case:

G1P0A0, GR 31 weeks + PLACENTA

ABRUPTION
Counsellor
dr. Gioseffi Sp.OG

Prepared by
Christine Surbakti - 406147010
Marcelly Raymando - 406147011
Melani Sugiarti Wijaya Kangmartono - 4060147014

OBSTETRICS AND GYNECOLOGY CLERKSHIP

TARUMANAGARA UNIVERSITY
RSUD CIAWI, BOGOR
Period Desember 29th 2014 March 7th 2015

Admitted to hospital on 9th February 2015

Patients Identity

Name

: Mrs.NH

Age

: 24 years old

Occupation

: Housewife

Education

: Elementary school

Race

: Sundanese

Religion

: Muslim

Address

: Kp.Sawah,Ciomas-Bogor

Patients Husbands Identity

Name

: Mr. I

Age

: 32 years old

Occupation

: self-employed

Education

: Senior High School

Race

: Sundanese

Religion

: Muslim

Address

: Kp.Sawah,Ciomas-Bogor

1. History Taking
Directly with the patient at 12.58 p.m. on February 9th 2015
Main complaint: Vaginal bleeding
Present Illness:
The patient came to the maternity ER with active vaginal bleeding since
12 p.m. The blood discharged was bright red. She mentioned that she had not
felt the fetal movement since 7.00 a.m. She also was having uterine
contractions, blurred vision, nausea and vomit. Her first day of the final
menstruation was on 10th July 2014.
Past Medical History:
-

Hypertension (-)

Diabetes mellitus (-)

Heart Disease (-)

Asthma (-)

Seizures (-)

Irregular menstrual cycle (-)

Menstruation:
-

Menarche

: 14 years old

Menstrual cycle

: 28 days

Duration

: 7 days

Diaper/day

: 2-3 x/days

Menstrual pain

: (-)

Marriage:
- Married: 1x, age 21th
Contraception : none
Operation: none
Antenatal Care: regular, monthly with midwife
supplement: fe & folic acid (+)
2. Physical Examination
On February 9th 2015, 12.58 pm

Overall condition : moderately pain

Awareness : full consciousness

Vital Sign: - Blood pressure: 110/80 mmHg

- Pulse: 120x/min
- Respiratory rate: 25x/min
- Temperature: 36.7oc

GENERAL EXAMINATION
Head

Eye

: Anemic conjuctiva +/+, icteric sclera -/Pupil diameter symmetrical, eyelid edema -/-

Ear

: tympany membrane intact +/+, earwax -/-

Nose : septal deviation -/-, mucous discharge -/-

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

Mouth : oral hygiene (+), mucosa normal

Neck : Trachea in the middle, normal lymph nodes and thyroid gland
Thorax

Breast : normal , Inverted nipple -/-

Lung : Inspection: Barrel chest(-), pectus excavatum(-), pectus

carinatum(-)
Palpation: tactile fremitus right=left
Percussion: Resonance +/+
Auscultation: vesicular +/+, crackles -/-, wheezing -/-

Heart : Inspection : Ictus cordis not visible

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

Obstetric Abdominal Examination

Inspection : striae gravidarum(+), scar (-), fetal movement (-)
Palpation:
Fetal parts were not palpable due to the presence of the severe abdominal pain
(defans musculaire).
Auscultation:

FHR: absent

External genitalia
-Inspection: condition of vulva / vagina normal
Bleeding (+)
- In-speculo: Not done

Internal Genitalia
-

Not done

Laboratory Test
Haematology

Hb

: 8,3 g/dl (12.0-15.0 g/dl)

Ht

: 24% (36-46 %)

Leucocyte

: 29100 /ul (4000-10000/ul)

Platelet count

: 125000 /ul (150000-45000/ul)

CT

: 1130 (6-11 minutes)

BT

: 330 (1-6 minutes)

Chemistry Screens

SGOT

: 32

SGPT

: 12

Ureum

: 25,5

Creatinin

: 1.27

Blood sugar

: 111

3. Resume
A 24 years old woman came to the maternity ER on 09th February 2015 because
active vaginal bleeding since 12 p.m. The blood discharged was bright red. She
mentioned that she had not felt the fetal movement since 7.00 a.m. She also was
having uterine contractions, blurred vision, nausea and vomit. Her first day of
the final menstruation was on 10th July 2014.

