English Case

G1P0A0L0 34-35 weeks of preterm pregnancy + severe preeclamsia on

maintenance dose of MgSO4 + oligohydramnios + suspect IUGR

Andalas University

Presented by:
dr. Mila Permata Sari
Resident of Obstetrics and Gynecology

Guidance:
dr. Ferdinal Ferry, Sp.OG, Subsp. Obginsos (K)

OBSTETRICS AND GYNECOLOGY DEPARTMENT

MEDICAL FACULTY OF ANDALAS UNIVERSITY
DR. M. DJAMIL CENTRAL GENERAL HOSPITAL
PADANG
2022

i
 SPECIALIST DOCTOR EDUCATION PROGRAM
OBSTETRY AND GYNECOLOGY
FACULTY OF MEDICINE ANDALAS UNIVERSITY
DR.M.DJAMIL CENTRAL HOSPITAL PADANG

VALIDITY SHEET OF CASE PRESENTATION

Name : dr. Mila Permata Sari

Semester : II

Has Finished English Case Presentation with title :

G1P0A0L0 34-35 weeks of preterm pregnancy + severe preeclamsia on
maintenance dose of MgSO4 + oligohydramnios + suspect IUGR

Padang, 06 July 2022

Approved by : Peserta PPDS
Preceptor Obstetric and Gynecoloy Resident

dr. Ferdinal Ferry, Sp.OG, Subsp. Obginsos (K) dr. Mila Permata Sari

Known by,
Head of Obstetric and Gynecology Study Program
Medical Faculty of Andalas University/Dr.M.Djamil Central Hospital

dr. Bobby Indra Utama, SpOG, Subsp. Urogin (K)

ii
 SPECIALIST DOCTOR EDUCATION PROGRAM
OBSTETRY AND GYNECOLOGY
FACULTY OF MEDICINE ANDALAS UNIVERSITY
DR.M.DJAMIL CENTRAL HOSPITAL PADANG

REPORT OF ASSESSMENT RESULTS

Name : dr. Mila Permata Sari

Semester : II

Has finished English Case Presentation with title:

G1P0A0L0 34-35 weeks of preterm pregnancy + severe preeclamsia on
maintenance dose of MgSO4 + oligohydramnios + suspect IUGR

NO Assessment Criteria Score Explanation

1
Knowledge

2
Skills

3 Attitude

Padang, 06 July 2022

Approved by,
Preceptor

dr. Ferdinal Ferry, Sp.OG, Subsp. Obginsos (K)

iii
 TABLE OF CONTENT

VALIDITY SHEET OF CASE PRESENTATION.................................................ii

REPORT OF ASSESSMENT RESULTS..............................................................iii
TABLE OF CONTENT..........................................................................................iv
LIST OF FIGURES.................................................................................................v
LIST OF TABLES..................................................................................................vi
CHAPTER I INTRODUCTION..............................................................................1
CHAPTER II CASE REPORT................................................................................4
CHAPTER III LITERATURE REVIEW..............................................................12
3.1. Definition.................................................................................................12
3.2. Epidemiology..........................................................................................14
3.3. Etiology...................................................................................................14
3.4. Risk Factor..............................................................................................17
3.5. Classification...........................................................................................18
3.6. Pathogenesis............................................................................................20
3.7. Pathophysiology......................................................................................21
3.8. Clinical Manifestation.............................................................................23
3.9. Diagnosis.................................................................................................24
3.10. Management............................................................................................27
3.11. Complication...........................................................................................32
3.12. Prognosis.................................................................................................35
4.1 Diagnosis......................................................................................................36
4.2 Management.................................................................................................40
CHAPTER V CONCLUSION...............................................................................44
REFERENCES.......................................................................................................45

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 LIST OF FIGURES

Figure 1. Physiologic transformation of the spiral arteries, failure of physiologic

transformation, and atherosis.................................................................................15
Figure 2. Probability of preeclampsia according to pre-pregnancy body mass
index.......................................................................................................................16
Figure 3. The etiological explanations of preeclampsia........................................17
Figure 4. Schematic of the pathogenesis of preeclampsia.....................................21
Figure 5. Diagnostic Criteria for Preeclampsia......................................................26
Figure 6. Preeclampsia with Severe Features........................................................27
Figure 7. Clinical management algorithm for severe preeclampsia at <34 weeks
31 Figure 8. Effects of preeclampsia on the foetus................................................33

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 LIST OF TABLES

Table 1. Clinical Definition of Preeclampsia.........................................................13

Table 2. Risk Factors for Preeclampsia.................................................................18
Table 3 Pregnancy-Related Classification and Diagnosis.....................................19
Table 4 Indicator of Severity of Hypertension in Pregnancy.................................20
Table 5. End organ dysfunction in preeclampsia...................................................22
Table 6. Signs and symptoms of pre-eclampsia per organ system........................24
Table 7. Magnesium Sulfate Dosage Schedule for Severe Preeclampsia and
Eclampsia...............................................................................................................29
Table 8. Antihypertensive Agents Used for Urgent Blood Pressure Control in
Pregnancy...............................................................................................................30
Table 9. Adverse impact of preeclampsia on fetus and mother.............................34

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 CHAPTER I
INTRODUCTION

Hypertensive disorders are a common complication of pregnancy that put

women and their fetuses at disproportionate risk for further complications, as well
as life-long sequelae. Ranging in severity, hypertensive disorders of pregnancy
include chronic hypertension—systolic blood pressure (BP) ≥140 mm Hg or
diastolic BP ≥90 mm Hg that predates the onset of pregnancy; gestational
hypertension—hypertension diagnosed after 20 weeks gestation without
concurrent proteinuria; preeclampsia-eclampsia—classically, new-onset
hypertension with new-onset proteinuria; and chronic hyper-tension with
superimposed preeclampsia—chronic hypertension with new-onset proteinuria or
other signs/symptoms of preeclampsia after 20 weeks or chronic proteinuria with
new-onset hypertension.1 With the greatest morbidity and mortality, preeclampsia
affects 5% to 7% of all pregnant women but is responsible for over 70 000
maternal deaths and 500 000 fetal deaths worldwide every year. In the United
States, it is a leading cause of maternal death, severe maternal morbidity, maternal
intensive care admissions, cesarean section, and prematurity.2,3 Delivery can
resolve most signs and symptoms; however, preeclampsia can persist after
delivery and, in some cases, can develop de novo in the postpartum period.1,4
In spite of advances in medicine, preeclampsia and eclampsia continue to
remain leading causes of maternal and perinatal mortality and morbidity
throughout the world. Severe Preeclampsia can lead to multiple life-threatening
complications like eclampsia, cerebral haemorrhage, cardiovascular complications,
hepatic failure, acute renal failure, pulmonary oedema, ARDS (Adult Respiratory
Distress syndrome), DIC (Disseminated Intravascular Coagulation) HELLP
syndrome (Haemolysis, Elevated Liver enzymes, Low Platelet), retinal
detachment, cortical blindness, hypoxic cerebral damage and even maternal
death.5
Fetal complications are mainly due to uteroplacental insufficiency leading
to IUGR (Intrauterine Growth Restriction), low birth weight babies, IUFD
(Intrauterine Fetal death) and complications due to prematurity. There are still no

