UMS Short and Long Case

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Obstetrics & Gynaecology

Short Cases
Wong Wen Hao & Low Qin Jian
Dr Win Win Than

Dr Helen
Dr Win Win Min
Wong & Low O & G Short Cases Record

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Our Aim : Made it easy to do it right!

Cases Compiled
Gynaecology
1. Uterine fibroid
2. Ovarian cyst
Obstetric
1. Uterus Larger than Date
2. Uterus Smaller than Date
3. Breech Presentation
4. Unstable Lie
5. Previous LSCS Scar
6. Multiple Pregnancy
7. Pregnancy Induced Hypertension
8. Gestational Diabetes Mellitus
Common Questions & Answers
Revised: 14 / 2 / 12
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Short Case Record for uterine mass (Fibroid)
Sir, this patient is a middle age Malay lady who appears to be well. She has a normal body built.
In the peripheral examination, there is no clubbing, palmar pallor, pulse rate is 80bpm. She has no
conjunctiva pallor or sclera icterus. No palpable cervical LN. No pedal edema.
In the abdomen examination, abdomen is distended at the suprapubic region. There are no cutaneous
stigmata of pregnancy, surgical scars or superficial veins noted. Umblicus is central & inverted. Hernia
orifices are intact.
On palpation, abdomen is soft, non-tender. The suprapubic mass corresponds to 14 weeks pregnancy size.
It is globular in shape, firm in consistency, smooth surface, regular margin, non-tender, mobile sideways
but not up & down, cannot get below the mass & scoop up sign negative. There is no sense of urgency
when pressure is applied over the mass. Both iliac fossa are empty. There is no other mass felt in the
abdomen. Liver & Spleen are not palpable. Kidneys are not ballotable. Percussion over the mass reveal
dullness. No flank dullness. No palpable inguinal lymph nodes!
On auscultation, I can hear normal bowel sounds, no bruit heard over the mass.
I would like to complete my examination by doing a speculum & bimanual examination.
In the speculum examination, I would like to look for any bleeding, local lesions on the cervix, and do a
Pap’s smear if the patient had not had one before.
In the bimanual examination, I would like to confirm the origin of the mass. If it’s a uterine mass, when
the mass is moved upwards, the cervix will move away along with the mass from the examining finger. If
it’s an ovarian mass, when the mass is moved upwards, the cervix will not move. I would also like to feel
at the adnexae for any mass, POD for bogginess as it suggests presence of fluid or nodularity which
suggest malignant infiltration.
In summary, I think the suprapubic mass is uterine in origin and most likely a fibroid (or leiomyoma). She
is clinically not anemic.
My differentials for this mass are:

Adenomyosis. Others are uterine sarcoma, tubo-ovarian inflammatory mass, ovarian neoplasm, pelvic
kidney, diverticular or inflammatory bowel mass & cancer of colon.
Differential diagnoses (depends on symptoms)

Menstrual symptoms: DUB, endometrial polyps, endometrial ca, endometriosis, chronic PID.
Mass: Ovarian tumour, pregnancy, adenomyosis, uterine sarcoma, tubo-ovarian abscess, others: tumour of
large bowel, appendix abscess, diverticular abscess.

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What are the investigations you would like to do?

To confirm my diagnosis, I would like to do an ultrasound imaging to distinguish between a fibroid from
an ovarian mass. I would like to determine the site, type, number & size of the fibroid. Also, I would like
to exclude hydronephrosis from pressure over ureters.
Besides, I would also like to do a UPT and hysteroscopy with biopsy (endometrial sampling).
To assess the general wellbeing of my patient, I would like to do FBC (Hb, platelet).
How would you manage her?

If the fibroid is small, not influencing her general health, lifestyle, she is asymptomatic or she is near
menopause, I would like to manage her conservatively/expectantly by routine surveillance 6-12 monthly,
monitor FBC & the growth of the mass.
Appropriate medical management with Mefenamic acid & Tranexamic acid should be offered for
menorrhagia along with hematinic. Heavy & prolonged menses can be controlled by oral contraception
(COC) or danazol. Levonorgestrel releasing intrauterine system (mirena) is effective in reducing fibroid
related menorrhagia provided the uterine cavity is not distorted. It can cause shrinkage of the fibroid as
well. Progesterone receptor modulators (asoprisnil) or progesterone receptor antagonist (mifeprostone)
may also be used.
If medical treatment fails, symptomatic menorrhagia, reproductive failure problem, rapidly growing
fibroids (12-14 weeks uterus), if it is subserous and pedunculated (prone to torsion), if it is likely to
complicate a future pregnancy, if tere is doubt about its nature, then surgery will be offered. The options
for surgery will be myomectomy or hysterectomy. Hysterectomy option will depend on her age & need
for fertility. I will counsel her about the advantages & possible complications of the surgery (like
hemorrhage, infection, recurrence). If she wants to preserve her fertility, myomectomy may be an option
if the number & size of the fibroids is limited. If there is uncontrolled bleeding during myomectomy, she
might need to undergo hysterectomy.
Submucosal fibroids may be resected hysteroscopically. Pedunculated, subserosal myomas can be

resected laparoscopically (usually asymptomatic, so can treat conservatively). If she has completed her
family, hysterectomy provides a definitive cure.
GnRH analogues have high adverse effects & should not be use > 6/12 as it can cause osteoporosis. They
can be used selectively to reduce the fibroid size, less bleeding intra-operatively & enable a suprapubic
incision rather than a midline abdominal incision.
What are the new methods for treating fibroid?

Medical – progesterone receptor modulators.
Surgical – Bilateral uterine artery embolisation, uterine artery ligation, high intensity focused ultrasound,
MRI guided laser ablation, laparoscopic myolysis, high intensity focused ultrasound (HIFU), laser
photocoagulation.
What is the incidence of uterine fibroids?

It is the commonest tumor of the female genital tract, being present in > 20% of women > 35 years old.
Peak age of incidence of symptoms is between 35-45 years old.
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What are the sites of origin?

(a) Intramural – Within uterine wall.
(b) Subserous – Projecting from the peritoneal surface of the uterus. Can be pedunculated.
(c) Intraligamentary – Between the layers of broad ligament.
(d) Submucous – Indenting the uterine cavity. Can be polypoidal.
(e) Cervical
What are the clinical features of leiomyoma?

Mostly asymptomatic. Pelvic pressure/congestion/bloating, feeling of heaviness in lower abdomen, lower
back pain. Pressure symptoms like frequency of urination (urinary retention).
Prolonged or heavy menses associated with intramural or submucosal myoma.
Intermenstrual bleeding may occasionally occur with submucous myomas ulcerating through endometrial
lining. Excessive bleeding may lead to anemia, weakness & dyspnea.
Generally no pain, but severe pain (may be due to uterine colic to abort the myoma, torsion of its pedicle,
degeneration, sarcomatous change, adhesion to other organs associated endometriosis) associated with red
degeneration. Submucosal myoma are associated with infertility because the tumour interferes with
implantation of the fertilized ovum, it hinders the ascent of the spermatozoa by distorting uterus and tubes.
What are the risk factors of developing fibroids?

Increase age during reproductive age (40% more than 40 y/0), ethnicity (African 3x > White ), nulliparity,
family history, high BMI, excessive estrogen stimulation.
What are the protective factors of developing fibroids?

Oral contraceptive pills & pregnancy.
What are the complications of fibroids?

Torsion of pedicle, infection, hemorrhage, red/hyaline/cystic degeneration, calcification, malignant
change (leiomyosarcoma) in 1:200 cases or less.
What the potential effects of fibroids on pregnancy?

Antenatal : Subfertility, miscarriage, preterm labour, malpresentation, red degeneration.,
Intrapartum : Cord prolapsed / obstructed labour (rare), third stage problems (uterine inertia).
Postpartum : Delayed involution postpartum, PPH.
What are the common associated conditions?

Follicular cysts of the ovary, endometrial hyperplasia, endometrial carcinoma, endometriosis
What is the rare association with fibroids?

Fibroids is rarely associated with polycythaemia. Cervical fibroid can cause acute retention of urine.
Broad ligament fibroid can cause hydroureter.
What is the pathogenesis of leiomyomas?

Leiomyomas have increased levels of estrogen & progesterone receptors compared with other smooth
muscle cells. Estrogen stimulates proliferation of smooth muscle cells, whereas progesterone increases the
production of protein that interferes with apoptosis. Leiomyomas also has higher levels of growth factors
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that stimulate production of fibronectin & collagen, major components of extracellular matrix that
characterizes these lesions.
Given a 14 weeks size suprapubic mass, how would you differentiate it between a bladder,
pregnancy or myoma?
Bladder : Cystic consistency, urge to urinate upon pressure.
Pregnancy : Cutaneous stigmata of pregnancy, fetal poles, external ballottement.
Myoma : Firm consistency.
How do you differentiate myoma from adenomyosis?
Myoma Adenomyosis
Epidemiology Commonest benign uterine tumor. Less common.
Age group 30-40 years old 40-50 years old (uptodate)
Clinical manifestation Menorrhagia Dysmenorrhea
Size Any size < 14 weeks size
Tenderness Non tender mass Usually tender mass
Facts about GNRH analogue
Mechanism of action These drugs work by initially increasing the release of gonadotropins,
followed by desensitization and downregulation to a
hypogonadotropic, hypogonadal state that clinically resembles
menopause.
Routes of administration Goserelin acetate (3.6 mg/month subcutaneously or 10.6 mg

subcutaneous implant every three months) Leuprolide acetate depot
(intramuscularly 3.75 mg/month or 11.25 mg/three months).
Ornafarelin acetate (administered as a twice daily intranasal spray).
Benefits Reduce fibroid size, less bleeding intra-operatively.

Enable a suprapubic incision rather than a midline abdominal incision
or facilitate vaginal rather than abdominal hysterectomy (Rapid
recovery & less post-operative complications).
Side effects Severe hypoestrogenism like hot flashes, sleep disturbance, vaginal
dryness, myalgias, arthralgias, possible impairment of mood &
cognition. Osteoporosis.
10 teachers : Obscure tissue planes around fibroids making surgery

more difficult.

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Short Case Ovarian Cyst
Sir, my patient is a middle-aged lady lying supine comfortably on the bed supported by one pillow. She is
not wasted/cachexic/emaciated, pale or jaundiced. There is also no facial flushing.
On peripheral examination, there are no stigmata of chronic liver disease, pulse rate is 80 beats/minute
with regular rhythm, no cervical lymphadenopathy and no pedal oedema. I would like to measure her
blood pressure.
Abdomen:
On inspection, the right/left iliac fossa is distended. Otherwise, the abdominal wall moves with respiration,
umbilicus is centrally located and inverted, no superficially dilated veins, hernial orifices are intact and no
visible peristalsis or pulsation seen.
On palpation, the abdomen is soft and non-tender. A mass can be appreciated at the right/left iliac fossa,
which measures 5cm X 6cm, oval in shape, has a smooth surface, cystic in consistency, has a well-defined
margin, mobile vertically and horizontally. I am able to get below the mass. I could not appreciate any
other mass at the contralateral side. There are no hepatomegaly, splenomegaly or ballotable kidneys. No
palpable inguinal lymph nodes.
On percussion, there is dullness over the mass. No signs of free fluid.
On auscultation, there is no bruit heard over the mass. Bowel sounds are present.
To complete my examination, I would like to examine the breast, inguinal and supraclavicular lymph
nodes and perform a bimanual examination. In the bimanual examination, if it is ovarian in origin the
cervix will not move along with the mass. Cleft sign can also be appreciated.
Discussion
Diagnosis
Based on the clinical findings, my impression is that the mass is of ovarian origin and it is benign. (if
elderly, malignant ovarian tumour). The reason I think is ovarian in origin is because of the location of the
mass, I can get below the mass & it is mobile in all direction. I think it is benign because the general
condition of the patient looks fit, not lethargic or cachexic, the mass is well defined, single, unilateral,
patient age, no hepatomegaly or ascites.
Since my patient is young, my differential diagnoses include benign functional (follicular, corpus luteal,
theca luteal), inflammatory (tubo-ovarian abscess, endometrioma – which are not freely mobile) and germ
cell (benign teratoma) tumours.
Since she is an elderly lady, my differential diagnoses include benign epithelial (serous cystadenoma,
mucinous cystadenoma, Brenner tumour) and sex cord stromal (fibroma, thecoma) tumours.
However, I would also like to consider the possibility of malignancy by calculating the risk of malignancy
index (RMI) score, which is the product of ultrasound scan score, menopausal status and Ca125 level.
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My differential diagnosis are pedunculated fibroid, appendicular mass, tumor arising from GIT especially
terminal ileum & rectum and bladder/kidney mass.
Investigations:
To confirm my diagnosis, I would like to proceed with transabdominal and transvaginal ultrasound scan,
which my yield information about the origin and nature (benign or malignant) of the mass. Besides, I
would also like to check the tumour marker levels, which include Ca125, Ca19-9, Inhibin, B-HCG and
AFP. Both USG and ca125 level will be used in the scoring of RMI.
To provide baseline data, I would like to do renal and liver function tests. Renal function may be impaired
if the tumour has caused obstruction urinary flow obstruction. Liver function may be deranged if there is
secondary metastasis.
Management
Since my patient is young and the tumour size is < 5 cm in diameter, I will manage her conservatively. If
the tumor is > 5cm I will also treat her conservatively if there is no signs or symptoms of malignancy.
I will re-examine in 12 weeks for diminution in size. If persists, she will be scheduled for follow-up
6monthly with USG and CA125 levels. However, if the tumour enlarges further evaluation may need to
be done by laparoscopy or laparotomy. If she becomes symptomatic, such as an acute painful episode,
emergency laparotomy/laparoscopy is indicated.
Since she is an elderly lady and the tumour size measures more than 5 cm, she should be offered surgical
management (TAHBSO).
What are the complications of ovarian cyst? THIN RIM
 Torsion, haemorrhage, infection, necrosis, rupture, intestinal obstruction, malignant change
Differentiate mass between ovarian and myoma
Ovarian Uterine
RIF/LIF Suprapubic
Cystic Firm
Mobile vertically/horizontally Mobile horizontally
Can get below Cannot get below
Cervix doesn’t move with mass Cervix moves with mass
Exception: Exception:
 Endometriosis causing adhesions  Pedunculated fiboid
Scoop up sign positive
Cleft sign positive

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Differentiate between benign and malignant ovarian tumor based on clinical features
Malignant:
 General: Elderly, Cachectic, pale

 Mass: pain and tenderness of mass, rapidity of growth, 75% are bilateral, consistency is party
solid-cystic, solid, nodular, irregular shape, poorly defined margin, irregular surface, limited
mobility
 Ascites: peritoneal metastases or ovarian capsule perforated. (in benign, fibroma and cystadenoma)
 Palpable liver, ballotable kidneys, inguinal lymph nodes enlargement
 Pleural effusion
 Oedema of the legs and vulva or evidence of venous obstruction
 Supraclavicular lymph nodes
 Irregular deposits in POD
Differentiate between benign and malignant ovarian tumour based on laparotomy findings
Malignant:
 Bloody ascitic fluid

 Mass: bilateral, consistency is solid or party solid-cystic, fungation through capsule, large vessel
on tumor, poorly defined margin, irregular surface, limited mobility (adhesion).
 Retroperitoneal nodes enlargement
 Omental cake
 Liver metastasis
How do you differentiate benign from malignant ovarian tumor through ultrasound?
Benign Malignant
Unilateral lesion Bilateral lesion
Thin wall Thick wall/septum, Breaching capsule
Simple cyst Solid tumor / Mixed solid & cystic mass
No loculations Multilocular cyst
Internal papillary projections
Ascites
Evidence of metastasis
Increased vascularity on Doppler

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Uterus Larger than Date
In summary, the SFH is > 37 cm, >3cm greater than the gestational age of 34 weeks. Clinically, amniotic
fluid is adequate. No pelvic mass felt.
To complete my examination, I would like to take a detailed history (LMP, EDD, GDM, Anomaly scan),
through examination (BMI) & relevant investigations to find the possible cause. I would also like to
arrange for an ultrasound to look for evidence of multiple pregnancies, pelvic mass, AFI, EFW, evidence
of placenta abnormality.
What are the causes for uterus larger than date?

Mother : Wrong date, wrong SFH measurement, obesity, pelvic mass.
Fetus : Macrosomia, multiple gestations, polyhydramnios, normal large-for-gestation.
Placenta : Choriangioma.
How would you manage this case?

I will like to manage according to the underlying cause. I will treat the patient conservatively if she is
asymptomatic & no pressure symptoms. If she is symptomatic, there is a role for medical treatment (*
Indomethacin 50-200mg od till 35 weeks  can be use in Polyhydramnios; COX 2 inhibitor) or serial
amniocentesis.

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Uterus Smaller than date
SFH is 3cm less than the gestational age in weeks.
Management
Dear Sir, my patient has uterus smaller than date. First of all, I would like to rule out wrong dates. Then, I
will proceed to look for the cause. Serial USG should be done and growth parameters plotted on growth
charts for the detection of IUGR. IUGR may be suspected if there is a single measurement below the 5 th
centile. Besides, an USG may also yield information about the liquor amount, as oligohydramnios may
also cause uterus smaller than date. A detailed fetal anomaly scan can also be done to detect congenital
anomalies, such as renal agenesis. Doppler study of the umbilical arterial flow maybe be done to detect
placental insufficiency as a cause of IUGR.
Other tests which may be valuable are urine dipstick for glycosuria and proteinuria, MOGTT and FBC.
GDM is associated with congenital anomalies (renal agenesis) and IUGR, if there is nephropathy and
vasculopathy. PIH and Pre-eclampsia is also associated with IUGR. Furthermore, anaemia in pregnancy is
associated with IUGR.
Once the cause is found, management is tailored accordingly to treat the cause.
FAQs
What are the causes of uterus smaller than date?
 Mother: wrong dates, oligohydramnios, missed miscarriage, IUD

 Fetus: IUGR (placental insufficiency, congenital infections), congenital anomalies (renal agenesis
– Potter’s sequence)
What do you understand by the term symmetrical and asymmetrical IUGR? What are the causes?
Symmetrical IUGR is less common, begins early in pregnancy, manifested as generalized growth
restriction. Causes of symmetrical IUGR include:
 idiopathic
 chromosomal abnormalities
 TORCH infections
 maternal smoking
 maternal alcohol/opiate abuse
 chronic maternal nutritional deficiency
 ionising radiation
 sickle cell disease
Asymmetrical IUGR is more common, usually begins late in pregnancy, manifested as restriction of
weight followed by length, but the head continues to grow at normal or near-normal rates.
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Causes of asymmetrical IUGR include:
 Idiopathic
 Uteroplacental insufficiency: pre-eclampsia, maternal renal or cardiac disease, multiple gestation,
anemia.
What are the complications of FGR?

Antenatal: fetal hypoxia  IUFD
In labour: intrauterine hypoxia/asphyxia  stillbirth
Neonate:
 hypoxic-ischaemic encephalopathy (HIE) including seizures, multiorgan damage in neonate
 neonatal hypothermia, hypoglycaemia, infection
 necrotizing enterocolitis
 cerebral palsy
Adult life:
 CVS complications (hypertension and ischaemic heart disease)
 Metabolic disorders (non-insulin dependent diabetes)

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Breech Presentation
In summary, SFH is … weeks. This is a singleton fetus in longitudinal lie, breech presentation, fetal back
on maternal left side. FHR 150 bpm, strong & regular. Amniotic fluid is clinically adequate. Estimated
fetal weight is 3kg.
Discuss management options for a breech presentation at 38 weeks.

I would like to counsel her regarding the presentation, various options for delivery & allow her to make
an informed consent. Recent Us (after 36 weeks) should be checked to confirm presentation, rule out
placenta praevia, fetal malformation.
I would like to offer her ECV by trained professionals at 38 weeks. Before that, I would exclude the
contraindications of ECV. It should be performed on the labor ward near facilities for emergency delivery.
Us guidance is helpful. CTG prior & after ECV reconfirms fetal wellbeing. Tocolysis is effective. ECV
carries a success rate of 50% and halves the rate of C-sections done for breech presentation. < 1% require
emergency C-section for fetal distress, placenta abruption, vaginal bleeding.
Postural management to promote cephalic version include knee chest position, elevation of pelvis using
cushion, moxibustion.
(No more Trial of vaginal breech delivery except for breech delivery of second twin!)
Elective C-section at 39 weeks is now the safest mode of delivery (Term breech trial). However, there is
inherent risk of a surgical procedure like thromboembolism, bleeding & infection. If spontaneous labour
start before scheduled surgery, EMLSCS maybe required which carries higher morbidity.
Finally, I would like to document meticulously the counseling & women’s decision in her case records.
What is the incidence of breech presentation?

4% of all term singleton pregnancies.
What are classifications of breech presentation at term?

Extented/frank breech (65%), Flexed/complete breech (25%), Footling/incomplete breech (10%).
What are the etiology of breech presentation?

Mother : Uterine anomaly (bicornuate uterus), CPD, pelvic tumors obstructing birth canal,
polyhydramnios/oligohydramnios.
Fetus/placenta : IUGR, congenital anomalies, extended legs preventing spontaneous version, prematurity,
multiple gestations, placenta praevia, IUD.
What are breech presentation associated with?

Fetal anomaly (hydrocephalus, anencephaly), preterm, multiple pregnancy.
What are the hazards of ECV?

PROM, transplacental haemorrhage, Preterm labour, placenta abruption, cord accident, uterine rupture
(previous scar), fetal distress, fetal bradycardia, rupture membrane  cord prolapsed.

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What are the contraindications to ECV?

Absolute CI : Multiple pregnancy, significant fetal anomaly, ruptured membranes, oligohydramnios, APH,
placenta praevia, caesarean section indicated for other reasons.
Relative CI : Mother (hypertension, rhesus iso-immunization, obesity), Previous C-section, FGR, anterior
placenta, polyhydramnios.
What are the prerequisites for ECV?

The gestation should be > 36 weeks. Recent ultrasound to confirm presentation, normal fetus, rule out
placenta praevia, adequate liquor volume. Reactive CTG. Informed consent of mother. Facilities for rapid
progression to C-section. If necessary, rhesus –ve women must be given anti-D Ig.
How are you going to monitor the mother post successful ECV?
My aim is to monitor both maternal & fetal wellbeing. For the maternal wellbeing, I will monitor her BP,
PR 4 hourly, ask her for any signs/symptoms of labour, per vaginal bleeding, unusual abdominal pain,
increased contraction pain. If mother is rhesus negative, I would like to give anti-D prophylaxis. For fetal
monitoring, I will do a post ECV CTG, measure the fetal heart rate by pinard stestoscope, fetal kick chart,
and look for contractions.
Which type of breech presentation is associated with the highest ECV success?
Flexed/Complete breech.
What are the prerequisites for breech vaginal delivery? (Singleton Vaginal breech delivery is no
longer practiced)
Type of breech (Flexed or extended, footling not allowed), Normal uterus with no scars or abnormalities,
no placenta praevia, fetal weight 2.5-3.5Kg, no hyper-extended head.
What are the possible complications of vaginal breech delivery? (Singleton Vaginal breech delivery
is no longer practiced)
Prolonged labour, fetal distress, entrapment of head (preterm head), maternal/fetal injury.
Which type of breech presentation is favorable for vaginal delivery? (Singleton Vaginal breech
delivery is no longer practiced)
Frank or extended breech.
What are the possible complications of breech vaginal delivery?

Umbilical cord prolapsed, head entrapment, intracranial hemorhage, birth asphyxia, birth trauma (Erb’s
palsy, fracture of bones, soft tissue injury of abdomen).
RCOG : How should delayed second stage of labour with breech presentation be managed?
Caesarean section should be considered if there is delay in the descent of the breech at any stage in the
second stage of labour.

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RCOG : How should delayed engagement in the pelvis of the aftercoming head be managed?
Suprapubic pressure by an assistant should be used to assist flexion of the head. The Mauriceau-Smellie-
Veit manoeuvre should be considered, if necessary, displacing the head upwards and rotating to the
oblique diameter to facilitate engagement.
RCOG : How should the aftercoming head be delivered?

The aftercoming head may be delivered with forceps, the Mariceau-Smellie-Veit manoeuvre or the Burns-
Marshall method (rare).

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Unstable Lie
In summary, SFH is … cm. This is a singleton fetus in transverse lie, with its head at the right
hypochondrium and back facing downwards. Amniotic fluid is adequate and estimated fetal weight is
3.0kg. Fetal heart rate is 142 bpm, strong and regular.
How would you manage this patient if the lie is changing everyday and she is currently at 36 weeks
of gestation?
My diagnosis for this condition is unstable lie. Antenatally, she should be managed expectantly, as 85 %
of fetal lies will become longitudinal before rupture of the membranes or labour. The causes for unstable
lie should be sought, such as wrong dates, mechanical causes like polyhydramnios, placenta praevia,
fibroids, multiple pregancnies; and pelvic size and shape may be assessed by pelvic examination. If no
abnormalities are detected, she should be reassessed at 37 weeks. If unstable lie persists, she should be
admitted to hospital until delivery. Fetal lie should then be monitored using a lie chart daily. She can be
discharged if there is longitudinal lie for 3 days. My patient should also be informed of need for prompt
admission to hospital if membranes rupture or when labour starts.
Immediate clinical assistance should be given if membranes rupture or there are signs of labour.
Intrapartumly, vaginal and pelvic assessment should be done to establish presentation, exclude cord
presentation and assess cervical dilatation. If the lie is longitudinal, it can be managed normally. If the lie
is not longitudinal, ECV may be considered early in labour and ARM done with caution. If the lie is not
longitudinal and cannot be corrected, Caesarean section should be done.
Alternatively, a stabilizing induction can be done at 38 weeks, if the cervix is favourable according to
bishop score.
FAQs
What is lie?
Relationship between the longitudinal axis of the fetus to the longitudinal axis of the mother.
What is the definition of unstable lie?

Fetal lie and presentation repeatedly change at beyond 36weeks of gestation.
What is the incidence of unstable lie?

At 26weeks is 40%, at 30week is 20%, at term is 3%.
What are the causes of unstable lie?
 Prematurity
 Prevention of head descending: Cephalopelvic disproportion, cervical fibroid, Placenta praevia,
Uterine surgery, Multiple gestation, Fetal abnormality (anencephaly), Fetal neuromuscular
disorder
 Condition that permit free fetal movement: Polyhydramnios, Uterine laxation (multipara)

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What are the possible complications of unstable lie?
 Cord prolapsed leading to fetal hypoxia/ fetal death.

 Compound presentation
 Uterine rupture
How are you going to manage an unstable lie case?

I would like to rule out causes of unstable lie like placenta praevia, polyhydramnios & pelvic tumors. If
the patient has reached term, I would like to put her on daily lie chart. If the fetus turns into cephalic
presentation, I would like to do stabilization induction if there are no contraindications to vaginal delivery.
I would also like to counsel the mother on the mode of delivery, if the fetus is not in longitudinal lie
LSCS will be offered.

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Previous LSCS Scar
In summary, SFH is 37 cm, there is a singleton fetus in longitudinal lie, cephalic presentation, fetal back
on maternal right side. FHR is 150 bpm, strong & regular. Clinically, amniotic fluid is adequate. EFW is
3kg. There is presence of a transverse suprapubic scar, measuring ?cm, healed by primary/secondary
intention, no scar tenderness or incisional hernia. (if new or recent scar comment on signs of
inflammation, infection, induration, tenderness.
To complete my examination, I would like to know the type of C-section, indication (emergency or
elective), how many times she had a scar, last scar date (>2 years for good healing), any complications
from previous C-section, any medical conditions complicating this pregnancy & the current baby
condition.
I would like to do an ultrasound to locate the placenta (r/o placenta praevia), confirm number of
pregnancy, lie/presentation of fetus, AFI, growth parameters, EFW.
Where and how would you manage her during labour?
Delivery should be conducted in suitably staffed and equipped delivery suit, with continuous
intrapartum care and monitoring, available resources for immediate CS and advance neonatal
resuscitation facilities.
During the first stage of labour, I will monitor her vital signs closely & do continuous electronic fetal
monitoring, monitoring progress with partogram. I will provide adequate analgesia. I would be extra
caution & vigilance in monitoring for evidence of scar dehiscence & rupture. I would do 4 hourly VE to
look for OS dilatation & fetus position. I would also prepare her as if she is going for OT by monitoring
her vital signs, insert 2 large bore cannula, GSH 4 units blood + FBC (hb), NBM (good hydration), counsel
& take consent.
In the second stage of labour, my aim is to monitor vigilantly. (2-3 fold increased risk of uterine rupture
and 1.5 fold increased CS rate in induced and augmented labour than spontaneous labour.)
IOL wit prostin in patient with previous LSCS is extremely high risk, need to carefully monitor patient.
I would like to actively manage the third stage of labour by giving IM syntocinon after the anterior
shoulder is out, early cord clamping, rubbing of uterine fundus & CCT. I would watch actively for signs of
PPH by monitoring her vital signs.
If during any stage of labour there is scar dehiscence or rupture, I would like to manage the patient in
the OT by doing laparotomy.
What are the possible complications of vaginal birth with previous scar?
Uterine rupture (disrupt uterine serosa), uterine dehiscence (intact uterine serosa).

19
What are the signs of scar dehiscence?

Mother : Suprapubic pain asynchronous with contraction with PV bleeding & Sudden cessation of
contraction, loss of sensation of the presenting part.
Fetus : Loss of fetal heart sound, Fetal distress seen on CTG
What are the signs of scar rupture?

Mother : Pale, tachycardia, hypotension, shock, chest pain/shoulder tip pain, sudden SOB.
Sudden cessation of contraction, loss of sensation of the presenting part easily palpable fetal part,
uterus separated from baby.
Abdominal distension/tender free fluid in peritoneum cavity, hematuria, PV bleed,
Also, post-delivery maternal collapse. Diagnosis is confirmed at laparotomy.
Fetus : Loss of fetal heart sound, fetal distress on CTG.
What are the indications for repeat LCSC?

Elective LSCS : CPD, 2 previous scar, breech/malpresentation, IUGR, placenta praevia, pelvic tumor.
Emergency LSCS : Fetal distress, cord prolapsed, placenta abruption.
Non- recurrent causes : Breech, Placenta praevia, secondary arrest, fetal distress, eclampsia.
Recurrent cause : Gross CPD
RCOG : What are the success rate of VBAC?

