case:

G1P0A0, GA 40 - 41 weeks stage 1 latent phase +

severe PE + PROM
Counsellor
dr. Gioseffi Sp.OG

Prepared by
Angela Jessica - 406138047
Krisnataligan - 406138114

OBSTETRICS AND GYNECOLOGY CLERKSHIP

TARUMANAGARA UNIVERSITY
RSUD CIAWI, BOGOR
Period November 24th 2014 - January 31st 2015

Admitted to hospital on 6th January 2015

Patients Identity

Name

: Mrs. EH

Age

: 33 years old

Occupation

: Housewife

Education

: Senior High School

Race

: Sundanese

Religion

: Muslim

Address

: Kp. Warung Pari 01/02

Pamoyanan

Patients Husbands Identity

Name

: Mr. J

Age

: 43 years old

Occupation

: driver

Education

: Junior High School

Race

: Sundanese

Religion

: Muslim

Address

: Kp. Warung Pari 01/02

Pamoyanan

1.Anamnesis
with auto anamnesis at 04.50 a.m. on January 6th 2015
Chief complaint: High blood pressure with watery and bloody mucous from vagina
Present Illness:
Patient came to the obstetric and gynecological clinic on 6th January 2015 referred by
midwife because of high blood pressure since entering the gestational age of 9 months. She
also complained about her uterine contraction getting more often and painful since yesterday
morning. In addition, she reported about bloody mucous discharge and watery discharge
from her vagina since 00.30 p.m. Patient often feel headache, epigastric pain, nausea, but she
denied vomiting, blurred vision and dyspnea. Fetal movement is still active.

Patient said she is pregnant with her 1st child, miscarriage (-), first day of her last period =
March 25th 2015, estimated delivery date = January 4th 2015.

Medical History:
-

Hypertension (-)

Diabetes (-)

Heart Disease (-)

Asthma (-)

Seizures (-)

Irregular menstruation cycle (-)

Menstruation History:
-

Menarche

: 14 years old

Menstrual cycle

: 30 days

Duration

: 7 days

Sanitary napkin/day

: 2-3 x/days

Menstrual pain

: (-)

History Marriage
- Married: 1x, age 31th
History Contraceptives : no experienced
Operation History : no experienced
Antenatal Care: regular, monthly with midwife
supplement: fe & folic acid (+)
2. Physical Examination
On January 6th 2015, 04.30 am

General Situation : moderate pain

Awareness : compos mentis

Vital Sign: - Blood pressure: 170/110 mmHg

3

- Pulse : 96x/min
- Respiratory rate : 23x/min
- Temperature : 36.7oc

Weight before pregnancy : 69 kg

Weight gain during pregnancy : 92 kg there is a weight gain 23 kg during

pregnancy

Height : 158 cm

GENERAL EXAMINATION
Head
-

Eye : Conjunctiva anemic -/-, sclera icteric -/Pupil isocor, palpebral edema -/-

Ear : membrane tympani intact +/+, secret -/-

Nose : deviation septum -/-, secret -/-

Thorax : T1-T1 normal, Faring hyperaemic (-)

Mouth : oral hygiene (+), mucosa normal, sulcus nasolabialis symmetric

Neck

: Trachea in the middle, lymph nodes and thyroid normal

Thorax
-

Mammae : normal , Inverted nipple -/-

Pulmo : Inspection: Barrel chest(-), pectus excavatum(-), pectus carinatum(-)

Palpation: Fremitus tactile right=left
Percussion: Sonor +/+
Auscultation: vesicular +/+, rhonchi -/-, wheezing -/-

Cor

: Inspection : Pulse ictus cordis can not be seen

Palpation : pulse of ictus cordis is not palpable at ICS V MCLS
Percussion : Dull, heart margins within normal limits.
Auscultation: Heart sounds I/II regular, gallop(-), murmur (-)

Extremities: Oedema (+/+ on the lower extremities)

Obstetric Abdominal Examination
Inspection : striae gravidarum(+), scar (-), fetal movement (-)

Palpation :

Leopold I

: A broader, softer, less defined presenting part is palpated (fetal buttocks)

Symphyseal-fundal height was 36 cm

Leopold II : Palpable a big bulge, firm, and smooth on the left side (fetal back)

Leopold III : A hard, firm, and round presenting part is palpated (fetal head)

Leopold IV : engaged

His : 2-3x/ 10 mins, each contraction:15-20 secs.