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widely accepted biochemical markers for early detection of Preeclampsia but
some maternal and pregnancy characteristics have been identified as risk factors,
these are nulliparity, previous history of preeclampsia, maternal age over 40,
multiple gestation, molar pregnancy, pregestational diabetes, vascular, endothelial
or renal diseases, maternal smoking, obesity and certain genetic factors.6
Preeclampsia has catastrophic consequences such as fetal and maternal
death. Moreover, it is tightly related to adverse perinatal outcomes including
increased cesarean section rate, low Apgar scores, prematurity, placental
abruption, HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome,
eclampsia, disseminated intravascular coagulation and increased maternal/fetal
intensive care unit requirement.7
Fetal growth restriction can be defined as an inadequate fetal growth
compared to the expected growth potential based on the estimated fetal weight
and/or abdominal Fetal growth restriction can be defined as an inadequate fetal
growth compared to the expected growth potential based on the estimated fetal
weight and/or abdominal circumference after adjusted for gestational age, race
and gender. It is related to perinatal mortality and morbidity. Furthermore, it
contributes to chronic diseases such as hypertensive disorders. In previous studies,
preeclamptic patients have increased odds of fetal growth restriction and fetal
growth restriction is claimed to be the indicator of severity of preeclampsia.8,9,10
Amniotic fluid is a liquid surrounding the fetus and providing optimal
environment for fetal development of fetal respiratory, gastrointestinal,
musculoskeletal and urinary system. Oligohydramnios can lead to fetal growth
restriction, pulmonary hypoplasia, cord compression, low Apgar scores, fetal
mortality and increased cesarean section rates. Oligohydramnios could be found
as a concomitant condition in 10–30% of preeclamptic patients with or without
fetal growth restriction.11,12
Placental insufficiency is claimed to have a key role in preeclampsia.
Similarly, fetal growth restriction could result from abnormal placentation leads to
inadequate uteroplacental blood flow.13 Another condition which arises from
placental insufficiency is oligohydramnios. Therefore, preeclampsia, fetal growth
restriction and oligohydramnios are the conditions rising from the same

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etiopathogenesis named as placental insufficiency.14 Thus, the clinical conditions
are in relationship with each other and affects adverse perinatal outcomes.
However, there are data in the literature evaluating the effect of oligohydramnios
and fetal growth restriction together in preeclampsia, there is no evidence about
the separate roles of oligohydramnios and fetal growth restriction in adverse
pregnancy outcomes in preeclampsia.15.
Based on this problem, the authors are interested in presenting cases of
preeclampsia with complications such as oligohydramnios and suspected IUGR.

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 CHAPTER II
CASE REPORT

A. Identity
Patient
Name : Mrs. N
Age : 29 years old
No. MR 163449
Address : Jr. Ampalu, Batusangkar
Occupation : Housewife
Education : Elementary school
Admission date : 16-6-2022

Husband
Name : Mr. B
Age : 30 years old
Address : Jr. Ampalu, Batusangkar
Occupation : Farmer

B. Chief Complaint
The patient came to the emergency room of Prof. Dr. MA Hanafiah SM
Batusangkar Hospital referred by polyclinic with diagnosed G1P0A0L0 34-35
weeks of preterm pregnancy + severe preeclampsia + oligohydramnios + suspect
IUGR. Previously, the patient came to Gurun Public Health Center because on the
previous pregnancy control the patient had hypertension, then the patient was
referred to polyclinic for further management.

C. Present Illness History

 Headache (-), Blurry vision (-), Epigastric pain (-)
 Pelvic pain referred to groin (-)
 Bloody show from the vagina (-)
 Fluid leakage from the vagina (-)
 Vaginal bleeding from vagina (-)
 Amenorrhea since 8.5 months ago

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 LMP: 20th October 2021. EDD: 27th July 2022
 Fetal movements have been felt since 3.5 months ago
 History early pregnancy: nausea (+) vomit (-) bleeding (-)
 Menstrual History: Menarche at 13 years old, regular cycle (28 days),
duration 4-6 days, 2-3 pad changes per day, menstrual pain (-)
 The first ANC went to the midwife when she was 2 months of pregnancy,
then the patient went to public health center every month. At the time of the
last ANC (15th June 2022) it was known that she has a hypertension. The
patient never had ANC to obstetrician.
 Shortness of breath (-), fever (-). History of contact with patients confirmed
positive for COVID-19 (-)

D. Previous Illness History

 History of heart disease, lung disease, liver disease, kidney disease, diabetes
mellitus is denied

E. Family Illness History

 There were no history of congenital, psychiatric and contagious disease

F. Obstetric History
 Marriage History : Once, at 2021
 History of pregnancy/Abortus/Labor : 1/0/0
o 1. Present
 History of Contraception : (-)
 History of immunization : (-)
 History of education : Elementary School
 History of Habits : Cigarette (-), Drugs (-), Alcohol (-)

G. Physical Examination
GA Cons BP HR RR T SpO2 Urine
Moderate CMC 160/90 94 24 36.7 98% 200cc/3 hour
(dark yellow)

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 Weight
o Before pregnancy : 60 kg
o During pregnancy : 65 kg
 Height :157 cm
 BMI : 24,3 ( normoweight)
 Head : Normocephaly
 Eyes : Conjunctiva wasn’t anaemic, sclera wasn’t
icteric
 Neck : JVP 5–2 cmH2O, there is no enlargement
in thyroid gland
 Chest : Heart and Lung : no abnormality was found
 Abdomen : Obstetrical record
 Genitalia : Obstetrical record
 Extremity : Edema -/-, Physiological reflex +/+ normal,
Pathological reflex -/-
 Obstetric Examination
Abdomen
o I : Abdomen according to preterm of pregnancy. Striae gravidarum
(+), linea mediana hyperpigmentation (+), cicatrix (-)
o L1: fundal uterine palpated between processus xyphoideus and
umbilical, A large, soft, nodular mass was palpated
o L2: Big resistance of baby was palpated on left side, small parts of
the baby was palpated on right side
o L3: A hard, round mass was palpated, not fixated
o L4: Not performed
 UFH : 27 cm
 EFW : 2170 gr
 Uterine contraction :-
 Fetal heart rate : 145- 155x/i
 Genitalia
o V/U within normal limit, vaginal bleeding (-)
o Vt : Not performed

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  Speculum Examination :
o Not performed
 CTG: 1st category

H. Supporting Examination
Laboratory Results (16/06/2022)
Hb : 13,8
Leukocyte : 17.020
Platelet : 235.000
Hematocrit : 37,4
CT : 5’30”
BT : 3’30”
SGOT 15
SGPT 14
Ur 14
Cr : 0.54
HIV : NR
HBsAg : NR
Urine Protein : -

Ultrasound Examination

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Fetal alive, singleton, intra uterine, head presentation

Fetal movement activity was good

Fetal Biometri :

BPD : 8.64 cm EFW : 1811 gram

AC : 28.05 cm FHR : 145

FL : 6.36 cm AFI : 3.27

Placenta implanted in fundus to anterior, Maturity grade II

Impression :

34-35 weeks of preterm pregnancy according fetal biometry

Fetal alive, singleton, intra uterine, head presentation, oligohydramnios

I. Diagnosis
 G1P0A0L0 34-35 weeks of preterm pregnancy + severe preeclamsia on
maintenance dose of MgSO4 + oligohydramnios + suspect IUGR
 Fetal alive, singleton, intrauterine, head presentation

J. Management
 Plan:
o Emergency CS

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  Instruction:
o Control GA, VS, FHR, impartu sign
o IVFD RL 20 + MgS04 inisial dose -> maintenance dose
o Inj Cefotaxime 2gr
o Metildopa 3x500 mg
o Nifedipin 3x10 mg
 Process
o G1P0A0L0 34-35 weeks of preterm pregnancy + Severe
preeclampsia on maintenance dose of MgSO4 + oligohydramnios +
suspect IUGR  LSCS

16-06-2022 at 16.45 LSCS was performed

Male baby was born at 16.55
BW : 2.060 gr
BL : 45 cm
A/S : 5/7

K. Post Operation Diagnose

 P1A0L1 post LSCS oi severe preeclamsia on maintenance dose of MgSO4
+ oligohidramnion + IUGR
 Mother and baby were in care

Instruction
 Control GC, VS, Vaginal Bleeding
 IVFD RL 500 cc drip oxytosine 20iu 28 tpm
 Inj. Cefotaxime 2 x 1 gr IV
 Pronalges supp if needed
 Metildopa 3x500 mg
 Nifedipin 3x10 mg
 Misoprostol 400mg / 4 hours
 Care in room obstetric
 Blood check 6 hours post operation

