroaching to the lower segment. This was confirmed in a study which showed

incidence of placenta previa of 0.55% for twin as compared to 0.31% in singleton

gestation.

5. Previous placenta previa (recurrence of 4.8%)

Williams reported recurrence in four consecutive pregnancies Gorodeski

recorded incidence of 3.2%, 6 times more compared to general population.

6. Previous cesarean delivery56,58

The incidence of placenta previa increase in a linear way with increase in

number of previous cesarean section. A retrospective analysis of 292 cases of

placenta previa by Clark and colleagues showed an incidence of 0.26% in a

unscarred uterus and 0.65% after one cesarean section. 2.2% after two and 10 to

16% after four or more previous cesarean sections.(Nielson et al 1989)61,62

It is biologically possible that scar in the lower segment impedes the

placental migration.

The risk of placenta previa is highest in pregnancy immediately following

cesarean section and with multiparous with previous lower segment caesarean

56

section. Failure of lower segment development due to scar tissue as well as

inability of low lying placenta to migrate across scar tissue.

Ligation of uterine vessels may further increase the risk of damage to the

endometrium and myometrium leading to low implantation of placenta in next

pregnancy (Taylor et al 1994)37.

Cesarean Section, termination of pregnancy and intrauterine surgery

(Ananth et al., 1996)56,58 and manual removal of placenta have shown risk of

placenta previa, is highest in the pregnancyimmediately following cesarean

delivery and increase with number of previous Cesarean Section. 2.6 fold increase

risk of placenta previa in subsequent pregnancy (Ananth et al 1999b)59,60,61.

One large scale population based study showed Cesarean Section for first

five birth is associated with 47% increase risk of placenta previa and 40% increase

risk of placental abruption in second pregnancy than with singleton (Yang et al

2007)60,61.

The risk of morbidity adherent placenta17,40,61,65, Placenta accreta is

increased in anterior placenta previa especially associated with previous Cesarean

Section.

The risk of placenta accreta is an unscarred uterus with placenta previa is

5%. This rises to 24% with placenta previa and one previous Cesarean Section

and increase to 67% with placenta previa and four or more Cesarean Section

(Clark et al 1985), prior Cesarean Section with placenta previa increase incidence

of Cesarean hysterectomy61 by 25%, Friederiksen and co-workers 1999 reported

25% hysterectomy rate in women with repeat section with praevia with only 6%

compared in primary cesarean for placenta previa40,65.

57

7. Endometrial damage and associated with previous abortions

Damage to the endometrium or myometrium has been shown to be a risk

factor for low implantation site.

There are significant association between placenta previa and previous

dilation and curettage.

Spontaneous abortion or evacuation or retained product of conception has

been described. A six fold increase in the risk of placenta previa following medical

termination of pregnancy in the first trimester has been reported however number

of other studies have been unable to demonstrate any association with therapeutic

abortion, method of suction evacuation as opposed to sharp curettage accounts for

different finding. Any of above procedure lead to endometrial damage, which is

turn lead to endometrial scarring, if significant would predispose to an abnormal

site of placental implantation and to increase placental surface area.

8. Preterm delivery

Spontaneous labour before 37 week is more commonly complicated by

bleeding from a low lying placenta than labour in a term pregnancy. A recent

study examined 198 placentas from preterm deliveries at gestation between 28-37

week and reported an incidence of 2.91% for placental previa and low

implantation. This may be due to delivery before the lower uterine segment not yet

well formed. Hence chances of placental migration is less.

Women with placenta previa the uterine contractions that normally occur

during gestation cause separation of the placenta from its implantation site in the

cervix and lower uterine segment causing bleeding in choriodecidual interface,

thrombin release, and activation of the final pathway of parturition. Another

58

possibility is that the uterine contractions are caused by stress activation of the

fetal hypothalamic-pituitary-adrenal axis secondary to fetal growth restriction that

is a common finding in women with abnormal placentation. In the majority of

patients with placenta previa, contractions occur simultaneously or shortly after a

bleeding episode and, similarly to what happens in women with abruption, they

are resistant to tocolysis.

9. Ethnic origin and socio-economic status

The effect of ethnic origin on the incidence of placenta previa was

considered in a study and higher incidence (OR 1.39-2.15, CI 95%) was found in

Asian women when compared with white women. Vietnamese (4.4/1000) had

lowest incidence, while the Philippine women had highest incidence (7.6/1000).

The incidence in Indian women was 4.5/1000.

Retrospective cohort study involved Taiwanese women:

Risk factor for placenta previa among the pregnancies analyzed, risk factors for

placenta previa included a prior preterm birth, technology-assisted conception,

smoking or working during pregnancy, maternal age of or greater than 35years

and previous induced abortion , concluded that risk factors for placenta previa

were found to be same for Asian women as those previously recorded for

American and European women, but additional factors were detected.

10. Uterine Scar and Pathology

Uterine scars from surgical procedures as myomectomy endometritis,

submucous fibroids, adenomyosis and uterine adhesions may all be predisposing

factors to placenta previa due to endometrial damage and then endometrial scar,

and under perfusion of placenta leads to enlargement of placenta, because of scar

59

formation in lower uterine segment placental migration hindered, defective

decidual vascularization, the possible end result of inflammatory and atrophic

changes.

11. Placental pathology

Placental membranacea is an extremely rare cause of placenta previa

marginal or velamentous cord insertions, Succenturate lobes, bipartite placenta

and fenestrated placenta are all commonly seen in placenta previa.

12. Assisted reproductive technique

Placenta previa is more common after assisted reproductive technique

including IVF and ICSI. The prevalence is 6 fold higher in IVF pregnancies

compared with spontaneous conception four fold higher in ICSI pregnancies after

adjusting for confounding factors like age, parity, smoking, previous cesarean

(Romundstad et al., 2006)66. The underlying mechanism not clear.

Embryo replacement may induce uterine contraction and lead to

implantation in the lower uterine segment and placenta previa.

CLINICAL PRESENTATION

1. Vaginal bleeding

It is usually painless and varies from minor to massive hemorrhage.

Bleeding may be intermittent but rarely continuous. The recurrence of the bleeding

is unpredictable and for unknown reasons the bleeding occurs at night. It is known

as warning hemorrhage or sentinel bleed.

Unprovoked painless vaginal bleeding which usually does not appear until

near the end of second trimester or afteroccasionally, however it may be provoked

60

by sexual intercourse, serve fits of coughing or sneezing, straining at stool, lifting

weight, jolting from automobile journey on rough road. Threatened miscarriage in

second trimester may precede placenta previa though such bleeding may be minor

or some case unreported.

The initial episode of bleeding has modal prevalence of about 34 weeks.

Women with Accidental Placental Hemorrhage had diagnosis of placenta previa

confirmed at earlier gestation had emergency cesarean and fetal distress occured in

over 50% before 36 weeks and only 2% after 40 weeks.

The number of bleeding episodes do not relate to the degree of placenta

previa or to prognosis for perinatal survival.

Absence of pain is often regarded, as a significant distinguishing factor

between placenta previa and placenta abruption, but 10% of women with placenta

previa will have co-existing abruption.

Such patient and those presenting for first time in labour and hence

experiencing uterine contraction may present diagnostic problem. Major degree of

placenta previa present with symptoms of bleeding earlier. The initial bleeding is

slight and ceases with small clot formation.

The most characteristic feature is the occurrence of hemorrhage without

any warning and associated pain, fortunately the initial bleeding is rarely so

profuse as to prove fatal on the other hand it may be so severe that the patient is

soon in extremes.

Although is some cases hemorrhage stop. a slight, serosanguinous

discharge may continue promoting degree of anemia. The commonest period when

hemorrhage occurs is during the last 10 or 12 weeks of pregnancy sometimes it

61

occurs much earlier and some cases of abortion are due to placenta previa around

30 weeks of gestation, the first bout of bleeding usually occurs.

According to Crenshaw et al 1/3 of patients have one bleeding episode

before 30 week of gestation 1/3 from 30-35 week and 1/3 after 36 week.

The hemorrhage is due to detachment of placenta and comes from the open

placental sinuses occasionally it may also be from rupture of the circular sinuses

of the placenta. In some cases separator may be initiated by same causes which

given rise to accidental hemorrhage that is diseased condition of uterus probably

associated with eclampsia.

The extent of hemorrhage depends upon the type of placenta previa and the

period of pregnancy at which it occurs, the hemorrhage is severe in later weeks of

pregnancy and in central placenta previa.

The earlier in the pregnancy the first bleeding episode occurs the worse is

the outcome of the pregnancy in fact the incidence of preterm delivery, the number

of bleeding episodes, the severity of bleeding and the number of units of blood

required for transfusion are higher for patients who begin bleeding before 28

weeks. The worst prognosis is for those patients with placenta previa who had

prior Cesarean Sections.

The severity of the bleeding and the need for blood transfusion usually

increase with each bleeding episode.

Fetal distress is unusual unless the hemorrhage is severe enough to cause

maternal hypovolemic shock. Uterine contraction occurs commonly in association

with episode of bleeding and may aggravate the bleeding tendency.

62

According to MacAfee and Johnson the really dangerous hemorrhage is

one which is provoked by vaginal examination. A case study 174 cases with

diagnosed placenta praevia stated better results are obtained by postponing pelvic

examination until such time when the termination of pregnancy is sought with all

preparation of caesarean section bleeding occurs from large maternal sinuses at

margin of placenta as this area is extremely vascular. Torrential bleeding was

associated with rupture of marginal sinus.

Hemorrhage from the placentation site continues after delivery because of

poor contraction of lower uterine segment and from the laceration in the friable

cervix resulting in postpartum hemorrhage.

2. Malpresentation17,46

Breech presentation or transverse lies were observed in 30% of cases.

In either case the effect claimed was reduced available length of the uterus and so

predispose to fetal position other than the longitudinal.

It has long been accepted that the previa position of placenta is cause of

oblique lie.

Women with placenta previa have a higher risk of fetal malpresentation

such as breech os transverse lie than women with normal placental sites.

Malpresentations are found in 30% of cases. It has been suggested that the

combination of marginal placenta previa and breech increase the no. of Cesarean

Section associated with placenta previa.

However as mechanism of malpresentaiton in placenta praevia is assumed

to be due to the bulk of the placenta in the lower segment preventing engagement

63

of fetal head. It is likely that malpresentation indicates situations with a significant

degree of placenta previa in whom safe vaginal delivery would be unlikely.

The primary indication for Cesarean Section will be the degree of placenta

previa, fetal malpresentation is not of importance in management decisions, but as

clinical indicator of possible placenta previa.

3. Congenital abnormalities

Brenner et al. suggested that women with placenta previa more frequently

delivered fetuses with serious congenital abnormalities (6.7 vs.3.2). No

mechanism for this effect has been described and the finding has not been repeated

in other studies.

4. Abnormal placentation

Abnormal placentation such as placenta accreta and percreta has an

association with placenta previa and in particular with the combination of previous

cesarean section done for placenta previa. In a study by Clark et al 5% of women

with an unscarred uterus had placenta previa and 24% of women with one

previous Cesarean Section done for placenta previa had accreta. The risk of

placenta accreta with each repeat Cesarean Section such that 40% of women with

2 or 3 previous Cesarean Section and 69% of women with 4 or more previous

Cesarean Section had placenta accreta.

64

5. Small for gestational age (SGA)

There is conflicting evidence regarding the association between placenta

previa and birth weight of less than 10th percentile for gestation, rates as high as

16% have been noted. The cause being decrease placental perfusion due to a sub

optimal placental site however then data has not been substantiated by others.

The effect of early and prolonged bleeding from a low lying placenta or

fetal growth as compared to uncomplicated previa is not reported but these women

seem to be at risk of SGA as well as early delivery.

6. PIH

Placenta previa been reported to protect against PIH. However the higher

incidence of delivery before 37 completed weeks and maternal characteristics such

as parity appear to explain the observed difference.

65

Fig.8. Vasaprevia

7. Vasaprevia

On rare occasion blood loss is fetal and not maternal. A child can be born

bled while from rupture of umbilical vessel, where the cord had a velamentous

insertion. Curl and Johnson (1968) demonstrated pulsating vessels within the

cervix whose constant compression caused fetal bradycardia.

MacAfee had recorded cases of abnormal cord insertion and cord

compression in 27%, as the major cause of fetal loss.

RCOG 2011-Vasa previa describes fetal vessels coursing through the

membranes over the internal cervical os and below the fetal presenting part,

unprotected by placental tissue or the umbilical cord.This can be secondary to a

velamentous cord insertion in a single or bilobed placenta(vasa praevia type1)or

from fetal vessels running between lobes of placentawith one or more accessory

lobes(vasaprevia type2).The reported incidence varies between 1 in 2000 and 1 in

6000 pregnancies.Unlike placenta previa vasaprevia carries no major maternal

66

risk,but is associated with significant risk to fetus. When the fetal membrane are

ruptured either spontaneously or artificially the unprotected fetal vessels are at risk

of disruption with consequent fetal hemorrhage.vasa previa therefore often

presents with fresh vaginal bleeding at the time of membrane rupture and fetal

heart rate abnormalities such as decelerations, bradycardia, a sinusoidal trace or

fetal demise. The mortality rate in this situation is around 60%, although

significantly improved survival rates of up to 97% have been reported where the

diagnosis has been made antenatally. More rarely, bleeding can occur in the

absence of membrane rupture because the fetal blood volume is around 80-

100ml/kg,the loss of relatively small amounts of blood can have major

implications for the fetus thus rapid delivery and aggressive resuscitation

including the use of blood transfusion if required are essential. Very rarely, fetal

heart rate abnormalities in the absence of bleeding may be present secondary to

compression of the fetal presenting part.

Risk factors for vasa previa include placental anomalies such as a bilobed

placenta or succenturiate lobes where the fetal vessels run through the membranes

joining the separate lobes together, a history of low lying placenta in the II

trimester,multiple pregnancy and in vitro fertilization, where the incidence of vasa

previa has been reported to be as high as one in 300.The reasons for this

association are not clear, but disturbed orientation of the blastocyst at

implantation, vanishing embryos and the increased frequency of placental

morphological variations in vitro fertilization pregnancies have all been

postulated.

67

Fig 9. Colour Dopler of Vasaprevia

8. Post placenta previa

A posteriorly situated placenta hinders easy engagement of the head and pressure

applied to the fetal head in cephalic presentation, will compress the placenta and

cause FHR to slow, the Stalworthy sign. It overlies the sacral promontory and

because of its bulk reduces the space available at the brim for the head to come

through cervix hence presenting part remains high and it will be found difficult to

push the head through. This type of placenta previa generally associated with

anomalies of umbilical cord like the battle door placenta in which cord is attached

to margin of placenta hence cord compression and irregular fetal heart rate pattern

and death.

Ultra sound scan of post placenta previa is likely if the distance between

post fetal skull bone and adjacent sacral margin is greater than 15 mm (Anderson

Wellin, 1992) with accuracy rate of 95%, false negative of 0.7%.

68

On Examination;

The general condition of patient depends on the amount of bleeding at the

time of admission and also history of previous vaginal examination, patient may

be anemic, increase pulse rate and low blood pressure.

Abdominal examination, uterus is usually not tender on palpation.

Malpresentation is common, if it is cephalic presentation, usually head is mobile

(cannot be pushed down into pelvis) this is usually present unless the patient is in

exsanguinated condition.

Abdominal examination reveals soft non tender uterus that relaxes between the

contractions if the patient is in labour. In Das series incidence of vertex

presentation are 82.2%, breech 17%. The oblique transverse unstable lies are

common because of the displacement of presenting part from lower uterine

segement by placenta. The presenting part is usually high or floating in central

(Types III and IV) and posterior placenta previa.

MacAfee and Johnson quotes to torrential bleeding is provoked by vaginal

examination in their series. They obtained better results by postponing pelvic

examination, deciding termination by caesarean section while pelvic examination

done in operation theater. This view was supported by Marshall and Moir (1972).

Certain factors like serum alfafeto protein, in 2nd trimester thick placenta,

major previa, echo free spaces at placental margin on ultrasound and turbulent

blood flow on Doppler are associated with higher incidence of antepartum

hemorrhage.

69

DIAGNOSIS:

Four percent of all pregnancies are complicated by bleeding in the 3rd

trimester and fifth of these are due to placenta previa. The differential diagnosis

depends on the gestation at which it occurs and includes bloody show, placental

abruption, local vaginal or cervical lesions and idiopathic antepartum

haemorrhage.

Placental localization is of importance in determining whether there is a

placenta previa and should be done prior to any vaginal examination.

Diagnosis of placenta praevia can seldom be established firmly by clinical

examination unless a finger is passed through cervix and placenta is palpated.

Such examination is never permissible unless the women in the operating room

with preparation of Caesarian Section. This type of examination should not be

performed unless delivery is planned for it may cause bleeding that necessitates

immediate delivery even though fetus is immature.

This double set up examination is rarely necessary because placental

location can almost always be obtained by sonography.

70

Fig 10. Transabdominal localization of placenta previa

Placental localization

Various radiological methods such as soft tissue placentography, radio

isotope radiography, pelvic angiography and thermography are no longer used.

MRI was reported to diagnose placenta previa accurately however

experience with this technique is limited and safety of magnetic field during

pregnancy has not been established.

Furthermore the cost of MRI equipment and its limited availability make

this approach impractical.

Localization of sonography

Gotterfeld advocated sonography in 1966 for the localization of placenta.

71

The diagnostic techniques include

1. Ultrasound 67,68– Trans abdominal, Transvaginal67,69, Translabial color Doppler

2. Soft tissue radiography

3. Radio isotope placentography

4. Air cystography

5. Infra redthermographicplacentography

6. MRI

Transabdominalsonography

Although the localization of the placenta can be made with 100% accuracy

by ultrasound the determination of whether the placenta crosses the cervix is less

accurate due to difficulty in precisely localizing the internal os of the cervix.

Anterior placenta previa is evident when the lower portion of the placenta is

detected inferior to the presenting parts and covers the region of the internal

cervical os. A posterior placenta previa will displace the presenting fetal part

anteriorly and cover the os. In order to diagnose partial or marginal placenta

previa,it is important to record the echoes from the cervical canal or posterior

vagina. This is best accomplished after maternal bladder has been distended to the

patient’s tolerance.

Although transabdominalSonography has become the method of choice for

diagnosing placenta previa, there are several technical problems when using

transabdominalSonography for outlining the exact location of placenta and its

relation to the internal os.

72

1. Patient obesity often causes the placenta to be out of focus

2. The posterior placenta and even a lateral placenta are not always well seen

3. The fetal head (when in the vertex position) may cast in acoustic shadow on

the internal os and the placenta

4. Over distended bladder may push the lower uterine segment to horizontal

position and lead to false diagnosis of placenta previa. On other hand an empty

bladder makes the examination more difficult as there is no acoustic window.

With the accuracy transabdominalSonography, the patient must be

rescanned to ascertain the diagnosis later in pregnancy. Even then there are times

when the diagnosis is difficult to establish and a double setup examination may be

required.

These factors lead to false positive diagnosis of placenta previa in 2 to 6%

of women scanned during third trimester. Most of the false positive results are due

to myometrial contractions and/ or an over distended bladder. Myometrial

contractions may simulate a placenta or displace the placental edge low down,

whereas, an over distended bladder approximates the anterior and posterior width

of the uterus giving false impression of previa.

73

Fig.11. Transabdominal sonography

Fig.12. Early placenta previa VS threatened abortion

74

Fig 13. Anterior placenta previea

Fig 14. Marginal placenta previa

75

A false positive diagnosis may lead to unnecessary restriction of activity

and hospitalization, costly ultrasound examination and patient anxiety.

A more accurate diagnostic mode could alleviate need for double setup

examination which may lead to unnecessary bleeding complication.

False negative diagnosis may incorrectly persuade the clinician that vaginal

examination can be done safely. The false negative rate of Transabdominal

Sonography done late in pregnancy is 2%.

In this study accuracy of 95% for placental localization and false positive

rate of 5% was seen.

The bladder distended with urine is an ideal structure to display because its

known fluid compensation is a standard to which other pelvic and abdominal

contents can be compared and its position and contour allow for the identification

of related anatomic structures. Therefore regions of the cervical canal and anterior

vaginal wall are known because of their continuity with the posterior bladder. In

addition an inferior placental margin may be clearly defined when contrasted to

the dome of the fluid distended bladder, but poorly delineated with the bladder

empty it is difficult to know in a patient with bleeding per vagina in early 3rd

trimester.

1. Bleeding will ease and fetus will eventually deliver vaginally.

2. The patient will bleed acutely and require emergency lower segment caesarian

section.

3. The patient will remain with a placenta previa until term and then require

Caesarean Section.

76

Unfortunately there is no way to predict into which of these categories a

patient will fall. It is mandatory to take necessary precautions and repeat ultrasonic

examination at 2 weeks interval until the position of the placenta is normal or the

fetus is full term whichever occurs first. It often happens, placenta previa is

discovered as an incidental finding and the patient is asymptomatic, follow up

examinations are advocated. This is done every 2 weeks if a large volume of the

placenta crosses the cervix.

If only a small part of placenta crosses the cervix in 2nd trimester and the

patient is asymptomatic, it is virtually certain that the placenta will be in normal

position at term.

The position of placenta with respect to cervix may change even as late as

38 weeks.

In case of posterior placenta with vertex presentation, the placenta is shadowed by

fetal head. In this instance a clear space between the fetal head and posterior

uterine wall is seen, rather than placenta behind the fetal head.

If the bladder is full a segment of placenta lying inferior to the head can be

identified. If a pressure is applied to the fetal head the distance from it and the

posterior uterine wall does not change. If there is no placenta between the head

and uterine wall, the head can be depressed so that it touches the posterior uterine

wall. Another maneuver is to place the patient in trendleberg position which

causes the head move out of the pelvis and permit visualization of posterior

placenta previa. A step like configuration of the placenta may be observed as it

crosses the cervix.

77

When fetus is in breech or in a transvers position there are usually limbs

moving in direction of cervix. Since the placenta is the barrier to the limb motion,

if the limbs can be seen to move in to the cervix the diagnosis of placenta previa

can be excluded. Otherwise one sees the limbs abutting against the placenta and

identifies the placenta as it is alternatingly visible and invisible depending up on

the position of fetal limbs. When there is a false wave contraction of the uterus it

appear as hypoechoic area and mimic placenta previa.

