This document discusses bleeding disorders in late pregnancy such as antepartum haemorrhage and its causes including placenta previa and abruption placentae. It describes the diagnosis, management and nursing considerations for women experiencing bleeding in the second half of pregnancy. Complications for both mother and baby are explained. The prognosis is generally good when cases are diagnosed early and properly managed in well-equipped hospitals with blood transfusion facilities and skilled practitioners.

1. BLEEDING
DISORDERS IN LATE
PREGNANCY
DEEPTHY P. THOMAS
II YEAR M.S.c. NURSING
GOVT. COLLEGE OF NURSING
ALAPPUZHA

2. ANTEPARTUM HAEMORRHAGE:
Antepartum haemorrhage is defined as
bleeding from or into the genital tract after the
28 week of pregnancy but before the birth of the
baby.

3. CAUSES
APH
Placental bleeding unexplained extra placental
Placenta abruptio local cervico
previa placenta vaginal lesions
-Cervical polyp
-Carcinoma cervix
-Varicose vein
-Local trauma

4. PLACENTA PRAEVIA
• When the placenta is implanted partially or
completely over the lower uterine segment it is
called placenta praevia.

5. INCIDENCE
0.5-1% amongst hospital deliveries.
One third of all cases of antepartum
haemorrhage are due to placenta previa.
Higher incidences have been reported in
multiparous, multiple pregnancies, elderly
woman [ over 35 years]

6. ETIOLOGY
Dropping theory
• The fertilized ovum drops down and implanted
in the lower uterine segment. Poor decidual
reaction in the upper uterine segment may be
the cause. Failure of zona pellucida to disappear
at time can be hypothetical possibility. This
explains the formation of central placenta
previa.

7. Persistence of chorionic activity
• Chorionic activity in the deciduas capsularis and
its subsequent development into capsular
placenta which comes in contact with decidua
vera of the lower segment can explain the
formation of lesser degrees of placenta previa.

8. Defective deciduas
• It results in the spreading of the chorionic villi
over wide area in the uterine wall to get
nourishment. During this process not only the
placenta become membraneous but encroaches
onto lower segment. Such a placenta may invade
the underlying decidua or myometrium to cause
placenta accrete, increta or percreta.

9. Big surface area of the placenta
• Big placenta as in twins may encroach onto
lower segment.

10. PREDISPOSING FACTORS
Multiparity
Increased maternal age
History of previous caesarean section or any
other scars in the uterus.
Placental size
Smoking
Leiomyomas distorting uterine cavity
Congenital malformations of the uterus.

11. PATHOLOGICAL ANATOMY
Placenta
• The placenta may be large and thin. This is often
tongue shaped extension from the main
placental mass. Extensive areas of degeneration
with infarction and calcification may evident.
The placenta may be morbidly adherent due to
poor decidual formation in the lower segment.

12. Umbilical cord
• The cord may be attached to the margin or into
the membranes. The insertion of the cord may
be close to the internal os or the fetus blood
vessels may run across the internal os in
velamentous insertion due to poor placental
formation

13. Lower uterine segment
• Due to increased vascularity, the lower uterine
segment and the cervix becomes soft and more
friable.

14. TYPES OR DEGREES
Type I (low lying)
Type II (marginal)

15. Type III (incomplete or partial central)
Type IV (central or total)

16. Dangerous placenta previa is the name
given to the type-II placenta previa.
• Because of curved birth canal major thickness of
the placenta overlies the sacral promontory,
thereby diminishing the antero-posterior
diameter of the inlet and prevents engagement
of the presenting part. This hinders effective
compression of the separated placenta to stop
bleeding.
• Placenta is more likely to compressed if vaginal
delivery is allowed.
• More chance of cord compression or cord
prolapsed.

17. CAUSE OF BLEEDING
• Thrombosis of the open sinuses.
• Mechanical pressure by the presenting part .
• Placental infarction.