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L. Documentation

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M. Follow Up

S/ Post operative pain (+) Fever (-) Vaginal bleeding (-)

O/ GA Cons BP HR RR T
Mdt CM 140/80 84 20 36.7
Abd :
Operation wound closed by verband. Uterine fundal palpated 2 fingers
below umbilical, contraction (+)
Genitalia :
V/U normal. Vaginal bleeding (-)
Urine : 150 cc/hours
A/ • P1A0L1 post LSCS oi Severe preeclamsia on maintenance dose of
MgSO4 + oligohidramnion + IUGR
• Mother and baby were in care
P/ Instruction
Control GA, VS, uterine contraction, vaginal bleeding, urine output
IVFD RL 500 cc drip oxytosine 20 iu 28 tpm
Inj. Cefotaxime 2 x 1 gr IV
Pronalges supp if needed
Metildopa 3x500 mg
Nifedipin 3x10 mg
Misoprostol 400mg / 4hours
Care in room obstetric
Blood check 6 hours post operation
Follow up 2 hours post operative June 16th 2022

Post Surgery Laboratorium : 17/06/2022

Hb : 11,9 g/dL
Leuko : 22.200 g/dL
Trombo : 162.000 g/dL
Ht : 34,5%

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 CHAPTER III
LITERATURE REVIEW

3.1. Definition
Classically, the American College of Obstetrics and Gynecology (ACOG)
defines preeclampsia as the presence of hypertension and proteinuria occurring
after 20 weeks of gestation in a previously normotensive patient. However, a
significant proportion of women develop systemic manifestations of preeclampsia
—such as low platelets or elevated liver enzymes—before the hallmark of
proteinuria is detectable, resulting in delayed diagnoses. The evolving
understanding of preeclampsia as a heterogeneous hypertensive disorder of
pregnancy led to ACOG’s hypertension 2013 task force to re-vise the definition of
preeclampsia to include the presence of severe features with or without proteinuria
and to exclude degree of proteinuria as a criterion of severe features (Table 1).
These criteria were confirmed more recently in an update of the ACOG’s practice
guidelines.16,17

Although hypertension and proteinuria are considered to be the classical

criteria to diagnose preeclampsia, other criteria are also important. In this context,
it is recommended that women with gestational hypertension in the absence of
proteinuria are diagnosed with pre-eclampsia if they present with any of the
following severe features: thrombocytopenia (platelet count less than 100,000 3
109/L); impaired liver function as indicated by abnormally elevated blood
concentrations of liver enzymes (to twice the upper limit of normal con-
centration); severe persistent right upper quadrant or epi-gastric pain and not
accounted for by alternative diagnoses; renal insufficiency (serum creatinine
concentration greater than 1.1 mg/dL or a doubling of the serum creatinine
concentration in the absence of other renal disease); pulmonary edema; or new-
onset headache unresponsive to acetaminophen and not accounted for by
alternative diagnoses or visual disturbances. Gestational hypertension is defined
as a systolic blood pressure of 140 mm Hg or more or a diastolic blood pressure of
90 mm Hg or more, or both, on two occasions at least 4 hours apart after 20 weeks

1
of gestation in a woman with a previously normal blood pressure. Women with
gestational hypertension with severe range blood pressures (a systolic blood
pressure of 160 mm Hg or higher, or diastolic blood pressure of 110 mm Hg or
higher) should be diagnosed with preeclampsia with severe features.16

Table 1. Clinical Definition of Preeclampsia17

Proteinuria during pregnancy is defined as 300 mg/dL of protein or more

in a 24-hour urine collection or a protein-to-creatinine ratio of 0.30 or more.
When quantitative methods are not available or rapid decisions are required, a
urine protein dipstick reading can be substituted. However, dipstick urinalysis has
high false-positive and false-negative test results. A test result of 1+ proteinuria is
false-positive in 71% of cases com-pared with the 300 mg cutoff on 24-hour urine
collection, and even 3+ proteinuria test results may be false-positive in 7% of
cases. Using the same 24-hour urine collection standard, the false-negative rate for
dipstick urinalysis is 9%. If urinalysis is the only available means of assessing
proteinuria then overall accuracy is better using 2+ as the discriminant value.18

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3.2. Epidemiology
Hypertensive disorders of pregnancy constitute one of the leading causes
of maternal and perinatal mortality worldwide. It has been estimated that
preeclampsia complicates 2–8% of pregnancies globally. In Latin America and the
Caribbean, hypertensive disorders are responsible for almost 26% of maternal
deaths, whereas in Africa and Asia they contribute to 9% of deaths. Although
maternal mortality is much lower in high-income countries than in developing
countries, 16% of maternal deaths can be attributed to hypertensive disorders. In
the United States, the rate of preeclampsia increased by 25% between 1987 and
2004. Moreover, in comparison with women giving birth in 1980, those giving
birth in 2003 were at 6.7-fold increased risk of severe preeclampsia.16

3.3. Etiology19
1. Uteroplacental Ischemia
The following evidence supports a causal link between placental ischemia
and preeclampsia: (1) experimentally induced ischemia in several animal models
leads to hypertension and proteinuria; (2) uterine blood flow is lower in patients
with preeclampsia than in women with a normal preg-nancy; (3) placental
histopathologic lesions indicative of ischemia (often referred to as maternal
vascular malperfusion) are frequent and consis-tent findings in preeclampsia and
eclampsia; (4) failure of physiologic transformation of the spiral arteries and
atherosis are typical features of pre-eclampsia; (5) the pulsatility index of the
uterine artery (a parameter to assess resistance to flow) is higher in patients with
preeclampsia than in women with a normal pregnancy; this can be observed
during the midtrimester of pregnancy, weeks or even months before the
development of disease; (6) the maternal plasma placental growth factor (PlGF) to
sFlt-1 ratio, a noninvasive marker of lesions of maternal vascular malperfusion, is
elevated at the time of disease onset and before the development of preeclampsia;
and (7) a blockage of sFlt-1 mRNA reduces hypertension and proteinuria.16 The
frequency of placental lesions of maternal vascular malperfusion, of abnormalities
in the uterine artery Doppler, and of alterations in biomarkers (eg, PlGF/sFlt-1) is
higher in preterm preeclampsia than in term pre-eclampsia, suggesting that
ischemia plays a different role in early-onset vs late-onset preeclampsia.

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 Figure 1. Physiologic transformation of the spiral arteries, failure of physiologic
transformation, and atherosis
2. Maternal Infection
Maternal infection has been implicated in the etiology of preeclampsia
and eclampsia since the beginning of the 20th century. Albert proposed that the
“toxins” responsible for eclampsia were the product of putrefactive changes in the
uterine cavity caused by the action of bacteria (“a latent microbic endometritis”).
Indeed, the microorganism “Bacillus eclampsiae” was proposed to be the cause.
This view progressively fell out of favor because preeclampsia and eclampsia do
not present the typical features of an infectious disease (eg, fever). Nonetheless,
the idea that micro-organisms may be involved in the genesis of preeclampsia and
eclampsia recurs in the literature every few years, and it has recently reemerged
on the basis of research on the relationship between preeclampsia and periodontal
disease, urinary tract infection, SARS-CoV-2 infection, or maternal gut dysbiosis.

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Gestational diabetes mellitus, maternal obesity, and metabolic syndrome
Gestational diabetes mellitus Gestational diabetes mellitus is an
independent risk factor for preeclampsia, after adjusting for confounders. In a
retrospective study of 647,392 pregnancies, women with gestational diabetes had
an increased risk of preeclampsia. Preexisting diabetes mellitus has also been
linked to the development of preeclampsia as reported in a systematic review.
Diabetes mellitus is considered to be strongly associated with late-onset rather
than early-onset pre-eclampsia. The Hyperglycemia and Adverse Pregnancy
Outcome (HAPO) Study Cooperative Research Group reported a significant
positive association between the degree of maternal hyperglycemia and
preeclampsia.

