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OBSTETRICS MATERIAL

BY :- DR. MOHAMMED ISMAIL KHAN


MBBS (GOLD MEDALIST), (MD, MRCOG)
Index

S.No. Chapter Page From Page To

1. Obstetric Anatomy 2 5
2. Basics of Reproduction 5 7
3. Placenta & Amniotic Fluid 7 12
4. Maternal Adaptations 12 18
5. Puerperium & its disorders 19 22
6. Diagnosis in Obstetrics 23 26
7. Foetal Medicine 26 32
8. Pregnancy Loss 32 39
9. Ectopic Gestation 39 45
10. Gestational Trophoblstic Diseases 45 52
11. Normal Labour 52 55
12. Induction of Labour 55 57
13. Pre-term, Post-dates, PROM 57 61
14. Abnormal Labour 62 66
15. AntePartum Haemorrhage 67 75
16. 3RD Stage Complications 75 79
17. Multifoetal Gestation 79 83
18. Operative Obstetrics 84 88

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CHAPTER - 1
OBSTETRIC ANATOMY

Maternal pelvis ➢ Inlet or the brim*


• The pelvis is the most important bone from the • it is formed by the following structures*
obstetric point of view • Pubic symphysis, pubic crest, pubic tubercle, pectineal
• The pelvis is considered as a single bone for all line, iliopubic eminence, ilio pectineal line, sacro iliac
obstetric purposes articulation, ala of sacrum and promontory of sacrum
• It is composed of 4 bones • It measures:
➢ The Innominate bones • Anteroposterior (AP) – 11cm*
➢ The sacrum (also called true or anatomical conjugate)
➢ The coccyx • Oblique – 12cm
• Transverse – 13 cm
• The bony pelvis has two parts :
➢ THE CAVITY
• The obstetric cavity is the plane of pelvis at the level
of ischial spines
• It is also called as the plane of least pelvic diameter
as the interspinous distance/ diameter* is 10cm
• The anatomical cavity is below the level of ischial
spines and above the outlet and measures 12cms in
all dimensions

THE SIGNIFICANCE OF ISCHIAL SPINES*


• OBSTETRIC SIGNIFICANCE:
➢ The false pelvis : the part of pelvis above the pelvic
➢ Internal rotation*
brim
➢ The zero station*
➢ The true pelvis : the brim of the pelvis and the part of ➢ The pudendal block
pelvis below the brim ➢ Deep transverse arrest*
➢ Forward curve (of carus)
• The true pelvis has three parts
➢ The inlet or the brim of the pelvis • GYNAECOLOGIC SIGNIFICANCE:
➢ The cavity or the mid pelvis or the plane of least pelvic ➢ The level of external os*
dimensions (obstetric cavity)
➢ The outlet ➢ THE OUTLET
• The outlet is represented by 2 triangles
❖ Types of pelvis • Formed by joining the S5, sacrotuberous ligaments,
• The following are the 4 major types of pelvis: ischial tuberosities and pubic symphysis
➢ Gynaecoid : the female type ( 50%)* • Dimensions are
➢ Android : the male type ( 20%) • AP – 13cm* (in non pregnant state 11cm)
➢ Anthropoid : the ape type ( 25%) • Oblique – 12 cms
➢ Platypelloid : the flat type ( 5%) • Transverse – 11cm
➢ Combinations* ______ AP OBLIQ TRANSVERSE
➢ Exceptions* INLET 11 12 13
✓ Anthropoplatypelloid CAVITY 12 12 12
✓ platypoanthropoid OUT LET 13 12 11
Non
preg:11

❖ The gynaecoid pelvis ❖ SPECIAL DIMENSIONS**


• It is the commonest type of pelvis* • The conjugates :

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➢ True conjugate measures 11 cm OC : Obstetric conjugate
➢ Obstetric conjugate measures 10 cm ❖ Special types of contracted pelvis
➢ Diagonal conjugate measures 12 cm ➢ Rachitic pelvis
➢ Posterior saggital diameter of the cavity: • Reniform shape of inlet with marked shortening of
• It is measured from S5 to the mid point of antero – posterior diameter without affecting the
interspinous line transverse diameter
• Measures 5cm • Sacrum is flat and tilted
➢ Posterior saggital diameter of the outlet* • Widening of transverse diameter of the outlet and
• It is measured from the tip of the coccyx to the pubic arch
midpoint of intertuberous line
• Measures 7.5cm ➢ Tri radiate pelvis
• Triradiate shape of inletQ
❖ CONTRACTED PELVIS • Approximation of the two ischial tuberosities*
• If any of the pelvic diameters are less than the critical • and marked narrowing of pubic arch.
pelvic diameters then it is described as contracted • Short sacrum with coccyx pushed forward.
pelvis
• The following are the critical diameters* ➢ Naegele’s pelvis : arrested development of one ala of
✓ Obstetric conjugate < 10cm the sacrum
✓ Diagonal conjugate < 11.5cm
✓ Transverse dia of inlet < 12 cm
✓ Interspinous diameter < 10cm
✓ Inter tuberous diameter < 8cm
✓ Inter spinous diameter + post saggital diameter of
cavity < 13.5cm

➢ Roberts pelvis : arrested development of both the ala


of sacrum

❖ Dystocia dystrophia syndrome


• The patient is stockily built with bull neck, broad
shoulder and short thigh.
• She is obese with a male distribution of hairs.
• Pelvis is of the android type*
• Occipito-posterior position is common.
• They are usually subfertile, having dysmenorrhoea,
oligomenorrhoea or irregular period
• There is increased incidence of preeclampsia and a
tendency for postmaturity during pregnancy.
• During labour, inertia is common* and there is a
tendency for deep transverse arrest or outlet dystocia
leading to either increased incidence of difficult
instrumental delivery or cesarean section.
AP: Anteroposterior • There are increase chances of lactation failure during
TC: True conjugate purperium.
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………………………………………………………………………………………….
FOETAL SKULL
➢ The sutures :
• The sagittal or longitudinal suture
• The coronal sutures
• The frontal suture
• The lambdoid sutures
• The Significance : moulding and internal examination
➢ FONTANELLE OF FOETAL SKULL
• 6 fontanelles are present in fetal skull.
• Anterior fontanelle (bregma) - 1
• Posterior fontanelle (lambda) - 1
• Anterolateral fontanelle - 2
• Posteriolateral fontanelle – 2

• Sub occipito bregmatic* (SOB) : complete flexion :


vertex presentation – 9.5 cm
• Sub occipito frontal(SOF) : incomplete flexion :
vertex presentation – 10cm
• Occipito frontal(OF) : neutral position : vertex
presentation – 11.5 cm
• Mento vertical*(MV) : little extension : brow
presentation – 14cm
• Sub mento vertical(SMV) : incomplete extension :
face presentation* – 11.5cm
• Sub mento bregmatic(SMB) : complete extension :
face presentation* – 9.5cm
➢ Anterior fontanelle/ bregma:
• It is formed by joining of the four sutures in the ❖ THE TRANSVERSE DIAMETERS OF FOETAL SKULL
midplane. • Bi mastoid : 7.5cm
• Its anteroposterior and transverse diameters • Bi temporal : 8cm
measure approximately 3 cm each. • Super sub parietal* : 8.5 cm
• The floor is formed by a membrane and it becomes • Bi parietal diameter* : 9.5cm
ossified 18 months after birth.
❖ BASIC OBSTETRIC TERMINOLOGY
• It becomes pathological, if it fails to ossify even after
24 months. • LIE : relationship between spine of foetus and
• Significance : internal examination & hydrocephalus longitudinal axis of the uterus
➢ Posterior fontanelle: It is formed by junction of
three suture lines — sagittal suture and lambdoid • PRESENTATION
suture ➢Cephalic presentation*
• It is triangular in shape and measures about 1.2 x 1.2 ➢Breech presentation
cm (1/2" x 1/2"). ➢ Shoulder presentation
❖ THE LONGITUDINAL DIMENSIONS OF FOETAL SKULL
• POSITION OF THE FOETUS
• The commonest foetal position is _________*
• The transverse dia of foetal head engages in the ____
dia of pelvic inlet*
• The most common longitudinal diameter during
engagement is _________ & measures _________ cm*
• The commonest foetal position is _________*
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• The transverse dia of foetal head engages in the ____ tissue.
dia of pelvic inlet* - Has got no radiation hazard, hence biologically safe*
• The most common longitudinal diameter during - But it is expensive, requires more time and expertise
engagement is _________ & measures _________ cm*

❖ Cephalopelvic Disproportion
• Cephalopelvic Disproportion (CPD) is the disparity in
the relation between the head of fetus and maternal
pelvis.
• CPD can be diagnosed : TYPES OF PELVIS AND OBSTETRIC OUTCOME
A. Clinically: By per abdomen examination / Bimanual
examination (Muller-Munrokerr method)

• The Bimanual method is superior to the abdominal


method as pelvic assessment can be done
simultaneously
• Limitations of clinical assessment: Tr: transverse
• - It can assess the disproportion of the brim and not of AP: anteroposterior
the midpelvis or outlet.
• - The fetal head can be used as a pelvimeter to elicit
only the contraction in the antero-posterior plane of ❖ GYNAECOID PELVIS
the inlet. ➢ INLET : Transverse oval : no dificulty in engagement (
• (If contraction affects the transverse diameter of the Tr > AP )
inlet, it is of less use).* ➢ OUTLET : Spacious : no difficulty in extension
➢ Sub pubic angle : 90
B.Radiographically: ➢ Outcome : normal vaginal delivery
➢ X-ray pelvimetry
• For complete evaluation 3 views are taken: ❖ ANDROID PELVIS
a) Antero-posterior ➢ INLET : Heart shaped – Tr > AP – diameters smaller –
b) Lateral engagement delayed
c) Outlet ➢ OUTLET : very small – prominent ischial spines –
• Hazards of X-Ray pelvimetry: deep transverse arrest
a) radiation exposure to fetus. ➢ Outcome : normal delivery very difficult
b) Radiation exposure to gonads ( 885 milli rads)
❖ ANTHROPOID
➢ INLET : AP oval : AP > Tr – engagement occurs in AP
➢ CT Scan: diameter – position is OP
- Involves less radiation (44-425 milli rad) ➢ OUTLET : Ischial spines prominent – non rotation
- Is easier to perform. ➢ OUTCOME : Face to pubis delivery
- Accuracy is greater than that of conventional X Ray
pelvimetry*. ❖ PLATYPELLOID
➢ INLET : Transverse oval – Tr >>> AP – engagement
➢ MRI: Is more accurate to assess the bony pelvis. delayed or non engagement as BPD can’t pass
- Also helpful to assess the fetal size and maternal soft through AP diameter( very small)
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✓ If engagement occurs there is marked asynctilism • Least common pelvis – Platypelloid pelvis*
with litzmann’s obliquity • The only pelvis with AP > Tr – Anthropoid pelvis*
➢ OUTLET : Spacious • Face to pubis is M/c in – Anthropoid pelvis*
➢ OUTCOME : • OP position is M/c in – Anthropoid pelvis*
✓ non engagement : cesarean • DTA is M/c in – Android pelvis*
✓ Difficult engagement : normal • Flat bowl shaped pelvis is – Platypelloid pelvis*
• Marked posterior asynclitism is seen in – Platypelloid
IMPORTANT POINTS pelvis*
• M/c pelvis – Gynaecoid*

CHAPTER – 2
BASICS OF REPRODUCTION

❖ SPERMATOGENESIS :
• The developmental process from spermatogonium
to sperm takes about 61 days* and the entire
process, including the transit time in the ductal
system takes approximately three months*
➢ The primordial germ cells remain as it is in the
testis from birth to puberty
➢ Shortly before puberty, the primordial germ cells
develop into spermatogonia in the wall of
seminiferous tubules by several generations of
mitosis
➢ With the onset of puberty the primordial germ cells
divide by meiosis to form the primary and
secondary spermatocytes
➢ Meiosis is a special type of cell division that reduces
the diploid
number of chromosomes (i.e., 46) to the haploid
number of 23.
➢ It involves two meiotic cell divisions, meiosis I and
meiosis II.
• The first metotic division is a reduction division
because the chromosome number is reduced from ❖ OOGENESIS :
diploid (46) to haploid (23).
• The 2nd meiotic division is similar to mitosis as
daughter cell formed contain the same haploid
number of chromosomes as the mother cell.

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• Therefore first polar body is released just prior to
ovulation*
• the secondary occyte then enters the second meiotic
division and gets arrested at metaphase of meiosis
• At the time of fertilization second division is
completed which results in the release of oocyte and
second polar body
• Therefore second polar body release occurs only at
the time of fertilisation*
❖ OVULATION

• The primitive germ cells take their origin from the


endoderm of yolk sac at about the end of 3rd week
• migrate to the developing gonadal ridge, at about
the end of 4th week.
• Oogenesis begins in the ovary at 6 - 8 weeks of
gestation. • LH SURGE precedes ovulation by 34-36 hours.
• The primitive germ cells in the ovary undergo • LH PEAK precedes ovulation by 10-16 hours.
extensive mitosis to form oogonium • Prior to ovulation :
• Maximum number of oogonia are in the ovary at ➢ Follicle reaches a size of 18-20 mm*
5th month/ 20 weeks of gestation of development ( Called Graafian follicle)
number ie 6-7 million ➢ Endometrium is 9 -10 mm thick*
• These oognia start undergoing the mitotic division ➢ Endometrium shows triple line on USG.*
when the baby is still intra uterine( they form the ➢ Ovulation occurs 14 days before the next
primary oocytes) menstruation.
• At birth no more mitotic division occur, all oogonia ➢ Maximum action of corpus luteum is at 22 day
are replaced by primary oocyte of menstruation (following which it starts regressing
• The primary oocytes formed then enter the meiotic ~ 8 days after ovulation
division but don’t form the secondary oocyte (they ➢ In absence of fertilisation and implantation the
get arrested in late prophase of the meiosis 1) corpus luteum persists for 12 -14 days.
• All female foetuses are born with primary oocytes in ➢ Maximum growth of corpus luteum of pregnancy
the ovary arrested in prophase* of meiosis 1 (2 is at 8th week of gestation and degenerates at 6
million primary oocytes) months of gestation.
• They remain arrested in this state till that oocyte is
chosen for development (puberty)
➢ FERTILISATION AND FURTHER DEVELOPMENT
• At puberty number is further decreased and is
300,000 – 500,000
• At puberty as a result of mid cycle preovulatory
surge, meiosis is resumed and completed just prior
to ovulation*
• This leads to the formation of secondary oocyte and
a polar body

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• In human, the blastocyst burrows in the uterine
cavity till whole of it lies within the thickness of
endometrium. This is called as interstitial
implantation.
• The Endometrium Is in the secretory phase
corresponding to 20 - 21 days of cycle" at the time
of implantation*
• After ovulation, the endometrium now
demonstrates a combined reaction to estrogen
and progesterone activity.
• Most impressive is that total endometrial height is
fixed at roughly its preovulatory extent (5- 6 mm)
despite continued availability of estrogen*
• At the time of implantation, on days 21-22 of
menstrual cycle the predominant morphologic
• Fertilisation occurs in the ampullary part of fallopian feature is EDEMAof the ENDOMETRIAL STROMA
tube* • After implantation of the embryo the uterine
• As fertilisation of the ovum occurs and a zygote is endometrium is called the "decidua".
formed, it undergoes cleavage to form 2, 4, 6 cell • Well developed endometrium has three layers-
stage. ✓ Superficial compact layer,
• This cleavage continues till it is 16 cell staged and is ✓ Intermediate compact layer
called as Morula* ✓ Thin basal layer.
• Zygote enters the uterine cavity in the form of- • Line of separation of placenta runs through the
Morula* intermediate compact layer.
• Zygote enters the uterine cavity - On 18th day of • After implantation of zygote into the compacta,
menstrual cycle i.e 4 days after the fertilisation* decidua is renamed as
• The morula now undergoes diffrentiation to form ➢ Decidua Basalis - The part of decidua where the
the inner cell mass(embryoblast) and the outer cell placenta is to be formed.
mass(trophoblast) ➢ Decidua Capsularis - The part of the decidua that
• From the time a fertilized ovum enters the uterine separates the embryo from the uterine lumen.
cavity from the fallopian tube (which occurs 3-4 ➢ Decidua Parietalis (Vera) - The part of the decidua
days after ovulation) until the time ovum implants lining rest of the uterine cavity.
the uterine secretions called uterine milk provides • At the end of pregnancy, the decidua is shed off
nutrition for the early dividing ovum* along with placenta and membranes.
• Some fluid passes from the uterine cavity into the
morula. So that the embryoblast attaches to
trophoblast on one side only. The morula now
becomes a 'blastocyst'.
• As the blastocyst develops further the
• inner cell mass/ embryoblast -into
• -ectoderm,
• -endoderm
• -mesoderm .
• Implantation of the zygote occurs in the form of
Blastocyst*
• Implantation occurs 7-8 days after fertilisation 21-
22 nd day of menstrual cycle*

➢ IMPLANTATION:
• Implantation occurs 7 - 9 days after ovulation

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INTRA UTERINE PERIODS • Some of this oxygen rich blood passes into the
➢ Ovular or Germinal Period : Fertilisation-2 weeks carotid and subclavian arteries to supply the brain,
➢ Embryonic Period : 3 weeks-8 weeks the head and neck and the upper extremities.
➢ Fetal Period : >8 weeks and till delivery • The rest of it gets mixed up with poorly oxygenated
blood from the ductus arteriosus.
FOETAL CIRCULATION : • The parts of the body that are supplied by branches
of the aorta arising distal to its junction with the
ductus arteriosus, therefore, receive blood with
only a moderate oxygen content.
• Much of the blood of the aorta is carried by the
umbilical arteries to the placenta where it is again
oxygenated and returned to the heart.
• As a result, the pressure inside the left atrium is
greatly increased. Simultaneously, the pressure in
the right atrium is diminished because blood from
the placenta no longer reaches it.
• The net result of these pressure changes is that
pressure in the left atrium now exceeds that in the
right atrium causing the valve of the foramen ovale
to close
Umbilical arteries Medial umbilical ligaments*
Left umbilical vein Ligamentum teres
Ductus venosus Ligamentum venosum*
Ductus arteriosus Ligamentum arteriosum*

➢ LUNG MATURITY
• The oxygen rich blood reaching the right atrium • L/S ratio :
through the inferior vena cava is directed by the • (Lecitine /springomyline) >2
valve of the inferior vena cava towards the foramen
ovale. • PHOSPHATIDYL GLYCEROL:
• Most of it passes through the foramen ovale into the
left atrium. • Fluorescence Polarization
• The rest of it gets mixed up with the blood returning
to the right atrium through the superior vena cava,
and passes into the right ventricle.
• From the right ventricle, the blood (mostly
deoxygenated) enters the pulmonary trunk.
• Only a small portion of this blood reaches the lungs
and passes through it to the left atrium.
• The greater part is short circuited by the ductus
arteriosus into the aorta.
• We have seen that the left atrium receives:
➢ Oxygenated blood from the right atrium, and IMPORTANT TIME LINES
➢ A small amount of deoxygenated blood from the Fertilization O HOUR
lungs. 16 cell stage 4TH DAY
• The blood in this chamber is, therefore, fairly rich in Morula enters uterine cavity 4TH DAY
oxygen. Blastocyst 5TH DAY
• This blood passes into the left ventricle and then Interstitial implantation occurs 7TH DAY
into the aorta.

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Placenta circulation established / 3rd WEEK Swallowing starts 12TH WEEK
Fetal circulation established and External genitalia formed 12TH WEEK
heart formed .
Internal gonads formed 8TH WEEK .
Fetal breathing movements 11TH WEEK • .

CHAPTER – 3
THE PLACENTA & AMNIOTIC FLUID

• The human placenta is discoid, because of its shape • Small cavities appear in the basal decidua called as
• hemochorial, because of direct contact of the lacunae which get filled with maternal blood
chorion with the maternal blood • The lacunae are separated from one another by
• deciduate, because some maternal tissue is shed at partitions of syncytium called as trabeculae.
parturition • Each trabeculas is, initially made up entirely of
syncytiotrophoblast.
❖ FORMATION OF PLACENTA • Chorionic villi can first be distinguished in the
human placenta on about 12th day after
fertilisation.

➢ PRIMARY VILLI
• Later cells of cytotrophoblast begin to multiply and
grow into each trabeculas. This is called as Primary
villi.

➢ SECONDARY VILLI
• Extra embryonic mesoderm then invades the centre
of each primary villus. This is now called as
secondary villus

➢ TERTIARY VILLI
• Placenta is formed by the trophoblast. • Soon thereafter, fetal blood vessels can be seen in
The trophoblast differentiates into- the mesoderm forming the core of each villus.
✓ syncytiotrophoblast • The villus is called as Tertiary villus.
✓ cyto trophoblast. • Thus the maternal blood in the lacuna is never in
• The syncytiotrophoblast all over its surface starts direct contact with fetal blood.
developing chorionic villi They are separated by: Syncytiotrophoblast -
• The chorionic villi in relation to decidua BASALIS Cytotrophoblast – extraembryonic Mesoderm -
develop further to form chorionic frondosum Endothelium of fetal capillaries
• The chorionic villi in relation to decidua ➢ This is known as placental barrier
CAPSULARIS degenerate to form a smooth surface
called chorionic levae
• The syncytiotrophoblast grows into the
endometrium ( decidua basalis) and erodes the
maternal blood vessels

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• FFN (fetal fibronectin) has been called trophoblast
glue to suggest a critical role for this protein in the
migration and attachment of trophoblasts to
maternal decidua.
• The presence of FFN in cervical or vaginal fluid can
be used as a prognostic indicator for preterm labor
• The stroma of placenta has fetal macrophages
called as Hofbauer cells.
• The tumors which can metastasize to placenta
are melanoma, leukemias, lymphomas and
➢ Further changes in villi breast cancer.
• Near term, thinning of the syncytial layer -
Vasculosyncytial membrane - These thin zones ❖ PLACENTAL CIRCULATION
(alpha zones) are for gas exchange. • Placental circulation consists of independent
• The thick - beta zones - patches are for hormone circulation of blood in two systems:
synthesis ➢ Uteroplacental circulation
➢ THE TERM PLACENTA ➢ Fetoplacental circulation
• The placenta, at term, is almost a circular disk with a • Uteroplacental circulation: It is concerned with
diameter of 15-20 cm and thickness of 3 cms at its the circulation of the maternal blood through the
center. intervillous space.
• It weighs 500 gms**, the proportion to the weight of • The blood is brought in through a high pressure
the baby being roughly 1:6 at term. system of uterine ARTERIS and taken away by a
• (At 16 weeks of gestation the weight of the placenta low pressure system of VEINS
and fetus are equal) • The uteroplacental circulation is established 9-10
• Occupies about 30% of the uterine wall. days after fertilization.
• It presents two surfaces, fetal and maternal, and a •
peripheral margin.
• Fetal surface: covered by the Smooth and • Fetoplacental circulation: The 2 umbilical
glistening amnion with umbilical cord attached at or ARTERIS carry the DEOXYGENATED blood from the
near its center. At term - four-fifths of placenta - fetus to the placenta and the umbilical VEIN carry
fetal origin. OXYGENATED blood from the placaenta to the
foetus
• Maternal surface: Rough and Spongy- Maternal
• The fetal blood flow through the placenta is about
blood gives it a dull red color. The maternal surface
400 mL/min.
has 15-20 convex polygonal areas known as
• Fetoplacental circulation is established 21 days post
lobes or cotyledons which are limited by fissures.
fertilization.
Maternal portion - less than one-fifth of the total
placenta.
❖ DISEASES OF PLACENTA
• The cotyledons are separated by fissures
• Each fissure is occupied by the decidual septum
• Placental infarction: These are the most common
which is derived from the basal plate. maternal
placental lesion. If they are numerous, placental
origin.
insufficiency may develop.
• When they are thick, centrally located and
➢ PATHOLOGICAL CORELATIONS
randomly distributed, they may be associated with
preeclampsia or lupus anticoagulant
• Folds of Hobokon - Umblical cord ( in tunica
• They can also lead to placental abruption.
media)
• Whartons jelly - Connective tissue of umblical
➢ Placentomegaly (big placenta) is seen in
cord
• Multiple pregnancies, Diabetes mellitus, Macrosomy,
• Peg cells - Fallopian tube
Hydrops fetails (immune and nonimmune), Syphilis
• Langhans cells - Cytotrophoblast

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• When fixed in their normally distended state, the
➢ Small placentas are seen in umbilical arteries exhibit transverse intimal folds of
• Postdatism, IUGR, Placental infarcts Hoboken across their lumen.
• The extracellular matrix, which is specialized
➢ Succenturiate placenta connective tissue consists of Wharton's Jelly.0
• When a small part of placenta is separated from the • Anatomically umbilical cord can be regarded as a
rest of placenta and forms a separate lobe - A leash fetal membrane.
of vessels connecting the mass to the small lobe • The 02 Supply to fetus is at the rate of 5 ml/kg min
through the membranes. and this is achieved with cord blood flow of 105-320
• In case the communicating blood vessels are absent, ml/min
it is ealled as Placenta spuria. • Its length is 50cm - 55cm
• It can be retained leading to PPH, sub involution, • If it is < 32 cms it is considered abnormally short
uterine sepsis and polyp formation • Folding and tortuosity of the vessels within the cord
itself creates false knots (which are essentially
varices).
• The two arteries are smaller in diameter than the
veins.
➢ SHORT CORD
• IUGR, Abnornal lie/presentation, Congenital
malformations, Prenature placental

➢ LONG CORD
• Cord entanglement, Cord around the neck of fetus,
Fetal distress, Cord prolapse , Fetal anomalies

➢ Circumvallate placenta ➢ Single umbilical artery


• When the peripheral edge of the placenta is covered • More common - diabetic patients, black patients,
by a circular fold of amnion & chorion and fetal with eclampsia,hydramnios and oligohydramnios,
surface has a central depression. epilepsy patients and in APH.
• It can lead to abortion, APH, IUGR, Preterm delivery ➢ Finding of a single umblical artery is significant and
and hydrorrhea gravidarum. is associated with - Renal anomaties. Genitourinary
anomalies and Trisomy 18 are common.
➢ Increased chances of abortion, prematurity, IUGR
and perinatal mortality
❖ ABNORMALITIES OF CORD
➢ Normal attachment of cord
• The umblical cord is attached to the placenta near
the centre
• Marginal - Cord is attached to the margin of the
placenta (this type of placenta is called Battledore
❖ THE UMBILICAL CORD placenta)
• Umbilical cord (or funis) extends from the fetal • Furcate - Here the blood vessels divide before
umbilicus to the fetal surface of the placenta reaching the placenta.
• It develops from the connecting stalk. • Velamentous - Here the blood vessels are attached
• In the EARLY fetal life, cord has 2 arteries and 2 veins to the amnion, where they ramify before reaching
but later right umbilical vein disappears, leaving the placenta
only the left vein
• Thus at term umbilical cord has 2 arteries and 1 vein

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Composition of Amniotic Fluid
• Water-98-99%
• Solids-1-2%-include
✓ organic solids like proteins,glucose,lipid,urea,uric
acid,creatinine and hormones like-Prolactin,insulin
and renin.
✓ Inorganic solids are-Na,K and CI
• Amniotic fluid usually has a pH of 7.0 to 7.5

Origin of Amniotic Fluid


➢ Amniotic fluid originates both from maternal and
fetal sources:
• In early pregnancy - As an ultrafiltrate of maternal
plasma.
• By beginning of the second trimester - It consists of
extracellular fluid which diffuses through the fetal
skin.
• After 20 weeks - Cornification of skin prevents this
diffusion and amniotic fluid is composed mainly of
fetal urine.
➢ Other minor contributors:
• Pulmonary fluid
• Fluid filtering through the placenta
✓ The water in the amniotic fluid is completely changed
and replaced in every 3 hours.

Colour of Amniotic Fluid


❖ AMNIOTIC FLUID ➢ NORMAL
✓ Early Pregnancy – Colourless
➢ Impotant Facts ✓ Near term - Pale straw coloured due to presence of
• Specific gravity of Amniotic fluid: 1.008 to 1.010 exfoliated lanugo hairs and epidermal cells from the
• Osmolality: 250 mosm/L fetal skin.
• It is completely replaced in 3 hours. ➢ Abnormal
• Rate of amniotic fluid turn over is 500cc/hr. ✓ Green - meconium stained - fetal distress/breech or
• Volume of Amniotic fluid maximum is between 36-38 transverse position/Listeria infection
weeks and then decreases such that at term it is
roughly 800-900ml.
✓ Golden yellow - Rh incompatibility (Because bilirubin levels are increased in amniotic fluid in case of Rh
incompatibility).
✓ Greenish yellow (saffron) - post maturity.

✓ Dark coloured - concealed hemorrhage.


✓ Dark brown (tobacco juice) - in case of IUD.

MEASUREMENT OF AMNIOTIC FLUID


➢ Techniques used for ultrasonographically measuring
are:
➢ Amniotic fluid index (AFI):

ARISE MEDICAL ACADEMY Dr. MIK | 13


• The deformities include alteration in shape of the
skull, wry neck, club foot, or even amputation of the
limb
• Fetal pulmonary hypoplasia (may be the cause or
effect)
• Cord compression and High fetal mortality.

➢ Maternal:
• Prolonged labor due to inertia, operative
interference due to malpresentation, increased
maternal morbidity.

