ABRUPTIO PLACENTAE

Dr Warfa
17 March 2009.

Case
24 yr old primigravida at 35/40 presented with
a 2 hr history of acute onset of abdominal
pain, all over the abdomen.
No hx of PV bleeding
Hx of minor trauma 8 hrs prior to the onset of
abd pain.
O/E pt in pain, Pale, BP 110/70 mmhg, pulse
98 bpm.

 PA abdomen tense , tender on palpation,

fetal heart heard.
CTG- Bradycardia with late decelerations,
hypertonic contractions.

 How should this patient be management.

Objectives

Definition
Risk factors
Pathogenesis
Clinical presentation
Management

Definition
Abruptio placentae defined as the premature
separation of the placenta, complicates
approximately 1% of births.
Cause of vaginal bleeding in the second half of
pregnancy and is associated with significant
perinatal mortality and morbidity.

Placental abruption and adverse perinatal outcomes. JAMA 1999;282: 164651.

 The immediate cause of the separation is

rupture of defective maternal vessels in the
decidua basalis, where it interfaces with the
placental anchoring villi.
Rarely, the bleeding can originate from the
fetal-placental vessels.

Types of Abruptio

red: hematoma; blue line: amnion; pink line: chorion.

(A) Concealed abruption.
(B) Complete placental separation.
(C) Subamniotic hemorrhage extends anterior to the placenta and is
contained between the amnion and chorion

 Clinical importance of Abruptio is in the

spectrum of disease that it may cause from
cases with;
Minor bleeding and little or no consequences,
Massive abruption leading to fetal death
Severe maternal morbidity.

Pathogenesis
Does abruptio placentae results from an acute
pathologic event or is the culmination of a
longer-standing disorder of the fetal-placental
interface ?

 In an acute event a single precipitating factor

(motor vehicle accident or fall) is the most
likely etiology.
In PPROM acute inflammation is the
precipitating event (placental/decidual
inflammation).

 Abruption is both a cause and a consequence

of PPROM.
Abruption-induced decidual thrombin
generation may promote increased protease
production, leading to both membrane
compromise and vascular destabilization.

Role of cytokines
(IL)-1 and TNF up-regulate the production
and activity of MMPs in the trophoblast.
Result in destruction of the extracellular
matrices and cell-cell interactions.
lead to disruption of the
placental attachment
premature separation of the placenta.
Histologic evidence of inflammation and risk of placental abruption. Am J Obstet Gynecol 2007;197

 Neutrophil infiltration into the decidua with

preterm PROM and placental abruption,
Abruptions are associated with a thrombinenhanced expression of IL-8, a potent
neutrophil chemo attractant, which leads to a
marked infiltration of decidual neutrophils.
Produce proteases that can degrade ECM leading
to PROM.

 The presence of pregnancy complications

associated with chronic utero placental
vascular insufficiency supports the hypothesis
of a chronic pathologic vascular process.
Utero placental/spiral artery vascular
thrombosis and failed physiological
transformation of utero placental vessels
suggest that underlying spiral artery
vasculopathy is a principal etiology of
abruption.

 Acute separation of the placenta deprives the

fetus of oxygen and nourishment, with the
consequence that the fetus frequently dies.

Coagulation cascade is activated consequent

DIC.

 Bleeding may occur into the uterine

myometrium, leading to a Couvelaire uterus.

Microscopic examination reveals hemosiderinladen macrophages and evidence of villous

hemorrhage.

Risk Factors
Trauma
Rapid uterine
decompression
Hypertension
Cigarette smoking
Cocaine abuse
Increasing parity

Preterm premature
rupture of membranes
Inherited thrombophilia
Multifetal gestation
Uterine leiomyoma
Previous abruption
Uterine or placental
anomalies

 Mechanical factors
Trauma (external compression-decompression
induced stress at the placental-decidual interface.
Rapid decompression
Polyhydramnios
Twin deliveries

Placental implantation over a uterine anomaly or

myoma.

 Hypertension -Severe abruption is associated

with chronic maternal hypertension,
preeclampsia superimposed on chronic
hypertension, and severe preeclampsia.

