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ABRUPTIO
PLACENTAE
CC JUANICO, CLAREEN MAE
JULY 23, 2020
 INTRODUCTION
INCIDENCE
ETIOLOGY
PREDISPOSING FACTORS
PATHOPHYSIOLOGY
OUTLINE
CLASSIFICATION
CLINICAL DIGANOSIS
COMPLICATIONS
MANAGEMENT
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• also known as Placental

Abruption, Accidental
Hemorrhage, or Placental
Apoplexy

• Premature Placental
Separation (of normally WHAT IS
planted placenta)
ABRUPTIO
• External vs. Concealed PLACENTAE?
Hemorrhage

• Total or Partial

• Acute or Chronic 3
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• 1:200 - 300 pregnancies –

Philippines/Worldwide

INCIDENCE
• more common in African
American women than in
white or Latin American
women

• Patients older than 35 years

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• Its etiology is not fully

understood.

• Impaired placentation, placental

insufficiency, intrauterine
hypoxia, and uteroplacental
underperfusion are considered
the key mechanisms. ETIOLOGY
• Rupture of maternal decidual
artery dissection of blood at
the decidual‐placental
interface, around placental
margin, or behind the
membranes
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• Most often presents clinically as

an Acute event.
 Shearing forces from trauma
 Sudden decompression of the over
distended uterus

ETIOLOGY
• Chronic process: Retroplacental
hemorrhage or hematoma
 Infarctions Underperfusion 
Increased placental resistance
destruction of blood vessels feto
maternal bleeding  placental
abruption
• Alpha Feto Proteins

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PREDISPOSING
FACTORS

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PREDISPOSING FACTORS
• AGE, PARITY AND FAMILIAL
FACTORS
• increases with maternal age. (40 years
were 2.3 times risk) • SUDDEN DECOMPRESSION OF
• incidence is higher in women of great THE UTERUS
parity
• Premature rupture of membranes: 3-fold
• woman had a severe abruption, then
risk of abruption with preterm rupture was
the risk for her sister is doubled further increased with infection.
• Rupture of membranes in a patient with
• SEVERE PREECLAMPSIA AND CHVD polyhydramnios, or delivery of a first
twin, can lead to a shearing effect on the
placenta as the uterus contracts, thus
• Most common predisposing factor causing abruption placentae.
• 10- fold among women with chronic
hypertension, and slightly more than 2-
foLd for women with pre‐eclampsia
• Damaged vascularization  ischemia
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PREDISPOSING FACTORS
• CIGARETTE SMOKING
• Predisposes to decidual necrosis and
development of hypertension
• twofold risk for abruption in smokers.
• five- to eightfold if smokers had
chronic hypertension, severe
preeclampsia, or both
• THROMBOPHILIAS
• Associated with thromboembolic
disorders during pregnancy.
• Factor V Leiden and prothrombin gene
mutation— are associated with
placental abruption and infarction as
well as preeclampsia.
• COCAINE ABUSE
• Hypertension due to decreased
reuptake of epinephrine and
norepinephrine which cause
vasoconstriction leading to increase BP.
• RETROPLACENTAL MYOMAS
• Placenta could not attach properly since
myoma can cause poor trophoblastic
invasion. It can also prevent contraction
post partum.
• HISTORY OF ABRUPTION
• 2 previous occurrences: 25% risk
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PATHOPHYSIOLOGY

Hemorrhage into
the decidua
basalis (most
commonly from
damaged or
ruptured small
maternal
decidual
arteries, with
the formation of
a hematoma.

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PATHOPHYSIOLOGY

Decidua separates because of localized anoxic necrosis

and pressure resulting from bleeding into a confined
space

As the hematoma expands, disruption and separation of

the basal plate from the decidua increases until
complete placental detachment results.

Compression from the hematoma obliterates the

overlying intervillous space.

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PATHOPHYSIOLOGY
Further damaging placental vessels.