Treatment:
• AIsolated oligohydramnios in the third trimester
with a normal fetus may be managed
conservatively.
• Oral administration of water increases amniotic
fluid volume.
• 10% fructose infusion improves the volume
• Amnioinfusion (prophylactic or therapeutic) for
✓ Uterus into four quadrants and measuring the meconium liquor is found to improve neonatal
largest vertical pocket of liquor in each of the four outcome
quadrants. ❖ POLYHYDRAMNIOS
✓ The sum of the four measurements is the AFI in cm.
• It is a condition where liquor amnii is in excessive
The range of 5 - 25 cm is considered normal. Less
amount i.e., > 2 litres at term.
than 5 is considered significant oligohydramnios
• Most common used definition is by ultrasound
and more than 25 as poly hydramnios
assessment i.e., when amniotic fluid index (AFI) is >
➢ Single deepest pocket (SDP):
25 cm
✓ It is the depth of a single cord free pocket of
• pocket of fluid measuring 8 cms or more in vertical
amniotic fluid. The normal range is 2 - 8 cm.
diameter.
• Over 8 cm is considered polyhydramnios. Less than
2 cm is considered as oligohydramnios. Grades of Polyhydramnios
• Mild defined as pockets measuring 8-11 cm in
vertical dimension (seen in 80% cases).
• Moderate defined as pocket measuring 12 -15 cms
in vertical dimension (seen in 15% cases).
• Severe defined as free floating fetus found in
❖ OLIGOHYDRAMNIOS pockets of fluid of 16 cms or more (seen in 5%
➢ Oligohydramnios is a condition where liquor amnii cases).
is deficient (< 200 ml at term).
➢ Sonographically it is defined as: Causes of Polyhydramnios
• Maximum vertical diameter of amniotic fluid pocket ➢ Fetus produces more urine for eg:
less than 2 cm or Amniotic fluid index less than 5 • Twin/multifetal pregnancy (number of fetus is
cms. more: more of urine)
• Maternal hyperglycemia/diabetes (Maternal
Complications hyperglycemia --- Fetalhyperglycemia --- Fetal
➢ Fetal polyuria --- increased amniotic fluid.)
• Abortion • Twin to Twin transfusion syndrome
• Deformity due to intra-amniotic adhesions or due to
compression. ➢ if fetal swallowing is impaired as in case of:

ARISE MEDICAL ACADEMY Dr. MIK | 14


• Cleft lip and cleft palate • Preeclampsia (25%), Malpresentation and
• Esophageal atresia or stenosis persistence of floating head, Premature rupture of
• Duodenal atresia or stenosis the membranes, Preterm labor
• Bowel obstructione.
• Anencephaly (swallowing is decreased + increased ✓ During labor:
transudation of CSF into amniotic fluid due to • Early rupture of the membranes, Cord prolapse
absence of cranial vault) • Uterine inertia, Increased operative delivery due to
malpresentation, Retained placenta, postpartum
➢ Placental Causes hemorrhage and shock. (The postpartum
• Chorangioma of placenta hemorrhage is due to uterine atony).
• circumvallate placenta
✓ Puerperium:
➢ Fetal Causes • Subinvolution, Increased puerperal morbidity due
• Hydropsfetalis to infection
• Rubella, syphilis, Toxoplasma infection of fetus
• Trisomy (note - Triploidy leads to oligohydraminos) Management
• Sacrococcygeal teratoma ➢ Serial amniocentesis
• Thallasemia of fetus • It is the TOC if the patient is in distress.
• Amount of fluid removed is 500 ml/hr, Maximum
Complications fluid removed is 1 . 5 - 2 litres.
➢ Indomethacin therapy
Fetal: • Potential hazard of Indomethacin therapy -
• There is increased perinatal mortality Premature closure of Fetal ductus arteriosus.
• The deaths are mostly due to prematurity and • So, the therapy should be stopped at 32 weeks
congenital abnormality (40%).
• Dangerous complications of amniocentesis
➢ Cord prolapse & Abruptio placenta
➢ Maternal
✓ During pregnancy—There is increased incidence of:

CHAPTER – 4
MATERNAL ADAPTATIONS IN PREGNANCY
➢ Uterus – 1 kg
MATERNAL WEIGHT GAIN ➢ Breasts – 0.4kg
• There is no such thing as absolute weight gain in ➢ Accumulated fats and proteins – 3.5kg
pregnancy ➢ Increase in blood volume – 1.3kg
• Average maternal weight gain during pregnancy is ➢ Increase in extra cellular volume – 1.2kg
11-12 kgs ✓ TOTAL AMOUNT OF WATER RETAINED AT TERM IS
• Weight gain is due to 6.5 – 7 LT
➢ Foetus – 3 kg
➢ Placenta – 0.5 kg ❖ Weight gain depends on several factors
➢ Liquor – 1 kg

ARISE MEDICAL ACADEMY Dr. MIK | 15


✓ Pre pregnancy weight: If the pre pregnancy weight ➢ Platelet count (Benign gestational
is more than normal (obese), there is a tendency to thrombocytopenia)
gain excessive weight during pregnancy. ➢ Clotting factor 11, 13
✓ Race and ethnicity: American women tend to put ➢ In normal pregnancy - Since plasma volume
on more weight during pregnancy as compared to increases more in comparison to Red cell volume so
Asians and Africans. viscosity of blood decreases
✓ Socio economic status: Women from higher socio ➢ Since total hemoglobin mass increases during
economic group have more weight gain as pregnancy. Therefore, oxygen carrying capacity of
compared to women from lower socio economic blood also increases
group. This is because malnutrition prevents ➢ in pregnancy hemoglobin mass increases up to the
optimum weight gain. extent of 18-20%) but hemoglobin concentration
✓ Associated conditions like women with decreases due to hemodilution.
gestational/over diabetes mellitus, twins and
polyhydramnios have higher weight gain during ❖ CHANGES IN IRON DYNAMICS
pregnancy • Serum Iron concentration -- Decreases
✓ Parity: Multigravida females tend to gain less weigh • Serum ferritin (Reflecting Iron stores) -- decreases
than primigravida • Serum Total iron binding capacity -- Increases
• Rapid weight gain i.e. more than 0.5 kg a week or 2 • Percentage saturation (Serum ferritin / TIBC) ---
kg per month is an early manifestation of Decreases
preeclampsia. • Serum Transferrin -- Increases
• Stationary or falling weight suggests IUGR or IUD • During pregnancy there is marked demand of extra
• Smoking does not affect maternal weight gain iron especially in the second half.
during pregnancy (smoking affects fetal weight gain • Even an adequate diet cannot provide the extra
and is one of the causes of lUGR) demand of iron.
• Thus pregnancy is always a state of physiological
iron deficiency.

❖ HAEMATOLOGICAL ADAPTATIONS • The two Ts i.e. Transferrin and TIBC increase during
pregnancy, rest all parameters of iron metabolism
• The following components of the haematological decrease during pregnancy.
system show an ‘increase’
➢ Blood volume - (30-40%) ❖ RENAL PHYSIOLOGY
➢ Plasma volume - (40-50%)
➢ Red blood cell volume - (20-30%) Since the increase ➢ Increase in
in RBC volume is less in comparison to plasma • Renal blood flow (+50%)
volume there is hemodilution during pregnancy. • GFR (+50%)
➢ Hb mass (in gm's) (as RBC volume increases) • Creatinine clearance
➢ WBC count (Neutrophilic leucocytosis) • Glucosuria
➢ All clotting factors (except 11 and 13) i.e. pregnancy
is a hypercoagulable state ➢ decrease in
➢ S. fibrinogen (Clotting factor I) increases by 50% • Plasma osmolality
➢ ESR ( 4 times) • S. creatinine
• S Uric acid
• The following components show a ‘decrease’ in • S. K+ and Na+
value during pregnancy • S. Cl -
➢ Hemotocrit • Progesterone leads to relaxation of the smooth
➢ Packed cell volume muscles of ureter.
➢ Viscosity of blood • Therefore activity of ureters decreases and leads to
➢ Hb conc (i.e. g/dl) as increase in plasma volume is urinary stasis.
more compared in packed cells ( 50 : 30 ) • Glomerular filtration rate is increased by 50% which
means filtering capacity of the kidney is increased

ARISE MEDICAL ACADEMY Dr. MIK | 16


so their is a decrease in maternal plasma levels of • Women are asymptomatic and their is no H/O
creatinine, blood urea nitrogen and uric acid bleeding.
• In pregnancy there is active retention of Na+, K+ • Condition is benign and has no risk to mother or
and water due to increased estrogen, progesterone, infant.
aldosterone and renin angiotensin activity • The only problem associated with it is - that
• And although there are increased total anaesthesioiogists are reluctant to give epidural or
accumulation of sodium and potassium, their serum spinal anaesthesia if platelet count is < 1 lakh/mm3.
concentrations are decreased slightly becasue of • Treatment with steroids and IgG or platelet
expanded plasma volume transfusion before delivery is sometimes necessary.
• The average plasma sodium concentration during
pregnancy is 136 meq/L. ❖ VENOUS THROMBO EMBOLISM
• This slight decrease in plasma sodiun concentration
during pregnancy is a result of the increased • Venous thromboembolism is the leading cause of
amount of filtered sodium caused by the increased maternal deaths in developed countries.
GFR. • Pregnancy increases the risk of thromboembolism 6
• In fact during pregnancy the amount of sodium times as all components of virchow's triad are
presented to the tubules for reabsorption is increased
approximately 30240 meq/L per day, whereas the • Left sided DVT is more common than Right sided
non-pregnant woman filters only about 26160 DVT.
meq/L per day. • Homans sign-i.e pain in calf muscles on dorsiflexion
• Although the efficiency of tubular sodium of foot is positive.
reabsorption during pregnancy is remarkable, the
serum sodiun equilibrates at slightly lower level
than it does in non-pregnant status maily due to ➢ Investigations
haemodilution • Recommended method during pregnancy : Doppier
ultrasound
❖ ADAPTATIONS IN BLOOD COAGULATION SYSTEM • Gold standard (in conditions other than pregnancy):
• Pregnancy is a hyper coagulable state all clotting Venography
factors are increased • Though objective evidence is ideal, treatment
• serum fibrinogen levels are raised by 50% from 200 should be started on clinical grounds if confirmatory
- 400 mg% in non pregnant to 300 - 600 mg% in tests are not available
pregnancy
• All the clotting factors show an increase except o ANTI COAGULANTS
factor XI and XIII • There are 2 main drugs for consideration as anti
• Factors II, VII, VIII, IX, X show a most increase and coagulants in pregnancy ie Warfarin and Heparin:
others show a slight increase
• Platelet count decreases called as benign ➢ WARFARIN
gestational thrombocytopenia • highly effective anticoagulant - Can cross placenta
➢ IMPORTANT: and Lead to-short stature, stippled epiphysis, Nasal
• Clotting time and bleeding remain unaffected in hypoplasia, Saddle nose and frontal Bossing if used
pregnancy. in 1st Trimester.
• This is known as ‘contradi hunerman syndrome’ or
➢ GESTATIONAL THROMBOCYTOPENIA/BENIGN foetal warfarin syndrome.
GESTATIONAL THROMBOCYTOPENIA
• It is the most common cause of thrombocytopenia ➢ HEPARIN
accounting for 80-90% of all cases of • Cannot cross placenta and so does not lead to
thrombocytopenia occuring during pregnancy. foetal defects
• Exact cause is not known (may be due to • It is not as effective as warfarin
hemodilution and increased platelet consumption.)
• Platelet count is rarely <70,000/mm3. o Keeping these things in mind, during pregnancy
anticoagulants are used as

ARISE MEDICAL ACADEMY Dr. MIK | 17


• Uptil 12 weeks – unfractionated heparin ( 1st ❖ ADAPTATIONS IN RESAPIRATORY SYSTEM
trimester avoid warfarin) ✓ The following parameters increase
• 12-36 weeks – warfarin can be used if indicated (TIdal voluMe Up)
• 36 weeks onwards and uptil 6hrs before delivery - ➢ Tidal volume, Minute ventilation, Inspiratory
Unfractionated heparin ( warfarin if used now may capacity, Minute oxygen up take
cause PPH after delivery)
• 6 hours before delivery or elective cesarean section ✓ The following parameters decrease
– no anti coagulant ( risk of bleeding during (Total Fuctional REserve)
delivery or surgery) ➢ Functional residual capacity, Expiratory reserve
• From 6 hrs after vaginal delivery and 24 hrs after volume, Residual volume, Total lung capacity
cesarean – IV HEPARIN
• 3rd day after delivery or surgery once INR is ✓ The following are unchanged
adjusted between (2-3) – stop heparin and start ➢ Respiratory rate, Vital capacity, Inspiratory reserve
warfarin (warfarin is completely safe during breast volume
feeding)
❖ CARDIOVASCULAR PHYSIOLOGAL ADAPTATIONS
• Cardiac output = Stroke volume x HR
• Parameters which ‘increase’ in pregnancy.
❖ SKIN CHANGES DURING PREGNANCY ➢ Cardiac output increase
• During pregnancy, skin undergoes varying degrees ✓ by 40% during pregnancy
of pigmentation, which varies among individuals. ✓ 50% during each uterine contraction in labour
• The dark line runn centrally below the umbilicus is ✓ 80% immediately postpartum
called the linea nigra. • Hence Maxmimum risk of cardiac failure or
• Chloasma It is hyperpigmentation of the skin eclampsia in pregnany is in
around the cheeks, forehead and eyes. The • immediate postpartum period > intrapartum
pigmentation is thought to be due to increased period > 32 wks of pregnancy
levels of endorphins and melanocyte stimulating
hormone and disappears spontaneously after • Parameters which ‘decrease’ in pregnancy
delivery • Peripheral vascular resistances (as progesterone has
• Striae gravidarum are stretch marks of pregnancy a smooth muscle relaxant effect)
found during pregnancy caused due to stretching of • Diastolic BP
collagen beyond physiological limits • Mean arterial BP
• Linea albicans are whitish stretch marks seen after • [Systolic BP + (Distolic BP * 2)] /3
delivery due to unsuccessful attempts at collagen
regeneration ➢ CLINICAL FINDINGS IN CARDIOVASCULAR
PHYSIOLOGY
❖ CHANGES IN PLASMA PROTEINS • Heart rate (resting) increases by about 10-15 bpm.
➢ Increase in • Apex beat shifts to the 4th intercoastal space, 2.5
• Total proteins (g) (+ 20 to 30%), Globulin (+5%) cms outside the mid clavicular line (as heart is
pushed upwards, outward, with slight rotation to
➢ Decrease in left).
• Plasma proteins concentration (measured in g/dl) (- • Slightly enlarged cardiac silhouette. (marked
10%), Albumin (-30%), Albumin/globulin ratio in- enlarged cardiac silhoute is not normal in
pregnancy - 1:1, In non pregnant- (1.5 to 1.7) : 1 pregnancy)
• Exaggerated splitting of the first heart sound (both
➢ Changes in blood chemistry components loud).
• During pregnancy the pH is 7.42 (non pregnant • Second heart sound : Normal
states - it is 7.9 • Third heart sound : Loud and easily auscultated.
• Pregnancy is a state of respiratory alkalosis with
metabolic acidosis. ➢ Murmurs : -

ARISE MEDICAL ACADEMY Dr. MIK | 18


• Grade II systolic ejection murmur is audible in aortic pregnant females are advised to lie in left lateral
or pulmonary area at about 10-12 weeks due to positions
expanded intravenous volume. It diappears in the • Femoral venous pressure is markedly raised in
begining of post partum period. pregnancy especially in later months.
• Mammary murmur. - Continuous hissing murmur • The pressure exerted by gravid uterus on the
audible over tricuspid area in left 2nd and 3rd common iliac veins (more on right side due to
intercoastal spaces known dextrorotation of the uterus
• ECHO - Shows increased left atrial and ventricular • causes pedal edema in pregnant women called as
diameters. physiological edema of pregnancy.
• ECG - Shows left axis deviation. • No treatment is required for physiological edema or
• Note : None of the arrythmias are normal during orthostatic edema. It subsides on rest alone.
pregnancy, rather their presence indicates heart • Diuretics should not be prescribed in case of
disease during pregnancy physiological edema.

❖ ARTERIAL HAEMODYNAMICS ❖ ENDOCRINOLOGY

• REGIONAL DISTRIBUTION OF BLOOD FLOW DURING • The following hormones are increased during
PREGNANCY: pregnancy
• Uterine blood flow is increased from 50 mL/min in ➢ Growth Hormone, Prolactin, ACTH, Aldosterone,
nonpregnant state to about750ml_ near term. The Cortisol , T3 and T4 and BMR, Testosterone and
increase is due to the combined effect of Androstenedione, Thyroid binding globulin, Insulin,
uteroplacental and fetoplacental vasodilatation. Insulin Resistance
• Pulmonary blood flow (normal 6000 mL/min) is
increased by 2500 mL/min (i.e. 40% increase). • In pregnancy, the following hormones decrease
• Renal blood flow (normal 800 mL) increases by 400 ➢ Follicle Stimulating Hormone, Leutinising Hormone,
mL/min (i.e. 50% increase) at 16th week and De Hydro Epi Aandrosterone, Serum Iodine
remains at this level till term.
• The blood flow through the skin and mucous • The following remain unchanged
membranes reaches a maximum of 500 mL/min by ➢ Thyroid Stimulating Hormone and Anti Diuretic
36th week. Hormone
• Heat sensation, sweating or stuffy nose complained
by the pregnant women can be explained by the ➢ In pregnancy there is hyperplasia of the Thyroid,
increased blood flow. Parathyroid, Pituitary and Adrenal Cortex
➢ Although the size of thyroid gland increases and the
❖ VENOUS HAEMODYNAMICS T3 and T4 released increase the patient remains
• SUPINE HYPOTENSION SYNDROME (POSTURAL euthyroid.
HYPOTENSION):
• During late pregnancy, the gravid uterus produces a ➢ OESTROGEN :
compression effect on the inferior vena cava when • The form of estrogen produced mainly by placenta
the patient is in supine position. is estriol.
• In 90% cases this, however, results in opening up of • Placenta cannot synthesise estriol unless it gets
the collateral circulation by means of paravertebral precursors from the fetual adrenals
and azygos veins. • so estriol is the marker for Feto-maternal-placental
• In some cases (10%), when collateral circulation wellbeing.
fails to open up, the venous return of the heart may • Estrogen is produced by placenta but not
be seriously curtailed. exclusively because the precursors for synthesis of
• This results in production of hypotension, estrogen are made available to the placenta by the
tachycardia and syncope called as supine fetal adrenal cortex, without which it cannot
hypotensive syndrome. synthesise estrogen
• The normal blood pressure is quickly restored by • The evidence is provided by anecephalic fetus
turning the patient to lateral position. That is why where adrenal glands are absent or diminished in

ARISE MEDICAL ACADEMY Dr. MIK | 19


size therefore there is limited availability of steroid • Estrogen(estriol,precursors of which come from
precursors and so rate of formation of placental fetus), Progesterone
estrogen is severely limited. ➢ Others:
• After ovulation the graafian follicle is converted to • Relaxin (also secreted by corpus luteum & decidua).
corpus leuteum
✓ FROM CYTOTROPHOBLAST
➢ PROGESTERONE • It produces hypothalamus like releasing factors
• The corpus luteum then secretes high amounts of ➢ Corticotrophin releasing hormone (CRH), Growth
progestrone whose main function now is hormone releasing hormone (GHRH), Neuropeptide
decidualisation Y , Gonadotrophin releasing hormone (GnRH),
• Decidua is the specialised highly modified Thyrotrophin releasing hormone (TRH)
endometrium of pregnancy.
• Decidual reaction/decidualisation is the conversion o HUMAN CHORIONIC GONADOTROPIN
of secretory endometrium into decidua and is • HCG is a glycoprotein
dependant on estrogen and progesterone. • It is synthesized by syncytiotrophoblast of the
• Decidual reaction is completed only with blastocyst placenta.
implantation. • HCG has 2 subunits ALPHA AND BETA
• Progesterone is secreted by the corpus luteum until ✓ ALPHA : biologically similar in LH, FSH and TSH.(i.e
6-7 weeks of gestation after which placenta is the non specific)
main source of production ✓ BETA : unique to HCG. (i.e specific)
• Progesterone is the main hormone which maintains • Structurally it is similar to - FSH, LH, TSH but
pregnancy functionally it is similar to LH (i.e luteotropic) helps
in maintaining corpus luteum.
➢ PROLACTIN • the main hormone which maintains activity of
• Maternal plasma levels of prolactin increase corpus luteum during pregnancy is HCG and in non
markedly during the course of normal pregnancy pregnant state is LH.
• Serum concentration levels are usually 10-fold • The half life of HCG is 36 hours.
greater at term (about 150 ng/ml) compared with • In early pregnancy the doubling time of HCG is 1.4
normal non pregnant women. - 2 days.
• Paradoxically, after delivery, the plasma prolactin • It can be detected in maternal serum as early as 8
concentration decreases even in women who are days following fertilisation/Day 22 of menstrual
breast feeding. cycle/5 days before missed period by radio
• During early lactation, there are pulsatile bursts immuno assay.
ofprolation secretion in response to sucking. • The level is 100 IU/L or mlU/mL around the time of
• Hormone responsible for lactation - Prolactin. the expected menses.
• Prolactin is synthesized by pitutary and decidua. • The levels progressively rise and reach maximum
• Prolactin suppresses GnRH, LH and FSH, causing levels by about 8-10 weeks 170 days/1 st trimester.
lactational amenorrhea • It then falls until about 16weeks and remains at low
level up to term.
➢ PLACENTAL HORMONES • HCG disappears from circulation by 2 weeks
following delivery.
✓ FROM SYNCYTIOTROPHOBLAST • Action :
➢ Protein hormones • Sustains the corpus luteum and thereby maintains
• HCG, Human placental lactogen – HPL, Human the hormonal support to the pregnancy in early
chorionic thyrotropin (HCT), Pregnancy specific weeks.
beta-1 glycoprotein PSBG, Pregnancy associated • Stimulates the Leydig cells of the male fetus to
plasma protein A (PAPPA) produce testosterone and thereby induces
➢ Growth factors development of the male external genitalia.
• Inhibin, Activin • Immunosuppressive action which helps in the
➢ Steroid hormones: maintenance of pregnancy.

ARISE MEDICAL ACADEMY Dr. MIK | 20


➢ Increased HCG values
• Pregnancy, Successful therapeutic insemination & in o SCHWANGERSHAFT PROTEIN OR PREGNANCY
vitro fertilization, Hydatiform mole, SPECIFIC BETA 1 GLYCOPROTEIN
Choriocarcinoma, Multifetal pregnancy, • Produced by trophoblast.
Erythroblastotic fetus, Down syndrome • Can be detected 18 days after ovulation.
• Ovarian, testicular teratoma , certain neoplasm of • Its concentration rises steadiiy and reaches
lung stomach & Pancreas 200mg/ml at term.
• Role - measure of placental function for fertility
➢ Decreased HCG values control
• Thereatened/spontaneous abortion, Ectopic
pregnancy & Trisomy 18 o INSULIN
• In pregnancy there is hyperinsulinemia ie increase
➢ MEASURING hCG in the secreted amount of insulin
• There are 2 types of tests • This is associated with insulin resistance in the
➢ Urine tests mother to essentially shunt glucose selectively to
➢ Serum tests the baby
✓ ELISA • On the whole the general plasma insulin level is
✓ Radioimmunoassay ( beta sub unit) increased, so as to ensure continuous supply of
✓ Immunoradiometric assay glucose to fetus.
• To be specific: The overall effect of pregnancy is
o HUMAN PLACENTAL LACTOGEN such that there is maternal fasting hypoglycemia
• It is also called human chorionic somatotropin. (due to fetal consumption), whereas postparandial
• It is a polypeptide hyperglycemia and hyperinsulinemia.
• It is secreted by the syncytiotrophoblast.
• It is similar to pituitary growth hormone and ➢ INCREASED SECRETION
prolactin. • During pregnancy insulin levels are increased
• It is first detected at 3rd wk after fertilisation or because of increased insulin secretion as well as
5menstrual week gestation age (both mean the increase in insulin resistance due to a number of
same thing) and rises progressively until 36 weeks. contra insulin factors.
✓ These are – Estrogen, Progesterone, Human
➢ Role of HPL placental lactogen (HPL), Cortisol and Prolactin
• HPL is mainly responsible for diabetogenic state
in pregnancy. (It antagonises the action of ➢ INSULIN RESISTANCE
insulin. • The main hormone responsible for insulin
• It leads to maternal lipolysis and increases level of resistance is HPL
circulating free Fatty Acid thus provides a source of • Insulin resistance is maximum between 24-28
energy for maternal metabolism and fetal nutrition weeks of pregnancy.
• It is a potent angiogenic hormone therefore, may
play important in fetal vasculature formation. ❖ VAGINAL CHANGES
• Levels of HPL are more in big babies and multiple
pregnancies, making them all prone to develop ➢ INCREASED VASCULARITY AND HYPEREMIA
gestational diabetes.
• As such HPL mainly plays role in maternal • causes - violet colour characteristic of Chadwick sign
endocrinal changes during pregnancy
• Due to it’s metabolic effects like in free fatty acids ➢ VAGINAL pH:
and aminoacids it can indirectly lead to fetal • decreases i.e. becomes acidic and varies from 3.5 to
growm. 6 and this mainly occurs due to increase in number
• Because hPL is secreted primarily into maternal of lactobacillus - inhibits the growth of pathogenic
circulation with only small amounts in cord blood bacteria.
• It’s role is more in maternal rather than in fetal ➢ Histopathology:
tissues

ARISE MEDICAL ACADEMY Dr. MIK | 21


➢ In early pregnancy • Fetal growth is predominantly controlled by :
• the vaginal epithelial cells are similar to those seen 1. IGF-1, 2. Insulin, 3. Other growth factors
in the luteal phase. • Growth hormone is required for postnatal growth
of fetus
❖ FETAL ENDOCRINOLOGY:
• All anterior pituitary hormones are secreted at 10 Miscellaneous changes
weeks ➢ The following parameters increase in pregnancy
• All posterior pituitary hormones along with insulin • Total cholesterol
are secreted at 12 weeks • LDL and HDL
• Fetal thyroid gland beings to concentrate iodine at • C reactive protein
10-12 weeks. • Total alkaline phosphatase (due to placental
• Synthesis and secretion of thyroid hormone by fetus alkaline phosphatase)
ensues at 20 weeks.
• At birth 30% of T4 in umbilical cord blood is Hormones which have alpha and beta subunits
maternal in origin. • HCG, LH, FSH, TSH, Insulin
• Glucagon is secreted at 8th week.

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ARISE MEDICAL ACADEMY Dr. MIK | 23
ARISE MEDICAL ACADEMY Dr. MIK | 24
CHAPTER 5
PUERPERIUM
• It starts after delivery and extends 6 – 8 weeks
• Puerperium is the time after child birth after child birth
GENERAL PHYSIOLOGICAL CHANGES IN PUERPERIUM ➢ Lochia serosa
• 5-9 days
• Pulse - Increases for few hours and then settles • the color is yellowish or pink or pale brownish.
down to normal • It consists of less RBC but more leukocytes,
wound exudate, mucus from the cervix and
• Temperature - In the first 24 hrs-temp should not microorganisms
be above 99 F / On day 3, due to breast ➢ Lochia alba
engorgement there may be slight rise of • 10-15 days.
temperature • It contains plenty of decidual cells, leukocytes,
• UTI must be ruled out if there is rise of temperature mucus, cholestrin crystals, fatty and granular
• Weight - Loss of 2 kg (5 lb) occurs due to diuresis. epithelial cells and microorganisms
• Blood volume - Decreases after delivery and returns
• The average amount of discharge for the first 5-6
to pre pregnant levels by the second week.
days, is estimated to be 250 mL.
• Cardiac output - Rises after delivery to 60% above • The normal duration may extend up to 3 weeks.
the pre-labour value, and returns to norm within • The red lochia may persist for longer duration
one week. especially in women who get up from the bed for
• Fibrinogen - Remain high upto the second week of the first time in later period.
puerperium ➢ Clinical importance:
• ESR - levels remain high. • The discharge is scanty following premature labors
or in case of infection
• Urinary tract - Retention of urine is common due to • It is excessive in twin delivery or hydramnios, or
oedema of vulva and pain from perineum subiinvolution of uterus and retained bits of
• Patient should be encouraged to pass urine conception.
following delivery. • If malodorous it indicates infection or retained plug
• GIT tract - Thirst increased or cotton piece inside the vagina
• Persistence of red color beyond the normal limit
• Constipation - due to intestinal paresis
signifies subinvolution or retained bits of conceptus.
• Duration of the lochia alba beyond 3 weeks
LOCHIA:
suggests local genital lesion.
• It is the vaginal discharge for the first fortnight
during puerperium INVOLUTION OF UTERUS
• The discharge originates from the uterine body, ➢ The process by which the post partum uterus
cervix and vagina. returns to its pre pregnant state is called as
• It has got a peculiar offensive fishy smell. Involution.
• Its reaction is alkaline tending to become acid ➢ Involution is achieved by decrease in the size of
towards the end. muscle fibres and not in the number
• Depending upon the variation of the color of the • Immediately following delivery, the fundus is just
discharge, it is named as: below the umbilicus 13.5 cms above the symphysis
pubis/ 20 weeks gestational age size.
➢ Lochia rubra • After 24 hours of delivery, height of uterus
decreases by 1.25 cm/day.
• 1-4 days.
• Uterus is a pelvic to organ by the end of 2 weeks.
• It consists of blood, shreds of fetal membranes
(Just after delivery uterus is 13.5 cms above pubic
and decidua, vernix caseosa, lanugo and
meconium. symphysis and thereafter its size decreases by 1.25
• It has bacteria like anaerobic streptococci and cm/ day which means by 10-12 days it will be an
staphylococci intra pelvic organ)

ARISE MEDICAL ACADEMY Dr. MIK | 25


• Uterus returns almost to its normal size (pre
pregnant size) by the end of 8 weeks.

