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ABRUPTIO PLACENTAE ABRUPTIO PLACENTAE DR V L DESHMUKH ASSO PROF DEPT OBGY GMCH A,BAD

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ABRUPTIO PLACENTAEABRUPTIO PLACENTAE

• DR V L DESHMUKH

• ASSO PROF

• DEPT OBGY

• GMCH A,BAD

Abruptio PlacentaeAbruptio Placentae

• Abruptio – tearing away from

• Placentae – placenta

• It is a Latin word

Synonyms Synonyms

• Accidental Haemorrhage (Great Britain)

• Ablatio Placentae

• Premature separation of placenta

Definition:

• It is one form of Antepartum Haemorrhage

where bleeding occurs due to premature

separation of normally situated placenta.

a) Retreoplacental haematomo b) Revealed c) Concealed d) Mixed

1. Revealed : Most common

Blood loss is visible as the blood drops down

between membrane & decidua & come out

through cervical canal.

2. Concealed : Rare

a) Effusion of blood behind the placenta but its

margins still remain adherent

b) Placenta completely separated but

membranes intact

c) Blood enter amniotic sac after breaking

membranes

d) Fetal Head closely applied to lower uterine

segment.

1. Mixed – quite common

- Some amount of blood is inside & some

expelled.

Incidence

- 1 in 150 deliveries

• Perinatal mortality – 15 – 20%

• Maternal mortality – 2 – 5 %

Etiology:

a) Maternal Hypertension: 44% of all cases

mechanism- Spasm of vessels in utero

placental bed i.e. of decidual spiral artery

causes endothelial damage & rupture of

vessels leading to haemorrhage.

b) Maternal trauma – 1.5 – 9.5 %

- Motor vehicle accidents (MVA)

- Assaults, falls.

c) Foetal trauma –

- Attempted external cephalic version

- Needle puncture at amniocentesis

d) Cigarette Smoking –

- Decidual necrosis

e) Cocaine abuse – Onset of labour with

placental abruption in 4 of 23 women

immediately after IV self infection of cocaine.

f) Short umbilical cord – Mechanical pull during

labour.

g) Sudden Uterine decompression

1. Delivery of first baby of twins

2. PROM

3. Sudden escape of liquor amni in hydramnios.

h) Advanced Maternal age

i) Thrombophilias

j) Folic acid deficiency

k) Sick placenta

l) Retroplacental fibromyoma

m) Idiopathic

n) Recurrence increase 10 fold.

Pathogenesis:

• Initiated by Haemorrhage into decidua basalis.

• The decidua splits leaving thin layer adherent

to the myometrium

• Subsequently there is development of decidual

Haematoma that leads to separation

compression & ultimate destruction of

placenta.

• Sometimes

– Decidual spiral artery rupture RP Haematoma separation of placenta inability of uterus to contract& control the torn vessels.

– Changes in other organs• Liver – Fibrin knots

• Kidney – Acute cortical necrosis or acute tubular necrosis, proteinurea.

• Blood coagulopathy – Due to excess consumption of plasma fibrinogen due DIC & RP bleeding.

Investigation :

• For evaluation of haemostatic system in

patients with abruptio placentae, most

laboratories use DIC profile.

• It includes

Test Normal Results

Fibrinogen 150 to 600 mg/dl

PT 11 to 16 sec.

PTT 22 to 37 sec.

Platelet count 120000 to 350,000/mm3

D-dimer <0.5mg / L

FDP < 10 mg / dl

Bleedin time (Duke) 1-3 mins

(IVY’s) 1 – 9 mins

Coagulation time (wright tube) 3 – 7 mins

(Lee & White) 4 – 9 mins.

• Clot observation test (weiner)

– 5 ml of venous blood placed in 15 ml dry test

tube & kept at 370C

– CT < 6min, fibrinogen level > 150 mg%

no clot < 30 min,fibrinogen level < 100 mg %

• FDP

– Latex agglutination test

– In DIC > 80 ug / ml

• D-dimer

– Specific component of fibrin break down

– Latex agglutination method.

– In DIC > 200 mg / L

• Estimation of fibrinogen

– Blood sample collected in EDTA vial critical

level 100 mg %

Diagnosis of abruptio placentae is more clinical Diagnosis of abruptio placentae is more clinical rather than USG findings.rather than USG findings.

S/S Frequency

Vaginal bleeding 78%

Uterine tenderness /back pain

66%

Fetal distress 60%

High frequency contractions 17%

Hypertonus 17%

Idiopathic preterm labour 22%

Dead fetus 15%

• Classification of placental abruption is based

on extent of separation (ie, partial vs complete)

and location of separation (ie, marginal vs

central). Clinical characteristics include the

following:

Class 0 is asymptomatic. Diagnosis is made

retrospectively by finding an organized blood

clot or a depressed area on a delivered

placenta.

Class 1 is mild and represents approximately 48%

of all cases. 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 is moderate and represents approximately 27% of

all cases 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 is severe and represents approximately

24% of all cases. 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

• Role of USG in Abruptio placentae – – locate RP clot (20-25%)

• Estimation of blood loss– Wt. of RP clot in gm x 3

• Pain due to RP clot causing intravasation of

blood & disruption of myometrial fibres.

• Couvelaire uterus (Uteroplacental apoplexy)

Microscopic appearance

• Due to more severe & wide spread extravasation of blood into the uterine musculature & beneath the uterine serosa.

• Occasionally seen beneath the tubal serosa, connective tissue of broad ligament, substance of ovaries & in peritoneal cavity

• Incidence (unpredictable)

• Myometrial Haemotomas seldom interfere with

uterine contractions to cause PPH.

• Hence not indication for hysterectomy.

• Naked eye appearance uterus of dark port

wine colour.