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PREFACE & ACKNOWLEDGEMENT

Special appreciation to our beloved seniors of MD UPM for their pioneering efforts in
compiling all these notes during their years of study.

In this edition, we humbly added several topics into this compilation and updated
some information from the latest guidelines.

This book of 11th Teachers is primarily a compilation of notes and tips that were
obtained throughout the O&G posting from lectures, bedsides teachings and the
“Fertility Lab late night classes”. Bear in mind, this is not a textbook. Go read your
10th Teachers and etc too.

We hope you find this book useful and informative as a guidance throughout your
posting in year 4 & 5!

Let us all pray for our beloved lecturers who are always dedicated in teaching and
guiding us all. May God bless and shower them and their family with all of His
kindness and His love.

Edition @ 2021
MD 21 El Salvador
Contributors: Reviewers:
1. Adib Farhan 1. Thamara
2. Afnan Azhar 2. Sandeep
3. Alicia 3. Ghananarth
4. Alvina
5. Anisah
6. Jegathis
7. Khalilah
8. Nik Qabila
9. Wan Iffah

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TABLE OF CONTENTS
PREFACE & ACKNOWLEDGEMENT 1
TABLE OF CONTENTS 2

CLERKING TIPS 5

1.0 DATING ULTRASOUND SCAN ASSESSMENT 8

2.0 EARLY PREGNANCY BLEEDING 12


2.1 ECTOPIC PREGNANCY 14
2.2 MISCARRIAGE 17
2.3 GESTATIONAL TROPHOBLASTIC DISEASE/ HYDATIDIFORM MOLE (MOLAR PREGNANCY) 19
3.0 ANTEPARTUM HAEMORRHAGE 24
3.1 PLACENTA PREVIA 27
3.2 PLACENTA ABRUPTIO 35
3.3 MORBIDLY ADHERENT PLACENTA 39
3.4 CERVICAL MALIGNANCY 40
3.5 INDETERMINATE APH 40

4.0 LEAKING LIQUOR (PROM, PPROM) 41


4.1 PREMATURE PRELABOUR RUPTURE OF MEMBRANE (PPROM) 45

5.0 ANEMIA IN PREGNANCY 54

6.0 DIABETES IN PREGNANCY 60


6.1 GESTATIONAL DIABETES MELLITUS 74

7.0 HYPERTENSIVE DISORDERS IN PREGNANCY 76


7.1 GESTATIONAL HYPERTENSION/ PREGNANCY-INDUCED HYPERTENSION (PIH) 79
7.2 PRE-ECLAMPSIA 83
7.3 ECLAMPSIA 85
7.4 CHRONIC HYPERTENSION IN PREGNANCY 89
8.0 TWIN/MULTIPLE PREGNANCY 90

9.0 BREECH PRESENTATION 97

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10.0 LABOUR 106

MANAGEMENT OF LABOUR 106


10.1 PROCESS OF NORMAL LABOUR 106
10.2 STAGES & ABNORMALITIES IN LABOUR 107
11.0 INDUCTION OF LABOUR 117
11.1 TYPES OF INDUCTION OF LABOUR (IOL): 120

12.0 OBSTETRICS EMERGENCIES 122


12.1 CORD PROLAPSE 122
12.2 SHOULDER DYSTOCIA 125
12.3 AMNIOTIC FLUID EMBOLISM 127
12.4 POSTPARTUM HAEMORRHAGE 129

13.0 INSTRUMENTAL DELIVERY 133

14.0 CESAREAN SECTION 136

15.0 MENSTRUAL DISTURBANCE 141

16.0 DYSFUNCTIONAL UTERINE BLEEDING (DUB) 147

17.0 DISORDER OF MENSTRUAL CYCLE 150

18.0 ENDOMETRIOSIS 154

19.0 ADENOMYOSIS 161

20.0 PELVIC INFLAMMATORY DISEASE (PID) 162

21.0 UTERINE FIBROIDS 165

22.0 POSTMENOPAUSAL BLEEDING 171

23.0 POSTCOITAL BLEEDING 173

24.0 CERVICAL CANCER 174


24.1 CERVICAL CANCER SCREENING 179

25.0 OVARIAN CANCER 182

26.0 HYPEREMESIS GRAVIDARUM 195

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APPENDIX 198
A1. PARTOGRAPH 198
A2. CARDIOTOCOGRAPHY (CTG) 199
A3. TYPE OF INSULIN VIALS 199
A4. MODIFIED BISHOP’S SCORE 200
A5. SHORT CASE OBSTETRIC DR QUE SCRIPT 201
A6. SHORT CASES IN GYNAECOLOGY DR QUE SCRIPT 206

REFERENCES 214

4
CLERKING TIPS

5
6
OBSTETRICS

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1.0 DATING ULTRASOUND SCAN ASSESSMENT
1. Singleton/multiple pregnancy and chorionicity (best assessed during 11+0 - 13+6 weeks)
2. Viability ( fetal heart should be seen if CRL>7mm around 7 weeks )
3. Confirmation of gestational age the earlier the better.
a. If gestational age calculated at 9th week, and another scan done at 12th week showing
4 days discrepancy, we stick with the first scan (9th week).

Rule in Deciding EDD


(References : ACOG)

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Ultrasound Assessment :
Parameter Notes

First Trimester 1. Dating scan 10-13 weeks


2. Best to detect ectopic pregnancy between 5-8 weeks
3. Full bladder is necessary for transabdominal scan in
early pregnancy
4. In transvaginal scan, empty bladder is necessary

Gestational Sac 1. Earliest sign of pregnancy


2. Can be as seen as early as 4.5-5 weeks using TVS
3. A normal GS grows by 1mm per day
4. GS > or equals to 25mm without visbile fetal pole:
likely to be a missed miscarriage
5. Yolk sac should be seen at GS diameter of 18mm
vaginally or 25mm abdominally

Crown Rump Length (CRL) 1. Measurement from the top to bottom or the crown
to rump, excluding the limbs
2. CRL > or equals to 7mm without heartbeat likely to
be missed miscarriage
Pregnancy is considered non-viable on TVS if :
1. No fetal pole when Mean sac diameter >25mm
2. No fetal heart beat when CRL > 7mm

2nd and 3rd Trimester ● Presence or absence of fetal heart activity, number
of fetus lie and presentation of fetus
Parameters:
1. BPD
2. HC
3. AC
4. FL
5. AFI/DVP
6. Placental

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Biparietal diameter (BPD) Landmarks;
1. Midline falx cerebri,
2. Cavum septum pellucidum (SCP),
3. Thalami,
4. Lateral ventricle,
5. Symmetrical margin of skull vault.

● Measure after 13 weeks (or CRL> 84mm)


● Diameter between the 2 sides of the head
● Measurement taken from the outer edge of the near
cranium to the inner edge far cranium

Head circumference (HC) Landmarks : Same as BPD


Measure the outer margin of the bony skull

Abdominal circumference (AC) Landmarks;


1. Spine and rib
2. Stomach bubble
3. Part of portal vein
4. Should be as round and smooth in shape
5. Measure the outer edge of circumference

● Reflects fetal size and weight


● Serial measurement useful in monitoring fetal
growth
● Should NOT be used for dating

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Femur length (FL) 1. Femoral shaft seen as a slightly curved, echogenic
structure that produces acoustic shadow
2. To monitor the growth of long bones
3. Measure the longest dimension of femoral shaft
4. The femoral epiphysis, seen as a spike at the end of
femoral shaft is not included in the measurement
5. Most accurate when the femur is perpendicular to
US beam
6. Femur image should be at angle to less than 45
degrees to the horizontal
7. Choose the femur closest to the transducer
8. Obtain longitudinal view of femur
9. Measure along femur diaphysis, exclude the distal
femoral epiphysis

AFI / DVP 1. A single measurement of deepest vertical pole


(normal is between 2-8cm)
2. A sum of measurement of maximum vertical pole in
each four quadrants of the uterus (normal between
5-25cm)
3. Transducer should be placed perpendicular to
patient’s spine/ floor
4. Measure the anterior-posterior diameter of the
largest empty pockets

Placenta 1. Examination of placenta should includes its position,


configuration and abnormalities such as
velamentous insertion, bilobed placenta and
succenturiate lobe
2. Should the placenta be low lying or covering the os,
a repeat examination at 28-30 weeks should be
performed to exclude placenta praevia

Adopted from Dr Ifitida’s Slides on “Ultrasound for Undergraduates”

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2.0 EARLY PREGNANCY BLEEDING
DEFINITION:
Bleeding in pregnancy before 24 weeks gestation (some practise says 22 weeks).

HISTORY:
● Quantify the blood loss (spotting/number of pads changed/any blood clot).
● Any abdominal pain?
● Passing out product of conception (POC)?
● Trauma (abdominal/perineal?)

PHYSICAL EXAMINATION:
● General : pallor, blood pressure, pulse rate, pulse volume
● Abdomen : uterus size, tenderness, guarding, rebound tenderness
● Speculum : Amt of bleeding, os dilatation, cervical mass, product of conception
● Vaginal examination: cervical excitation, adnexal mass/tenderness

INVESTIGATION
● UPT
● FBC
● TAS/TVS

DIFFERENTIAL DX (ΔΔ):
1. Ectopic pregnancy
2. Miscarriage
3. Molar pregnancy
4. Pregnancy of unknown location
5. Local causes (trauma/tumour)

IMPORTANT

For any woman at reproductive age presenting with per vaginal bleed or abdominal
pain, MUST RULE OUT ECTOPIC PREGNANCY! MUST DO UPT!

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2.1 ECTOPIC PREGNANCY

DEFINITION:
● Gestation that implantation occurs outside the uterine cavity.

RISK FACTORS:
1. History of tubal inflammation (ie; PID / endometriosis)
2. History of tubal surgery
3. Use of Assisted Reproductive Technologies
4. Previous history of ectopic pregnancy

SITES OF ECTOPIC PREGNANCY:

CLINICAL FEATURES:
● Symptoms
○ Triad of missed menses + PV bleed + lower abdominal pain
○ Ipsilateral shoulder pain (phrenic nerve irritation) in ruptured ectopic
● Signs
○ Pallor
○ Abdominal tenderness
○ Abdominal distension
○ Vaginal exam : slight enlarged uterus, tender adnexae, positive cervical excitation

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INVESTIGATIONS:
● UPT
● Serum B hCG (low)
● Pelvic ultrasound (Transvaginal Ultrasound, TVS)
○ Empty uterus
○ Free fluid in POD
○ Double ring sign (non-rupture)

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POSSIBLE CASE SCENARIO @ SCRIPT FOR ECTOPIC PREGNANCY

CHIEF COMPLAINT

Madam _____ is a ____ year old Malay housewife, gravida __ para __ at ___ weeks of
period of amenorrhea (POA), was admitted to the ward due to lower abdominal pain 2 day prior
to the admission that associated with per vaginal bleeding.

HISTORY OF PRESENT PREGNANCY

The first day of her last normal menstrual period (LMNP) was on ___________. She was
sure of the date. Her menstrual cycle was regular, she was not on oral contraceptive pills (OCP)
and not breastfeeding at that time. Therefore, her expected date of delivery (EDD) is on
__________.

This is a planned pregnancy. Her pregnancy was confirmed by a positive urine pregnancy
test (UPT) done by herself after her period was delayed for ______ weeks and she had
symptoms of early pregnancy such as nausea, vomiting and headache.

Her pregnancy was well and she had no complaints until 2 days prior to the admission
which corresponded to 8 weeks POA where she started to have lower abdominal pain that is
more to the left side. The pain was sudden onset, colicky in nature, continuous and
non-radiating. It was aggravated by movement and relieved by rest. However she did not take
any medication to relieve the abdominal pain. Beside that, she also experienced per vaginal
bleeding which was fresh blood with no blood clot, no vesicle or product of conception. She had
to wear 1 pad per day which was partially soaked. Furthermore, she had no fever, giddiness,
shoulder tip pain, palpitation or syncope attack. She also had no nausea, vomiting, bladder or
bowel problems. Therefore, she went to HKL to seek treatment. Ultrasound scan was performed
in Early Pregnancy Assessment Unit (EPAU) and she was told that her uterine cavity was empty
and presence of extrauterine cystic mass with fetal heart activity found at ?

Therefore, she was admitted to wad 15 for further management. Physical examination
was done by the doctor and found that there was tenderness at the left lower quadrant.
Abdominal ultrasound and transvaginal ultrasound were performed in the ward to reconfirm the
presence and the site of the extrauterine pregnancy. She was told that there was a viable
extrauterine fetus in a gestational sac which was located at the left fallopian tube. The fetus was
corresponding to eight weeks of POA. She was advised by the doctor to terminate the pregnancy
because it may jeopardize her life if the sac ruptures. Therefore, she was planned for an
emergency laparoscopic salpingectomy.

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2.2 MISCARRIAGE

DEFINITION:
Fetal loss between the time of conception & the time of fetal viability (at 24 weeks gestation) OR
expulsion of a fetus or embryo weighing <500g

● Product of conception :
○ Placental tissues
○ Fetal tissues

CAUSES OF MISCARRIAGES:

General maternal factors Local Maternal Factors

1. Advanced maternal age 3. Congenital uterine abnormalities


2. Maternal medical conditions 4. Acquired uterine abnormalities
a. DM ➝ fetal anomaly a. Submucous fibroid
b. Hypo/Hyperthyroid b. Endo polyps
c. CKD c. Asherman syndrome
d. SLE 5. Cervical incompetence
e. Antiphospholipid syndrome ➝
antibody production

Fetal Abnormalities

Often due to chromosomal abnormalities

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TYPES AND CLINICAL FEATURES OF MISCARRIAGES:

Miscarriage Assessment TAS / TVS Management

THREATENED ● Minimal bleeding IUGS with viable embryo Conservative


● Os closed

INCOMPLETE ● Usually significant ● Previous scan with IUGS Suction and


bleeding ● Current scan no IUGS + curettage
● Os opened intrauterine thickness of >
15mm

COMPLETE ● Bleeding usually ● Previous scan with IUGS/ No Conservative


stops after Previous scan but patient bring
passing out POC POC
● Os closed ● Current scan without IUGS and
intrauterine thickness of
<15mm

INEVITABLE ● Bleeding with ● IUGS with viable/non viable Conservative


abdominal pain embryo Analgesia
● Os opened

MISSED ● Usually minimal ● IUGS with mean sac diameter Conservative


bleeding (MSD) >25mm but no embryo Suction and
● Os closed OR curettage (pt
● IUGS with embryo CRL > 7mm preference after
but non-viable (no fetal heart counselling)
activity)

SEPTIC ● Cervical excitation Can be incomplete/ inevitable/ IV Cefuroxime


● Sign of sepsis missed miscarriage Metronidazole
(fever/ Suction and
tachycardic/ curettage
hypotensive/
acidotic)

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2.3 GESTATIONAL TROPHOBLASTIC DISEASE/ HYDATIDIFORM
MOLE (MOLAR PREGNANCY)

TYPES OF MOLAR PREGNANCIES:


1. Hydatidiform (Complete mole)
2. Partial mole
3. Choriocarcinoma*
4. Invasive mole (rare)
5. Placenta site trophoblastic tumour, PSTT (rare)

*Choriocarcinoma: can arise from normal pregnancy but rare, presented as secondary postpartum
haemorrhage

CLINICAL APPROACH:
1. Molar pregnancy
○ Age: (at 2 extreme ages)
■ Scenario 1 : 20yo, primigravida came with PV bleed, differential
diagnosis- ectopic pregnancy, molar pregnancy, miscarriage
■ Scenario 2 : 40yo with PV bleed-miscarriage due to chromosomal
abnormalities, molar pregnancy
○ History of previous molar pregnancy
○ ABO group (A>O in choriocarcinoma)

CLINICAL FEATURES:

Classical presentation Physical examinations

1. PV bleeding in early pregnancy 1. Increased BP


2. Passing out vesicles 2. Uterus larger than date
3. Excessive symptoms of early pregnancy 3. Palpable mass in L/R adnexa
4. Hyperthyroid symptoms 4. Consistency of uterine mass is doughy
5. Acute abdomen (rare) in case of torted
or ruptured theca lutein cyst

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EXAM TIPS

Q1 : Why do we need to differentiate between complete and partial mole?


A1 : To determine the frequency of follow up due to the higher risk of getting choriocarcinoma
in complete mole compared to partial mole

Q2 : How do we confirm molar pregnancy?


A2 : By doing HPE

Q3 : Do all patients presented with these?


A3 : NO, only complete mole patients can present with all these symptoms and signs BUT NOT
ALL

Q4 : Why do patients with partial mole may not/ rarely be presented with ALL these sm + sn?
A4 : Because, usually in partial mole, B-HCG is just slightly higher than in normal pregnancy as
compared to complete mole. Therefore patients with partial mole may not/ rarely be presented
with all these sm + sn.

INVESTIGATIONS:
Q5 : How to diagnose molar pregnancy?
A5 :
1. USS: multiple sonolucent appearance with various shapes and sizes in the uterine
cavity (snowstorm appearance), fetal echo (present: partial, absent: complete),
presence/absence of ovarian cyst (theca lutein cyst)
2. Blood test: Beta HCG> 100, 000IU/L

Q6 : But can both of the tests confirm the diagnosis?


A6 : NO, they can only suspect. Therefore, to confirm we need to do HPE.

**Theca lutein cyst most likely appears in complete mole, because to have the TLC, very high levels
of B-HCG is needed, which can be found in complete mole.

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MANAGEMENTS:
Once diagnosed with molar pregnancy:

1. Admit the patient to ward


2. Do a suction and curettage (S&C)
3. Do FBC, coagulation profile, GXM because worry of bleeding during S&C
a. Why do we worry about bleeding in S&C?
i. because placenta is very vascularised
ii. because uterus is very soft, therefore easy to perforate
iii. because uterus is contracted following S&C, therefore risk of uterine
atony
4. Acquire consent from the patient.
5. S&C done by specialists because : they are more aware of the complications such as
uterine atony and give oxytocin to contract uterus making it hard and not easily
perforated.
6. Do blood test for Beta HCG monitoring.
7. Discharge the patient after 2 days and follow her up at the molar clinic: need to
follow up because risks of choriocarcinoma, follow up 1 week later to see whether
there are any complications of the S&C done, to review the HPE results and to see
the B-HCG levels.

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POSSIBLE CASE SCENARIO @ SCRIPT FOR MOLAR PREGNANCY

CHIEF COMPLAINT

Madam X, a __ year-old Malay housewife, in her __ pregnancy presented with per


vaginal bleeding for the past 5 days. Currently, she was at ____weeks POA, admitted because
suspected of molar pregnancy and for further management.

Her first date of her last normal menstrual period (LMNP) was on __. She was sure of
the date. Her menstrual cycle was regular, she was not on an oral contraceptive method and not
breastfeeding at that time. Therefore, her expected date of delivery (EDD) is on __.

HISTORY OF PRESENT PREGNANCY

This is unplanned but wanted pregnancy. She was suspected that she had been pregnant
after she missed her period for ___ weeks and experienced symptoms of early pregnancy such
as nausea, vomiting, lethargy and headache. She complained about having episodes of excessive
vomiting for 3 days, and realized that those pregnancy symptoms are worse than symptoms that
she experienced for her other child. It was severe since she cannot do her housework when the
symptoms attack. Indeed, the pregnancy was confirmed by +ve UPT done at the private clinic.
However, no ultrasound was performed for her at that clinic.

Two weeks later which is at 8 weeks POA, she experienced one episode of abdominal
pain. (Describe the pain – SOCRATES). Because of this problem, she presented herself for the
2nd time to the same private clinic. She was examined and had been given injection which I
assume was analgesics. Then, the pain was relieved.

After that, she complained of brownish per vaginal bleeding for 5 days continuously. She
used 3 pads per day which were totally soaked. There are no blood clots and no flooding. She
claimed that she had passed out vesicles at that time. However, she denied having any
symptoms of anaemia such as lethargy, breathlessness and palpitation. She became worried of
miscarriage so she seek treatment at the same private clinic. Since there is no ultrasound facility
in that private clinic, then she was referred to MHKL for further management of her problem on
the same day. Upon further questioning, she still complained of symptoms of early pregnancy
such as nausea, vomiting and headache. However, she has no symptoms of thyrotoxicosis such
as heat intolerance, tremor, palpitation, loss of weight and increased appetite.

At MHKL, early ultrasound was done to confirm the diagnosis. She was told that the
result suggestive of molar pregnancy which I think showed a snow storm appearance. Blood was
sent for investigations which I assumed was FBC, beta hCG and renal profile. Chest X-ray was
also performed for worries of metastasis. She was kept nil by mouth on that night and suction
and curettage was performed on the next day.

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3.0 ANTEPARTUM HAEMORRHAGE
DEFINITION:
APH can be defined as any bleeding from the genital tract that occurs in a pregnant lady after 22
weeks of gestation and before the onset of labour. (RCOG defined at 24 weeks)

The possible causes of APH include:


1. Placental causes
a. Placenta praevia (which is the most common)
b. Abruptio placenta
c. Vasa praevia
2. Local causes (very rare)
a. Trauma
b. Cervical ectropion *erosion
c. Cervical polyps
d. Cervical malignancy
3. Medical causes particularly Von Willebrand dz (but rare)
4. Patient on anticoagulant which is uncontrolled
5. Indeterminate APH

COMPLICATIONS:
● The possible cx is increased maternal morbidity and mortality as well as fetal morbidity &
mortality.
● If massive bleeding, it will cause hypovolemic shock which if not treated will lead to DIVC &
subsequently will cause maternal death.
● As massive bleeding requires blood transfusion, it will increase risk of blood borne dz such
as Hepatitis B, HIV. If mismatch happens it will cause maternal death.
● In certain cases of APH, it increases risk of preterm delivery which will lead to
○ Premature baby
○ Birth asphyxia (baby collapse with 0 Apgar score, can coz cerebral palsy)
○ IUD (massive bleeding)

How do you manage a patient who presented with bleeding (APH)?

● Firstly, I would like to admit the pt to the ward. Any patient who presented with per vaginal
bleeding after 24 weeks POA have to be admitted to the ward.
● I need to assess the severity of the bleeding by putting the patient on a pad chart.
● If pt presented with massive bleeding, I would like to stabilize the pt by resuscitating and
start with ABC.
● Once pt is hemodynamically stable, I would like to ask detail hx, do thorough P/E and
relevant Ix to rule out underlying causes.
○ If the bleeding a/w abdominal pain and hx of blunt trauma such as MVA, it may be
suggestive of abruptio placenta,

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○ If it is painless PV bleeding, it is most likely due to PP or other causes,
○ I would like to ask previous hx of PP,
○ Besides that, I would like to ask about the RISK FACTORS of PP such as:

Maternal RF Fetal RF

1. Previous uterine surgery 1. Macrosomic baby


a. Caesarean section 2. Multiple pregnancy
b. Myomectomy
c. ERPOC
2. Advanced maternal age
3. Multiparity
4. Smoker, drug abuse, alcohol
5. Previous hx of PP

○ I would also like to ask what type of pain – regular abdominal pain which increases
in intensity is most likely due to labour pain that sometimes present with heavy
show,
○ (Local causes) I would like to ask whether pt had any gynaecological hx such as
cervical polyps, cervical malignancy, cervical ectropion and vasa praevia,
○ Any significant hx of gynaecological symptoms such as intermenstrual bleeding or
prolonged menses which may give the idea of cervical polyps.
○ Besides that, I would like to ask whether the pt have done a recent pap smear test
or not. If she had done, where?, when?, and the result?
○ (Medical hx) I would like to ask for any coagulation disorder such as VWD.
○ I also would like to ask whether pt is on anticoagulant or not? If yes, is it controlled
or uncontrolled?
*** Further management of APH depends on the causes and POA.

What to do during physical examination?

1. General examination – any sign of anaemia? pallor, tachypnoeic


2. Vital sign – PR,b/p,T
3. Local causes – any foreign body?
4. Per abdomen look for
a. Any evidence of abruptio
b. Tense and tender abdomen
c. Any evidence of trauma
d. Presentation of fetus
e. Scar in the abdomen
f. Baby alive or not

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### V/E is strictly contraindicated in APH unless PP is excluded ###
INVESTIGATIONS:

1. I would like to proceed with ultrasound to


a. Locate the placenta
b. Confirm the lie & presentation of fetus
c. Look for fetal growth
d. Look for transplacental clot (in abruptio)
2. I would also like to do FBC, PT and APTT to assess the pt’s condition
3. If it is not PP, we need to do a speculum examination to look for local causes.

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3.1 PLACENTA PREVIA

AETIOLOGY:
1. Previous uterine surgery (myomectomy, TOP, CS)
2. Advanced maternal age
3. Multiparous
4. Multiple pregnancy
5. Previous history of PP
6. Smoking

Can we suspect major PP by palpation?


YES, if presenting part not engaged and there is unstable or abnormal lie

Can we locate the type of PP (whether anterior/posterior) by palpation?


YES, if the presenting part is easily felt-posterior

LONG TERM COMPLICATIONS


● Risk of recurrent PP
● Risk of scar dehiscence/rupture
● High risk of placenta accreta/increta/percreta

MANAGEMENT OF PP:
Depends on factors: Symptomatic /asymptomatic? What is POA? How severe is the bleeding?

● All PP have to be admitted to the ward following Mcafee Regime (1945) which is to admit
patients in tertiary centers until delivery, blood bank back-up available, 24 hours OT
facilities, close monitoring of any PV bleeding and liberal use of LSCS.
● Exclude morbidly adherent placenta by asking for previous history of uterine surgery
(including history of caesarean section), history of retained placenta and previous PP
anterior major.
● If bleeding is massive and hemodynamically pt is not stable, then we have to stabilize the pt
1st by giving colloid or crystalloid. Blood transfusion if indicated. Send blood for FBC,
coagulation profile and GXM at least 4 pint.
● If there is minimal bleeding, we have to manage the pt expectantly till 38 weeks POA
provided there is no evidence of fetal compromise.
● If asymptomatic PP, during my daily ward round I would like to ask whether there is
presence of bleeding or not, sign and sx of labour- abdominal pain, fetal movement present
or absent, monitor vital sign, check FHR.
● However, there is a role to manage PP minor as an outpatient provided the pt knows what
are the consequences of PP, what to do if she has bleeding or sx of labour, their house is
near to hospital and transport is available 24 hours.

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During daily ward rounds
● I will ask mother whether there is
○ Any PV bleeding
○ Any abdominal pain (worry about pt is going to labour)
○ How the Fetal movement (put pt on FMC)
● Do physical examination
○ Look the general physical examination (particularly signs of anemia)
○ BP/PR
○ Palpate abdomen (for contraction, SFH, fetal heart)

For the fetus


Monitor fetal surveillance in the ward
● FMC
● CTG depend on POA
● Serial ultrasound for fetal growth (every 2 weeks)

***There is a role of antenatal corticosteroid from 24 to 33+6 weeks and can consider until 36
weeks of gestation (IM DEXA 12mg in 2 doses) unless contraindicated because of increased risk of
prematurity
***Need to consider role of MgSO4 for neuroprotection from 24-32 weeks of gestation

INVESTIGATIONS:
1. FBC to look for Hb level (at least once every 2 weeks)
2. Urinalysis
3. Ultrasound to look for growth parameter of the fetus (every 2 weeks)
4. Blood cross match
5. Give Rogem to pt who had Rhesus –ve to avoid rhesus isoimmunization because it can lead
to agglutination (we give when the bleeding occur)
6. IM DEXA for fetal lung maturity.

When to deliver in cases of PP?

1. In asymptomatic patients and minimal bleeding usually at 38 weeks POA (Mcafee


Regime).
2. In symptomatic (ie severe bleeding) that causes pt to be hemodynamically unstable then
we have to deliver immediately BUT need to resuscitate pt first.
3. In cases of fetal compromise, we also have to deliver immediately.

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How to deliver?

● All PP major – I will manage expectantly until 38 weeks POA provided there is no evidence
of maternal and fetal compromise and delivered by LSCS.
● But if the pt develops sx of labour, I will consider to do emergency LSCS after stabilizing the
pt.
● There are certain precautions that have to be considered before performing LSCS.
○ Do a FBC to identify and correct anaemia
○ Do GXM to alert the blood bank to prepare for at least 4 pint of blood because
certain blood groups are difficult to get and furthermore, it is a major operation.
○ Because LSCS for PP major is a major operation, there are a lot of cx that may arise
following the surgery either intra-op, post-op and long term.
■ Intra operatively, pt may get cx of GA eg: Mandelson’s syndrome,
complication following surgery itself eg: massive bleeding, injury to baby,
bowel and bladder.
■ Post-operatively, the pt may get PPH (due to adherent or retained placenta),
infection or DVT.
■ Long term complication is, if the patient has recurrent PP especially PP
major or anterior located placenta in future pregnancy, she has a high risk of
developing placenta accreta, increta or percreta.
○ She has to be counseled that many cx may arise eg: massive bleeding that may end
up with hysterectomy if the pt has completed the family, or internal iliac, ovarian
and uterine arteries ligation if the pt is still young.
○ I would like to do USS to reconfirm the localization of the placenta and to do
mapping because we don’t want to cut through the placenta during the surgery.
○ Keep pt NBM at least 6 hours.
○ Inform anaest and paeds.
● However, there is a role to deliver pt with asymptomatic anterior PP minor (Type 1 anterior
and posterior & Type 2 anterior) with vaginal delivery provided she presented with
spontaneous labour and the pt is asymptomatic (no pv bleeding).

