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1. Pre term labour

3. DEFINITION
Preterm labour is defined as one where the labour
starts before the 37
th
completed weeks counting from
the first day of the last menstrual period

4. INCIDENCE
5 – 10%

5. ETIOLOGY
HISTORY
Abortion
Bacteriuria or recurrent UTI
Smocking
Low socio-economic and nutritional status

6. COMPLICATIONS IN THE PRESENT
PREGNANCY
Maternal
Pregnancy complications
•Pre eclampsia
•APH
•PROM
•Polyhydramnios
Uterine anomalies
•Cervical incompetence
•Malformations of the uterus

7. Contd...
Medical and surgical illness
•Acute fever
•Acute pyelonephritis
•Diarrhoea
•Acute appendicitis
•Toxoplasmosis
•Abdominal operations
Genital tract infection
•Bacterial vaginosis
•Chlamydia
•Mycoplasma

8. Contd…
Fetal
Multiple pregnancy
Congenital malformations
IUD
Placental
Infarction
Thrombosis
Placenta previa or abruption
IATROGENIC
IDIOPATHIC

9. Etiopathogenesis
Decidual cells and macrophages produce
cytokines
Increase synthesis of prostaglandins and
leukotrienes
Initiate pre term contraction

10. Diagnosis
Regular uterine contraction with or without pain
( 1 in 10 minute)
Dialation (2cm)
Effacement ( 80%)
Pelvic pressure
Back ache
Vaginal discharge

11. Management
OBJECTIVES
1.To prevent pre term onset of labour
2.To arrest pre term labour
3.To minimise perinatal mortality and
morbidity
4.Appropriate management of labour
5.Effective neonatal care

12. Prevention
Identification of risk factors
Rest
Nutritional supplement
Avoidance of smocking
Encerclage operation
Premature effacement with irritable uterus and early engagement
of head
 Tocolytic agent
Bed rest
Be sure about the gestational age before induction
Selective continuation of complicated pregnancy
Rest
Appropriate therapy
Early hospitalisation

13. Investigations
FBC
Urine for routine and c/s
Endocervical swab
USG
Serum electrolyte and glucose when
tocolytic agents are to be used
Fibronectin

14. To arrest pre term labour
Adequate rest
 Left lateral position
Adequate sedation
Diazepam 5mg
Phenobarbitone 30- 60 mg
Adequate hydration
Antibiotic if there is infection
Tocolytic agents ( short and long term therapy)

15. Short term therapy
Objectives
1. To delay delivery for at least 24 hrs for
glucocorticoid therapy
2.In utero transfer of patient

16. Contd…
Contraindications
1. Maternal
•Diabetes
•Thyrotoxicosis
•Hypertension
•Cardiac disease
•Haemorrhage
2.Fetal
•Fetal distress
•Fetal death
•Congenital malformation
•Pregnancy beyond 34 weeks
3.Others
•Rupture of membrane
•Cervical dialatation more than 4 cm
•Chorioamnionitis

17. Long term therapy
Pregnancy prior to 34 weeks
Pregnancy can be continued for at least one week
Benificial when pregnancy beyond 48 hours but less than 7
days
Glucocorticoid therapy
 Betamethasone 12mg IM every 12hrs - 2 doses
 Dexametasone 8mg IM every 12 hrs - 3 doses
Contraindication
PROM
Pre eclampsia
Delivery time is outside 24hrs – 7 day interval

18. Management during labour
Objective
•To prevent asphyxia
•To prevent birth trauma

19. First stage
Patient is put to bed to prevent PROM
Ensure adequate oxygenation
Strong sedatives and acceleration should be avoided
Watch during labour
Delay - LSCS

20. Second stage
Birth should be gentle and slow
Liberal episiotomy
Tendency to delay curtailed by forceps
Cord is to be clamped immediately to prevent hypervolemia
and hyperbilirubinemia
Place baby in NICU

21. LSCS
 Before 34 wks with breech
Lower segment or j shaped incision is preferred

22. Nursing Diagnosis
1.Altered cardiopulmonary tissue perfusion related to the
effects of tocolytic agents
2.Fear related to the uncertainity of outcome and effects of
preterm labour on fetus
3.Impaired gas exchange related to lung immaturity
4.Pain related to uterine contraction
5.Ineffective management of therapeutic regimen related to
the lack of knowledge and complexity of therapy
6.Diversional activity deficit related to the imposed bed rest

23. Contd…
7.Constipation related to decreased gastrointestinal motility
from prolonged bed rest / adverse effect of tocolytic agent
8.Situational low self esteem related to the feeling of
inadequacy from pre term labour complications
9.Knowledge deficit related to the treatment of preterm labour

24. Premature Rupture of Membranes
(PROM)

25. Definition
Spontaneous rupture of the membranes any time
beyond 28
th
week of pregnancy but before the
onset of labour is called premature (pre labour)
rupture of membranes.

26.  TERM PROM
When the rupture occurs beyond 37
th
week but before the onset
of labour it is called term PROM
PRE TERM PROM
When the rupture occurs before the 37
th
completed weeks it is
called preterm PROM
PROLONGED RUPTURE OF MEMBRANE
Rupture of membrane for 24 hours before delivery is called
prolonged rupture of membrane

27. INCIDENCE
10 % of all pregnancies

28. Causes
Increased friability of the membranes
Decreased tensile strength of the membranes
Polyhydramnios
Cervical incompetence
Multiple pregnancy
Infection – Chorio-amnionitis, UTI, lower genital tract
infections

29. Diagnosis
 Subjective symptom is
Escape of watery discharge per vagina either as a gush or
slow leak.
 Usually confused with
1.Hydrorrhoea gravidarum
2.Incontinence of urine

30. Confirmation of Diagnosis
1.Speculum examination
2.Examination of the collected fluid from posterior fornix
for
Detection of pH ( 6 – 6.2)
Ferning pattern
3.0.1% Nile blue sulphate test – orange blue colouration of
cells
4.USG

31. Investigations
Complete blood count
Urine analysis and culture
High vaginal swab for culture
Vaginal pool to estimate phosphatidyl glycerol
USG
NST

32. Dangers
Preterm labour and prematurity
Ascending infection
Cord prolapse
Dry labour
Fetal pulmonary hypoplasia
R.D.S

35. Management
- Assess gestational age and fetal weight
- Patient not in labour
- Absence of infection and fetal distress
- biophysical profile and NST
To monitor maternal pulse, temperature, FHS and start prophylactic antibiotics
Pregnancy < 34 weeks Pregnancy > 34 weeks Pregnancy > 37 weeks
Expectant management Wait for spontaneous onset Wait for spontaneousto
continue for fetal maturity. of labour for 24 – 48 hours labour for 24 hours
Transfer patient with “fetus in FAILS FAILS
Utero” to equipped centre
Induction of labour Induction of labour
with oxytocin with oxytocin

39. Meaning
Any deviation of the normal pattern of
uterine contractions affecting the
course of labour is called abnormal
uterine action

40. Etiology
Advancing age of the mother
Prolonged pregnancy
Over distention of the uterus due to twins
Psychological Factors
Contracted pelvis
Malpresentations
Full bladder

41. Types

42. `

43. Precipitate LabourPrecipitate Labour
Definition:
A labour lasting less than 3 hours
Etiology: More common in multipara when there are
strong uterine contractions
roomy pelvis
small sized pelvis
minimal soft tissue resistance

44. Complications
Maternal:
Lacerations of the cervix, vagina
and perineum.
Shock. 
Inversion of the uterus.
Postpartum haemorrhage:
no time for retraction,
lacerations.
Sepsis due to:
lacerations,
inappropriate surroundings.
Foetal:
Intracranial haemorrhage due to
sudden compression and
decompression of the head.
Foetal asphyxia due to:
strong frequent uterine
contractions reducing placental
perfusion,
lack of immediate resuscitation.
Avulsion of the umbilical cord.
Foetal injury due to falling down.

45. Management
Before delivery
Patient who had previous precipitate labour should be hospitalized
before expected date of delivery as she is more prone to repeated
precipitate labour.
During delivery
Inhalation anaesthesia: as nitrous oxide and oxygen is given to
slow the course of labour.
Tocolytic agents: as ritodrine (Yutopar) may be effective.
Episiotomy: to avoid perineal lacerations and intracranial
haemorrhage.
After delivery
Examine the mother and foetus for injuries.