Auscultation:

FHR: (+), located at the left of the mother's abdomen, 152x/mins

Rhythm: Regular

Intensity: Strong

External genitalia
-Inspection : condition of vulva / vagina normal
Bleeding (-)
- Speculum examination : not done
Internal Genitalia
-Examination of vaginal (vaginal touch): v/v normal, portio thick and soft, opening of
ostium uteri externa 3cm, amniotic sac (-), presentation of head , H 2
Laboratory Test
Haematology

Hb

: 12.8 g/dl (12.0-15.0 g/dl)

Ht

: 38% (36-46 %)

Leucocyte

: 11800 /ul (4000-10000/ul)

Platelet count

: 256000 /ul (150000-45000/ul)

CT

: 1030 (6-11 minutes)

BT

: 230 (1-6 minutes)

Chemistry Screens

SGOT

: 45

SGPT

: 16

Ureum

: 16.7

Creatinin

: 0.79

Glucose tolerance test : 94

5

Urinalisa

Protein : ++/POS2

The others examination within normal limit

3. Resume
A 33 years old woman came to the obstetric and gynecological clinic on 6th January 2015
referred by midwife because of high blood pressure since entering the gestational age of 9
months. She also complained about her uterine contraction getting more often and painful
since yesterday morning. In addition, she reported about bloody mucous discharge and
watery discharge from her vagina since 00.30 a.m. Patient often feel headache, epigastric
pain, nausea, but she denied vomiting, blurred vision and dyspnea. Fetal movement is still
active. Patient said she is pregnant with her 1st child, miscarriage (-), first day of her last
period = March 25th 2015, estimated delivery date = January 4th 2015

Vital Sign

: - Blood pressure: 170/110 mmHg

- Pulse : 96x/min
- Respiratory rate : 23x/min
- Temperature : 36.7oc

Eye

: Ca -/-, SI -/-, light reflex +/+

Thorax

: within normal limits

Abdomen

Inspection : striae gravidarum(+), scar (-), fetal movement (-)

Palpation :
Leopold I

: A broader, softer, less defined presenting part is palpated (fetal buttocks)

Symphyseal-fundal height was 36 cm

Leopold II : Palpable a big bulge, firm, and smooth on the left side (fetal back)
His : 2-3x/ 10 mins, each contraction:15-20 secs.
Leopold III : A hard, firm, and round presenting part is palpated (fetal head)
Leopold IV : engaged
Auscultation:
FHR

: (+), located at the left of the mother's abdomen, 152x/mins

Rhythm

: Regular

Intensity

: Strong

External genitalia
-Inspection : condition of vulva / vagina normal
Bleeding (-)
- Speculum examination : not done
Internal Genitalia
-Examination of vaginal (vaginal touch): v/v normal, portio thick and soft, opening of
ostium uteri externa 3cm, amniotic sac (-), presentation of head , H 2
Laboratory Test

Increased in SGOT

Increased leucocyt

Urine protein ++/POS2

Working Diagnosis : G1P0A0, GA 40 - 41 weeks, stage 1 latent phase + severe PE +

PROM
4. Management:
Conservatif

IVFD RL 2000cc/ 24 hours, 20 gtt

Oxygen 3-4 L

Urine catheter

CTG

MgSO4 40 % : loading dose (4gr in 15 mins), maintanance dose (6gr in D5% 500 cc)

Methyldopa 3 x 500 mg tab

Nifedipin 3 x 10 mg tab

Observation of vital sign and labor progress

5. Follow Up (6 th January 2015, at 05.00 am)

S

:-

: CM/moderate pain

Vital Sign:

BP

: 160/110 mmHg

Pulse

: 92 x/mins

RR

: 21 x/mins

Temperature

: 36.6oC
7

General exam

Eye

: CA -/- , SI -/-

Thorax

: C/P within normal

Abdomen

: symphyseal-fundal height: 36cm, FHR: 152 bpm

His : 2-3x/10mins

Gen

: v/v normal, thin and soft portio, 3cm, amniotic sac (-),
presentation of head, H 2

Extremities : Oedema (+/+) on the lower extremities

A

: G1P0A0, GA 40 - 41 weeks stage 1 latent phase + severe PE + PROM

: MgSO4 according to guideline

Nifedipin 3 x 10 mg
Methyldopa 3x500 mg
Cefadroxil 2x500 mg
Observation of vital sign and labour progress
Pro Partus Pervaginam

(06.00 am) MgSO4 loading 4 gram (bolus)

(06.30 am) MgSO4 maintenance 6 gram (drip)
(08.00 am)
S

: Labour pain was getting stronger and more often (4-5x / 10 mins @ 30-40)

: CM/moderate pain , FHR: 148bpm

Vital Sign:
BP

: 150/100 mmHg

Pulse

: 96 x/mins

RR

: 19 x/mins

Temperature

: 36.6oC

A : G1P0A0 parturian 40 - 41 weeks + severe PE + ROM

P : Observation of vital sign and labour progress and tell her to relax
09.00 am
Patient wanted to bear down
(VT) complete dilation of cervix, amniotic fluid (-), presentation of fetal head
8