An overtly distended urinary bladder may compress the anterior

myometrium of the lower uterus against the posterior myometrium, resulting in

apparent localization of internal cervical os several centimeters proximal to its true

location. A distended urinary bladder may distort pelvic anatomy whereas partially

fill bladder becomes important in cases in which the anterior cervical lips has to be

emphasized on a sagittal scan in case of suspected placenta previa or cervical

anatomy need to be delineated.

The only limitation to accuracy in the diagnosis of Placenta previa is

identification of cervix. When the bladder is full the cervix lies at the point where

the bladder uterus interface intersects with the posterior wall. Sanders point out

that the internal os is slightly above that point. To decide how to manage the

patient suspected placenta previa at term. Sanders advocated the following

strategy- the interpretation of no placenta previa should not be rendered unless the

inferior placental margin is seen remote from the internal os.

If placenta previa is excluded without doubt by ultra sound there is no need

to avoid vaginal examination. Conversely, if the placenta previa has been

78

diagnosed with certainty, vaginal examination is not indicated and may be

dangerous

Placental migration

It was demonstrated rate of placental migration was 0.1mm per week when

it covered the os and 4.1mm per week when the placental age was more than 3cm

from the os. The clinical implication of this study is that major degree placenta

previa is likely to persist as previa at term rather than the one away from os.

Placental migration is less likely if placenta is posterior, thick and the lower edge

is less than 2cm from the os, or with the history of previous cesarean section.

This theory was put forward by King in year 1973 and was based on fact

that only a small percentage of patients diagnosed placenta previa persist as previa

till term considered misnomer today.

79

Fig 15. Placenta previa with abruption

In a study done by Mecure (1990) of 25% of patient diagnosed as placenta

praevia at 18 weeks only 7 persisted. In another study by Sanderson (1991) of the

12% of cases of placenta previa at 18-20 weeks only those covering the internal os

persisted as previa and those not covering the internal os did not persist as praevia.

Early pregnancy Ultra Sound scan shows the placenta more towards the

cervix on covering it hence 5-8% show placenta praevia.

After second trimester scanning 95% migration is seen, extension of lower

segment from 0.5 cm at 20 weeks to 5 cm at term in cause for this seemingly

upward movement of the placenta for distance of 3-9 cm this is consistent with

observation of degree of elongation of the lower segment so repeat scan must be

done at 30-32 weeks.

80

The appropriate movement of low lying placenta is explained by the

differential growth of upper and low uterine segment as pregnancy progresses and

the inability to define the relationship in a 3D manner using a 2D ultrasonography

in early pregnancy.

Ultra sound criteria of placenta accrete

Greyscale:

Loss of the retro placental son lucent zone

Irregular retro placental son lucent zone

Thinning or disruption of the hyper echoic serosa-bladder interface

Presence of focal exophytic masses invading the urinary bladder

Abnormal placental lacunae.

Transvaginalsonography

Trans Vaginal Sonography is safe and most accurate method especially in

posterior place and provides better resolution with visualization of the internal os

and placental edge (Sherman et al., 1986). It is not only accurate but has the

benefit of reduced scanning time with sensitivity of 87.5% and specificity of

98.8%. (Leerentred et al., 1990)

The transabdominal scan has a higher false positive rate compared with

transvaginalsonography. There are number of potential theoretical advantages to

use of trans vaginal sonography in this situation because, imaging is better and

patient do not need full bladder (Lancet, 1989), thus avoiding both maternal

discomfort and distortion of anatomy of lower segment and cervix.

81

It is seen that 26-60% of cases in second and 12.5% in third trimester

diagnosed as Placenta Previa by transabdominal scan reclassified by

transvaginalsonography as normally placed placenta (Sheormen et al., 1986) more

than 90% of low lying placenta detected in early pregnancy move out of Lower

Segment to Upper Segment as pregnancy progresses.

Women with placenta praevia which reaches or extends over internal

cervical os during anomaly scan should be offered a further scan in 3rd trimester.

Follow up imaging can be left until 36 week in asymptomatic minor

placenta previa whereas with asymptomatic major previa it should be performed at

32 weeks to plan for further management and delivery. (RCOG 2011)

The distance between placental edge and internal os is measured distance

less than 3 cm is used for diagnosis of placenta previa. Tai Pale and colleagues

observed that if placenta overlaid the internal os by 25 mm or more at 18-23 week,

the positive predictive value for placenta previa at delivery is 40%.

82

Becker and associates showed that if overlay >25 mm at 22-23 week 100%

predictive value. Placenta previa diagnosed in later pregnancy has higher chance

of persistence until delivery.

Darsche and colleagues showed that only 34%, 4 cases persisted as

placenta previa if diagnosed at 20-23 week as against 73% of those present at 32-

35 week persisted at delivery.

Some of the advantages

1. The proximity of the probe to internal os and placenta results in less signal

attenuation.

2. This proximity enables the use of higher frequency 5.0-7.5 mHz which results

in better resolution.

3. The image obtained by transvaginalsonography can be magnified with little or

no loss of resolution.

4. The technical problems with Trans-abdominal sonography (obesity, bladder,

fetal head, and posterior placenta) are avoided with vaginal approach.

The vaginal probe is inserted under direct imaging scrutiny and the relation

of the tip of the probe to the cervix is continuously assessed. The focal zone of

high frequency probe is 2-8 cm, if the probe is advanced to a distance of 2 cm

remote from the external os, the internal os and placenta are within the focal zone

and therefore clearly visible.

A careful real time examination in different planes can distinguish between

blood vessels in uterus and cervix and marginal sinus. Bloody cysts can be easily

distinguished from placenta, unclotted blood in less ecogenic and is easily seen

even in small quantities.

83

A Japanese study done today demonstrate zero risk, of any iatrogenic

bleeding due to transvaginalsonography scan probe, if the probe is inserted not

more than 4 cm in the vagina.

The positive value of transvaginalsonography is diagnosing placenta previa

is 71% as opposed to 31% by transabdominalsonography.

SOGC clinical practice guidelines 2011 according to TVS.

Transvaginalsonography if available may be used to investigate placental location

at any time in pregnancy when the placenta is thought to be low lying it is

significantly more accurate.

Sonographer encouraged to report the actual distance from the placental edge to

the internal cervical os at transvaginalsonography. A placental edge is exactly

reaching the internal os is 0mm. when the placental edge reaches or overlaps the

internal os on transvaginalsonography between 18 – 24 weeks gestation (Incidence

2-4%). Follow up examination for placental location in 3rd trimester is

recommended. Overlap of more than 15mm is associated with increased likelihood

of placenta previa at term.

When placental edge lies between 20 mm away from the internal os and

20mm of overlap after 26 weeks ultra sound should be repeated at regular interval

depending up on gestational age. Overlap of 20 mm or more with 3rd trimester is

highly predictive of need for caesarean section. The os – placental edge distance

on TVS after 35 weeks gestation is valuable for planning the route of delivery.

When placental edge lies more than 20 mm away from cervical os, woman can be

offered a trial of labour.

84

The distance of 20 – 0 mm away from the os is associated with higher

caesarean rate.

Any degree of overlap more than 0 mm after 35 weeks is an indication for

Cesarean Section.

Out patient management of placenta previa may be appropriate for stable

woman with house support with close proximity to the hospital and readily

available transportation on telephone communication.

There is insufficient evidence to recommend the practice of cervical

cerclage to reduce bleeding in placenta previa.

Regional anesthesia may be employed for Cesarean Section in presence of

placenta previa.

Woman with placenta previa and prior Cesarean Section are at high risk for

placenta accreta. If there is imaging evidence of pathological adherence of

placenta delivery be planned in an appropriate setting with adequate resources.

Comparison with placenta previa and placenta accreta, diagnosis and

management RCOG guidelines No: 27, Oct 2011.

The likelihood of persistent placenta previa was effectively zero, when placental

edge reached but did not overlap os (0 mm) and increased significantly beyond 15

mm overlap such that the distance of more than 25 mm likelihood of placenta

previa delivery 40% and 100% respectively.

An average migration rate of more than 1 mm per week high predictive of

normal outcome.An average of more than 20 mm after 26 weeks was predictive of

need for Cesarean Section.

85

In retrospective study to investigate the relationship between the cervical

length and maternal adverse out comes, cervical length was transvaginaly

measured between 24 weeks to 33 weeks of gestation. After bladder evacuation,

sagittal plane was obtained to visualize the full length of cervical canal. The

median age of longer cervical length is longer than 30 mm, shorter cervical length

is shorter than 30mm. More over cervical length of 30mm or less was a significant

risk factor for massive estimated blood loss at cesarean section and placental

adherence. (Kotaro Fukushima, Jan 2012)

Color Doppler

Color Doppler imaging improves the diagnostic accuracy in the prediction

of placenta accreta in patient with persistent placenta previa. Placental lacunae

exhibiting marked or turbulent blood flow from within the placenta extending into

the surrounding tissue should alert the physician to possibility of placenta accreta.

Color Doppler in placenta accreta

Diffuse or focal lacunar flow

Vascular lakes with turbulent flow(peak systolic velocity over

15cm/s)

Hypervascularity of serosa-bladder interface

Markedly dilated vessels over peripheral subplacental zone.

Three dimensional power Doppler:

Numerous coherent vessels involving the whole uterine serosa-

bladder junction(basal view)

Hyper vascularity(lateral view)

86

Inseparable cotyledonal and intervillous circulations, chaotic

branching, detour vessels(lateral view).

Soft tissue radiography

Soft tissue radiography or direct visualization of placenta has a reliable

technique before sonar imaging was developed, this method still has place where

sonar is not available.

A positive diagnosis of placenta previa can be made by observing the

displacement of presenting part from mid coronal or mid saggital plane of pelvic

brim. It is helpful only when the fetus present by vertex. When placenta is on

posterior wall it is different to define because of overlying bony pelvis and muscle

mass but it may be demonstrated by its ability to displace the presenting part

forwards when patient is x-rayed in sitting position.

Radioisotope placentography

This is an acceptable alternative when sonar is not available. This method

uses an IV injection of 99mTc bound to red blood cells or radioactive albumin

bound to B2I. The placenta is detected because of the greater blood pool in relation

to the adjacent myometrium. It was originally described by Browne and Veal in

1950. It has diagnostic accuracy of 87%. It is useful only in 3rd trimester of

pregnancy when placenta is of maximal size. There is difficulty in differentiating

low lying placenta, partial placenta previa and complete placenta previa

from low normal implantation. The isotopes used are considered safe in pregnancy

87

because of their short half life and procedure involves only minimal discomfort to

mother.

Air cytography

This method mainly applicable to vertex presentation and can detect

placentapraevia in the anterior and anterolateral position of lower uterine segment.

In normal cases only 0.8 to 1.5 cm of soft tissues lie between bladder and fetal

head. If the head is displaced upwards by a mass of tissue such as placenta the

distance increases upto 3 or 4 cm.

Thermographic (infrared) placentagraphy

Since the placenta has greater degree of vascularity, then the adjacent

myometrium the temperature is higher so a larger amount of infra red radiation is

produced. These emissions are detectable from anterior and laterally located

placentas by existing thermographic techniques.

Magnetic resonance imaging (MRI)

MRI is a technique that represents a complimentary imaging modality to

ultrasound for the evaluation of fetus and gravid uterus. Its use is advocated when

sonographic findings are equivocal or when sonography is non diagnostic

secondary to technical limitations.

MRI similar to ultra sound involves no ionizing radiation is non-invasive

can provide images in multiple planes. Unlike ultra sounds it is not operator

88

dependent and MR image are not limited by interference from intervening skeletal

fatty and air filled structures.

The placental tissue tends to demonstrate a fairly homogenous appearance

on MR images. MRI easily depicts placental tissue. This may facilitate the

diagnosis of placental enlargement as seen with Rh incompatibility, maternal

anemia and diabetes as well as those conditions in which placental tissue is

smaller than normal. It also provides complementary technique to us in the

detection of succenturate lobes.

In case of placenta praeviasonographic diagnosis is problematic when fetal

head obscures a posterior praevia or when a low lying placenta is laterally located

sagittal MRI can precisely delineate the relationships of the inferior aspects of the

placenta to internal cervical OS.

MRI more accurate in the precise definition of the degree of placenta

previa.

MRI features of placenta accreta:(Trop et al 1998)67

Uterine bulging

Heterogeneous signals intensity within the placenta

Dark intraplacental bands over T2- weighted imaging

Direct placentography

Calcaneous deposits in the placenta were identified by Blare Heartley

Manchester 1954, after 32 weeks of pregnancy accuracy was 99.5%.

89

Pelvic angiography

Nelson et al. (1961) and Eisenmass (1961), Annaworth and Gillaman

(1964) contributed to this and stated an accuracy upto 95% beyond 42 week.

Retrograde catheterization of femoral artery and injection of radio opaque dye.

90

MANAGEMENT:

The earlier dictum was to control bleeding from the placenta site even at

the cost of fetal life.

In early 19th century Gillaman recommended podalic version for this

complication. Mauriceau followed it and delivery was hastened.

Sir James Simpson believed that in order to arrest the bleeding placenta

should be completely separated as it was though that bleeding was from detected

placental site. Beenes stressed on this (1886). Leroux thought of plugging the

vagina. Baudelque believed in plugging the cervix. It was Denman who pointed

out low bleeding was controlled by pulling down the leg.

In later part of 19th century Braxton Hicks bipolar version as a method of

control bleeding came into practice. But the idea seems to have lost support.

Lawson Tai in 1890 recommended rupture of membrane. In 1927 Arthur Bill

advocated the idea of adequate blood transfusion and CS. At present junction the

line of management can be expectant or active Management of placenta previa by

version as emergency procedure has been abandoned. It may save the patient

especially primi from uterine scar which limp her obstetric carrier when babies are

dead deformed premature.

Aim of management of placenta previa is to

1. Maintain hcE>30

2. To keep neonatal mortality as low as 5% and even lower, women with placenta

previa it may be considered as follows.

(a) Those in whom the fetus in preterm but there is no pressing need for

delivery.

91

(b) Those in whom fetus is reasonably mature.

(c) Those in labour.

(d) Those in whomhaemorrhage is so severe as to mandate delivery despite

fetal immaturity.

It depends on:

1. The degree of placenta previa17,

2. Gestational age17,48,63

3. Amount of blood loss17,51

4. Maternal and fetal well being48,63

92

Fig 16

92

Fig 16

92

Fig 16

93

Expectant Management

Over years the preferred method of managing the patient with placenta

previa progressively changed from “active management” with frequent one of

vaginal delivery to expectant management with frequent use of caesarean section.

Expectant management women with placenta previa was first described by

MacAfee and Johnson (1945). After this the trend in the management of placenta

previa completely changed. The aim was to allow the pregnancy to continue until

the baby has grown sufficient enough to survive ex utero.

The management protocol includes:

1. Avoidance of vaginal examination.

2. Prolongation of pregnancy until fetal maturity

3. Transfusion support

4. Delivery by caesarean section

The fact that the warning haemorrhage is seldom severe and could be the

only one in milder degree of placental previa. Such line of management helps to

improve the fetal prognosis.

Mills (1948), Stallworthys (1957) and Duncan (1947) have all followed

MacAfee’s regime and reported a steady fall in perinatal mortality. Pedowitz

(1980) concluded that expectant management is more successful in partial then in

total placenta previa.

A word of warning regarding the expectant line of management is that it

should be carried in a well equipped hospital with competent staff.

94

Selection of patients

1. Mother is haemodynamically stable and with wide margin of safety to withstand

further bouts of haemorrhage if it occurs. Hb% should be ideally 10 g% or

more.

2. Duration of pregnancy less than 37 weeks.

3. Active vaginal bleeding absent.

4. FHS is satisfactory.

5. Lethal congenital anomalies of fetus should be ruled out.

It includes

1. Hospital admission40

2. Fetal monitoring

3. Cross match (2-4U of blood) should be readily available.

4. Steroids should be used for fetal lung maturity in all cases with bleeding from

24-34 weeks.

5. Kleihauer testing should be performed in all Rh –ve women for each episode of

bleeding and anti D given appropriately.

Termination of expectant management should be done

1. At completion of 37 week of gestation.

2. Recurrence of brisk hemorrhage which does not abate.

3. Fetus is dead.

95

Definitive management

1. Asymptomatic patients

2. Symptomatic patients

1. Asymptomatic patients

1/3 of all women with placenta praevia will not bleed antenatally. The main

controversy regarding the management of placenta praevia revolves around the

question of whether asymptomatic women, should be admitted for observation and

bed rest in third trimester or managed as outpatients.

Outpatient management has resulted in fetal and maternal morbidity.

Bleeding due to placenta previa is unpredictable, which may be one of main

reasons for traditional inpatient management of women with placenta previa.

During third trimester, Inpatient management is indicated (RCOG, 2011). But the

financial and emotional cost to the women and her family from prolonged

hospitalization must always be considered.

With improvement in transportation facilities and ambulance services

highly motivated women who clearly understand the necessity of restriction of

activity and are within 15-30 min of hospital, Perhaps may be monitored at home

applicable only to grade I-III and asymptomatic grade IV, apart from reduced

length of hospital stay. There was little evidence of any clear advantage or

disadvantage of policy of home versus hospital management, ask to return if there

is bleeding or contraction. As risk of haemorrhage increase with advancing

gestation women should be admitted at approximately 34 weeks if they have

warning haemorrhage (Love et al., 2004).

96

Criteria of outpatient management of patient with placenta previa:40

1. Inpatient observation for 72 hour without vaginal bleeding.

2. Stable serial hematocrit > 35%.

3. Reactive NST at the time of discharge.

4. Telephone available, 24 hr transportation between home and hospital.

5. Bed rest compliance at home.

6. Patients families’ comprehension of potential complications.

7. Weekly clinical follow up until delivery including serial Hb% and repeat

ultrasound.

There is need for future research to find clinical methods for prediction of risk of

bleeding in placenta previa determine the suitability for hospital

management70,79

1. Raised serum alpha feto protein level at 15 to 20 weeks

2. Thick Placenta

3. Turbulent flow with Doppler, are at risk of bleeding and

suitable for out patient management

In developing countries like ours, since it is very difficult to meet the above

criteria better to manage as an inpatient only.

Serial scanning of women diagnosed as having placenta previa in the third

trimester is important (particularly in women identified as having type I and type

II) to check for resolution of placenta previa, as lower uterine segment forms.

Placental localization beyond 38 weeks is unnecessary as there is little growth of

the lower uterine segment after this time and so as a significant change in a degree

of placenta previa will not occur.

97

As women with placenta previa are at high risk of antepartum and

postpartum haemorrhage, haematinics should be given to maintain an Hb level at

the upper end of the normal range.

Caesarean section is the appropriate mode of delivery for all women with a

type II, III and IV placenta previa. There is no evidence to indicate an advantage

in doing this before 37 weeks gestation. Patient with type I placenta previa should

be rescanned at 36-37 weeks and if the fetal biparietal diameter is below the lower

edge, they can safely be left to go into labour. Bleeding from placenta previa

usually causes contraction, which will force the fetal head further into the pelvis

and thus will control the bleeding by compression.

Symptomatic patients:

The following parameters should be evaluated first who is bleeding

because of placenta previa.

1. The mother condition as evidenced by the degree of obstetric haemorrhage.

2. Fetal condition including in particular gestational age estimation.

3. The ability of the neonatal unit to handle as infant of that gestational age.

Evaluation of severity of bleeding

Placenta previa has a classic presentation of painless vaginal bleeding. Pain

may be a feature of initial presentation and suggests the possibility of concurrent

placental abruption or the onset of painful contraction. This is the initial and

decisive step in the management of patients with placenta previa. However an

adequate evaluation of the severity of the bleeding episode is difficult. The degree

98

of bleeding is variable slight spotting of fresh blood to torrential hemorrhage.

However first warning bleeding from placenta previa is rarely severe and delivery

may be delayed for a period of time. Blood pressure, pulse rate, haematocrit,

haemoglobin levels and measurement of blood volume may be inaccurate in a

hypervolemic pregnant woman shortly after a bleeding episode.

Mild bleeding

(The patient has lost less than 15% of her intravascular volume)

1. No change in vital signs

2. No postural hypotension

3. No peripheral evidence of circulatory volume deficit.

4. Normal urinary output

Moderate bleeding

(the patient has lost between 15% and 30% of her blood volume)

1. Postural changes in pulse rate (increase in pulse rate of 10-20 bpm when

changing from supine to the upright position). And drop in diastolic blood

pressure of 10 mm Hg or more

2. Evidence of inadequate circulatory volume (dypnea, thirst, pallor, tachycardia,

clammy extremities), mental status changes may also be present (apathy or

agitation).

Severe bleeding

(the patient has lot 30-40% of her blood volume)

1. Patient is in shock with decreased or unrecordable blood pressure.

99

2. Persistent loss of fresh bleed from the vagina.

3. Fetus may be dead or showing signs of distress.

4. Oliguria or anuria.

Assessment of severity of bleeding

I II III IV

Blood loss (ml)<750

<15%

750-1500

15-30%

1500-2000

30-40%

>2000

>40%

Pulse rate (bpm) <100 100-120 120-140 >140

Blood pressure Normal Decreased Decreased Decreased

RR (per min) 14-20 20-30 30-40 >40

UOP (ml/hr) >30 20-30 5-15 Negligible

CNS symptoms Normal Anxious Confused Lethargic

Management of patients with mild bleeding

Fetal pulmonary maturity dictates the management of patients with mild

bleeding. Immediate delivery of mature fetuses is the appropriate course,

regardless of the minor degree of bleeding. If the fetal lungs are immature or

gestational age <36 weeks, the patient becomes a candidate for expectant

management.

100

Management of patients with moderate bleeding

The gestational age and fetal pulmonary maturity dictate the management

of patients with moderate bleeding. Caesarean section is performed if the

pregnancy is 36 weeks or more. If the patients is <36 weeks fetal pulmonary

maturity is evaluated as soon as bleeding stops and the patient is

haemodynamically stable. Delivery accomplished if the fetal lungs are mature (if

the fetal lungs are immature) and the patient has moderate bleeding, then she is put

under intensive monitoring in labour and delivery unit for period of 24-48 hours.

AHb% of roughly 10 gm% should be maintained by transfusion. The uterus

should be kept quiescent by tocolytics, Steroids to accelerate fetal lung maturation.

