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CASE REPORT

Supervisor:

dr. Sigit Diptoadi, Sp.OG

Presented by:

Elke tjahja 2012-061-174

Suwandi 2013 061048

Agnes Hermawan 20130 061050

Suryadi Limardi 2013 061- 053

Department of Obstetrics and Gynecology

School of Medicine Atma Jaya Catholic University of Indonesia

2014


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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 10th2014

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.


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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 20th, 2013

Obstetrics History

No. DateGestational

AgeLabor History Sex Birth Weight Breast feeding

1 1994 9 months

Spontaneous

vaginaldelivery

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

10th,

2014


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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 : 36,7o C

Body Weight : 66 kg

Body Height : 150 cm

BMI : 29,3 kg/m2(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 thintercostal space.

P: No cardiomegaly impression

A : 1stand 2ndheart sounds regular, murmur -, gallop


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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+


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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 .


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Planning

Inpatient

MgSO4 loading dose 4 gram MgSO4diluted 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 drip11.50 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 + MgSO4IV 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


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- 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: 36,5oC

Eyes: anemic conjunctiva -/-, icteric sclera -/-

Oral: wet oral mucosa

Thorax:

Cor: regular Ist

and IInd

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


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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

-


- Mefenamic acid 3 x 500 mg PO


-

Nifedipin 3 x 10 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: 36,3oC



Thorax:


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Cor: regular Ist and IInd heart sound, gallop - , murmur -

Pulmo: vesicular breath sound +/+, wheezing -/-, crackles -/-


Abdomen: I: convex, linea nigra +, striae gravidarum +

P: supple, tenderness -

P: tympany all around abdomen regio

A: bowel sound +, 6 x/min


reflex -/-

Obstetric Examination :

Mobilization: active

Fundal height: 1 cm below the umbilical, strong contraction





P :


-




-

Nifedipin 3 x 10 mg PO

Follow-up 13/7/2014

S:coughs with secrets, headache -, defecation -

O:



Vital signs:

BP: 170/90 mmHg HR: 64 bpm


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RR: 20 x/min

Temperature: 36,5oC



Thorax:




Abdomen:

I: convex, linea nigra +, striae gravidarum + P: supple, tenderness -

P: tympany

A: bowel sound +, 5-6 x/min


reflex -/-

Obstetric Examination


Fundal height: 1 cm below the umbilical, strong contraction





P :


- Cefadroxil 3 x 500 mg PO



- Nifedipin 3 x 10 mg PO


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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: 37,2oC



Thorax:




Abdomen:

I: convex, linea nigra +, striae gravidarum +

P: supple, tenderness - P: tympany

A: bowel sound +, 6 x/min


reflex -/-

Obstetric Examination


Fundal height: 2 cm below the umbilical, strong contraction Lochia: rubra, 10 cc





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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


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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 hashistory 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 36,7o 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.


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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 MgSO4. 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 typeII diabetes mellitus


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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 Nifedipine, methyldopa 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


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pregnancy

Chorioamnionitis

Women with a large fetus,

multipel fetuses or hydramnions

cause overdistended uterus andthen 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 membraneUterine 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


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catheter for administration of

blood or fluids

Bimanual Compression and

Massage

Operative management :

Ligation, B-Lynch Brace suture


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Systemic lupus erythematosus

Advanced maternal age ( older than 40 years)

Etiology1.

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.


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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 ofIV 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.


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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.


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Diagnosis

Diagnostic criteria for hypertensive disorder in pregnancy are summarized in table a. 3

Tabel a. Diagnosis Criteria of Hypertensive Disorders Complicating Pregnancy3

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


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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

Pregnancy4

Table 2. Common Oral Hypertensive Agents in Pregnancy4

Antepartum management of women with superimposed preeclampsia include

the administration of antenatal corticosteroids and use of magnesium sulfate for


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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

Eclampsia3

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 beterminated 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


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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 of500 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


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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


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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


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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.


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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


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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 F2 (PGF2) to control bleeding was initially described in 1976.

Intravaginal or rectal prostaglandin suppositories, intrauterine irrigation with


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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


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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.


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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 PGF2 (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


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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

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