“COMPARATIVE STUDY OF PLACENTAL

CYTOARCHITECTURE IN MILD AND SEVERE

HYPERTENSIVE DISORDERS OCCURRING DURING
PREGNANCY.”

Mrs. P. Sridevi ,Tutor

, .
RIMS Medical College,
Srikakulam , AndhraPradesh
Guide:

Dr.ANITHA ROY
Associate Professor and H.O.D,
Department of Pharmacology,
Saveetha Institute of Dental sciences,
Poonamallee, Chennai,
Tamilnadu.

Signature of the Guide

Co-guide:

Dr.S.Ravindra Kishore,
Professor and H.O.D,
Department of Anatomy,
R.I.M.S Medical College,
Srikakulam,
Andhra Pradesh.
INTRODUCTION

3
 INTRODUCTION
Hypertensive disorders complicating pregnancy are common
and form a deadly triad along with haemorrhage and infection
that contributes greatly to maternal mortality and morbidity.
Incidence of hypertensive disorders in pregnancy is 5-10%,
whereas incidence of preeclampsia is 3.9% of all
pregnancies1. In developing countries, a woman is seven times
more likely to develop preeclampsia than a woman in a
developed country. 10-25% of these cases will result in
maternal death 2.
 The current Maternal Mortality Rate (MMR) of India is 178
per one lakh live births. Major causes of maternal mortality in
India remain haemorrhage (38%), sepsis (11 %), abortions
(8%), hypertensive disorders (5%) and other causes (3%).
Hypertensive disorders of pregnancy are strongly associated
with both maternal and fetal complications 1.
4
Placenta is essential for maintenance of pregnancy and
for promoting normal growth and development of fetus
which functions to help developing fetus to derive its
nutritional substances and obtain its metabolic and
4
immunological requirements .
The Aetiology and pathological mechanism in the
development of hypertensive disorders of pregnancy is
still controversy, however it is generally accepted that
the placenta is the key organ in the pathogenesis of this
disease and important mechanism involved is defective
remodeling of the spiral arteries, that could contribute to
the hypoxic environment and there by placental
insufficiency which can lead to the maternal and fetal
complications. 5,6
The maternal and fetal complications in hypertensive
disorders complicating pregnancy are associated with
significant pathological changes in the placenta depending on
the severity of the hypertension, whether it is mid or severe
hypertensive disorder complicating pregnancy.7
Various studies and trails in recent years focused their
attention towards these changes in the placenta and reviewed
whether these placental changes are the causal agents for
complications associated with mother and fetus in
hypertensive disorders of pregnancy.8,9
Several studies have shown that utero-placental blood flow
is decreased in PIH due to maternal vasospasm10. This
leads to constriction of fetal stem arteries and has been
associated with the changes seen in the placenta of
preeclamptic women11. The placental examination will help
in understanding the specific atiologies of adverse outcome
which will lead to specific treatment and preventive
measures for those with the risk for
recurrence in subsequent pregnancies and long term
sequelae in hypertensive disorders of pregnancy

As placenta is the mirror of maternal and fetal status, it

reflects the changes due to maternal hypertension. The
present study has been undertaken to record the data on
the morphology, morphometry, and histopathology of
placenta from mothers with PIH and correlate the findings
with the birth weight of the new born babies.
PROPOSAL
 AIMS AND OBJECTIVES:

To study the morphology, morphometry and histopathology of the placenta

in cases of mild and severe Hypertensive disorders of Pregnancy.

To correlate the pathological changes in the placenta with the severity of
Hypertension.

To study the spectrum of features in placenta that could be responsible for
the manifestations of complications of pregnancy.

To study the birth weight of the fetus delivered by pregnancy induced
hypertensive mothers.

9
 REVIEW
OF
LITERATURE
 REVIEW OF LITERATURE

The placenta is a vital structure which establishes connection between the mother and fetus through
the umbilical cord.

Structure of the placenta:1,12

By the beginning on the fourth month, placenta has two components, a fetal plate formed by chorion
frondosum and a maternal plate formed by the deciduas basalis. The placenta covers approximately
15 to 30 % of the internal surface of the uterine cavity.

The placenta at term:1,13 Placenta is a flattened discoid structure with a circular or oval in outline.
Weight 500 gms (1/6th of the fetal birth weight), diameter 22 cms, central thickness of 2-2.5 cms.
Average numbers of maternal cotyledons are 15-20.

