Tmbool’s Notes

in
Obstetrics and Gynecology

Notes from Dr. M Tmbool revision sessions for

Batch 88 “Qasawir”
February 2017

Written and revised by Hala Abdellaziz Altahir

 Topic Page Anemia 41
no. Antiphospholipid syndrome 42
Obstetrics DVT 44
Pulmonary Embolism 45
Bleeding in early 1
Malaria 45
pregnancy
HIV 46
Miscarriage 1
Diabetes 49
Notes on Anti D 9
Miscellaneous conditions 53
Gestational trophoblastic 10
Preterm labour 53
disease
Caesarean section 56
Ectopic Pregnancy 11
VBAC 58
Antepartum Hemorrhage 14
Induction of labour 59
Placenta Previa 14
Malposition and 61
Abruptio Placentae 16
malpresentation
Vasa Previa 18
IUFD 64
Hypertensive Disorders in 19
Obstetric Cholestasis 66
Pregnancy
Acute Fatty Liver 67
PIH 19
IUGR 68
Preeclampsia 20
Eclampsia 24 Gynecology
Chronic HTN 26 Menstrual cycle 70
Obstetric Emergencies 26 Abnormal Menstrual cycle 71
Postpartum Hemorrhage 26 Amenorrhea 71
Shoulder Dystocia 29 Dysmenorrhea 76
Cord Prolapse 31 Menorrhagia 77
Uterine Inversion 32 PCOS 80
Amniotic Fluid Embolism 32 Contraception 82
Uterine Rupture 33 Subfertility 88
Morbid Adherent Placenta 34 Infections 94
Medical Disorders in 35 Tumors 100
Pregnancy Uterine tumors 100
Epilepsy 35 Cervical tumors 102
Cardiac diseases 37 Ovarian tumors 106
*Rheumatic Heart disease 39
 Obstetrics

Bleeding in early pregnancy

Case:

27 years old married female presented at 11 th week GA C/O vaginal bleeding, on

examinations vital signs are stable, USS inconclusive.

1. mention the differential diagnosis?

2. outline the management plan?

DDx:

1. first trimesteric miscarriage

2. gestational trophoblastic disease (GTD)
3. ectopic pregnancy
4. Co-incidental cause (cervical erosion, polyps…)

Miscarriage
Expulsion of conception before viability i.e. before 24 weeks gestation.

Types:

Complete Incomplete

Threatened Septic

Inevitable Missed

Recurrent

General approach for any miscarriage:

- Make the right diagnosis.

- Carry out investigations in form of:

• ΒhCG
• USS
• Blood grouping and Rh status
• CBC for Hb
• Urine analysis

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- Suspect when there is period of amenorrhea in a lady with positive ΒhCG and now
presents with vaginal bleeding.

Complete miscarriage:

Hx: there is bleeding and pain then the pain subsides .

O/E: cervix is closed

Do USS twice; immediately => to exclude retained products of conception (RPOC), then
after 2 weeks do another USS.

*Nothing more on its management plan.

Incomplete miscarriage:

Hx: vaginal bleeding and pain.

O/E: cervix is open.

* (cervix is regarded closed when it is < 2 cm and open when > 2 cm).

Do USS => there will be heterogonous mass that is mixture of gestational sac and fetal
parts, and you can't differentiate between the fetal part and the sac (unlike in normal
preg.)

Management plan:

Expectant, medical or surgical management.

a) Expectant: admit and observe, if failed go for:

b) Medical management:
1. oxytocin infusion (but uterus rarely responds to uterotonic drugs in an
early GA => you will need high dose).
*more advanced GA => more effective induction
2. misoprostol orally or vaginally (at least 1 mg = 1000 mcg)
*unlike ordinary induction => 25-50 mcg is used

Surgical management: evacuation.

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Threatened miscarriage:

Hx: minimal vaginal bleeding and minimal pain

O/E: cervix is closed

On USS:

1. gestational sac
2. fetal pole/part
3. fetal heart activity

Missed miscarriage:

Hx: cessation of symptoms of pregnancy.

No abdominal pain and vaginal bleeding

O/E: is not remarkable and the cervix is closed.

On USS:

1. gestational sac > 25 mm and no fetal heart activity.

2. fetal parts of at least 7 mm.

*If fetal parts are not found it is either (GA usually < 6 weeks):

blighted ovum or an early pregnancy.

Note: the gestational age should be > 6 weeks to diagnose missed miscarriage.

Management:

Expectant, medical and surgical management (you give her the options).

Expectant:

Observe and follow up

• The expectant management should not be continued for more than 4 weeks
(risk of DIC)
• The lady should come immediately at any time if there is vaginal bleeding or
abdominal pain not responding to simple analgesia.

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 • Should come after 2 weeks for follow up => if nothing changed, she should come
after more 2 weeks for evacuation.

Medical management:

Benefit is to avoid the surgery and its complications.

Disadvantages are:

• Failure
• More time of hospitalization
• Medications side effects

The most effective method: Start with oral mifepristone (progesterone antagonists) and
wait for 24-48 hours then give misoprostol (PGE1 analogue) vaginally and admit the pt,
and repeat it after 4-6 hours.

Surgical Mx:

(D&E) = Dilatation and evacuation (by suction or non-suction evacuation)

*Note: (D&C) = Dilatation and curettage is used for endometrial biopsy.

Complications:

1. Injuries to
a. Cervix => can lead to cervical weakness
*Cervical injury can be avoided by giving vaginal misoprostol (to dilate)
4-6 hours earlier.
b. Uterus => Ashermann syndrome, or uterine perforation.
2. Infections
a. UTI
b. Endometritis and its complications.
3. Psychological trauma.

Procedure & Instruments:

• Lithotomy position
• Light source
• Cusco's or Sims speculum
• Tenaculum\Vulsellum forceps; to hold the anterior tip of cervix
• Hegar cervical dilator
• Uterine sound; to measure the length of the uterine cavity;

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 (but it’s the commonest cause of perforation during D&E)
• Ovum forceps; to remove the gestational sac
• +/- Curette; if there’s any RPOC.

Inevitable miscarriage:

Hx: severe pain and vaginal bleeding

O/E: the cervix is open

On USS: gestational sac +/- fetal pole, fetal heart activity presents in early stages but no
fetal heart activity in late stages.

Management:

Medical and surgical management same as missed miscarriage but here there is no
expectant management.

Septic miscarriage:

It is the most severe miscarriage.

Either:

1. secondary to induced miscarriage (abortion) in an illegal pregnancy, or

2. evacuation of incomplete miscarriage under septic conditions.

Hx: vaginal bleeding and abdominal pain + features of sepsis:

*Local features: mal-colored and offensive vaginal discharge.

*systemic features: fever, rigor, tachycardia, malaise.

Septic miscarriage can be complicated by:

1. severe sepsis and septic shock => leading to acute kidney injury and multi-organ
failure.
2. infection of genital tract organs => endometritis, tubo-ovarian abscess & pelvic
abscess.
3. DIC.

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Management :

• Admission
• NPO
• IV fluids
• Antipyretics
• Analgesics
• IV broad spectrum antibiotics (combination of 3rd generation cephalosporin –
ceftriaxone- and metronidazole).
• Urine analysis
• High vaginal/endocervical swab for C/S.
• Blood culture
• Blood for CBC, coagulation profile

*Wait for 4-6 hours up to 8 hours before any surgical evacuation.

Note: the uterus can be ruptured or perforated very easily in septic miscarriage and
gestational trophoblastic disease (GTD).

Recurrent miscarriage:

= 3 or more consecutive miscarriages from the same biological father

Either:

• recurrent first trimesteric miscarriage or

• Recurrent second trimesteric miscarriage

Causes of recurrent first trimesteric miscarriage:

1. antiphospholipid syndrome
2. polycystic ovary disease
3. persistent TORCH

Causes of recurrent second trimesteric miscarriage:

1. cervical weakness
2. uterine anomalies

(uterine anomalies also cause preterm labour)

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Second trimesteric miscarriage:

Mainly due to Cervical weakness.

Causes of cervical weakness:

1. D&E
2. D&C
3. cone biopsy
4. LLETZ (large loop excision of transformation zone)
5. previous passage of sizable macrosomic baby
6. Manchester operation for genital prolapse
7. forceps delivery
8. cervical tear after labor

Presentations of cervical weakness:

• Early second trimesteric miscarriage

• Painless gush of liquor in a women with amenorrhea and *documented*
pregnancy *(by USS or ΒhCG).
(*Because stress incontinence is a differential diagnosis)

Management of cervical weakness:

If presented at 14 weeks => Exclude:

1. uterine anomalies
2. vaginal bleeding
3. infections

If any one of the above; it is contraindication for cerclage.

Another contraindication is multiple pregnancy.

Cervical cerclage:

Carried out using Mersilene tape

2 types:

1. McDonald’s operation: at lower border by local anesthesia.

2. Shirodkar operation: at upper part of the cervix done under GA, it is more
effective but it carries a risk of more complications due to GA.

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When to reverse cerclage?

• If the lady went into a labor

• 37-38 weeks (term)
• Antepartum hemorrhage
• IUFD

When to apply?

If Hx is typical for cervical weakness, do elective cervical cerclage between 13-14 weeks.

It is not done earlier; to exclude the causes of first trimesteric miscarriage and to
exclude chromosomal anomalies.

If atypical Hx => come back in 1-2 weeks to confirm.

Dx of cervical weakness:

Clinical evaluation

History

Examination: (done inter-pregnancy i.e. in a non-pregnant women) => the cervix is

dilated and funnel shaped

Investigations: HSG (done outside pregnancy) => shows funnel shaped cervix.

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Anti D:

Given to avoid Rh sensitization of a Rhesus negative mother from a Rhesus positive

fetus.

The full dose is 500 IU

Half the dose is 250 IU

Full dose is given if: GA > 20 weeks gestation

Half dose is given if:

1. GA between 12-20 weeks gestation.

2. major bleeding at less than 20 weeks.
3. if she underwent any intervention.

No indication for anti D if:

1. GA < 12 weeks
2. minimal bleeding

no intervention (for example complete miscarriage without need for D&E)

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 Gestational Trophoblastic Disease
Range of diseases characterized by:

- hyperplasia of villi and swelling of trophoblastic cells

- with or without fetal parts
- ultimate diagnosis is by direct visualization of placental tissue

it ranges from: Molar Pregnancy to Invasive Mole to Choriocarcinoma

Molar Pregnancy

Partial Complete
Ovum Normal ovum Empty ovum
Sperm By 2 sperm By 1 sperm & duplication of
paternal sex
Karyotype (Triploid) 69 XXX/XXY/XYY (Diploid) 46 XX/XY
Fetal Parts on USS Present Absent
Symptoms ↓↓ ↑↑
Uterus Enlargement -- ↑↑

Clinical Presentation of Molar pregnancy:

- early pregnancy bleeding, passage of grape like tissue.

- exaggerated symptoms of pregnancy (+ Hyperemesis Gravidarum)
- early onset pre-eclampsia (also caused by multiple pregnancy)
- Hyperthyroidism (α subunit of βhCG is nearly identical to α subunit of TSH)
- Theca luteal cyst

Notes: (revise physiological changes during pregnancy)

• 1st half of Pregnancy:

(βhCG ↑) → TSH ↓, Total T3 & T4 ↑, Free is normal, (Estrogen↑) → TBG ↑
• 2nd half of Pregnancy:
(As βhCG ↑ at 7 day and peaks at 8-12 weeks then ↓ & plateau at 20 weeks)
→ TSH ↑, Total T3 & T4 ↓ initially, Free is normal in all pregnancy

* The α subunit of the βhCG resembles: LH, FSH, TSH

* βhCG → progesterone → ↓ motility and reverse it in GIT leading to Nausea and

Vomiting → Hyperemesis Gravidarum

* βhCG act as LH → theca luteal cyst → Abdominal pain, unilateral or bilateral

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Risk Factors

- Previous History
- Extremes of age
- Asian Population

Diagnosis

- Transvaginal USS (Snowstorm appearance & theca luteal cyst in complete mole)
- ↑βhCG not proportional to gestational age
- Urine analysis, RFT, RBS, CBC

Approach: (Benign mole)

- Suction and evacuation of molar pregnancy and follow up by βhCG until it

reaches zero IU/dl and give contraception.
- Suction and evacuation can be augmented by oxytocin after > half of products
expelled to avoid amniotic fluid embolism.
- Another option: medical management → Methotrexate

Ectopic pregnancy
• Any female with amenorrhea & ↑ βhCG is ectopic pregnancy until proven
otherwise by visualization of fetal parts in USS.
• Implantation of Zygote outside the uterus (ampulla of fallopian tube is the
commonest site) could also be in the abdomen, cervix, ovary.