18. Placental Migration
The term placental migration could be explained
in two ways:
• With progressive increase in the length of lower
uterine segment, the lower placental edge
relocates away from the cervical os .
• Due to trophotropism (growth of trophoblastic
tissue towards the fundus), there is resolution of
placenta previa.

19. CLINICAL FEATURES
Symptoms
• Vaginal bleeding
sudden onset, pain less, apparently causeless
and recurrent

20. Signs
Abdominal examination
• Size of the uterus is proportionate to the
period of gestation.
• The uterus feels relaxed, soft and elastic
without any localized areas of tenderness.
• Persistence of malpresentations
• The head is floating in contrast to the period
of gestation.

21. • The FHS is usually present unless there is major
separation of the placenta. Slowing of the FHS
on pressing the head down into the pelvis which
soon recovers promptly as the pressure is
released is suggestive of the presence of low
lying placenta specially of posterior type it is
known as Stallworthy’s sign.

22. Vulval inspection :
• Only inspection is to be done to check whether
bleeding is still occurring or has ceased
• In placenta praevia the blood is bright red as the
bleeding occurs from the separated utero
placental sinuses close to the cervical opening
and escape out immediately.
• Vaginal examination must not be done outside
the operation theatre in the hospital.

23. DIAGNOSIS
History and clinical features
• Painless and recurrent vaginal bleeding
in the second half of pregnancy should be
taken as placenta praevia unless provoked
otherwise.

24. Placentography
• Sonography
Transabdominal
• The accuracy after 30th week of gestation is
about 98%.
Transvaginal (TVS)
• The probe is very close to the target area. it is
more accurate than TAS.
Transperineal (TPS)
• It is well accepted by patients. Internal os is
visualized in 97-100% of cases.

25. Color doppler flow study
• Prominent venous flow in the hypo-echoic areas
near the cervix is consistent with the diagnosis
of placenta praevia.
MRI
• It is a non invasive method without any risk of
ionizing radiation.

26. Clinical confirmation of placenta preavia
• Double set up examination (vaginal
examination)
• it is less frequently done these days.
Indications are
• inconclusive USG report
• USG reveals type I placenta preavia
• USG facilities not available

27. Visualization of the placental implantation on the
lower segment can be confirmed during
caesarean section.
Examination of the placenta following vaginal
delivery reveals;
• a tongue shaped, thin segment of placental
tissue projecting beyond the main placental
mass with evidences of degeneration.
• Rent on the membranes on the margin of the
placenta.
• Abnormal attachment of the cord.

28. DIFFERENTIAL DIAGNOSIS
• Vasa preavia
• The local cervical lesions
• Circumvallate placenta

29. COMPLICATIONS
Maternal
During pregnancy
• APH with varying degrees of shock.
• Malpresentation is common.
• Premature labour: either spontaneous or
induced.

30. During labour
• Early rupture of membranes.
• Cord prolase.
• Slow dilatation of the cervix.
• Intrapartum haemorrhage.
• Increased incidence of operative interference.
• Post partum haemorrhage
• Retained placenta

31. During puerperium
• Sepsis is increased due to operative interference.
▫ Placental site near the vagina
▫ Anemia and devitalized state of the
patient
• Subinvolution
• Embolism

32. • Fetal
• Low birth weight
• Asphyxia:
 Early separation of placenta
 Compression of the placenta or
 Compression of the cord
• Intrauterine death
• Birth injuries
• Congenital malformation

33. PROGNOSIS
Maternal
• Early diagnosis
• Omission of internal examination outside the
hospital.
• Free availability of blood transfusion facilities.
• Potent antibiotics.
• Wider use of caesarean section with expert
anaesthetist.
• Skill and judgement with which the cases are
managed.

34. fetal
judicious extension of expectant treatment
thereby reducing the loss from prematurity
liberal use of caesarean section which greatly
lessens the loss from anoxia
 improvement in the neonatal care unit.

35. MANAGEMENT
Prevention
• Adequate antenatal care.
• Antenatal diagnosis of low lying placenta.
• Significance of “ warning haemorrhage”.
• Family planning and limitation of births.