Placental examination: Placentae has been examined macroscopically and microscopically for a
variety of reasons-diagnostic, either for the mother or for the neonate and – prognostic – prediction of
future pregnancies, investigative and for legal purpose.14 Naeye opines that all placentae should be
examined grossly and an immediate microscopic examination indicated for those cases with adverse
pregnancy outcome15. Driscoll supports this view that the obstetrician should grossly examine all
placentae and triage those placentae requiring further gross and microscopic study by a pathologist16.
Salafia and Vintzileos have recommended that pathologists should examine all specimens by light
Microscope to ensure tissue examination of potential cases of litigation, since clinical appearance of
neurological disturbances in children is unpredictable and may be delayed for many years.17 Practice
guidelines for Examination of the placenta was developed by the placental pathology practice
guideline development task force of the college of American pathologists in 199718
 Benefits of placental examination18:
1. Categorization of various aetiologies of adverse outcome.
2. Improved management of subsequent pregnancies for those shown to
have conditions that have recurrence risk and may be either treatable or preventable.
3. Understanding of antenatal and intra-partum events that contribute to long term
neurodevelopmental sequelae with early identification of such changes making possible early
interventions and improvement in long term outcome.
4. Assessment of factors contributing to poor outcome as a factual basis for resolving medico legal
issues. Indications for histopathological examination of placenta18:

Recommended Maternal indications

Systemic disorders with clinical concerns for mother or infant (eg.

Severe diabetes, impaired glucose metabolism, hypertensive disorders, collagen disease,
seizures, severe anaemia, Premature delivery <34 weeks gestation, Peripartum fever and / or
infection, Unexplained third trimester bleeding or excessive bleeding>500 cm3.Clinical concern for
infection during this pregnancy (e.g. Human immune deficiency virus, syphilis, cytomegalovirus,
primary herpes, toxoplasma, rubella), Severe oligohdramnios, Unexplained or recurrent pregnancy
complication (e.g. intrauterine growth retardation, stillbirth, spontaneous abortion, premature
birth), Invasive procedures with suspected placental injury, Abruption, Thick and / or viscid
meconium.
Other maternal indications

Premature delivery from >34to37 weeks gestation, Severe

unexplained polyhydramnios, History of substance abuse, Gestational
age at 42 weeks, Severe maternal trauma, Prolonged (>24hours)
rupture of membranes.

Recommended fetal/neonatal indications:

Admission or transfer to other than a level 1 nursery, Stillbirth or

perinatal death, Compromised clinical condition defined as any of the
following: Cord blood pH<7.0; Apgar score of 6 at 5 minutes; ventilator
assistance for>10minutes; ventilator assistance for>10minutes; or
severe anemia, hematocrit<35%, Hydrops fetails, Birth weight<10th
percentile, Seizures, Infection or sepsis, Major congenital anomalies,
dysmorphic phenotype, or abnormal karyotype, Multiple gestation with
same sex infants and fused placentas.

Other fetal/neonatal indications:

Birth weight>95th percentile, Asymmetric growth, Multiple gestations

without other indication, Vanishing twin beyond the first trimester.
Placental pathology in hypertensive disorders of pregnancy:

No single lesion is invariably found in preeclampsia and other hypertensive disorders

complicating pregnancy, in major number of cases placenta shows the effects of low
uteroplacental flow.

Placental weight:At term, usually placenta weighs one sixty of the fetal weight, but in
hypertensive disorders of pregnancy, placental weight reduced may be due to the
reduced blood flow which may be due to the ischemic changes in the vessels19 .

Placental diameter:

Average placental diameter at term 20-25 cms, there will be a marked

reduction in the diameter of the placenta in PIH( pregnancy induced hypertension)20

Placental thickness:

Normal placental thickness at term is >2 cms and 32 weeks >1.5 Cms. Thickness
seemed to be reduced in hypertensive disorders of pregnancy21 according to a study
done by Sabita Singh. T S Gunapriya et al observed decrease in placental thickness in
hypertensive disorders22.
MORPHOLOGY:

Infarction:Infarcts are significant when they are more numerous, and centrally located.
They may be old or fresh. A fresh placental infarct is well demarcated, dark red (<2-3 days) and
firm. As the infarct ages, it becomes progressively hard and its colour changes successively to
brown yellow and white (after 1 week). An old infarct thus appears as a hard white plaque, with a
smooth or slightly granular, amorphous cut surface.
Histologically, the early infarct is characterized by aggregation of villi in the affected area,
with marked narrowing and often obliteration of the intervillous space. As the infarct ages, the
syncytial nuclei eventually disappear and there is a progressive coagulative necrosis of the villi,
undergo haemolysis and the endothelium of these vessels degenerates. The old infarct simply
consists of crowded ghost villi, without any fibrosis or cytotrophoblastic proliferation. Infarction is
the dramatic and easily recognized visible sign of maternal uteroplacental vascular
insufficiency23. Infarcts can occur in about 25% of normal term pregnancies. Infarcts are more
significant when they are central and greater than 3 cm in greatest dimension or infarcts occur in
the first and second trimester. Infarction is associated with significant perinatal mortality and
morbidity, including IUD, fetal hypoxia24. Thus extensive infarction occurs only against a
background of markedly abnormal maternal vasculature and a decreased maternal blood flow to
the placenta and it is these factors, rather than the destruction of villi due to infarction, which are
the real cause of the fetal complications23.
Retro Placental hematoma:

It is a clot located between the basal plate of the placenta and the
uterine wall. These are less common, occurring in about 12-15% all
preclamptic cases25. Microscopically this change is characterized by the
presence of red cells and fibrin. As the lesion age increases proportion
of fibrin increases and red cells degenerates. They are associated with
high incidence of fetal hypoxia and death. Other types of placental
hematomas are sub amniotic, Marginal, Massive subchorial hematoma.

Calcifications:

Often calcifications are visible on gross examination. Fibrin or

fibrinoid material containing placentas often shows calcifications. They
produce a multifocal blue color with haematoxylin and eosin staining.
Low uteroplacental blood flow may be the cause for these changes.
Severe and diffuse calcification often associated with the hypoxic
newborns.26
Tenny parker change:

Syncytial knots can be seen in normal placenta but more than 30%
are indicative of perfusional compromise. They are more significant when they
present in the central portion of the placenta, because peripheral portion has
already low placental blood supply23. When the villi are small with excessive
syncytial knots, it is known as Tenny-Parker change.27

Acute atherosis:

Acute atherosis is another pathological change associated with

spiral arteries, it also known as acute necrotizing arteriopathy. This is
characterized by the fibrinoid necrosis of the vessel wall, accumulation of lipid
laden cells, and perivascular mononuclear infiltrate. This change results in
infarcts and retroplacental haematomas. But, examination of spiral arteries is
difficult because they found rarely in random sections of the placenta. They
usually seen near the centre of a cotyledon. It can also be seen in unexplained
still birth, idiopathic IUGR, and in prematurity.23
 Hyperplastic arteriosclerosis:

Hyperplastic arteriosclerosis characterized by the marked medial thickening of

the vessel wall, intimal hyperplasia and narrowing of lumen and this is most
commonly associataed with the chronic hypertension. Super imposition of the
acute atherosis on the hyperplastic arteriosclerosis can be seen in cases with
preeclampsia superimposed on chronic hypertension22

Fibrin deposition:

With progression of pregnancy there is increased deposition of fubrin and

thrombotic material under the foetal surface. The eventual outcome of the foetal
activity is associated with the subchorionic deposition of fibrin.28 When this
deposition of fibrin surrounds more than half of the villous tissue it is considered
to be massive intervillous fibrin deposition. In maternal floor infarction, there is
excessive fibrin at the maternal floor around the basal villi. This condition is most
often associated with still birth, growth retardation and preterm delivery with
possibility of recurrence in subsequent deliveries.29 Redline and Patterson
observed that perivillous fibrin deposits that entrapped more than 20% of the
terminal villi in the central basal portion of the placenta, which is the primary
region of the gas and nutrient exchange, were significantly associated with the
IUGR and low placental weight.30,31
Chorangiosis:

Chorangiosis is said to be present with the presence of at least ten villi that
have ten capillary lumina in each villus, in ten different microscopic fields in ten
different placental areas. It never occurs in normal placetas.30 Mostly this change
is associated with preeclampsia31 and other neonatal morbidity and mortality.32

Villous hypermaturity:

Villous hypermaturity has been thought as a compensatory mechanism to

counter the effects of an inadequate uteroplacental blood flow in conditions like
preeclampsia. It is defined as the appearance of numerous small terminal villi
before the 40th week and numerous small cross-sections of highly capillarized
terminal villi.7

Avascular villi:

Avascular villi were diagnosed when a group of at least 5 fibrotic avascular

villi without inflammation and without mineralization were seen. Avascular villi is
noted in placenta from babies of low birth weight. 7 They can be seen in
placentas of IUGR, oligohydramnios, and maternal coagulation disorders.
DEFINITION AND CLASSIFICATION OF HYPERTENSIVE DISORDERS
PREGNANCY1,34,35:

Multiple classifications have been proposed to classify the hypertensive

disorders of pregnancy. The Working Group of National High Blood Pressure
Education Programme (2000) recommended the following classification.
Hypertensive disorders of pregnancy are classified as
1.Gestational hypertension.
2.Preeclampsia and Eclampsia syndrome.
3.Chronic hypertension of any aetiology.
4.Preeclampsia superimposed on Chronic hypertension.