Ampullary Ectopic Pregnancy:

Risk Factors

- Previous History (18–20%)

- PID (> 25% of cases)
- IUCD, POPs
- Previous pelvic surgery
- Endometriosis if gets pregnant
- Tubal anomalies (diverticulum)
- Assisted reproductive technique

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Clinical Presentation

Acute:

- Due to rupture of fallopian tube, results in massive hemoperitoneum, syncope

and shock, shoulder tip pain, minimal brownish vaginal bleeding. with severe
abdominal pain in one side.

Chronic:

- Abdominal pain unilaterally

- Anemia (accumulation of blood)

Fate:

1. Expulsed
2. Reabsorbed
3. Ruptured

Diagnosis

a. Early pregnancy assessment:

1. Serial quantitative βhCG

2. Transvaginal USS.

βhCG

* βhCG normally in pregnancy

- > 1500 IU if fetus is viable, discriminatory zone

- Doubles or at least > 66% rising every 48 hours

* βhCG in ectopic

- 1500 IU
- Will never double or increase by 66% every 48 hours

TVU

Outside Uterus:

- Ectopic sac
- Fluid in Douglas pouch

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 Inside Uterus

- Pseudo-gestational sac = centrally-located within the uterine cavity

*N.B.: The normal: eccentric location of gestational sac – embedded in the

endometrium.

b. Gold standard: Laparoscopy

*(also in endometriosis and endometrial PID, Laparoscopy is diagnostic and therapeutic)

Management

1. Resuscitation
2. Blood grouping, cross matching
3. Urgent laparotomy (better than laparoscopy in acute ruptured)

In laparotomy

1. Confirm diagnosis
2. Abdominal wash and packing to stop bleeding
3. Look at the other tube to see if it’s normal → do salpingectomy (remove and
resect), if not → do salpingostomy.

Salpingectomy is better, why?

1. Decrease risk of recurrence of ectopic

2. Choriocarcinoma 25%
3. Decrease the risk of persistent trophoblastic disease

Abdominal ectopic

- Follows expulsion of tubal pregnancy from fimbrial end -without rupture-.

- Formation of very huge placenta abdominal distention
- Recurrent syncope
- Anemia & Jaundice

Treatment

Laparoscopy, remove the fetus, irrigate umbilical cord and get out, then give
intraperitoneal methotrexate. Don't remove placenta.

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Cervical Ectopic

- Main risk factor is D&C

- Remove by dilatation of cervix
- Present as early bleeding
- Dx: TVU

Management of chronic ectopic

1. Expectant
2. Medical = Methotrexate and follow up
3. Surgical = laparoscopy superior to laparotomy
➢ Expectant and medical treatment, if:
- No symptoms of acute rupture
- Size < 3-5 cm
- βhCG < 3000 IU
➢ Surgical treatment, if:
- Size > 3 cm
- βhCG > 3000 IU
- Symptoms

Antepartum Haemorrhage (APH)

Def.: vaginal bleeding after 20 weeks GA

Causes:

1. Minor placental abruption or marginal sinus separation

2. Abruptio placenta
3. Placenta previa
4. Vasa previa
5. Local cause: cervical polyp, malignancy, erosion, cervicitis
6. Bloody show

Placental Previa

Insertion of placental tissue in lower segment of uterus after 32 week GA

*before that (< 32 weeks) it’s low lying placenta.

Dx: by TVU

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Types:

1. Minor: not covering the cervical opening

(PP latralis = more than 2 cm from cervical OS,
PP marginalis = less than 2 cm from cervical opening)
2. Major: covering the cervical opening (Asymmetrical/Symmetrical)

Risk factors

1. Previous history
2. Multiple pregnancy
3. Previous scar (C-Section, Uterine rupture, Myomectomy)
4. Uterine anomalies (also causes abruption)
5. Hypoxia - Smoking / COPD / High altitude

Presentation

*Vaginal Examination is contraindicated

1. Painless, causeless bleeding after 24 weeks (first spotting, not massive bleeding
then after a while becomes massive)
* (abruption is massive bleeding then spotting)
* Painful PP follows trauma
2. Malposition and malpresentation
3. IUGR/IUFD
4. Fetal anomaly
5. Oligohydraminous
(Uterus is soft and no contractions)

Management

• Admission from 34 weeks and onwards

• C-Section at 37⁺ weeks
• The decision of delivery depends on:
• absence or presence of fetal distress and GA
o < 37 + distress → C/S
o > 37 ± distress→ C/S
o < 37 – distress → wait till 37
• Anti – D

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 • No vaginal deliveries → C/S:
Major degree & marginalis, lie posteriorly
• Can deliver vaginally:
Minor latralis PP; that should lie anterior

➢ Consent pt with PP because:

- Normal C/S, cross match 2-4 units, while
- In C/S with PP cross match ≥ 6 units
- Consent woman for hysterectomy and tubal ligation

Abruptio Placentae

- Early separation of placenta after 24 weeks & before onset of labour

Risk Factors:

- Uteroplacental insufficiency
- PIH/Pre-eclampsia
- Uterine over distention (polyhydramnios/multiple pregnancy)
- Trauma
- ECV
- Smoking and cocaine use
- Uterine anomalies
- Previous history
- Antiphosphlipid syndrome

Presentation:

- Severe pain (labour like)

- Vaginal bleeding (minimum/massive), concealed or revealed or mixed.

Diagnosis:

is clinical => History & examination

O/E:

- Hemodynamic unstable features

- Hard tender uterine wood-like ± Uterine contraction
- Fetal tachy\ bradycardia → distress.
* N.B.: fetal distress is unusual presentation of palcenta previa

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 at theatre:

- Do PV => vaginal bleeding seen (important)

Categories:

0 Separation with retroplacental clots.

1 Separation, minimal bleeding & no maternal or fetal distress.
2 Fetal distressed but mother not distressed
3 Both of them distressed ± DIC
(1-3) → bleeding

Management:

0-1 (minor) → expectant & follow up of fetal & maternal.

2-3 → For delivery (termination of pregnancy)

The delivery depend on:

- Presence / absence of fetal distress.

- Presence / absence of maternal hemodynamic instability.
- Bishop’s score.
- Malposition, malpresentation

Examples:

Distressed fetus, Maternal not stable, Bishop unfavourable => C/S

Bishop unfavourable, Maternal stable, fetus not stable => C/S

Bishop favourable, maternal, fetus stable => vaginal delivery

Complications:

• Bleeding, DIC, shock.

• Fetal distress & demise.
• PPH, How?
- Couvelaire uterus (Blood in myometrium) => lead to atony
- DIC, Thrombosis
- Intrapartum abruptio
- Risk factors of abruptio placentae can also cause PPH

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Vasa Previa: (fetal source)

Normally, the umbilical cord should be at the centre of the placenta, covered by the
thick chorionic membrane.

a condition in which babies' blood vessels cross or run near the internal opening of the
uterus. These vessels are at risk of rupture when the supporting membranes rupture, as
they are unsupported by the umbilical cord or placental tissue.

It has a triad of fetal distress, associated with minimum bleeding after the onset of the
rupture of membranes.

Risk factors:

• Placenta Previa
• Accessory placental lobes (succenturiate or bilobate placenta)
• Velamentous insertion of cord
• Multiple pregnancy
• Assisted reproductive technique - IVF

Screening for at-risk mothers is by colour flow Doppler

Diagnosis:

➢ Clinical
➢ Diagnostic test (Apt test = Alkali denaturation test) => detects the presence of fetal
hemoglobin in vaginal blood; as fetal hemoglobin (HbF) is resistant to denaturation
in presence of 1% NaOH (+ve).

Management:

Emeregncy CS within 15-30 minutes,

If not done, the fetus usually died and can be delivered vaginally.

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* Uterine artery Doppler (Screening test) → notch is found, predicts the following:

o Pre-eclampsia

o IUGR

o Placental abruptio

Hypertensive Disorders in Pregnancy

PIH Pre-eclampsia Chronic HTN

*** Regarding BP, normal physiological changes during pregnancy:

* in early pregnancy: expansion of plasma volume → increase in HR up to 15
from the baseline and increase in stroke volume → increase in COP, these
changes are supposed to increase BP but because of progesterone effect
(=>vasodilatation and ↓ PR) → BP in first half of pregnancy tend to be reduced
and reach the maximum reduction at 24th week of gestation
* after 24 weeks the progesterone level will decline → so the peripheral
resistance will increase → and BP will increase to pre-pregnancy level.

PIH = Pregnancy-induced HTN

Def: It is elevation of blood pressure more than 140/ 90 in 2 readings, at least 4 hrs
apart and after 20 weeks gestation, and not associated with proteinuria in previously
normotensive patient.

* Also called gestational non-proteinuric hypertension.

* It is the most common HTN in pregnancy 10%

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Management:

1. Exclude secondary causes of HTN

2. Exclude pre-eclampsia → by doing urine analysis, to look at the amount of
protein in urine using protein/creatinine ratio
Normally it is 10 mmol creatinine : 1 mg protein
If the ratio is increased => it means that there is proteinuria
3. Then follow the approach
➢ Give a period of expectant management; usually up to 4-6 weeks, i.e.
restricted salt intake and exercise.
➢ if failed, go to medical treatment (as the treatment of Pre-eclampsia).

Pre-eclampsia:

Def: It is elevation of blood pressure more than 140/90 in 2 readings, at least 4 hrs apart
and after 20 weeks, and proteinuria of more than 300 mg/dl on 24-hr urine collection
or dipstick with one cross (+) ± present facial and hand oedema.

Diagnosis:

- Def.

- Can be by made out if one reading was 160/110

- Or already Hypertensive pt with systolic BP increase by 30 mmHg and diastolic BP

increase by 15 mmHg => it’s called superimposed pre-eclampsia

Risk Factors:

• Previous history (most important) Antiphospholipid syndrome is a

• The extremes of age, usually age < 20 years risk factor for:
• Obesity, BMI > 30 • Pre-eclampsia
• Primagravida • Placental abruptio
• Gestational DM • Recurrent miscarriage
• Preterm labour
• Family Hx, 1st degree relative
• DVT
• Molar pregnancy and multiple pregnancy
• Pulmonary embolism
• Increased interval between pregnancies. • IUGR

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• Antiphospholipid syndrome
• chronic kidney disease, DM, connective tissue disease, thrombophilia

** N.B. smoking is protective factor

Clinical Features:

Remember that: it’s a disease of sign not a disease of symptoms; once pre-eclampsia
become symptomatic this indicates severity

Signs:

• Elevation of BP,..

Symptoms:

• Headache
• Blurring of vision, blindness, or enlarged blind spot
• Epigastric or right hypochondrial pain
• Nausea and vomiting

Sever pre-eclampsia if:

➢ Symptomatic pre-eclampsia
➢ Proteinurea > 5 mg/dl
➢ BP > 160/110
➢ Signs of cerebral irritation: Papilledema, hyperreflexia and clonus
➢ Development of Eclampsia, HELLP and other complications..

Complications:

- Eclampsia - Subcapsular liver hematoma, risk

- HELLP of rupture
- CVA, Cerebral oedema - DIC
- Cerebral haemorrhage - Abruptio placentae
- ARDS, or suffocation - Fetal distress
- Laryngeal oedema - IUGR, IUFD
- Acute kidney injury

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Investigations:

Investigate by tests which are known as Pre-eclamptic toxaemia plot:

• Blood:
- CBC:
↑ RBCs => ↑ Hct due to hemoconcentration or ↓ due to HELLP
WBC count doesn’t change but as differential will change
- PLT count is normally up to 100 in pregnancy due to 2 causes: dilutional
thrombocytopenia or gestational thrombocytopenia (due to ↓
production of platelets)
if < 100 → HELLP
- Coagulation profile is indicated if PLT count < 100
- Blood grouping
• Biochemical:
- LFT & enzymes
- RFT : U&E
- Uric acid test → It is prognostic test
• Imaging:
TAU for:
- Fetus viable or not
- Liquor volume, because baby is IUGR → oligohydramnios

Management:

Usually pre-eclampsia is divided to mild, moderate and severe depending on signs,

symptoms and BP.