If the patient’s condition remains unstable with steady blood loss in

moderate amounts she should be delivered in spite of early gestational age or lack

of fetal lung maturation. If the patient’s condition becomes stable she becomes a

candidate for expectant management. However in the presence of complicating

factors such as PROM other maternal medical conditions of fetal distress,

continuation of pregnancy seems inappropriate

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Fig 17

101

Fig 17

101

Fig 17

102

Management of patients with severe bleeding

Initial management involves rapid assessment of maternal cardiovascular

status and rate of continuing blood loss followed by fetal assessment. IV access

with 18 gauge cannula should be established in all women regardless of the degree

of bleeding. Baseline investigation, Hb%, blood group and Rh typing, cross

matching and in women with heavy bleeding clotting studies are indicated. Fluid

replacement with crystalloid is appropriate initially. This may be supplemented

with colloid with heavy blood loss. In women requiring delivery because of heavy

bleeding transfusion of cross matched blood should begin as soon as possible. In

these cases an efficient management plan including life support measures and

immediate operative intervention are only hope of avoiding a maternal death.

It includes constant observation and monitoring, administration of blood,

plasma expanders, IV fluids, assessment of renal function and intravascular status,

assessment of fetus and delivery.

Frequent monitoring of vital signs, precise measurement of fluid input and

urinary output recording, the amount of vaginal bleeding, and keeping complete

records of what has transpired are essential for positive outcome.

Haemoglobin, pulse and blood pressure can all be misleading in the

presence of decreased urine output. A peripherally inserted CVP line especially if

there is a coagulopathy, internal jugular will provide information for safe and

rapid expansion of intravascular space.

Patient with placenta previa and severe bleeding should be delivered by

caesarean section irrespective of type of placenta previa. The anaesthesia of choice

is general anaesthesia with endotracheal intubation. Systemic maternal disease

103

must be quickly evaluated as a history of hypertension, diabetes mellitus or renal

disease may alter management and choice of anaesthesia.

The type of incision over the uterus to be decided by surgeon. In low

transverse incision bleeding sinus at placental site can be dealt better under direct

vision and as such the decision to preserve or remove the uterus can easily be

made.

Placenta accreta if accidentally present can also be tackled effectively. The

disadvantages are the engorged vessels on the anterior lower segment which may

bleed profusely when they are cut. In case of transverse lie or preterm infant

delivery may be difficult through this incision. In anterior placenta praevia, the

placenta may haveto be cut or separated to deliver the baby. Chances of fetal

exsanguinations during such delivery is a real threat to the baby. The edges of the

cut margins become so vascular and friable that the tissues may cut through during

suturing.

In classical caesarean section the operation can be done more quickly and

baby is delivered without disturbing the placenta so there is no fetal

exsanguination. The disadvantage is that the lower segment over which the

placenta is implanted cannot be visualized and as such it is difficult to control

bleeding.

If there are engorged vessels on the anterior uterine wall, put two ligatures

and cut in between while making transverse incision.

The placenta underneath the incision should be separated manually to get

the margin and then membranes are ruptured or the placenta may have to be cut

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promptly to enter into the amniotic sac to deliver the baby. In either case, the cord

should be clamped quickly to prevent further fetal exsanguination.

After the placenta is expelled the lower segment should be inspected for

any oozing points. If hemostasis by sutures fails and the uterus is to be preserved

tight intra uterine packing is to be done, to give firm pressure on the oozing area.

Lowering the plane of anaesthesia quick suturing of uterine incision,

oxytocic’s and massaging the uterus almost bring back the uterine tone.

Intrapartumhaemorrhage:surgical techniques to stanch the flow

• In the event of massive haemorrhage,immediate compression of the aorta

below the level of the renal arteries will reduce the bleeding enough to allow time

to evaluate the situation.At the same time,aggressive IV fluid resuscitation and

blood transfusion should begin.Reevaluate coagulation status after every 5 to 10U

of blood

•. Focoused repair may be effective:In some situations,thehaemorrhage may

be controlled by oversewing and repairing the focal placental site defects.

• Bracketing the bleeding area:Another measure is a circular suture

technique in which an interrupted sutures are placed on the serosal surface of the

anterior and posterior aspects of the uterus and as deeply as possible into the

endometrium in a circumferential mannar,bracketing the bleeding area.

• The argon beam coagulator can be used to achieve hemostasis; it is more

effective than traditional bipolar cautery at ensuring hemostasis in extensive areas.

105

• Stepwise devascularization was effective in 100% of 103 women with

postpartum haemorrhage who did not respond to traditional management.It

involves 5 procedures to be performed in sequence until hemostasis is

achieved.Unilateral uterine vessel ligation, bilateral uterine vessel ligation, low

uterine vessel ligation, unilateral ovarian vessel and bilateral ovarian vessel

ligation.

• Hypogastric artery ligation is another option,but it is technically

challenging and successful in less than 50% of cases.In fact the time spent on this

technique may actually lead to increased blod loss.

Pelvic vessel embolization

Elective embolization or occlusion of the hypogastric or uterine arteries has

proved to be safe and effective for postpartum haemorrhage,with a success rate of

more than 90% in women with normal coagulation.

In addition, elective catheterization with a balloon-tipped catheter can be used

prophylactically to reduce blood flow to the placenta.Prophylactic catheterization

of the anterior division of the internal iliac arteries can be performed right before

the scheduled caesarean section. An axillary approach is technically easier for

fluoroscopically guided catheterization of the internal iliac. The actual fluoroscopy

time is minutes,so the risk of fetal exposure to radiation and irreversible ovarian

damage is minimal.

The fetus is monitored during the procedure and the balloons are left in the

deflated state until after delivery, reducing the risk of uteroplacental

106

insufficiency.Balloon inflation after delivery occludes the hypogastric arteries and

diminishes uterine arterial blood flow during surgery. In some cases, the

temporary occlusive effect of the balloons may control intraoperative bleeding

completely . if substantial bleeding persists,subsequent embolization of the uterine

arteries is advised, using absorbable gelfoamparticles,which are temporary and do

not damage pelvic organs. Mentruation is not impaired,and normal pregnancies

have been reported after this procedure.

In women who undergo cearean delivery under regional

anesthesia,placemant of a dry epidural catheter for later dosing of anesthetic

agents should be considered prior to balloon catheterization, since the patient’s

mobility is restricted after placement of balloon tipped catheter. This therapy is

especially useful when there is a high index of suspicion of placenta accrete.

Recommendations at the time of delivery

• Ensure IV line access with a large-bore cannula.

• Give prophylactic antibiotics, and take steps to prevent

thromboembolism,eg,by fitting of sequential compression devices.

• Choose appropriate anaesthesia .In a haemorrhaging women with evidence

of maternal hypovolemic and coagulopathy, general anaesthesia is preferred. For

planned caesarean in a stable patient, regional anaesthesia is acceptable. In fact,

regional anaesthesia techniques were associated with substantially lower blood

loss and a reduced need for transfusion, based on a review of data from 514

women.

• Choose the skin incision carefully based on the patients body habitus.If

placenta accreata is suspected,adequate exposure is required. A wide pfannenstiel

107

incision may be possible in a thin patient,but extension to a modified cherney

incision may be necessary if exposure is inadequate. A vertical incision provides

optimal exposure.

• Inspect the uterus for prominenet blood vessels within visceral peritoneum

covering the uterus,which suggests placenta accrete. Also for direct invasion of

placenta accrete into surrounding structures,such as the bladder or parametrium.If

the lower aspect of the uterus is highly vascularized,a low transverse uterine

incision should be avoided in favour of classical incision. Make every effort to

avoid incising the placenta because it would lead to massive maternal

haemorrhage and marked fetal blood loss.

• Determine management of placenta.Spontaneous delivery of placenta is

best to minimise blood loss. However,if there is strong evidence of

accrete/perecreta, leave the placenta in situ and perform hyaterectomy.

(Note:Several cases reports have described successful conservative management

of placenta accrete in carefully selected.hemodynamically stable patients who

wish to preserve their fertility.The placenta was left in place in part or in full,and

methotrexate and antibiotics were given.Rigorous follow-ups and and intensive

monitoring with diagnostic imaging and serial human chorionic gonadotropin

measurements are required.However as an American college of obstetricians and

gynaecologists committee opinion observes,this approach should be considered

investigational.

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Hysterectomy for placenta previa, placenta accreta

This procedure is technically challenging when there is a markedly enlarged uterus

with engorged collateral vessels. One useful method, delayed ligation technique,

was originally described by Dyer et al on the Tulane obstetrics service at Charity

Hospital of New Orleans.This technique facilitates quick control of all uterine

vasculature with rapid hemostasis.Later modification of this method involves

successive clamping and severing of all vascular pedicles supplying the uterus,

prior to their suture ligation, for quick control of bleeding.

109

Fig 18

109

Fig 18

109

Fig 18

110

Summary of mode of delivery72

Mode of delivery is based on clinical and ultrasound findings. Caesarean

section should be carried out at 38 weeks of the placental margin is within 2 cm of

the internal os and more so if it is posterior and bulky (Bhide et al., 2003).

Women should be counseled and consented regarding possible blood transfusion

and hysterectomy where placenta accreta is suspected. Multidisciplinary

involvement is necessary in delivery of women with accreta, inereta, percreta

(Catanzarite et la., 1996). Delivery should be attended by an experienced

obstetrician and anesthetist.

Anesthesia72,73

The blood loss and blood transfusion requirements are both high with

general anaesthesia compared with regional anaesthesia. Caesarean section should

be performed through a transverse uterine incision however it should be

remembered that the lower segment can be poorly formed and thick (placenta

might be incised if it is anterior). Uncontrollable haemorrhage may occur

following placental removal due to relative atony of lower segment (prostaglandin

F2 alpha initial dose 250 mg) can be repeated every 15 min upto 8 doses maximum

to control bleeding. Recently prothrombin complex and recombinant factor 7a are

used in massive postpartum haemorrhage in placenta praevia. Several uterine

tamponed methods have been developed to control postpartum haemorrhage and

avoid major surgical intervention. They are less hazardous and have the advantage

of preserving fertility. Various balloons including Foley’s catheter sengstaken

Blackmore tube, urological and prostatic balloons have been used to produce

avascular compression of the bleeding surface.

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Tocolysis in placenta previa

Bleeding from placenta previa is usually associated with uterine activity. A

vicious cycle where small changes in cervical effacement and dilatation which

occur as a physiologic phenomenon in many women, precipitate placental

bleeding. This in turn stimulates the release of prostaglandins from the lower

segment and thereby uterine contractions, which will aggravate the amount of

bleeding. Here tocolytics play a role in inhibiting uterine contractions and then

prolong pregnancy allowing time for steroid administration to promote fetal lung

maturity. There is no evidence to support the theory that by causing uterine

relaxation tocolytics increase the amount of bleeding.

Beta sympathomimetic cause maternal tachycardia and hypotension and

thus reduces the ability of the patient to compensate for blood loss. They should

therefore be given under intense supervision with double venous access.

Calcium channel blockers such as Nifedipine cause profound hypotensive

changes and are not suitable for use in women with existing haemodynamic

instability.

Magnesium sulphate has been advocated by some as it is associated with

less haemodynamic disturbance and its tocolytic efficacy is comparable with Beta

sympathomimetic. It however requires careful monitoring as its toxicity can cause

respiratory and cardiac arrest.

Prostaglandin synthetase inhibitors such as indomethacin seem to be the

drug of choice as they are not associated with maternal cardiovascular effects, but

they should be used on a short term basis as they may cause marked

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oligohydramnios and over 32 weeks gestation, they have a theoretical risk of

premature closure of fetal ductusarteriosus and/or fetal pulmonary hypertension.

The benefits of corticosteroids in promoting lung maturity have been

established Betamethasone 12 mg intramuscularly repeated once 12 hours later

should be given without delay to all women with known placenta previa

presenting with antepartum haemorrhage from 24-32 weeks gestation.

In a retrospective study, it was found that treatment with tocolytics was

associated with greater prolongation of pregnancy and higher birth weight;

however numbers are too small to make any conclusion (Sharma, et al., 2004;

Besinger, et al., 1995). Selective use of tocolytics should be used with extreme

caution and involvement of senior personnel. MgSO4 is better tocolytic agent

(Morgan Arul Kumaran, 2003)22,70.

Cervical Cerclage:71,22

Cervical cerclage has been used to try to prevent the physiological dilation

of cervix which occurs with increasing gestation. A randomized trial by Arias in

25 patients with placenta previa had 13 patients receiving cerclage compared with

12 control subjects. The patients with cerclage achieved a more advanced

gestational age at delivery (34.9 3.0 compared with 31.6 2.9 weeks) and had

less maternal bleeding. Although numbers are small, they provide an interesting

series from which to consider the use of cerclage in patients with symptomatic

placenta previa early in gestation. Other reports on the efficacy of cerclage in

placenta previa need corroboration.

113

In a study of Fernando Arias cervical cerclage as a temporizing measure for

the treatment of patients with placenta previa was evaluated in 25 patients. All had

vaginal bleeding severe enough to justify their admission to hospital. Twenty had

complete previa and five had partial placenta previa demonstrated by ultra sound

scan. They were assigned to cerclage treatment (cervical cerclage group) or

conventional expectant management (control group). Control patients were treated

with bed rest in the hospital until delivery Terbutaline (2.5 mg) orally every four

to six hours was given to prevent preterm contraction and glucocorticoid treatment

was given to accelerate fetal lung maturity.

The cerclage was placed after cessation of all bleeding. The procedure was

performed under General anesthesia using 5 mm mersilene band in purse string

fashion as described by McDonald. Indomethacin 50 mg rectal suppository was

given one hour before surgery followed by 25 mg orally every six hour for eight

doses to prevent uterine contraction during periopertive period.

The patient in both study and control groups had ultrasound examination

every three weeks to reconfirm the placental localization and follow the fetal

growth patients in both groups were delivered if the frequency of severity of their

bleeding indicated delivery or if amniotic fluid analysis demonstrated fetal lung

maturity.

Gestational age at delivery, prolongation of pregnancy and birth weight

were greater in patients treated with cerclage than in those who received

conventional expectant management. The number of units of blood transfused

between randomization and delivery was significantly higher for patients in the

control group than those for cerclage group. Neonatal complications occurred

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more frequently in patients treated with conventional expectant management. The

most frequent complication was hyaline membrane disease.

Since the introduction of expectant management in 1945 the perinatal

mortality associated with placenta praevia was decreased steadily. However there

is strong possibility that this improvement in perinatal outcome is more the result

of continuous advances in neonatal care than of sophisticated obstetric therapy.

In 1956, Lovset and later extended by the von Freisen presented evidence

supporting a beneficial role for the use of an encircling suture of the cervix for

treatment of patients with placenta previa, because the most likely mechanism for

bleeding in praevia was partial detachment of placenta, brought about by

progressive formation of lower uterine segment. Thus, the cervical cerclage was

thought to act by halting the placental separation. In 1990, William B. Cameron

presented additional evidence concerning theadvantages of this procedure at the

meeting of the central association of obstetricians and gynecologists. Using

cerclage to treat 14 patients with placenta previa he achieved a mean pregnancy

prolongation of 6.75 weeks and one of his patients delivered because of further

bleeding. Cervical cerclage to reduce bleeding and prolong pregnancy has been

suggested but sufficient evidence is not available to justify its use (Lobo et al.,

1998).

Although studies support the proposed value of cervical cerclage in patient

with placenta previa there are several potential problems. The, first is possibility of

using cerclage in patients who are misdiagnosed for placenta previa especially

those who were diagnosed in II trimester. The second potential problem with the

cerclage treatment is the false sense of security given to the patient by initial

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results of surgery. A third potential problem is the possibility of concealed

bleeding after the cerclage operation. These patients should be followed with

periodic ultrasound examination with special attention to search for retro placental

clots.

However the results of various studies suggest that the use of cervical

cerclage in patients with symptomatic placenta previa in early gestation has fetal

advantages without increasing maternal morbidity.

Artificial rupture of membranes

Unlike in abruption placenta this is not so effective except in case of type I

or type IIA. MacAfee (1942) and Stallworthy (1951) have shown that prognosis is

very bad for a fetus after ARM in case of posteriorly located placenta especially so

when ARM has been earlier to the engagement of head and when, engagement

occurs, placenta is liable to excessive pressure by presenting part of fetus. In

carefully selected cases, surgical induction at 31-38 weeks gives a satisfactory

response almost always accelerated with syntocinon drip. If bleeding were to

continue in spite of ARM caesarean section is indicated.

Management of placenta previa by version as an emergency treatment has

been abandoned in modern obstetrics contemplated only if infant is dead seriously

deformed or previable, only if a lesser degree of placenta praevia exists. Only

attraction of the version is to save especially primigravidae from uterine scar

which may limp her obstetric carrier.

Gun (1997) and Menon (1963) used willet forcept is 15%. This has been

abandoned because of morbidity due to infection. If the fetus is dead and mild

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bleeding persists scalp traction with willet forceps, the cervix should be 2/5th or

more dilated, membranes ruptured. Traction with 1-½ pound weight attached to

the foot of the bed is then applied. The traction is not continued for more than 4-6

hours. The head is then brought to compress the placental site if this procedure is

applied when the fetus is alive it is associated with a higher fetal mortality and so

caesarean section is preferred.

Caesarean Section:

Anaesthesia for cesarean section for placenta previa is controversial, while

many anaesthetists believe that general anaesthesia is mandatory for cesarean

section for placenta previa. Recently the view has seen changing to considering

regional anesthesia for placenta previa depending up on the position of placenta

previa, the urgency of the situation and the extend of any continuing antenatal

blood lose. Compared to general Anaesthesia, spinal anaesthesia allowed easier

intra pelvic manipulation and uterine atony was unusual, less hemorrhage from

placental site and obstetric shock was rare with spinal anaesthesia (BRJ anaesth

2000).

While all types of placenta previa in the interest of the baby and mother

need caesarean section in modern times. Type I placenta previa is invariably

managed by vaginal route as it seldom end up in catastrophic bleeding episodes.

Type II placenta previa anterior, management can be done on the same line but

occasionally they had caesarean section in interest of mother and fetus. If the fetus

is premature hopelessly moribund it is better to resort to vaginal delivery looking

into amount of bleeding and condition of patient on contrary if pregnancy, beyond

117

36 weeks especially inprimigravidae (elderly) it is better to do caesarean section.

Even in milder varieties, in all cases of severe bleeding through closed and

unaffacedos, type III, IV and type II posterior placenta previa caesarean section is

indicated. Stallworthys (1951) stated that aim in modern obstetrics should be bring

down the perinatal loss to 10%. Munrokerr states that choice of approach is

caesarean section for placenta previa. Classical incision may be resorted to, when

the patient is poor risk and rapid delivery indicated for the sake of mother and to

save the child in present pregnancy, due to reduced bleeding, should not be sought

unless she is multi. Classical caesarean section has been advocated when placenta

is implanted anteriorly. Now-a-days lower segment approach is universally

preferred and where large vessels are encountered bleeding can be controlled by

ligating or by prompt clamping of the vessels.

Due to increased vascularity in the lower uterine segment Abdul and Karim

prefers to incise the lower uterine segment vertically. But they also state that

whatever may be the type of section, bleeding at the site of placental separation is

difficult to control. It is better to find an edge of the placenta and push it aside in

order to extract the baby rather than to cut through it, if this is not feasible and is

either case because of the fetal haemorrhage the cord should be clamped as soon

as possible in all cases.

In women with active bleeding at start of surgery, General Anesthesia may

be safer for mother and fetus, because of risk of further lowering of BP during

epidural or spinal anaesthesia. Opinion vary from regarding placenta previa as an

absolute contraindication to the belief that with the appropriate experience all

cases are suitable for regional anaesthesia. From an obstetric view point in women

118

at high risk of having placenta accreta such as those with a history of previous

caesarean section General Anesthesia is preferable.

Current recommendations are that the operator at a caesarean section for

placenta praevia should be senior specialist. In one series women with scarred

uterus and placenta praevia had 16% risk of undergoing caesarean hysterectomy,

because of placenta accreta and severe haemorrhage. Women should be informed

the risk of need for hysterectomy during preoperative counseling.

Fetal survival rates have been improved by abdominal delivery and

therefore the majority opinion is that there are virtually no indications for an

attempt vaginal delivery, if the fetus is viable.

The use of so called double set up where an examination in theatre (with or

without anaesthesia) is performed to decide whether delivery by caesarean section

is required or whether should be induced has no place in modern obstetrics.

Management decision should be made on the basis of ultrasound appearance of the

placental localization and the presence of the presenting part below the lower edge

of placenta. Vaginal delivery with careful supervision may be attempted in cases

of Grade I, II and III placenta previa complicated by intra uterine fetal death or

premature labour at previable gestation. Blood should be cross matched as

transfusion may be necessary. In cases with grade IV, placenta previa vaginal

delivery is unlikely to be safe for the women and caesarean section will be

necessary with the exception of second trimester losses.

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Management of Placenta Previa- Flow chart

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120

MATERNAL OUTCOME

MATERNAL MORBIDITY AND MORBIDITY

In developing countries like India, obstetric haemorrhage is the commonest

cause of maternal death. Even though antepartum haemorrhage is less common than

postpartum haemorrhage, it contributes to a significant number of cases. Placenta

praevia is less common than abruption placenta in our country.

In general the maternal mortality rates have improved in regard to placenta

previa because of

a. Improvement in the health status of the pregnant women by antenatal care.

b. Early diagnosis by routine use of Ultra Sound Scan.

c. Free availability of blood transfusion facilities.

d. Omission of internal examination in case of accidental placental hemorrhage.

e. Wider number of caesarean section.

f. Potent antibiotics.

In spite of above measures the patient with placenta previa has an increased

maternal morbidity and mortality because of the following factors.

1. Shock

This can be ante, intra or postpartum period.

Antepartum – In majority of cases the first bout of bleeding is seldom severe but

torrential haemorrhage can be easily provoked by internal examination. A woman

who is anaemic in such a situation is placed at an even greater risk.

Intrapartum –

In cases of minor degree placenta previa allowed for vaginal delivery all

measures are to be taken to counter the effects of intrapartumhaemorrhage. Also

121

labour is prolonged due to slow dilation of cervix because of attachment of placenta

on the lower segment.