• Placental site involution: Immediately after delivery SYNTHESIS AND SECRETION OF BREAST MILK
placental site is palm size. By the end of 2 weeks it
is 3-4 cm in diameter.
Stage Description Main hormone Supportive
hormones
Mammogenesis Mammary • Estrogen (for • Hpl For milk
Growth and Ductal growth) • Growth hormone Secretion to
Development • Progesterone • Insulin thyroxine occur
(For alveolar growth) Nursing effort
is not
Essential
Lactogenesis Initiation of Prolactin Estrogen
Milk secretion
Galactokinesis Ejection of milk Oxytocin Suckling of
Or let down Breast
reflex
Galactopoiesis Mantainence of Prolactin Continous
lactation suckling

• It has higher specific gravity and higher protein,


Breast milk vitamin A, D, E, K, immunoglobulin, sodium and
chloride content than mature breast milk.
➢ Composition of Breast Milk: • It has lower carbohydrate, fat and potassium than
✓ Carbohydrate - Lactose is present in high mature milk.
concentration in breast milk. ➢ Advantages
✓ Protein content is low, as the baby cannot • Antibodies (IgA, IgG, IgM) and humoral factor
metabolise a high protein diet. The proteins are (lactoferrin) provide immunological defence to the
mainly lactalbumin and lactoglobulin, which are new born.
easily digestible. • Laxative action due to fat globules.
• It is also rich in the aminoacids taurine and cysteine, • It is an ideal natural starter food.
which are necessary for neurotransmission and
neuromodulation.
✓ Fats - Breast milk is rich in polyunsaturated fatty
acids (PUFA) needed for myelination.
✓ Water and electrolytes - The water content is 86 -
87%. Lactation amenorrhea
✓ Immunological superiority - Breast milk contains
immunoglobulins, especially IgA and IgM, lysozyme, • After child birth the normal menstrual cycles
lactoferrin (which protects against enterobacteria), cessate/ stop for some time, this period is called
bifidus factor (to protect against E.coli), PABA lactational amenorrhoea
(which protects from malaria).
CONTRACEPTION IN PUERPERIUM
➢ The Rule of 3's :
➢ Colostrum • In the presence of FULL breast feeding, a
• It is a deep yellow serous fluid secreted from contraceptive method should begin in the 3rd
breasts starting from pregnancy and for 2-3 days postpartum month.
after delivery.
➢ Composition

ARISE MEDICAL ACADEMY Dr. MIK | 26


• With PARTIAL breast feeding or no breast feeding,
a contraceptive method should begin during the 3rd 1. Necrotizing enterocolitis (NEC)
postpartum week. 2. Otitis media
• But it is not a reliable method if mother is nursing 3. Bottle feeding
only in day time. Waiting for first menses involves a • Carries a huge risk of infections due to unsterile
risk of pregnancy because ovulation usually conditions
antedates menstruation. 4. Hypocalcemia
CONTRACEPTIVES IN PUERPERIUM The only benefit……
➢ 1st contraceptive of choice in lactating mother • In formula feeds vitamin K is added in higher levels
• Progesterone only pill or progesterone implant or than in breast milk to reduce the risk of
DMPA injection. hemorrhagic diseases in new born. So, vitamin K
➢ 2nd choice is lUCD's deficiency can never be a complication of formula
• Can be used as an alternative to progesterone only fed babies.
pills by lactating mothers but only following
complete uterine involution in woman who are CAUSES OF INADEQUATE MILK PRODUCTION
sexually active. (LACTATION FAILURE)
• Infrequent suckling.
FORMULA FEEDS vs. BREAST MILK • Depression or anxiety state in puerperium
• Reluctance or apprehension to nursing.
• There is no substitution of formula milk for breast • Poor development of nipples/retracted nipple.
milk • Painful breast lesion viz cracked nipple/ breast
• Breast milk is the best milk for the child and has no abscess.
replacement • Endogenous suppression of prolactin.
• The following are few potentially dangerous side
effects of formula feeds
LACTATION SUPRESSORS GALACTOGOUGES/ LACTATION STIMULATORS
BROMOCRIPTINE/ CABERGOLINE STIMULATION OF NIPPLE/ GENITALS
TESTOSTERONE METOCLOPRAMIDE
ETHINYL OESTRADIOL INTRANASAL OXYTOCIN
PYRIDOXINE
SULPIRIDE

BREAST DISEASE ASSOCIATED WITH LACTATION


CONTRAINDICTIONS TO BREASTFEEDING
➢ Mastitis:
• Mother on IV drug abuse/excess alcohol.
• In females undergoing treatment for breast cancer
• Mother on anticancer drugs or other teratogenic
drugs.
• Active Herpes simplex lesions of the breast.
• Active/untreated pulmonary tuberculosis in
mother.
• Galactosemia and congenital lactose intolerance in
infant.
• HIV-positive mother
• Hepatitis B/C infections in the mother are not • It is parenchymatous infection of breast.
contraindications to breast feeding. Infants of
seropositive hepatitis B mothers should be given
Hepatitis B Immunoglobulin (I.M.) within 12 hours
of birth

ARISE MEDICAL ACADEMY Dr. MIK | 27


• M/C site of Puerperal infection - Placental site.
➢ Most common organism causing breast infection • M/C manifestation of Puerperal infection -
Staphylococcus aureus Endometritis.
• The immediate source of organism that cause • M/C/C of Puerperal sepsis - Streptococcus.
mastitis is almost always the infant's nose and • M/C route of infection - Direct spread.
throat
PUERPERAL BLUES/ 3 DAYS BLUES / BABY BLUES
➢ Others: • It is transient state of mental illness observed 4-5
• Coagulase negative Staphylococci days after delivery in nearly 50% of post partum
• Viridian Streptococci. women.
• Postpartum blues occurs at the height of hormonal
➢ Symptoms changes
• appear in the 3rd or 4th week • It is due to a sudden increase in oestrogen and
• Characterised by pain, swelling, redness and progesterone
tenderness • Patients present with depression, anxiety,
• Infection is almost always unilateral tearfulness, insomnia, helplessness and negative
• Predisposing factors : fissures / abrasions or cracks feelings towards infant.
in nipples • It may last from a few days to 2-3 weeks.
• Generally self limited, 20% of women may develop
➢ Treatment depression in the first postpartum year.
• Mastitis is not a contraindication for breast feeding. • Treatment: Reassurance and psychological support
• DOC : Dicloxacillin (In patients not sensitive to of family members.
penicilin )
• Eythromycin (In patients sensitive to penicillin) Post-partum Depression
• Treatment to be given for 10-14 days. • It is observed in 10 - 20% of mothers.
• About 10% of women with mastitis develop an • It is more gradual in onset over the first 4 - 6
abscess due to variable destruction of breast tissue. months following delivery or abortion.
• If abscess is formed - surgical drainage is done • Changes in hypothalarno-pituitary-adrenal axis may
under general anaesthesia be a cause.
• Manifested by loss of energy and appetite,
insomnia, social withdrawal, irritability and even
Puerperal pyrexia suicidal attitude.
• It is defined as a rise of temperature reaching • Risk of recurrence 50 -100% in subsequent
100.4° F (38° C) or more (measured orally) on pregnancies.
separate occasions at 24 hours apart (excluding first • Treatment: Should be started early. Fluoxetine or
24 hours) within first 10 days following delivery. paroxetine is effective and has fewer side effects.
• Any infection of genital tract which occurs as a
complication of delivery is called as Puerperal
sepsis.

CHAPTER – 6

DIAGNOSIS OF PREGNANCY

PREGNANCY IS DIAGNOSED BY THE FOLLOWING ➢ CLINICAL METHODS ( TRIMESTER WISE)


METHODS ➢ ULTRASONOGRAPHIC METHODS
➢ BIOCHEMICAL/ IMMUNOLOGICAL METHODS

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SIGN DESCRIPTION SEEN AT / SEEN IN
GOODELS SIGN SOFTENING OF CERVIX (CERVIX FEELS LIKE LIP OF 6TH WEEK OF
MOUTH WHEREAS IN NON PREGNANT STATE IT PREGNANCY & IN OC
FEELS LIKE TIP OF NOSE) PILL USERS
HEGARS SIGN ON BIMANUAL EXAMINATION WITH 2 FINGERS IN 6 – 10 WEEKS
ANTERIOR FORNIX & FINGERS OF OTHER HAND
BEHIND THE UTERUS, THE ABDOMINAL & VAGINAL
FINGERS SEEM TO APPOSE BELOW THE BODY OF
UTERUS. IT OCCURS BECAUSE OF SOFTENING OF
ISTHMUS
JACQUIMER’S SIGN OR CHADWICK’S DUSKY HUE OF VESTIBULE AND ANTERIOR 8TH WEEK AND IN
SIGN VAGINAL WALL DUE TO PELVIC CONGESTION PELVIC TUMORS LIKE
FIBROID
OSIANDERS INCREASED PULSATION FELT THROUGH THE 8TH WEEK AND IN PID
LATERAL FORNICES

o SECOND TRIMESTER SIGNS

• QUICKENING - It refers to the perception of active


fetal movements felt by 18 weeks of pregnancy in
primipara and 2 weeks earlier in multiparae.

• Chloasma - Pigmentation over forehead & cheeks

• Breast changes - 12 weeks of pregnancy -


Appearance of secondary areola and tubercles of
montegomerry
• Size of the uterus - The uterus becomes an
abdominal organ in second trimester • Elicited between 16 - 20 weeks of pregnancy
➢ Braxton hick contractions • Ballottement of uterus on bimanual examination
• Starts early and persists till term - Irregular, gives the impression of a floating object inside the
infrequent, spasmodic & painless contractions uterus.
without any effect on dilatation of the cervix • It may also be seen in case of uterine fibroid, ascites
• Intrauterine pressure is <8 mm of Hg or ovarian cyst
• Symptomatised as tightening of abdomen • External ballotment is elicited by 20 weeks and
internal ballotment from 16 – 28 weeks

➢ Palpation of fetal parts & active fetal movement


• Elicited by 20 weeks
• They are positive signs of pregnancy

➢ Ballottement of foetus ➢ Auscultation of fetal heart sound


• Most conclusive sign of pregnancy
• Begin in early pregnancy & continue till term
• Heard by stethoscope between 18-20 weeks of
pregnancy
• Fetal cardiac motion can be detected by doppler by
10 weeks

ARISE MEDICAL ACADEMY Dr. MIK | 29


• It is based on the rationale of
➢ Uterine souffle ➢ First trimester for exact SEDD
➢ Funic or fetal souffle ➢ Second trimester scan for congenital anomalies
➢ Third trimester scan for placenta, presentation, AFI
o SIGNS OF THIRD TRIMESTER etc

➢ LIGHTENING
• It is a sense of relief from the pressure symptoms THE FIRST TRIMESTER SCAN
due to engagement of the presenting part.
• lt is felt at 38th week in primigravida • The first definitive sign of confirming pregnancy is
• the visualisation of gestational sac
ULTRASONGRAPHIC DIAGNOSIS • The first sign of confirming intrauterine gestation is
the visualisation of yolk sac
• Ultrasound is the safest and best diagnostic tool in • Best parameter to assess the foetal age is crown
pregnancy rump length
• It is recommended that a patient undergoes 3 scans • It is always possible to visualise gestational sac,
in pregnancy, one in each trimester yolk sac and cardiac activity earlier by TVS than by
• The radiologists rule for calculating the gestational TAS
age is from the menstrual age and not from the
hour of fertilisation
VISUALIZATION TVS TAS
GESTATIONAL SAC 4w5d 5w3d
YOLK SAC 5 WEEKS 7 WEEKS
CARDIAC ACTIVITY 6 WEEKS 7 WEEKS

• Gestational sac is visualised with TVS at 4 and a half 5weeks - Gestation sac, embryo yolk sac
weeks and corresponds with 1000 mIU/L of hCG in
serum 6weeks - Fetal pole, cardiac activity
• Gestational sac is visualised with TAS at 5 and a half
weeks and corresponds with 6000 mIU/L of hCG in 7weeks - Lower limb buds, midgut herniation
serum (physiological)
• Using transvaginal transducers with frequency of 5
MHz, the size threshold for sac detection is 2 - 3 8weeks - Upper limb buds, stomach
mm.
• Mean sac diameter + 30 gives the gestational age 9weeks - Spine. Choroid plexus
• Failure to visualise the embryo when MSD is 6
indicates pregnancy loss CROWN RUMP LENGTH

• Best method of assessing gestational age


THE YOLK SAC THE SECOND TRIMESTER DIAGNOSTIC SCAN
• The yolk sac appears by 5 weeks in TVS and by 7 ➢ The intercerebellar or the trans cerebellar
weeks in TAS diameter is the best indicator of gestational age
• Absence of yolk sac denotes a blighted ovum or
when the scan is being performed between 14 – 28
miscarriage weeks
• The trans cerebellar diameter in mm equals the
gestational age in weeks
WEEKS OF MENSTRUAL AGE AND USG FINDINGS • The other parameter used in the second trimester
for age estimation is BPD ( bi parietal diameter)
4 week - Choriodecidual thickness, chorionic sac

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• The bi parietal diameter is measured in the trans • But, fertilization usually occurs about 14 days after
thalamic view at the level of the thalami and cavum the first day of the period. Thus, the true gestation
septum pellucidum period is to be calculated by subtracting 14 days
➢ Cephalic index = BPD divided by occipito frontal from 280 days, i.e. 266 days.
diameter (OFD) • This is called fertilization or ovulatory age and is
• It head shape is flattened (dolichocephaly) or widely used by the embryologist.
rounded (brachycephaly), then HC is more reliable
than BPD.
➢ Best indicator of fetal growth -Abdominal PSEUDOCYESIS or PHANTOM PREGNANCY or
circumference SPURIOUS PREGNANCY or FALSE PREGNANCY.
• So the best USG parameter to detect IUGR is
Abdominal circumference. • It is a psychological disorder where the women has
• The best USG parameter to detect Macrosomia is a false but firm belief that she is pregnant,
Abdominal circumference. although no pregnancy exists.
• AC is measured from the skin surface of the foetus • Patient is often infertile and has an intense desire to
at the level of stomach, left umbilical vein and have a baby.
portal sinus and spine visible
➢ Patient presents with:
• Cessation of menstruation.
FOETAL ANOMALIES IN SECOND TRIMESTER SCAN • Enlargement of abdomen (due to deposition of fat).
• Secretions from breasts.
• Fetal anomaly which can be earliest detected by • Fetal movement (actually intestinal movement).
USG- Anencephaly.

➢ On examination:
FOETAL ANOMALIES IN SECOND TRIMESTER SCAN • No positive signs of pregnancy are found i.e. fetal
heart sound is not heard, no fetal movement felt
• The two best ultrasonographic markers of Down and no fetal parts palpable by the examiner.
syndrome in first trimester are.
➢ Absent or hypoplastic nasal bone
➢ USG and Xray do not reveal any signs of
➢ Increased nuchal translucency
pregnancy.
➢ If a single ultrasound examination is planned for the
purpose of evaluating fetal anatomy, it is to be
performed at 18-20 weeks*. BASICS OF ANTENATAL CARE
➢ It is possible to demonstrate foetal skeleton
radiologically by 16th week THE ANTENATAL VISITS

➢ Ideally the schedule for antenatal visits should be:


THE THIRD TRIMESTER DIAGNOSTIC SCAN • Monthly visits upto 28 weeks.
• Two weekly visit between 28 and 36 weeks.
• The best parameter to detect gestational age in • Weekly visit from 36 weeks onwards
third trimester is femur length • This means a total of 12-15 visits.
• The best parameter to assess foetal growth is
abdominal circumference
DURATION OF PREGNANCY ➢ WHO recommends atleast 4 visits
• 1 st at - 16 weeks
• The duration of pregnancy has traditionally been • 2nd at - 24-28 weeks
calculated by the clinicians and radiologists in terms • 3rd at - 32 weeks
of ‘10 lunar months’ or ‘9 calendar months and 7 • 4th at - 36 weeks
days’ or ‘280 days’ or ‘40 weeks’, calculated from
the first day of the last menstrual period. ➢ As per Indian scenario - minimum 4 visits are
• This is called menstrual or gestational age. essential according to central guidelines

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• The first visit that a woman makes to a health care
facility is called the booking visit. VACCINATION IN PREGNANCY
• A booked case is one that has at least 4 ante natal
visits with at least two in the last trimester and • Killed vaccine are safe in pregnancy.
two doses of tetanus toxoid • Live vaccines are best avoided in pregnancy.
• Avoid all vaccines except tetanus toxoid in
FOLIC ACID pregnancy except indicated otherwise

• Folic acid is used to reduce the risk of neural tube KIEGELS EXERCISE
defect
• Prophylactic dose : ( to be given to avoid NTD) it is ➢ Kegels exercises - Time for initiating kegels
400mcg or 0.4mg exercise:
• Therapeutic dose : (to be given in females with • Pregnancy-1st trimester
previous history of baby with NTD) - 4mg. • After vaginal delivery-after 24 hrs
• Duration: should be started 1 month before • After cesarean section-after 24 hrs.
conception and continued till first 6-12 weeks of
pregnancy.

CHAPTER – 7

DIAGNOSIS IN OBSTETRICS AND FOETAL MEDICINE


FOETAL MEDICINE

SOURCES OF FOETAL TISSUE • A catheter is passed through the cervix or through


the abdominal wall into the uterus under
• Chorionic villus sampling ultrasound guidance, and a sample of chorionic villi
• Amniocentesis surrounding the sac is obtained.
• The chorionic villi are formed by trophoblast and
hence study material is trophablast.
• Chorionic villus sampling :

• Amniocentesis

• It can be performed trans abdominal method or


trans cervical
• Performed at 10-13 weeks.

ARISE MEDICAL ACADEMY Dr. MIK | 32


• It is an invasive procedure performed between 15 studied simultaneously by recording them ( graphy )
to 20 weeks for detecting fetal karyotype. on a single time frame
• It is done under ultrasound guidance using a 22 • A cardio tansducer is applied on the abdomen at
gauge spinal needle. the level of foetal heart ( measures the FHR) and a
• The spinal needle is passed through the mothers toco transducer is applied over the fundus of the
lower abdomen into the amniotic cavity inside the uterus ( measures the pressure)
uterus and 10-20 ml of amniotic fluid is collected.
• Amniotic fluid has cells from amnion, fetal skin and • Measurements on a CTG
lungs which are collected and cultured for fetal ✓ Baseline FHR – Tachycardia, Bradycardia, Baseline
karyotyping, biochemical and metabolic analysis. variability
✓ Accelarations
✓ Decelarations
MONITORING FOETAL WELL BEING • Baseline FHR
• Normal baseline FHR’s are

• Foetal well being is monitored by the following


• 12 – 30 weeks : 140 – 180 bpm
ways • 30 – 40 weeks : 120 – 160 bpm
• Cardiotocography • A normal component of foetal FHR is ‘ baseline
variability ’
• Non Stress Test
• Biophysical Profile and Manning Scores
• Abnormalities in baseline FHR are manifested as
• Foetal Scalp pH
• Foetal Tachycardia

• Umbilical artery Doppler


• Foetal Bradycardia

• MCA Doppler
CARDIOTOCOGRAPHY ✓ Baseline variability
• Unlike normal adult HR which is more or les fixed at
a particular level FHR is not fixed
• It is found to vary between 5 – 15 beats every 10 –
20 seconds
• Hence it changes at the frequency of 3 – 6 beats per
minute
• Due to this the FHR seen on CTG is saw toothed in
appearance
• ‘Baseline variability’ is best assessed during periods
of uterine relaxation during labour
• Too little or too much variability is abnormal

• Variability
• < 5 bpm : omnious
• 5 – 10 bpm : normal but keep under observation
• 10 – 20 bpm : healthy
• 20 – 25 bpm : normal but keep under observation
• > 25 bpm : critical observation
• It is a procedure wherein the foetal heart activity ( o Sinusoidal pattern
cardio) and the uterine contactions ( toco) are • Fixed or flat short-term variability.

ARISE MEDICAL ACADEMY Dr. MIK | 33


• Oscillation of the sinusoidal waveform above or • The dip is ‘ v’ shaped - The tip of ‘ V ‘ coincides with
below a baseline (smooth wave) the apex of uterine contaction - It starts
• Absence of accelerations. immediately after beginning of a contraction ( early)
- ----- - Ends with the end of contraction
✓ Foetal tachycardia • Short lived
• FHR >160 bpm observed over 10 minutes • Baseline FHR and baseline variability remain normal
• Mild tachycardia – upto 180 in between contactions
• Severe tachycardia – beyond 180
o Causes
o Causes
• Head compression
• Maternal fever due to 'amnionitis' is the
commonest cause, Maternal
parasympathomimetics (atropine) or ✓ Late decelaration
sympathomimetics (terbutaline), Epidural analgesia • The deceleration starts a little after the begenning
• ‘May’ indicate fetal compromise of contraction ( late decel) the time gap between
contaction and decel is called as lag phase
✓ Bradycardia : • Doesn’t reach the base line after the end of
contraction - It is usually ‘ U’ shaped and wide
• FHR <110 bpm observed over 10 minutes
mouthed - The lowest point of ‘U’ doesn’t co incide
with the height of contraction
o Causes • It is long lasting
• Hypoxemia, Due to mild head compression in the • FHR may not reach baseline between late
second stage of labour, Mild cord compression decelarations
• Indicates serious fetal compromise
- ------ • Always indicates foetal distress
• Accelarations
✓ Variable deceleration
• It is defined as a sudden increase in FHR by at least
15bpm for at least 15 seconds
• As the word suggests they are variable with no
• At least one contraction should occur in 15 minutes
relation with uterine contactions
• Presence of accelarations is indicative of a normal
• They may come sometimes during contractions also
foetus with intact neurohumoral and cardio
co incidentally
vascular system

• Absence of accelarations is a sign for concern
- ------ • Always indicates a disturbance in umbilical blood
flow
• Deceleration
• A decrease in FHR by at least 15 bpm for atleast 15 Non Stress Test
seconds is called deceleration
• A deceleration shouldn’t last longer than 2 minutes
otherwise it is considered more of a bradycardia
• It is of three types
• Early deceleration ( type 1 dip)
• Late decelation ( type 2 dip)
• Variable deceleration
• Presence of any type of deceleration is indicative of
distress or problem

✓ Early deceleration

ARISE MEDICAL ACADEMY Dr. MIK | 34


o Non reactive test
• To be called as non reactive, there should be <2
accelerations or no accelerations in a period of n40
minutes (to exclude those cases in which fetus
might be sleeping in first 20 minutes)
• A non reactive non stress test should be followed by
contraction stress test.
• Most common condition for non reactive NST - fetal
hypoxia.
• Sometimes a sleeping normal foetus gives a non
reactive NST
• For this problem we can either do
✓ A vibroacoustic stimulation which wakes up the
sleeping foetus
✓ Wait for the foetus to wake up

• It is the most commonly used test for antepartum • Timing


evaluation of the fetal status.
• Testing should begin by 32 to 34 weeks.
• Principle :
• In pregnancies with severe complications, begin at
• The test looks for the presence of temporary 26 - 28 weeks.
accelarations of fetal heart rate (FHR) associated
with fetal movement.
• In case test is being performed before 32 weeks,
accelerations are defined as having 10 bpm or more
• Presence of spontaneous fetal heart rate above baseline for 10 seconds or longer ( not 15 )
acceleration associated with fetal movements is an
indicator of fetal well being
• Interval between NST testing
• Absence of fetal reaction suggests the possibility of
fetal hypoxia
•Ideally - repeat weekly
✓ Method : •In high risk pregnancies like diabetes mellitus,
IUGR and Gestational hypertension twice
• Place patient in the semi-Fowler's position. weekly
• Apply the tococardiographic equipment to the •In severe preeclampsia remote from term -
maternal abdomen, and observe the uterine activity done daily
and FHR for 10 minutes.
• Instruct the patient to push the calibration button
of the uterine contraction tracing every time she Biophysical Profile (BPP)
feels fetal movement. Biophysical score
• Interpretation :
o Reactive or Positive NST - 2 or more accelerations
of at least 15 beats per minute, each lasting for at
• Manning proposed a method using 5 fetal
biophysical variables to assess the status of fetal
least 15 seconds and occurring within 20 minutes of
well being antenatally.
the beginning of the test.
• If in 20 minutes test is not reactive, do a 20 minute
repeat test to account for fetal sleep cycle before • These 5 variables are
concluding the test or awaken the foetus by • Fetal Tone
vibroacoustic stimulation • Fetal Breathing Movements (seen in 30 minutes)
• Reactive test means that fetus is in no danger for at • Fetal gross body Movements (seen in 30 minutes)
least 7 days. • Amniotic Fluid Volume
• Non stress test

ARISE MEDICAL ACADEMY Dr. MIK | 35


• Diastolic flow is inversely related to peripheral
• The variables are observed for atleast 30 minutes resistance
and assigned a score of 2 each to normal variables • If there is a reduction in the EDF and increase in the
and a score of to abnormal variables. resistance indices it suggests increased resistance to
• Thus the highest score possible for a normal fetus is flow as in preeclampsia ( placental vessel spasm)
10. and IUGR.
• A score of 8 to 10 is normal, 6 is equivocal and 5 or
less is abnormal • There are three abnormal flow patterns
• reduced EDF
• absent EDF
DOPPLER STUDIES
• reversal of flow.
• Doppler ultrasound is used to assess the uterine,
placental and fetal arterial and venous system.
• Doppler detects the direction of blood flow, the
amount of blood flow and the velocity of flow
• Two special tests used are
• Umbilical artery doppler
• Middle cerebral artery doppler

• UMBILICAL ARTERY DOPPLER

• Umbilical artery vessels:


• Blood flow across the umbilical arteries provides a Middle Cerebral Artery (MCA) Doppler
comprehensive overview of the maternal - fetal
blood supply and helps in detecting fetal circulatory
compromise.
• Normally the middle cerebral vessels have high
• The systolic component of blood flow reflects the resistance flow and are characterised by little
cardiac pump diastolic flow.
• The diastolic component the distal vascular bed ( • In case of IUGR a brain-sparing effect is seen with a
placenta) reduction in the resistance indices in the middle
• cerebral vessels (i.e. increased flow) due to the
• The umbilical artery is characterised by forward low shunting of blood to the brain in IUGR.
resistance flow.
• As gestation increases, there is gradual fall in all the
resistance indices so the amount of forward Fetal Scalp Ph
diastolic flow increases
• Normal fetal scalp pH ranges from 7.25 to 7.35.

ARISE MEDICAL ACADEMY Dr. MIK | 36


• Fetal hypoxia is indicated by 'acidosis' or fall in fetal It is used to corroborate the significance of fetal
scalp pH to values below normal

FETAL GROWTH

• Fetal growth is characterized by sequential patterns of tissue and organ growth, differentiation, and maturation.
• Fetal growth has been divided into three phases.
• The initial phase of hyperplasia occurs in the first 16 weeks and is characterized by a rapid increase in cell number.
• The second phase, which extends up to 32 weeks' gestation, includes both cellular hyperplasia and hypertrophy
•After 32 weeks, fetal growth is by cellular hypertrophy, and it is during this phase that most fetal fat and glycogen are
accumulated.

GESTATIONAL AGE AND BIRTH WEIGHT

• Previously, the birth weight of < 2500 g was taken as the index of prematurity without taking any consideration of
the gestational period or any other factors.
• But now it is not so
• Gestational age has to be correlated with the weight to get an idea of the condition of the baby
• Therefore, survival outcome of an infant depends both on the gestational age as well as on the birth weight

TERMINOLOGY

• Small for gestational age (SGA): Birth weight less than 10th percentile for gestational age
• Appropriate for gestational age (AGA): Birth weight lies between the 10th and 90th percentiles for gestational age
• Large for gestational age (LGA): Infant's birth weight above the 90th percentile for gestational age
• Low birth weight (LBW) infant is defined as one whose birth weight is less than 2500 g irrespective of the
gestational age.
• Very-low birth weight (VLBW) infants weigh 1500 g or less
• Extremely-low birth weight (ELBW) infants weigh 1000 g or less

ARISE MEDICAL ACADEMY Dr. MIK | 37



Types of SGA Fetus

• Based on clinical evaluation and ultrasound examination there are two types of SGA babies ie type 1 and type 2

• Type 1 – 70% (apparent IUGR)


• Type 2 – 30% (true IUGR)
• symmetrical – 20% (more dangerous)
• assymmetrical – 80% (less dangerous)

• Type 1
• Fetuses that are small and healthy
• They have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course.
• They constitute about 70% of SGA infants
• Birth weight below the 10th percentile are found normally grown.
• They are constitutionally small and not at any increased risk for adverse outcome. They present at the end of the
normal spectrum for growth

• Type II
• They constiturte 30% and are truly growth restricted.
• Fetuses where growth is restricted by pathological process (true IUGR)
• All these babies are growth retarded and as such are considered abnormal/ pathological
• These are further divided into symmetrical IUGR (20%) and asymmetrical IUGR (80%).