▪ Mild: BP 140/90-150/90 and no symptoms

=> need regular follow up every 2 weeks + aspirin.
▪ Moderate: systolic BP > 150 but < 160 , and diastolic BP > 90 and < 100-110
▪ Severe: > 160/110 with symptoms

=> In moderate and severe:

o Admission
o Do previous investigation
o Give antihypertensive drugs - for moderate:
➢ ᾳ-methyldopa (safest medication but needs time to reduce BP 48 hrs
and the pt may develop HSR)

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 ➢ Nifedipine, start with 10 mg bd then increase up to 20 mg 6-hourly
(SE: peripheral oedema & headache → it will mask the symptoms of
severe pre-eclampsia, and you can’t determine whether the pt is
improving or not)
➢ Labetalol, start with small dose 250 mg tds, and titrate until
maximum 1 g 6-hourly (4 g/day)
➢ Atenolol lead to IUGR, so it’s no longer used and replaced by labetalol
o Severe:
➢ no rule for methyldopa
➢ Nifedipine: given orally
*avoid sublingual Nifedipine for that it results in rapid reduction of BP
leading to stroke *MSQ*
➢ Add labetalol (1st line in severe pre-eclampsia management) *MCQ*
➢ Hydralazine, start by loading dose to reduce the BP, then repeat every
5-15 minutes, then maintenance dose of hydralazine in normal saline.

*N.B.: Mg-sulphate is given in D5%

Other aspects of management:

o Fluid restriction: to prevent pulmonary oedema, restrict up to 1 ml/kg/hr

o Monitor: accordingly;
- UOP, but the patient is oliguric and susceptible to pulmonary oedema; so go
for
- Central venous pressure, if no pulmonary symptoms
- Pulmonary capillary wedge pressure, if the patient has pulmonary symptoms
o Indications for termination:
1. MAP > 125
2. Refractory pre-eclampsia, (resistance to 3 drugs on maximum dose)
3. Eclampsia
4. Fetal compromise detected by: CTG (pathological), UA Doppler (reversed end
diastolic flow)
*N.B.: reduced or absent EDF in UA Doppler is indication for admission for daily
CTG, → if shown pathological CTG → this indicates termination,
→ if not; → repeat UA Doppler after 1 week,
→ if still reduced or absent → give dexamethasone if preterm and deliver within
maximum of 10 days.
5. HELLP
6. Uric acid > 7 mg

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 7. Term
8. Placental abruption

*RULE: → C/S if 2 risk factors present

e.g.: Pre-eclampsia + Placenta Previa

Eclampsia:
- mainly postpartum

- can develop in a normotensive

Def.: Occurrence of generalized tonic clonic convulsions in pre-eclamptic patient

* N.B.: Unlikely to be eclampsia if there was:

- Sphincteric disturbance
- Multiple attacks in 24 hrs
- Fits while on Mg sulphate

Main cause of death:

At hospital: CVA or cerebral haemorrhage

At home: Airway obstruction or suffocation, usually associated with pulmonary oedema

Management Approach:

1. Call for help

2. Left lateral position
3. ABCD
➢ Airway management: mouth gauge
➢ Breathing: high flow O₂
➢ Circulation: fluid-restriction
➢ Drugs:
I. To abort and prevent the seizure:
Mg-sulphate, usually given as loading dose 4 g over 10-20 minutes, → then
maintenance dose (infusion) 1 gm/hr for 24 hrs from the last fit.

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 If the pt is already on medication and has developed another fits, give ½ of
the loading dose i.e. 2 gm over 10-20 minutes, and continue the
maintenance dose.
* N.B.: Mg-sulphate is given in D5%
SE: areflexia => reflexes should be monitored
* note: monitor as follows: the biceps reflex if the patient is under epidural
anaesthesia, if not; use the knee reflex
Toxicity:
- Depress respiration => hypoventilation
- Cardiac depression
- Renal: oliguria → anuria
II. To control BP:
1. Labetalol: can be given alone, it’s a non-selective ß blocker; and block
α₁ receptors as well => reduce effect of renin and abort reflex
tachycardia
2. Hydralazine: not usually given alone, it’s a vasodilator => ↓ renal
perfusion → activates renin-aldosterone → fluid retention and
oedema. So it needs to be combined with a diuretic to reduce
oedema and a selective ß₁ blocker (bisoprolol or atenolol)

=> So labetalol is preferred as 1st line here, because diuretics are

contraindicated in pregnancy, they are indicated in combination with
hydralazine only in case of laryngeal oedema or severe heart failure.

Target:
- BP 150/90
- and of more importance is to maintain diastolic between 90-100
- Or MAP 90-100

Continue medications till the pt is stabilized.

4. Mechanism of last resort (antepartum eclampsia) => Termination of pregnancy:

➢ Mode of TOP? dependent on 2 factors:
- Presence or absence of fetal distress
- Bishop score
➢ Induction and normal vaginal delivery: no fetal distress, Bishop score is
favourable
➢ Elective C/S: fetal distress + eclampsia

25
 Chronic HTN:
Medications: in general depends on the age, then ethnicity:

> 55, African-Caribbean → thiazide or CCB

< 55, DM → ACEI/ARBs

* pt already on CCB can continue drug during pregnancy

* drugs that are contraindicated:

- Thiazide diuretics, interfere with normal physiological response of pregnancy
- ACEI/ARBs cause fetal renal agenesis

* hypertensive drugs like Ergometrine & Syntometrine (oxytocin + Ergometrine) are CI in

management of 3rd stage of labour in preeclamptic pt, but Syntocinon can be given.

Obstetric Emergencies

PPH Uterine Inversion

Shoulder Dystocia Amniotic Fluid Embolism

Cord Prolapse Uterine Rupture

PPH
- Postpartum Haemorrhage: any vaginal bleeding in the 1st 6 weeks that lead to
hemodynamic instability, can be primary (in 1st 24 hrs) or 2ndry (up to 6 weeks).

Stages of blood loss:

Stage 1 = 10-15 % Stage 2 = 15-30%

Stage 3 = 30-40 % Stage 4 > 40 %

Stage 3 & 4 = blood loss 1.5 – 2 liters

26
Causes of primary PPH:

1. Atonia (in 90%)

2. Trauma
3. Tissue
4. Thrombin

1- Atonia:

a. Uterine over-distension (polyhydramnios, multiple pregnancy)

b. Placental abruptio
c. Endometrial/myometrial mass
d. Drugs: oxytocin
e. Induction of labour
f. Epidural analgesia
g. Uterine infection
h. Retained product

2- Trauma:

a. forceps
b. episiotomy
c. vaginal delivery (shoulder dystocia, macrosomic baby, breech delivery)

3- Tissue:

- retained products

4- Thrombin:

- DIC secondary to abruptio placentae, severe preeclampsia, septic/missed

miscarriage.

Causes of secondary PPH:

1. Infection due to retained products

2. Persistent trophoblastic disease

27
Management Approach:

1- call for help!

2- manage the pt as 3 zones:

Zone 1 = head => Anaesthetist:

o maintain airway N.B.: high flow O₂ is not

o high flow O₂ always indicated in all
o monitor consciousness level emergencies
o suction; of any secretions
o auscultate chest for symmetrical breathing

Zone 2 = arms => Nurse + Physician:

o 2 wide bore cannula

o monitor (pulse, BP, capillary refill)
o inflow arm: loading dose of 2 L crystalloid + 1,5 L colloid
o outflow arm: take samples (blood group + cross matching &=>
preparation of 8 units, CBC, ABG, coagulation profile)

Zone 3 = vagina => Obstetrician

o palpate uterus for presence of contraction, if it’s not contracted this is

atonia, go for:
1. uterine massage
2. bimanual compression
o if not controlled go for drug management:
1. Oxytocin
loading dose 10 IU, then maintenance dose 40 IU over 4 hrs
2. Ergometrine: 0.25-0.50 mg given IM ONCE
3. Misoprostol: up to 4-5 tabs = 800-1000 mg rectally ONCE
4. Carboprost: IM or intramyometrium (need a consultant) given up to 8
doses (1 dose = 250 mcg) but if the pt is not responding after the 2nd
dose, do not give more!

* In the meantime, at Zone 2, start giving blood and fresh frozen plasma as follows: after
the 1st 2 units of blood, give 1 unit of fresh frozen plasma for each unit of blood given
furtherly- that’s a general rule.

28
 o if not improved go for surgical management, but inspect at first for any
tears to repair & any retained products to be removed.
at laparotomy (step by step):
1. B-lynch suture or vertical compression suture if the pt has
initially respond to Bimanual compression
2. Ligation; of the following arteries as needed respectively:
i. uterine artery
ii. tubal branch of ovarian artery
iii. internal iliac artery
3. Compress the aorta
4. Hysterectomy
a. total: uterus + cervix’, done if Placenta Previa or
morbidly adherent placenta
b. subtotal, for other cases
this one prevents vault prolapse due to preserved
cervical support

Once elected for laparotomy, Sengstaken–Blakemore tube can be used initially to compress the uterus
till laparotomy
(transient method)
Therapeutic => stop the bleeding
Diagnostic => if really stopped, it’s due to atonia

Shoulder Dystocia
Def.: impaction of the anterior shoulder against symphysis pubis of the mother after
delivery of the head by more than 60 sec

Risk factors:

- previous history - DM
- macrosomic baby - prolonged 2nd stage of labour
- short & obese mother - instrumental delivery
- postdate pregnancy - oxytocin augmentation
- induction of labor

29
Why it’s an emergency??

Umbilical cord impaction under symphysis pubis leads to fetal distress and acidosis:

1 minutes compression → drop by 0.04 in fetal pH

5 minutes compression → acidosis → maximum time

the fetus can tolerate shoulder dystocia Fetal pH
7.35 normal
Management: < 7.25 acidosis

▪ HELPERR (see ‫ طلب‬.‫) شيت د‬

H call for Help

E Evaluate for episiotomy; to facilitate internal manoeuvre

L Legs (the McRoberts manoeuvre = hyperflexed, hyperabducted)

P Suprapubic Pressure (Rubin I)

E Enter manoeuvres (internal rotation): including (Rubin II, wood screw and
reversed wood screw)

R Remove/Release the posterior arm

R Roll on 4, and repeat all manoeuvres except Rubin I

If all failed, go for:

▪ Symphysiotomy
▪ Cleidotomy, done in upward direction to avoid
lung injury Indications of symphysiotomy:

▪ Zavanelli maneuver (cephalic replacement): ▪ shoulder dystocia

- give a tocolytics to stop uterine contractions, ▪ breech presentation
it’s beneficial for it decreases the force upward in obstructed labour

and reduce pressure over the umbilical cord, as

well as it aids in reversal of the stages of labour
- perform C/S
▪ Document and debrief

Remember:

▪ Shoulder dystocia is unpredictable & unpreventable

▪ 50% are not macrosomic

30
 Cord Prolapse
Def.: Prolapse of the umbilical cord below the presenting part with rupture of the
membrane (if without ROM, it’s simply cord presentation)

Risk factors:

o Polyhydramnios
o Multiple pregnancies
o Cord presentation
o Breech presentation
o Transverse lie

- pH ↓ in each minute by 0.04, leading to fetal acidemia within 5 minutes

Management:

▪ Call for help

▪ Position: Keep cord inside: Knee-to-chest/Trendelenburg/By hand (NS gauze)
▪ Avoid excessive touch and manipulation
▪ Inflate the urinary bladder (to move the presenting part upward)
▪ Infuse vagina by warm normal saline
▪ Cover the Os by the Ventouse cup
▪ Tocolytics; to stop the presenting part from compression
▪ Deliver the baby, depending on:
- Stage of Labor
- Bishop score
- Fetal viability
✓ Fetus dead → vaginal
✓ 1st stage → C/S
✓ 2nd stage → according to Bishop score:
→ Favorable: VD with forceps and ventouse
→ Unfavorable: Emergency C/S

31
 Uterine inversion:
Risk factors:

▪ Fundal insertion of placenta

▪ Short umbilical cord
▪ Fundal insertion of morbidly adherent placenta
▪ Poor management of 3rd stage of labour
▪ Previous history of uterine inversion

Clinical presentation:

Severe lower abdominal pain may lead to neurological shock associated with vaginal
bleeding

On examination:

▪ Dimple in the abdomen

▪ PV: features of palpable fundus in vagina

Management:

▪ Call for help

▪ Reduce the fundal part of the uterus upward manually by palm of the hand
▪ Never try to separate placenta!
▪ Give tocolytics; to stop contractions and aid reversion;
If failed;
▪ Hydrostatic pressure reduction
If failed;
▪ Surgical management : Laparotomy & reversion of the inverted part by your hand

Amniotic fluid embolism:

Def.: Embolism of fetal tissue / amniotic fluid in the maternal circulation

Risk factors:
Contraindications
▪ ARM (Artificial rupture of membranes) > ¾ the cases of ARM: IUFD,
▪ Molar pregnancy, if given oxytocin during early evacuation Cord presentation
▪ IUFD → ARM

32
Clinical presentation:

▪ Neurological: Focal signs up to encephalopathy

▪ Cardiovascular: Heart failure
▪ Respiratory: Signs and symptoms of Pulmonary embolism
▪ Haematological: DIC

Management: (Multi-disciplinary team approach)

▪ Support
▪ ICU admission (intubate and ventilate)
▪ Correct DIC (FFP, vitamin K, Fresh blood)
▪ NS and Inotropes

Diagnosis:

Mainly post-mortem; by demonstration of fetal part on maternal blood

Uterine rupture:
Def.: Separation of all layers, from endometrium up to serosa.