36. Management at home
• The patient is immediately put to bed.
• Assess the blood loss.
• Quick but gentle abdominal examination.
• Vaginal examination must not be done.

37. • Hospital treatment
• Shift the patient to an equipped.
• An intravenous dextrose saline drip.
• Patient should be accompanied by 2/3 persons
fit for donation of blood if necessary.
• All cases of APH should be

38. TREATMENT ON ADMISSION
1. Immediate attention
• Amount of blood loss.
• Blood samples are taken for grouping, cross
matching and Hb.
• A large bore IV cannula is sited and an infusion
of normal saline is started.
• Gentle abdominal palpation.
• Inspection of the vulva.
• Confirmation of diagnosis.

39. • Formulation of line of treatment
 Expectant management
 Active management

40. Expectant management
• Vital prerequisites
• Availability of blood for transfusion
• Facilities for caesarean section
• Selection of cases
• Mother is in good health status.(Hb >10 gm%,
haematocrit >30%)
• Duration of pregnancy is <37 weeks.
• Active vaginal bleeding is absent.
• Fetal well being is assured by USG.

41. Expectant management
• Bed rest.
• Investigations.
• Periodic inspection.
• Supplementary haematinics.
• When the patient is allowed out of bed a gentle
speculum examination is made to exclude local
cervical and vaginal lesions for bleeding.
• Use of tocolytics and cervical encirclage are not
helpful.

42. • Expectant management is done in home
• Patient lives close to hospital
• 24 hour transportation is available
• Bed rest assured
• Patient is well motivated to understand the risks

43. Termination of the expectant treatment
• The expectant management is carried upto 37 weeks
of pregnancy. By this time baby become mature.
• Premature termination is done in conditions such as
 Presence of brisk haemorrhage and which is continuing.
 The fetus is dead.
 The fetus is found congenitally malformed on
investigation.
Steroid therapy
• It is indicated when duration of pregnancy is
<34 weeks. Betamethasone reduces the risk of
respiratory distress of the new born when preterm
delivery is considered.

44. Active management (Delivery)
• Bleeding occurs at or after 37 weeks of
pregnancy.
• Patient is in labour
• Patient in exsanguinated state on admission.
• Bleeding is continuing and of moderate degree.
• Baby is dead/congenitally deformed.

45. DEFINITIVE MANAGEMENT
• Vaginal examination in OT followed by
 Lower rupture of membranes or
 Caesarean section
• Caesarean section without internal
examination

46. Vaginal examination
• Contraindications
• Patient in exsanguinated state
• Diagnosed cases of major degrees of placenta
preavia confirmed by USG.
• Associated complications like malpresentations,
elderly primigravida, pregnancy with h/o
previous caesarean section, contracted pelvis etc.

47. Low rupture of membranes
• Low rupture of membrane is done using long
Kocher’s forceps in lesser degrees of placenta
praevia (type I & type II anterior).
Precautions during vaginal delivery
• steps to restore the blood volume.
• Methergine 0.2 mg.
• Proper examination of the cervix should be done
soon following delivery.
• Baby’s blood Hb level is to be checked.

48. Caesarean section
Indications
• Severe degree of placenta praevia .
• Lesser degree of placenta praevia where
amniotomy fails to stop bleeding or fetal distress
appears.
• Complicating factors associated with lesser
degrees of placenta praevia where vaginal
delivery is unsafe.

49. Caesarean section without internal
examination
• If precise location of placenta.
• It should be performed by senior obstetrician
with the help of a senior anesthetist.
• Regional anaesthesia is generally avoided.
• If patient is in shock, and the bleeding
continues, operation has to be performed
immediately along with restorative measures.
• Low transverse abdominal incision is to be
avoided; intra umbilical longitudinal incision is
preferred.

50. NURSING CONSIDERATIONS
• strict bed rest
• Teaching
• home visits for comprehensive fetal and
maternal assessment
• specific, information about the condition of the
fetus.
• Make the family understands

51. In patient care
• Nursing assessments
• Periodic electronic fetal monitoring
• Immediate delivery

52. ABRUPTIO PLACENTAE-DEFINITION
• It is one form of anteparum hemorrhage where
the bleeding occurs due to premature separation
of normally situated placenta.