• Symmetrical IUGR (20%):


• The fetus is affected from the noxious effect very early in the phase of cellular hyperplasia.
• The total cell number is less.
• This form of growth retardation is most often caused by structural or chromosomal abnormalities or congenital
infection (TORCH).
• The pathological process is intrinsic to the fetus and involves all the organs including the head
• Good feeding after birth doesn’t resolve the problem

• Asymmetrical (80%)
• The fetus is affected in later months during the phase of cellular hypertrophy.
• The total cell number remains the same but size is smaller than normal.
• The pathological processes that too often result in asymmetric growth retardation are maternal diseases extrinsic to
the fetus.
• These diseases alter the fetal size by reducing uteroplacental blood flow or by restricting the oxygen and nutrient
transfer or by reducing the placental size.(intra uterine malnutrition)
• Good feeding after birth resolves the problem

CAUSES OF IUGR

ARISE MEDICAL ACADEMY Dr. MIK | 38


➢ MATERNAL CAUSES :
✓ Constitutional, Small mothers, Poor maternal
nutrition during pregnancy, Social deprivation
✓ Toxins: Alcohol, Smoking, Heroin, Morphine, CEPHAL HAEMATOMA AND CAPUT SUCCEDANEUM
Cocaine
✓ Drugs: Chemotherapeutic agents, Warfarin and ➢ Cephalhaematoma:
Phenytoin
• Maternal diseases - Chronic hypertension/PIH,
Thrombophilia, Hemoglobinopathy, Heart diseaseQ
Class III and IV, Chronic renal disease, Collagen
vascular disease, Diabetes with vascular lesion,
Sickle cell anemia

✓ FOETAL CAUSES - Structural anomalies,


Cardiovascular, Renal, Osteogenesis imperfect,
Chromosomal abnormalities - Trisomy 13, 18, 21,
Turner syndrome, Infections
➢ Placental :
• Causes leading to poor uterine blood flow to the
placental site for long time, i.e. placental
insufficiency - Placenta praevia, Abruption
Infarction
• Collection of blood in between the pericranium (
COMPLICATED CAUSES
periosteum of skull bone) and the flat bone of the
skull due to rupture of a small emissary vein from
➢ Maternal Anaemia:
the skull.
• Maternal anemia does not causes fetal growth
restriction
• It may be associated with fracture of the skull bone.
• Usually unilateral.
➢ Maternal Diabetes and IUGR • Lies over a parietal bone.
• Insulin dependant diabeties, Diabetic Vasuclopathy • Caused generally by forceps delivery but may also
and excessively tight control of diabetes mellitus in be met with following a normal labour.
pregnancy has been linked to intrauterine growth • Ventouse application does not increase the
restriction incidence of cephalhaematoma.
• Gestational diabetes is associated with macrosomia • It is never present at birth but gradually develops
after 12-24 hours of birth and disappears by 6-8
weeks
➢ Maternal short stature and IUGR • It is circumscribed, soft, fluctuant, and
• While an arbitrary measurement of 5ft. is incompressible.
considered as short stature in western countries, it
is 4'7" in India considered the low average height. • The swelling is limited by the suture lines of the
• A short statured mother has a constitutionally small skull as the pericranium is fixed to the margins of
baby and not IUGR the bone.
• No active treatment is necessary.
➢ Maternal Smoking and IUGR • Prognosis is good.
• It is the single most preventable cause of IUGR ➢ Caput succedaneum

ARISE MEDICAL ACADEMY Dr. MIK | 39


• Presents at about 7 - 10 days after birth.
• Situated at the junction of upper and middle third
of the muscle.
✓ Etiology
• Rupture of sternocleidomastoid muscle fibres and
blood vessels due to
- Hematoma and cicatricial contracture

- Difficult breech delivery


• This is a localised swelling of the scalp due to - Attempted delivery after shoulder dystocia
effusion of serum above the periosteum.
• There is obstruction of venous and lymphatic return - Excessive lateral flexion of neck following normal
of the foetal head due to pressure by the cervix. delivery.
• This leads to stagnation of fluid and oedema over
scalp ✓ Clinical features : Transient torticollis
• Site of the caput depends upon the position of the ✓ Treatment:
head. – No treatment required, disappears spontaneously
• It is present at birth and disappears by about 24 - by 6 months
36 hours. – Gentle movements and stretching of muscle done
• The size indicates the amount of pressure on the after feeds
head. – Do not massage
Sternomastoid tumour / Hematoma

ARISE MEDICAL ACADEMY Dr. MIK | 40


CEPHALHAEMATOMA CAPUT SUCCEDANEUM

Sharply circumscribed Diffuse

Soft but does not pit on pressure Soft and pits on pressure

Under the periosteum Above the periosteum

Does not cross suture lines Lies over and crosses suture lines/midiine

Fixed in one place Movable over dependant part

May be associated with fracture Not associated with fracture

Appears some time after birth, grows larger Largest at birth

disappears only after weeks or months Immediately starts to

regress and disappears in a few hours

CHAPTER – 8

ABORTION

✓ Blighted ova: Those early pregnancy losses in which


fetal development is not observed with ultrasound
➢ Nomenclature (so that only a gestational sac is present with or
• Abortion is the expulsion or extraction from its without a yolk sac) and fetal tissue is absent on
mother of an embryo or fetus weighing 500 g or histologic examination of the products of
less when it is not capable of independent survival conception.
(WHO).
• This 500 g of fetal development is attained ✓ Early Fetal demise: Those early pregnancy losses in
approximately at 22 weeks (154 days) of gestation. which fetal development is clearly observed by
ultrasound and fetal tissue is found on the
histologic examination.
EARLY PREGNANCY LOSS
• The difference between these two types of abortion
• Early Pregnancy loss is of two main types
is of fundamental importance.
➢ Blighted ovum
➢ Early Foetal demise
• The lack of development of fetal structures as in
blighted ovum defines a subset of abortions of

ARISE MEDICAL ACADEMY Dr. MIK | 41


genetic origin. Therefore, the patients with blighted
ova do not require extensive work up
[ foetal pahology] • Incomplete Abortion
• Here the entire products of conception are not
• In contrast, the early interruption of fetal life is a expelled but a part is left inside the uterine cavity.
complex phenomenon with multiple
✓ C/o - ongoing moderate to heavy bleed
etiologies.these are those patients who have
aborted cytogenetically normal fetuses and need an
✓ O/E - Uterus – less than gestational age & Cx -
Internal os is open
extensive search for non genetic factors responsible
for the pregnancy loss. [maternal pathology] ✓ USG – products of conception in uterine cavity
SPONTANEOUS ABORTION

Spontaneous abortion: unexplained natural abortion is ➢ Missed Abortion


called spontaneous abortion • When the fetus is dead and retained inside the
uterus for a variable period, it is known as missed
Recurrent abortion: It is defined as a sequence of three abortion
or more consecutive spontaneous abortion before ✓ C/o - no bleed, no morning sickness and regression
20 weeks. of breast changes
✓ O/E - Uterus – lesser than gestational age ( arrested
Its types are – Threatened, Inevitable, Complete, at the stage when foetus was lost) Cx - Internal os
Incomplete & Missed is closed
✓ USG – dead foetus
• Threatened Abortion
• It is a clinical entity where the process of abortion
has started but has not progressed to a state from SPONTANEOUS ABORTION
which recovery is impossible
✓ C/o - Slight bleeding ➢ Incidence:
✓ O/E - Uterus - corresponds to gestational age, Cx - • Of all the spontaneous abortions 50-75% are due to
Internal os is closed chromosomal anomalies (Germplasm defect).
✓ USG - live foetus with subchorionic haemorrhage

➢ Aetiology
• Inevitable Abortion • Maternal
• It is a clinical entity where process of abortion has • Foetal
progressed to a state from where continuation of
pregnancy is impossible
✓ C/o - heavy bleeding and severe pain ➢ Foetal
• Chromosomal abnormalities
✓ O/E - Shock, Uterus - corresponds to gestational
• Hydropic degeneration of villi
age or less, Cx - Internal os is open
• Multiple pregnancy
✓ USG – dead foetus

➢ Maternal
• Complete Abortion • Maternal infections like: TORCH infections, malaria,
• Here the products of conception are expelled en ureoplasma, chlamydia, brucella and spirochaetes
masse. • Maternal medical disorders like: Hypertension,
✓ C/o - severe bleed which stopped Chronic renal disease, Cyanotic heart disease and
✓ O/E – Shock, Uterus – less than gestational age, Cx - Hemoglobinopathies
Internal os is closed • Endocrine problems like: Luteal phase defect
✓ USG – empty uterine cavity (deficiency of progesterone), Thyroid abnormalities

ARISE MEDICAL ACADEMY Dr. MIK | 42


hypothyroidism, Poorly controlled diabetes mellitus
and PCOD
• Immunological causes: Antiphospholipid antibody 1.Parental peripheral blood karyotyping with banding
syndrome, Inherited thrombophilias technique
• Anatomical factors: Cervical incompetence,
Mullerian anomalies, Large and multiple submucous • Karyotyping of the both partners is recommended
leiomyoma, Ashermann syndrome & DES exposure in recurrent miscarriage.
in utero • Prenatal diagnosis is usually advised in the next
• Others like Trauma; Subchorionic hematoma; pregnancy.
Defective placentation
• Environmental factors like: Alcohol, Caffeine,
Exposure to radiation (> 5 rads) and Anaesthetic 2. Assessment of the intrauterine cavity with either
gases office hysteroscopy or hysterosalpingography.

• Anatomic malformations and diseases like big


➢ CHROMOSOMAL ANOMALIES AS AN AETIOLOGICAL
fibroid can cause recurrent pregnancy loss
FACTOR FOR SPONTANEOUS ABORTION

3. Thyroid function tests


• Majority of genetically originated abortions occur
before 8 weeks and are blighted ova
• Hypothyroidism is an important cause of recurent
• Commonest cause of early miscarriages are due to abortions
chromosomal abnormality
• Commonest chromosomal abnormality is
autosomal trisomy - Commonest chromosome - 4. Anticardiolipin antibody and lupus anticoagulant
chr. 16 testing (aPTT or Russell Viper venom testing)
• Other common trisomies are of chromosome 13,
18, 21 and 22, although any chromo-some except • This is an important cause of recurrent abortions
chromosome 1 can be involved • SLE is an established cause for recurrent abortion
• Apart from trisomies, triploidy, monosomy X and • SLE is associated with antiphospholipid syndrome
tetraploidy are also seen frequently (anti-cardiolipin antibodies)

RECURRENT ABORTIONS 5.Parental blood grouping and coombs test


It is defined as a sequence of three or more consecutive • Rh incompatibility is a known cause for
spontaneous abortion before 20 weeks. spontaneous abortion and may lead to recurrent
abortions if it remains unrecognized
➢ Aetiology
• The most common cause of recurrent abortions is
incompetent cervix 6.Thrombophilia testing:
• The most common cause of recurrent first trimester
abortions is chromosomal anomalies of which most • Factor V leiden, prothrombin gene mutation, Protein
common is balanced translocation in mother S activity.
• The most common cause of recurrent second • In the presence of a family or personal history of
trimester abortion is incompetent cervix venous thromboembolism, protein C and
• Infections don’t cause recurrent abortions **** antithrombin activity

➢ WORKING UP OF A CASE OF RECURRENT 7. Blood Glucose and Hb A1C


PREGNANCY LOSS

ARISE MEDICAL ACADEMY Dr. MIK | 43


• In women with recurrent pregnancy loss, evaluation ➢ SEQUELAE:
with blood glucose and HbA 1 C level is indicated for • Chronic pelvic pain & Tubal block and infertility
those with known or suspected diabetes, but
otherwise it is unwarranted
ANTIPHOSPHOLIPID ANTIBODY SYNDROME
8.Serum homocysteine level.

➢ INFECTIONS AS AN AETIOLOGICAL AGENT FOR It is a treatable, autoimune disorder associated with


RECURRENT PREGNANCY LOSS recurrent second trimester pregnancy loss

• All causes of spontaneous abortion may cause Antiphospholipid antibodies are acquired antibodies
recurrent abortions EXCEPT infections targeted against a phospholipid.
• TORCH profile should not be included in the set of
investigations done to find out the cause of They can be IgM, IgG or IgA
recurrent abortion
• Syphillis lead to recurrent abortions. *** Most important antiphospholipid antibodies are:

✓ Lupus anticoagulant
Septic Abortion ✓ Anticardiolipin antibody
✓ BFP-ST
Septic abortion: Any abortion associated with clinical
evidences of infection of the uterus and its contents is
called Septic abortion. THE SYNDROME

➢ CRITERIA FOR SEPTIC ABORTION: ➢ PATHOGENESIS


• Rise of temperature is at least 100.4-degree F for 24 The antiphospholipid antibody syndrome is
hours or more. characterised by an increased tendency for
• Presence of offensive or purulent vaginal thrombosis
discharge.
• Presence of other evidence of pelvic infection such Placetal thrombosis decreases the blood supply to
as lower abdominal pain and tenderness. placenta causing - Smaller size of placenta, PIH,
• In majority of the cases the infection occurs Foetal loss, IUGR
following illegal induced abortion but may occur
following spontaneous abortion. ➢ Clinical features
• Infection is polymicrobial from the normal flora of
✓ General Medicine
genital tract and is due to gram positive, gram
• It is due to arterial occlusion(less common) or
negative and anaerobic pathogens.
venous occlusion(more common)
• The following are its manifestations
➢ CLINICAL PRESENTATION
1. Venous thrombosis (more common)
• Patients will present with fever, abdominal pain,
2. CNS – Stroke
purulent offensive vaginal discharge and vomiting.
3. Heart - Myocardial infarction
4. Lungs - Pulmonary hypertension
5. Kidney - Glomerular Thrombosis due to Renal
➢ COMPLICATIONS:
artery occlusion
• Uterine infection i.e. endomyometritis (M/C
6. Bones - Avascular Necrosis
manifestaion) parametritis, peritonitis, septecemia
• ARDS (M/c cause of death) , DIC and Acute renal
failure
➢ Clinical features

ARISE MEDICAL ACADEMY Dr. MIK | 44


➢ Obstetrics ➢ DIAGNOSIS:
1.Recurrent spontaneous abortions
2.Pregnancy induced hypertension ✓ History: The typical history of painless rupture of
membranes followed by the quick delivery of a live
(Preeclampsia and eclampsia) fetus in midtrimester is very suggestive

3. Placental insufficiency/Abruption ✓ Non pregnant state


• The internal os allows the passage of a No. 8 Hegar's
4. Intrauterine Growth retardation cervical dilator or Foley's catheter filled with 1 ml
water without resistance.
5. Post partum comlicatons like pulmonary infiltrates,
• Premenstrual Hysterocervicography will show the
fever and cardiac symptoms typical funneling of
the internal os
Management

• Treatment as proposed by ACOG is a combination ✓ In Pregnancy:


of low dose aspirin (81 mg) daily and low molecular • Transvaginal ultrasound is the ideal method to
weight heparin (LMWH) in prophylactic doses (e.g. follow up and detect early incompetence.
dalteparin 5000 units S/C twice daily), started as • The normal cervical length at 14 weeks is 35 - 40
soon as pregnancy is confirmed, mm.
• A cervical length less than 25 mm and funneling of
the internal os > 1 cms on USG indicates cervical
CERVICAL INCOMPETENCE
incompetence.
Cervical incompetence is characterised by painless
cervical dilatation in the second or early third
➢ TREATMENT
trimester • The treatment is surgical by a cervical circlage.
It is characterised by ballooning of the amniotic sac into
the vagina, followed by rupture of membranes and ➢ Time of operation:
expulsion of a usually live fetus.
• Cervical circlage is usually delayed up to 12 -14
The usual timing is 16 to 24 weeks. weeks so that miscarriage due to other causes can
be eliminated
➢ AETIOLOGY: • it should be done atleast 2 weeks earlier than the
lowest period of earlier wastage (but never earlier
✓ Congenital than 1O weeks).
• Developmental weakness of cervix.
• Associated with uterine anomalies like septate
uterus. ➢ Note: Sonography should be done prior to circlage
• Following in utero exposure to diethyl stilbestrol. to confirm a live fetus and to rule out anomalies.

✓ Acquired due to previous cervical trauma ➢ Removal of Cerclage Stitch:


• Forcible dilatation during MTP and D and C. • The Stitch should be removed at 37 - 38 week or
• Conisation of cervix. earlier if labour pain starts or features of abortion
• Cauterisation of cervix. appear.
• Amputation of cervix or Fothergill's operation.
➢ Circlage is of two types

ARISE MEDICAL ACADEMY Dr. MIK | 45


✓ Vaginal circlage • Only a qualified registered medical practitioner
• Mc Donald’s suture possessing prescribed experience can terminate
• Shirodkars suture pregnancy.
• ChiefMedical Officer of the district is empowered
to certify that a doctor has the necessary training to
✓ Abdominal circlage do abortions based on these criteria
1. RMP with 25 MTPS done in approved institution

MEDICAL TERMINATION OF PREGNANCY 2. 6-month housemanship in Obstetrics and


Gynecology
Medical Termination of Pregnancy Act, 1971
3. Post graduate qualification in Obstetrics and
In India, the MTP act was passed in August 1971 and Gynecology
came into effect from April 1972.
4. 3 years practice in Obstetrics and Gynecology who
In extends to the whole of India except in the state of are registered before 1971
Jammu and Kashmir.
5. 1 year practice in Obstetrics and Gynecology for
➢ Indications those registered on or after the date of
commencement of the act
✓ Therapeutic:
• When the continuation of pregnancy endangers the
life of woman or may cause serious injury or harm ➢ WHERE CAN IT BE DONE
her physical or mental health. • The pregnancy should be terminated in
Government hospitals, or in the hospitals
recognised by the Government for this purpose
✓ Humanitarian • Non-governmental institutions may take up
• When pregnancy has been caused by rape. abortion if they obtain a licence from Chief Medical
Officer of the district

✓ Social:
• When pregnancy has resulted from the failure of ➢ PATIENT PROTECTION
contraceptive methods in case of a married • The consent of the woman is required before
woman, which is likely to cause serious injury to conducting abortion.
her mental health. • Written consent of the guardian is required if the
• When social or economic environment, actual or woman is a minor (<18 years) or a mentally ill
reasonably expected can injure the mother's health. person.
• Consent of husband is not necessary.
• Abortion cannot be performed on the request of
the husband, if the woman herself is not willing.
• The woman need not produce proof of her age/
✓ Eugenic: Sexual assault
✓ When there is risk of the child being born with • The statement of the lady is accepted without any
serious physical or mental abnormalities. doubt and she need not prove it.
• It is enough for the woman to state that she was
raped, and it is not necessary that a complaint was
LEGISTATION RULES lodged with the police.
• Professional secrecy has to be maintained.
➢ WHO CAN DO THE MTP • The Admission Register for the termination of
pregnancies is secret document, and the

ARISE MEDICAL ACADEMY Dr. MIK | 46


information contained therein should not be • Dilatation and evacuation (Rapid method/Slow
disclosed to any person. method)

➢ WHEN CAN THE TERMINATION BE DONE ➢ SECOND TRIMESTER


• If the period of pregnancy is below 12 weeks, it can ✓ Medical
be terminated on the opinion of a single doctor. • Prostaglandins PGE1 (Misoprostol), 15
• If the period of pregnancy is between 12 and 20 methylPGF2a (Carboprost), PGE2 (Dinprostone)
weeks, two doctors must agree that there is an and their analogues (used-intravaginally,
indication and once the opinion is formed, the intramuscularly or intra-amniotically)
termination can be done by any one doctor. ✓ Surgical
• Termination is permitted upto 20 weeks of • Dilation and evacuation
pregnancy only. • Intrauterine instillation of hyperosmotic solutions
- Intra-amniotic hypertonic urea (40%), saline (20%)
- Extra-amniotic—Ethacrydine lactate,
➢ EXCEPTION Prostaglandins
• In an emergency, pregnancy can be terminated by - (PGE2, PGF2a)
a single doctor, even without required training • Hysterotomy (abdominal)— less commonly done
(even after twenty weeks even without consulting
a second doctor, in a private hospital which is not
recognised.) ➢ Most suitable method for 2nd trimester abortions is
by prostaglandins

➢ PUNISHMENT
• The termination of pregnancy by a person who is ➢ Mifepristone + Misoprostol
not registered medical practitioner, the person • 200 mg of mifepristone is given orally on day 1
concerned is punishable followed 2 days / 48 hrs later by
• The termination of pregnancy in an unrecognised • Vaginal misoprostol 800 mcg (4 tablets of 200mcg
hospital , the administrative head) shall be punished each) is placed in the posterior fornix of vagina
• with rigorous imprisonment for a term which shall •
not be less than two years, but which may extend to • The combipack of 1 tablet mifepristone and 4
seven years. tablets misoprostol (i.E. 5 tablets) is approved by
DGHS, govt, of india.

• Mifepristone blocks progesterone receptors in the


endometrium which leads to disruption of the
embryo, production of prostaglandins and a
decrease in human chorionic gonadotropin levels.
METHODS OF PERFORMING MEDICAL TERMINATION • Combination of mifepristone and misoprostol is
OF PREGNANCY effective for inducing abortion within 63 days of
amennorhea
➢ FIRST TRIMESTER
✓ Medical MENSTRUAL REGULATION
• Mifepristone and Misoprostol (PGE,)
✓ Surgical • Consists of aspiration of contents of uterine cavity
by means of plastic cannula (Karman's cannula) and
• Menstrual regulation
a plastic 50 cc syringe.
• Vacuum Aspiration (MVA/EVA)
• Suction evacuation and/or curettage

ARISE MEDICAL ACADEMY Dr. MIK | 47


• It is carried out effectively within 14 days of missed ➢ Dilatation and currettage
period. • it is the second most common method of first
trimester abortion
➢ Suction Evacuation • The cervix is dilated with hegars dilators
• It is the most suitable method for 1st trimester • The whole uterine cavity is curetted with a curette
abortions.
• It is done under local anaesthesia / paracervical
block. ➢ Intrauterine extra amniotic instillation
• The cervical os is first dilated using Hegar's dilators. • Ethacridine lactate is drug of choice for extra-
• Instrument used for evacuation is Karman suction amniotic instillation
cannula. • Available as injection Emcredil (0.1%)
• Diameter of suction cannula should be equal to the • Foleys catheter is introduced into extra-amniotic or
weeks of gestation. extra-ovular space and bulb is inflated by 10-20 ml.
• Suction pressure is 60-70 cms of water of Ethacridine solution.
• The end point of suction is denoted by: • Dose is calculated as 10ml/week of gestation upto
1 No more material sucked out. maximum of 150 ml
• Catheter is left for 6 hrs.
2. Gripping of the cannula by the contracting smaller • Uterine action begins in 16-18 hrs.
uterus. • In 30% cases abortion is incomplete and requires
3. Grating sensation. oxytocin drip or supplementation with
4. Appearance of bubbles in the cannula. prostaglandin.

CHAPTER – 9

ECTOPIC GESTATION

An ectopic gestation is the one in which the fertilized


ovum implants and develops outside the normal
endometrial cavity ✓ Uterine ectopics (1.5%)
• Cervical ( 1% ) - commonest
• It could be • Angular
✓ uterine ( 1.5%) • Cornual
✓ extra uterine ( 98.5%) • Scar ( cesarean )

ARISE MEDICAL ACADEMY Dr. MIK | 48


• Contraception failure
• Previous genital infection
✓ Extrauterine ectopics (98.5%)
• Multiple partners
• Tubal (97%) – commonest
• In utero DES exposure.
• Abdominal ( 1%)
• Ovarian ( 0.5% )
✓ Slight risk

The criteria
• Previous pelvic or abdominal surgery
• Smoking
• Douching
• Intercourse before 18 years
✓ Primary Abdominal Pregnancy
✓ Studiford criteria
Risk Factors In Ectopic

✓ Ovarian pregnancy ✓ Contraception


✓ Speilberg’s criteria • With any form of contraceptive, the absolute
number of ectopic pregnancies is decreased
because pregnancy occurs less often.
✓ Cervical pregnancy
✓ Rubin’s criteria
✓ Pelvic Inflammatory Disease
• M/C cause of ectopic pregnancy is PID
TUBAL PREGNANCY

• It refers to the implantation in the fallopian tube


• It order of occurrence they are
✓ Ampulla ( 55% )
✓ Isthmus ( 25 %)
✓ Infundibulum ( 18%)
✓ Interstitial ( 2% )
Pathology of Ectopic Gestation
• Risk Factors for ectopic pregnancy:
✓ Decidualisation in ectopic pregnancy
✓ High risk
• In ectopic pregnancy under the hormonal
• Tubal corrective surgery (M/c risk factor) influence of Progesterone and Estrogen uterine
• Tubal sterilization endometrium is converted to decidua (Similar to
• Previous ectopic pregnancy Intrauterine pregnancy)
• Artificial reproductive technology • But ectopic can not survive for a long time
• Pelvic inflammatory disease • When the ectopic is interrupted
• Documented tubal pathology • Levels of progesterone and Estrogen decrease
• Congenital tubal anomalies withdrawal of support to uterine endometrium
(decidua) leads to it’s shedding off in the form of
Decidual cast
✓ Moderate risk
• Infertility treatment with CC

ARISE MEDICAL ACADEMY Dr. MIK | 49


✓ Arias Stella Reaction • “ History of acute abdominal catastrophe with
• It is a histological change seen in endometrium fainting attack and collapse i.e. shock following
when it is undergoing decidualisation if the short period of amenorrhea, in a woman of child
progesterone support to it is suddenly lost bearing age always points towards ectopic
• It indicates loss of hCG stimulus to release pregnancy (ruptured) unless proved otherwise “
progesterone • The above triad may be accompanied by nausea,
• Seen in - ectopic pregnancy, blightening of vomiting, fainting attacks or syncope.
conceptus, abortion • Patient may present in shock with pallor,
tachycardia, hypotension and cold clammy
extremities.
o Villi are absent – it is an ectopic • Internal hemorrhage floods the peritoneal cavity
o Villi are present - it is a failed intrauterine and irritates the undersurface of diaphragm and
pregnancy phrenic nerve, the patient complains of shoulder
tip and epigastric pain.

PRESENTATION OF A TUBAL PREGNANCY


✓ General Examination:
• A patient with a tubal pregnancy may present to us • Pallor + VE
in two ways
• BP - decreased
✓ Unruptures ectopic
• Slight intermittent pyrexia due to absorption of
✓ Ruptured ectopic products of degeneration.

• The diagnostic methods, investigative approach ✓ Per abdominal Examination


and management techniques vary according to the
• Per Abdomen - Abdomen is tense, tender and
presentation
distended.
• Shifting dullness may be present (depending on
❖ Ruptured ectopic pregnancy the amount of hemorrhage).
• Ectopic pregnancy is the leading casue of early • Rigidity / muscle guarding
pregnancy related deaths. • Cullen's sign - bluish discolouration around the
• Most common casue of death in ectopic pregnancy umbilicus may be present.
is tubal rupture —> severe hemorrhage —> death.
✓ Symptoms - In Ectopic pregnancy triad of:
• Abdominal pain (seen in 100% cases, it is the most ✓ On Bimanual examination
consistent symptom of ectopic pregnancy). • Vaginal mucosa appears blanched.
• Amenorrhea (seen in 75% cases) • Uterus: normal size / slightly bulky.
• Appearance of vaginal bleeding are seen • Extreme tenderness on cervical movement
• Amenorrhoea followed by pain followed by vaginal • Fornices – tender
bleed (tenderness in pelvis is the most constant sign of
• Amenorrhoea of 1 – 2 months Ectopic pregnancy).
• Abdominal pain is severe and localised to lower • U/L adnexal mass is palpable in one third to half of
abdomen, spasmodic in nature
patient and usually well separated from ovary
• Vaginal bleed almost always small but persistent
and consists of dark altered fluid blood or dark
coagulated blood. ✓ Culdocentesis:

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• It is a simple technique used to identify • Most common and the most consistent symptom
hemoperitoneum. of ectopic pregnancy (undisturbed) is Abdominal
• Fluid is aspirated from cul-de-sac via posterior pain.
fornix with the help of a needle. • It is seen in 95-100% cases.
• If non clotting blood is obtained, it is indicative of • Pain is located in the lower abdomen / pelvic
an intraperitoneal bleed and probably a ruptured region.
ectopic. • It can be unilateral or bilateral.
• If the aspirated blood clots, it may have been • The confusing points are
obtained from an adjacent blood vessel rather than ✓ Absence of vaginal bleed
from bleeding ectopic pregnancy.
✓ Abdominal pain follows vaginal bleed
( cf Ruptured ectopic)
❖ Unruptured Ectopic Pregnancy
✓ Patient is stable and vitals are normal
✓ An adnexal mass on palpation
• It is also called chronic or sub acute ectopic ✓ Culocentesis may or may not reveal blood
• It is very difficult to daignose • Because of several diagnostic difficulties several
• Ectopic awareness and ectopic mindedness of the investigative tests are done to diagnose an
physician alone helps to diagnose an unruptured unruptured ectopic
ectopic • Diagnosing an unruptured ectopic can help save
the life of that patient, avoid permanent damage to
the tubes and prevent operational morbidity and
✓ It features are: mortality
✓ Pain abdomen

feature Ruptured ectopic Unruptured ectopic

Synonyms Acute ectopic Chronic ectopic

Sub acute ectopic

Presentation 6 – 8 weeks amenorrhoea followed by a 4 - 6 weeks amenorrhoea presenting with


catastropic abdominal pain, vaginal abdominal pain moderate.
bleed and syncopal attacks
(confused with n. preg)

General Condition Shock Stable

Risk of peritonoitis Vitals normal

Pallor proportionate to bleed No pallor

Risks Risk of death due to internal RISK OF IMMINENT RUPTURE

haemorrhage or operative / ‘TIME BOMB’

anaesthetic complications

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‘ BOMB BLAST ’

Symtomatology Amennorhoea then abd pain then vaginal Abdominal pain is always present
bleed
Vaginal bleed may or may not be present
Vaginal bleed is always present

Diagnostic work up Don’t waste time All investigations possible to confirm ectopic

UPT – confirm hCG

USG – confirm absence of intrauterine


gestation

Blood grouping and typing – blood for resus

No other investigation

Management Emergency laparotomy and resuscitation Conservative management

‘OPEN AND SEE’ Medical management

Surgical management ( if medical fails or is


contra indicated only)

‘WAIT AND SEE WHAT HAPPENS’

• Fluid in the pouch of Douglas (Cul-de-sac).