* N.B.: Separation of endometrium and Myometrium with intact serosa is called

“Uterine Dehiscence”

Clinical presentation:

❖ Uterine Dehiscence:
o Sudden onset of severe localizing pain (just like that of red degeneration
of fibroid), not associated with fetal distress or bleeding (or minimum
bleed)
❖ Uterine Rupture:
o Severe pain localized then becomes generalized
o Antepartum or Intrapartum
o Minimal vaginal bleed
o Maternal shock
o Fetal part palpable abdominally but not vaginally
i.e. Loss of station

33
Risk factors:

▪ Previous scar
▪ Uterine hyperstimulation
▪ Obstructed labor in multiparous
❖ In primiparous → leads to Fistula more than rupture (Fistula: between
cervix/vagina and surrounding tissue)

Management:

▪ Call for help

▪ Resuscitate
▪ Laparotomy:
o Hysterectomy, or
o Repair with tubal ligation (to prevent recurrence)

* you have to counsel the pt for both and consent.

Morbid adherent placenta

Def.: a placenta that’s adherently attached to a multiple layers of uterine wall.

Types:

1. Accreta: attached to the outer part of myometrium – not deep

2. Increta: to the uterine wall deep into the myometrium
3. Percreta: deep to the serosa and adjacent organs (intestines, urinary bladder)

The most common is accreta, followed by increta then percreta being the least
common.

Risk factors:

▪ Previous scar
▪ Placenta previa

Presentation:

▪ Any placenta should be delivered within 30 mins if actively managed 3rd stage of
labour or within 1 hour of physiologically managed 3rd stage of labour
▪ If it is still there despite genital traction → morbid adherent placenta

34
▪ Gold Standard for Dx: MRI (just like adenomyosis)

Management:

▪ Total hysterectomy
▪ Selective embolization of placental bed

Medical Disorders in Pregnancy

(Oxford is the best Ref. here)

Epilepsy
Epilepsy: tendency to have two or more unprovoked seizures.

Major types: Generalised tonic clonic then Absence,

* But remember in general any pregnant woman with generalised tonic clonic
convulsions is considered eclampsia until proved otherwise!

Effect of pregnancy on epilepsy:

A. If already epileptic:
- 50% have no change in seizure frequency,
- 30% improve, and
- 20% have increased seizure frequency.
(its better to check these percentages from oxford O&G latest edition)
B. If an epileptic pregnant woman develops status epilepticus, the fetus may
develop hypoxia leading eventually to IUFD.
C. Trauma secondary to status epilepticus may lead to Abruptio Placentae.
D. There is a higher risk of the fetus developing congenital anomalies, even if the
mother is not on antiepileptics!
E. the newborn baby has a higher tendency to develop epilepsy at an older age!

35
Management:

1. Before pregnancy – Preconception:

▪ review control of seizures.

▪ decrease number of drugs to a monotherapy at its lowest dose.
(replace the drugs that are likely to cause congenital malformation)
▪ give her folic acid 5 mg (also indicated in Diabetes, previous NTD, Obesity,
Nutritional deficiency and maternal haemolytic anaemias)
▪ consider Contraception if the seizures are not well controlled!
It’s better to use an IUCD cause most of antiepileptics are enzyme inducers
(decrease the efficacy of contraceptives and increase the chances of unwanted
pregnancy) - Carbamazepine, Phenytoin and Phenobarbital - If you must use
them then just increase the dose of COCs, Others are enzyme inhibitors -Na
Valproate, in this case you give lower doses of COCs.

2. During pregnancy:

▪ If already on specific medication, don’t change it or the dose to avoid the risk of
developing status epilepticus which is more worse than the side effects of the
drugs.
▪ Stop aggravating factors: alcohol, sleep deprivation,…
▪ Continue folic acid 5 mg up to 12 week or (usually) throughout pregnancy
▪ More follow up in Antenatcal care:
- Dating scan (8-13 weeks): by measuring crown-rump length,
if > 13 wk then we measure femur length and the biparietal diameter.
- Anomaly scan (18-22 weeks): for better detection of cardiac anomalies at
this period.
- Serial growth scan in the 3rd trimester.
- α-fetoprotein and acetylcholine esterase (more specific) both for
screening for neural tube defects.
▪ Vitamin K injection (if she’s on phenytoin) at last month of pregnancy to avoid:
1. Haemorrhagic disease of the newborn 2. PPH

3. Delivery:

• C/S only indicated for usual obstetric indications.

• The lady is delivered by normal vaginal delivery, with precautions.

36
 but Labour is a stressful condition and may precipitate status epilepticus so in
order to avoid that we have to:
1. Shorten the second stage of labour by instrumental delivery.
2. Antiepileptic during delivery.
* Benzodiazepines can cause maternal and fetal respiratory depression leading
to hypoxia and academia, so single dose of phenytoin is better! (one dose of it
won’t increase risk of haemorrhagic disease of the newborn)

Antiepileptic Drugs:

Drugs with high risk of congenital anomalies: Na valproate and Topiramate

Drugs with lower risk of congenital anomalies: Lamotrigine and Carbamazepine

*Lamotrigine has recently discovered to be safer than Carbamazepine

*the problem is that you need to increase the dose in pregnancy, and higher doses may
also increase the risk of toxicity leading to erythema multiform or a more severe form
known as Steven Johnson syndrome! But in general it’s the safest drug in pregnancy!

Congenital malformations among epileptic mothers’ newborns :

▪ NTDs
▪ Cleft lip and palate
▪ Cardiac anomalies (mostly phenytoin)

Cardiac diseases and pregnancy

Women with cardiac diseases have variable mortality rates if they get pregnant, they
can be categorized as low, moderate and high risk.

▪ The mortality rates according to different groups are as follows:

- low risk group: 8-15%
- Moderate risk group: 25%
- High risk group: 50 % (advised not to get pregnant)

37
High risk group:

- Pulmonary hypertension and Eisenmenger

- Aortic root dilatation > 4 .5 (Marfans)
- Coarctation of the Aorta
- Peripartum cardiomyopathy

Moderate risk group:

- Severe Mitral stenosis (calcified valve)

- Uncorrected TOF
- Aortic stenosis of any type

Low risk group:

- ASD/VSD not associated with Eisenmenger

- Corrected TOF
- Non calcified mitral stenosis

*Severe Mitral Stenosis:

1. valve orifice < 1 cm 2. Symptoms of PHTN 3. Thromboembolic phenomena

*HOCM: moderate to high risk

*HCM: low to moderate risk

*Pulmonary hypertension:
Most of the drugs used to treat it are contraindicated in pregnancy, so it’s better to
terminate the pregnancy (option is up to the mother after counselling)

*Peripartum cardiomyopathy:
It’s in the period between the last months of pregnancy and 5-6 months postpartum.
It has a high risk of recurrence and mortality.

*Rheumatic Heart disease:

Regurgitant valve conditions tend to improve during pregnancy, while stenotic valves
tend to get worse.

38
 Rheumatic Heart Disease (MS)
1. Before pregnancy:

▪ A cardiologist has to prove the diagnosis and assess the severity of the condition
– assess the risk, by assessing the presence of:
1. Heart failure 2. Pulmonary hypertension
=> If they are present, then this is a high risk pregnancy.
▪ If the woman is using warfarin, it should be stopped and replaced by injected
LMWH, because warfarin is teratogenic and increases the risk of fetal bleeding.
▪ Stop diuretics are contraindicated.
▪ Best management for elected pregnancy is: catheter Ballon Valvuloplasty.
This modality is contraindicated if there was: calcification, regurgitation or Lt
atrial thrombus.
▪ Then valvuotomy ( closed/open) and mitral valve replacement.
Tell her that her baby is at risk of developing congenital cardiac malformation,
especially if the mother has congenital heart disease.
▪ In case of severe MS, offer contraception:
o IUCD: risky, can introduce infection.
o COCS: increase risk of thromboembolism.
o POPs, implanon or injectable progesterone are the best.

2. During pregnancy:

▪ Dating scan
▪ Anomaly scan
▪ Fetal Echocardiography
▪ Maternal Echo and follow up for Heart failure and Pulmonary hypertension
▪ Management options:
- Continue warfarin throughout pregnancy.
- Stop warfarin and replace it with LMWH throughout pregnancy (best option)
- Stop warfarin at 6 weeks and replace it with LMWH up to 13-14 weeks and
then continue with warfarin.

* monitor LMWH with activated factor X, the dose is in the form of S.C. injection
single or twice daily.

* prolonged use of heparin causes: osteoporosis, heparin-induced

thrombocytopenia, bleeding.

39
 ▪ if symptoms deteriorate:
Valvotomy is contraindicated but valvuloplasty can be done at any time during
pregnancy.
▪ As she approaching 36 -37 week, after choosing the appropriate way of labour,
therapeutic dose of heparin is stopped 24 hours before the onset of labour while
prophylactic stopped before 12 hours only.

3. During delivery:

▪ Epidural analgesia can be used but with caution because Ejection Fraction is
limited.
▪ 1st stage:
o Be followed by partogram
o Follow the fetus by CTG
o Keep lady in left lateral position
o ive prophylactic doses of antibiotic to protect against Infective
Endocarditis.
▪ 2nd stage:
o shorten by forceps or ventose.
o Oxytocin and misoprostol should be avoided because they can cause fluid
retention and hyponatremia aggravating the condition. (oxytocin has
ADH-like effect, PGE is a vasodilator)
o Extra effort should be made to decrease blood loss.
*Hb of 10.5 is compatible with vaginal delivery and should be corrected.
▪ rd
3 stage of labour:
o Active management but avoid using Ergometrine and Syntometrine
(oxytocin can be used).

4. Postpartum:

▪ The most critical time for developing pulmonary edema and pulomary
hypertension is 24 hours after delivery. Accordingly, the lady s hould be admitted
for 2-3 days.
= After delivery, the blood that was going to placenta (500 ml/min) will now all
enter the circulation and overload the heart.
▪ Admit in cardiac bed with oxygen supply and mannitol, if she develops
pulmonary edema then transfer into the ICU (revise the management of
pulmonary edema)
▪ Start warfarin.
▪ Refer to a cardiologist.

40
 Anemia in Pregnancy
Defined as haemoglobin less than 10.5 g/dl

Causes: physiological causes, iron deficiency (IDA) is the most common cause, followed
by folic acid deficiency.

IDA causes: increased fetal demands.