Women considering their options for birth after a single previous caesarean should be informed that,
overall, the chances of successful planned VBAC are 75-80 %.
Indications / Option for VBAC?
 Women with prior history of one uncomplicated LSCS

 Women with an otherwise uncomplicated pregnancy at term
 Women with no contraindication to vaginal birth
Final decision for mode of delivery

Should be agreed between women and her obstetrician before planned delivery date (ideally by 36
weeks of gestation)
Counseling
Should include maternal and perinatal risk and benefits of planned VBAC versus elective LSCS.

20
Risk factors for unsuccessful VBAC

Induced labour, no previous vaginal birth, BMI >30, previous CS for dystocia (49% success rate)
Contraindications to VBAC
 Women with a prior history of one classical CS (200-900/10000 risk of uterine rupture)
 Previous uterine rupture (risk is unknown)
 3 or more previous CS (risk is unknown)
Rupture rates
 Inverted T or J incision (190/10,000 risk)
 Low vertical incision (200/10,000 risk)
 LSCS (22-74/10,000 risk)
Caution in VBAC (uncertainty in safety)

 Twins
 Macrosomia
 Short interdelivery interval

21
Multiple Pregnancy
In summary, the SFH is …cm. There are 2 fetuses, both in longitudinal lie. The leading twin is in cephalic
presentation, whereas the second twin is non-cephalic. The head of the leading twin is 3/5 palpable, hence
not engaged. Estimated fetal weight of the individual twins is 2.0kg. The liquor amount is adequate. Fetal
heart rate of the leading twin is … bpm, whereas the second twin is …bpm (at least 10 bpm difference,
different intensity, audible at 2 different areas)
Remark : In a twin pregnancy, both fetal back will be at the maternal sides.
How would you manage a case of twin pregnancy?
A twin pregnancy should ideally be managed by 1 consultant or specialist.
Antenatally, regular clinic attendance is strongly advised because all the major hazards of pregnancy are
increased. Maternal complications such as anaemia, pregnancy-induced hypertension or pre-eclampsia,
gestational diabetes mellitus, preterm prelabour rupture of membranes and placentae praevia should be
identified, monitored and treated appropriately. Iron and folic acid supplementation from the 1st trimester
is recommended. I also like to monitor for fetal growth and well-being. (As for the fetus, an early dating
scan, ideally in the 1st trimester should be done and chorionicity determined.) A monochorionic twin
require much greater surveillance as the perinatal mortality is 5 times greater than dichorionic twins. A
detailed anomaly scan should be done at 20 weeks of gestation. Serial growth scans should also be done,
2 weekly for monochorionic and 4 weekly for dichorionic, as fetal growth restriction complicates 30% of
twin pregnancies. Complications such as TTTS, TRAP, IUGR and IUD should be identified. Fetal well-
being should also be monitored regularly, in the form of fetal kick counts, fetal heart rate and
cardiotocography. My patient should counseled that if pain, contractions and leaking of liquor occur, she
should seek medical attention immediately. If it is preterm, corticosteroids should be given.
If no complications arise, the timing of delivery should be at 38 weeks. The mode of delivery of choice is
vaginal delivery, as the leading twin is in cephalic presentation.
Intrapartumly, 2 neonatologists, 2 senior obstetricians, 1 midwife and 2 neonatal resuscitation trolleys

should be present. Continuous CTG monitoring of both the fetuses is indicated. The leading twin should
be delivered normally. The second twin’s lie and presentation should be assess thereafter, and stabilized
in longitudinal lie. Amniotomy can be performed when the presenting part descended to stimulate or
augment uterine contraction. Watch out for cord prolapsed. The second twin can be delivered as cephalic
or breech. For abnormal lie, ECV, IPV can be done. If complications arise, second twin may be delivered
by CS. After delivery of the second twin, syntometrine can be given, provided there is no undiagnosed
triplet. Third stage should be managed actively.

22
FAQs
What is the role of ultrasound in multiple pregnancy?

Early : Number of fetus, chorionicity (first trimester), sac.
18-20 weeks : Fetal anomaly scan
Third trimester : Lie, presentation, monitor fetal growth & wellbeing (discordant growth/IUGR),
placenta localization, AFI (high risk of polyhydramnios), , TTTS, TRAP
What is Hellin’s rule? Expected incidence in twins is 1:80, triplets is 1:802, and so on.
What are the complications of multiple pregnancy?
Mother Fetus
Antepartum  Excessive symptoms of  Miscarriage
(Divide into pregnancy  Unexplained IUD
1st, 2nd, 3rd o Hyperemesis gravidarum  IUGR
trimesters) o Backache, abd discomfort  Congenital malformations
o Varicose veins, haemorrhoids  TTTS
o Edema  TRAP
 Anaemia  Prematurity
 PIH/PE (5-10x more common)
 PPROM/PROM
 APH (Placenta praevia)
 Compressive symptoms (e.g.
dyspnea)
Intrapartum  Prolonged labour  Preterm labour
 Increased likelihood for  Malpresentation
operative delivery (instrumental,  Fetal hypoxia/distress
LSCS)  Cord prolapsed
 Uterine rupture (due to internal  Retained 2nd twin
podalic version, prolonged  Fetal trauma
labour)  Difficulty in monitoring 2 fetus
Postpartum  PPH, Retained placenta, delayed  Prematurity associated problems
uterus involution. (RDS, sepsis, jaundice, hypothermia
 Puerperium infection.  Cerebral palsy
 Highest risk of pre-eclampsia in
48 hours.
 Social, financial, personal
problems (breastfeeding and
care for 2 babies)
Types of multiple pregnancy : Monozygotic and dizygotic (MCMA, MCDA, DCDA)
Why is there higher risk of PPH in multiple gestation?

Larger placenta site & uterine over-distension.

23
What are the causes of morbidity & mortality in twins?

RDS, birth trauma, cerebral hemorrhage, birth asphyxia/anoxia, congenital anomalies, still births,
prematurity.
Before discharge, what are you going to counsel her?

I would like to talk about contraception & benefits of family planning to her. Arrange follow-up to
monitor maternal & fetal wellbeing. Provide reading pamphlets & contact details of local multiple
pregnancy support group.

24
Pregnancy Induced Hypertension
In summary, she has PIH diagnosed at 30 weeks POA. BP is 130/80mmHg & there is no signs &
symptoms of IE.
I would like to complete my examination by measuring her weight, performing a complete examination of
the cardiovascular system, neurological examination to look for neurological deficits, clonus,
hyperreflexia; fundoscopy do look for hypertensive retinopathy & dipstick urine for proteinuria.
When will you deliver her (sole PIH case)?

Deliver is consider when prolonging the pregnancy offers no benefit to mother & fetus and there is
increasing risk of deterioration of both parties.
In an uncomplicated asymptomatic PIH case with no evidence of fetal/maternal compromise, I would like
to manage conservatively until 40 weeks but do not allow post date (risk of placenta insufficiency 
Sudden IUD).
If she is on anti-hypertensive & BP well controlled, no evidence of fetal/maternal compromise, there is a
role of managing her expectantly till 38 weeks.
If she develops severe PE, eclampsia or any evidence of fetal/maternal compromise, I will like to deliver
her immediately regardless of POA.
How will you monitor her during labor?

Intrapartum monitoring includes continuous electronic fetal monitoring, monitor labor by partogram,
anti-hypertensive medications continued. I will also establish IV line, keep NBM & provide adequate
analgesia as pain can increase BP. I will monitor her BP/PR every 15 minutes. In the second stage of
labor, I will try to assist her to shorten this stage. In the third stage of labor, I will give her syntocinon
after the delivery of the baby. I will monitor closely her urine output by strict I/O charting. Restriction of
fluids to < 1 liter following delivery of women with severe PE reduces risk of pulmonary oedema.
I will inform the pediatrician to be be standby at delivery.
How would you manage her if she develop eclampsia?

I will like to resuscitate her according to airway, breathing, circulation (ABC).
I will place her in left lateral position & secure airway, give O2. I will also insert an urinary catheter to
monitor urine output. I will like to check for disorders of electrolyte imbalance & DIC. To control the
convulsions, MgSO4 is the drug of choice as it reduces neuromuscular irritability & cerebral vasopasm.
A suggested regime is a loading dose of slow bolus of 4g iv over 5-10 minutes followed by iv infusion of
1g for 24 hours. Treat recurrent seizures with further iv bolus of 2g over 5 minutes. If seizure persists
despite on MgSO4, I would consider giving diazepam or thiopentone under anaesthetic guidance. If BP >
160/110 mmHg, I will consider staring hypertensive crisis regime. Finally, when eclampsia is under
control, I will like to deliver her immediately by C-section if vaginal delivery is unfavorable. If she is in
labour, delivery may be possible.

25
What are the predisposing factors for hypertensive disorders during pregnancy?
Primigravida, genetic (mother & fetal), predisposing factors medically (essential hypertension,
thrombophilia, migraines, DM), socioeconomy (Poor maternal nutrition).
What is the strong association with hypertensive disorders during pregnancy?

Multiple pregnancy (particularly monochorionic twins), fetal triploidy/trisomy 13, hydatidiform mole,
placenta hydrops.
What is the timing of eclampsia seizures?

38% antenatally, 18% intrapartum, 44% postpartum.
What are the sign & symptoms of impending eclampsia?

Symptom : Epigastric pain, nausea & vomiting, frontal headache.
Signs : Severe hypertension & proteinuria. Papilloedema, retinal oedema/hemorrhages.
What are the signs of MgSO4 toxicity?

Respiratory suppression (<16 bpm), urine output (< 25ml/hr), absence knee jerks.
What is the antidote for MgSO4 overdose?

IV Calcium gluconate 1g over 10 minutes.
What is the proposed etiology of pre-eclampsia?

Genetic predisposition  Abnormal immunological response Deficient trophoblast invasion 
Hypoperfused placenta  Circulating factors released  Vascular endothelial cell activation  Clinical
manifestation of disease.
Why pre-eclamptic / eclamptic patient who goes for emergency LSCS bleeds more?
Hypertension & Thrombocytopenia (HEELP).

26
Gestational Diabetes Mellitus
Management
Since my patient has GDM, I would like to manage her by a multidisciplinary team, which consists of
obstetricians, physicians and dieticians. Antenatally, the aims of my management are to achieve a good
blood glucose control and to prevent complications. To control the blood sugar level, a strict diet
control should be adopted. This can be achieved by taking high fibre diet with correct calorific intake as
advised by the dietician. If indicated, an insulin therapy may be initiated. The usual insulin treatment is
combined soluble intermittent soluble insulin with each meal and an intermediate-acting insulin in the
evening. If my patient is on insulin, she should be instructed on the use of glucagon for hypoglycaemic
attacks. To assess her blood glucose control, blood sugar profile monitoring should be done for 2-3 times
per week. Ideal pre and post-prandial levels are <5.0 and <7.0 respectively. Urinalysis should also be
done at each visit for glycosuria and evidence of UTI (leucocyte esterase, nitrites). HbA1c or
fructosamine tests may also be done regularly to assess blood glucose control.
For maternal health, her weight, optic fundi, blood pressure and renal function should be monitored
regularly. Fetal monitoring, on the other hand, consists of fetal well-being and growth. This can be done
by counting of fetal movements by the mother and recording it on a fetal kick chart (>10 in 12 hours),
symphysiofundal height, fetal heart rate and CTG should be done at each follow up. Serial USG should
also be done fortnightly to assess for fetal growth, as GDM is associated with macrosomia. Liquor
amount should also be assessed as GDM is associated with polyhydramnios. A detailed anomaly scan
should be done at 20 weeks, as there is associated increase in incidence of congenital anomalies (e.g.
cardiac and cranio-spinal defects) in DM mothers.
For labour and delivery, if diabetes is well-controlled and pregnancy is uncomplicated, the timing of
delivery should be at 38 weeks, by induction of labour. I will not allow post date. The mode of delivery of
choice is normal vaginal delivery, unless contraindicated. During labour, close control of blood glucose is
achieved by a continous infusion of soluble insulin using a sliding scale, and a separate infusion of
dextrose and KCl. Regular blood glucose control monitoring should be undertaken (hourly DXT) and the
insulin infusion titrated to keep levels between 5-7 mmol/L. If a syntocinon infusion is needed, should be
made up using normal saline. Continous electronic fetal monitoring should be done.
If my patient is going for ELSCS, keep her NBM from 12 midnight. Baseline U&E and RBS should be sent
at 6am. Morning dose of insulin is omitted. DXT to be monitored regularly. Close control of blood
glucose is achieved by hourly assessment of BS level, a continuous infusion of soluble insulin using a
sliding scale, and a separate infusion of dextrose and KCl.
Shoulder dystocia and fetal distress should be anticipated.
During the post partum period, following the delivery of placenta, insulin infusion should be discontinued.
DXT for both mother and baby to be checked before transferred out to post-natal ward. Mother should be
encouraged to commence breast feeding early. Blood glucose level should be maintained at 4-10mmol/L.
Contraception should be advised.

27
FAQs
What are the risk factors for the development of DM in pregnancy?
 Increasing age
 Certain ethnic groups (Asian, African Americans, Hispanic/Latino Americans and Pima Indians)
 High BMI before pregnancy (three-fold risk for obese women compared to non-obese women)
 Smoking - it doubles the risk of GDM
 Change in weight between pregnancies - an inter-pregnancy gain of more than three units (of BMI)
doubles the risk of GDM
 Short interval between pregnancies
 Previous unexplained stillbirth
 Previous congenital anomaly
 Previous macrosomia
 Family history of type 2 diabetes or GDM - more relevant in nulliparous than parous women
What are the effects of pregnancy on diabetes?
 Change in eating pattern

 Increase in insulin dose requirements
 Greater importance of tight glucose control
 Increased risk of sever hypoglycaemia
 Risk of deterioration of pre-existing retinopathy
 Risk of deterioration of established nephropathy
What are the effects of diabetes on pregnancy?
 Increased risk of miscarriage

 Risk of congenital malformation
 Risk of macrosomia
 Increased risk of pre-eclmpsia
 Increased risk of still birth
 Increased risk of infection
 Increased operative delivery rate
Factors associated with poor pregnancy outcomes in diabetes
 Maternal social deprivation

 No folic acid intake pre-pregnancy
 Suboptimal approach of the woman to managing her diabetes
 Suboptimal pre-conception care
 Suboptimal glycaemic control at any stage
 Suboptimal maternity care during pregnancy
 Suboptimal fetal surveillance of big babies
28
Who to be screened for GDM? (Carol)
 Age > 25 years old

 BMI >27 kg/m2
 Glycosuria @ 1st antenatal / booking visit
 Previous macrosomic baby (≥4kg) or LGA
 Previous GDM
 First-degree relative with diabetes
 Family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle
Eastern)
 Previous unexplained stillbirths, recurrent abortions, birth defects
 Current obstetric problems – polyhydramnios, current use of steroids, persistent glycosuria.
How would you screen for GDM in a pregnancy?

In the presence of GDM risk factors but gestation < 12 weeks, I will perform a RBS.
If GDM risks present but gestation is > 12 weeks but patient has hyperemesis, I will deter OGTT till later.
If gestation is > 12 weeks & she has no hyperemesis, I will do OGTT.
I would like to repeat OGTT at 24-28 weeks if the first OGTT is normal.
How you diagnose GDM?

MOGTT : FBS ≥5.6 and / or 2nd hr ≥ RBS 7.8

29
Common Q & A
What is the definition of labour?

Labour is defined as the presence of regular contractions with increasing intensity & frequency associated
with progressive dilatation & effacement of the cervix with descent of the presenting part.
What are the features of normal labour?

Spontaneous onset; single cephalic presentation, 37-42 weeks; no artificial interventions; unassisted
spontaneous vaginal delivery; dilatation ≥ 1cm/2 hours in active first stage; active second stage < 2 hours
in primiparous, < 1 hour in multiparous; third satge < 30 minutes with active management.
How to differentiate true from false labour pain?

In false labour, the cervix remains undilated & uterine contractions remain impalpable or infrequent.
What is the evidence of obstructed labour?

Secondary arrest of cervical dilatation & descent of presenting part, large caput, third degree moulding,
cervix poorly applied to presenting part, oedemtous cervix, ballooning of lower uterine segment,
formation of retraction band, maternal/fetal distress. Thick meconium stained liquor.
What are the signs of separation of the placenta?

Lengthening of the cord, small gush of blood, rising of uterine fundus to above umbilicus, fundus become
hard & globular compared to soft & broad prior to separation.
How are you going to present a vaginal examination finding?

Vulva & Vaginal no abnormalities detected. Os 2cm. Cervix canal length 2cm, station -1, medium
consistency, membrane intact, no cord felt, vertex presentation. (0/5 = +2cm, 1/5 = +1cm, 2/5 = 0cm
@ischial spine; head engaged, 3/5 = -1 cm, 4/5 = -2cm, 5/5 = -3cm)
Where would you place your Pinard stethoscope?

Anterior shoulder.
(Alternatively, Fetal back, identify the anterior shoulder then move 3.75 cm (1.5-2 inch) laterally).
If mother complained of reduced fetal movement, what will you do?

I will take a complete history & PE. I will use a pinard stestescope to measure fetal heart rate.
Next, I will like to proceed to US to look at fetal heart activity, measure the growth parameter (BPD, AC,
FL, AFI and weight), lie & presentation, biophysical profile. I will also like to do a Doppler US to look
for reversed diastolic flow, CTG, and ask the mother to plot a fetal kick chart.
What is a biophysical profile? Score 0-10

A biophysical profile is a long US scan (30 minutes) which identify antenatal hypoxia. It takes into
account of a non-stress CTG, fetal breathing movements, fetal body movements, fetal tone & amniotic
fluid volume.

30
What is a modified biophysical profile?

The modified biophysical profile combines the non-stress test (CTG) with the amniotic fluid index.
The modified biophysical profile is considered normal if the nonstress test is reactive and the amniotic
fluid index is greater than 5 cm and abnormal if the nonstress test is nonreactive or the amniotic fluid
index is 5 cm or less.
What is Bishop score? Score 0-13

Dilatation of cervix, consistency of cervix, length of cervical canal, position, station of presenting part.
How do you determine fetal well being?

By CTG & Biophysical profile.
What is active management of third stage of labour?

Syntocinon, controlled cord traction, early clamping of cord, uterine massage.
What are the indications of doing a emergency LSCS in a major placenta praevia case?
Major bleeding, in labour, fetal distress, placenta abruption.
What are the complications of post date?

IUFD secondary to placenta insufficiency, fetal hypothermia or hypoglycemia, fetal distress during labour,
increase risk of caesarean section, meconium stained liquor.
What should be excise in hysterectomy?

Broad ligament, round ligament, cardinal ligament/paracervical & vaginal vault.
Landmark trial to quote in exams Findings
ORACLE1 & 2 : Erythromycin in PPROM
Magpie trial
Mnemonics in Obstetrics & Gynaecoogy
Prerequisites for instrumental delivery : FORCEPS

Fully dilated cervix (8cm for ventouse)
OA/OP
Ruptured membranes
C – No CPD, catheterize patient, contraction satisfactory.
Episiotomy, Engage (0/5)
Pain relief, position( (Lithotomy)
Supervision, sterility, skill

2009/2010
2009
Long Case Examination for Phase III Medical Students (Obstetric Cases)
List and Answer to Commonly Asked Questions by Lecturers
Muhamad Na’im B Ab Razak

University Science Malaysia
jacknaim@gmail.com
www.jacknaimsnotes.blogspot.com
Long Case Examination for Phase III Medical Students
Important and Common Cases Needs to be Covered in Obstetric Section.

1) Normal labour
2) False labour
3) Unsure of Date
4) Induction of Labour
5) Caesarian Section
6) Pregnancy Induce Hypertension
7) Pre eclampsia
8) Hypertension in Pregnancy
9) Diabetes Mellitus in pregnancy
10) Gestational Diabetes Mellitus
11) Oligohydramnios
12) Polyhydramnios
13) Reduced Fetal Movement
14) Threatened pre term labour
15) Premature birth.
16) Post Date
17) Post Term
18) PPROM
19) PROM
20) Placenta previa
21) Unstable lie
22) Breech presentation
23) Multiple pregnancy
24) Heart disease in pregnancy
25) Anemia in pregnancy
26) Fibroids
27) Anti phospholipids syndrome
28) Teenage pregnancy
And We have enjoined on man (to be good) to his parents: in travail upon travail did his
mother bear him, and in years twain was his weaning: (hear the command), "Show
gratitude to Me and to thy parents: to Me is (thy final) Goal [Q31:14]]
Anti tetanus toxoid Macrosomic baby (page 18)

Type of immune (page 36) Management (page 16, 17)
When to give (page 36) MOGTT, when to do (page 15)
MOGTT, Indication (page 16)
Anemia in pregnancy (page 44,45) Shoulder dystocia (page 18)
Spontaneous vaginal delivery ((page 18)
Breech presentation (page 36) Weight gain in pregnancy (page 15)
Causes and complication
Mode of delivery Heart disease in pregnancy (page 40, 41,
42, 43)
Candidosis Aspirin, IV
Drug (page 24) Contraindication for pregnancy (page 43)
Failure (page 40)
Caesarian section (page 9) Eisenmenger syndrome (page 41)
Anterior abdominal wall layer (page 10) Warfarin (page 41)
Impending scar rupture (page 10)
Preparation pre op and post op (page 9) Episiotomy
Pfannensteil scar (page 32) Definition (page 4)
Trial of scar (page 9) Layer cut (page 4)
Cervix Fibroids (page 46)

Normal cervical length (page 3)
cervical effacement (page 1) Hypothyroidism (page 50)
cervical dilatation in nulli vs multiparity
(page 1) Labour
Bishop score (page 1, page 3)
Cervical cerclage (page 26) Braxton Hicks contraction (page 2)
definition of labour (page 5)
Chorioamnionitis Discharging patient in latent phase of
Common organism (page 8) labour (page 3)
Management (page 8) engagement (page 4)
Show (page 5)
Diabetes Melitus in pregnancy True vs false labour (page 2)
GDM (page 15) Management of active phase of labour
Complication of GDM (page 16) (page 2)
Diagnosis and level of sugar control (page Mechanism of labour (page 4)
15)
Screening test (page 15) Induction of labour
Diabetogenic hormone (page 15) definition (page 7)
Hydrocephalus (page 19) Indication (page 7)
Mehtod (page 7) Ultrasound

placenta (page 6)
Oligohydramnios (page 20)
Premature labour (page 24)
Parity Definition
Pseudoprimid (page 5) Premature contraction (page 25)
Grand multiparity (page 26) Management
Great grand multiparity (page 49)
Reduce fetal movement (page 22, 23)
Polyhydramnios (page 21) Tocolytic
Fetal kick chart
Post date (page 27)
Tradisional medicine (page 23)
Post term (page 28, 29)
PPROM (page 30) Twin pregnancy (page 37, 38, 39)
Fever Classification
Positive findings complication
Management Physical examination
Twin to twin transfusion reaction
PROM (page 31)
Unsure of date (page 7)
Placenta Neagele's rule (page 7)
seperation, sign and symptoms (page 2) Comfirmation of date
Placenta previa (page 32, 33)
Unstable lie (page 34, 35)
Prostin Causes
Complication (page 7) Complication
dose (page 8) Management
Instruction to patient (page 8) Mode of delivery
with presence of contaction pain (page 1,
page 3)
Uterus
Pregnancy induced hypertension support (page 4)
definition (page 11)
Essential hypertension (page 14)
Management (page 11)
Pre eclampsia (page 12)
Impending eclampsia (page 13)
Magnesium sulphate (page 13)
25 years old Malay lady, G1P0 at 37W+ 2/7 are

admitted because of contraction pain but not
associated with show or leaking.
Questions
1) How do you access the favorable of
cervix?
2) What is cervical effacement?
3) Are there any differences if the cervix is
1 cm dilated in primid vs. Multipara
who presented with contraction pain at
term? Image from: Joan Pitkin et al, Obstetrics and
4) Can we induce the labour with Prostin Gynaecology: An Illustrated colour Text
with the present of recorded contraction
pain? Differences if the cervix is 1 cm dilated in
primid vs. Multipara who presented with
Answer contraction pain at term?
Cervical score
In HUSM, we used Modified Bishop Score. Nulliparous women have small external os at
Cervix is favorable if Bishop score > 5 cervix center. In multiparous woman, cervix is
bulkier and the external os has a more slit like
appearance. Therefore, dilatation of 1 cm is
significant in primid and not in multigravida.
In multiparous, it is usually normal if cervix

dilatation is 1 cm. Diagnosis of false labour
should be made if it did not progress.
Role of Prostin in the presence of recorded

contraction pain.
Recorded contraction pain is by evidence of

CTG reading plus typical history of contracting
Mnemonics: DiCoLePoS (Dilatation, pain.
consistency, length, Position and Station)
[Credited to Dr Ramli Ibrahim, HUSM] Once it present, Prostin should never being use
as it will predispose mother to uterine hyper
Cervical Effacement stimulation and cause fetal distress to the baby.
Cervical changes prior to onset of labour where
cervix become shorter, softer and moves from its Other mode of induction of labour should be
position in the posterior vaginal fornix towards considered.
anterior vaginal fornix [Joan Pitkin et al,
Obstetrics and Gynaecology: An Illustrated
colour Text]
1
Case: G1P0, Post EDD, currently in labour (VE Impression: Patient is already in active phase of
5cm) first stage of labour.
Post date patient who are already in labour will
Question: not change the management and spontaneous
a) Patient is a primid, never experience vaginal delivery should be expected except there
before, how are you going to ask her in is indication for caesarian section or
Hx whether it is a true labour. instrumental deliveries.
b) How to manage this patient
General management
Notes: A Braxton Hicks contraction is a normal 1) Transfer patient to Labour room
irregular uterine contraction starts occurring 2) FBC and GSH
from fourth months of pregnancy. It acts as
preparation for uterus to contract properly later. First stage of labour
1) Review history and problems
True vs. False Labour pain 2) Abdominal exam and VE +ARM
1) Timing of contractions 3) Starts partogram
False Labor: Often are irregular and do not 4) Review patient after 4H since cervix is
get closer together <6cm (if >6cm VE when full dilatation
True Labor: Come at regular intervals and as is expected)
time goes on, get closer together. Contractions 5) Monitor
last about 30-70 seconds. a) Maternal BP, PR, Uterine
contraction
2) Change with movement b) 4H temperature
False Labor: contractions stop in association c) FHR auscultation/ CTG
with walking or change in position.
True Labor: Contractions continue, despite Second stage of labour
movement or changing positions 1) Leave patient for 30 minutes if no
pushing contraction. Notify MO if not
3) Strength of contractions deliver after 1H of active pushing
False Labor: Contractions are usually weak 2) Episiotomy
and do not get much stronger (may be strong
first, then get weaker) Third stage of labour (30 Minutes)
True Labor: Contractions steadily increase 1) Syntometrine (Oxytoxin 5U+
in strength ergometrine 0.5 mg) IM
2) Delivery of placenta by controlled cord
4) Pain of contractions traction
False Labor: contractions are usually only 3) Repairing of episiotomy wounds
felt in the front of the abdomen or pelvic region
True Labor: Contractions usually start in the Signs of placenta separation
lower back and move to the front of the - Uterus contract and fundus become
abdomen. Referred pain from uterus felt at the globular and firm
buttock. - Small gush of blood flow out
- Lengthening of umbilical cord.
Management of this patient
2
28 years old Malay lady, G1P0 at 38W + 5/7 Before, any decision to discharge this patient,
days POA was admitted because of contraction few measures needs to be look at.
pain. There is no show or leaking liquar.Below 1) If the contraction pain starts to subside
is her Bishop score on admission. 2) Pre discharge vagina examination did
not show any cervical progression
3) No Pre labour ruptures of membrane.
4) CTG has been performed and reactive
5) Baby is not in mal presentation.
6) Patient can easily come back to hospital
if anything happen.
a) Short distance
b) Access to transportation
c) People to take care of her.
7) With advice that patient must come to
hospital if any PROM or show or if the
contraction become strong and in close
intervals.
Questions Induction of labour

1) Comment on the Bishop score
2) What is the normal length of the cervix - Induction with prostin is not indicated as
in non pregnant lady? contraction is already there. It will only
3) If this patient requested to be increase risk for uterine hyper
discharged, can you allow that? Support stimulation and abruptio placenta.
your answer. - ARM could be done if cervical
4) Will you induce this patient for labour? dilatation more than 3 cm.
Bishop Score
Based on assessment on Bishop Score, patient is

already in latent phase of labour as evidence of
os is dilated. However the cervix is not favorable
for labour yet.
Normal cervix length for non pregnant lady
3.5 CM
Requested to be discharged
This patient is in the latent phase of labour. In

primid, the latent phase could be as short as one
day but may extend up to one week.
3
23 years old Malay lady at 39W+3/7 POA Mechanism of labour

was transferred into ward from labour room
because of contraction pain associated with Changes in position of the fetal head during
show on the day of admission. No leaking of passage through the birth canal in the vertex
presentation.
liquor reported and fetal movement was
good.
(EDFIERE!)
Questions
1) Engagement
1) Types of pelvis
2) Descent
2) What is engagement
3) Flexion
3) Outline the mechanism of labour
4) Internal rotation
4) What is the layer cut during the
5) Extension
episiotomy procedure?
6) External rotation
5) The structures supporting the uterus.
7) Expulsion
What is episiotomy and layer cut during the

procedures?
Episiotomy is a surgical cut that is made to the

perineum during the pushing stage of labour.
Layers of cutting:
1) Skin
2) Subcutaneous tissue
3) Vaginal mucosa
4) Bulbospongiosus muscle
5) Deep and superficial transverse perineal
muscle
Engagement
Descent of the biparietal diameter of the fetal