Hematoma that results may remain localized and may

not extend to a point at which it becomes manifest
clinically (CONCEALED HEMORRHAGE)

Bleeding from placental separation extends to the edge

of the placenta and continue to dissect between the
chorion and decidua vera until it reaches the internal
cervical os and vagina. (REVEALED OR EXTERNAL
BLEEDING)

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PATHOPHYSIOLOGY

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CLASSIFICATION
EXTENT OF COVERAGE

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CLASSIFICATION

REVEALED or CONCEALED 15
CLASSIFICATION
CONCEALED ABRUPTION
• Likely when:
• Bleeding observed is not
appropriate with signs and
symptoms presented
• Patient is pale, hypovolemic but
with minimal bleeding
• Presents in only a small
percentage of patient with
abruptio placenta
• Poor prognosis due to under
management of the physicians.
 Effusion of blood behind the
placenta (margins still adhered)
 Placenta is completely separated,
yet the membranes retain their
attachment to the uterine wall.
 Blood gains access to the
amnionic cavity after breaking
through the membranes
 Fetal head is so closely applied to
the lower uterine segment that
blood cannot make its way past.
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CLASSIFICATION
REVEALED ABRUPTION

• Bleeding is visible as the edge of placenta has been separated allowing

retroplacental hematoma to regress out of vagina
• Better prognosis
• Bleeding observed is proportional with signs and symptoms presented

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SIGNS AND SYMPTOMS

CPG: WHEN IS ABRUPTION PLACENTAE
SUSPECTED?

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Diagnosis of abruptio placenta is a clinical one and it is suspected in women who:
vaginal bleeding or abdominal pain or both, a history of trauma, or those
who present in otherwise unexplained preterm labor.

Classical symptoms are vaginal bleeding and abdominal pain but may occur with neither or
just of one of these signs. Diagnosed clinically when 2 or more of the following criteria are
present:

• Significant unexplained vaginal bleeding after 20 weeks gestation.

• Uterine irritability manifested as high frequency uterine contractions or uterine
hypertonus.
• Uterine tenderness or back pain – significant in the presence of sonographic evidence of a
posterior placenta.
• Evidence of fetal distress on electronic fetal heart rate monitoring(Fetal death)

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CLASSIFICATION
IN RELATION TO CLINICAL SIGNS AND SYMPTOMS
MILD
• No to mild vaginal bleeding
• Slightly tender uterus
• Normal maternal BP and
heart rate
• No coagulopathy
• No fetal distress
MODERATE
• No to moderate vaginal bleeding
• Moderate to severe uterine tenderness
with possible tetanic contractions
• Maternal tachycardia with orthostatic
changes in BP and heart rate
• From 25 to 50% of placental surface is
separated.
• Fetal monitoring may show
tachycardia, decreased variability, or
mild late decelerations.
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CLASSIFICATION
IN RELATION TO CLINICAL SIGNS AND SYMPTOMS

SEVERE
• No vaginal bleeding to heavy vaginal bleeding
• Maternal shock
• Symptoms are usually abrupt with a continuous knifelike uterine pain.
• Greater than 50% of placental separation occurs.
• Fetal monitor shows severe late decelerations, bradycardia, or even fetal
death.
• Severe disseminated intravascular coagulation (DIC) may occur. Ultrasound
visualization of a Retroplacental hematoma may be seen.

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 NO lab nor diagnostic tests available to detect
lesser degrees of abruptio placenta (more on
clinical presentation)

*Decreasing serial haematocrit

DIAGNOSIS *Amniocentesis – Port wine amniotic fluid (seen

in concealed hemorrhage as blood stains the AF

Continuous monitoring of uterine activity assist

the clinician in the assessment of the severity
of the abruption.

