Case DR Dipto

1
CASE REPORT

Supervisor:
dr. Sigit Diptoadi, Sp.OG

Presented by:
Elke tjahja 2012-061-174
Suwandi 2013 061 048
Agnes Hermawan 20130 061 050
Suryadi Limardi 2013 061- 053

Department of Obstetrics and Gynecology
School of Medicine Atma Jaya Catholic University of Indonesia
2014

2

CHAPTER I
CASE REPORT

Identity
Name : Mrs. T
Age : 40 years old
Ethnic : Indonesia
Religion : Moslem
Occupation : Housewife
Education : Junior High School
Date of Admission : July 10
th
2014
Resume
Chief complain
Patient complains mucous vaginal discharge and blood within it 4 hours before
admission.
History of Present Illness
10 hour before admission patient complaint about abdominal discomfort that
radiate to the back, intensified and worsen gradually. 4 hours before
admission patient complaint about mucous vaginal discharge and blood within
it. Later on patient was taken to Atma Jaya hospital. At this time, patient had
no complaint about blurred vision, headache, epigastric pain and swelling of
the feet.
History of Past Illness
o History of hypertension was confirmed since third pregnancy which is 15
years ago. Patient consume Captopril routinely before this pregnancy.
o History of diabetes mellitus denied
o History of allergy denied
o History of asthma denied
o History of trauma was confirmed 6 days before admission on a sitting
potition. No vaginal bleeding and no other complaints.

3

History of Menstrual
o Patient menarche at 16 years old
o Menstrual cycle: 30 days
o Regularly, once a month for 4 days, dysmenorrhea is denied
o First day last menstrual : October 20
th
, 2013

Obstetrics History

No. Date
Gestational
Age
Labor History Sex Birth Weight Breast feeding
1 1994 9 months
Spontaneous
vaginal
delivery
Male 2700 gr Yes
2 1997 9 months
Spontaneous
vaginal
delivery
Female 3000 gr Yes
3 1999 9 months
Spontaneous
vaginal
delivery
Female 2500 gr Yes
4 2004 9 months
Spontaneous
vaginal
delivery
Female 2600 gr Yes
5 2007 9 months
Spontaneous
vaginal
delivery
Female 2500 gr Yes
6 2011 9 months
Spontaneous
vaginal
delivery
Male 2800 gr Yes
7
July
10
th
,
2014

4

Obstetric data :
ANC : 5 times in public health center without USG, she had hypertension
(>140/90 mmHg).
EDD : July 27
th
2014

Physical Examination
General condition : Moderately ill
Level of consciousness : Compos mentis, GCS 15 (E4V5M6)
Vital Signs
Blood pressure : 160/90 mmHg
Heart rate : 80 bpm
Respiration rate : 24 x/minutes
Temperature : 36,7
o
C
Body Weight : 66 kg
Body Height : 150 cm
BMI : 29,3 kg/m
2
(obese)
General Examination
o Eyes : anemic conjunctiva -/-, icteric sclera -/-
o Mouth : wet oral mucous membrane
o Thorax
Lung :
I : symmetrical chest movement
P : symmetrical chest movement, symmetrical fremitus tactile
P : Sonor bilaterally
A : Vesicular breath sounds +/+ regular, rhonchi -/-, wheezing -/-

Heart :
I : Ictus cordis unseen
P : Ictus cordis was palpable at midclavicular line 4
th
intercostal space.
P: No cardiomegaly impression
A : 1
st
and 2
nd
heart sounds regular, murmur -, gallop

5

Mammae: areola hyperpigmentation +/+, nipples retraction -/-, breast milk -/-

o Abdomen
Inspection : convex, lineanigra (+), striae gravidarum (+)
Palpation : supple, pain on palpation (-)
Percussion : tympanic in all quadrants
Auscultation : bowel sounds (+), 5x/minute

o Extremities : Warm, Edema -/-, CRT < 2 seconds, physiologic reflexes
+/+/+/+, pathologic reflexes -/-

Obstetrics Examination
Fundal height : 32 cm
Fetal weight estimation : 3255 grams
Uterine Contraction : 3 times in 10 minutes for 20 - 30 seconds
Fetal heart rate : 148 x/minute
Leopold Maneuver :
Leopold I : breech
Leopold II : right side of the back
Leopold III : head
Leopold IV : 3/5
Genitalia :
I : Vulva within normal limit
In speculo : was not performed
Vaginal toucher : vaginal wall within normal limit, portio was thin and
tender, cervical dilatation 8 cm, cervical effacement 90%, amnion sac
(+), head presentation, hodge III.
Laboratory Examination
Hb : 11,6 g/dL
Ht : 34 %
Leukocyte : 8.100 cells/l
Thrombocyte : 248.000 cells/l
Blood type : O/rh+
6

Proteinuria : +++
AST/SGOT : 14 u/L (5 - 40 u/L)
ALT/SGPT : 7 u/uL (7 56 u/L)

CTG:

o Baseline: 150 bpm
o Variable: normal
o Acceleration: +
o Deceleration: + (variable)
o Fetal movement: 10 times in 20 minutes.
o His: -
o Result: reassuring

Admitting Diagnosis
G7P6, 40 years old, gravid 38-39 weeks based on first day of last menstrual
period, in labor, with superimposed preeclampsia on chronic hypertension with
single live fetus intrauterine, head presentation .

7

Planning
Inpatient
MgSO
4
loading dose 4 gram MgSO
4

diluted in 10 ml aqua bidestilata for
15 20 minutes and maintenance 1gram/hour in 500 ml RL in 24 hours.
Oxytocin 5 IU IV drip start from 12 dpm until his adequate.
Amniotomy
Misoprostol 3 x 200 mcg perrectal
Nifedipine tab 10 mg P.O.