5 COMMON QUESTIONS IN EXAM (PLACENTA PREVIA)

1. WHAT ARE THE RISK FACTORS?

There are several possible risk factors that may associate with placenta praevia which include:

1. Advanced maternal age


2. Multiparity
3. Previous uterine surgery such as C-Section, myomectomy and ERPOC
4. Previous history of placenta praevia
5. Multiple pregnancy

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6. Foetal anomalies such as hydrop fetalis

2. COULD YOU EXAMINE ABDOMEN IN PATIENT WHO IS DIAGNOSED WITH PP? WHAT IS THE
MOST LIKELY FINDING?

The possible findings that usually we expect during abdominal examination are mainly
malpresentation and abnormal lie. Besides that, the abdomen is soft and non-tender in those
who presented with per vaginal bleeding.

3. ARE YOU WORRIED OR NOT/ WHAT ARE YOU WORRIED OF?

Yes, I’m worried sir, because I’m worried of preterm contraction that may lead to preterm
delivery. (Besides that, she had PP anterior with a history of previous scar. Therefore, there is a
higher risk of getting placenta accreta intra operatively.)

4. SO, HOW WOULD YOU ANTICIPATE OR WHAT ARE THE PRECAUTIONS?

I would like to do:


● FBC as for haemoglobin baseline
● GXM whereby we have to call the blood bank in order to prepare at least 4 pines of
blood and blood products (cryoprecipitate, fresh frozen plasma, platelets and
cryosupernatant). Besides that, we also want to look for the rhesus blood of the patient.
● I would give the patient antenatal steroid such as dexamethasone two doses 12mg 12
hours apart to promote and enhance fetal lung maturity if the patient is at risk of
preterm delivery.
● I will inform the patient and the couple regarding the possible complication of having
placenta previa. In view that she had placenta accreta and history of LSCS, she may end
up with hysterectomy.
● I will inform the neonatologist, senior obstetrician, and anesthesiologists.
● Before the operation I need to do an ultrasound to confirm that the patient has placenta
praevia and to map the placenta. This is so that we can avoid cutting through the
placenta. Besides that, if the foetus is in transverse lie I would like to know the back of
the baby to make the surgeon easily grab the fetal leg.
● The operation must be done by the senior obstetrician.

5. HOW WOULD YOU MANAGE HER FROM NOW TILL DELIVERY?

Scenario: 30 weeks POA, no PV bleeding, had previous history of LSCS

● I will admit the patient based on hospital protocol (Hospital Serdang at 36 weeks,
Hospital Kajang at 34 weeks) and manage her expectantly following the Mcafee Regime
(1945) till 38 weeks POA provided there is no maternal or foetal compromise by elective
LSCS.

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● During my daily ward round, I will make sure whether she has any PV bleeding or not,
fetal movement is good or not, sn and sx of labour.
● PE will done 4 hourly, by doing:
○ Vital signs
○ Abdominal examination to know the growing and the viability of the baby.
● Then I would like to do investigations such as:
○ FBC to know whether the patient is anemic or not. If she is anaemic, we correct
the anemia by giving hematinics or blood transfusion depending on severity. We
do it once a month or once in three weeks.
○ Then, I would like to do blood GXM in order to know whether the patient is
having rhesus positive or negative. Besides that, the blood bank must be ready
and available all the time.
○ Then, I would like to do an ultrasound to see the foetal growth by measuring the
fetal head circumference, biparietal diameter, abdominal circumference and also
femur length. Besides that, I also want to confirm whether pts is having PP or not
and also to confirm the gestation age of the foetus. By doing ultrasound also, I
can do mapping of the placenta so that we can avoid cutting through the placenta
during the operation.
● After 32 weeks POA, I also would like to do CTG or Pinard stethoscope in order to know
the viability of the foetus.
● There is a role of giving antenatal steroids such as dexamethasone (12mg, 12 hours
apart) because it can enhance foetal lung maturity. Not only that, it also can reduce risk
of getting infection such as NEC and also can reduce risk of having intraventricular
hemorrhage. We give that up to 34 weeks POA (but in our practice in HKL are usually up
to 36 weeks POA).
● If there is no maternal or fetal compromise, I will then perform an elective LSCS at 38
weeks POA.
● Before that, I will take all the precautions (as mentioned above)
● However, if the patient has PV bleeding, I will assess the bleeding first whether it is
excessive or minimal. If excessive and hemodynamically is not stable, I will resuscitate
the patient by maintaining the ABC.
● Once the patient is stable, I will perform an emergency LSCS. But before that, I will give
pts antenatal steroid and also take all the precautions (as discussed above).
● If the bleeding is so minimal, I will manage her expectantly following the Mcafee Regime
(as discussed above)

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POSSIBLE CASE SCENARIO @ SCRIPT FOR PLACENTA PREVIA 1

Chief complaint
Madam X, ___ year old, ______ housewife, in her ___ pregnancy, currently at ___ weeks POA ,
was admitted to the ward for expectant management of PP. The placenta praevia was
accidentally found during ultrasound scan at ____ weeks of POA.

Her date of LNMP was on______. She was sure of the date. Her menstrual cycle was regular. She
was not on OCP at that time & not breastfeeding at that time. Therefore,her EDD was_______.
Currently, she was at ____ weeks POA.

HOPP
This is a planned pregnancy. Her pregnancy was confirmed by +ve UPT done at private clinic
when she missed her period for ____ weeks associated with symptoms of early pregnancy such
as nausea, vomiting, headache and lethargy. Unfortunately, no early ultrasound was done to her
to date the pregnancy.
OR

This is a planned pregnancy. Her pregnancy was confirmed by +ve UPT done by herself after she
had missed her period for ____ weeks and she experienced symptoms of early pregnancy such
as nausea, vomiting, headache and lethargy. Then, she presented herself to the private clinic
and the pregnancy was confirmed by +ve UPT at the clinic. Unfortunately, an early ultrasound
was not done at that time.

Her antenatal visit/booking was done at ____ weeks POA at clinic_______. She had no
complaint at that time and her pregnancy was well. She had no sx of pregnancy. During the
check up, physical examination was performed. The blood pressure was taken and she was
found to be normotensive. The urinalysis shows no abnormality was detected. Then, the
antenatal blood investigation was taken and her blood gp is ____. HIV, Hep B and VDRL
screening were non-reactive. The u/s scan was performed to confirm the date of pregnancy. The
result shows that there was a singleton viable fetus and the pregnancy corresponded to
_____POA. However, she was told that she has a low lying placenta.

She had regular follow up at 1 month interval at 16, 20, 24 and 28 weeks POA at the same clinic.
During each visit, her b/p remained normotensive and her urinalysis no abnormality detected.
Unfortunately, no detail u/s and no growth u/s were performed. Otherwise, her pregnancy
progressed well.

In her subsequent antenatal follow up which at 30 weeks POA done at the same clinic she was
being told by the doc that she had PP major, no gross anomaly detected, liquor was adequate,
growth parameter was corresponded to date, fetus in transverse lie and FHR was detected. She
was referred to MHKL on the same day for further mx. Another u/s was performed to her and
confirmed that dx was PP major, fetus in transverse lie, FHR detected, fetal growth was

31
corresponded to date and the liquor was adequate. She was counseled and advised for
admission.

During her admission to the ward, the patient denied having PV bleeding and abdominal pain.
According to her, the fetal movement was good, more than 10 kicks per day. Besides that, there
is no sign and symptoms of labour. Currently, she was admitted for expectant management of PP
major.

POSSIBLE CASE SCENARIO @ SCRIPT FOR PLACENTA PREVIA 2

Chief Complaint
Madam JR, a __ year-old Malay housewife, in her __ pregnancy and she has __ children (with __
previous history of miscarriage), currently at __ weeks and __ days of period of amenorrhea
(POA), was admitted to the ward for expectant management of placenta praevia type IV. The
placenta praevia was accidentally found during ultrasound scan at __ weeks of POA. Her first day
of her last normal menstrual period (LMNP) was on __. She was sure of the date. Her menstrual
cycle was regular; she was not on oral contraceptive method and not breastfeeding at that time.
Therefore, her expected date of delivery (EDD) is on __.

HOPP
This is a planned and wanted pregnancy. Her pregnancy was confirmed by a urine pregnancy
test (UPT) done at the private clinic after she missed her period for __ month and experienced
symptoms of early pregnancy such as nausea, vomiting, headache and lethargy for a few days.
Unfortunately, an early ultrasound was not done at that time.

Her first antenatal booking was done at __ weeks of gestation at Maternity Hospital Kuala
Lumpur (MHKL). She had no complaint at that time and her pregnancy was well. During that
visit, she was normotensive and urine analysis was done and the result was normal. Antenatal
blood investigation was performed. Her blood group is __, HIV, hepatitis B and VDRL screenings
were non-reactive. Hemoglobin level was normal and she’s not anaemic.

The subsequent follow up is 4 weeks later which was at 12 weeks of POA. During the follow up,
her pregnancy was well. She remained normotensive and urinalysis was normal. Fortunately, her
first ultrasound scan was performed and she was told that her pregnancy corresponded to the
date which was at 12 weeks of POA. It was an intrauterine, single and viable fetus. No gross fetal
anomaly was detected. Subsequently, she was told to do modified glucose tolerance test
(MGTT) since she is obese, advance maternal age (>35 year old), previous history of macrosomic
baby and she had first degree family history of diabetes mellitus).

MGTT was done during her 3rd antenatal visit which is at 16 weeks period of amenorrhea. She
has been found to have (impaired glucose tolerance/abnormal glucose level). She was told to do
a blood sugar profile on the next day. Her fasting blood sugar was abnormal which 7.4mmol/l for

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fasting blood sugar and 9.1mmol/l for 2 hour postprandial was. She was only advised on diet
modification by the doctor since she was asymptomatic from any hyperglycaemic symptoms
such as polyuria, nocturia, lethargy and polydipsia. She was planned for first blood sugar profile
at 20 week period of gestation. Blood pressure and urinalysis were performed and no
abnormalities were detected.

Her 4th and 5th antenatal follow up which was at 20 weeks and 24 weeks period of amenorrhea
respectively, BP and urinalysis were performed and no abnormalities were detected. During
each follow up her pregnancy was well. BSP was also performed each visit and she claimed that
the results were all normal. She still remained asymptomatic from having any hyperglycaemic
symptoms. However, no ultrasound was done to her.

Her last antenatal visit at MHKL was at 28 weeks period of amenorrhea. BP and urinalysis were
performed and no abnormalities were detected. BSP also has been performed and she claimed
that the results were normal. She never experienced any symptoms of hyperglycemia at that
time. During the follow up, ultrasound scan was done and she was told that the fetal growth
corresponded to the date, liquor volume was adequate, no gross abnormalities detected and
the fetus was in longitudinal lie with cephalic presentation. At the same time, she was diagnosed
to have placenta praevia type IV. However, her pregnancy was well and she was asymptomatic.
She did not complain of any painless per vaginal bleeding or leaking at that time. She was
advised for admission for expectant management of placenta praevia type IV.

In the ward, she was given 2 injections at the buttock which I think it was IM Dexamethasone as
she was told it was for fetal lung maturity. The patient was monitored strictly and was put under
a pad chart to watch out for any per vaginal bleeding, leaking or any contraction pain. Her pulse
rate and blood pressure was monitored regularly.

For fetal monitoring, ultrasound scan was done 2 times and confirmed placenta praevia type IV
(major). The pregnancy was corresponding to the date, single and viable fetus in oblique lie and
adequate amount of liquor. Intermittent CTG was carried out and were reactive. She was
planned for an elective lower segment caesarean section at 37 weeks of gestation on __.

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3.2 PLACENTA ABRUPTIO

DEFINITION:
Premature separation of the placenta from the uterine wall (occurs usually in the 3rd trimester).
Separation of a normally located placenta after 22 weeks gestation prior to the delivery of the
fetus.

AETIOLOGY:
Mother Fetus and Placenta

1. Hypertension (established/PIH) 1. Multiple pregnancy


2. Abdominal trauma (blunt) 2. The ‘sick placenta’
3. PPROM/PROM
4. Polyhydramnios
5. Infections (eg. chorioamnionitis)
6. Pelvic mass (eg. uterine fibroid)
7. Multiparity
8. Advanced maternal age (>35y/o)
9. Autoimmune disease (eg. SLE)
10. Previous h/o placenta abruptio
11. Smoking, cocaine and other drug abuse
12. Folic acid deficiency

RISK FACTORS:
● Hypertension/Severe preeclampsia
● Smoking
● Trauma to maternal abdomen
● Cocaine use
● Alcohol use
● Polyhydramnios
○ When sudden massive leaking occurs
○ The sudden gushing out of amniotic fluid separates the placenta from the uterus
● Multiple pregnancy
● Fetal growth restriction

CLINICAL FEATURES:
● Painful PV bleeding
● History of abdominal trauma
● Tender abdomen (uterine irritability)
● Abdomen tense (woody hard)
○ May be soft if the placenta is posteriorly implanted (complaints instead of
backache)

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● Fetal parts are difficult to palpate
● Fetal heart is difficult to be heard
○ If absent, fetus may be dead
● Uterus larger than date (concealed)

TYPES OF PLACENTA ABRUPTIO:

***In concealed abruption, there is significant separation but the blood is concealed between the
placenta and uterus = minimal vaginal bleeding
***Patient usually complaint of back pain

GENERAL EXAMINATION:
1. Painful pv bleeding with tense rigid abdomen
2. Abdominal pain
3. Sweating
4. Hypovolemic shock
5. Hypotension
6. Tachycardia
7. Reduced/absent fetal movements
8. CTG showing fetal distress

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INVESTIGATIONS:
● Transabdominal USS (plays little role in diagnosis)
○ To look for presence of retroplacental hematoma

MANAGEMENT:
Placenta abruptio is diagnosed clinically in the presence of
1. Painful pv bleeding
2. Constant and tense abdominal pain

● Once the diagnosis has been made, assess the condition of the pt by which
the pt’s condition may reflect the severity/degree of abruptio
● If the maternal condition is not stable then we have to resuscitate first.
a. Initiate red alert
b. Resuscitate with ABC
c. SET 2 IV line (large branula at least size 16 ),
d. Monitor vital signs (BP/PR)
e. Consider colloid and crystalloid while waiting for blood
f. Send all necessary investigation GXM, coagulation profile, FBC
g. Consider to transfuse blood and DIVC regime if patient in DIVC
● Once the pt’s condition is stable then monitor the fetus condition (CTG).
***In general, once placenta abruptio is diagnosed, we have to deliver immediately

How to deliver?

● Possible early delivery is usually vaginal delivery


● The role of vaginal delivery is in
1. The pregnant woman who is already in labour and delivery is around the corner (3-4
hours) especially grand multipara, PROVIDED fetal is not compromised
2. Reactive CTG provided there is no maternal and fetal compromise
● If there is fetal compromise, then perform CS immediately or instrumental delivery (if OS is
FULL and ALL prerequisite is fulfills)
● LSCS is indicated when
1. Persistently abnormal fetal heart rate pattern
2. Evidence of continued bleeding

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REMEMBER

In certain cases of abruptio placenta, the abdomen may be soft and NOT tense and tender
ESPECIALLY when the placenta is at the posterior segment. Patient will only complain of
backache.

Placenta abruptio may be due to hypertensive crisis when the blood pressure is more than
160/110 mmHg, or there is a direct trauma to the abdomen.

What are the dangers/complications of placenta abruptio?

Mother Fetal

● Preterm labour ● Fetal hypoxia/IUD


● Hypovolemic shock ● IUGR
● DIVC ● Rh isoimmunization
● Acute renal failure ● Prematurity with
● PPH ○ Patent ductus arteriosus
● Amniotic fluid embolism ○ Necrotising enterocolitis
*** Last but not least all these factors will lead ○ Periventricular leukomalacia
to maternal morbidity and mortality *** Perinatal morbidity and mortality is high

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3.3 MORBIDLY ADHERENT PLACENTA
1. Placenta Accreta: invade myometrium, bleeding on removal of placenta, type II, III, IV ant
PP most likely to get
2. Placenta Increta: invade myometrium and reach serosa
3. Placenta Percreta: invade myometrium and through serosa

Can we predict placenta accreta?


YES, in all patients with PP anterior major, history of retained placenta, D&C, previous LSCS and
myomectomy are at risk of developing placenta accreta, increta or percreta.

How to predict?
1. USS
a. Measure thickness of lower segment (anterior part)
b. Look for loss of placental endometrial interface
c. Look for loss of retroplacental clear zone
2. Doppler US
a. Assess blood flow at lower segment
b. Look for blood vessels crossing myometrium
c. Look for blood vessels reaching bladder

Case in point: G8P6+1 presented with PP type III posterior with previous scar and D&C

Precautions to take pre-op, intraop, and postop


● Informed consent about the procedure, possibility required more than 4
pints blood, cx of op to the pt before the operation.
● Send blood for cross match (at least 4 pints)
● Optimize the Hb becoz we worried of severe anaemia during op d/t massive bleeding
● Post op – PPH, we give oxytocin 40 unit to prevent blood loss

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3.4 CERVICAL MALIGNANCY

In case of cervical malignancy

● If PP was excluded, I would like to do speculum to check for local causes


● If I see growth, take biopsy and send for HPE
● If come back as cervical ca, we must stage the ca first

Principle of management of pregnant women with cervical ca

● I will treat the pt same like other non-pregnant woman depending on the stage
● Stage 2A and below – do Wertheim’s hysterectomy
● Stage 2B onwards – consider radiotherapy

1. Patient with cervical ca at 28 weeks POA


Of course I’m in a dilemma whether to keep the pregnancy since the baby is still immature
or to treat the cervical ca if pt presented at 28 weeks POA. I have to weigh between
keeping the pregnancy till term or to treat cervical ca. I need to discuss it with a senior
obstetrician and neonatologist.

One alternative is:


● Complete Dexamethasone
● Prepare ventilator for baby
● I will deliver the baby by classical C-section
● Then, followed by Wertheim’s hysterectomy (if 2A below) but I’m aware this
is a bloody surgery OR followed by radiotherapy (if 2b onwards).

2. Patient with cervical ca stage 2A below at <10 weeks POA


I will terminate the pregnancy and do Wertheim’s hysterectomy

3. Patient with cervical ca stage 2B onwards at <10 weeks POA


I will terminate the pregnancy and do radiotherapy

3.5 INDETERMINATE APH

In the case of Indeterminate APH

Usually pt is stable, so we manage the pt expectantly the same like other APH because they still
have high risk to get in utero placental insufficiency.

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4.0 LEAKING LIQUOR (PROM, PPROM)
*important to differentiate because management is different

DIFFERENTIAL DIAGNOSIS:
1. Leaking liquor
2. Preterm labour
3. Urinary stress incontinence
4. Excessive PV discharge (candidiasis)
5. Semen (sexual intercourse)

RISK FACTORS:
1. Current infection: a) Local infection (recurrent eg: bacterial vaginosis,vaginacandidiasis)
b)Systemic chronic infections (dengue fever, sepsis, pyelonephritis,
chorioamnionitis, recurrent UTI (ascending infections), TB,
pneumonia)

hints: recent history of admission to the ward (~1 week)

2. Previous history of PROM/PPROM


3. Trauma: MVA, iatrogenic (amniocentesis/amnioreduction)

What are the differences between amniocentesis & amnioreduction?

Amniocentesis Amnioreduction

● diagnostic ● therapeutic
● 20cc taken ● 200-300cc taken

4. Smoking, drug abuse (especially cocaine)


5. Uterine abnormalities
6. Congenital anomalies: cervical damage, fibroid
7. Multiple pregnancy
8. Polyhydramnios

CLASSICAL PRESENTATIONS:
- Sudden gush of colorless and odourless fluid per vaginally followed by dribble (*typical: after a
few days of fever/trauma)
- Clothing wear at the time
- Ask whether had previous admission recently

CONFIRMATION:

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Sterile speculum examination: if I see liquor coming out from the cervical os, it is confirm that it is
liquor OR if I see a pooling of liquor at the posterior fornix, I will confirm by doing the litmus test
OR if there is no presence of liquor, i will ask the patient to cough/ lift up the head/press the
abdomen/strain and confirm the liquor by litmus paper

INVESTIGATIONS FOR CONFIRMING LIQUOR:


- Litmus test (turns red to blue)
- Nitrazine paper or amnicator test (turns dark blue/black)
- Examine for ferning using microscopy

*once diagnosed with leaking liquor, admit the patient and differentiate whether it’s PPROM or
PROM

COMPLICATIONS:
1. PPROM:

Maternal Fetal

● Risk of chorioamnionitis ● Risk of prematurity


● Risk of operative delivery ● Risk of birth asphyxia
● Risk of IUD
● Risk of lung hypoplasia (in early leaking
liquor)
● Risk of skeletal deformities
● Risk of neonatal infection

2. PROM

Maternal Fetal

● Risk of chorioamnionitis ● Risk of neonatal infection


● Risk of operative delivery

MANAGEMENT FOR PROM:

Once diagnosis of PROM is made, deliver immediately because the fetus is at term. Therefore
there is no risk of prematurity. However, the risk of infection to the mother is high which warrants
immediate delivery. Allow 24 hours for spontaneous labour, however if there is no spontaneous
labour, patient can be induced with IOL

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There is a role of antibiotic in PROM
1. For GBS +ve mother, give IV ampicillin stat and IOL (no need to wait 24h)
2. For GBS -ve mother, start IV ampicillin after 18 hours of leaking and no S&S of labour
3. If patient is already in labour, start on IV Ampicillin 2g stat then 1g QID for non GBS
mother OR 1g 4 hourly for GBS mother and discontinue post delivery

MANAGEMENT OF PPROM:
(read below for more detailed information)

- Admit the patient


- Monitor sm+sn of chorioamnionitis
- Monitor other complications of leaking liquor towards mother such as labour, abruptio
placenta
- Rest in bed
- Pad chart
- Blood investigations: FBC [done twice weekly] ESR/CRP
- IM Dexamethasone
- Prophylactic erythromycin 800mg bd for 10 days
- For fetus, FKC
CTG fetal tachycardia? [done 2 times per day]
USS : to see fetal heart activity, AFI, number of fetus

SCENARIO: when there is maternal or fetal compromise, I will need to deliver immediately
*Maternal compromise (develop sm+sn of chorioamnionitis)

Symptoms Signs

● Fever ● Increased temperature


● Palpitation ● Tachycardia
● Abdominal pain ● Tender abdomen
● Foul smelling PV discharge ● Foul smelling PV discharge
● Fetal tachycardia
*Fetal compromise: non-reassuring CTG, meconium-stained liquor

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SCENARIO: Can we discharge patients with PPROM?
YES if after 48 hours:
1. Vital signs are normal
2. There is no more leaking liquor
3. No sn+sm of chorioamnionitis or any other complications

● Patient must be followed up once a week and on visit, must do FBC


● Patient is advised to check temperature at home
● TCA if fever
● Delivery preferably as near term as possible

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4.1 PREMATURE PRELABOUR RUPTURE OF MEMBRANE
(PPROM)

DEFINITION:
Rupture of membrane that occur before 37 weeks & after 24 weeks of POA/POG

AETIOLOGY (exact etiology is unknown):

Mother Fetal

● Infection (chorioamnionitis, bacterial ● Multiple pregnancy


vaginosis, group B β-hemolytic strep) ● Polyhydramnios
● Cervical incompetence (hx of recurrent ● Fetal anomaly
miscarriage : 2nd trimester loss in ● Hydrops fetalis
which the pattern is decreasing eg first
pregnancy 20w, 2nd at 18w and 3rd at
16w)
● Uterine anomaly (e.g., septate or
bicornuate uterus)
● amnioreduction
● Smoking, drug & EtOH abuse
● Malnutrition
● Poor socioeconomic status
● Previous hx of PPROM

HOW TO SUSPECT PT WITH PPROM???


From History Taking:
● sudden gush of fluid (colourless & odourless) vaginally than continue to leak till wet the
undergarment
● reduced fetal movement
● presence of abdominal pain / contraction

*need to distinguish wt UTI symp- frequency, dysuria, urgency & incontinence

HOW TO CONFIRM LEAKING OF LIQUOR?


● To confirm leaking of liquor, I would like to do a sterile speculum examination.
● Firstly, I would like to inspect any leaking of liquor from the cervical os. If it is present,
confirm that it is liquor.
● If there is no leaking from the cervical os, then i want to inspect a pooling of liquor in the
posterior fornix.

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● However, if there is no presence of liquor, I will ask the patient to cough.
● If there is a presence of liquor, I would like to test by using Litmus paper. If it turns from
red to blue, it is more suggestive of liquor as liquor is alkaline.

False +ve : semen, blood, vagina infection


False –ve : prolonged rupture of membrane

Symptoms Signs

● Sudden gush of nearly colorless fluid Abdominal Examination


● Pervaginally ● Oligohydramnios
○ Continue leaking until wetting ● Fetal part is easily palpable
the undergarment followed by ● Uterus smaller than date
dribbling Vaginal Examination
○ Presence of meconium stained? ● Speculum examination (Pool test)
○ Foul smelling? ○ Pooling of liquor at the
● Reduced fetal movement posterior fornix
● Abdominal pain (pre or post-leaking) ○ If no pooling, ask patient to
○ Differentiates PPROM & cough
preterm labour ○ Exclude cord prolapse &
extruding of fetal extremity
*differentiate from urinary incontinence (UI) & ● Litmus paper test (90 -98% sensitivity)
excessive PV discharge ○ Changes from red to blue
● Ask about other urinary symptoms e.g. (alkaline)
dysuria, urgency, frequency ○ False positive (semen, blood or
vaginal infections)
● Ferning test (85- 98% sensitivity)
○ Fern pattern on slides due to
crystallization or arbotization
when amniotic fluid interact
with protein & salt
● High Vaginal Swab (HVS)
○ To rule out any infections

45
COMPLICATIONS:

Maternal Fetal

● Chorioamnionitis that can lead to ● Prematurity


septicaemia ● Cord prolapse
● Jeopardized future pregnancy ● Lung hypoplasia esp in cases PPROM
(chorioamnionitis => ascending occur early
infection => PID => tubal blockage => ● Skeletal deformity esp in cases PPROM
subfertility) occur early
● Placental abruptio ● Baby asphyxia secondary to cord
● Preterm labour prolapse
● Increased risk of operative delivery ● Neonatal infection
● Postpartum hemorrhage

Signs & Symptoms of CHORIOAMNIONITIS:

Symptoms Signs

● Maternal pyrexia ● Febrile


● Palpitation ● Maternal tachycardia
● Abdominal pain ● Abdominal tenderness
● Foul smelling PV discharge ● Foul smelling discharge
● Fetal tachycardia

INVESTIGATIONS:
● There are several investigations indicated in the patient with leaking of liquor.

FOR THE MOTHER:


● During the speculum examination, I would like to do HVS and send it for culture &
sensitivity in order to confirm the presence of infection by looking for organisms that are
responsible for infection as well as antibiotic sensitivity & cx from the leaking. If the
result is negative, i would like to repeat again if the patient complaints of foul smelling
discharge. If the first result reveals that there is positive-bacteriological isolation, I will treat
it accordingly and repeat HVS after 10 days.
● In addition, I would like to do FBC to look for WBC level whereby an increase in total WBC
may indicate infection.
● Other than that, CRP as well as ESR also can be done to look for evidence of infection.
However, these 2 tests are not specific enough. The frequency of these investigations

46
depends on the severity of the previous result. I will do it more frequently if there is a sign
of chorioamnionitis.

Blood ● FBC
○ look for evidence of infection (leukocytosis) e.g.,
chorioamnionitis
○ trend of WCC
○ frequency
○ normal = biweekly; ↑ WCC = every alternate day
● ESR & CRP (non-specific but can suggest infection)

HVS ● to confirm the presence of infection


(done during initial ● if negative, repeat again another 2 weeks
speculum
examination)

FOR FETUS :
● Other than that, i also want to perform an ultrasound in this patient to check for:
○ Fetal growth (every 2 week) as well as fetal well being by looking at the biophysical
profile which contains AFI (every week), tone, movement and breathing.
● Access fetal viability by access FHR by Daptone < 32 wk and CTG > 32 wk.

What is your approach for PPROM?

● When the patient comes with leaking of liquor, i will do a speculum examination to confirm
a diagnosis. Then, as the diagnosis is confirmed, I will admit the patient into the ward.
● I have to weigh the risk of delivery premature baby & cx that may develop if we prolong
the pregnancy which is chorioamnionitis
● I will manage the patient expectantly as near term as possible provided there is no fetal
and maternal compromise such as chorioamnionitis and fetal distress.
● During the daily ward round, i will ask the patient whether :
○ she still has leaking or not.
○ I will ask about the amount of leaking based on no. of pads used
○ colour of liquor whether it is clear colour or yellowish colour that most probably
meconium stain and suggestive fetal distress.
○ Besides that, i will ask the patient about the smell of the liquor whereby foul
smelling may indicate infection (chorioamnionitis).
○ Besides that, i would like to ask whether the patient has an abdominal tenderness,
palpitation or fever that may indicate chorioamnionitis or abdominal tense that
may indicate abruptio placenta. This is strongly important because
chorioamnionitis can cause maternal septicaemia.

47
○ As the PPROM is associated with preterm delivery, I would like to ask about the
symptoms of labour such as abdominal pain which is increasing in frequency and
intensity and a/w show may indicate that the patient is in labour.
○ Then, I will examine the vital signs in this patient such as temperature, pulse rate
and blood pressure as pyrexia and tachycardia are the signs of chorioamnionitis.
○ Besides that, I also would like to monitor the fetal kick chart (FKC) that has been
given to the patient as PPROM may cause reduced fetal movement.