46. EXCESSIVE UTERINE CONTRACTION AND
RETRACTION
Physiological Retraction Ring
It is a line of demarcation between the upper and lower uterine segment
present during normal labour and cannot usually be felt abdominally.
Pathological Retraction Ring (Bandl’s ring)
It is the rising up retraction ring during obstructed labour due to marked
retraction and thickening of the upper uterine segment while the relatively
passive lower segment is markedly stretched and thinned to accommodate
the foetus.
The Bandl’s ring is seen and felt abdominally as a transverse groove that
may rise to or above the umbilicus.
Clinical picture: is that of obstructed labour with impending rupture
uterus.
Obstructed labour should be properly treated otherwise the thinned lower
uterine segment will rupture.

48. HYPOTONIC UTERINE INERTIA
Definition: The uterine contractions are infrequent, weak and of
short duration
General factors:
Primigravida particularly elderly.
Anaemia
Nervous and emotional as anxiety
and fear.
Hormonal due to deficient
prostaglandins or oxytocin as in
induced labour.
Improper use of analgesics.
Local factors:
Overdistension of the uterus.
Developmental anomalies of the uterus
Myomas of the uterus interfering
mechanically with contractions.
Malpresentations, malpositions and
cephalopelvic disproportion. The
presenting part is not fitting in the
lower uterine segment leading to
absence of reflex uterine contractions.
Full bladder and rectum

49. Types
Primary inertia: weak uterine contractions from the start.
Secondary inertia: inertia developed after a period of good uterine
contractions when it failed to overcome an obstruction so the uterus is
exhausted.
Clinical Picture
Labour is prolonged.
Uterine contractions are infrequent, weak and of short duration.
Slow cervical dilatation.
Membranes are usually intact.
The foetus and mother are usually not affected apart from maternal anxiety
due to prolonged labour.
More susceptibility for retained placenta and postpartum haemorrhage due to
persistent inertia.
Tocography: shows infrequent waves of contractions with low amplitude

50. Management

51. HYPERTONIC UTERINE INERTIA
Types
Colicky uterus: incoordination of the different parts of the uterus in contractions.
Hyperactive lower uterine segment: so the dominance of the upper segment is lost.
Clinical Picture
The condition is more common in primigravidae and characterized by:
Labour is prolonged.
Uterine contractions are irregular and more painful.
High resting intrauterine pressure in between uterine contractions detected by
tocography (normal value is 5-10 mm of Hg).
Slow cervical dilatation.
Premature rupture of membranes.
Foetal and maternal distress.

52. Management
General measures: as hypotonic inertia.
Medical measures:
€Analgesic and antispasmodic as pethidine.
€Epidural analgesia may be of good benefit.
Caesarean section is indicated in:
€Failure of the previous methods.
€Disproportion.
€Foetal distress before full cervical dilatation

53. CONSTRICTION (CONTRACTION) RING
Definition
It is a persistent localised annular spasm of the circular uterine muscles.
It occurs at any part of the uterus but usually at junction of the upper and
lower uterine segments.
It can occur at the 1st, 2nd or 3rd stage of labour.

55. Aetiology
Unknown but the predisposing factors are:
Malpresentations and malpositions.
Clumsy intrauterine manipulations under light anaesthesia.
Improper use of oxytocin e.g.
use of oxytocin in hypertonic inertia.
IM injection of oxytocin.
Diagnosis
The condition is more common in primigravidae and frequently
preceded by colicky uterus.
The exact diagnosis is achieved only by feeling the ring with a
hand introduced into the uterine cavity.

56. Management
Exclude malpresentations, malposition and disproportion.
In the 1st stage: Pethidine may be of benefit.
In the 2nd stage: Deep general anaesthesia is given to relax the
constriction ring:
If the ring is relaxed, the foetus is delivered immediately by forceps.
If the ring does not relax, caesarean section is carried out with lower
segment vertical incision to divide the ring.
In the 3rd stage: Deep general anaesthesia is given followed by
manual removal of the placenta

57. CERVICAL DYSTOCIA
Definition
Failure of the cervix to dilate within a reasonable time in spite of good
regular uterine contractions.
Varieties
Organic (secondary) due to
Cervical stances as a sequel to previous amputation, cone biopsy, extensive
cauterisation or obstetric trauma.
Organic lesions as cervical myoma or carcinoma.
Functional (primary):
In spite of the absence of any organic lesion and the well effacement of the
cervix, the external os fails to dilate.
This may be due to lack of softening of the cervix during pregnancy or
cervical spasm resulted from overactive sympathetic tone.

58. Complications
Annular detachment of the cervix: the bleeding from the cervix is
minimal because of fibrosis and avascular pressure necrosis leading
to thrombosis of the vessels before detachment.
Rupture uterus.
Postpartum haemorrhage: particularly if cervical laceration extends
upwards tearing the main uterine vessels.
Management
 Organic dystocia:
♣Caesarean section is the management of choice.
 Functional dystocia:
♣Pethidine and antispasmodics: may be effective.
♣Caesarean section: if
♣medical treatment fails or
♣foetal distress developed.

60. Prolonged labour

62. Definition
The labour is prolonged when the combined duration of the
first and second stage is more than the arbitrary time limit
of 18 hours.
[ D.C.Dutta]
Prolonged labour is defined when the first and second
stage of labour last more than 24 hours, currently duration
is taken as more than 18 hours. Duration of labour is
calculated from mother’s subjective estimate of labour
onset
[Dawn]

63. Prolongation due to
Protracted cervical dilatation in the first stage
Inadequate descent of the presenting part during the first or
in the second stage
Labour considered prolonged when the cervical dilatation
rate is < 1 cm/hr and the descent of the presenting part is <
1 cm/hr for a period of minimum 4 hours observation.

64. Types of prolonged labour
 Hypotonic uterine dysfunction: due to low intensity
uterine contractions.
general factors local factors
Elderly primi gravida over distention of uterus
Anemia developmental anomalies
Nervousness, anxiety myomas of uterus
and fear
Hormonal mal presentations, CPD
Improper use of malpositions
analgesics full bladder and rectum

65. Cont…
 Hypertonic uterine dysfunction: it can be
a. Incordinate uterine action
b. colicky uterus
c. Asymmetrical uterine dysfunction
d.Hyperactive lower segment
e.Constriction ring dystocia
Cervical dystocia: cervix becomes thin and fails to dilate
within a reasonable time inspite of good uterine
contractions.

66. Cervical
dystocia
In coordinate uterine
action

67. Incidence
Primi gravidae 25%
Multi gravidae 2%

68. Risk factors of prolonged labour
 age and parity: commonly primigravidae, more in elderly
one
 CPD and fetal malposition
 Uterine distention- twins, hydramnios
 Uterine defect- fibroid, malformation
 Nervousness, fear and emotion
 injudicious use of analgesia in labour
 injudicious induction of labour by ARM and oxytocin
drip.
 unknown cause.

69. Causes of prolonged labour
Faults in power [commonest cause]
*inefficient uterine dysfunction
*constriction ring
*cervical dystocia
*over dose of sedative and analgesics
* epidural analgesia
*improper use of oxytocics

70. Cont…
Faults in passage:
 PROM
 Contracted pelvis
CPD
Cervical stenosis
Fibroid or carcinoma
Ovarian tumor
Uterine fibroid 20%

71. Engagement & descent of the
foetal head -
presence of cephalopelvic
disproportion

72. Engagement & descent of the foetal
head -
presence of cephalopelvic
disproportion

73. Cont…
Faults in passenger:
Occipito posterior positions of vertex
 Other malpresentations
 Twins
 Hydramnios[ 30%]

74. Labour disorders due to inefficient
uterine action
prolonged latent phase beyond 12 hours
a.Hypotonic or hypertonic dysfunction
b.Predisposing factors are sedation, anaesthesia , false
labour,unknown cause.
Prolonged active phase[ protraction disorder]
Slow rate of cervical dilatation below 1cm/hr in
nullipara and 1.5 cm/hr in multipara
Caused by hypotonic dysfunction, hyperactive lower
segment.
Predisposing factors :CPD,fetal malpositions and
sedation

75. Cont…
secondary arrest of cervical dilatation or head descent
Arrest of cervical dilatation is taken when there is no
cervical change for 2 hrs.
 there is head descent less than 1cm/hr in nullipara or
less than 2cm/hr in multipara and no head descent for
one hour.
Due to hypotonic dysfunction and incordinate uterine
dysfunction.
 The causative factors are occipito posterior positions
[70%], pelvic contraction ,excessive sedation.

76. DIAGNOSIS
Clinical features
Hypotonic
dysfunction
[more frequent]
Hypertonic
dysfunction
[ less frequent]
1. Timing of
dysfunction
[more
frequent]
At latent phase
from start of labour
usually running to
active phase
Latent phase from start of
labour
2.Labour pains
Less painful, short
lasting,
infrequent
abdominal pain
and no back ache
Severely painful ,prolonged
lasting, frequent pain as
abdominal colic or as
backache ,desire to bear
down during contraction
with incompletely dilated
cervix.

