Presentation about Abruptio placentae and its various problems

1. Dr.Rupa Rajshekar MBBS, MD
Specialist in Obg
Al Bukariya general hospital
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2. Definition
 Abruptio Placentae is the premature separation of the
normally implanted placenta from the uterine wall
after the 20th week of gestation until the 2nd stage of
labor.
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4. Epidemiology
 1/3 of all ante-partum bleeding is due to A P
 Incidence ranging from 1 in 75 to 1 in 225 births
 AP recurs in 5 to 17% of pregnancies after 1 prior
episode
 Up to 25% after 2 prior episodes
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5. Etiology
 Primary cause of A P is uncertain
 Several associated conditions identified:
 Increase in age & parity: 1.3-1.5%
 Pre-eclamsia: 2.1-4%
 Chronic hypertension: 1.8-3%
 Preterm ruptured membranes: 2.4-4.9%
 Multifetal gestation: 2.1%
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6. Etiology
 Cigarette smoking: 1.4-1.9%
 Cocaine abuse: NA
 Prior abruption: 10-25%
 Uterine leiomyoma: NA
 Hydromnios: 2%
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7. Classification
 Revealed type: Bleeding is revealed.
 Concealed type: No obvious bleeding.
 Mixed type: Combination of 1&2 above.
 In the concealed type(20%), the hemorrhage is confined
within the uterine cavity, detachment of the placenta may
be complete, and the complications are often severe.
 In the revealed type(80%) the blood drains through the
cervix, placental detachment is more likely to be
incomplete, and the complications are fewer and less
severe
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10. Pathophysiology
Placental abruption initiated by hge into decidua basalis
Haematoma formation
In concealed type blood accumulates &
seeps into myometrium
Couvelaire’s uterus
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11. Couvelaire’s uterus
 Also called as Utero-placental apoplexy
 First described by Couvelaire in early 1900
 Extravasation of blood into uterine musculature &
beneath uterine serosa
 Demonstrated only at laparotomy
 These myometrial hge interfere with uterine
contraction to produce PPH
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12. Couvelaire’s uterus
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13. Pathophysiology
Blood gains access to amniotic fluid
through rupture membranes
With disrupted placental site there is reduced
metabolic exchange
Process continues with release
Fetal hypoxia of tissue thromboplastin in
maternal circulation
DIC
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14. Complications
Maternal:
1. Maternal mortality
2. Hypovolaemic shock
3. Renal failure
4. DIC
5. PPH
6. Rhesus sensitization
7. Complication of massive transfusion
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15. Complications
Fetal:
1. Fetal death
2. Hypoxic brain injury
3. IUGR
4. Neonatal anemia
5. Congenital malformations (CNS)
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16. Signs & symptoms
 Vaginal bleeding: 78%
 Uterine tenderness: 66%
 Back pain: 60%
 Fetal distress: 22%
 Hypertonus: 17%
 Fetal demise: 15%
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17. Diagnosis
 Basis of diagnosis consists of :
 History & physical examinations
 Triad of external bleeding through cervical Os, Uterine
or back pain and fetal distress should be of high
suspicion
 Defer digital cervical examinations until PP & VP are
ruled out
 Ultrasound – limited value but for large abruptions
hypoechoic areas seen underlying placenta
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18. Ultrasound
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19. Ultrasound
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21. Laboratory tests
1. Complete blood cell count
2. Blood type & screen
3. Urine analysis,
4. Liver function tests
5. Renal function tests
6. Prothrombin time/ aPTT
7. Fibrinogen levels
8. FDP – Fibrin degradation products
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22. Classification of A P depending on
history & investigations
Grade O : Asymptomatic –incidental finding of retro-
placental clot
Grade 1 : Vaginal bleeding, no maternal or fetal
compromise – uterine tenderness present
Grade 2 : Fetal distress
No evidence of maternal shock
Vaginal bleeding may not be present
Grade 3 : Maternal shock & fetal demise present
Marked uterine tetany & tenderness
Vaginal bleeding may not be present
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23. Management
 Depends on condition of mother & gestational age of
fetus:
 Large bore IV access obtained
 Fluid resuscitation
 Foley’s catheter
 Maternal vitals close monitoring
 Continuous FHR monitoring
 Rh D immunoglobulin administered to Rh (-) patients
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24. Management
 Term gestation, hemodynamically stable:
 Plan for vaginal delivery with CS for usual indications
 Follow serial hematocrit & coagulation studies
 Continuous fetal monitoring
 Term gestation, hemodynamic instability:
 Aggressive fluid resuscitation
 Transfuse packed RBC, fresh frozen plasma & platelets
as needed
 Maintain Fibrinogen level > 150 mg/deciliter,
hematocrit > 25% & platelet over 60000/μ L
 Urgent CS unless vaginal delivery is imminent
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25. Management
 Preterm gestation hemodynamically stable:
 In absence of labor, preterm AP should be followed with
serial USG for fetal growth
 Steroids should be given to promote fetal lung maturity
 If maternal instability or fetal distress arises delivery
should be performed, if not labor can be induced at
term
 Preterm gestation hemodynamically unstable:
 Delivery should be performed after appropriate
resuscitation
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26. Conclusion
 Abruptio Placentae is an important cause of fetal and
maternal morbidity and mortality. The etiology is poorly
understood , various management options are however
available.
 The principle of initial assessment of the patients
condition and subsequent planned management aimed at
resuscitation and prolongation of pregnancy if possible or
immediate delivery either for fetal or maternal indications.
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