09.10 am (a baby girl was born and spontaneously crying, 3260 grams, 48cm, A/S:9/10)
09.20 am
umbilical cord delivered completely, weight: 500 grams, 20 x 20 x 1,5 cm
uterine contraction: good, fundal height: 1 cm below belly button.
Perineum hecting with chromic catgut 2.0
09.30 am
S

:-

: BP

: 140/100 mmHg

Pulse

: 82 x/mins

RR

: 19 x/mins

Temperature

: 36.5oC

: P1A0 spontaneous normal delivery + severe PE

: Mefenamic acid 3 x 500 mg

Cefadroxil 2 x 500 mg
SF 1 x 1
Nifedipin 3 x 10 mg
Methyldopa 3 x 500 mg

15.30 pm (TERATAI A)
S

:-

: BP

: 130/90 mmHg

Pulse

: 88 x/mins

RR

: 19 x/mins

Temperature

: 36.6oC

: P1A0 spontaneous normal delivery + severe PE

: Mefenamic acid 3 x 500 mg

Cefadroxil 2 x 500 mg
SF 1 x 1
Nifedipin 3x 10 mg
Methyldopa 3x500 mg

7th January 2015 07.00 am

S

:-

: CM/ mild pain

BP

: 120/80 mmHg

Pulse

: 80 x/mins

RR

: 17 x/mins

Temperature

: 36.4oC

Eye

: CA -/- , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm under belly button, uterine
contraction: good

Gen

: v/v normal, blood + minimal

Extremities

: Minimal edema (+/+) on the lower extremities

: P1A0 spontaneous normal delivery + severe PE

: Mefenamic acid 3 x 500 mg

Cefadroxil 2 x 500 mg
SF 1 x 1
Nifedipin 3x 20 mg
Methyldopa 3x500 mg

Laboratory Test
Haematology
Hb

: 12.5 g/dl (12.0-15.0 g/dl)

Ht

: 36% (36-46 %)

Leucocyte

: 10200 /ul (4000-10000/ul)

Platelet count

: 296000 /ul (150000-45000/ul)

Chemistry Screens
SGOT

: 24

SGPT

: 14

Ureum

: 13.7

Creatinin

: 0.62
10

 Glucose tolerance test : 102

Urinalisa
Protein : +/POS1
The others examination within normal limit
8th

January 2015 07.00 am

S

:-

: CM/ mild pain

Eye

BP

: 120/80 mmHg

Pulse

: 88 x/mins

RR

: 17 x/mins

Temperature

: 36.6oC

: CA -/- , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm under belly button, uterine
contraction: good

Gen

: v/v normal, blood + minimal

Extremities

: Minimal edema (+/+) on the lower extremities

: P1A0 spontaneous normal delivery + severe PE

: Mefenamic acid 3 x 500 mg

Cefadroxil 2 x 500 mg
SF 1 x 1
Nifedipin 3x 10 mg
Methyldopa 3x500 mg

5. Case analysis
1. In this case, the patient has severe PE and she was treated with MgSO4 40% (loading
and maintenance dose), but MgSO4 was only given once. Theorically, severe PE
should be given MgSO4 until 24 hours after labouring or 6 hours after labouring until
the tension is normal and stable.

11

2. Lab check should be done everyday and we should check complete blood count,
blood plasma glucose, complete urinalysis, and MgSO4 blood level. But in this
patient we didnt check MgSO4 blood level.
6. Conclusion
Based on the analysis that has been done in this case, it can be set some conclusions:

In this case, the patient has severe PE and she was treated with MgSO4 40% (loading
and maintenance dose), but MgSO4 was only given once. Theorically, severe PE
should be given MgSO4 until 24 hours after labouring or 6 hours after labouring until
the tension is normal and stable.

Lab check should be done everyday and we should check complete blood count,
blood plasma glucose, complete urinalysis, and MgSO4 blood level. But in this patient
we didnt check MgSO4 blood level

12

PRE-ECLAMPSIA

DEFINITION
Preeclampsia is a pregnancy complication characterized by high blood pressure and signs
of damage to another organ system, often the kidneys. Preeclampsia usually begins after
20 weeks of pregnancy in a woman whose blood pressure had been normal. Even a slight
rise in blood pressure may be a sign of preeclampsia.
Left untreated, preeclampsia can lead to serious even fatal complications for both
you and your baby. If you have preeclampsia, the only cure is delivery of your baby.
If you're diagnosed with preeclampsia too early in your pregnancy to deliver your baby,
you and your doctor face a challenging task. Your baby needs more time to mature, but
you need to avoid putting yourself or your baby at risk of serious complications.