Postpartum haemorrhage–

It is mainly due to imperfect retraction and contraction of lower uterine

segment on which placenta is implanted.

Presence of large endometrial vessels at placental site.Large surface area of

placenta with atonic uterus due to pre-existing anemia.

Trauma to cervix and lower segment because of extreme softness and

vascularity.

Occasional association of morbidly adherent placenta.

2. Difficulties during operative delivery

The problems associated with placenta previa during caesarean section are:

1. Very vascular lower uterine segment.

2. Lateral extension of uterine incision.

3. Morbidity adherent placenta.

4. Bleeding from the placental bed.

3. Puerperium

These women are prone for sepsis because of

1. increased operative interference.

2. Placenta site near to the vagina.

3. Anemia in devitalized state of placenta.

122

All these factors put the women at very high risk. More so if the patients were

anemic.

Maternal risk

Maternal mortality due to hemorrhage has fallen from 5% to <0.1% since

introduction of conservation management consisting of hemodynamic support and

expectant management where possible.

1. Anesthetic and surgical complication especially in those women with major

praevia delivered by emergency CS where preparation for surgery in suboptimal.

2. Air embolism occurs where the sinuses in the placental bed are torn.

3. Postpartum hemorrhage and postpartum sepsis.

4. Placenta accreta occurs up to 15% of women with placenta previa.

5. Placenta malformations like biparitate, succenturate and membranacea and

fenestrate are encountered with placenta previa.

6. Battle dore insertion and velamentous distribution of vessels are common

features.

Air embolism – common as the placenta sinuses are open.

Fetal risk74,75

Preterm birth neonatal mortality rate was three fold in pregnancies

complicated by placenta previa because of increase preterm birth. There was also

increase risk of neonatal mortality in those delivered at term.

PNMR associated with placenta previa was 2.5% compared to 0.75% with

normal singleton pregnancy and was explained by gestational age at delivery

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association of congenital anomalies and maternal age, no increased occurrence of

IUGR seen in placenta previa.

Respiratory distress syndrome was frequently with an odds ratio of 4.9%.

Incidence of serious malformation is increased 2.5 fold in women with

placental previa.

Umbilical cord prolapse, malpresentation, fetal anemia, unexplained IUD due

to rupture of vasoprevia or from severe maternal hypovolemic shock.

Placenta Previa should be considered as a marker for possible obstetric

complication. Hence detection of placental previa should encourage a careful

evaluation with timely delivery in order to reduce the associated maternal end

perinatal complication.

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FETAL OUTCOME

PERINATAL MORTALITY AND MORBIDITY

The perinatal mortality for placenta previa has been reduced considerably

from as high as 50% to 5%. Under the present day circumstances the perinatal

mortality should not exceed 10%.

The chief causes of fetal/neonatal death in case of placenta previa are.

Intrauterine asphyxia

The placental separation irrespective of the cause can result in asphyxia.

However the maternal hypotension due to the haemorrhage or the shock can lead to

fetal hypoxia/anoxia.

Prematurity

This happens to be one of the leading contributors to the perinatal death.

However, the modern expectant management of placenta previa has significantly

reduced this hazard. 126/1000 to 42 – 81/1000 live birth.

The hazards of delivery

The cases of malpresentation especially take their own toll. The premature

infants especially are more prone to intracranial haemorrhage more so in case of

breech deliveries.

125

Respiratory distress syndrome

This condition is commonly associated with prematurity resulting from

placenta previa.

Fetal abnormalities

These are more commonly associated with placenta previa. MacAfee reported

an incidence of 3.4%. The most likely forms are spina bifida, hydrocephalus and

anencephaly. Cardiovascular/respiratory/gastrointestinal system.

Prematurity

A preterm neonate is defined as that baby born before 37 completed weeks of

gestation or by weight criteria a newborn with birth weight less than 2500 gms.

The chief problems associated with prematurity are as follows.

Respiratory

The premature infants have difficulty adapting to air breathing. This may first

present itself as perinatal depression and low Apgar scores. Respiratory distress

syndrome may occur due to surfactant deficiency, and apnea can also occur due to

immaturity of the breathing apparatus. The premature infants are at risk for

bronchopulmonary dysplasia or chronic pulmonary insufficiency.

Cardiovascular

The premature infants may be subject to hypotension due to hypovolemia,

cardiac dysfunction and or vasodilatation due to sepsis. This blood or fluid loss may

be further exaggerated due to their small sizes.

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Neurologic

Premature infants are at risk for acute neurologic problems such as intracranial

haemorrhage and perinatal depression.

Haematologic

Fetal anaemia is not common in cases of placenta previa, more common in

anterior placenta previa.

Infants with hyperbilirubinemia need special attention as even the low level of

bilirubin may be toxic to the nervous system of immature infant. It is common in

emergency caesarian section as high as 7.7% than in elective caesarian section 2.9.

Metabolic

Disorders in glucose and calcium metabolism are more common in premature

infants especially those infants who are malnourished and sick.

Immunologic

Due to deficiencies in both humoral and cellular immune response, the

premature infant is at a greater risk for infection.

In addition the premature neonate faces other problems as nutritional and

gastrointestinal. It is at more risk for necrotisingenterocolitis. The kidneys being

immature they have a low glomerular filtration rate and are unable to handle the water

and solute load.

The premature infants are also more prone to hypothermia and hyperthermia.

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Intracranial haemorrhage

Intracranial haemorrhage may result form trauma, or asphyxia, primary

haemorrhagic disturbances or congenital vascular anomaly. Intracranial haemorrhages

often involve the ventricle (intraventricularhaemorrhage) of premature infants

delivered spontaneously without apparent trauma.

Pathogenesis

Intraventricularhaemorrhage occurs in gelatinous subependymal germinal

matrix in case of the premature infant. The immature blood vessel in the

periventricular area is subjected to varied forces and has a poor tissue support.

Prematurity, respiratory distress syndrome, hypoxic ischemic and hypotensive injury

are some of the relevant factors which act as predisposing factors for

intraventricularhaemorrhage. These factors cause the rupture of germinal matrix blood

vessels. These factors produce cortical intra parenchymal echodensities which later on

develop to periventricular leukomalacias.

Clinical manifestation

The incidence depends on birth weight, being 10-20% in infants weighing

1000-1500 gms but it may be as high as 60-70% in infant weighing 500-750 gms. The

common symptoms are poor muscle tone, lethargy, apnea, somnolescence, decreased

or absent Moro’s reflex. There may be periods of apnea, pallor, cyanosis, failure to

suck well, abnormal eye signs, a high pitch shrill cry, muscular paralysis, metabolic

acidosis and shock. The fontanellae may be tense, bulging. The neurological

depression progresses to coma depending on the severity of the

intraventricularhaemorrhage. Periventricular leukomalacia is usually asymptomatic.

128

Diagnosis

Intracranial haemorrhage can be diagnosed based on history, clinical

manifestation, transfontanal cranial ultrasonography or CT scan.

Respiratory Distress Syndrome

This is an acute illness usually of preterm infants manifesting 4-6 hours after

delivery and characterized by a respiratory rate of more than 60 per minute

accompanied by dyspnea or respiratory distress.

The incidence varies according to gestational age and birth weight being 15-

30% between 32 and 36 weeks and about 60-80% in infants less than 28 weeks.

Etiopathogenesis

Surfactants are synthesized and stored in type II alveolar cells. In the

immature neonate the amounts produced are relatively insufficient to meet the

demands. In addition there are many other abnormalities in the lungs of premature

babies. The immature lung structures, cell damage, proteinaceous exudation on to the

alveolar surface are important factors. Asphyxia, hypoxemia and pulmonary ischemia

in association with hypovolemia, hypotension and cold suppress surfactant synthesis.

Alveolar atelectasis, hyaline membrane formation and interstitial edema make the

lung less compliant requiring greater pressure to expand the smaller alveoli and

airways. The highly compliant chest wall of premature infants offers less resistance

than those of mature infant against the natural tendency of the lungs to collapse.

129

Clinical manifestation

The signs manifest within minutes. The respiration becomes shallow and rapid

the rate exceeding 60 per minute. There is a prominent audible grunting, intercostals

and subcostal retraction, nasal flaring and duskiness.

As the infant gets exhausted apnea and irregular respiration occurs. There is

mixed respiratory – metabolic acidosis, edema, ileus and oliguria. The condition

rarely progress to death in severely affected neonates. In the mild cases the signs and

symptoms reach a peak within 7 days after which gradual improvement sets in. Death

usually occurs between the second to the seventh day.

Diagnosis

The diagnosis is made on the basis of clinical manifestations, the chest X-

ray, blood gas and the acid-base values. The chest X-ray appearance is characteristic

but not pathognomic. The X-ray shows fine reticular granularity of parenchyma and

air bronchogram. The typical X-ray pattern usually develops after 6-12 hours. The

initial firms may be normal.

Fetal growth restriction:

It occurs in upto 16% of cases and incidence is higher in multiple episodes of

antepartum haemorrhage.

Malpresentation:

Breech in commoner than transverse lie.

Placenta accreta merits a special attention as a part of placenta praevia. Joyce

Morgan quotes as incidence of 1.6%.

MacAfee also mentions that placenta accreta as the cause of death of one

patient in this series.

130

Fig 19. Hysterectomy Specimen of Placenta Accreta

131

PLACENTA ACCRETA

Abnormal adherence of placenta to uterine wall as a consequence of partial or

total absence of deciduasbasalis and imperfect development of nitabuch layer where

the placental villi are attached only to myometrium. It has been propose that the

abnormality of the placental uterine interface in women with placenta accrete will

lead to leakage of fetal alpha protein in to maternal circulation resulting in elevated

level of MSAFP.

Kupferminc76 and colleges reviewed 44 cases of women who had caesarean

hysterectomy found that 9.6 (45%) with placenta accrete had elevated MSAFP levels

(between 2.7- 40.3 MOMS). Similarly Zelop and colleagues foundelevated second

trimester MSAFP level (2.3-5.5MOMS) in 45% of 11 women with placenta accrete.

Placenta accretatotalis:17,48,56,72

The abnormal adherence of all cotyledons of placenta.

Partial placenta accreta:

Few to several cotyledons are attached to uterine wall.

Focal placenta accreta:

A single cotyledon is adherent to myometrium.

Bernischke and Kaufman (2012) showed that histological diagnosis of accreta

to be made from placenta and entire uterus or curettings from the myometrium are

necessary.

132

Fig 20

132

Fig 20

132

Fig 20

133

Incidence:40,65

It occurs in 1:2500 deliveries (ACOG, 2012) and a 10 fold increase over past

50 years. In the presence of a placenta praevia there is 5% to 10% in invasive

placenta. The risk is 20-25% with history of one caesarean delivery increasing to 40-

50% with a history of 2 or more caesarean deliveries (ACOG, 2012; Clark, 2004).

With the presence of placenta previa, the risk of placenta accrete was

3%,11%,40%,61%,and 67% for the first, second, third, fourth, and fifth of greater

repeat cesarean deliveries respectively.

Placenta increta:

Invasion of chronic villi into one-third of myometrium.

Placenta percreta:

Invasion of chronic villi beyond serosa and bladder.

Etiology

Age > 35 years

Parity > 4

Previous uterine scar

Uterine curettage

Down’s syndrome

134

Diagnosis

Antepartum

Ultrasonogical examination in placenta praevia is very important. Lam and

colleagues (2002) showed that ultrasound is only 33% sensitive in diagnosis77,78.

Ultrasound Doppler mapping, Twickler and colleagues (2000) found that

following factors had high predictive value in invasion of the myometrium.

Sensitivity is 100% and positive value is 78%.

1. A distance <1 mm between uterine serosa and bladder interface and retro placental

vessels.

2. Presence of large intraplacental lakes (Swiss Cheese Appearance).

3. Placental villous tissue in the bladder as exophytic growth or nodular or as

thickened bladder wall.

Women at high risk of a morbidly-adherent placenta need further imaging by

color Doppler or MRI. Doppler imaging has a sensitivity of 82.4% and a specificity of

96.8% (Chou et al., 2000). The final diagnosis and management is made only

intraoperatively and by histopathological examination of placenta and specimen as

false positives can occur.

MRI has better diagnostic role in invasive placenta. A sagittal sequence MRI

oriented in the plane of cervix is used to assess placental margin. It is more useful in

posterior placenta.

Postpartum

Spontaneous delivery of placenta does not occur and partial separation in focal

placenta accreta, and non-separation in total placenta accreta.

135

Maternal and Fetal Effects

Fetus is rarely affected unless uterine rupture or extensive bleeding occurs

during pregnancy.

Serious maternal complications are:

1. Severe intractable postpartum haemorrhage

2. Infection

3. Pelvic organ damage

4. Shock and death with a high rate of maternal mortality being 7% (ACOG, 2002).

136

Fig 21 Colour Doppler study of placenta accreta

Fig 22. MRI Scan of Placenta Accreta

137

MANAGEMENT

Definitive Management

Placenta previa with previous uterine scar should have consent for peripartum

hysterectomy. It is the most common indication for peripartum hysterectomy (Kastner

and associates, 2002).

According to RCOG 2012 guidelines care bundle for suspected placenta

accrete should be applied in all cases where there is placenta previa and a previous

cesarean sections or an anterior placenta underlying the old cesarean scar

Consultant obstetrician planned and directly supervising delivery

Consultant anesthetists planned and directly supervising anesthetic at delivery

Blood and blood products available

Multi-disciplinary involment in pre-op planning

Discussion and consent includes possible interventions(such as hysterectomy,

leaving the placenta in place, cell salvage and intervention radiology)

Local availability of a level 2 critical care bed.

Supportive therapy:

Along with maintenance of airway, breathing and circulation it needs.

1. Multiple blood and its products are necessary.

2. Auto transfusion also has a role.

3. Recombinant factor 7a in severe cases.

Conservative Management

Medical line of management with methotrexate.

Surgical management includes internal iliac artery ligation or uterine artery

embolization.

138

When the placenta previa is complicated by placenta accreta which makes

difficult to control bleeding from the placental bed by conservative means other

method of haemostasis are necessary over sewing the implantation site with chromic

catgut no. 10 may provide haemostasis.

In some cases bilateral uterine artery ligation is helpful and in others bleeding

controlled with internal iliac artery ligation. Cho and colleagues have described

placing circular interrupted sutures around the lower segment above and below the

transverse incision which controlled haemorrhage. Durfin (1989) successfully

controlled haemorrhage by tightly packing the lower uterine segment. Conservative

treatment with methotraxate has also provided satisfactory results.

If these methods fail then hysterectomy is necessary. Attention to asepsis is

important because peurperial sepsis is very liable because the placental site being both

low in genital tract and larger than usual provides portal of entry for ascending

infection.

139

Recommendation and conclusions ACOG(2012)

Women at greatest risk of placenta accrete are those who have myometrial

damage caused by an earlier cesarean delivery with either an anterior or

posterior placenta previa overlying the uterine scar.

Grayscale ultrasonography is sensitive (77-87%) and specific (96-98%) for the

diagnosis of placenta accrete.

If there is a strong suggestion of the presence of abnormal placental invasion,

health care providers practicing at small hospitals or at institutions with in

sufficient blood bank supply availability of subspecialty and support personal

should consider patient transfer to a tertiary perinatal care center

To enhance patient safety, it is important that the delivery be performed in an

operating room by an experienced obstetric team that includes an obstetric

surgeon, urologist, general surgeons, and gynecologic oncologists, available if

necessary. Improved outcomes have been demonstrated when women with

placenta accrete give birth in specialized tertiary centers.

Preoperative patient counseling should include discussion of the potential need

for hysterectomy, the risk of profuse hemorrhage, the risk of profuse

hemorrhage, and possible maternal death.

Although a planned delivery is the goal, a contingency plan for emergency

delivery should be developed for each patient, which may include following

an institutional protocol for maternal hemorrhage management.

The timing of delivery should be individualizes,depending on patient

circumstances. Combined metarnal and neonatal outcome is optimized in

stable patients with a planned delivery at 34 weeks of gestation without

amniocentesis.

140

The decision to administer antenatal corticosteroids and the timing of

administration should be individualized.

Generally the recommended management of suspected placenta accrete is

planned preterm cesarean hysterectomy with the placenta left in situ because

removal of placenta is associated with significant hemorrhagic morbidity.

However, surgical management of placenta accreta may be individualized.

141

PART – II

METHODOLOGY

“The patient is the centre of medicine universe around which all our works resolve

and towards which all our efforts tread”

J. B. Murphy (1857-1916)

Materials and Methods of study:

Analysis of maternal and neonatal outcome in case of placenta previa occurring over a

period of 1 year (Nov 2011 – Oct 2012). This study was carried out at

CHELUVAMBA HOSPITAL, MYSORE MEDICAL COLLEGE AND RESEARCH

INSTITUTE, MYSORE.

Study Design:

The present study group consists of 61 cases of placenta previa, during one year of

study period.

Inclusion Criteria:

Pregnant women with placenta previa confirmed by ultra sonography and gestational

age beyond 28 weeks were selected irrespective of their parity, type of placenta previa

and with live or dead fetus.

Methodology:

The ethical committee of hospital approved the study. Before recruiting an eligible

patient in the study, an informed consent was taken from the patient’s attender's or

patient herself.

142

Data Collection:

On admission, the history of the patient consisting of name, age, address, duration of

bleeding, associated pain, h/o appreciation of fatal movements were recorded. The

obstetric history was recorded in detail. Personal history was also noted.

The clinical examination included nutritional status, pallor, edema and signs of shock

.PR, BP and respiration were noted. CVS and RS examined. The height of uterus in

weeks, uterine contractions, lie, presentation and position of fetus, mobility and

engagement of fetal head and FHS was noted, and also examined for uterine

tenderness. Regular records of vital parameters were maintained. Input and output

charts were maintained.

IV lines were secured and blood samples collected for investigation

Investigations included Hb%, blood grouping and Rh typing, bleeding time, clotting

time and CRT. Cross matching samples were drawn in case blood transfusion was

required. Urine examined for albumin, sugar and microscopy. All patients were

subjected to USG if it was not done previously or not done after 28 completed weeks

of gestation.

Cases were managed according to the degree of placenta previa and gestational age,

taking into account the fetal and maternal condition. Minor degree of placenta previa

cases were allowed for vaginal delivery and caesarean section resorted to in case of

complications. Major degree of placenta previa cases underwent emergency caesarean

section. Anticipating PPH, Oxytocics, Methergin or prostaglandins were used.

143

All the delivered babies were managed with proper care paying attention to the

resuscitation of the asphyxiated ones. Babies requiring special care were admitted to

NICU.

The fetal and maternal outcome and complications was recorded in each case and the

patients and babies assessed at the time of discharge. The duration of hospital stay

was recorded in each case.

144

STATISTICAL METHODS APPLIED:

Frequencies:

The Frequencies procedure provides statistics and graphical displays that are useful

for describing many types of variables.

Chi-square test:

The Chi-Square Test procedure tabulates a variable into categories and computes a

chi-square statistic. This goodness-of-fit test compares the observed and expected

frequencies in each category to test either that all categories contain the same

proportion of values or that each category contains a user-specified proportion of

values.

Crosstabs (Contingency coefficient test)

The Crosstabs procedure forms two-way and multi-way tables and provides a variety

of tests and measures of association for two-way tables. The structure of the table and

whether categories are ordered determine what test or measure to use.

All the statistical calculations were done through SPSS 16.0 (2007) for windows.

145

Management of the cases were based on the following criteria:

1. Mother’s condition –

Degree of obstetric haemorrhage– Mild, Moderate or severe.

2. Fetal condition –

Gestational age, live/dead

3. Ability of the neonatal unit to handle an infant of that gestational age.

Characteristic of Bleeding

Severe Modarate Mild

>36 weeks orImmatureL/S ratio

< 36 weeksImmatureL/S ratio

<36weeksImmatureL/S ratio

TocolysisCorticosteroids

Blood Tranfusion

PatientUnstable

PatientStable

Cesarean Section ExpectantManagement

Moderate

146

According to RCOG (2011)40 guidelines the Initial management should follow the

ABCD pathway.

A and B – Assess airway and breathing

A high concentration of oxygen (10–15 litres/minute) via a facemask should be

administered.

C – Evaluate circulation

Establish two 14-gauge intravenous lines; a 20 ml blood sample should be taken and

sent for diagnostic tests,

including full blood count and assessment of FMH if RhD-negative, coagulation

screen, urea and electrolytes

and cross match (4 units)

D – Assess the fetus and decide on delivery

The four pillars of management:

1. communication between all members of the multidisciplinary team

2. Resuscitation (see Appendix 2)

3. Monitoring and investigation

4. Arrest bleeding by arranging delivery of the fetus (see section 14).

These management strategies have been adapted from RCOG Green-top Guideline

No. 52 Prevention and

Management of Postpartum Haemorrhage.12 The differences in management options

between APH and PPH are that there are two individuals to care for (should the fetus

still be alive) and that a very specific method

147

of controlling the haemorrhage is available in the event of an APH (delivery of the

fetus and placenta).

Delivery of the fetus and placenta will control bleeding by allowing the uterus to

contract and stop bleeding

from the site of placental separation, and will also remove placental tissue, a source of

production ofcoagulation activators which predisposes to the development of DIC.

The principles of fluid replacement and administration of blood products (from

RCOG (2011)40 Green-top Guideline No. 5212)

Basic measures for haemorrhage up to 1000 ml with no clinical shock:

● intravenous access (14-gauge cannula x 1)

● commence crystalloid infusion.

Full protocol for massive haemorrhage (blood loss > 1000 ml or clinical shock):

● assess airway

● assess breathing

● evaluate circulation

● oxygen by mask at 10–15 litres/minute

● intravenous access (14-gauge cannula x 2)

● position left lateral tilt

● keep the woman warm using appropriate available measures

● transfuse blood as soon as possible

148

● until blood is available, infuse up to 3.5 litres of warmed crystalloid Hartmann’s

solution (2 litres) and/or

colloid (1–2 litres) as rapidly as required

● the best equipment available should be used to achieve rapid warmed infusion of

fluids

● special blood filters should not be used, as they slow infusions.