Anemia problems in pregnancy:

Maternal complications during pregnancy:

1. Anemic heart failure.

2. DVT: *hypoxia leads to increased levels of RBCS and Platelets *pressure on inferior
vena cava *Fatigue and decreased physical activity
3. infection and sepsis
4. APH (placental hypoxia) and PPH
5. exaggeration of edema and fatigue

Postpartum:

1. Puerperal pyrexia
2. Puerperal sepsis
3. puerperal psychosis
4. DVT and pulmonary embolism

Fetus problems:

1. Preterm
2. Low iron stores and Anemia
3. IUGR

Management:

Iron supplements are not routinely recommended.

41
Diagnosis:

- Clues: low Hb , high PLT, low MCH, MCV and MCHC.

- Iron studies:

▪ Serum iron (low or N)

▪ Serum ferritin (gold standard in preg.)
▪ TIBC (normaly high in preg.)
▪ Transferrin

Management:

▪ depend on the pt. condition:

If Hb ≤ 6 or anemic HF → indication for BT
▪ Otherwise start iron replacement:
- Oral: ferrus sulfate, ferrus fumerate , ferrus gluconate (SE of all: nausea,
vomiting and constipation).
- IM: F. sorbitol (painful, twice per week).
- IV: iron dextran (can cause a rate of HSR up to anaphylactic shock, so It has
been withdrawn), I/V iron sucrose is better for it has less tendency to cause
allergic reaction
▪ If BT is done, combine to it with oral iron Not IV .
▪ follow up: the ↑ in iron should be 0.8 -1 g /dl per week

General indication of BT:

▪ Anemic HF ▪ if approaching term & Hb < 10.5

▪ Hb ≤ 6 ▪ DVT
▪ if high risk of C/S or instrumental ▪ PE
delivery
During labour :

▪ Hydrate pt by N saline and prepare blood.

▪ Shorten the 2nd stage by instrumental delivery.
▪ Continuous fetal monitoring by CTG.
▪ Prophylactic antibiotics.
▪ Active management of the 3rd stage of labour.
▪ Only if needed as indicated by investigations, give LMWH.

42
 Antiphospholipid Syndrome
Acquired thromboembolic disorder that maybe present as:

▪ 1ry (most common type), or

▪ 2ry; associated with 2ry autoimmune disease e.g.( SLE) malignant disorder (CLL)
or by medications (phenothiazine).

Diagnosis Criteria:

Clinical:

1. Recurrent (≥3) 1st trimesteric miscarriages < 10 weeks.

2. 1 or more pregnancy loss > 10 weeks .
3. 1 or more preterm delivery prior to 34th week due to conditions precipitated by
APS like preeclampsia.
4. Venous or arterial thrombosis.

Lab:

1. Anticardiolipin Ab. Level (moderate to high titre twice at least 6 weeks apart)
2. Lupus anticoagulant (2 readings of moderate to high level in at least 2 weeks
apart)
3. Anti ß₂ glycoprotein Ab. (indicate 2ry APS)

Manifestations:

1st / 2nd tri miscarriages, preterm labour, preeclampsia, IUGR, IUFD, abruptio placenta,
PPH, anemia, DVT and PE.

Other: can be associated with non-infective endocarditis, PHTN and systemic HTN,
chorea in pregnancy.

*(causes of chorea in pregnancy: antiphospholipid, Rh fever, chorea gravidarum,

thyrotoxicosis)

Management:

Aspirin and LMWt heparin.

Aspirin to be started when ßhCG +ve till detection of fetal heart activity then start
LMWH and continue till 34 week and stop it (won’t cause preterm after that).

43
 DVT
Common due to the physiological changes of pregnancy:

1.high coagulation factors (1,8,9,10)

2.Lower anticoagulants (mainly anti thrombin III being lost in urine)
3.Progesterone vasodilator and cause stasis
4.Compression of uterus and IVC
5.Bed ridden
6.Other causes:
▪ Acquired: (immobility, surgery, dehydration, trauma)
▪ Hereditary: (anti thrombin III deficiency, protein C & S deficiency, factor V
leiden deficiency, prothrombin gene mutation, S.C. anaemia).
❖ Generally DVT affects vessels in the calf, but in pregnancy it tends to affect
proximally the thigh and pelvis, resulting in high risk of PE.
❖ > 80 % are Lt sided due to compression of the Lt iliac vein by external iliac artery.

Clinical presentation:

Pain, swelling, tender limb,

Presentation of PE: sudden onset dyspnoea, chest pain, haemoptysis, syncope

Investigations:

▪ Duplex scan or Doppler compression sonography of the affected leg.

▪ General: CBC, PBP, coagulation profile, LFT, U&E, urine analysis, serum Ca.
 D dimer is usually high in pregnancy.

Management: of DVT during pregnancy:

1- Admission 3- Hydration
2- Immobilization 4- Analgesia
5- Anticoagulation:
i. Unfractionated Heparin if LMWH not available or DVT has precipitated
massive PE.
ii. LMWH
▪ Types of LMWH: Enoxaparin - Tinzaparin , given b.d as s/c injections
▪ Monitoring: measure Factor X level before LMWH dose, and then re-measure
3 hrs after the dose.
▪ Screen for RFT (C.I. in ESRD)

44
• Continue till 6 months in complete therapeutic dose, if 6 months has passed and
she’s still pregnant yet, reduce to prophylactic dose up to 6 week postpartum.
• DVT in pregnancy is a provoked condition, no need for long term management or
prophylactic heparin in the next pregnancy.
• For a woman who had 2 or more DVT in one pregnancy, should be elected for s/c
prophylactic LMWH injection during next pregnancy.

PE
 CTPA: high radiation dose => ↑ risk of breast cancer .
 V/Q scan: high risk of childhood malignancy especially ALL, AML.
 and they are Not done if the pt. not stable or had an abnormal CXR.
 So if you confirm DVT you don’t need to confirm PE because management is
similar.
 Thrombolytic is C.I.

Malaria During Pregnancy

❖ Tend to be severe, why?
Due to placental sequestration of the plasmodium if replicate there => excessive
load.

Problems with pregnancy:

▪ 1st and 2nd trimesteric miscarriage

▪ preterm labour
▪ Still birth IUGR ,IUFD
▪ high risk of anemia (hemolysis), PPH
▪ Congenital malaria: in form of neonatal sepsis (p. falciparum)
▪ Low birth Wt, chronic anemia: (p. ovale)

Diagnosis:

PFFM can be false so repeat 3 times.

Clinical malaria: positive symptoms and signs, negative PFFM. => start treatment

45
Management:

depends on trimester:

1st tri: Quinine oral / IV infusion.

2nd and 3rd: 1st line Quartum (Artemether and lumefantrine )

2nd line Quinine

Stable malaria transmission zone area “Endemic Malaria” => are given prophylactic
anti-malarial agent “Fancidar” 2 doses; 1st at quickening and 2nd one month later.

HIV
HIV doesn’t make the pregnancy of high risk.

HIV infection leads to AIDS as a result of deficiency of CD4 lymphocytes and

macrophages → due to HIV-induced apoptosis → high risk of infection and malignancy.

TH1 deficiency → ↑ TH2 humoral immune response → lead to

hypergammaglobulinemia.

Main methods of transmission: Blood transfusion (highest), sexual T, vertical MTCT,

contact with fluid in injured pt., needle stick

Disease progression:

i. IP: 3-6 weeks with max 3 months.

ii. Seroconvertion illness (= primary HIV infection; Glandular-fever-like illness):
fever, headache, pharyngo-tonsillitis, skin rash, abdominal pain, vomiting,
hepatosplenomegaly, hepatitis, meningitic picture, epistaxis.
usually resolve spontaneously, then pt. enter into,
iii. latent period: CD4 count plateau but decrease with time.
iv. AIDS: CD4 count < 200 and any detectable viral RNA.

AIDS defining conditions:

▪ Bacterial infections: mycobacteriam TB , mycobacterium avium complex,

salmonella typhi
▪ Parasitic infections: Pneumocystic Carinii , toxoplasmosis, disseminated visceral
lieshmaniasis.

46
 ▪ Viral infection: CMV (encephalitic/retinitis)
▪ Mycological: invasive candidiasis, aspergillosis., Cryptococcal meningitis
▪ Malignancy: Kaposi sarcoma, primary CNS lymphoma, cervical carcinoma, non-
Hodgkin lymphoma .

In pregnancy:

no changes in usual progression of HIV, despite cellular immune response decrease in

2nd half of pregnancy but humeral increase. (=> this results in flare up of autoimmune
diseases, except SLE)

Diagnosis:

Screen by ELISA, confirm by western blot.

If both negative: maybe window period seroconversion, so do (HIV-RNA-PCR).

Then quantify CD4 level after confirming positive diagnosis.

When to start Treatment?

1. CD4 < 350

2. Pregnant lady regardless of viral load or CD4
3. AIDS defining condition (e.g. mycobacterium avium complex infection)
4. HIV nephropathy
5. HBV, HCV co-infection

How HIV affects pregnancy?

▪ Mother: Preterm labour, PROM

▪ Fetus: IUGR, but usually cause No congenital malformations

N.B.: HIV screening is recommended in the 1st trimester, offered at booking.

Management:

▪ If she requests treatment for her health, start at any time

▪ If she requests treatment for her baby’s health: 22-32 weeks, optimum time 28
weeks (to avoid side effects of medications).

47
Types of medications:

• NRTI • Protease • Integrase

• Non-NRTI inhibitor inhibitor
• Fusion inhibitor
Triple therapy = 2 NRTI + 1 other

▪ If the woman can’t tolerate triple therapy and doesn’t need it, give zidovudine
monotherapy (NRTI).

Indications of HAART (If the patient didn’t voluntarily request it):

1. Viral load > 10,000/ml or > 50 copies

2. CD4 < 350
3. HBV/HCV +ve

If she doesn’t have any of these (1,2,3), offer zidovudine monotherapy only, otherwise
offer HAART.

Follow up pregnancy normally. (N.B.: HIV is not a high-risk pregnancy)

Base line CD4 (repeat every 4-6 weeks) and viral load (at 36 weeks gestation), also do
CD4 count at 36 weeks to choose method of delivery, either:

▪ C/S if: Viral load > 10000, CD4 < 350, HBV/HCV +ve, or HCV RNA detectable
despite treatment.
▪ Vaginally if: CD4 > 350, Viral load < 50 copies, HCV RNA undetectable.

Always with precautions:

▪ Do not induce ARM (wait for spontaneous)

▪ Do not shorten the 2nd stage by forceps or ventouse
▪ Do not do fetal scalp sampling or invasive fetal monitoring

What to do:

▪ Stop any other antiretroviral therapy and start infusion of zidovudine during
labour for all HIV patients regardless of CD4 count or viral load; stop it once you
clamp the umbilical cord.
▪ Advice the mother to avoid breastfeeding and use formula (But here in Sudan,
it’s not an absolute C/I, because here the risk of malnutrition outweighs the risk
of HIV)

48
 ▪ If the baby’s viral load at 36 weeks is > 10000 or copies > 50, start HAART for 6
weeks; or if the mother’s viral load at 36 weeks is < 50, start zidovudine
monotherapy.

The following can decrease the MTCT from 25% to 2%:

✓ C/S delivery at 38 weeks

✓ Giving the mother HAART
✓ Avoiding breast feeding
✓ Giving the child therapy (HAART or Zidovudine)

Diabetes and Pregnancy

GDM = DM + Polyuria, polydipsia and polyhydramnios

Risk Factors of Gestational DM:

• Previous Hx of GDM,
• Previous Hx of delivery of a macrosomic baby
• Previous unexplained fetal death
• Polyhydramnios
• Recurrent glycosuria
• BMI > 30
• Multiple pregnancy
• First degree relative with DM

Management:

• Diet control, if failed

• Oral hypoglycaemic agents are safe but insulin is preferred:
 Intermediate-acting insulin twice daily injection
• Follow up:
 Measure blood glucose 4 times/day
 More antenatal visits
 More frequent USS for amniotic evaluation and serial growth scan to
detect macrosomia especially in 3rd trimester.