CAUSE
The exact cause of preeclampsia is unknown. Experts believe it begins in the placenta
the organ that nourishes the fetus throughout pregnancy. Early in pregnancy, new blood
vessels develop and evolve to efficiently send blood to the placenta. In women with
preeclampsia, these blood vessels don't seem to develop properly. They're narrower than
normal blood vessels and react differently to hormonal signaling, which limits the amount
of blood that can flow through them.
Causes of this abnormal development may include:

Insufficient blood flow to the uterus

Damage to the blood vessels

A problem with the immune system

Certain genes
Other high blood pressure disorders during pregnancy
13

Preeclampsia is classified as one of four high blood pressure disorders that can occur
during pregnancy. The other three are:

Gestational hypertension. Women with gestational hypertension have high blood

pressure but no excess protein in their urine or other signs of organ damage. Some women
with gestational hypertension eventually develop preeclampsia.

Chronic hypertension. Chronic hypertension is high blood pressure that was present
before pregnancy or that occurs before 20 weeks of pregnancy. But because high blood
pressure usually doesn't have symptoms, it may be hard to determine when it began.

Chronic hypertension with superimposed preeclampsia. This condition occurs in

women who have chronic high blood pressure before pregnancy who then develop
worsening high blood pressure and protein in the urine or other health complications
during pregnancy.

Preeclampsia as a Two-Stage Disorder

Observations that abnormal interfaces between maternal, paternal, and fetal tissues may cause
preeclampsia have led to hypotheses that the syndrome is a two-stage disorder. In this
scenario, there is a spectrum to include "maternal and placental preeclampsia " (Ness and
Roberts, 1996). According to Redman and colleagues (2009), stage 1 is caused by faulty
endovascular trophoblastic remodeling that downstream causes the stage 2 clinical syndrome
(Fig. 34-1). There certainly is evidence that some cases of preeclampsia fit this theory.
Importantly, stage 2 is susceptible to modification by preexisting maternal conditions that
include cardiac or renal disease, diabetes, obesity, or hereditary influences. Such
compartmentalization seems artificial, and it seems logical that there likely is a continuous
process. Thus, although perhaps helpful to classify the syndrome for research purposes
preeclampsia is clinically more realistically a continuum of worsening disease. Moreover,
evidence is accruing that many "isoforms" exist as discussed below.

14

Etiology
Instead of being simply "one disease," preeclampsia appears to be a culmination of factors
that likely involve a number of maternal, placental, and fetal factors. Those currently
considered important include:
1. Placental implantation with abnormal trophoblastic invasion of uterine vessels
2. Immunological maladaptive tolerance between maternal, paternal (placental), and
fetal tissues
3. Maternal maladaptation to cardiovascular or inflammatory changes of normal
pregnancy
4. Genetic factors including inherited predisposing genes as well as epigenetic
influences.

Abnormal Trophoblastic Invasion

In normal implantation, shown schematically in Figure 34-2, the uterine spiral arterioles
undergo extensive remodeling as they are invaded by endovascular trophoblasts (see also
Chap. 3, Invasion of Spiral Arteries). These cells replace the vascular endothelial and
muscular linings to enlarge the vessel diameter. The veins are invaded only superficially. In
preeclampsia, however, there may be incomplete trophoblastic invasion. With such shallow
invasion, decidual vessels, but not myometrial vessels, become lined with endovascular
trophoblasts. The deeper myometrial arterioles do not lose their endothelial lining and
musculoelastic tissue, and their mean external diameter is only half that of vessels in normal
placentas (Fisher and colleagues, 2009). Madazli and associates (2000) showed that the
magnitude of defective trophoblastic invasion of the spiral arteries correlates with the severity
of the hypertensive disorder
15