53. VARIETIES
• Concealed
• Mixed
• Revealed

54. ETIOLOGY
• High birth order pregnancies with
gravid 5 and above- three times more
common than in first birth.
• Advancing age of the mother.
• Poor socio economic condition.
• Malnutrition.
• Smoking

55. • Hypertension in pregnancy
• Trauma
• Sudden uterine decompression
• Short cord
• Supine hypotension syndrome
• Placental anomaly

56. PATHOGENESIS
• premature separation is initiated by
haemorrhage into the deciduas basalis. The
collected blood (decidual haematoma)
• The decidual hematoma may be small and self
limited
• If major spiral artery ruptures, a big hematoma
is formed.
• As the uterus remains distended by the
conceptus, it fails to contract and therefore fails
to compress the torn bleeding points.

57. • Couvelaire Uterus( Utero placental
apoplexy )
It is a pathological entity in association with
severe form of concealed abruption placentae.
There is massive intravasation of blood into the
uterine musculature upto the serous coat. The
condition can only be diagnosed on laprotomy.

58. • Changes in other organs
• In the liver presence of fibrin knots in the
hepatic sinusoids.
• Kidneys may show acute cortical necrosis or
acute tubular necrosis.
• Shock protenuria

59. Blood coagulopathy:
• Blood coagulopathy is due to excess
consumption of plasma fibrinogen due to
disseminated intravascular coagulation and
retro placental bleeding .There is overt hypo
fibrinogenemia (< 150 mg / dl) and elevated
levels of fibrin degradation products and
D- dimer

60. Clinical Classification
• Grade -0 :
• Clinical features may be absent .The diagnosis
is made after inspection of placenta following
delivery.
• Grade -1 (40% ) :
• Vaginal bleeding is sight .
• Uterus : Irritable , tenderness may be minimal
or absent.
• Maternal BP and fibrinogen levels unaffected.
• FHS is good.

61. • Grade -2 (45% ):
• Vaginal bleeding mild to moderate.
• Uterine tenderness is always present .
• Maternal pulse is always increased, BP maintained .
• Fibrinogen level may be decreased.
• Shock or even death occurs.
• Grade -3 (15% ):
• Bleeding is moderate to severe or may be concealed
• Uterine tenderness is marked .
• Shock is pronounced .
• Fetal death is the rule .
• Associated coagulation defect or anuria may
complicate.

62. CLINICAL FEATURES OF ABRUPTIO
PLACENTAE
The clinical features depend on :
• Degree of separation of placenta ,
• Speed at which separation occurs and
• Amount of blood concealed inside the uterine
cavity

63. DIFFERENTIAL DIAGNOSIS
Revealed type:
• Confusion with intermediate causes of APH is
difficult to eliminate.
Mixed or concealed type:
• Rupture uterus, rectus sheath hematoma,
appendicular or intestinal perforation, Twisted
ovarian tumour, Volvulus, acute hyramnios,
tonic uterine contraction.

64. COMPLICATIONS OF ABRUPTIO
PLACENTA
Maternal
• In revealed type
• maternal risk is proportional to the visible
blood loss and maternal death is rare.
• In concealed variety
• Haemorrhage
• Shock
• Blood coagulation disorders
• Oliguria and anuria
• Postpartum haemorrhage
• puerperal sepsis.

65. Fetal :
• In revealed type, the fetal death is to extent of
25- 30% .
• In concealed type, however, the fetal death is
appreciably high, ranging from 50-100%.

66. MANAGEMENT OF ABRUPTIO
PLACENTAE
Prevention:
• Elimination of known factors likely to produce
placental separation.
• Correction of anemia during antenatal period so
that the patient can withstand blood loss.
• Prompt detection and institution of the therapy
to minimize the grave complication namely
shock, blood coagulation disorders and renal
failure.