Gestational hypertension:

BP > 140 mm of Hg for first time during pregnancy after 20 weeks of

gestation, with no proteinuria, with BP returning to normal within 12 weeks
postpartum.

Preeclampsia:

BP > 140/90 mm Hg after 20 weeks of gestation, with significant proteinuria (>

300mg / 24 hours or > 1+dip stick).
Eclampsia:

Seizures that cannot be attributed to other causes in a woman with

preeclampsia.

Preeclampsia super imposed on chronic hypertension:

New onset proteinuria > 300mg/24hours in hypertensive women but

no proteinnuria before 20 weeks gestation. A sudden increase in
proteinuria or blood pressure or platelet count <1,00,000/mm3 in women
with hypertension and proteinuria before 20 weeks gestation.

Chronic hypertension:

BP > 140/90 mm of Hg before pregnancy or diagnosed before 20

weeks of gestation and
persistent after 12 weeks postpartum.
 TABLE 1- Indicators of severity in hypertensive disorders of pregnancy1

Abnormality Mild HTN Severe HTN

Diastolic blood pressure <110mmHg >110 mm Hg

Systolic blood pressure <160 mm Hg >160 mm Hg

Proteinuria None to positive None to positive

Headache Absent Present

Visual disturbances Absent Present

Upper abodominal pain Absent Present

Oliguria Absent Present

Convulsion Absent Present

Serum creatinine Normal Elevated

Thrombocytopenia(<1,00,000/ Absent Present

ul)

Serum transaminase elevation Minimal Marked

Fetal growth restriction Absent Obvious

Pulmonary oedema Absent Present

22
Definition of hypertension according to ISSHP36:

(The international society for study of hypertension in pregnancy)

A diastolic pressure of 90 mm Hg, but measured twice at least 4 hours
apart, diminishing the influence of “white coat hypertension” or A diastolic
pressure of 110 mm Hg is sufficient for the diagnosis even if measured only
once.

Blood pressure measurement protocol:38

Blood pressure should be measured with the woman in the sitting position and
with the arm at the level of the heart.An appropriately sized cuff (i.e., length –
1.5 times the circumference of the arm) should be used.Korotoff phase V
should be used to designate diastolic blood pressure.If blood pressure is
consistently higher in one arm, the arm with the higher values should be used
for all blood pressure measurements.Blood pressure can be measured using a
mercury sphygmomanometer, a calibrated aneroid device, or an automated
blood pressure machine that has been validated for use in
preeclampsia.Automated blood pressure machines that have not been
validated for use in women with preeclampsia may underestimate or
overestimate blood pressure in those women; a comparison of readings using
mercury sphygmomanometry or a calibrated aneroid device is recommended.
 Risk factors for Hypertensive disorders of pregnancy:1,12,38,39

Extremes of maternal age (young and old age), Race and ethnicity,
Environmental factors, Socioeconomic factors, Genetic predisposition , Primi
Gravida, Previous history of preeclampsia,New paternity,Multiple pregnancy,
Hydatidiform mole, Chronic hypertension,Diabetes,Obesity, Renal disease,Anti
phospholipid antibody syndrome, Inherited thrombophilias,Hyper homocysteinemia,
Metabolic syndrome, Connective tissue disorders like systemic lupus
erythematosus.
Aetiopathogenesis of hypertensive disorders of pregnancy:
The exact aetiology of hypertensive disorders of pregnancy remains unknown,
but there are a number of theories which can explain to some extent.

1.TWO STAGE DISORDER THEORY:40

According to this, stage 1 is caused by faulty endovascular

trophoblastic remodeling of uterine vessels which causes placental hypoxia. Stage 2
is caused by oxidative stress which causes release of placental factors into the
maternal circulation, this in turn sets up a systemic inflammatory response and
endothelial cell activation, which results in clinical syndromes of preeclampsia.
2.ABNORMAL TROPHOBLASTIC INVASION THEORY:1,32,42

In normal pregnancy, during placental implantation there will be

proliferation of endovascular trophoblasts, which invade the deciduas and
extend into the walls of the spiral arterioles to replace the endothelium and
muscular wall and creates a dilated low-resistance flow in the vessel. Where
as in HDP, there is incomplete invasion of the spiral arteriolar wall by
endovascular trophoblasts, results in a small-caliber vessel with high
resistance flow. The magnitude of defective trophoblastic invasion appears to
be positively correlated with the severity of the hypertensive disorder.