Vital Sign

: - Blood pressure: 110/80 mmHg

- Pulse : 120x/min
- Respiratory rate : 25x/min
- Temperature : 36.7oc

Eye

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

Thorax

: within normal limits

Abdomen

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

Palpation : Leopold examination could not be done because the fetus

was not palpable

External genitalia
Inspection : condition of vulva / vagina normal
Bleeding (+)
Speculum examination : not done

Internal Genitalia : Not done

Laboratory Test
-

Decreased hemoglobin, hematocrite, thrombocytes

Increased leucocytes

Working Diagnosis : G1P0A0, GA 31 weeks + placental abruption

4. Management:
Conservative treatment

IVFD RL 2000cc/ 24 hours, 20 dpm

Oxygen 3-4 L

Urine catheter

Observation of vital signs

Kalnex 500 mg

Vit K

Gelofusin loading dose

Ceftriaxone 2gr in NaCl 100cc

SC Cito

16.00 :the operation began

16.50 : post op instructions:
- IVFD 2000cc/24 hrs
- Ceftriaxone 1x2 gr IV
- Kaltrofen supp 3x1
- Check post op Hb
- Bed rest in supine position for 24 hrs
- Observe vital signs
- Oxytocin 20 IU per 500 cc

- Misoprostol 800 mg per rectal

17.00 : patient has been transfered to ICU
23.22 :Check Lab
Laboratory Test
Haematology
Hb

: 6,0 g/dl (12.0-15.0 g/dl)

Ht

: 18% (36-46 %)

Leucocyte

: 29200 /ul (4000-10000/ul)

Platelet count

: 101000 /ul (150000-45000/ul)

Chemistry Screens
Natrium

: 135 mEq/L

Kalium

: 7.4 mEq/L

Chlorida

: 107mg/dL

Glucose tolerance test : 107 mg/dL

01.00 : get lasix 1Amp(IV)
02.00 : get blood transfusion 3 bags
Follow Up ( 10th February 2015, at 07.00 am at ICU)

: abdominal pain

: CM/moderate pain

Vital Sign:

BP

: 109/45 mmHg

Pulse

: 78 x/mins

RR

: 22x/mins

Temperature

: 36.6oC

General exam :
Eye

: CA +/+ , SI -/-

Thorax

: C/P within normal limit

Abdomen

: flat, supple, bowel sound +, fundal height:

2cm below umbilicus, uterine contraction:
good,post operation wound covered verban

Gen

: v/v normal, bleeding(+)

Extremities

: Oedema (-/-)

: P1A0 mature parturition with SC for indication placental

abruption(POD I)
P

: RL 2000 cc per 24 hrs

1 bag of blood
Ceftriaxone 1x2gr IV
Kaltrofen supp 3x1
Gradual mobilization
Feeding test

07.45 : infus RL 500cc + Oxytocin 1 Amp + Tramadol 1 Amp every 6 hrs

15.00 : ceftriaxone
kaltrofen supp
PRC 250 cc
Follow Up ( 11th February 2015, at 07.00 am at ICU)
S

: pain in post operation wound

: CM/moderate pain

Vital Sign:

BP

: 100/60 mmHg

Pulse

: 82 x/mins

RR

: 20x/mins

Temperature

: 36.6oC

General exam :
Eye

: CA +/+ , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm below

umbilicus,

uterine contraction: good ,post operation

wound covered verban

Gen

: v/v normal, bleeding(+)

Extremities

: Oedema (-/-)

: P1A0 mature parturition with SC for indication placental

abruption (POD II)

P

: RL 2000 cc per 24 hrs

Cefriaxone 1 x 2gr

Asam Mefenamat 3x500 mg

Oxytocin
get blood transfusion 2 bags
Laboratory Test
Haematology

Hb

: 6,9g/dl (12.0-15.0 g/dl)

Ht

: 20% (36-46 %)

Leucocyte

: 25100 /ul (4000-10000/ul)

Platelet count : 105000 /ul (150000-45000/ul)

Ureum

: 84,7

Creatinin

: 3,89

Follow Up ( 12th February 2015, at 07.00 am at Teratai A)

