i
“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
i
“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
i
“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
ii
iii
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).
iv
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.
v
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.
vi
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.
vii
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
viii
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
ix
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
x
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
xi
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
xii
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
1
PART - I
PLACENTA PREVIA
2
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.
3
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.
4
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.
5
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.
6
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.
7
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
8
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
9
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.
10
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
11
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.
12
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.
13
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.
14
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.
15
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
16
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.
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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.
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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
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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.
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• 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
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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
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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.
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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.
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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
116
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
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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
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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
119
Management of Placenta Previa- Flow chart
119
Management of Placenta Previa- Flow chart
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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.
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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
123
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.
127
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
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
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
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
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
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%.
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
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
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
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
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
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
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
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
1 2 3 4
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
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
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
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
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
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
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
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
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
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
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
Coefficient.014 .912
N of Valid Cases 61
187
Graph 9
Symmetric Measures
Value
Approximate
Significance
Nominal by Nominal Contingency
Coefficient.014 .912
N of Valid Cases 61
187
Graph 9
Symmetric Measures
Value
Approximate
Significance
Nominal by Nominal Contingency
Coefficient.014 .912
N of Valid Cases 61
188
Table 26. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Nominal by Nominal Contingency
Coefficient.525 .000
N of Valid Cases 61
188
Table 26. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Nominal by Nominal Contingency
Coefficient.525 .000
N of Valid Cases 61
188
Table 26. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Nominal by Nominal Contingency
Coefficient.525 .000
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%.
Table 27. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Coefficient.356 .014
N of Valid Cases 59
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
Coefficient.356 .014
N of Valid Cases 59
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
Coefficient.356 .014
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
Table 28. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Table 28. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
Table 28. CORRELATION BETWEEN PERINATAL MORTALITY AND
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
193
Symmetric Measures
Value
Approximate
Significance
Nominal by
Nominal
Contingency
Coefficient.475 .000
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
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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
ed/u
nboo
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Am
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(in m
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Dur
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Prio
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BP(
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Abd
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Ges
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nal
Age
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Pres
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exam
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PVex
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Sex
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C.O
.D
Feta
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Plac
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alie
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Typ
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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
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Am
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hoea
(in m
onth
a)
Dur
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n of
ble
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g PV
(hrs
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Pain
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Prio
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PAR
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alie
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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
-
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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
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.D
Feta
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-mal
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Typ
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pla
cent
apr
evia
COMPLICATIONS
HO
SPIT
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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