3.IMMUNOLOGICAL FACTORS:

Loss or dysregulation of maternal immune tolerance to paternally

derived placental and foetal antigens seemed to be one of the aetiology. The
histological changes at the maternal placental interface resemble an acute
graft rejection, which may explain the high prevalence of preeclampsia in first
pregnancy, molar pregnancy and in cases where paternal load increased
conditions like trisomies.
 4.ENNOTHELIAL CELL DYSFUNCTION:43

Although HDP appears to originate in the placenta, the tissue affected most is the
maternal endothelium. The clinical manifestations of preeclampsia reflect widespread
endothelial dysfunction, with vasoconstriction and end organ ischemia..Endothelial
dysfunction may be manifested by the altered synthesis and release of endothelial cell
products. Oxidative stress caused by, cytokines such as tumor necrosis factor-α (TNF- α)
and the interleukins (IL). This results in release of reactive oxygen species and free radicals
which helps in formation of self propagating lipid peroxides. This result in imbalance in nitric
oxide production, and interfere with prostaglandin balance. This further leads to activation of
microvascular coagulation and increased capillary permeability resulting in edema and
proteinuria.

5.ALTERATION IN NITRIC OXIDE AND PROSTAGLANDINS:43

According to a study done by R R C Venuto and M D. Lindheimer it

was found that the tissue and urine analysis of normal pregnant women showed higher
levels of nitric oxide whereas those with preeclampsia showed relatively lower levels.
Damaged or activated endothelial cells may produce less nitric oxide and secrete
substances that promote coagulation and increase sensitivity to vasopressors. In
preeclmpsia there is a reduction in prostacyclin and nitric oxide, which are vasodilators and
increase in thrombaxane A2 production which is a vasoconstrictor. This imbalance results in
vasospasm, platelet and coagulation system activation.
6.RENIN ANGIOTENSIN SIGNALING:46,47

In preeclampsia there is loss of vascular insensitivity to the pressor effect of

the angiotensin II, which results in vasospasm and increase in vascular
resistance and increase in blood pressure. According to a study done by G.
Walluikut, V. Homuth et al, they reported the presence of angiotensin II type 1
receptor agonistic antibody (AT1-AA) found circulating in preeclamptic women.
7.ROLE OF ENDOTHELINS:43
Plasma endothelin I (ET-I) levels increased more in preeclamptic women
which is a potent vasoconstrictor.
8.ROLE OF ANGIOGENIC AND ANTIANGIOGENIC FACTORS:48,49,50

A According to a study done by S.E. Maynard, J.Y. Min, et al,

. preeclampsia was associated with increased expression of soluble fms-
like tyrosine kinase (sFlt1), together with decreased. placental growth
factor(PGF) and vascular endothelial growth factor (VEGF).
B (b) Soluble endoglin (sEng) – This solube form of endoglin
. inhibits various TGFβ isoforms from binding to endothelial receptors and
results in decreased endothelial nitric oxide dependent vasodilation. This
type of endothelial abnormality would be requisite to account for the
disseminated intravascular coagulation seen in
patients with severe preeclampsia.
9. GENETIC FACTORS: 51,52,53

The risk factors for preeclampsia are both genetic and environmental.
The relative risk of preeclampsia in a women increases by 2 to 4 fold with
first degree relatives. The most common genetic abnormally associated
with preeclampsia is polymorphism in sFlt1 and VEGF which have been
associated with severity of preeclampsia. Trisomy 13 fetuses have a higher
incidence of preeclampsia suggesting that gene dosage or copy number
variation may contribute to the development of preeclampsia. Both material
as well as paternal (or fetal) genotypes have been suggested to contribute
for the risk of preeclampsia.

COMPLICATIONS OF HYPERTENSIVE DISORDERS OF PREGNANCY

The outcome and complications of pregnancy in hypertensive disorders can

be affected by multiple factors like gestational age at onset, severity of
disease, and the presence of co morbid conditions like diabetes mellitus,
renal disease, thrombophilia, or preexisting hypertenstion. These
complications can be divided into short term and long term complications.
Short term complications are mainly maternal.
Short term complications:
Maternal complications:

CNS injuries such as seizures (Eclampsia), Cerebrovascular accident,

like haemorrhagic and ischemic storkes which may lead to residual neurological
deficit such as hemiplegia, Visual disturbances like cortical blindness, retinal
detachment,HELLP syndrome (haemolysis, elevated liver enzymes, low platelet
count), Pulmonary edema,Acute respiratory distress syndrome,Acute left
ventricular failure, Renal dysfunction may be in the form of reduction in the
GFR or minimal. proteinuria to reversible acute renal failure or acute tubular
necrosis to even irreversible renal failure secondary to renal cortical necrosis,
Microangiopathis haemolytic anaemia, Hepatic failure, DIC (Disseminated
intravascular coagulation), Increased frequency of caesarean delivery, preterm
delivery, and abruption placetae and Induced labour.

