SEVERE PREECLAMPSIA ON MULTIGRAVIDE

FULLTERM PREGNANCY IN LABOUR 1ST STAGE OF

ACTIVE PHASE
By :
Andika Pratama
Advisor : Professor. Dott. Antonio Mauora
CASE REPORT
Mrs.VM , 38 y.o , female
 Patient Identity

 Name : Mrs.VM

 Age : 38 y.o

 Address : Via Cristiano No. 12A

 Examination Date : August 14th, 2017 (12 AM)

 Registration Number : AC897xxx

 History of Presenting Complaint
(July 4th , 2017)

 Mrs.CM, a 38-year-old woman, G3P1A1, was admitted to an obstetric

ward with uterine contraction. She was in 38 weeks pregnant. Her
blood pressure was 160/100 mmHg and she has been examined with
the finding of proteinuria +1. She had a bloody show but without
amnion fluid leakage. She felt well in herself except for swollen legs.
 Patient History
Past Gynaecological
Past Medical History
History

 Mrs.VM did not have any problems during the first  Patient had her menarche at 14 years
trimester. In the early second trimester at 16 weeks
gestation, the patient presented to antenatal clinic of age, her menstrual cycle were
with cellulitis , significant lower limb oedem, and regular ranging from 28 to 30 days
her blood pressure was 150/100. Because of these
findings, the doctor referred her to the Arnas Civico with the length of her menses were 7
Hospital. days.
 She denied had history of allergic, asthma, cardiac
disease, kidney disease,hypertension.
 Patient History

Obstetric History
 I : female, 17 years old, 1600 gr, Marriage History and Family
spontaneous vaginal delivery
 Mrs. VM is married once when she
was 20Planning History
years old and lives with her
 II : abortion, 3 month, curettage husband
 III: this pregnancy
 She was never on any form of
 Last menstrual period : 11th October, 2016 contraception
 Estimated date of delivery: 18th July, 2017

 Gestation age : 38 month

 Physical Examination
(August 15th , 2017 (12 AM))
 General state: compos mentis, looks obese  Head : mesocephal

 Vital sign:  Eyes : anemic conjungtive (-/-), ictric sclera

(-/-)
BP: 160/100 mmHg,

HR: 88 x/min

RR : 20 x/min

T : 36.5 C

Weight : 90 kg

Height : 160 cm
 Physical Examination
(Thorax)
1) Cor 2) Pulmo

 Inspection: ictus cordis unseen  Inspection: chest expansion symmetric

 Palpation: ictus cordis normal  Palpation: tactile fremitus normal

 Percussion: normal  Percussion: sonor// sonor

 Auscultation: heart sound I-II normal  Auscultation: vesicular breath sound

intensity, reguler (+/+), rales (-/-), wheezing (-/-)
 Physical Examination
(Abdomen)

 Inspection : striae gravidarum (+)

 Auscultation : bowel sound (+) normal

 Palpation : the abdomen was soft and non tender. The abdomen was distended
compatible with pregnancy, the foetus was palpable in a longitudinal lie and the
presentation was cephalic. The frequency of uterine contraction was 3 times/10
min. The fetal heart rate was audible and of normal rate (150 times/minute). The
fundal height was 28 cm.

 Percussion : timpani
 Physical Examination
(Genital and Extremity)

 Vulva and urethra in normal condition and also vaginal wall.Portio of

cervix flattening 4 cm with effacement 75 %,cephalic presentation,head
descent in Hodge II,amnion membrane intact,bloody show (+),amnion
fluid(-)

 Oedema :Upper extremities:(-),Lower extremities:(+)

 Cold limb :Upper extremities:(-), Lower extremities:(-)

 Additional Examination

 Blood Lab.(14 th August 2017):

 Homeostasis
Hb : 12.4 g/dl Clinical Chemistry
PT : 12,0 detik
Hct : 38% GDS : 87 mg/dl
APTT : 30.4 detik
AL : 10,4 x103/Ul SGOT: 15 u/l
INR : 0,940
AT : 296 x103/uL SGPT : 10 u/l
Hepatitis
AE : 4.34 x103/uL Creatinine: 0.6 mg/dl
HbsAg Rapid : nonreactive
Ureum : 19 mg/dl
Urinalisis
Qualitative Protein +1.
LDH : 135 u/l (↓)
Albumin : 19 dL
 USG
 Appeared Single Fetal, alive , Inta Uterine , longitudinal lie , Cephalic
presentation, FHR (+)
 Fetal Biometry :
Biparietal Diameter 9.16 cm
Abdominal Circumference 31.90
Femur Length 6.47
Estimated Fetal Weight 2570 gr
 Umbilical cord insertion on corpus (grade II)
 Amniotic fluid single deepest pocket 4.78 cm
 Congenital abnormality unseen
 Conclusion : foetus is in good condition
 CARDIOTOCOGRAPH

The CTG shows :

 Baseline : 145 beats/min
 Variability : more than 5 beats/min.
 Acceleration : (+)
 Deceleration (-)
 Contraction (+)
= CST 1 Category.
 CONCLUSION

 Mrs VM, G3P1A1, 38 years old at 38 weeks pregnant. She had good fertility history but
poor obstetric history, palpable single foetus, alive, intrauterine, cephalic presentation,
back foetus on the left, soft portio delated 4 cm, fetal head enter the Hodge II. She denied
have history of allergic, asthma, cardiac disease, kidney disease, hypertension.