: no complaint

: CM/moderate pain

Vital Sign:

BP

: 110/60 mmHg

Pulse

: 86 x/mins

RR

: 20x/mins

Temperature

: 36.6oC

General exam :
Eye

: CA -/- , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm

below umbilicus, uterine contraction:good,post operation wound

no blood,and pus

Gen

: v/v normal, bleeding(+) minimal

Extremities

: Oedema (-/-)

: P1A0 mature parturition with SC for indication placental

abruption(POD III)
P

: Ceftriaxone 1x2 gr

-12.00 : Check Lab

Laboratory Test
Haematology

Hb

: 7,3g/dl (12.0-15.0 g/dl)

Ht

: 20% (36-46 %)

Leucocyte

: 15500 /ul (4000-10000/ul)

Platelet count : 120000 /ul (150000-45000/ul)

Ureum

: 86,2

Creatinin

: 2,34

Potasium

: 1,29

Kalium

Chlorida

: 106

GDS

: 76

-23.30

: 4,0

: patient has been transfered to Teratai A

Follow Up ( 13th February 2015, at 07.00 am at Teratai A)

S

: no complaint

: CM

Vital Sign:

BP

: 120/70 mmHg

Pulse

: 75 x/mins

RR

: 16x/mins

Temperature

: 36.6oC

General exam :
Eye

: CA +/+ , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm below

umbilicus , uterine contraction: good

Gen

: v/v normal, bleeding(-)

Extremities

: Oedema (-/-)

: P1A0 mature parturition with SC for indication placental

abruption(POD IV)
P

: Cefadroxil 500 mg 2x1

Asam Mefenamat 500mg 3x1

SF 1x1
-19.30 : get blood transfusion

Follow Up ( 14th February 2015, at 07.00 am at Teratai A)

S

: no complaint

: CM

Vital Sign:

BP

: 120/70 mmHg

Pulse

: 75 x/mins

RR

: 16x/mins

Temperature

: 36.6oC

General exam :
Eye

: CA -/- , SI -/-

Thorax

: C/P within normal

Abdomen

: flat, supple, bowel sound +, fundal height: 2cm below

umbilicus, uterine

contraction: good

Gen

: v/v normal, bleeding(-)

Extremities

: Oedema (-/-)

: P1A0 mature parturition with SC for indication placental

abruption(POD V)
P

: Cefadroxil 500 mg 2x1

Asam Mefenamat 500mg 3x1
SF 1x1

-09.00 : Check Lab

Laboratory Test
Haematology

Hb

: 8,2g/dl (12.0-15.0 g/dl)

Ht

: 23% (36-46 %)

Leucocyte

: 13300 /ul (4000-10000/ul)

Platelet count : 200000 /ul (150000-45000/ul)

5. Case analysis

We agreed the patient has a severe placenta abruption because from sign
and symptom that we found are same from references, there are :
- Vaginal bleeding
- Absence of fetal heart sounds
- Uterine tenderness
- Defans musculare
- Shock
- Trombositopenia
- Hypofibrinogenemia

We agreed the treatment in the case is caesarean delivery because

in the references, the treatment of severe plancenta abruption is
caesarean delivery.

PLACENTAL ABRUPTION
Placental abruption (or abruption placentae) is defined as the separation
of the placenta from its site of implantation before delivery. Placental abruption
complicates approximately 1 in 20 deliveries. As a significant cause of thirdtrimester bleeding associated with fetal and maternal morbidity and mortality,
placental abruption must be considered whenever bleeding is encountered in the
second half of pregnancy. Some of the bleeding of placental abruption usually
insinuates itself between the membranes and uterus, and then escapes through
the cervix, causing external hemorrhage. Less often, the blood does not escape
externally but is retained between the detached placenta and the uterus, leading
to concealed hemorrhage. Placental abruption may be total or partial. Placental
abruption with concealed hemorrhage carries with it much greater maternal and
fetal hazards, not only because of the possibility of consumptive coagulopathy,
but also because the extent of the hemorrhage is not appreciated and the
diagnosis typically is made later (Chang and co-workers, 2001).

1.