Fetal complications:

Intrauterine fetal growth restriction ,Oligohydromnios, Prematurity, Antepartum

and intropartum asphyxia, Increased frequency of admission
into NICU, Intrauterine fetal death, Long term cardiovascular morbidity (fetal
origins of adult disease)
Long term complications:

Risk of Recurrence: It varies with the severity and onset of the

disease in women primigravida with the severe and early onset disease tend to
develop high risk of recurrence in the subsequent pregnancies (25- 65%)
Cardiovascular complications:

women with significant past history of HTN, will have significantly increased risk to
develop chronic hypertension, ischemic heart disease, stroke, type II diabetes, and
venous thromboembolism in future. These complications are more likely to develop in
women with early onset preeclampsia, recurrent preeclampsia, severe preeclampsia,
gestational hypertension, or preeclampsia with onset as a multipara.
Renal disease:

There is an increased risk for women with history of preeclampsia to develop end-
stage renal disease (ESRD). This risk increases with increased recurrent episodes of
preeclampsia in two or more pregnancies. In one study done by Vassiliki Krielessi,
Nikos Papantoniou et al7 (2013), compared placental pathology with the severity of
the hypertension, in mild and severe hypertensive group compared to the mild
hypertensive group. They observed the presence of villous fibrinoid necrosis, villous
hypermaturity, and placental infarction were significantly more in the severe
hypertensive placentas and also avascular villi, calcifications, thickened vessels and
lymphohistiocytic villitis were noted more often in the severe hypertension group than
mild hypertension group, but these results were not statistically
significant.7Chakravorty (1967) et al60 and Udainia, A, Jain M.L, et al61 observed
similar results of decreased placental weight in severe hypertensive group. In a study
done by SauriyaRanjan Das, Pradeep Kar et al62, observed that placental diameter
was reduced the severe hypertensive group compared to the mild group.
 Miamoona Ahmed, Rekha G. Daver et al63, (2013) done a Study on
‘placental changes in pregnancy induced hypertension’ observed that mean
fetoplacental weight ratio was decreased in severe hypertensive group as
compared to the mild group. They also observed that calcifications,
retroplacental hematoma, infarction were associated with the severe
hypertensive group.

Bandana Das, Dutta D. Chakraborty et al (1996) studied placentas from

different categories of hypertensive disorders and concluded that placental
changes are directly proportional to the duration of the disease process and
its severity and foetal outcome is adversely influenced by the pathological
changes observed in the placenta.

Kaizad R et al65, (1989) studied the placental changes in the hypertensive

disorders of pregnancy and correlated with the fetal outcome, concluded that
low weight placentas associated with the low birth weight infants.In one
study, G.B. Doddamani, Usha Doddamani et al67(2012) studied perinatal
outcome in hypertensive disorders of pregnancy and concluded that poor
perinatal outcome associated with the severity of the hypertension.Maimoona
Ahmed, Rekha G. Daver et al68 (2009) done a study on ‘fetomaternal
outcome in hypertensive disorders of pregnancy’, concluded that poor fetal
outcome with more number of NICU admissions were noted in the severe
hypertensive group.
METHODOLOGY
 MATERIALS AND METHODS

Study Design: Hospital based prospective study.

Source of Data: Pregnant women with hypertensive disorders in the

Department of Obstetrics and Gynaecology in RIMS Medical College, Srikakulam, Andhra
Pradesh.

Study population: Women with hypertensive disorders complicating pregnancy

including gestational hypertension, preeclampsia, eclampsia, pre eclampsia
superimposed on chronic hypertension, and chronic hypertension were taken in this
study.

Selection criteria:

Inclusion Criteria: Antenatal women with hypertensive disorders including

• Gestational hypertension
• Preeclampsia, Eclampsia,
• Preeclampsia superimposed on chronic hypertension,
• Chronic hypertension ,
• Singleton pregnancy
.
Exclusion Criteria: Antenatal women with molar pregnancy.
Antenatal women with multiple pregnancy.