INVESTIGATIVE WORK UP IN RUPTURED ECTOPIC


• Adnexal mass clearly separated from the ovary.
• Gestational sac in the adnexa surrounded by a
✓ USG hyperechoic ring (Bagel sign/ tubal ring sign)
• Transvaginal / transabdominal ultrasound is the • Ring of fire on US Doppler
investigation most commonly done to diagnose
ectopic pregnancy.
• Transvaginal ultrasound is more informative.
✓ Findings in case of ectopic pregnancy:
• Absence of intrauterine pregnancy with positive
pregnancy test.

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✓ Specific
• Fetal pole / cardiac activity / yolk sac seen outside
the uterus in tubal ring (bagel sign)
• Demosntration of an extra uterine gestational sac
appearing as fluid containing structure with an
echogenic ring (the tubal ring sign)

✓ Nonspecific
• Absence of intrauterine gestational sac
INVESTIGATIVE WORK UP IN UNRUPTURED ECTOPIC • Complex adnexal mass clearly separated from
ovary
✓ Urinary hCG or Gravidex • Fluid in pouch of douglas
• Simple urine testing is positive • Rarely cardiac motion may be seen in an
• Disadvantage - Not specific just confirms unruptured tubal ectopic pregnancy
pregnancy

Doppler sonography
✓ Serum beta hCG measurement
• It is used to diagnose those cases of ectopic
• Results : Abnormally low level of beta hCG for
pregnancy which cannot be identified by TVS
gestational age
• Ring of fire pattern (placenta)
• Rise in hCG < 66% in 48 hours
• Blood flow pattern outside uterus

✓ Serum progesterone
✓ Combination of hCG & sonography
• Levels are lower in ectopic pregnancy than in • it gives a greater accuracy for diagnosing ectopic
viable pregnancy pregnancy.
• Levels > 25 ng = normal l/U pregnancy • β hCG levels above the discriminatory zone but no
• Levels < 5ng = abnormal (? Ectopic / uterine intrauterine gestational sac visualized.
abortion) o Discriminatory levels :
• The minimum level of hCG at which a G.sac is
visualised by TVS is 1500mIU/ml (or 1000mIU/ml)
at 4 weeks 5 days usually
• The minimum level of hCG at which G.sac is
visulalised by TAS is 6000mIU/ml at 5 weeks 3
days
➢ Sonography(TVS/TAS)
• Culdocentesis
• Reserved for emergency situation when USG is not
• Transvaginal USG is the logical first step for
possible
diagnosing ectopic pregnancy
• Transvaginal ultrasound is the best available • Laparoscopy
diagnostic modality for diagnosing ectopic
✓ Results
pregnancy.
• Direct visualization of pelvis specially the tube
• Also identifies endometriosis, adhesions
The following are the usg findings ✓ Advantages
• Gold standard for identification of ectopic preg.

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• Therapeutic management can also be done at the be undertaken only in appropriately selected and
same time counseled women
• Feasible in hemodynamically stable patient. • Minimal side effects of methotrexate make it
preferable to avoid the prolonged surveillance the
of expectant management and associated patient
TREATMENT GUIDELINES FOR RUPTURED ECTOPICS anxiety.

• Immediate laparotomy should be done along with ➢ Medical management


- general resuscitative measures together • It involves the use of a sysytemic agent to treat
• Even in those cases where there is doubt of an unruptured ectopic
ruptured ectopic pregnancy - Laparotomy should • Drug most commonly used: Methotrexate
be done to open and see
• Even if blood is not available then also a
laparotomy is done ✓ Methotrexate
• Immediate laparotomy and clamping of the • It is a folic acid analogue which inhibits
bleeding vessels may be the only means of saving dehydrofolate reductase
the life of moribund patient • This leads to a deficiency in folic acid
• This prevents synthesis of DNA.
• This will lead to cytological death of the
✓ Surgery of choice- conceptus and trophoblastic tissue
• Salpingectomy
✓ Indications
TREATMENT GUIDELINES FOR UNRUPTURED o Absolute requirements
ECTOPICS • Patient should be hemodynamic stable
• No evidence of acute intra-abdominal bleeding
➢ Unruptured • Reliable commitment to comply with required
• Depending on the patient's condition & other follow-up care
criteria there are 3 types of treatment • No contraindications to treatment viz woman
✓ Expectant management should not be breast feeding / renal / hepatic
✓ Medical management management dysfunction ( for methotrexate)
✓ Laparoscopy • Serum beta HCG level less than 10,000 IU/L (best
✓ Laparotomy results seen with HCG < 2000 IU/L
• Absent heart activity
• Ectopic gestational mass less than 4 cms in
➢ Expectant management diameter
• Only observation is done in hope of spontaneous
resolution. ✓ Single Dose Medical Treatment Protocol For
✓ Indication: Ectopic Pregnancy.
• Decreasing serial hCG titres
• No evidence of intraabdominal bleeding or • Day 0 / Day I = Measure serum hCG, TLC, DLC,
rupture assessed by vaginal sonography Liver Function Test and Renal Function Test
• Diameter of the ectopic mass less than 3.5 cms. • Day 2 = Single dose Methotrexate 50 mg/m2 IM
given
• Baseline HCG < 1000 IU/L & falling
• Day 4 = S. hCG and counts repeated
• Day 7 = S. hCG and counts repeated
• The potentially grave consequences of tubal • hCG titres on day 4 and day 7 are decisive
rupture and the established safety of medical and
surgical therapy, require that expectant therapy
✓ Prognosis and futher treatment

ARISE MEDICAL ACADEMY Dr. MIK | 54


• The main factor here is the difference in hCG • It is done in all those patients who do not fulfill
between day 4 and day 7 the criteria laid down for medical management
o If the decline is > 15% - No further treatment is • Surgical management could be done either by
required laproscopy or laparotomy
• If the decline is < 15% - Repeat another cycle of 7
days
✓ Disadvantages of medical management ✓ Laparoscopy
• It fails in 10 – 15% of all the patients • Indicated in hemodynamically stable patients and
✓ Don’ts during medical management not in emergencies
• Sexual intercourse, Alcohol to be avoided, Folic
acid
✓ Laparotomy
• Patient is hemodynamically unstable
✓ Surgically administered medical management: • Ruptured ectopic pregnancy
• Extensive abdominal & pelvic adhesion making
laparoscopy difficult
• Certain drugs can also be administered into the • Any ectopic gestation other than tubal pregnancy
gestational sac directly under laparoscopic or
ultrasonographic guidance.
• The method delivers a high concentration of the TYPES OF TUBAL SURGERY
drug to the site of implantation
• Tubal surgeries for ectopic are of 2 types
➢ Conservative
o Drugs used are • Salpingostomy
• Methotrexate (1 mg/kg) • Salpingotomy
• Prostaglandins • Segmental resection
• Hyperosmolar urea • Fimbrial expression
• Mifepristone (RU486)
• Actinomycin D
➢ Radical
• Vasopressin
• Salpingectomy
• KCI (Potassium Chloride)
➢ Fate Of The Ovary
• Salpingo-oophorectomy i.e. removal of tubes
along with the ovaries is not recommended in
➢ Surgical management young patient
• It should be done in all cases of ruptured ectopic

CHAPTER – 10
GESTATIONAL TROPHOBLASTIC DISEASES
• Definition
• Gestational Trophoblastic Disease (GTD) ➢ Classification
encompasses a spectrum of proliferative ✓ Conventional classification
abnormalities of trophoblasts associated with • Hydatidiform mole
pregnancy. • Invasive mole
• Persistent GTD (persistently raised (hCG) is referred • Choriocarcinoma
as gestational trophoblastic neoplasia (GTN) • Placental site trophoblastic tumor (PSTT).
ARISE MEDICAL ACADEMY Dr. MIK | 55
➢ Complete Mole
• Complete H. mole shows no evidence of fetal tissue
HYDATIDIFORM MOLE at all.
• Hydatidiform mole is a benign neoplasm of • Complete hydatiform moles exhibit characteristic
chorion with malignant potential. swelling and trophoblastic hyperplasia.
• It is the most common form of gestational • Most common karyotype is 46XX 90%
trophoblastic disease. • 10% may have a 46XY karyotype
• It is an abnormal condition of the placenta where • The molar chromosomes are entirely of paternal
there are partly degenerative and partly origin (although mitochondrial DNA is of maternal
proliferative changes in the young chorionic villi. origin.)
• Characterised by multiple grape like vesicles filling
➢ TYPES
and distending the uterus, usually in absence of an
• There are two types of hydatidiform moles intact fetus
✓ Complete mole
✓ Partial mole ✓ Origin
• The complete moles arises from an ovum that has
✓ Complete mole been fertilized by a haploid sperm, which then
duplicates its ownchromosomes called as
Androgenesis.
➢ EPIDEMIOLOGY • The ovum nucleus may be either absent or
inactivated!
✓ Incidence
• Incidence is maximum in Asia and South America ➢ Partial Mole
and least in U.S. • Some embryonic or fetal tissue is identifiable.
• Maximum incidence is in Philippines (1 in 80). • Chorionic villi of varying size with focal hydatidiform
• In India it is 1 in 400 pregnancies. swelling, cavitation, and trophoblastic hyperplasia
(whereas complete mole shows diffuse
✓ Risk Factors hydatidiform swelling and trophoblastic
• Risk is more in women too elderly (> 35) or too hyperplasia.)
younger (< 18 years). • Marked villous scalloping.
• Low socioeconomic status. • Prominent stromal trophoblastic inclusions.
• History of molar pregnancy.
• Diet deficient in protein, folic acid and vitamin A. ✓ Origin
• Blood group ‘A blood group’ lady married to ‘O • Partial moles generally have a triploid karyotype (69
blood group’ man. chromosomes); the extra haploid set of
chromosomes usually is derived from the father.
• Partial mole is linked to the use of oral
contraceptive pills and history of irregular • When a fetus is present in conjunction with a partial
menstruation. mole, it generally exhibits the stigmata of triploidy,
including growth retardation and multiple
➢ Genetics congenital malformations such as syndactyly and
• Familial repetitive hydatidiform mole has been hydrocephaly
linked to a missense mutation in the NLRP7 locus on
chromosome 19;
• This mutation is present in 60% of patients who had
two molar pregnancies

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• DIFFERENCES IN COMPLETE AND PARTIAL MOLE:

CHARACTER COMPLETE MOLE PARTIAL MOLE

KARYOTYPING 46XX - 90% or 46XY - 10% i.e. 69XXX or 69XXY i.e. it is triploid
it is diploid
Embryo/fetus ABSENT PRESENT
Trophoblastic DIFFUSE OVERALL AFFECTION FOCAL AFFECTION
hyperplasia
Fetal RBC in ABSENT PRESENT
villi
Hydropic PRONOUNCED AND DIFFUSE VARIABLE AND FOCAL
degeneration
of villi

➢ Clinical Features ✓ Signs


• The fundal height of uterus is more than the period
✓ Symptoms of amenorrhea
• Amenorrhea ( The size of the uterus is more than that
• It is of varying duration followed by continuous or expected for the period of amenorrhea in 70%,
intermittent brown or bloody discharge (usually not corresponds with the period of amenorrhea in 20%
profuse) evident by 12 weeks (Three fourths of and smaller than the period of amenorrhea in 10%.
these patient present prior to the end of the first )
trimester) • Uterus is doughy in consistency (due to absence of
• uterine bleeding is all most universal (it is the most amniotic fluid).
common presenting feature , occuring in more than • Fetal parts will not be felt.
90% of patients with molar pregnancies). • Fetal heart sounds will not be heard (even on
• Passage of vesicles per vaginum doppler).
3. Hyperemesis (due to the high levels of circulating • External and internal ballottement can not be
HCG). elicited.
➢ Patient complaining of extremes of nausea, • Adnexal mass felt on P/V examination – theca leutin
vomiting + bleeding in first trimester + size of cyst
uterus more than the period of amenorrhea-
think of Molar pregnancy

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➢ SPECIAL POINTS • Done to rule out lung metastasis
• Patients with partial mole do not have dramatic • Straight X ray of chest should be carried out as a
clinical features of complete molar pregnancy. In routine, for evidence of pulmonary embolization
general these patients have signs and symptoms of even in benign moles.
incomplete or missed
• When hypertension appears before 24 weeks, it is 4. CTscan
important to rule out hydatidiform mole. • Done to rule out brain and liver metastasis.
• Clinical Thyrotoxicosis seen due to the
5. Gold Standard
thyrotrophin-like effect of hCG
• Definitive diagnosis is done by histological
examination of products of conception.
➢ Investigations :
➢ MANAGEMENT OF H. MOLE
1. Ultra sono graphy 1. Suction curettage
• USG is a reliable and senstive technique for the • It is the treatment of choice irrespective of uterine
diagnosis of molar pregnancy. size
• USG alone is adequate, quick and a safe procedure • Suction evacuation is done first. After most of the
• Ultrasound shows "Snow storm" appearance in molar tissue has been removed by aspiration,
the uterus. oxytocin is given.
• Once the myometrium has contracted, thorough
but gentle curettage with a large sharp curette is
performed.
• Intraoperative ultrasonographic examination may
help document that the uterine cavity has been
emptied
• As far as pulmonary embolisation in concerned -
acute pulmonary insufficiency due to pulmonary
embolization of trophoblastic cells can occur during
suction evacuation

✓ In case of complete molar pregnancy: 2. Hysterectomy:


• Chorionic villi exhibit diffuse hydropic swelling ✓ Indications
• Absence of fetal shadow. • Female has completed her family irrespective of age
✓ In case of partial molar pregnancy: • Age of patient - >35 years (as chances of malignancy
• Focal cystic spaces are seen in placental tissue are more).
• Some fetal tissue is identifible. • Uncontrolled haemarrhage during scutum
evacuation
➢ In either case theca lutein cyst may be seen.
✓ Advntages
2. Serum beta hCG • In women aged 40 or older because atleast a third
• Serum beta hCG levels are very high in case of of these women will go on to develop gestational
molar pregnancy. trophoblastic neoplasia.
• Levels more than 40,000 as detected by radio • Hysterectomy when performed in molar pregnancy
immunoassay are seen in trophoblastic diseases. significantly decreases the chances of developing
• Rapidly increasing serum values of HCG are also choriocarcinoma (by 5 fold times)
suggestive of molar pregnancy. ✓ Disadvantages
• Following hysterectomy, persistent GTD is
3. Chest X-ray observed in 3-5% cases and hence does not
eliminate the necessity of follow up

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✓ Guidelines • Chemotherapy is not indicated as long as these
• The enlarged ovaries (theca lutein cysts) found serum levels continue to regress.
during operation should be left undisturbed as they • A rise or persistent plateau in the level demands
will regress following removal of mole. evaluation for gestational trophoblastic neoplasia
• But, if complication arises, like torsion, rupture or and usually treatment by chemotherapy.
infarction then the ovaries can also be removed ▪ Median time for resolution of partial mole is 7
weeks and for complete mole is 9 weeks.
➢ Fate of a complete mole
• Spontaneous expulsion occurs at around 16 weeks ➢ Contraceptive Advice during follow up
and rarely delayed beyond 28 weeks. • All patients with H. mole have to compulsorily
• Complete moles have a potential for local invasion avoid pregnancy during the followup period
and dissemination after molar evacuation • Estrogen-progestin contraceptives or depot
• Persistent - 15-20%, medroxyprogesterone is usually used to prevent a
subsequent pregnancy during the period of
• metastatic disease-5%, surveillance.
• recurrence - 1-4%, • Contraceptive of choice being combined oral pills.
• Choriocarcinoma - 2-10%. • Earlier the contraceptive of choice was Barrier
method.
➢ Fate of a partial mole
• Persistent tumour - 2-4% . • Earlier patient was advised to avoid pregnancy for
atleast 1 year after H mole evacuation but now it is
• Most of the pregnancies are aborted restricted to 6 months following a negative hCG
titre
➢ Following-up Molar Pregnancy
• Routine follow up is mandatory for all cases for
atleast 6 months following molar pregnancy.
• The chances of persistent trophoblastic disease and ➢ Prophylactic Chemotherapy
choriocarcinoma are high after evacuation of H. ✓ Indications
mole therefore regular follow up is mandatory. • Initial high levels of β HCG (> 100,000 mill/ml)
• Doing hysterectomy does not negate the need for • If hCG fails to becomes normal by stipulated time
followup. (10-12 weeks) normal time being 9 wks and 7 wks
✓ First B-hCG level is obtained 48 after evacuation. • Reelevation of serum HCG after reaching normal
✓ Then patients should be monitored with weekly levels
determinations of beta -subunit HCG levels until • Evidence of metastasis irrespective of HCG levels.
these levels are normal for 3 consecutive weeks • Post evacuation hemorrhage.
✓ (The average time to achieve the first normal HCG • Age : patient >35 years.
level after evacuation is about 9 weeks ) • Theca lutein cysts > 6 cms.
✓ After normal levels are achieved monthly
determinations for 6 consecutive months
• After a patient achieves a nondetectable hCG level, ✓ Drug used : Methotrexate / Actinomycin D
the risk of developing tumour relapse is very low
and may approach zero ✓ Methotrexate
• 1mg/kg is given on days 1, 3, 5 and 7
• Prevent pregnancy for a minimum of 6 months
• Alternately give folinic acid 0.1 mg/kg on day 2, 4, 6
following normal levels of hCG
and 8
• After 6 months of monitoring pregnancy is allowed
• A total of 3 such courses can be given
( previous guidelines to avoid pregnancy for a period
of 1 – 2 years are not followed) • hCG falls within 4 days to 1 week following single
cycles

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• It refers to a spectrum of diseases with invasive,
✓ Actinomycin D malignant or metastatic potentials.
• Can be given as 12mcg/kg iv for 5 days • It is composed of 4 variants
• More costly ✓ Persistant Hydatidiform mole
• Less toxic ✓ Invasive Mole
✓ Choriocarcinoma
✓ Placental site Trophoblastic Tumor

➢ Theca lutein cysts: ➢ Invasive mole :


• They vary in size from microscopic to 10 cms size. • Also called chorioadenoma destruens
• Yellow coloured. • It accounts for 15 % of all GTN
• It occurs due to overstimulation of the luteal • It has extensive penetration abilities through all the
elements by the large amounts of circulating hCG
layers of uterus
especially in complete moles to about 25 – 60 %
• It may present with multiple purple perforated
• Persistent trophoblastic disease is more likely in areas with massive intra peritoneal haemorrhage
women with theca lutein cysts >6 cms ( FIGO
guidelines) • Later may metastasize to vagina or distant sites
• Patients with theca lutein cysts (> 6 cms) have high • Excessive trophoblastic over growth and extensive
risk of developing choriocarcinoma (FIGO and WHO penetration by the trophoblastic cells including the
) villi.
• Theca lutein cyst regress spontaneously after • The villus structure is retained well without signs of
suction evacuation & do not need any specific muscle necrosis
management.

✓ Complications
• It may undergo torsion, infarction or hemorrhage

✓ Management
• If found during hysterectomy they are left
untouched – NO OOPHORECTOMY
• It may undergo torsion, infarction or hemorrhage
and if found pathological during hysterectomy then
oophorectomy may be done ➢ Placental Site Trophoblastic Tumor(PSTT) :
• It arises at the placental implantation site
• It is the rarest variant of GTN
➢ PERSISTENT GESTATIONAL TROPHOBLASTIC
DISEASE
• The tumor arises from the intermediate
trophoblasts Local invasion occurs into the
• Definition: Persistent GTD is defined where there is myometrium and lymphatics
persistence of trophoblastic activity as evidenced by
clinical, imaging, pathological and or hormonal
• This tumor metastasises less commonly into the
vasculature (different from choriocarcinoma)
study following initial treatment.
• This may be following treatment of hydatidiform • Patient presents with vaginal bleeding.
mole ( called post molar GTD) • These tumors have been associated with
• A postmolar GTD may be benign or malignant. modestly elevated serum beta - hPL (human
placental lactogen) is also a tumor marker for these
tumors.
• GESTATIONAL TROPHOBLASTIC NEOPLASIA

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✓ Treatment • Columns and sheets of trophoblastic cells
• PSTT is not responsive to chemotherapy. penetrating the muscle and blood vessels
Hysterectomy is the preferred treatment • Cellular atypia

✓ MC mode of spread is hematogenous

➢ METASTASIS
• Most common sites of metastases in
choriocarcinoma are
• Lung (80%) > Vagina (30%) > Pelvis (20%) > Liver
(10%) and Brain (10%)
➢ Choriocarcinoma • The sites associated with lesser risk is lung and
vagina
• Metastasis to brain and liver are associated with
worse prognosis
• Patients with brain or liver metastasis are at great
risk of sudden death from hemorrhage from these
lesions
• Therefore it is a standard practice to include whole
brain or whole liver irradiation concomitantly with
combination chemotherapy

➢ Lung Metastasis
• It is seen in 80% cases
• Patient presents with respiratory symptoms like
dyspnoea, hemoptysis, chest pain etc.
• Most malignant tumor of uterus • On X-ray it may produce the following four patterns
• It arises from the chorionic epithelium ✓ An alveolar snow storm pattern
• It is not a tumor of uterus but the uterus is ✓ Discrete rounded densities or canon ball
secondarily affected appearance
• Mostly presents as irregular bleeding or uterine ✓ Pleural effusion
hemorrhage following an abortion, a molar ✓ An embolic pattern caused by pulmonary arterial
pregnancy or a normal delivery occlusion

✓ Gross :
➢ Vaginal Metastasis
• It usually starts at any place in the uterus
• It is seen in 30% cases
• May rarely start from the fallopian tube or ovary
• Metastasis occurs in suburethral or in fornicesQ
• Usually appears as localised nodular lesion
• Metastasis appears as purple hemorrhagic
projections which are highly vascular and bleed on
✓ Histopathology :
touch (pathognomic of choriocarcinoma)
• Absence of villous pattern
• Where else do we see purplish spots in the fornices
_____________?

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➢ CHEMOTHERAPY
• It is of two types
✓ Single agent chemo
✓ Combination chemo

✓ Single agent chemo


• Methotrexate is the drug of choice. ✓ NEO ADJUVANT CHEMOTHERAPY
• If the patient has jaundice then actinomycin D should • It is preferable to start chemotherapy 3 days before
be given. surgery
• Given on day 1, 3, 5 and 7 • Then perform the surgery followed by chemotherapy
• Alternating with folinic acid on day 2, 4, 6 and 8 as per schedule.
• Repeat every 7 days ✓ Metastatic resections
• Lung resection (thoracotomy) is done in pulmonary
✓ Combination chemo metastasis in drug resistant cases.
• Most commonly is Bagshaw regime consisting of- • Craniotomy is for control of bleeding.
o E = etoposide
o M = methotrexate ➢ Radiation
o A = actinomycin D ✓ Brain metastasis:
o C = cyclophosphamide • Whole-brain radiation therapy (3000 cGy over 10
o O = vincristine (oncovin) days).
• EMA-CO regimen results in response rates of about • Intrathecal high dose methotrexate may be
90% and survival rates of 80-100%. administered to prevent hemorrhage and for
tumor shrinkage.
• Treatment must be continued until beta HCG
✓ Liver metastasis:
titres return to nondetectable levels. • Interventional radiology (hepatic artery ligation or
embolization) or whole liver radiation (2000 cGy over
• Complete remission is documented after 3
10 days) along with chemotherapy maybe effective.
consecutive weekly normal beta HCG titres
• It is recommended that all high risk patient should
• Hepatic metastasis has a poor prognosis
receive at least three courses of triple agent
chemotherapy after beta HCG titres have returned to
➢ Prognosis
normal
• The cure rate is almost 100 percent in low risk
• about 70 percent in high risk metastatic groups.
➢ SURGERY • Follow up is mandatory for all patients at least for 2
✓ Total hysterectomy years.
• It is done if required in choriocarcinoma . • Serum hCG is measured weekly until it is negative for
• The ovaries are usually not involved and if involved, three consecutive weeks.
can be effectively cured with postoperative • Thereafter it is measured monthly for 6 months and 6
chemotherapy, hence bilateral salpingoopherectomy monthly thereafter for life.
is not done.

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CHAPTER – 11
NORMAL LABOUR
• Normal labour is defined as a series of events that
take place in the genital tract in order to expel the
viable products of conception from the uterus to the
outside world through the vagina
➢ TRUE VS FALSE*
THE EDD
True labour pains False labour pains
• The Expected Date of Delivery is calculated by the
Naegele’s formula • Sharp pain • Dull pain
• The formula is d+7 / m+9 for the LMP • Intensity , duration • Intensity , duration and
• 4% of females deliver on the EDD* and frequency frequency don’t
• 50% of the females deliver within one week of the increase progressively increase
EDD* • Associated with show • Not associated with
• The EDD calculated by the first trimester ultra sound • Associated with show
scan is most accurate* cervical dilatation and • Not associated with
effacement cervical dilatation and
• Associated with effacement
➢ ONSET OF LABOUR descent of presenting • Not associated with
part descent of presenting
• Mainly due to increase in the level of oestrogen
• Associated with bag of part
relative to progesterone
membrane formation • Not associated with
• The raised levels of Oestrogen then cause:
• Not relieved on bag of membranes
✓ Increase the release of oxytocin*
sedation / enema • Relieved on sedation /
✓ Increase oxytocin receptors ______ times *
enema
✓ Increases Prostaglandin synthesis
✓ Increases exitability of the myometrial cell
✓ Increases contractility of the myometrium*

➢ THE LABOUR PAINS


THE BIOPHYSICS OF LABOUR
• Causes are :
TONE/TONUS
1) Uterine angina*
2) Peritoneal stretching • The tone or intensity refers to the intra uterine
3) Compression of nerve ganglion
pressures
✓ The distribution of pain* is along the cutaneous
nerves T10 to L1 • During pregnancy it is 2mm Hg
4) Cervical dilatation and stretching*
✓ The distribution is along the sacral plexus • During Braxton Hicks* it is < 8 mm Hg

• During first stage* of labour it is 40 – 50 mm Hg

ARISE MEDICAL ACADEMY Dr. MIK | 63


• During second and third stage* it is 100 – 120 mm Hg

• Other units measured are montevideo units

• MONTEVIDEO = intensity(mm hg) x frequency


(/10mins)*

FREQUENCY ❖ THE FIRST STAGE


• The number of contractions in a period of 10 minutes

• In first stage of labour it is usually 1 contaction in 10


minutes

• In second stage it is atleast 3 contractions in 10


minutes*

DURATI0N

• The time each contraction lasts is the duration

• During first stage it lasts for 30second each

• During second stage it lasts for 45seconds to 90


seconds
➢ It consists of some important events :
❖ STAGES OF LABOUR ✓ Cervical dilatation
✓ Cervical effacement
✓ Formation of bag of waters
1ST STAGE • ONSET OF TRUE ✓ Cervical effacement
LABOUR PAINS TO ✓ Taking up of the cervix by the uterus
FULL DILATATION OF ✓ Effacement occurs before dilatation in primis*
CERVIX* ✓ Effacement and dilatation occur together in multis
✓ ( Primi* 12-18 hrs ;
multi 6 - 8 hrs) ➢ Clinically the first stage of labour is divided into:
• Latent phase
2ND STAGE • FULL DILATATION OF • Active phase
CERVIX TO EXPULSION
OF THE BABY Latent phase Active phase
✓ (Primi 2 hrs ; multi 30
mins) • It is the preparatory • The cervix dilates
phase of cervical from 3cm to 10cm
3RD STAGE • EXPULSION OF THE dilatation in this phase
PLACENTA • It is 8 hrs in primi • This is the phase of
✓ (Expectant 15 mins ; and 4hrs in multi* actual quick cervical
active* 5 mins) • The cervix dilates dilatation
only 3 cms during • The cervix dilates @
the latent phase* 1cm/hr in primis
4TH STAGE • STAGE OF and @ 1.5cm/hr in
OBSERVATION* – 1Hr multis

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• Rate of dilatation in • Time of active phase • Decision for referral to higher centre ________
latent stage is of stage 1 in primis is • Decision for ARM* _________
_______ --------------------- • Decision for cesarean section* __________
• Time taken for active • Distance between alert line and action line is
phase of stage 1 in _________
multis is ---------------- • A senior obstetrician is informed if _________
--

❖ THE SECOND STAGE


❖ PARTOGRAM
• The second stage starts after full dilatation of cervix
and ends with the expulsion of the baby
• The membranes rupture after full dilatation of cervix*
• Sometimes they rupture immediately after full
dilatation and sometimes a little later after the start of
second stage of labour*

• A partogram is the best method to assess the


progress of labour
• Though a partogram has several components the
most important components are :
➢ Cervical dilatation : accessed by vaginal
examination
➢ Descent of head : accessed by abdominal
examination
• Cervical dilatation is plotted as cervical dilatation in
cms on Y axis against time in hours on X axis
• Descent of head is accessed as 5/5 method
( descent of head is a part of both first and second
stage of labour starts at 7cm and ends with the
second stage) *
➢ The partogram is best to diagnose prolonged labour
at the earliest and intervene timely
• It is a comprehensive record in cases of referral to
higher centres
• It is a guideline for senior intervention and surgical
decision making

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( ______ = ______ cm) enters the brim of the pelvis
• Engagement occurs at the end of 37th week in primi*
and with the onset of labour in multi*
• M/c position – LOT then LOA*
• M/c diameter for the entry of head – transverse*
• M/c the BPD enters along the – AP diameter*
❖ THE MECHANISM OF LABOUR* • Internal rotation occurs at the level of ischial spines*
• The timing of episiotomy is decided by crowning*
• Defined as the series of movements on the foetal • The head is born by the process of extension*
head in order to adapt to the maternal pelvis
They are as follows*:
❖ THIRD STAGE OF LABOUR
It is composed of 2 important steps:
✓ Placental separation
✓ Placental expulsion

❖ PLACENTAL SEPARATION

There are 2 ways of palcental separation:

1. Central separation: Schultz mechanism


2. Peripheral: Duncan mechanism.

1) Engagement* 1. Central separation:


2) Descent
3) Flexion • Most commonly during placental delivery, a
4) Internal rotation* retroplacental hematoma forms and pushes the
5) Crowning* center forward
6) Extension* • This causes it to separate toward the uterine cavity.
7) Restitution • Weighted by this hematoma, the placenta descends,
8) External rotation drags the membranes, and peels them from their
uterine attachment.
❖ Engagement: • Consequently, the glistening amnion, covering the
placental surface, presents at the vulva.
• It is defined as the process by which the largest • The retroplacental hematoma either follows the
transverse diameter of foetal head placenta or is found within the inverted sac.