Epidemiology
The frequency of abruptio placentae in the United States is
approximately 1%, and a severe abruption leading to fetal death occurs in
0.12% of pregnancies (1:830).
Abruptio placentae also occurs in about 1% of all pregnancies
throughout the world.
Race predilection

Placental abruption is more common in African American women than in

white or Latin American women. However, whether this is the result of
socioeconomic, genetic, or combined factors remains unclear.
Age predilection
An increased risk of placental abruption has been demonstrated in
patients younger than 20 years and those older than 35 years
2. Etiology
The primary cause of placental abruption is usually unknown, but
multiple risk factors have been identified. However, only a few events have
been closely linked to this condition.
3. Risk factor
Risk factors in abruptio placentae include the following:

Maternal hypertension - Most common cause of abruption, occurring in

approximately 44% of all cases

Maternal trauma (eg, motor vehicle collision [MVC], assaults, falls) Causes 1.5-9.4% of all cases

Cigarette smoking

Alcohol consumption

Cocaine use

Short umbilical cord

Sudden decompression of the uterus (eg, premature rupture of

membranes, delivery of first twin)

Retroplacental fibromyoma

Retroplacental bleeding from needle puncture (ie, postamniocentesis)

Idiopathic (probable abnormalities of uterine blood vessels and decidua)

Previous placental abruption

Chorioamnionitis

Prolonged rupture of membranes (24 h or longer)

Maternal age 35 years or older

Maternal age younger than 20 years

Male fetal sex

Low socioeconomic status

Elevated second trimester maternal serum alpha-fetoprotein (associated

with up to a 10-fold increased risk of abruption)

Subchorionic hematoma

T. Boisram a,b,, N. Sanans b,c, G. Fritz b, E. Boudier b, G. Aissi a, R. Favre a,

B. Langer . Placental abruption: risk factors, management and maternalfetal
prognosis.

Department of GynecologyObstetrics, Strasbourg University

Hospitals, Centre Mdico-Chirurgical Obsttrique (CMCO), Strasbourg Cedex,

France . 2014
4. Classification of placental abruption
Classification of placental abruption is based on extent of separation (ie,
partial vs complete) and location of separation (ie, marginal vs central).

Clinical classification is as follows:

Class 0 Asymptomatic

Class 1 - Mild (represents approximately 48% of all cases)

Class 2 - Moderate (represents approximately 27% of all cases)

Class 3 - Severe (represents approximately 24% of all cases)

A diagnosis of class 0 is made retrospectively by finding an organized

blood clot or a depressed area on a delivered placenta.
Class 1 characteristics include the following:

No vaginal bleeding to mild vaginal bleeding

Slightly tender uterus

Normal maternal BP and heart rate

No coagulopathy

No fetal distress

Class 2 characteristics include the following:

No vaginal bleeding to moderate vaginal bleeding

Moderate to severe uterine tenderness with possible tetanic

contractions

Maternal tachycardia with orthostatic changes in BP and heart rate

Fetal distress

Hypofibrinogenemia (ie, 50-250 mg/dL)

Class 3 characteristics include the following:

No vaginal bleeding to heavy vaginal bleeding

Very painful tetanic uterus

Maternal shock

Hypofibrinogenemia (ie, < 150 mg/dL)

Coagulopathy

Fetal death

5.

Pathology
Placental abruption is initiated by hemorrhage into the decidua basalis.
The decidua then splits, leaving a thin layer adherent to the myometrium.
Consequently, the process in its earliest stages consists of the development
of a decidual hematoma that leads to separation, compression, and the
ultimate destruction of the placenta adjacent to it.
In its early stage, there may be no clinical symptoms. The condition is
discovered only on examination of the freshly delivered organ, which has a
circumscribed depression measuring a few centimeters in diameter on its
maternal surface, and is covered by dark, clotted blood. Undoubtedly, it
takes at least several minutes for these anatomical changes to materialize
Thus, a very recently separated placenta may appear no different from a
normal placenta at delivery. According to Benirschke and Kaufmann
(2000), and in our experiences, the "age" of the retroplacental clot cannot
be determined exactly.
In some instances, a decidual spiral artery ruptures to cause a
retroplacental hematoma, which as it expands disrupts more vessels to
separate more placenta. The area of separation rapidly becomes more
extensive and reaches the margin of the placenta. Because the uterus is still
distended by the products of conception, it is unable to contract sufficiently
to compress the torn vessels that supply the placental site. The escaping
blood may dissect the membranes from the uterine wall and eventually
appear externally or may be completely retained within the uterus.
CONCEALED HEMORRHAGE.
Retained or concealed hemorrhage is likely when:
1. There is an effusion of blood behind the placenta but its margins still
remain adherent.
2. The placenta is completely separated yet the membranes retain their
attachment to the uterine wall.
3. Blood gains access to the amnionic cavity after breaking through the
membranes.