Fluid therapy and blood product transfusion:

Crystalloid up to 2 litres Hartmann’s solution

Colloid up to 1–2 litres colloid until blood arrives

Blood cross-matched

If cross-matched blood unavailable and the clinical situation is urgent, give

uncrossmatched

group-specific blood or give O RhD-negative blood consider the use of red-cell

salvage if available

Fresh frozen plasma 4 units of FFP (12–15 ml/kg or total 1 litre)

(i) for every 6 units of red cells or

(ii) if prothrombin time and/or activated partial thromboplastin time (PT and aPTT)

are greater than 1.5 x mean control Platelets concentrates if platelet count < 50 x 109/l

Cryoprecipitate if fibrinogen < 1 g/l.

149

With continuing massive haemorrhage and whilst awaiting coagulation studies, up to

4 units of FFP and 10 units of cryoprecipitate (two packs) may be given empirically.

Apply clinical judgement in each situation.

The main therapeutic goal of the management of massive blood loss as outlined in

Green-top Guideline No. 52 summarises the main therapeutic goal of management of

massive blood loss is to maintain:

● haemoglobin > 8 g/dl

● platelet count > 75 x 109/l

● prothrombin time < 1.5 x mean control

● activated partial prothromboplastin time < 1.5 x mean control

● fibrinogen > 1.0 g/l.

150

OBSERVATIONS AND DISCUSSION:

In the present study, the following results have been discussed under the following

headings:

1. The incidence of placenta previa

2. Correlation of maternal age and placenta previa.

3. Correlation of parity and placenta previa.

4. Risk factors in placenta previa.

5. Antenatal complications associated with placenta previa.

6. Intra and post-operative complications noted in the cases studied.

7. The perinatal morbidity in placenta previa.

8. The perinatal mortality rate.

9. Comparison of the causes of death.

10. Correlation between perinatal mortality and type of placenta previa.

11. Correlation between perinatal mortality and mode of delivery.

12. Correlation between perinatal mortality and gestational age.

13. Correlation between perinatal mortality and birth weight of infants.

151

Table 1. INCIDENCE OF PLACENTA PREVIA:

Period of Study: from November 2011 to October 2012.

Total no. of births 14712

Total no. of cases of placental previa 61

Incidence of placenta previa 0.41%

Total no. of perinatal deaths due to placenta previa 4

General perinatal mortality rate 18/1000

Perinatal mortality rate in placenta previa 6.5

NICU admission 44.3%

Maternal death due to placenta previa 2

152

Table 2. INCIDENCE OF PLACENTA PREVIA BY DIFFERENT AUTHORS

AUTHOR INCIDENCE PERCENTAGE

Daftery (1960) 1:142 0.70%

Purandare (1962) 1:188 0.53%

Menon (1963) 1:205 0.49%

Hibbard and Jeffcot (1966) 1:119 0.84%

Ratnam (1968) 1:213 0.47%

Das.B (1970) 1:139 0.70%

Motwani Seth (1988) 1:135 0.73%

BhaskarRao (1988) 1:192 0.52%

Hemmadi (1995) 1:250 0.40%

Rani.P.R (1999) 1:175 0.57%

Mahesh.R (2000) 1:125 0.80%

Kondur Pallavi (2001) 1:141 0.70%

Shonali Mayerkar (2008) 1:418 1.80%

Present study 1:137 0.40%

153

The above table shows the incidence of placenta previa in various studies. The

incidence of placenta previa varies with the availability of antenatal care and

sonographic evaluation.

Das.B from 1940-197044 analysed and gives incidence of placenta previa -

1:139(0.7%)

Ratnam (2007)45 gives incidence of placenta previa 1:213 (0.47%)

Motwani and sheth (1990)46 from Wadiahospital,Mumbai noted the incidence of

placenta previa – 1:135 (0.73%)

K.BhaskarRao (1988)47 from Maternity hospital, Chennai reported the incidence of

placenta previa – 1:192 (0.52%)

Hemmadi (1995)5 gives incidence of placenta previa 1:250 and Rani.P.R (1999) from

JIPMER, Pondicherry reported the incidence – 1:175.

Mahesh.R (2000) from Cheluvamba hospital, Mysore gives incidence of 1:125

(0.80%)

ShonaliMayerkar (2008) Gulburga Medical college gives the incidence of Placenta

previa 1.80%

154

Table 3. INCIDENCE OF PLACENTA PREVIA ACCORDING TO VARIOUS

STUDIES:

NAME OF THE INSTITUTE PREVIA APH% PLACENTA PREVIA

Medical college and hospital Rohtak (82-87) 4.8% 69%

Dhaka medical college, Bangladesh (1986) 1.30% 64.1%

Sirraj hospital Thailand (1983) 0.60% 64.7%

Eden hospital and medical college (89-92) 1.13% 45.8%

Maternity hospital, Kualalmpur 1.24% 74.3%

National university of Singapore 2.1% 63.4%

Sharma BD Post Graduate Hospital, Hariyana (2007) 3.1% 52.64%

Scandinavian Study (2008) 4.5% 28.0%

155

Table 4. INCIDENCE OF PLACENTA PREVIA IN CHELUVAMBA

HOSPITAL:

YEAR INCIDENCE TOTAL No: OF DELIVERIES

1995-1996 1:135 6342

1996-1997 1:118 6250

1997-1998 1:109 6361

1998-1999 1:142 6990

2000-2001 1:125 13351

Present study 1:137 14712

156

Table 5. CORRELATION OF MATERNAL AGE AND PLACENTA PREVIA:

Present study:

Graph 1

Age No. of cases Percentage

<19 1 1.63

20-29 45 73.77

30-35 12 19.67

>35 3 4.91

Total 61 100.0

156


Present study:

Graph 1


<19 1 1.63

20-29 45 73.77

30-35 12 19.67

>35 3 4.91

Total 61 100.0

156


Present study:

Graph 1


<19 1 1.63

20-29 45 73.77

30-35 12 19.67

>35 3 4.91

Total 61 100.0

157

Test Statistics

As shown in the table above, in the present study the incidence of placenta

previa was highest in the age group of 20-29 years i.e., 73.77% , followed in

descending order by women in the 30-35 year age group, above 35 year age group

and less than 19year age group, i.e.,19.67%, 4.91%, 1.63% respectively.

The mean maternal age in our study was 26.07 years which is similar to

observation made by Das et al (1999) with the main age of 28.6 years and Singhal et

al (2008) as 26.2.

In a recent study Shonali Mayerkar (2008) regarding the maternal age, the

maximum number of Patients i.e., 35 (70%) women were between the age group of

20-29 years, followed in descending order by 8 (16%) women in 30-35 years age

group. 6 (12%) women were more than 35 years and one woman (2%) was less than

19 years.

In the study done by Patricia Mcshane (1985)52 the mean age was 29.8 years.

CORN

Chi-Square 76.797

Df 3

Asymptotic

Significance.000

158

Table 6. COMPARATIVE STUDIES OF AGE DISTRIBUTION IN

PLACENTA PREVIA.

Authors Max age group

Macafee (1945) 25-30

Das.B (1970) 29.6

Steven Clark (1985) 25 – 29

Michelle A williams (1987-88) 20 - 29

Handler (1994) 20-29

Hemmadi (1995) 20-29

Rani P.R (1999) 20-29

MaheshKumar (2000) 21-25

Kondur Pallavi (2001) 20-29

Shonali Mayerkar (2008) 20-29

Gurol Urganci (2011) 20-29

Present Study 20-29

159

Table 7. CORRELATION OF PARITY AND PLACENTA PREVIA:

In the present study, the incidence of placenta previa was highest (63.9%) in

multigravidas (with two to three viable births). The incidence in Grand multi (>4

viable births) was 1.6% and in Primi it was 34.4%.

Test Statistics

PRESENT STUDY No of cases Percentage

primi 21 34.4

Multi(2-3) 39 63.9

Grand multi(>=4) 1 1.6

Total 61 100.0

PARITY

Chi-Square 35.541

Df 2

Asymptotic

Significance.000

160

Graph 2

In the study done by Michelle A Williams (1993)53 the correlation between placenta

previa and parity was as follows, with the highest incidence in the multiparous group

(61.2%).

In the study done by Steven Clark et al(1985)54 the relationship of placenta previa to

maternal parity is 21.2% in primi gravida. 2nd gravida 18.7%.

160

Graph 2



(61.2%).



160

Graph 2



(61.2%).



161

Table 8. COMPARITIVE STUDY OF DISTRIBUTION OF PARITY INPLACENTA PREVIA:

Williams (1991)55 in his studies found that 65.2% incidence of Placenta previa is

between para 2-4.

Rani P.R (1999)10 found that maximum incidence in multigravida-69%.

Mahesh Kumar (2000), in his study found that 65.42% incidence of placenta previa

multi para.

Kondur Pallavi (2001) in her study stated that 78.4% incidence of placenta previa

multi para.

Shonali Mayankar (2008) in her study found that 56% incidence of placenta previa

multi para.

Gopleurd in his study showed that as the parity increases the risk of placenta previa

also increases independant of other risk factors.

As it has been noted in the other studies, the incidence of placenta previa is higher in

women of high parity and women who are well into reproductive span of life.

In present study, there were 34.4% primigravida. 63.9% were Multi between 2-3

and 1.6% is above 4.

Auther Incidence (PARA)Williams (1991) 65.2% (2-4)Rani P.R (1999) 69% (Multi)Mahesh Kumar (2000) 72% (2-4)Kondur Pallavi (2001) 78.4% (Multi)Shonali Mayankar (2008) 56% (Multi)Present Study 63.9% (2-3)

162

Table 9. PRESENCE /ABSENCE OF PAIN ABDOMEN IN PLACENTA

PREVIA:

Pain abdomen No. of cases Percentage

Present 2 3.27%

Absent 59 96.72%

Total 61 100%

The above table shows that in majority of cases pain abdomen was absent (96.72%)

and remaining 2 cases pain abdomen was present.

Usually pain abdomen is absent in placenta previa unless the patient is in labour, and

when associated with abruption placenta in 2 of our cases were retroplacental clot was

present.

163

Table 10. RISK FACTORS FOR PLACENTA PREVIA:

Present Study

Graph 3

RISK FACTORS No of cases Percentage

Caesarean section 4 6.6

Abortion 6 9.8

Twin gestation 0 0

Rh isoimmunation 6 9.8

Myomectomy 1 1.63

None 44 72.13

Total 61 100.0

163


Present Study

Graph 3



Abortion 6 9.8

Twin gestation 0 0


Myomectomy 1 1.63

None 44 72.13

Total 61 100.0

163


Present Study

Graph 3



Abortion 6 9.8

Twin gestation 0 0


Myomectomy 1 1.63

None 44 72.13

Total 61 100.0

164

The above table showed 4 cases had a history of 1 prior caesarean sections 6 cases of

abortion out of which 3 cases had undergone D and C., 1 case had previous history of

myomectomy. RH isoimmunisation was for 6 cases and no twin gestation in the

study.

Damage to the endometrium or myometrium has shown to be a risk factor for low

implantation of placenta.

RISK

Chi-Square 77.557

Df 3

Asymptotic

Significance.000

165

Risk factors for placenta praevia40–43,45–47

According to RCOG (2011)40:

Previous placenta praevia (adjusted OR 9.7)45–47

Previous caesarean sections (RR 2.6, 95% CI 2.3–3.0 with a background rate of

0.5%)46

One previous caesarean section OR 2.2 (95% CI 1.4–3.4 with a background rate of

1%)47

Two previous caesarean sections OR 4.1 (95% CI 1.9–8.8)

Three previous caesarean sections OR 22.4 (95% CI 6.4–78.3)

Previous termination of pregnancy

Multiparity

Advanced maternal age (>40 years)

Multiple pregnancy

Smoking

Deficient endometrium due to presence or history of:

• uterine scar

• endometritis

• manual removal of placenta

• curettage

• submucous fibroid

Assisted conception

166

Table 11. THE RELATIVE RISK OF PLACENTA PREVIA ASSOCIATED

WITH PREVIOUS CEASAREAN SECTION

The incidence of placenta previa increases with the increase in number of

previous caesarean section. Retrospective analysis of 292 cases of placenta previa

showed an incidence of 0.26% in an unscarred uterus, 0.65% after caesarean section

and rising to 10% in a woman with more than 2 abdominal deliveries. The risk of

placenta previa is highest in a pregnancy immediately following caesarean section.

Clark et al proposed that lower uterine scar impedes the migration of placenta away

from internal OS that would otherwise occur in late pregnancy.

David et al (1980)57, noted interesting clinical features of study that history of

abortions and previous D&C increased the risk 5 times and prior caesarean section

Study ID Odds Ratio

Hendricks-1999 2.64

Lydon Rochelle-2001 1.40

Gilliam-2002 1.28

Tuzovic-2003 2.00

Hossian-2004 0.45

Olive-2005 1.96

Getahun-2006 1.50

Kennare-2007 1.66

Daltveit-2008 1.50

Rahim-2009 1.70

Rosenberg-2010 1.76

167

increased the risk 6 times and increased the incidence of placenta previa. Post-

operatively, there was an unexplained increase in the incidence of male infants in the

mother having placenta previa. In the study, 37% patients had a history of prior

abortions, 14.6% had previous caesarean sections and 2.3% had a placenta previa in

early pregnancy.

Recurrence rate following placenta previa is 4-8% but in the present study

there was no history of previous placenta previa.

In a study done by Milosevic J et al: (2009)39 May-Jun, retrospective study of

10-year period about the placental complication after a previous caesarean section.

The incidence of placenta previa in control group was 0.33% opposite to 1.86% after

1 caesarean section, 5.49% after 2 caesarean sections and as high as 14.28% after 3

caesareans sections.

Rani .P.R. (1999)10, shows that prior caesarean section in 11% and 9% had

abortion, majority had no risk factors.

According to Mahesh (2000), shows that prior caesarean section in 9.35%, abortion in

14%.

KondurPallavi (2001), abortions in 18.3%, prior caesarean section in 21.7%

and twin gestation 1.7%.

Shonali Mayarkar (2008), in her studies showed that 6(12%) women had one

or more previous LSCS, 9(18%) had under gone abortions previously out of which

4(8%) women had D&C done, And twin gestation had one case.

L.G. Johnson et al (2003)59. international journal of gynaecology and

obstetrics 81, showed that risk of placenta previa increased with no. of sharp curettage

168

abortions. (OR 2.9, 95% CI 1.0-8.5 for >3). Vaccum aspiration abortion was not

associated with an increased risk of placenta previa (OR 0.9,95% CI o.6-1.5).D and C

is more likely to cause damage or scarring of the uterus than VA, multiple D and C

abortions may be associated with greater scarring and greater risk of placenta previa.

CandeV.Ananth, John C. Smulian(2003)19 meta-analysis of association of

placenta previa with history of caesarean delivery and abortion. Relative risks were

4.5 after 1, 7.4 after 2, 6.5 for 3 and 44.9 for 4 or more prior cesearean deliveries.

Women with history of spontaneous or induced abortion had a relative risk of

placenta previa of 1.6% and 1.7% respectively.

In the study done by Ananth CV et al: (2003)19, the prevalence rate of placenta

previa is 4.0/1000 births and advancing maternal age multi parity, previous caesarean

delivery and abortion smoking cocaine use during pregnancy and male foetuses all

confirmed increased risk for placenta previa.

In the study done by Victoria Taylor (1993)47 the incidence of spontaneous

and induced abortions was 36% and 29% respectively.

In the present study, the incidence of prior spontaneous or induced abortions

followed by check curettage was 9.8%.

In the present study the incidence of twin gestation was 0% and in the study

done by McShane (1985)2 the incidence of twin gestation was 0.60%.

169

Table 12. ANTENATAL COMPLICATIONS IN THE PRESENT STUDY:

COMPLICATIONS COUNT & % OF COMPLICATIONS

Minor(N=23) Major(N=38) Total(N=61)1STTrimister bleeding 1 1 2

3.27%2nd Trimester bleeding 9 11 20

32.7%Severe anemia<7gm 3 9 12

19.67%Malpresentation 3 7 10

16.3%Transverse lie 2 4 6

9.83%

Breech2 3 5

8.1%PIH 0 5 5

8.1%IUD 1 0 1

1.63%

Presentation Carlyle-

1969

Baskar

Rao-

1976

Rani

P.R-

1999

Mahesh

R-2000

Kondur

Pallavi

2001

Shonali

Mayarkar

2008

Present

study

Vertex 71% 67.3% 80% 65.42% 77% 36% 39%

Breech 11% 23.3% 7% 24.30% 18% 14% 8.3%

Tr.lie 17% 8.6% 12% 10.28% 5% 0% 4.1%

170

Symmetric Measures

Value

Approximate

Significance

Nominal by

Nominal

Contingency

Coefficient.278 .550

N of Valid Cases 59

Graph 4

According to Fishman, Shire et al JPM (2011)60, of 113 singleton pregnancies

with placenta previa, 54(48%) delivered at term and 59(52%) delivered preterm.

Fifty-one(45%) experienced antepartum bleeding at a median gestational age of 31

170

Symmetric Measures

Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 59

Graph 4




170

Symmetric Measures

Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 59

Graph 4




171

weeks(29-33 weeks) with a median interval of 20days(11-33 days) between first

bleeding episode and delivery. Women with antepartum bleeding were more likely to

be delivered for hemorrhage (36 of 51 vs. 8 of 62,p<0.001). Antepartum bleeding

before 34 weeks has a positive predictive value of 88% for preterm birth and 83% for

emergent delivery.

In the present study Ante partum bleeding was present in 35.97% and severe

anemia (Hb% <7gm %) was found in 16% of cases.

In a study done by P. Reddi Rani and Chaturvedula (1999)10 anemia

complicated 20% of cases.

In the present study the incidence of malpresentation was 20% . In the study

done by P.Reddi Rani (1999)10 the incidence of malpresentation was 20% and in the

study done by McShane (1985)2 the incidence of malpresentation was 27 . These two

studies correlate with the present study.

In the present study PIH complicated 4.4%of cases whereas in the study done by

McShane (1985)2 PIH complicated only 1% of cases. In the study done by P.Reddi

Rani (1999)10 PIH complicated 15% of cases.

Above table shows majority of cases have vertex presentation that is 39% almost

all had an unengaged head.

A patient with term pregnancy with unengaged head along with bleeding pv,

most probably placenta previa.

Disproportion, malpresentation and multiparity have to be kept in mind.

George R Henry (1974) says that whenever an abnormal presentation found in

primigravida patient, an obstetrician should suspect placenta previa, contracted pelvis

and pelvic tumors

172

In emergence with placenta previa, antepartum bleeding is a strong predictor of

preterm delivery. 1st trimester bleeding is a risk factor for preterm delivery.

Table 13. DEGREE OF PLACENTA PREVIA

Out of 61 cases of placenta previa 23 had minor degree (Type I, Type IIA) and 38 had

major degree of placenta previa (Type II B, Type III & Type IV).

59 cases delivered by CS, 2 cases delivered vaginally. Active management was

carried out in 58 cases and 3 cases were subjected for expectant management by

Macafee regime, 2 women continued with pregnancy till 37 weeks and taken for

elective LSCS were as one woman had two episodes of severe bleeding and was taken

for emergency LSCS.

Degree of Placenta Previa No of Cases Percentage

Minor degree 23 37.70%

Major degree 38 62.29%

173

Table 14. ULTRA SOUND OF DIFFERENT TYPES OF PLACENTA PREVIA:

Type of placenta previa Frequency percentage

Type1 8 13.1%

Type2 26 42.6%

Type3 7 11.4%

Type4 16 26.2%

Graph 5

In one case placenta at the mid trimester scan at 20weeks showed type 4 and

subsequent scan at 34 weeks showed type1. Owing to the development of lower

uterine segment occurs during II and III trimester but it is less likely to occur if

placenta is posterior or if there has been a previous caesarean section. In case of

asymptomatic women with suspected minor previa follow up imaging can be left until

0 1

type3

type1

type4

type2

173



Type1 8 13.1%

Type2 26 42.6%

Type3 7 11.4%

Type4 16 26.2%

Graph 5






1 2 3 4

173



Type1 8 13.1%

Type2 26 42.6%

Type3 7 11.4%

Type4 16 26.2%

Graph 5






5

Series 3

Column2

Column1

174

36 weeks of gestation, done for 3cases. In case of asymptomatic women with

suspected major previa or a question of placenta accrete imaging must be performed

at around 32weeks of gestation to clarify the diagnosis and allow the planning for III

trimester management, further imaging delivery done for 4 cases-1case with previous

caesarean section with major placenta previa with type IV. There was thin anterior

myometrial segment (<5mm), loss of sub placental lucent zone, blood vessels in the

bladder where peripartum hysterectomy was done.

Serial scans in II trimester were placenta remained <20mm from internal OS

elective LSCS was done.

When placental edge was more than 20mm from the internal cervical OS

vaginal delivery was done for 2 cases.

175

Table 15. MANAGEMENT PROTOCOL:

Management No: cases Percentage

Active 58 95.08%

Expectant 3 4.91%

Expectantly managed delivery there was no perinatal mortality while in actively

managed groups perinatal mortality was 6.55%.

Table 16. Route of delivery: Abdominal

Route of delivery No: of Cases Percentage

Emergency 35 57.37%

Elective 7 11.4%

Table 17. Cesareans Section in placenta previa in different study:

Author CS Rate

Chakraborthy 1992 81.8%

Rani P.R 1999 64%

Mahesh R 2000 70.09%

KondurPallavi 2001 24.3%

Shonali Mayarkar 2008 82%

Present study 68.7%

There has been a profound increase in cesareans section rate and improvement in

perinatal maternal outcome has been attributed to this.

176

Table 18. Route of delivery: Vaginal

Route of delivery No: of Cases Percentage

Augmented with Oxytocin 1 1.63%

Spontaneous 1 1.63%

Augmented with Oxytocin was IUD of 28 weeks with transverse lie with low lying

placenta previa. One more cases was spontaneous delivery due to Preterm of 32

weeks with low lying placenta previa.

Table 19. Vaginal delivery in placenta previa in different study:

Chakraborthy 1992

Hemmadi 1995

Rani P.R 1999

Mahesh R 2000

KondurPallavi 2001

Shonali Mayarkar 2008

Present study

177

Table 20. INTRA AND POST OPERATIVE COMPLICATIONS:

PRESENT STUDY: Type of placenta

Complications Minor(N=23) Major(N=38) Total

(N=61)

Percentage

Shock/Hypotension 0 2 2 3.7%

Sepsis 0 0 0 0

Febrile Morbidity 0 0 0 0

PPH 6 9 15 27.8%

Blood transfusion 12 12 33 61.1%

Hysterectomy 3 1 4 7.46%

Adherent placenta 0 1 1 1.9%

Value

Approximate

Significance

Nominal

by

Nominal

Contingency

Coefficient .228 .565

N of Valid Cases 54

178

Graph 6

Table 21. Blood components.