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• blood from the placental site pours into the • the placenta separates first at the periphery. As a
membrane sac and does not escape externally until result, blood collects between the membranes and the
after extrusion of the placenta. uterine wall and escapes from the vagina.
• In this circumstance, the placenta descends sideways,
2. peripheral separation: and the maternal surface appears first"
In the other method of placental extrusion, known as the • Placenta separates after the birth of the baby and the
Duncan mechanism: line of separation is through the decidua spongiosum.
✓ the placenta separates first at the periphery. As a
result, blood collects between the membranes ❖ ACTIVE MANAGEMENT OF THIRD STAGE
and the uterine wall and escapes from the vagina. • The third stage of labour is potentially the most
✓ In this circumstance, the placenta descends dangerous of all stages
sideways, and the maternal surface appears • The active management includes the following as
first". recommended by the WHO
✓ Placenta separates after the birth of the baby and ➢ Administer oxytocin immediately after delivery of the
the line of separation is through the decidua baby*
spongiosum. ➢ Deliver the placenta by controlled cord traction and
counter traction*
➢ Delayed cord clamping*
SIGNS OF PLACENTAL SEPARATION
❖ CORD CLAMPING
PER ABDOMEN FINDINGS : • Immediately after birth hold the baby below the level
• Uterus becomes globular, firm and ballotable ( of the vaginal interoitus*
earliest sign) • Clamp the cord approximately 1- 2 mins after
• Supra pubic bulging complete expulsion of the baby*
• The cord doesn’t retract on pushing the uterus • This is to facilitate transfer about 100ml of blood from
upwards(Kustner’s sign) the placenta to the baby
• A slight raise in supra pubic height (Schroeder’s sign) • The WHO has advocated early cord clamping in the
following conditions:
PER VAGINAL FINDINGS ➢ HIV positive mothers
• Gush of fresh blood ➢ Rh negative mothers
• Permanent leghthening of the cord ➢ Diabetic mothers
➢ Preterm baby
PHYSIOLOGICAL HAEMOSTASIS ➢ Birth asphyxia

• The uterine arteries pass through the uterine ❖ LEVEL OF UTERUS AFTER DELIVERY
musculature
• The contraction of uterus leads to compression of • After 2nd stage the uterus is at the level of the
these arteries leading to haemostasis ( stoppage of umbilicus*
bleeding) • After 3rd stage the uterus is below the level of the
• Which layer* of uterine myometrium forms the living umbilicus*
ligatures _______ • Anterior asynclitism is common in multis*
• In the other method of placental extrusion, known as • Posterior asynclitism is more common in primis
the Duncan mechanism

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CHAPTER – 12
INDUCTION OF LABOUR

• Induction: Implies stimulation of contractions


before the spontaneous onset of labor ➢ ABSOLUTE CONTRINDICATIONS
• Often the cervix is closed and uneffaced, labor (Most High CAPUT)
induction is commenced by first making cervix soft, • Macrosomia
the process is called as cervical ripening. • Severe hydrocephalus
• Contracted pelvis /advance cancer cervix
• Augmentation of labor implies increasing the • Active genital herpes, high viral load of active HIV
strength of uterine contractions such that labor • Placenta previa, cord prolapse
progresses fast. • Uterine scar due to
• Induction of labor is indicated in all those conditions - 2 or more LSCS
when the benefits to either mother or fetus outweigh - Previous classical cesarean section
those of pregnancy continuation. - Myomectomy entering the endometrium
- Hysterotomy
INDICATION - Unification surgery
• Transverse lie
➢ MATERNAL INDICATIONS
• Preeclampsia/eclampsia ➢ RELATIVE CONTRAINDICATIONS
• Maternal medical complications like • Breech presentation
- Diabetes mellitus • Oligohydramnios
- Chronic renal disease • Multiple gestation
• Abruptio placenta • Grand multipara
• Premature rupture of membrane • Prematurity
• Chorioamnionitis
• Chronic hydramnios/Oligohydramnios
BISHOP SCORE
➢ FOETAL INDICATIONS • It is a quantitative method for prediction of
• Intrauterine fetal death successful induction of labour.
• IUGR • It includes the following parameters:
• Prolonged pregnancy ➢ D = Cervical Dilatation(most important parameter)
• Rh incompatibility ➢ P = Cervical Position
• Lethal malformation ➢ E = Cervical Effacement
• Unstable lie after correction into longitudinal lie ➢ S = Head Station
(versions) ➢ C = Cervical Consistency
• Fetus with major congenital anomaly
• Non reassuring fetal statues

CONTRAINDICATIONS OF INDUCTION OF LABOUR

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THE SCORING SYSTEM
SCORE CERVICAL CERVICAL CERVICAL HEAD CERVICAL
DILATATION POSITION EFFACEMENT STATION CONSISTENCY

0 CLOSED POSTERIOR 0 – 30 % - 3 FIRM


1 1 – 2 CM MID 40 – 50 % -2 MEDIUM
2 3 – 4 CM ANTERIOR 60 – 70 % -1, 0 SOFT
3 > 5 CM > 80 % 1, 2

• It involves rupturing the membranes overlying the


cervix using a Kocher's forcep
➢ CLINICAL SIGNIFICANCE • Stripping of Membranes is the digital separation of
• Induction is successful only if scores are more than 9 membranes from the wall of the cervix and lower
• If scores are less than 4 then ripening of cervix uterine segment
should be done before starting induction of labour
➢ ADVANTAGES:
Techniques for cervical ripening • Promotes labour, encourages application of the fetal
➢ Pharmacological method head to the cervix, Colour of the liquor can be
✓ Prostaglandin observed and meconium staining ruled out
• Dinoprostone gel (PGE2) - it is the gold standard for
cervical ripening ➢ DISADVANTAGES:
• Misoprostol (PGE1) tablet - vaginal or oral • Cord prolapsed, Amnionitis, abruption in case of
➢ Non Pharmacological method polyhydramnios.
✓ Stripping the membrane • Vasa-previa
✓ Mechanical dilators:
PROSTAGLANDINS

ARTIFICIAL RUPTURE OF MEMBRANES

• For obstetric purposes the following prostagladins are


used
➢ PG E1 – Tab. Misoprost
➢ PG E2 – Gel. Dinoprost
➢ PG F2 alpha – Inj Carboprost

FORMULATIONS AND DOSAGES


• ARM is a method for inducing and augmenting ➢ PG E1
labour. • Tab Misoprost
• Available as 200mcg tablet

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➢ PG E2 • The analogue of prostaglandin which is
• Available as tablet dinoprostone and gel dinoprostone contraindicated in scarred uterus and should not be
• Tablet dinoprostone 3mg used in previous LSCS patients-PGE1
• Gel as 0.5 mg single use gel is syringe and catheter • The analogue of prostaglandin which is not used for
➢ PG F2alpha inducing labour PGF-2 alpha
• It is available only as injection carboprost • The analogue of prostaglandin which is used only in
• It is available as 250 mcg in a 1ml ampoule PPH -PGF-2 alpha

USES OF PROSTAGLANDINS VAGINAL BIRTH AFTER CESAREAN DELIVERY


➢ PG E1 (VBAC)
• Abortion/ MTP 1st trimester
✓ 200mcg P/V or P/O 4 tablets fourth hourly (48 hrs
after mifepristone)
• Induction of labour –
✓ 25mcg P/V every 4th hourly upto max 8 times
✓ 50mcg P/V every 3rd hourly upto max 6 times
✓ 50mcg P/O every 4th hourly upto max 6 times
• PPH
✓ 1000mcg P/R stat

➢ PG E2 / dinoprostone
• Ripening of cervix prior to induction of labour
✓ Gel dinoprost 0.5mg in cervical canal taking care not
to go beyond internal os ➢ selection of candidate for inducing a VBAC
✓ Tab Dinoprost 3mg P/V twice 6 hours apart • No more than one prior LSCS.
• Clinically adequate pelvis (no CPD).
➢ PG F2alpha • No other uterine scars or previous rupture.
• PPH • Physician immediately available throughout active
✓ Inj 250 mcg intramuscular ( gluteal) labour who is capable of monitoring labour and
✓ Inj 125 mcg intramyometrial performing emergency cesarean.
• Availability of anesthetist and operation theatre
GOLD STANDARDS facilities.
• The gold standard agent for cervical ripening is PGE2 • Availbility of blood and resuscitation
i.e dinoprost gel. • absolutely contraindication in VBAC induction
• The gold standard agent for inducing labour is PGE2 • Induction and trial of scar is absolutely
• The analogue of prostaglandin recently approved by contraindicated in CPD/contracted pelvis.
ACOG for cervical ripening – PGE1 (misoprost) • In case of previous classical cesarean section, the risk
of rupture of uterus during trial is 4-9%, hence trial of
scar is an absolute NO

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CHAPTER – 12
PRETERM, POST DATED, PROM & PPROM

PRETERM LABOUR (PTL) • Medical and surg. disorders in preg : fever,


• Preterm labour is defined as labour (regular, painful pyelonephritis, diarrhoea, acute apendicitis,
frequent uterine contractions causing progressive abdominal surgery
effacement and dilatation of cervix) occurring before
37 completed weeks of gestation ✓ Iatrogenic : indicated disorder for termination of
pregnancy
➢ High risk factors
✓ Idiopathic : majority of the cases

✓ Foetal : multiple pregnancy, congenital


malformations, IUFD

✓ Placental : infarction, thrombosis, previa, abruption

• Most common cause of preterm labour is idiopathic


followed by infection like urinary tract infection,
vaginal infections
• Other common cause is short Cx
• Most common organisms responsible for preterm
labour: Ureoplasma urealyticum and Gardenerella
vaginum causing bacterial vaginosis.

✓ History ➢ CERVIX AND PRE TERM LABOR


• Past H/o preterm labor, Pregnancy after ART,
Asymptomatic bacteriuria, Smoking, Low socio
• Length of cervix (measured by TVS) <2.5 cm and
economic and nutritional status, Maternal stress
tunneling of internal os is an important risk factor for
preterm
✓ Maternal • Shape of Cx and Correlation
• Pregnancy complications : pre eclampsia, APH,
polyhydramnios, PROM, short Cx
SHAPE OF CERVIX CORELATION

T shaped Normal
Y shaped Suspicious of preterm labor

U shaped Funneling of os -seen in incompetent os , preterm


labor

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DIAGNOSIS OF PRETERM LABOUR • Steroids are recommended for all women in preterm
• Regular uterine contractions with or without pain (at labour before 32 weeks with or without membrane
least one in every 10 min). ruptures in whom there is no evidence of
• Dilatation (> 2 cm) and effacement (80%) of cervix. chorioamnionitis.
• Resting pressures more than 20mm hg • Steroid of choice for lung maturity is
• Fetal fibronectin if present in vaginal /cervical Betamethasone.
secretions before 37 weeks • Dosage is 2 doses of 12 mgs of steroid (i.e., 3
➢ Fetal fibronectin equal to or more than 50 ng/ml and ampules) are given i/m - 24 hours apart.
cervical length <2.5 cm on TVS are the best
predictors especially in a woman with a prior history
of preterm birth. ➢ Advantage:
• Steroids reduce the rate of respiratory distress
➢ Fetal Fibronectin: syndrome, intraventricular hemorrhage and
necrotising enterocolitis in the newborn.
• It also prevents periventricular leukomalacia

➢ Adverse effects of steroid therapy

✓ On Mother
• Pulmonary edema, Infection, More difficult glucose
control in diabetic women, No long term maternal
adverse effect

✓ On Foetus
• Early onset neonatal sepsis, Chorioamnionitis,
Neonatal death
• It is a fetal glycoprotein.
• Normally it is found in the cervico vaginal discharge
➢ CONTRAINDICATIONS
before 22 weeks and again after rupture of • Corticosteroids can be given even in presence of
membranes. maternal hypertension or diabetes mellitus
• If detected in cervicovaginal secretions prior to • Be avoided if PROM is associated with definitive
rupture of membranes, it indicates disruption of the evidence of chorioamnionitis / overt infection
maternal-fetal interface and may be predictive of
impending preterm labour. ➢ Tocolysis:
• When the test is negative it reassures that delivery • Tocolytics are not given with the aim to arrest
will not occur within next 7 days. preterm labor for a long time, but to prolong the
labor for 48 hours.
➢ MANAGEMENT ✓ This servers the following purposes:
• Glucocorticoids : to reduce RDS, IVH and NEC - The corticosteroids get time to act.
• Tocolysis : To allow the steroids to act and gives time - Allows time for transport of the woman to better
to allow the mother to be shifted to higher centre obstetrical centre.
• Antibiotics : if indicated to avoid infections and
Neonatal sepsis ➢ Antibiotics:
• Rescue circlage ( debatable) • Do not have a role in preterm pregnancy with intact
membranes.
➢ Steroid therapy in preterm labour:
ARISE MEDICAL ACADEMY Dr. MIK | 72
• Ruptured membranes - avoid the spread of infection
from vagina to the uterus / foetus - main organism -
group B streptococcus

TOCOLYTIC DRUGS

➢ BEST CHOICE FOR PATIENT

• Best first line tocolytic—Nifedipine


• Overall tocolytic of choice – Nifedipine
• Most efficacious tocolytic agent – Nifedipine • Premature Rupture Of Membrane ( PROM) is defined
• 2nd line tocolytic—Betamimetic agents like ritrodine, as spontaneous rupture of membranes before the
salbutamol. onset of labour
• Safest tocolytic agent – Atosiban • Preterm premature rupture of membranes (PPROM)
is defined as premature rupture of membranes before
• Tocolytic preferred in heart disease – Atosiban >
MgSO4 37 completed weeks.
• Tocolytic with maximum side effects-Betamimetic
agent
➢ Risk factors for PROM:
• Incresing friabilty/decreased tensile strength of
➢ Most commonly used tocolytics in case of preterm membranes
previa. • Infections like bacterial vaginosis
✓ Nifedipine • Polyhydramnios
✓ Magnesium sulphate • Multiple pregnancy
• Cervical incompetence
➢ Tocolytics which are not used in preterm previa • Previous H/O PROM.
• Terbutaline and Ritodrine: They cause tachycardia
and make the assessment of patient's pulse rate
unreliable. • The predominant risk for patients with PROM
• Indomethacin: It causes inhibition of platelet cyclo between 28 and 32 weeks is hyaline membrane
oxygenase system and prolongs the bleeding time. disease. Administration of glucocorticoids and
prolongation of the latent phase are beneficial for
these patients if they do not have clinical or
subclinical chorioamnionitis.
• The predominant risk for patients with PROM
between 32 and 36 weeks is chorioamnionitis.
Therefore the dominant tendency in their
management should be toward delivery.
• The most probable cause of PROM is a reduction in
membrane tensile strength caused by the effect of
PREMATURE RUPTURE OF MEMBRANES bacterial proteases or by repeated stretching caused
by uterine contractions
(PROM) • Most common infection is bacterial vaginosis (
Chlamydia and group B streptococcus)

➢ Definition PRESENTATION

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• The membranes probably are intact if the color of the
• Patients present with a typical history of sudden paper remains yellow or changes to olive-yellow (pH
gush of clear or pale yellow fluid leaking from 5.0 to 5.5).
vagina.
• However many women may present with history of • False result: Antiseptic solution, urine, blood, and
intermittent or constant leaking of small amounts of vaginal infections alter the vaginal pH and cause false-
fluid or just sensation of wetness within the vagina ( positive results.
confused with vaginal discharge)
➢ Fern test
➢ O/E :
• Per speculum examination - First step in the
diagnosis of PROM is a sterile per speculum
examination to demonstrate leaking.
• Pooling of fluid in the posterior fornix or leakage of
fluid from the cervical os confirms the diagnosis of
PROM.
• A per vaginal examination should not be done as it
increase the risk of intrauterine infection and
preterm labour.
• If the condition is still doubtful some tests are done

Tests done to confirm amniotic fluid


• Ferning results from the drying of salts contained in
the amniotic fluid.

• Nitrazine Test and


• To perform the test, a sample of fluid is placed on a
glass slide and allowed to dry.
➢ Nitrazine test for Diagnosis of PROM : • The preparation is observed under the microscope,
looking for a crystallization pattern that resembles a
fern, which is the seen if membrane have ruptured.
• The accuracy of the test is affected by blood,
meconium and cervical mucus.
• The diagnosis of PROM is close to 100% reliable if the
vaginal fluid gives both positive nitrazine and
positive fern tests

• Principle: The vaginal pH is normally 4.5 to 5.5,


where as amniotic fluid usually has a pH of 7.0 to 7.5. MANAGEMENT
• Test: Nitrazine paper is smeared with vaginal ➢ PPROM without amnionitis and foetal distress
secretions. • < 34 weeks : expectant management with
antimicrobials in a high obstetric dependency unit
• Result: Nitrazine paper will turn deep blue if
with well equiped NICU
amniotic fluid is present in vagina i.e. if membranes
have ruptured • 34 – 37 weeks : wait for spontaneous onset of labour
for 24 – 48 hrs, if it fails then LSCS
• This is because pH will become alkaline.

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• > 37 weeks : wait for spontaneous onset of labour for ➢ Post Dated Pregnancy : Confused Doctor &
24 – 48 hrs, if it fails then LSCS Patient
• Most common cause is wrong dates
➢ CHORIOAMNIONITIS and PROM • If the patient is sure about her date - regular cycles - ,
it is reliable
• Acute Chorioamniotis is diagnosed Clinically in • The previous well documented antenatal records of
presence of fever ( >100 for 37.8 C) and atleast two of first visit in first trimester if available, are useful
the following: guides.
• a. Maternal Tachycardia • If not available then consider any other EDD
• b. Fetal Tachycardia
• c. Uterine tenderness
• d. Foul smelling amniotic fluid COMPLICATION
• e. Maternal leucocytosis
❖ FOETAL COMPLICATION

• When chorioamnionitis is diagnosed, fetal and ➢ Still Birth


maternal morbidities increase and delivery is ✓ Ageing of placenta – foetal hypoxia – foetal
indicated regardless of the fetus's gestational age. acidosis – foetal distress – foetal death

➢ Foetal macrosomia
POST DATED PREGNANCY ✓ Increased weight gain by the baby – macrosomia -
--difficulty in vaginal birth
• A pregnancy continuing beyond two weeks of the
expected date of delivery (> 42 weeks or >294 days) ➢ Shoulder dystocia and cord prolapse
is called postmaturity or post-term pregnancy ✓ Gestation increases – amniotic fluid decreases –
oligogydramnios – more chances of shoulder
➢ Causes of Post term pregnancy: dystocia and cord prolapse

• Wrong dates: due to inaccurate LMP (most common). ➢ Meconium Aspiration Syndrome
• Biologic variability (Hereditary) may be seen in the ✓ Foetal distress and oligohydramnios
family.
• Maternal factors: Primipara / elderly multipara / H/o ➢ IVH
previews prolonged pregnancy, sedentary habit. ✓ Oligohyramnios – less proper engagement – less
• Fetal factors: Congenital anomalies: Anencephaly - moulding
(Abnormal fetal HPA axis), adrenal hypoplasia
(Diminished fetal Cortisol response). ❖ Neonatal complications:
• Placental factors: Sulphatase deficiency (Low ✓ Chemical pneumonitis, atelectasis and pulmonary
oestrogen). hypertension due to meconium aspiration.
✓ Hypoxia and respiratory failure.
✓ Hypoglycemia & Polycythemia.

CHAPTER – 14
ABNORMAL LABOUR

UTERINE RUPTURE

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➢ Rupture Uterus 1. Spontaneous
• Disruption in the continuity of the all uterine layers 2. Scar rupture
(endometrium, myometrium and serosa) any time 3. Iatrogenic
beyond 28 weeks of pregnancy is called rupture of the
uterus. • Each of them is further classified as
• Any disruption before 28 weeks is called as ✓ During pregnancy
perforation ✓ During labour

1. SPONTANEOUS RUPTURE

➢ During pregnancy
• It is rare for an apparently uninjured uterus to give
way during pregnancy. -
o The causes are:
• (1) Previous damage to the uterine walls following
dilatation and curettage operation or manual removal
of placenta
• (2) Grand multiparae ( due to weak uterine walls)
• (3) Congenital malformation of the uterus (bicornuate
variety)
❖ PATHOLOGICAL CLASSIFICATION
• (4) In Couvelaire uterus.
• Uterine rupture can be complete and incomplete
o Spontaneous rupture during pregnancy is usually
depending on whether the peritoneal coat is involved
complete, involves the upper segment and usually
or not.
occurs in later months of pregnancy
• Incomplete rupture usually results from rupture of
the lower segment scar or extension of a cervical tear
into the lower segment with formation of a broad
➢ During labor:
• Spontaneous rupture which occurs predominantly in
ligament hematoma.
an otherwise intact uterus during labor. It is due to:
• Complete rupture usually occurs following disruption
o Obstructive rupture—This is the end result of an
of the scar in upper segment.
obstructed labor. The rupture involves the lower
segment and usually extends through one lateral side
❖ CLINICAL CLASSIFICATION
of the uterus to the upper segment.
➢ Scar dehiscence:
o Non-obstructive rupture—Grand multiparae are
✓ Disruption of part of scar and not the entire
usually affected and rupture usually occurs in early
length
labor. The rupture usually involves the fundal area
✓ Fetal membranes remain intact and
and is complete.
✓ Bleeding is almost nil or minimal.
➢ Scar rupture:
2. SCAR RUPTURE
✓ Disruption of the entire length of the scar
✓ The incidence of lower segment scar rupture is
✓ Complete separation of all the uterine layers
about 1-2%, while that following classical one is 5-
including serosa
10 times higher.
✓ Rupture of the membranes with
✓ Uterine scar, following operation on the non-
✓ Varying amount of bleeding from the margins or
pregnant uterus such as myomectomy or
from its extension
metropiasty hardly rupture.
✓ Uterine cavity and peritoneal cavity become
✓ Uterine scar following hysterotomy behaves like
continuous
that of a classical scar.
• During pregnancy :
❖ TYPES OF RUPTURE
➢ Classical cesarean or hysterotomy scar is likely to give
• The causes of rupture of the uterus are broadly
way during later months of pregnancy.
divided into:
• Lower segment scar rarely ruptures during pregnancy.

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➢ During labor : • Use of prostaglandins for induction of abortion or
➢ The classical or hysterotomy scar is more vulnerable labor
to rupture during labor. lower segment scar • Forcible external version specially under general
predominantly ruptures during labor, although rare anesthesia

➢ During labor.
• Internal podalic version—specially following
obstructed labor
• Destructive operation
• Manual removal of placenta
3.IATROGENIC OR TRAUMATIC • Application of forceps or breech extraction through
incompletely dilated cervix
➢ During pregnancy: • Injudicious administration of oxytocin for
• Injudicious administration of oxytocin augmentation of labor

---------------------------------------------------------------------------------------------------------------------------------------------------------------
✓ Mother will immediately go into shock and may die
on the labour table itself
❖ RECURRENCE RATES IN SCAR RUPTURE
✓ Classical : 2-9 % ❖ MORTALITY
✓ One low-transverse : 0.2-1.8 % ✓ With rupture and expulsion of the fetus into the
peritoneal cavity, the chances for intact fetal
❖ Clinical features of Ruptured Uterus survival are dismal
✓ Foetal Morality rates range from 50% to 75%.
➢ Impending Sear Rupture (Scar Dehiscence) ✓ Maternal mortality rates are very high,
✓ Unexplained maternal tachycardia emergency cesarean with caesarean
✓ Weak, thready & fast pulse hysterectomy are the only options
✓ Hypotension shock
✓ Fetal tachycardia
✓ Persistent fetal bradycardia
✓ Variable and late decels
✓ Uterine scar tenderness.
✓ Bleeding p/v SHOULDER DYSTOCIA
✓ Hematuria
➢ Definition
➢ Ruptured uterus • The term shoulder dystocia is used to define a wide
✓ Electronic fetal monitoring finding is sudden, severe range of difficulties encountered in the delivery of
heart rate decelerations that may evolve into late the shoulders.
decelerations, bradycardia, and undetectable fetal • A head to body delivery time exceeding 60 secs
heart action. defines shoulder dystocia
✓ In some cases in which the fetal presenting part has
entered the pelvis with labor, loss of station may be ➢ Risk factors:
detected by pelvic examination. • Shoulder dystocia can occur in all those conditions
✓ If the fetus is partly or totally extruded from the site where fetus is too big or in case of mismanaged
of uterine rupture, abdominal palpitation or vaginal labour.
examination may be helpful to identify the presenting • Maternal diabetes
part, which will have moved away from the pelvic • Maternal obesity and fetal obesity i.e macrosomia
inlet. • Post term pregnancy
✓ A firm contracted uterus may at times be felt • Anencephaly
alongside the fetus. • Fetal ascites

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❖ COMPLICATIONS
➢ MATERNAL
• Intrapartum chorioamnionitis, Laceration of birth
canal, Rupture uterus, Genital fistula, Urinary or anal
incontinence, Genital organ prolapse, PPH
➢ FOETAL
• Most common complication of shoulder dystocia is
Brachial plexis injury
• Death due to asphyxia
• Meconium aspiration syndrome
• Erb’s paralysis ( C5,C6, C7) adducted, internally ➢ 3rd Line
rotated and pronated arm • Cleidotomy (# clavicle of baby)
• Klumpke’s paralysis ( C8, T1) claw hand • Symphiosotomy (divide pubic symphysis of mother)
• Clavicle or Humerus # • Zavaneilli manouvre
• Sternocleidomastoid tumor (push head backand do cesarean)

❖ SHOULDER DYSTOCIA DRILL


• It is a series of events done in order to deliver a
shoulder dystocia

➢ McRoberts' manoeuvre

➢ 1st Line of management


• Stop giving fundal pressure
• Can give supra-pressure
• Best/most effective pubic pressure manouvre Mc
Roberts manouvre • It consists of forcible abduction of patients legs by
(flexion and abduction of thigh) sharply flexing them on the abdomen.
• It is the single most effective manoeuvre and should
➢ 2nd Line :Woods Corkscrew manouvre be the first manoeuvre to be performed in case of
shoulder dystocia.
• McRobert's manoeuvre results in straightening of the
sacrum relative to the lumbar vertebra along with

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rotation of symphysis pubis towards the maternal ✓ Maternal:
head and it decreases the angle of pelvic inclination. • Contracted pelvis/CPD.
• Sometimes, over zealous use of McRobert's • Pelvic tumours like fibroids or ovarian tumours.
manoeuvre may result in separation of the maternal • Cervical dystocia due to previous scarring.
pubic symphysis and injury to lateral cutaneous
nerve of thigh. ✓ Fetal:
• Malposition (persistent occipito-posterior or deep
❖ Partum Neuropathies transverse arrest).
• Prolonged second stage of labour can injure the • Malpresentations (neglected shoulder, brow or
Common Fibular Nerve caused by inappropriate leg persistent mentoposterior).
positioning in the stirrups • Macrosomia.
• M/C Nerve injury seen in post partum females = • Fetal anomalies (hydrocephalus, fetal ascites and
✓ Lateral femoral Cutaneous nerve followed by abdominal tumours, conjoined twins).
femoral nerve
✓ Nerve injuries seen with cesarean delivery
include iliohypogastric and ilioinguinal nerves. ❖ Clinical Features
➢ General examination:
Risk factors for neuropathy
• The mother is exhausted, dehydrated, febrile and
✓ Nulliparity
urine may show ketone bodies.
✓ Prolonged second stage of labor
✓ Pushing for a long duration in the semi fowler position • Hematuria i.e., blood is present in urine

➢ Abdominal examination:
• Uterus may be tonically contracted over the fetus.
• Difficulty in palpating the fetal parts.
• Bandl's ring running obliquely over the uterus and
OBSTRUCTED LABOUR rising up.
• The upper and lower segments will be sharply
➢ DEFINITION demarcated.
• Evidence of fetal distress/Fetal heart sounds are
usually absent.
➢ Vaginal examination:
• Vagina is usually hot and dry and there may be
offensive discharge
• Cervix is fully dilated and may be felt hanging loose.
• Membranes are absent
• Presenting part is usually jammed in pelvis.
• There may be hand prolapse in a neglected shoulder
presentation.
• In cephalic presentations, there will be a large caput
and irreducible moulding.
✓ Labour is said to be obstructed when despite • So the lower pole may appear to be quite low even
good uterine contractions, there is arrest of when the major part of the head is above the pelvic
progress due to mechanical factors causing inlet and palpable per abdomen.
obstruction to delivery.
✓ The uterine contractions are normal ( power is ➢ BLADDER IN OBSTRUCTED LABOUR
normal) • In obstructed labour the bladder becomes an
✓ There is a problem in passage or passenger abdominal organ due to compression of urethra
between the presenting part and symphysis pubis
➢ Causes: • The patient fails to empty the bladder.