Type I DM: usually tend to be primagravida, managed with insulin injections

Type II DM: tend to be multiparous

49
Before pregnancy:

• Assess degree of glycaemic control => Measure FBG , 1-2h postprandial and
HbA1c:
 FBG = 3.5-5.6 , 2h PP < 7 , HbA1c = 6.5
• Improve her glycaemic control:
 Tightening dose of insulin injections
 Frequent exercise
 Stop smoking and alcohol
 Diet control
• Contraception: Avoid COCs, they are absolutely contraindicated in any diabetic
pt who has diabetes for > 20 years, replace with IUCD or POPs, if < 20 years COCs
can be used with precautions.
• Look for diabetes complications by consultation: Retinopathy, nephropathy,
neuropathy and cardiac
• Pregnancy should be avoided if:
 Recent MI
 ESRD
 proliferative retinopathy (pregnancy will result in permanent blindness)
• review to control complications and give 5 mg folic acid

During pregnancy:

• firstly, confirm pregnancy by linear βhCG

• Assess glycaemic control and assess for complications regularly and in every
trimester
• 1st trimester: should have dating USS at 8-13 weeks
• 2nd trimester:
o anomaly scan at 18-22 weeks
o uterine artery Doppler and trans-cervical length at 23 weeks for
prediction of preterm labour and utero-placental insult.
o Urine for proteinuria
• While approaching 28 weeks, if she has nephropathy or vascular complication of
DM, the fetus tend to develop IUGR, if not; the fetus tend to be macrosomic with
polyhydramnios.
 Start Serial growth scan for detection of macrosomia and polyhydramnios
which are good indicators of glycaemic control, usually done every 2-4
weeks.
 Assess fetal wellbeing => biophysical profile + CTG

50
 • At 36 weeks, USS to determine the mode of delivery
 largely dependent on the type of DM:
Type I: usually primagravida, 50 % of them are delivered by C/S
Type II: usually older, multiparous, responsive to induction and normal
vaginal delivery
o USS showed any estimated fetal WT of ≥ 5.5 → for C/S
o Otherwise, C/S done for its usual indications.
o Induction to be done at 37-38 weeks, to prevent sudden unexpected fetal
death.

Delivery:

• Blood glucose control by sliding scale

• 1st stage: partogram, continuous fetal monitoring by CTG, offer epidural
analgesia, start sliding scale infusion of insulin – using infusion pump if available,
measure blood glucose every 1-2 hours and correct accordingly
• 2nd stage: anticipate for shoulder dystocia, avoid use of forceps and ventouse
• 3rd stage: active management (with I.M. oxytocin)

Postpartum:

• Once the baby is delivered, the requirement for insulin will halved
• When the mother start to eat, start s/c insulin injections, then stop the sliding
scale.
• Remember: regarding oral hypoglycaemic agents, sulfonylurea is C.I with
breastfeeding => replace with metformine
• Anticipate for PPH
• Follow up: has to come at 3 weeks and 6 months to do OGTT => in order to
determine the type of diabetes
• Offer contraception; (as mentioned above).

Complications and risks:

Maternal:

1. Recurrent hypoglycaemia
2. DKA (type I)
3. Increase risk of infections
4. DM complications flare up: retinopathy, nephropathy, neuropathy, and MI

51
Fetal:

1. Fetal macrosomia, IUGR

2. Miscarriage
3. Sudden unexpected fetal death
4. Fetal anomalies:
a. Cardiac: Transient HCM (Commonest cardiac malformations), VSD
b. Neural tube defects
c. Sacral agenesis
d. Hypoplastic left colon (Short left colon): also occurs if mother or child has
cystic fibrosis or meconium ileus, and in the contracted area of the colon
in Hirshsprung disease
5. Shoulder dystocia
6. Postnatal: infant of diabetic mother

Uteroplacental insufficiency:

1. Preeclampsia
2. Abruptio placentae

52
 Miscellaneous conditions
Preterm labour
Preterm labour:

• onset of labour after 24 weeks but before 37 weeks.

• Main cause of neonatal mortality and morbidity.

Risk factors:

• Previous Hx of recurrent • Maternal Infection (HIV, Malaria,

Miscarriage or preterm labor
• Uterine over-distension
(Multiple
Pregnancy/Polyhydramnios)
Pyelonephritis)
• Hypertensive disorders
• Abnormal placentation
(abruptio)
• Medical conditions (DM, GDM)

Presentation:

Same as normal labour

Usually 1/3 of cases are associated with PROM, the other 2/3 are
spontaneously/Iatrogenic (Iatrogenic like induction of labour or amniocentesis)

Diagnosis:

1. Symptoms and signs of labour

2. TVUS for trans-cervical length
a. > 15mm – unlikely to develop preterm labor
b. < 15mm – likely to be completed within 7 days
3. Fetal fibronectin= normal physiological protein secreted throughout pregnancy;
except between 22-34 weeks, if it’s secreted during this period it indicates
separation of membranes.
4. Hx: Gush of clear fluid.
5. O/E: Sterile speculum examination => looking for membrane in vagina, discharge
of fluid from endocervical os, or pooling of fluid in posterior fornix.
(Can ask mother to cough/Valsalva – if there was increase in fluid it’s more likely
in post. fornix)
6. Ferning test – part of fluid is taken looking for arborization of membrane, which
indicates amniotic origin.

53
 7. Nitrazine test – Nitrazine dye: Depends on pH of amniotic fluid, alkaline colour
=> changes to Blue => indicates rupture of membranes.
8. Urinalysis to exclude pyelonephritis as cause
*Differentiate btw urine (acidic), stress incontinence and amniotic fluid (alkaline)

Monitoring & management:

1. Decrease fetal complications – Steroid injection to mother

(dexamethasone/betamethasone)
2. Allow time for steroid to act by giving tocolytics – nifedipine, atozepam,
terbutaline, salbutamol (any B₂ agonist), NSAIDS (indomethacin)
a. Atozepam = safest and most effective, disadvantage: expensive,
unavailable
b. Nifedipine = fluid retention, edema & headache
c. Indomethacin = C/I after 32 weeks gestation, causes premature closure
of PDA
d. Terbut/salbut = B₂ receptor stimulation – tachycardia, hypokalaemia,
hypotension (vasodilation)
e. Steroids effect start to act in 1 day and peak in 2-3 days.
3. A paediatrician should be attending and an incubator available .

Prevention:

Factors that decrease incidence of preterm labor are the same as those that combat the
risk factors of preterm labour, such as:

• Control of DM to avoid • Treatment of bacterial vaginosis

polyhydramnios,
• control ART,
• regular follow up at antenatal
clinic for pre-eclampsia and for
control of conditions that lead to
preterm labour,
• better control of infectious
disease and HIV,
(by metronidazole/clindamycin -
> preferred in pregnancy).
* [Metronidazole is safe but can
induce IUGR in high doses (safe
in usual dose)]
• and management and Treatment
of pyelonephritis.

54
Problems of PROM:

▪ precipitate preterm labor ▪ Fetal lung hypoplasia, RDS and

▪ Abruptio placentae and APH limb agenesis – due to
▪ Cord prolapse oligohydramnios
▪ Psychological trauma
Management of PROM:

1. Admission
2. Maternal and Fetal assessment:
a. Vital signs and abdominal examination (daily)
b. TWBC and CRP (3x daily)
c. (Weekly/2x Weekly) USS looking for fetal viability and liquor volume
d. CTG (2x Weekly)
3. Antibiotics to the mother (erythromycin)
a. Decrease risk of chorioamnionitis
b. Other erythromycin benefits: Acts as a tocolytic,
*Not for vaginal examination, because it can induce chorioamnionitis
4. Ask mother to notice any increase in pain, malodorous discharge, bleeding and
monitor for chorioamnionitis signs until she reaches term (37 weeks)
 If labour/abruptio/FD/Chorioamnioitis = terminate pregnancy
5. At time of delivery add gentamycin and metronidazole (in addition to
erythromycin)

55
 C-section
Definition = delivery of fetus through an abdominal incision *Remember:
after 32 weeks gestation. Pathological CTG should
be confirmed by fetal
* The lower uterine segment is not formed before this time, so
scalp blood sampling for
incision < 32 weeks = hysterotomy. fetal academia (pH <7.2)
Indications of C section (6 categories):

Category 1 - Emergency/cold crash C/S (delivery within maximum of 30 minutes)

1. Cord prolapse 4. Fetal acidemia pH < 7.2

2. Abruptio placentae 5. Uterine rupture
3. Vasa previa 6. Shoulder dystocia
Category 2 - Urgent/cold urgent C/S (Should be done up to 2 hrs from diagnosis of any
condition that causes fetal distress with non-reassuring CTG):

1. Failure of progression

Category 3 - Scheduled C/S:

1. Severe preeclampsia.
2. Eclampsia
3. Malposition and malpresentation
..and any indications other than category 1,2 and 4

Category 4 – Elective C/S:

1. Previous/recurrent C/S
2. Monochorionic monoamniotic twin
3. Not-cephalic 1st twin
4. HIV infection
5. Genital herpes simplex infection in the 3rd trimester
6. Previous repaired fistula
7. Major degree Placenta Previa
8. Suspected cephalo-pelvic disproportion (e.g. macrosomia)
9. Prima gravida with breech presentation

Category 5 – Emergency/cold crash Peri-mortem C/S:

the mother is expected to die within 5 minutes and the fetus is alive

56
Category 6 – Emergency/cold crash Post-mortem C/S:

the mother has died, the fetus should be delivered within 5 minutes

Types:

Lower-segment transverse C/S Upper-segment C/S

advantages disadvantages
Intraoperative:
Decrease risk of Excessive blood loss
bleeding
Formation of
adhesions and
Better healing Less adhesions
persistent lower
abdominal pain
Lower risk of bowel More risk of bladder More risk of bowel injury
injury injury But lower risk of bladder injury
Lower risk of
Rupture easily with recurrent pregnancy
rupture
Indications:
1- Post-mortem or peri-mortem
2- severe prematurity
3- transverse lie
4- major degree anterior placenta previa
5- lower segment masses
(endometrial/cervical polyps, fibroids)
6- contractions due to adhesions from
previous C/S.

Approach:

1. Counsel the mother and take an informed Consent; including hysterectomy and
tubal ligation especially in case of placenta previa and uterine rupture
2. Fasting, that’s more prolonged; 6-8 hrs prior to the C/S
3. Consent also for possible general anaesthesia, because spinal anaesthesia might fail.
4. Urinary catheterization to empty the bladder to decrease the risk of bladder injury.
5. Give: antacids, prophylactic antibiotics and appropriate analgesia
6. Prepare 2-4 units of blood

57
Postoperatively:

1. Continue analgesia, antibiotics, fluids, and

2. give LMWtH s/c injections in prophylactic dose for 7 days

Follow up:

2 visits: after 2 weeks and at 6 weeks => Look for the healing of scars and
development of persistent abdominal pain

VBAC
VBAC = Vaginal Birth After Cesarean, aka TOLAC = Trial of Labour After Cesarean

Effective up to 72-76% of women

2 major contraindications:

1. previous 1 upper segment C/S

2. 2 or more lower segment C/S

Factors that decrease success rate:

1. Short ladies
2. Obese, BMI > 30
3. Previous delivery by C/S due to macrosomia
4. Shoulder dystocia
5. Preterm labor

If had a C/S in less than 2 years:

6. Foetal macrosomia
7. postdate pregnancy
8. Use of epidural analgesia
9. Male fetus

Factors that increase success rate:

• A previous successful VBAC (the strongest predictor)

• The reverse of the above factors

58
Approach:

Counsel: define VBAC, give her the C/S option

Disadvantages: Advantages:

• Failure => C/S • Avoid major surgery, anaesthesia

• Rupture or dehiscence of scar => and its complications
C/S and hysterectomy • Increase future success of VBAC
• High risk of bleeding and huge • Decrease the risk of Transient
need of blood transfusion tachypnea of newborn
• Prolonged VBAC can lead to fetal
distress => hypoxic ischemic
encephalopathy => fetal death

After delivery, you document and debrief.

Induction of labour
Def.: a planned initiation of labour before its spontaneous onset after 24 weeks of
gestation.

Indications:

1. Postdate pregnancy (major 7. Chorioamnionitis

indication) 8. Foetal distress
2. Utero-placental insufficiency 9. General medical conditions: DM,
3. IUGR, IUFD uncontrolled HTN, uncontrolled
4. Eclampsia Thyroid problem, some cases of
5. Obstetric cholestasis myasthenia gravis and Guillian
6. Placental abruption barre
How?