In the present study, 61.1%of patients received blood transfusion and 3.7%of

patients went in for hypotension and/or shock. No patients had febrile morbidity in

the post-operative period. The incidence of PPH was 27.9%, hysterectomy was done

Components Frequency

Platelets 4

PRBC 44

FFP 20

Cryoprecipitate 8

178

Graph 6






Platelets 4

PRBC 44

FFP 20

Cryoprecipitate 8

178

Graph 6






Platelets 4

PRBC 44

FFP 20

Cryoprecipitate 8

179

in 4 cases(7.46%). In this study 3 case of peripartum hysterectomy was for anterior

placenta previa. Adherent placenta was seen in 1case (1.9%).

Zlatnik MG et al (2007)31 Patient with previa were more likely to be

diagnosed with postpartum haemorrhage (59.7% vs. 17.3%;p< 0.001) and to receive a

blood transfusion(11.8% vs. 1.1%;p<0.001).

North Am J Med SC 2011: The incidence, indications, risk factors and

outcome of emergency peripartum hysterectomy ranged from 0.24 to 8.7 per 1000

deliveries. Emergency peripartum hysterectomy was found to be more common

following caesarean section than vaginal deliveries. The predominant indication for

emergency peripartum hysterectomy was abnormal placentation (placenta

previa/accrete) which was noted in 45 to 73.3%, uterine atony in 20.6 to 43% and

uterine rupture in 11.4 to 45.5%. The risk factors included previous caesarean section,

scarred uterus, multiparity, older age group. The maternal morbidity ranged from 26.5

to 31.5% and the mortality from 0 to 12.5% with a mean of 4.8%. the decision of

performing total or subtotal hysterectomy was influenced by the patient’s condition.

The indication for emergency peripartum hysterectomy in recent years has changed

from traditional uterine atony to abnormal placentation. Patients with placenta previa

and scarred uterus had 16% risk of undergoing emergency peripartum hysterectomy

compared to 3.6% in patient with unscarred uterus.

Total hysterectomy is the recommended surgical method of emergency

peripartum hysterectomy due to the potential risk of malignancy developing in the

cervical stump and the need for regular cytology.

North Am J 2011: The pre-operative risk factors like previous history of CS,

placenta previa and accreta should be identified and referred to the tertiary centre

180

proper surgical measures such as haemostatic sutures or uterine or hypo gastric artery

ligation or embolization are options in whom future fertility is important and who are

relatively haemodynamically stable. When conservative treatment is not feasible or

has failed, prompt emergency peripartum hysterectomy is performed failing which the

delay would contribute to the maternal morbidity and in unfortunate cases mortality.

In the study done by Suk- Joo Choi et al: (2008)35, concluded that women with

placenta previa, history of abortion as well as prior CS and total previa are strong

antepartum risk factor for peripartum hysterectomy.

In the study done by Dong Gyu Gang et al: Dept of Obg&Gynec, The catholic

University of Korea, Seoul. Reported in their study that complications like Massive

blood transfusion, Placenta accreta and hysterectomy was more in anterior placenta

previa.

In the present study, all the 4 case was done for uterine atony, after all

conservative measure to arrest bleeding with uterotonic drugs, uterine artery ligation,

haemostatic sutures failed and all the 4 had total hysterectomy.

The Histopathology reports of all these hysterectomy specimens were showing

edematous myometrial tissues.

Uterine atony is an indication for emergency peripartum hysterectomy in

27.8% of all the cases

As per ACOG committee opinion, July 2012, the incidence of Placenta accrete

has increased and seems to parallel the increasing caesarean delivery rate. Researchers

have reported the incidence of placenta accrete as 1 in 533 pregnancies for the period

181

of 1982 – 2002(5). This contrasts sharply with previous reports, which ranged from 1

in 4,027 pregnancies in 1970s, increasing to 1 in 2,510 pregnancies in 1980s(6,7)

In my present study, compared to the placenta previa, placenta accrete is less

contributing to caesarean hysterectomy was nil.

In the study done by Meshane et al (1985) the major post partum

complications were Hysterectomy 28.6%, Febrile morbidity 28.6%,Urinary tract

infection 28.6% and Shock 14.3%.

Table 22. PERINATAL MORBIDITY IN THE PRESENT STUDY:

Graph 7

MORBIDITY No of cases Percentage

Resuscitation 1 1.6

NICU admission 27 44.3

No 33 54.1

Recovered 24 39.34

181









Graph 7


Resuscitation 1 1.6


No 33 54.1

Recovered 24 39.34

181









Graph 7


Resuscitation 1 1.6


No 33 54.1

Recovered 24 39.34

182

In the present study, 1.6%, 44.3% of babies received resuscitation and NICU

admission. 39.34%of babies recovered.

In the study done by McShane et al (1985) 22% of babies required

resuscitation. The Mean+/-SD of Apgar at 1’ and 5’ was 5.0+/-1.3 and 6.7+/-1.0

respectively. Int.J.Med.Sci.2011

Mcshane reports a correlation between neonatal anemia and the amount of

intrapartum maternal blood loss. When the placenta is in anterior position, through

direct placenta incision, quickly causing maternal and fetal hemorrhage. Although

mothers can sometimes tolerate this hemorrhage, it might be sufficient to cause

neonatal anemia/

In conclusion, in this study anterior placental location was an independent risk

factor of neonatal anemia in placenta previa patients. Thus to manage neonatal

anemia, obstetricians should make every effort to detect anterior placental location

rather than complete previa and develop better surgical methods to avoid direct

placental incision.

Jang DG et al (2011) Int j med science anterior placental location OR 2.48,

95% CI 1.20 – 5.11 was an independent risk factor of neonatal anemia .placenta

previa with preterm birth with neonatal anemia is a major factor of 4-8% risk of

perinatal mortatility in placenta previa patient.

183

Table 23. THE PRENATAL MORTALITY RATE ACCORDING TO

VARIOUS AUTHORS

The table above shows that the PNMR in our setup is still quite high and

efforts should be made to bring down the mortality rates.

John L Kiely (1985), studied interaction between parity and age, such that

mother of 34years old having their first birth were at high risk for perinatal mortality

Clery Goldman(2005) obstetrics & gynaecology, noted PNM, adjOR 2.2 was

noted in women in 40 years and older.

Year Study PNMR

1985 John L kiely OR 2.20

1999 Crane Joan OR 2.30

2001 E.Sheiner OR 2.60

2003 Salihu 2.30%

184

Table 24. CAUSES OF PERINATAL MORTALITY IN THIS STUDY:

Graph 8

CAUSE OF DEATH NO of cases Percentage

Asphyxia 2 3.27

Prematurity 1 1.63

IVH o -

RDS 1 1.63

None 56 91.8

184


Graph 8


Asphyxia 2 3.27

Prematurity 1 1.63

IVH o -

RDS 1 1.63

None 56 91.8

184


Graph 8


Asphyxia 2 3.27

Prematurity 1 1.63

IVH o -

RDS 1 1.63

None 56 91.8

185

Out of 4 cases of perinatal deaths, asphyxia and prematurity were the major

contributors to the extent of 3.27% and 1.63% respectively. This was followed by

RDS (1.63%)

In the study by Ananth CV et al: (2003)19, Neonatal mortality was 10.7% with

previa. In the present study it is 6.5%.

Preterm delivery as result of placenta previa is major cause of perinatal death.

In 1997 linked birth and infant death data sets for united states. Salihu and associates

2003 reported the neonatal mortality rate to be three fold increased in pregnancies

complicated by placenta previa. This was finally because of increased preterm birth

rates.

Ananth and Associates (2003b)19 reported increased risk of neo natal death

even for those foetuses delivered at term. Some of this risk appears related to fetal

growth restriction and limited prenatal care and increased congenital mal formation

and previa is confirmed by Crane and co-workers (1999).

Ananth and associates (2001a)64 found most of the association between

placenta previa and low birth weight was from preterm birth and only to the lesser

extent from growth restriction.

DEATH

Chi-Square 145.230

df 3

Asymptotic

Significance.000

186

According to Zlatnik et al in (2010)31: Survival curves were constructed to

compare preterm delivery in pregnancies complicated by previa vs. no previa.

Survival curves demonstrate the risk of preterm delivery at each week and showed an

overall higher rate of preterm delivery for patients with a placenta previa.

Table 25. CORRELATION BETWEEN PERINATAL MORTALITY AND

TYPE OF PLACENTA PREVIA:

Present study:

The perinatal mortality in cases of both types of placenta previa was almost

similar, for minor it was 91.3%and major it was 92% .Thus the perinatal mortality did

not show any major difference based on the type of placenta previa.

TYPE No. of cases Perinatal deaths Percentage

Minor 23 2 91.3

Major 38 3 92

Total 61 5 91

187

Graph 9

Symmetric Measures

Value

Approximate

Significance

Nominal by Nominal Contingency


N of Valid Cases 61

187

Graph 9

Symmetric Measures

Value

Approximate

Significance



N of Valid Cases 61

187

Graph 9

Symmetric Measures

Value

Approximate

Significance



N of Valid Cases 61

188


MODE OF DELIVERY IN PLACENTA PREVIA:

Graph 10

Symmetric Measures

MODE OF DELIVERY No. of cases Perinatal death Percentage

Vaginal 2 2 100%

Abdominal 59 2 3.3%

Total 61

Value

Approximate

Significance



N of Valid Cases 61

188



Graph 10

Symmetric Measures


Vaginal 2 2 100%

Abdominal 59 2 3.3%

Total 61

Value

Approximate

Significance



N of Valid Cases 61

188



Graph 10

Symmetric Measures


Vaginal 2 2 100%

Abdominal 59 2 3.3%

Total 61

Value

Approximate

Significance



N of Valid Cases 61

189

In the present study of 61 cases, of the 2 cases which delivered vaginally, there

were 2 perinatal deaths with a perinatal mortality of 100% and of the 59 cases which

delivered by caesarean section, there were 2 perinatal deaths with a perinatal mortality

of 3.3% .This shows that the PNM varies with mode of delivery.

The liberal use of caesarean section reduces in the PNM in placenta previa.

In the study done by Khosla et al(1980)31, the perinatal mortality in those

delivered vaginally was 57.2%. and in those delivered by caesarean section was 35%.


GESTATIONAL AGE, IN PLACENTA PREVIA:

Present study:

Gestational age (Wks) No. of cases Perinatal deaths Percentage

28-33 23 5 78%

34-36 14 0 0

37+ 22 0 0

total 59 5 91.5%

190

Graph 11

In the present study perinatal deaths were higher in the gestational age group

of 28-33 weeks and the perinatal mortality was 78%. The perinatal mortality 34-

36weeks group was 100% and in term infant it was 100%. This shows that the PNM

rates are low for term fetus.

The overall perinatal mortality rate ranges between 4 – 8%. The important

causes are Aspyxia, prematurity, abdominal presentation, congenital malformation

and associated placental abruption. The onset of bleeding before 20 weeks carries a

Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 59

190

Graph 11








Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 59

190

Graph 11








Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 59

191

poor fetal prognosis. Most of the neonatal mortality ia attributed to prematurity with

its associated risk, particularly respiratory distress syndrome and intracranial

haemorrhage. Although the expectant management of placenta previa has gone a long

way towards minimizing the effects of this hazard, placenta previa still accounting for

12% of preterm deliveries.

Malpresentation, in case of premature infants, who has got high risk of

intracranial haemorrhage, especially in breech delivery. Neonatal anemia may occur

secondary to maternal blood loss. There is no significant increase in the incidence of

growth restriction with placenta previa.

In a study done by Khosla et al (1989)66, the perinatal mortality for term

infants and preterm infants was 61.5% and 75.3% respectively.

In the study done by Zlatnik MG et al: (2007)31, concluded that placenta

previa is associated with preterm delivery prior to 28 weeks 3.5%, 32 weeks 11.7%

and 34 weeks 16.1%

192


BIRTH WEIGHT OF INFANTS:

Present study:

BIRTH WT 500-999 1000-1499 1500-1999 2000- 2499 >2500

BIRTHS 0 0 18 25 18

DEATHS 1 0 4 0 0

Total 1 0 22 25 18

Percentage 1.5% 0 33.3% 37.9% 100%

Graph 12

192



Present study:

BIRTH WT 500-999 1000-1499 1500-1999 2000- 2499 >2500

BIRTHS 0 0 18 25 18

DEATHS 1 0 4 0 0

Total 1 0 22 25 18

Percentage 1.5% 0 33.3% 37.9% 100%

Graph 12

192



Present study:

BIRTH WT 500-999 1000-1499 1500-1999 2000- 2499 >2500

BIRTHS 0 0 18 25 18

DEATHS 1 0 4 0 0

Total 1 0 22 25 18

Percentage 1.5% 0 33.3% 37.9% 100%

Graph 12

193

Symmetric Measures

Value

Approximate

Significance

Nominal by

Nominal

Contingency


N of Valid Cases 66

a Assuming the alternate hypothesis

b Using the asymstd error ...

In the present study, PNM rates were higher in the 1500-1900gms groups and

lowest in>2500gms group. In the study done by McShane et al, the PNM rates were

lowest in the >2500gms group. These figures correlate with the present study.

In the study done by McShane et al the perinatal mortality by Birth weight was

as follows:

BIRTH

WT

500-999 1000-

1499

1500-

1999

2000-

2499

>2500 Percentage

BIRTHS 10 15 13 27 78 91.6%

DEATH 7(70%) 3(20%) 0(0%) 0(0%) 2(25%) 8.4%

Total 10 15 13 27 78 100%

194

Table 29. MATERNAL MORTALITY IN PLACENTA PREVIA BY

DIFFERENT AUTHOR

The table shows that maternal mortality was bought down to 1.7%(Motawari

and Sheth-Wadia Hospital, Bombay) from 9%(Chakraborthy 1937).This was achieved

by early hospitalisation without pelvic examination, prompt and adequate transfusion

of blood with caesarean section improves maternal prognosis. One has to guard

against delayed postpartum haemorrhage and coagulation failure whether the delivery

is vaginal or abdominal.

Maternal mortality rate in India because of placenta previa was 6.6-9.0 .Now it

varies between 0.9 to 3.4 as shown in the table

In the Menon (1929-61)67, the gross mortality rate in PP was 8.7%. in the last

series of study 1954-61 it reduce to 2.2%. the cause of mortality was excessive

haemorrhage.

Author No of cases Percentage

Das B 1970 1333 2.1

Motwani 1988 810 0.97

BhaskarRao 1989 462 3.44

Mahesh R 2000 107 0.93

Oyelese & Smulian 2006 1000 3.00

Present study 61 3.27

195

Gun 1954 showed 1 (0.46%) maternal death in PP. Purandare 1962 showed 1.7%(7

death in 400 cases). Leela et al 1969 showed 1.7% (6 death in 340 cases). K bhaskar

Rao 1984 showed 3.44% (16 deaths in 462 cases)

A marked reduction in maternal mortality rates from placenta previa was

achieved during the last half of the 20th century but still placenta previa is an

important cause of morbidity and mortality. In the recent review Oyelese and

Smulian(2006) cite an approximately 3 fold increase in the maternal mortality ratio of

30 per 100,000.

Macafee(1962), gets the credit for demonstrating the benefit of expectant

management by which achieved a maternal mortality of 0.57% in contrast to the

earlier figure of 6.7% mortality for placenta previa. With improving obstetric service,

the mortality rate in recent studies as expected is much lower, the centre for Disease

Control and Prevention (USA) reporting a mortality rate of 0.03%. The major cause

of mortality and morbidity are haemorrhage (both antepartum & peripartum), Anemia,

Sepsis and Placenta accrete. Pregnancies with low lying placenta are associated with

high incidence of postpartum haemorrhage. A history of previous caesarean section

and complete previa increase maternal morbidity due to increased risk of massive

haemorrhage, placenta accrete and chances for hysterectomy.

The reduced maternal mortality in recent years is mainly attributable to the

increased use of blood transfusion, effective antibiotic therapy and better

understanding of the management of shock and renal failure. The increased use of

caesarean section, preceded by expectant treatment has been universally adopted in

cases of placenta previa. which has reduced the maternal mortality to nil and the fetal

mortality to less than 10%.

196

In present study two maternal deaths case no.50 G2P1L1 with 34 weeks with

transverse lie with previous LSCS with central placenta previa. At the time of her

admission she was in shock, pulse 120 BP-90/60 Hb%- 6.8 immediately resuscitative

measures taken ,she was shifted to OT. Emergency LSCS under GA and extracted

alive female 2kg at 4.44pm at 28/06/12.

As there was placental bed oozing with atonic PPH, uterine artery ligation and

utero ovarian anastomosis ligation done , bleeding not stopped subtotal hysterectomy

done with intra cervical foleys bulb inflated with 40cc.

Patient was shifted to ICU, inotropoic started with o2+N20+IPPV. Transfused

with 1 PRBC, 6FFP, 4 cryoprecipitate but patient could not be revived with all the

resuscitation hence declared dead. Patient died because of hypo volemic shock

because of PPH.

Case no: 55, G2P0L0 gravida 2, abortion 1 at term gestation with marginal

placenta previa with sever PE. In third trimester She was admitted in CHE with scan

report showing single live intra uterine gestation of 32 weeks with marginal placenta

previa done 25/08/2012, Hb was 9gm and transfused 1 point of PRBC and 400gm of

Iron sucrose discharged after correcting anemia discharged after 3 days to review as

soon as possible in any bleeding PV and for regular A&C chck up weekly. But patient

had come only after two months with history of bleeding PV, head ache and pedal

edema. At time of admission BP was 160/110, urine albumin 4+, with history of

bleeding PV, inj Labetolol 20mg IV bolus, inj MgSo4, Pritchards regime started and

taken for emergency LSCS. And extracted alive female baby of 2.1kg at 6 am on

11/10/2012, Intra OP was low lying placenta anteriorly there was intra OP PPH which

was managed conservatively with uterotonics and patient received 2 point of PRBC,

197

the uterus contracted and retracted well, during the closure of rectus sheath patient

developed sudden hypo tension was started inotropics , shifted to ICU after half an

hour the patient had sudden cardiac arrest. CPR was started the patient revived and

put on ventilator. Later patient developed pulmonary edema again she had cardiac

arrest inspite of all resuscitation patient was declared dead. The patient died because

of sudden amniotic fluid embolism. Those patient attenders were not giving consent

for post mortem.

198

SUMMARY

Placenta previa accounts for approximately 0.5% of all deliveries but still

remains major cause of perinatal mortality and morbidity. It is clearly evident from

our study that the majority of our patients were from rural areas with poor educational

standard, from low socioeconomic status and they were unaware of the importance of

antenatal visits.

It is observed that the patient who had no antenatal check ups and admitted to

hospital as an emergency admission had maximum incidence of maternal morbidity

and perinatal mortality.

A good antenatal care, early detection of placenta previa by ultrasound and the

conservative management including the aggressive use of antepartum blood

transfusion in cases of moderate to severe bleeding and early elective termination of

pregnancy by judging the fetal maturity along with the development of neonatal

intensive care unit appears to have great contribution to the dramatic reduction in the

perinatal mortality in placenta previa.

Improved transport communication and proper health education by

paramedical staff, regarding the MCH services, family planning – to the patient

individually, to the public in general is necessary in the rural and semiurban areas for

the better management and prognosis of patients with placenta previa. Women with

placenta previa stayed for longer in hospital and had a higher rate of caesarean

section, but perinatal mortality remains high and the principal cause was prematurity.

The increasing use of caesarean section will result in increase in the incidence

of placenta previa and placenta accreta. The linear rise in the incidence of both these

199

conditions with repeated abdominal delivery is an argument for a trial of scar

whenever possible after one abdominal delivery. Expectant antenatal management

will reduce but not totally avoid perinatal mortality. Anticipation of the complications

at caesarean section is an important factor in reducing maternal morbidity.

In the present study, the incidence of placenta previa contributed to 0.40%

cases. The general perinatal mortality was 18 per 1000 live births and that due to

placent previa was 84 per 1000 live births. The maternal mortality rate due to

placenta previa in the study was 3.27%.

As the maternal and perinatal morbidity and mortality due to placenta previa is

preventable, efforts should be made to bring down these rates. This can be achieved

by spacing pregnancies, limitation of family size, antenatal registration of all pregnant

women, routine use of USG in pregnancy and early referral of high risk pregnant

women to tertiary care centres. Awareness should be brought about in the rural public

to avail the facilities provided by the Government.

These measures will definitely help in a better outcome for both mother and fetus in

all high risk pregnancies.

200

CONCLUSION

1. In present study, 61 cases of placenta previa were studied regarding the type of

clinical presentation, the clinical course, the perinatal and material outcome. The

information obtained was arranged statistically.

2. In the present study the cases of placenta previa were highest in the maternal

age group 20-29 years i.e. 72.9%, it was in the age group 30-35 years, 20.3% in

the age group <=19 years and 1.7% in the >35 age group. The mean age +- SD in the

present study was 25.8+- 4.9 years.

3. In the present study incidence of placenta previa was highest in 63.9% the

multiparous group. It was 34.4% in the primi group and 1.6% in grand multi group.

4. In the present study, the risk factors studied were previous caesarean section,

abortion and twin gestation. The incidence of prior caesarean section was6.6% , prior

abortion was 9.8% and no twin gestation in present and Rh isoimmunisation in 9.8%

and myomectomy in 1 case.

5. Of the complications studied, in the present study severe anaemia contribution

to 16% , malpresentations contributed to 20%(breech 8.3%, transverse lie 4.1%) ,I

trimester bleeding complicated 3.3% of cases, II trimester bleeding contributed to

17% of complications PIH was found in only 4.4% of cases.

6. In the present study 61.1% of cases required blood transfusion and

shock/hypotension was noticed in 3.7% of cases, PPH was noticed in 27.8% of cases,

adherent placenta noticed in 1.9% cases, 4 cases of placenta previa required

caesarean hysterectomy to control the bleeding in the immediate post-operative period

201

.Post-operative febrile morbidity was not seen in any of cases and no sepsis

complications.