77. Cont…
3.membranes Remains intact Ruptures early
4.Cervical
dilatation
slow Slow .it hangs thick
lipped without
pressure of head.
5.Fetal head Caput
develops late
Caput develops even
before rupture of
membranes
6.Fetal distress
Appears late Appearing early

78. Cont…
7.Maternal
effect
little
She becomes
distressed in pain,
goes to dehydration
and acidosis early.
8.Difficult
labour
Same in both
groups

79. Cont…
Other measures such as :
 radiography, CT or MRI
 Abdominal and vaginal examination.
 partograph

80. Cont…
First stage: is considered prolonged
 When the duration of labour is more than 12 hrs
The rate of cervical dilatation is < 1 cm / hr in a primi and
< 1.5 cm/ hr in a multi
 when the cervicograph crosses the alert line and falls on
zone2
 Intervention is required when the cervico graph crosses
the action line and falls on zone 3

81. Cont…
Secondary arrest : is defined when the active phase of
labour ( cervical dilatation ) commences normally but
stops or slows significantly for 2 hrs or more prior to
full dilatation of the cervix. It is commonly due to
malposition or CPD

84. Cont…
Second stage: is considered prolonged
When it lasts for more than 2 hrs in primi and 1 hr in
multi.
Diagnosis :
Sluggish or non descent of the presenting part even
after full dilatation of the cervix.( failure of head
descent within 1 hr of full dilatation is called
protraction of descent.)
Variable degrees of molding and caput formation in
cephalic presentation.
Identification of the course of prolongation.

85. Dangers(Complications)
Maternal effects:
Distress
PPH
Trauma to genital tract
Increased operative delivery
Puerperal sepsis
Sub involution.

86. Cont…
Fetal effects :
Hypoxia
Intra uterine infection
Intra cranial stress or hemorrhage
Increased operative delivery

87. Management
Prevention :
Antenatal or early intra natal detection of the factors
likely to produce prolonged labour.
 Use of partograph
Selection and judicious augmentation of labour by
low rupture of the membranes followed by oxytocin
drip.
Change of posture in labour, other than supine to
increase uterine contractions, avoidance of
dehydration in labour and use of adequate analgesia
for pain relief.

88. Cont…
Actual Rx:
Careful evaluation to find out
Cause of prolonged labour
Effect on the mother
Effect on the fetus

89. Cont…
Definitive Rx :
First stage
patient is referred to level 11 care without any solid food.
Only water is allowed orally.
Maintain partograph
Identify or diagnosis of hypotonic and hypertonic labour
dysfunction.
Monitor maternal vital signs and FHS
Identify CPD or fetal mal position.
Maintain I.V line with 5% DW/RL
Antibiotics ( cefazoline ) 1 gm I.V and repeated after 6 hrs on
PROM

90. IN CASE OF PROM
GROUP A: Hypotonic uterine
dysfunction
Os 3 cm on 12 hrs labour since
admission on vertex presentation.CPD
excluded.FHS normal
Artificial rupture of membrane , if liquor
shows meconium CS. If liquor clear


wait for 60min. for improvement of
contractions Otherwise – oxytocin 5
units.
500ml 5% dectrose in primi or 2 units in
500ml DW in multi.
Fetal monitoring is done. If failure to
progress or fetal distress


CS
GROUP B: Hypertonic uterine dysfunction
Os 3 cm at 12 hrs labour since admission;
i.v. 5% DW and RL is set up
Nothing by mouth
Inj. Pethedine 100 mg, phenergan 25mg,
continuous epidural or caudal analgesia if
available.CPD is evaluated
FHR monitoring done on recovery from
sleep , her hypertonic
dysfunction may improve.
Uterine hyper tone Uterus
Persists, fetal distress relaxes
AROM


C.S oxytocin, wait for
Vaginal delivery

CS

91. Cont..
Group A:Second stage
Head at outlet,FHS normal; AROM.
If membranes present followed by
oxytocin drip for uterine
dysfunction
Failure to progress
Low forceps/ vacuum extraction
if late referral/ dead fetus/malformed
fetus
Oxytocin drip
Craniotomy delivery
Group B:Second stage
Cervical dystocia,
Duhrssen’s incision is
made at 3 o’ clock and 9 o’
clock position on cervical
lip by applying forceps or
vacuum extractor, thus
delivery is done.
For constriction ring, vaginal
delivery can be done under
deep general anaesthesia if
fetus is not distressed

92. Cont…
Third stage actively managed
Neonatal care is important due to meconium aspiration

93. Nursing diagnosis
Risk for injury to mother and fetus
Fatigue and exhaustion related prolonged efforts and
pain
Anxiety related to process and outcome of labour
Knowledge deficit related to labour process

95. OBSTRUCTED LABOUR.

97. ETIOLOGY.
FAULT IN THE PASSAGE.
FAULT IN THE PASSENGER.

98. FAULT IN THE PASSAGE.
Bony obstruction.
Soft tissue obstruction.

99. I.BONY
e.g. Contracted pelvis

100. e.g.Cephalopelvic disproportion

101. 2)SOFT TISSUE OBSTRUCTION
e.g.Cervical dystocia:

102. e.g.Cervical or broad ligament fibroid

103. e.g. Impacted ovarian tumor

104. e.g.Non gravid horn of a bicornuate uterus:

106. Transverse lie.
Brow presentation.
Congenital malformations.
Big baby.
Occipito posterior positions.
Compound presentation.
Locked twins.

107. Transverse lie

108. Brow presentation

109. Congenital malformations

110. Big baby

111. Occipito posterior positions.

112. Compound presentation

113. Locked twins

114. Fetal Ascitis

115. MORBID ANATOMICAL CHANGES
 BLADDER
 UTERUS

116. UTERUS:
Formation of bandl’s ring

117. BLADDER:
Bladder become an abdominal organ.
Patient fails to empty the bladder.
Bladder walls get traumatized.
Blood stained urine.
Pressure necrosis.
Genito urinary fistula.

118. Genito urinary Fistula

119. SIGNS OF OBSTRUCTED LABOUR.
EARLY SIGNS:
PRESENTING PART DOES NOT ENTER THE PELVIC
BRIM.
SLOW CERVICAL DILATATION.
LOOSELY HANGING CERVIX.
EARLY RUPTURE OF MEMBRANE OR FORMATION
OF A LARGE ELONGATED SAC OF FORE WATERS.

120. LATE SIGNS:
I.MOTHER MAY BE DEHYDRATED AND KETOTIC AND IN
CONSTANT PAIN.
II.CLINICAL SIGNS:-
a)PYREXIA, TACHYCARDIA.
b)DIFFICULT ABDOMINAL PALPATION.
c)DIFFICULT ABDOMINAL EXAMINATION.
d)COMPLICATED VAGINAL EXAMINATION .

121. CONTI…
e)LESS URINE OUTPUT,HAEMATURIA.
f)EVIDENCE OF FETAL DISTRESS.
g)PHYSIOLOGIC RETRACTION RING.
h)VISIBLE RETRACTION RING OR BANDL’S RING.
i)HOT,DRY VAGINA.
j)PRESENTING PART WILL BE HIGH AND
IMMOVABLE.

122. Multiple Pregnancy

123. DEFINITION
When more than one fetus
simultaneously develops in the
uterus ,it is called multiple
pregnancy.

124. According to their number, they could be
categorized into:
Twins (most common)
 Triplets
Quadruplets
Quintuplets
Sextuplets

125. Types
Monozygotic
Identical/Uniovular
Fertilization of a single ovum,
Similar sex.
Identical in every way including
the HLA genes
Not genetically determined
Dizygotic
Fertilization of 2 seperate
ova
Fraternal /Dizygotic

126. Monozygotic Twins…
Different Scenarios of Cleavage
If the separation takes place just after the first cellular
division [1
st
3 days ]/ prior to morula stage
both of the twins will have their own placenta and an
amniotic sac each.
Scenario 1
Monozygotic twin
  pregnancy 
Di-Amniotic and Di-Chorionic
or D/D

127. Scenario 2
Monozygotic twin
  pregnancy
 

Di-amniotic - Mono-chorial
and or D/M
Separation can also take place a little
later in the development [4-8 days after
the formation of inner cell mass when
chorion has developed]
of the embryonic cells but before the
blastocyte has defined the roles of each
cell.
Twins will be in the same placenta, but
they will have 2 amniotic sacs.

128. Scenario 3
Monozygotic twin
  pregnancy
 

Mono-amniotic and Mono-
chorial
Separation takes place at the stage when the amniotic bag is
already being formed
[day 8-14]
Twins will be in the same placenta, and in the same amniotic
sac.