1. Risk of preterm delivery, there is a role of giving antenatal steroids such as


IM Dexamethasone (DXM) 2 doses 12 mg 12 hrs apart BD to promote
lung maturity by increasing the production of surfactant by type 11
pneumocytes.
2. Prophylactic Ab = Tab Erythromycin 800mg bd given for 10 days
3. If patient is already established labour, give IV ampicillin

Role of Dexamethasone
- accelerate lung maturity by enhancing surfactant production.
- reduce the risk of Necrotising Enterocolitis (NEC)
- Reduce the risk of Intraventricular haemorrhage

EXAM TIPS

How to ask whether a patient was injected with DXM?


Injections (IM) in her buttock, 2 times in a day.

Contraindication for DXM (antenatal steroid)


- Chorioamnionitis
- Tuberculosis
- Porphyria
- uncontrolled DM

PHYSICAL EXAMINATION:
● Then, I would like to perform an abdominal examination on this patient.
● I will look for any tenderness, irritability or tense of the abdomen.
● Besides that, i also want to check SFH, whether the uterus is smaller than date, the lie of
the uterus and also whether the fetus is easily palpable as this may indicate
oligohydramnios.
● I also want to check for fetal heart since PPROM may be complicated by fetal distress.
● Vaginal examination will not be performed in this patient as it may introduce infection to
the patient unless if the patient is in labour. However, a sterile Speculum examination will
be performed if the patient complained of foul smelling PV discharge.

48
SUMMARY

Mother Fetal

● Still leaking or not? ● Fetal kick chart


○ Amount of leaking (pad chart) ● Any reduction in fetal movement
○ Colour of liquor i.e. meconium ● Abdominal US
stained? ● Check for AFI weekly
○ Foul smelling? ● Fetal growth 2 weekly
(Chorioamnionitis) ● Biophysical profile
● Symptoms of labour ● CTG daily
○ Contraction pain
○ Show
● Symptoms of chorioamnionitis
○ Fever
○ Abdominal Pain
○ Palpitation
● Abdominal Examination
○ Uterus smaller than date
○ Uterine irritability
(chorioamnionitis)
○ Lie of the fetus
○ Oligohydramnios
● Vaginal examination
○ DVE only when patient in labour
(avoid introduction of infection)
○ Speculum examination to
exclude PV discharge
● Consider IM Dexamethasone
○ To accelerate fetal lung maturity
● Tocolytic agents (exclude CIs)
○ Only if premature contraction to
but some time for steroid to act
● Erythromycin 800 mg BD (ORACLE 1)
○ Prolonged pregnancy up to 1
week
○ Dec. the risk of neonatal
infection

49
MODE OF DELIVERY:
● Mode of delivery depends on favourability of the cervix & vaginal delivery is the best
mode of delivery.
● I will allow vaginal delivery if there is no evidence of maternal or fetal compromised.
● However, if there is obstetric complications such as malpresentation, 2 previous scar,
cervical fibroid or CPD, i would like to do LSCS
● PPROM and chorioamnionitis are not an indication of LSCS becoz in chorioamnionitis,
spillage of liquor to the peritoneal cavity can cause spread of infection leading to
generalize peritonitis.
● However, if there is contraindication for vaginal delivery in cases of chorioamnionitis, LSCS
is allowed but with extra precaution by putting abdominal padding & early suction of the
liquor. ( other case we put abdominal padding in rhesus mother & if bowel disturbed
view)

WHEN TO DELIVER???

● If there is evidence of chorioamnionitis or fetal distress (thick meconium stained liquor), I


will deliver the baby straight away regardless of period of gestation.l
● If there is no evidence of maternal or fetal compromise, I would like to manage the patient
expectantly until … (depends on when the leaking occur)
○ If continue leaking, I will manage expectantly until as near term as possible and wait
for SVD
○ If stop leaking, I will allow the patient to deliver at term (37 weeks)
● If the patient is at 36 weeks and comes with signs of labour, I will allow the patient to
deliver.

ROLE OF TOCOLYTIC- in case of preterm contraction to allow pt complete steroid


● why not take uric acid postpartum – because it comes from the placenta and indicator of
fetal distress if high => deliver the baby immediately.

Intrapartum

● If there is infection (+ve HVS), I will give IV antibiotics to the mother after delivering the
baby, I will handle the baby to the pediatrician for further management.
● I assume that the pediatrician will draw blood from the baby for C&S and start with IV
antibiotics.
● If the result shows no infection, IV antibiotic will be stopped after 5 days.
● If the result is positive, IV antibiotics will be continued until the blood result reveals no
infection.

50
HOW LONG TO ADMIT PATIENT?

● Duration of hospital stay depends on gestational age & severity of the leaking.
● If the leaking stops & after 2-3 days there is no more leaking & no evidence of
chorioamnionitis or maternal & fetal compromise, I will discharge the patient.
● However, ideally I should keep the patient for at least 1 week. I would also advise the
patient to come for follow-up at the hospital weekly.

Don’t you worry about the risk of infection by giving DXM?

Of course I’m worried. However, giving antenatal steroids provide more benefit to the baby. It is
not only to promote lung maturation but also reducing the risk of NEC as well as risk of
intraventricular haemorrhage. Furthermore, the dose that are given is small in dosage and pt is on
antibiotics.

How do you manage the patient at 30 weeks POA, presence with PPROM and ultrasound
showed that the fetal is anencephaly ?
a
In this kind of case, i would like to terminate the pregnancy as soon as possible because prolonging
the pregnancy offers no benefit to the mother as well as to the fetus. Furthermore, it will reduce
the risk of chorioamnionitis and risk of operative delivery to the mother. However, i need to
discuss with the couple first, whether she want to terminate the pregnancy or keep the pregnancy

POSSIBLE CASE SCENARIO @ SCRIPT FOR PPROM

Madam ___ a __ years old (race) , (occupation), in her __ pregnancy, was admitted due
to sudden leaking of clear and non foul smelling liquor . Her first day of (lnmp) was on __. She
was sure of the date. Her menstrual cycle was regular, she was not on oral contraceptive pills
(ocp) and not breastfeeding at that time. Therefore, her expected date of delivery (edd) is on __.
Currently she at __ weeks of period of amenorrhea (poa)

History of present pregnancy

This is unplanned but wanted pregnancy. She suspected that she was pregnant when
she missed her period for __ weeks and also after she experienced symptoms of early pregnancy
such as nausea, vomiting, headache and lethargy for a few days. Then, she presented herself to
the private clinic and indeed her pregnancy was reconfirmed by a positive urine pregnancy test.
Unfortunately, an early ultrasound was not done at that time.

51
Her first booking was done at __ weeks of pregnancy at __. She had no complaint at
that time and her pregnancy was well. She had no symptoms of early pregnancy. During that
visit, she was normotensive and urine analysis was done and no abnormality was detected.
Routine antenatal blood investigation was performed. Her blood group is __, hiv, hepatitis b and
vdrl screenings were non-reactive. Unfortunately, ultrasound was not done as there was no
ultrasound scan available there. She also experienced her first quickening on __ weeks of
gestation.

Subsequent antenatal follow up which is 1 month interval at 21, 25 & 30 wk of


gestation. The routine examination and investigations revealed no abnormalities. She remained
normotensive and the urine test was normal. However, on __ which was on __ weeks of
amenorrhea, she complained of a sudden gush of warm fluid running down her thigh
continuously while she was doing some housework. The fluid was clear in colour with no
meconium stained and non-foul smelling. She had to wear 2 sanitary pads and the pads were
fully soaked. She claimed during that time, she could feel that her fetal movement was reduced.
However, there were no per vaginal bleeding, presence of show or abdominal pain. She also had
no history of trauma or other local or systemic infection. She has no fever and there was no sign
and symptoms of uti such as frequency, urgency, leakage and dysuria. On assessing this patient,
risk factor, there was no history of abdominal trauma and she had no history and symptoms of
vaginal infection such as foul smelling discharge, and pruritus.

As the leaking worsens (she had to use 8 pads from 11.00 am to 7.30 pm), she seeks
medical attention at PAC of mhkl. The doctor there performed a speculum examination and
litmus test was carried out and confirmed amniotic fluid. High vaginal swab is also done to rule
out any organism that causes infection. Then she was admitted to ward for expectant
management of her pprom. Since in the ward, there is still leaking liquor and she used about 3
pads daily with totally soaked. The liquor is still clear and not smelly. In the ward an ultrasound
scan was performed and revealed the fetus in longitudinal lie and cephalic presentation, liquor
volume is adequate and no oligohydramnios, no fetal abnormality and placenta located at upper
segment. She has been given twice injection intramuscularly at her buttock. I think it was a
dexamethasone injection as she said that the injection helps to promote lung maturity.

Since admitted, ultrasound scan was repeated and she was prescribed antibiotics and
dexamethasone. She was admitted to the ward for close monitoring. Blood investigation was
done and showed normal results. However, she denied having any contraction or abdominal
pain.

52
5.0 ANEMIA IN PREGNANCY
❖ Definition

Time Hb Level

1st Trimester < 11 g/dL

2nd and 3rd Trimester < 10.5 g/dL

❖ Classification

Severity Hb Values (g/dL)

Mild 10 - 10.9

Moderate 7 - 9.9

Severe <7

Very severe <4

❖ Epidemiology
➢ Occurs in 20-60% of pregnant women ( 95% are IDA type)

❖ Pathophysiology
➢ Physiological anemia
1. Due tu hemodilution as there is disproportionate increase in plasma volume
& RBC (50% vs 30%)
2. Increase in iron requirement in 2nd,3rd trimester due to production of fetal
RBCs
➢ Magnitude related to
1. Fetal weight or size
2. Gravidity (more in multipara or closed gravida)
3. Multiple pregnancy
❖ Aetiology
➢ Anemia in pregnancy is not a complete diagnosis!!
➢ A cause must be identified to ensure effective treatment.
➢ Other causes must be explored if the patient is not responding to hematinics.

53
Causes of anemia in pregnancy Diagnosis

Obstetric ● Physiological - due to haemodilution


● Multigravida
● Poor spacing in between pregnancies
● Multiple pregnancy
● APH - Placenta Previa, Placenta Abruptio
● Previous PPH

Gynecological ● Recurrent menorrhagia


● Uterine fibroid

Parasitology ● Parasite infection


● Malaria

Medical ● Haemorrhoids
● UTI
● Peptic Ulcer disease

Haematological ● Thalassemia

Social ● Diet (Vegetarian) - IDA or Folate deficiency

54
Features suggestive of IDA ;

1. Previous or early booking Hb with normal MCH and MCV


2. Microcytic hypochromic anemia
3. Mentzer index > 13
4. Transferrin saturation ; <16% indicates inadequate iron supply for erythropoiesis
5. Confirmatory test for IDA : Serum Ferritin <15ng/mL

IDA Thalassemia

Serum ferritin Low Normal

RDW** High Normal

Mentzer index >13 <13


** RDW high in IDA, folate deficiency and vitamin B12 deficiency

❖ Complications

Mother Fetus

Antepartum;
1. Infections 1. IUGR
2. Preterm labour 2. SGA or Low Birth Weight
3. Left failure 3. IUD
4. Cardiac failure of fetus → non immune
Intrapartum ; hydrops fetalis
1. Cardiac failure
2. PPH
3. Shock

Postpartum;
1. Increase morbidity & mortality (unable
to sustain bleeding during labour)
2. Heart failure
3. Puerperal sepsis
4. Uterine sub-involution

55
❖ Investigations

Investigations Details

FBC HB, MCV,MCH,RDW,Mentzer Index

Peripheral Blood Film IDA : target cells,pencil shape

Iron Study To know iron level & related parameters


(Serum ferritin, Total Iron, TIBC ,transferrin & transferrin
saturation)

Hb electrophoresis Beta thalassemia

Hb DNA analysis Alpha thalassemia

Serum folate & Vit B12 If suspect macrocytic anemia

Stool for ova and cyst Parasitic infection

Stool for occult blood GIT bleeding

❖ Classification

Severity Hb Values (g/dL)

Mild 10 - 10.9

Moderate 7 - 9.9

Severe <7

❖ Management

■ Depends on :
1. Types of anemia
2. Severity of anemia
3. Period of gestation

56
Treatment of Iron Deficiency Anemia
■ 4 main modality of treatment

1. Iron rich food 2. Oral iron 3. Parenteral iron 4. Blood


diet supplement transfusion

1. Iron Rich Food Diet


❖ Haem iron : red meat, fish, poultry (2-3x easier absorption)
❖ Vitamin C enhances iron absorption
❖ Avoid iron absorption inhibitors : tea, coffee, cereals, and calcium

2. Oral Iron Supplement


❖ General rules of Iron Supplement requirement;
➢ Prophylaxis : ~ 60mg elemental iron/day
➢ Treatment : ~ 100-200 elemental iron /day
❖ Prophylaxis is given to all mothers > 12 weeks POG
❖ Response towards oral iron therapy will increase Hb by around 1 g/dL per week.

Types of Iron Supplement Elemental Iron Notes

Obimin 30mg 1. Correct way of taking : on empty stomach,


1 hour before meals with source of
Sangobion 35mg vitamin C (juice).
2. Avoid taking with antacids.
Ferrous fumarate 65mg 3. Explore on compliance and tolerance to
iron supplement (Blackish stool )
Maltofer 100mg

Iberet 105mg

Zincofer 115mg

2. Parenteral Iron

57
1. Iron Dextran ( Cosmofer ) OR Iron Sucrose ( Venofer )
2. Indications
■ Failure to respond to oral iron
■ Non compliant/intolerant of oral iron
■ Clinical need to deliver iron rapidly
3. Contraindications
■ Hx of allergy/anaphylaxis to parenteral iron
■ 1st trimester
■ Acute & chronic infection
■ Chronic liver disease
3. Blood Transfusion
❖ Indications;
➢ Severe anemia (Hb < 7 g/dL)
➢ Symptomatic anemia
➢ Hb < 8 g/dL and >36 weeks
➢ Anemia associated with obstetric problems (e.g. APH, early pregnancy bleeding)
➢ Anemia with heart disease (need to be caution)

❖ Risks of ;
➢ Blood transfusion reaction
➢ Blood borne diseases (HIV, Hep B, Hep C)

Antepartum Admit patient for further assessment


● FBC (Hb, platelets, MCV)
FBP
● Peripheral blood film (e.g. Malaria)
● Serum ferritin & TIBC (Iron studies)
● Urine FEME
● Stool ova and cyst

Treatments are based on the underlying causes

Intrapartum Depends on severity of anemia


● Mild GSH 2 pints
● Moderate - Transfuse 2 packed cells
● Transfuse slowly with IV Furosemide in between

Postpartum Continue oral medication (for mild & moderate)

58
6.0 DIABETES IN PREGNANCY
A good medical student should know:
● Definition and type of diabetes.
● How to diagnose diabetes in pregnancy.
● What are risk factors?
● Important to know
○ Effects of pregnancy towards diabetes
○ Effects of diabetes on mother and fetus.
● How to manage;
○ Pre-pregnancy.
○ Antenatal
○ Intrapartum
○ Post-partum
________________________________________________________________________________

DEFINITION & TYPES OF DIABETES:

Types Explanation Details

Pre-existing DM DM existed before pregnancy TYPE 1 : juvenile onset, inherited.


TYPE 2 : maturity onset, lifestyle.

Gestational DM DM occurs during pregnancy but It is a retrospective diagnosis.


disappears after delivery After 6 weeks postpartum repeat
MGTT.;
➔ if normal – GDM.
➔ if abnormal type 2 DM.

**Impaired glucose tolerance = abnormal glucose tolerance test.

PHYSIOLOGICAL CHANGES:

● During pregnancy, there is a state called diabetogenic . This is due to an increase in


hormones (such as human placental lactogen, cortisol, insulinase) produced by placenta
have an antagonist effect on maternal insulin.

● Usually in pregnant ladies, fasting blood sugar is low whereas postprandial is high
compared to non-pregnant ladies.

59
● During pregnancy also the glomerular filtration rate is increased and this leads to
decreased tubal function which then can cause glycosuria (this is physiological changes).
That’s why this is not one of the risk factors of GDM. However if glycosuria is detected on 2
occasions we can say that this patient is at risk of GDM, so we need to screen the patient
by doing MGTT.

How to diagnose GDM?

60
Oral Glucose Tolerance Test (OGTT) Modified Oral Glucose Tolerance Test
(MOGTT)

1 hour before glucose given 1 hour before glucose given

50 g anhydrase is given 75 g anhydrase is given

1 or 2 hour postprandial 2 hours postprandial.

Normal Range ( CPG Diabetes in Pregnancy 2017 )

MGTT Fasting : ≤ 5.1 mmol/L


AND/OR
2HPP : ≤ 7.8 mmol/L

Blood Sugar Profile Fasting : ≤ 5.3 mmol/L


2HPP : ≤ 6.7 mmol/L

61
BLOOD SUGAR PROFILE

● After MOGTT is done and if the result is abnormal, we need to do BSP to know whether the
patient required treatment in which patient needs insulin or not or just enough diet
modification.
● Normal reading for BSP : 5 / 6 / 6 / 7 OR between 4-6 mmol/L
● BSP can be done either as in-patient or out-patient.
○ 1st: in the morning, ½ an hour before breakfast.
○ 2nd: at 12 noon before meal.
○ 3rd: at 7 pm pre – dinner.
○ 4th: at 10 pm post – dinner.

RISK FACTORS:
Current history:
➔ Age > 25 yrs old .
➔ Obesity > 80 kg BMI >27kg/m
➔ Glycosuria in > 2 occasions.
➔ Recurrent vaginal candidiasis / other infection.
➔ Ultrasound show features of macrosomic fetus ,abnormal fetus .
➔ Current Obstetric problems
◆ Polyhydramnios
◆ Essential / Pregnancy induced hypertension
◆ Use of corticosteroids

Past history:
➔ Family history of DM.
➔ Previous pregnancy complicated with GDM.
➔ Previous history of macrosomic baby (> 4 kg).
➔ History of congenital anomalies.
➔ History of unexplained IUD
➔ History of recurrent miscarriage.

When to screen?
When patient is having the risk factors no matter what is the POA .
For example, Patient < 10 weeks of POA, do MGTT

● If the result is normal, repeat MOGTT at 24-28 weeks (because placental hormones are at
maximum during that period).
● If the result is abnormal, I would like to subject the patient to do BSP either as in–patient or
out-patient.

Why it is important?
GDM have high risk of maternal / perinatal morbidity and mortality.

62
EFFECTS OF PREGNANCY TO DIABETES:

➔ Increased requirement for insulin towards the 2nd and 3rd trimester due to increased
hormone levels which antagonize insulin (such as glucagons, insulinase, hpL).
➔ Pregnancy may exacerbate diabetes and patients may develop retinopathy, nephropathy or
neuropathy or if a patient already has the above complications then it may WORSEN.

** Is retinopathy commonly seen in pre-existing DM pregnant mothers ?


➔ UNCOMMON. Because most pregnant ladies are young. Retinopathy usually takes more
time to develop. Unless patient with Type 1 DM patients/ pre-existing Type 2 DM.

EFFECTS OF DIABETES TO PREGNANCY:

Mother:
➔ Recurrent infection ➝ such as UTI, vaginal candidiasis.
➔ Increased risk of preeclampsia.
➔ Increased risk of operative delivery due to …unstable lie / presentation / macrosomic baby
and etc ..
➔ Polyhydramnios ➝ abdominal discomfort, SOB , unstable lie, malpresentation, PPROM ,
preterm contraction which may lead to preterm labour and delivery.
➔ Possible risk of termination of pregnancy if DM nephropathy.

*** How uncontrolled DM causes polyhydramnios?


1. Fetal anomaly e.g. GIT obstruction.
2. Fetus is the same as a normal adult human being in uncontrolled DM - polyuria.
3. Big baby - high urine output compared to small baby (↑ body surface area).
4. High osmotic diuresis.

Fetus :

1st Trimester Miscarriage : in pre-existing DM (may be due to abnormal fetus)


(all cx is due to Teratogenic condition for organogenesis.
pre-existing DM not
GDM) Congenital anomalies;
Eg:
1. CNS system, most common such as neural tube defect
2. Cardiac anomaly , most common TGA,VSD & AVD
3. Renal agenesis
4. Sacral agenesis (RARE)
- but if present, pathognomonic for Pre-existing DM

2nd Trimester -

3rd Trimester Unexplained IUD (Glycosylated hemoglobin)

63
Macrosomia (if uncontrolled GDM).
Risk of prematurity ( may be indirectly due to complications of DM) eg
Preeclampsia, Poly⇾ PPROM

Intrapartum Shoulder dystocia (big baby)


Birth asphyxia
Risk of operative delivery.

Postpartum Prematurity
Hypoglycemia
Hypocalcemia
Polycythemia
Jaundice
Respiratory Distress Syndrome (delay in lung maturity ).

** Why shoulder dystocia in uncontrolled GDM ?


➔ Causes of shoulder D can either be due to GENETIC or GDM.
➔ In GDM, the fat distribution more to the trunk causing ‘stuck in AP plane during labour’.

** Why macrosomia in uncontrolled GDM ?


➔ Maternal hyperglycemia ➝ fetal hyperglycemia ➝ high insulin production in fetal pancreas
(insulin-like growth factor -IUGF) ➝ IUGF responsible for macrosomia.

** Why IUD in uncontrolled GDM ?


➔ Maternal hyperglycemia ➝ high glycosylated hemoglobin ➝ low oxygen carrying capacity
➝ fetal hypoxia ➝ SUDDEN IUD.

MANAGEMENT:
1. Pre-pregnancy in cases of established/ pre-existing DM :

1. Advice regarding diet, weight, smoking and alcohol.


2. Optimizing glycaemic control
3. Medication review
4. Folic acid supplementation
5. Screening and management of diabetes complications
6. Information on pregnancy risk to the mother, including particular risks of hypoglycaemia
and DKA
7. Information on pregnancy risk to the baby— risk of congenital abnormalities, preterm
birth, and risk of macrosomia and growth restriction
8. Increased risk of hypertensive disease in pregnancy
-pre eclampsia prophylaxis in 1st trimester
9. Importance of pregnancy planning and accessing multidisciplinary care in early pregnancy

64
2. Antenatal care:
Management is dependent on the pre-existing DM or GDM.

Patient with Pre-Existing DM


Mother:

● We need to optimize the diabetic control in the patient.


● If a patient of oral hypoglycemic agent, we have to change it into insulin therapy but the
dose this depend on the BSP level. (Blood sugar level is poorly controlled during pregnancy
with OHA as compared to Insulin ). Usually patients require admission for insulin therapy
unless the patient is already familiar with therapy (ie how to inject ,where to inject ,what to
do when she encounters the hypoglycemic attack ).
● If a patient is already on insulin, we just continue the treatment. Insulin is commonly given
in a soluble form pre meal (pre breakfast/pre lunch/pre dinner ).Usually it is advisable to do
dextrostix test pre insulin therapy . If Low just ignore the dose . Sometimes may need to
consider long acting (monotard) or intermediate (ie insulatard)
● We would also refer patient to the dietician to advise her on how to control the diet
(carbohydrate intake, reduce fat intake and increase fiber intake as well as exercise )
● Try to detect whether patients have the risk to develop retinopathy, neuropathy or
nephropathy. Then, we refer her to the respective physician.
● We will also prescribe patients with folic acid to prevent neural tube defects in the fetus. As
recommended practice we have to give 3 months before she gets pregnant and will
continue until 3 months pregnancy .
● If possible, patients need to be followed up in the Combined Clinic under consultant follow
up. Frequency of ANC visits depend on the severity of the disease as well as POA .
● In each visit ,for Mother
1. ask any symptoms hypo or hyperglycemia and sign of,
2. ask any symptoms of possible complications of DM such as PPROM, Preterm
contractions , Infection (UTI,vaginal candidiasis..etc …)

● Perform thorough physical examination in each visit

1. Look patient as a whole (general physical examination)


2. BP,PR
3. Fundoscopy
4. Any evident of skin infection (oral, below breast ,groin OR at injection site)
5. The abdomen: Look evident of polyhydramnios, macrosomic fetus ,lie and
presentation especially at 36 weeks onwards as well as fetal heart .

65
● For investigations

1. Performed BSP. Aim between 4-6 mmol /l . If severe enough do weekly, if under
controlled do every 2 weeks.
2. Urinalysis
3. HbA1c will be performed in the 1st trimester to monitor how bad the glucose
control for the past 3 months, if > 10 % fetal anomaly is about 25% and if < 8% fetal
anomaly is about 5 %. It can also be done one in each trimester.

Fetus:
● Perform dating scan in early first trimester.
● Fetal surveillance:
1. Abdominal examination: SFH
2. Fetal movement chart / fetal kick chart.
3. Serial ultrasound scan every 2 weeks : growth parameters and AFI.
4. Fetal anomaly scan at 20 – 22 weeks.
5. CTG.
6. Doppler ultrasound scan if complicated with PE .

Patient with GDM


Mother:
Example if detected at 28 weeks , the MOGTT is abnormal:

● We need to do BSP to know whether to require treatment or just require diet


modifications.
● If BSP abnormal ex : 8 / 8 / 8 / 8. We should consider the insulin, short acting pre-meal (SC
actrapid) usually as in patients. We need to teach patient how , where to inject and what to
do when she encounter the hypoglycemic attack
● Then, we have to repeat BSP 1-2 days after insulin given to see whether the dose is
adequate or not. If not adequate , we have to adjust the dose accordingly (ie normal BSP
level 4-6 mmol/l .
● If normal, then continue the same dose and can allow the patient home.
○ Educate the patient
○ Compliance of the diet and treatment

*** Other measures are pretty much the same as pre-existing DM.

Fetus:
● Dating scan.
● Fetal surveillance.

66
The aim of antenatal care is to control blood glucose level at 4 – 6 mmol / l to avoid complications
of DM to occur.

When to deliver?

● If there is no evidence of maternal or fetal compromise, we have to manage the patient


expectantly until 40 weeks in case, where the patient did not require treatment and only
on diet modifications. However, we won’t allow post dates because of the risk of IUD,
macrosomic baby and fetal hypoxia.
● If patient on treatment, we manage the patient expectantly until 38 weeks.
● In case of poorly controlled, early delivery may be indicated, but the risk of respiratory
syndrome and neonatal jaundice is high, thus dexamethasone should be administered.
● Remember dexamethasone MAY JEOPARDISE the DM controlled therefore in most cases ,
IV insulin infusion is indicated together with monitoring dextrose stick hourly, to prevent
hypo/hyperglycemia and possible ketoacidosis.

SUMMARY

GDM

i. On diet control without complications 40 weeks

ii. On treatment 37+0 - 38+6 weeks

iii. With maternal or fetal complications Before 37 weeks

Pre-existing DM

i. Without complications 37+0 - 38+6 weeks

ii. With maternal or fetal complications Before 37 weeks


** Adopted from PRIMEOG

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Mode of delivery:

➔ If good control, the baby is not macrosomic, therefore, SVD can be opted.
➔ Remember wound healing in DM may be delayed therefore the morbidity is high
➔ CS is justified in cases of macrosomic baby or any other obstetrics complications such as in
twins pregnancy , 2 previous scars, abnormal lie or breech presentation or mother with a
history of subfertility .

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How to manage women with GDM or DM in Labour ??

Mother in labour:

Stage Management

Intrapartum 1st stage


Mother:
● Monitor progression of labour using partograph.
○ BP, PR, Temp.
○ Monitor the contractions every 30 minutes
○ Abdominal palpation to check lie,engagement
○ Vaginal examination every 4 hourly OR earlier if
indicated.
● Diabetic control by IV insulin infusion (DKA regime).
● Monitor blood sugar level using dextrose sticks hourly.
● Nutrition: IV drip, NBM preparation.
● Pain killer: epidural (ideally), i/m pethidine, s/c morphine,
Enthonox.. Etc.
● Urine acetone 1 hourly to detect ketoacidosis.

Fetus
● Continuous CTG monitoring in high risk patients.

2nd stage
● Encourage patients to push and conduct delivery the
same like other normal pregnancy.
● Continue CTG monitoring.
● If prolonged 2nd stage, ask a senior obstetrician to assess
the patient due to worry of shoulder dystocia or CPD.
● This is to assess whether a patient can fit for instrumental
delivery or C section.

3rd stage
● Give syntocinon / syntometrine.
● Early cord clamping.
● CCT
# active management of 3rd stage of labour.

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Postpartum ● Hands baby to pediatrician.
● Monitor blood sugar level (dextrose stick premeal).
● Treat accordingly to the dextrose stick.
● IF GDM : stop insulin.
● IF Pre-existing DM: cut 1/3 of the dose then continue
regime as before pregnancy if patient on insulin therapy
BUT if patient previously on oral hypoglycemic agent ,just
continue the same dose what she took before pregnant
once patient can take normal diet .
● Then repeat MOGTT after 6 weeks to know whether it is
GDM or pre-existing DM.
● Usually we need to discuss with the couple regards to
Family planning

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71
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6.1 GESTATIONAL DIABETES MELLITUS

HISTORY TAKING:

Establishing the ● When MGTT was done?


diagnosis of GDM ● What was the indication of MGTT?
○ maternal age > 35
○ maternal weight > 80 kg
○ glycosuria on > 2 occasions
○ ultrasound shows macrosomic baby
○ presence of polyhydramnios
○ history of macrosomic baby
○ history of recurrent vaginal candidiasis
○ family history of DM in 1st degree relative
○ previous history of GDM
○ history of unexplained IUD
● How was the result?
● How many BSP were done and how was the result?
● Any signs and symptoms of hyperglycemia (polydipsia,
polyuria, polyphagia, fatigue,LOW)?
● Any complications (maternal or fetal)?