7. In the present study, perinatal morbidity was studied as the percentage of

babies requiring resuscitation and NICU admission. It was 44.3% of the cases.

8. In the present study, the percentage of perinatal deaths was 8.3% Asphyxia

was the major contributor to perinatal deaths i.e. 2 cases followed by prematurity 1

cases, and respiratory distress syndrome contributed 1 case.

9. The perinatal mortality was the same in both the clinical types of placenta

previa i.e. chi square value was 1.28 which is not significant.

10. The perinatal deaths were more in the cases delivered vaginally than those

delivered abdominally i.e. 100%then those delivered abdominally 1.7%.

11. The perinatal mortality was more in the 28-33 weeks gestation group i.e.

78%, whereas in the 34-36 weeks and 37+ weeks gestation, group it was nil.

12. New born with birth weights above 2500gms had a good survival rate with

PNM being 5.5% and infants with weights <1000 gms had a very poor survival rate.

202

BIBLIOGRAPHY

1. Harvey A, Gabert. Corrilation between placeta previa and fetal growth. Amj

Obstet& gyncol. 1971:38: 403-406.

2. McShane P M, Heyl P S, Epstein M F. Maternal perinatal morbidity Resulting

from placent previa. Jbostet & Gynecology 1985; 65: 176-182.

3. Tariq Khasbhoggi, Arab board. Correlation of placenta previa with maternal

& neonatal out come. Ann Saudi Med. 1995; 15(4)

4. Taylor Y M, Peacock S , Kramer T L, Vaughan. Placenta previa in asian

origin women: incidence and out come. J obstet and gynecol 1995; 86: 805 -

808

5. Hemmadi. etal., 1989. : "Recent trends in the management of placenta

previa". Ind. J of Obstet Gynaecol; 39(71) : 365-368

6. Edward T Way, Angie, Mallozzi, Toan F, Rodis, James F X, Egan Antohny

M, Vintzilos, Winster A C. Association of baby weight with gestationa age in

placenta previa. Intl J obstet & gynecol.1996; 90: 120-128.

7. Catanzaria VA, Lorrain MS, Schimmer Dr et al. Managing placenta previa

accrete contemp Obstet Gynecol1996; 41: 66-95.

8. Miller DA, Choller JA, Goodwin. TM. Clinical risk factors for placenta previa

accrete. AJOG 1997, 177: 210-4

9. Ananth CV, Savitz DA, Bowes WA Je, Luther ER. Influence of hypertrnsive

disorders and cigarette smoking on placental abruption and uterine bleeding

during pregnancy. BJOG 1997;104:572-8.

10. Reddi P. Rani, et al., 1999. : "Placenta previa - An analysis of 4 year

experience". Indian J of Obstet Gynaecol; 19 (3): 53-55.

11. Bhide A, Thilaganathan B.Recent advance in the management of placenta

previa.Curr opin Obstet Gynecol 2004 Dec:16(6):447-51.

12. Schutte JM, Schuitemaker NW, van Roosmalen J, Steegers EA. Substandard

care in maternal mortality due to hypertensive disease in pregnancy in the

Netherlands. BJOG 2008; 115:732-6.

13. Saftlas.A, Olson D, trash H, et al. national trends in the incidence of abruption

placenta. Obstet Gynecol.2001; 78:1081-1086.

203

14. Buttler, Erim, Dashe, Ramus, Ronald. Association between maternalserum

alfa-feto protein and adverse outcome in pregnancy withplacenta previa. Intl J

Obstet & Gynecol. 2001; 97(1): 35-38.

15. Sheiner E, Shoham-Vardi I, Hallak M, et al. Placenta previa Obstetric risk

factors and pregnancy outcome. J Matern Fetal Med. 2001 Dec; 10(6):414-9

16. Gillian M, Rosenberg D, Davis F. The likelihood of Placenta previa with

greater number of cesarean deliveries and higher parity. Obstet Gynecol

2002; 99;976-80

17. Konje JC, Taylor DJ.Bleeding in late pregnancy, in: James JD, Steer PJ,

Weiner CP, Gonik B, 3rd edition. High risk pregnancy management options.

Philadepia : Saunders.2006.p:1259-1274:

18. A.S. faaiz and C.V. Ananth. Etiology and risk factors for placenta previa: an

overview and meta – analysis of observational studies. 2003, Vol. 13, No. 3,

Pages 175-190.

19. Ananth CV, Smulian JC, Vintzileos AM. The effect of Placenta previa on

neonatal mortality: A population – based study in the United States, 1989

though 1997. AMJ Obstet Gynecol. May 2003; 188(5): 1299-304

20. Tuzovic L, Djelmis J, Illijic M. Obstetric risk factors inplacentaprevia.Croat

Med J. 2003; 44: 727-733.

21. Razia Mehboob, Nazir Ahmed. Maternal and fetal outcome in placenta previa.

Pakistan J Med. Res. 2003; 42(1).

22. Sharma A, Suri V, Gupta I. 2004. Tocolytic therapy in conservative

management of symptomatic placenta praevia. International Journal of

Gynaecology and Obstetrics 84:109-113.

23. Jackson RA, Gibson KA, Wu YW, Croughan MS. Perinatal outcomes in

singletons following in vitro fertilization: A meta-analysis. Intl J Obstet &

Gynecol. 2004 Mar; 103 (31): 551-63.

24. Emily C Olive, Christine L, Roberts Charles S, Algert & Jonatha MM.

Placenta previa: Maternal morbidity and place of birth. Aus & NZ J Obstet &

Gynecol. 2005; 45(6): 499-504.

25. Richard LN. Abruptio & placenta previa frequency, perinatal outcome and

cigarette smoking. Intl J Obstet & Gynecol. 2005; 106(5): 986-991.

26. Oyelue, Yinka, Smiltian J. Placenta previa, placenta accrta, vasa previa. Intl J

Obstet Gynecol. 2006; 107(9): 927-941.

204

27. Ananth CV, WiloxAJ, Cavitz DA, Bowes WA Jr, Luther ER. Effect of

maternal age and parity on risk of uteroplacental bleeding in pregnancy. Intl J

Obstet & Gynecol. 2006; 2: 511-6.

28. Allen VM, Wilson RP, Cheung A. Pregnancy outcome after

assistedreproductive technology. Reproductive EndocrinologyInfertility

Committee (SOGC). Intl J Obstet & Gynecol.Canada. 2006; 28(3): 220-250.

29. Jaswal A, Manaktala U, Sharma JB. Cervical encirclage in expectant

management of placenta previa. Intl J Obstet & Gynecol. 2006; 93(1): 51-2.

30. Oppenheimer I. Guidelines: diagnosis and management of Placenta previa. J.

Mar 2007; 29(3): 261-73.

31. Zlantnik MG, Cheng YW, Norton ME. et al. Placenta previa and the risk of

preterm delivery. J Matern Fetal eonatalMed.2007 Oct;20(10):719-23

32. Gobman, William, Gorshovez, Landon, Mark, Sporg et al. Correlation of

number of previous LSCS and placenta previa. Intl J Obstet & Gynecol.

2007; 110(6): 1249-1255.

33. Qiuying Yang, Shi Wu, Yen, Sharon Caugh EY, Daniel, Krewski,

Lumingsum, Mark C Walker. Placenta previa: Its relationship with race and

the country of origin among Asian Women. Acta Obstetrica & Gynecologica

Scandinavica. 2008; 87(6): 612-616.

34. Savita Rni, Singhal, Nymphaea, Smitinanda. Maternal and perinatal outcome

in APH. Intl J Obstet & Gynecol. 2008; 9(2).

35. Suk-Joo Choi, Seung Eun Song, Kyung-Lan Jung, et al. Antepartum risk

factors associated with peripartum cesarean hysterectomy in women with

placenta previa. American journal of Perinatology (2008) volume: 25, Issue:

1 Pages: 37-41

36. El Sherbiny M. placenta previa after previous CS: the new nightmare. The 9th

annual conference of the department of obstetrics & gynecology – Cairo

University, Cairo Marriott Hotel- Zamelek. April 3-4, 2008.

37. Victoria Taylor, et al., 1994. : "Placenta previa and prior caesarean delivery

Flow strong is the association". Obstet Gynaecol; 84:55-7.

38. Vergani P, Ornaghi S, Pozzi I Bertta P et al. Placenta previa: Distance to

internal OS and mode of delivery. AM J obstet Gynecol. Jul 2009;23.

205

39. Milosevic J, Lilac V tasic m Rodovic- Janosevic D, Stefanovic M, et al.

Placental complication after a previous cesarean section. Med pregl. May –

Jun 2009; 62(5-6):212-6

40. RCOG. Guideline: Placenta previa, placenta previa accreta and Vasa previa:

Diagnosis and Management. Jan 2011. (www.rcog.org)

41. Gorodeski IG, Bahar CM. the effect of placenta previa localization upon

maternal and fetal- neonatal outcome. Dept of Obstetricsand gynecology “B”,

Meir hospital, Kfar Saba, Israel. J Perinat Med. 1987; 15(2): 169-77.

42. Sheiner E, Shoham-Vardi I, Hallak M, et al. Placenta previa Obstetric risk

factors and pregnancy outcome. J Matern Fetal Med. 2001 Dec; 10(6):414-9.

43. Richard E. Besinger, Charles W. Moniak, Lind S. Paskiewicz et al. the effect

of tocolytic use in the management of symptomatic placenta previa.

American Journal of Obstetrics & Gynecology. Volume 172, Issue 6, Pages

1770-1778, June 1995.

44. Das.B. Antepartum haemorrhage in three decades.Obs Gyn india 1975; 25:

636-41.

45. Ratnam SS et al. Obstetrics & Gynecology for Postgraduates. 2nd edition

India. Orient Longman. 2007; 78-88.

46. Bhide A, Thilaganathan B.Recent advance in the management of placenta

previa.Curr opin Obstet Gynecol 2004 Dec. 14, 12

47. Bhaskar Rao K, Manorama S, Maternal prognosis in placenta previa . Obsgyn

india 1975; 25:642 – 46.

48. Pankaj D, Narendra M, Duru S.Antepartum haemorrhage. Sukanta In

Principles and practice of Obsterics and Gynecology for post graduates.3rd

edition45:403-417.

49. Gargano JW, Holzman CB, Senagore PK, Reuss ML, pathak DR, Friderici

KH, et al. polymorphisms in thrombophilia and rennin-angiotensin system

pathways, preterm delivery, and evidence of placental hemorrhage. AM J

Obstet Gynecol 2009;201:317el-9.

50. Ananth CV, Demissie K, Smulian JC, Vintzileos AM. Placenta previa in

singleton and twin births in the United States, 1989 through 1998: a comparison

of risk factor profiles and associated conditions. Am J Obstet Gynecol

2003;188:275-81.

206

51. Bhide A, Prefumo F, Moore J, Holhs B, Thilaganathan B. 2004. Placental

edge to internal os distance in the late third trimester and mode of delivery in

placenta previa. British Journal of Obstetrics and Gynaecology 110:860-864.

52. Patricia M. McShane. et al., 1985. : "Maternal and perinatal morbidity

resulting from placenta previa" Obstetrics Gynaecology: 65 (2): 176-182.

53. Williams M. 1991. : "Cigarette smoking in pregnancy in relation to placenta

previa". Am J Obstet & Gynaecol; 165:28-32.

54. Steven Clark, et al., 1985. : "Placenta previa / Accreta and prior caesaren

section". Obstet Gynaecol; 66: 89.

55. Michelle A Williams, et al., 1993. : "Increasing maternal age as a determinant

of placenta previa". J of Rep Med; 38(6) : 425-428.

56. Ananth CV, Smulian JC, Vintzileos AM. The effect of placenta previa on

neonatal mortality: a population-based study in the United States, 1989 through

1997. Am J Obstet Gynecol 2003;188:1299-304.

57. Addis A, Moretti ME, Ahmed Syed F, Einarson TR, Koren GFetal effects of

cocaine: an updated meta – analysis. Reprod Tosicol 2001;15:314-69

58. Cesarean rates for low-risk women: United States, 1990-2003. Natl Vital Stat

Rep 2005;54:1-8.

59. Paterson-Brown S, Fisk NM. Caesarean section: every woman's right to

choose? Curr Opin Obstet Gynecol 1997;9:351-5.

60. Lydon-Rochelle M, Holt VL, Easterling TR, Martin DP. First-birth cesarean

and placental abruption or previa at second birth(l). Obstet Gynecol 2001

;97:765-9.

61. Getahun D, Oyelese Y, Salihu HM, Ananth CV. Previous cesarean delivery

and risks of placenta previa and placental abruption. Obstet Gynecol 2006 ;

107 : 771-8.

62. Prochazka M, Happach C, Marsal K, Dahlback B, Lindqvist PG. Factor V

Leiden in pregnancies complicated by placental abruption. BJOG

2003;110:462-6.

63. Saftlas.A, Olson D, trash H, et al. national trends in the incidence of abruption

placenta. Obstet Gynecol.2001; 78:1081-1086.gestational duration, and small-

forgestational –age births. Epidemiology1995;6:391-5-21

64. Ananth CV, Peedicayil A, Savitz DA. Effect of hypertensive diseases in

pregnancy on birthweight,

207

65. Thorn EA, et al. Maternal morbidity associated with multiple repeat cesarean

deliveries. Obstet Gynecol 2006;107:1226-32.

66. Romundstad LB, Romundstad PR, Sunde A, von Du" ring V,Skjaerven R,

Vatten LJ. 2006. Increased risk of placenta previa in pregnancies following

IVF/ICSI; a comparison of ART and non-ART pregnancies in the same mother.

Human Reproduction 21:2353—2358

67. Catanzarite V, Maida C, Thomas W, Mendoza A, Stanco L, Piacquadio KM.

2001. Prenatal sonographic diagnosis of vasa praevia: ultrasound findings and

obstetric outcome in ten cases. Ultrasound in and Gynecology 18:109-115.

68. Chou MM, Ho ES, Lee YH. 2000. Prenatal diagnosis of placenta praevia

accreta by transabdominal color Doppler ultrasound.Ultrasound in Obstetrics

and Gynecology 15:28-35.

69. Dumont A, Tourigny C, Fournier P. improving Obstetric care in low resource

settings: implementation of facility –based maternal death review in five pilot

hospitals in Senegal. Hum Resour Health 2009;7:61.

70. Ononeze BO, Ononeze VN, Holohan M. 2006. Management of women with

major placenta praevia without haemorrhage: A questionnaire-based survey of

Irish obstetricians. Journal of Obstetrics and Gynaecology 26:620-623.

71. Besinger RE, Moniak CW, Paskiewicz LS, Fisher SG, Tomich PG. 1995. The

effect of tocolytic use in the management of symptomatic placenta praevia.

American Journal of Obstetrics and Gynecology 172:1770-1778.

72. Bhide A, Prefumo F, Moore J, Holhs B, Thilaganathan B. 2004. Placental

edge to internal os distance in the late third trimester and mode of delivery in

placenta previa. British Journal of Obstetrics and Gynaecology 110:860-864.

73. Breathnach F, Tutie DJ, McEniff, Byrne P, Geary MP. 2007. Uterine artery

embolisation as an interval adjunct to conservative management of placenta

praevia increta. Journal of Obstetrics and Gynaecology 27:195.

74. Merkus JM. Perinatal mortality in The Netherlands: an audit is now more

necessary than ever. Ned Tijdschr Geneeskd 2008;152:603-5. Confidential

enquiries into maternal mortalitya 2010.

75. Previa: an overview and meta-analysis of observational studies. J Matern Fetal

Neonatal Med 2003;13:175-90.

76. Benirschke K, Kaufmann P. 2000. Pathology of the human placenta. 4th ed.

New York: Springer

208

77. Chou MM, Ho ES, Lee YH. 2000. Prenatal diagnosis of placenta praevia

accreta by transabdominal color Doppler ultrasound.Ultrasound in Obstetrics

and Gynecology 15:28-35.

78. Akthar Ali, Sultan Zaffar et al.Obstetrical renal failure from frontier province.J

Pondicherry medical science: 18:109-116.

79. Love CD, Fernando KJ, Sargent L, Hughes RG. 2004. Major placenta praevia

should not preclude outpatient management. European Journal of Obstetrics,

Gynaecology and Reproductive Biology 117:24-29.

80. Practical guide to high risk pregnancy and delivery 3rdedition pp 342.

Fernando Arias

81. Iandonalds practical obstetric problems 6thedition pp-312-313

82. SOGC clinical practice guidelines no 189 march 2007.

83. Machado LSM, emergency peripartomy hysterectomy incidence, indications,

risk factor and outcome.North Am J Med Sci 2011;3:358-361.

84. Dong gyu Jang International journel of medical science pp-554-557 2011.

85. Fishman,Shire et al JPM.2011.125,Novenber 2011.

86. Gofferfeld K. et al., 1966. : Ultrasonic placentography : a new method for

placental localisation. Am J Obstr Gynaecol: 96: 538-547.

87. Ian Donald : Text book of practical Obstetric problems - Fifth Edition pp 423-

454.

88. Iyasu. et al., 1993. : "Epidemiology of placenta previa in the United States".

Am J Obstet Gynaecol; 168 : 1424-9.

89. Rigby E(1775) An essay on the uterne haemorrhage,which precedes the delivery

of the full grown fetus.(JJohnso, London) 6th ed,(1822)

90. Singhal, Nanda:Maternal and perinatal outcome in antepartum haemorrhage: A

Study at a tertiary hospital.The internet journal of Gynecology and

obstetrics.2008.Vol.9.Number 2.

91. Arora R, Devi U ,MajumdarR. Perinatal morbidity and mortality in antepartum

haemorrhage.J Obstet Gynaec India 2001:51(3): 102-4

92. Barret J. et al, 1981. : "Induced abortion - A risk factor for placenta previa".

AMJ Obstet Gvnaec: 141: 769-772.

93. Brenner W. et al., 1978. : "Characteristics of patients with placenta previa

and results of expectant management. Am J Obstr Gynaecol; 132: 180-189.

94. Campbell S : Ultrasound in obstetrics and Gynaecology 1992.

209

95. Chervanak F. et al., 1984. : Role of attempted vaginal delivery in the

management of placenta previa. Obstet & Gynaecol: 64: 798-801.

96. Cotton D. et al., 1980. : The conservative aggressive management of

placenta previa. Am J Obstr Gynaecol; 137: 687-695.

97. D'Angelo. etal., 1983. : Conservative management of placenta previa-A cost

benefit analysis. Am J Obstr Gynaecol: 149: 320-326.

98. Farine D. et al., 1988. : Vaginal USG for diagnosis of placenta previa. Am J

Obstr Gynaecol: 159: 566-569.

99. George Macones. etal., 1997 : "Association between maternal cocaine use

and placenta previa". Am J Obstet Gynaecol: 177: 1097-1100.

100.Leerenvelt. et al. 1990. : Accuracy and safety of TVS localisation of placenta.

Obstet Gynaecol; 76: 759-762.

101.Mabie WC. 1992. : Placenta previa clinical perinatology. 19,425-435.

102.McClure. et al., 1988. : Early identification of placenta previa. Br J Obstet

Gynaecol; 159: 566-569

103.Newton E. et al., 1984. : "The epidemiology and clinical history of

asymptomatic midtrimester placenta previa". Am J Obstet Gynaecol; 149 :

743-746.

104.Richard Naeye. 1980. : "Abruptio placentae and placenta previa frequency,

perinatal mortality and cigarette smoking". Obstet Gynaecol; 55 (6): 701-704.

105.Sand H. 1997. : Ultrasonic diagnosis of placenta previa. Acta Obstet

Gynaecol Suppl; 56: 105-108.

106.Silver, etal., 1984. : Placenta previa aggresive expectant management. Am J

Obstet Gynaecol; 156: 15-21.

107.Singh P. et al., 1981. : "Placenta previa and prior caesarean section". Acta

Obstet Scand ; 60: 367-368.

108.Steven Clark, et al., 1985. : "Placenta previa / Accreta and prior caesaren

section". Obstet Gynaecol; 66: 89.

109.Strong T. et al., 1989. : "Placenta previa in twin gestation". J of Rep Med; 34:

415-416.

110.Studd : "Progress in obstetrics and Gynaecology" Vol.11, pp 161-178.

111.Timor Trisch. et al., 1986. : Confirming the safety of TVS in patients

suspected of placenta previa. Am J Obstr Gynaecol; 154: 565-569.

210

112.Placental haemorrhage and PTD” 2010 The Authors Journal compilation”

RCOG 2010 GJOG An international Journal of Obstetrics and Gynaecology

455.

113.Lewis G. Confidential Enquiry into Maternal and Child Health (CEMACH).

Saving Mother’s Lives: Reviewing Maternal Deaths to Make Motherhood

Safer – 2003-2005. The Seventh Repot on Confidential Enquiries into

Maternal Deaths in the United Kingdom.London: CEMACH 2007.

114.Tuffnell DJ, Shennan AH, Waugh JJS, Walker JJ.Gren Top Guideline. The

Management of Severe Preeclampsia/Eclampsia. London : Royal College of

Obstetricians and Gynaecologists, 2006

115.Tuffnell DJ, Jankowica D, Lindow SW, Lyons G, Mason GC, Russell IF,

Walker JJ. Outcomes of severe pre-eclampsia/eclampsia in Yorkshire

1999/2003. BJOG 2005;112:875-80.

116.Drife J, Maternal Mortality in well-resourced countries:is there still a need for

confidential enquiries ? Best Pract Res Clin Obstet Gynaecol 2008:22:501-15.

117.Yang J, Hartmann KE, Savitz DA, Herring AH, Dole N, Olshan AF,et

al.Vaginal bleeding during pregnancy and preterm birth. AM JEpidemiol

2004;160:118-25.

118.Green NS, Damus K, Simpson JL, Iams J, Reece EA, Hobel CJ, et al.Researeh

agenda for preterm birth: recommendations from the March of Dimes. Am J

Obstet Gynecol 200;193:626-35

119.HHossain R, Harris T, Lohsoonthor V, Williams MA.Risk of preterm delivery

in relation to vaginal bleeding in early pregnancy, Eur J Obstet Gynecol

Reprod Biol 2007;135:158-63

120.Weis JL, Malone FD, Vidaver J, Ball RH, Nyberg DA, Comstock CH, et al.

threatened abortion: a risk factor for poor pregnancy outcome, a population

based screening study, Am J Obstet Gynecol2004; 190:745-50

121.Fox H.Macroscopic abnormalities of the placenta. In: Livolsi VA,editor.

