This document discusses abruption placenta, which is defined as hemorrhaging during pregnancy caused by separation of the normally situated placenta. It grades abruption based on severity and lists risk factors like preeclampsia, thrombophilias, and trauma. Abruption can be revealed, concealed, or mixed based on whether bleeding is visible. Complications include shock, renal failure, and fetal death. Management involves resuscitation, monitoring, prompt delivery to save the fetus if possible, and treating coagulation disorders. Other causes of antepartum hemorrhaging like placenta praevia, circumvallate placenta, and vasa praevia are also summarized.

2. CAUSES
 Placenta praevia
 Abruptio placenta
 Local causes like polyp,cancer cervix,varicose
veins and local trauma
 Circumvallate placenta
 Vasa praevia
 Unclassified or indeterminate haemorrhage

3. ABRUPTIO PLACENTA
DEFINITION
• It is defined as hemorrhage
occuring during pregnancy due to
separation of normally situated
placenta.
• Also called accidental hemorrhage
or premature separation of
placenta.

4. GRADING
Sher and statland’s grading
It is of prognostic significance and
differentiates between a live and
dead fetus.
GRADE 1:Unrecognised clinically
before delivery,but evidence of
retroplacental clots on examining
the placenta

5. GRADE 2:Intermediate with
classical signs of abruption,but no
maternal distress and live fetus
GRADE 3:severe abruption with the
fetus dead
A.with coagulpathy
B.without coagulopathy

6. INCIDENCE
1% and is leading cause for perinatal
mortality

7. AETIOLOGY
The following are some of the risk
factors that are implicated
1.Medical factors
Preeclampsia and hypertension are
associated in 50% cases
Another strong correlation is with
chorioamnionitis secondary to
preterm premature rupture of
membranes

8. 2.Thrombophilias
Congenital and acquired thrombophilias
are associated with abruption.
Aquired type is antiphospholipid
syndrome-thrombosis,recurrent
miscarriage,early onset of preeclampsia
and fetal growth restriction in addition to
abruption
Congenital ,includes prothrombin gene
mutation factor v mutation protein C and S
deficiency are also associated with
abruption

9. 3.Hyperhomocystinaemia
Elevated levels of homocysteine-damage
vascular endothlium-causes abruption
This is the basis for association noticed
in women with folate deficiency
4.trauma
Blunt trauma to the abdomen
Amniocentesis
External cephalic version
Sudden uterine
decompression(hydramnios and
following delivery of 1st twin)

10. 5.Other associations
Previous abruption
Smoking and cocain abuse
Raised serum α fetoprotein level
Myomas esp. submucus myomas

11. CLASSIFICATION
Vasospasm→myometrial
contraction→venous engorement and
arteriolar rupture into decidua basalis
→dev. of decidual hematoma→
seperation of placenta
Abruption is divided into 3 based on
the type of hemorrhage:
Revealed(60%):
effused blood dissects the membranes
away from the uterine wall and make
its way through cervix into vagina.

12. Concealed(35%):
blood is retained in the uterus
Due to loss of tone of uterine muscle and
absence of uterine contractions
Uterus distends to accommodate the
blood
Sometimes amnion may rupture and
there is bleeding into amniotic sac
Concealed type is more likely to lead to
couvelaire uterus and cause fetal demise
and maternal complications

13. Mixed(5%):
In this partly revealed and partly concealed

14. COUVELAIRE UTERUS
 There can be extensive extravasation of blood into uterine
musculature beneath serosa esp. in concealed type.
 uterus show ecchymoses and tubes and ovaries drain blood.
 Peritoneal cavity is also filled with blood.
 This is called couvalaire uterus or uteroplacental apoplexy.
 Already there is fetal hypoxia due to placental seperation
 Tetanic contraction brought about by the seepage of blood
into myometrium in abruption cause ↑sed intrauterine
pressure.
 this cuts off placental blood flow adding to fetal
hypoxia.thus sudden fetal death is common.
 Concealed abruption is more likely to lead to couvelaire
uterus and cause fetal demise and maternal complications

16. DIAGNOSIS
 SYMPTOMS
Severe and constant abdominal
pain(more in concealed and less in
revealed)
Bleeding is present in revealed and
mixed types but may be absent in
concealed type.

17.  SIGNS
Pallor which is out of proportion to the
extent of bleeding
Hypertension(if there is associated
preeclampsia)
Uterus larger than the expected for the
period of amenorrhoea
Uterus may be tense and tender and
even rigid(woody hard)
Difficulty in palpating underlying fetal
parts easily
Fetal distress or absent FHS.