Maternal components Diabetic control ○ Well controlled or not?


○ Referral to dietician.
○ Advice diet.
○ If on treatment, symptoms of
hypoglycaemia (palpitation, dizziness, cold
sweat, trembling).
○ Change of treatment.
○ Admission required/ how many times?

Associated problems ○ Infections (UTI, vaginal candidiasis, skin


infection)
○ Hypertension
○ Excessive weight gain
○ Polyhydramnios (abdominal discomfort,
unstable lie, malpresentation, preterm
labour, PPROM)

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Fetal components ● Fetal growth
● Fetal abnormality
● Macrosomia
● Polyhydramnios
** detected during Transabdominal Ultrasound (TAUS)

PHYSICAL EXAMINATION:

General Examination
● Weight, BMI ⇾ obese or not
● Blood pressure
● Pallor (if a/w chronic renal failure)
● Skin lesion / scratch marks (below breast, armpit, groin, perineum)
● Injection site ⇾ atrophy, hypertrophy, cellulitis (deltoid, thigh)
● Heart / lung / breast / funduscopy (CWS, haemorrhage, neovascularization, papilloedema)

Abdominal Examination
● Fundal height / SFH ⇾ uterus > date due to macrosomic baby or polyhydramnios
● Lie and presentation ⇾ may cause abnormal lie due to polyhydramnios
● EBW larger ⇾ macrosomic baby
● Fluid thrill positive ⇾ polyhydramnios
● Fetal heart rate ⇾ worried about IUD

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7.0 HYPERTENSIVE DISORDERS IN PREGNANCY
Hypertension Systolic blood pressure of ≥ 140 mmHg and/or diastolic blood pressure ≥90
mmHg, with at least 2 measurements, taken at least 4 hours apart.

Classification 1. Preeclampsia (PE)*


a) PE de novo
b) PE superimposed on chronic HTN
2. Gestational hypertension*
3. Isolated office hypertension (a.k.a. white coat hypertension)
4. Chronic hypertension

*after 20 weeks gestation

DEFINITION:
Isolated Office ● BP ≥140/90 mmHg only in the clinic with normal BP demonstrated by
Hypertension ambulatory BP monitoring (ABPM) either awake or during sleep
● In the absence of ABPM device, HBPM can be used
● Risk of gestational hypertension (50%)
● Risk of PE is 8%

Chronic Either 1 of the following:


hypertension
in pregnancy 1. HPT diagnosed before pregnancy
2. HPT diagnosed before 20 weeks of gestation
3. HPT diagnosed after 20 weeks of gestation but not normalized after 3
months postpartum.

● Risk of PE is 25%

Causes:
● Primary/ Essential
● Secondary
○ Renal: renal artery stenosis, GN, polycystic KD, diabetic nephropathy,
nephritic syndrome, SLE, antiphospholipid syndrome
Pheochromocytoma
○ Coarctation of aorta

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Gestational ● Hypertension detected after 20 weeks and normalize within 3 months
hypertension postpartum.
● Risk of PE is 25% (especially if presented before 34weeks)

Preeclampsia Hypertension diagnosed after 20 weeks gestation associated with any of the
following:

Significant proteinuria ● Urine dipstick +2


● Spot urine protein-creatinine ratio ≥30
mg/mmol
● 24hr urine sample ≥300 mg protein

Renal insufficiency serum creatinine ≥90μmol/l or oliguria

Liver disease raised transaminases and/or severe right


upper quadrant or epigastric pain

Neurological problems convulsions (eclampsia), hyperreflexia with


clonus or severe headaches, persistent visual
disturbances (scotoma)

Haematological thrombocytopenia, coagulopathy, haemolysis


disturbances

Fetal growth restriction Reduced fetal movement, uterus smaller than


date, IUGR from TAS

Eclampsia The presence of tonic-clonic convulsions in a woman with pre-eclampsia and


in the absence of any other identifiable cause.

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RISK FACTORS OF PRE-ECLAMPSIA:
Moderate risk 1. Primigravida
2. Age > 40 years old
3. Pregnancy interval > 10 years
4. BMI >35 kg/m² at first visit
5. Family history of PE
6. Multiple pregnancy

High risk 1. Hypertensive disease during previous pregnancy


2. Chronic kidney disease
3. Autoimmune disease (Eg: SLE, APS)
4. T1 or T2 Diabetes Mellitus
5. Chronic Hypertension

IMPORTANCE OF RISK STRATIFICATION:


● To screen for high risk mothers for initiation of PE prophylaxis;
○ Low dose aspirin (100-150mg) at 12-16 weeks of gestation until delivery (based on
CLASP trial, low dose aspirin 60-100mg has moderate benefit (10%) in prevention of
pre-eclampsia and its consequences. Especially beneficial in women with a prior history
of severe, early onset pre-eclampsia.)
○ Calcium supplement 500-1000mg/day (CPG Malaysia) or 1.5g/day (RCOG) before 20
weeks gestation (52% reduction of risk)
● Start PE prophylaxis when there is at least 1 high risk or at least 2 moderate risk factors

COMPLICATION OF GESTATIONAL HYPERTENSION (PIH, PE, ECLAMPSIA):

Maternal Fetal Placenta

1. Eclampsia 1. IUGR 1. Placenta infarction


2. HELLP syndrome 2. SGA
3. Coagulopathy (DIVC) 3. IUD
4. Renal impairment 4. Complications of
5. Cerebral haemorrhage prematurity
6. Retinal detachment
7. Risk of preterm delivery
8. Risk of operative delivery
9. Liver impairment
10. Pulmonary oedema

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7.1 GESTATIONAL HYPERTENSION/ PREGNANCY-INDUCED
HYPERTENSION (PIH)

SCENARIO 1
26 y/o, primid, 32 weeks, on ANC BP was found to be 150/90 mmHg.
How do you manage this patient?

● Admit to ward
● Advise patient for bed rest
● Monitor PE chart
● Monitor BP every 4 hours
○ If BP remains high (150/100mm Hg), start on oral antihypertensives either
Methyldopa or Labetalol
● Ask for symptoms of impending eclampsia (IE): headache, giddiness, BOV, nausea +
vomiting, epigastric pain
● Do blood investigations: FBC (thrombocytopenia and anaemia), RP, serum uric acid,
coagulation profile, LFT
● Do urine dipstick
○ If contains albumin, do a 24H urine collection to quantify whether amount is
significant or not
○ If there is significant albumin - PE
○ If not, still PIH
○ OR if on dipstick albumin is 1+, do UFEME, if SG>1.030 indicates UTI
● For fetus, do: FMC
● CTG
● USS: look at growth parameters for evidence of IUGR, measure AFI for oligohydramnios,
look for calcifications of placenta

If the patient is normotensive, blood investigation results are normal and the CTG is reassuring,
then I will discharge the patient with advice to her and also the husband:
● to be compliant to the medication
● TCA if there are any symptoms of IE
● Ask patient to monitor her BP at the nearest clinic
● Follow up at a tertiary center where there are specialists/consultants

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SCENARIO 2
Patient who is a primigravida, with PIH on treatment, currently at 32 weeks of POA

HISTORY TAKING:
● Ask about symptoms of impending eclampsia- headache, giddiness, blurring of vision,
nausea and vomiting, epigastric pain, RHC pain
● Ask whether patient is compliant to treatment or not
● Advise bed rest to lower down BP (if BP is high)
● Monitor closely BP and PR
● Fetal movement chart
● On physical examination:
○ Vital signs
○ General examination: toxic-looking, edematous, do fundoscopy
○ RS: lung crepitations for pulmonary edema
○ Abdominal examination: uterus tense and hard(abruptio placenta), SFH uterus
smaller than date(IUGR)
○ Neurological examination: hyperreflexia, ankle clonus

INVESTIGATIONS:
● For the mother, I will do blood investigations which include FBC to look for
thrombocytopenia and anaemia
● Renal profile
● Coagulation profile
● Serum uric acid
● LFT
● Urine dipstick for any evidence of proteinuria

While for the fetus, I will do FKC, CTG and USS because in PIH, there is a possibility of having an
IUGR fetus (BPP and Doppler US only in severe cases)

If the patient is normotensive, blood investigation results are normal and the CTG is reassuring,
then I will discharge the patient with advice to her and also the husband:
● to be compliant to the medication
● TCA if there are any symptoms of IE ( headache, BOV, n/v, epigastric pain)
● Ask patient to monitor her BP at the nearest clinic
● Follow up at a tertiary center where there are specialists/consultants

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SCENARIO 3
On follow up at 34 weeks POA
● Same history taking
● Same PE
● If blood investigations are normal and there is no evidence of maternal or fetal
compromise, then I will manage her expectantly until 38 weeks POA.
● If there is evidence of fetal compromise (evidence of IUGR on USS), I will not prolong her
pregnancy until 38 weeks of POA. Do serial growth scan, monitor with previous scan
records.

SCENARIO 4
IUGR diagnosed at 34 weeks POA. Would you deliver the baby?

● I will not deliver yet because the fetus is still premature. However I will monitor the fetal
well-being closely.
● My main concern is prematurity and the risk of RDS
● Therefore, I will give IM Dexamethasone (2 doses) and monitor the fetus well-being closely
by FKC, CTG and Doppler US.
● If the results show that there is maternal or fetal distress, then I will deliver immediately
● However, as long as the fetus does not show any evidence of distress, i will prolong the
pregnancy until 38 weeks of POA (lungs already matured)

SCENARIO 5
IUGR diagnosed at 36 weeks POA. What would you do?

Since there is fetal compromise, I will deliver immediately by emergency LSCS

SCENARIO 6
High BP diagnosed at 38 weeks. Outline your management.

● Admit to ward
● Advice for bed rest
● Monitor BP
● If persistent, start on oral Labetalol 100mg tds
● Do blood investigations
● Do fetal monitoring
● Review BP and biochemical markers
● When BP is well controlled, deliver the baby
● Mode of delivery: do USS to see lie, presentation and EFW
- If fit for SVD, wait for spontaneous labour for 24H, if still not reach labour, induce the
patient
- If SVD not feasible, LSCS

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SCENARIO 7
Patient with PIH diagnosed with abruption placenta

● This is an obstetric emergency, therefore I will initiate a red alert


○ Monitor the patient’s vital signs, determine whether she is hemodynamically stable
or not
● If there is evidence of haemodynamic shock, resuscitate the patient
● Maintain the airway, breathing and circulation
○ Set large bore iv cannula and draw blood for investigations (FBC, coagulation profile,
GXM) +/- blood transfusion
● If we suspect the mother has DIVC, activate the massive transfusion protocol (MTP) and
start on the DIVC regime (6 cryoprecipitate, 4 blood, 4 platelets, 2 FFP).
● While waiting for the lab results (FBC, coagulation profile, fibrinogen), we can give one
cycle of the DIVC regime.
● If the lab results show no DIVC, proceed with Massive Transfusion Therapy (MTP).
● If there is presence of DIVC, continue with the DIVC regime.
● Once mother is stable, deliver the fetus via emergency LSCS
○ *Is there an occasion whereby an abruption placenta patient can deliver
vaginally? Yes, there is, provided if:
■ The CTG is reactive
■ Multiparous who is already in labour and therefore can give AOL to hasten
the delivery
■ Primigravida already in 2nd stage, os fully dilated and can use instrumental
delivery

*however, if a multiparous already in labour with abruption placenta and breech presentation,
must deliver by emergency LSCS because of complicated breech

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7.2 PRE-ECLAMPSIA

SCENARIO:
23yo, at 12 weeks POA, came in for the ANC. On examination, SFH was 16cm.

Possible cause ● Wrong date


● Pregnancy with pelvic mass
● Multiple pregnancy
● Molar pregnancy

List the investigation you would like to do Transabdominal Ultrasound (TAS) to:
and justify ● Confirm date of pregnancy
● Number of fetus
● Presence of mass

On examination by MO, the SFH was found to be 14cm. At 28 weeks POA, she came for the ANC.
BP was found to be 150/110mm Hg and urine albumin was 3+. On examination, SFH was 23cm.

Diagnosis (Δ): Pre-eclampsia with suspected IUGR

IMPORTANT HISTORY TO ELICIT:


● Ask for symptoms of IE.
● Fetal movement?
● Leaking liquor?
● Contraction?
● Abdominal pain?

OUTLINE YOUR MANAGEMENT:


● Admit patient to HDW
● Advice for bed rest
● Monitor BP closely every 15 min
● Watch for sm of IE
● Do blood investigations: FBC, RP, serum uric acid, coagulation profile, LFT

If persistent DBP>110mm Hg, give oral Nifedipine 10mg stat first, then oral Labetalol 100mg TDS (if
no tachycardia, can give methyldopa 250mg TDS)
● Do fetal monitoring by FMC, CTG, USS and consider doppler umbilical artery (in view of
IUGR), if absent or reversed end diastolic flow (EDF) -> deliver immediately.
● Give IM Dexamethasone

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○ If biochemical markers came back as abnormal (maternal compromise), deliver
immediately.
○ If BP is well controlled, discharge the patient and follow up weekly.
SEVERE PRE-ECLAMPSIA: Management
● Admit to HDW
● Advice patient to bed rest
● Monitor BP closely every 15 min
● Set 2 large bore IV cannula and draw blood for FBC, RP, serum uric acid, coagulation profile,
LFT)
● If DBP remains >110mm Hg with sm of IE, give IV Hydralazine 5mg bolus if patient not
tachycardic
● Control and stabilize BP at 140/90mm Hg
● Give prophylaxis 4mg of MgSo4 as slow bolus and prepare MgSo4 infusion at 1g/h as
maintenance dose. (MgSO4 is also used as a neuroprotection and anti-hypertensive)

Once patient became stable,


● assess sm of IE
● ask about fetal movement
● any PV bleeding/abdominal pain
● Do PE (neurological examination and fundoscopy)
● Put patient on input-output chart
● Do fetal monitoring by CTG and USS
● Deliver immediately

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7.3 ECLAMPSIA

ECLAMPSIA PROPHYLAXIS:
1. Start Magnesium Sulphate (MgSO4) and continue for 24 hours after the last fit or
delivery, whichever event is later.
2. Consider delivery once decision for MgSO4 has been made

Magnesium Sulphate regime

Regime Route Regime

Loading Dose IV 4g (8mL) MgSO4 with 12 mL normal saline (NS)


(either IV or IM) given over 15 minutes

IM 10g to be given as 5g (10mL) MgSO4 at each upper


quadrant of patient buttock (add 1mL of lignocaine
2%)

Maintenance Dose IV 24.7 (10 ampoules) MgSO4 with 500 mL NS to run


(either IV or IM) at 1g/hour (21 mL/hour)

IM 5g (10 mL) MgSO4 deep IM in alternate buttock


every 4 hours

Recurrent seizure IV 2g (4mL) + 8 mL NS given over 15 minutes and


continue with maintenance dose of 1g/hour

Magnesium Sulphate, MgSO4


1 vial = 2.47 g/5ml (50% concentration)

Monitoring toxicity - MgSO4 chart (hourly)


● ECG for prolonged PR interval and wide QRS complex
● Deep tendon reflexes must be present
● Urine output should be > 30ml/hour (0.5 ml/kg/hr)
● Respiratory rate between 12-16 /min
● Oxygen saturation should be > 95%
● Assess AVPU.

ANTIDOTE:
1gm Calcium gluconate (10 ml of 10% solution) given slow IV bolus over 3 min

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SCENARIO 1
18 y.o, primigravida, at 38 weeks POA with BP = 160/110 mmHg suddenly develops fit at the
labour room. How do you manage her?

1. Eclampsia is considered as obstetric emergency


2. Firstly, i've to initiate RED alert
3. Then, position the patient on L lateral position to prevent aspiration
4. Maintain ABC
○ Give O2 to the mother
○ Make sure the airway is patent and put ET tube to prevent airway obstruction &
biting tongue
○ Ask the nurse to put 2 large bore IV cannula at least 16 gauge & draw blood at the
same time
○ Send blood for FBC, GXM, RP, LFT & coagulation profile (in case pt will end up with
C-section)
5. Stop fitting - give slow bolus IV MgSO4 4g loading dose over 10-15 min followed by
maintaining dose 1g/hour
○ or give IM if IV assess is not available - 5g loading
○ dose over 4 hour once injection 2.5g to each buttock
○ once MgSO4 is administered, pt is monitor by MgSO4 chart

6. MgSO4 charting

● BP & PR manually monitoring every 15 minutes


● RR monitoring every 30 minutes
● patellar reflex hourly
● urine output >30ml/hr
● serum Mg level must be within 1.7-3.5mmol/L

If pt is anuric, or other features of MgSO4 toxicity*, do not administer MgSO4 until urine
output become normal

7. When the pt stop fitting, check vital signs (BP/PR)


8. If blood pressure >160/110mmHg, give antihypertensives such as:

IV hydralazine 5mg bolus at least 2min (s/e - tachycardia, severe headache)


OR
IV labetalol 50mg bolus over 2-5 min (s/e - bradycardia, severe headache)

9. Once pt is stable, monitor the fetal by CTG


○ if CTG reactive, os fully dilated, no contraindication of VD
○ if CTG reactive , os not fully dilated there is a role of vaginal delivery provided that
the mother is alert & conscious

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○ majority of eclampsia cases that occur antenatal as well as intrapartum reQ
C-section
○ if CTG not reactive (indicate fetal distress → fetal hypoxia → cerebral palsy-->
C-section immediately

10. Majority of pt undergo C-section reQ GA. Bear in mind the risk of failed intubation is high
due to edematous larynx.
○ There is a role for regional anesthesia for C-section in stable pt but make sure
PT/aPTT is not prolonged becoz it is contraindicated in regional anesthesia.

11. Majority of pt after C-section reQ monitoring in HDW/ICU. in pt who are not stable, may
need monitoring in ICU for cerebral resuscitation.
○ After C-section, we worry about the risk of bleeding because eclampsia incidence of
thrombocytopenia/ coagulopathy is high.

12. In HDW/ICU, continue MgSO4 for 24 hours post fit or delivery, whichever is later &
antihypertensive drugs.

13. As pt is bedridden, she is at risk of DVT, so i have


○ s/c heparin 5000unit (usually give 6hours post-op)
○ advice for compression stocking

EXAM TIPS

* Signs of Magnesium Sulfate (MgSo4) toxicity: BURP

Bradycardia (cardiac arrest)


Urine Output decrease (oliguria)
Respiratory Rate decrease (resp. distress)
Patellar reflex absent (loss of tendon reflex)

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SCENARIO 2
Primigravida, at 34 weeks POA, with BP of 140/100 mmHg, suddenly develops fit in the labour
room. As a HO, what would you do?

1. ECLAMPSIA is an obstetric emergency, therefore I will initiate red alert (call for help from
nurses, sister-in-charge, neonatologist, anaesthetist, senior obstetrician)
2. Position the patient in the left lateral position
3. Maintain ABC:
■ Give O2 mask
■ Ensure the airway is patent, put ET tube to prevent airway obstruction and
tongue biting
■ Set up 2 large bore IV cannula (16G) and draw blood
■ Send blood for FBC, GXM, RP, LFT, coagulation profile
4. Give slow bolus 4g IV MgSo4 loading dose over 10-15 min followed by maintaining dose
1g/h OR give IM MgSo4 5g if vein is not accessible and need to monitor patient by MgSo4
chart
5. MgSo4 chart:
○ BP, PR, RR manually monitored every 15 min
○ Check pulse oximetry
○ Patellar reflex hourly
○ Urine output> 30 ml/h (CBD insertion)
6. MgSo4 toxicity:
○ Cardiac arrest
○ Respiratory arrest
○ Loss of tendon reflex
○ Oliguria
○ Then, give antidote- calcium gluconate
7. When fitting stops, check vital signs, pulse oximetry
8. If BP> 160/110 mm Hg give IV Hydralazine 5mg bolus of at least 2 min OR give IV Labetalol
50mg bolus over 2-5 min
9. Once the patient is stable, do CTG monitoring
10. Deliver immediately by LSCS

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7.4 CHRONIC HYPERTENSION IN PREGNANCY

SCENARIO:
Madam H, 28 y/o, with one previous scar, currently a twin pregnancy. At 10 weeks gestation, her
BP was noted to be 140/90 mmHg and repeated BP was 148/92 mmHg.

How would you manage her?

1. Take a detailed history to look for symptoms of PE / impending eclampsia such as: increase
in weight, facial edema, shortness of breath, limb swelling, nausea and vomiting, RUQ /
epigastric pain, frontal headache, blurring of vision, giddiness, seizures.

○ Also look for any evidence of complications of preeclampsia in the history such as:
Generalized abdominal pain, per vaginal bleeding (placental abruption)

2. Proceed with a complete physical examination of any signs and complications of PE.
3. For investigations, check her urinalysis for any evidence of significant proteinuria.

4. On fetal wellbeing, perform regular ultrasound scan to look for:


○ The growth parameters and estimated fetal weight of the fetuses for any growth
discrepancy by 20%
○ The AFI / MVP to look for any poli-oli sequence
○ The Doppler ultrasound of the middle cerebral artery to look for any Twin Anemia
Polycythemia Sequence (TAPS)
○ Fetal anomaly scan at 18-22 weeks

5. The patient should be on regular follow up every 2 weekly at the KK. During each follow-up,
assess for:
○ Symptoms of preeclampsia
○ Blood pressure
○ Urinalysis
○ Fetal growth

6. At 12 weeks of gestation, start the patient on PE prophylaxis consisting of low dose aspirin
(100-150mg) and calcium supplement (500-100mg).

7. Discuss the mode and timing of delivery.


○ Timing:
i) MCMA: 32-34 weeks
ii) MCDA: before 36 weeks
iii) DCDA: before 37 weeks
○ Mode: As the patient has 1 previous scar, the best option for her is elective LSCS as
there is increased risk of uterine rupture.

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8.0 TWIN/MULTIPLE PREGNANCY
DEFINITION:
● Dizygous (non-identical or fraternal twin)
○ increase incidence of DZ d/t assisted reproductive technologies (AST).
○ have familial predisposition.
● Monozygous (identical or maternal twins) / incidence constant every year/ 3.9 per 1000.

OVERVIEW:
● Maternal & perinatal mortality high.
● Perinatal mortality in twins is 5x more common compared to singleton.
● Triplets up to 10x mortality.
● Cerebral palsy 3x more common in twins.

TYPE OF MULTIPLE PREGNANCY: (is divided based on its)


1. Zygosity
2. Chorionicity
3. Amnionicity

Source:https://link.springer.com/article/10.1007/s00467-019-04418-0/figures/2

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Chorionicity Zygosity

● Important for risk stratification ● 2/3 DZ and 1/3 MZ


● 100% accuracy if determined during ● all DZ pregnancies are DC
the 1st trimester. ○ have separate chorions &
● Signs of DC are (acronym LDSS): amnions
○ Lambda or twin-peak sign at ○ no significant vascular
membrane insertion communication between
○ Dividing membrane > 2mm fetuses
○ Different Sex fetuses ● MZ pregnancies may become
○ Widely Separated 1st trimester ○ DC (within 3 days)
sac or separated placenta ○ MC (4 days) but 2 amnions
○ MC MA (after 7 days)
○ Conjoined twins (14 days twins)
● Most MC placentas have interfetal
vascular connections

Why is chorionicity important?


● Perinatal mortality in MC 5x more compared to DC
● Cerebral palsy:
○ MC = 30%
○ DC = 3%

SUMMARY

1. Division of embryo before trophoblast differentiation leads to 2 chorions, 2 amnions


(days 2 – 3).
2. Division of embryo after trophoblast differentiation but before amnion formation leads
to 1 placenta, 1 chorion, 2 amnions (days 4 – 8).
3. Division of embryo after amnion formation leads to 1 placenta, 1 chorion, 1 amnion
(days 9 – 13).

Important US features:

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Conjoined twins
● Are monozygotic multiples that do not fully separate from each other d/t incomplete
division of fertilized ovum.
● The individuals will be connected at certain points of the body & may share tissue, organ or
limbs.

RISK FACTORS:
● Assisted fertilization specifically women who had undergone medically assisted conception
(MAC) either using induction of ovulation (clomiphene citrate), hMG.
● Previous/Family history of multiple pregnancy.
● Method of contraception e.g. 20% with ovulation induction.
● Ethnicity (esp. Black race from Africa/Nigeria).

WHAT IS THE APPROACH (WHEN TO SUSPECT?):


From history taking,
● Excessive symptoms of early pregnancy.
Upon Physical Examination,
● Uterus larger than date.

On Inspection Stretching striae gravidarum


Dilated veins
Fundal height is increased

On Palpation SFH> date


Multiple fetal poles
Unable to determine lie and presentation (abdomen globular shape)
Unable to determine fetal heart
Tenderness on superficial palpation
Fullness of flank

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EXAM TIPS

Timing of scan:
1. First trimester (Booking)
Viability of pregnancy, number of fetus, gross fetal anomaly (hydrops fetalis,
anencephaly), dating.
2. Second trimester (Detailed Scan)
18-22w- useful for dating in late booker, liquor, fetal anomaly scan.
3. Third trimester (Growth Parameters)
28-32- fetal growth, placental localization.

Why in multiple pregnancy, there is increased risk of operative delivery?


Because multiple pregnancy is associated with abnormal lie, malpresentations and
complications such as IUGR, PIH and GDM.

**Deliver earlier with the presence of complications

COMPLICATIONS:
Mother Fetal

Antenatal Excessive symptoms of pregnancy ● Miscarriage


which might requires recurrent ● Unexplained IUD
admissions, such as: ● Congenital anomalies/
● Hyperemesis gravidarum/ malformations (anencephaly,
backache/ varicose veins/ DS, NTD)
edema/ discomfort & ● Twin-to-twin transfusion
dyspnea syndrome (TTTS)
Possible comorbidities: ● Twin reversed arterial
● Anemia in Pregnancy perfusion sequence (TRAP)
● Hypertensive disorder such ● IUGR
as Pre-Eclampsia ● Prematurity (d/t preterm
● Diabetes Mellitus delivery)
● PPROM/PROM
● APH from placenta previa

Intrapartum ● Prolonged labour ● Preterm labor


● Increase likelihood for ● Malpresentation
operative delivery ● Fetal hypoxia
(instrumental or C-section) ● Retained 2nd twin
● Uterine rupture ● Fetal trauma
● Risks of internal podalic
version, ICV, intrauterine

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manipulation as opposed to
ECV (2nd twin in transverse
lie)

Postpartum ● PPH ● Prematurity (Respiratory


● Retained product of distress syndrome, sepsis,
conception (placenta) jaundice, hypothermia)
● Psychological issues such as ● Cerebral palsy (Hypoxic
how the mother will cope on babies), Erb’s Palsy
breastfeeding and taking (Macrosomic babies)
care of the babies.

Quintero staging system for Twin-Twin Transfusion Syndrome (TTTS):

CLERKING TIPS

Quintero staging: Presence of Growth Discordance >20%


1: Poly/oli sequence (>8/<2 MVP)
2: Absence of bladder in donor
3: Abnormal doppler (Umbilical artery doppler & MCA doppler): MCA PSV (30x2)- 60, (15x2)- 30
4: Hydrops of recipient
5: IUD

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How to manage multiple pregnancy? Must know the complications in order to manage
● Where to f/up
● Frequency of f/up
● Mode of delivery

MANAGEMENT:
1. Counseling (perinatal risk). Early detect of possible comorbidities are crucial:
○ Anemia in pregnancy
○ Preterm labor
○ PIH/PE
○ IUGR
○ GDM

2. Dating scan to determine the chorionicity in the 1st trimester or early 2nd trimester.
○ Confirm date of pregnancy.
○ Determine chorionicity because there are much more complications in
monochorionic (MC) twins compared to dichorionic (DC) twins, therefore the
management is different.

3. Routine US scan, done at tertiary centre with feto-maternal specialists because multiple
pregnancy is a high risk pregnancy:
○ 2 weekly for MC
○ 4 weekly for DC

4. Detailed US scan at 20 – 22 weeks (for detection of fetal structural anomaly).

5. Fetal well being:


○ Growth scan to rule out IUGR
○ Fetal kick chart
○ Doppler US

6. Haematinic supplementation:
○ Ferrous fumarate 200mg TDS
○ Folic acid 5mgOD
○ Vitamin C
○ Vitamin B complex

7. Follow-up at hospital under one consultant.

8. Refer fetal medicine (fetomaternal specialists) unit if complications of MC.

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9. Factors influencing Mode of Delivery for multiple pregnancy:
○ Number of fetuses
■ Timing of delivery:
1. MCMA 32 - 34 W
2. MCDA < 36 W
3. DCDA < 37 W (May
treat as normal labour)
○ Presentation and lie of leading twin:
■ Aim for vaginal delivery IF leading twins in cephalic
presentation, longitudinal lie and both fetal condition adequate.
■ If vaginal delivery is contraindicated, consider C-section.
○ Presence of complications
■ Subfertility
■ Maternal problems

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9.0 BREECH PRESENTATION
Epidemiology

❖ More common in preterm (40% at 20 weeks, 25% at 32 weeks, 10% at 36 weeks)


❖ Fetus is fairly mobile due to relatively small size compared to the liquor volume
❖ Fetal lie usually stabilize by 36 weeks
❖ At term = ~3-5% (chance of spontaneous version after 38 weeks is < 4%)

Etiology

Mother Fetus & Placenta

● Wrong date (commonest) ● IUGR (20-30%)


● Uterine anomaly (septate/bicornuate) ● Congenital anomaly
● Large pelvic mass (e.g., cervical fibroid) (eg; hydrocephalus, anencephaly)
○ prevent engagement ● Placenta previa
● Polyhydramnios ● Prematurity (especially if < 32 weeks)
● Oligohydramnios ● Multiple pregnancy
● Lax uterus (multiparous women) ● IUD
● CPD (small or contracted pelvis)

Types of Breech Presentation

Frank ➔ A.k.a extended breech (65%(


➔ Both hips flexed and both knees extended

Complete ➔ A.k.a flexed breech (25%)


➔ Both thigh & legs are flexed

Incomplete ➔ A.k.a footling (10%)


➔ One or both of the hips are not flexed so that foot lies below

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Management

❖ All women with breech presentation at term should be offered external cephalic version
unless there is an absolute contraindication.