Pathology of the placenta, 2nd edn. London: W.B.Saunders Company Ltd.,

1997.pp.102-50

122.Kelly R, Holzman C, Senagore P, Wang J, Tian Y, Rahbar MH, et al.

Placental vascular pathology findings and pathways to preterm delivery. Am J

Epidemiol 2009;170:148-58.

211

123.Benirschke K, Kaufmann P, Baregen R, Materanl diseases complicating

pregnancy: diabetes, tumors, preectampsia, lupus anticoagulant. In:

Benirschke K, Kaufmann P, Baergen RN., Pathology of the Human Placenta.

New york: Springer:2006,pp,596-656.

124.Operative Obstetrics. Saunders Elsevier.Munrokerr’s 11th Edition;

page.no.210-220.

125.Hiralal Konar. Dutta DC textbook of Obstetrics. 7th ed;241-252.

212

PROFORMA

Maternal & Fetal Outcome In Placenta Previa

Name: Hospital:

Age: I.P.No:

Occupation: D.O.A:

Address: D.O.D:

Distance Traveled: Booked / Referred from:

Socio Economic Status:

Informant: Total Hospital Stay

Presenting Complaints:

Amenorrhea : ………… Months

Bleeding P/V : Yes/ No

No of Episodes :

Duration :

Pain Abdomen : Yes / No

Fetal movement: Yes / No

213

Threatened Abortion:

Congenital Anomaly :

Twins :

Obstetric History:

Obstetric score :

Married Life : Year / Consanguineous / Non consanguineous

Detailed History of Previous Pregnancy:

Abortions :

MTP / D&C : Yes/No

Blood Transfusion :

Deliveries : Vaginal / Cesarean Section

Menstrual History:

Age of Menarche :

Menstrual cycles : Regular/ irregular LMP:

EDD:

Corrected EDD/GA :

214

Past History:

Past Medical disorders & Its Details :

Past Surgical procedures & Its Details :

Family History

Family history of multiple pregnancies:

Personal History:

Diet : Sleep :

Appetite : Smoking :

Bladder functions : Bowel function :

General Physical Examination:

Level of Consciousness :

Hemodynamic stability : Yes / No

Pallor : Mild / Moderate / Severe:

Pulse : BP :

CVS : RS :

Per Abdominal Examination:

Uterus : ……… Weeks

215

Relaxed or Acting :

Symphsio Feudal Height : In Cm & Weeks:

Abdominal Girth in Cms :

Lie :

Presentation :

FHS :

Genital Examination:

External Genitalia :

Vulva :

Per-Speculum Examination:

Vagina : Any Lesion

Cervix : Any Lesion

: Presence of Placenta over laying it:

: Effacement:

: Dilatation:

216

: Status of Membrane:

: Presenting Part:

: Amount of Bleeding:

Clinical Diagnosis:

Investigations :

1. HB% :

2. Urine : Albumin

: Sugar:

: Micro:

3. Bl. Grouping& Rh Type:

4. Bleeding time :

5. Clotting time :

6. VDRL :

7. HBSAG :

8. HIV :

217

9. Blood Sugar :

10. Trans Abdominal Ultra sound:

Ante partum Management:

Conservative :

Duration :

Mode of delivery

Vagainal/Cesarean Section :

Duration of Labor :

1st stage :

2nd Stage :

3rd Stage :

Active Management 3rd Stage : Yes/No

Caesarean : Emergency

Date GestationalAge

PlaecntalLocation

Presentation EFW Anomalies Others

218

Elective

Indication

Anaesthesia

Placental Implantation site : Low Lying

PP - Anterior

Posterior

Intra operative blood loss :

Mode of Baby delivery :

PPH :

Drugs Dosage Frequency

Date & Time of Delivery:

3rd stage complication: Management: Medical

PPH : Atonic Surgical

: Traumatic Both

: Mixed

Examination of Placenta:

Weight :

Adherent Clots :

Final Diagnosis:

Neonatal Outcome: Live / Fresh still Born / Macerated

Term / Preterm

Sex: Weight:

219

Apgar: At 1 minute

: At 5 minute

NICU Admission: Yes/No

Maternal Outcome: Morbidity: 1. Anaesthesia

2. Major-Haemorrhage

3. Anemia

4. Peri Partum hysterectomy

Minor : Febrile Morbidity

Blood Transfusions Date NO:

Whole blood/ Packed RBC

Component Transfusions

FF

Platelet

Cryoprecipitate

220

Maternal Outcome

Fetal Outcome

Follow up:

Lactation& brest feeding:

Contraceptive Advice:

Risk Factors

Age

Parity

Multiple Pregnancy

Poly hydraminios

Mal presentation

Previous MTP

Previous CD

No of Previous CD

Previous History ofPlacenta Previa

Preterm

Term

LBW

Fresh still born

IUGR

Sepsis

NICU

221

SL-

Nam

e

Age

IP book

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ked

Am

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(in m

onth

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Feta

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Prio

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PV

PAR

ITY

AB

OR

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(end

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MG

)

Priv

ious

H/o

LSC

S

Gen

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con

ditio

ns

Pulse

(bea

ts/m

in)

BP(

mm

IIg)

Abd

omen

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ense

,tend

er

Ges

tatio

nal

Age

(wks

)

Pres

enta

tion

FHS

Loc

al e

xam

inat

ion

P/S

exam

inat

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PVex

amin

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Hb

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M%

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Blo

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usio

n

Mod

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Bab

y-al

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d

WT

of th

e ba

by

Sex

of th

e ba

by

NIC

Uad

miss

ion

APG

AR

C.O

.D

Feta

lA-M

AL

Y

Plac

enta

l/cor

dA

-m

alie

s

Typ

e of

pla

cent

apr

evia

COMPLICATIONS

HO

SPIT

AL

ST

AY

RE

MA

RK

S

AP IP PP Operative

G P L

INTR

A

POST

1 Bindumathi25

947 U 8 1 A P A 2 1 1 - G 104130/86 A 32 B P N N ND 9.2 Y 1

EMCS L 1.75 F Y G - - IV - - - - - 6

2 Pavithra 20 1622 U 8 1 A P A 1 - G 86120/80 A 32 VX P N N ND 10.8 Y 2

EMCS D 1.5 M

ASP - - IV - - -

BICUTR - 5

3 Nagamma 30 3978 U 8 8 A P A 2 1 1 - G 106160/100 A 30 VX P N N ND 7.3 Y 2

ELCS L 1.75 F G - - IIP - - - - 6

4 Sudha 22 5686 U 9 6 A P A 21SA - G 88

110/70 A 38 VX P N N ND 8.6 Y

EMCS L 3 M G - - IIP - - - - 6

5 Seema 30 6816 U 8 3 A P A 2 1 1 - G 88120/80 A 32 VX P N N ND 9.3 Y

ELCS L 1.3 F G - - IIA

ITRI

BL - - - 5

6 Mubintaj 32 6711 U 8 6 A P A 4 2 21SA - G 88

130/80 A 32 B P N N ND 8 Y 1

EMCS L 1.2 M G - - IIA - - - PPH - 6

7 Pavithra 24 12604 U

7.5 6 A P A 1 - G 86

110/70 A 32 B P N N ND 8

P IN T OS

1ELCS L 1 F Y G - - IIIA - - -

PPH 3

8 Bhagya 32 U 810 A P A 3 2 2 - G 88

110/70 A 32 VX P N N ND 9.7

M A P P E

1EMCS L 1.5 F Y G - - IIA - - - PPH - 8

9 Savitha 25 10340 U 8 7 A P A 2 1 1 - G 80110/70 A 32 VX P N N ND 9.8 Y 2

EMCS L 2.25 F Y G - - IV - - - HYPO - 8

R H D

10 Thara 21 10044 U 9 4 A P A 1 1 - G 88110/80 A 36 VX P N N ND 10 Y 1

EMCS L 2.5 M G - - IIIA - - - PPH - 5

R H - V E

11 Savitha 20 12984 U 8 2 A P A 2 1 0 - G 98140/100 A 34 VX P N N ND 8.3 Y 2

EMCS L 2.4 M G - - IIA

IITRIBL

PIH - - 6

12 Mahadevi 26 12207 U 9 1 A P A 1 - G 80110/70 A 32 VX P N N ND 8.8 Y 1

EMCS L 1.8 M G - - IIA - - - PPH - 8

13 Chandramani 19 14133 U 9 2 A P A 1 - G 80110/70 A 40 VX P N N ND 10.8 Y 1

EMCS L 3 M G - - IV - - -

PPHUAL - 7

14 Shakunthala 22 13950 U

7.5 5 A P A 2 1 0 - G 120

110/70 A 28 VX P N N ND 4.7 Y

2,F

FP EMCS D 0.5 F

ASP - - IV - - -

PPHIAL - 7

RH - VE

15 Lakshmi 25 13984 U 9 3 A P A 21SA 1 G 80

110/70 A 36 VX P N N ND 7.3 Y 1

ELCS L 2.25 M Y G - - IV - - - - 8

16 Puttalakshmi 21 16688 U 8 9 A P A 2 1 1 - G 80110/70 A 34 VX P N N ND 6.8 Y

2,2

FF P,2

CP P EM

CS L 1.5 M Y G - - IIA

IITRIBL - -

PPHHYST - 7

17 Manjula 24 14976 U

8.5 3 A P A 1 - G 98

130/80 A 30 VX P N N ND 9.5 Y

EMCS L 3 M Y G - - IIA - - - PPH - 8

18 Mahadevi 26 12207 U 8 1 A P A 1 - G 110140/90 A 32 VX P N N - 7.3 Y 1

EMCS L 1.8 M Y G - - IIA -

PIH - PPH - 8

19 Gowri 23 8159 U

8.5 3 A P A 2 1 1 - G 89

130/80 A 36 VX V N N ND 7.3 Y 1

EMCS L 2 F Y G - - IV - - - - 7

O-VE

20 Choodamani 19 14134 U 7 2 A A A 1 - G 80120/80 A 28 T A N N ND 7.5 Y 1

VAGS

IUD 900 M - - 1A - - - - - 7

222

SL-

Nam

e

Age

IP Boo

ked/

unbo

oked

Am

e-rr

hoea

(in m

onth

a)

Dur

atio

n of

ble

edin

g PV

(hrs

)

Pain

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omen

Feta

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ts

Prio

r ep

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leed

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PV

PAR

ITY

Abo

rtio

ns/(e

ndo

DM

G)

Priv

ious

H/o

LSC

S

Gen

eral

con

ditio

ns

Pulse

(bea

ts/m

in)

BP(

mm

IIg)

Abd

omen

-Ten

se,te

nder

Ges

tatio

nalA

ge(w

ks)

Pres

enta

tion

FHS

Loc

al e

xam

inat

ion

P/S

exam

inat

ion

PV e

xam

inat

ion

Hb

ING

M%

Ultr

a so

und

Blo

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ansf

usio

n

Mod

e of

del

iver

y

Bab

y-al

ive/

Dea

d

WT

of t

he b

aby

Sex

of th

e ba

by

NIC

Uad

miss

ion

APG

AR

C.O

.D

Feta

l A-M

AL

Y

Plac

enta

l/cor

d A

-m

alie

s

Typ

e of

pla

cent

a pr

evia COMPLICATIONS

HO

SPIT

AL

ST

AY

RE

MA

RK

S

AP IP PP Operative

G P LINTRA PO

ST

21 Asha 24 13301 U 9 1 A P A 2 1 1 - G 80120/80 A 36 VX P N N ND 12.6 Y 1 EM CS L 2.4 F G - - IV - - -

PPHPBS - 5

22 Sushela 30 6777 U 8 4 A P A 3 2 1 1 - G 84120/80 A 30 VX P N N ND 9 Y 1 EL CS L 7.6 M Y G - - III - - - Anem 7

23 Jyothi 27 4538 U 9 1 A P A 1 - G 84120/80 P 40 VX P N N ND 9.5 Y 1 EM CS L 3.5 F G - - 1A - PHYD - Anem 7

24 Chaithra 20 3346 U 8.5 2 A P A 2 1 1 - G 89120/80 A 32 B P N N ND 9 Y 1 EM CS L 1.7 F Y G - - 1A - - -

PPH UTTAMP - 11 CM

25 Suma 28 7672 U 7 1 A P A 2 1 1 - G 84120/80 A 30 VX P N N ND 9.5 Y EM CS L 1.2 M Y G - - 1A - - - - 7

26 Raziya 26 9828 U 9 4 A P A 2 1 1 - G 84120/80 A 40 VX P N N ND 9.5 Y EM CS L 3.1 F G - - IIP

IITRIBL - - Anem 9

AB-VE

27 Jabben 20 23196 U 9 1 A P A 2 1 1 - G 94110/70 A 40 VX P N N ND 9 Y 2 EM CS L 2.75 F G - - IIA

IITRIBL - -

UAL &IAL - 9

28 Sameena 20 23088 U 9 1 A P A 1 - G 89110/80 A 40 VX P N N ND 9 Y 2 EM CS L 2.5 M G - - IIA

IITRIBL - -

UAL &TAMP - 11

29Sumithra 34 16816 U 9 5 A P A 2 1 1 - G 88

130/80 A 40 VX P N N ND 9.5 Y EM CS L 2.8 F G - - IV - - - - 12

30 Arthi 22 21809 U 9 2 A P A 3 1 1 1 - G 84120/80 A 40

TRALIE P N N ND 5.4 Y 1 EM CS L 2.1 F Y G - - IIA

IITRIBL - - - 12

RH-VE

31 Asiya 26 21648 U 9 4 A P A 2 1 1 - G 89120/80 A 40 VX P N N ND 9.5 Y 2 EM CS L 2.5 F G - - IIA

IITRIBL - - ADH PL

Anemia 7 CM

32 Reshma 21 20637 U 8 1 A P A 1 - G 89120/80 A 34 VX P N N ND 9.3 Y EM CS L 2.2 M Y G - - IIP

IITRIBL - - - 8 CM

33 Lakshmi 30 18266 U 7 1 A P A 2 1 1 - G 92110/80 A 30 B P N N ND 9.3 Y 1 EM CS D 1.2 M G

RDS

- - IV - - -PPHPBS - 7

34 Lakshmi 22 18227 U 8 2 A P A 2 1 1 - G 89110/80 A 36 VX P N N ND 9.3 Y 2 EM CS L 2 M G - - IIP

IITRIBL - - - 7

35 Manjula 35 16895 U 9 1 A P A 1 - G 92110/80 A 32 VX P N N ND 9.3 Y 2 VAG D 1.5 M

PMT G

IUA

-

-

1A - - - - 12

36Jaylakshmi 25 18177 U 8.5 1 A P A 3 2 2 - G 84

140/96 A 34 VX P N N ND 7.5 Y EM CS L 2 F Y G - - III - PIH - - 4

37Rathnamma 33 19656 U 8 1 A P A 1

M0my - G 86

110/80 A 32 VX P N N ND 7.1 Y EM CS L 2.1 M G - - IV - - - - 5

38 Jyothi 30 2478 U 7.5 3 A P A 2 1 1 - G 89110/80 A 30 VX P N N ND 9.4 Y 4 EM CS L 1.8 M Y G - - IIP - - -

RPC100GMHYST - 13

39Nagarathna 25 22406 U 9 4 A P A 3 1 1 1 - G 88

110/80 A 40 VX P N N ND 5.85 Y 2 EM CS L 3.5 F G - - IV

IITRIBL - -

PL INCRUP Hyst 10

223

C.O.D:cause of death,B-Booked,U-unbooked,RDS-Respiratory distress syndrome,ASP:Asphyxia,ITRI BL-1st trimester bleeding,IITRI BL-2ndtrimester bleeding,ADHP-Adherent placenta,PPH-Postpartum hasmorrhage,Hypo-hypotension,HYST-peripartum hysterecotomy,VX-vertex,B-Breech,TRANS-transverlie,1SA-1 spontaneous abortion, BIC UTR-Bicorunate uterus, UAL-uterine artery ligation, IAL-internal artery ligation, UT TAMP Uterine tamponade ,RPC-Retro placental clot, PLINC RUP-Posterior wall incomplete rupture,POWLDIS-Posterior wall desection,ANEM-Anemia,COUT-Coulevire Uterus,CM-Consevative management PBS-Placental Bed Stitch, M-Maternal mortality

SL-

Nam

e

Age

IP Boo

ked/

unbo

oked

Am

e-rr

hoea

(in m

onth

a)

Dur

atio

n of

ble

edin

g PV

(hrs

)

Pain

abd

omen

Feta

l mov

emen

ts

Prio

r ep

isode

s of b

leed

ing

PV

PAR

ITY

Abo

rtio

ns/(e

ndo

DM

G)

Priv

ious

H/o

LSC

S

Gen

eral

cond

ition

s

Pulse

(bea

ts/m

in)

BP(

mm

IIg)

Abd

omen

-T

ense

,tend

er

Ges

tatio

nal

Age

(wks

)

Pres

enta

tion

FHS

Loc

alex

amin

atio

n

P/S

exam

inat

ion

PV e

xam

inat

ion

Hb

ING

M%

Ultr

a so

und

Blo

odtr

ansf

usio

n

Mod

e of

del

iver

y

Bab

y-al

ive/

Dea

d

WT

of t

he b

aby

Sex

of th

e ba

by

NIC

Uad

miss

ion

APG

AR

C.O

.D

Feta

l A-M

AL

Y

Plac

enta

l/cor

dA

-mal

ies

Typ

e of

pla

cent

apr

evia

COMPLICATIONS

HO

SPIT

AL

STA

Y

RE

MA

RK

S

AP IP PP Operative

G P L INTRA POST

40 Noorjan 20 13301 U 9 4 a P A 1 - G 88110/80 A 40 VX P N N

ND

9.8 Y 1 EM CS L 3 F G - - III

1 TRIBL - - - 7

41 Sumithra 24 16816 U 9 5 A P A 2 1 1 - G 88120/80 A 40 VX P N N

ND 9 Y EM CS L 2.8 F G - - IV

IITRIBL - - PPH MM - 7

42 Savitha 21 17562 U 8 2 A P A 2 1 1 1 G120

110/80 A 34 VX P N N

ND

9.8 Y EM CS L 2.2 M G - - IIP - - - - 7

43Farzanabanu 28 21488 U 9 1 A P A 2 1 1 - G 80

149/100 A 38 VX P N N

ND

9.8 Y 1 EM CS L 2.5 M G - - IIP

IITRIBL PIH - - 7

44 Dhakshainni 28 1456 U7.5

48 A P A 2 1 1 - G 88

110/80 A 32 VX P N N

ND

9.5 Y EM CS L 2.4 M G - - IIA - - - - 8

45 Roopa DC 21 1822 U 9 2 A P A 1 - G 88140/100 A 38 VX P N N

ND

9.5 Y EM CS L 2.2 F G - - IV

IITRIBL PIH - - 7

46 Suguna 30 1416 U 9 1 A P A 3 1 1 1 1 G 88110/80 A 40 VX P N N

ND

8.8 Y EM CS L 3 F G - - IV

IITRIBL - - -

47 Pavithra 26 4858 U 8 1 A P A 3 1 1 - G 90110/60 A 34 VX P N N

ND

9.2 Y 2 EM CS L 2.4 F Y G - - IIA

IITRIBL - - - 5

48 Shobha 20 1771 U 9 2 A P A 1 - G 86120/80 A 34 VX P N N

ND

9.2 Y 1 EM CS L 2.5 M Y G - - IIA

IITRIBL - - -

12

49 Hemavathi 28 16991 U 8 2 A P A 2 1 1 - G100

120/80 A 36 VX P N N

ND

9.8 Y EM CS L 2.9 F G - - IIP

IITRIBL - -

PPHPBS - 5

50 Padhma 35 13271 U 9 2 A P A 2 1 1 1 G120

100/60 A 32

TRANS P N N

ND

8.8 Y 3 EM CS L 2.4 F Y G - - IV - - - PPH

HYPO- M

51 Rathna 22 12267 U 9 2 A P A 1 - G 86160/100 A 40 VX P N N

ND 11 Y EM CS L 2.7 F G - - IA

IITRIBL - - - 1

52 Savitha 22 19845 U 8 2 A P A 2 1 1 - G 80130/80 A 32 VX P N N

ND

7.8 Y EM CS L 2.1 M Y G - - IIP - - - - 7

53Zaheerabanu 35 14234 U 8 3 A P A 3 2 2 - G 88

120/80 A 34

TRANS P N N

ND 8 Y EM CS L 1.5 M Y G - - IIP

IITRIBL - - PPH - 8

54 kamala 30 20336 U 9 8 A P A 2 1 1 - G 9094/7

0 A 32

TRANS P N N

ND

8.5 Y EM CS L 2.1 F Y G - - III

1 TRIBL

HYPO - - 7

55 Rani 2622064

8 B 9 4 A P Y 2SA - G 80

160/101 A 40 VX P N N

ND

9.8 Y 2 EM CS L 2.1 F G - - IIA - PIH - PPH

HYPO M

56 Jabeena 26 20719 B 9 4 A P A 1 A - G 80120/80 A 38

TRANS P N N

ND 10 Y EM CS L 2.5 F G - - IIP

IITRIBL - -

POWLDIS - 8

B-VE

57Sarasvti 30 16696 U 9 3 A P A 1 - G 80

110/80 A 38 VX P N N

ND 10 Y EL CS L 2.25 M G - - IA - - - - 8

58 norfatima 21 15883 U 9 4 A P A 1 - G 80120/80 A 38 VX P N N

ND 11 Y EL CS L 3 M G - - IA - - - - 8

59 Pavithra 26 1597 U 9 4 P P A 2 1 1 - G 80110/60 P 34

MHD P N N

ND

9.6 Y 2 EM CS L 2 F Y G - - IIP -

RT100GM - - 8

60 Rekha 27 881 U 9 4 A P A 1 - G 80120/80 A 38 VX P N N

ND 10 Y EM CS L 2.7 M Y G - - IIA - - - - 8

61 Madhu 33 15641 U 8 3 P A A 3 2 1 A - G 80100/70 P 32 VX A N N

ND

9.3 Y EMCS D 1.7 M - - III - - - CO UT

RT200GM

Documents

“MATERNAL FETAL OUTCOME IN PLACENTA PRAEVIA”