Figure 2. Probability of preeclampsia according to pre-pregnancy body mass

index
Sleep disorders
Sleep-disordered breathing, a term encompassing obstructive sleep
apnea, snoring, periodic episodes of hypoxia, central apnea, and sleep hypopnea,
is a risk factor for preeclampsia during pregnancy. The proposed mechanisms
linking sleep disorders and preeclampsia involve intravascular inflammation and
endothelial cell dysfunction.

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 Figure 3. The etiological explanations of preeclampsia
3.4. Risk Factor
Risk factors for the development of preeclampsia have been studied
extensively (Table 2). Major risk factors include a history of preeclampsia,
chronic hypertension, pregestational diabetes mellitus, antiphospholipid syndrome,
and obesity, among others. Other risk factors include advanced maternal age,
nulliparity, history of chronic kidney disease, and use of assisted reproductive
technologies. Relatively rare risk factors are a family history of preeclampsia and
mother carrying a trisomy 13 fetus. Genetic susceptibility to preeclampsia has
been extensively studied. A 2017 genome-wide association study analysis of
neonates from 4380 cases of preeclampsia and 310 238 controls found a genome-
wide susceptibility locus (rs4769613; P=5.4×10−11) near the FLT1 (FMS-like
tyrosine kinase 1) gene, the protein product of which is a well-established
pathogenetic factor in preeclampsia. rs4769613 has a higher frequency in late-
onset preeclampsia, exerts effects only in the fetal—not maternal—genome, and
has no difference in transmission of disease association with parental sex

1
inheritance, making the effects of imprinting unlikely. However, maternal genetic
susceptibility may play a role as well. A multiethnic maternal preeclampsia
genome-wide association study discovered a genome-wide susceptibility locus at
rs9478812 (P=5.90×10−7), an intronic region of protein PLEKHGI im-plicated in
BP regulation.

Table 2. Risk Factors for Preeclampsia

3.5. Classification
The hypertension classification has a major importance for the study of all
of the aspects of hypertension disease in pregnancy. In the literature there is a
large number of hypertension HBT classifications, both on the part of national and
on the part of various international associations. The confusion significantly slows
down the basic research in PE aetiology and pathophysiology and also impacts the

1
recommendations and prevention protocols as well as the treatment of the
hypertension disease in pregnancy. Since 2013, after a guide was published by the
ACOG workgroup (American College of Obstetricians and Gynaecologists), there
has been a tendency of wider implementation of new diagnostic criteria into
national guides also of other countries and associations. This classification
basically and primarily leans on the new understanding of PE pathophysiology
and also to extensive epidemiological studies. The ACOG hypertension
classification has the tendency to be simple, precise and easy for clinical
application. According to this classification, hypertension can be divided into four
basic groups:20
1. Pre-eclampsia/eclampsia
2. Chronic hypertension
3. Chronic hypertension with superimposed pre-eclampsia
4. Gestational hypertension
Table 3 Pregnancy-Related Classification and Diagnosis21

1
Table 4 Indicator of Severity of Hypertension in Pregnancy21

3.6. Pathogenesis17
A placental disease, preeclampsia progresses in 2 stages: (1) abnormal
placentation early in the first trimester followed by (2) a “maternal syndrome in
the later second and third trimesters characterized by an excess of antiangiogenic
factors (Figure 6). While the mechanism of abnormal placentation is controversial,
animal models have demonstrated that uteroplacental ischemia drives the
hypertensive, multi-organ failure response observed in the maternal preeclamptic
syndrome(stage 2). A number of theories have been proposed for the placental
dysfunction observed in stage 1, including oxidative stress, abnormal natural killer
cells (NKs) at the maternal-fetal interface, and genetic and environmental factors,
though none have conclusive evidence in humans. However, substantive evidence
supports the idea that the diseased placenta leads to release of soluble toxic factors

2
in the maternal circulation that result in inflammation, endothelial dysfunction,
and maternal systemic disease.

Figure 4. Schematic of the pathogenesis of preeclampsia.

Genetic factors, immunologic factors, other maternal factors cause placental dysfunction which in
turn leads to the release of antiangiogenic factors (such as sFLT1 [soluble fms-like tyrosine
kinase 1] and sENG [soluble endoglin]) and other inflammatory mediators to induce
preeclampsia.

3.7. Pathophysiology22
A The exact pathophysiology of preeclampsia remains unknown. However,
there are several theories that have been put forth that may explain most of the
abnormalities seen in this disease process.
1. Abnormal placentation
Preeclampsia is primarily a disease of the placenta as it may be encountered
in molar pregnancies. One of the most accepted theories in preeclampsia revolves
around abnormal placentation. In normal pregnancies, trophoblast begins invasion
into the myometrial blood vessels by remodeling the maternal spiral arteries,
transforming them from small, muscular, higher resistance arterioles into large
caliber arteries with high capacitance and free flow of blood. Remodeling
typically begins in the late first trimester and is completed by 18-20 weeks of
gestation. Failure of this process of complete remodeling leads to persistence of
high resistance spiral arteries that impede placental perfusion thereby leading to a
state of "relative hypoxemia" which culminates into maternal endothelial cell

2
dysfunction. Maternal systemic endothelial cell dysfunction manifests in signs and
symptoms that are reflective of maternal vasoconstriction and multi-organ damage
outlined in Table 5. Placental hypo perfusion is both a cause and effect of
abnormal Placentation that becomes more pronounced with growing needs of the
feto-placental unit as pregnancy progresses. Late pathologic changes that are seen
in the placental tissue correlate with ischemia including atherosis, fibrinoid
necrosis, thrombosis, sclerosis of the arterioles, and infarction.
Table 5. End organ dysfunction in preeclampsia.

2. Immunologic factors
Preeclampsia tends to affect the first pregnancy (naïve to the paternal/fetal
antigens) and repeat exposure to paternal/fetal antigens tends to lower the risk of
the disease. Additionally, other situations that limit exposure to paternal antigens
such as a new partner in a subsequent pregnancy and long inter-pregnancy
intervals, use barrier contraception, or conception through artificial insemination
lead to a higher risk of preeclampsia. It is also known that women who conceive
through egg donation have more than double the risk of preeclampsia than other
forms of assisted reproduction. Pregnancies conceived through assisted
reproductive techniques had a four-fold increase in preeclampsia compared to
naturally conceived pregnancies. Abnormalities seen in preeclampsia are similar
to those seen in graft versus host disease. The interaction between the extra villous
trophoblast antigens and the natural killer cells dictates placental implantation. In
preeclampsia abnormal placental implantation is thought to be due to the
increased NK cell activity due to the conflict between the maternal and paternal
genes. This may partly be mediated through the dendritic cell activity as increased
dendritic cell infiltration is seen in placental bed biopsies in preeclampsia.

2
3. Inflammation and/or infection
Signs of inflammation are seen in normal pregnancies at term, but these
changes are exaggerated in women with preeclampsia. It is thought that debris of
the outer layer of trophoblast contributes to maternal inflammation and some
features of the syndrome. Placental DNA released into the circulation of the
mother and the fetus (maternal circulation) could have a role in the characteristic
inflammation involved with preeclampsia. In studies that looked at the connection
between maternal infection and preeclampsia, it was found that the risk of
preeclampsia was increased in women with urinary tract infection and periodontal
disease.
4. Genetic factors
Genetic factors are thought to have a role in getting the disease.
Observations that suggest this are that women who are pregnant for the first time
and have a family history of preeclampsia have a higher risk of getting it than
women who are pregnant for the first time and do not have a family history of
preeclampsia [20]. The risk of preeclampsia is significantly increased in women
who previously had preeclampsia. The partners of men who whose mothers had
preeclampsia are more likely to get preeclampsia. A woman who gets pregnant by
a man whose previous spouse had preeclampsia is at a higher risk of the disease.
Most of the data suggests that the mother's and father's genes have a role in the
defective formation of the placenta and subsequent preeclampsia.
To summarize, placental hypoxia and ischemia are the ultimate pathways in
the pathogenesis of preeclampsia by release of vasoactive factors into the maternal
circulation and endothelial cell dysfunction leading to the signs and symptoms of
preeclampsia.