129. Conjoined Twins
If the division occur after 2 weeks
of the embryonic disc formation,
incomplete or conjoined twins
will occur.
They may be joined
anteriorly [thoracopagus-
commonest],
posteriorly [pyopagus]
cephalic [craniopagus] o
caudal [ischiopagus].

130. Dizygotic twin pregnancy
Di-chorial and Di-amniotic.
Dyzygotic twins, are descended from a double ovulation and a double fertilization.
The 2 eggs are completely independent.
This configuration represents two thirds of all twin pregnancies.

132. Superfecundation
It is the fertilization of two different ova
released in the same menstrual cycle,by
separate act of coitus within a short period of
time.

133. Superfetation
It is the fertilization of two ova released in
different menstrual cycle
One fetus over another
Possible until decidual space is obliterated by
12 weeks of pregnancy

134. Fetus papyraceous or compressus
One fetus dies early
Dead fetus is flattened and compressed
between the membranes of the living fetus
and the uterine wall

135. Fetus acardicus
Occurs only in monozygotic twins
Part of the fetus remains amorphous and
becomes parasitic without a heart

136. Hydatidiform mole
Hydatidiform mole from one placenta
And a normal fetus and placenta

137. Vanishing twins
USG in early pregnancy revealed occassional
death of one fetus and continuation of
pregnancy with surviving one

138. ETIOLOGY
Race – Highest among negroes and lowest among mongols
Hereditary- Transmitted through female
Advancing age of the mother- Maximum between 30-35 years
Parity – 5
th
gravida onwards
Iatrogenic – Gonadotrophin(20-40%),clomephene citrate(5-
6%)

139. Maternal physiological changes
Increase weight gain and cardiac out put
Plasma volume is increased by an additional of
500ml
Increased fetoprotein level and GFR

140. History…
Patient profile:
Etiological factors; with positive past history and family history
specially maternal.
Early pregnancy
 Hyperemesis, bleeding.
Mid-pregnancy
 Greater weight gain than expected
 Abdominal size > period of amenorrhea
 early PIH symptoms, persistent fetal activity.
Late pregnancy
Pressure symptoms (dyspnea, dyspepsia, UTI, piles, edema and
varicose veins in LL).

141. Examination
General:
 An early increase weight gain,
Pallor
Less mid-trimisteric fall blood pressure
Early PIH
Eary edema, and varicose veins in LL.
Abdominal:
Fundal level > amenorrhea especially in mid-pregnancy
 exclude other causes.
Palpation: Multiple fetal
 identify presentations.
Auscultation of FHS:
2 different recordings by 2 observers and a difference > 10 bpm a Gallop between 2
points[ Arnoux sign]
Pelvic: Specially during the course of labor
small presenting part compared to abdominal size

142. Types of Twin Lie and Presentations
1
st
twin 2
nd
twin%
Vertex Vertex35
Vertex Breech20
Breech Vertex15
Breech Breech10
Cephalic or transverseTransverse or cephalic10
Breech or transverseTransverse or breech 5
Transverse Transverse 5

143. Selective Embryo Reduction
The presence of > 3 fetuses carries the risk of losing
them all (preterm delivery).
The number is reduced to twins only by injecting
potassium chloride intracardiac under U/S guidance
(about 1.5 ml of 15% solution).
Potassium chloride may diffuse and affect other fetuses.

144. Maternal Complications
DURING PREGNANCY
Nausea and vomiting
Anaemia
Pre eclampsia
Hydramnios
Antepartum haemorrhage
Malpresentation
Preterm labour
Mechanical distress

145. Maternal Complications
DURING LABOUR
Early rupture of membranes and cord prolapse
Prolonged labour
Increased operative interference
Bleeding
Postpartum haemorrhage
DURING PUERPERIUM
 Sub involution
Infection
Lactation failure

146. Fetal Complications
 Miscarriage rate is increased
Premature rate
Growth problem
Intrauterine death of one fetus
Fetal anomalies
Asphyxia and still birth

147. Antenatal Management
ANTENATAL ADVISES
Diet – extra 300 Kcal, extra protein
Increased rest at home
Travel restriction
Supplementary therapy – Fe 60-100mg,Additional Ca, Vitamin
and Folic acid
Frequent antenatal visit
Prophylactic os tightening
Fetal surveillance
HOSPITALISATION

148. How are they going to be delivered?

149. Management During Labour
DELIVERY OF THE FIRST BABY
Same as singleton pregnancy
Liberal episiotomy
Forceps delivery
Do not give IV ergometrine with the delivery of the anterior
shoulder of the first baby
Clamp cord at two places and cut in between
Leave at leat 8-10 cm of the cord
Label bay as no 1

150. Contd….
DELIVERY OF THE SECOND BABY
External cephalic version
Rupture fore water after correcting the lie
Wait for 10min for spontaneous delivery
Syntocinon drip
Vaccum extraction or Breech extraction

151. Contd….
CESAREAN SECTION
Severe PIH
Bad obstetrics history
Long history of infertility
Elderly primi
Preterm delivery
Breech presentation

152. MANAGEMENT OF THIRD STAGE AND PUERPARIUM
Prevention of PPH
Treatment of anemia
Psychological adjustment
Family planning advice

153. Twin to Twin transfusion
Vascular communication between 2 fetuses,
mainly in monochorionic placenta (10% of
monozygotic twins),
Twins are often of different sizes:
Donor twin = small, pallied, dehydrated (IUGR),
oligohydramnios (due to oliguria), die from
anemic heart failure.
Recipient twin = plethoric, edematous,
hypertensive, ascites, kernicterus (need
amniocentesis for bilirubin), enlarged liver,
polyhydramnios (due to polyuria), die from
congestive heart failure, and jaundice.

157. FETAL DISTRESS

158.   DEFINITION
•Fetal distress is the term commonly used to describe Fetal distress is the term commonly used to describe
fetal fetal hypoxiahypoxia
•It is a clinical diagnosis made by It is a clinical diagnosis made by indirectindirect methods and methods and
should be defined as: should be defined as:
Hypoxia that may result in fetal damage / death if not Hypoxia that may result in fetal damage / death if not
reversed or the fetus delivered immediatelyreversed or the fetus delivered immediately
•It includes It includes acuteacute distress and distress and chronicchronic distress distress

159. ETIOLOGY
Maternal:Maternal:
poor placental perfusionpoor placental perfusion
hypovolaemiahypovolaemia
hypotensionhypotension
myometrial hypertonusmyometrial hypertonus
prolonged laborprolonged labor
excess oxytocinexcess oxytocin

160. Fetal:Fetal:
cord compressioncord compression
 oligohydramniosoligohydramnios
 entanglemententanglement
 prolapseprolapse
pre-existing hypoxia or growth retardationpre-existing hypoxia or growth retardation
infectioninfection
cardiaccardiac
ETIOLOGY

161. MECHANISM
There are potentially limitless causes for fetal distress, but There are potentially limitless causes for fetal distress, but
several key mechanisms are usually involvedseveral key mechanisms are usually involved
Contractions reduce temporarily placental blood flow and can Contractions reduce temporarily placental blood flow and can
compress the umbilical cordcompress the umbilical cord

If a women is in labor longer then this can cause fetal distress via If a women is in labor longer then this can cause fetal distress via
the above mechanismthe above mechanism

162. MECHANISM
Acute distress can be a result of:Acute distress can be a result of:
placental abruptionplacental abruption
prolapse of the umbilical cordprolapse of the umbilical cord (especially with breech presentations) (especially with breech presentations)
hypertonic uterine stateshypertonic uterine states
use of oxytocinuse of oxytocin
HypotensionHypotension can be caused by either epidural anesthesia or the can be caused by either epidural anesthesia or the
supine position, which reduces inferior vena cava return of blood to supine position, which reduces inferior vena cava return of blood to
the heartthe heart
The decreased blood flow in hypotension can be a cause of fetal The decreased blood flow in hypotension can be a cause of fetal
distressdistress

163. SIGNS AND SYMPTOMSSIGNS AND SYMPTOMS
Acute fetal distressAcute fetal distress

164.  Cardiotocography signs:Cardiotocography signs:
Increased / decreased fetal heartIncreased / decreased fetal heart (tachycardia and bradycardia), (tachycardia and bradycardia),
especially especially duringduring and and afterafter a contraction decreased varibility in the a contraction decreased varibility in the
fetal heart ratefetal heart rate
Abnormal fetal heart rateAbnormal fetal heart rate (< 120 or > 160 bpm) (< 120 or > 160 bpm)
A normal fetal heart rate may slow during a contraction but usually recovers to A normal fetal heart rate may slow during a contraction but usually recovers to
normal as soon as the uterus relaxesnormal as soon as the uterus relaxes
A very slow fetal heart rate in the absence of contractions or persisting after A very slow fetal heart rate in the absence of contractions or persisting after
contractions is suggestive of fetal distress contractions is suggestive of fetal distress 
SIGNS AND SYMPTOMS