Support of the Uterus
head below the plane of the pelvic inlet.
Clinically, if the lowest portion of the occiput is
1) Tone of levator ani muscle
at or below the level of the maternal ischial
2) Perineal body
spines (station 0), engagement has usually taken
3) Ligaments
place. Engagement can occur before the onset of
a. Transverse cervical or cardinal
true labor, especially in nulliparous patients [The
ligament
John Hopkins Manual of Gynecology and
b. Pubocervical
Obstetrics 3rd ed.]
c. Sacrocervical
4
36 years old Malay lady, G3P0 at 37 weeks of Differential diagnosis

pregnancy was admitted to ward after noticing - In labour
spotting blood mixing with mucous on her - False labour
underpants after waking up from sleep. The - PROM
same event occurs two times in ward. However, - Bleeding from PP or Placenta abruptio.
there is no recorded abdominal pain. - Discharge from urinary tract infection
- Trauma to the perineal region.
Question
1) What is mature pseudo primid? Management to this patient
2) What is labour
3) Terminology for blood mixing with 1) Full history and physical examination
mucous a) Correct dating of pregnancy
4) Differential diagnosis b) Elicit any risky pregnancy
5) Management to this patient. c) Eliminating the differential
diagnosis.
Answer d) It is important to exclude PROM as
patient at term and chorioamnionitis
Mature pseudo primid could be disastrous for fetus.
- Mature means age of mother > 35 years 2) Observation of vital sign
old 3) Fetal kick chart (some doctor
- Pseudo primid means patient has been recommend this) and labour progression
pregnant but never deliver the baby. chart (LPC)
- The term ‘mature’ should alert the 4) Speculum examination to access the
doctor in carefully managing this patient cervix and excludes PROM, infection.
because of many complication can occur 5) Assessment of fetal well being (CTG
in this age group. Furthermore, this and ultrasound)
could be her last pregnancy 6) Blood investigation (FBC to look for
evidence of infection)
Labour 7) Urine FEME to exclude UTI.
- Process by which fetus is expelled from 8) Observe the patient in wards for 2-3
the uterus and into the outside world. days. If patient is stable and the labour
- Three stages of labour does not progress, then the diagnosis is
a) 1st stage- onset of contraction till false labour. Patient can be safely
full dilatation of cervix discharge and ask her to come back
b) 2nd stage- full dilatation of cervix till again once the sign and symptoms of
delivery of fetus labor starts.
c) 3rd stage- delivery of placenta 9) If patient in labour, then proceed with
- Sign and symptoms of labour includes the management for labour
abdominal contracting pain, show
(discharging blood mixing with
mucous), gushing of clear fluid (liquor)
5
Notes on U/S about placenta Placental thickness judged subjectively
Vascularity But if measure at midposition or cord

insertion 2-4 cm = normal
Very vascular – has 2 blood supplies
Blood from fetus through 2 (sometimes 1) Grade 0

umbilical arteries through umbilical cord 1.Late 1st trimester-early 2nd trimester
from fetal hypogastric arteries to placenta 2.Uniform moderate echogenicity
3.Smooth chorionic plate without indentations
1 umbilical vein carries blood back to fetal
left portal vein Grade 1
1.Mid 2nd trimester –early 3rd trimester (~18-29
Blood from mom through branches of wks)
uterine arteries through the myometrium 2.Subtle indentations of chorionic plate
(arcuate arteries) through the basilar plate 3.Small, diffuse calcifications (hyperechoic)
(spiral arteries) into the placenta
randomly dispersed in placenta
The two circulations intertwine in the
Grade 2
placenta but do not mix
1.Late 3rd trimester (~30 wks to delivery)
Exchange of oxygen and nutrients occurs 2.Larger indentations along chorionic plate
over the large vascular surface area 3.Larger calcifications in a “dot-dash”
configuration along the basilar plate
Maternal venous channels in the placenta are
hypoechoic or anechoic spaces called Grade 3
venous lakes (usually small, but can be 1.39 wks – post dates
large) 2.Complete indentations of chorionic plate
through to the basilar plate creating
Anatomy on US “cotyledons” (portions of placenta separated by
the indentations)
Inner border of placenta against the uterine 3.More irregular calcifications with significant
wall has the combined hypoechoic shadowing
myometrium and interposed basilar layer = 4.May signify placental dysmaturity which can
hypoechoic band called the decidua basalis cause IUGR
(contains maternal blood vessels) 5.Associated with smoking, chronic
hypertension, SLE, diabetes
Outer surface abutting the amniotic fluid =
chorionic plate (chorioamniotic membrane)
Sources:
= bright specular reflector
http://www.learningradiology.com/notes/gunote
s/placentapage.htm
6
Case: Unsure LMP/ Unsure of Date to pregnancies at gestations greater than the
legal definition of fetal viability (24 weeks).
Questions
a) Neagele’s rule Divided into mechanical (Sweep & scratch,
b) Investigation ARM,) and pharmacological (IV Syntocinon,
c) Management Prostin).
d) Induction of labour
e) Complication of Prostin Others; breast stimulation, relaxin,
hyaluronidase, sexual intercourse, acupuncture,
Neagele’s rule homeopathic method
1) Sure of date
2) Menstrual cycle is regular of 28 days
(ovulation occur 14 days prior to the Indication for IOL
next menses) 1) Fetal
3) Not on any form of hormonal a) IUGR
contraception within 3 months b) PIH/PE
4) Not lactating within 2 months c) GDM at 38w
d) Post EDD
Investigation e) Twin at term
1) Cardiatocography (CTG) to access fetal f) Hx of unexplained APH
well being g) Transverse oblique/unstable lie
2) Ultrasound for physical biometry of the h) Hemolytic disease
baby, and amniotic fluid index i) Fetal abnormality incompatible with
life (anencephaly)
2) Maternal
Management a) Medical disorder aggravated by
1) Confirmation of the date of pregnancy pregnancy like DM, SLE, PE, Renal
a) Early ultrasound scan (<20w) disease.
b) 1st UPT positive (6-8w) b) IUD with risk of DIC
c) Quickening c) Spontaneous/ PROM>24h
d) Uterine size correspond to d) Abruption of placenta
pregnancy
e) Onset of signs and symptom of
pregnancy Complication of prostin
f) Conception date 1) Failed IOL (require c-sec)
2) Bishop score (>5 is favorable) 2) Uterine hyper stimulation
3) Elicit any medical problem. 3) Uterine rupture.
4) Fetal distress.
Induction of labour 5) C/I in patient with asthma/glaucoma
An intervention designed to artificially initiate 6) Abruptio placenta
uterine contractions leading to progressive
dilatation and effacement of the cervix and the
birth of the baby. The term is usually restricted
7
27 years old Malay lady, G2P1 at 38 weeks of In woman whom deliver more than two babies
pregnancy was admitted to ward because of (not grand Multipara) and 1 caesarean section
PROM more than 24 hours. She was council for scar, the dose for each cycle is 1.5 mg.
induction of labour.
If labour is not progress after the second dose,
Question then it is considered as failed induction [NICE
1) Common organism causing Guidelines] and emergency C-sec will be done.
chorioamnionitis in PROM and how to HUSM did not follow this guidelines and IOL
manage. with prostin is based on clinical experience.
2) Dose of Prostin
3) Instruction to the patient before inserting Some might consider failed induction after the
the Prostin third dose, 6 hours after the second dose.
(Controversy)
Answer
Notes: Prostin is contraindicated if presence of
Common organism causing chorioamnionitis uterine contraction to avoid uterine hyper
in PROM and how to manage? stimulation.
1) Risk of getting infection arises after 12 Instruction to patient before inserting the
hours of PROM. Prostin
2) Antibiotic prophylaxis should be given
based on common isolated organism 1) Ask the patient to urinate first because
which is group B Streptococcus (IV she needs to lie on bed for one hour
Penicillin) 2) Ask the patient to lie down on bed for
3) Chorioamnionitis is more dangerous to one hour
fetus as compared to mother 3) Ask the patient to inform the doctor if
4) IOL should be suggested to the mother the contraction pain is strong.
if PROM > 24 hours. 90% of patient 4) Do CTG after one hour to access uterine
with ruptured membrane will deliver the contraction and any evidence of fetal
baby within 24 hours. distress
5) If chorioamnionitis develop, patient 5) After one hour, do the VE to access the
should be covered with antibiotic cervical dilatation.
against GBS, gram negative and 6) If cervix is more than 3 cm, remove the
anaerobes. residual Prostin and sent patient to
labour room.
Dose of Prostin 7) If less than that, and suspect uterine
Notes: I suppositories equals to 3 mg. hyper stimulation, remove the residue
Prostin as well and send patient to
In primid, we can insert 1 suppository and labour room and monitor with CTG.
access the Bishop score 6 hours later. If cervix is KIV tocolytic agents (salbutamol). If
favorable, then we may proceed with artificial fetal distress, emergency cs.
rupture of membrane. If not, second dose of 8) If CTG normal, patient can regain her
Prostin may be given. activity. Recheck cervical score 6 hour
later.
8
Case: 3 Previous C-sec scars 3) To cover the surgery

a) Consent form signed
Question b) Baseline blood investigation (FBC,
a) Investigation GSH, LFT, BUSE/Creat)
b) Management c) Blood cross match (2U Pack cell)
c) Post op-acute management d) IV ampicillin 1g stat for
prophylactic
Trial of Scar e) Bladder catheterization
Notes: According to ACOG guidelines on f) Pre med (IV Ranitidine 50mg in 10
vaginal birth after Caeserean Section, trial of ml by slow injection, IV Maxalon
scar is not recommended in patients at high risk 10 mg by slow injection, Sodium
for uterine rupture. One of the contraindication citrate 30 ml orally)
including this case. 4) Anesthetist with at least one year
experience
1) Two prior uterine scars and no vaginal 5) Ideally use regional block except contra
deliveries indicated (major placenta previa, local
2) Previous classical or T-shaped incision skin sepsis, severe heart disease,
or extensive transfundal uterine surgery coagulation disorder, severe fetal
3) Previous uterine rupture distress, cord prolapsed, eclampsia)
4) Medical or obstetric complication that 6) Present of obstetrician.
precludes vaginal delivery 7) Reduce risk of thromboembolic
5) Inability to perform emergency cesarean phenomenon after surgery
delivery because of unavailable surgeon, a) Early ambulation
anesthesia, sufficient staff, or facility b) Anti embolic stocking/Flowtron
c) Anti coagulant for high risk cases.
Notes: The management of this patient should [The practical Labour Suite Management- Dr Adibah Ibrahim]
emphasize more on caesarean section and

anticipating in possibility of uterine rupture. It Post op management
also includes advice for tubal ligation. (Practice 1) Recovery area (one to one observation until
in Malaysia to do BTL after 4 Caesarian patient has airway control, cardio respiratory
Section) stability and can communicate)
2) In wards (1/2hly observation RR, HR, BP,
Investigation pain and sedation) for 2H, then hourly if stable
Fetal investigation 3) Intrathecal opiods- hourly observation for RR,
- Ultrasound (AFI, Estimated fetal Sedation and pain scores for 12h for
weight, exclude placenta previa, accrete diamorphines and 24h for morphines)
or abruptio, biometry) 4) For epidural opiods and patient-controlled
- CTG analgesia with opiods (hourly monitoring during
CS, plus 2h after discontinuation)
Maternal (preparation for C-sec) 5) Post natal care (analgesic, monitor wound
1) For patient in labour (fluid diet and T. healing, signs of infection)
Ranitidine 150 mg q.d.s) 6) consider CS complication (endometritis,
2) Patient at high risk of anesthetic( sips of thromboembolism, UTI, urinary tract trauma)
water+ IV fluid if indicated) [NICE Guidelines on Caesarian Section]
9
26 years old Malay lady, housewife, G2P1 at 38 4) Forceps application and breech extraction
weeks of gestation with second husband and once full cervical dilatation achieves
history of previous caesarean section was 5) Elective caesarean section
admitted because of c-sec scar tenderness. 6) Explore the genital tract after difficult or
instrumental delivery
Questions 7) Blood FBC and GSH
1) S&S of impending scar rupture
2) Management for patient come with Once the ruptured occur
impending scar rupture
3) Elicit the scar tenderness on PE 1) Secure the ABC. 02 100%, 3L/min increase
4) The anterior abdominal wall layer cut oxygenation to tissue if hemorrhage occurs.
during the c-sec operation. 2) 2 large bore IV line
3) Blood transfusion and shock management
Uterine scar rupture 4) Emergency laparatomy
5) Delivery of fetus and placenta
A complete uterine rupture is a tear through the 6) Exploration of the rupture site
thickness of the uterine wall at the site of a prior a) Try to repair the lesion
cesarean incision. b) Hysterectomy of not salvageable
7) Internal iliac artery ligation in case of broad
Patient might present with: ligament hematoma because uterine artery is
usually retracted and difficult to be identified.
1. Fetal distress evidence by abnormalities 8) Vaginal repair if there is cervical tear
in fetal heart rate
2. Vaginal bleeding Layer cut through caesarean section
3. Sharp onset of pain at the site of (Pfannenstiel approach)
previous scar
4. Sharp pain between contractions 1) Curved transverse cut just below hair
5. contraction become less intense (finally border
lead to atony) a) skin
6. Diminished baseline uterine pressure b) superficial fascia (Camper and
7. Abdominal tenderness Scarpa)
8. Recession of the presenting fetal part c) Rectus sheath (contains fascia of
9. Hemorrhage EO, IO and TM)
10. shock
2) Vertical incision for access into lower
Management to impending scar ruptures abdomen
Management a) Separation of rectus abdominis
muscle in midline
Prophylactic management b) Dividing of the fascia transversalis
c) periperitoneal fat tissue
1) Close monitoring for woman with high risk of d) peritoneum
uterine rupture
2) Early detection of causes of obstructed labour
3) Use Oxytoxin with caution
10
Case: PIH being, abnormal surveillance basic

blood test (BP and urine dipstick at least
Questions 3X per week, weekly PE profile and
a) Differential diagnosis CTG.)
b) Management 6) Starts anti hypertensive when diastolic
c) Drugs (SE&MOA) BP > 90 mmHg
d) Drugs contraindicated in PIH a) T. Methyldopa 250 mg tds to max
dose of 3g/day or
Definition b) T. labetolol 100 mg tds to max 300
BP more than or equal to 140/90 mmHg in mg tds
previously normotensive patient, @ A rise in 7) IM dexamethasone 12 MG 12 hourly for
systolic BP of > 30 mmHg or diastolic BP > 15 two doses for expectant prem delivery.
mmHg compared with pre-conception or first
trimester value in two recording of at least 4H In case of severe PE
apart 1) Manage in hospitals
2) Close monitor BP 4Hly, reflex, clonus
Differential diagnosis 3) Check fundus
- Chronic hypertension (long or before 20w) 4) Twice weekly(or more based on
- Pre eclampsia (>20W+new onset proteinuria) severity) PE, CTG, biophysical profile
- PE with superimposed chronic HPT and doppler
New onset or A) acutely worsen proteinuria, B) 5) Anti-hypertensive but aim for 20-25
sudden increase in BP, C) thrombocytopenia or reduction only and not normal by using
D) elevated liver enzymes after 20 week hydrallazine or labetolol
gestation in women with pre existing HPT
- Gestational HPT (after 20w without In labour
proteinuria) 1) BP stabilization
2) Watch for fluid overload (monitor UO)
Management 3) Seizure prophylaxis in severe PE
1) if detected <20W, must exclude molar 4) Epidural analgesic is the best
pregnancy by US and after exclusion, 5) Oxytoxin only to augment labour.
being investigate for primary or 6) Never allow woman with severe PE to
secondary HPT push excessively. If BP high, consider
2) If pre existing HPT during Booking, instrumental delivery.
should be managed by obs+internist 7) C/I to ergometrine/syntometrine in third
3) Every other day BP check at local clinic stage due to hypertensive effect.
if BP is first high during any ante natal
check up.
4) Investigation for PE profile (platelet Drugs contraindicated for PIH includes ACE
count, uric acid, serum creatinine level, inhibitor and ARB as it can cause renal
AST, urine albumin). If PE is diagnosed, dysgenesis of the baby.
then it should be repeated once a week
5) If BP sustained at >100mg/ >25
increment mmHg or clinical suspicious
of IUGR, poor maternal-feternal well
11
Case: 41/M/F, G1P0 at 29W+2d POA 5) PE profile twice a week (severe PE) or
High blood pressure and proteinuria 3+ once a week(mild PE) compose of
a) Platelet count (decrease)
Question b) Uric acid (1st indication of renal
a) Investigation and reason impairment)
b) Treatment plan c) Sr Creatinine level (renal function)
c) Time of delivery and why? d) Liver enzyme, AST (liver damage)
e) Urine albumin as mention in above.
My impression: High blood pressure with 6) Clotting study if platelet < 100 x 106/l
proteinuria could lead to Pre eclampsia which is 7) Input/output Fluid Chart.
worrisome due to serious complication. 8) CTG for fetal well being.
Therefore, PE should be ruled out first before 9) Serial ultrasound measurements of fetal
considering other condition that may falsely give size, umbilical artery Doppler and liquor
positive result to proteinuria like UTI volume
PE is defined as: Treatment plan

Hypertension unique to pregnancy, diagnosed
after 20W of gestation and associated with new Mild PE
onset proteinuria; Eclampsia if seizure occurs. T. Methyldopa 250mg tds, max 3g/day or
T. Labetolol 100 mg tds, max 300mg tds
If woman already having pre existing HPT but Or, Tab. Nifedipine 10 mg tds stat dose
after 20W she develops new onset proteinuria,
sudden increase in BP, thrombocytopenia or Severe PE
elevated liver enzymes, then PE with IV hydrallazine start 5mg, double if no effect
superimposed on chronic hypertension must until 35mg. change drug if fails or
be suspected. IV Labetolol start 10 mg, double if no effect
until max 300mg/day)
HELLP (Hemolysis, Elevated liver enzyme, low
platelet) is a variant of PE with involvement of ** MgSo4 slow infusion 4g 10-15 minutes.
liver giving rise to tender epigastric pain, and Maintenance dose IV ig/hour
finally DIC.
When to Deliver
Investigation 1. Delivery is definitive treatment if mother life
1) Repeat Dipstick testing within 6H is compromised. (Very high uncontrolled BP,
PE shows by urinary albumin platelet <100, AST>150 iU/L
>300mg/24 hour@ >1g/l in 2 random 2. Can wait until term if well controlled and fetal
urine 6 hour a part. is not compromised.
1+ = 0.3 g/l, 2+ = 1 g/l and 3+ = 3 g/l. 3. If gestation >34W, then delivery after
2) 24 Hour proteinuria to see severity of stabilization is recommended
PE. Severe PE >5000mg/24 hr. 4. In this case, prolong delivery for 24 Hr to give
3) BP should be checked every 15 minutes steroid injection for lung maturity
until women are stable. Then, [RCOG Guideline No. 10(A) March 06]
4) Close monitoring of BP (at least
4Hourly) + reflex, clonus.
12
Case: 19/M/F, G1P0 at 32W of pregnancy 1g/h for at least 24h after last seizure or delivery
diagnosed with pre eclampsia at 28W of Add 4 vials (10g) to 50cc of normal saline & run
gestation. at 5cc/h
Question If further fits occur give a further

furth slow IV dose
a) Signs and symptoms of impending of 2g & continue the maintenance infusion
eclampsia
b) Magnesium sulphate Contraindications for Magnesium Sulfate:
Cardiac failure
Signs and symptoms of impending eclampsia Acute renal failure
1) Headache
2) N & V Drug monitoring:
3) Visual Disturbances Clinical
4) Right upper quadrant pain 1) Patellar reflex:
5) Progressively oedema (non dependant) - After completion of loading dose
6) Frothy urine (proteinuria - Half hourly whilst on maintenance
maintenanc infusion
- use elbow reflex if epidural in situ
Magnesium sulphate 2) Respiratory rate: should be >16/min
Magnesium sulfate is superior to other AED 3) Hourly urine output: should be >25ml/h
(phenytoin, diazepam). (urine output is critical as serum Mg level
depends on renal excretion)
Indications:
1) Eclampsia 4) Pulse Oximetry : must remain >90%
2) Fulminating severe PE either:
a) Severe hypertension (MAP: >125 Serum Mg level should be checked when:
mmHg, SBP: >170 mmHg, DBP: >110 Oliguria (<25ml/h)
mmHg); OR Respiratory rate <16/min
b) Hypertension with proteinuria (BP: Pulse oximetry <90%
>180/90 mmHg, proteinuria: Continuing fit
>0.3g/24h), AND one of the following:
i. Clonus (>3 beats) Toxicity (therapeutic range: 2-4
2 mmol/l @ 4-8
ii. Severe persistent headache mg/dl)
iii. Visual disturbance Loss of patella reflex
iv. Epigastric pain Weakness
v. Platelet count <100 x 103/dL Nausea
Feeling of warmth 5mmol/l
Protocol for use of Magnesium Sulfate: Flushing
(5ml vial contain 2.5g MgSO4 ~0.5g/ml) Double vision
Slurred speech
Loading Dose – 4g Magnesium Sulfate Muscle paralysis 6-7 mmo/l
8ml (4g) + 12ml 0.9% saline IV over minimum Respiratory arrest
of 10 - 15 minutes Cardiac arrest >12 mmol/l
[Labor suite Management by Dr Adibah Ibrahim]
Maintenance Dose
13
Case: 34/M/L, G2P1 C/C-High blood pressure Investigation

Dx- Essential hypertension. 1) ECG
2) Urine dipstick test
Question: Hx and Pe only 3) Fasting Lipid profile
4) BUSE and creatinine,
Essential hypertension
-Primary elevation of blood pressure without Management
known causes which can be ameliorated only by
lifelong pharmacological therapy [Kumar& Non pharmacological
Clark 6th edition] 1. Lifestyle medication with light exercise.
2. Reduce the intake of salt and fat.
Risk factor
- Genetic Pharmacological
- Low birth weight 1. Stop ACE inhibitor and ARBs. Atenolol
- Environmental factor can cause IUGR and Labetolol is
a) Obesity relatively contraindicated in Asthmatic
b) Alcohol intake patient.
c) Sodium intake 2. T. Methyldopa 250mg tds, max 3g/day
d) Stress or
e) Smoking 3. T. Labetolol 100 mg tds, max 300mg tds
- Humoral mechanism (insulin resistance) or
4. Tab. Nifedipine 10 mg tds stat dose
Cardiac output rises in pregnancy, however there ** Do not give Methyl dopa together
is relative greater fall in peripheral resistance, with Nifedipine.
therefore BP in pregnant woman is usually low 5. High calcium supplementation of 1.5
than those not pregnant [Kumar& Clark 6th g/day to prevent PE
edition] 6. Avoid Combined vitamins C and E (in
the form of tocopherol from soybean) as
Important history to be elicited it may cause IUGR
1) Risk factor to develop pre eclampsia Others measurement

1. Routine ante natal check up.
a. existing chronic medical disorders such 2. Advise patient to come immediately to
as obesity, hypertension, diabetes hospital if develop signs and symptoms
mellitus, renal disease, connective tissue of impending PE.
disease and thrombophilia, 3. Urinary Dipstick to screen new onset of
b. Previous history of preeclampsia or proteinuria.
eclampsia or IUGR or unexplained 4. CTG and ultrasound to monitor fetal
stillbirth well being.
c. Family history of preeclampsia or 5. Re assurance to the patient.
eclampsia, and 6. Can allow delivering via SVD unless
d. Extremes of reproductive age (below 20 there is indication for C-Sec.
or above 40 years old)
14
25 Years Old Malay lady, Nurse, G1P0 at date b) 2 hour post glucose load: 7-8
+ 5/7 was admitted to wards because of mmol/L
contraction pain and URTI. Patient also was 2) Level of blood glucose control: Blood
investigated for GDM because of excessive Sugar Profile (4-6 mmol/L) and Serum
weight gain during 21 week of pregnancy. HBA1c concentration (< 6.5%)
Questions Screening test for GDM before performing the

1) What Is GDM? MOGTT
2) How do you diagnose GDM
3) Screening test for GDM a) Random blood sugar (> 11.1 mmol/L)
4) When to do MOGTT b) Urinary glucose level (≥ 1+ on more
5) Name the diabetogenic hormone in than one occasion or ≥ 2+ on one
pregnancy occasion)
6) What is normal weight gain in c) Mini Glucose Tolerance Test (> 7.8
pregnancy? mmol/L)
Answer When to do MOGTT
What is GDM? 1) Candidates for MOGTT is offered for

this test at 16-18 weeks of pregnancy
A syndrome of glucose intolerance appears 2) If normal, then repeat at 26-28 weeks of
during pregnancy and usually disappears after pregnancy. If it negative, then no need
pregnancy is terminated. It affects 7% of all to re-do it as HPL diabetogenic effect
pregnancy. starts to plateau even though it’s serum
level continue to increase
It is a metabolic disorder of multiple aetiology proportionally.
characterized by chronic hyperglycemia with
disturbances of carbohydrate, fat and protein Diabetogenic hormone in pregnancy
metabolism resulting from defects in insulin
secretion, insulin action, or both. a) Human Chorionic Somatomammotropin
(HCS) or formerly known as Human
Previously, it is categorized into impaired Placental Lactogen (HPL)
glucose tolerance test and GDM based on fasting b) Estrogen (stimulate production of
and 2 hour post glucose load in MOGTT. prolactin)
However, current guidelines stated that GDM c) Progesterone
includes impaired glucose tolerance test. d) Cortisol
Notes: In GDM, besides of anti-diabetogenic
Diagnosing Diabetes Mellitus and the level of hormone, there will be increased in insulin
blood sugar control degradation by placental enzymes
1) Diagnose: Based on MOGTT Normal weight gain in pregnancy

Normal level of MOGTT is
a) Fasting: 5-6 mmol/L 1) First 5 months: 0.5 kg/months
2) Followed with: 0.5 kg/ week.
15
Case: 28/M/F, G3P2 at 28W P.O.A admitted in Neonate

view of uncontrolled blood sugar level. a) Congenital abnormalities
Diagnosed as GDM at 26W P.O.A. Previous b) Shoulder dystocia, birth asphyxia & traumatic
pregnancy also complicated with GDM and birth
macrosomic baby requiring LSCS. Positive c) Hypoglycemia – fetal islet cell hyperplasia
family history of DM on maternal side. d) Jaundice
e)Respiratory distress syndrome –
Questions hyperinsulinaemia diminished surfactant
a) Complication of GDM production
b) Indication for MOGTT f) Hypocalcaemia and hypomagnesaemia
c) Management to this patient
Indication for MOGTT
Complication of GDM 1) Significant glycosuria on 2 or more
Maternal occasions during pregnancy
a) Hypertension, ↑ incidence of pre- 2) Maternal obesity (i.e. maternal weight
eclampsia (if a/w nephropathy) >80 kg or BMI >27 at booking)
b) ↑ incidence of infection – UTI, 3) Family history of diabetes in first-degree
vulvovaginitis etc relatives
c) Polyhydramnios 4) Previous big baby (weighing >4 kg)
d) Pre-term labour 5) Women >35 years old
e) Coronary artery disease 6) Previous unexplained stillbirths,
f) Thromboembolic disease recurrent abortions, birth defects
g) Risk of caesarean delivery 7) Previous history of gestational diabetes
8) Polyhydramnios in current pregnancy
Fetus 9) Big baby in current pregnancy
1. Early pregnancy 10) Congenital abnormality
a) Spontaneous abortion
b) Congenital anomalies → 40% of perinatal Management for this patient
death in diabetic pregnancies My point of view: This patient was diagnosed as
c) Cardiac defects GDM at 26W of pregnancy. Now is her 28W of
d) Neural tube defects pregnancy and her blood sugar level is
e) Renal anomalies uncontrolled. Obviously DM diet is not working.
f) Caudalregression synd (rare) Therefore, I see the role of giving insulin
injection to her.
2. Later pregnancy
a) Macrosomia Therefore for this current admission, BSP should
b) Polyhydramnios be done after giving insulin injection to look for
c) IUGR (intrauterine growth restriction) the blood sugar level and further adjustment of
d) Unexplained intrauterine death. May be insulin dosage.
secondary to:
Chronic hypoxia Pregnancy shouldn’t be allowed beyond 38W
Polycythemia due to risk of unexplained IUD.
Lactic acidemia
Ketoacidosis
16
36 years old Malay lady, teacher, G4P3 at 37W Caesarean section