67. • Prevention of known factors likely to cause
placental separation are :
• Early detection and effective therapy of pre-eclampsia
• Needle puncture during amniocentesis should be
under ultra sound guidance.
• Avoidance of trauma–specially forceful external
cephalic version under anesthesia.
• To avoid sudden decompensation of the
• To avoid supine hypotension
• Routine administration of folic

68. • Treatment:
• At home
• In the hospital :
▫ Revealed type
• Amount of blood loss.
• Maturity of the fetus
• Whether the patient is in labor or not (usually
labor starts).
• Presence of any complication.
• Type and grade of placental abruption.

69. • Emergency measures:
• Blood is sent.
• Ringer solution drip is started with a wide bore
cannula and arrangement for blood transfusion
is made for resuscitation.
• Close monitoring of maternal and fetal
condition is done.

70. 1.Definitive treatment
(immediate delivery):
• The patient is in labour:
▫ Vaginal delivery is favored in cases with :
 Limited placental abruption .
 FHR tracing is reassuring .
 Facilities for continuous (electronic )
fetal monitoring is available .
 Prospect of vaginal delivery is soon as or
 Placental abruption of a dead fetus.

71. The patient is not in labour:
Pregnancy 37 weeks or greater:
 Induction is done by low rupture of
membranes with or without oxytocin.
 Indications of caesarean section are:
 Appearance of fetal distress.
 Amniotomy couldn’t be done or amniotomy
fails to control.
 Associated complicating factors.

72. • Pregnancy less than 37 weeks:
 Bleeding more to severe and continuing- low
rupture of membranes is quite effective.
Oxytocin drip may be added.
 Bleeding slight or has stopped- the patient is
put on conservative treatment as outlined in
placenta praevia.

73. Induction of labour is done by low rupture
of membrane
• Oxytocin may be added to expedite delivery.
• Placenta with varying amount of retro-placental
clot is expelled in most often simultaneously
with the delivery of the baby.
• Inj. oxytocin 10.IU IV slowly or IM or Inj.
methergin 0.2 mg IV is given with the delivery of
the baby to minimize postpartum blood loss.

74. Caesarean Section :
• Severe abruption of with live fetus.
• Amniotomy could not be done (un-favorable
cervix).
• Prospect of immediate vaginal delivery despite
amniotomy failed to arrest the process of
abruption (rising fundal height).
• Appearance of adverse (fetal distress, falling
fibrinogen level, oliguria).
• Anesthesia during caesarean section :
• Regional anesthesia is generally avoided when
there is significant hemorrhage.

75. • 2.Expectant management in case of
placental abruption is an exception and
not the rule :
• Cases where bleeding is slight and has stopped
(grade I abruption), fetus reactive (CTG ) and
remote from term, may be considered.
• Continuous electric fetal monitoring
• Patient should be observed in the labour ward
for 24-48 hours.
• betamethasone is given to accelerate fetal lung
maturity in the event preterm delivery has to be
contemplated.

76. Management of complications :
The major complications of placental abruption
are :
• Haemorrhagic shock .
• DIC
• Renal failure.
• Uterine atony and post partum haemorrhage.

77. NURSING MANAGEMENT OF BLEEDING
IN LATE PREGNANCY
Nursing assessment:
• Amount and nature of blood
• Pain type and location
• Maternal vital signs.
• Uterine contractions.
• Obstetric history: gravid, para, previous abortions,
preterm infants, previous pregnancy outcomes.
• Length of gestation:LMP, fundal height, co-orelation
of fundal height with estimated gestation.
• Laboratory data

78. Nursing diagnosis
• Deficient fluid volume related to excessive vascular lose
as evidenced by hypotension, increased pulse rate,
decreased/concentrated urine.
• Ineffective utero-placental tissue perfusion related to
hypovolemia as evidenced by changes in fetal heart rate
and activity.
• Activity Intolerance related to enforced bed rest during
pregnancy secondary to potential for hemorrhage
• Anxiety related to unknown effects of bleeding and lack
of knowledge of predicted course of management

79. THANK
YOU…..