11.27 Patient was given MgSO4 loading and maintenance dose.
11.32 Patient was given Oxytocin 5 IU IV drip
11.50 Amniotomy was performed
11.55 Blood pressure : 200/110 mmHg, patient was given nifedipine 10 mg PO.
13.00 Vaccum extraction was performed
13.10 Male baby was born with birth weight of 3550 grams, birth lengths 51cm, and
APGAR 7/9 .
Patient was given oxytocin IM 10 IU
13.15 Placenta was born, sized 35cm x 20cm x 2cm, cord length 40 cm, weighted 820
gram, intact cotiledon and membrane, no calfication, no hematoma, stool cell
+, central implantation of the cord.
13.20 Estimated blood loss 1020 ml
13.21 On examination : fundal height 3cm above umbilicus, moderate contraction,
intact birth canal, laceration -.
13.23 Patient was given misoprostol 3 tab per rectal.
13.30 Uterine tamponade was performed.
14.30 Observation : no vaginal bleeding, uterine contaction : strong
15.00 Hb postpartus : 10 g/dl.
Planning :
- Patient was given RL 1500 ml in two IV lines, consisted of :
Line I : RL 500 ml + MgSO
4
IV 1 gram given until 24 hours postpartum.
Line II: RL 1000 ml + oxytocin 5 IU
- Cefadroxil 3 x 500 mg PO.
- Mefenamic acid 3 x 500 mg PO
8

- Misoprostol 2 x 1 tab PO
- Nifedipin 3 x 10 mg PO
Final Diagnosis
Mother: P7, 40 y.o. post term labor, by assisted vacuum extraction due to
superimposed pre-eclampsia on chronic hypertension and history of early onset post
partum haemorrage caused by hypotonic uterine.

Baby :
Term nenonates, gestational age 38 to 39 weeks based on New Ballard Score,
APGAR score 7/9, birth weight 3550 grams, birth length 51cm, male, is diagnosed
with healthy neonates.

Follow-up 11/7/2014
S: abdominal tenderness +, headache, chest pain on coughing
O:
General appearance: Moderately ill
Consciousness: Compos mentis, GCS 15
Vital signs:
BP: 200/120 mmHg
HR: 80 bpm
RR: 16 x/min
Temperature: 36,5
o
C
Eyes: anemic conjunctiva -/-, icteric sclera -/-
Oral: wet oral mucosa
Thorax:
Cor: regular I
st
and II
nd
heart sound, gallop - , murmur -
Pulmo: vesicular breath sound +/+, wheezing -/-, crackles -/-
Mammae: areolar hyperpigmentation +/+, nipple retraction -/-, breast milk +/+
Abdomen:
I: convex, linea nigra +, striae gravidarum +
P: supple,tenderness +
P: tympany
A: bowel sound +, 5x/min
9

Extremity: warm, CRT < 2sec, edema -/-, physiologic reflex +/+/+/+, pathologic
reflex -/-
Obstetric Examination :
Mobilization: active
Fundal height: 2 cm above the umbilical, strong contraction
Lochia: rubra, 30 cc

A: P7, 40 y.o. post term labor, by assisted vacuum extraction due to superimposed
pre-eclampsia on chronic hypertension and history of early onset post partum
haemorrage caused by hypotonic uterine.

11.15 Therapy:
- Continuing Oxytocin and MgSO4 until 24 hours post partum
- After 24 hours post partum aff IV line, catheter and tamponade
- Metyldopa 3x250 mg PO

Follow-up 12/7/2014
S: coughs with secrets, headache - , chest pain
O:
General appearance: Slightly ill
Vital signs:
BP: 170/100 mmHg
HR: 68 bpm
RR: 24 x/min
Temperature: 36,3
o
C

Thorax:
10

Cor: regular I
st
and II
nd
Abdomen:
P: supple, tenderness -
P: tympany all around abdomen regio
A: bowel sound +, 6 x/min
reflex -/-
Obstetric Examination :
Fundal height: 1 cm below the umbilical, strong contraction


P :

Follow-up 13/7/2014
S: coughs with secrets, headache -, defecation -
O:
Vital signs:
BP: 170/90 mmHg
HR: 64 bpm
11

RR: 20 x/min
Temperature: 36,5
o
C

Thorax:
Cor: regular I
st
and II
nd
Abdomen:
P: tympany
A: bowel sound +, 5-6 x/min
reflex -/-
Obstetric Examination


P :
- Cefadroxil 3 x 500 mg PO

12

Follow-up 14/7/2014
S: coughs with secrets, headache -, defecation +
O:
Vital signs:
BP: 160/90 mmHg
HR: 60 bpm
RR: 24 x/min
Temperature: 37,2
o
C
Thorax:
Cor: regular I
st
and II
nd
Abdomen:
P: tympany
A: bowel sound +, 6 x/min
reflex -/-
Obstetric Examination


13

14/7/2014 06.30 Patient discharged home with medications:
- Ambroxol 3x1 tab
- Misoprostol 2x1 tab
- Mefenamic acid 3x500mg
- Metyldopa 3x250 mg
- Nifedipine 3x10 tab
- Edukasi pasien
14