+ 6/7 was admitted to wards for further 1) This is possibly a best option but this
management in view of will put patient in high risk category for
next pregnancy which is 2 caesarean
1) Establish DM for three years. scars with no successful VBAC.
Previously on OHA but now changed to 2) If patient wish to pregnant again, she
insulin. However, blood sugar is will require caesarean section for the
uncontrolled. Currently there is no following pregnancy.
complication of DM develops.
2) Last pregnancy is by caesarian section Management for this patient
because of transverse lie. Antenatal
1) Fetal surveillance with ultrasound for
Questions biophysical profile and CTG.
1) Option of mode of delivery and pre 2) Blood sugar profile with adjustment of
requisite for it. insulin dosage.
2) Management for this patient. 3) Diabetic diet
Answer Intrapartum
1) Management based upon modes of
Patient with uncontrolled diabetes mellitus delivery either chooses induction of
should not be allowed to proceed with labour with spontaneous vaginal
pregnancy beyond 38 weeks of pregnancy. delivery or caesarean section.
2) Patient should be started on DKI
Therefore, it is crucial to determine the correct regimes (5% dextrose solution with 1
date of pregnancy to avoid pre term delivery. gram KCL) together with sliding scale
Furthermore, fetus of diabetic mother is insulin infusion. If patient go for c-sec,
associated with delay lung maturity. morning dose of insulin should be
omitted.
Mode of delivery 3) Presence of senior obstetrician to
In this patient, mode of delivery should be standby in case any complication occur.
balanced between benefit and risk. The decision 4) Pediatrician needs to be informed
should always be discussed with the patient. regarding this case.
Spontaneous vaginal delivery with induction of Post partum

labour. 1) Baby should be observed in NICU for
1) Should be done carefully if using 24 hours before discharged.
Prostin because of history of c-sec with 2) After the delivery, insulin can be stop
no successful VBAC. Dosage is 1.5 mg and patient may continue taking OHA.
for each cycle. Membrane sweeping 3) Referral to internal medicine team for
could be considered. further management
2) Need to elicit the lie of the fetus in 4) Advise for contraception.
cephalic presentation. 5) Counseling on blood sugar control if
3) Excludes macrosomic baby. patient wish to get pregnant again
17
35 Years old Malay lady, G1P0 at 37W + 5/7 b) > 4,250 g = elective caesarean section
with gestational Diabetes Mellitus was admitted Notes: Ultrasound is specific for determination of
for review for intrapartum management estimated fetal weight but only with sensitivity of 60-
70% at term. There will be a + of 500 mg
Questions discrepancy of estimated and real fetal weight.
1) What should you elicit before allowing Macrosomic baby of diabetic vs. non diabetic
patient to deliver by vagina delivery? mother
2) What is macrosomic baby?
3) Are there any differences between Macrosomic baby of non diabetic mother is at
macrosomic baby who is belonging to low risk for developing shoulder dystocia as
diabetic mother and non diabetic compared to baby of diabetic mother. This is due
mother? to present of excessive fat tissue growth at
4) If this patient keen on SVD even though shoulder region in baby of diabetic mother. The
the estimated fetal weight is 4 Kg and disproportionate excessive growth of the
the labour is complicated with shoulder shoulder will predispose them to the risk of
dystocia, what would be your shoulder dystocia during SVD.
management?
Steps in managing Shoulder dystocia
Answer
1) Call for help, inform senior obstetrician
and pediatric colleague
Before allowing diabetic mother deliver via
SVD, few thing needs to be excluded first. 2) Experienced obstetrician should be
present during second stage of labour
1) The size of baby is not macrosomic 3) Mc Roberts’ maneuvers (Flexion and
2) Cephalic presentation abduction of the maternal hips,
3) Longitudinal lie positioning the maternal thighs on her
4) Not a candidate for Caesarean section abdomen)
a) Major placenta previa 4) If not successful, apply suprapubic
b) Footling or flexion breech pressure together with Mc Roberts
c) 2 previous c-sec scar without prior (External suprapubic pressure is applied
normal delivery in a downward and lateral direction to
d) Unstable lie push the posterior aspect of the anterior
e) Any obstruction to descending of shoulder towards the fetal chest )
fetus (fibroid, ovarian cyst, 5) If fail, proceed with Wood-Corkscrew
Cephalopelvic disproportion) Maneuvers (The hand is placed behind
the posterior shoulder of the fetus. The
Macrosomic Baby shoulder is rotated progressively 180° in
a corkscrew manner so that the impacted
For undergraduate level, macrosomic is the anterior shoulder is released.
estimated weight of fetus > 4 kg. However, it is 6) If still fail, then deliver the posterior arm
further classified into categories first.
a) 4,000 - 4,250 g (discuss with patient 7) If fail, do Zavanelli maneuvered (push
regarding mode of delivery) the baby back) and prep for emergency
C-sec
18
Case: DM with hydrocephalus baby 2) Observation of fetal condition through

serial ultrasound. Check for any
Question abnormality like spina bifida (associated
a) H(x) and P(e) with hydrocephalus)
b) Investigation and management 3) 30 minutes CTG monitoring for fetal
condition.
History 4) FBC and GSH for the mother
1) Regarding DM 5) Blood sugar profile, Hba1c level of the
a) Since when? Pre existing or during mother.
this pregnancy 6) Check for any complication of diabetes
b) Any history of macrosomic baby, mellitus.
Polyhydramnios or unexplained
IUD during previous pregnancy? Management
c) Are there family risk factor?
d) Is MOGTT done? (normally early 1) Prenatal
pregnancy and repeated at24-28w in a) Pre term delivery is unlikely in this case;
high risk group in which initial test therefore corticosteroid injection is not
is negative) needed.
e) Now on diabetic diet, OHA, or b) Admit the patient at obstetric wards to
insulin. observe the blood sugar level. Starts
f) Ever being admitted due to DM with diabetic diet. If fails, starts insulin.
complication like hypoglycaemia, c) Inform the pediatrician and neonatal
diabetic foot. neurosurgeon regarding delivery of baby
g) Any complaint of DM complication and next intervention. (most likely
like heart disease, peripheral caesarian section at 38-39w to prevent
vascular disease, diabetic head entrapment)
nephropathy, diabetic retinopathy. d) Counseling to the patient regarding the
baby condition. Congenital abnormality
2) Regarding hydrocephalus in DM is low. On next pregnancy should
a) How did the patient know that? take folic acid to reduce risk of
Through US (usually diagnosed hydrocephalus.
after >24w)? Who confirmed it? e) Termination of pregnancy is against
b) Did mother took/compliance to folic medical ethics and Islamic law. Only
acid? fetus which is dead in vitro or no chance
c) Did previous baby having of living can be terminated.
congenital anomaly? 2) Intrapartum
d) The weight of the baby? a) Prep for C-sec
e) P(e) for unstable lie. 3) Post natal
1) Check CBS of the baby and mother
Investigation 2) Admit baby to the NICU for further
1) Find the causes of hydrocephalus. management.
TORCHES? Bleeding? Edward 3) Counsel mother to control diabetes and took
syndrome? folic acid before next pregnancy
19
Case: Oligohydramnios In the term or post-term gestation,

oligohydramnios is frequently associated with
Question thick meconium (a/w Meconium Aspiration),
a) Complication of oligohydramnios deep decelerations in the fetal heart rate, and
b) How to detect the dysmaturity syndrome. One team reported
c) Management a 13-fold increase in perinatal mortality rate
(to 57/1,000) when the sonogram showed
Definition amniotic fluid volume to be marginal, and a 47-
Reduce in AFI <5 based on ultrasound fold increase (to 188/1,000) with severe
[additional of vertical amniotic fluid pocket oligohydramnios.
depths volume in four quadrant.] Some specialist
may consider AFI <8 as oligohydramnios (AP In 62 cases of second-trimester
Dr Nik Hasliza). oligohydramnios, another team reported a 43%
perinatal mortality rate, with lethal pulmonary
Amniotic fluid production hypoplasia complicating 33% of cases. If
A) Production of amniotic fluid is from amniotic fluid was essentially absent
1. Inward transfer of solute across the ("anhydramnios"), 88% had lethal outcomes,
amnion with water following passively in compared with 11% of those with moderate fluid
early gestation. reductions.
2. Water transport across the highly
permeable skin of the fetus during the first Diagnosis
half of gestation (keratinization of skin at - Via ultrasound
22-25W)
3. Baby's urination (first starts at 8-11W Management
and is major source of production. it is Other Investigation
recycled when baby swallows it) 1) intrauterine instillation of dye to
4. Secretion of large volumes of fluid each diagnose PROM [confirm if the dye is
day by the fetal lungs after second half of found in the vagina]-not practically done
gestation (2nd source) 2) Furosemide test to visualize fetal
B) Increase amniotic fluid from 8-43W bladder
gestation linearly until 32W (700-800 mL- ! Both test not practically done
constant until term) Others
-C) After 40W, declines at rate 8% per 1) Amnioinfusion of 200 ml Normal saline
week until 300ml at 42W (not practically done)
2) Maternal rehydration.(controversial)
Causes 3) frequent fetal biophysical testing and
1) PROM or PPROM appropriately timed delivery
2) fetal urinary tract anatomy (renal and 4) Rule out fetal structural and
ureter most common) chromosomal anomalies
3) Uteroplacental insufficiency 5) Earlier delivery in baby incompatible
4) Pulmonary hypoplasia with life.
Complication Notes: risk of fetal asphyxia and death is high in

IUGR
20
35 years old Malay lady, G3P2 at 26W POA moderate (AFI 30.1-35) and severe (AFI >35)
was admitted for further management after she [Naser Omar et al]
persistently worried about her current
pregnancy because her belly was too big Causes of polyhydramnios
compared to previous pregnancy
1) 60% is idiopathic
Questions 2) Maternal causes
1) What is polyhydramnios and how do a) Gestational diabetes mellitus
you grade them? 3) placental abnormalities (placental
2) What is the causes of polyhydramnios abruption, placenta accreta)
3) How do you manage this patient? 4) Fetal factor
a) congenital anomalies ( anencephaly,
Answer hydrocephalus, spina bifida,
tracheoesophageal fistula, duodenal
atresia, hydrops fetalis and many
more)
b) Multiple pregnancy
95th percentile c) chromosomal abnormalities such as
Down's syndrome and Edwards
Mean value syndrome
5) Skeletal dysplasia and syndrome.
5th percentile 6) others like chorioangioma of the
placenta
Management to this patient

Source:http://emedicine.medscape.com/article/40485
6-overview 1) Reassure the mother
2) Excludes the causes of polyhydramnios
a) This patient should be offered to do
MOGTT
Polyhydramnios
b) Ultrasound examination and
proceed to Doppler and full scan if
Polyhydramnios may be defined as an amniotic
necessary
fluid index above the 95th centile for gestational
3) Assessment of fetal well being
age [Moore& Cayle].
a) Access while doing ultrasound +
CTG.
Previously, it is defined when the deepest
4) Treat the underlying causes
vertical pool is more than 8 cm, but currently
5) Treat the hydramnios
based on measurement on 4 quadrant > 25.
a) Mild & Moderate: Indomethacin or
(Based on ultrasound)
sulindac
b) Severe: Amnioreduction
It complicates approximately 0.4-3.5 % of
6) Corticosteroid if anticipating pre term
pregnancies and it can be divided into three
delivery.
groups: mild (amniotic fluid index 25-30),
21
Case: 32/M/F, G2P1, decreased fetal movement Tocolysis has also been advocated for the
management of intrapartum fetal distress,
Question impaired fetal growth, pre term labour and to
1) H(x) and P(e) facilitate external cephalic version at term
2) Management of decrease fetal
movement MgSO4
3) Use of tocolytic (function/type) 1. works as membrane stabilizer,
4) Fetal kick chart (indication and competitive inhibition of Ca; therapeutic
component) at 4-7 mEq/L
2. SE: flushing, nausea, lethargy, pulm
Reduce fetal movement? Baby goes through edema
normal sleep cycle. As long as baby moves 3. Toxicity: cardiac arrest (tx: calcium
every couple of hour, then it’s fine. gluconate), slurred speech, loss of
patellar reflex (@ 7 -10), resp problems
History (@15-17), flushed/warm (@9-12),
Exclude Abruptio placenta muscle paralysis (@15-17), hypotonia
-Decreased fetal movement, abdominal pain, (@10-12)
bleeding after 22w
-shocks, tender uterus, fetal distress/absent fetal Nifedipine
heart sound 1) calcium channel blocker: 10 mg q 6 h;
se: nausea and flushing
Exclude fetal distress
-Decreased/absent fetal movement, abnormal B2 agonist
fetal heart rate 1. ritodrine/ terbutaline
- Thick meconium stained fluid 2. dec. uterine stimulation; may cause
DKA in hyperglycemia, pulm edema,
Other history n/v, palpitations (avoid with h/o cardiac
- What did patient do? Working mother seems to disease or if vaginal bleeding) 0.25 mg
perceive less fetal movement. sq q 20-30 min x 3 then 5 mg q 4 po
- Any history of trauma?
- Elicit maternal medical illness Indomethacin/prostaglandin synthesis inhibitor
1. 50 mg po/100 mg pr SE: premature
PE and investigation closure of PDA in an
1) Auscultation of fetal heart rate and hour,oligohydramnios
confirmation with ultrasound.
2) CTG monitoring for ½ hour. Fetal kick chart
3) Umbilical artery Doppler ultrasound in 1) Screening by caregivers to alert them about
high risk cases. their fetal condition which might compromised.
This will aid early intervention to reduce
Tocolysis perinatal mortality.
The administration of medications to stop 2) Routine or done in women with increased risk
uterine contractions during premature labor of complication in baby
3) Decision of management shouldn’t be made
based on fetal kick chart.
22
Case: Reduce fetal movement about decrease in fetal movement as

compared with multi para.
Question 2) Identification of maternal risk factor
a) Regarding traditional medicine, how to which might contribute to perinatal
advice patient mortality.
b) Line of thinking to get diagnosis - age, smoking, overweight/obesity,
c) Management. previous stillbirth or neonatal death
Traditional medicine 3) What actually the causes of reduce or

A doctor has no right to order patient to stop absent fetal movement?
taking traditional medicine. However, lack of a) Placenta Abruptio
study and information between interaction of b) Intra uterine growth restriction
traditional medicine and modern medicine may c) Syndromic baby
cause few un-expected side effect. d) Placenta insufficiency.
e) Mother’s perception.
Furthermore, few manufacturers being dishonest
by adding some ‘hidden’ ingredient inside their 4) Investigation to support diagnosis
product which may cause serious side effect in
reaction to certain drugs. Therefore, as a doctor Management
we can advise patient to
1. Choose either taking only traditional or 1) Take full history and elicit risk factor
modern medicine or not combining that might compromise fetal condition.
them. 2) Fetal well being assessment
2. Suggest to them to stop traditional (recommended by NICE guideline)
medicine while pregnant because afraid CTG, Ultrasound.
of unexpected side effect with 3) Fetal kick chart (not recommended by
prescribed medicine. NICE and others as it will cause more
3. Avoid herbal base traditional medicine. anxiety to the mother.) however, some
4. Use alternative traditional medicine that says it is better than doing nothing.
known scientifically not harmful like 4) If CTG or ultrasound shows fetal
honey. compromise, admit patient to the wards
and do serial monitoring of fetal
Line of thinking to get the diagnosis condition
1) Is mother really paying full attention 5) Re assures the mother.
about fetal movement 6) Patient can be safely discharge after
a) Fetal movement is rather perception fetal monitoring shows normal result in
of woman. Busy mother tends to three consecutive days. Discharge
feel less fetal movement. patient with
b) Working in busy environment may a) TCA at antenatal wards weekly or
cause less perception of fetal twice weekly
movement. b) To come again to ward if reduce
c) A woman which is first time fetal movement
pregnant may become too anxious c) Instruction to use fetal kick chart.
about fetal condition and notice
23
Case: Premature labour with PV Bleeding glucose tolerance, osteoporosis and

depression of fetal/maternal adrenals
Questions 2) Tocolytic
a) 4 drugs in management of premature Nifedipine
labour - calcium channel blocker: 10 mg qds;
b) Drugs for candidiasis - se: nausea and flushing
c) Function, complication and monitoring B2 agonist
of the drugs - ritodrine/ terbutaline
d) Doses of drugs - dec. uterine stimulation; may cause
DKA in hyperglycemia, pulm edema,
Definition of preterm n/v, palpitations (avoid with h/o cardiac
1) Onset of labour after the gestation of viability disease or if vaginal bleeding) 0.25 mg
i.e 24 weeks and before 37 completed weeks of sq q 20-30 min x 3 then 5 mg q 4 po
pregnancy.
2) The onset labour may be determined by 3) Antibiotic therapy
documented uterine contractions and rupture - For women at risk of preterm delivery
membranes or documented cervical change with because of PPROM, prophylactic
an estimated length of less than 1 cm and/or antibiotics delay delivery and reduce
cervical dilatation of more than 2 cm. maternal and neonatal infective
morbidity.
Types - Not recommended in risk of preterm but
a) Threatened (uterine contraction without with intact membranes
cervical changes) - Erythromycin 500mg qds plus co-
b) Actual/establish (uterine contraction+ cervical amoxyclav (Augmentin) 375mg tds for
changes) 7 days OR clindamycin 150mg qds for 7
Additional: occurs in around 7% of all days.
pregnancies and is a major cause of infant
mortality and morbidity. [Scottish guidelines] Drug for candidiasis in pregnancy
Survival rate: 23 w 0-8% 24w 15-20% Imidazoles are best but pregnant women may
25w 50-60% 26-28w 85% 29w 90% need longer (7 not 4 day) courses. Thrush is a
common vaginal infection in pregnancy causing
Drugs in management of premature labour itching and soreness. There is no evidence that
1) Corticosteroid therapy this yeast infection harms the baby. Antifungal
- Betamethasone, 12mg, IM, 24 hours creams are effective. Imidazoles (such as
apart. clotrimazole) are more effective than older
- In USM, Dexamethasone, 12 MG, IM, treatments such as nystatin and hydrargaphen.
12 hours apart. Longer courses (7 days) cured more than 90% of
- Function is to increase lung maturity. women whereas standard (4 day) courses only
Usage of corticosteroid below 24w is no cured about half the cases. [Cochrane Database
beneficial since pneumocyte not develop of Systematic Reviews, Issue 4, 2009]
yet. Also not recommended >34W.
- Possible long-term effects on cognitive
or neurological development, impaired
24
Case: 33 years old, G3P2 present at 24W+5D 4) Re assure the patient

POA with premature contraction. No history of 5) Give IM Dexamethasone 12mg bds, 12 hours
UTI, Vaginal discharge, trauma. apart.
6) Keep patient nil by mouth and anticipate for
Question caesarian section.
A) How to differentiate premature 7) Hydrate patient adequately with 2 pints NS
contraction and true labour contraction and 3 pints D5%
B) Management of this patient 8) Take blood for investigation including FBC,
C) How to discharge this patient GSH.
9) Urine dipstick (nitrogen, albumin= indicate
Premature contraction UTI) and Urine FEME.
Uterine contraction after the gestation of 10) Allocate possible causes of premature
viability. i.e 24W and before 37 completed contraction.
weeks of pregnancy. It could progress to 11) Monitor 4 hourly BP, 20 minutes CTG
premature labour. 12) Inform Pediatrician regarding patient's
condition and keep in view to book for
It is called threatened pre term labour if ventilator.
contraction is not associated with cervical 13) Monitor the labour progression by labour
dilatation. progression chart.
14) Ultrasound examination for fetal well being.
If it is associated with cervical dilatation, hence 15) Administer tocolytic for example Nifedipine
it is termed as Establish Pre term labour. 5mg (some specialist give 10 mg)
16) Observe patient for one day. if contraction
Characteristic of a true labour subside, discharge patient to ante natal wards for
1) At term further observation.
2) Come at regular interval i.e once in one 17) If contraction subsides for two consecutive
hour and finally can goes to once in five days in ante natal wards, then patient can be
minutes near labour. discharged
3) The timing of each contraction is last
about 30-70 seconds Discharging the patient
4) The intensity of pain increase by time. 1) After no contraction within 2 days in ante
Pain is at the back due to referred pain natal wards
of cervix. 2) Ensure that patient already took
5) The pain does not relief by walking or dexamethasone.
changing in posture. 3) CTG reactive.
6) Presence of show and liquor. 4) Follow up at ante natal clinic within 2 weeks.
5) Fetal Kick Chart (some protocol say it is not
Management of this patient indicated)
1) Obtain full history and perform relevant

physical examination.
2) Admit patient to premature room in labour
room.
3) Inform the case to MO in charged
25
Case: 42/M/F G11P7+3A at 36/52 with history fetal, placenta abnormalities (PE, Anruptio
of 5 premature deliveries, electively admitted for placenta, PP), multiple pregnancy, Medical
removal of cervical cerclage condition like Hypertension, DM and anemia,
aneuploidy and fetal anomalies, increase
Questions maternal mortality. [The older obstetric patient,
a) Risk of grandmultiparae Current Obstetrics & Gynecology (2005) 15,
b) Risk of pregnancy at old age 46–53]
c) How to prevent PPH in this patient
d) Indications of cervical cerclage Cervical cerclage
e) When to do and remove cervical
cerclage. Cervical cerclage is a procedure in which sutures
are inserted around the cervix in women
Grandmultiparae suspected to have cervical weakness. This is
Definition: a woman who has had five or more thought to prevent cervical dilatation and
pregnancies resulting in viable fetuses. Great membrane exposure, thus helping the uterus to
grand multipara if > 10 retain the pregnancy in women who are prone to
miscarrying, mostly in the mid-trimester.
The results showed high in incidence of anemia [Cervical cerclage, Current Obstetrics &
(80%). Cesarean section (38% vs 35%), Gynaecology (2006) 16, 306–308]
inversion of uterus (0.2% vs nil) and rupture of
uterus (0.2% vs nil), hypertension and PIH Cervical cerclage can be classified as an elective
superimposed on chronic hypertension (12.5- procedure (based on previous history and/or
25% vs 8-14%). The incidence of postpartum investigation), a selective procedure (based on
hemorrhage, abruptio placentae, preterm labour, evidence obtained by ultrasound examination
obstructed labour, puerperal sepsis and wound that shows shortening of the cervix) or an
infection was also high in grand multi parous emergency procedure (when the cervix is dilated
group. There were 9 maternal deaths out of 1000 with the membranes seen or bulging via the
cases of study group as compared to 4 deaths in cervical os).
control group. Similarly the perinatal mortality
rate was 180/1000 births as compared to An elective procedure is performed around 12–
150/1000 in para 2-4. [Grand Multiparity: Still 14 weeks’ gestation (Dr Amir HUSM-16W)
an Obstetric Risk Factor,Khadija H Asaf. Pak J after confirming fetal viability. The TAC is
Obstet Gynaecol May 1997;10(1,2):24-8] performed around the same time. Emergency
cerclage is performed when the cervix is noted
Pregnancy at old age to be dilating.[Cervical cerclage, Current
an age over 35 years for the ‘elderly Obstetrics & Gynaecology (2006) 16, 306–308]
primigravida’(FIGO, 1958)Improvements in
women’s general health have led to this term It is removed when term is achieved or
tending to be reserved for pregnancies in women premature contraction (Dr Amir HUSM)
at or above 40 years of age.[Current Obstetrics
& Gynaecology (2005) 15, 46–53]
Risk of pregnancy at old age: Miscarriage,

ectopic pregnancy, chromosomal disorder in
26
Case: Post EDD + PIH (exact case is unknown For PIH

so discussion is random) 1) For baby(similar to post EDD)
2) For mother
Question a) Hourly BP monitoring
a) Differential diagnosis b) PE Profile (platelet count, uric acid,
b) Investigation serum creatinine level, Liver
c) Management enzymes- AST, Urine albumin)
Term Management for Post date and post Term

Period of gestation 37 to 42 week Based on scientific evidence
1) Women with post term gestations who
Post date have unfavorable cervices can either
Post date is a term to describe any pregnancy undergo labor induction or be managed
that goes beyond expected date of delivery (40 expectantly.
W) but does not exceed term. 2) Prostaglandin can be used in post term
pregnancies to promote cervical
Current practice in HUSM and KKM is to avoid ripening and induce labor.
the delivery of post term baby due to the 3) Delivery should be effected if there is
increase perinatal morbidity and mortality evidence of fetal compromise or
associated with post term. Therefore, induction oligohydramnios.
of labour should be initiated if pregnancy goes
beyond the post date. Based on expert experiences
1) Antenatal surveillance for post term
Approach to this patient pregnancies between 41 weeks (287
days; EDD +7 days) and 42 weeks (294
1) Absolute treatment for PIH is the days; EDD +14 days) of gestation
termination of pregnancy. because of evidence that perinatal
2) Post EDD itself is an indication for morbidity and mortality increase as
induction of labour to prevent post term gestational age advances.
delivery.
3) However, the exact POG needs to be 1. Twice-weekly testing with some
established to avoid delivery of pre term evaluation of amniotic fluid volume
baby. beginning at 41 weeks of gestation. A
nonstress test and amniotic fluid volume
Investigation assessment (a modified BPP) should be
For Post EDD adequate.
1) Biophysical profile of the baby
• Fetal tone Drug commonly use in PIH
• Movement of the body or limbs a) Methyl dopa
• breathing movement b) Labetolol
• Amniotic fluid volume c) Nifedipine
• Heart rate (CTG) analysis. d) Magnesium Sulphate (pre eclampsia)
2) Doppler ultrasound
27
31 years old Malay lady, G6P5 at date + 9/7 In this patient, we however need to go through a
with 1 previous scar for transverse lie and 4 broad perspective before deciding the
VBAC management for this patient. Patient’s problem
is
1) What is post term? a) Post date
2) What is the complication of the post b) 1 previous c-sec with successful 4
term? VBAC (low risk patient)
3) In this patient, how will you manage her c) Grand multi para (deliver > 5 times)
and give reasons.
Therefore, risk and benefit on method of
Post term
A pregnancy that has extended to or beyond 42 delivery should be considered.
weeks of gestation (294 days, or estimated date
of delivery [EDD] +14 days) [ACOG Roughly, this is the overview of the
guidelines] management.
1) Antenatal surveillance at 42 to 42 week

Complication of the post term including at least non stress test and
assessment of amniotic fluid volume.
1) To the baby 2) Estimating the fetal weight.
a) Uteroplacental insufficiency 3) Considering the induction of labour
b) Oligohydramnios causing cord a) Prostin and oxytocin is not a good
compression syndrome choice.
c) Meconium aspiration syndrome b) May consider membrane sweeping
d) Intrauterine infection c) After excludes macrosomic baby,
e) Macrosomia and complication related to breech presentation and severe
it oligohydramnios.
f) Fetal dysmaturity syndrome 4) If we considering Caesarian section
g) Increased risk for neonatal a) Indicated if it is a macrosomic baby
encephalopathy b) But this will put mother on higher
risk on next pregnancy because of
2) To mother two c-sec scar and grand Multipara.
a) Severe perineal injury if delivering big Risk of uterine atony and rupture is
baby high
b) Increase rate for caesarian section c) Advise on bi tubal ligation for the
c) endometritis, thromboembolic disease, mother.
hemorrhage. d) Indicated if breech presentation.
d) Psychological (anxiety and frustration) e) Indicated in severe oligohydramnios
for carrying the baby longer than 5) Present of senior MO and pediatrician
expected. during delivery.
Management for this patient

Women with an uncomplicated pregnancy who
reach 41 to 42 weeks’ gestation should be
offered elective delivery [SOGC]
28
A healthy 25-year-old nulliparous woman has such events. Contraction stress tests assessing
an uncomplicated pregnancy at 42 weeks. fetal heart responses to oxytocic-induced
Induction of labour is fully discussed, suggested contractions have largely gone out of use as the
and declined. Evaluate the tests that may be high false-positive rate has led to a high level of
arranged to monitor fetal health until labour intervention. They also take longer and are more
begins. [Journal review] complicated to conduct than NSTs.
Where the advice over induction is unacceptable The assessment of liquor volume that may be
to the patient, various measures may be used to related to placental function and fetal health has
review fetal health. Several tests are described become an accepted part of surveillance of
for this situation, but the problem remains that women such as this. A measurement of the
no test or group of tests has been shown to amniotic fluid index of less than 5 cm or of the
improve the perinatal outcome. maximum vertical pocket depth of less than 2
cm (various other levels are quoted) suggest
Fetal movement charts have long been used in fetal compromise and lead to a recommendation
late pregnancy as a form of fetal monitoring. for delivery. The biophysical profile combines
They require the woman to note the time taken an ultrasound assessment of fetal movements
for 10 fetal movements. A large randomised- and tone, breathing movements and amniotic
controlled trial (RCT), however, demonstrated fluid volume. This combination would seem to
no reduction in fetal mortality compared with be the most appropriate, but a recent RCT
the control group, and the use of these charts showed no advantage over CTG with amniotic
may increase anxiety without a beneficial depth measurement. Doppler studies of
effect. Various forms of fetal acoustic umbilical artery velocimetry have not been
stimulation test have been developed using a shown to be of benefit in predicting outcome.
transabdominal sound source and assessing the
fetal reaction in terms of cardiotocograph (CTG) There are clearly considerable limitations in the
changes and fetal movements. Although such value of all these tests in detecting fetal
tests have the advantage of taking less time than compromise and enabling rescue, but NICE
other tests, there is no evidence for an improved recommends twice-weekly CTG and
perinatal outcome. measurement of amniotic pool depth, and this
will remain the advice until further advice based
The standard non-stress test (NST) using a on RCTs is available. The advice and its reasons
CTG relies on the observation of two or more must be discussed with this woman, and a
episodes of fetal cardio acceleration of 15 beats sensitive approach is most likely to lead to a
or more occurring within 20 minutes of the onset compromise, although there remains a
of the test. It is generally thought, and advised possibility that the woman will wish for no tests
by the National Institute for Health and Clinical and will await nature’s decision.
Excellence (NICE), that twiceweekly tests
should be performed, although the optimum Simon G. Crocker Department of Obstetrics &
scheme is not known. Furthermore, the NST Gynaecology Norfolk & Norwich University
used alone has a low sensitivity. The most Hospital, Colney Lane, Norwich NR4 7UY, UK
common cause of perinatal death in such cases is [OBSTETRICS, GYNAECOLOGY AND
meconium aspiration due to an acute asphyxial REPRODUCTIVE MEDICINE 17:1,2007
event, and the NST is not adequate to preclude Published by Elsevier Ltd.]
29
Case: PPROM 1) Clear watery and alkaline per vaginal

discharge. (pH 7.1-7.3 compared with
Question: vaginal pH 4.5-6.0)
a) Symptoms of fever 2) Arborization (ferning) under
b) Positive findings in PPROM microscopic visualization
c) Ix and Mx 3) Oligohydramnios
d) Causes of unstable lie [ACOG Practice Bulletin, VOL. 109, NO. 4,
APRIL 2007]
PPROM Symptoms of chorioamnionitis: High grade
Membrane rupture that occurs before 37 weeks fever, maternal and fetal tachycardia, tender
of gestation is referred to as preterm PROM uterus.
Intraamniotic infection has been shown to be Investigation and management

commonly associated with preterm PROM, **Based on period of gestation but basically
especially if preterm PROM occurs at earlier
gestational ages. In addition, factors such as low 1. Determination of gestational age, fetal
socioeconomic status, second- and third- presentation, and well-being
trimester bleeding, low body mass index less 2. Expeditious delivery in patient with
than 19.8, nutritional deficiencies of copper and evident intrauterine infection, abruptio
ascorbic acid, connective tissue disorders (eg, placenta, or evidence of fetal
Ehlers–Danlos syndrome), maternal cigarette compromise
smoking, cervical conization or cerclage, 3. swabs for diagnosis of Chlamydia
pulmonary disease in pregnancy, uterine trachomatis and Neisseria gonorrhoeae
overdistention, and amniocentesis have been if immediate delivery not indicated
linked to the occurrence of preterm PROM 4. Group B antibiotic prophylaxis
5. CTG monitoring for umbilical cord
The risk of recurrence for preterm PROM is compression or asymptomatic uterine
between 16% and 32%. contraction.
Fever Causes of unstable lie

Fever is considered as temp above 100.40 (380C) 2. Prevention of head descending
but feverish sensation may occur when body a) Cephalopelvic disproportion
temp above 98.60 (370C) b) Fibroid
c) Ovarian cyst
Symptoms d) Placenta previa
1) Patient complaints of body become hot e) Uterine surgery
and sweating (increase temperature and f) Multiple gestation
diaphoresis) g) Fetal abnormality (anencephaly)
2) Can also a/w with tachycardia, altered h) Fetal neuromuscular disorder
consciousness, chills & rigor, headache,
muscle and joint pain. 3. Condition that permit free fetal
movement
Positive findings in PPROM a) Polyhydramnios (AFI>8)
b) Uterine laxation
30
25 years old Malay lady, G3P2 at 40 weeks + Management