Mechanical:

• Usually used in postdate pregnancy

• Stretch and sweep
• Usually done at 40 weeks GA

59
Chemical:

Based on assessment by modified bishop score: (> 6 = favourable, < 6 = unfavourable)

• Favourable => induce by Artificial ROM

- Primagravida + favourable => AROM and start oxytocin infusion immediately

- Multiparous + favourable => AROM and wait for 2 hours then start oxytocin
infusion

• Unfavourable => make it favourable, use prostaglandin analogue, misoprostol

(tabs) or prostin

- Primagravida: misoprostol 25 mcg with baseline CTG before the dose and 6-hrs
after it, if there’s no improvement of bishop score and CTG is normal give
another 25-50 mcg

- Multiparous: use 1 dose only, and seek for consultation if more is needed, due
to high risk of uterine hyperstimulation and rupture

*rule: wait for 6-8 hours after PG analogue, before you start oxytocin

Approach:

1. Bring the mother early

2. Abdominal examination, full obstetric examination
3. Control DM,…
4. Baseline CTG

Failure of induction:

Failure to rupture the membranes after 2 or more trials

Failure of bishop score to become favourable after recurrent positioning of misoprostol

Complications:

1. Failure of induction
2. Uterine hyperstimulation and rupture (more risk with use of misoprostol)
3. Oxytocin can cause fluid retention and dilutional hyponatremia, and neonatal
jaundice
4. PG analouge may cause HSR: skin rash, bronchoconstriction, diarrhoea and
hypotension due to vasodilatation

60
 5. Iatrogenic prematurity Uterine hyperstimulation:
6. PPH and fetomaternal haemorrhage
> 7 contractions per 10 mins
7. Cord prolapse
8. Fetal distress and death Reverse contractions by:

• Positioning of the mother

• Proper hydration
• Tocolytic agent (atozemap)

Malposition and Malpresentation

Important Definitions:

Lie: relation of the long axis of the fetus to the long axis of Reference point for describing fetal
the uterus (longitudinal, transverse, oblique or unstable) position:

Presentation: fetal part presenting at pelvic outlet • Occiput for cephalic presentation
(cephalic –vertex, face, asynclitic-, • Sacrum for breech presentation
breech –complete, frank, footling-, • Mentum for face presentation
transverse –shoulder-,
compound- fetal extremity as cord prolapses along with presenting part)

Position: position of presenting part of the fetus relative to the maternal pelvis (OA, OP,
OT)

*N.B: Normal lie; longitudinal, may lead to abnormal position and presentation

Abnormal lie (transverse, oblique or unstable lie)

Risk factors for abnormal lie:

• Uterine anomalies/masses • Multiple pregnancy

(fibroids) • Congenital fetal anomalies
• Placenta Previa • Multiparity
• Polyhydramnios • Contracted pelvis
O/E:

• Fundal height less than expected for GA (less for date)

• Empty pelvis with no presenting part downward
• Palpation of the fetal pool on the Rt and Lt flanks
• Abnormal position of fetal heart sounds

61
Management:

• Generally, if presented in labour => for C/S

• If not in labour => admission at 37 weeks, aim to increase GA to give a chance for
spontaneous reversion to longitudinal lie
• If has not corrected spontaneously, offer more complicated procedure which is
only done by a senior consultant obstetrician => stabilization induction +
amniotomy: ECV and amniotomy
- Complications: cord prolapse and abruptio placentae
• If has not corrected spontaneously and/or no place for stabilization induction,
arrange for elective C/S at 39-40 weeks; also giving a chance for spontaneous
reversion

Abnormal presentation:

Vertex presentation: sub-occipito-pregmatic = 9.5 cm

OP position: sub-occipito-frontal = 10.5 cm

Occipito-frontal = 11.5 cm

Brow presentation: Mento-vertical = 13.5 cm

• Very large diameter

• Management: expectant or C/S

Face presentation: sub-mento-pregmatic = 9.5 cm

• Mento-anterior: compatible with vaginal delivery, most common type of face

presentation
• Mento-transverse: unstable; might progress to mento-posterior or downgrade to
mento-anterior
• Mento-posterior: 1- expectant management: wait for spontaneous resolution to
mento-anterior, or otherwise => 2- C/S

*Face presentation case: Thyroid goiter, cystic hygroma

Shoulder presentation:

• For C/S , high risk of cord prolapse

62
Breech presentation:

Risk factors:

• maternal: multiparity, uterine anomalies, mass, previous breech.

• fetal: multiple pregnancy, hydrocephalus
• placental: placenta previa
• polyhydramnios and oligohydramnios
• preterm labour (while at term the rate is only 1%)

O/E:

• fundal level is normal, fundus is occupied by head, fetal heart is upward, soft
presenting part.

Types of breech:

1. extended: commonest type, 70 %

2. flexed: 15 %
3. footling: 15 %

Problems: cord prolapsed especially with footling, but all of them can cause it.

Management:

• Optimum management: C/S

• Primigravida: C/S as a rule
• Candidate for Normal Vaginal Delivery:
o Mother: multiparous + adequate pelvis -no previous history of obstructed
labour, no previous history of C/S, no uterine masses/abnormalities-
o Fetus: GA > 34 weeks (less than that is for C/S) + no fetal distress +
extended breech + head is not extended + estimated baby weight is 2.5-
3.5 Kg.
• ECV: external cephalic version can be done for a multiparous at 37 weeks, a
primigravida at 36 weeks GA.
o Do baseline CTG to exclude fetal distress
o Blood grouping to determine Rh +/-
o Prepare blood
o Give a small dose of tocolytic (uterine contractions will increase failure
rate of ECV)

63
 Complications of ECV: placental abruptio, PROM, cord prolapse, fetal
distress, feto-maternal hemmorrhage

Contraindications: polyhydramnios, abruptio placentae, multiple

pregnancies, uterine anomalies, Rh-isoimmunization, HTN, severe
preeclampsia, IUGR

Compound presentation:

= Two or more presenting fetal parts

RFs: same as breech presentation

Examples: nuchal arm (head+arm), arm+leg,

Mood of delivery:

• Most of compound presentations revert spontaneously to cephalic and delivered

normally
• If not, most of them can be delivered normally as well
• If there is anticipation for fetal distress with normal delivery, go for C/S

Asynclitism:

• Degree of polarism between fetal head and maternal pelvis

(synclitism) = anterior parietal and posterior parietal are
equally presented.
• Post. Asynclitism = posterior parietal pole is the presenting
part
• Ant. Asynclitism = anterior parietal pole is the presentencing part

IUFD
Def.: death of the fetus in uterus after 24 weeks of gestation

Causes:

• Idiopathic (most common) • Maternal endocrinological

• Chromosomal abnormalities abnormality
• Fetal anomaly • Uteroplacental insufficiency
• Maternal infection • Placental abnormality

64
Clinical presentation: O/E:

• Cessation of symptoms of • ↓ fundal height

pregnancy • Absent fetal heart sound (most
• ↓ fetal movement specific indicator)
• ↓ peripheral edema
• Galactorhea (most commonly
noticed symptom)
Investigations:

• USS: absent fetal heart sound, oligohydramnios, The Spalding sign (overlapping
of the fetal skull bones caused by collapse of the fetal brain, appears usually a
week or more after fetal death in utero).
• ßhCG, serum progesterone

Management:

• counsel the mother kindly that the fetus has demised

• offer her options for management: a week of expectant management and
spontaneous ROM, if has failed; use induction of labor: misoprostol
*Remember: avoid here AROM
• ask her if she want to be investigated for the cause of IUFD; including
examination of fetal and placental tissues, BP measurement, urine proteins,
OGTT, Thyroid function test, autoimmune screening, chromosomal analysis .
• To tell her that the cause was never detected in > 50% of IUFD, and very likely
her future pregnancy may pass uneventfully.
• Post termination counselling
• Contraception: offer IUCD immediately after Contraception after normal
labor pregnancy:
• can be given as early as possible
• Drug to supress milk production: rd
from the 3 week of delivery, as
bromocriptine I.M. medroxyprogesterone acetate
(Depo-Provera) – the only best
Follow up: choice,
• optimum time from the 6 th week
- Come after 6 weeks
forward, any type except COCs.
- Delay investigations till the pt is ready

65
 Obstetric Cholestasis
Occurs usually during the 3rd trimester, especially in multiparous or who had previous
history, or during COCs.

Retention of bile acids and salts due to obstruction

Clinical Presentation: Complications:

- itching without rash - Precipitate PPH if associated

- nausea and vomiting can occur with vitamin K deficiency
- very rarely jaundice - Preterm labor
- Sudden unexpected fetal death
Diagnosis:

History, Examination &

Investigations:

- LFT: ALT, AST should not be elevated > 3x (if so it indicates ongoing hepatocyte
injury), massive increase in ALP level
- Abdominal USS: to exclude other causes
- CBC and coagulation profile
- Hepatitis infection workup
* hep A is the most common in pregnancy
* hep E is the most severe spectrum in pregnancy - acute liver failure
- Autoimmune hepatitis workup

Management:

- Symptomatic:
o antihistamine drugs: decrease pruritus, SEs: sedation and associated with
NTD.
o Cholestyramine, SEs: bloating and diarrhoea.
o Urodeoxycholic acid => most effective and safe => ↓ bile salt & bile acids
- Vitamin K injection to the mother to prevent PPH and haemorrhagic disease of
newborn.
- Monitoring:
o USS and CTG: but usually unsuccessful, it doesn’t reduce the risk of fetal
death; so it’s controversial issue.
- Delivery:

66
 o Optimum time: 37-38 weeks
o Induction is recommended to avoid sudden death.
- Follow up:
o Repeat LVF after labor and a week later
=> complete resolution confirm the diagnosis of OC
 High recurrence rate, especially with the use of COCs; so use POPs instead.

Acute Fatty Liver

- The most severe spectrum of obstetric cholestasis, that it may result in acute liver
failure.

Risk factors:

- Previous Hx - Multiple pregnancy

- Family Hx - Male fetus
Clinical presentation:

Mimic spectrum of acute viral hepatitis: anorexia, low grade fever, nausea and vomiting
→ jaundice → acute liver failure → complications

▪ Complications: (list from the most frequent to the least)

1. hepatic encephalopathy and 3. bleeding tendency,
cerebral edema, 4. bacteremia and sepsis,
2. hypoglycaemia, 5. hepatorenal syndrome and AKI
Management:

- Symptomatic:
• ICU • Vitamin K and FFP
• 45⁰ bed • Broad spectrum antibiotic (in
• Mannitol infusion case of proven sepsis and
• D 10% (avoid NS → Pul. edema) bacteraemia)
• CVP line for monitoring
- For HRS:
• Fluids • Prophylactic Abx: cefotaxime
• Terlipressin + 20% salt-free • TIPS
Albumin • Liver Transplant

67
- renal dose of dopamine, to increase GFR, increase diuresis and improve renal function;
and prevent pul. edema.

- high risk of mortality and morbidity, IUFD

- follow by CTG and abdominal USS

- Delivery: Induction of labor

- repeat LFT and USS after labor

- refer to a physician; (acute fatty liver in pregnancy is considered a genetically

predetermined condition associated with enzymatic deficiency).

- HB vaccination to be offered after delivery to the mother.

IUGR
Def.: failure of fetus to reach normal growth potential

Risk factors:

Maternal: Placental:

• Chronic diseases: CKD, DM, HTN, • Chronic marginal sinus

CHD, COPD separation (minor abruptio
• SLE placentae)
• Thrombophilia • Placenta previa
• Low socioeconomic status • Morbidly adherent placenta
• Phenylketonuria • Tumor
• Nutritional deficiencies • Calcification (by 40 weeks GA)

Uterine: Fetal:

• Scar • Chromosomal abnormalities

• Fetal anomalies
• TORCH

Multiple pregnancy (causes are: 1.