CHAPTER II
CASE ANALYSIS

Mrs. T G7P6 40 years old, gravid 38-39 weeks based on first day of last
menstrual period, 10 hour before admission patient complaint about abdominal
discomfort that radiate to the back, intensified and worsen gradually. 4 hours before
admission patient complaint about mucous vaginal discharge and blood within it.
Later on patient was taken to Atma Jaya hospital. At this time, patient had no
complaint about blurred vision, headache, epigastric pain, swelling of the feet.
Patient has history of hypertension since third pregnancy which is 15 years ago and
patient consume Captopril routinely before this pregnancy. There is history of trauma
6 days before admission. No vaginal bleeding and no other complaints. Patient has
ANC visit 5 times in public health center.
On physical examination we found that the blood pressure is 160/90 mmHg,
heart rate 80 bpm, respiration rate 24 x/minutes, with temperature 36,7
o
C. General
examination within normal limits. On obstetrics Examination, the fundal height is 32
cm, fetal weight estimation is 3255 grams, uterine contraction 3 times in 10 minutes
for 20 -30 seconds, fetal heart rate 148 x/minute. Leopold maneuver finding is leopold
I: breech, leopold II: right side of the back, leopold III: head, and leopold IV : 3/5.
Vaginal toucher found that the vaginal wall within normal limit, portio was thin and
tender, cervical dilatation 8 cm, cervical effacement 90%, amnion sac (+), head
presentation, hodge III. In speculo was not performed. Laboratory examination result
hemoglobin 11,6 g/dL, hematocrit 34 %, leukocyte 8.100 cells/l, thrombocyte
248.000 cells/l, blood type O/rh+, proteinuria +++, AST/SGOT 14 u/L (5 - 40 u/L),
and ALT/SGPT 7 u/uL (7 56 u/L). Cardiotocography impression is reassuring.
In this patient, from our history taking and physical examination we concluded
some differential diagnosis : chronic hypertension and superimposed preeclampsia on
chronic hypertension. To exclude the differential diagnosis, we decide to check urine
protein level. And in this patient, the protein urine level was +3. This result
confirmed that this patient has superimposed preeclampsia on chronic hypertension.
Criteria diagnosis of superimposed preeclampsia on chronic hypertension is
proteinuria > 300 mg/24 hours in hypertensive women but no proteinuria before 20
weeks gestation or a sudden increase in proteinuria or blood pressure or platelet count
100,000/L in women with hypertension and proteinuria before 20 weeks gestation.
15

Because the patient had high blood pressure (200/100mmHg), nifedipine tab 1 x 10
mg was given to lower the blood pressure. To prevent eclampsia, the patient was
given MgSO
4
. By considering patient condition, which is in stage 1 active phase with
risk of increasing blood and intracranial pressure caused by maternal expulsive
efforts, assisted delivery with vacuum extraction was chosen. After the completion of
stage 2 of labor, the patient was given oxytocin 10 IU IM for helping the delivery
process of placenta and prevent prolonged stage 3 of labor. Methylergomethrine was
not given to this patient because it can increase arterial contraction which worsening
hypertension condition. Then, for the uterotonic medication, oxytocin and
misoprostol was chosen. During delivery process, total estimated blood loss volume
was 1020cc. This is an evident that this patient had early onset postpartum
hemorrhage (PPH). We found that the contraction of this patient uterus is inadequate,
no birth canal laceration and intact placenta. From these findings, we concluded that
this patient was suffering early onset PPH e.c. hypotonic uterine.
In this patient, we also found the risk for hypotonic uterine such as grand
multipara and augmented labor. The management of this case is to continue the
uterotonic agent and uterine tamponade to stop the bleeding. Then the patient was
still given the magnesium sulfate until 24 hours postpartum to prevent eclampsia. To
control the blood pressure, the patient was given nifedipine and methyldopa. After
several days of follow up, we found that the patient had cough with white secrete. By
this finding, the patient was given ambroxol as mucolytic to relieve the symptom.

Comparison of the case based on theoretical analysis

Comparison Case Theory PE
Risk factor - Chronic hypertension
- Advanced Maternal age
(older than 40 years old)
- Primiparity
- Previous preeclamptic
pregnancy
- Chronic hypertension or
chronic renal disease or both
- History of thrombophilia
- Multifetal pregnancy
- In vitro fertilization
- Family history of preeclampsia
- Type I diabetes mellitus or type
II diabetes mellitus
16

- Obesity
- Advanced maternal age ( older
than 40 years)
Clinical
findings
- Proteinuria (+3 dipstick)
- There is no facial edema or
feet edema
- Blood pressure: 160/90
mmHg
- Capillary leak (proteinuria,
ascites, pulmonary edema)
- excessive weight gain by the
edema
- or a spectrum of abnormal
hemostasis.
- Facial edema and pleural
effusion as the other
manifestations of capillary
leakage.
- Patient can present with
symptoms such as epigastric
pain, severe headache, nausea
or vomitting, and bleeding.
Management 1. Nifedipine, methyldopa 1. 1. Antihypertnsive Agent
Patient was given MgSO4
loading and maintenance
dose.
2. Magnesium sulfate for
seizure prophylaxis.
Corticosteroid is not given
because gestational age > 34
weeks.
3. Corticosteroid (for maturity
of the fetal lung) :
Betamethasone,
Dexamethasone