2/7 of pregnancy presented to you because of 1) Close observation of vital sign
gushing of clear fluid from vagina for 1 day 2) Review patient regularly especially
duration. However, there is no contraction pain palpation of uterus.
a) Elicit uterine tenderness
Questions b) Lie and presentation of the fetus
1) Differential diagnosis and further c) Estimated fetal weight.
history to support your diagnosis 3) Assessment of fetal well being (CTG
2) What complication that should concern and ultrasound )
you that may occur to the mother and 4) Rehydrate the patient
baby. 5) IV ampicillin as prophylaxis against
3) How do you manage this patient GBS (rate of infection rise after 12 hour
rupture of membrane)
Differential diagnosis 6) Corticosteroid is not indicated.
1) Pre labour rupture of membrane 7) Notify the pediatric team regarding the
- Establish that the fluid is truly amniotic possibility to admit the baby because of
fluid and not urine. infection.
- Contraction pain 8) This patient should not be discharged
- Liquor color and induction of labour should be
discussed with patient if not deliver after
2) In labour >24 hour. Usually 90% of patient with
- Contraction pain that become shorten in PROM will deliver within 24 hour.
intervals
Notes:
3) Bacterial vaginosis Student must be able to differentiate between the
- Foul smelling discharge PPROM and PROM.
- Itchiness of vagina
- Yellow or cream color discharge PPROM is premature rupture of membrane. i.e;
- Any systemic sign for infection. membrane rupture during the period of fetal
viability (>24 W) but not reach term yet.
Complication to look for
1) Chorioamnionitis Meanwhile, Prelabour rupture of membrane,
Notes: chorioamnionitis must be PROM is the ruptured membrane before labour.
anticipated in patient presented with The patient already at term.
PPROM or PROM as it can cause death
to the mother and fetus. In PPROM, the focus is 1) to prolong the
pregnancy so that the chances for fetus to
Beware sign and symptoms of survive remain high and 2) to prepare the baby
chorioamnionitis for possibility to be delivered prematurely.
a) Fever
b) Maternal tachycardia In PROM, a focus should be stress on possible
c) Tender uterus infection to the mother and also to the fetus.
d) Fetal tachycardia Lung complication to the fetus is unlikely as
lung maturation already completed.
31
Case: Placenta Previa Investigation to order

1) Transvaginal or Abdominal US
Question 2) FBC, GSH, Rh compatibility
a) Management 3) CTG
b) Other name for low transverse scar
c) Types of placenta previa
d) Investigation to order Management
e) Complication 1) Admission to ward for PP Major.
f) How to differentiate between placenta 2) Bed rest and serial US as placenta
previa and abruptio. migration can occur.
3) Transfuse blood if needed i.e
Definition: symptomatic or near delivery, (target Hb
Placenta implanted in the lower segment of the at delivery is at least 8) + haematinic.
uterus, presenting ahead of the leading pole of 4) Tocolysis and corticosteroid if prem
the fetus. It occurs in 2.8/1000 singleton delivery is anticipated
pregnancies and 3.9/1000 twin pregnancies 5) Avoid Sexual intercourse
[MARCH JOGC MARS 2007] 6) PP Minor can be allowed for SVD
7) Counseling to the patient.
Grade.
I Placenta Lateral Minor Complication:

encroaches on the Antepartum
lower uterine -APH (3rd trimester) and Cx of blood transfusion
segment but does -Unstable lie
not reach the - Perinatal death
cervical os. - Pre term labour
-Thromboembolism
Thromboembolism d/t prolongs bed rest.
II Placenta reaches marginal major if - Placenta abruption
the margin of the posterior
cervical os but located
Intrapartum
does not cover it.
- Excessive bleeding during SVD
- C- section and its complication (major PP)
III Placenta partially
covers the os.
- Hysterectomy
IV Placenta is Complete Major Post partum

symmetrically -DIC
implanted in the - Intra uterine adhesion
lower uterine -Recurrent PP
segment - Placenta accrete
PP VS Placenta abruptio
Other name for low transverse scar Association with pain: PP is painless
Pfannenstiel (traditional) scar, Joel--Cohen scar. US: abruptio shows Retro placental blood clot
32
21 Years Old Malay Lady, G1P0 at 36/52 + 4/7 Management for this patient
was admitted since 30 Week POA after history 1) FBC to access the level of hemoglobin
of sexual intercourse and strenuous activity. of this patient
Currently, there are no more bleedings. 2) GSH as patient may lose lot of bloods
Ultrasound reveals placenta previa type III during delivery. GXM 2 unit should be
prepared before delivery.
Questions 3) Tocolysis as bleeding in PP patient may
1) How to differentiate PP type III and PP also due to contraction of uterus (not the
type IV on ultrasound lower segment)
2) What is the risk factor for placenta 4) Assessment of fetal well being
previa 5) Complete bed rest and avoid any
3) Can this patient be discharged? excessive activity.
4) Management for this patient 6) Discuss with patient regarding caesarian
section as mode of delivery.
How to differentiate PP type III and PP type IV Prior to delivery, all women with
on ultrasound placenta praevia and their partners
PP type III- Placenta partially covers the os. should have had antenatal discussions
PP type IV- Placenta is symmetrically implanted regarding delivery, hemorrhage,
in the lower uterine segment possible blood transfusion and major
surgical interventions, such as
Risk factor for placenta previa hysterectomy, and any objections or
- Multiple gestation queries dealt with effectively.[RCOG]
- Previous caesarian section 7) To prepare the patient for caesarian
- Uterine structure anomaly section.
- Assisted conception
- Dilation & Curettage Notes:
1) Trans vaginal ultrasound is safe in the
Can this patient be discharged? presence of placenta praevia and is more
No, accurate than trans abdominal
ultrasound in locating the placenta
Women with major placenta praevia who have [RCOG Guideline No. 27
previously bled should be admitted and managed 2) Placenta migration occurs during second
as in patients from 34 weeks of gestation. and third trimester except in posteriorly
[RCOG] located PP and present of C-sec scar.
3) A scan should be performed at 32 weeks
All women at risk of major ante partum in case suspected PP major and 90% of
hemorrhage should be encouraged to remain the patient who is diagnosed with PP
close to the hospital of confinement for the major will remains so.
duration of the third trimester of pregnancy 4) Elective caesarean section should be
[Royal Australian and New Zealand College of deferred to 38 weeks to minimize
Obstetricians and Gynecologists] neonatal morbidity.
Women with placenta praevia who have bled

tend to deliver earlier
33
Case: 42/M/F G9P8 with unstable lie Management
a) Causes of unstable lie 1) Admit patient to antenatal wards

b) Management a) Daily observation for fetal lie
c) Complication b) Provide active management to
correct lie
c) Provide immediate clinical
assistance upon membrane rupture
Unstable lie 2) Exclude factors contributing to unstable
1. Fetal lie and presentation repeatedly lie
change at beyond 36/52 of gestation. 3) Expectant vs. Emergent management
2. by 36W, fetal movement is limited, fetal
should present as cephalic) Expectant
3. Incident at 26/32 is 40%, at 30/52 is A) Daily observation for fetal lie
20% & at term is 3% B) Discharge if longitudinal lie for 3
consecutive days
Causes of unstable lie C) Review patient in a week time
4. Prevention of head descending D) Wait for spontaneous labour
i) Cephalopelvic disproportion
j) Fibroid Active management
k) Ovarian cyst
l) Placenta previa A) Caeserean section
m) Uterine surgery B) ECV
n) Multiple gestation C) Stabilizing induction of labour
o) Fetal abnormality (anencephaly)
p) Fetal neuromuscular disorder
Complication
5. Condition that permit free fetal
movement 1) Cord prolapsed leading to fetal hypoxia/
c) Polyhydramnios (AFI>8) fetal death.
d) Uterine laxation 2) Compound presentation
3) Uterine rupture
History
a) Make sure that the date is correct
cause unstable lie is physiological
<36/52.
b) Find any risk factor associated with
unstable lie.
c) Elicit any problem during pregnancy
34
Case: Unstable lie

Option for this patient
Question: A) Passive management by observation
a) Physical examination (abdomen) in hope that the lie will return to
b) Level of exposure normal position during term.
c) Clinical evidence of head and buttock B) Caeserean section
d) Management for this patient C) ECV [Relative contraindication]
e) Option for this patient Results vary from 30% up to 80% in
f) What is unstable lie different series. Race, parity, uterine
g) Causes of unstable lie tone, liquor volume, engagement of
the breech and whether the head is
Unstable lie palpable, and the use of tocolysis,
1. Fetal lie and presentation repeatedly all affect the success rate.
change at beyond 36/52 of gestation. [Greentop]
2. by 36W, fetal movement is limited, fetal D) Stabilizing induction of labour
should present as cephalic)
3. Incident at 26/32 is 40%, at 30/52 is Notes: B-D is active management.
20% & at term is 3%
Complication
Clinical evidence of head and buttock 1) Cord prolapsed leading to fetal hypoxia/
Head: Hard, round and ballotable fetal death.
Buttock: Soft, broad and not ballotable. 2) Compound presentation
3) Uterine rupture
Management
Causes of unstable lie
1) Admit patient to antenatal wards Prevention of head descending
a) Daily observation for fetal lie a) Cephalopelvic disproportion
b) Provide active management to b) Fibroid
correct lie c) Ovarian cyst
c) Provide immediate clinical d) Placenta previa
assistance upon membrane rupture e) Uterine surgery
2) Exclude factors contributing to unstable
f) Multiple gestation
lie g) Fetal abnormality (anencephaly)
3) Expectant vs Emergent management h) Fetal neuromuscular disorder
Expectant Condition that permit free fetal

A) Daily observation for fetal lie movement
B) Discharge if longitudinal lie for 3 a) Polyhydramnios (AFI>8)
days b) Uterine laxation
C) Review patient in a week time
D) Wait for spontaneous labour
35
Case: Breech
Mode and timing of delivery
Questions
a) Causes and complication of breech <28 weeks, weight <1 SVD
b) Management, mode of delivery and time kg
of delivery for breech.
c) ATT- Type of immune 28-32 weeks, weight LSCS
1.0 - 1.5 kg
Breech
It is the most common type of malpresentation. 32-37 weeks Weight Depend on case
Presentation of the fetal buttocks and feet in 1.5 – 2.5 kg 1) Assisted
labour breech
delivery for
Incidence: 26W 40%, 30W 20%, term 3% Extended and
Type: Extended, Flexed, Footling flexed
2) LSCS for
footling
Causes breech
1) Multiparous woman with lax uterus and > 37 weeks Preferably Caesarean
abdomen section
2) Prematurity
3) Fetal structural anomalies; anencephaly, ATT
hydrocephalus Tetanus vaccine is an inactivated toxin (toxoid)
4) Uterine anomalies; uterus bicornu, made by growing the bacteria in a liquid
fibroids medium and purifying and inactivating the toxin.
5) Multiple gestation; twins Type II Immune response
6) Hydramnios; oligo or poly
7) Placenta previa It is administer once the quickening felt and can
8) Contracted maternal pelvis be repeated 2-3 months after first injection in
9) Pelvic tumours primid women as a booster injection. (Usually
5th and 7th months of pregnancy)
Complication
1) PROM Notes: It is different from Anti tetanus human
2) Cord prolapsed [common in footling immunoglobulin which are preparation
presentation and lesser in flexed breech containing IgG immunoglobulin derived from
presentation] plasma of donors sensitized to tetanus toxoid. It
3) Difficulty in delivering the shoulder acts by The IgG antibodies acts to neutralize the
4) Difficulty in delivering the head[ may free circulating exotoxisn of clostridium tetani
lead to intracranial bleeding d/t tear of and prevent its fixation in tissue and its
tentorium or delay delivery of head can consequences.
cause prolonged compression of cord
and asphyxia]
5) Birth trauma such as fracture, viscera
damage, Erb Duchenne paralysis,
dislocation of hip joint.
36
35 years old Malay lady, G5P5 (1 pair twin) at b) Number of fertilized egg (zygosity;
26/52 of pregnancy was admitted to wards mono,di)
because of premature contraction and twin c) Number of placenta (chorionicity)
pregnancy. d) Number of amniotic cavity (amnionicity)
Questions Complication of multiple pregnancies

1) What history that could give you idea
that you are dealing with cases of To the mother
multiple pregnancy? 1) Hyperemesis gravidarum and in fact all
2) How do you diagnosed multiple physiological response towards
pregnancy through physical examination pregnancy will be exaggerated.
3) How do you classify multiple pregnancy 2) Exacerbation of chronic illness
4) Complication of multiple pregnancy 3) Severe anemia in pregnancy
4) DIC secondary to fetal death.
Answer 5) Miscarriage
6) Preterm labour.
Notes: Account for only 3% of all live births, 7) Polyhydramnios
they responsible of a disproportionate share of 8) Pre eclampsia.
perinatal morbidity and mortality 9) Placenta abruptio
10) Post partum hemorrhage.
History 11) Higher risk for developing GDM
- Accelerated weight gain Others: acute fatty liver, pulmonary
- Hyperemesis gravidarum embolism
- Sensation of moving of more than one
fetus To the fetus
- Infertility treatment by ovulation- 1) IUD of one fetus
inducing agents or gamete/zygote 2) IUGR
transfer 3) Fetal abnormality
- family history of dizygotic twins 4) Pre term delivery
Notes: certain race like Africa has higher risk 5) Low birth weight
factor to have multiple pregnancies. 6) Acute respiratory distress syndrome.
7) Congenital abnormality (mental
Physical examination retardation, Siamese twin, cerebral
- Presence of more than 2 poles (need to palsy)
excludes fibroid) Others: twin-to-twin transfusion syndrome,
- Usually, the abdomen size is bigger than Twin reversed arterial perfusion (TRAP)/
corresponds date acardiac twinning
- Polyhydramnios
- Presence of two or more fetal heart
sounds on pinnard auscultation.
Classification of multiple pregnancies

a) Number of fetus (twin, triplet, quadruplets)
37
29 Years old Malay lady, G1P0, twin pregnancy Management to this patient
at 24/52 was admitted because of frothy color 1) Evaluation on severity of the pre
urine and headache. eclampsia
- Close monitoring of blood pressure (15
Questions minutes interval until BP stable)
- Repeat Dipstick testing within 6H
1) What is your provisional diagnosis and - 24 hour urinary protein
justify your answer? - PE Profile (platelet count, uric acid
2) What is twin to twin transfusion level, sr Creatinine level, liver enxyme)
syndrome? - Clotting study if platelet < 100 x 106/l
3) Factors contributes to preterm delivery 2) Management of hypertension
4) How do you manage this patient?
Mild PE
T. Methyldopa 250mg tds, max
Answer 3g/day or
T. Labetolol 100 mg tds, max 300mg
Provisional diagnosis tds
Pre eclampsia Or, Tab. Nifedipine 10 mg tds stat
- Occur at 24w of gestation. dose
- Primigravida
- Twin pregnancy Severe PE
- Symptoms of impending pre eclampsia IV hydrallazine start 5mg, double if
no effect until 35mg. change drug if
(frothy urine suggestive of proteinuria
fails or
and headache.)
IV Labetolol start 10 mg, double if
no effect until max 300mg/day)
Twin to twin transfusion syndrome
** MgSo4 slow infusion 4g 10-15
- Intrauterine blood transfusion from minutes. Maintenance dose IV
donor twin to another recipient twin ig/hour
- Donor twin has smaller size and anemic 3) Fetal surveillance
- Recipient twin will be plethoric - CTG for fetal well being.
- Only occur in monozygotic twin with - Biophysical profile (Ultrasound
monochorionic placenta monitoring of fetal movement, fetal tone
and fetal breathing, ultrasound
Factors contributes to preterm delivery assessment of liquor volume with or
without assessment of fetal heart rate)
- Lower and upper genital tract infection
- Uterine over distension 4) Anticipating in preterm delivery by
- Cervical incompetence giving IM Dexamethasone, 12 MG, and
- Maternal medical complications, 12 hours apart.
maternal stress
- Fetal, placental or uterine abnormalities 5) Others
- Bed rest
- Reduce physical activity
- Reduce high cholesterol and salty diet.
38
Multiple Pregnancies
Summary of recommendation from Clinical

Management Guidelines for Obstetrician-
Gynecologists Number 56, October 2004
Level B Evidence
Tocolytic agents should be used judiciously in Cerclage, hospitalization, bed rest, or home
multiple gestations uterine activity monitoring has not been studied
in high order multiple gestations, and, therefore
Women with high-order multiple gestations should not be ordered prophylactically. There
should be queried about nausea, epigastric pain currently is no evidence that their prophylactic
and other unusual 3rd-trimester symptoms use improves outcome in these pregnancies
because they are at increased risk to develop
HELLP syndrome, in many cases before Because the risks of invasive prenatal diagnosis
symptoms of preeclampsia have appeared. procedures such as amniocentesis and chorionic
villus sampling are inversely proportional to the
The higher incidence of gestational diabetes and experience of the operator, only experienced
hypertension in high-order multiple gestations clinicians should perform these procedures in
warrants screening and monitoring for these high-order multiple gestation.
complication.
Women should be counseled about the risks of
Level C (expert opinion) high order multiple gestation before beginning
ART
The national Institutes of Health recommends
that women in preterm labor with no Management of discordant growth restriction of
contraindication to steroid use be given one death of one fetus in a high-order multiple
course of steroids regardless of the number of gestations should be individualized, taking into
fetuses consideration the welfare of the other fetus (es)
39
36 years old Malay lady, housewife, G5P4 at 2. Prop up the patient 45o.
30W+ 5/7 POA with known history of chronic 3. Oxygen 100% 3L/min via nasal prong
rheumatic heart disease and on single drug 4. Intravenous access.
therapy presented with sudden onset shortness 5. Take the blood for arterial blood gas
of breath on the day of admission, cannot lie flat (ABG).
on night and reduce effort tolerance. There was 6. 12 lead ECG.
no sign and symptoms suggestive of lung 7. Intravenous furosemide, 40 – 80 mg stat
infection. Currently she is not in labour and and maintenance.
fetal movement is good. 8. Intravenous digoxin and intravenous
diamorphine 2.5 – 5 mg slowly –
Questions depending on medical request.
1) What sign and symptoms that you
would like to elicit to suggest that this is Further management:
a case of heart failure 1. Admit the patient to antenatal ward.
2) How do you manage this patient 2. Carry out all the investigations as
mentioned above.
Answer 3. Continue oxygenation.
4. Prop up the patient 45o.
Sign and symptoms of heart failure 5. Close monitoring of
Cardiac symptoms: exertional dyspnoea, a) vital signs
orthopnea, paroxysmal nocturnal dyspnoea, b) input output chart
dyspnoea at rest, acute pulmonary edema, chest c) Cardiotocography ( CTG )
pain, palpitation. 6. Continue IV furosemide. May change to
tablet form when necessary.
Non cardiac symptoms: anorexia, nausea, weight 7. Tab slow potassium.
loss, bloating, fatigue, weakness, oliguria,
8. Consider IM dexamethasone 12 mg b.d,
nocturnal, and cerebral symptoms 6 hours apart to anticipate pre term
delivery.
Physical examination: Clubbing, prolong 9. Should be managed together with
capillary refilling, weak, rapid, and thready medical team.
pulse, tachycardia, diaphoresis, pallor,
Advice on discharge:
peripheral cyanosis with pallor and coldness of
the extremities, pulmonary rales, edema, 1. Semi bed rest at home and avoid
hepatomegally, pleural effusion, ascites, vigorous activity
cardiomegally, murmurs. 2. Regular follow up at combined clinic.
3. If the patient develops any symptoms of
Management to this patient urinary tract infection, upper respiratory
Acute management tract infection or chest infection, come
early to the hospital.
Similar to managing non pregnant patient where 4. Advise to deliver in the hospital.
the aim is to stabilize the patient 5. Admit when the patient at term OR
admit earlier if the patient has symptoms
1. Secure the ABC – airway, breathing and of HF.
circulation.
40
29 years old Malay lady, G3P2 at 27/52 W POA withstand stress of normal labour. The
with mitral valve prolapses (not in failure) same thing goes for Induction of labour.
3. Patient should be placed on high risk
Questions category with present of senior
1) What is Eisenmenger’s syndrome obstetrician and consultation from
2) How do you manage this patient cardiologist.
4. Close monitoring of vital signs, CTG
Answer and oxygen saturation. Each patient
must be attended by one staff nurse or
Heart disease complicates approximately 1% of all mid wife
pregnancy with chronic rheumatic heart disease is 5. Patient must be in prop up position with
the commonest cause in Malaysia apart from oxygen is freely available.
congenital heart disease, cardiomyopathies, 6. Pain management – in form of epidural
myocarditis and coronary artery diseases.
anesthesia (if the patient has no
contraindication) or opiates.
Eisenmenger’s syndrome
7. Prophylactic antibiotic to give adequate
Pulmonary hypertension secondary to
protection: Ampicillin or Gentamicin or
uncorrected congenital heart disease
Amoxicillin
characterized with right-to-left shunting and the
8. Prolonged second stage labour must be
associated cyanosis
assisted
9. Syntocinon is used in third stage of
Management to this patient
labour instead of ergometrine or
syntometrine.
Antenatal
1. Should be managed in combined clinic.
Management of postpartum:
2. Advice on
1. Adequate rest for maternal.
a) Avoid doing vigorous activities
2. Encourage breast feeding unless she
b) Avoid from getting infection – i.e.
cannot cope with it.
good oral hygiene, treat UTI or
3. Continue oral antibiotic for 5 days.
URTI.
4. Adequate anti coagulant prophylaxis i.e
3. Medication – T.frusemide, hematinic,
warfarin to prevent deep vein
folic acid and anticoagulant prophylaxis
thrombosis and thromboembolism.
i.e. LMWH
5. Discussion about family planning.
4. Come to the hospitals if develops any
Based on
symptoms of heart failure, UTI, URTI
a. Severity of the heart disease
or chest infection
b. Completed family
5. Advise to deliver in the hospital.
6. Admit when the patient at term OR
Methods:
admit earlier if the patient has symptoms
a. Hormonal contraception - COC will
of HF.
increase risk of TE.
b. IUCD should be discouraged due to
Management of intrapartum:
risk of infection.
1. Aim for SVD
c. Sterilization
2. C-sec if any obstetric problem or in
view of cardiologist that patient cannot
41
19 Years old Malay lady, G2P0+1(abortion) at microcephaly, optic atrophy, and blindness,
39 W POA with history of chronic rheumatic seizures, Dandy-Walker syndrome, and focal
heart disease with mitral valve replacement, cerebellar atrophy),absent or non-functioning
infective endocarditis and completed treatment kidneys, anal dysplasia, deafness, hemorrhagic
and history of overwafarinization at 15W POA complications, premature births, spontaneous
currently admitted for elective heparin infusion abortions, stillbirths, and death
Questions How to access functional cardiac status during

1) Should warfarin be used in pregnancy pregnancy
2) How to access functional cardiac status
during pregnancy
3) Why do you think this patient admitted
for heparin infusion?
Answer
Should warfarin be used in pregnancy?
Warfarin (Coumadin®) is an oral anticoagulant

that inhibits synthesis of vitamin K–dependent
clotting factors, including factors II, VII, IX, and
X, and the anticoagulant proteins C and S
[Shirin Abadi et al]
Literature suggests a strong association between

maternal warfarin use and fetal adverse effect
[Shirin Abadi et al]
If possible, warfarin therapy should be avoided

during pregnancy. If warfarin therapy is Clinical Practice Guideline on "Management of
essential, it should be avoided at least during the Heart failure", KKM
first trimester (because of teratogenicity) and
from about 2 to 4 weeks before delivery to Why do you think this patient admitted for
reduce risk of hemorrhagic complications heparin infusion?
[Shirin Abadi et al] Pregnancy itself predispose patient to risk of
thromboembolism. Furthermore, this patient has
Using warfarin between 6 and 12 weeks’ been on prosthetic mitral valve which further
gestation is associated with “fetal warfarin increases the risk of thromboembolism.
syndrome,” which is most commonly manifested
by nasal hypoplasia, stippled epiphyses, limb Unfractionated heparin or low molecular weight
deformities, and respiratory distress heparin could be substituted when appropriate
because these agents do not cross the placenta
Other complication includes central nervous and are considered the anticoagulant drugs of
system abnormalities (mental retardation, choice during pregnancy. [Shirin Abadi et al]
42
38 Years old Malay lady, housewife, due to any structural or functional cardiac
G9P6+2(abortion) at 12/52 POA and known conditions [Hunt SA et al]
case of Mitral Valve Prolapse with mild Mitral
regurgitation for more than 10 years According to European Society of Cardiology,
HF is a syndrome whereby the patient should
Questions have the following features; typically shortness
1) Type of murmur in mitral regurgitation of breath at rest or exertion, and/fatigue sign,
and stenosis and Pathophysiology signs of fluid retention and objective evidence of
2) What is heart failure? an abnormality of the structure or function of the
3) Contraindication for pregnancy in heart heart at rest.
disease
There have been a confusing in defining the type
Types of murmur and Pathophysiology of heart failure especially involving the acute or
chronic state. Furthermore, many clinicians use
Mitral regurgitation it interchangeably to refer to severity of the
- Pan systolic murmur disease. Therefore, the ESC guidelines have
- Occur when ventricles leak to a lower come across with new definition which
chamber or vessel because there is distinguishes between new onset HF, transient
pressure gradient from the moment HF and chronic HF.
ventricle begin to contract.
- Blood then flow and murmur begin at New onset HF is self-explanatory and refers to
beginning of first heart and continue first presentation.
until the pressure equalize
- Other causes of pan systolic murmur Transient HF refer to symptomatic HF over a
include tricuspid regurgitation, VSD, limited time period, although long-term
and Aortopulmonary shunts. treatment may be indicated, for examples;
patient with mild Myocarditis with nearly
Mitral stenosis complete recovery, patient with MI who needs
- Mid diastolic murmur. diuretic in CCU but not require it in long term
- Begin later in diastolic and may be short treatment or transient HF caused by ischemia
or extend right up to first heart sound. that resolve with revascularization
- Due to impairs flow during ventricular
filling either because of stenosis, or Meanwhile chronic heart failure is a persistent
obstruction by tumor mass (atrial heart failure with stable, worsening or
myxoma) decompensated state.
- Can also due to Austin Flint murmur of
aortic regurgitation and Carey Coombs Contraindication for pregnancy
murmur of acute rheumatic fever,. 1) Pulmonary hypertension
2) Eisenmenger’s Syndrome
What is Heart failure? 3) Aortic dilatation > 4cm and this should
be suspected in Marfan syndrome
Heart failure is a syndrome manifesting as the 4) Mother on warfarin treatment.
inability of the heart to fill with or eject blood 5) Severe cyanotic heart disease with low
oxygen saturation and high hematocrit
43
18 years old Malay lady, G1P0 at 32/52 POA 6) Excludes the differential diagnosis of
was admitted because of severe lethargy, lethargy, shortness of breath and light-
shortness of breath and light-headedness. headedness
a) Cardiovascular problem
Questions b) Respiratory tract infection
1) Define anemia c) Multiple pregnancy
2) Common cause of anemia in pregnancy d) Diabetes mellitus
3) Management to this lady 7) For iron deficiency anemia
4) What is haematinic a) Iron supplement like ferrous
5) 1 pack cell blood can increase how sulphate and ferrous fumarate
much hemoglobin level (increase approximately 1 Hb in 1
6) Complication of anemia week)
# may consider double hematinic
(doubling the dose)
Answer b) Parenteral iron
c) Packed cell transfusion.
Anemia 8) Maternal transfusion should be
Hemoglobin concentration <11.0 g/dL [WHO] considered for fetal indications in cases
a) Mild (Hb 8-10 g/dL) of severe anemia.
b) Moderate (Hb 5-8 g/dL) 9) Course of treatment should be based on
c) Severe (Hb less than 5 g/dL clinical judgment and individualized;
period of gestation, severity of anemia,
Common cause of anemia in pregnancy type of anemia.
1) Microcytic anemia (Iron deficiency
anemia. Needs to exclude Thalassemia Haematinic
as both will give low MCV of <85 fL) a) Iron
2) Macrocytic anemia (folate deficiency) b) Folate
3) Trauma c) Vitamin C (increase absorption of iron)
4) Hemolytic anemia
a) Sickle cell syndrome One packed cell
b) Sickle cell disease - Is 450 ml of blood. Ideally it will
c) Sickle cell traits increase 1 Hb level
d) Sickle cell hemoglobin C disease.
Complication of anemia
Management for this lady 1) To mother
1) Admit to wards for observation a) Aggravate heart failure
2) Monitoring of vital sign. b) Risk of post partum hemorrhage
3) Full blood count (pay attention on c) Increase risk of infection
hemoglobin level for grading and MCV
for type of anemia), serum ferritin level, 2) To fetus
total iron binding capacity. a) Fetal hypoxia
4) Full blood picture if iron deficiency b) IUGR
anemia is unlikely c) Spontaneous abortion.
5) Establish the causes of anemia
44
Clinical Management Guidelines for Obstetrician–Gynecologists

Number 95, July 2008
Anemia: Hgb (g/dL) and Hct (percentage)