4. The fetal head is so closely applied to the lower uterine segment that the
blood cannot make its way past it.
Most often, however, the membranes are gradually dissected off the uterine
wall, and blood sooner or later escapes.

6.

Clinical Presentation
Women presenting PA had metrorrhagia in 81.9%, uterine hypertonia in
26.1%, abdominal pains in 27.8% and abnormal fetal heart rate (aFHR) in
64.8% of cases. Overall, the classic clinical triad of metrorrhagia, uterine
hypertonia and abdominalpelvic pain, was found in 24 women (9.7%).
Among women who presented metrorrhagia in the second or third trimester,
it was linked to PA in 13.1%: metrorrhagia was therefore the only clinical
presenting sign in 60.5% of cases. Metrorrhagia plus aFHR was the most
common association, found in 39.3% of PA cases.

T. Boisram a,b,, N. Sanans b,c, G. Fritz b, E. Boudier b, G. Aissi a, R. Favre a,

B. Langer . Placental abruption: risk factors, management and maternalfetal
prognosis.

Department of GynecologyObstetrics, Strasbourg University

Hospitals, Centre Mdico-Chirurgical Obsttrique (CMCO), Strasbourg Cedex,

France . 2014

7.

Diagnostic
PA diagnosis was made either on the basis of direct visualisation of a
hematoma at the time of placental delivery or in a frank clinical setting
(association of several clinical signs including: metrorrha- gia, abdominal
pelvic pain, uterine hypertonia, non-reassuring fetal status, gestational
hypertension, preterm premature rupture of membranes (PPROM),
premature labor and IUFD). In some cases, PA was directly visualised on
antenatal ultrasonography. Patho- logical examination was usually
requested when PA was suspected.

8.

Physical Examination
The physical examination of a patient who is bleeding must be targeted
at determining the origin of the hemorrhage. Simultaneously, the patient
must be stabilized quickly. With placental abruption, a relatively stable
patient may rapidly progress to a state of hypovolemic shock.
Do not perform a digital examination on a pregnant patient with vaginal
bleeding without first ascertaining the location of the placenta. Before a
pelvic examination can be safely performed, an ultrasonographic
examination should be performed to exclude placenta previa.[17] If placenta
previa is present, a pelvic examination, either with a speculum or with
bimanual examination, may initiate profuse bleeding.
a.

Vaginal bleeding
Bleeding may be profuse and come in "waves" as the patient's
uterus contracts. A fluid the color of port wine may be observed when
the membranes are ruptured.

b.

Contractions/uterine tenderness
Uterine contractions are a common finding with placental
abruption. Contractions progress as the abruption expands, and
uterine hypertonus may be noted. Contractions are painful and

palpable. Uterine hyperstimulation may occur with little or no break

in uterine activity between contractions
c.

Shock
Patients may present with hypovolemic shock, with or without
vaginal bleeding, because a concealed hemorrhage may be present. As
with any hypovolemic condition, blood pressure drops as the pulse
increases, urine output falls, and the patient progresses from an alert
to an obtunded state as the condition worsens.

d.

Absence of fetal heart sounds

This occurs when the abruption progresses to the point of fetal
death

e.

Signs of possible fetal jeopardy

Signs of possible fetal jeopardy include the following:

f.

Prolonged fetal bradycardia

Repetitive, late decelerations

Decreased short-term variability

High Fundal height

This may increase rapidly because of an expanding intrauterine
hematoma.

9.