Comparison Case Theory HPP
Risk factor - Induced or augmented labor
(misoprostol)
- High parity (grand
multipara)
- The use of some general
anesthetics
- Overdistended uterus,
- Prolonged labor,
- Very rapid labor,
- Induced or augmented labor,
- High parity (grand multipara)
- Uterine atony in previous
17

pregnancy
- Chorioamnionitis
- Women with a large fetus,
multipel fetuses or hydramnions
cause overdistended uterus and
then cause uterine atony.
Clinical
findings
- Bleeding >500 mL - Usually steady bleeding more
than 500 mL
- Hypovolemia
- Failure of the pulse and blood
pressure to undergo more than
moderate alterations until large
amounts of blood have been
lost.
Management - Oxytocin 5 IU started from
12 dpm until his adequate
- Misoprostol 2 x 1 tab
Uterotonic Agents: oxytocin
(either low-dose IV or IM)
- No laceration on birth canal
- Intact placenta, cotiledon,
and membrane
- Uterine tamponade
-
-
Evaluation of Persistent
Bleeding
1. Manually compress the
uterus.
2. Obtain assistance.
3. If not already done, obtain
blood for typing and cross-
matching.
4. Observe blood for clotting to
rule out coagulopathy.
5. Begin fluid or blood
replacement.
6. Carefully explore the uterine
cavity.
7. Completely inspect the cervix
and vagina.
8. Insert a second intravenous
18

catheter for administration of
blood or fluids
Bimanual Compression and
Massage
Operative management :
Ligation, B-Lynch Brace suture

19

CHAPTER III
BASIC THEORY

Hypertension in Pregnancy
Hypertensive disorders of pregnancy represent a group of conditions associated
with high blood pressure during pregnancy, proteinuria, and in some cases
convulsions.

Epidemiology
Hypertensive disorders complicate 5 to 10 percent of all pregnancies, and
together they form one member of the deadly triad, along with hemorrhage and
infection, that contribute greatly to maternal morbidity and mortality rates. Williams
In the Global Burden of Diseases (GBD) 1990, hypertensive disorders of
pregnancy ranked 75th in terms of Disability-Adjusted Life Years (DALYs) and were
responsible for 6% of the burden of all maternal conditions. In developed country, 16
percent of maternal deaths were due to hypertensive disorders.
1

It is believed that 16% of maternal mortality in developing countries is due to
HDP, greater than other causes, such as hemorrhage, abortion, and sepsis. In
Indonesia, hypertension in pregnancy is the cause of 30-40% perinatal mortality.
2

Classification of Hypertensive Disorders :
1. Preeclampsia-eclampsia
2. Chronic hypertension (of any cause)
3. Chronic hypertension with superimposed preeclampsia
4. Gestational hypertension

Risk Factor
Primiparity
Previous preeclamptic pregnancy
Chronic hypertension or chronic renal disease or both
History of thrombophilia
Multifetal pregnancy
In vitro fertilization
Family history of preeclampsia
Type I diabetes mellitus or type II diabetes mellitus
Obesity
20

Systemic lupus erythematosus
Advanced maternal age ( older than 40 years)

Etiology
1. Abnormal Trophoblastic Invasion of uterine vessels
2. Immunological maladaptive tolerance between maternal, paternal (placental), and
fetal tissues.
3. Maternal maladaption to cardiovascular or inflammatory changes of normal
pregnancy.
4. Genetic factors including inherited predisposing genes as well as epigenetic
influences

Abnormal trophoblastic invasion of uterine vessels
In normal implantation, the uterine spiral arterioles undergo extensive
remodelling as they are invaded by endovascular trophoblast. These cells replace the
vascular endothelial and muscular linings to enlarge the vessels diameter. In
preeclampsia, there may be incomplete trophoblastic invasion. With such shallow
invasion, desidual vessels, but not myometrial vessels, become lined with
endovascular trophoblast. The deeper myometrial arterioles do not lose their
endothelial lining and musculoelastic tissue, and their mean external diameter in onlu
half that of vessels in normal placentas.
The abnormally narrow spiral arteriolar lumen impairs placental blood flow.
Diminished perfusion and a hypoxic environment eventually blead to release of
placental debris taht incites a systemic inflammatory response.

21

Immunological Factors
Another cause of preeclampsia is dysregulation of maternal immune tolerance to
paternally derived placental and fetal antigens. The histological changes at the
maternal-placental interfere are suggestive of acute graft rejection. Tolerance
dysregulation might also explain an increased risk when te paternal antigenic load is
increased.
Endothelial Cell Activation
Inflammatory changes are thought to be a continuation of the defective
placentation. Antiangiogenic and metabolic factors and other inflammatory mediators
are thought to provoke endothelial injury.
Nutritional Factors
Insuffiency of nutrition consists of antioxidant can be one cause of hypertension
in pregnancy
Genetic Factors
Ward and Lindheimer (2009) preeclampsia incidence :
20 - 40 % for daughters of preeclamptic mothers,
11-37% for sisters of preeclamptics women
22-47% in twin studies.

Pathogenesis
1. Cardiovascular System
Severe disturbances of normal cardiovascular in preeclampsia and eclampsia
patient are related to increased cardiac afterload because of the hypertension,
diminished cardiac preload pathologically, or increased cardiac preload iatrogenically
by IV crystalloid or colloid solution, and endothelial activation with extravasation of
IV fluid into the extracellular space (lungs).
2. Thrombcytopenia
In preeclampsia-eclampsia pateient, platelet aggregation is decreased compared
with the normal characteristic of pregnancy likely is due to platelet exhaustion, might
be caused by immunological processes or simply platelet deposition at sites of
endothelial damage.