18.  In revealed uterus fundal height may
correspond to period of gestation
FHS are present
Initial presentation may be as preterm
labour with an irritable uterus and there
should be a high index of suspicion
Due to association of preeclampsia BP
may be normal even with severe
abruption.Hence findng of a normal BP
is not always reassuring

19.  VAGINAL EXAMINATION
 Performed after ruling out placenta praevia
 Usually patient will be in labour with fixed
presenting part and on artificial rupture of
membranes,liquor will appear to be uniformly blood
stained
 ULTRASOUND
 Less significant role
 Mainly useful to rule out placenta praevia
 Sometimes retroplacental hematoma may be seen
 Negative findings do not exclude abruption
 Abruption is essentially a clinical diagnosis and not
an ultrasound diagnosis

20. DIFFERENTIAL DIAGNOSIS
 Placenta praevia
 Other causes of APH
 Preterm labour
 Acute polyhydramnios(absence of pallor and
ultrasound is diagnostic)
 Rupture uterus(esp. incomplete rupture)
 Red degeneation,pyelonephritis,and other causes
of acute abdomen

21. COMPLICATIONS
 MATERNAL
 1.shock
 2.renal failure
 3.disseminated intravascular coagulation
(liberation of thromboplastin from placenta →intravascular
coagulation→ consumption of all coagulation factors →
fall in fibrinogen level →bleeding).
4.Postpartum hemorrhage(due to atonicity and
coagulation failure)
FETAL
1.Prematurity
2.Hypoxia and fetal death

22. MANAGEMENT
 Immediade management
 Similar in all cases of APH
 Resuscitation with blood and crystalloids and prompt
delivery
 Blood transfusion
 Indwelling catheter introduced and monitered
 Central venous pressure line inserted
 Blood taken for Hb,PCV,grouping,cross matching and
coagulation profile
 Coagulation profile includes fibrinogen ,fibrin
degradation products , partial thromboplastin time,
prothrombin time and platelet count
 (best marker –fibrinogen)
 Clotting time,clot retracton test,stability of the clot is
also looked for
 Ultrasound to confirm normal placenta and live fetus

23.  Obstetric management
 Immediate delivery is vital in abruption
 Mode of delivery depends on gestational
age and condition of mother and fetus
 fetus is alive
 Ceasarian is the best method
 In mild cases of revealed
abruption,imminent vaginal dlivery is
carried out

24.  Fetus is dead
 Vaginal delivery preferred unless bleeding is so severe or
there are other obstetric complications
 Hence artificial rupture of membranes and immediate
infusion of oxytocin to hasten delivery
 If delivery is not imminent after reasonable
time,caesarean section may have to be resorted to
 Caesarean section
 Done by experienced person with the help of an expert
anaesthetist
 PPH must be anticipated
 Indications for caesarean section:
 Fetus is alive and capable of survival
 Severe bleeding and vaginal delivery is not imminent
 Failure to progress after artificial rupture of membranes
and oxytocin

25. o Coagulation failure
o It is treated by blood tranfusion
o Human recombinant activated factor
vii is best agent but very expensive
o Cryoprecipitate used if fibrinogen is
very low
o Vaginal delivery is preferred ,if
caesarean becomes
neccesary,coagulation defect is
corrected before proceeding.
o Plenty of cross matched bood should
be available

28. OTHER TYPES OF APH
 CIRCUMVALLATE PLACENTA
 In this condition chorionic plate which is on the fetal
side is smaller than than basal plate on maternal side
 Fetal surface of placenta presents a central
depression surrounded by thickened greyish white ring
 These pregnancies may be complicated by IUGR,↑sed
chance of fetal malformations
 Bleeding is usually painless
 Antenatal diagnosis is unlikely and diagnosis usually
made after examination of placenta post delivery

30. VASA PRAEVIA
 When the fetal vessels in the membrane cross the
region of the internal os and are ahead of
presenting part the condition is called vasa
praevia.
 Occurs in 2 situations
 Type 1-velamentous to cord insertion where cord
insertion is into the membranes
 Type 2-presence of fetal vessels running between
lobes of a placenta with one or more accessory
lobes
 these can remain undiagnosed and and it can
rupture during artificial rupture of membranes
leading to death of the fetus

32.  Apts test or singer’s alkali denaturation test can
be used to confirm vasa praevia
 Principle-fetal Hb more resistant to alkali
denaturation
 When water and blood are mixed with NaOH it
remains pink for longer if fetal in origin or turns
yellow brown in 2 min if maternal in origin
 Risk factors-
 Succenturiate lobe
 Multiple pregnancy
 IVF

33.  Sometimes vessels can b palpated on vaginal
examination
 Prenatal diagnosis is rarely possible by
ultrasound and doppler
 Vaginal bleeding associated with variable
deccelerations on cardiotocography alerts one to
diagnose vasa praevia

34. Unclassified or intermediate APH
 Exact cause of APH is unknown
 There is mild bleeding but no features of
abruption or placenta praevia
 Speculum examination may not reveal local
cause
 Apt test-exclude VP
 IUGR and poor perinatal outcome are
associated
 If there is recurrent bleeding and GA is 37
weeks or more,risk factors like fetal growth
restriction delivery is preferred
 In majority of cases marginal sinus rupture
is later found to be the cause