Work Up
No laboratory studies have been shown to definitively help with the
differential diagnosis of abruptio placentae; however, multiple laboratory
studies may be helpful in the management of this problem.

a. CBC Count
A complete blood cell (CBC) count can help to determine the
patient's current hemodynamic status, but findings are not reliable for
estimating acute blood loss.
In an acute hemorrhage, the fall in hematocrit value lags several
hours behind the bleeding and may be falsely decreased by the
administration of crystalloid fluids during resuscitation.
b. Fibrinogen examination
Pregnancy is associated with hyperfibrinogenemia; therefore,
modestly depressed fibrinogen levels may represent significant
coagulopathy. A fibrinogen level of less than 200 mg/dL suggests that
the patient has a severe abruption.
The goal should be to keep the fibrinogen level above 100
mg/dL, which can be accomplished via transfusion of fresh frozen
plasma or cryoprecipitate, as necessary.
c. Prothrombin Time/Activated Partial Thromboplastin Time
Some form of DIC is present in up to 20% of patients with severe
abruptions. Because many of these patients require cesarean delivery,
knowing a patient's coagulation status is imperative.
d. Blood Urea Nitrogen/Creatinine
The hypovolemic condition brought on by a significant abruption
also affects renal function. The condition usually self-corrects without
significant residual dysfunction, if fluid resuscitation is timely and
adequate.

e. Ultrasonography
Ultrasonography is a readily available and important imaging
modality for assessing bleeding in pregnancy. The quality and
sensitivity of ultrasonography in detecting placental abruptions has
improved significantly; however, it is not a sensitive modality for this
purposefindings are positive in only 25% of cases confirmed at
delivery, and the negative predictive value is low at around 50%.
In addition, there does not appear to be any clinical difference in
presentation between women who have an abruption seen on
ultrasonography and those who do not. Ultrasonographic studies do
1help to quickly diagnose placenta previa as the etiology of bleeding, if
present.
Placental abruption shows as a retroplacental clot on an
ultrasonographic image, but not all abruptions are ultrasonographically
detectable. In the acute phase, a hemorrhage is generally hyperechoic,
or even isoechoic, compared with the placenta; a hemorrhage does not
become hypoechoic for nearly a week.
Ultrasonography can help to exclude other causes of thirdtrimester bleeding. Possible findings consistent with an abruption
include (1) retroplacental clot (ie, hyperechoic to isoechoic in the acute
phase, changing to hypoechoic within a wk), (2) concealed
hemorrhage, or (3) expanding hemorrhage.
f. Nonstress Test
External fetal monitors often reveal fetal distress, as evidenced
by late decelerations, fetal bradycardia, or decreased beat-to-beat
variability.
An increase in the uterine resting tone may also be noticed, along
with

frequent

contractions

that

may

progress

hyperstimulation, as seen in the fetal tracing below.

to

uterine

h. Histologic Findings
After delivery of the placenta, a retroplacental clot may be noted.
Another possible finding involves extravasation of blood into the
myometrium, which produces a purple discoloration of the uterine
serosa. This phenomenon is known as a Couvelaire uterus.
10. Differential Diagnoses
Ectopic Pregnancy

Ovarian Cysts

Ovarian Torsion

Placenta Previa

Preeclampsia

Pregnancy Trauma

11. Managament
In contrast to the more conservative trend that characterizes the
management of placenta previa, management of abruptio placentae has for
the most part become more aggressive. In the past, studies have noted the
numerous deaths among viable fetuses alive at the time of admission and
have urged more liberal use of cesarean section for the delivery of patients
with placental abruption. However, some patients may be candidates for
closely monitored ambulatory obstetric management. This includes patients
who are in stable condition with a small resolving abruption, no increased
uterine activity, and reassuring results of fetal surveillance.
In general, the longer the interval between diagnosis and delivery, the
greater the risk for maternal complications and the poorer the outlook for
fetal or neonatal salvage. If DIC occurs, its onset usually takes place within
8 hours of placental abruption. Pritchard and Brekken report that all
patients in whom potentially serious hypofibrinogenemia develops have it
develop within this time period.
The timing and method of delivery depend on maternal and fetal
condition, gestational age, and cervical status. The premature fetus with a
mild abruption and minimal bleeding may be managed expectantly with
close observation, because this often is a self-limiting event. Tocolysis may