22

3. Kidney
With development of preeclampsia, there may be a number of reversible
anatomical and pathophysiological changes. Renal perfusion and glomerular filtration
is reduced.
Mildly diminished of glomerular filtration may result from a reduced plasma
volume. Most of the decrement is probably from increased renal afferent arteriolar
resistance that may be elevated. Diminished filtration causes serum creatinine value to
rise. Plasma uric acid concentration is typically elevated in preeclampsia due to
enhanced tubular reabsorption.
Proteinuria happen when there is evidence that endothelial swelling results form
angiogenic factor withdrawal. The angiogenic protein is crucial for podocyte health
and its anivaction leads to podocyte dysfunction and endothelial swelling. Increased
excretion of urinary podocyte cells with eclampsia, shared by other proteinuric
disorder.
4. Liver
In preeclampsia-eclampsia patient, found extensive necrosis and infarction in
hepatic cell which can increase AST or ALT level. Symptomatic involvement,
typically manifest by moderate to severe right-upper or midepigastric pain and
tenderness.

Clinical Manifestation
Preeclampsia has various clinical manifestations. Although hypertension is
considered as the hallmark for the diagnosis of preeclampsia, preeclampsia can
manifest as either a capillary leak (proteinuria, ascites, pulmonary edema), excessive
weight gain by the edema, or a spectrum of abnormal hemostasis. Patients can have
facial edema and pleural effusion as the other manifestations of capillary leakage.
Excessive weight gain can be considered when weight increment per week exceeding
5 pounds (~2,2 kg). Patient can present with symptoms such as epigastric pain, severe
headache, nausea or vomitting, and bleeding.

23

Diagnosis
Diagnostic criteria for hypertensive disorder in pregnancy are summarized in table a.
3
Tabel a. Diagnosis Criteria of Hypertensive Disorders Complicating Pregnancy
3

Management
The goal of management in hypertension in pregnancy is preventing acute
complications of hypertension in the woman and maintaining a healthy pregnancy for
as long as possible. Another goal is to minimizing risks to the fetus that are
attributable to hypertension, vascular disease, and the possible effect of
antihypertensive medications that may alter maternal hemodynamics and reduce
uteroplacental perfusion or that may cross placenta and be harmful to the fetus.
Management of the hypertension with antihypertensive agent can be used to
treat severe hypertension. Pharmacologic antihypertensive therapy should be used for
24

women with severe hypertension (systolic blood pressure of 160 mmHg or higher or
diastolic blood pressure of 105 mmHg or higher) or at even lower blood pressure if
there is any evident of end-organ involvement to prevent acure maternal
cerebrovascular and coronary events .
4
Acute lowering of severe hypertension may be
accomplished by intravenous or oral medications (table 1). Long-term treatment of
blood pressure should maintain blood pressure level below severe range (table 2).

Table 1. Antihypertensive Agents Used for Urgent Blood Pressure Control in
Pregnancy
4

Table 2. Common Oral Hypertensive Agents in Pregnancy
4

Antepartum management of women with superimposed preeclampsia include
the administration of antenatal corticosteroids and use of magnesium sulfate for
25

seizure prophylaxis. Corticosteroids used to maturating fetal lung and administered to
women who receive expectant management at less than 34 weeks.
4
Delivery was
mandatory when severe features presents. Magnesium sulfate is used to orprevent
convulsions. It is administered perenterally and an effective anticonvulsant that avoids
CNS depression in the mother and the infant. It is given during labor and for 24 hours
post partum. Dosages for severe preeclampsia is summarized in table 3.
3

Table 3. Magnesium Sulfate Dosage Schedule for Severe Preeclampsia and
Eclampsia
3

The definitive treatment of severe preeclampsia is termination of the pregnancy.
When women with superimposed preeclampsia is complicated by uncontrollaable
severe hypertension, eclampsia, pulmonary edema, abruptio placenta, disseminated
intravascular coagulation, and nonreassuring fetal status, pregnancy should be
terminated soon after maternal stabilization irrespective of gestational age or full
corticosteroid treatment. If the gestational age less than 34 weeks and the maternal
and fetal conditions are stable, expectant management can be done by hospitalitation
and close monitoring. Termination can be done at 34 weeks gestational age. If the
women have severe superimposed preeclampsia, expectant management beyond 34
weeks of gestation is not recommended.
4

26

Complications
Complications can occured due to chronic hypertension and severe
preeclampsia. In acute setting, eclampsia can complicate severe preeclampsia.
Chronic hypertension will increase cardiovascular and neurovascular morbidity such
as ischemic heart disease, stroke, and thromboembolism. Renal failure was associated
with a fourfold increased risk when preeclampsia occured.
3

Postpartum hemorrhage
Postpartum hemorrhage is an event rather than a diagnosis that cause by
bleeding from the reduce of uterine tone, placental implantation site, trauma to the
genital tract or coagulation disorder. Postpartum hemorrhage defined as the loss of
500 ml of blood or more after completion of the third stage of labor. Early onset
postpartum hemorrhage defined as bleeding before 24 hours postpartum. Late onset
postpartum hemorrhage defined as bleeding between 24 hours and 12 weeks
postnatally.
5
Normal when the placenta separate from uterine wall, spiral arteries are avulsed
and then cause bleeding from placental implantation site. Hemostasis from this site is
achieved by contraction of the myometrium that compresses these vessel. And then,
this is followed by subsequent clotting and obliteration of their lumens.
Most postpartum hemorrhages are caused by uterine atony. There are several
predisposing factors that cause uterine atony or uterine hypotonic, such as use of some
general anesthetics, overdistended uterus, prolonged labor, very rapid labor, induced
or augmented labor, high parity, uterine atony in previous pregnancy and
chorioamnionitis. The overdistended uterus is due to hypotonic after delivery.
Women with a large fetus, multipel fetuses or hydramnions cause overdistended
uterus and then cause uterine atony. The woman whose uterine activity is remarkably
vigorous also cause postpartum atony. When the labor initiated or augmented with
oxytoxics can cause atony and hemorrhage. High parity may be a risk factor for
uterine atony. Another risk factor is prior postpartum hemorrhage, hasten placental
delivery can cause uterine atony.
3