MRI and Doppler Imaging

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DIAGNOSIS
THE CLINICAL TESTS MOST USEFUL
ARE THE ULTRASONOGRAPHIC
EXAMINATION OF THE UTERUS AND
PLACENTA AND ELECTRONIC FETAL
HEART RATE MONITORING.
Fetal heart rate monitoring: tachycardia, loss of
variability, sinusoidal pattern, pseudosinusoidal
pattern, or late decelerations.
Ultrasonographic Criteria for Diagnosis of
Abruptio Placenta
• Preplacental collection under the chorionic
plate (between the placenta and amniotic fluid)
• Jello-like movement of the chorionic plate with
fetal activity
• Retroplacental collection
• Marginal hematoma
• Subchorionic hematoma
• Increased heterogenous placental thickness
(more than 5 cm in a perpendicular plane)
• Intra-amniotic hematoma
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 HYPOVOLEMIC SHOCK
COUVELAIRE UTERUS
ACUTE RENAL FAILURE
SHEEHAN SYNDROME
CONSUMPTIVE COAGULOPATHY/ DIC
COMPLICATIONS
MATERNAL AND FETAL
FETAL DEATH
INTRAUTERINE GROWTH
RESTRICTION
PRETERM AND LOW BIRTH WEIGHT

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• Placental abruption may be complicated
by massive and sometimes torrential
haemorrhage due to maternal blood loss.

• Blood loss in these women often

amounted to at least half of their
HYPOVOLEMIC
pregnant blood volume.
SHOCK
• Importantly, massive blood loss and shock
can develop with a concealed abruption

• End point is asphyxia the immediate

treatment is replacement of the
intravascular volume deficit as rapidly as
possible
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• There may be widespread

extravasation of blood into the
uterine musculature and beneath
the uterine serosa

• Such effusions of blood are also

occasionally seen beneath the
COUVELAIRE
tubal serosa, between the leaves
of the broad ligaments, in the UTERUS
substance of the ovaries, and free
in the peritoneal cavity

• Bruised appearance

• Its precise incidence is unknown

because it can be demonstrated
conclusively only at laparotomy.
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• Seen with severe placental abruption. It is more
common if treatment of hypovolemia is delayed
or incomplete.

• Seriously impaired renal perfusion is the

consequence of massive hemorrhage.
ACUTE RENAL
• Renal vasospasm and hypoperfusion are likely
intensified FAILURE
• Prompt and vigorous treatment of hemorrhage
with blood and crystalloid solution usually
prevents clinically significant renal dysfunction.

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• Severe intrapartum or early postpartum
hemorrhage rarely followed by pituitary failure.

• Failure of lactation, amenorrhea, breast atrophy,

loss of pubic and axillary hair, hypothyroidism,
and adrenal cortical insufficiency.

• Exact pathogenesis is not well understood.

SHEEHAN
SYNDROME
• Develop infrequently even in women who
hemorrhage severely.

• There may be varying degrees of anterior

pituitary necrosis and impaired secretion of one
or more trophic hormones.

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• Placental abruption is one of the most
common causes of clinically significant
consumptive coagulopathy

• Hypofibrinogenemia—plasma levels <150

mg/dL—is found coupled with elevated
levels of fibrinogen-fibrin degradation
products and/or D-dimers.
CONSUMPTIVE
COAGULOPATHY
• Major mechanism is activation of
intravascular coagulation with varying
degrees of defibrination. Its consequence is
the activation of plasminogen to plasmin,
which lyses fibrin microemboli to maintain
microcirculatory patency

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 CONSUMPTIVE
COAGULOPATHY
The most effective and definitive
treatment is correction of the underlying
process 
Replacement therapy with blood components
(give only what patient lacks)

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• Fetal anoxia, exsanguination (because rupture of
fetal placental vessels can occur), and
prematurity main causes of fetal death FETAL DEATH,
• Mechanism of effect of placenta abruption on
IUGR still not clear: suggested that IUGR is
INTRAUTERINE
related to response to the chronic effects on the
placenta damage(uteroplacental blood perfusion GROWTH
insufficiency)
RESTRICTION,
• Haemorrhage induces thrombin from decidual
tissue factor, result to PPROM and Preterm PRETERM AND
delivery. Severe, acute abruption can lead to
maternal and fetal mortality.
PROM
• Thrombin also promotes neutrophil trafficking
and uterine contractility increasing risk of
pretern delivery