165. A A rapid fetal heart raterapid fetal heart rate may be a response to: may be a response to:
maternal fever maternal fever
drugsdrugs
hypertension hypertension
amnionitisamnionitis
In the absence of a rapid maternal heart rate, a rapid fetal heart In the absence of a rapid maternal heart rate, a rapid fetal heart
rate = a sign of fetal distressrate = a sign of fetal distress
For a diagnosis of fetal distress to be made, one or more of the For a diagnosis of fetal distress to be made, one or more of the
following must be present: following must be present:
persistent severe variable decelerationpersistent severe variable deceleration
persistent and non-remediable late declarationspersistent and non-remediable late declarations
persistent severe bradycardiapersistent severe bradycardia
SIGNS AND SYMPTOMS

166. Amniotic fluid is contaminated by Amniotic fluid is contaminated by meconiummeconium

There are 3 degrees about contaminatedThere are 3 degrees about contaminated

I - I - slight slight contaminationcontamination
The color of the amniotic fluid = The color of the amniotic fluid = slight greenslight green
IIII

--

mildmild contamination contamination
Color of the amniotic fluid = Color of the amniotic fluid = dark greendark green
III - III - severesevere contamination contamination
Color of the amniotic fluid is dark yellow. Color of the amniotic fluid is dark yellow.
If the amniotic fluid is severely contamination, it suggests the, If the amniotic fluid is severely contamination, it suggests the, fetal distressfetal distress - -
it must be managed as soon as possibleit must be managed as soon as possible
SIGNS AND SYMPTOMS

167. Decreased fetal movement felt by the motherDecreased fetal movement felt by the mother
Biochemical signs - assessed by collecting a small sample of Biochemical signs - assessed by collecting a small sample of
baby‘s blood from a scalp prick through the open cervix in baby‘s blood from a scalp prick through the open cervix in
labor:labor:
Fetal acidosis elevated fetal blood lactate levels Fetal acidosis elevated fetal blood lactate levels

A fetal scalp A fetal scalp pH < 7.2pH < 7.2 , , PoPo
22 >60mmHg >60mmHg suggests fetal distress suggests fetal distress
SIGNS AND SYMPTOMS

168. Chronic Fetal Distress

169.  Decreased or disappear fetal movement:Decreased or disappear fetal movement:

< 10 times per 12 hours is regarded as decreased< 10 times per 12 hours is regarded as decreased
With the first effect of hypoxia, the fetal movement is increasedWith the first effect of hypoxia, the fetal movement is increased
If the hypoxia persists, the fetal movement is decreased, and may If the hypoxia persists, the fetal movement is decreased, and may
disappeardisappear

If the fetal movement lost, the fetal heart beat will be disappearing If the fetal movement lost, the fetal heart beat will be disappearing
within 24 hourswithin 24 hours
Cautions: Dangerous for the fetus if the fetal movement disappear. Cautions: Dangerous for the fetus if the fetal movement disappear.
Management immediately!!Management immediately!!
SIGNS AND SYMPTOMS

170. Abnormal cardiotocography signs:Abnormal cardiotocography signs:

Slow fetal heart rate(<120bpm) or rapid fetal heart rate Slow fetal heart rate(<120bpm) or rapid fetal heart rate
(>180bpm) (>180bpm) last more than 10 minlast more than 10 min in the absence of in the absence of
contractions contractions is suggestiveis suggestive of fetal distress of fetal distress
The fetal heart rate > 160 bpm , especially > 180 bpm, it The fetal heart rate > 160 bpm , especially > 180 bpm, it
suggests suggests early hypoxiaearly hypoxia, unless the maternal heart rate is faster, unless the maternal heart rate is faster
SIGNS AND SYMPTOMS

171. FHR < 120bpm, typically less than 100bpm FHR < 120bpm, typically less than 100bpm
It is very danger for fetusIt is very danger for fetus
The fetal heart rate normally show continuous minor The fetal heart rate normally show continuous minor
variations, with a range of about 5 bpm, loss of base line variations, with a range of about 5 bpm, loss of base line
variability implies that the cardiac reflexes are impaired, variability implies that the cardiac reflexes are impaired,
either from the effect of either from the effect of hypoxiahypoxia or of or of drugsdrugs such as such as valiumvalium
It may be seriousIt may be serious
SIGNS AND SYMPTOMS

172. Early decelerationEarly deceleration: with each contraction the rate often slows, but : with each contraction the rate often slows, but
it returns to normal soon after removal of the stressit returns to normal soon after removal of the stress
The early deceleration in the heart rate start within 30 seconds of The early deceleration in the heart rate start within 30 seconds of
the onset of the contraction and return rapidly to the baseline rate the onset of the contraction and return rapidly to the baseline rate
It is not of serious significanceIt is not of serious significance as a rule and indicate that while the as a rule and indicate that while the
fetus is undergoing some stress the cardiac control mechanisms are fetus is undergoing some stress the cardiac control mechanisms are
responding normallyresponding normally
SIGNS AND SYMPTOMS

173.  
EARLY DECELERATIONEARLY DECELERATION

174. Variable decelerationVariable deceleration: no consistent relationship with uterine : no consistent relationship with uterine
contraction. contraction.
It is sometimes caused by compression of the umbilical cord It is sometimes caused by compression of the umbilical cord
between the uterus and the fetal body, or because it is looped between the uterus and the fetal body, or because it is looped
round some part of the fetusround some part of the fetus
Provided that it does not persist for more than a few minutes it Provided that it does not persist for more than a few minutes it
may have little significance, but may have little significance, but persistence for more than 15 persistence for more than 15
minutesminutes would call for treatment would call for treatment
SIGNS AND SYMPTOMS

175. VARIABLE DECELERATIONVARIABLE DECELERATION

176. The most serious pattern of heart rate changes is The most serious pattern of heart rate changes is fetal bradycardiafetal bradycardia
with loss of baseline variability and with loss of baseline variability and late decelerationslate decelerations
Decrease (defined as onset of deceleration to nadir =30 seconds) Decrease (defined as onset of deceleration to nadir =30 seconds)
and return to baseline FHR associated with a uterine contraction. and return to baseline FHR associated with a uterine contraction.
The deceleration is delayed in timing, with the nadir of the The deceleration is delayed in timing, with the nadir of the
deceleration occurring after the peak on the contractiondeceleration occurring after the peak on the contraction
SIGNS AND SYMPTOMS

177. LATE DECELERATIONLATE DECELERATION

178. Biophysical Profile:Biophysical Profile:
Amniotic Fluid Volume Normal = 2 Points Amniotic Fluid Volume Normal = 2 Points
Non-Stress Test Result Positive = 2 Points Non-Stress Test Result Positive = 2 Points
Fetal Breathing Movements Active = 2 Points Fetal Breathing Movements Active = 2 Points
Fetal Extremity/Trunk Movements Active = 2 PointsFetal Extremity/Trunk Movements Active = 2 Points
Fetal Movements Active= 2 PointsFetal Movements Active= 2 Points
If Biophysical Profile scores If Biophysical Profile scores < 4< 4 suggest fetal distress suggest fetal distress
Placental Insufficiency: Low estriol levels, EPlacental Insufficiency: Low estriol levels, E
33 in urine in urine < <
10mg/24h10mg/24h
BIOPHYSICAL PROFILE

179. TREATMENT
Reposition patient: left-side-lying positionReposition patient: left-side-lying position

Administer oxygen by maskAdminister oxygen by mask

Perform vaginal examination to check for prolapsed cordPerform vaginal examination to check for prolapsed cord
Ensure that qualified personnel are in attendance for resuscitation Ensure that qualified personnel are in attendance for resuscitation
and care of the newbornand care of the newborn
Note: each institution shall define in writing the term qualified Note: each institution shall define in writing the term qualified
personnel for resuscitation and care of the newbornpersonnel for resuscitation and care of the newborn

180. Each of the following actions should be performed and Each of the following actions should be performed and
documented prior to starting a Cesarean section for fetal distress:documented prior to starting a Cesarean section for fetal distress:
 Perform vaginal exam to rule out imminent vaginal deliveryPerform vaginal exam to rule out imminent vaginal delivery

Initiate preoperative routinesInitiate preoperative routines

Monitor fetal heart tones (by continuous fetal monitoring or by Monitor fetal heart tones (by continuous fetal monitoring or by
auscultation) immediately prior to preparation of the abdomen auscultation) immediately prior to preparation of the abdomen
TREATMENT