Cigarette smoking - ischemic peripheral

necrosis of the decidua is observed in smokers
and predisposes to vascular disruption .

 Maternal parity maybe related to endometrial

scarring, impaired decidualization, or aberrant
uterine vasculature.
Maternal age could be related to underlying
vascular disease in older women.

1. Impact of Maternal Age on Obstetric Outcome. Obstet Gynecol 2005 May;105(5):983-990.

2. Placentae Previa and Abruptio Placentae: Maternal Fetal Medicine, 4th ed.

 Inherited thrombophilias have been

associated with an increased risk of maternal
venous thromboembolism, fetal death and
abruption. Commonly asso with
heterozygosity for the factor V Leiden
prothrombin G20210A gene mutations,
Homozygosity for the thermo labile allele of the
methylene tetrahydrofolate reductase gene
causing hyperhomocysteinemia

 Cocaine-induced acute vasoconstriction

leading to ischemia, reflex vasodilatation, and
disruption of vascular integrity.

Clinical presentation
Varies widely from totally asymptomatic cases
to those where there is fetal death with
severe maternal morbidity.
Correlation between the extent of placental
separation and the risk of stillbirth ( > 50%
placental separation )

Clinical presentation

Vaginal bleeding (>80 percent of patients)

Abdominal pain (>50 percent)
Uterine contractions
Uterine tenderness
Nonreassuring FHR tracing
Backache

Grade 0 -retrospective diagnosis of abruptio

placentae.
Grade 1 vaginal bleeding

Grade 2 vaginal bleeding, concealed

hemorrhage, uterine tenderness, NRFS

Grade 3 vaginal bleeding, shock, extensive

concealed hemorrhage, uterine tenderness, fetal
death, and sometimes coagulopathy
3a absent coagulopathy
3b presence of coagulopathy
.

Diagnosis
The diagnosis of abruptio placentae is
primarily clinical.

Ultrasonography
Depends on
Size and location of the bleed
Duration between the abruption and the time the
ultrasonographic examination was done.

Fresh retroplacental clot has acoustic

characteristics which may be very similar to
those of the placenta itself.

Ultrasonographic features to diagnose

abruptio
Preplacental collection under the chorionic plate
(between the placenta and amniotic fluid).
Retroplacental collection.
Marginal hematoma
Subchorionic hematoma
Increased heterogenous placental thickness (more
than 5 cm in a perpendicular plane)
Intra-amniotic hematoma.

ultrasound
Rule out other causes of bleeding
Fetal viability
Concealed abruption

Diagram showing the different sites at which ultrasonographic

evidence of abruption may be observed.

Lab diagnosis
No lab diagnostic test is used for abruptio.

Plasma fibrinogen level below 200 mg/dL

Thrombocytopenia (less than 100,000/microL)
Used to support a diagnosis of severe abruptio.

Management
Individualize management on a case-by-case
basis.
Rapid assessment on admission
Longer decision delivery intervals are associated
with poorer perinatal outcomes.

IV access, blood FHG, coag profile, cross

match blood, urinary catheter.

Management

Oyelese and Ananth, Placental Abruptio Obstet Gynecol 2006;108:100516

Trauma
Following trauma RTA or intimate partner
violence Admit patient for 24 observation.
CTG for 4 hours if reactive then observe.
In presence of uterine contractions or
irritability put patient on continuous CTG.

Obstetrics and Gynaecology clinics vol 34 issue 3 Pg 357-368 Sep 2007.

outcomes
Fetal
Perinatal mortality
(PNM),
Fetal growth restriction
(IUGR)
Prematurity
Stillbirth

Maternal

Hemorrhage
DIC
Blood transfusion
Renal failure (ATN or
acute cortical necrosis)
Hysterectomy
Maternal death

 Recurrence..
Recurrence has been reported as 5 to 15 percent.
After 2 previous abruptio risk increases to 25%

Management in subsequent pregnancies

Modifying reversible risk factors smoking , cocaine
? Non recurrent causes
Thromboprophylaxis in patients with
thrombophilias