3.8. Clinical Manifestation

A Pre-eclampsia is a multisystemic disease characterized by the
development of hypertension after 20 weeks of gestation in a previously
normotensive woman, with the presence of proteinuria or, in its absence, of signs
or symptoms indicative of target organ injury. The clinical signs involve multiple
organs, including the liver, kidneys, heart, lungs, brain, and pancreas (Table 6).

2
These complications can result in maternal and fetal adverse outcomes that can
lead to intrauterine growth restriction, placental hypoperfusion, premature
placental disruption or, in most serious situations, termination of pregnancy and
fetal and maternal death. This disease can be divided into mild and severe forms,
according to the severity and type of the symptoms presented. The mild form of
pre-eclampsia is characterized by systolic blood pressure (SBP) ≥140 mmHg or
diastolic blood pressure (DBP) ≥90 mmHg, and proteinuria >300 mg/24 h. The
severe form of pre-eclampsia is characterized by severe hypertension (SBP > 160
mmHg or DBP > 110 mmHg), or severe proteinuria (>2 g/24 h), or signs and
symptoms of target organ damage. Women with severe pre-eclampsia may
present headaches, visual disturbances (including blindness), epigastric pain,
nausea and vomits, hepatic and renal insufficiency, and pulmonary edema.23

Table 6. Signs and symptoms of pre-eclampsia per organ system

3.9. Diagnosis
A Preeclampsia is a disorder of pregnancy associated with new-onset
hypertension, which occurs most often after 20 weeks of gestation and frequently
near term. Although often accompanied by new-onset proteinuria, hypertension
and other signs or symptoms of preeclampsia may present in some women in the
absence of proteinuria. Reliance on maternal symptoms may be occasionally
problematic in clinical practice. Right upper quadrant or epigastric pain is thought

2
to be due to periportal and focal parenchymal necrosis, hepatic cell edema, or
Glisson’s capsule distension, or a combination. However, there is not always a
good correlation between the hepatic histopathology and laboratory abnormalities.
Similarly, studies have found that using headache as a diagnostic criterion for
preeclampsia with severe features is unreliable and nonspecific. Thus, an astute
and circumspect diagnostic approach is required when other corroborating signs
and symptoms indicative of severe preeclampsia are missing. Of note, in the
setting of a clinical presentation similar to preeclampsia, but at gestational ages
earlier than 20 weeks, alternative diagnoses should to be considered, including but
not limited to thrombotic thrombocytopenic purpura, hemolytic–uremic syndrome,
molar pregnancy, renal disease or autoimmune disease. Although hypertension
and proteinuria are considered to be the classical criteria to diagnose preeclampsia,
other criteria are also important. In this context, it is recommended that women
with gestational hypertension in the absence of proteinuria are diagnosed with
preeclampsia if they present with any of the following severe features:
thrombocytopenia (platelet count less than 100,000 3 109/L); impaired liver
function as indicated by abnormally elevated blood concentrations of liver
enzymes (to twice the upper limit of normal concentration); severe persistent right
upper quadrant or epigastric pain and not accounted for by alternative diagnoses;
renal insufficiency (serum creatinine concentration greater than 1.1 mg/dL or a
doubling of the serum creatinine concentration in the absence of other renal
disease); pulmonary edema; or new-onset headache unresponsive to
acetaminophen and not accounted for by alternative diagnoses or visual
disturbances (figure 7). Gestational hypertension is defined as a systolic blood
pressure of 140 mm Hg or more or a diastolic blood pressure of 90 mm Hg or
more, or both, on two occasions at least 4 hours apart after 20 weeks of gestation
in a woman with a previously normal blood pressure. Women with gestational
hypertension with severe range blood pressures (a systolic blood pressure of 160
mm Hg or higher, or diastolic blood pressure of 110 mm Hg or higher) should be
diagnosed with preeclampsia with severe features. These severe ranges of blood
pressure or any of the severe features listed in Box 3 increase the risk of morbidity
and mortality.16

2
 Figure 5. Diagnostic Criteria for Preeclampsia
Proteinuria during pregnancy is defined as 300 mg/ dL of protein or more in
a 24-hour urine collection or a protein -to-creatinine ratio of 0.30 or more. When
quantitative methods are not available or rapid decisions are required, a urine
protein dipstick reading can be substituted. However, dipstick urinalysis has high
false–positive and false–negative test results. A test result of 1+ proteinuria is
false–positive in 71% of cases compared with the 300 mg cutoff on 24-hour urine
collection, and even 3+ proteinuria test results may be false– positive in 7% of
cases. Using the same 24-hour urine collection standard, the false–negative rate
for dipstick urinalysis is 9%. If urinalysis is the only available means of assessing
proteinuria then overall accuracy is better using 2+ as the discriminant value.16

2
 Figure 6. Preeclampsia with Severe Features

3.10. Management
Management of preeclampsia begins with early diagnosis and intervention,
focusing on adequate blood pressure control and seizure prevention. Fetal
evaluation should also include ultrasonography of amniotic fluid index, estimated
fetal weight, and antenatal testing, such as non-stress tests and biophysical
profiles. Fetal status may also play a major role in determining delivery versus
expectant management in preeclamptic patients.24
Ultimately, the definitive treatment of preeclampsia is the delivery of the
fetus. While continued observation is permissible for preterm gestations in
patients with either well-controlled gestational hypertension or preeclampsia
without severe features in the setting of normal antepartum testing, risks of
expectant management exist. If expectant management is undertaken in stable
patients, serial ultrasonography, weekly antepartum testing, and close observation
of symptoms and blood pressure and laboratory values should be employed. As
per ACOG, it is recommended that patients at 37 0/7 weeks gestation diagnosed
with gestational hypertension or preeclampsia without severe features should
undergo delivery rather than expectant management.24

2
 It is also recommended that patients diagnosed with preeclampsia with
severe features at or beyond 34 0/7 weeks gestation undergo delivery after
maternal stabilization and should not be delayed to accommodate steroid
administration. In cases where patients less than 34 0/7 weeks gestation are
diagnosed with preeclampsia with severe features, proper stabilization of both
maternal and fetal well-being should be initiated and may be followed with
expectant management.24
While neonatal and maternal outcomes may benefit from delivery or
expectant management, informed decision-making regarding benefits and risks
must be discussed with the patient. Antepartum admission with close monitoring
of maternal and fetal conditions may be employed with a low threshold for
delivery if maternal or fetal deterioration is suspected. Findings that indicate
expeditious delivery after stabilization regardless of gestational age can be
described as fetal and maternal factors.24

3.10.1 Seizure Prophylaxis

The prevention of eclampsia is empirically based on the concept of timely
delivery, as previously discussed, once preeclampsia has been diagnosed. A
significant body of evidence attests to the efficacy of magnesium sulfate to
prevent seizures in women with preeclampsia with severe features and eclampsia.
Magnesium sulfate is more effective than phenytoin, diazepam, or nimodipine (a
calcium-channel blocker used in clinical neurology to reduce cerebral vasospasm)
in reducing eclampsia and should be considered the drug of choice in the
prevention of eclampsia in the intrapartum and postpartum periods.
Benzodiazepines and phenytoin are justified only in the context of antiepileptic
treatment or when magnesium sulfate is contraindicated or unavailable
(myasthenia gravis, hypocalcemia, moderate-to-severe renal failure, cardiac
ischemia, heart block, or myocarditis).25