181. Ensure that qualified personnel are in attendance for Ensure that qualified personnel are in attendance for
resuscitation and care of the newborn (each institution shall resuscitation and care of the newborn (each institution shall
define in writing the term qualified personnel for resuscitation define in writing the term qualified personnel for resuscitation
and care of the newborn)and care of the newborn)

STOPSTOP using using oxytocinoxytocin ! !
Oxytocin can strengthen the contraction of uterine which Oxytocin can strengthen the contraction of uterine which
affects the baby's heart rateaffects the baby's heart rate
TREATMENT

182. DEFINITIONS MUST GRASPED
Baseline FHRBaseline FHR::

approximate mean FHR rounded to increments of 5 bpm approximate mean FHR rounded to increments of 5 bpm
during a 10-minute segment, excluding periodic or episodic during a 10-minute segment, excluding periodic or episodic
changes, periods of marked FHR variability, and segments of changes, periods of marked FHR variability, and segments of
the baseline that differ by > 25 bpmthe baseline that differ by > 25 bpm
In any 10-minute window, the minimum baseline duration In any 10-minute window, the minimum baseline duration
must be at least 2 minutes or the baseline for that period is must be at least 2 minutes or the baseline for that period is
indeterminate indeterminate

183. Baseline FHR variabilityBaseline FHR variability::
Fluctuations in the baseline FHR =2 cycles / minFluctuations in the baseline FHR =2 cycles / min

These fluctuations are irregular in amplitude and frequency, and are These fluctuations are irregular in amplitude and frequency, and are
visually quantitated as the amplitude of the peak to the trough in beats visually quantitated as the amplitude of the peak to the trough in beats
per minute as follows: per minute as follows:
amplitude range undetectable, absent FHR variability; amplitude range undetectable, absent FHR variability;
amplitude range greater than undetectable but = 5 bpm, minimal FHR amplitude range greater than undetectable but = 5 bpm, minimal FHR
variability; variability;
amplitude range 6 bpm to 25 bpm, moderate FHR variability; amplitude range 6 bpm to 25 bpm, moderate FHR variability;
amplitude range >25 bpm, marked FHR variabilityamplitude range >25 bpm, marked FHR variability
DEFINITIONS MUST GRASPED

184. BradycardiaBradycardia::
a baseline FHR <120 bpma baseline FHR <120 bpm
TachycardiaTachycardia::
a baseline FHR >160 bpma baseline FHR >160 bpm
DEFINITIONS MUST GRASPED

185. Early decelerationEarly deceleration::
a visually-apparent, gradual decrease (defined as onset of a visually-apparent, gradual decrease (defined as onset of
deceleration to nadir =30 seconds) and return to baseline FHR deceleration to nadir =30 seconds) and return to baseline FHR
associated with a uterine contractionassociated with a uterine contraction
The decrease is calculated from the most recently determined The decrease is calculated from the most recently determined
portion of the baselineportion of the baseline

It is coincident in timing with the nadir of the deceleration occurring It is coincident in timing with the nadir of the deceleration occurring
at the same time as the peak of the contractionat the same time as the peak of the contraction

In most cases the onset, nadir, and recovery of the deceleration are In most cases the onset, nadir, and recovery of the deceleration are
coincident with the beginning, peak, and ending of the contraction, coincident with the beginning, peak, and ending of the contraction,
respectivelyrespectively
DEFINITIONS MUST GRASPED

186. Variable decelerationVariable deceleration::
a visually-apparent, abrupt decrease in FHR below the baselinea visually-apparent, abrupt decrease in FHR below the baseline
The decrease is calculated from the most recently determined portion The decrease is calculated from the most recently determined portion
of the baselineof the baseline

The decrease in FHR below the baseline is =15 bpm, lasting =15 The decrease in FHR below the baseline is =15 bpm, lasting =15
seconds and =2 minutes from onset to return to baselineseconds and =2 minutes from onset to return to baseline
DEFINITIONS MUST GRASPED

187. Late decelerationLate deceleration::
a visually-apparent, gradual decrease (defined as onset of a visually-apparent, gradual decrease (defined as onset of
deceleration to nadir = 30 seconds) and return to baseline FHR deceleration to nadir = 30 seconds) and return to baseline FHR
associated with a uterine contraction associated with a uterine contraction
The decrease is calculated from the most recently determined The decrease is calculated from the most recently determined
portion of the baselineportion of the baseline
The deceleration is delayed in timing, with the nadir of the The deceleration is delayed in timing, with the nadir of the
deceleration occurring after the peak on the contractiondeceleration occurring after the peak on the contraction
DEFINITIONS MUST GRASPED

188. DIAGNOSIS:DIAGNOSIS:
Absence of uterine growthAbsence of uterine growth
Serial ß-hcgSerial ß-hcg
Loss of fetal movementLoss of fetal movement
Absence of fetal heartAbsence of fetal heart
Disappearance of the signs & symptoms of pregnancyDisappearance of the signs & symptoms of pregnancy
X-ray X-ray Spalding signSpalding sign
Robert’s signRobert’s sign
U/S U/S 100% accurate Dx100% accurate Dx
DEFINITION:DEFINITION:
• dead fetuses or newborns weighing > 500g or > 20 dead fetuses or newborns weighing > 500g or > 20
wks gestationwks gestation
4.54.5 / /10001000 total birthstotal births
INTRAUTERINE FETAL DEATH (IUFD) INTRAUTERINE FETAL DEATH (IUFD)

189. Fetal causes 25-40%Fetal causes 25-40%
•Chromosomal anomaliesChromosomal anomalies
•Birth defectsBirth defects
•Non immune hydropsNon immune hydrops
•InfectionsInfections
Placental 25-35%Placental 25-35%
•AbruptionAbruption
•Cord accidentsCord accidents
•Placental insufficiencyPlacental insufficiency
•Intrapartum asphyxiaIntrapartum asphyxia
•P PreviaP Previa
•Twin to twin transfusion STwin to twin transfusion S
•ChrioamnionitisChrioamnionitis
Maternal 5-10%Maternal 5-10%
•Antiphospholipid antibodyAntiphospholipid antibody
•DMDM
•HPTHPT
•TraumaTrauma
•Abnormal laborAbnormal labor
•SepsisSepsis
•Acidosis/ HypoxiaAcidosis/ Hypoxia
•Uterine ruptureUterine rupture
•Postterm pregnancyPostterm pregnancy
•DrugsDrugs
•ThrombophiliaThrombophilia
•Cyanotic heart diseaseCyanotic heart disease
•EpilepsyEpilepsy
•Severe anemiaSevere anemia
Unexplained 25-35%Unexplained 25-35%
CAUSES OF IUFDCAUSES OF IUFD

190. A systematic approach to fetal death is valuable inA systematic approach to fetal death is valuable in
determining the etiologydetermining the etiology
11--HISTORYHISTORY
A-Family historyA-Family history
•Recurrent abortionsRecurrent abortions
•VTE/ PEVTE/ PE
•Congenital anomaliesCongenital anomalies
•Abnormal karyptypeAbnormal karyptype
•Hereditary conditionsHereditary conditions
•Developmental delayDevelopmental delay
B-Maternal HistoryB-Maternal History
I-Maternal medical conditionsI-Maternal medical conditions
•VTE/ PEVTE/ PE
•DMDM
•HPTHPT
•ThrombophiliaThrombophilia
•SLESLE
•Autoimmune diseaseAutoimmune disease
•Severe AnemiaSevere Anemia
•EpilepsyEpilepsy
•ConsanguinityConsanguinity
•Heart diseaseHeart disease
II-Past OB HxII-Past OB Hx
•Baby with congenital anomaly / hereditary Baby with congenital anomaly / hereditary
conditioncondition
•IUGRIUGR
•Gestational HPT with adverse sequeleGestational HPT with adverse sequele
•Placental abruptionPlacental abruption
•IUFDIUFD
•Recurrent abortionsRecurrent abortions

191. Current Pregnancy HxCurrent Pregnancy Hx
•Maternal age Maternal age
•Gestational age at fetal deathGestational age at fetal death
•HPTHPT
•DM/ Gestational DDM/ Gestational D
•Smooking , alcohol, or drug abuseSmooking , alcohol, or drug abuse
•Abdominal traumaAbdominal trauma
•CholestasisCholestasis
•Placental abruptionPlacental abruption
•PROM or prelabor SROMPROM or prelabor SROM
Specific fetal conditionsSpecific fetal conditions
•Nonimmune hydropsNonimmune hydrops
•IUGRIUGR
•InfectionsInfections
•Congenital anomaliesCongenital anomalies
•Chromosomal abnormalitiesChromosomal abnormalities
•Complications of multiple gestationComplications of multiple gestation
Placental or cord complicationsPlacental or cord complications
•Large or small placentaLarge or small placenta
•HematomaHematoma
•EdemaEdema
•Large infarctsLarge infarcts
•Abnormalities in structure , length Abnormalities in structure , length
or insertion of the umbilical cordor insertion of the umbilical cord
•Cord prolapseCord prolapse
•Cord knotsCord knots
•Placental tumorsPlacental tumors
11--HISTORYHISTORY