 From the physical examination obtained blood pressure 160/100 mmHg. The abdomen
palpation was soft and non tender. The fundal height was 28 cm, abdomen was distended
compatible with pregnancy, palpable single foetus, alive, intrauterine, cephalic
presentation, and back foetus on the left. The frequency of uterine contraction was 3
times/10 min. The fetal heart rate was audible and of normal rate (150 times/minutes).
Portio of cervix flatening 4 cm with effacement 75%, head descent in Hodge II, amnion
membrane intact, bloody show (+), amnion fluid (-). Blood lab results obtained Hb: 12.4
g/dl ,Hct: 38% , GDS: 87 mg/dl, OT : 15 , PT 10 , LDH: 135 u/l , Albumin : 19 dL. From
the Urinalisis obtained Qualitative Protein +1.
 DIAGNOSIS:

Severe preeclampsia on multigravide fullterm pregnancy in labour 1st

stage of active phase.

 PROGNOSIS:

Dubia
 THERAPY

1. Continued the labour delivery and second stage lightened with vacum
extraction

2. 10 steps observation

3. Severe preeclampsia procedures:

1. O2 3 lpm
2. IVFD RL 12 drops/min
3. Inj. MgSO4 20% 4 gr in 15 min, continue with Inj. MgSO4 20% 1 gr/hour in 24
hour

4. Evaluate after 2 hour

 FOLLOW UP
( Evaluation on 7th July, 2017 (12 A.M) )

 Para 2 Abortion 1, 38 years old

 Chief complain : (-)

 General examination :

a. General appearance : compos mentis, looks obese

 FOLLOW UP
( Evaluation on 17th August , 2017 (12 A.M) )
b. Vital sign :
Blood Pressure : 150/100 mmHg
Heart Rate : 82 x/menit
Respiratory Rate : 20 x/menit
Temperatur : 36,5 C
c. Eye : anemic conjungtive (-/-), ictric sclera (-/-)
d. Neck : enlarge lymph node (-)
e. Thorax : cor and pulmo were normal
 FOLLOW UP
( Evaluation on 17th August , 2017 (12
i. Abdomen A.M) :)
Inspection : striae gravidarum (+)

Auscultation: bowel sound (+) normal

Palpation : the abdomen was soft and non tender.

Fundal

height was 2 cm under the umbilical

Percussion : timpani
 FOLLOW UP
( Evaluation on 17th August , 2017 (12 A.M) ))

h. Genital : blood (-), discharge (-), rubra lochea

(+)

 Assesment : post vacum extraction by indication severe preeclampsia

on multiparous fullterm pregnancy
 Treatment :

1. Cefradoxil 500 g/ 12 hour p.o

2. Mefenamat acid 500 g/8 hour p.o

3. Vitamin C 50 G/12 hour p.o

4. Severe preeclampsi guidelines:

a. O2 3 lpm

b. IVFD RL 12 drops/ min

c. Inj. MgSO4 20% 4 gr in 24 hour (until 8TH JULY 2017, 7 PM)

d. Nifedipin 3x 10 g (if the blood pressure more than 160/100)

5. Plan for 4 hourly blood pressure, heart rate, respiratory rate ( becarefull with the sign of
impending eclampsia )
Working Diagnosis

SEVERE
PREECLAMPSIA ON
MULTIGRAVIDE
FULLTERM
PREGNANCY IN
LABOUR 1ST STAGE OF
ACTIVE PHASE
 Definition

“Preeclampsia is pregnancy-specific
hypertensive disease with
multisystem involvement”
 Risk Factor

 Primigravida

 Family history with preeclampsia

 History of preeclampsia in pregnancy

 The presence of chronic hypertension or chronic kidney disease or both

 Pregnancy Age

Preeclampsia in the first pregnancy with delivery with 32 weeks to 36 weeks gestation will increase
the risk of preeclampsia in second pregnancy by 25.3%.
 Risk Factor

 Obesity

Women with body mass index (BMI) <20 kg / m2 had a risk of 4.3% and those with BMI> 35 kg /
m2 had a risk of 13.3%