27

Clinical Characteristics
Postpartum bleeding may begin before or after placental separation. Instead of
sudden massive hemorrhage, there usually is steady bleeding. At any given instant, it
appears to be only moderate, but may persist until serious hypovolemia develops.
Especially with hemorrhage after placental delivery, constant seepage can lead to
enormous blood loss. The effects of hemorrhage depend to a considerable degree on
the nonpregnant blood volume and the corresponding magnitude of pregnancy-
induced hypervolemia. A treacherous feature of postpartum hemorrhage is the failure
of the pulse and blood pressure to undergo more than moderate alterations until large
amounts of blood have been lost. The normotensive woman initially may actually
become somewhat hypertensive in response to hemorrhage. Moreover, the already
hypertensive woman may be interpreted to be normotensive although remarkably
hypovolemic. Accordingly, hypovolemia may not be recognized until very late.
The woman with severe preeclampsia or eclampsia does not have normally
expanded blood volume. Some studies documented a mean increase above
nonpregnant volume of only 10 percent in 29 eclamptic women at delivery. Thus,
these women are very sensitive to, or even intolerant of, what may be considered
normal blood loss. When excessive hemorrhage is suspected in the woman with
severe preeclampsia, efforts should be made immediately to identify those clinical and
laboratory findings that would prompt vigorous crystalloid and blood administration
to resuscitate hypovolemia. In some women after delivery, blood may not escape
vaginally but instead may collect within the uterine cavity, which can become
distended by 1000 mL or more of blood. In some, the attendant may massage a roll of
abdominal fat mistaken for the postpartum uterus. Thus, observation of the uterus
postpartum must not be left to an inexperienced person.
3

Diagnosis
Except possibly when intrauterine and intravaginal accumulation of blood is not
recognized, or in some instances of uterine rupture with intraperitoneal bleeding, the
diagnosis of postpartum hemorrhage should be obvious. The differentiation between
bleeding from uterine atony and that from genital tract lacerations is tentatively
determined by predisposing risk factors and the condition of the uterus. If bleeding
persists despite a firm, well-contracted uterus, the cause of the hemorrhage most
likely is from lacerations. Bright red blood also suggests arterial blood from
28

lacerations. To confirm that lacerations are a cause of bleeding, careful inspection of
the vagina, cervix, and uterus is essential. Sometimes bleeding may be caused by both
atony and trauma, especially after major operative delivery. If easily accessible, such
as with conduction analgesia, inspection of the cervix and vagina should be performed
after every delivery to identify hemorrhage from lacerations. Palpation of the uterine
cavity and inspection of the cervix and entire vagina is essential after internal podalic
version and breech extraction. The same is true when unusual bleeding is identified
during the second stage of labor.

Management
Immediate Postpartum Period
Uterotonic agents can be administered as soon as the infant's anterior shoulder is
delivered. Recent studies show a significantly lowered incidence of postpartum
hemorrhage in patients receiving oxytocin (either low-dose IV or IM) at the time of
delivery of the anterior shoulder and controlled cord traction compared to patients
receiving IV oxytocin following placental delivery. There was no greater incidence of
placental retention. However, populations without ultrasound screening for twins have
a potential risk for entrapment of an undiagnosed second twin, and oxytocin should
only be given after placental delivery. Routine administration of oxytocics during the
third stage reduces the blood loss of delivery and decreases the chances of postpartum
hemorrhage by 40%. Oxytocin, 1020 U/L of isotonic saline, or other intravenous
solution by slow intravenous infusion or 10 U intramuscularly can be used. Bolus
administration should not be used because large doses (> 5 U) can cause hypotension.
Ergot alkaloids (eg, methylergonovine maleate 0.2 mg intramuscularly) also can be
routinely used, but they are not more effective than oxytocin and pose more risk
because they rarely cause marked hypertension. This occurs most commonly with
intravenous administration or when regional anesthesia is used. Ergot alkaloids should
not be used in hypertensive women or in women with cardiac disease.

Repair of Lacerations
If bleeding is excessive before placental separation, manual removal of the
placenta is indicated. Otherwise, excessive manipulation of the uterus should be
avoided. The vagina and cervix should be carefully inspected immediately after
delivery of the placenta, with adequate lighting and assistants available. The
29

episiotomy is quickly repaired after massage has produced a firm, tightly contracted
uterus. A pack placed in the vagina above the episiotomy helps to keep the field dry;
attaching the free end of the pack to the adjacent drapes reminds the operator to
remove it after the repair is completed. The tendency of bleeding vessels to retract
from the laceration site is the reason for 1 of the cardinal principles of repair. Begin
the repair above the highest extent of the laceration. The highest suture is also used to
provide gentle traction to bring the laceration site closer to the introitus. Hemostatic
ligatures are then placed in the usual manner, and the entire birth canal is carefully
inspected to ensure that no additional bleeding sites are present. Extensive inspection
also provides time to confirm that prior hemostatic efforts have been effective.
A cervical or vaginal laceration extending into the broad ligament should not be
repaired vaginally. Laparotomy with evacuation of the resultant hematoma and
hemostatic repair or hysterectomy is required. Large or expanding hematomas of the
vaginal walls require operative management for proper control. The vaginal wall is
first exposed by an assistant. If a laceration accompanies the hematoma, the laceration
is extended so that the hematoma can be completely evacuated and explored. When
the bleeding site is identified, a large hemostatic ligature can be placed well above the
site. This ensures hemostasis in the vessel, which is likely to retract when lacerated.
The hematoma cavity should be left open to allow drainage of blood and ensure that
bleeding will not be concealed if hemostasis cannot be achieved. If no laceration is
present on the vaginal side wall when a hematoma is identified, then an incision must
be made over the hematoma to allow treatment to proceed as outlined.
Following delivery, recovery room attendants should frequently massage the
uterus and check for vaginal bleeding.