The following recommendations are based
levels below 11 g/dL and 33%, respectively,
primarily on consensus and expert opinion
in the first trimester; 10.5 g/dL and 32%,
(Level C):
respectively, in the second trimester; and 11
g/dL and 33%, respectively, in the third
- All pregnant women should be
trimester
screened for anemia, and those with
iron deficiency anemia should be
Summary of Recommendations and
treated with supplemental iron, in
Conclusions
addition to prenatal vitamins.
The following conclusion is based on good
- Patients with anemia other than iron
and Consistent scientific evidence (Level A):
deficiency anemia should be further
evaluated.
- Iron supplementation decreases the
prevalence of maternal anemia at
- Failure to respond to iron therapy
delivery.
should prompt further investigation
and may suggest an incorrect
The following recommendation and
diagnosis, coexisting disease,
conclusions are based on limited or
malabsorption (sometimes caused by
inconsistent scientific data (Level B):
the use of enteric-coated tablets or
concomitant use of antacids),
- Iron deficiency anemia during
noncompliance, or blood loss.
pregnancy has been associated with
an increased risk of low birth weight,
preterm delivery, and perinatal
mortality. Severe anemia with
maternal Hgb levels less than 6 g/dL
has been associated with abnormal
fetal oxygenation resulting in non
reassuring fetal heart rate patterns,
reduced amniotic fluid volume, fetal
cerebral vasodilatation, and fetal
death. Thus, maternal transfusion
should be considered for fetal
indications.
45
28 Years old Malay lady, housewife, G2P1 at Management of pregnant lady with fibroids
38W + 5/7 POA was admitted in view of
1) Management of fibroids during
1. One Previous scar a year ago due to pregnancy is just a monitoring of its
fetal distress, uncomplicated CS growth. Drugs rarely being prescribed.
2. Uterine fibroid diagnosed during first 2) Fibroids can cause miscarriage.
pregnancy Therefore, advise patient not to
undergone vigorous activity.
Questions 3) Corticosteroid injection if pre term
labour is anticipated.
1) Why fibroid increase in size during 4) Monitoring of the fetus for fetal well
pregnancy being, lie and presentation.
2) What fibroid changes can occur during 5) Observation of fetal lie and presentation
pregnancy is crucial before allowing patient to go
3) Expected findings during PE for SVD.
4) How do you manage the pregnancy 6) Furthermore, obstructed labour should
patient with fibroids? be excluded.
7) If patient is scheduled for caesarean
Answer section, do not remove the fibroid
during the surgery as it will cause heavy
Why fibroid increase in size during pregnancy bleedings.
8) Fibroids will shrink after pregnancy.
Fibroid is an estrogen-dependant for its growth. Management post pregnancy includes
During pregnancy, the level of estrogen rise a) Ablation of the fibroids
steadily until term. b) Surgery to remove the fibroids
c) Hysterectomy
Fibroid changes during pregnancy d) Medications to shrink the fibroids
Red degeneration can occurs between 12th and

22nd week of pregnancy where the blood supply
to the fibroid is cut off. As a result, the fibroid
turn red and die. Red degeneration can cause
intense abdominal pains and uterine contraction
which could lead to early labour or miscarriage
Expected findings during PE
1) More than 2 fetal pole palpated

2) Some fibroids may cause unstable lie or
breech presentation.
46
16 years old Malay lady, single parent with e) Leading causes of death for girls aged
G1P0 at 37 w + 6/7 POA with history of 15 to 19 in developing countries
f) Predispose to un safe abortion
1) Bronchial asthma on MDI salbutamol g) High risk for HIV infection due to
and MDI inflammide unprotected sex
2) Anemia on double hematinic. History of
blood transfusion at 26/52 Dexamethasone
3) Ante partum hemorrhage secondary to
PP type I at 34/52. Completed Pre term labor associated with complication of
dexamethasone. respiratory distress syndrome, intraventricular
4) Currently admitted because of hemorrhage and necrotizing enterocolitis.
contraction pain. Multiple randomized controlled trials has
5) Pre marital sex demonstrated that the admission of
corticosteroid to the mother resulting significant
reduction in these complication.
Questions Both betamethasone and dexamethasone can

cross the placenta. In USM, dexamethasone is
1) What is the effect of Salbutamol used instead of betamethasone. Betamethasone
(ventolin) on uterine contraction may be a better choice because it can reduce the
2) Complication of teenage pregnancy risk of cystic periventricular leukomalacia.
3) Principles of Dexamethasone and
dosage. It can be given in doses of 6 mg every 12 hours
for four doses, and 12 mg every 12 hours for 2
doses during period of gestation of 24 W to 34
Answer through IM route.
In term of lung maturity, no benefit has been

Salbutamol action on uterus
demonstrated in infants beyond 34 weeks
Salbutamol stimulates beta 2 receptor in the gestation. However, it is still being given in
uterus and causing muscles in the wall of uterus many centers because of no harm to the baby
to relax. and mother. Furthermore, it still can improve the
complication of intraventricular hemorrhage and
Complication of teenage pregnancy necrotizing enterocolitis.
Teenage pregnancy is defined as a teenage girl, Beware when used in mother with poorly
usually within the ages of 13-19, becoming controlled diabetes in pregnancy,
pregnant. [UNICEF] chorioamnionitis and immunosuppressed
mothers
a) Highest global incidence for premature
birth and low birth weight Corticosteroid shows maximum effect after 24
b) High risk for anemia in pregnancy hour and lasted 7 days. Repeated use of
c) Difficulties in labour due to corticosteroid should be avoided as it may
underdeveloped pelvis impose complication to mother and fetus.
d) High risk for obstructed labour, causing
obstetric fistula if c-sec is not readily
accessible
47
33 Years old Malay lady, housewife, G7P6 at 38 2) Counseling on mode of delivery and
W POA was admitted for further management in reason why patient can not be allowed
view of for SVD.
3) Plan for Caesarean section. Can be
1) Grand multi para performed at 38 week to 39 week of
2) Maternal obesity but MOGTT test is gestation.
normal 4) Counseling for bi tubal ligation because
3) Placenta previa type III anterior but no patient is in high risk to develop uterine
history of APH. rupture, hemorrhage and uterine atony
4) Biggest baby is 3.9 kg. after this c-sec delivery due to
5) Clinically, suspected macrosomic baby. a) Grand multi para
On ultrasound, estimated fetal weight is b) 1 c-sec scar.
4.0 to 4.2 kg.
6) Not in labour yet. Intrapartum management
Question 1) Preparation for c-sec (refer c-sec

preparation)
1) What is the mode of delivery and justify 2) Blood GSH because anticipating in
your answer blood loss because we will cut through
2) How do you manage this patient the placenta.
Answer 3) Presence of senior obstetrician in case of
complication to mother during operation
Mode of delivery and pediatrician for management of
baby.
After thorough view on this patient presentation,
caesarian section is the most appropriate mode Post partum
of delivery because of
1) Baby should be check for capillary
1) Placenta previa type III in which blood sugar and early feeding is
descending of fetal head into pelvic encouraged
brim is impossible due to obstruction to 2) Baby should be managed by pediatrician
cervical os. and kept in NICU for observation.
2) Maternal obesity and macrosomic baby 3) Mother should be offered with other
will predispose to complication type of contraception if she refused bi
especially shoulder dystocia. tubal ligation.
3) Induction of labour also impossible 4) Daily inspection on c-sec scars to look
because of grand multi para with for any infection or ruptured scar.
macrosomic baby. 5) Referral to the mother to dietitian and
internal medicine team for further
Management to this patient management on obesity.
6) Mother should be offered MOGTT
Ante natal management
screening on the next pregnancy.
1) Daily CTG for fetal surveillance.
Ultrasound should also be done.
48
40 Years old Malay lady, housewife, G15P12+2 than in the multiparous group (P < .05). Similar
(abortion) at 36W + 3/7 from low frequency of maternal diabetes, infection,
socioeconomic status presented with this uterine wall scar rupture, variations in fetal heart
problem list rate, fetal death, and neonatal mortality was
found in the 3 groups. [Agota Babinszki et al]
1) Elderly pregnancy
2) Great grand Multipara (para >10) Principles of management in this patient
3) Unstable lie
1) Daily observation for fetal lie
Questions 2) Exclude factors contributing to unstable
lie such as fetal abnormality, placenta
1) Complication associated with great previa, uterine abnormality
grand Multipara 3) Pelvic abnormality
2) Principles of management in this patient 4) Polyhydramnios
3) What is the contraindication for ECV? 5) Discuss on mode of delivery which is
Answer expectant vs. active management (C-sec,
ECV or stabilizing induction)
Notes: The risk of cord prolapses leading to fetal 6) Advise on contraception. Tubal ligation
hypoxia and fetal death is very high once the should be offered in view of
membrane ruptures. Therefore, it is highly a) Advanced maternal age
recommended that patient with unstable lie b) Great grand multi parity
should be admitted to antenatal wards at 37 c) Two history of abortion.
weeks onward for observation [The Practical d) Low socio economic status.
Labour suite Management] ! As a Muslim, permanent method of
contraception should only be performed
Complication associated with great grand if specialist agrees that next pregnancy
Multipara will be harmful to the patient’s life.
The incidence of malpresentation at the time of Contra indication for ECV
delivery, maternal obesity, anemia, preterm
delivery, and meconium-stained amniotic fluid Absolute contraindication
increased with higher parity, whereas the rate of 1) Multiple pregnancy
excessive weight gain and cesarean delivery 2) APH
decreased. Compared with grand multiparas, 3) PP
great-grand multiparas had significantly elevated 4) PROM or PPROM
risks for abnormal amounts of amniotic fluid, 5) Significant fetal abnormality
abruptio placentae, neonatal tachypnea, and 6) Any indication for caesarean section.
malformations but lower rates of placenta
previa (P < .05). The incidence of postpartum Relative
hemorrhage, preeclampsia, placenta previa, 1) Previous c-sec
macrosomia, postdate pregnancy, and low Apgar 2) IUGR
scores was significantly higher in grand 3) Severe proteinuric hypertension
multiparas than in multiparas, whereas the 4) Rhesus iso-immunization
proportion of induction, forceps delivery, and 5) Evidence of macrosomia
total labor complications was significantly lower 6) Any suspected fetal compromise.
49
26 Years old Malay lady, G1P0 at 38 W POG a) Severe cognitive, neurological and
currently presented with this problem developmental activity
1. Extended breech Management to this lady

2. Persistent proteinuria
3. Hypothyroidism on Tab Thyroxine 50 1) The management in view of breech is
microgram OD and undergone total similar to normal pregnancy
thyroidectomy in 2002 2) Excludes the causes of proteinuria. Take
notes that primid with proteinuria and
Questions hypothyroidism should increase
1) Hormones affecting level of thyroid suspiciousness to pre eclampsia even
hormone during pregnancy. though it is already near term.
2) What is the effect of hypothyroidism in 3) For the management of hypothyroidism
pregnancy a) WHO recommends intake of 200
3) Management to this lady micrograms/day of iodine during
pregnancy to maintain adequate
thyroid hormone production
Answer b) Dosage of maintenance thyroxine
could be increased during pregnancy
Hormones interacting with thyroid hormones up to 50-200 microgram daily dose.
(Doubling the dose by 25% to 50%)
1) High level of human chorionic c) Thyroid function tests every 6-8
gonadotropin will decrease the level of weeks during pregnancy to ensure
TSH during first trimester normal thyroid function throughout
2) Estrogen will increases the amount of pregnancy.
thyroid hormone binding proteins in the 4) Screening for congenital
serum hence increases the total thyroid hypothyroidism to the baby using the
hormone levels in the blood. However, umbilical cord blood during delivery.
free hormone remains normal
Effect of hypothyroidism on pregnancy
1) Mother
a) No symptoms in mild
hypothyroidism
b) Maternal anemia
c) Maternal myopathy
d) Congestive heart failure
e) Pre eclampsia
f) Placental abnormalities
g) Low birth weight infants
h) post partum hemorrhage
2) Baby
50
In Pursuit to Excel MCQ Exam for Professional III Examination (MCQ)
Asherman’s syndrome (intrauterine Fibroids, due to their mere presence, cause the
adhesion) is associated with: entire uterus to enlarge, thereby stretching the
blood vessels that supply the various parts of the
A) Amenorrhea uterus. When the fibroids are removed, the
B) Placenta previa remaining uterus collapses down to a smaller
C) Subfertility volume and some of the blood vessels that
D) Salphingitis supply the endometrium may become blocked.
E) Menorrhagia Because of the lack of oxygen and nutrients, that
area of tissue may die and a scar may form
leading to Asherman’s syndrome.
History: Named after Dr Asherman, an Israeli
gynaecologist, who first described the condition Other cause: radiation cause ischemia to
in the mid 20th century when he noted that some myometrium tissue
women who had surgical treatments at the
time of pregnancy stopped having periods Signs and symptoms
after this treatment 1) Oligomenorrhea, amenorrhea
2) Pain (increase work by uterine muscle to get
Def: A reduction or absence in menstruation rid blood through scar tissue)
that may be due to scar tissue formation inside 3) Infertility
the uterus and can occur as a result of 4) Haematometra (large bruise inside uterus that
pregnancy and delivery, infection or diagnosed by pelvic US)
gynaecological surgical procedure
Complication
**differ from endometrial ablation: induce
1) Placenta previa, accrete
scar tissue in the uterus to prevent heavy periods
2) Infertility
Classification according to 17th Congress of the 3) IUGR
Federation of Frenchspeaking Societies of 4) Ectopic pregnancy
Gynaecology and Obstetrics [1957]
(1) Traumatic synechiae connected with surgical Investigation:

or obstetrical evacuation of the uterus. 1) Hysteroscopy
(2) Spontaneous synechiae of tuberculous origin. 2) Hysterosalpingogram (HSG)
(3) Synechiae occurring after myomectomy.
(4) Synechiae secondary to the attack of Management
chemical or physical agents and, likewise, those
resulting fromatrophic changes. 1) Admission to wards
2) Investigation to confirm the diagnosis
Pathophysiology: Severely damaged decidua 3) Surgical excision of scar tissue by
basalis are replaced with granulation tissue and hysteroscope under General anesthesia.
opposing uterine wall adhere to form scar tissue.
It is later infiltrated by myometrial cells and Answer: T, T, T, F, F
covered by endometrium.
1
Concerning heart disease in pregnancy a. Non pharmacological (mild)

A. Mitral stenosis carries a better - limiting strenuous exercise
prognosis than atrial defect - adequate rest
B. Pregnancy should be induced at 38 - maintaining a low salt diet
weeks in cases with grade IV - treating anemia and infections early
dyspnoea - frequent antenatal examinations
C. Rheumatic heart disease is more
common than congenital heart disease Pharmacological
D. Ergometrine should be avoided in - Sublingual GTN
most cases - Digoxin
E. Mitral volvotomy is contraindicated. - Diuretic(used with care as may impair uterine
blood flow. No teratogenic effect)
Introduction: About 0.5 – 4% of pregnant - Beta blocker (used with care;intrauterine
women have cardiac disease. Common causes of growth retardation, apnea at birth,fatal
HF in pregnancy are hypertension, eclampsia, bradycardia, hypoglycaemia and
undetected valvular heart disease especially hyperbilirubinemia)
mitral stenosis, congenital heart disease, and - ACEI and ARB are contraindicated in
occasionally peripartum cardiomyopathy. pregnancy.
Peripartum cardiomyopathy occurs in 1:3,000 -warfarin is teratogenic in early trimester.
life births in Malaysia [Management of HF Heparin can be used LMW subcutaneous.
Malaysia]
Labour is spontaneous except in fetal
NYHA classification did not show any marked compromise (consider pre mature delivery)
differences in outcome.
Epidural anaesthesia during labour is
Eismenger’s syndrome and pulmonary recommended.
hypertension carries 40-50% mortality rate (can
be caused by mitral stenosis). TOF 5% if no Ergometrine causes 1. Vasoconstriction, HPT
pulmonary HPT. and heart failure. So must be avoided. Used
syntocinon only.
Normal haemodynamic changes that occur in
pregnancy are: Antibiotic prophylaxis in structural heart
1) Cardiac output increases by 30–50% during abnormality during labour (IV ampiillin 1.0g 6h
normal pregnancy. X 3doses, IV gentamycin 80 mg 8 hourly X 3)
2) Cardiac output increases to 80% above - Surgical volvotomy ideally be performed
baseline during labour and delivery. before pregnancy although it is safe to do it
during pregnancy
**Haemodynamic changes return to baseline 2 - Marfan syndrome is an autosomal dominant
– 4 weeks after vaginal delivery and up to 6 connective tissue abnormality that may lead to
weeks after caesarian delivery. mitral valve prolapsed and aortic regurgitation,
aortic root dilatation and aortic rupture (50% in
Management pregnancy)
1) Manage by multidisciplinary team consist of
physician, obstetrician and pediatrician Answer: F, F, T, T, F
2
Pyelonephritis in pregnancy Investigation

A. Occur in 0.1% of pregnant woman 1) Full blood count
B. If unilateral, is most often right sided 2) Urinalysis:Positive results for nitrites,
C. Caused predominantly by staph. leukocyte esterase, WBCs, RBCs, and protein
Aureus suggest UTI.
D. Common in diabetic patient 3) Urine culture: A colony count of 100,000
colony-forming units (CFUs) per milliliter has
Def: Pyelonephritis is the most common urinary historically been used to define a positive culture
tract complication in pregnant women, occurring result
in approximately 2% of all pregnancies. 4) Renal ultrasonography
5) Evaluation of fetal status
Symptoms of pyelonephritis include the 6) Renal function test
following:
1. Fever (Often, the temperature is very high.) Treatment
2. Chills -Ampicillin 2 g IV q6h for treatment of
3. Nausea and vomiting pyelonephritis; use in conjunction with an
4. Costovertebral angle (CVA) or flank pain aminoglycoside for treatment of pyelonephritis
-Paracetamol
Flank tenderness is right-sided in more than half of -Amoxicillin 7-Day regimen: 250 mg PO q8h or
patients, bilateral in one fourth of patients, and left- 3-Day regimen: 500 mg PO qid
sided in one fourth of patients. Pain may also be -Amoxicillin/clavulanate potassium
found suprapubically with palpation. (Augmentin), 500 mg PO tid for 7-10 d
-Ceftriaxone (Rocephin)
Other symptoms may include nausea, vomiting,
frequency, urgency, and dysuria.
Complication
- Bacteremia
Women with additional risk factors - Respiratory insufficiency due to bacterial
(immunosuppression, diabetes, sickle cell endotoxin damage to the alveoli, causing
anemia, neurogenic bladder, recurrent or pulmonary edema; therefore, fluid overload
persistent UTIs prior to pregnancy) are at an - Renal dysfunction
increased risk of a complicated UTI - PPROM
- Pre term birth
Common organism
1. Escherichia coli (most common, in as Answer; F, T, F, T
many as 70% of cases)
2. Group B Streptococcus (10%)
3. Klebsiella or Enterobacter species (3%)
4. Proteus species (2%)
Physiological changes include urinary retention

caused by the weight of the enlarging uterus and
urinary stasis due to ureteral smooth muscle
relaxation
3
STD include Answer: T, T, T, F, F

A. Trichomonas vaginitis
B. Condyloma accuminata
C. Chlamydial infection
D. Type 1 herpes hominis
E. Toxoplasmosis
Bacterial STDs include syphilis, gonorrhea,

chancroid, lymphogranuloma venereum,
granuloma inguinale, and chlamydial,
mycoplasmal, and Ureaplasma infections.
Viral STDs include genital and anorectal warts

(Condylomata acuminata :HPV types 6 and 11),
genital herpes, molluscum contagiosum, and
HIV infection
Parasitic infections that can be sexually

transmitted include trichomoniasis (caused by
protozoa), scabies (caused by mites), and
pediculosis pubis (caused by lice).
Type 1 herpes hominis causes classic “cold

sores” or “fever blisters”, commonly known as
herpes simplex, herpes genitals, herpes labialis
Toxoplasmosis is caused by infection with

Toxoplasma gondii, an obligate intracellular
parasite. The infection produces a wide range of
clinical syndromes in humans, land and sea
mammals, and various bird species.Individuals
at risk for toxoplasmosis include fetuses,
newborns, and immunologically impaired
patients. Congenital toxoplasmosis is usually a
subclinical infection. Among immunodeficient
individuals, toxoplasmosis most often occurs in
those with defects of T-cell–mediated immunity,
such as those with hematologic malignancies,
bone marrow and solid organ transplants, or
AIDS.T gondii oocysts are ingested in material
contaminated by feces from infected cats.
Oocysts may also be transported to food by flies
and cockroaches
4
Uterine rupture may be associated with Consequences of Uterine rupture in fetal

A. Previous c-section 1) Fetal hypoxia or anoxia
B. Myomectomy 2) Fetal acidosis
C. Oxytoxin infusion 3) Admission to a NICU
D. Prostaglandin administration 4) Fetal or neonatal death
E. Breech extraction
Consequences of Uterine rupture in mother
Uterine rupture in pregnancy is a rare and often 1) Maternal bladder injury
catastrophic complication with a high incidence 2) Severe maternal blood loss or anemia
of fetal and maternal morbidity. Several factors 3) Hypovolemic shock
are known to increase the risk of uterine rupture, 4) Need for hysterectomy
but, even in high-risk subgroups, the overall 5) Maternal death
incidence of uterine rupture is low. From 1976-
2005, 19 peer-reviewed publications that Risk Factor
described the incidence of uterine rupture 1) Previous cesarean delivery
reported 1654 cases of uterine rupture among 2) Previous myomectomy
2,504,456 pregnant women, yielding an overall 3) Congenital uterine anomaly
rupture rate of 1 in 1514 pregnancies (0.07%). 4) Pregnancy considerations
Grand multiparity, Maternal age,
Uterine rupture is defined as a full-thickness Placentation (accreta, percreta, increta,
separation of the uterine wall and the overlying previa, abruption)
serosa.
Cornual (or angular) pregnancy
Differs from uterine scar dehiscence: Separation of a Overdistension (multiple gestation,
preexisting scar that does not disrupt the overlying polyhydramnios)
visceral peritoneum (uterine serosa) and that does Dystocia (fetal macrosomia, contracted
not significantly bleed from its edges. In addition, the
pelvis)
fetus, placenta, and umbilical cord must be contained
within the uterine cavity, without a need for cesarean Trophoblastic invasion of the myometrium
delivery because of fetal distress. 5) Labor status
Induced labor
Uterine rupture results in: + With oxytocin
• bleeding;
+ With prostaglandins
• rupture of the amniotic sac (bag of
waters); Augmentation of labor with oxytocin
• partial or full delivery of the fetus into Duration of labor, Obstructed labor
the abdominal cavity; and 6) Obstetric management considerations
• loss of oxygen delivery to the fetus. Instrumentation (forceps use)
Intrauterine manipulation (external
Classic symptoms of rupture include: cephalic version, internal podalic version, breech
• pain above and beyond normal labor
extraction, shoulder dystocia, manual extraction
pain;
• discontinuation of uterine contractions; of placenta)
• signs of fetal heart rate abnormalities; Fundal pressure
• hemorrhage; and 7) Uterine trauma
• Hypovolumic shock Direct uterine trauma and Violence
Answer: All True
5
Labour may be obstructed by

A) Ovarian tumor
B) Cystocoele
C) Ectopic kidney
D) Distended bladder
E) Vaginal septum
Obstructed labour means that, in spite of strong

contractions of the uterus, the fetus cannot
descend through the pelvis because there is an
insurmountable barrier preventing its descent.
Obstruction usually occurs at the pelvic brim,
but occasionally it may occur in the cavity or at
the outlet of the pelvis. [WHO]
Causes of obstructed labour:
1) cephalopelvic disproportion
(small pelvis or large fetus)
2) abnormal presentations, e.g.
- brow
- shoulder
- face with chin posterior
- aftercoming head in breech
presentation
3) Fetal abnormalities, e.g.
- hydrocephalus*
- locked twins*
4) abnormalities of the reproductive
tract, e.g.
- pelvic tumour*
- stenosis of cervix or vagina**
- tight perineum.**
* Rarer causes.
** This may be associated with scarring caused
by female genital mutilation, or previous
“gishiri” cut.
Answer: All true
6
During pregnancy and puerperium, fibroid However, without pathologic examination of the
A) increase in size uterus, this determination is not possible.
B) Undergo red degeneration Uterine leiomyosarcomas are found in
C) Become infected approximately 0.1% of women with leiomyomas
D) May undergo sarcomatous changes and are reported to be more frequently
E) Cause post partum hemorrhage associated with large or rapidly growing
fibroids.
Uterine leiomyomas, commonly known as
fibroids, are well-circumscribed, non-cancerous The two most common symptoms of fibroids
tumors arising from the myometrium (smooth (also called leiomyomas) are abnormal uterine
muscle layer) of the uterus. In addition to bleeding and pelvic pressure.
smooth muscle, leiomyomas are also composed
of extracellular matrix (i.e., collagen, Leiomyomas are also associated with a range of
proteoglycan, fibronectin). Other names for reproductive dysfunction including recurrent
these tumors include fibromyomas, fibromas, miscarriage, infertility, premature labor, fetal
myofibromas, and myomas. malpresentations, and complications of labor.
Leiomyomas are usually detected in women in Diagnosis

their 30's and 40's and will shrink after 1. bimanual pelvic examination
menopause in the absence of post-menopausal 2. ultrasonography, MRI (magnetic
estrogen replacement therapy. (Dependent on resonance imagery), and CT
estrogen for growth) 3. Hysterosalpingography,
sonohysterography, and hysteroscopy
Two to five times more prevalent in black
women than white women Red degeneration: obsolete term for necrosis,
with staining by hemoglobin, which may occur
Leiomyomas are classified by their location in in uterine myomas, especially during pregnancy;
the uterus. Subserosal leiomyomas are located marked by softening and a red color resembling
just under the uterine serosa and may be partly cooked meat. [stedman]
pedunculated (attached to the corpus by a
narrow stalk) or sessile (broad-based). Medical treatment
Intramural leiomyomas are found 1) NSAIDS for dysmenorrhea
predominantly within the thick myometrium but 2) antifibrotic drug, pirfenidone
may distort the uterine cavity or cause an 3) GnRH agonist (Specifically, uterine
irregular external uterine contour. Submucous volume has been shown to decrease
leiomyomas are located just under the uterine approximately 50% after three months
mucosa (endometrium) and, like subserosal of GnRH agonist therapy.)
leiomyomas, may be either pedunculated or - Use to reduce fibroid size few
sessile. Tumors in subserosal and intramural months before surgery or
locations comprise the majority (95%) of all - When menopause is within few
leiomyomas; submucous leiomyomas make up months
the remaining 5%. Others; Cervical,
Intraligamentary (within broad ligament, cause Surgical treatment
uteric compression) and Parasitic(attached Myomectomy (pt wish to reproduce)
outside the uterus, i.e. the bladder) Hysterectomy
Transformation of uterine leiomyomas (benign) Answer: T, T, F, F, T

to uterine leiomyosarcomas (malignant smooth
muscle tumors of the uterus) is extremely rare,
and, in fact, many researchers and clinicians
believe this type of transformation never occurs.
7
Placenta previa is associated with * Multiple gestation (larger surface area of the
A) Painless vagina bleeding placenta)
B) Abnormal fetal heart rate * Erythroblastosis
C) Twin pregnancy * Prior uterine surgery
D) Android pelvis * Recurrent abortions
E) Diabetes Melitus * Nonwhite ethnicity
* Low socioeconomic status
Placenta previa involves implantation of the * Short interpregnancy interval
placenta over the internal cervical os. Variants * Smoking
include complete implantation over the os * Cocaine use
(complete placenta previa), a placental edge * Other causes include digital exam, abruption
partially covering the os (partial placenta previa) (pre-eclampsia, chronic hypertension, cocaine
or the placenta approaching the border of the os use, etc) and other causes of trauma (eg,
(marginal placenta previa). A low-lying placenta postcoital trauma).
implants in the caudad one half to one third of
the uterus or within 2-3 cm from the os. Grade.
A leading cause of third trimester hemorrhage,
placenta previa presents classically as painless I Placenta Lateral Minor
bleeding. Bleeding is thought to occur in encroaches on
association with the development of the lower the lower
uterine segment in the third trimester. Placental uterine segment
attachment is disrupted as this area gradually but does not
thins in preparation for the onset of labor. When reach the
this occurs, bleeding occurs at the implantation
cervical os.
site as the uterus is unable to contract adequately
and stop the flow of blood from the open
vessels. Thrombin release from the bleeding II Placenta marginal major if
sites promotes uterine contractions and a vicious reaches the posterior
cycle of bleeding-contractions-placental margin of the located
separation-bleeding. cervical os but
does not cover
Placental migration occurs during the second
it.
and third trimesters, owing to the development
of the lower uterine segment, but it is less likely
if the placenta is posterior or if there has been a III Placenta
previous caesarean section. partially cover
the os.
Causes
IV Placenta is Complete Major
* Hemorrhaging, if associated with labor,
would be secondary to cervical dilatation and symmetrically
disruption of the placental implantation from the implanted in the
cervix and lower uterine segment. The lower lower uterine
uterine segment is inefficient in contracting and segment
thus cannot constrict vessels as in the uterine
corpus, resulting in continued bleeding.
* Advancing age (>35)
* Multiparity
* Infertility treatment Answer: T, F, T, F, F
8
Complication of abruptio placenta corrected to ensure adequate hemostasis in the

A) Eclampsia case of a cesarean
B) Acute renal failure
C) DIVC Prematurity: Delivery is required in cases of
D) Fetal death severe abruption or when significant fetal or
E) Post partum hemorrhage maternal distress occurs, even in the setting of
profound prematurity. In some cases, immediate
Abruptio placentae is defined as the premature delivery is the only option, even before the
separation of the placenta from the uterus. administration of corticosteroid therapy in these
Patients with abruptio placentae typically premature infants. All other problems and
present with bleeding, uterine contractions, and complications associated with a premature infant
fetal distress. A significant cause of third- are also possible.
trimester bleeding associated with both fetal and
maternal morbidity and mortality, abruptio Signs and symptoms
placentae must be considered whenever bleeding
is encountered in the second half of pregnancy. 1) Vaginal bleeding
- Vaginal bleeding is present in 80%
Hemorrhage into the decidua basalis occurs as of patients diagnosed with placental
the placenta separates from the uterus. Vaginal abruptions.
bleeding usually follows, although the presence - Bleeding may be significant enough
of a concealed hemorrhage in which the blood to jeopardize both fetal and maternal
pools behind the placenta is possible. health in a relatively short period.
- Remember that 20% of abruptions
If the bleeding continues, fetal and maternal are associated with a concealed
distress may develop. Fetal and maternal death hemorrhage and the absence of
may occur if appropriate interventions are not vaginal bleeding does not exclude a
undertaken. The primary cause of placental diagnosis of abruptio placentae.
abruption is usually unknown, but multiple risk 2) Contractions/uterine tenderness
factors have been identified. - Contractions and uterine hypertonus
are part of the classic triad observed
Complication with placental abruption.
- Uterine activity is a sensitive marker
Cesarean delivery: Cesarean delivery is often of abruption and, in the absence of
necessary if the patient is far from her delivery vaginal bleeding, should suggest the
date or if significant fetal compromise develops. possibility of an abruption,
If significant placental separation is present, the especially after some form of
fetal heart rate tracing typically shows evidence trauma or in a patient with multiple
of fetal decelerations and even persistent fetal risk factors.
bradycardia. A cesarean delivery may be 3) Decreased fetal movement
complicated by infection, additional - This may be the presenting
hemorrhage, the need for transfusion of blood complaint.
products, injury of the maternal bowel or - Decreased fetal movement may be
bladder, and/or hysterectomy for uncontrollable due to fetal jeopardy or death.
hemorrhage. In rare cases, death occurs.
Hemorrhage/coagulopathy: Disseminated
intravascular coagulation (DIC) may occur as a Answer: F(risk factor), T, T, T, T(uterine atony)
sequela of placental abruption. Patients with a
placental abruption are at higher risk of
developing a coagulopathic state than those with
placental previa. The coagulopathy must be
9
A patient with severe placental abruption will 2. Early Rupture of Membranes (AROM)
need 3. Internal Fetal Monitoring (fetal scalp
A) CVP line electrode)
B) Artificial Rupture Of Membrane 4. Tocometry
C) Sedation with morphine 5. Intrauterine Pressure Catheter
D) Beta adrenergic drug 6. Cautious use of Pitocin
E) Arterial Blood Gas analysis E. Risks
1. Preterm birth
Sher Severity Grading system 2. Intrauterine Growth Retardation
1. Grade 1: (Herald bleed) Management: Emergent