Endothelial Cell Activation

In many ways, inflammatory changes are thought to be a continuation of the stage 1 changes
caused by defective placentation discussed above. In response to placental factors released by
ischemic changes or by any other inciting cause, a cascade of events is set in motion (Taylor
and colleagues, 2009). Thus, antiangiogenic and metabolic factors and other inflammatory
mediators are thought to provoke endothelial cell injury.
It has been proposed that endothelial cell dysfunction is due to an extreme activated state of
leukocytes in the maternal circulation (Faas, 2000; Gervasi, 2001; Redman, 1999, and all
their colleagues). Briefly, cytokines such as tumor necrosis factor(TNF) and the
interleukins (IL) may contribute to the oxidative stress associated with preeclampsia. This is
characterized by reactive oxygen species and free radicals that lead to formation of selfpropagating lipid peroxides (Manten and associates, 2005). These in turn generate highly
toxic radicals that injure endothelial cells, modify their nitric oxide production, and interfere
with prostaglandin balance. Other consequences of oxidative stress include production of the
lipid-laden macrophage foam cells seen in atherosis and shown in Figure 34-2; activation of
microvascular coagulation manifest by thrombocytopenia; and increased capillary
permeability manifest by edema and proteinuria.
These observations on the effects of oxidative stress in preeclampsia have given rise to
increased interest in the potential benefit of antioxidants to prevent preeclampsia.
Antioxidants are from a diverse family of compounds that function to prevent overproduction
of and damage caused by noxious free radicals. Examples of antioxidants include vitamin E (
-tocopherol), vitamin C (ascorbic acid), and
-carotene. Dietary supplementation
with these antioxidants to prevent preeclampsia has thus far proven unsuccessful and is
discussed further in Dietary Manipulation.
16

Nutritional Factors

John and co-workers (2002) showed that in the general population a diet high in fruits and
vegetables that have antioxidant activity is associated with decreased blood pressure. Zhang
and associates (2002) reported that the incidence of preeclampsia was doubled in women
whose daily intake of ascorbic acid was less than 85 mg. These studies were followed by
randomized trials to study dietary supplementation. Villar and associates (2006) showed that
calcium supplementation in populations with a low dietary calcium intake had a small effect
to lower perinatal mortality rates, but no effect on the incidence of preeclampsia (see Dietary
Manipulation). In a number of trials, supplementation with the antioxidant vitamins C and E
showed no beneficial effects.

Genetic Factors

Preeclampsia is a multifactorial, polygenic disorder. In their comprehensive review, Ward and

Lindheimer (2009) cite an incident risk for preeclampsia of 20 to 40 percent for daughters of
preeclamptic mothers; 11 to 37 percent for sisters of preeclamptic women; and 22 to 47
percent in twin studies. In a study by Nilsson and co-workers (2004) that included almost 1.2
million Swedish births, they reported a genetic component for gestational hypertension as
well as preeclampsia. They also reported 60-percent concordance in monozygotic female
twin pairs.
This hereditary predisposition likely is the result of interactions of literally hundreds of
inherited genesboth maternal and paternalthat control myriad enzymatic and metabolic
functions throughout every organ system. Thus, the clinical manifestation in any given
woman with the preeclampsia syndrome will occupy a spectrum as discussed under the twostage concept in Preeclampsia as a Two-Stage Disorder. In this regard, phenotypic expression
will differ among similar genotypes depending on interactions with environmental factors.

SIGNS AND SYMPTOMS

Preeclampsia sometimes develops without any symptoms. High blood pressure may
develop slowly, but more commonly it has a sudden onset. Monitoring your blood
pressure is an important part of prenatal care because the first sign of preeclampsia is
commonly a rise in blood pressure. Blood pressure that is 140/90 millimeters of mercury
(mm Hg) or greater documented on two occasions, at least four hours apart is
abnormal.
Other signs and symptoms of preeclampsia may include:

Excess protein in your urine (proteinuria) or additional signs of kidney problems

Severe headaches
17

Changes in vision, including temporary loss of vision, blurred vision or light

sensitivity

Upper abdominal pain, usually under your ribs on the right side

Nausea or vomiting

Decreased urine output

Decreased levels of platelets in your blood (thrombocytopenia)

Impaired liver function

Shortness of breath, caused by fluid in your lungs

Sudden weight gain and swelling (edema) particularly in your face and hands often
accompanies preeclampsia. But these things also occur in many normal pregnancies, so
they're not considered reliable signs of preeclampsia.

When to see a doctor

18

Make sure you attend your prenatal visits so that your care provider can monitor your
blood pressure. Contact your doctor immediately or go to an emergency room if you have
severe headaches, blurred vision, severe pain in your abdomen or severe shortness of
breath.
Because headaches, nausea, and aches and pains are common pregnancy complaints, it's
difficult to know when new symptoms are simply part of being pregnant and when they
may indicate a serious problem especially if it's your first pregnancy. If you're
concerned about your symptoms, contact your doctor.

RISK FACTOR
Preeclampsia develops only as a complication of pregnancy. Risk factors include:

History of preeclampsia. A personal or family history of preeclampsia significantly

raises your risk of preeclampsia.

First pregnancy. The risk of developing preeclampsia is highest during your first
pregnancy.

New paternity. Each pregnancy with a new partner increases the risk of preeclampsia
over a second or third pregnancy with the same partner.

Age. The risk of preeclampsia is higher for pregnant women older than 40.

Obesity. The risk of preeclampsia is higher if you're obese.

