Professional Documents
Culture Documents
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
❖ 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)
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.
➢ IMPLANTATION:
• Implantation occurs 7 - 9 days after ovulation
➢ 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.
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
➢ LONG CORD
• Cord entanglement, Cord around the neck of fetus,
Fetal distress, Cord prolapse , Fetal anomalies
➢ 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:
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
❖ 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
• 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
• 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
CHAPTER – 6
DIAGNOSIS OF PREGNANCY
➢ 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
➢ 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
• 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
• Amniocentesis
• 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.
✓ Early deceleration
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.
•
• 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
• Based on clinical evaluation and ultrasound examination there are two types of SGA babies ie type 1 and type 2
• 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%).
• 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
Soft but does not pit on pressure Soft and pits on pressure
Does not cross suture lines Lies over and crosses suture lines/midiine
CHAPTER – 8
ABORTION
➢ 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
• 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
✓ 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
➢ 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.
CHAPTER – 9
ECTOPIC GESTATION
The criteria
• Previous pelvic or abdominal surgery
• Smoking
• Douching
• Intercourse before 18 years
✓ Primary Abdominal Pregnancy
✓ Studiford criteria
Risk Factors In Ectopic
anaesthetic complications
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
No other investigation
✓ 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.
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
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
✓ 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
➢ 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
_____________?
DURATI0N
❖ PLACENTAL SEPARATION
• 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
➢ 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
T shaped Normal
Y shaped Suspicious of preterm labor
✓ 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
➢ Definition PRESENTATION
➢ 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
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.
➢ 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
➢ McRoberts' manoeuvre
➢ 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.
CHAPTER – 15
ANTEPARTUM HAEMORRHAGE
✓ 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
✓ 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
➢ 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.
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
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
CHAPTER – 16
COMPLICATIONS OF THE THIRD STAGE
➢ Secondary PPH
• Vaginal birth after cesarean
✓ 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.
CHAPTER – 17
MULTIFETAL GESTATION
➢ Route of delivery:
➢ INTRAPARTUM
✓ 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
➢ 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)
➢ Maternal
➢ Types of Episiotomy:
➢ 3° - Involves the vaginal mucosa, skin and perineal ➢ Structures cut in Mediolateral episiotomy (Very
body and the anal sphincter is also disrupted. Important)