1. Less than 100cc of uterine bleeding
2. Uterus non-tender Rapid management is critical as fetal death
3. No Fetal Distress occur in up to 30% within 2h. Do not wait for
2. Grade 2 US as it is clinically diagnosed
1. Uterus tender
2. Fetal Distress 1. Brisk bleeding
3. Concealed hemorrhage 2. Unstable vital signs
4. Progresses to Grade 3 without delivery 3. Fetal Distress
3. Grade 3 4. Grade II or III placental abruption
1. Fetal death
2. Maternal shock Immediate interventions
3. Extensive concealed hemorrhage 1. Oxygen
4. Coagulopathy 2. Trendelenburg position
1. Absent: 3A (66% of patients) 3. Obtain immediate Intravenous Access
2. Present: 3B (33% of patients) 1. Two large bore IV (16-18 gauge)
2. Initiate Isotonic crystalloid bolus
Management: Stable patient (Grade I) 1. Normal saline or Ringers
4. Call for immediate Obstetric and
A. General neonatal support
1. Obstetrics Consultation 5. Delivery within 20 minutes if Fetal
2. RhoGAM if Maternal blood Rh -ve Distress** Cesarean Section unless imminent
B. Criteria Vaginal Delivery
1. Reassuring Fetal Heart Tracing 6. RhoGAM if Maternal blood Rh -ve
2. No coagulopathy
3. Normotensive without Preeclampsia Monitoring
4. Nontender uterus 1. Orthostatic Blood Pressure and pulse
5. Negative ultrasound with normal AFI 2. Monitor Intake and output
C. Preterm gestation *Keep Urine Output over 30cc per hour
1. Consider Tocolysis with Magnesium 3. Monitor Hemoglobin or Hematocrit q1-
Sulfate. Contraindicated in all but mild 2 hours prn
abruption <34 weeks**Controversial and risky 1. Keep Hemoglobin >10 g/dl or
2. Steroids to promote lung maturity Hematocrit >30%
3. Consider Amniocentesis for lung 2. Packed Red Blood Cell transfusion
maturity studies as needed
4. External Fetal Monitoring 4. Monitor coagulation studies
5. Observe during short term 1. Fresh Frozen plasma transfusion as
hospitalization needed
D. Term gestation or mature lung studies 2. Platelet transfusion as needed
1. Active management labor towards rapid
fetal delivery Answer: T, F(once pt stable), T, F, T
10
The following are associated with placental Twin-to-twin transfusion syndrome (TTTS) is
insufficiency the result of an intrauterine blood transfusion
A) Diabetes Mellitus from one twin (donor) to another twin
B) Post maturity
(recipient). TTTS only occurs in monozygotic
C) Twin pregnancy
D) Cigarette smoking (identical) twins with a monochorionic placenta.
E) Dieting during pregnancy The donor twin is often smaller with a birth
weight 20% less than the recipient's birth
Definition: weight. The donor twin is often anemic and the
Placental insufficiency is the failure of the recipient twin is often plethoric with hemoglobin
placenta to supply nutrients to the fetus and differences greater than 5 g/dL. [EMedicine
remove toxic wastes.
article 271752]
In post maturity of the baby [before term,
growth of placenta is proportional to growth of
fetus. However after term, placenta start to Answer: T, T, T, T, T
regress while the baby continue to grow]
Causes [from Ten Teachers]

Reduced uteroplacental perfusion: Inadequate
trophoblast invasion, anti phospholipid
syndrome, diabetes mellitus, Sickle cell disease,
multiple gestation, collagen vascular disease.
This will result in small placenta with gross

morphological changes. Usually infarct and
basal hematoma.
Reduce feto placental perfusion: Single

umbilical artery, twin-twin transfusion
syndrome.
Antiphospholipid syndrome (APS) is a disorder

that manifests clinically as recurrent venous or
arterial thrombosis and/or fetal loss.
Characteristic laboratory abnormalities in APS
include persistently elevated levels of antibodies
directed against membrane anionic
phospholipids (ie, anticardiolipin [aCL]
antibody, antiphosphatidylserine) or their
associated plasma proteins, predominantly beta-
2 glycoprotein I (apolipoprotein H); or evidence
of a circulating anticoagulant. [EMedicine
article 333221]
11
Hydatidiform mole is associated with Failure of the placental-site trophoblastic tumor

increased urinary output of to produce large amounts of estrogen, in contrast
to normal pregnancy and Hydatidiform mole,
a) estrogen resulted in marked androgen/estrogen
b) human chorionic gonadotrophin imbalance, high circulating concentrations of
c) prostaglandin free testosterone, and Virilization. [Nagelberrg
d) pregnanediol SB& Rosen SW, 1985] A decrease of E3 in
e) human placental lactogen
these abnormal pregnancies would result mainly
in a lower level of tissue P450arom
Gestational trophoblastic disease encompasses concentration [Takara Yamamoto et al, 1997]
of several disease processes that Originate from
placenta HPL Value increased in multiple pregnancies
a) Complete mole (no fetal tissue, 90% 46 (twins or more), Placental site trophoblastic
XX and 10% 46 XY) tumor, intact molar pregnancy, Diabetes, Rh
b) Partial mole (69, XXX or 69, XXY with incompatibility and deccreased in Toxemia,
fetal tissue present) Aborting hydatidiform mole, Choriocarcinoma
c) Placental site trophoblastic tumors and Placental insufficiency [Medline Plus]
d) Choriocarcinomas
e) Invasive moles PGDH activity in neoplastic tissues was found
to be one tenth or less of that in normal term
Neutral steroids in urine were determined human placentae. PGDH may be important in
quantitatively with gaschromatography on the accumulation of PGs in neoplastic tissues. If
capillary columns in a case of benign choriocarcinoma cells were able to synthesise
hydatidiform mole associated with bilateral prostaglandin E2 or PGF2α then the very limited
theca-lutein cysts. A remarkable finding was the amounts of PGDH in these cells would allow
very high levels of 17-hydroxypregnanolone considerable quantities of these prostaglandins
and pregnanetriol, which continued to rise until to be produced. The lack of PGDH in these cells
the 15th day after molar evacuation.[Vanluchene suggests that very little or no PGE2 is
E et, al, 1977] synthesised in choriocarcinoma cells.
Rapid urine qualitative hCG assays may not be Answer: T, T, F, F, T

reliable in the presence of markedly elevated
hCG levels found in molar pregnancy. [Davison
CM et al, 2004]
Urinary pregnanediol levels, on the other hand

are frequently decreased. [Clinical Laboratory
Medicine by Richard Ravel]
Decreased urinary pregnandeniol level but

increased in serum progesterone and estradiol-
17 beta suggest molar pregnancy
12
Prolactin the nipples and mammary gland, as occurs

a) is secreted by the posterior pituitary during nursing, leads to prolactin release. This
b) is necessary for mammary ductal effect appears to be due to a spinal reflex arc
growth that causes release of prolactin-stimulating
c) level in plasma is unaffected by hormones from the hypothalamus.
smoking
d) is necessary for the establishment of
lactation Estrogens provide a well-studied positive control
e) secretion is controlled by an inhibiting over prolactin synthesis and secretion. Increase
factor blood concentrations of estrogen during late
pregnancy appear responsible for the elevated
Prolactin is a single-chain protein hormone levels of prolactin that are necessary to prepare
closely related to growth hormone secreted by the mammary gland for lactation at the end of
lactotrophs in the anterior pituitary. It is
synthesized as a prohormone. gestation.
Prolactin induces lobuloalveolar growth of the Excessive secretion of prolactin -

mammary gland. Alveoli are the clusters of cells hyperprolactinemia - is a relatively common
in the mammary gland that actually secrete milk. disorder in humans. This condition has
numerous causes, including prolactin-secreting
Prolactin stimulates lactogenesis or milk tumors and therapy with certain drugs.
production after giving birth. Prolactin, along
with cortisol and insulin, act together to Common manifestations of hyperprolactinemia
stimulate transcription of the genes that encode in women include amenorrhea (lack of
milk proteins. menstrural cycles) and galactorrhea (excessive
or spontaneous secretion of milk). Men with
hyperprolactinemia typically show
hypogonadism, with decreased sex drive,
decreased sperm production and impotence.
Such men also often show breast enlargement
(gynecomastia), but very rarely produce milk.
http://www.vivo.colostate.edu/hbooks/pathphys/endo
crine/hypopit/prolactin.html
Dopamine serves as the major prolactin-
inhibiting factor or brake on prolactin secretion. A minimum of 5 cigarettes significantly
It is secreted into portal blood by hypothalamic decreases prolactin concentration in smokers. A
neurons, binds to receptors on lactotrophs, and matched pair’s comparison confirmed that
inhibits both the synthesis and secretion of smoking reduces the level of prolactin [Gabriela
prolactin. Agents and drugs that interfere with et al, 1995]
dopamine secretion or receptor binding lead to
enhanced secretion of prolactin. Answer: F, T, F, T, T
Prolactin secretion is positively regulated by

several hormones, including thyroid-releasing
hormone, gonadotropin-releasing hormone and
vasoactive intestinal polypeptide. Stimulation of
13
With regards of the blood volume and its [Wikipedia] In pregnancy, liver produces more
composition during pregnancy transferrin.
Serum Ferroxidase I and II are progressively

a) the total RBC falls by about 20%
increased with serum Total Iron Binding
from the normal non-pregnant
Capacity (TIBC) and unsaturated iron binding
volume
capacity (UIBC) as pregnancy advances
b) the packed cell volume falls
[Agroyannis B et al]
c) there is rise in the iron binding
capacity
The total iron-binding capacity exceeded normal
d) the blood cholesterol rises
starting in the sixth lunar month in the
e) the protein bound iodine level falls
nontreated group and in the seventh lunar month
in the treated group, and it decreased slightly in
the latter toward term and had returned to
Physiology of anemia in pregnancy
normal in both groups by the fourth postpartum
A disproportionate increase occurs in plasma
week [George D. Malkasian]
volume (25% to 50%) compared to red blood
cell mass (10% to 25%) during pregnancy, with
Serum protein bound iodine levels increased
resultant hemodilution and reduction in
significantly with age in both sexes and in
hematocrit of 3% to 5%. These changes begin at
pregnant women, while it decreased
approximately 6 weeks gestation and normalize
significantly in alcoholics, cigarette smokers and
by 6 weeks postpartum. [The John Hopkins
marijuana addicts [O M Ebuehi et al]
Manual of Gynecology and Obstetrics 3rd Ed.]
It is well known that with the effect of hormonal
Packed cell volume (PCV) is determined by
changes during pregnancy, plasma lipid levels
measuring the height of the red cell volume in a
increase. Expected elevations for triglyceride
micro-hematocrit capillary filled with whole
and cholesterol levels during a normal
blood, after centrifugation. It is a directly
gestational period usually do not exceed 332
measured value, Meanwhile hematocrit (Hct) is
mg/dL and 337 mg/dL, respectively
the corresponding calculated value (RBC X
(corresponding 95th percentile values).
MCV), PCV and Hct are interchangeable even
However, elevations over the 95th percentile
though PCV is slightly higher than the more
values can be observed during pregnancy, and
accurate Hct due to plasma trapping (between
patients with levels over these expected
the packed cells in a centrifuged capillary).
adaptation levels can be divided into 2 groups:
(1) supraphysiologic hyperlipoproteinemia
In present study hemoglobin percent and packed
during pregnancy and (2) extreme
cell volume was significantly decreased in 2nd
hyperlipoproteinemia limited to gestational
and 3rd trimester of pregnancy when compared
period (triglyceride level >1000 mg/dL)
with the control group and same category of
[Basaran A.]
women who were not supplemented with iron. It
is evident that the significantly low hemoglobin
percent and packed cell volume (PCV) in
Answer: F, T, T, T, F
pregnant women is due in part to dietary iron
deficiency. Therefore, iron therapy in pregnancy
is helpful to maintain the hemoglobin percent
and packed cell volume nearer to that of non
pregnant normal women. [Wahed F et al]
Total iron-binding capacity (TIBC) is a medical

laboratory test which measures the blood's
capacity to bind iron with transferrin.
14
Ovulation in human become vigorous and the mesosalpinx contracts

to bring the tube in more contact with the ovary
a) is associated with surge of LH while the fimbria contracts rhythmically to
b) is characteristically followed by the sweep over the ovarian surface. As progesterone
development of secretory level rises 4-6 days after ovulation, it inhibits
endometrium tubal motility. This may lead to relaxation of the
c) is associated with an increased in tubal musculature to allow passage of the ovum
motility of the Fallopian tube into the uterus by the action of the tubal cilia.
d) is associated with a sustained fall in The effects of estrogen and progesterone on
the basal body temperature oviductal motility and morphology is mediated
e) followed by a rise in urinary through these steroids' receptors. The changes in
pregnanetriol receptors levels are critical in determining the
functional state of the oviduct.[Diaa M. EI-
Mowafi, MD;Zagagig University, Egypt]
The midcycle LH surge is responsible for a
dramatic increase in local concentrations of In women, ovulation causes an increase of one-
prostaglandins and proteolytic enzymes in the half to one degree Fahrenheit (one-quarter to
follicular wall. These substances progressively one-half degree Celsius) in basal body
weaken the follicular wall and ultimately allow a temperature (BBT); monitoring of BBTs is one
perforation to form. Ovulation most likely way of estimating the day of ovulation. The
represents a slow extrusion of the oocyte tendency of a woman to have lower
through this opening in the follicle rather than a temperatures before ovulation, and higher
rupture of the follicular structure [Novak temperatures afterwards, is known as a biphasic
Gynecology 14 ed] pattern. Charting of this pattern may be used as a
component of fertility awareness.[Wikipedia]
During the normal menstrual cycle the excretion

of pregnanetriol increased on the day that the
excretion of oestrone and oestradiol reached a
maximum during the follicular phase.
Pregnanediol excretion did not begin to increase
until 2 days later. The excretion of pregnanetriol
reached a peak and began to decrease before that
of pregnanediol. Thus the pattern of
pregnanetriol excretion was different from that
of the excretion of oestrogens or pregnanediol.
[K. Fotherby]
It is found that the cyclic change in urinary

pregnanetriol excretion is variable in extent but
there is a correlation between the urinary
excretion of oestrogens, pregnanediol and
pregnanetriol during the ovulatory cycle [Mary
TP & Ian FS]
Peristaltic movement of fallopian tube is
primarily regulated by three intrinsic systems:
the estrogen-progesterone hormonal milieu, the
Answer: T, T, T, F, T
adrenergic-nonadrenergic system, and
prostaglandins. Before ovulation, contractions
are gentle, with some individual variations in
rate and pattern. At ovulation, contractions
15
Pre eclampsia is associated with booking (1.55, 1.28 to 1.88), or maternal age ≥
A) Diabetes Mellitus 40 (1.96, 1.34 to 2.87, for multiparous women).
B) Rhesus iso immunization Individual studies show that risk is also
C) Urinary tract infection increased with an interval of 10 years or more
D) Polyhydramnios since a previous pregnancy, autoimmune
E) Twin pregnancy disease, renal disease, and chronic hypertension.
[Duckitt & Harrington]
Severe pre-eclampsia and eclampsia are
relatively rare but serious complications of The most significant risk factors for developing
pregnancy, with around 5/1000 maternities in pre-eclampsia are a history of pre-eclampsia and
the UK suffering severe pre-eclampsia and 5/10 the presence of Antiphospholipid antibodies.
000 maternities suffering eclampsia. In [Duckitt & Harrington]
eclampsia, the case fatality rate has been
reported as 1.8% and a further 35% of women Pre-existing diabetes and a pre-pregnancy BMI
experience a major complication [RCOG of ≥ 35 almost quadruple the risk; nulliparity, a
Guideline No. 10(A)] family history of pre-eclampsia, and twin
pregnancy almost triple the risk; and maternal
Who is at risk of getting pre-eclampsia? age ≥ 40, a booking BMI of ≥ 35, and a systolic
1) First pregnancy blood pressure ≥ 130 at booking double the risk.
2) First pregnancy with a new partner [Duckitt & Harrington]
3) Aged 40 or over
4) Mother or sister had pre-eclampsia Pre-existing hypertension, renal disease, chronic
during pregnancy autoimmune disease, and ≥ 10 years between
5) Pre-eclampsia in a previous pregnancy pregnancies increase the risk but it is not clear
6) Body mass index (BMI) of 35 or more by how much. [Duckitt & Harrington]
(you weigh 90 kg or more)
7) Multiple pregnancy These data demonstrates a significant positive
8) Medical problem such as high blood relation with maternal age, diabetes in
pressure, kidney problems and/or pregnancy, and fetal macrosomia with
diabetes. polyhydramnios. Anemia during pregnancy,
9) Pregnant from egg (oocyte) donation. cesarean delivery rate, and congenital anomalies
were significantly higher in the study
Controlled cohort studies showed that the risk of group.[Mathew Mariam et al]
pre-eclampsia is increased in women with a
previous history of pre-eclampsia (relative risk Answer: T, F, F, F, T
7.19, 95% confidence interval 5.85 to 8.83) and
in those with antiphospholipids antibodies (9.72,
4.34 to 21.75), pre-existing diabetes (3.56, 2.54
to 4.99), multiple (twin) pregnancy (2.93, 2.04
to 4.21), nulliparity (2.91, 1.28 to 6.61), family
history (2.90, 1.70 to 4.93), raised blood
pressure (diastolic ≥ 80 mm Hg) at booking
(1.38, 1.01 to 1.87), raised body mass index
before pregnancy (2.47, 1.66 to 3.67) or at
16
In normal labour It is widely accepted that prostaglandins play a

central role in parturition through their actions
a) endogenous oxytocin is responsible on uterine contractility and on cervical ripening.
for the initiation of uterine In both human and nonhuman primates, the
contraction major intrauterine sources of prostaglandins are
b) there is progressive increase in the fetal membranes and the deciduas [George J.
normal cortisol Haluska et al]. PGs have also been shown to
c) the uterine contractions is increased play an important role in up-regulation of the
by release of endogenous fetal hypothalamic-pituitary-adrenal axis,
prostaglandin membrane rupture and the maintenance of
d) during the first stage of labour, the uterine and placental blood flow [McKeon &
maternal arterial pressure rises Challis]
during each uterine contraction
13, 14-dihydro-15-keto-prostaglandin F (PGFM)
levels increased a labor progressed, and reached
They are four major hormonal systems involve maximal levels before placental separation had
during labor which are oxytocin, endorphins, occurred. Peripheral plasma concentrations of
epinephrine& Norepinephrine and prolactin. oxytocin did not change significantly at any
stage of labor or 2 hours post partum. These
Oxytocin causes the rhythmic uterine results suggest that prostaglandins have a role in
contractions of labor, and levels peak at birth the third stage of labor, and this finding may
through stimulation of stretch receptors in a have important clinical implications. [SM
woman’s lower vagina as the baby descends. Sellers et al]
The high levels continue after birth, culminating
with the birth of the placenta, and then gradually With active labor there are clear identifiable
subside. The baby also has been producing changes in arterial compliance and cardiac load
oxytocin during labor, perhaps even initiating as reflected in rapid ejection times (RETs) and
labor; [Dr Sarah J Buckley MD] pulse wave arrival times (PWATs), respectively.
These findings are absent in Prelabour. [Edward
These results give further support to the H. Hon et al]
hypothesis that maternal stress leads to a
reduced concentration of prolactin and increased Serial measurements of cardiac output and mean
concentration of cortisol whereas relief of pain arterial pressure were performed in 15 women
and maternal anxiety with meperidine lessens during the first stage of labour and at one and 24
both effects.[E. Onur et al] hours after delivery.....Over the same period
basal mean arterial pressure also
Maternal plasma Cortisol levels in 62 increased......There were also further increases in
primiparous women rose during labour and mean blood pressure during contractions.[S C
remained high for 20 minutes after delivery. Robson et al]
Umbilical cord Cortisol levels were substantially
lower than maternal levels. The maternal Answer: T, T, T, T, T
Cortisol level was slightly lower in those who
required oxytocin. This relationship between
maternal Cortisol levels and the use of oxytocin
was not affected by the use of epidural
analgesia. The mean maternal Cortisol level rose
to a lesser extent in the women who had epidural
analgesia than in those who did not.[Haddad &
Morris]
17
Regarding ectopic pregnancy
a) the common site is the cornu of uterus

b) anaemia is due to thrombocytopenia
c) hemoperitoneum results from tubal
rupture
d) ovary is another common site
e) shock may follow tubal rupture
Ectopic pregnancy refers to the implantation of a

fertilized egg in a location outside of the uterine Pictures from
cavity, including the fallopian tubes, cervix, http://emedicine.medscape.com/article/258768-overview
ovary, cornual region of the uterus, and the
abdominal cavity. This abnormally implanted The classic clinical triad of ectopic pregnancy is
gestation grows and draws its blood supply from pain, amenorrhea, and vaginal bleeding (50%).
the site of abnormal implantation. As the Patients may present with other symptoms
gestation enlarges, it creates the potential for common to early pregnancy, including nausea,
organ rupture because only the uterine cavity is breast fullness, fatigue, low abdominal pain,
designed to expand and accommodate fetal heavy cramping, shoulder pain, and recent
development. Ectopic pregnancy can lead to dyspareunia.
massive hemorrhage, infertility, or death.
38 year-old woman presented with gynaecologic
[Vicken P Sepilian] It is occur in 2% of all
haemorrhage, pelvic pain and hypovolemic
pregnancy
shock. Without any ambiguity, the diagnosis
Anything that impairs migration of embryo to was directly made during contrast enhanced
the andometrial cavity will predispose a woman Multidetector Computed Tomography (MDCT).
to ectopic pregnancy. this includes pelvic Massive hemoperitoneum with fresh blood clots
inflammatory disease, history of prior ectopic in the hypogastric area, active free peritoneal
pregnancy, History of tubal surgery and extravasation of intravascular contrast material
conception after tubal ligation, Use of fertility and dramatic peripheral enhancement, - "ring of
drugs or assisted reproductive technology, Use fire" sign - of an adnexal cystic structure were
of an intrauterine device, Increasing age, the key signs. [Coulier B et al]
smoking, Salpingitis isthmica nodosum,
Finding of hemoperitoneum on ultrasound
diethylstilbestrol (DES) exposure, a T-shaped
examination may not be an absolute
uterus, prior abdominal surgery, failure with
contraindication to conservative management of
progestin-only contraception, and ruptured
tubal ectopic pregnancy [Bignardi & Condous]
appendix.
Rupture may be heralded by sudden, severe
Sites and frequencies of ectopic pregnancy. By
pain, followed by syncope or by symptoms and
Donna M. Peretin, RN. (A) Ampullary, 80%;
signs of hemorrhagic shock or peritonitis. Rapid
(B) Isthmic, 12%; (C) Fimbrial, 5%; (D)
hemorrhage is more likely in ruptured cornual
Cornual/Interstitial, 2%; (E) Abdominal, 1.4%;
pregnancies [The Merck Manuals]
(F) Ovarian, 0.2%; (G) Cervical, 0.2%.
Answer: F, F, T, F, T
18
Endometriosis or inadequacy of ovulation. Some studies say

that up to 50 percent of patients with
a) commonly affects the ovaries endometriosis have some degree of ovulatory
b) is usually not associated with dysfunction and this should certainly be taken
infertility into account in the treatment of patients with
c) intestinal obstruction is a possible endometriosis and infertility. [Endometriosis -
complication if bowels are involved
d) often present with dysmenorrhea The '90s Outlook]
e) is primarily an acute inflammatory
Usually, the pain associated with endometriosis
process
is right before or during the menstrual period in
the initial stages; however, as the disease
Endometriosis is the presence of endometrial- progresses, it may occur throughout the cycle.
like tissue outside the uterine cavity, which The pain may be acute or chronic. In about half
induces a chronic inflammatory reaction. It can of the patients with severe or extensive
occur in various pelvic sites such as on the endometriosis, the pain is chronic all through the
ovaries, fallopian tubes, vagina, cervix, or cycle which gets worse right before and during
uterosacral ligaments or in the rectovaginal menstruation, and during or shortly after
septum. It can also occur in distant sites intercourse. [Endometriosis - The '90s Outlook]
including laparotomy scars, pleura, lung,
diaphragm, kidney, spleen, gallbladder, nasal Endometriosis may invade the rectovaginal
mucosa, spinal canal, stomach, and breast. [Ami septum and the anterior rectal wall. It may also
K Davé, MD] involve the upper rectum and sigmoid colon,
infiltrating the muscularis. Cyclical rectal
Ovaries is the most common site for bleeding (hematochezia) is pathognomonic of
implantation of the endometrial cell (up to 75%) endometriosis. However, transmural bowel
because 1) through the theory of retrograde involvement by endometriosis remains a rarity.
menstruation, ovaries are adjacent to the opening The ileum, appendix, and cecum may also be
of the tube in the pelvic area and that location involved, leading to intestinal obstruction.
alone will make the ovaries more prone to be Cicatrization as a consequence of endometriosis
contaminated with the regurgitated menstrual may lead to symptoms of obstruction even in
flow.2) ovaries have the highest level of steroid postmenopausal women. [Ami K Davé, MD]
hormone compared to any other organ and hence
they represent an ideal environment for
implantation and growth of the endometrial
Answer: T, F, T, T, F
tissue.
Infertility in endometriosis are due to 1) increase

level of prostaglandin production which is
interfering with sperm-ovum interaction, embryo
growth, interfering with sperm motility, and
interfering with the function of some central
nervous system areas that are responsible for
control of reproduction and 2) The presence of
endometrial tissue in the pelvic and peritoneal
cavities will cause some degree of abnormality
19
Question1: Which of the following statements alone have been described. The Cochrane
are true regarding the pharmacological induction Database indicates that with the available
of fetal respiratory maturity? evidence, antenatal TRH cannot be
recommended for clinical practice at the present
a) Maternally administered thyroid releasing time. Adverse maternal side-effects were
hormone (TRH) alone may cause lung significant for women receiving antenatal TRH
maturation. and these included hypertensive episodes.
b) Antenatal TRH has no maternal side-effects.
c) Treatment with antenatal corticosteriods Q11: Beta sympathomimetic drugs:
between 28 and 32 weeks reduces the incidence a) Increase maternal stroke volume.
of fetal intraventricular haemorrhage. b) Decrease fetal heart rate.
d) The use of antenatal cortiosteriods between c) Increase maternal bowel motility.
28 and 32 weeks with pre-labour ruptured d) Decrease intracellular potassium in maternal
membranes is associated with a significant cells.
increase in neonatal infection. e) Decrease maternal urinary output.
e) Antenatal corticosteriods may cause long-
term cognitive disabilities in infants treated Answer: T, F,F,F,T
prenatally.
Beta adrenergic agonists, currently the most
a) False widely used tocolytic drugs in the UK, include
b) False ritodrine, salbutamol and terbutaline. These
c) True pharmacological agents act via Beta-1 and Beta-
d) False 2 adrenergic receptors. Beta-I receptor responses
e) False include an increase in maternal heart rate and
stroke volume, a decrease in bowel motility and
The meta-analysis of 36 prospective studies an increase in metabolic lipolysis. The Beta-2
indicate that treatment between 28 and 32 weeks adrenergic response includes an increase in renal
with antenatal corticosteriods prior to the onset renin production and a decrease in urinary
of premature labour resulted in a substantial output.
reduction in the incidence of respiratory distress
syndrome. The reduction in respiratory Question, answer and discussion are taken from
morbidity was associated with overall reductions Self-assessment questions: Premature labour, by
in the incidence of neonatal intraventricular M.Kilby, Current Obstetrics & Gynaecology
haemorrhage, necrotizing enterocolitis and early (1996) volume 6 issue 3
neonatal death. There was no strong evidence of
any adverseeffects of corticosteroids in these
trials. Long-term follow-up of children in
several of these studies indicated no adverse
effect on growth, physical development or
cognitive skills.
Trials investigating the improved efficacy of

antenatal TRH given with antenatal
corticosteriods, as compared to corticosteriods
20
Question 2: The following are contraindications significantly reduces intraventricular