External Cephalic Version

❖ Aim : Maneuvering the infant to a vertex position

❖ Timing of procedure :
Nulliparous : 36 weeks gestation
Multiparous : 37 weeks gestation

❖ Intended benefits :
➢ Successful rate : 50%
➢ Success ECV
■ ↓chances of non-cephalic presentation
■ ↓ chances of Caesarean section

How to do ECV

1) Admit pt and NBM midnight


2) Do baseline Ix (in case of EMLSCS)
3) Do CTG
4) U/S to;
a) Types of breech
b) Position of fetal spine
c) AFI
d) EFW
e) Location of placenta
5) Obtain, inform & written consent
6) Terbutaline ( S/C or IV ) 250μg (to relaxed uterus ; when maternal HR > 110 bpm)
7) 20 mins later ➝ Attempt ECV
8) ECV done in 5 mins with maximum 3 attempts
9) Use ‘forward roll, backward slip’ technique
10) Do U/S to confirm presentation
11) CTG post ECV ;
a) If normal ➝ TCA 1/52
b) If suspicious ➝ arrange for EMLSCS

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Contraindications

Mother Fetus

● Previous uterine scar (e.g., LSCS, full ● Multiple pregnancy


thickness myomectomy) ● IUGR
○ ↑ risk of uterine dehiscence/ rupture
● APH (may worsen or increase the risk of
placental separation)
● Preeclampsia
● Bad obstetrics hx

Absolute Relative

● Absolute contraindication for vaginal ● Previous C-sec


delivery (PP, classical Cesarean section, ● IUGR
pelvic mass obstructing labour) ● Oligohydramnios
● Placenta abruptio ● Unstable lie
● Major uterine abnormality ● Severe hypertension or other medical
● Rupture of membrane disorders
● Abnormal fetal Doppler or CTG
● Multiple pregnancy
● Current or recent (<1 week) vaginal
bleeding
● Mother refusal
● Severe preeclampsia

Complications

Mother Fetus & Placenta

● Placenta abruptio ● Placenta abruptio


● Uterine scar dehiscence or rupture ● Cord entanglement
● PPROM ● Transplacental hemorrhage
● Preterm labor
● Rh sensitization (in Rh negative
mother)
● Emergency C-sec

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Trial of Breech Vaginal Delivery

❖ Planned Caesarean section (Canadian Breech Trial) is recommended over Breech Vaginal
Delivery because of the reduced number of perinatal mortality.
❖ A safe vaginal breech birth requires highly skilled intrapartum care.
❖ Approximately 40% of planned vaginal breech births require an emergency Caesarean section.

Contraindications

CPD 1. An absolute CI to VD
2. Exclude CPD by clinical or radiological pelvimetry (X-ray/CT)
a. AP diameter of pelvic inlet < 11cm

EFW 1. Size of the baby is estimated clinically or by USS (especially look at


the abdominal circumference)
2. Contraindicated if EFW > 3.5kg

Fetal Neck 1. Hyperextension of fetal neck by USS is absolute contraindication


2. Can consider VABD in flexed fetal neck.

Others Exclude other causes that can prevent normal vaginal delivery eg placenta
previa, large pelvic mass (e.g., cervical fibroid)

Methods

❖ Breech pregnancies > 36 weeks will be yellow-tagged (followed-up by specialist &


delivered in hospital)

1st Stage ➔ As for any other normal deliveries


➔ Do pelvic examination (VE) to exclude cord presentation or prolapse
(common in flexed breech)
➔ Adequate anesthesia (preferably epidural)

2nd Stage ➔ Perform episiotomy to facilitate the delivery of after-coming head


➔ Pinard manuever to facilitate delivery of feet in frank breech.
➔ Lovset’s maneuver can be performed for delivery of extended arm
➔ Delivery of head has 3 ways:
1. Burns-Marshall maneuver
2. Mauriceau Smellie-Veit maneuver
3. Outlet forceps (Piper / Wringley forceps)

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Complications

Fetal hypoxia ➔ Cord prolapse or compression


➔ Early placenta separation
➔ Delay in delivery of the fetal head (> 10mins)
➔ Premature inhalation (inhalation of mucus - obstruct the
airway)

Intracranial hemorrhage ➔ Due to rapid descent of the after-coming head causing


sudden compression followed by subsequent
decompression
◆ tentorial tear & intracranial hemorrhage

Entrapment ➔ Entrapment of the after-coming head

Trauma ➔ Widespread bruising


➔ Shoulder dystocia with or without # of the humerus
➔ Brachial plexus injury (e.g., Erb’s palsy, Klumpke’s paralysis)
➔ Damage to the internal organs (viscera)
➔ Spinal cord transection
➔ Fractured femur
➔ Dislocated hip (e.g., DDH)

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(Short case) Breech presentation

Scenario – 32 y.o, G4P3 at 37 weeks POA presented to you with breech presentation. How
do you manage her?

1. In this particular lady, I would like to identify the possible causes of the abnormal
presentation.
2. There are several causes which can be divided into mother & fetal causes :

Mother Fetus & Placenta

● Wrong date (commonest) ● IUGR (20-30%)


● Uterine anomaly (septate/bicornuate) ● Congenital anomaly
● Large pelvic mass (e.g., cervical fibroid) (eg; hydrocephalus, anencephaly)
○ prevent engagement ● Placenta previa
● Polyhydramnios ● Prematurity (especially if < 32 weeks)
● Oligohydramnios ● Multiple pregnancy
● Lax uterus (multiparous women) ● IUD
● CPD (small or contracted pelvis)

3. Thus, I would like to take detail hx and do relevant Ix.

HISTORY

Detailed hx include :

1. I will ascertain the date by asking pt when her LNMP?


➔ she was sure of the date or not
➔ her menses is regular or not
➔ she was on OCP or not
➔ she breast feeding or not

2. I also want to ask whether she has the benefit of early dating u/s in 1st trimester or
not. If she had benefit of early u/s;
➔ Is it consistent with her POA?
➔ Is there any evidence of multiple pregnancy?

3. I would like to ask whether she had detail u/s at 20-22 week POA. If she had, what are
the findings which give an idea for me to rule out any fetal anomaly which leads to
polyhydramnios.

4. Besides that, I would like to ask whether she had been diagnosed to have GDM/DM
or not. If yes, whether her blood glucose level is well controlled or not?

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Because uncontrolled DM associated with polyhydramnios (refer to chapter GDM)
which leads to abnormal presentation.
5. I also would like to ask the patient whether she had been diagnosed as having PIH /
PE which was complicated with IUGR/SGA.

Because complication of the PIH/PE is IUGR/ IUD that may cause breech presentation.

6. Other than that, I also would like to ask the pt whether she had any history of
gynaecological problems such as fibroid or ovarian cyst which give an idea about
pelvic mass.

7. I also would like to ask her whether she had done recent u/s or not?
If yes,
➔ Where is the location of placenta? (to exclude PP)
➔ How is the liquor? (to exclude polyhydramnios / oligohydramnios)
➔ EFW? (to exclude macrosomic)

*** If pt is G3 P0+2, I would like to ask pt whether (TRO uterine anomaly)...


➔ she had recurrent misscariage
➔ she had difficulties to conceive/ subfertility
➔ she had hx of abnormal lie
➔ she had been told by the surgeon that she had abnormal uterus or not

PHYSICAL EXAMINATION

8. During P/E, generally, I want to measure the height of the patient because the
majority of the short stature patient is associated with non-gynaecoid pelvic.

9. Abdominal examination , I would like to examine whether;


➔ uterus larger / smaller than date (polyhydramnios / IUGR)
➔ multiple pole can be felt or not
➔ confirm the lie and presentation
➔ liquor volume
➔ clinical EFW

INVESTIGATION

10. I would like to arrange for ultrasound to look for;


➔ Evidence of pelvic mass
➔ Reconfirm the lie & presentation
➔ Physical biometry (HC and AC for IUGR)
➔ AFI
➔ EFW
➔ Localization of placenta

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MANAGEMENT

11. Management of breech presentation highly depends on the underlying causes and
POA.

12. In uncomplicated breech presentation, there is 3 options that we can offer to the
mother,
a) Vaginal delivery (in extended only)
b) External cephalic version
c) LSCS

However, based on Canadian term breech trial study showed that the elective LSCS for
uncomplicated breech at term offer better outcome to the fetal & mother as compared to
the vaginal delivery .

There is a role of SVD in this uncomplicated breech after we exclude all contraindication of
VD and
➔ Normal size baby (3.0kg)
➔ Adequate pelvic
➔ Flexed neck
➔ Multiparous
➔ Engaged & extended breech
➔ Pt understood about possible cx
➔ Skilled surgeon

# these are all prerequisites

This is because the risk of birth asphyxia is higher in vaginal delivery compared to LSCS. It is
may be due to:
➔ Risk of cord prolapse or compression is higher
➔ Damage to the internal organ (viscera)
➔ Spinal cord transection
➔ Fracture of the humerus and clavicle
➔ And the most dangerous cx is head entrapment

However, in certain cases, LSCS is strongly indicated in breech presentation. The indications
include:

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Maternal:

a) CPD
b) Previous uterine scar (2 LSCS / 1 classical scar)
c) Severe medical / obstetric problem (severe PE / heart disease)
d) Precious pregnancy (hx of subfertility, medically assisted conception, hx of stillbirth)

Fetus :

a) Macrosomia
b) Very small fetus
c) Premature fetus (unable to cope with stress of BVD)
d) Hyperextended neck ( increase risk of head entrapment, detected by USS)

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10.0 LABOUR
MANAGEMENT OF LABOUR

10.1 PROCESS OF NORMAL LABOUR


Labour Stages of labour Phases of labour

Definition: 1st stage Begins with the onset of Latent phase ● Cervix effaced and dilated from 0 to 3 cm
regular, painful
Presence of uterine contractions and cervical Active phase ● Cervix effaced and dilated from 4-10 cm
contraction that dilations until the cervix ● Cervical os dilates 1 cm/hr for primigravida
increases in frequency reaches full dilatation. ● Normal duration: <16 hours
and intensity which
leads to cervical 2nd stage ● Cervix is fully dilated (10 Passive phase ● When the os is fully dilated, the fetal head is able to
dilatation & cervical cm) descend through the pelvis
effacement with ● Presenting part ● This phase occurs until the fetal head has descend up to
descend of presenting descended down birth the pelvic floor
part of fetus. canal
● Mother has the urge to Active phase ● The fetus undergoes flexion -> internal rotation ->
push hyperextension -> external rotation -> delivery of anterior
● Painful uterine
● Delivery of the baby shoulder
contractions that
● The mother has a strong urge to push in coordinate to the
increases in intensity
regular contraction
● Leaking liquor*
● Presence of show* 3rd stage Begins after delivery of the fetus until the expulsion of placenta and its membranes.

*supporting points

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10.2 STAGES & ABNORMALITIES IN LABOUR

1st stage of labour Routine management Possible complications Management of complications

Latent Phase: ● +/- Induction of labour Prolonged latent phase (>8 hours) ● Not in labour: No immediate action
● In labour: Consider amniotomy / oxytocin
Cervix effaced and ● Evidence of obstruction: EMLSCS
dilated from 0 to 3 ● Evidence of fetal distress: EMLSCS
cm
Uterine hyperstimulation upon ● Stop the procedure
prostin insertion ● Perform VE
● A single contraction that lasts ● Remove prostin from posterior fornix
>2 minutes ● Rinse cervix with normal saline
● >5 contractions in 10 minutes ● Monitor CTG
● Consider tocolysis (Terbutaline, Salbutamol)

Active Phase: ● Diagnosis of Uterine hyperstimulation upon ● Stop infusion of oxytocin


established labour augmentation with oxytocin ● Maintain hydration
Cervix effaced and ● Artificial Rupture of ● Place patient on her left side
dilated from 4-10 Membrane ● Monitor CTG
cm ● Augmentation with ● Consider tocolysis (Terbutaline, Salbutamol)
oxytocin
Cervical os dilates 1 ● Pain relief Poor progress in active phase: ● Monitor if CTG is reactive
● Cervical dilatation: <1cm/hr for ● Abdominal examination: fetal lie and presentation
cm/hr for ● Maintain hydration
2-4 hr (malpresentation)
primigravida ● Partogram 4 hourly
● Feeding ● Vaginal examination: signs of obstructed labour in CPD,
Possible causes: presenting part (malposition)
Duration: <16 hours ● Hydration + IV Cannula
● Power: maternal exhaustion, ● Ultrasound scan: EFW, pelvic mass
/ GSH
inadequate uterine contraction ● Monitor Parthogram
● CTG monitoring
● Passage: CPD, pelvic mass

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Low risk patients: ● Passenger: macrosomia, ● Consider EMLSCS in obstructed labour
Intermittent (2 hourly) malpresentation (OT, OP),
High risk patients: malpresentation
Continuous

Normal CTG pattern Non-reassuring CTG ● Investigate cause


● Baseline heart rate: ● Baseline heart rate: 100-110 / ● Left lateral position
110-150 bpm 160-180 bpm ● Monitor maternal VS
● Baseline variability: 5 - ● Baseline variability: <5 for ● Stop oxytocin
25 bpm (NICE, 2017) ≥40-90 minutes ● Maintain oxygen and hydration
● Acceleration: ≥2 in 20 ● Deceleration: Early ● VE: Cervix dilatation, exclude cord prolapse
minutes decelerations, prolonged ● Consider: Internal CTG, expedite labour if os is full, LSCS
● Deceleration: Absent decelerations (up to 3 minutes) is not indicated

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Diagnosis of established labour Oxytocin augmentation Regime Partogram: Signs of satisfactory progress

● Cervix >3cm dilated Function: ● Contractions: good and regular


● Regular contractions ● To increase the frequency and strength of ● Contractions: ↑ duration and frequency
● Fetal descend uterine contraction (3 in 10 minutes each ● Rate of cervical dilatation: 1cm / hr
lasting >45 seconds) ● Presenting part: well applied to cervix
● To correct coordination of uterus

Pain relief Regime:

● Psychological ● Infuse 10 units of oxytocin (1ml) in 500ml NS


● Entonox (50% NO + 50% O2) also known as / 5% Dextrose solution
laughing gas ● Start infusion at 2 mU/min
● IV / IM Pethidine ● Via IV infusion syringe pump / IV drip
● IM Morphine +/- Naloxone ● Increase dose every 30 minutes
● Pudendal nerve block ● Maximum dosage
● Epidural anaesthesia Primid: 32 mU/min
Multip: 16 mU/min
Prev scar: 8 mU/min

Precautions:
● Previous scar
● Grand multipara
● Underlying heart disease

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CTG abnormality Figure

Early deceleration (type 1)

● Uniform in shape, occur with each contraction.


● Appear in a mirror image of the contraction.
● The onset of the deceleration is at the onset of contraction.
● The heart rate reaches its lowest point at the peak of the contraction,
recovers to baseline by the end of contraction.
● The amplitude of the deceleration is usually 40 bpm or less.

Causes:

● Compression of fetal head at perineum causing increased vagal


impulse.
● Iatrogenic: Mother on pethidine.
● Fetal sleeping.

Late deceleration (type 2)

● Uniform in shape and depth, occur after each contraction.


● Any deceleration whose lowest point occurs more than 15 seconds
after the peak of the contraction is said to be late.

Causes:

● A decrease in uterine blood flow:


○ Fetal hypoxia
○ Cord compression.

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CTG abnormality Figure

Variable decelerations

● Inconsistent in shape, frequency and relation to contraction.


● Tend to have an amplitude of 40 bpm or more.
● Atypical variable decelerations: indicates fetal compromise.

Causes:

● Umbilical cord entanglement:


○ Umbilical cord around the neck or body
○ True knot in the umbilical cord
○ Prolapsed umbilical cord.

Prolonged deceleration

● Described as a drop in the fetal heart rate of 30 bpm or more, lasting


for a period of at least 2 minutes.

Causes:

● Cord prolapse.
● Maternal hypotension due to the use of local anaesthetic via an
epidural catheter.
● Uterine hypercontractility.
● Vaginal examination or ARM.

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CTG abnormality Figure

Sinusoidal pattern

● Pattern: smooth, undulating, sine wave-like baseline.


● Variability is absent.
● The amplitude of the undulations is usually 5–15 beats and the
frequency 2–5 per minute
● Amplitude of 20 beats or more, and a frequency of 1–2 oscillations per
minute: suggestive of fetal hypoxia and are an indication for
immediate delivery.

Causes:

● Cessation of umbilical venous blood flow: Umbilical cord compression,


increased. intraperitoneal pressure, ascites
● Fetal anaemia: rhesus incompatibility, TTTS, APH.
● Fetal thumb-sucking
● Administration of narcotic analgesia (eg: pethidine).

Source: (CTG Made Easy, 4th Edition by Gauge S.)

111
2nd stage of labour Routine management Possible complication Management of complications

Passive phase: ● Lasts for: Prolonged second stage of labour Instrument assisted delivery:
<1 hour (primid) (>1hr) ● Ventouse assisted delivery
When the os is fully <30 mins (multip) ● Forcep assisted delivery
dilated, the fetal <120 minutes (on epidural)
head is able to ● Position the patient: Lithotomy
descend through position
the pelvis ● Secure IV access
● CTG monitoring for high risk
This phase occurs patients
until the fetal head ● Catheterization
has descend until ● Delivery
the pelvic floor ● Episiotomy (8’ o clock
mediolateral)
● Administer IM Syntometrine
(Ergometrine + Oxytocin) after
delivery of shoulders

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3rd stage of labour Routine management Possible complication Management of complications

Expulsion of placenta ● Palpate the abdomen (if there Perineal tears Repair of perineal tears
and its membrane is other fetus)
1st Injuries to the perineal skin
● Active management of 3rd
only IMPORTANT
stage of labour: Administer IM
2nd Injuries to the perineum Episiotomy = 2nd Degree Perineal Tear
Oxytocin (Pitocin)
Early cord clamping 3rd Injuries to the anal sphincter
(EAS/IAS)
Controlled cord traction
4th Injuries to the anal muscosa
Uterine massage
● Signs of placental detachment:
Gush of fluid Post partum haemorrhage 1. Call for help - RED ALERT
2. Resuscitate - ABC, Monitor vital
Uterus contracts signs & GXM
Uterine fundus rises 3. Medical management:
a. IV Oxytocin
Uterine fundus becomes b. IV bolus: 5IU
globular c. Infusion: 40IU in 500ml
Hartmans at 125ml/hr
● Check for completeness of d. IM Syntometrine 1 ampule
placenta (look for any missing (500mcg ergometrine + 5IU
oxytocin)
lobules in the placenta) e. IM Carboprost (hemabate)
● Check perineum for tear and 250mcg
4. Non surgical:
need for repair a. Uterine massage
● Send cord blood for TSH and b. Bimanual compression of uterus
c. Aortic compression

113
G6PD d. Bakri balloon
5. Surgical:
● Note blood loss
a. Compression haemostatic
● Documentation sutures: B lynch, Hyman
b. Systematic pelvic
● Encourage breastfeeding
devascularization, uterine a.,
internal a. ligation
c. Total hysterectomy
d. Subtotal hysterectomy

Retained placenta - Endometrisis Manual removal of placenta


secondary to RPOC Suction & Curettage

114
CLERKING TIPS

Labour Room Rotation Presentation:

1. Patient details (Name, Age, POA/POG, G/P, presenting complaint (what phase of labour? latent/active,
show/leaking/contraction).
2. Details of Admission:
a. Time of Admission
b. Contraction progress
c. VE findings: Os progress
3. ANC Book (as pts are not fit to be clerked):
a. Look for important RF
b. Fetal well being (FH, FKC)
c. REDD vs EDD (u/s findings are within 7 days of calculated EDD based on LMP)
4. Partograph (interpret from below => top) *REFER APPENDIX
5. CTG (Basal Heart Rate, Variability, Acceleration, Deceleration, MC => Impression?)
6. Labour summary (can be found in ANC booklet)

**LESS ASKING, MORE LOOKING

115
11.0 INDUCTION OF LABOUR
REASON/ IMPORTANCE:
Induction of labour is considered when the prolonging the pregnancy may harm to fetus and
mother or both.

DEFINITION:
● Planned initiation of labour prior to its spontaneous onset.

INDICATIONS:

MATERNAL FETAL

Pre-eclampsia Post date ( most common)

GDM Polyhydramnios

Chronic illness: SLE, chronic kidney disease IUD/IUGR/SGA

APH- placenta previa IOL is contraindicated Fetal Distress- reduced fetal movements

Chorioamnionitis Multiple pregnancy > 38 weeks

Social reason: husband not around, no Unstable lie @term @ cephalic presentation
caregiver, horoscope induction

Bad obstetric history previously (recurrent


abortion, previous hx of IUD baby, case of RH
immunization)

CONTRAINDICATIONS:

MATERNAL FETAL

Cardiac disease Preterm fetus with immature lungs

Cephalopelvic disproportion (CPD) Acute fetal distress

Prior c-section Malpresentation

Prior uterine surgery Vasa praevia

Wrong dates Cord prolapse

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Grandmultipara

Active HSV (prior symptoms for sexually


transmitted infection)

What is the prerequisite for induction ???


1. Ascertain the date (make sure the date is correct).
2. Certain about the indication.
3. Exclude the contraindication for vaginal delivery:
■ make sure baby is not macrosomia (clinical evidence and ultrasound)
■ make sure the lie is longitudinal.
■ make sure the presentation is normal (cephalic).
■ exclude placenta previa.
■ make sure fetal is not compromised .as evident by CTG)
4. Exclude the CPD.
5. Counsel patient and obtain consent
6. Obtain GSH- in case of prepare patient for C-sec
7. Exclude the possibility of coagulopathy (in cases of IUD)
8. Make sure that the patient is not having contractions.

METHODS:
Methods of induction of labour is depend on Modified Bishop’s score:
1. Cervical dilatation.
2. Cervical effacement.
3. Cervical consistency.
4. Cervical position.
5. Station (distance between the presenting part and ischial spine).

Factors Score

0 1 2

Dilatation 1 2 >3

Effacement (cm) 1.5 or more Intermediate 0.5 or less

Station -2 or higher -1 0 or lower

Consistency Firm Intermediate Soft

Position Posterior Axial Anterior

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If favourable (6 and more) - do surgical induction/mechanical e.g. ARM followed by Oxytocin
infusion.
If less favourable (< 6) go for medical induction such as Prostin, Foley catheters.

● If less than < 6 – cervix needs to be ripen (by prostaglandin).


● If 6 or more-favourable just do ARM

118
11.1 TYPES OF INDUCTION OF LABOUR (IOL):

1. Medical method:
● PGE2 : Dinoprostone / prostin (use only at term > 38 weeks and alive fetus )
○ sulprostone / nalador (use in IUD, less than 28 weeks)
● PGE1 : Gameprost / cervagem (IUD less than 28 weeks, missed abortion).
○ Misoprostol (only in US : not license in UK and Malaysia))
● Mifepristone (use in missed abortion only).

2. Mechanical method:
a. Sweep and stretch in multipara.
b. Foley’s catheter
c. Hydrostatic method (Dilapan)
■ Usually used for multipara.
■ IUGR.
■ Previous scar.

Disadvantage: respond slow, delay and need more than 1 dilapan


Advantages: no risk of uterine hyperstimulation, fetal distress & uterine rupture

d. Surgical- Artificial Rupture of Membrane (ARM).

COMPLICATIONS:

Mothers Fetal

● Failed induction (diagnose when ● Fetal distress


patient is not in labour after 3 times ● Cord prolapse
prostin was inserted .
● Uterine hyperstimulation
○ which can lead to uterine
rupture, abruptio placenta &
fetal distress.
● Inadvertent preterm delivery (if date is
uncertain).
● Primary postpartum haemorrhage.
● Increase risk of operative delivery.

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Therefore, we need to monitor patient and the fetus post induction:

Mothers Fetal

● rest in bed for one hour ● CTG after one hour post induction but
● check / time contraction. ideally as soon as induction was
● check the blood pressure and pulse started.Then do another CTG 5 hours
rate. post- IOL
● pad chart (PV bleeding). ● Then, repeat VE after 6 hour or earlier
if the patient complains of bearing
down:
○ if not favourable (Bishop’s score
less than 6) give another
prostin.
○ if more than 3 prostin consider
failed induction. Consider the
LSCS in view of a failed IOL.

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12.0 OBSTETRICS EMERGENCIES
12.1 CORD PROLAPSE

Definition

Cord prolapse is an obstetric emergency where the cord passess through the os in front of the
presenting part of the baby.

This occurs especially when the membrane ruptured or is ruptured with a high presenting part.

● Overt umbilical cord prolapse: when the umbilical cord lies in front of the presenting part
and the membranes have ruptured.

● Umbilical cord presentation is when the umbilical cord lies in front of the presenting part
and the membranes are intact.

● Occult umbilical cord presentation or prolapse is when the umbilical cord lies trapped
beside the presenting part rather than below it.

● Birth asphyxia occurs as a result of cord compression or vasospasm.

Associated factor:

Cord prolapse following ARM in pt with the unengaged presenting part is the most common
Iatrogenic cause of cord prolapse.

Risk Factors of Cord Prolapse

MATERNAL 1. Grand multiparity


2. Polyhydramnios
3. True/relative CPD
4. Pelvic mass
5. Malpresentation
6. Abnormal lie

FETAL 1. Multiple pregnancy


2. Fetal anomaly
3. Abnormal lie - transverse/oblique
4. Malpresentation - footling breech
5. Unengaged presenting part

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6. Prematurity
7. Small fetus (IUGR/SGA)

PLACENTA AND CORD ABNORMALITIES 1. Placenta praevia


2. Long cord
3. Velamentous insertion of cord

IATROGENIC 1. Amniotomy
2. Manual rotation of head
3. Placement of cervical ripening balloon
catheter
4. Vaginal manipulation of fetus with ruptured
membranes
5. ECV

Assessment

1. Gestational age
2. Fetus still alive or dead?
3. How much is the cervix dilated?

Diagnosis
1. Clinical:
a. Fetal heart may show sudden alteration in rate and rhythm following ROM
b. Loop of cord seen at vulva
c. On VE, loops of cord felt in the vagina following ROM
2. USS :
a. Routine scan shows herniation of membranes with loops of cord below the
presenting part (cord presentation)- impending cord prolapse

Management

1. If the cord is palpated before ARM (cord presentation) → proceed with C-section
2. If the cord is prolapsed:
a. since cord prolapse is consider obstetric emergency, i will initiate RED alert
b. apply certain maneuver which may prevent further compression of presenting part
towards cord such as
i. Raise the foot end of the bed & put 1/2 pillow beneath patient's buttock
(Trendelenburg position)

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ii. Do VE and displace the presenting part upward by gently pushing the fetal
head upwards, away from the maternal pelvis. Use the other hand to apply
suprapubic pressure to keep the fetus from the pelvis.
iii. (do not handle the cord itself as there is risk of spasm, bradycardia +/-
asystole, thus false diagnosis of FSB
iv. inflate the bladder with 300-500 ml normal saline
c. if the cord inside the vagina, i will put sanitary pad firmly to the vulva
d. if cord outside the vagina, i will replace it back within the vagina with minimal
cord manipulation
e. if the cervix is fully dilated and there is a role of immediate instrumental delivery
(forceps/ventouse)
f. however, if the cervix is not fully dilated and fetal is alive & normal, proceed with
emergency C-section under GA or rapid spinal anaesthesia

**Majority of cord prolapse delivered by C-section

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12.2 SHOULDER DYSTOCIA

Definition:
The difficulty in delivering the shoulder after the delivery of the baby’s head.

Shoulder dystocia is also defined as vaginal cephalic delivery that requires additional obstetric
maneuvers to release the shoulder after routine traction has failed.

Risk factors:
1. Macrosomic fetus
2. Uncontrolled DM/GDM
3. Baby boy
4. Maternal obesity
5. Previous history of shoulder dystocia
6. Post-term/post-date delivery
7. Multiparity (next baby tends to be larger than the last because increasing size of placenta)

Signs:
1. Prolonged 1st stage
2. Prolonged 2nd stage
3. Assisted delivery
4. Turtle-neck sign (head remains tightly applied to the vulva or may even retract)
5. Failure of restitution of the fetal head.
6. Failure of the shoulders to descend.
7. Difficulty with delivery of the face and chin.