Multiple pregnancy. Preeclampsia is more common in women who are carrying

twins, triplets or other multiples.

Interval between pregnancies. Having babies less than two years or more than 10
years apart leads to a higher risk of preeclampsia.

History of certain conditions. Having certain conditions before you become

pregnant such as chronic high blood pressure, migraine headaches, type 1 or type 2
diabetes, kidney disease, a tendency to develop blood clots, or lupus increases your
risk of preeclampsia.

COMPLICATION

19

The more severe your preeclampsia and the earlier it occurs in your pregnancy, the
greater the risks for you and your baby. Preeclampsia may require induced labor and
delivery. Surgical delivery (cesarean section or C-section) isn't always advantageous
unless other problems are present, such as a baby in breech presentation, or if a speedy
delivery is necessary. If you have severe preeclampsia or you're at less than 30 weeks
gestation, a C-section may be necessary.
Complications of preeclampsia may include:

Lack of blood flow to the placenta. Preeclampsia affects the arteries carrying blood
to the placenta. If the placenta doesn't get enough blood, your baby may receive less
oxygen and fewer nutrients. This can lead to slow growth, low birth weight or preterm
birth. Prematurity can lead to breathing problems for the baby.

Placental abruption. Preeclampsia increases your risk of placental abruption, in

which the placenta separates from the inner wall of your uterus before delivery. Severe
abruption can cause heavy bleeding and damage to the placenta, which can be lifethreatening for both you and your baby.

HELLP syndrome. HELLP which stands for hemolysis (the destruction of red
blood cells), elevated liver enzymes and low platelet count syndrome can rapidly
become life-threatening for both you and your baby. Symptoms of HELLP syndrome
include nausea and vomiting, headache, and upper right abdominal pain. HELLP
syndrome is particularly dangerous because it represents damage to several organ
systems. On occasion, it may develop suddenly, even before high blood pressure is
detected.

Eclampsia. When preeclampsia isn't controlled, eclampsia which is essentially

preeclampsia plus seizures can develop. Symptoms that suggest imminent eclampsia
include upper right abdominal pain, severe headache, vision problems and change in
mental status, such as decreased alertness. Because eclampsia can have serious
consequences for both mom and baby, delivery becomes necessary, regardless of how far
along the pregnancy is.

Cardiovascular disease. Having preeclampsia may increase your risk of future heart
and blood vessel (cardiovascular) disease. The risk is even greater if you've had
preeclampsia more than once or you've had a preterm delivery. To minimize this risk,

20

after delivery try to maintain your ideal weight, eat a variety of fruits and vegetables,
exercise regularly, and don't smoke.
TEST AND DIAGNOSIS
To diagnose preeclampsia, you have to have high blood pressure and one or more of the
following complications after the 20th week of pregnancy:

Protein in your urine (proteinuria)

A low platelet count

Impaired liver function

Signs of kidney trouble other than protein in the urine

Fluid in the lungs (pulmonary edema)

New-onset headaches

Visual disturbances
Previously, preeclampsia was only diagnosed if a pregnant woman had high blood
pressure and protein in her urine. However, experts now know that it's possible to have
preeclampsia, yet never have protein in the urine.
A blood pressure reading in excess of 140/90 mm Hg is abnormal in pregnancy. However,
a single high blood pressure reading doesn't mean you have preeclampsia. If you have one
reading in the abnormal range or a reading that's substantially higher than your usual
blood pressure your doctor will closely observe your numbers. Having a second
abnormal blood pressure reading four hours after the first may confirm your doctor's
suspicion of preeclampsia. Your doctor may have you come in for additional blood
pressure readings and blood and urine tests.
Tests that may be needed
If your doctor suspects preeclampsia, you may need certain tests, including:

Blood tests. These can determine how well your liver and kidneys are functioning and
whether your blood has a normal number of platelets the cells that help blood clot.

Urine analysis. A single urine sample that measures the ratio of protein to creatinine
a chemical that's always present in the urine may be used to make the diagnosis.

21

Urine samples taken over 24 hours can quantify how much protein is being lost in the
urine, an indication of the severity of preeclampsia.

Fetal ultrasound. Your doctor may also recommend close monitoring of your baby's
growth, typically through ultrasound. The images of your baby created during the
ultrasound exam allow your doctor to estimate fetal weight and the amount of fluid in the
uterus (amniotic fluid).

Nonstress test or biophysical profile. A nonstress test is a simple procedure that

checks how your baby's heart rate reacts when your baby moves. A biophysical profile
combines an ultrasound with a nonstress test to provide more information about your
baby's breathing, tone, movement and the volume of amniotic fluid in your uterus.