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• The transverse depression at the junction of the ➢ Pathophysiology :
superior border of the bladder and the distended • In case of obstructed labour, the upper segment of
lower segment is often confused with the Bandles the uterus contracts and retracts vigorously, in an
ring. attempt to overcome the obstruction while the lower
• The bladder wall gets traumatised which may lead to segment dilates.
blood stained urine, a common finding in obstructed • With each contraction there is myometrial shortening,
labour so that the actively contracting upper segment
• The bladder wall compressed between the foetal becomes progressively thicker and shorter.
head and pubic symphysis may undergo pressure • The passive lower segment is progressively stretched
necrosis and lead to formation of VVF and becomes thinner.
✓ Though hematuria can also indicate impending • The junction between the two segments stands out
uterine rupture but for that obviously the patient prominently as a pathological retraction ring or
should have a previous scar Bandl's ring.
• Situation: It runs obliquely and is always situated at
❖ Management Of Obstructed Labor the junction of upper and lower segment.
✓ Three main principles in ther are-
➢ On abdominal examination:
• Never wait and watch
• Uterus is tense and tender
• To control sepsis.
• Fetal parts are not easily felt
• Never use oxytocin.
• Ring is felt as a groove placed obliquely
✓ In case of obstructed labor there is a problem with
• FHS is absent
either the passage or the passenger bur the uterus • Round ligaments are palpable.
contracts adequately, so if we increase uterine
contractions by giving oxytocin it will lead to uterine
➢ On vaginal examination: Ring cannot be felt
rupture.
vaginally.
➢ Management of obstructed labor-
❖ Schroeder's ring
• Management of dehydration- by giving i:v fluids
• It is also called as constriction ring
• Antibiotics are given to prevent infection
• Constriction ring is a form of incoordinate uterine
• Most important step is to relieve obstruction
action where there is localised spastic contraction of a
➢ The mode of relieving obstruction is based on foetal
ring of circular muscle fibres ofthe uterus.
viability
• Usually situated at the junction of the upper and lower
segment around neck in cephalic presentation.
✓ Viable foetus • It forms a constriction through which the foetus cant
• Immediate cesarean pass
✓ Dead foetus
• Perform a destructive procedure and relieve the ➢ Management:
obstruction • If the ring is diagnosed at the time of cesarean
• If the obstetrician is not well versed with destructive section: it should be cut vertically to deliver the baby.
procedures then immediate cesarean • If there is failure to deliver the head even after
• Immediate cesarean even in a dead baby because
correct application of forceps: constriction ring
even a dead baby causing obstruction can lead to
should be suspected and LSCS should be done.
rupture or severe infections
• If the ring is diagnosed at the time of manual removal
of placenta, plane of anesthesia should be deepened.
❖ Bandl's ring
• It is also called as Pathological retraction ring.
• It is formed in cases of obstructed labour0.

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FEATURE RETRACTION RING CONSTRICTION RING
BANDL’S RING SCHROEDER’S RING

NATURE END RESULT OF TONIC CONTRACTIONS IN AN RESULT OF IN CO ORDINATE UTERINE


OBSTRUCTED LABOR CONTRACTION
CAUSE OBSTRUCTED LABOUR UNDUE IRRITABILITY AND IN CO ORDINATE
ACTIVITY
SITUATION BETWEEN UPPER AND LOWER SEGMENTS USUALLY BETWEEN UPPER AND LOWER
MOVES PROGRESSIVELY UPWARDS SEGMENTS
CAN BE FORMED ELSEWHERE
DOESN’T MOVE UPWARDS
UTERUS UPPER SEGMENT CONTRACTS AND RETRACTS UPPER SEGMENT TONICALLY CONTRACTED
WITH RELAXATION AND THICK
LOWER SEGMENT REMAINS THICK AND LOWER SEGMENT PROGRESSIVELY THINS OUT
LOOSE

GENERAL CONDITION EXHAUSTED, KETOTIC, DEHYDRATED AND GOOD


SEPTIC

P/A UTERUS TENSE & TENDER UTERUS NON TENDER


FOETAL PARTS NOT FELT FOETAL PARTS FELT
RING FELT AND MOVES UP RING NOT FELT
ROUND LIG. – TAUT AND FELT ROUND LIG. – NOT FELT
FHS ABSENT FHS PRESENT

P/V FEATURES OF OBSTRUCTION PRESENT FEATURES OF OBSTRUCTION


RING NOT FELT ABSENT
RING FELT

END RESULT BAD GOOD

CHAPTER – 15
ANTEPARTUM HAEMORRHAGE

ANTE PARTUM HAEMORRHAGE


• Ante partum haemorrhage is defined as bleeding ➢ CAUSES of Antepartum Hemorrhage
from or into the genital tract after foetal viability or • Placenta previa
upto viability • Abruptio placenta
• Viability is considered upto 28 weeks • Vasa previa
• Latest developments in obstetrics and neonatology • Circumvallate placenta
has lowered the cut off age to 22 weeks

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▪ Local causes like: Polyp, Carcinoma cervix, Varicose ✓ Principle:
veins, Trauma • Fetal blood has fetal hemoglobin (HbF) and maternal
• Unclassified or indeterminate blood has adult hemoglobin (HbA). - HbF is resistant
to alkali denaturation (not HbA) - when KOH/NaOH is
➢ GUIDELINES FOR ADEQUATE BLOOD added, it remains pink if blood is of fetal origin.
TRANSFUSION • If it is maternal blood it turns yellow brown in 2
• Maintainence of minutes as HbA is denatured easily.
• Central venous pressure at 10 cm of water.
• Hematocrit = 30%
✓ Application
• Urinary output = 30 ml/hour
• Used to detect the presence or absence of fetal blood
(qualitative) in a vaginal discharge
• FOETAL AND MATERNAL BLOOD ADMIXTURES
• To detect the origin of a neonatal blood vomiting,
upper Gl hemorrhage or swallowed maternal blood
during delivery or from cracked nipple.
✓ In ante partum haemorrhage the bleeding occurs per
vagina
➢ Kleihauer Bhetke test
• This bleeding could be from the uterine maternal
sinuses or from the foetus or both mixed in various
proportions
• It is a quantitative method of detecting how much
foetal blood has leaked into maternal circulation

✓ In Rh incompatibility
✓ Principle
• At the time of birth few foetal RBC’s enter maternal
• A standard blood smear is prepared from the
circulation
mother's blood, and exposed to an acid bath.
• This leads to foeto maternal admixture
• This removes adult hemoglobin, but not fetal
hemoglobin, from the red blood cells.
• In order to detect these and to differentiate foetal
blood from maternal blood the following tests are
done
✓ Rationale
➢ Alkali denaturation test
➢ Kleihauer Bhetke test • When fetal blood needs to be differentiated from Apt
test is used (Qualitative estimation) maternal blood
➢ Singers alkali denaturation test • When the amount of fetal bleeding needs to be
estimated Kleihauer-Betke test is used (Quantitative
estimation)
• Also called as ‘Apt test’ or Apt Downey Test
• It was invented by a paediatric ophthalmologist
Leonard apt

--------------------------------------------------------------------------
• It is rare condition and occurs in 1 in 2000 - 3000
VASA PREVIA deliveries but is a dreaded condition
• Blood loss which occurs is fetal in origin and so there
• It is a condition in which the fetal blood vessels is increased fetal mortality - (75 to 90%), maternal
unsupported by either umbical cord or placental mortality is not increased
tissue overlies the internal os and is vulnerable to
rupture when supporting membrane rupture. ✓ Vasa previa is associated with high fetal mortality
• Thus bleeding in case of vasa previa is of fetal origin because
and not maternal origin (unlike placenta previa and • Wharton's jelly is absent around the fetal vessels,
abruptio) hence they can be easily lacerated at the time of

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rupture of membranes leading to severe fetal • Emergency LSCS should be done if it is diagnosed
bleeding. intrapartum.
• Vessels can be easily compressed by the fetal
presenting part during uterine contractions leading to
fetal exsanguination.

✓ Vasa previa should be suspected if


• Velamentous cord insertion
• Bilobed placenta
• Succenturiate lobed placenta
• Placenta previa /low lying placenta in second
trimester ➢ Circumvallate placenta
• Pregnancy resulting from IVF
• Multiple pregnancies • It is an uncommon cause of antepartum hemorrhage,
• In this condition, the chorionic plate which is on the
fetal side of the placenta is smaller than the basal
plate on the maternal side.
• The fetal surface of the placenta presents a central
depression surrounded by a thickened grayish white
ring.
• These pregnancies may be complicated by IUGR and
an increased chance of fetal malformations.
• Bleeding is usually painless
• Antenatal diagnosis is unlikely and the diagnosis is
usually made after examination of the placenta post
delivery

✓ Diagnosis

o Antenatal
• Doppler examination can also reveal fetal blood
vessels traversing below the presenting part

o Intra partum
• In all cases of antepartum and intrapartum
hemorrhage, the possibility of vasa previa should be
kept in mind and blood should be tested for fetal
hemoglobin characterized by resistance to
denaturation by alkaline reagent (Singer alkali
denaturation test/Apt test)
• When bleeding occurs: Sinusoidal fetal heart rate
pattern seen
DIC – DISSEMINATED INTRAVASCULAR
COAGULOPATHY
• Management-
• In a diagnosed case of vasa previa elective cesarean
section should be done

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• It is a pathological condition associated with
inappropriate activation of coagulation and LABORATORY FINDINGS IN DIC
fibrinolytic system.
• This leads to coagulation inside the blood vessels ✓ Pathological findings
• This extensive coagulation all over the body leads to • The platelet count is low.
usage (consumption) of platelets and all clotting • Blood film shows the features of microangiopathic
factors hemolytic anaemia.
• Hence the platelet and coagulation factor deficiency • There is presence of schistocytes and fragmented red
leads to bleeding tendencies, haemorrhages and cells (helmet shaped)
death • These fragmented cells are formed due to damage
• It is secondary phenomenon resulting from an caused by trapping and passage through the fibrin
underlying disease state. thrombi.
• Several system disease can lead to DIC but obstetric
diseases have special predisposition to DIC ✓ Biochemical findings
• Prothrombin Time (PT) elevated to 11 – 16 secs
OBSTETRIC CAUSES OF DIC (N is 12 – 13 secs)
• Activated Partial Thromboplastin Time aPTT is
➢ More common - Intrauterine fetal death, Amniotic prolonged to > 40 secs
fluid embolism, Pre eclampsia- Eclampsia, HELLP (N is 22 – 37 secs)
syndrome, Placenta Abruption, Septic Abortion
• Plasma fibrinogen levels are reduced < 200mg/dl
(N is 200 – 400 mg/dl)
➢ Less common
• Chorioamnionitis, Pyelonephritis in pregnancy, H. • Fibrin degradation products (FDPs) are raised
(N is < 10 mcg/dl)
mole, Instillation of intraamniotic hypertonic saline,
Feto maternal bleed, Incompatible blood transfusion, • D-dimer levels are raised (N is < 0.5 mcg/dl)
Viremia -HIV, varicella, CMV hepatitis • Platelets are reduced (N is 1.5 – 3.5 lakh / cumm)

AMNIOTIC FLUID EMBOLISM


PATHOGENESIS ➢ It occurs due to sudden entry of amniotic fluid into
systemic circulation
➢ Endothelial injury is the inciting factor which leads to
tissue distruction ➢ Onset
• Damaged tissue releases thromboplastin • It usually may present on the labour table when the
• This thromboplastin acts as factor III and activates the patient is at the height of uterine contraction
coagulation cascade • It is usually fatal and is characterised by an abrupt
• The activated cascade then causes deposition of fibrin onset of respiratory distress and coagulopathy.
and platelets onto the vessel lumen • It should be considered in all cases of peripartum
• This leads to consumption of all platelets and clotting collapse.
factors • Classically a woman in late labor or immediate
• Deposition of fibrin in vessels leads to microvascular postpartum gasps for air, has bronchospasm,
occlusion which can further lead to ischemia of becomes cyanotic and undergoes immediate collapse
several organs firstly kidney and cardiorespiratory arrest usually accompanied by
• The fibrin activates anti fibrinolytic pathways leading haemorrhage
to conversion of plasminogen to plasmin • Sudden death is usual.
• Plasmin then degrades fibrin to form fibrin
degradation products (FDP’s) ➢ Timing:
• These FDP’s cause further bleeding • After ARM and at cesarean section.

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• In labor with strong uterine contractions. • Deliver foetus immeditely to avoid cord compression
• Immediate postpartum. and distress

➢ Pathogenesis • Named classifications and Regimes


• Embolic component causes acute respiratory distress
syndrome and ultimately death. ➢ Macaffee and Johnson Regime
• Coagulation failure causes hemorrhage, DIC and • Expectant management of placement previa
consumptive coagulopathy. ➢ Page classification
• Abruptio plcenta
➢ Risk factors: ➢ Sher classification
• Advanced maternal age • abruption placenta
• Multiparity
• Tetanic uterine contraction ➢ Clarke's classification
• Use of uterine stimulants • Classification of heart disease based on
maternal mortality
• Uterine rupture
➢ Lytic cocktail regime (used 3 drugs -
• Cesarean section chlorpromazine, Promethazine and pethidine)
• Premature separation of placenta • Proposed by Menon for management of
• Intra uterine fetal death. convulsion in eclampsia
• Amniotic fluid enters maternal circulation as a result ➢ Whites classification
of breech in the physiological barrier that normally • Earlier used for classification of diabetes in
exists between maternal and fetal compartments pregnancy
zso, any cause leading to this mixing like cesarean ➢ Caldwell and mohoy classification
section, premature separation of placenta, rupture • Types of pelvis
uterus etc predisposes to amniotic fluid embolism.

➢ Management
• Aimed at minimizing hypoxemia with supplemental
oxygen, mantaining blood pressure and managing
associated coagulopathy
PLACENTA PREVIA ➢ Type 4 Central Placenta covers the internal os even
when fully dilated
➢ Definition
• Placentra praevia is defined as a placenta located
partly or completely in the lower uterine segment.
The bleeding
• It is called inevitable or unavoidable haemorrhage as
dilatation of the internal os inevitably results in
haemorrhage.

➢ Browne's classification for placenta previa


➢ Type 1 Lateral Placenta-dipping into the lower
segment but not reaching uptothe os
➢ Type 2 Marginal Placental edge reaches the internal
Os • Incidence of placenta previa ranges from 0.5 to 1%
➢ Type 3 Incomplete central Placenta covers the among hospital deliveries.
internal os when closed, but not when fully dilated • According to 2003 birth certificate data in the US,
placenta previa complicated almost 1 in 300 deliveries

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• Type 1 and 2 are called minor degrees and type 3 and • Fetal heart sounds will usually be heard (c.f.
4 called major degrees of placenta previa. abruption).
• Type 1 and 2 can be anterior or posterior. • Slowing of the fetal heart rate on pressing the head
down into the pelvis and prompt recovery on release
➢ Dangerous type of the pressure is termed Stallworthy's sign and is
Type 2 posterior placenta is also called the 'dangerous suggestive of posterior placenta previa.
type' as it is more likely to be compressed producing • VAGINAL EXAMINATION SHOULD NOT BE DONE IN
cord compression. SUSPECTED PLACENTA PREVIA
This can cause fetal asphyxia and even death.

➢ P/V in placenta previa


➢ Risk Factors • In placenta previa P/V examination is contraindicated
• Previous history of placenta previa (12 times more since the finger passes beyond the internal os inorder
risk)-most important risk factor. to know the exact location of the placenta
• Multiparity and increased maternal age • This in turn can lead to more separation of the
• H/O any previous uterine surgery (4 time more risk) placenta and cause torrential haemorrhage
• Previous uterine currettage
• Increased placental size as in multifetal pregnancy ➢ Stallworthy's sign:
• Succenturiate lobe • Slowing of the fetal heart rate on pressing the head
• Smoking (due to defective decidual vascularisation) - down into the pelvis and prompt recovery upon
two fold times release of the pressure is termed
• Elevated prenatal maternal serum alpha fetoprotein • It is suggestive of posterior placenta previa.
levels (unexplained) • Presence of this sign is not always significant because
it may be due to fetal head compression even in an
CONTRACEPTION AND PREVIA other normal case.
• Increased family planning acceptance with limitation
and spacing of birth, lowers the incidence of placenta INVESTIGATIVE WORK UP
previa.
• Hence previa is less in the developed world ➢ Investigation of choice: TVS
• Though P/V examination is contraindicated TVS is safe
- the probe never touches the cervix or maximally is
Clinical Features kept in the cervical canal

➢ SYMPTOMS ➢ Double set up examination


• The classical presentation is painless antepartum • This refers to the P/V examination in the operation
haemorrhage. theatre with all arrangements of cesarean section
• The typical history is of the woman waking up lying in • These days the need for double set up has decreased
a pool of blood. as the placental location can always be ascertained
• The bleeding is usually massive in amounts sonographically.
• This is a more bookish approach wherein if the margin
➢ SIGNS of placenta is beyond 2cm from internal os then a
• Pallor, if present, will be proportionate to the amount vaginal delivery can be attempted
of bleeding (cf abruptio)
• Size of the uterus corresponds to the period of
amenorrhoea. (cf abruptio) ➢ Avoid double set up examination in
• Uterus is soft and non tender. (cf abruptio) • Double set up should be avoided in those patients
• Malpresentations are common and if it is a cephalic where there is an emergency so no point in wasting
presentation, the head if usually floating. time to know the type of placenta previa by vaginal

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examination and taking the risk of occurrence of brisk • Patient is admitted for the rest of the pregnancy
hemorrhage • Complete bed rest with only bathroom previledges
• These conditions mandate cesarean section • Periodic inspection of vulval pads
• Avoid a P/v even in OT • Correct anaemia if any by blood transfusion
• Inj betamethasone is given to hasten the lung
maturity of the fetus
• Blood is crossmatched and kept ready just in case
patient starts bleeding again
• Tocolysis if bleed is associated with uterine
contractions
MANAGEMENT • Should be continued till 37 weeks only and not
beyond that even if all the criteria are met
There are two types of management for placenta previa • If anytime during expectant management patient
based on certain criteria rebleeds, pregnancy should be terminated
They are: immediately with out foetal concerns
➢ Expectant management • Anti D injection to all Rh –ve patients
➢ Active management

▪ The most important guiding principle is when the ➢ Active management


mother’s life is at risk don’t think about saving the
baby ➢ Goal: To terminate pregnancy immediately
irrespective of gestational age to save the mother
➢ Expectant management Baby is not of prime concern
• It is called as Macaffee and Johnson regime
➢ Indications
➢ Goal • If active bleeding is present
• To carry pregnancy till term without putting mother’s • Hemodynamically unstable/shock
life at risk with an aim to achieve fetal lung maturity. • Gestational age >37 weeks and patient in labour
• Fetal distress present/ FHS absent
➢ Indications • USG shows fetal anomaly or dead fetus
• No active bleeding present
• Hemodynamically stable and haematocrit > 30%
• Gestation age <37 weeks ➢ Mode of delivery
• CTG-should be reactive • Mode of delivery practically in all patients of placenta
• No fetal anomaly on USG previa is -Cesarean section
• Co operative or educated patient with supportive • Earlier it was said that for minor degrees of placenta
family previa, vaginal delivery can be tried
• Presently irrespective of degree of placenta previa,
➢ Pre requisites for Macafee cesarean section is done and recommended.
• 24 hours blood bank services with readily available
blood (kept cross matched for the patient)
• Round the clock surgical obstetrician to immediately COMPLICATIONS OF PREVIA
perform cesarean section and terminate the
pregnancy if required ➢ Maternal
• Round the clock anaesthetist and operative OT’s • Antepartum haemorrhge, Intrapartum hemorrhage,
• Possible only for co – operative patients Postpartum haemorrhage, Malpresentation, Cord
prolapsed, Retained placenta, Preterm labour,
Protocol: Premature rupture of membranes, Slow dilatation of
cervix

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➢ Fetal
• Asphyxia, Birth injuries, Low birth weight, Congenital
malformation, Intrauterine death, M/C fetal
complication of placenta previa: Low birth weight
baby

➢ Placenta previa and PPH


• A major problem with placenta previa, is that after
delivery of fetus, it leads to PPH as bleeding occurs
from the placenta site. ➢ Concealed
• There is a greater chance to bleed from the lower In this the bood gets collected behind the placenta and
segment because it is deficient in muscles and the forms the retro placental clot
muscles in this segment lack power hence it is more Sometimes it may be due to collection between the
difficult for natural ligatures to be applied decidua and membranes but it can’t present at vagina
• This should be managed like PPH & if all conservative because the presenting part is firmly pressed over the
measures fail-hysterectomy is done. cervix

➢ Placenta previa and placenta accreta are M/C causes


of peripartum hysterectomy.

➢ Placenta previa and placenta accreta


• These both conditions are neither the cause or effect
of each other
• But they are related because
• Placenta previa is implantation in lower uterine
segment ➢ Mixed
In this type it is partly revealed and partly retroplacenta
• Placenta accreta is more common in lower uterine
segment due to poor decidual reaction
• Hence they are both related by ‘lower uteruine
segment’

ABRUPTIO PLACENTA

➢ Definition
• Abruptio placenta is defined as haemorrhage
occurring in pregnancy due to the separation of a
normally situated placenta.
➢ Risk Factors
• It is also called accidental haemorrhage or premature
• The risk factors usually are not diagnosable at the
separation of placenta.
time of presentation

➢ Types of abruption
➢ Usual risk factors are
• Hypertension (most important predisposing factor)
➢ Revealed
• High birth orders (> 5) – three times more than in
In this type the blood seeps between the decidua and the
primi
membranes to present at the vagina

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• History of previous abruption (5 – 17 % recurrence)
• Advanced age of mother, Low socio economic areas
• Maternal malnutrition, Maternal smoking

➢ Other causes include


• External trauma, Sudden decompression of uterus,
Short cord, Supine hypotension syndrome,
Circumvallate placenta, Sick placenta, Uterine
myomas, Torsion uterus, Cocaine abuse,
Thrombophilias, Folic acid deficiency

➢Pre eclapsia and abruption


• Pre eclampsia causes spasm of the vessels in the
utero placental bed (decidual spiral artery) - anoxic
endothelial damage - leads to bleeding from the
damaged vessel - collects as blood beneath the
placenta and clots (retroplacental clot)

Couvelaire Uterus
• It is also called as utero placental apoplexy ➢ Incidence
• It occurs due to massive extravasation of blood into • It is 1: 200, It is less than previa
the myometrium upto the serosa - Spreads from the • Accounts for 5 % maternal mortality and 20%
cornua - May spread to broad ligament (haematoma) perinatal mortality
• Uterus appears as dark port wine discoloration diffuse
or patchy - petechial haemorrhages appear beneath
the peritoneal layer CLINICAL FEATURES
• Blood may spill in the peritoneal cavity
• The only diagnosis is laprotomy ➢ Symptoms
• Conservatively managed with regular coagulation ➢ Severe and constant abdominal pain
screening Bleeding is present in the revealed and mixed types, but
• If bleeding is not controlled hysterectomy may be absent in the concealed type
More in the concealed and less in the revealed types
➢ Bleeding per vaginum.
➢ Loss of fetal movements.

➢ Signs
➢ Pallor, which is usually out of proportion to the extent
of bleeding especially is conceled and mixed
➢ Hypertension (if there is associated pre-eclampsia)
➢ The uterus will be larger than expected for the period
of amenorrhoea especially in concealed and mixed
➢ Uterus may be tense and tender and even rigid
(woody hard) - couvelaire uterus
➢ Difficulty in palpating the underlying fetal parts easily
➢ Fetal distress or absent fetal heart sound

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• Haematocrit and Hb%
COMPLICATIONS
➢ Ultra sonography
➢ Maternal
• The complications in revealed variety is usually • Early bleed presents as hyperechoic or isoechoic
proportionate to the amount of blood lost, • Concealed variety presents as a retroplacental blood
complications are less, less severe and death is rare clot
• The complications in concealed are out of • Abruption may be diagnosed on USG as a diagnosis of
proportionate to blood loss, complications are more, exclusion
more dangerous and permanent morbidity or
➢ Coagulation profile
mortality is common
• Of DIC

➢ The complications are ➢ Warnings:


• Haemorrhage, Maternal shock, DIC, Oliguria and • Never give tocolytics in patients of abruptio
anuria, Post partum haemorrhage, Puerperal sepsis,
➢ Mode of Termination
Sheehan’s syndrome
– Fetus dead
➢ Foetal • Vaginal delivery without wasting time (ARM +
• Foetal death is very common with abruption oxytovin)
• In revealed variety it is 25 – 30% • LSCS if there is the presence of severe torrential bleed
• In concealed variety it is 50 – 100% not controlled even by massive blood transfusions
• Death is due to anoxia or sometimes due to and other indicative obstetrical factor.
prematurity (delivered alive at an earlier date)
– Fetus living
INVESTIGATIVE WORK UP • Fetal distress present – LSCS without wasting time
➢ The most important investigations are • No fetal distress and vaginal delivery is obstetrically
• Ultra sonography possible - vaginal delivery without wasting time (ARM
+ oxytocin)
• Coagulation profile

CHAPTER – 16
COMPLICATIONS OF THE THIRD STAGE

POST PARTUM HAEMORRHAGE ✓ Quantitative definition


• Post Partum Hemorrhage (PPH) is blood loss of more
• As the word suggests PPH is the haemorrhage or than 500 ml from the genital tract following child
bleeding after birth of the baby birth
• It is usually referred to the bleeding in anytime after • Major PPH: blood loss more than 1000ml
the second stage of labour
• The most common of rapid death in obstetrics is PPH ✓ Operational definition
• In PPH we can lose a patient within minutes • PPH is the amount of bleeding sufficient enough to
• In India PPH is the largest contributor to maternal cause a considerable fall in BP and an appreciable rise
mortality rate in heart rate
• It is the most dreaded labour complication
✓ According to ACOG
• PPH is defined as a drop in hematocrit of 10%.
➢ The Definitions

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Types of PPH Traumatic PPH

➢ Primary PPH • Genital tract injuries like, lacerations of the cervix,


• Hemorrhage occurring within 24 hours following child vagina, perineum, Colporrhexis and Rupture uterus
birth • It occurs due to
• Most common cause: Atonic PPH • Instrumental delivery

➢ Secondary PPH
• Vaginal birth after cesarean

• Hemorrhage occurring after 24 hours and upto 6 • Face to pubis delivery


weeks postpartum • Precipitate labour
• Most common cause: Retained placenta • Macrosomia
• Mismanaged labour / improper surgical skills and
inexperienced hands
➢ Causes of PPH:
✓ Atonic PPH (Tone) Coagulation Defects
✓ Traumatic PPH (Trauma)
✓ Coagulopathy (Thrombin) • Disseminated intravascular coagulation (DIC) and
hypofibrinogenemia are rare causes of PPH
✓ Retained placenta / membranes (Tissue)
• It occurs due to
• Abruption
Atonic PPH • Sepsis
• Intrauterine death
• It is the most common cause of primary PPH • Severe preeclampsia
accounting for 90% of cases. • HELLP syndrome
• The bleeding occurs as the blood vessels are not
obliterated by contraction and retraction of uterine Retained products of conception
muscle fibres
• All the products of conception relate to the
o The causes of atonicity are connection between the foetus and mother
• Grand multipara • All these are supposed to be expelled outside
• Malnutrition/Anemia • If any of these products remain attached to uterus it
• Previous H/o atonic PPH causes bledding (from uterine maternal blood
• Antepartum hemorrhage sinuses)
• Overdistended uterus due to multiple pregnancy, • It may occur due to
hydramnios and macrosomia • Morbidly adherent placenta
• Uterine malformations or fibroid uterus • Retained placenta
• Precipitate labour and prolonged labour • Succenturiate lobe of placenta
• Mismanaged third stage of labour • A big clot of blood covering the placental site
• Inadvertent use of oxytocin
• Use of general / epidural anaesthesia especially MANAGEMENT OF PPH
halothane
➢ Primary PPH
• Step 1 – resuscitative, investigative and immediate
management of cause
• Step 2 – medical methods
• Step 3 – mechanical methods

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• Step 4 – surgical methods
• The use of the 'shock index' (SI) is invaluable in the
➢ Secondary PPH monitoring and management of women with PPH.
• D and C • It refers to heart rate divided by the systolic BP.
• The normal value is 0.5-0.7 (80 / 120 = 0.6)
Step 1: General Measures • With significant haemorrhage, it increases to 0.9-1.1.
• The change in SI of an individual patient appears to
• Including Resuscitative Measures + Investigations + correlate better in identifying early acute blood lost
Confirmation of Diagnosis
• It is better than monitoring HR, SBP or diastolic blood
• The first and basic step in the management of PPH is pressure used in isolation.
resuscitation of the patient which includes:
• Securing I/V lines Step 2: Medical management
• Volume restoration by crystalloids (normal saline/
Ringer lactate) • Atonicity is the most common cause of PPH
• Oxygen inhalation • Any drug which increases the tone of uterus or the
• Crossmatching and arranging for blood. force of contraction is used to control PPH and is
• The Cause of PPH i.e., whether it is atonic (diagnosed called oxytocic.
by abdominal palpation) or traumatic should be • Commonly used oxytocics in the management of PPH
looked and managed accordingly. are
• At the same time investigations like Blood group, ✓ Oxytocin
Hemoglobin, plotting time, Coagulation profile, ✓ Methergin
Electrolytes should be sent ✓ Misoprost (PG E1)
✓ Carboprost (PG F2α)
• When diagnosis of Atonic PPH is confirmed - Uterus
should be massaged continuously and medical
methods should be adopted. ✓ Oxytocin
• When diagnosis of traumatic PPH is confirmed – • Immediately start RL or NS through two wide bore iv
immediately try to stop the bleeding by repairing the cannular on both hands
defect
• Add 20 units in both the iv fluids and give slow
• When diagnosis is retained placenta immediately infusion, never give bolus
send for an anaesthetist and OT
• Other routes: im
• When diagnosis is a coagulative disorder immediately
order for FFP and blood
• Side effects: nausea, water intoxication
• Warning: never give bolus oxytocin
• It is a drugs used for prevention and treatment of PPH
➢ acute management of PPH
• a 'rule of 30' has been proposed. ➢ Oxytocin pharmacology
• If the patient's • It is a nonapeptide (Peptide of nine amino acids).
✓ systolic blood pressure (SBP) falls by 30 mm Hg • Released by posterior pituitary and synthesized in the
✓ heart rate (HR) rises by 30 beats/min supra optic and paraventricular nucleus of
hypothalamus
✓ respiratory rate increases to >30 breaths/min
✓ haemoglobin or haematocrit drop by 30% • Half life 3-4 mins.
✓ urine output is < 30 ml/hour, then • Mechanism of action - Acts through calcium
mediated channels to initiate myometrial
• the patient is most likely to have lost at least 30% contractions
of her blood volume and is in moderate shock
leading to severe shock
✓ Methergin

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• Injection methergin 0.2 mg is given im stat and can be • Warning: never give to a hypertensive or cardiac
repeated every 2- 4 hours if required patient and in pre eclamptics /eclamptics
• Other routes: iv and im
• Side effects: Nausea, vomiting and hypertension --------------------------------------------------

✓ Family is completed
✓ Misoprostol • Hysterectomy
• Available as 200mcg tablets
• Place 1000 mcg or 4 – 5 tablets P/R stat
• Other routes – po UTERINE INVERSION
• Side effects: fever and tachycardia
• Uterine inversion is a condition in which there is
inside out turning of the uterus.
✓ 15 methyl PG F2α
• Injetion carboprost 0.25 mg or 250 units given im can
• It is a rare cause of postpartum collapse but collapse
occurs suddenly after labour.
be repeated every 15-90 mins to a maximum of 8
doses • It is acute in onset.
• Other routes: intra myometrial • Mostly uterine inversion is complete i.e. of third
degree
• Side effects: Nausea, vomitings, chills and diarrhoea
➢ Aetiology
• Warning: never give to patient with bronchial asthma
or active cardiac, renal or hepatic disease
• Mismanagement of the third stage (M/C cause) -
Attempting to deliver a placenta by cord traction that
has not yet separated
Step 3: Mechanical methods
• When medical methods fail to control PPH the
• Spontaneous inversion can occur with an atonic
uterus (in 40% cases).
following mechanical methods are adopted:
• Bimanual compression
• Placenta accreta is a rare cause.
• Uterine packing under anesthesia
• Balloon tamponade with a sengstaken tube inserted
into the uterus.
• Shivkars pack i.e condom inflated with saline can also
be used as a tamponade.