*Why do babies from GDM mothers are prone to have shoulder dystocia?
Due to the unequal fat distribution which is more focus around the shoulders

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Management

Adopted from Clinical Protocols In Obstetrics & Gynaecology For Malaysian Hospitals.

H Call for HELP; senior staff must be called in


● Inform mother to stop pushing
● Do not apply fundal pressure
● Mother is lie flat and buttocks are drawn to the edge of the bed

E Evaluate and perform EPISIOTOMY to facilitate obstetric maneuvers

L MacRobert’s position (flex and abduct hips) so as straighten lumbosacral angle and
increase A-P diameter of pelvis

P Suprapubic pressure (Rubin I) is applied continuously for 30 seconds followed by


rocking pressure for 30 seconds as efforts are made to deliver the baby
● Reduces bis-acromial diameter
● Dislodges impacted shoulder
● Facilitates movement to oblique position to permit subsequent delivery with
gentle traction.

E ENTER vagina for internal manoeuvres


● Rubin II : 2 fingers applied to posterior aspect of anterior shoulder and forward
pressure is applied to adduct the shoulder so s to move it to oblique position
(disimpact shoulder)
● Wood’s Screw : If above fails, 2 fingers of opposite hand is used to press on
anterior aspect of posterior shoulder
● Can be combined with Rubin II maneuver
● Reverse Wood’s : If unsuccessful, place 2 fingers on posterior shoulder to
rotate to opposite direction.

R REMOVAL of posterior arm : Fingers introduced to fetal axilla to bring the shoulder
down and deliver the posterior arm

R ROLL woman onto all FOURS (GASKIN manoeuvre) if required

Others If all manoeuvres fails;


● Zanavelli manoeuvre : fetal head is replaced and caesarean section performed.
Clearly the delivery time is prolonged and fetal hypoxia is imminent.
● Cleidotomy and symphysiotomy are other procedures included as last resort
measures though rarely done.

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Complications

Maternal Fetal

1. Genital tract trauma 1. Asphyxia


2. Uterine atony 2. Erb’s palsy (C5,6,7), brachial plexus
3. PPH injury
4. Infection 3. Brain damage
5. High risk of operative delivery 4. Humerus and clavicle fracture
6. Bladder atony 5. Spinal cord injury
7. Femoral neuropathy 6. Stillbirth
8. Psychological trauma

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12.3 AMNIOTIC FLUID EMBOLISM

CAUSES:
● Strong uterine contractions
● Excess amniotic fluid (polyhydramnios)
● Disruption of uterine vasculature

DIFFERENTIAL DIAGNOSES:
● Pulmonary embolism
● Primary PPH
● MI

RISK FACTORS:
● Multiparous
● Advanced maternal age
● CS/instrumental delivery
● Eclampsia
● Polyhydramnios
● PP/placenta abruptio
● Uterine rupture
● IOL
● Obesity
● ECV
● Amniocentesis
● Abdominal trauma

SYMPTOMS (ACUTE ONSET OF):


● Hypoxia and respiratory arrest
● Hypotension
● Fetal distress
● Convulsions
● Shock
● Altered mental status
● Cardiac arrest

INVESTIGATIONS:
● ABG
● Electrolytes
● FBC
● Coagulation profile
● CXR (pulmonary oedema)
● ECG (ischemia and infarction)

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MANAGEMENT - OBSTETRIC EMERGENCY:
● Call for help (RED ALERT)
● Pulmonary artery wedge pressure monitoring
● Blood aspirate via catheter
● Oxygen mask
● IV access for fluid, blood, blood products
● Direct-acting vasopressors (phenylephrine)
● Manage DIVC
● Deliver immediately

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12.4 POSTPARTUM HAEMORRHAGE

SCENARIO:
40 year old, para 6, delivered a 4kg baby after AOL for prolonged 1st stage. She was induced at 38
weeks for diabetes in pregnancy and pre-eclampsia. 2 hours after delivery, she experienced PV
bleeding of 1000cc.

DIAGNOSIS (Δ): Primary PPH

RISK FACTOR BASED ON THE SCENARIO:


1. Advanced maternal age
2. Multiparous
3. AOL
4. Macrosomic baby
5. Prolonged 1st stage
6. IOL

Suddenly her BP became 90/40mm Hg and her PR is 110bpm

OUTLINE YOUR MANAGEMENT

1. Activate obstetric red code


2. Resuscitate the patient, maintain ABC
3. Give oxygen mask
4. Set 2 large bore IV cannula (16G) and draw blood for GXM, FBC, coagulation profile and
blood urea and electrolytes
5. Infuse patient with crystalloids or colloids
6. If the BP is still low, consider transfusing blood/blood products
7. If DIVC, give DIVC regime
8. Monitor the urine output
9. Once stable, find the source of bleeding

On examination, the uterus is 30 weeks in size and vaginal examination is normal

DIAGNOSIS (Δ): Uterine atony

OUTLINE YOUR MANAGEMENT

1. I would do a uterine fundal massage to encourage uterine contraction.


2. And give 10iu bolus IV Syntocinon in 500ml of saline followed by a maintenance dose of
40-80 IU.

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3. If still bleeding, give IV Ergometrine 0.25mg OR
a. straightaway give IM Carboprost/Hemabate 250µg, can be repeated after 15-60 min
for a maximum of 3 doses (C/I in heart disease, renal disease, pulmonary edema)
b. Other option: IV Nalador 500µg

In spite of all the above measures, the bleeding persist:


● Other options
1. Bimanual compression of the uterus (internal or external)
2. Aortic compression

In spite of that, the patient still bleeds.

1. Name one surgical management


Hysterectomy

2. Other alternative surgical convention management


○ B Lynch suture @ Suture of Aid (Done before hysterectomy itself)
○ Bilateral uterine artery ligation
○ Bilateral internal iliac artery ligation
○ Utero-ovarian artery anastomosis ligation
○ Arterial embolization

EXAM TIPS

Primary PPH Blood loss of 500ml or more from genital tract during the first 24hours
after delivery.

Secondary PPH Excessive bleeding from the genital tract occurring after 24 hours of
delivery of baby and up to 6weeks postpartum.

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Causes of PPH (4 Ts)

Tone 1. Polyhydramnios
(Uterine atony) 2. Multiple pregnancies
3. Fetal macrosomia
4. Prolonged rupture of membranes
5. Fever
6. Myomas
7. Rapid labour
8. Prolonged labour
9. Placenta previa
10. Uterine anomalies
11. Bladder distension
12. Medications e.g. terbutaline, magnesium sulphate, and nifedipine

Trauma 1. Genital tract lacerations


2. Uterine rupture
3. Caesarean section tears
4. Uterine inversion

Tissue Retained product of conception

Thrombin 1. DIC e.g. in abruption, fetal demise and amniotic fluid embolism
2. Haemophilia
3. Idiopathic thrombocytopenic purpura
4. HELLP syndrome

131
13.0 INSTRUMENTAL DELIVERY
Instrumental delivery includes:
● Forceps
● Ventose (Vacuum)

Types of Forceps:
Types Outlet forceps Low forceps Mid forceps

Examples Wrigley's forceps Simpson's, Neville Kielland's forceps


Barnes & Anderson's
forceps

Indication Station +3 Station +2 or lower Asynclitism

From left: Wrigley's forceps, Simpson’s forceps & Kielland's forceps.


Source: https://elearning.rcog.org.uk//easi-resource/forceps/types-forceps
* Specialized forcep, Pipers forcep after-coming head in breech delivery.

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Types of vacuum:

Types Metal cup Silicone (Semi-Rigid) Kiwi Omnicup


cup

Images

● Maintain neck flexion of the babies to give the smallest AP diameter = 9.5 cm.
● Apply the cup at the flexion point, 3cm from the posterior fontanelle.
● Stop pressure once the head is delivered.

Source: https://www.whattoexpect.com/pregnancy/labor-and-delivery/procedures-and-interventions/vacuum-extraction.aspx

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Prerequisite for instrumental delivery (forceps/vacuum):
Acronym FORCEPS

F Fully dilated cervical os

O OA/OP [OT cannot] - Presenting part

R Rupture of Membrane

C CPD excluded, catheterization*

E Engagement, Episiotomy**

P Pain relief (Epidural)

S Station at least 0, Sterile space

* to facilitate fetal descent (fetus vs. loaded bladder/rectum).


** to facilitate fetal descent, to avoid any unnecessary injuries (vaginal tear) & to provide spaces for
instruments.

Complication of instrumental delivery:


Maternal Fetal

1. Genital Tract Trauma 1. Fetal Injuries


a. Labia majora/minora a. Facial laceration
b. Vagina b. Facial nerve injury
c. Cervical tear c. Ocular trauma
d. Uterine rupture d. Skull fracture
e. Haematoma 2. Fetal hypoxia
2. PPH 3. Intracranial haemorrhage
3. Gential infections 4. Fetal death
a. Endometritis
4. Uterovaginal prolapse
5. Incompetence

EXAM TIPS

Why are premature babies known as an absolute contraindicated for ventouse delivery?
Fontanelles gaping may result in serious injuries.

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14.0 CAESAREAN SECTION
MAJOR INDICATIONS
1. Previous C-section - 1 previous classical c-section scar, 2 and more LSCS
2. Malpresentation - breech, brow
3. Suspected acute fetal distress
4. Failure to progress in labour
5. Abnormal lie (transverse/oblique)* CONTROVERSIAL

INDICATION
1. Abnormal progress of labour
2. Malpresentation
3. Myomectomy
4. Placenta Previa

Types:
1. Classical C-section: (Vertical incision @upper segment)

Indication Disadvantage

● Preterm breech ● Eliminate VBAC in all subsequent


● Transverse lie back down fetal position pregnancy
● Poor success to LSCS d/t fibroids, ● Increase risk of uterine rupture
adhesion ● Increase risk of PPH/ infection

2. LSCS
➢ Disadvantage:
- Limited ability to extend laterally to enlarge incision
- Increased incidence of placenta praevia / placenta accreta

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Complications

Intra Op Post-Op Long Term

- Anesthesia risk - PPH - DVT

- Bleeding - Infection( UTI/ - Post-op adhesion


endometritis)

- Injury to surrounding - Longer hospital stay Future pregnancy


organ and recovery - uterine rupture increase
eg;bowl/bladder/fetus - PP/Placenta accreta risk
increases

Factors to consider before Vaginal Birth after C-section (VBAC) :


1. Number of scar
2. Type of scar
3. When was the scar
4. Intra op complication- any extended tear
5. Postpartum complication
6. Current pregnancy problem

Contraindications for VBAC:


a. Placenta accreta/ Praevia
b. Review previous operative notes: eg: classical c-sect, myomectomy breeching
endometrium, uterine perforation
c. Medical or obstetric conditions that preclude VBAC.

Likelihood of successful of VBAC

● Without previous vaginal birth : 75% ( 3 out of 4)


● At least one previous vaginal birth :90 % ( 9/10)
● Factors increasing likelihood of
○ Successful VBAC
■ spontaneous onset of labour, higher Bishop score, engaged head or lower
station.
■ Greater maternal height
■ Maternal age < 40 yrs old

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■ Gestation < 40 weeks
■ estimated fetal weight < 4kg
■ previous C-section for malpresentation

○ Unsuccessful VBAC more likely in:


■ induced labour
■ no previous vaginal birth
■ BMI> 30
■ Previous labour for shoulder dystocia

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Brief Comparison between VBAC and elective repeat LSCS

VBAC Elective Repeat LSCS

ADVANTAGES

Faster recovery Predicted time of birth

Shorter hospital stay Avoid risk of uterine rupture/dehiscence

No surgical/ anaesthetic risk if successful VBAC No risk associated with assisted vaginal
delivery and anal spinchter injury

Increase likelihood of future vaginal birth Reduces risk of pelvic organ prolapse and
urinary incontinence

Option for sterilisation if fertility is no longer


desired

MATERNAL RISK

Uterine rupture in 5:1000 Uterine rupture < 2 in 10000

Blood transfusion 2 in 100 Blood transfusion 1 in 100

Maternal mortality : 4 per 100,000 MAternal mortality 13 per 100000

Anal spinchter injury : 5% Surgical and Anaesthetic risk

EMLSCS or assisted vaginal delivery if not PP/ morbidly adherent placenta in future
successful pregnancy

FETAL/NEWBORN RISK

Transient respiratory morbidity 2-3 per 100 Transient respiratory morbidity 4-6/100

Hypoxic ischemic encephalopathy(HIE) - HIE < 1 per 10000


8/1000

Antepartum stillbirth beyond 39 weeks while


waiting spontaneous labour 10/10000

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GYNAECOLOGY

139
15.0 MENSTRUAL DISTURBANCE
Important definitions from 10 Teachers:

Last menstrual period (LMP) Date of last menstrual bleed.

Primary Amenorrhoea Girls fail to menstruate by 16 years of age.

Secondary Amenorrhoea Absence of menstruation for more than 6 months in a


normal female of reproductive age that is not due to
pregnancy, lactation or the menopause.

Oligomenorrhea Infrequent menstrual bleeds more than 35 days apart


(Normal menstrual cycle is 21 - 35 days)

Dysmenorrhoea Painful menstrual bleeding (primary or secondary).

Menorrhagia @ Heavy Menstrual Bleed Excessive menstrual blood loss, more than 80ml of blood
per cycle.

CLASSIFICATIONS

1. Gynaecological problems according to age:

Adolescent Fibroid
Dysfunctional uterine bleeding
Hypothyroid

30 - 45 year olds Fibroid


Adenomyosis
Endometrial hyperplasia
Endometrial polyps
Endometrial carcinoma (>40y/o)
Irritable bowel syndrome

> 50 year olds Endometrial hyperplasia


Endometrial carcinoma
Dysfunctional uterine bleeding

140
2. Gynaecological problems according to types of bleeding and pain:
(These are the chief complaints with which patients come with. Patients may have other
associated symptoms that may or may not direct to a different diagnosis.)
*Common cases
MENORRHAGIA SECONDARY DYSMENORRHEA

Uterine fibroid* Endometriosis


Endometrial hyperplasia* Adenomyosis
Endometrial carcinoma* Endometrial polyps
Adenomyosis* Fibroid
Endometriosis (rare) Ovarian cysts (Endometrioma/ Luteal)
Hypothyroid Pelvic inflammatory disease
Irritable bowel syndrome Copper IUCD
Coagulopathy

POST MENOPAUSAL BLEEDING POST COITAL BLEEDING


(from the cervix and vagina)
Endometrial carcinoma
Endometrial hyperplasia Cervical polyps
Endometrial polyps Cervical ectropion
Cervical carcinoma Cervical carcinoma
Endometriosis Genital infection;
Atrophic vaginitis -Cervicitis
Granulosa cell ovarian cyst -Vaginitis

DYSPAREUNIA CHRONIC PELVIC PAIN

Deep dyspareunia Superficial dyspareunia Endometriosis


Endometriosis Atrophic vaginitis Adenomyosis
Cervicitis Pelvic inflammatory disease
Cervical carcinoma Tubo ovarian abscess
Cervical polyps Ovarian cyst
Irritable bowel syndrome

PER VAGINAL DISCHARGE


Pelvic inflammatory disease
Endometrial carcinoma
Genital infection/STI

Bacterial vaginosis Candidiasis Trichomoniasis

Yeast infection Gonorrhea Chlamydia

141
3. Gynaecological problems according to the causative organs:

Organ Diagnosis

Uterus Abnormal Growth/Deposition:


(Can be further divided into Uterine fibroid
layers: Endometrial hyperplasia
Endometrium, Endometrial polyps
Myometrium, Endometriosis (rare)
Serosa layer) Adenomyosis

Cancerous:
Endometrial carcinoma
Leiomyosarcoma

Follapian tube Pelvic Inflammatory Disease


Ectopic Pregnancy

Ovaries Benign ovarian growth


Malignant ovarian tumour
Endometriosis - Endometrioma

Cervix Cervical polyps


Cervical ectropion
Cervical carcinoma
Genital infection - Cervicitis

Vagina Pelvic inflammatory disease


Endometriosis (rare)
Genital infection - Vaginitis

Others Blood coagulopathy


Thyroid disorder
Medication (antiplatelets, anticoagulant, hormonal)

142
4. Gynaecological problems according to the classical textbook recommendations
(PALM-COEIN) by FIGO:

Structural Non-structural
(evaluation by imaging or biopsies) (underlying condition that results in AUB)

P Polyps C Coagulopathy

A Adenomyosis O Ovulatory disorders (PCOS,


Thyroid Disorders)

L Leiomyoma E Endometrial

M Malignancy I Iatrogenic

N Not classified causes (DUB)

EXAM TIPS

Students tend to forget to ask anything regarding BLOOD & THYROID DISORDER!
Exclude them in the summary.

PE - look for evidence of blood disorders (bruises), thyroid disorders

143
Approach to Heavy Menstrual Bleed: History taking

Tip: Begin with presenting the menstrual history so we can compare the changes that occur after the
onset of menstrual disturbances. “I would like to begin the history of presenting illness with the
patient’s menstrual history.”

Points Menstrual history Onset of HMB Any worsening of Currently at the


episodes? time of interview

Age / timing She attained She was well until


menarche at the __ years ago.
age of __ y/o

Regularity

Duration

Volume (number and


types of pads used)

Presence of blood
clots or flooding

Anaemic symptoms

Impairment due to -
symptoms

Associated -
symptoms*

Management -
(investigations**,
treatment, follow up)

Response to -
treatment (adherence
to medication, reason
for non-compliance,
medication side
effects, improvement
of symptoms)
**Need to know the routine investigations (not textbook investigations) for patients first presenting
to the gynae clinic with HMB and actively ask the patient during history taking.
*Associated symptoms

144
Symptoms Diagnoses

Structural Other per vaginal bleeding:


causes Intermenstrual bleed Endometrial polyp
Post coital bleed Cervical cancer

Per vaginal discharge PID, endometrial cancer

Pain symptoms:
Cyclical pain, secondary dysmenorrhea, deep Endometriosis
dyspareunia, dyschezia, dysuria, infertility

Worsening of pain, secondary Adenomyosis


dysmenorrhea, deep dyspareunia, infertility

Infertility (if large) Endometrial fibroids


Compressive symptoms:
Bowel (constipation, abdominal distention)
Urinary (frequency, urgency)

Constitutional symptoms Malignancy

Non - Easy bruising, history of blood transfusion Coagulopathy


structural
causes Cold intolerance, weight gain Hypothyroidism

Warfarin use, jamu Iatrogenic

145
16.0 DYSFUNCTIONAL UTERINE BLEEDING (DUB)
● Definition : Bleeding not d/t :
b. Local dz in the genital tract
c. Pelvic infection
d. Cx of pregnancy

● Incidence: at 2 extreme ages (<30yo, >40 yo)


● Diagnosis by exclusion
● Pathophysiology: unknown
● Hypotheses:
○ Fibrinolytic system
○ Production of prostaglandin

● Causes :
○ Alteration balance of:
■ Gonadotrophins (FSH and LH)
■ Ovarian hormones
■ Endometrial prostaglandin

● Types :
1. Ovulatory cycle
2. Anovulatory cycle
3. Endometrial hyperplasia

1. Ovulatory cycle

a) Insufficient Corpus luteum

CL doesn’t last long →E2 and P4 reduces early →Bleeding

b) Too sufficient CL

CL last too long → E2 + P4 very high→ very high E2 and P4→abnormally thick endometrium

2. Anovulatory cycle DUB

➢ Similar to the situation of insufficient CL


➢ In this case→no ovulation→no dev. of CL
➢ Therefore, no secretory phase to take over proliferative phase early shedding occur

146
3. Endometrial hyperplasia

d/to absent –ve feedback of high E2 to FSH



No –ve feedback to FSH

FSH ↑↑

E2 continue rising d/t many follicular development



Continue thicken the uterus

Eventually E2 level ↓

Excessive bleeding

147
TREATMENT

Medical Treatment

Non-hormonal Hormonal
(dosage is the same as for family planning)

1. Anti-fibrinolytic agents 1. COC pill


(tranexamic acid-50% reduction) 2. Progesterone pill – dydrogesterone
2. Prostaglandin synthesis inhibitor (Duphaston)
(mefenamic acid-25-50% reduction) a. medroxyprogesterone acetate
(Provera)
3. Noretisterone (Norculut)
4. IUCD (Mirena)
a. - for >40 yo (90-95% reduction)
5. Gestrinone (not recommended
because of the side effect-irreversible
breast atrophy)
6. Danazol (has masculinizing effects)
7. GnRH (menopause issues)

Surgical Intervention
(older age group>35 yo, failed medical tx, patient’s wish

1. Radical: hysterectomy
2. Conservative (keep uterus):
a. Excision (advantage-can send for HPE)
b. Ablation

148
17.0 DISORDER OF MENSTRUAL CYCLE
EXCESSIVE AND IRREGULAR UTERINE BLEEDING (> 80 ml)

Definition : Excessive menstrual bleeding that occurs with regular/irregular cycles.

Pattern :
1) Regular heavy – anovulatory
2) Irregular and heavy – anovulatory
3) Intermenstrual spotting / post-coital bleeding

149
Differential diagnosis

1) REGULAR HEAVY MENSES


● DUB
● Fibroids (usually periods painless) but can be painful in submucosal fibroid
● Adenomyosis (period painful)
● Polyps (cervical polyps, endometrial polyps)

2) IRREGULAR MENSES
● PCOS
● Weight changes
● Infection
● Abnormal pregnancy states –miscarriage, molar, ectopic pregnancy
● Neoplasia – polyps (cervical, endometrial)
- CA (cervical, endometrial)
● Hormone induced – non-compliance

3) INTERMENSTRUAL SPOTTING/ POST-COITAL BLEEDING


● Midcycle bleed – a/w Mittelschmerz
● Premenstrual – defective CL/progesterone insufficiency
● Neoplasia – benign polyps (cervical/ endometrial/ fibroid)
- malignant (cervix/ corpus)
● Infection - Cervicitis/ infected polyps causing contact bleeding
● Post-coital bleeding – classical symptoms of cervical CA
● can be caused by cervicitis

History
1) Ask about LMP
2) Ask about severity of bleeding
- how many pads
- how often change the pad
- totally soaked or not
- duration of bleeding
- a/w flooding/ clots??
3) Types of bleeding
- IMB
- Post-coital bleeding
- Post-menapausal bleeding
- a/w
4) Is the bleeding cyclical or not
5) Ask any cyclical symptoms :
- dysmenorrhea- severe and progressive adenomyosis
- abdominal bloating

150
6) Symptoms of anaemia
- SOB
- Palpitation
- Dizziness
- Lethargy
- Reduce effort tolerance
7) Any past/ recent contraceptive use
- POP- irregular bleeding/spotting
- OCP- compliance or not
- Bleeding d/t stopped OCP
- IUCD (coz bleeding)
8) Any pap- smear clinic
9) Sexual hx
- age of first SI
- multiple sexual partner
- unprotected/protected SI
- HPV infection, STD
10) Past Medical and Surgical
- VWD
- On anticoagulant or not
- Immunocompromised or not (DM, HIV, on steroid)
11) Past O&G
- infertility
12) Social hx
- Smoking
- Alcoholic
13) Pressure effect – to exclude fibroid
- constipation
- urinary incontinence/retention
- dyspareunia
- pelvic pain
- hemorrhoids
- hydronephrosis a/w edema
14) Infertility – endometriosis, adenomyosis, fibroid.
15) Mx of trauma

Physical Examination
1) Vital sn.
2) Ht., Wt., BMI
3) Look pt as general
- hirsutism
- striae
- thyroid skin pigmentation – petechiae, ecchymosis
4) Palpate abdomen for mases

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5) Speculum examination
- take vaginal swab if +ve sn of infection
- cervical smear if indicated
6) Vaginal examination
- feel for adnexal mass
- local causes

Investigation
1) FBC
2) Serum B-hCG – to exclude pregnancy
3) TFT
4) Coagulation profile – to exclude coagulopathy
5) Serum LH / FSH
6) Serum prolactin
7) Serum androgen – PCOS
8) Ultrasound ( abdominal/vaginal) – endometrium thickness
- detect abnormalities at the cavity eg: polyps
- Visualize the ovary & POD and uterus - polycystic
ovaries
9) Endometrial biopsy – women > 40 y.o presented wt. IMB/ menorrhagia
-Pipelle sampling
Hysteroscopy (goal standard)
-

10) Pap Smear / cervical smear if indicated

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18.0 ENDOMETRIOSIS
Definition

It is defined as the presence of endometrial tissue (stroma and glands) outside of the
uterine cavity.

Pathogenesis
1. Retrograde menses / Sampson’s Implantation theory.

- Menstrual blood containing endometrial tissue follows the pathway of retrograde


menstruation. The common sites of endometriosis are the structures that are being hit
first:
Ovary → broad ligament → uterosacral ligament → pouch of Douglas

- This theory explains why endometriosis commonly occurs in ovary, broad ligaments, pouch
of Douglas and uterosacral ligaments.
- However, the shortcomings for this theory is, it cannot explain endometriosis in distant
parts such as mediastinum and pleural.

2. Coelomic metaplasia theory

- Coelomic epithelium in the pleural is the same origin from coelomic epithelium in the
Mulerian duct.
- Metaplasia of coelomic epithelial to endometrial like tissue can occur in the other part.
- This theory can explain endometriosis in distant parts such as the pleural and mediastinum.

3. Lymphatic and intravascular dissemination

- Endometrial cells enter the lymphatic and vascular circulation and embolize to the ectopic
site.

Risk Factors
1. Family history of endometriosis
- Inheritance
2. Conditions associated with prolonged estrogen exposure:
- Nulliparous
- Delayed childbearing
- High economic status (associated with low parity)

Endometriosis is an estrogen-dependent disease.


More common in women with regular menstruation, reproductive age group

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Clinical Presentation

❖ Some women do not have any symptoms, accidental findings during laparoscopic.
❖ There is a poor relationship between severity of the symptoms and severity of the disease.
❖ Most common clinical presentation is PAIN .

Nature of the pain largely depend on site and extent of the lesion;

1. Deep dyspareunia ( If endometriosis located in the utero-sacral ligament)


2. Secondary dysmenorrhoea
3. Chronic pelvic pain
4. Cyclical pain – eg dysuria, hematuria, pain during defecation and per rectal
bleeding, hemoptysis, nose bleeding
5. Menstrual disorders
a. Menorrhagia (in cases of adenomyosis )
b. Intermenstrual bleeding ( In cases of bilateral endometrioma)
6. Infertility
a. HOW?
a. Altered ovarian function (endometrioma) – causing anovulatory cycle
b. Cause tubal damage (due to adhesion) .
c. Deep dyspareunia – so it will reduce coitus frequency
d. Hostile environment because in endometriosis, the prostaglandins
concentration is higher, so increase the number of macrophage.
Macrophage interferes with sperm motility, acrosome reaction and
fertilization.

How to Diagnose?

Diagnosis of endometriosis is made when women of reproductive age group with risk
factors coming with the classical presentation of endometriosis.

➢ In ABDOMINAL EXAMINATION, on palpation, the abdomen is tender. There may be a mass


that is located in right or left iliac fossa with irregular border and restricted mobility (the
only type of endometriosis that is palpable is endometrioma). Cannot get below due to
adhesion. The consistency is cystic in nature and there were no ascites.

➢ In SPECULUM EXAMINATION, can see bluish nodules in the posterior fornix (due to pooling
of blood at pouch of douglas). However, we need to exclude other differential diagnosis
that is molar pregnancy

➢ In VAGINAL EXAMINATION, there is tender POD, thickening of uterosacral ligament/


multiple tender nodules at uterosacral ligament, tender adnexal mass and fixed retroverted
uterus (being pulled down by thickened uterosacral ligament).

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➢ In BIMANUAL EXAMINATION, there is a retroverted uterus, we can feel for adnexal mass.

➢ ULTRASOUND is not specific but highly suspicious if mass found in adnexae in a woman
of reproductive age group with risk factors coming with the classical presentation of
endometriosis . Presence of kissing ovaries indicating endometrioma.

➢ LAPAROSCOPIC is a gold standard for diagnosis of endometriosis. During laparoscopic,


staging is made according to the AFS (American Fertility Society ).

➢ There is a role of CA-125 in investigation of endometriosis to exclude ovarian ca. It may


also be used after treatment of endometriosis to see effectiveness of treatment.

Treatment

Treatment may be medical or surgical or combination of both and depend on several factors such
as :
1. Symptomatic / asymptomatic
2. Extent of the disease
○ Need to score according to American Fertility Society
4 stages →
■ Stage I – mild
■ Stage II – moderate
■ Stage III – severe
■ Stage IV – extensive
During staging, we look at :
- Ovary – size, bilateral/ unilateral, adhesion
- Peritoneum - adhesion, ectopic spot
- Tube- bilateral/ unilateral blocked, adhesion
3. Age of the patient → complete the family or not (if patient has not completed family
yet or in young age, I will consider conservative treatment can be either medical or
surgical)
4. Patient’s wish

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Medical treatment

1. Principle of treatment is to ABOLISH or STOP the menses NEED to counsel PATIENT that;

● Only temporary measure at least 6 months


● The side effects
● Recurrence after treatment is common

Oral
○ Continuous OCP for 6 months because of side effect
(nausea) -Danazol – increased dosage until no menses may
reach 200 mg bd
○ Continuous progesterone gestrinone – twice a week
○ Visanne (Dienogest) - progestin

Injection / IV
○ GnRH analogue – have negative feedback mechanism

2. No medical treatment is indicated in asymptomatic or minimal endometriosis in patient


who wish to conceive

3. If after treatment bleeding does not stop, try to look for other causes of bleeding.

Table 1. Medical therapies for endometriosis

156
4. In patient taking GnRh agonist, we have to advise the patients in regards to:
● May present with climacteric symptoms such as vasomotor symptoms and vaginal
dryness etc.
● Can cause osteoporosis if prolonged use. (can’t use more than 6 months)

Combined treatment

1. There is a role for combined medical and surgical treatment especially in cases of
endometrioma after evisceration or cystectomy because not all active ectopic foci can be
removed or diathermized .