TREATMENT
The only cure for preeclampsia is delivery. You're at increased risk of seizures, placental
abruption, stroke and possibly severe bleeding until your blood pressure decreases. Of
course, if it's too early in your pregnancy, delivery may not be the best thing for your
baby.
If you're diagnosed with preeclampsia, your doctor will let you know how often you'll
need to come in for prenatal visits likely more frequently than what's typically
recommended for pregnancy. You'll also need more-frequent blood tests, ultrasounds and
nonstress tests than would be expected in an uncomplicated pregnancy.
Medications
Possible treatment for preeclampsia may include:

Medications to lower blood pressure. These medications, called antihypertensives,

are used to lower your blood pressure if it's dangerously high. Blood pressure in the
140/90 millimeters of mercury (mm Hg) range generally isn't treated. Although there are
many different types of antihypertensive medications, a number of them aren't safe to use
during pregnancy. Discuss with your doctor whether you need to use an antihypertensive
medicine in your situation to control your blood pressure.

22

Corticosteroids. If you have severe preeclampsia or HELLP syndrome, corticosteroid

medications can temporarily improve liver and platelet function to help prolong your
pregnancy. Corticosteroids can also help your baby's lungs become more mature in as
little as 48 hours an important step in preparing a premature baby for life outside the
womb.

Anticonvulsant medications. If your preeclampsia is severe, your doctor may

prescribe an anticonvulsant medication, such as magnesium sulfate, to prevent a first
seizure.
Bed rest
Bed rest used to be routinely recommended for women with preeclampsia. But research
hasn't shown a benefit from this practice, and it can increase your risk of blood clots, as
well as impact your economic and social lives. For most women, bed rest is no longer
recommended.

Hospitalization
Severe preeclampsia may require that you be hospitalized. In the hospital, your doctor
may perform regular nonstress tests or biophysical profiles to monitor your baby's wellbeing and measure the volume of amniotic fluid. A lack of amniotic fluid is a sign of poor
blood supply to the baby.
Delivery
If you're diagnosed with preeclampsia near the end of your pregnancy, your doctor may
recommend inducing labor right away. The readiness of your cervix whether it's
beginning to open (dilate), thin (efface) and soften (ripen) also may be a factor in
determining whether or when labor will be induced.
In severe cases, it may not be possible to consider your baby's gestational age or the
readiness of your cervix. If it's not possible to wait, your doctor may induce labor or
schedule a C-section right away. During delivery, you may be given magnesium sulfate
intravenously to prevent seizures.
After delivery, expect your blood pressure to return to normal within 12 weeks but
usually much sooner. If you need pain-relieving medication after your delivery, ask your
doctor what you should take. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
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ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve), can increase your
blood pressure. Acetaminophen (Tylenol, others) is usually a safe alternative.
PREVENTION
Researchers continue to study ways to prevent preeclampsia, but so far, no clear strategies
have emerged. Eating less salt, changing your activities, restricting calories, or consuming
garlic or fish oil doesn't reduce your risk. Increasing your intake of vitamins C and E
hasn't been shown to have a benefit, and the research into vitamin D is ongoing.
In certain cases, however, you may be able to reduce your risk of preeclampsia with:

Low-dose aspirin. If you had preeclampsia in a previous pregnancy that resulted in

delivery before 34 weeks' gestation or you had preeclampsia in more than one previous
pregnancy, your doctor may recommend a daily low-dose aspirin between 60 and 81
milligrams beginning late in your first trimester.

Calcium supplements. In some populations, women who have calcium deficiency

before pregnancy and who don't get enough calcium during pregnancy through their
diets might benefit from calcium supplements to prevent preeclampsia. However, it's
unlikely that women from the United States or other developed countries would have
calcium deficiency to the degree that calcium supplements would benefit them.
It's important that you don't take any medications, vitamins or supplements without first
talking to your doctor.
Before you become pregnant, especially if you've had preeclampsia before, it's a good
idea to be as healthy as you can be. Lose weight if you need to, and make sure other
conditions, such as diabetes, are well-managed.
Once you're pregnant, take care of yourself and your baby through early and
regular prenatal care. If preeclampsia is detected early, you and your doctor can work
together to prevent complications and make the best choices for you and your baby.

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PREMATURE RUPTURE OF MEMBRANE

Definition
Premature rupture of membranes (PROM) is a rupture (breaking open) of the membranes
(amniotic sac) before labor begins. If PROM occurs before 37 weeks of pregnancy, it is
called preterm premature rupture of membranes (PPROM).
PROM occurs in about 8% to 10% of all pregnancies. PPROM (before 37 weeks) accounts
for one-fourth to one-third of all preterm births.