be considered and has been used with caution in certain cases. It may be
beneficial in the scenario of a stable mother and fetus without distress or
complications, with positive sonographic signs of abruptio placentae, and
who has only mild bleeding that is associated with uterine contractions.
There is evidence that such pregnancies may be successfully prolonged
(which would allow corticosteroid administration for fetal lung maturity
enhancement) without increased jeopardy to the mother or fetus.
Magnesium sulfate is the tocolytic agent of choice because betamimetic
agents can have adverse hemodynamic effects on a bleeding patient by
accentuating further signs of hypovolemia (hypotension and tachycardia).
In the premature fetus with persistent, heavy vaginal bleeding, however, use
of tocolytics would be contraindicated, and expeditious delivery is
recommended. In general, any attempt at tocolysis should be weighed
against the severity of abruption and likelihood of neonatal survival and
morbidity.
An important aspect of the treatment is continuous, careful monitoring
of mother and fetus for any signs or symptoms of deterioration. If the
abruption is adversely affecting maternal or fetal condition, delivery should
be performed. In cases of premature placental separation, cesarean delivery
should be performed liberally for maternal or fetal reasons.
The route of delivery for patients with placental abruption and a viable
fetus generally should be by rapid cesarean delivery unless vaginal delivery
can be expected promptly. Many patients with placental abruption already
have contractions; therefore, cesarean delivery may not be necessary.
Abruption may even cause a rapid and tumultuous labor. A recent study
suggests that in the absence of life-threatening hemorrhage, approximately
50% of patients with placental abruption but a normal fetal heart rate
tracing could have vaginal delivery. In such cases, neonatal outcomes
comparable with those obtained in infants born by cesarean delivery were
reported. There is no specific time limit imposed on a trial of vaginal
delivery as long as intensive maternal and fetal surveillance show no
significant progression in abruption severity and labor is progressing
satisfactorily. Oxytocin may be used to augment uterine contractions. Its
use has been questioned and challenged in that it might enhance the escape

of thromboplastin into the maternal circulation and therefore initiate or

augment consumptive coagulopathy. However, there is no evidence to
support this hypothesis. However, remember that the fetal condition may
rapidly deteriorate. Patients may present with a live fetus, only to have that
fetus die undelivered while awaiting vaginal delivery. In a recent study it
was found that in cases of placental abruption, for those fetuses alive on
admission, cesarean delivery was associated with a significant reduction
(odds ratio: 0.10; 95% confidence interval: 0.050.20) in neonatal
mortality. With an immature fetus or after intrauterine fetal death, attempts
at vaginal delivery using oxytocin should be implemented if needed.
However, a deteriorating clinical situation with increasing blood loss or a
worsening coagulopathy may dictate operative intervention for maternal
indications.
Management is most difficult and controversial in patients who have
placental abruption and are admitted with clinical DIC. If bleeding is
excessive, the condition must be promptly treated after evaluation of the
previously mentioned hemostatic parameters. The most effective and
definitive treatment is correction of the underlying process (i.e., the release
of tissue thromboplastin into the circulation by the damaged placenta) by
delivery of the placenta and fetus. If vaginal delivery is accomplished
quickly without trauma, prompt restoration of the hemostatic mechanism
usually results. Even in the most severe cases, clinically evident
coagulopathy usually resolves by 12 hours after delivery. There is a
decrease in the fibrin deposition products that interfere with thrombin
action and platelet function and an increase in fibrinogen, factor V, and
factor VIII. The platelet count returns to normal at a slower rate. This delay
is caused by the time required for maturation and release of new platelets
from the bone marrow. The expected order of normalization of the
coagulation tests is PT followed by fibrinogen, FDP, and platelets. A
clinical trial has found that the use of activated protein C intravenously in
cases of placental abruption complicated by DIC resulted in rapid
improvement of the DIC picture within 1 to 2 days. No adverse events
related to the use of activated protein C were observed. Further study is
needed to elucidate its value in DIC.