2. Used GnRH analogue or danazol after surgical treatment

Surgical treatment

1. Conservative - In young patient who wish for further fertility


a) Laser vaporization / electrical diathermy in cases when active foci / spot seen during
laparoscopic.
b) Cystectomy / Evisceration in cases of huge masses > 5 cm in size, considered in view of
infertility as well as in smaller cyst.

2. Radical – TAHBSO is definitive treatment because endometriosis is estrogen dependent

3. Laparoscopic is a gold standard for diagnosis of endometriosis. It can be both a diagnostic


and therapeutic approach of endometriosis. If the lesion is small , I will use electrical
diathermy, but if the lesion is more than 5 cm I will consider to do evisceration. After that,
continue with combined medical treatment because not all active ectopic foci can be
removed or diarthermize. Usually we give GnRH analogue or danazol to stop pseudo
pregnancy and stop the menses as well.

a. Where do you want to do laparoscopic?


At Palmar Point ( 2 cm below subcostal)

I will do laparoscopic , in a patient that did not have any previous pelvic surgery. If there are
any adherent structure, I will proceed to laparotomy

b. When do you know it is recurrent?

6 months after treatment, high risk of recurrent, if within 6 month after treatment, it is not
recurrent , maybe incomplete evisceration of lesion.

157
POSSIBLE CASE SCENARIO @ SCRIPT FOR ENDOMETRIOSIS

Chief Complaint

Madam _______ a __ year old Malay/ Indian/ chinese lady, parity ___ was admitted on the
___ due to abdominal pain for __days prior to admission.

History of Presenting Illness

Madam __is an administrative officer who presented herself into HKL after she experienced
severe lower abdominal pain for __ days. The pain was located in the ___ region. The pain was
sudden in onset, occurring at the rest while she was watching television and continuously
throughout the days. The pain was pricking in nature. There was no aggravating factor as well as
relieving factor and the pain was not radiated. The abdominal pain interfered with his daily
activity since she cannot sleep for the __ days and she had to take leave from the employer for
__ days as well.

However, the pain was not associated with menses and no associated symptoms such as
dyspareunia, post- coital bleeding, low back pain, intermenstrual bleeding, per rectal bleeding
and hematuria. However, she experienced dysmenorrhea as well as menorrhagia for the first
__days menses. She had to use 7 to 8 pads per day and the pads were totally soaked and there
was a presence of blood clots. She also experienced flooding. However, she denied any
symptoms of anemia such as palpitation, shortness of breath, lethargy and giddiness. Besides
that, there was no fever, no loss of weight and no loss of appetite. In addition, she has no
symptoms of urinary tract infection such as dysuria, frequency and hematuria as well as
gastrointestinal symptoms such as diarrhea, constipation, nausea and vomiting.

This was not her first episode as she experienced abdominal pain. The left iliac fossa pain
started since __ years ago. She was apparently well before that until 2000 when she
experienced severe abdominal pain at the ____ region which was not related to the menses.

The nature of the pain was similar with the current pain. Because of the pain, she presented
herself into the private clinic and was given IM analgesic and tablets in order to relieve her pain.
Then, Madam __ was referred from that private clinic to the HKL and was admitted there for __
days. Several investigations were done to her. She claimed that the blood was taken and
ultrasound was performed. However, she was told that the results were normal. Then, she was
subjected for laparoscopic examination and later was told by the doctor that there was no
abnormality detected during the examination. At that time, she was diagnosed as having
Chronic Pelvic pain. Before discharging from the ward, she was given Tablet Buscopan in order to
relieve her pain. In addition, she also was put under gynae follow up but defaulted treatment as

158
she felt no improvement at all. During this time, she also experienced severe dysmenorrhea
until disturbing her works as well as her routine activity.

Since __years ago, she was admitted to the hospital for about __ times due to the same problem
which was left iliac fossa pain and the last admission into the HKL was on ___, which was last
year. At that time, she also presented with severe left iliac fossa pain that was not relieved with
medication. At first, she was admitted into the surgical ward. However, she was referred to the
gynaecological unit after she was suspected of having an ovarian cyst after CT scan of the
abdomen was done to her. She was discharged after __ days admitted and claimed to be given
tablet Tramal. She was put under follow-up. However, she defaulted that follow up because
according to her, the pain was relieved after taking tablet Tramal.

From __ until ___, the patient still experienced severe abdominal pain on and off as well as
severe dysmenorrhoea and only went to the private clinic to seek a treatment. She claimed that
the pain was relieved by medications given by the doctor at the private clinic. Usually, she was
given IM analgesic at the clinic.

During the admission into the ward, several blood investigations were done to her as a pre
operative assessment as a laparotomy was planned for her. During these days, the patient is still
having continuous lower abdominal pain and in the ward she was given tablet simplex in order
to relieve her pain.

159
19.0 ADENOMYOSIS

Definition
A disorder in which endometrial glands and stroma are found deep within the myometrium.

Risk Factors
1. Multiparous
2. Late 30s, early 40s
3. Early menarche
4. Short menstrual cycles
5. Surgery involving disruption of endometrial-myometrial border
6. Smoking

Clinical features
1. Severe secondary dysmenorrhea which is increasing in severity
2. Heavy menstrual bleeding which is increasing in severity
3. Chronic pelvic pain
4. Uterine enlargement

Physical examination findings


- Bulky and tender ‘boggy’ uterus

Investigations
Ultrasound: localized, haemorrhage-filled distended endometrial glands. Irregular nodular. Loss of
endometrial myometrial junction.
MRI: more sensitive, moderate-severe adenomyosis

Management
Any treatment that induces amenorrhea - to make ectopic endometrium quiescent, relieve pain
and excessive bleeding.
1. Conservative
- Progestin-containing long-acting reversible contraception (LARC) : LNG-IUS (Mirena) and
depo provera
- Short term GnRH agonist
2. Uterine artery embolization (UAE)
3. Surgical
- Hysterectomy (definitive treatment) : high intensity focused U/S to thermally ablate the
adenomyotic foci.

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20.0 PELVIC INFLAMMATORY DISEASE (PID)

Definition
It is a polymicrobial infection of the upper genital tract.

Risk factors
1. Factors related to sexual behaviour (young age of first SI, multiple partner, recent partner
having multiple sexual partner, past history of STI)
2. Termination of pregnancy (as it predisposes to infection)
3. Instrumentation of cervix

Common organisms
1. Chlamydia (most common)
2. Neisseria gonorrhoeae
3. Mycoplasma genitalium

Typical clinical presentation/symptoms

Acute
1. Fever with chills
2. Suprapubic pain
3. Deep dyspareunia
4. Dysmenorrhea
5. Purulent vaginal discharge
6. Urinary symptoms (eg: dysuria)

Chronic
1. Chronic pelvic pain
2. Pressure symptoms from the mass
3. Deep dyspareunia
4. Vaginal discharge
5. Lower back pain
6. Subfertility
7. Menstrual irregularities

Physical examination

General examination
1. Vital signs
2. Observe appearance of patient whether ill or not
3. Monitor for any signs of sepsis (fever, tachycardia)

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Abdominal examination
1. Tender/ guarding/ rigid abdomen
2. Abdominal distension

Vaginal examination
1. Speculum : purulent discharge seen at cervix, presence of bleeding
2. Bimanual: positive cervical excitation, tender pelvic mass with restricted mobility, swelling
in pouch of douglas (POD) if there is pelvic abscess, retroverted uterus due to dense pelvic
adhesion in chronic PID.

Investigations
1. Full blood count (FBC) : anemia, leukocytosis
2. Vaginal swab : to identify the type of organism
3. Ultrasound: to detect hydrosalpinx, adnexal mass, tubo-ovarian abscess
4. Urine analysis: to exclude UTI
5. UPT: to rule out ectopic pregnancy

How to confirm diagnosis?


(based on CDC guidelines)
● 1 minimum criteria:
○ uterine tenderness
○ adnexal tenderness
○ cervical motion tenderness
● Additional criteria:
○ temperature > 38℃
○ abnormal vaginal discharge
○ increase in WBC count
○ elevated ESR/CRP
● Specific criteria:
○ ultrasound show hydrosalpinx or tubo ovarian abscess
○ laparoscopic finding of PID

Management

Mild
● Treat as outpatient
● Risk factor identified and corrected (if the cause of it is IUCD, we might have to remove it)
● Give empirical antibiotic (IM ceftriaxone 250mg TDS, followed by doxycycline 100mg BD
with or without metronidazole 400mg BD for 2 weeks)

Hospitalise patient if:


1. Unable to confirm PID
2. Suspected pelvic abscess or peritonitis

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3. Presence of sepsis
4. PID in pregnancy
5. Not responding to treatment as outpatient

Mx at hospital
● Bed rest until vital signs stable
● IV fluid (give NSAIDS for pain relief)
● IV antibiotic given for every 6 hours then switch to oral for 2 weeks

Surgical treatment
● Drainage of pelvic abscess
● Indicated in tuboovarian abscess when:
- size of abscess > 10cm
- ruptured tube with pyoperitoneum
- no response to antibiotic after 48-72 hours
● Drainage of abscess laparoscopically
● Send pus for culture and sensitivity

Long term complications


1. Blockage of fallopian tube
2. Ectopic pregnancy
3. Recurrent or chronic PID
4. Infertility

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21.0 UTERINE FIBROIDS
❖ Is a benign tumour of uterine smooth muscle a.k.a leiomyoma
❖ Gross appearance : well demarcated, firm, whorled tumour
❖ Common in nulliparous, obese and family history
❖ Oestrogen dependant → substantially increase in size especially during pregnancy
(hyperestrogenic state)
❖ 3 degenerative changes :
➢ Red : Hemorrhage and necrosis typically during mid second trimester p/w
acute pain
➢ Hyaline : Asymptomatic softening and liquefaction
➢ Cystic : Asymptomatic central necrosis. Rarely turn into malignant

Symptoms Examination findings suggestive of fibroids

Most fibroid are small and asymptomatic but ● General : signs of anemia
can present with ass/ sx “: ● Abdominal examination : visible or
● AUB (usually HMB and IMB) palpable abdominal mass arising from the
● Reproductive failure pelvis
● Subfertility ● Bimanual examination : enlarged, firm,
● Recurrent pregnancy loss smooth or irregular, non tender
● Bulk effect on adjacent structures in the
pelvis
● Pressure and pain
● Bladder and abdominal dysfunction
● Abdominal distension

164
How can you differentiate mass from uterus and from ovary?

On inspection

1. I will look at the site of the mass → If the mass is at centre, it is more likely to be uterine in
origin, as compared to ovarian mass which is more likely located at the LIF/RIF.

On palpation

2. I will look at the consistency of the mass → If the mass is firm in consistency, it is more
likely to be uterine in origin but if it is soft in consistency, it is more likely to be ovarian cyst

3. Margin → Mass with well defined margin is more likely to be uterine in origin and mass
with irregular margin is more likely to be ovarian in origin.

4. Mobility → If the mass is only mobile from side to side, it is more likely to be uterine in
origin as compared to ovarian mass which is usually mobile in all directions.

5. Lower border → usually if the mass is uterine in origin, I cannot get below the mass,
however if the mass is ovarian in origin, I can get below the mass.

6. Ascites → If there is present of ascites, the mass more likely to be ovarian tumour

On bimanual examination

7. The cervix usually moves away from my finger when I push the mass upwards.

BUT not always, there are certain cases of ovarian mass which adhere to the uterus will
also move when we push the mass upwards. However if the mass is ovarian in origin, the
cervix usually does not move away.

Management

Mx of fibroid depends on certain factors :

a. Whether the patient is symptomatic or not


b. Wish for fertility
c. Age of the patient
d. Patient comorbidities
e. Patient wish
f. Availability of treatments

165
There are 3 treatment modalities that can be offered which are :
1. Medical treatment,
2. Surgical treatment
3. Radiological

Modalities Explanation

Medical Is there a role of medical treatment in uterine fibroid?


treatment

Yes, there is a role of medical treatment using GnRH analogue in uterine


fibroid but ONLY to patients who plan to undergo surgery and for
patients who have huge fibroid. However it cannot be used for more
than 6 months because of the side effects.

Mirena, tranexamic acid, mefenamic acid and COCP tend to be


ineffective in presence of submucous fibroid or an enlarged uterus that
is palpable abdominally more than 12 weeks size.

What are the advantages and disadvantages?

Advantages

1. Shrink the fibroids → by reducing the bulk and vascularity of the


fibroids. This can make operation much easier, maybe instead of
though laparotomy, I can do laparoscopic assisted vaginal
hysterectomy (LAVH).
2. Treat the symptom → reduce the heavy flow
3. Optimise the Hb
4. Reduce the bleeding intraoperatively → less postoperative
complications (infection).

Disadvantages

1. Expensive
2. Side effect is osteoporosis
3. Rebound post treatment (small fibroid will disappear during
treatment and regrow to their previous dimensions)
4. Difficult to evacuate the fibroid during myomectomy (due to
pseudo-capsule)

Surgical 1. Myomectomy → There is a risk of bleeding during surgery that may


treatment even necessitate a hysterectomy. Myomectomy is associated with

166
greater morbidity than hysterectomy because of haematoma
formation in the cavity of the excised fibroid and also because of the
infection.
2. Hysterectomy

Complication of surgery

1. Intra-Operative
a. Anaesthesia
i. Spinal : Hypotension/shock/meningitis
ii. GA : Pulmonary complication
b. Hemorrhage
c. Trauma to surrounding organ

2. Post-Operative
a. Anesthetic complication – giddiness
b. Aspiration pneumonia
c. Wound infection
d. DVT / PE
e. Shock
f. Wound infection

3. Risk of scar dehiscence → patient have to undergo complicated


C-section in further pregnancy (↑ risks of intraoperative morbidity)

4. Therefore, in the patient who will undergo surgical treatment, I need


to counsel the couple the complication that may occur:
a. During operative
b. Post-operative
c. Further complication on their subsequent pregnancy.

Uterine UAE is a procedure where the tiny balls made of plastic or gelatin sponge
Artery the size of grains of sand are pumped through the catheter into both the
Embolization right and left uterine artery where they block the blood supply to the
(UAE) fibroids. Without blood, the fibroid shrinks and dies.

** Newer modality available : (good to know)


1. High Intensity Focused Ultrasound
2. MRgFUS

167
[SCRIPT] How would you manage a patient with fibroid?

1. As the patient is still young (<35 y.o), and has not completed the family yet, I will offer her to
do myomectomy either by laparoscopic or by doing laparotomy. Prior to this surgery, I will
give the patient GnRH analogue to shrink the fibroid. However, I will counsel her that there
is a risk that the fibroid may recur, and this is the major operation which may end up with
severe hemorrhage which later surgery may end up with hysterectomy.

2. As this patient's age is ___ (42< age <45), I will offer her to do a hysterectomy as she has
completed her family and there is a long way for her to be menopause (conserve the ovary).
However I will counsel her that she might be having premenopausal symptoms in about 2
years time.

3. As this patient's age is already ___(>45 y.o), I will offer her for TAHBSO and I will counsel her
that she will be menopause and there is a role of HRT for her.

Example Case scenario :

40 y.o women, single and nulliparous, presented with mass 20 weeks of gravid uterus associated
with heavy, irregular and prolonged menses. How would you manage this patient?

Answer:

a) I would like to discuss with the patient regarding the choice of treatment in this case since
she is single and did not have any child.
b) I will discuss whether she will get married or not and I will tell her that the chance for her
to conceive is reduced.
c) If she wants to get pregnant, I will offer her conservative medical and surgical treatment.
d) I will start her on GnRH analogue for 6 months to shrink the fibroid.
e) Then I will proceed to do myomectomy. However I will advise the patient the complication
of doing myomectomy which is :
➢ There is a risk of bleeding during surgery that may even necessitate a hysterectomy.
➢ Myomectomy is associated with greater morbidity than hysterectomy because of
haematoma formation in the cavity of the excised fibroid and also because of the
infection.

168
Complications of Fibroids in Pregnancy

Timeline Complications

Maternal

Antenal 1. Red degeneration (mid-second trimester)


2. Preterm contraction
3. Placenta abruptio
4. Placenta previa

Intrapartum 1. ↑ risks of operative delivery d/t


a. Placenta previa
b. Abnormal lie
c. Prolong labour
d. Obstructed labour

Postpartum 1. PPH
➢ Due to incoherent contractions of uterus
➢ Leading to uterine atony

Fetus / Neonates

1. ↑ risk of prematurity
2. IUGR / SGA
3. Birth asphyxia due to cord prolapse

Question : If a patient went for LSCS, will myomectomy be done right after taking out the fetus ?
Answers : NO. Because the uterus is very vascularized at that time hence increased risk of
bleeding.

169
22.0 POSTMENOPAUSAL BLEEDING
SCENARIO: 60 year old lady, nulliparous, presented with PV spotting for 3 months duration,
menopause 2 years ago.

Differential diagnosis;

1. Endometrial cancer
2. Atrophic vaginitis
3. Local causes of cervix:
○ cervicitis
○ cervical erosion
○ cervical polyp
○ cervical cancer

4. Local causes of endometrium: polyp, hyperplasia


5. Medical causes: hypothyroidism, bleeding disorders
6. patient on anticoagulant
7. HRT (unlikely in 60 year old patients)

History

1. Endometrial cancer: other associated sm such as foul smelling PV discharge,


constitutional sm, risk factors (unopposed stimulation of endometrium with estrogen,
obesity, nulliparity, late menopause, early menarche, PCOS, personal or family hx of
breast or colon ca, tamoxifen therapy, functioning ovarian tumours)
2. Cervical cancer: foul smelling PV discharge, blood stained discharge, if still sexually
active-post coital bleeding?, risk factors
3. If on HRT-compliance?

Physical examination

1. General : nutritional status, pallor, bruising, Virchow’s node, leg edema


2. Breast : mass (Krukenberg), axilla LN
3. RS : effusion, consolidation
4. Abd : distended, mass, scar, ascites
5. Pelvic : inspect perineum, speculum examination

170
Investigations
(TRO causes, to know sequelae)

1. Routine blood ix: FBC, GXM, coagulation profile, LFT if suspect malignancy, RP
2. USS: to see ET (>4mm-endometrial ca), mass in uterus, mass in ovary
3. Hysteroscopy guided biopsy under GA (>60 yo or nulliparous women)
4. Pipelle endometrial tissue sampling (<60yo)
5. If HPE (to know grading and type of tumour) result came back as positive for
endometrial cancer;
■ Do staging by surgical and histopathological
6. CT scan to see involvement of LN
7. Tumour marker: estrogen

Treatment
(principal: remove source of estrogens)

1. Surgery
2. Radiotherapy
3. Chemotherapy

Irrespective of the patient’s age, do;

a. TAHBSO (remove all source of estrogens)


➢ +/- pelvic lymphadenectomy
b. KIV adjuvant radiotherapy (if the removed LN is positive and the grading of tumour is
poor/moderately differentiated/notorious type of tumour such as clear cell or papillary)
c. Follow-up patient closely within 2 years (in case of recurrence) with gynae-oncologist
d. If patient complaint of PV spotting, do speculum examination, take biopsy and send for HPE
e. If recurrent (at vagina vault), start on chemotherapy
f. In case of clear cell or serous papillary cancer (poorly differentiated) - straightaway do
TAHBSO + pelvic lymphadenectomy + adjuvant radiotherapy

*Subtype:
endometrioid, most common
adenocarcinomas
adenosquamous
Papillary serous
clear cell

171
23.0 POSTCOITAL BLEEDING
SCENARIO: 44 year old lady complained of postcoital bleed for 5 months duration, single but
sexually active

Differential Diagnosis
1. Cervical causes: cervicitis, polyp, erosion, cervical cancer
2. Vaginal causes: vaginal cancer, vaginitis
3. Vulva causes: squamous cell carcinoma

History
Cervical cancer:
● Foul smelling PV discharge
● Abnormal vaginal bleeding (irregular menses)

Risk factors:
1. Multiple sexual partners (>3) : STD mainly HPV infection (might come from partner)
2. Partner with multiple sexual partners
3. Early sexual exposure (young age of first SI, <17years old) : the earlier the exposure, the
higher the chance of getting HPV infection
4. Unprotected sexual intercourse
5. Exposure to and persistent HPV infection (undiagnosed/undetected) : highly associated
with cervical ca
6. Co-infection with Chlamydia and HSV : related to unprotected sex
7. Usage of contraception (OCP) > 10 years
8. Women with precancerous lesion : high tendency to have malignant changes
9. Multiparity (≥7 children) : highly associated with HPV infection
10. Immunocompromised : DM, HTN, smoking, drugs
11. Low socioeconomic status
12. Pap smear

172
24.0 CERVICAL CANCER
Histological type of cervical CA

1. Squamous cell carcinoma (SCC) : ≈ 90%


2. Adenocarcinoma
3. Adenosquamous : less common

Typical clinical presentation /symptoms

1. Typical :
- PCB
- vaginal discharge : foul smelly (yellowish, bloody) [dt fast growth, fast death]
2. Possible sx :
- IMB
3. Rare :
- Abdominal pain
- Bowel : tenesmus, LGIB
- Urinary sx : hematuria, dysuria

Physical Examination

1. General: nutritional status, pallor, ill-looking, cachexic, jaundice, Virchow’s node


2. Lymphadenopathy : supraclavicular, inguinal
3. Respi : effusion, consolidation, PE
4. Abdo : distended, mass, scar, hepatomegaly, ascites
- mass (blocked passage dt cervical stenosis bcs of the mass : hematometra-->pyometra) if
distant mets, hydronephrosis d/t obstructive uropathy
5. Pelvic : inspect perineum, speculum examination (any erosion or abnormal growth)
- Speculum : lesion or cauliflower-like mass at cervix, discharge
- Bimanual : vaginal wall involvement
6. DRE : mass or lesion due to direct infiltration

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Investigations

1. Routine blood investigations


2. USS: to look for mass in uterus and ovary, hematometra, pyometra
3. PAP smear: conventional / LBC - normal, HSIL or LSIL (screening) if abnormal do colposcopy
(look for acetowhite area), take biopsy and send for HPE
- If on speculum examination there is an abnormal growth, straightaway do punch biopsy
and send for HPE
4. Colposcopy: green filter for angiogenesis, iodine (unstained is abnormal) & acetic acid
(stained is abnormal, more nucleus more white), appearance grading — high or low grade
5. Biopsy: LLETZ & cone
6. HPV testing: 16,18,31,33,45

If HPE result came back as positive for cervical cancer:


a. Do staging clinically under EUA:
b. Do digital rectal examination (DRE) to see involvement of
parametrium
c. Cystoscopy
d. Sigmoidoscopy
e. CT scan for involvement of lymph nodes and distant
metastases

Staging: Clinicopathological
Diagnosis: HPE

➢ During examination : if see mass or features suggestive of cancer, → DIRECTLY DO BIOPSY


and send for HPE
➢ If examination normal, but high risk or sx suggestive of cervical ca : pap smear + HPV
testing (if abnormal result)

Once confirmed cancer, steps to do before proceed with the treatment:

1. CT TAP +/- MRI


2. EUA (clinical staging)
3. Cystoscopy
4. Sigmoidoscopy
5. CXR
6. U/S KUB (not mandatory as there is CT already)
7. IVU
8. FBC , Crossmatch, LFT, RP, ECG (pre-op assessment)

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Management

For Screening :

1. Pap smear & HPV DNA Testing


2. Colposcopy
i. If low grade
- conservative management
- repeat PAP smear & HPV testing in 6 months monitor till normal
ii. If high grade
- ablation / excision
- choices: LLETZ, cone, cold coagulation

Then, review again in 6 months


- PAP & HPV
- if present: repeat colposcopy and remove residual lesions
- if negative: cervical screening in 3 years

If confirmed cancer by biopsy :


Treatment modalities for cervical CA:
1. Surgery
2. Radiotherapy
3. Chemotherapy

Management: Stage Dependent

1. Preclinical IA
- remove cervical cancer from the cervix
- clear margin excision (LLETZ / cone biopsy)

2. Clinically invasive IB - IV

A. Stage IB - IIA :
○ Wertheim’s hysterectomy [uterus, paracervical tissue, upper 1/3 of vagina +/- LN]
(elderly) ;
○ Radical trachelectomy [removal of cervix and upper part of the vagina] + PLND
(fertility sparing)

B. Stage IIB and beyond: concurrent chemoradiotherapy

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FIGO Staging of Cervical Cancer

Complications of treatment

➔ CCRT : peripheral neuropathy, nausea and vomiting, diarrhea, nephrotoxicity, ototoxicity,


subacute obstruction, radiation prostatitis/cystitis, fistula
➔ Surgery : Hemorrhage, urinary and bowel injury, fistula, atonic bladder, pulmonary
embolism, lymphedema

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How to follow up?

Post tx :
1. f/up every 3 months for 1st year → every 4 months in 2nd year → every 6 months in 3rd -
5th year → annually
2. Complication of surgery
3. Recurrent of disease (any stage) : do as when you suspected pt to has cervical cancer
4. Obtain history : any active complaints
5. Discharge, abnormal vaginal bleeding
6. Edema
7. LOW, LOA
8. Physical examination

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24.1 CERVICAL CANCER SCREENING
1. What is the advantage of HPV screening over Paps smear?

HPV DNA test Pap smear

Advantages ● Has better sensitivity Cheaper


(more accurate as it detects the
specific HPV DNA)
● Self collected, easy to perform
● Less painful

Disadvantages More expansive More uncomfortable as the


clinician will need to visualise the
cervix using Cusco speculum
during sample collection

2. What are the worrying strains?


a. The oncogenic strains that are associated with high grade CIN and cervical cancer

3. What are oncogenic strains and non-oncogenic strains?


a. Oncogenic strains: 16, 18, 31, 33, 45
b. Non-oncogenic strains: 6, 11 (genital warts), 52, 58

4. What is the management for oncogenic and non-oncogenic strains?

Non-oncogenic strain Monitor 3 yearly

Oncogenic strain ● Indicated for colposcopy examination

● During colposcopy, we first rinse the cervix with normal


saline. Then, we apply 5% acetic acid and observe for the
presence of acetowhite area.

After that, we apply the Lugol's iodine and monitor for the
staining of the dye. Biopsy of the abnormal areas is taken
after the Lugol’s iodine test.

● Acetowhite area indicates the presence of areas with


increased cell turnover including CIN. Areas with increased
cell turnover have high nucleoprotein content that will
coagulate and turn white when exposed to the acetic acid.

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● Schiller's test is positive when Lugol's iodine does not stain
the area of the cervix. This also indicates the presence of
areas with increased cell turnover or CIN. These areas fail
to take up the stain because it lacks intracytoplasmic
glycogen.