192. 2-EVALUATION OF STILL BORN INFANTS2-EVALUATION OF STILL BORN INFANTS
Infant descriptionInfant description
•MalformationMalformation
•Skin stainingSkin staining
•Degree of macerationDegree of maceration
•Color-pale ,plethoricColor-pale ,plethoric
Umbilical cordUmbilical cord
•ProlapseProlapse
•Entanglement-neck, arms, Entanglement-neck, arms,
legslegs
•Hematoma or strictureHematoma or stricture
•Number of vesselsNumber of vessels
•LengthLength
Amniotic fluidAmniotic fluid
•Color-meconium, bloodColor-meconium, blood
•VolumeVolume
PlacentaPlacenta
•WeightWeight
•StainingStaining
•Adherent clotsAdherent clots
•Structural abnormalityStructural abnormality
•Velamentous insertionVelamentous insertion
•Edema/hydropic changesEdema/hydropic changes
MembranesMembranes
•Stained Stained
•ThickeningThickening

193. 33--INVESTIGATIONSINVESTIGATIONS
Maternal investigationsMaternal investigations
•CBCCBC
•Bl Gp & antibody screenBl Gp & antibody screen
•HB A1 CHB A1 C
•Kleihauer Batke testKleihauer Batke test
•Serological screening for RubellaSerological screening for Rubella
•CMV, Toxo, Sphylis, Herpes & CMV, Toxo, Sphylis, Herpes &
ParovirusParovirus
•Karyotyping of both parents (RFL,Karyotyping of both parents (RFL,
Baby with malformationBaby with malformation
•Hb electrophorersisHb electrophorersis
•Antiplatelet anbin tibodiesAntiplatelet anbin tibodies
•Throbophilia screening Throbophilia screening
(antithrombin(antithrombin
Protein C & S , factor IV leiden,Protein C & S , factor IV leiden,
Factor II mutation, , lupus Factor II mutation, , lupus
anticoagulant, anticoagulant,
anticardolipin antibodies)anticardolipin antibodies)
•DICDIC
Fetal investigationsFetal investigations
•Fetal autopsyFetal autopsy
•Karyotype Karyotype
((specimen taken from cordspecimen taken from cord
blood, intracardiac bloodblood, intracardiac blood,,
body fluid, skin, spleenbody fluid, skin, spleen,,
placental wedge, or amnioticplacental wedge, or amniotic
fluidfluid))
•FetographyFetography
•RadiographyRadiography
Placental investigationsPlacental investigations
•Chorionocity of placenta inChorionocity of placenta in
twins twins
•Cord thrombosis or knots Cord thrombosis or knots
•Infarcts, thrombosis, Infarcts, thrombosis,
abruptionabruption
•Vascular malformationsVascular malformations
•Signs of infectionSigns of infection
•Bacterial culture for E.coli, Bacterial culture for E.coli,
Listeria, gp B strptListeria, gp B strpt..

194. IUFD COMPLICATIONSIUFD COMPLICATIONS
• Hypofibrinogenemia Hypofibrinogenemia  4-5 wks after IUFD 4-5 wks after IUFD
• Coagulation studies must be started 2 wks after Coagulation studies must be started 2 wks after
IUFDIUFD
• Delivery by 4 wks or if fibrinogen Delivery by 4 wks or if fibrinogen  < 200mg/ml < 200mg/ml

195. PSYCHOLOGICAL ASPECT & COUNSELINGPSYCHOLOGICAL ASPECT & COUNSELING
• A traumatic eventA traumatic event
• Post-partum depressionPost-partum depression
• AnxietyAnxiety
• PsychotherapyPsychotherapy
• Recurrence 0-8% depending on the cause of IUFDRecurrence 0-8% depending on the cause of IUFD

197. RETAINED PLACENTA

198. DEFINITION
The placenta is said to be retained when it is
not expelled out even 30mts after the birth of
the baby.
C.S. Dawn

199. Gross anatomy of mature placenta
Shape - Circular disc
Diameter - 15-20cm
Thickness- 2.5cm at its centre,
thin off towards the edge
By touch - It feels spongy
Weights - about 500gm
Surface - fetal surface and

maternal surface
Margin - Peripheral margin

200. Phases in expulsion of placenta
1.Separation through the spongy layer of
decidua
2.Descent into the lower segment and vagina
3.Finally its expulsion to outside

201. Causes of retained placenta
-Poor voluntary expulsive efforts
-Uterine atonicity in cases of grand multipara overdistension
of uterus, prolonged labour, uterine malformation
-Incarcerated placenta following partially or completely
separated. It is due to constriction ring (hour – glass
contraction)

202. -Morbid adherent placenta – partial or rarely, complete
- Placenta accreta
- Placenta increta
- Placenta percreta

204. DANGERS:
They are:
1.Post-partum haemorrhage.
2.Shock – mainly due to haemorrhage.
3.Puerperal sepsis.
4.Thrombophlebitis – in the pelvic and leg veins.
5.Embolism
6.Placental polyp.

205. Diagnosis
Diagnosis is made by an arbitary time spent following
delivery of the baby
Dangers
1.Haemorrhage
2.Shock is due to a. Blood loss
b. Retained more than one hour
c. Frequent attempts of abdominal
manipulation
3. Puerperal sepsis
4. Risk of its recurrence in next pregnancy

206. Management
Period of watchful expectancy
•Watch for bleeding
•Note the signs of separation of placenta
•The bladder should be emptied using a rubber catheter
•Any bleeding during the period should be managed.
Placenta is separated and retained
- To express the placenta out by controlled cord traction. - -
Unseparated retained plaenta
- Manual removal of placenta under G.A

207. Management of unforseen complications during manual
removal
1. Hour glass contraction – placenta either inseparated or
separated – partially or completely, may be trapped by a
localised contraction of circular muscles of the uterus.
This ring should be made to relax by
a. Deepening the plane of plane of anaesthesia (halothane)
b. Subcutaneous injection of .5ml of 1 in 1000 adrenaline Hcl.

208. c. Inhalation of two amyl nitrate capsules of 5 minim each.
If the ring is too tight and bleeding is absent
•Operation is to be postponed
•The patient is to be sedated by morphine 15mg Im
after the manual removal.
•Watch for a period of 4-6hrs
If the ring is not too tight and bleeding is continuing
The ring is to be manually stretched by the cone shaped
hand and the separation of the placenta is preferably
done from above down wards to minimise bleeding.

209. Morbid adherent placenta
-Manual removal
Management of complicated retained placenta
1. Retained placenta with shock but no haemorrhage
• To treat shock
• Manual removal of placenta when the condition
improves.
2. Retained placenta with haemorrhage
• To assess the amount blood loss and to replace the lost
blood
• Manual removal

210. 3. Retained placenta with sepsis
• Intrauterine swabs are taken for culture
• Administer broad spectrum antibiotic
• Blood transfusion
4. Retained placenta with an episiotomy wound
•The bleeding points of the episiotomy wound are to be
secured by artery forceps
•Manual removal of placenta followed by repair of
episiotomy wound.

211. Placenta Acreta (morbid adherent placenta)
•The placenta is directly anchored to the myometrium partially
or completely without any intervening decidna.
•Probable cause is defective decidual formation
•The condition is usually associated when the placenta
happens to be implanted in lower segment.

212. Management
•In case of partial morbid adherent placenta
•Manual removal if there is effective uterine contractions with
haemostasis
•If the uterus fails to contract an early decision of hystrectomy may
have to be taken.

213. In total placenta accreta hysterectomy is indicated
•It the patient desiring to have a child conservative
management.
•Antibiotics
•Placenta accreta – choriomic villi invade up to the
myometrium
•Placenta increta – Choriomic villi invade the myometrium
•Placenta percreta – chronic villi penetrate the whole uterine
wall to the serosal layer.

214. Manual Removal of the Placenta
One hand is inserted through the vagina and into the uterine
cavity.
1.Insert the side of your hand in between the placenta and the
uterus.
2.Using the side of your hand, sweep the placenta off the uterus.
3.After most of the placenta has been swept off the uterus, curl
your fingers around the bulk of the placenta and exert gentle
downward and outward traction. You may need to release the
placenta and then re-grab it.
4.Then pull the placenta through the cervix. Most placentas can
be easily and uneventfully removed in this way. A few prove to
be problems.