If a cesarean delivery is to be performed, the patient should be receiving

fluids, oxygen, and replacement products. Coagulation factors should be
given during the surgery. If given before surgery, they may provide little
improvement at the time of surgery as a result of the ongoing DIC. Surgery
should be performed quickly but in a meticulous manner. The surgeon
should avoid unnecessary trauma to the tissues and should ligate or
cauterize all bleeding points, even small bleeders that otherwise might be
overlooked. The abdominal incision should be drained by a closed system.
If vaginal delivery is expected, which in some cases, depending on maternal
and fetal status, may be the preferred route, the obstetrician should attempt
an amniotomy as soon as possible, because it may benefit labor and also
allows the placement of internal monitoring if desired. If the fetus is
immature, it may be best to leave the membranes intact. The intact sac may
be a better dilatory wedge than a small fetal part that can be poorly applied
to the cervix. After delivery, uterine blood loss can be decreased by quick
infusion of oxytocin and appropriate uterine massage. The episiotomy, if
needed, should be repaired meticulously and the cervix and vagina carefully
examined for lacerations.
In a patient with extensive uterine involvement and uncontrollable
blood loss, a hysterectomy may be indicated. A bruised Couvelaire uterus is
by itself not a reason for hysterectomy. In this situation, there often is fear
of uterine hemorrhage secondary to atony; however, this usually is not the
rule. In most cases, the uterus will still be able to contract sufficiently, even
in response to oxytocin, to prevent postpartum hemorrhage.
Treatment depends on the severity of the separation, location of the
separation and the age of the pregnancy. There can be a partial separation
or a complete (also called a total) separation that occurs. There can also be
different degrees of each of these which will impact the type of treatment
recommended.
In the case of a partial separation, bed rest and close monitoring may be
prescribed if the pregnancy has not reached maturity. In some cases,
transfusions and other emergency treatment may be needed as well.

In a case with a total or complete separation, delivery is often the safest

course of action. If the fetus is stable, vaginal delivery may be an option. If
the fetus is in distress or the mom is experiencing severe bleeding, then a
cesarean delivery would be necessary.
Unfortunately, there is no treatment that can stop the placenta from
detaching and there is no way to reattach it.
Any type of placental abruption can lead to premature birth and low
birth weight.

In cases where severe placental abruption occurs,

approximately 15% will end in fetal death.

12. Prognosis
If the bleeding continues, fetal and maternal distress may develop. Fetal
and maternal death may occur if appropriate interventions are not
undertaken.
The severity of fetal distress correlates with the degree of placental
separation. In near-complete or complete abruption, fetal death is inevitable
unless an immediate cesarian delivery is performed.
If an abruption occurs, the risk of perinatal mortality is reported as 119
per 1,000 people in the United States, but this can depend on the extent of
the abruption and the gestational age of the fetus. This rate is higher in
patients with a significant smoking history.
Currently, placental abruption is responsible for approximately 6% of
maternal deaths.
The risk of recurrence of abruptio placentae is reportedly 4-12%. If the
patient has abruptio placentae in 2 consecutive pregnancies, the risk of
recurrence rises to 25%.
If the abruption is severe and results in the death of the fetus, the risk of
a recurrent abruption and fetal demise is 7%.

REFERENCES
Clark SL. Placentae previa and abruptio placentae. In: Creasy RK, Resnik R,
eds. Maternal Fetal Medicine. 5th ed. Philadelphia, Pa: WB Saunders;
2004:715
Cunningham GF, Gant NF, Leveno JK, Gilstrap LC, Hauth JC, Wenstrom
KD. Williams Obstetrics, 23rd ed. New York: McGraw-Hill, 2010: 761-9.

 Lami Yeo, Cande V. Ananth and Anthony M. Vintzileos. Placental Abruption.

Lippincott Williams & Wilkins.
Markhus VH, Rasmussen S, Lie SA, Irgens LM. Placental abruption and
premature rupture of membranes. Acta Obstet Gynecol Scand. 2011;90:1024
9
Meguerdichian D. Complications in late pregnancy. Emerg Med Clin North
Am. Nov 2012;30(4):919-36.
Pariente G, Shoham-Vardi I, Kessous R, et al. Placental abruption as a
significant risk factor for long-term cardiovascular mortality in a follow-up
period of more than a decade. Paediatr Perinat Epidemiol. Jan
2014;28(1):32-8.
Shad H Deering, MD Medical Director, Andersen Simulation Center,
Madigan Army Medical Center . Abruptio Placentae . American College of
Obstetricians and Gynecologists, Association of Professors of Gynecology
and Obstetrics, and Society for Maternal-Fetal Medicine. 2014