This parenterally administered agent is an effective anticonvulsant and

avoids producing central nervous system depression. It may be given
intravenously by continuous infusion or intramuscularly by intermittent injection.
A third option is intermittent, intravenous, 2-g injections. Dosages for severe

2
preeclampsia mirror those for eclampsia. Because labor and delivery is a more
likely time for seizures to develop, women with severe preeclampsia or eclampsia
usually are given magnesium sulfate during labor and for 24 hours postpartum. In
the United States, magnesium sulfate is almost universally administered
intravenously. Of concern, magnesium sulfate solutions, although inexpensive to
prepare, are not readily available in all parts of the developing world. Even if
solutions are available, the technology to infuse them may not be. Thus, the drug
can be administered intramuscularly, and this is as effective as intravenous
infusion.25

Table 7. Magnesium Sulfate Dosage Schedule for Severe Preeclampsia and

Eclampsia21

3.10.2 Antihypertensive Approach: Drugs and Thresholds for Treatment

The objectives of treating severe hypertension are to prevent congestive
heart failure, myocardial ischemia, renal injury or failure, and ischemic or
hemorrhagic stroke. Antihypertensive treatment should be initiated expeditiously
for acute-onset severe hypertension (systolic blood pressure of 160 mm Hg or
more or diastolic blood pressure of 110 mm Hg or more, or both) that is
confirmed as persistent (15 minutes or more). The available literature suggests
that antihypertensive agents should be administered within 30–60 minutes.
However, it is recommended to administer antihypertensive therapy as soon as
reasonably possible after the criteria for acuteonset severe hypertension are met.

2
Intravenous hydralazine or labetalol and oral nifedipine are the three agents most
commonly used for this.25

Table 8. Antihypertensive Agents Used for Urgent Blood Pressure Control in

Pregnancy25

3.10.3 Delivery
Delivery remains the ultimate treatment for preeclampsia. Although
maternal and fetal risks must be weighed in determining the timing of delivery,
clear indications for delivery exist. When possible, vaginal delivery is preferable
to avoid the added physiologic stressors of cesarean delivery. If cesarean delivery
must be used, regional anesthesia is preferred because it carries less maternal risk.
In the presence of coagulopathy, use of regional anesthesia generally is
contraindicated. Women with preeclampsia and preterm pregnancy can be
observed on an outpatient basis, with frequent assessment of maternal and fetal
well-being. Women who are noncompliant, who do not have ready access to
medical care, or who have progressive or severe preeclampsia should be
hospitalized. Women whose pregnancy is remote from term should be cared for in
a tertiary care setting or in consultation with an obstetrician or family physician
who is experienced in the management of high-risk pregnancies.25
Indications for delivery in Preeclampsia:

3
 1. Fetal indications
 Severe intrauterine growth restriction
 Nonreassuring fetal surveillance
 Oligohydramnios
2. Maternal indications
 Gestational age of 38 weeks or greater*
 Platelet count below 100 × 103 per mm3 (100 × 109 per L)
 Progressive deterioration of hepatic function
 Progressive deterioration of renal function
 Suspected placental abruption
 Persistent severe headache or visual changes
 Persistent severe epigastric pain, nausea, or vomiting
 Eclampsia

Figure 7. Clinical management algorithm for severe preeclampsia at <34 weeks21

3
3.11. Complication
Preeclampsia (PE) is a profound complication of pregnancy, where it affects
3–8% of all pregnancies and dramatically increases the risk of all-cause mortality,
especially in women who experienced early, severe, preterm episode.
Preeclampsia negatively affects both the mother and fetus. Concerning the latter,
preeclampsia may cause intra-uterine fetal growth restriction (IUGR), placental
abruption, preterm delivery and associated complications including, neonatal
respiratory distress syndrome, cerebral palsy, necrotizing enterocolitis retinopathy
of prematurity and even perinatal death. Besides its deleterious impact on the
fetus, preeclampsia also affects the pregnant woman, where it is associated with
hypertension, kidney damage, liver injury/failure, central nervous system (CNS)
damage, stroke, cardiomyopathy, pulmonary edema, adult respiratory distress
syndrome, and even death. Actually, preeclampsia is responsible for more than
60,000 maternal deaths annually worldwide, placing it as the third cause of
maternal mortality after bleeding and embolism. Higher mortality rate was
observed when preeclampsia is associated with HELLP (hemolysis, elevated liver
enzymes, low platelets), syndrome liver hemorrhage or rupture, acute kidney
injury (AKI), oliguria, disseminated intravascular coagulation (DIC), and
pulmonary edema. Preeclampsia is of special relevance in the developing
countries, where the maternal mortality is ~15% compared with 0–1.8% in the
developed countries. This difference is largely attributed to inadequate perinatal
care in poor regions of the world, and subsequently missing timely detection of
hypertension, generalized or local edema, and proteinuria to detect preeclampsia
at early stages.26

3
 Figure 8. Effects of preeclampsia on the foetus27

Placental perfusion is decreased in preeclampsia, and the primary

consequences are intrauterine growth restriction of the fetus and oligohydramnios.
Perinatal death is primarily related to premature delivery, placental abruption, and
intrauterine asphyxia.22 Placental insufficiency is claimed to have a key role in
preeclampsia. Similarly, fetal growth restriction could result from abnormal
placentation leads to inadequate uteroplacental blood flow. Another condition
which arises from placental insufficiency is oligohydramnios. Therefore,
preeclampsia, fetal growth restriction and oligohydramnios are the conditions
rising from the same etiopathogenesis named as placental insufficiency. Thus, the
clinical conditions are in relationship with each other and affects adverse perinatal
outcomes. However, there are data in the literature evaluating the effect of
oligohydramnios and fetal growth restriction together in preeclampsia, there is no
evidence about the separate roles of oligohydramnios and fetal growth restriction
in adverse pregnancy outcomes in preeclampsia.15

Oligohydramnios, can be found in otherwise uncomplicated pregnancies or

as an additional finding in 10%-30% of preeclamptic pregnancies with or without
fetal growth restriction (FGR). The common belief was that a fetus with
oligohydramnios is suffering from utero-placental insufficiency, requiring a

3
preferential shunting of blood flow away from nonessential organs such as the
kidneys thus decreasing renal blood flow and urine output. Placental vascular
abnormalities at the fetal, maternal or at both maternal and fetal compartments is
considered the common pathway mechanism in pregnancy complications such as
FGR, preeclampsia as well as oligohydramnios. Particularly, at the maternal
compartment, failure of deep placentation has been associated with preeclampsia,
FGR and preterm labor.15

IUGR, or failure to reach one’s birth potential, is one of the most common
complications during pregnancy and generally results from placental insufficiency.
IUGR is generally not recognized before delivery, and treatment options for
IUGR are limited, with early delivery being the most common. Preeclampsia is
often a contributory cause of IUGR, and numerous studies indicate that
individuals exposed to a preeclamptic pregnancy exhibit a higher body mass index
and blood pressure during childhood and adult life. Individuals born with IUGR
also demonstrate an increase in blood pressure later in life. This association forms
the basis for the developmental origins of health and disease and indicates that
adverse influences during fetal life that slow fetal growth program an individual
for greater cardiovascular risk in later life.15

Table 9. Adverse impact of preeclampsia on fetus and mother

3
3.12. Prognosis
A Early diagnosis, timely medical intervention, and appropriate maternal
and fetal surveillance significantly improve maternal and fetal outcomes. As
preeclampsia continues to be responsible for up to a quarter of maternal deaths in
certain ethnic backgrounds (the Caribbean and Latin American population,
followed by Asian and African populations), prompt care and routine monitoring
decrease morbidity and mortality.24