5. HPV vaccines

● HPV is part of the national vaccination programme targeted for all female aged 13 - 15
years old

● Why given at 13 -15 years old:


1. Those younger will have a better immune response towards the vaccine
2. The vaccine will prevent the covered types of HPV if they are given before exposure
to the virus (SI)

● The function;
1. Vaccination against HPV will protect against CIN and Cervical cancer
2. Protects against genital warts

● Dossage (0-1-6):
1. Consist of 3 injections
2. Second - 1 month after the first injection
3. Third injection - 6 months after the second injection

● Types of HPV vaccines and it’s coverage (advantage)

Types Strains Coverage Examples

Bivalent vaccine 16, 18 Oncogenic strains Cervarix

Quadrivalent 6, 11, 16, 18 Oncogenic strains Gardasil-4


(75%) Genital warts

Nanovalent 6, 11, 16,18, 31, 33, 45, Oncogenic strains Gardasil-9


(95%) 52, 58 Genital warts
Can offer in man

● Criteria for HPV vaccination


1. Offered in age between 13-15 years old
2. Recommended in everyone older than 15 years old if they were not adequately
vaccinated
3. No prior exposure to virus (sexual intercourse)

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25.0 OVARIAN CANCER
*no role of screening for ovarian cancer
Screening for cervical ca → pap smear

Types of Ovarian Neoplasms


Secondary metastases account for 4-8% of ovarian malignancies; primary ovarian neoplasms can
be classified based on cell population they are derived from:

(i) epithelial ovarian tumours (80-85%)

(ii) germ cell tumours (10-15%)

(iii) specialized gonadal stromal cell tumours (3-5%)

1. Epithelial Ovarian Tumours


(derived from the mesothelial lining of the ovary & peritoneum; may be differentiated along the
Müllerian or Wolffian pathway)

1. Serous tumours

● Most common epithelial ovarian tumour


● Resemble fallopian tube epithelium (Müllerian)
● Bilateral in 10% of cases
● Varying degrees of malignancy:
○ 70% benign (serous cystadenoma)
○ 5-10% borderline
○ 20-25% malignant (serous cystadenocarcinoma)
● Pathology of serous tumours:
○ Grossly: unilocular (small) or multilocular (large) cysts containing clear
serous fluid
○ Histologically: psammoma bodies, papillary bodies
● Clinical implications:
○ Worst prognosis (for cystadenocarcinoma)

2. Mucinous tumours

● Resemble endocervical epithelium (Müllerian)


● Bilateral in <10% of cases
● Varying degrees of malignancy:

- 85% benign (mucinous cystadenoma)


- Borderline

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- Malignant (mucinous cystadenocarcinoma)
● Pathology of mucinous tumours:
- Grossly: multilocular, huge cysts containing mucous-like contents; often the
largest of all ovarian masses, can grow to the extent of filling up the pelvis &
abdomen in a patient
- Histologically: locules containing mucin
● Clinical implications:
- Described association with a mucocele of the appendix (hence
appendicectomy usually also performed during surgery)
- Rare complication occurs when a mucinous tumour ruptures & seeds the
surface of the peritoneal & bowel surfaces, producing large quantities of mucus
(pseudomyxoma peritonei)

3. Endometrioid tumours

● 20% of all ovarian neoplasms


● Resemble endometrium (Müllerian)
● Mostly malignant
● Clinical implications:
- 10-15% associated with endometriosis (even though malignant transformation
of endometriosis occurs in <1% of patients)
- 20% associated with primary endometrial cancer of the uterus

4. Clear cell (mesonephroid) tumours

● Uncommon (5% of all ovarian neoplasms)


● Wolffian differentiation
● Malignant
● Pathology of clear cell tumours:
- Grossly: may be solid or cystic
- Histologically: large sheets of epithelial cells with clear cytoplasm,
tubules & hobnail nuclei
● Clinical implications:
- Worst prognosis alongside serous cystadenocarcinomas amongst the
epithelial ovarian tumours
- 25% occur in conjunction with endometriosis

5. Brenner tumours

● Uncommon (2-3% of all ovarian neoplasms)


● Resemble transitional epithelium (Wolffian)
● Predominantly benign (<2% are malignant)
● Pathology of Brenner tumours:

181
- Grossly: small (1-8cm) smooth solid mass
- Histologically: nests of urothelial-like cells with
coffee bean nuclei within a dense fibrous stroma

● Clinical implications:
- 10% of Brenner tumours occur in conjunction with a mucinous
tumour or a dermoid cyst in the same or contralateral ovary

2. Germ Cell Tumours


(derived from the germ cells – ovum – of the ovary)

1. Benign cystic teratoma (mature teratoma; dermoid cyst)

● Tumour differentiation into embryonic tissue


● Most common benign ovarian neoplasm
● Pathology:
- Can take on a great variety of forms, with virtually all adult tissue
types represented within the tumour mass
- Commonly features ectodermal tissue types (skin, hair, sweat &
sebaceous glands, teeth, neural) with some mesodermal (bone,
cartilage) & rarely endodermal elements
- Cyst lumen contains a nipple/mammary body/hillock-like
protuberance (Rokitansky tubercle)
- Rarely, may be composed of functional thyroid tissue (struma ovarii),
which can lead to clinical hyperthyroidism
● Clinical implications:
- Rarely may result in acute abdominal pain if tumour ruptures &
releases sebaceous material which causes peritonism
- 15-20% bilateral

2. Malignant teratoma (immature teratoma)

● Tumour differentiation into embryonic tissue


● 2nd most common malignant germ cell tumour
● Majority seen in the 1st 2 decades of life
● Pathology:
- Neural elements most frequently seen, but cartilage & epithelial
tissues also common

182
● Grading system for malignant teratomas:
- Grade 1 = rare foci of immature neuroepithelial tissue occupying <1 per
low power field (40x) in any slide
- Grade 2 = 1-3 per low power field per slide
- Grade 3 = large amounts
● Clinical implications:
- Do not produce any tumour markers
- Grow rapidly (like most malignant germ cell tumours) & can cause
pain early

3. Gonadoblastoma

● No tumour differentiation
● Benign tumour
● Almost all gonadoblastoma are seen in women with dysgenetic gonads
● Pathology:
- Technically a mixed ovarian neoplasm composed of cells resembling those of
dysgerminoma & others resembling granulosa & Sertoli cells
- Psammoma bodies characteristically seen
● Clinical implications:
- 50% will eventually become dysgerminoma or other malignant germ cell
tumours
- Bilateral oophorectomy indicated if dysgenetic gonads present to prevent
subsequent development of dysgerminoma

4. Dysgerminoma
● No tumour differentiation
● Most common malignant germ cell tumour
● Majority seen in children & young women

- Occasionally seen in patients with gonadal dysgenesis or testicular


feminization syndrome (in which case dysgerminoma may arise from a pre-
existing gonadoblastoma)

● Pathology:
- Grossly: large, firm, bosselated external surface; soft & fleshy
- Histologically: nests of monotonous tumour cells with clear glycogen-filled
cytoplasm bound within fibrous septa filled with lymphocytes
● Clinical implications:
- Produces lactate dehydrogenase (LDH)
- Highly radiosensitive tumour (but nowadays chemotherapy is first-line
treatment instead)
- 10% are associated with other germ cell malignancies
- 10% are bilateral

183
5. Choriocarcinoma

● Tumour differentiation into extraembryonic tissue


- A non-gestational form of choriocarcinoma
- Choriocarcinoma can occur in a gestational form in the setting of molar
pregnancies or from the trophoblastic tissue of ectopic & normal
pregnancies
● Clinical implications:
- Produces hCG
- Rarely bilateral

6. Endodermal sinus tumour (yolk sac tumour)

● Tumour differentiation into extra-embryonic tissue


● Highly malignant tumour
● Exclusively seen in young children & young women
● Pathology:
- Yolk sac differentiation
- Schiller-Duval bodies (central space surrounded by malignant cells)
- Immunohistochemical stain for AFP positive
● Clinical implications:
- Produces alpha-fetoprotein (AFP)
- Rarely bilateral

7. Embryonal carcinoma

● Clinical implications:

- Produces both AFP & hCG


- Rarely bilateral

3. Specialized Gonadal Stromal Tumours


(derived from the bipotential gonadal stroma/sex cords)

1. Granulosa-theca cell tumours


● Feminine differentiation of stromal cells
● Can occur at any time, but most common in post- menopausal age group
● Pure thecomas are rarely malignant; granulosa cell tumours are the most
common malignant stromal cell tumours
● Pathology:

- Thecomas exhibit plump spindle cells with lipid droplets

184
- Granulosa cell tumours comprise groups of lipid laden luteinized cells
in a follicular pattern (Call-Exner bodies); cells exhibit coffee bean
nuclei; strongly positive for inhibin

● Clinical implications:
- Functioning tumour producing female hormones, resulting in
feminizing signs & symptoms (precocious puberty, premenarchal
uterine bleeding in infancy & childhood, menorrhagia, endometrial
hyperplasia, endometrial cancer, breast tenderness, fluid retention)

2. Sertoli-Leydig cell tumours (Arrhenoblastomas)

● Masculine differentiation of stromal cells


● Commonly seen in young women
● Low grade malignant potential (3-5% malignant)
● Clinical implications:
- Functioning tumour producing male hormones, resulting in
virilizing signs & symptoms (hirsutism, temporal baldness, voice
deepening, clitoromegaly, muscular build)

3. Gynandroblastoma
● Combination of granulosa-theca & Sertoli-Leydig cell

4. Lipid cell tumours (hilar cell tumours)

● Usually located in the ovarian hilus


● Rarely malignant
● Clinical implications:
- Occasionally produce adrenal corticosteroids resulting in Cushing’s
syndrome
5. Fibroma

● Pathology:
- Solid encapsulated smooth-surfaced tumour
- Composed of interlacing bundles of fibrocytes
- May occasionally contain theca cell elements (fibrothecoma)
● Clinical implications:
- Occasionally results in transudation of fluid from the tumour, resulting
in ascites & subsequently flow of the ascitic fluid through
transdiaphragmatic lymphatics to result in right-sided pleural effusion
(Meig’s syndrome)

185
4. Metastatic Tumours
- Usual features of metastatic tumours to the ovaries:
● Bilateral involvement
● Cytokeratin 7 negative (CK 7, a marker for primary ovarian neoplasm)
● Friable & necrotic with vascular invasion

- Common sites of primaries:

● Breast
● Gastrointestinal tract
- Specific type of metastasis from gastric cancers histologically
comprising signet-ring cells known as Krukenberg tumour
● Uterus, fallopian tubes
● Peritoneum

● Summary on types of Ovarian CA

1. Epithelial tumours

Mnemonic

1. Serous carcinoma S

2. Mucinous carcinoma M

3. Endometrioid carcinoma E

4. Clear cell carcinoma → worse prognosis C

5. Mixed Mullerian Tumour → brenner B

2. Germ cell tumours (young) → unilateral salpingo-oophorectomy

Mnemonic

1. Dysgerminomas D

2. Yolk sac tumours/endodermal sinus tumour Y

3. Immature teratomas I

4. Choriocarcinoma C

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3. Sex cord stromal tumours → menorrhagia/PMB

- Granulosa cell tumour → PMB

- Theca cell tumour

- Androblastoma

Risk Factors of Ovarian CA

1. Family history of malignancy of ovary, endometrial, colon and breast

64 years old → accidental


84 years old → presented with family history of malignancy as above

2. ‘incessant ovulation’ theory (every menses cycle, oocytes will ruptured and thus can
cause damage/ exposure to long duration of menses) :
- early menarche
- late menopause
- nulliparous
- small family number → low parity

3. Endometriosis → endometrioid carcinoma & clear cell carcinoma (endometriosis is


associated with these carcinomas)
4. Smoking → mucinous carcinoma
5. Obesity
6. IUCD insertion

Protective factors

● Multiparity
● COCP → ↓ovulation
● Tubal ligation
● Salpingectomy
● Hysterectomy

187
Clinical Presentation

1. Asymptomatic in early stage


2. Late stage: SOB, abdominal swelling
3. Classical: constitutional sm, abdominal discomfort and pain, feeling of lump, urinary
sm

● How to diagnose?

1. USS to see the origin of the mass and the presence or absence of features of malignancy:

1. Size>5cm → ovary 2-3cm


2. Uni/bilateral (bilaterality)
3. Multiloculated/multiseptated
4. Solid/cystic
component-echogenicity
5. Papillary invasion
6. Ascites
7. hypervascularity

188
2. Blood investigations
Tumour markers (if on USS the mass arises from the ovary)

a. Epithelial:
● CA 125 (80%) → serous
→usually can also be elevated in fibroids, endometriosis, appendicitis, early
pregnancy
● CA 19-9,
● AFP,
● B-HCG,
● CEA→ mucinous

b. germ cell: AFP, B-HCG, LDH, inhibin


*if USS and blood ix is suggestive of cancer

Tumor markers used in ovarian cancer diagnosis and follow-up:

Tumor marker Tumor type Uses

CA-125 Epithelial ovarian ca, (Serous) Preoperative, f/u


borderline ovarian tumors

CA 19-9 Epithelial ovarian ca, Preoperative, f/u


(Mucinous) borderline ovarian
tumors

HCG Dysgerminoma, Preoperative, f/u


Choriocarcinoma

Inhibin Granulosa cell tumor f/u

Alpha-fetoprotein Endodermal yolk sac, Preoperative, f/u


teratoma

3. CT scan
To see the extent of tumour, to help counsel the patient on the prognosis
→paraaortic region→liver→lung

4. Additional blood test: LFT, RP, FBC


→ Correct anemia
→Associated baseline

189
➔ Fit for surgery or not

5. CXR if clinically, I think the patient has pleural effusion → presented with only SOB

6. ECG if elderly patients


*uterine mass: pregnancy (young pt), fibroid, sarcoma, bladder pathology (retention, cancer)
*ovarian mass: benign (hemorrhagic cyst, huge endometrioma), malignancy; well OR moderately
OR poorly differentiated

Risk of Malignancy Index(RMI) in ovarian cancer


RMI- predict risk that an adnexal mass is malignant

Risk of Malignancy Index (RMI)

Criteria Scoring system

Menopausal status (M)


Premenopausal 1
Post menopausal 3

Ultrasound features (U)


Multiloculated None = 0
Solid areas 1 feature = 1
Bilateral lesions >1 feature = 3
Ascites
Metastasis

Serum CA-125 titre Absolute value in U/ml

Calculation & interpretation of RMI:


RMI = M X U X CA-125

Low risk RMI : <25 (<3% risk of malignancy)


Moderate risk RMI : 25-250 (20% risk of malignancy)
High-risk RMI : >250 (75% risk of malignancy)

190
Treatment

1. Benign ovarian tumour; eg: teratoma

- Oophorectomy if the tumour is so huge because usually there is almost no


more normal tissue left
- Cystectomy if the tumour is small
- If too small <5cm just leave it be (border: >5cm- remove because tend to get
twisted and ruptured and will start developing sm)

2. Ovarian cancer

- Surgery (for epithelial tumours ONLY): TAHBSO + omentectomy (debulking)


+/-pelvic lymphadenectomy (LN sampling) +/- appendicectomy
- Chemotherapy
- Radiotherapy

Before considering TAHBSO, look at;


a. Severity of disease (extent of dz)
b. Young age
c. Desire for fertility
d. Patient’s wish
e. Comorbidity

Fertility sparing surgery (unilateral salpingo-oophorectomy) →germ cell tumor→young

Carboplatin → 6 cycles → 3 weeks apart


Side effects
Long term : neutropenia, immuno-compromised,.....

● Once do TAHBSO + omentectomy- straightaway do adjuvant chemotherapy


(carboplatin/cisplatin and paclitaxe(Taxol)) for 6 cycles
● For germ cell tumour patients (young)→ Do salpingo-oophorectomy + adjuvant
chemotherapy (cisplatin in combination with bleomycin and etoposide BEP) straightaway
● How to confirm? By doing biopsy and send for HPE
● For patient with germ cell→can recur post-op: advice to marry quickly
● Advice family members for early screening

191
Follow up

- At gynae-oncology clinic → how to f/u

1. Epithelial cancer:

- Do CA 125 only for monitoring


- USS

2. Germ cell cancer:

- CA 125, AFP
- USS

192
26.0 HYPEREMESIS GRAVIDARUM
Definition
HG can be diagnosed when there is protracted nausea and vomiting of pregnancy (NVP) with the
triad of more than 5% pre pregnancy weight loss, dehydration and electrolyte imbalance.

Pathogenesis
● Metabolic and endocrine factors:
● B-HCG levels which is high in molar and multiple pregnancy
● Estrogen
● Progesterone levels which peaks during 1st trimester just when n+v peaks

Clinical features
a. Excessive vomiting
b. weight loss (5% pre pregnancy)
c. Symptoms suggestive of dehydration (oliguria, giddiness, fatigue)
d. Symptoms suggestive of electrolyte imbalance (fatigue, confusion, epigastric pain)
e. Symptoms of complications:
○ Wernicke’s encephalopathy: restlessness, insomnia, convulsions, coma
○ Korsakoff’s psychosis: mental confusion, short term memory loss
○ Peripheral neuritis
○ Ophthalmic complications: blurring of vision, diplopia
f. Clinical Signs:
○ Anxious appearance
○ LOW >5% of TBW
○ Sunken eyes
○ Loss of skin elasticity
○ Dry tongue with ketotic odour of breath
○ Tachycardia
○ Hypotension
○ Fever
○ Confirmation of pregnancy
○ Size of uterus: larger than date in multiple and molar pregnancy

Differential diagnosis
1. Peptic ulcer disease
2. Acute gastroenteritis

193
3. Appendicitis
4. Severe gastroesophageal reflux
5. Cholelithiasis and cholecystitis

Pathology
● Liver: centrilobular fatty infiltration without necrosis
● Kidneys: fatty change in cells of first convoluted tubules
● Brain: small haemorrhages in hypothalamic region- Wernicke’s encephalopathy
● Starvation leads to depletion of glycogen stores, causing fat stores to produce ketone
bodies, excreted in urine and breath.
● Electrolyte disturbances due to dehydration: hyponatremia, hypokalemia, hypochloremia
● Hepatic dysfunction leads to elevated blood urea nitrogen and uric acid
● Prolonged starvation causes hypoglycemia, hypovitaminosis and hypoproteinemia
● Haemoconcentration due to dehydration, and mild leukocytosis with eosinophilia

Investigations
1. Blood test
a. Serum electrolytes
b. BUN
c. Hematocrit
d. LFT
2. Urine analysis
a. Reduced volume
b. Dark color
c. High specific gravity
d. Ketones
e. Acidic pH
f. Diminished or absent chlorides
3. Hormones
a. Diminished TSH
b. Elevated free T3
4. ECG - changes of hypokalemia
5. Fundoscopy - retinal haemorrhages and detachment

Complications
● Jaundice due to hepatic dysfunction
● Stress ulcers in stomach due to excessive vomiting

194
● Neurological complications as a result of vitamin deficiency : Wernicke’s
encephalopathy, Korsakoff’s psychosis, peripheral neuritis
● Ophthalmic complications

Management
● Simple n+v in pregnancy
● Reassurance that these sm are common and almost self-limited
● Dietary modifications:
● Avoid emetogenic foods and odours
● Frequent small meals every 2-3 hours
● Low protein and low fat diet
● High, easily digestible carb diet
● Avoid iron supplements
● Exclude other causes
● Trial of medications

Treatment
1. Admit the patient.
2. Monitor the vital signs.
3. Monitor urine output and fluid intake.
4. Intravenous hydration accomplished with dextrose and dextrose saline helpsin correcting
hypovolaemia and ketosis.
5. Intravenous potassium supplementation in few patients with close monitoring.
6. Parenteral vitamins in prolonged HG, particularly because of thiamine deficiency
(Wernicke’s encephalopathy).
7. Total parenteral nutrition in extreme cases.
8. Afterwards, small frequent meals gradually advanced from liquids to solid.
9. Antiemetics: phenothiazines (Chlorpromazine and Prochlorperazine 25 mg every 8 hours
orally, IM or rectally as needed).
10. Promotility agents: Metoclopramide 10mg orally up to 4 times a day.
11. Corticosteroids: 40 mg prednisolone daily in 2 divided oral doses.
12. Alternative therapy: acupressure, psychotherapy, etc.
13. Therapeutic abortion: if all therapeutic measures fail, only when maternal life is
threatened.

195
APPENDIX
A1. PARTOGRAPH

196
A2. CARDIOTOCOGRAPHY (CTG)

A3. TYPE OF INSULIN VIALS


● Actrapid - Yellow
● Insulatard - Green
● Mixtard - Chocolate

197
A4. MODIFIED BISHOP’S SCORE

Factors Score

0 1 2

Dilatation 1 2 >3

Effacement (cm) 1.5 or more Intermediate 0.5 or less

Station -2 or higher -1 0 or lower

Consistency Firm Intermediate Soft

Position Posterior Axial Anterior

198
A5. SHORT CASE OBSTETRIC DR QUE SCRIPT

199
200
201
202
203
A6. SHORT CASES IN GYNAECOLOGY DR QUE SCRIPT

MASS FOUND IN THE ABDOMEN

You should know the technique of physical examination (abdominal and vaginal examination) in
gynae U need to describe the mass properly i.e. site of the mass, consistency, margin, surface,
mobility either able to get above or below the mass as well as presence or absence of ascites.

You should know how to differentiate between mass from uterus and ovary.

1) How can you differentiate mass from uterus and ovary??

ON INSPECTION

SITE OF THE MASS

If the mass is at the centre, it is more likely to be uterine in origin, as compared to ovarian
mass which is more likely located at LIF/RIF.

ON PALPATION,

1. CONSISTENCY OF THE MASS

If the mass is firm in consistency it is more likely to be uterine in origin, and if it is soft in
consistency, it is more likely to be ovarian cyst.

2. MARGIN OF THE MASS

If the margin of the mass is a well defined margin it is more likely to be uterine mass and if
it is irregular margin than it is more likely to be ovarian mass.

3. MOBILITY OF THE MASS

If the mass is only mobile for side to side(laterally), it is more likely to be uterine mass as
compared to ovarian mass which is usually mobile in all directions.

4. GET BELOW AND ABOVE THE MASS

Usually, if the mass is uterine in origin, I only can get above the mass and cannot get below
the mass during palpation,however if the mass is ovarian in origin, I can get below as well
as above the mass.

204
5. ASCITES

If the mass is associated with the presence of ascites,then it is more likely the mass is
ovarian in origin .

ON BIMANUAL VAGINAL EXAMINATION

If the mass is uterine mass in origin, when I push the mass upwards using my left hand, the
cervix usually moves away from my finger. However, if the mass is ovarian in origin, the cervix
usually does not move. BUT not always so , there are certain cases of ovarian mass (ie ovarian
mass which was adhered to the uterus) in this case the cervix will also move away when we push
the mass upwards .

YOU SHOULD HAVE THE SCRIPT HOW TO PRESENT THE MASS FROM UTERUS AS WELL AS MASS
FROM OVARY

MASS FOUND IN THE ABDOMEN

What U WANT TO DO ?

1. I want to get more detail history from my patient and do the relevant investigations in
order to find the possible courses

2. Detail of history include;

a. Age ,parity, chief complaint of patient


b. Any history that may directed U to the provisional diagnosis
In case of uterine mass(ex: fibroid )
c. Ask whether the typical clinical presentation is present or not ?
d. Menstrual disturbance such as menorrhagia (majority of cases) or intermenstrual
bleeding(polyp)
e. Compression symptoms ? bowel or urinary ?
f. History of subfertility

Remember the symptoms are usually related to site (type) and size of fibroids . Age is very
important if reproductive age is it is more likely to be fibroid BUT if menopause may be
leiomyosarcoma.

In the case of ovarian mass ; Age is very important here. If a young patient, it is more likely to be
benign mass such as teratoma or if menopause may be malignancy. Ask if the patient got any risk
factor for malignancy .

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What investigations that you would to do?

I will do investigation, to find the origin of the mass either from uterus OR ovary as well as
nature of the mass (either benign or malignancy)

If the patient presented with menorrhagia, I would like to do FBC to assess her
haemoglobin status to see whether she is anemic or not.

CENTRAL ABDOMINAL MASS


Upon inspection of the abdomen, there was distension noted over the suprapubic area.
There was no surgical scar, no dilated vein and the abdomen moves with respiration. The umbilicus
was centrally located and inverted. Hernia orifices were intact.

The abdomen was soft and non-tender. There was a palpable mass located at the
suprapubic area corresponding to ___ weeks gravid uterus measuring ___ (mention the
dimension). It was non-tender, firm in consistency, smooth surface with regular margin, mobile
from side to side but not vertically, I can get above but cannot get below the mass and it was dull
on percussion. There was no organomegaly or ballotable kidney. Shifting dullness was negative and
bowel sounds were present. There was no bruit heard over the mass (aortic/ renal bruit). (if PPU:
hard, x mobile in all direction)

I would like to complete my examination by doing a bimanual palpation in which I would


insert my right index and middle fingers per vaginally touching the cervix while my left hand on the
abdomen pushing the mass upwards. If the mass is from the uterine in origin, the cervix will move
away from my examining fingers and vice versa.

My provisional diagnosis is fibroid.

My differential diagnosis are :


● Adenomyosis (globular, tender uterus)
● Physiological (pregnancy) – If young patient
● Distended bladder
● Ovarian mass→endometrium

I would like to do a transabdominal ultrasound scan to confirm the origin of the mass.

● If it is uterine in origin, I would like to know the size, position and number of
fibroid/ adenomyosis
● If it is an adnexal mass (size, location, endometrioma,cyst), I would like to
identify features of malignancy :
1. Bilaterality
2. Solid component
3. Papillary projection

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4. Hypervascularity
5. Multiloculated
6. Presence of free fluid
7. Size >5 cm (suggestive of malignancy)

Management for Fibroid ( most commonly asked )


-refer to Topic on Fibroid-

A. MEDICAL TREATMENT

Medical treatment → NO significant benefit for medical treatment. Given for those with
menorrhagia and uterus palpable more than 12 weeks. Furthermore, medical treatment is
conservative.

GNRH agonist - Lucrin → prior to surgery 3months

Role of GnRH / Advantages

● Reduce vascularity ( reduce bleeding intraoperatively and need for transfusion, lesser
post-op infection)
● Shrink fibroid ( more easier operation → can do myomectomy instead of hysterectomy →
lesser post-op analgesic requirement and shorter hospital stay)
● Cause amenorrhea
● Treat the symptom – reduce the heavy flow
● Optimise the Hb

Disadvantage of GnRH

● In case of multiple size fibroid, the smaller size fibroid will become very small and cannot
be found during operation → it will grow bigger again once the effect of the medication
finish (rebound)
● Difficult to inoculate the fibroid (due to pseudocapsule), difficulty to remove the fibroid
during myomectomy
● Expensive
● May cause menopausal symptoms (since Gonadotropin suppresses oestrogen)
● May cause osteoporosis

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Don't give if;
● Small size fibroid
● Patient is asymptomatic
● Pt plan to do hysterectomy

B. SURGICAL TREATMENT

1. MYOMECTOMY
Need to counsel about :
● It is a major surgery which can be complicated by haemorrhage and may need
hysterectomy
● Fibroid may recur and subsequent operation may be difficult due to adhesion
● Presence of adhesion colic
● Fertility problem (if plan to conceive) due to adhesion
● If able to conceive, high risk for miscarriage, placenta praevia and abruptio placenta

2. HYSTERECTOMY

3. UTERINE ARTERY EMBOLIZATION

** HOW WOULD YOU MANAGE PATIENT WITH FIBROID?

A few factors that i have to consider before offering treatment;

➔ Whether the patient is asymptomatic or not


➔ Wish for fertility
➔ Age of the patient
➔ Patient’s fitness (any other underlying illness)
➔ Availability of treatment

1. As the patient is still young (<35 y.o), and has not completed the family yet, I will offer her to do
myomectomy either by laparoscopic or laparotomy. Prior to the surgery, I will give the patient
GnRH analogue to shrink the fibroid. However, I will counsel her regarding the risk for
recurrence, and it is a major operation which may end up with severe haemorrhage which may
end up with hysterectomy.

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2. As this patient's age is ___ (40 - 45) and the patient has completed the family, the best option is
total abdominal hysterectomy (TAH) as fibroid has risk for recurrence and subsequent operation
may be complicated by adhesion. There is also a lower chance for pregnancy at this age group.

3. As this patient's age is already ___ (>45), I will offer her for TAHBSO and I will counsel regarding
the early menopause and role of HRT for her.

Strategy to reduce bleeding:


Pre-operatively
Optimise Hb before operation

Intraoperatively-strategy to reduce bleeding

1. Iv tranexamic acid
➔ 1gram
➔ Anti fibrinolytic
2. Vasopressin
➔ Inject to the fibroid
➔ vasoconstrictor
3. Ligate → internal iliac artery

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OVARIAN MASS
Script short case in Gynae

On Examination of the abdomen,

➢ The abdomen is distended/ not distended and symmetry/ not symmetry,


➢ The umbilicus is centrally located and inverted/ everted/ flat.
➢ There was transverse/ oblique / midline / no scar seen at ____ area measure about
__cm.
➢ There is no keloid or hypertrophy seen
➢ There is also no/ present dilated vein.

Mass from Ovary

The abdomen is soft and non tender. There is a mass at the LIF/RIF region measure _ X_ cm. The
mass is irregular in margin, smooth surface, normal in temperature and soft in consistency. The
mass is mobile in all directions and I can get above & below the mass. The mass is dull on
percussion. There is no hepatosplenomegaly and both kidneys are not ballotable. There is positive
fluid thrill & shifting dullness indicating the presence of ascites. The bowel sound is present/ not.

My differential dx are dermoid cyst (incre 20-40 y/o), serous cystadenoma, mucinous
cystadenoma, tubo ovarian abscess (increase in young pt), endometrioma, ovarian ca, non gynae
causes (CRC, appendicular abscess etc.)

If I were given an opportunity:

1. I would like to get the history from the patient


2. I will do ultrasound (TAS/TAV) to confirm the origin of the mass
a. If the origin is from the ovary, I would like to look for features of malignancy
such as bilateral, papillary projection, multiloculated, solid, thick septate,
free fluid, and increased vascularity.
3. Then, I would like to do blood investigation for tumor marker level which include
CA125, CA19-9 (old), inhibin, BHCG and AFP (young). (CA125, USS and menopausal
status will be used as scoring in risk malignancy index, RMI).
4. I also would like to do CT/MRI to know the extension of the mass

How would you manage ovarian tumor?:

1. If the patient is young and there is no sign and symptoms of malignancy, I will do a cystectomy
(in a viable ovary - small and benign ovarian cyst). However, I will do oophorectomy if there are;

a. Twisted cyst and necrosis,


b. Too large/huge ovarian cyst (benign)
c. No more normal ovarian tissue left (benign)

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d. Malignant

2. If it is ovarian malignancy and..;


a. Patient is young (germ cell): I would offer unilateral salpingo-oophorectomy with 6 cycles
chemotherapy. I will counsel patient to marry early/ complete family early due to
recurrence and the normal ovary might be affected by chemotherapy
b. If patient is older → Epithelial tumor : I would offer TAHBSO + omentectomy + Chemo
(carboplatin + paclitaxel) 6 cycle, 3W apart

Chemotherapy

1. Epithelial tumours – 6 cycles


➢ TAHBSO + Omentectomy + paraaortic and pelvic lymph node dissection
2. GC tumour – 3-4 cycle
➢ Young (unilateral salpingo-oophorectomy)

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REFERENCES
1) 10th Teacher O&G
2) Latest CPG Guideline
3) Clinical Protocols in Obstetric and Gynaecology For Malaysian Hospitals
4) Obstetrics & Gynecology : Primary Care Medical Officer Survival Guide (PRIMEOG)

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