Risk Factor
Rupture of the membranes near the end of pregnancy (term) may be caused by a natural
weakening of the membranes or from the force of contractions. Before term, PPROM is often
due to an infection in the uterus. Other factors that may be linked to PROM include the
following:

Low socioeconomic conditions (as women in lower socioeconomic conditions are less
likely to receive proper prenatal care)
Sexually transmitted diseases, such as chlamydia and gonorrhea

Previous preterm birth

Cigarette smoking during pregnancy

Trauma

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Vitamin C and collagen deficiency

Why is premature rupture of membranes a concern?

PROM is a complicating factor in as many as one-third of premature births. A significant risk
of PPROM is that most babies are born within a week of the membrane rupture. Another
major risk of PROM is development of a serious infection of the placental tissues called
chorioamnionitis. This can be very dangerous for mother and baby. Other complications that
may occur with PROM include placental abruption (early detachment of the placenta from
the uterus), compression of the umbilical cord, cesarean birth, and postpartum (after delivery)
infection.

Sign and symptom

The following are the most common symptoms of PROM:

Leaking or a gush of watery fluid from the vagina

Constant wetness in underwear

Diagnosis
In addition to a complete medical history and physical exam, PROM may be diagnosed in
several ways, including the following:

An exam of the cervix (may show fluid leaking from the cervical opening)
Testing of the pH (acid or alkaline) of the fluid

Looking at the dried fluid under a microscope (may show a characteristic fern-like
pattern)

Ultrasound. A diagnostic imaging technique that uses high-frequency sound waves

and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are
used to view internal organs as they function, and to assess how much fluid is around
the baby.

Treatment for premature rupture of membranes

Hospitalization
Expectant management (in very few cases of PPROM, the membranes may seal over
and the fluid may stop leaking without treatment, although this is uncommon unless
PROM was from a procedure, such as amniocentesis, early in gestation)

Monitoring for signs of infection, such as fever, pain, increased fetal heart rate, and/or
lab tests.

Giving the mother medications called corticosteroids that may help mature the lungs
of the fetus (lung immaturity is a major problem of premature babies). However,
corticosteroids may mask an infection in the uterus.
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Antibiotics (to prevent or treat infections) and to prolong the time to delivery

Tocolytics. Medications used to stop preterm labor.

Women with PPROM usually are induced to deliver at 34 weeks if stable. If there are
signs of abruption, chorioamnionitis, or fetal compromise, then early delivery would
be necessary.)
AFTER 37 WEEKS

If your pregnancy is past 37 weeks, your baby is ready to be born. You will need to go
into labor soon. The longer it takes for labor to start, the greater your chance of
getting an infection.
You can either wait for a short while until you go into labor on your own, or you can
be induced (get medicine to start labor). Women who deliver within 24 hours after
their water breaks are less likely to get an infection; so if labor isnt starting on its
own, it can be safer to be induced.
BETWEEN 34 AND 36 WEEKS

If you are between 34 and 37 weeks when your water breaks, The doctor will likely
suggest that you be induced. It is safer for the baby to be born a few weeks early than
it is for you to risk an infection.
BEFORE 34 WEEKS

If your water breaks before 34 weeks, it is more serious. If there are no signs of
infection, the doctor may try to hold off your labor by putting you on bed rest. Steroid
medicines are given to help the babys lungs grow quickly. The baby will do better if
its lungs have more time to grow before being born.
You will also receive antibiotics. They will help prevent infections. You and your
baby will be watched very closely in the hospital. Your doctor may do tests to check
your babys lungs. When the lungs have grown enough, your doctor will induce labor.

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REFERENCES

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1. Cunningham GF, Gant NF, Leveno JK, Gilstrap LC, Hauth JC, Wenstrom KD. Williams
Obstetrics, 21st ed. New York: McGraw-Hill, 1997: 101-5.
2. Grable IA. Cost-effectiveness of induction after preterm premature rupture of the membranes. Am
J Obstr&Gynecol 2002; 187:1153-8.
3. Romero R, Chaiworapongsa T, Espinoza J, Gomez R, Yoon Bh, Edwin S, et al. Fetal plasma
MMP-9 concentration are elevated in preterm premature rupture of the membranes. Am J
Obstr&Gynecol 2002; 187: 1101-8.
4. Williams Obstetrics, 21th ed, 423-469
5. Mercer, MB. High risk pregnancy series: an experts view. Preterm premature rupture of the
membranes. Am J Obstr&Gynecol 2003; 189: 111-8.
6. Sibai BM. Hypertensive disorders in women. 2001.
7. Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol
1998;92:883-9.
8. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet
Gynecol 2003;102:181-92.
9. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol 2005;105:40210.

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