3
 CHAPTER IV
DISCUSSION

4.1 Diagnosis
A 29 years old woman was admitted to the emergency room of Prof. Dr.
MA Hanafiah SM Batusangkar Hospital, June 16 th 2022, referred by polyclinic
with diagnosed G1P0A0L0 34-35 weeks of preterm pregnancy + severe
preeclampsia + oligohydramnios + suspect IUGR. This diagnose was based on :

a. Anamnesis
Patient has came with first pregnancy and no abortion history. Last
menstrual period on 2nd October 2021 and amenorrhea since 8.5 months ago.
Based on the last menstrual period, gestational age was 34-35 weeks. Previously,
the patient came to Gurun Public Health Center because on the previous
pregnancy control, the patient had hypertension, then the patient was referred to
polyclinic of Prof. Dr. MA Hanafiah SM Batusangkar Hospital for further
management. The patient did not complain of headache, blurred vision and
epigastric pain. Previous history of hypertension was denied.
b. Physical Examination
Examination of vital sign obtained blood pressure 160/90 mmHg, pulse 94
x/min, RR 24 x/min, temperature 36,7o C. Urine output 200cc/3 hour (dark
yellow). Physical examination of head, neck, chest and extremity was normal.
Uterine fundal height was 27 cm, fundal uterine palpated between processus
xyphoideus and umbilical. Estimated fetal weight was 1811 grams. Fetal heart
rate was 145-155 x/minute. The patient only found out about high blood pressure
at 35 weeks of gestation. According to the ACOG diagnostic guidelines, the
criteria for preeclampsia include systolic blood pressure of 140 mm Hg or more or
diastolic blood pressure of 90 mm Hg or more on two occasions at least 4 hours
apart after 20 weeks of gestation in a woman with a previously normal blood.
pressure and proteinuria or in the absence of proteinuria, new-onset hypertension
with the new onset of any of the following : thrombocytopenia, Renal
insufficiency, impaired liver function, pulmonary edema or new-onset headache

3
 unresponsive to medication and not accounted for by alternative diagnoses or
visual symptoms. In this patient found according to the criteria, then preeclampsia
can be established.28
c. Supporting examination
Impression of Ultrasound examination were 34-35 weeks of preterm
pregnancy according fetal biometry and fetal alive, singleton, intra uterine, head
presentation, oligohydramnios (AFI : 3,27).

Preeclampsia is a disorder of pregnancy associated with new-onset

hypertension, which occurs most often after 20 weeks of gestation. Although
often accompanied by new-onset proteinuria, hypertension and other signs or
symptoms of preeclampsia may present in some women in the absence of
proteinuria. Although hypertension and proteinuria are considered to be the
classical criteria to diagnose preeclampsia, other criteria are also important. In this
context, it is recommended that women with gestational hypertension in the
absence of proteinuria are diagnosed with preeclampsia if they present with any of
the following severe features: thrombocytopenia (platelet count less than 100,000);
impaired liver function as indicated by abnormally elevated blood concentrations
of liver enzymes (to twice the upper limit of normal concentration); severe
persistent right upper quadrant or epigastric pain and not accounted for by
alternative diagnoses; renal insufficiency (serum creatinine concentration greater
than 1.1 mg/dL or a doubling of the serum creatinine concentration in the absence
of other renal disease); pulmonary edema; or new-onset headache unresponsive to
acetaminophen and not accounted for by alternative diagnoses or visual
disturbances.28

Gestational hypertension is defined as a systolic blood pressure of 140 mm Hg

or more or a diastolic blood pressure of 90 mm Hg or more, or both, on two
occasions at least 4 hours apart after 20 weeks of gestation in a woman with a
previously normal blood pressure. Women with gestational hypertension with
severe range blood pressures (a systolic blood pressure of 160 mm Hg or higher,
or diastolic blood pressure of 110 mm Hg or higher) should be diagnosed with
preeclampsia with severe features.28

3
 Preeclampsia complicates approximately 6-10% of all pregnancies.
Further rise in the rate of this syndrome is expected following the increasing rates
of advanced maternal age, obesity, and multiple gestations.29

Oligohydramnios is a relatively common complication of pregnancy and

such case is often encounter in clinical practice. It refers to amniotic fluid volume
that is less than expected for gestational age. It is typically diagnosed by
ultrasound examination and may be described qualitatively (e.g, normal,reduced)
or quantitatively (e.g, amniotic fluid index [AFI] <5).

Oligohydramnios is often to describe pregnancies with AFI <5 cm and

borderline/ low normal amniotic fluid volume to describe pregnancies with AFI 5
to 8 cm. Alternatively, some clinicians prefer the single vertical pocket (SVP)
with severe oligohydramnios defined as SVP less than 1 cm and mild
oligohydramnios defined as SVP 1 to 2 cm. An adequate volume of amniotic fluid
is critical to allow normal fetal movement and growth, and to cushion the fetus
and umbilical cord. Oligohydramnios may inhibit these processes and can lead to
fetal deformation, umbilical cord compression and death.30 In this case, an AFI
3.27 was found according to the criteria for oligohydramnios. According to a
study conducted by Ozgen, oligohydramnios is caused by utero-placental
insufficiency, requiring a preferential shunting of blood flow away from
nonessential organs such as the kidneys thus decreasing renal blood flow and
urine output. Placental vascular abnormalities at the fetal, maternal or at both
maternal and fetal compartments is considered the common pathway mechanism
in pregnancy complications such as FGR, preeclampsia as well as
oligohydramnios. Especially, at the maternal compartment, failure of deep
placentation has been associated with preeclampsia, FGR and preterm labor.15

Oligohydramnios, can be found in otherwise uncomplicated pregnancies

or as an additional finding in 10%-30% of preeclamptic pregnancies with or
without fetal growth restriction (FGR). The common belief was that a fetus with
oligohydramnios is suffering from utero-placental insufficiency, requiring a
preferential shunting of blood flow away from nonessential organs such as the
kidneys thus decreasing renal blood flow and urine output. Placental vascular

3
abnormalities at the fetal, maternal or at both maternal and fetal compartments is
considered the common pathway mechanism in pregnancy complications such as
FGR, preeclampsia as well as oligohydramnios. Particularly, at the maternal
compartment, failure of deep placentation has been associated with preeclampsia,
FGR and preterm labor. Interpretation of the clinical significance of
oligohydramnios in women with preterm preeclampsia is under debate. Sibai et al
consider parturients with preterm severe preeclampsia, oligohydramnios or
oligohydramnios and growth restriction poor candidates for expectant
management beyond completion of antenatal corticosteroid therapy, due to the
increased risk of adverse outcomes including perinatal death. Our results indicate
that oligohydramnios and gestational age are independent risk factors for early
neonatal morbidity in preterm preeclampic patients. AFI < 5 cm can be used as
one component in the educated decision for delivery of these patients.29

IUGR is a common cause of iatrogenic prematurity, as a manifestation of

ischemic placental disease—a syndrome of placental insufficiency found in
several pregnancies terminated prematurely due to fetal conditions. IUGR is
diagnosed when ultrasound-estimated fetal weight is below the 10th percentile for
gestational age. Small for gestational age (SGA) is another term that defines a
fetus with an estimated weight below the 10th percentile; however, the term SGA
does not imply a pathological condition causing low fetal weight. Approximately
70 % of SGA fetuses are constitutionally small, meaning they are small but
healthy. The remaining are fetuses with IUGR, which are at high risk for perinatal
complications and therefore require more intensive surveillance. In this case, the
baby's weight on ultrasound examination was 1811 grams, according to the IUGR
criteria.31

Causes of intrauterine growth restriction (IUGR) are generally classified

as maternal, fetal, or placental. Impaired fetal growth not only results in elevated
risk for short-term complications, with intrauterine fetal death being the most
severe, but low birth weight also predisposes the child to cardiovascular disease.31

The etiology, the degree of IUGR, the time of its initiation and the time of
delivery, determine the management needs and the long term prognosis. Perinatal

3
asphyxia, meconium aspiration, hypoglycemia, polycythemia, pulmonary
hypertension, anoxic ischemic encephalopathy and NEC are the most significant
early neonatal complications. They require prompt recognition and therapy. The
long term prognosis of IUGR children varies considerably because of their
heterogenicity.32

Based on the literature, the diagnosis in this case was appropriate.