Evaluation of Persistent Bleeding
If vaginal bleeding persists after delivery of the placenta, aggressive treatment
should be initiated. It is not sufficient to perform perfunctory uterine massage, for
instance, without searching for the cause of the bleeding and initiating definitive
treatment. The following steps should be undertaken without delay:
1. Manually compress the uterus.
2. Obtain assistance.
3. If not already done, obtain blood for typing and cross-matching.
4. Observe blood for clotting to rule out coagulopathy.
30

5. Begin fluid or blood replacement.
6. Carefully explore the uterine cavity.
7. Completely inspect the cervix and vagina.
8. Insert a second intravenous catheter for administration of blood or fluids.
Manual Exploration of the Uterus
The uterus should be explored immediately in women with postpartum
hemorrhage. Manual exploration also should be considered after delivery of the
placenta in the following circumstances: (1) when vaginal delivery follows previous
cesarean section; (2) when intrauterine manipulation, such as version and extraction,
has been performed; (3) when malpresentation has occurred during labor and delivery;
(4) when a premature infant has been delivered; (5) when an abnormal uterine contour
has been noted prior to delivery; and (6) when there is a possibility of undiagnosed
multiple pregnancyto rule out twins.
Ensure that all placental parts have been delivered and that the uterus is intact.
This should be done even in the case of a well-contracted uterus. Exploration
performed for reasons other than evaluation of hemorrhage also should confirm that
the uterine wall is intact and should attempt to identify any possible intrauterine
structural abnormalities. Manual exploration of the uterus does not increase febrile
morbidity or blood loss. Uterine rupture detected by manual exploration in the
presence of postpartum hemorrhage requires immediate laparotomy. A decision to
repair the defect or proceed with hysterectomy is made on the basis of the extent of
the rupture, the patient's desire for future childbearing, and the degree of the patient's
clinical deterioration.

Bimanual Compression and Massage
The most important step in controlling atonic postpartum hemorrhage is
immediate bimanual uterine compression, which may have to be continued for 2030
minutes or more. Fluid replacement should begin as soon as a secure intravenous line
is in place. Typed and cross-matched blood is given when it is available. Manual
compression of the uterus will control most cases of hemorrhage due to uterine atony,
retained products of conception (once the products are removed), and coagulopathies.
Insert a Foley catheter into the bladder during compression and massage because
vigorous fluid and blood replacement will cause diuresis. A distended bladder will
31

interfere with compression and massage, will contribute to the patient's discomfort,
and may itself be a major contributor to uterine atony.
Curettage
Curettage of a large, soft postpartum uterus can be a formidable undertaking
because the risk of perforation is high and the procedure commonly results in
increased rather than decreased bleeding. The suction curette, even with a large
cannula, covers only a small area of the postpartum uterus, and its size and shape
increase the likelihood of perforation. A large blunt curette, the "banjo" curette,
probably is the safest instrument for curettage of the postpartum uterus. It can be used
when manual exploration fails to remove fragments of adherent placenta.
Curettage should be delayed unless bleeding cannot be controlled by
compression and massage alone. Overly vigorous puerperal curettage can result in
focal complete removal of the endometrium, particularly if the uterus is infected, with
subsequent healing characterized by formation of adhesions and Asherman's
syndrome (amenorrhea and secondary sterility due to intrauterine adhesions and
uterine synechiae). If circumstances permit, ultrasonic evaluation of the postpartum
uterus may distinguish those patients who will benefit from curettage from those who
should be managed without it.
Uterine Packing
Although once widely used for control of obstetric hemorrhage, uterine packing
is no longer favored. The uterus may expand to considerable size after delivery of the
placenta, thus accommodating both a large volume of packing material and a large
volume of blood. The technique also demands considerable technical expertise
because the uterus must be packed uniformly with 5 yards of 4-inch gauze, sometimes
with the aid of special instrumentation (Torpin packer). However, this method has
been used successfully, avoiding conversion to laparotomy in 9 reported cases. As a
last resort, uterine packing may be particularly appropriate in centers where an
interventional radiologist is not immediately available.
Uterotonic Agents
Oxytocin 2040 U/L of crystalloid should be infused, if not already running, at
a rate of 1015 mL/min. Methylergonovine 0.2 mg can be given intramuscularly but
is contraindicated if the patient is hypertensive. Intramyometrial injection of
prostaglandin F
2
(PGF
2
) to control bleeding was initially described in 1976.
Intravaginal or rectal prostaglandin suppositories, intrauterine irrigation with
32