Step 4: Surgical methods

• When all other methods fail - Surgical intervention ➢ Clinical Features


should be carried. • Patient present with shock and hemorrhage
• The choice of surgery is dictated by the condition of • degree of shock being out of proportion to the
the patient and her family status amount of bleeding (due to vagal shock)
• Bleeding is due to attempts to detach the placenta
✓ If Family is not completed before correcting the inversion.
• Application of B lynch sutures • Vaginal examination reveals a soft, globular swelling
• Radiographic embolization of pelvic vesels in the vagina or cervical canal.
• Uterine and ovarian artery ligation • On abdominal palpation, the fundus of the uterus is
felt to be absent
• Internal iliac artery ligation
• If these methods fail then hysterectomy is done as ➢ Complications
final resort.
• Neurogenic shock

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• Hemorrhage
• Pulmonary embolism ➢ Classification/Variants
• Uterine sepsis and subinvolution • Placenta accreta - chorionic villi are attached to the
superficial myometrium (< 50%)
➢ Management • Placenta increta - villi invade the myometrium (> 50
• Resuscitation and replacement of inverted uterus %)
should be done simultaneously. • Placenta percreta - villi penetrate the full thickness
✓ Manual replacement or Johnsons maneuver myometrium up to the serosal layer, sometimes also
involving the bladder and rectum
• Best step if diagnosis is made immediately.
• The part which comes out first i.e fundus should be ➢ Risk Factors
last to reposited
• Placenta previa in present pregnancy, History of
• After replacing oxytocics should be given to promote operative interferences, Previous cesarean section,
contraction. This is called as! Previous curettage, Previous manual removal,
Previously treated Ashermann syndrome,
✓ Hydrostatic or O’ sullivan method Synechiolysis, Myomectomy, Multiparity, Advanced
• Warm saline is run into vagina with labia apposed to maternal age > 35 years
prevent leakage.
• The vagina ballons with the fluid and the inversion ➢ Diagnosis (intra partum)
corrects on its own. • Presents as retained placenta
• during attempted manual removal of placenta the
diagnosis is made
• It is made when the plane of cleavage between the
• SUDDEN POST PARTUM COLLAPSE placenta and uterine wall cannot be made out.
➢ The causes are
• Amniotic fluid embolism ➢ Diagnosis (ante partum)
• PPH ✓ Transvaginal sonography - absence of the
subplacental sonoluscent zone (which represents the
• Uterine inversion
normal decidua basalis) indicates a placenta accreta.
• Eclampsia. ✓ Doppler imaging-shows
RETAINED PLACENTA • A distance less than 1mm between the uterine
serosal bladder interface and retroplacental vessels.
• Retained placenta is defined as failure of the placenta • Presence of large intraplacental lakes.
to be expelled within 30 min of delivery of the fetus.
➢ Complications
➢ Morbidly Adherent Placenta • Antepartum haemorrhage (due to associated placenta
• A condition wherein the placenta is firmly adherent to previa) and Uterine rupture before labour (due to
the uterine wall and doesn’t separate during the third myometrial invasion by placental villia at the site of
stage previous C.S. scar.
• Postpartum haemorrhage
✓ Pathological Findings • Infection
• Absence of decidua basalis or improper decidua • Inversion of uterus (rare).
basalis formation
• Absence of Nitabuch's fibrinoid layer ➢ Management
• The trophoblasts completely invade the endometrium
and have the potential to invade the myometrium ✓ Complete Morbid Adherent Placenta
o If female has completed her family

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• Hysterectomy • The patient should be given antibiotics and
methotrexate in hope of autolysis.
o If has not completed her family • Monitor βhCG levels
• Cut the umblical cord as high as possible and leave ✓ Placenta increta and percreta are treated by
the placenta as such. hysterectomy alone

CHAPTER – 17
MULTIFETAL GESTATION

• It is defined as simultaneous development of more DIZYGOTIC TWINS


than one foetus in the uterus • Dizygotic twins are more frequent than monozygotic
twins (3:1).
• Two Foetuses – Twins, Three Foetuses – Triplets Four • They are also called as non identical twins
Foetuses – Quadruplets, Five Foetuses – Quintuplets, • They are formed from different ova and sperm so
Six Foetuses - Sextuplets they are 2 different individuals
• They may be of the same sex or opposite sexes
INCIDENCE
➢ According to Hellin's rule
• They are not identical but ‘may’ show a degree of
resemblance no more than that of brothers and
• The mathematical frequency of multiple pregnancy is: sisters from different births
• Twins 1 in 80 • This is the reason they can be called as "fraternal
• Triplets 1 in (80)2 twins".
• Quadruplets 1 in (80)3 and so on
MONOZYGOTIC TWINS
• The incidence of twins is highest in Nigeria (1 in 20) • It is less common than binovular twins 25% of all twin
• It is lowest in far Eastern countries births
• Incidence in India - 1 in 80. • These twins are formed from the same ova and sperm
• Incidence of twins is increasing in India because of the hence are genetically similar
use of ovulation inducing drugs like clomiphene and • They are hence called identical twins
gonadotropins • Monozygotic / uniovular twins are always of the same
sex and are identical in appearance, resembling each
ZYGOSITY OF TWINS other both physically and mentally
• Twin pregnancy can be Dizygotic (binovular) or • They also show the same pathological tendencies.
monozygotic (uniovular)
✓ Dizygotic / binovular twins refer to release of 2 ova CHORIONICITY AND AMNIONICITY OF TWINS
and their fertilisation by 2 sperms leading to the • After fertilisation the zygote forms the morula which
formation of 2 zygotes (hence DI ZYGOTIC) then forms the blastocyst
✓ Monozygotic / uniovular twinning occurs due to • The blastocyst has an outer cell mass / trophoblast
fertilisation of 1 ovum by a 1 sperm leading to which forms the placenta
formation of 1 zygote but then followed by fission of • From the inner cell mass develops the whole body of
single fertilized ovum leading to formation of two the baby and the amnion
‘cell’ groups
• Chorion development occurs before amnion
• Each ‘cell’ group develops into an embryo development

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• Monochorionic Diamniotic
➢ IN DIZYGOTIC TWINS
• As they develop from two distinct embryos they have
two different chorions and amnions
• Dichorionic Diamniotic Dizygous twins

➢ IN MONO ZYGOTIC TWINS


• Development of chorion and amnion in monozygotic
twins is not that simple
• It is dependent upon the time at which the fission
occurs
• For our convineance we shall study them as
✓ before 3rd day of life
✓ 4th to 8th day of life ➢ After the 8th day
✓ After 8th day of life • By this time both the chorion and amnion are
✓ After 14th day of life formed
➢ Before 3rd DOL • Hence there is a single chorion (mono
• The fission occurs before the third day chorionic) and 1 placenta and a single amnion
• The outer cell mass is formed after the fission (mono amniotic)
hence there are 2 outer cell mass ie. 2 chorions • Monochorionic Monoamniotic
(dichorionic) and hence 2 placentas
• Later the amniotic cavity is formed hence each
developing ovum forms it’s own amnion ie 2
amnions (di amniotic)
• Dichorionic Diamniotic

➢ After 14th day


• By this time the germ disc is also formed hence any
fission after this will lead to conjoined twins ie they
share similar body parts
➢ 4th to 8th day of life • It is also called as Siamese twins
• If the fission is occuring after the 3rd day (when
the outer cell mass is being formed), the outer CHORIONICITY AND CLINICAL IMPLICATION
cell mass which is already formed can not
divide later hence it has 1 chorion (mono • Dichorionic twins, whether monozygous or dizygous,
amniotic) and one placenta develop as two distinct individuals and are hence not
• The amniotic cavity doesn’t form before the 8th at increased risk of complications.
day hence there is formation of 2 amniotic • Monochorionic twins are at increased risk because of
cavities (di amniotic) the vascular anastomosis between the two
circulations.

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• Chorionicity can be detected prenatally by ultrasound.
(Best time - 6 to 9 weeks of gestation). ➢ Fetal papyraceous or compressus
• It is a state which occurs if one of the fetus dies early -
TERMINOLOGY dead fetus is compressed between the membranes of
the living fetus and the uterine wall.
➢ Superfecundation
• It is the fertilization of two different ova released in ➢ Fetal acardiacus
the same cycle, by separate acts of coitus within a • Here one fetus does not possess a heart and the
short period of time. development of upper part of the body is almost
absent - normal twin is called "pump twin".
➢ Superfetation • It occurs only in monozygotic twin
• It is the fertilization of two ova released in different
menstrual cycles.
• This is theoretically possible until the decidual space is
obliterated by 12 weeks of pregnancy.
Terminology Feature

THORACOPHAGUS TWINS JOINED IN REGION OF THORAX


( COMMONEST)
ISCHIOPHAGUS TWINS JOINED IN THE REGION OF PELVIS
PYOPAGUS TWINS JOINED IN THE REGION OF BACK
CRANIOPAGUS TWINS JOINED THE REGION OF HEAD
DICEPHALUS DOUBLE HEADED MONSTERS IN WHICH THE LOWER PARTS ARE MORE OR LESS
FUSED INTO ONE.
SYNCEPHALUS SINGLE HEADED MONSTER WHICH SHOW DUPLICATION OF THE LOWER LIMB
AND SOME TIMES OF THE LOWER PART OF THE TRUNK.

➢ Route of delivery:

OBSTETRIC PRESENTATIONS IN TWINS ✓ In case of discordant growth vaginal delivery is


➢ LIE indicated if:
• In twins most common lie of both the fetus at term is • Cervix is ripe
longitudinal. • Presentation is vertex / vertex
• Rarest lie is both the twins transverse. • Weight of smaller twin is > 1500gms

➢ PRESENTATIONS TWIN TO TWIN TRANSFUSION SYNDROME (TTTS)


• Both vertex (Most common) 60%
• Vertex (1ST) - Breech (2ND) 20% • It is always seen in monochorionic placenta.
• Breech (1ST)-Vertex (2ND) 10% • There is an arteriovenous malformation such that
• Both Breech 8-10% there exists a communication from the umbilical
arterial system of the "donor" twin to the umbilical
➢ Interlocking of twins is a rare complication seen in vein of the "recipient" twin.
twins with 1STBreech presentation and 2ND vertex • The donor twin is growth restricted, hypovolemic, has
presentation. oligohydramnios and is anemic because it gives blood
to the recipient twin.

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• The recipient is larger, hypervolemic, has • Dysfunctional labour, Malpresentations, Increased
polyhydramnios and is plethoric, CHF—due to volume chance of operative delivery, Postpartum
overload and can have thrombosis since it has hemorrhage, Retained placenta
polycythemia
• It has also been termed as ‘Twin Oligohydramnios - FOETAL COMPLICATIONS IN TWIN PREGNANCY
Polyhydramnios Sequence’ (TOPS). • ANTEPARTUM
• The earlier the TOPS appears, worse will be the • Prematurity, IUGR, Single fetal demise,
prognosis. Monochorionic monoamniotic twins, Twin-twin
• TTTS is more common in female fetuses. transfusion syndrome, Vanishing twin and abortion
• TTTS can cause Preterm delivery due to • Congenital anomalies including acardiac fetus and
Polyhydramnios, IUGR or fetal demise. conjoined twins

➢ Diagnosis of TTTS ➢ INTRAPARTUM


• It is based on two criteria • PROM and cord prolapsed, Abruption in the second
✓ Presence of a monochorionic diamnionic pregnancy twin, Interlocking of twins (extremely rare)
✓ One twin having polyhydramnios and the other twin ➢ Complications Specific to Monochorionic twins
having oligohydramnios
• Hydramnios defined if the largest vertical pocket is > 8 • Twin-twin transfusion syndrome, Monoamniotic
twinning, Conjoined twinning, Acardiac fetus
cm in one twin
INVESTIGATIVE WORK UP IN TWINS
• Oligohydramnios defined if the largest vertical pocket
is < 2 cm in the other twin.
• Ultrasound Determination of Chorionicity

➢ Number of Sacs: This is applicable only before 10


weeks when 2 sacs indicate dichorionic and single sac
➢ Management
indicates monochorionic pregnancy.
• The preferred management these days is laser ➢ Placenta: Two placentae indicate a dichorionic
ablation of individual anastomosis. pregnancy.
• Selective reduction can be considered if severe
amniotic fluid and growth disturbances develop ➢ Sex: Discordant sex indicates dichorionicity but
before 20 weeks. concordant sex does not imply monochorionicity.
➢ Intertwin membrane: is thicker and more echogenic
MATERNAL COMPLICATIONS IN TWIN PREGNANCY in dichorionic twins, whereas it is thin in
monochorionic. It is best examined between 16-24
➢ ANTEPARTUM weeks, near the placental insertion of membranes.
• Hyperemesis, Hydramnios, Pre-eclampsia, Pressure
symptoms, Anaemia, Antepartum hemorrhage

➢ INTRAPARTUM

Twin peak or lambda sign:

• It is characteristic of dichorionic pregnancies and


is due to the chorionic tissue between the two layers
of the intertwin membrane at the placental origin.
• A potential space exists in the intertwin
membrane which is filled by proliferating piancental
villi, giving rise to a twin peak sign.

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• (5) Appearance of fetal distress.

➢ Extraction of The Second Twin

• A rational scheme is given below which depends on


the lie, presentation and station of the head.

✓ Head
• Twin peak appears as a triangle with base at chorionic
• - If low down, delivery by forceps
surface and apex in interwin membrane. • - If high up, delivery by internal version under general
✓ In monochorionic twins there is no chorionic tissue, anesthesia
and interwin membrane is composed of 2 Amnion
only giving rise to the "T" sign on ultrasound. ✓ Breech should be delivered by breech extraction

• Monochorionic pregnancies have a dividing ✓ Transverse lie—internal version followed by breech


membrane that is so thin, it may not be seen until the extraction under general anesthesia.
second trimester. o If, however, the patient bleeds heavily following the
• The membrane is generally less than 2mm thick and birth of the first baby, immediate low rupture of the
magnification reveals only 2 layers (of amnion) membranes usually succeeds in controlling the blood
loss.

➢ Delivery of twins INDICATIONS OF CESAREAN IN TWINS


• In twins, the chances of vaginal delivery are high if the
first twin or presenting twin is cephalic
• Twins with bad prognosis viz- Conjoint twins and
• The interval between delivery of twins should be less
than 30 minutes. If there is a delay of more than 30 • Monochorionic and monoamniotic twins
mins, interference should be done • Twin to twin transfusion syndrome (seen in
monochorionic twins)
➢ Indications of urgent delivery of the second baby: • Discordant twin with weight of smaller twin less than
• (1) Severe (intrapartum) vaginal bleeding 1500gms
• (2) Cord prolapse of the second baby • Severe IUGR of one or both twins
• (3) Inadvertent use of intravenous ergometrine with • First twin non vertex
the delivery of the anterior shoulder of the first baby • All other obstetric (maternal and foetal) which are
• (4) First baby delivered under general anesthesia indications for cesarean

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CHAPTER – 18
OPERATIVE OBSTETRICS
EXTERNAL CEPHALIC VERSION
CONTRAINDICATIONS
• ECV is the procedure where presentation other than
➢ Maternal causes
cephalic is converted by external manipulation into a
cephalic presentation • APH - Placenta previa/abruptio placentae, Pre
eclampsia (hypertension), Precious pregnancy as bad
• It can be carried out in breech presentation or in
obstetrics history, Elderly primigravida, Multiple
transverse lie.
pregnancy, Obesity
• It is more successful in transverse lie.
• Ruptured membranes (because liquor has drained),
Oligohydramnios, Contracted pelvis, Congenital
➢ Indications:
abnormalities of uterus, APH - Placenta
• Breech presentation, Transverse lie. previa/abruption, Placentae

➢ Timing:
• A prior uterine incision is a relative contraindication
• It should be done after 35 weeks, Ideal time is 36 ➢ Foetal causes
week.
• Precious pregnancy, IUGR, Significant fetal
anomalies/dead Fetus, Compromised foetal status,
➢ Factors associated with successful version
Foetal distress, Short cord
• Multiparity,
• Adequate liquor. FORCEPS
• Unengaged fetus.
• Tocolysis ➢ THERAPEUTIC INDICATIONS
• Fetal distress in the second stage like in case of
➢ Procedure: abruptio placentae or cord prolapsed, Maternal
• The manoeuver is carried out after 35 weeks under distress in the second stage, Cardiac disease, PIH,
the effect of. Terbutaline 0.25 mg s.c. or Isoxsuprine Chorioamnionitis, Maternal exhaustion in 2nd stage,
50-100 mcg IV Prolonged second stage, Inadequate contraction,
• Ultrasound examination is done to confirm the Ineffective maternal effort
diagnosis and adequacy of amniotic fluid volume.
• A reactive NST should precede the manoeuver.
• Then ECV is attempted
• This is followed by a repeat NST after the procedure.

➢ Complications
➢ PROPHYLACTIC INDICATIONS
• PROM, Abruption, Fetomaternal hemorrhage,
Amniotic fluid embolism, Uterine rupture (very rare)

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• Medical diseases like cardiac disease and pre-
eclampsia, Low brith weight infants (No obvious ➢ PROCEDURE
advantage), After coming head in breech. • Vacuum cup should be applied over the sagittal
suture at the median flexion point located 3cm
➢ PRE REQUISITES anterior to the posterior fontanelle.
• The fetal head must be engaged • Maximum pressure created by vaccum = 0.8 kg/cm2
• The cervix must be fully dilated • The direction of pull of vaccum should follow the
• The membranes must be ruptured Curve of Carus, i.e. downwards and backwards; then
• The position and station of the fetal head must be downwards and finally upwards (similar to forceps).
known with certainty • Delivery should occur within three pulls over a period
• No major cephalopelvic dispropor tion by clinical of 15 mins.
pelvimetry
• Bladder must be emptied
• Adequate analgesia
COMPLICATION OF FORCEPS DELIVERY

➢ Maternal

✓ Immediate • If the cup slips, despite correct application or delivery


• Injury -Vaginal laceration or sulcus tear, extension of does not occur after three pulls-cesarean section is
episiotomy to involve the vaginal vault, complete indicated.
perineal tear, cervical tear
• Nerve injury -Femoral (L2, 3, 4), Lumbosacral trunk ➢ Indications:
(L4,5) • As an alternative to forceps operation.
• Postpartum hemorrhage may be traumatic or atonic • As an alternative to rotational forceps in occipito
or both transverse or posterior position.
• Anaesthetic complications following local or general • Delay in descent of the head in case of the second
anaesthesia baby of twins.
• Puerperal sepsis and increased maternal morbidity • Deep transverse arrest
• To cut short the second stage of labour as in heart
➢ Foetal disease patients.

• Facial bruising, Facial palsy, Intracranial hemorrhage ➢ Prerequisite:


(rupture of the great vein of Galen), • Bladder should be empty
Cephalhematoma, Skull fracture, Cervical spine injury
• Cervix should be at least 6 cm dilated
(rotational forceps), Asphyxia
• Vertex presentation
• Head should be engaged
VENTOUSE • No bony resistance below the head / No evidence of
CPD
➢ Ventouse/Vaccum extraction
VENTOUSE APPLICATION FOR MALPRESENTATION
• Ventouse is an instrument which assists in delivery by
creating a vaccum between it and fetal scalp.
➢ Ventouse can be applied in:
• Vertex presentation:
• Occipito anterior position

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• Occipito transverse/posterior position
• Deep transverse arrest COMPLICATIONS

➢ Ventouse should not be applied in: ✓ Maternal


• Face presentations (Mento anterior and posterior) • (In ventouse maternal complications are less than
with forceps)
• Breech presentation
• Brow presentation • Soft tissue injuries to the vagina, cervix & perineum
• Annular detachment of the cervix
CONTRAINDICATIONS: • Traumatic PPH
• Prematurity (< 34 weeks or weight < 2 kg) as chances
of scalp avulsion or sub periosteal hemorrhage are ✓ Foetal
more (In ventouse foetal complications are more than with
• Fetal coagulopathy forceps)
• Fetal macrosomia (wt > 4 kg) • MC is retinal hemorrhage
• Non engaged fetal head • Scalp injury
• Fetal distress where urgent delivery is needed • Cephalhematoma (More common with vacuum)
Intracranial hemorrhage
• CPD
• Presentation other than vertex (including face • Subgaleal hemorrhage (More common with vacuum)
(50: 10000)
presentation)
• Contraindication - recent scalp blood sampling • Neonatal jaundice (More common with vacuum)
• Asphyxia in difficult vacuum
ADVANTAGES • Shoulder dystocia (More common with vacuum)
• Erb paralysis
• The 2 main advantages of vaccum are • 6th and 7th nerve palsy.
• It can be applied through incompletely dilated cervix
(not undilated cervix)
• Can be used in unrotated or malrotated
occipitoposterior position of head e.g. in deep
transverse arrest with adequate pelvis.
FORCEPS ADVANTAGES VENTOUSE DISADVANTAGES

No maternal effort needed, therefore Requires maternal effort


Suitable in case of Requires maternal effort hence unsuitable
maternal heart disease
Quick in cases of fetal distress Takes time in fetal distress
Less cephalhematomas More cephalhematomas/subgaleal
hematoma/jaundice
Can be used in preterm Cannot be used in preterm (< 34 weeks)
Can be used in face and breech Cannot be used in other presentations

Requires anaesthesia No need for anaesthesia


Maternal injuries may occur Less maternal injuries

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No autorotation, occupies space at the sides Promotes autorotation, can be used in
unrotated or malrotated occipito posterior
position of the head
Requires full dilatation Does not require full cervical dilatation
Can be applied if cervix > 6 cm dilated
More traction force needed Less traction force needed

• If the patient presents late (after 24 – 48 hrs) don’t


EPISIOTOMY repair leave it for secondary healing

➢ Types of Episiotomy:

• It is defined as a surgical incision made over the


perineum and vulva during delivery to increase the
diameter of the vulval outlet (and not the whole of ✓ The oldest was median episiotomy which is not done
birth canal) during child-birth and to prevent perineal now in modern obstetrics as it has a high incidence of
tears. grade 3 tears
• Thus episiotomy is a planned surgically given perineal ✓ Mediolateral is the most common type and is the
tear of second degree. most accepted
(Commonly a right mediolateral episiotomy is
• Perineal Tears performed, angled at
➢ 1° - Is a laceration of the vaginal mucosa and the 45 from the vulvar rim)
perineal skin, but not the underlying fascia and ✓ Lateral episiotomy gained some importance in past
muscle. but is now discontinued as it injures the bartholins
glands
➢ 2° - Involves the vaginal mucosa, perineal skin, and ✓ J shaped is less accepted because repair is difficult as
the fascia and muscles of the perineal body. perineal anatomy is very badly destroyed

➢ 3° - Involves the vaginal mucosa, skin and perineal ➢ Structures cut in Mediolateral episiotomy (Very
body and the anal sphincter is also disrupted. Important)

➢ 4° - In addition, the rectal mucosa is also torn. • Posterior vaginal wall


• Superficial and deep transverse perineal muscles,
• All perineal tears (whatever reason) should be bulbospongiosus and part of levator ani
repaired immediately • Fascia covering those muscles

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• Transverse perineal branches of pudendal vessels and • Hence tensile strength is more and so the chance of
nerves scar rupture in the next pregnancy is minimal.
• Subcutaneous tissue and skin.
➢ Cesarean hysterectomy
• Cesarean hysterectomy refers to an operation where
cesarean section is followed by removal of the uterus.
CESAREAN SECTION
• Peripartum hysterectomy is the surgical removal of
the uterus either at the time of cesarean delivery or
➢ Common indications
vaginal delivery or in the immediate postpartum
period
• Cephalopelvic disproportion
• Malposition and malpresentation (transverse lie and ✓ M/C cause of cesarean/peripartum hysterectomy is
breech) PPH
• Fetal distress ✓ Second most common cause is morbidly adherent
• Placenta previa placenta
• Preeclampsia and eclampsia remote from term ✓ Couvelaire uterus in abruption is not an indication for
• Multiple gestation hysterectomy.
• Fetal abnormalities (hydrocephalus)
• Cervical cancer
VAGINAL BIRTH AFTER CESAREAN SECTION (VBAC) OR
• Active herpes infection TRIAL OF SCAR
• Patients choice (now gaining popularity).
• Earlier previous cesarean section was considered as
➢ Types of Cesarean section an absolute contraindication for the next vaginal
• Classical section delivery
• Lower segment section • The rule was once a cesarean always a cesarean
• But now this statement is considered as an
➢ Classical cesarean: exaggeration
Indications of classical section in modern obstetrics
• Now the rule is once a cesarean try vaginal next time
• Dense adhesions (due to previous surgery) if possible
• Severe CP (osteomalacia or rickets) • All VBAC’s are trial of labour but all trial of labour are
• Big fibroid lower segment not VBAC
• Ca Cx
• Severe placenta previa with engorged vessels ➢ Essential Criteria
• Post mortem CS • One prior low - transverse cesarean delivery.
• Clinically adequate pelvis. (No CPD)
➢ Lower segment cesarean section • No other uterine scars or previous rutpure.
• Physician immediately available throughout active
• It is the only cesarean section performed now-a-days labor who is capable of monitoring labor and
(unless there is an indication for classical) performing emergency cesarean delivery.
• Here the insision is given in the lower segment of • Availability of anesthesia and personel for emergency
uterus (identified as the UV reflection) cesarean delivery.
• After identifying the lower segment an incision is
given either (transverse >99%) or vertical (1%) ➢ Vaginal delivery can be tried in post LSCS cases in
• Healing of the lower segment incision is better as it is institutions equipped with facilities and personell to
located in the lower segment which is quiescent. respond to emergencies (i.e., rupture uterus) with
physicians immediately available to provide
emergency care at any time

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➢ VBAC and trial of scar are synonyms of each other but Symphysiotomy
VBAC and trial of labor have two different meanings
• Symphysiotomy is the operation designed to enlarge
➢ Contraindications: the pelvic capacity by dividing the symphysis pubis.
• Prior classical or T or J-shaped uterine incision or • It is not prctised in modern obstetrics
extensive transfundal uterine surgery (eg,
myomectomy).
• Previous 2 or more LSCS DESTRUCTIVE PROCEDURES
• Previous history of uterine rutpure • There is no place for destructive operations in
• Contracted pelvis or CPD modern day obstetrics.
• Medical or obstetrical complications that preclude • They are - Craniotomy, Craniocentesis, Decapitation,
vaginal birth (eg, placenta previa), malpresentations Cleidotomy, Spondylotomy, Embryotomy or
• Previous history of puerperial infection evisceration
• Inability to perform emergency CS due to factors
related to the facility, surgeon, anesthesia, or nursing
staff.

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