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 MANAGEMENT
Depends on: Gestational Age, Maternal Status and Fetal Status
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GESTATIONAL AGE
Term pregnancy:
 without fetal distress + diagnosis uncertain, Mother
stable: close observation
 with fetal distress or if diagnosis of AP is certain:
Immediate intervention

Preterm pregnancy
 without fetal distress: Delay delivery
 with fetal distress: Immediate delivery

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 MATERNAL STATUS
• Monitor BP, CR, RR, Fluid Intake Urine
Output
• Blood typing and crossmatch
• Correct hypovolemia, anemia, hypoxia
before surgery
• Urine output should be 30ml/hr
• Blood studies – CBC, platelet count, plasma
fibrinogen and fibrin degradation products,
PTT (prone to develop DIC)
FETAL STATUS
• Fetal Monitor
• Fetal Distress – immediate delivery
CPG 2009
1. Nasal oxygen
2. Intravenous hydration using large bore
catheter
3. Type and crossmatch for 4 units of packed
red blood cells (RBC)
4. Evaluation of hematologic and clotting
studies (complete blood count,
prothrombin time, partial thromboplastin
time, fibrinogen, platelet count)
5. Monitoring of urinary output with
indwelling bladder catheter
6. Continuous electronic fetal heart rate and
uterine activity monitoring
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EXPECTANT MANAGEMENT IN PRETERM PREGNANCY
With labor well established, expectant management in abruptio placenta
is an option when both maternal and fetal status are reassuring or when
there is fetal demise as long as the mother is stable.

• When both maternal and fetal status is reassuring, conservative management,

with the goal of vaginal delivery, is reasonable.

• Term pregnancy with labor established should be allowed to progress, otherwise

induction of labor should be considered.

• Both mother and fetus should be monitored closely during labor.

• In severe abruptio with fetal death, regardless of gestational age, expectant

management is acceptable as long as the mother is stable.

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TOCOLYSIS

It seems reasonable to use tocolytics with caution in stable women who

have partial abruptio placenta but are remote from term.

• Side effects such as tachycardia could mask the clinical signs of blood loss

• Tocolysis for the preterm patients appeared to be beneficial in prolonging

gestation and did not increase the likelihood of cesarean delivery, hemorrhage,
or fetal distress.

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CESAREAN DELIVERY
At term or near term with a live fetus, prompt delivery is indicated once
there is evidence of fetal compromise, severe uterine hypertonus, life-
threatening vaginal bleeding or DIC when vaginal delivery is not
imminent. Cesarean delivery should be performed promptly because
total placental detachment could occur without warning.

• Rapid delivery of the fetus who is alive but in distress practically always means
cesarean delivery.

• Longer decision-delivery intervals were associated with poorer perinatal

outcomes.

• In severe abruptio placenta complicated by fetal bradycardia, a decision to

delivery interval of 20 minutes or less was associated with substantially reduced
neonatal morbidity and mortality
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VAGINAL DELIVERY
If placental separation is so severe that the fetus has died, then vaginal
delivery is usually preferred.
Minimal bleeding without signs of fetal distress.

• Oxytocin may be used for contractions to be regular (promoting rhythmicity; do

under flow surveillance)

• Amniotomy for quick delivery

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CONSERVATIVE APPROACH WHEN THERE IS ABRUPTIO PLACENTA
IN VERY PRETERM PREGNANCIES (20-34 WEEKS GESTATION)
When there is only partial abruptio placenta and the maternal and fetal status
are reassuring, the patient may be managed conservatively.

• Preterm birth is the leading cause of perinatal death in women with abruptio, and to
optimize perinatal outcomes, it is desirable, if possible, to prolong gestation

• Prolonged Hospitalization for extreme close monitoring maybe necessary.

• Steroids should be administered to promote fetal lung maturation.

• Serial ultrasonography is recommended to evaluate progression or regression of the

abruptio.

• Patient may be managed in out patient department if the fetal status is reassuring once
they have remained stable for several days.
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THANK YOU

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