to tocolytic inhibition of preterm labour: haemorrhage.
d) Antibiotic administration significantly
a) Abruptio-placenta. reduces maternal infective morbidity in
b) Chorioamnionitis. prelabour ruptured membranes.
c) Pre-labour ruptured membranes. e) Intrapartum antibiotic therapy significantly
d) Severe pregnancy induced hypertension. reduces fetal infective morbidity in prelabour
e) Mild intrauterine growth restriction. ruptured membranes.
a) True
a) True b) False
b) True c) False
c) False d) True
d) True e) True
e) False
Analgesia and anaesthesia of choice for preterm
Antepartum haemorrhage of whatever cause is a labour and delivery are not well established.
contraindication to the suppression of preterm Epidural anaesthesia may well have benefits
labour as is intrauterine infection and severe especially in the management of the first and
pregnancy induced hypertension which may be second stage of a preterm vaginal breech
life threatening to the mother. In prelabour delivery. However, such a choice of analgesia is
rupture of membranes, although there is no contraindicated in chorioamnionitis. Although
absolute contraindication to tocolysis as long as both an elective episiotomy and low forceps
there is no overt evidence of delivery have been historically discussed as
chorioamnionitis,there is little evidence to useful in reducing the length of second stage and
suggest that tocolysis significantly improves protecting the premature fetus at delivery, there
perinatal mortality. In selected cases of mild are no data to support this as a potential benefit
intrauterine growth restriction in which the fetus to the fetus.
is not compromised, it may be beneficial to
suppress labour to allow antenatal Administration of antibiotics prophylactically to
corticosteriods to be administered. women with prelabour ruptured membranes
preterm delays delivery and reduces both
However, any evidence of fetal compromise maternal and neonatal infection. No effect has
should lead to prompt delivery of the fetus. yet been shown demonstrating an improvement
in perinatal mortality. In particular, in women
known to be carrying Group B Streptococci,
Question3: During a preterm delivery: intrapartum antibiotics should be adopted as
standard care.
a) Epidural anaesthesia is contraindicated if
chorioamnionitis is present. Question, answer and discussion are taken from
b) Elective episiotomy is advised for all vaginal Self-assessment questions: Premature labour, by
deliveries. M.Kilby, Current Obstetrics & Gynaecology
c) The elective use of low outlet forceps delivery (1996) volume 6 issue 3
21
Q4: The following drugs significantly reduce There is no evidence that corticosteriod
preterm labour when administered: administration suppresses preterm labour and
there is anecdotal evidence indicating that intra-
a) Ritodrine. amniotic injection of betamethasone may
b) Indomethacin. actually be used to induce labour.
c) Nifedipine.
d) Pethidine. Q5: The following are useful predictors of
e) Dexamethasone. preterm labour:
a) A previous history of preterm labour.
ANSWER 4 b) Maternal plasma oestradiol concentration 14
a) True days prior to onset of labour.
b) False c) Fetal fibronectin.
c) False d) Multiple pregnancy.
d) False e) Uterine anomaly.
e) False
Answer: T, F, T, T, T
Although beta-sympatho-mimetics themselves
may not have beneficial effects for the fetus they The background rate of preterm labour in the
are effective at postponing delivery, especially UK is approximately 7%. If a patient has had a
for short intervals of up to 24 h. This suggests previous preterm labour this rises to between 14
that they may have a place if, for instance, and 18%. A uterine anomaly is proven in
corticosteriods could be administered to promote between 5 and 16% of all preterm deliveries.
pulmonary maturity. However, injudicious use Multiple pregnancy is associated with preterm
of corticosteriods and beta-sympathomimetics delivery and this is paticularly true with
have been reported to precipitate acute monochorionic placentation. The majority of
pulmonary oedema. The only statistically biochemical prediction indices, including serum
significant differences in prospective trials oestradiol concentrations, have a poor predictive
comparing the use of calcium antagonists with index at detecting preterm delivery. Fetal
beta-sympatho-mimetics have indicated that fibronectin, a component of the extra cellular
there were fewer neonates of less than 2.5 kg matrix in the cervix, has been shown both in
and there were more admissions to neonatal' cross sectional studies, and more recently in
intensive care after the treatment with calcium longitudinal studies, to have a positive predictive
antagonists. At the present time, only a small value of preterm delivery in high risk patients of
number of prospective studies are reported. 46%.
Meta-analysis from the Cochrane Database does
not support the use of calcium antagonists or Question, answer and discussion are taken from
magnesium sulphate in preference to beta- Self-assessment questions: Premature labour, by
sympatho-mimetics in the suppression of M.Kilby, Current Obstetrics & Gynaecology
preterm labour. (1996) volume 6 issue 3
Pethidine may suppress both fetal and maternal

respiration and has no proven benefit in the
management of preterm labour.
22
Q6: Regarding the lecithin-sphingomyelin ratio: c) True

a) This test is carried out on amniotic fluid. d) True
b) Sphingomyelin is a general membrane lipid. e) False
c) The ratio for normal pregnancies is greater
than 0.5 at 20 weeks. Cervical incompetence is a dysfunction in the
d) If the ratio is less than 2 there is less than a integrity ofthe internal cervical os. It is
10% chance of the baby developing respiratory characterised by painless cervical dilatation in
distress syndrome. the mid second trimester. With regard to
e) Lecithin is produced by type II pneumocytes. aetiology, several factors are important. In-utero
exposure of Diethylstilboestrol carries a 45%
Answer: T, T, F, F, T risk of pregnancy loss due to cervical
incompetence. Acquired factors include cervical
The L/S ratio was introduced by Gluck in 1971. trauma. This includes over zealous mechanical
Amniocentesis allows the collection of fluid and dilatation of the cervix prior to diagnostic
the results are expressed as the ratio of lecithin curettage. Loop excision of the transformation
(phosphatylcholine) fraction enriched by cold zone is rarely associated with cervical
acetone precipitation. The sphingomyelin is used incompetence. With contemporary cervical
as a control because amniotic fluid volume cerclage, the majority of patients have their
changes during gestation cannot be accurately operation during pregnancy. The classical
measured clinically. In normal pregnancies the Shirodkar's suture and McDonald's suture have
L/S ratio is less than 0.5 at 20 weeks. The value approximately the same success rate in
of 2.0 indicates a low risk of respiratory distress prevention of premature labour. Ritodrine alone
syndrome at any point in gestation. The L/S ratio will not stop the contractions due to cervical
is not reliable if amniotic fluid is heavily incompetence and there is little prospective
contaminated with blood or meconium. Lecithin evidence to confirm that ritodrine therapy has a
and other phosphatyl-lipids are produced by the role to play perioperatively in cervical cerclage.
type II pneumocytes within the lungs.
Question, answer and discussion are taken from

Q7: With cervical incompetence: Self-assessment questions: Premature labour, by
a) In-utero exposure to Diethylstilboestrol (DES) M.Kilby, Current Obstetrics & Gynaecology
is a causative factor. (1996) volume 6 issue 3
b) A history of loop diathermy excision of the
transformation zone of the cervix for treatment
of CIN is a common association.
c) Shirodkar and McDonald cerclage techniques
carry the same success rates.
d) When the amniotic membranes are ruptured
then cervical cerclage is contraindicated.
e) This may be treated by oral Ritodrine.
ANSWER 7
a) True
b) False
23
QUESTION 8: In preterm labour complicated syncytio-trophoblast of patients with preterm

by a low-grade infection: labour.
a) Bacterial phospholipases cause a direct
release of arachidonic acid from the amnion and Q9: Relaxin:
decidual cells. a) Has a stimulatory effect on the myometrium.
b) Bacterial lipopolysaccharides stimulate b) Has an inhibitory effect that is more rapid
increased production of interleukin-I (1L-I) from than progesterone.
amnion and decidual cells. c) Affects frequency modulation of uterine
c) IL-1 stimulates the decidual production of IL8 contractions.
d) Corticotrophin releasing hormone (CRH) d) Elevates uterine cyclic AMP concentrations.
does not stimulate prostaglandin production e) Stimulates prostocyclin production by the
from decidual cells. myometrium.
e) Annexin production by the trophoblast and
decidua decrease with the onset of labour. Answer: F, T, T, T, T
ANSWER: T, T, T, F, T Experimental animal models have suggested that

Relaxin has an inhibitory effect on myometrial
Approximately 30% of all preterm labours are activity. This is separate from that induced by
associated with some mild chorioamnionitis. progesterone. The inhibitory effect of Relaxin is
Bacterial phospholipases directly release more rapid in onset than that of progesterone.
arachidonic acid which are precusors of many Although spontaneous myometrial contractility
eieosanoids from decidual cells. Also is suppressed, sensitivity to oxytocin is
lipopolysaccharides stimulate decidual cells to maintained and its primary effects are one of
increase cytokines such as IL-I and tumour frequency modulation of contractions. Relaxin
necrosis factor from amnion and decidual cells. also elevates uterine cyclic AMP production in
The cytokines are elevated in the amniotic fluid common with other uterine relaxants. It is
from patients with preterm labour and infection unknown whether Relaxin has its effect directly
and may secondarily release other cytokines on the myometrium, but experimental evidence
such as IL-8 which are chemotaxtic peptides for indicates that cultured myometriai cells, when
neutrophils and T-cells. Cortieotrophin releasing stimulated with Relaxin, produce prostacyclin.
hormone is produced by the syncytio-trophoblast
and stimulates prostaglandin production from
cultured decidual cells. The prostaglandins Question, answer and discussion are taken from
produced may have a direct effect upon the Self-assessment questions: Premature labour, by
myometrium which is adjacent to the chorion, M.Kilby, Current Obstetrics & Gynaecology
amnion and decidual cells.The annexins are (1996) volume 6 issue 3
substrates for tyrosine kinases and influence
phospholipase A2 production and, therefore,
may increase myometrial intracellular free
calcium concentration. It is believed that they
bind to phospholipids preventing phospholipase
A2 from gaining access to its substrate. Both
annexin protein and mRNA are decreased in the
24
Q7: which of the following statements Q5: Concerning placenta praevia, which of the
concerning placental abruption is/are true: following statements is/are true:
a) The incidence of placenta praevia is 1 in
a) In western society placental abruption is 5000.
commonly associated with poor nutrition. b) Placenta praevia is more common in
b) Placental abruption can occur in association Caucasian women.
with external cephalic version. c) Owing to the position of the placenta in
c) Placental abruption is more common with placenta praevia, prolapsed cord is much less
multiple pregnancy. likely.
d) Placental abruption is more common with a d) Previous lower segment Caesarean section is
history of previous abruption. a risk factor for placenta praevia.
e) Postpartum haemorrhage is a common e) There is no association between the incidence
complication of placental abruption, which often of placenta praevia and maternal age.
requires hysterectomy to control the bleeding.
a) False. The true incidence is 0.3-1.0%.
a) False. Poor nutrition has previously been b) False. Placenta praevia is more common in
reported as being associated with placental black women.
abruption, but within the western world this is c) False. Prolapsed cord is up to three times
now a rare finding. more likely with placenta praevia.
b) True. External cephalic version is associated d) True.
with placental abruption, especially if the e) False. More common in older women and
manoeuvre is carried out under general multiparous women.
anaesthetic. Presumably, if the manoeuvre is
carried out under general anaesthetic, the Question, answer and discussion are taken from
operator exerts more 'energy' into the procedure Self-assessment questions: The Placenta, by
as she/he does not have the benefit of S.Smith, Current Obstetrics & Gynaecology
appreciating the maternal perception of (1998) volume 8 issue 1
discomfort.
c) True.
d) True.
e) False. Postpartum haemorrhage is a common
sequel of placental abruption, but only rarely is
hysterectomy required for its control. Senior
obstetric input is mandatory in the management
of postpartum haemorrhage under these
circumstances, as it is of the utmost importance
that a hysterectomy is performed neither too
early nor too late.
25
Question 4: Anti phospholipid syndrome: Question, answer and discussion are taken from
a) The mechanism of action of antiphospholipid Self-assessment questions: Recurrent Abortion
antibodies is unknown. by H.J.A. Carp, Current Obstetrics &
b) In the presence of antiphospholipid Gynaecology (1999) volume 9 issue 1
antibodies, pregnancy losses occur with equal
frequency in all three trimesters.
c) The treatment of choice is with steroids and
aspirin.
d) Anticardiolipin antibody is a very specific
marker of pregnancy loss.
Answer: T, F, F, F, T
Various pathways have been suggested to

explain the action of antiphospholipid
antibodies: coagulation in small vessels leading
to the placenta, vasoconstriction owing to
inhibition of prostacycline, and disruption of the
phospholipid intracellular bridges between
elements of trophoblast.
In the presence of antiphospholipid antibodies,

approximately 60% of pregnancy losses will be
in the first trimester, but there is a heavy
preponderance (40%) of second- and third-
trimester losses. Various treatment regimens
have been used. At present heparin (or low-
molecular-weight heparin) and low-dose aspirin
seems to be the most effective regimen. Steroids
are no longer widely used owing to the possible
side effects. However, the issue is far from
settled.
Anticardiolipin antibody is a very non-specific

marker of pregnancy loss. It can be raised after
viral infections etc. It is only of real significance
if a high level is present, or if thromboses and/or
other autoantibodies are present.
Treatment of thrombophilias, has mainly been

found to be effective in cases of late pregnancy
loss rather in first trimester miscarriage.
26
Question 1: Regarding the diagnosis and Question 2: Concerning the epidemiology of

classification of hypertension in pregnancy: preeclampsia:
a) The phase 5 Korotkoff sound is more reliably a) The incidence of preeclampsia in primigravid
detected in pregnancy than the phase 4 sound. mothers in the UK is 1%.
b) ‘Significant proteinuria’ is denoted by the b) Preeclampsia is more common in the black
presence of 500 mg of protein in a 24 h population.
collection. c) The incidence of preeclampsia is higher in
c) The combination of hypertension and triploid pregnancy.
proteinuria always signifies the presence of d) The incidence of preeclampsia is higher in
preeclampsia. lower socio-economic groups.
d) The presence of oedema is a useful diagnostic e) The risk of developing preeclampsia is
sign. decreased in a pregnancy complicated by
e) Preeclampsia never presents before 20 weeks’ placenta praevia.
gestation.
Answer: F, T, T, T, T
Answer: T, F, F, F, F The incidence of pre-eclampsia in privigravid
women in the UK is between 7 and 10%. Some
Pre-eclampsia is generally defined as ethnic groups appear to be at increased risk and
hypertension of at least 140/90 mmHg measured in particular the black population is said to have
on at least two separate occasions and arising de an increased risk. It is, however, difficult to
novo after the 20 weeks’ gestation, in the separate this risk from other predisposing factors
presence of 300 mg of protein in a 24 h such as parity, obesity and an inherited tendency
collection of urine.While the rapid appearance of to essential hypertension. There is a well-
oedema (particularly when it involves the face) documented relationship between
may herald the advent of pre-eclampsia, this hyperplacentosis and the development of pre-
sign is not part of the diagnostic pattern and, eclampsia; thus, multiple, molar and triploid
indeed, is present in two-thirds of normal pregnancy are all associated with an increased
pregnant women. The combination of incidence of pre-eclampsia. Placenta praevia is
hypertension and proteinuria does not always traditionally said to confer a decreased risk of
signify preeclampsia. Renal disease often developing pre-eclampsia and certainly the
presents with proteinuria and may or may not be incidence of one is lower in the presence of the
accompanied by hypertension. This is the more other. However, the protective effect of placenta
likely diagnosis if the presentation is before 20 praevia may merely reflect the increased
weeks’ gestation. However, a hydatidiform mole incidence of earlier delivery associated with this
can rarely present in the first trimester with condition. A higher incidence of pre-eclampsia
preeclampsia. The measurement of blood has been reported in lower socio-economic
pressure in pregnancy has long been the subject groups. This difference most likely reflects
of much controversy. The evidence at present differences in age, parity, levels of antenatal
suggests that Korotkoff phase V sound is the care and smoking.
most reproducible endpoint in pregnancy.
Question, answer and discussion are taken from
Self-assessment questions: The pathogenesis of pre-
eclampsia, by L.C. Kenny, Current Obstetrics &
Gynaecology (1999) volume 9 issue 4
27
Question 3: Pre-eclampsia is associated with: d) Decreased maternal levels of vitamin E.

a) An increase in the maternal platelet count. e) An increase in the maternal ratio of
b) An increase in the maternal mean platelet prostacyclin to lipid peroxides.
volume.
c) A decrease in maternal thromboxane Answer: F, F, T, T, F
production.
d) An increase in circulating maternal levels of There are many emerging similarities between
b- the condition of atherosclerosis and pre-
thromboglobulin. eclampsia. The two conditions share a similar
e) An increase in platelet adhesion. lipid profile; low maternal maternal serum
concentrations of HDL cholesterol, raised
Answer: F, T, T, T, T concentrations of serum triglycerides, and
increased formation of small, dense LDL
Longitudinal analysis of the peripheral platelet particles. Furthermore, many of the risk factors
count in pregnancy has revealed that pre- for the two disorders are similar; obesity, black
eclampsia is associated with thrombocytopaenia. race, lipid abnormalities, insulin resistance and
As a result the mean platelet volume has been raised homocysteine concentrations all
reported to increase in preeclampsia. The predispose to atherosclerosis and pre-eclampsia.
population of larger platelets in this condition These similarities and the generally accepted
may be explained by increased consumption, role of oxidative stress in atherosclerosis,
leading to an increase in the proportion of support the emerging concept that reduced
immature, larger platelets in the peripheral placental perfusion interacts with maternal
circulation. There is substantial evidence of factors to generate oxidative stress in pre-
platelet activation in pre-eclampsia. Circulating eclampsia. The most important lipid-soluble
levels of factors stored within platelets reflect anti-oxidant in human plasma is vitamin E. In
platelet activation Several studies have reported normal pregnancy plasma levels of prostacyclin
increased levels of the platelet granule protein b- and vitamin E increase, whereas thromboxane
thromboglobulin in women with pre-eclampsia levels are decreased and serum levels of lipid
as compared with normal pregnant controls and peroxide remain relatively constant. In pre-
this elevation precedes the development of eclampsia, there is an imbalance in the
clinical signs by at least 4 weeks. Thromboxane thromboxane to prostacyclin ratio with elevated
production, as measured by urinary metabolites, maternal levels of lipid peroxides and decreased
is increased in women with pre-eclampsia. This levels of vitamin E.
increase in thromboxane production leads to an
increase in platelet adhesion and aggregation Question, answer and discussion are taken from
. Self-assessment questions: The pathogenesis of
Question 4: Pre-eclampsia is associated with: pre-eclampsia, by L.C. Kenny, Current
a) Increased maternal serum concentrations of Obstetrics & Gynaecology (1999) volume 9
highdensity issue 4
lipoprotein cholesterol.
b) Decreased maternal concentrations of serum
triglycerides.
c) Increased maternal serum homocysteine
concentrations.
28
Question 5: Maternal cardiovascular changes Question 8: Liver function:

associated with preeclampsia include: a) Normal pregnancy is associated with a
a) An increase in maternal plasma volume. decrease in maternal alkaline phosphatase.
b) A decrease in the maternal haematocrit. b) During normal pregnancy maternal levels of
c) A rise in the maternal plasma oncotic alanine transaminase (ALT) and aspartate
pressure. transaminase (AST) fall.
d) An exaggerated maternal arterial response to c) The principal pathological finding in the liver
angiotensin II. in pre-eclampsia comprises of periportal fibrin
e) An exaggerated maternal arterial response to deposition, haemorrhage and hepatocellular
bradykinin. necrosis.
d) An increase in maternal levels of
Answer: F, F, F, T, F transaminases in pre-eclampsia reflects
hepatocellular damage.
In normal pregnancy, plasma volume increases e) Lactate dehydrogenase levels are a reliable
by about 40% and leads to a fall in the marker of haemolysis.
haematocrit. The traditional and most widely
accepted model of the haemodynamic Answer: F, T, T, T, T
characteristics of pre-eclampsia is one of a
relatively reduced plasma volume, The relative haemodilution of normal pregnancy
vasoconstriction and resulting hypoperfusion of leads to an approximate 20% reduction in the
organs such as the placenta and kidneys. Thus, level of circulating liver enzymes in pregnancy,
the haematocrit in pre-eclampsia is typically with the exception of alkaline phosphatase,
increased. The reduced plasma volume which normally increases with increasing
associated with pre-eclampsia reflects the shift gestation. Abnormal liver function in pre-
of fluid into the extravascular space across leaky eclampsia reflects liver dysfunction occurring as
capillary membranes. Increasing proteinuria in a result of vasoconstriction of the hepatic bed.
pre-eclampsia leads to marked Elevated levels of transaminases reflect
hypoalbuminaemia and a fall in plasma oncotic heptocellular necrosis. Haemolysis may increase
pressure. In normal pregnancy, a relative arterial asparate transaminase, but will
refractoriness to angiotensin II develops. This disproportionately increase lactate
can be detected as early as 8 weeks and is dehydrogenase levels with serial measurements
maximal at term. In women who develop pre- providing a reliable indicator of the degree of
eclampsia, the pressor response to angiotensin II haemolysis present. The histopathology of the
remains relatively greater than in normal liver in pre-eclampsia comprises peri-portal
women. Ex vivo studies have demonstrated that fibrin deposition, haemorrhage and heptocellular
endothelium- dependent relaxation to numerous necrosis. It is thought that segmental hepatic
substances, including bradykinin, is impaired in vasospasm leads to localized coagulopathy
arteries isolated from women with pre- allowing fibrin deposition while endothelial and
eclampsia. The combination of these two liver-cell necrosis produce haemorrhage.
findings may contribute to the relative
vasoconstriction associated with pre-eclampsia. Question, answer and discussion are taken from
Self-assessment questions: The pathogenesis of pre-
eclampsia, by L.C. Kenny, Current Obstetrics &
Gynaecology (1999) volume 9 issue 4
29
Question 7: Changes in the coagulation system levels of fibrinopeptides in women with pre-
in pre-eclampsia include: eclampsia as compared with normal pregnant
a) An increase in maternal levels of antithrombin women. Anti-thrombin III is produced by the
III. liver and is an important inhibitor of
b) An increase in maternal levels of factor VIII coagulation. Levels are unchanged in normal
related antigen. pregnancy but are decreased in the majority of
c) A decrease in maternal levels of women with pre-eclampsia. The decline in anti-
fibrinopeptide A. thrombin III activity is thought to result from
d) A decrease in maternal levels of protein C. increased consumption and has been reported to
e) An increase in maternal levels of protein S. precede the development of clinical signs by as
much as 13 weeks. Protein C is a potent
Answer: F, T, T, T, F inhibitor of activated factor V and VIII, and is
an activator of fibrinolysis. Levels are
In normal pregnancy, the overall state of the substantially reduced in pre-eclampsia.
coagulation system is one of activation. Activated protein C resistance resulting from a
Evidence for this comes from studies which mutation in coagulation factor V has now
report increased concentrations of clotting emerged as a leading cause of thrombosis in
factors and raised levels of highmolecular- pregnancy and a recent report links the HELLP
weight fibrinogen complexes. Sensitive studies syndrome with factor V mutation. Protein S
of coagulation factors provide evidence that serves as a cofactor for activated protein C.
pre-eclampsia accentuates a state of Levels of protein S in pregnancy may decrease
hypercoagulability already created in normal to levels similar to those with congenital protein
pregnancy. During normal pregnancy, the levels S deficiency. Furthermore, levels of protein S
of factor VIII coagulation activity and factor- decrease further in women with pre-eclampsia,
VIII-related antigen show a proportional rise as compared with normal pregnant controls.
and, thus, their ratio remains constant. In pre-
eclampsia, there is an early rise in the factor- Question, answer and discussion are taken from
VIII-related antigen:coagulation activity ratio Self-assessment questions: The pathogenesis of
which correlates with the severity of the disease. pre-eclampsia, by L.C. Kenny, Current
This increased ratio is a result of increased Obstetrics & Gynaecology (1999) volume 9
levels of factor- VIII-related antigen. This issue 4
substance is synthesized by endothelial cells and
megakaryocytes and is released by aggregating
platelets. It, therefore, seems probable that the
increase in circulating levels is a result of
endothelial damage and platelet aggregation.
The action of thrombin on fibrinogen is a crucial
step in the coagulation cascade. Thrombin
cleaves two pairs of peptides, fibrinopeptides A
and B from fibrinogen to produce fibrin.
Fibrinopeptide concentrations are considered to
be the best markers of accelerated thrombosis.
The majority of studies have reported increased
30
Question 6: Concerning renal function in pre- Question 10: Eclampsia:

eclampsia: a) Is an absolute indication for delivery.
a) The proteinuria of pre-eclampsia results b) Complicates 15 in 10 000 maternities in the
mainly from a loss of intermediate weight UK.
proteins. c) Can occur in the absence of significant
b) The rate of increase in the amount of hypertension.
proteinuria is both a sensitive and specific d) Leads to death most commonly by cerebral
predictor of maternal outcome. haemorrhage.
c) Glomerular filtration deteriorates first and is e) Can result in cortical blindness.
followed by a deterioration in tubular function.
d) Hyperuricaemia generally develops before Answer: T, F, T, T, T
proteinuria.
e) Glomerular endotheliosis is present in all The principal and clinically most disturbing
cases of established pre-eclampsia. cerebral sequelae of pre-eclampsia are eclamptic
convulsions. Eclampsia is defined as the
Answer: T, F, F, T, F occurrence of one or more convulsions, not
attributable to other cerebral conditions in a
Renal function deteriorates in pre-eclampsia in patient with pre-eclampsia. It should be noted,
two stages. The first stage involves impairment however, that eclampsia can rarely present in the
of tubular function and this is reflected by a absence of significant hypertension. The
reduction in uricacid clearance and the reported incidence varies geographically; figures
development of hyperuricaemia. Later, from the UK suggest the incidence to be 4.9/10
glomerular filtration becomes impaired and 000 maternities. Eclampsia is thought to result
proteinuria of intermediate selectivity develops. from focal cerebral vasospasm and
An increasing plasma urate is thus an early sign hypoperfusion leading to abnormal electrical
in the evolution of pre-eclampsia and proteinuria activity and seizures. The lack of any
is conventionally recognized as a late sign. The neurological deficit following uncomplicated
presence of proteinuria heralds a poorer eclampsia supports the concept that vasospasm
prognosis for the fetus, but the actual amount of precipitates the convulsions. This is in contrast
proteinuria and the rate of increase have been to convulsions caused by thrombosis and
found to be poor predictors of maternal or haemorrhage, as is often the case in postpartum
perinatal outcome. Renal biopsy in established eclampsia, when significant cortical damage
cases of pre-eclampsia demonstrates a may occur, including the development of
characteristic non-inflammatory lesion cortical blindness. The commonest cause of
commonly referred to as glomerular death in women dying with eclampsia is cerebral
endotheliosis. This primarily involves a haemorrhage.
combination of swelling of the glomerular
endothelial cells and sub-endothelial ‘fibrinoid’ Question, answer and discussion are taken from
deposits, which encroach on and occlude the Self-assessment questions: The pathogenesis of pre-
capillary lumen. This lesion is characteristic, but eclampsia, by L.C. Kenny, Current Obstetrics &
not pathognomonic of pre-eclampsia, as normal Gynaecology (1999) volume 9 issue 4
renal pathology has been described in some
cases.
31
Question 9: Regarding drug treatment in pre- intrauterine growth retardation, oliguria, renal
eclampsia: failure and neonatal anuria in late pregnancy,
and are thus contraindicated in pregnancy.
a) Angiotensin-converting enzyme inhibitors are
not associated with serious side effects in the Question, answer and discussion are taken from
antenatal period. Self-assessment questions: The pathogenesis of pre-
b) Peak plasma levels of methyldopa are reached eclampsia, by L.C. Kenny, Current Obstetrics &
24 h after an oral dose. Gynaecology (1999) volume 9 issue 4
c) Labetolol is a combined a- and b-
adrenoceptor blocker.
d) Nifedipine can be safely used concomitantly
with magnesium sulphate.
e) Hydrallazine has no effect on uteroplacental
blood flow.
Answer: F, F, T, F, F
The hypertension of pre-eclampsia is caused by

increased peripheral resistance and drug
treatment is directed towards relieving this
without compromising cardiac output.
Methyldopa has been extensively studied in
pregnancy and is the agent of choice for chronic
blood-pressure control. It reduces systemic
vascular resistance without significantly altering
heart rate or cardiac output. Peak plasma
concentrations are reached after 2 h, although
the maximum fall in arterial pressure occurs 4–8
h after an oral dose. Labetolol is a combined a-
and b-adrenoreceptor blocker. The a1 blockade
induces vasodilatation with little change in the
cardiac output. Nifedipine can be used for acute
or chronic treatment and appears to be safe in
pregnancy. It lowers systemic vascular
resistance and improves cardiac output without
adversely comprising uteroplacental blood flow.
It is, however, best avoided in combination with
magnesium sulphate as profound hypotension
may result. Hydrallazine is used for the acute
management of hypertensive crises. It too lowers
systemic vascular resistance, but it has a variable
effect on uteroplacental blood flow and can
occasionally lead to fetal distress. Angiotensin-
converting enzyme inhibitors are associated with
32

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1

Obstetrics & Gynaecology

Dr Win Win Than

Wong & Low O & G Short Cases Record

Our Aim : Made it easy to do it right!

Common Questions & Answers

Short Case Record for uterine mass (Fibroid)

I would like to complete my examination by doing a speculum & bimanual examination.

My differentials for this mass are:

Differential diagnoses (depends on symptoms)

Wong & Low O & G Short Cases Record

What are the investigations you would like to do?

How would you manage her?

Submucosal fibroids may be resected hysteroscopically. Pedunculated, subserosal myomas can be

What are the new methods for treating fibroid?

What is the incidence of uterine fibroids?

What are the sites of origin?

What are the clinical features of leiomyoma?

What are the risk factors of developing fibroids?

What are the protective factors of developing fibroids?

What are the complications of fibroids?

What the potential effects of fibroids on pregnancy?

What are the common associated conditions?

What is the rare association with fibroids?

What is the pathogenesis of leiomyomas?

Epidemiology Commonest benign uterine tumor. Less common.

Age group 30-40 years old 40-50 years old (uptodate)

Clinical manifestation Menorrhagia Dysmenorrhea

Size Any size < 14 weeks size

Tenderness Non tender mass Usually tender mass

Facts about GNRH analogue

Routes of administration Goserelin acetate (3.6 mg/month subcutaneously or 10.6 mg

Benefits Reduce fibroid size, less bleeding intra-operatively.

10 teachers : Obscure tissue planes around fibroids making surgery

Wong & Low O & G Short Cases Record

Short Case Ovarian Cyst

On percussion, there is dullness over the mass. No signs of free fluid.

What are the complications of ovarian cyst? THIN RIM

 Torsion, haemorrhage, infection, necrosis, rupture, intestinal obstruction, malignant change

Differentiate mass between ovarian and myoma

Wong & Low O & G Short Cases Record

 General: Elderly, Cachectic, pale

 Bloody ascitic fluid

Wong & Low O & G Short Cases Record

Uterus Larger than Date

What are the causes for uterus larger than date?

How would you manage this case?

Wong & Low O & G Short Cases Record

Uterus Smaller than date

SFH is 3cm less than the gestational age in weeks.

What are the causes of uterus smaller than date?

 Mother: wrong dates, oligohydramnios, missed miscarriage, IUD

Causes of asymmetrical IUGR include:

What are the complications of FGR?

Wong & Low O & G Short Cases Record

Discuss management options for a breech presentation at 38 weeks.

What is the incidence of breech presentation?

What are classifications of breech presentation at term?

What are the etiology of breech presentation?