4.2 Management
On 16th June 2022 patient was diagnosed with G1P0A0L0 34-35 weeks of
preterm pregnancy + severe preeclampsia + oligohydramnios + suspect IUGR.
Patient was planned for emergency section caesarea. Definitive treatment of
preeclampsia is the delivery of the fetus.28

Management of preeclampsia begins with early diagnosis and intervention,

focusing on adequate blood pressure control and seizure prevention. At the initial
evaluation, a complete blood count with platelet estimate, serum creatinine, LDH,
AST, ALT, and testing for proteinuria should be obtained in parallel with a
comprehensive clinical maternal and fetal evaluation. Fetal evaluation should
include ultrasonographic evaluation for estimated fetal weight and amount of
amniotic fluid, as well as fetal antepartum testing. Subsequent management will
depend on the results of the evaluation and gestational age. The decision to deliver
must balance the maternal and fetal risks.

Continued observation is appropriate for a woman with a preterm fetus if

she has gestational hypertension or preeclampsia without severe features.
Continued monitoring of women with gestational hypertension or preeclampsia
without severe features consists of serial ultrasonography to determine fetal
growth, weekly antepartum testing, close monitoring of blood pressure, and
weekly laboratory tests for preeclampsia.

The prevention of eclampsia is empirically based on the concept of timely

delivery. A significant body of evidence attests to the efficacy of magnesium
sulfate to prevent seizures in women with preeclampsia with severe features and
eclampsia. Magnesium sulfate is more effective than phenytoin, diazepam, or

4
nimodipine in reducing eclampsia and should be considered the drug of choice in
the prevention of eclampsia in the intrapartum and postpartum periods. Women
with severe preeclampsia or eclampsia usually are given magnesium sulfate
during labor and for 24 hours postpartum.25

The available literature suggests that antihypertensive agents should be

administered within 30–60 minutes. However, it is recommended to administer
antihypertensive therapy as soon as reasonably possible after the criteria for
acuteonset severe hypertension are met. Intravenous hydralazine or labetalol and
oral nifedipine are the three agents most commonly used for this.25

The patient was given 4-6 g loading dose of MgSO4 diluted in 100 ml of
IV fluid administered over 15-20 minutes. For the blood pressure lowering
regimen, Methyldopa 3x500 mg and Nifedipine 3x10 mg were given.

Preeclampsia without severe features, the balance should be in favor of

continued monitoring until delivery at 37 0/7 weeks of gestation in the absence of
abnormal antepartum testing, preterm labor, preterm prelabor rupture of
membranes or vaginal bleeding.

The risks associated with expectant management in the late preterm period
include the development of severe hypertension, eclampsia, HELLP syndrome,
placental abruption, fetal growth restriction and fetal death; however, these risks
are small and counterbalanced by the increased rates of admission to the neonatal
intensive care unit, neonatal respiratory complications and neonatal death that
would be associated with delivery before 37 0/7 weeks of gestation.28

Preeclampsia with severe features can result in acute and long-term

complications for the woman and her newborn. Maternal complications include
pulmonary edema, myocardial infarction, stroke, acute respiratory distress
syndrome, coagulopathy, renal failure, and retinal injury. The clinical course of
preeclampsia with severe features is characterized by progressive deterioration of
maternal and fetal condition. Therefore, delivery is recommended when
gestational hypertension or preeclampsia with severe features is diagnosed at or
beyond 34 0/ 7 weeks of gestation, after maternal stabilization or with labor or

4
prelabor rupture of membranes. Delivery should not be delayed for the
administration of steroids in the late preterm period.

In women with preeclampsia with severe features at less than 34 0/7 weeks
of gestation, with stable maternal and fetal condition, expectant management may
be considered. If delivery is indicated at less than 34 0/7 weeks of gestation,
administration of corticosteroids for fetal lung maturation is recommended,
however, delaying delivery for optimal corticosteroid exposure may not always be
advisable.28

Antenatal care (ANC) is a key strategy for reducing maternal and neonatal
morbidity and mortality rates because adequate utilization of antenatal health care
services is associated with improved maternal and neonatal health outcomes.
Three main reasons have been advanced to explain the importance of ANC for
pregnant women: promotion of health during pregnancy through counseling and
educational activities, screening, identification and referral of women with risk
factors; and health monitoring throughout pregnancy. Women with irregular
antenatal care attendance are much more prone to pregnancy complications such
as preeclampsia, eclampsia and anemia besides higher adverse birth outcomes
including preterm birth, intrauterine growth retardation, low birth weight and
stillbirth.33

IUGR in preeclampsia is 3 to 4 times more than normal. Even in some

studies, preeclampsia is considered as a factor for the occurrence of IUGR.
Preeclampsia is divided into two categories: early- and late-onset preeclampsias.
Lateonset preeclampsia is occurred at 34 weeks of gestation and is accompanied
by normal fetal development. Early-onset preeclampsia occurs before the 34th
week of gestation and is characterized by IUGR.34

Major risk factors include a history of preeclampsia, chronic hypertension,

pregestational diabetes mellitus, antiphospholipid syndrome, and obesity, among
others. Other risk factors include advanced maternal age, nulliparity, history of
chronic kidney disease, and use of assisted reproductive technologies. Relatively
rare risk factors are a family history of preeclampsia and mother carrying a
trisomy 13 fetus. This was the patient's first pregnancy.20 Ten percent of

4
primiparous women with pre-eclampsia delivered before 34 weeks of gestation.
The risk of such severe pre-eclampsia was 0.42% in the first pregnancy and
0.14% in later pregnancies.35

Suggestions for this patient, regular antenatal care including to the

obstetrician in the next pregnancy because of the high risk of severe preeclampsia
again. Aspirin is effective in secondary prevention of preeclampsia mainly in
patients with a history of preeclampsia. low doses of aspirin are effective in
secondary prevention of preeclampsia in high-risk patients, mainly those with a
history of preeclampsia. Aspirin inhibits thromboxane A2 production by platelets
and so increases the prostacyclin/TXA2 ratio and reduces platelet aggregation. It
also decreases production of the tissue factor thrombin. Aspirin should be
administered once a day in the evening at low doses ranging from 80 to 150 mg.
Aspirin in the prevention of preeclampsia in high-risk patients showed that low-
dose aspirin (60–160 mg) reduced the risk of preeclampsia by 15%. The effect of
low-dose aspirin on preeclampsia and its complications was consistent, regardless
of whether treatment is started before or after 16 weeks of gestation.36

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 CHAPTER V
CONCLUSION

1. The American College of Obstetrics and Gynecology (ACOG) defines

preeclampsia as the presence of hypertension and proteinuria occurring
after 20 weeks of gestation in a previously normotensive patient.
2. Management of preeclampsia begins with early diagnosis and intervention,
focusing on adequate blood pressure control and seizure prevention.
3. In this case, the patient was diagnosed with severe peeclampsia. The way
to establish the diagnosis and treatment of the patient was correct.
4. Placental perfusion is decreased in preeclampsia, and the primary
consequences are intrauterine growth restriction of the fetus and
oligohydramnios.
5. Severe preeclampsia is a pregnancy problem with hypertensive disorders
worldwide that increases the risk of maternal and newborn mortality and
morbidity
6. In this case, a patient with severe preeclampsia is presented with
complications of a suspected Intrauterine growth restriction fetus and has
received treatment according to immediate termination by sectio caesarea.
7. This patient is a high risk patient in the next pregnancy, so it needs to be
comprehensive when health facilities are adequate.

4
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