A detailed history will be taken regarding the symptoms of hypertensive

disorders complicating pregnancy at the time of admission. A detailed
menstrual history, relevant past obstetric history, significant past medical
history, history of previous surgeries, relevant family history, personal
history, related to the hypertensive disorders complicating pregnancy had
been taken. A thorough general physical examination including Body Mass
Index, pulse rate, Blood Pressure, Temperature, respiratory rate were
noted.

Method of Blood Pressure measurement:

BP measurements will obtained by a mercury sphygmomanometer in all

subjects three consecutive times with a gap of 5 mins. Blood pressure was
measured with the woman in the sitting position with the arm at the level of the
heart with an appropriately sized cuff (i.e length 1.5 times the circumference of
the arm).
Korotkoff phase V was used to designate diastolic blood pressure.
In cases where blood pressure is consistently higher in one arm, the arm with
the higher values will be taken for all blood pressure measurements
The mean of the three systolic values and the mean of the three diastolic values of the same
patient were taken as the mean systolic blood pressure (SBP) and the mean diastolic blood
pressure (DBP), respectively.

Definitions of mild and severe hypertension:

1.. Mild hypertension defined and taken as the BP elevation of > 140/90 mm of Hg to < 160/110
mm of Hg
2. Severe hypertension defined and taken as BP elevation greater than
160/110mm of Hg
Detailed systemic examination including Cardiovascular system, Central nervous system,
Respiratory System, and obstetrical examination performed. After thorough examination,
following investigations will be sent to the laboratory. Investigations performed
Hb%,
PCV,
Blood grouping & Rh typing,
RBS, Platelet count,
Bleeding time,
Clotting time,
Serum uric acid,
Liver function tests,
Renal Parameters like Serum creatinine and Blood urea,
Urine: Albumin,
sugar,
microscopy,
Fundoscopy,
Obstetrical ultrasonography.

In the present study, 50 cases of mild and 50 cases of severe

hypertensive disorders complicating pregnancy will be taken, those cases
will be followed till delivery, the placenta wil be collected immediately after
delivery in a clean tray, washed under tap water, placental weight,
thickness, diameter were measured. Fetal surface, maternal surface,
membranes, umbilical cord examined and any abnormalities will be noted.
Then placenta will be sent to the laboratory in a container with 10% formal
saline solution for examination and processing. In the pathology lab,
sections will be taken from the different sites, umbilical cord, insertion of the
umbilical cord, membranes, sections from 4 different quadrants of the
placenta and from any gross lesion.
Processing will be done and microscopic slides will be prepared and stained with haematoxylin
and eosin and will be studied under microscope. The following parameters will be observed in
placental specimen:
• Weight,
• Diameter,
• Thickness,
• Maternal surface,
• Fetal surface,
• No. of cotyledons,
• Any cord anomalies,
• Calcifications,
• Retroplacental hematoma,
• Infarction,
• Microscopic features like,
• Tenny Parker changes,
• Villous hypermaturity,
• Avascularvilli,
• Fibrindeposition,
• Calcifications,
• Retroplacental hematoma,
• Infarction.
At the time of delivery, fetal condition including APGAR score at 1minute and 5
minutes and baby birth weight will be noted. Neonates with NICU admission shall
be followed and outcome will be noted. Gross and microscopic placental changes
in the mild and severe cases of hypertension will be studied with the help of
pathologist and comparision will be done along with fetal outcome.

Examination Results will be analyzed with the help of chi-square test and T
test and association of the placental lesions with the severity of the hypertension
were noted.

Women with hypertensive disorders of pregnancy especially with severe

hypertension, have been shown to have nearly a two fold increase in risk for
ischemic heart disease, stroke and venous thromboembolic disease in the five to
fifteen years after the pregnancy. Due to these long term risks of specific
cardiovascular risk factors should be addressed and recommendations be made for
addressing them with dietary and lifestyle modification, including exercise,
maintenance of ideal body weight.
 PROFORMA
All the following details of the patients would be taken using this Proforma
I.P/0.P NO:
Sr No: Date:
Name:
Age: Sex: occupation:
Address:
Socioeconomic status: LMP:
Rellgion: EDD:
Chief complaint: POG:
Obstetrical formula:
Menstrual history:
Marital life:
Past obstetric history:
Past medical history:
Past surgical history:
Personal history:
Family history:
General Examination: Built and nourishment
Height:
Weight: BMI:
Pallor/lcterus/Cyanosis/Clubbing/Pedal edema /Lymphadenopathy
Vital parameters: Temp: PR: RR:
Blood pressure recordings: 1st : 2nd 3rd
Mean SBP: Mean DBP
Systemic examination:
CVS:
RS:
CNS:
Obstetrical examination:
Diagnosis:
Investigations:
Hb%: PVC:
Blood grouping & Rh D typing:
RBS:
Urine: Albumin: Sugar: Microscopy:
Serum uric acid:
Platelets:

BT:
CT:
Liver function tests:
Renal parameters: Serum creatinine: Blood urea:
Urine albumin:
Fundoscopy:
Diagnosis :
Onset of labour: Mode of delivery
Birth weight of baby: Apgar score at 1min:
NICU Admission: Apgar score at 5min:
Fetal outcome:
Examination of Placenta:
Gross Morphology:
Size:
Shape:
Weight:
Diameter:
Thickness:
Maternal surface:
Fetal surface:
No. of cotyledons:
Any cord anomalies:
Histopathological Examination:
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JOURNALS LIST:
1.COMPARITIVE STUDY OF PLACENTAL CHANGES IN MILD AND SEVERE
HYPERTENSIVE DISORDERS OF PREGNENCY.
Article in Journal of Evolution of Medical and dental sciences6(90):6368- 6372.november
2017.

DOI:10.14260/jemds/2017/1385.
2.A STUDY OF PLACENTAL WEIGHT AND FETAL OUTCOME IN DIFFERENT GRADES
OF PREGNENCY INDUCED HYPERTENSION

Raghavendra.a.y*1,Vinay.K.V,Veena Pai.
Web site:International Journal of Anatomy and Reasearch ISSN 2321-4287

Received 26 sep 2014

Peer REVIEW:26 sep 2014 published (o):31 oct 2014

Accepted:15oct 2014Published(P):31Dec 2014.

International Journal of Anatomy And Research,

Int J Anat Res 2014, Vol2(4):625-29.ISSN 2321-4287 DOI:10.16965/ijar.2014.509.

3.Study of Placental changes in pregnancy induced hypertension Maimoona Ahmed*,Rekha

G.Daver

International journal of Reproduction,contraception,obstetetries and Gyneocology

Ahmed et al.Int J Reported contracept obstet Gynecol.2013:2(4):524-527

PISSN2320--1770/eISSN 2320-1789

DOI;10.5455/2320-1770.ijrcog 20131207

Received 12 September 2013

Accepted 21 September 2013

placental morphology in hypertensive disorders and its correlation to neonatal outcome

Sudha Tangirala,Durga kumara.

International Archives of Integrated Medicine,Vol,2,Issue 11,November,2015.

Copy right 2015,IAIM,All Rights reserved. ISSN:2394-0026(9)

ISSN:2394-0034(0)

4.Placenta in normal pregnancy vs.placenta in pregnancy in included hypertention:A morphological and

histopathological study .

Journal of evidence Based Medicine And Healthcare PISSN 2349-2562 eISSN 2349-2570

ICV 2017 88.59

2015 Month :Noveber Volume :2 ISSUE :45 page 8142-8145.

5.Placental pathology And BLOOD Pressures Level in Women with hypertensive Disorders in pregnancy

Article May 2012

Histopathological study of placenta in pregnancy with Hypertension in western odisha.

IOSR Journal of ntal and Medical Sciences(IOSR_JDMS) e-ISSN:2279-0853,p-ISSN:2279-

0861.Volume 16,issue
6Ver.v(june.2017),pp 100-104

6.placental morphology and its co-relation with foetal outcome in pregnancy-Induced Hypertension

International Journal of Basic and Applied Medical Sciences ISSN:2277- 2103

2012 VOL.293) September-december,pp.120-125/pasricha navbir.

7.A Study of placenta in Normal and Hypertensive Pregnencies.

J.anat.soc.India54(2)1-9(2005) Majumdar SIPGMER Kolkata.

Placental Weight and Fetal Outcome in Pregnency induced Hypertension Asian journal of Bio

medical and Pharmaceutial Sciences,2016.

8.Placental parthology and pressures level in women with Hypertensive disorders in pregnancy.

Obstetrics and Gynecology International Volume 2012,Article ID 684083, 6 pages

http/dx.doi.org/10.1155/2012/684083.

3rd session American Journal of Obstetrics& Gynecology1.

9.Placenta associated pregnancy complications in pregnancies complicated with placenta previa.

Taiwanese Journal of Obstetrics and Gynecology Volume 56, Issue 3,
June 2007, pages 331-335
10. Study of Placental Diameter and Surface Area in Normal and Hypertensive
Pregnancies.
Anatomica Karnataka, Vol-7, (3), Page 18-22 (2013) Raghavendra AY
THANK YOU