 Donors of oocyte or donor insemination and history of thrombophilia

 Urinary tract infections, diabetes mellitus, collagen vascular disease, hydatidiform mole, and
periodontal disease
 Risk Factor

 Mother Age

Women who are pregnant at age 35 or older are at higher risk for preeclampsia

 Race

In the United States, preeclampsia in white women is 1.8% and 3% in black women

 Additional factors that affect the occurrence of preeclampsia are multiple pregnancies, poor
placentation and some other things that increase placental mass and poor placental
Pathogenesis
Although the cause of preeclampsia
remains unknown, evidence for its
manifestation begins early in
pregnancy with covert
pathophysiological changes that
gain momentum across gestation
and eventually become clinically
apparent
  During the past two decades,
Pathogenesis
(Endothelial Cell Injury)
endothelial cell injury has become the
centerpiece in the contemporary
understanding of preeclampsia
pathogenesis .In this scheme, protein
factor(s)—likely placental—are secreted
into the maternal circulation and
provoke activation and dysfunction of
the vascular endothelium. Many of the
face of the clinical syndrome of
preeclampsia are thought to result from
these widespread endothelial cell
changes.
  Endothelial activation causes
vascular constriction with increased
Pathogenesis resistance and subsequent
(Vasospasm) hypertension. At the same time,
endothelial cell damage causes
interstitial leakage through which
blood constituents, including
platelets and fibrinogen, endothelial
cells, modify their nitric oxide
production, and interfere with
prostaglandin balance.Activation of
microvascular coagulation manifest
by thrombocytopenia;and increased
capillary permeability manifest by
edema and proteinuria.
  Women with early preeclampsia,
Pathogenesis however, have increased vascular
(Increased Pressor reactivity to infused norepinephrine
Responses) and angiotensin II.Moreover,
increased sensitivity to angiotensin
II clearly precedes the onset of
gestational hypertension
  Several prostanoids are thought to
be central to preeclampsia syndrome
Pathogenesis pathophysiology.
(Prostaglandins)
 Specifically, the blunted pressor
response seen in normal pregnancy
is at least partially due to decreased
vascular responsiveness mediated
by endothelial prostaglandin
synthesis.
  This potent vasodilator is synthesized from
l-arginine by endothelial cells. Inhibition of
nitric oxide synthesis increases mean
Pathogenesis arterial pressure, decreases heart rate.
(Nitric Oxide)  In humans, nitric oxide likely is the
compound that maintains the normal low-
pressure vasodilated state characteristic of
fetoplacental perfusion .

 It also is produced by fetal endothelium,and

here it is increased in response to
preeclampsia, diabetes,and sepsis).

 The effects of nitric oxide production in

preeclampsia are unclear). It appears that
the syndrome is associated with decreased
endothelial nitric oxide synthase
expression,thus increasing nitric oxide
inactivation.
  These 21-amino acid peptides are potent
Pathogenesis vasoconstrictors,and endothelin-1 (ET-1)
(Endothelins) is the primary isoform produced by
human endothelium .

 Plasma ET-1 levels are increased in

normotensive pregnant women, but
women with preeclampsia have even
higher levels
  Placental vasculogenesis is evident by
21 days after conception.There is an
Pathogenesis ever-expanding list of pro- and
(Angiogenic and antiangiogenic substances involved in
placental vascular development.
Antiangiogenic Proteins)
 The families of vascular endothelial
growth factor (VEGF) and angiopoietin
(Ang) are most extensively studied.
 Angiogenic imbalance is used to
describe excessive amounts of
antiangiogenic factors that are
hypothesized to be stimulated by
worsening hypoxia at the uteroplacental
interface.
 Trophoblast of women destined to
develop preeclampsia overproduces at
least two antiangiogenic peptides that
enter the maternal circulation
 Diagnosis

 Minimal Criteria of preeclampsia

 Hypertension

Blood pressure of at least 140 mmHg systolic or 90 mmHg diastolic at

two examinations within 15 minutes using the same arm

 Proteinuria

Protein in urine more than 300 mg in 24 hours or dipstick test > +1.
 Diagnosis

 If we cannot find protein in urine, hypertension followed by

 Thrombocytopenia : Thrombocyt <100.000/microliter
 Kidney Disorders: Serum creatinine above 1.1 mg / dL or we find an elevated serum
creatinine level than before in a condition where there is no other renal abnormality.
 Liver Disorders: An increase in transaminase levels 2 times normal and or the
presence of pain in the epigastric region / upper right region of the abdomen
 Oedem Pulmo
 Neurologic Disorders: Stroke, Headache, visus disruption
 Uteroplacenta Circulation Disorders:Oligohidramnion,Fetal Growth Restriction(FGR)
or we find absent or reversed end diastolic velocity(ARDV)
 Diagnosis
 Severe Preeclampsia Criteria, The diagnosis of preeclampsia is met and if any of the following
conditions are found:

1. Hypertension

Blood pressure of at least 160 mmHg systolic or 110 mmHg diastolic at two

examinations within 15 minutes using the same arm

2. Thrombocytopenia : Thrombocyt <100.000/microliter

3. Kidney Disorders: Serum creatinine above 1.1 mg / dL or we find an elevated

serum creatinine level than before in a condition where there is no other renal abnormality.
 Diagnosis

4. Liver Disorders: An increase in transaminase levels 2 times normal and or

the presence of pain in the epigastric region / upper right region of the

abdomen

5. Oedem Pulmo

6. Neurologic Disorders: Stroke, Headache, visus disruption

7. Uteroplacenta Circulation Disorders:Oligohidramnion,Fetal Growth

Restriction(FGR) or we find absent or reversed end diastolic velocity(ARDV)

 ADMINISTRATION OF MEDICAL
THERAPY

 Immediately entered the hospital

 The bed rests tilted to the left intermittently

 IVFD Ringer Laktat or Ringer Dekstrose 5%

 Provision anti seizures MgSO4 as a prevention and treatment of seizures

 ADMINISTRATION OF MEDICAL
THERAPY
 Anti hypertensive
Given : When tension ≥ 160/110
Type of Drug:
• Nifedipine : 10-20 mg oral, repeat after 30 minutes, maksimum 120
mg in24 hours.
• Nicardipine-HCl : 10 mg in 100 or 250 cc NaCl/RL given IV for 5
minutes, if failure within 1 can be repeated with a dose of 12,5 mg for 5
minutes. If still fail in 1 hour, can be repeated once again with dose 15
mg for 5 minutes.
 Complications

 Epigastricpain indicates the occurrence of damage to liver in form of a

possibility:

1. Subcapsular bleeding

2. periportal sistem blleding and liver infarction

3. Edema of the liver parenkim

4. Increase liver enzyme expenditure

 Complications

 Blood pressure may increase resulting in a failure of the autonomic system

capability of central nervous system’s bllod flow and resulting in various
pathological forms as follows:
1. Cerebral edema due to incresaed capillary permeability.
2. Iskemia that causes serebral infarction
3. Edema and bleeding cause necrosis
4. Edema and bleeding in the brainstem and retina
5. Can occur brainstem herniation that suppress the vital center of the
medulla Oblongata
 Prognosis

 The Prognosis of severe preeclampsia and eclampsia is said to be ugly

because of maternal mortality between 9,8 – 20,5%, and infant
mortality is higher,is 42,2–48,9%. Death is due to lackof perfect
antenatal surveillance,in addition to eclampsia patients usually late to
get help.Maternal death is usually due to cerebral hemorrhage,
decompensatio cordis, pulmoner edema, renal liver and gastric
aspiration. Because of infant mortality due to prematurity and
intrauterin hypoxia
 CASE ANALYSIS

 Mrs S, G3P1A1, 38 years old at 38 weeks pregnant. She had good fertility history but
poor obstetric history, palpable single foetus, alive, intrauterine, cephalic
presentation, back foetus on the left, soft portio delated 4 cm, fetal head enter the
Hodge II. She denied have history of allergic, asthma, cardiac disease, kidney
disease, hypertension.
 From the physical examination obtained blood pressure 160/100 mmHg. The
abdomen palpation was soft and non tender. The fundal height was 28 cm, abdomen
was distended compatible with pregnancy, palpable single foetus, alive, intrauterine,
cephalic presentation, and back foetus on the left. The frequency of uterine
contraction was 3 times/10 min. The fetal heart rate was audible and of normal rate
(150 times/minutes). Portio of cervix flatening 4 cm with effacement 75%, head
descent in Hodge II, amnion membrane intact, bloody show (+), amnion fluid (-).
Blood lab results obtained Hb: 12.4 g/dl ,Hct: 38% , GDS: 87 mg/dl, OT : 15 , PT 10 ,
LDH: 135 u/l , Albumin : 19 dL. From the Urinalisis obtained Qualitative Protein +1.
 CASE ANALYSIS

 Severe Preeclampsia is is defined as systolic blood pressure ≥ 160

mmHg or diastolic blood pressure ≥ 110 mmHg or higher twice on
examination for at least 15 minutes.For our patient from the physical
examination obtained blood pressure 160/100 mmHg. And patient
admitted her blood pressure before pregnancy was never high.
 CASE ANALYSIS

 The patient was administered preeclampsia treatment guideline to

prevent patient from falling into eclampsia or impending eclampsia.As
for preeclampsia treatment guidline is oxygenation with 3 lt per
minute by nasal canulla, infusion of ringer lactate12 drops per minute,
injection. MgSO4 20% 4 gr in 24 hour. MgSO4 the given a seizure
prophylaxis, tocolytic, antihypertensives and diuretics.
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