prostaglandins, and intramyometrial injection of prostaglandins also have been
reported to control hemorrhage from uterine atony. Intramuscular administration of
15-methylprostaglandin analogue was successful in treating 85% of patients with
postpartum hemorrhage due to atony. Failures in these series occurred in women who
had uterine infections or unrecognized placenta accreta. Side effects usually are
minimal but may include transient oxygen desaturation, bronchospasm, and, rarely,
significant hypertension. Transient fever and diarrhea may occur.
Radiographic Embolization of Pelvic Vessels
Embolization of pelvic and uterine vessels by angiographic techniques is
increasingly common and has success rates from 8595% in experienced hands. In
institutions with trained interventional radiologists, the technique is worth considering
in women of low parity as an alternative to hysterectomy. With the patient under local
anesthesia, a catheter is placed in the aorta and fluoroscopy is used to identify the
bleeding vessel. Pieces of absorbable gelatin sponge (Gelfoam) are injected into the
damaged vessel or into the internal iliac vessels if no specific site of bleeding can be
identified. If bleeding continues, further embolization can be performed. This
technique has the advantage of being effective even when the cause of hemorrhage is
extrauterine and in the presence or absence of uterine atony.
Operative Management
The patient's wishes regarding further childbearing should be made clear as
soon as laparotomy is contemplated for the management of postpartum hemorrhage. If
the patient's wishes cannot be ascertained, the operator should assume that the
childbearing function is to be retained. Whenever possible, the spouse or family
members should also be consulted prior to laparotomy.
Pressure Occlusion of the Aorta
Immediate temporary control of pelvic bleeding may be obtained at laparotomy
by pressure occlusion of the aorta, which will provide valuable time to treat
hypotension, obtain experienced assistants, identify the source of bleeding, and plan
the operative procedure. In the young and otherwise healthy patient, pressure
occlusion can be maintained for several minutes without permanent sequelae.
Uterine Artery Ligation
During pregnancy, 90% of the blood flow to the uterus is supplied by the uterine
arteries. Direct ligation of these easily accessible vessels can successfully control
33

hemorrhage in 7590% of cases, particularly when the bleeding is uterine in origin.
Recanalization can occur, and subsequent pregnancies have been reported.
Internal Iliac Artery Ligation
Bilateral internal iliac (hypogastric) artery ligation is the surgical method most
often used to control severe postpartum bleeding. Exposure can be difficult,
particularly in the presence of a large boggy uterus or hematoma. Failure rates of this
technique can be as high as 57% but may be related to the skill of the operator, the
cause of the hemorrhage, and the patient's condition before ligation is attempted.
B-Lynch Brace Suture
An alternative to the vessel ligation techniques is placement of a brace suture to
compress the uterus in cases of diffuse bleeding from atony or percreta. A small case
series shows success and avoidance of hysterectomy using this novel approach.
Hysterectomy
Hysterectomy is the definitive method of controlling postpartum hemorrhage.
Simple hemostatic repair of a ruptured uterus with or without tubal ligation in a
woman of high parity or in poor condition for more extensive surgery may be
preferred unless she has intercurrent uterine disease. The procedure is undoubtedly
lifesaving.
Blood Replacement
Blood and fluid replacement are required for successful management of
postpartum hemorrhage. Massive transfusions may be necessary in patients with
severe hemorrhage. Component therapy is advocated, with transfusion of packed
cells, platelets, fresh-frozen plasma, and cryoprecipitate when indicated. Blood
products should be obtained and given without delay when needed, because
postponing transfusion may only contribute to the development of disseminated
intravascular coagulation.
Management of Delayed Postpartum Hemorrhage
Delayed postpartum hemorrhage is almost always due to subinvolution of the
placental bed or retained placental fragments. Involution of the placental site is
normally delayed when compared with that of the rest of the endometrium. However,
for unknown reasons, in subinvolution the adjacent endometrium and the decidua
basalis have not regenerated to cover the placental implantation site. The involutional
processes of thrombosis and hyalinization have failed to occur in the underlying blood
vessels, so bleeding may occur with only minimal trauma or other (unknown) stimuli.
34

Although the cause of subinvolution is unknown, faulty placental implantation,
implantation in the poorly vascularized lower uterine segment, and persistent infection
at the implantation site have been suggested as possible factors. Uterine compression
and bimanual massage, as previously described, control this type of bleeding, but it
may be necessary to continue compression and massage for 3045 minutes or longer.
As previously mentioned, transvaginal ultrasound may aid in diagnosis of retained
placental products. If imaging studies suggest intracavitary tissue, curettage is
warranted. Broad-spectrum antibiotics should be started when resuscitation allows.
Oxytocin 10 U intramuscularly every 4 hours or 1020 U/L intravenous solution by
slow continuous infusion, 15-methyl PGF
2
(Prostin 15M) 0.25 mg intramuscularly
every 2 hours, or ergot alkaloids, such as methylergonovine maleate 0.2 mg orally
every 6 hours, should be administered for at least 48 hours.
3

35

CHAPTER IV
REFERENCES

1. Dolea C, AbouZahr C. Global burden of hypertensive disorders of pregnancy in
the year 2000. Evid Inf Policy EIP World Health Organ. 2003;
2. BPPK Depkes. Riset Kesehatan Dasar (RISKESDAS 2007). Badan Penelit Dan
Pengemb Kesehat Dep Kesehat Repub Indones. 2008;
3. Cunningham F, Leveno K, Bloom S, Hauth J, Rouse D, Spong C. Williams
Obstetrics. 23rd ed. United States of America: McGraw Hill; 2010.
4. Hypertension in pregnancy. Washington DC: The American College of Obstetric
and Gynecologist; 2013.
5. Postpartum Haemorrhage, Prevention and Management (Green-top 52) [Internet].
2009 [cited 2014 Jul 19]. Available from: http://www.rcog.org.uk/womens-
health/clinical-guidance/prevention-and-management-postpartum-haemorrhage-
green-top-52

Case DR Dipto

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Case DR Dipto

Uploaded by

Copyright:

Available Formats

1

You might also like