215. Placenta Accreta and Percreta
When you manually remove the placenta, be prepared to
deal with an abnormally adherent placenta (placenta accreta or
placenta percreta). These abnormal attachments may be partial or
complete.
•If partial and focal, the attachments can be manually broken and
the placenta removed. It may be necessary to curette the
placental bed to reduce bleeding. Recovery is usually satisfactory,
although more than the usual amount of post partum bleeding will
be noted.
•If extensive or complete, you probably won't be able to remove
the placenta in other than handfuls of fragments. Bleeding from
this problem will be considerable, and the patient will likely end up
with multiple blood transfusions while you prepare her for a life-
saving, post partum uterine artery ligation or hysterectomy. If
surgery is not immediately available, consider tight uterine and/or
vaginal packing to slow the bleeding until surgery is available.

216. Separate the placenta from the uterus with a sweeping motion

217. After the placenta is mostly separated, curl
your palm around the bulk of it.

218. Continue to grasp the placenta as you remove it
from the uterine cavity

219. RETAINED PLACENTA ON HOME DELIVERY:
•Prophylactic IV ergometrine or inj. Ergometrine 0.5mg and
oxytocin 5 units IM  controlled cord traction on birth of baby
 placenta is delivered.
•If the nurses are trained she can do manual removal under
injection diazepam IV 10-20mg.
•If she is not trained, patient is sent in a transport to the nearest
health unit.
•ANM accompanies the patient during transport.
•IV fluid on flow.
•At hospital, manual removal is done early on resuscitation of
the patient.
•Adequate blood transfusion is given.

222. Definition
Placenta accreta occurs when there is a defect of
the decidua basalis, in conjunction with an
imperfect development of the Nitabuch
membrane (a fibrinoid layer that separates the
decidua basalis from the placental villi)
resulting in abnormally invasive implantation
of the placenta
The ACOG committee

223. According to Mudhaliar and Menon
Placenta accreta is defined as the abnormal adherence,either in
whole or in part,of the afterbirth to the unlying uterine wall.
According to D.C.Dutta
Placenta accreta in extremely rare form in which the placen is
directly anchored to the myometrium partially or completely thout
any intervening decidua.

225. Incidence
From 1930 to 1950--one case in 30,000 deliveries.
From 1950 to 1960, one in 19,000, deliveries.
by 1980 to one in 7,000.
the incidence has now risen to one in 2,500
deliveries
The ACOG committee

226. Degrees of severity/ Types of Placenta
Accreta
(1) Accreta, in which the placenta adheres to the myometrium
without invasion into the muscle.
(2) Increta, in which it invades into the myometrium.
(3) Percreta, in which it invades the full thickness of the uterine
wall and possibly other pelvic structures, most frequently the
bladder.

229. Depending on the area of involvement
1.Total
2.Partial
3.Focal

230. Risk factors
Placenta previa with or without previous
uterine surgery.
previous myomectomy.
previous cesarean delivery.
Asherman's syndrome.
submucous leiomyomata.
maternal age of 36 years and older.

231. Risk of developing placenta accreta in
women with placenta previa
No previous C/S 1% - 5%
One previous C/S30%
Two or more C/S 40% and higher

232. Etiology
Defective decidual formation
Implantation in lower uterine segment
Caesarean scar
Uterine incision or curettage
Manual removal of placenta
Abortive agents
Uterine infections

233. Clinical Course
Maternal Serum Alpha Fetoprotein level -
increased
Ante partum hemorrhage
Uterine rupture before labour

234. Diagnosis
Ultrasound
loss of the normal hypoechogenic zone between
the placenta and myometrium
abnormality of the smooth interface between the
uterus and bladder
a Swiss-cheese appearance to the placenta,
pulsatile flow of maternal blood
MRI

235. Swiss cheese appearance

236. Management
Partial Morbid Adherent Placenta
“Playing with the placenta with fingers”
Oxytocics
Intrauterine plugging
Hysterectomy

237. Total Placenta Accreta
Hysterectomy
Conservative :
1.Cutting umbilical cord
2.Antibiotics
Other measures
Blood replacement
Uterine and internal iliac artery ligation
Angiographic embolization
Argon beam coagulation

238. A tiny angiographic catheter is maneuvered into the uterine
artery in preparation for embolization

239. Complications
Hemorrhage
Shock
Infection
Sub involution of uterus
Secondary postpartum hemorrhage
Formation of placental polyp

241. INDUCTION OF INDUCTION OF
LABOURLABOUR

242. DEFINITION
Induction of labour means deliberate termination
of pregnancy beyond 28 weeks (Period of viability)
by any method which aims at initiation of labour and
a vaginal delivery.

243. Indications
Fetal
Maternal
Combined
Post maturity
History of IUD
DM
IUGR
Rh-isoimmunisation
Unstable lie
Fetal
IUD
Chronic polyhydramnios
Congenital malformations Maternal
Pre –eclampsia
Minor degree of placenta praveia
Abruptio placenta
PROM
Chronic HTN
Chronic renal disease
Combined

244. CONTRAINDICATIONS
Contracted pelvis and CPD
Persistent malpresentation
Pregnancy with previous caesarean section
Elderly primigravida
Heart disease
High risk pregnancy with compromised fetus
Pelvic tumour

245. SUCCESS OF INDUCTION depends on
Period of gestation
Case profile
Sensitivity of the uterus
Pre induction scoring

246. METHODS OF INDUCTION
Medical
Drugs used oxytocin, prostaglandins
LRM
AROM HRM
Surgical
Stripping of membranes
Combined

247. Merits and demerits of each method
Prostaglandin
Advantages
Effective method in IUD or cases with unfavourable cervix
No antidiuretic effect
Drawbacks
More systemic side effects when used orally or I/V
Hyper stimulation

248. OXYTOCIN
Advantages
Wider availability
Less systemic side –effects
HAZARDS OF AROM
Cord prolapse
Uncontrolled escape of amniotic fluid
Injury to cervix or presenting part
Rupture of vasapraevia leading to fetal blood loss.
Amnionitis

249. Injury to the placenta
Accidental injury to the uterine wall
Injury to the fetal parts especially eye.
Displacement of presenting part
Intra –ammotic infection
Longer induction – delivery interval compared to LRM

250. SCHEME OF INDUCTION PROTOCOLSCHEME OF INDUCTION PROTOCOL
CX – favourable
Surgical
Medical
CX – unfavourable
Oxytocin or
prostaglandin E
2

Prostaglandin more
effective
LRM
HRM
•APH
•Severe PIH
•Eclampsia
Ch.
Polyhydramnios
Combined
(common)
CX – unfavourable
Prostaglandin E
2 gel/
Oxytocin infusion
Cervix –ripe
LRM + OXYTOCIN
CX – favourable
LRM + OXYTOCIN

251. NURSING CARE
Technique of oxytocin administration
Indications for stopping the drip
Nursing measures Consent, explain to the patient
Monitoring
Supervision and recording of findings
Pain relief

252. Observation
 Rate of flow
 Uterine contractions
 FHR
 Progress of labor
 Maternal conditions
- Vital signs
- Urine for ketoacidasis
- Intake and output chart
- Watch for prolapse of cord

253. Observation
 Rate of flow
 Uterine contractions
 FHR
 Progress of labor
 Maternal conditions
- Vital signs
- Urine for ketoacidasis
- Intake and output chart
- Watch for prolapse of cord

254. Observation
 Rate of flow
 Uterine contractions
 FHR
 Progress of labor
 Maternal conditions
- Vital signs
- Urine for ketoacidasis
- Intake and output chart
- Watch for prolapse of cord

255. Augmentation Of Labour:
.

256. DEFINITIONS
Series of events that take place
in the genital organs in an
effort to expel out the viable
products of conception out of
the womb through the vagina
into the outer the world is
called as LABOUR

257. AUGMENATION OF LABOUR
Induction of labour means
initiation of uterine contractions
(after a period of viability) by
any method (medical, surgical
and combined) for the purpose
of the vaginal delivery.

258. AUGMENTATION
Augmentation is the
process of stimulation of
the uterine contraction
that are already present
but found to be
inadequate.

259. ELECTIVE INDUCTION OF LABOUR
Elective Induction Of Labour
means termination of pregnancy
without any acceptable medical
induction. (It is done for the
convenience of the patient,
obstetrician or the hospital.)

260. CONFUSION

261. ASSESSMENT

262. FETAL ASSESSMENT

263. CERVICAL RIPENING

264. CERVICAL STRIPPING

267. UTERINE RUPTURE

269. HYDRAMNIOS

270. PLACENTA PREVIA & ABRUPTIO
PLACENTAE.

271. CONTRACTED PELVIS & LIE

272. CORD PROLAPSE

273. HERPES SIMPLEX VIRUS

274. STERILE

275. METHOD

276. TEAM WORK