Crowdedness 2. Dizygotic twin with sex
difference 3. TTTS 4. TRAP)

68
Complications: IUFD

Screening of high risk:

1. Fundal height < GA

2. Fetal heart sound
3. Fetal movement # per 12 hr
4. Serial USS => measurements of AC/HC (symmetrical vs. asymmetrical IUGR)
=> diagnostic

Confirmation:

At 33 weeks: Uterine artery Doppler looking for a notch (to exclude uteroplacental
insufficiency)

Then do Doppler for fetal vessels:

1. UA (Umbilical artery): end diastolic flow ( ↓ , absent , reverse )

Reverse => indication of termination of pregnancy
Sensitive to uteroplacental insufficiency
Very sensitive before IUGR appear
2. MCA (middle cerebral artery)
In case of expected fetal anemia and fetal hydrops
3. DV (Ductus venosus)
Any change is a Late sign and terminal event
Indicate fetal academia and death

- CTG for monitoring

Management:

Deliver if:

1. Liquor amount is progressively decreasing

2. Pathological CTG
3. Reversed UA Doppler

69
 Gynecology
Menstrual cycle
Menstrual cycle:

• Secretion of GnRH is low and continuous → no puberty.

When it became pulsatile → stimulates pituitary gland to secrete FSH and LH in a
pulsatile manner.

Stages of female puberty:

1. Adrenarche: at 6 years
2. Gonadarche: sex hormones from ovaries
3. Thelarche: breast development
4. Menarche: menstrual cycle, between 11-13 years - mean age is 12.5

- Irregular cycle at onset of menarche and pre-menopause; due to anovulation.

Normal cycle:

GnRH → FSH/LH → act on ovaries. The cycle has 2 parts: ovarian and uterine.

Ovarian:

1. Follicular phase: irregular and variable – it’s the main determinant of the length
of the cycle
2. Ovulation
3. Luteal phase: fixed at 14 days; corpus luteum is viable for 14 days.

- 1st day of the cycle is the 1st day of bleeding, level of FSH/LH is high. Progesterone and
oestrogen become low, leading to decidualization/sluffing of endometrium.

- FSH/LH act on ovaries. LH act on theca cells to make progesterone and

androstenedione. FSH act to promote development of follicle. FSH act on granulosa cells
to convert testosterone to estrogen,↑proliferation and size of granulosa cells and
ovarian follicle => 18 mm = the ultimate size of dominant follicle, other follicles become
atrophied.

- Then ovulation occur due to LH surge caused by estrogen peak. (N.B.: The high
estrogen levels at this time send positive feedback to the pituitary)

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- After ovulation occur, dependent on secretion of LH, corpus luteum develops and
starts to secrete progesterone to affect endometrium.

- if fertilization occur, corpus luteum is maintained by hCG -secreted by cytotrophoblast-

and continue to secrete progesterone. If not, LH will decrease before the onset of
menstrual cycle and the corpus luteum is converted to corpus albicans.

- luteal phase is associated with large amount of progesterone but estrogen is constant.
Death of luteum lead to ↓ progesterone and decidualization => the start of another
cycle.

Uterine and cervical changes:

1. proliferative phase: due to oestrogen => endometrial and stromal hyperplasia.

Thick and long mucus in the cervix, that showed Spinnbarkeit up to 8-10 cm.
2. secretory phase: proliferation stop, there’s maturation of glands and
vasodilatation of uterine and spiral arteries. This phase is due to progesterone.
Thin watery cervical mucus, Spinnbarkeit 1-2 cm, ease penetration of sperms.
3. Decidualization: followed secretory phase

Abnormal menstrual cycle

• Normal length: 28 ± 7 days (21-35).
• Days of bleeding: average 3-7 days, range from 1-7 days.
• Amount of bleeding is variable (35-80 ml),

Remember: in normal vaginal delivery, bleeding up to 500 ml is considered normal.

Amenorrhea:
• Primary amenorrhea: failure to
start menstruation by age of 16
• Secondary amenorrhea: cessation
years with presence of secondary
of menses for 6 months.
sexual characteristics, or by age
of 14 years without secondary
sexual characteristics.

Causes:

1. Constitutional delay (most common cause).

2. Hypothalamic-pituitary-ovarian axis abnormality (hormonal):
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▪ Hypogonadotropic hypogonadism: failure of pituitary or hypothalamus by:
• anorexia nervosa
• excessive exercise
• tumor – craniopharyngioma
• inflammatory – autoimmune,
• infiltrative lesions – sarcoidosis, TB, iron
• genetic: idiopathic – Kallmann syndrome: X-linked or autosomal
recessive, failure to develop a hypothalamus and absent olfactory
bulb → anosmia, skeletal and renal malformation.
• systemic disease that suppress hypothalamus – DM, Addison
▪ Ovarian:
• Primary Gonadal dysgenesis/agenesis: resulting from failure of
migration of germ cells from the yolk sac to the genital ridge.
• Turner syndrome (hypergonadotropic hypogonadism)
= there is only streak of the ovaries, stroma only and absent follicles;
occurs due to deletion of 1 X (45 XO).
Features:
* external phenotype: short and webbed neck, wide chest, broad
separated nipples, cubitus valgus, lymphedema, no breast
development and no axillary or pubic hair, naivie, short 4th and 5th
metacarpals.
* internal phenotype: Cardiac anomaly: bicuspid aortic valve (most
common), coarcitation of the aorta. Renal anomaly: horse-shoe
kidney, system duplication. Cystic hygroma (neck or retroperitoneal).
Ovaries: streaks.
Diagnosis is clinical and by karyotyping.
Management:
1- attain normal skeleton and growth: give GH
(N.B. other indications: it’s also given for pituitary gland failure and
chronic kidney disease).
2- attain normal pubertal development: give estrogen but cautiously
to avoid excessive endometrial hyperplasia,
3- then give progesterone once the patient has attained normal
pubertal development.
• PCO is the most common cause of anovulatory cycle.
• POF: premature ovarian failure = presented as failure of occurrence
of normal MC before the age of 40 years, also called accelerated
menopause, usually associated with other autoimmune diseases

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 (Addison disease, Hashimoto thyroiditis, autoimmune hepatitis).
Follicles are absent! Other Causes: infections "mumps oopheritis",
radiation for cervical and rectal cancers, chemotherapy, wedge
resection of ovary in treatment of PCO -in the past, nowadays they do
laparoscopy-.
• Resistant ovary syndrome: normal ovaries and follicles, but FSH & LH
fails to act.
3. Genital tract abnormalities:
*N.B. Paramesonephric ducts (Müllerian ducts) fuse with the lower part of
urogenital sinus => develop into Fallopian tube and the upper art of the vagina.
• Müllerian agenesis: complete or partial, MRKH syndrome.
• Failure of fusion of the ducts: 2 uteruses => Uterus Didelphys (double
system).
• Partial fusion of the ducts: can result in either Bicornuate Uterus or Septate
Uterus.
- Discovered during pregnancy, presents with 2nd trimesteric miscarriage,
preterm labour, abnormal lie or presentation, abruptio placentae.
• Transverse vaginal septum: paramesonephric ducts fails to fuse with
urogenital sinus.
- Presentation: hematocolpus, that may lead to hematometrium, =>
cyclical dysmenorrhea with no bleeding (primary amenorrhea),
abdominal distention and acute urine retention. Management is surgical.
• Imperforate hymen: urogenital sinus fails to perforate
- Present as cryptomenorrhea = cyclical dysmenorrhea with no bleeding
(primary amenorrhea), O/E: bulging bluish membrane. Management:
cruciate incision.
4. Chromosomal abnormalities - 2nd most common cause, e.g.: Turner syndrome.
5. Physiological causes of amenorrhea: pregnancy, lactation, menopause.
6. Endocrinological abnormalities:
• CAH: Congenital adrenal hyperplasia: autosomal recessive, failure of normal
hormone synthesis by adrenal gland, resulting in high level of ACTH from
pituitary, resulting in hyperplasia. Has 5 main types, common one is 21a-
hydroxylase deficiency. Present with either:
- salt loosing CAH: in males, severe mineralocorticoid deficiency, presents
with symptoms of Addison disease.
- non-salt loosing CAH: 2 types:
a. classical: present at delivery with ambiguous genitalia in female.

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 b. Non-classical: primary amenorrhea and failure of secondary sexual
characteristics. (Main DD of PCOS).

Diagnosis of CAH: by detection of accumulation of metabolites before the

deficient enzyme. It’s mainly 17-hydroxyprogesterone in non-classical
type.

Management of CAH: replace at early age: glucocorticoid (by

hydrocortisone not prednisolone to reduce side effects) and
mineralocorticoid.

• Androgen insensitivity syndrome (previously: Testicular feminization

syndrome):
- Genetic sex: determined at fertilization XX or XY.
- Gonadal sex: at 12 weeks gestation.
- Phenotypic sex : 2ndry sexual characteristics.

Normal development and fertilization => XX or XY

- Y chromosome has SRY gene that is responsible of secretion of a

hormone (testicular differentiating factor) targeting the gonads for its
development into testis.

The testis has 2 type of cells: leydig cells and sertoli cells that secret:

1. AMH (anti-Mullerian hormone) => agenesis of paramesonephric duct.

2. Cholesterol => formation of primary (inactive) testosterone.

When testosterone becomes activated, it leads to normal development of

internal genital tracts: vas deference, seminal vesicles and epididymis.
Testosterone is also converted to dihydrotestosterone which is responsible
for external features.

Failure of any step lead to => Male genotype and female phenotype.

- in this syndrome there is Normal secretion of testosterone but resistant

response by the gonads, leading to:
- normal testis and testosterone secretion
- absent vas deferens, seminal vesicles and epididymis.
- female phenotype but no female internal organ (due to failure of
dihydrotestosterone to act) => blind ended vagina (urogenital sinus
that form vagina is independent on hormones)

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 Presentation: raised as females, primary amenorrhea.

Management: multidisciplinary; including psychological support, they are

given estrogen and should undergo gonadectomy to reduce malignancy.

Approach to amenorrhea:

History, examination (weight, height, 2ndry sexual characteristics).

Investigations:
- hormonal
- karyotyping
- abdominal and pelvic USS
* If there were no 2ndry sexual characteristics => mainly ovarian problem
If the above were normal;
- 17-hydroxyprogesterone level
- pituitary MRI
- progesterone withdrawal test:
=> useful to localize the cause of amenorrhea
This test is dependent upon presence of normal hypothalamus, normal pituitary,
normal ovaries, normal endometrium and no obstruction in outflow tract.
In a normal female who is given progesterone for 5 days then stopped, this will
result in decidualization and menstrual bleeding.
- If bleeding occurs after 5 days the cause of amenorrhea is usually anovulatory
cycle (most likely PCO) = due to excessive amount of estrogen which results in
unopposed stimulation of the endometrium.
Then do => LH/FSH ratio and abdominal USS.
- If there were no bleeding => exclude anovulatory cycle => give estrogen with it,
- if there is no bleeding => it is an obstructive problem or uterine
abnormality - absence of Mullerian duct.
- if there is bleeding => the cause is hormonal: hypothalamus, pituitary,
ovary.
Then investigate accordingly.

= elevated LH => more than 35 IU/dL "menopausal range"

Measure and repeat twice → POF, Turner, gonadal dysgenesis.

Management: cause-dependent, and according to fertility.

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 Dysmenorrhea:
Def.: feeling of excessive pain at time of menstruation as described by the patient
herself, i.e. it is subjective.

* N.B.: Normally the pain is due to:

- vasospasm "ischemic pain"
- effect of prostaglandins that cause: uterine contractions, and increase nerve
sensitivity to pain.

Primary Dysmenorrhea:
• No underlying cause
Secondary Dysmenorrhea:
• Risk factors are: early menarche,
Starts > 24 hrs premenstrual, increases
family history, heavy cycle.
in severity after onset, doesn’t end until
• Starts 24 hrs premenstrual,
menstruation ends or may extend
increases in severity and reaches
the peak at onset of bleeding, beyond that.
then decreases and ends before
the menses ends.

Causes of Secondary Dysmenorrhea:

a. infective: PID (2nd most common cause )

b. endometriosis (the most common cause), adenomyosis
c. IUCD
d. fibroid and polyps
e. cervical stenosis
f. Ashermann syndrome
g. theca luteal cyst/ovarian cyst
h. pelvic congestion

Approach:

If typical primary: no investigation is needed

Atypical => 1st investigation: Pelvic US for all possible causes

If US normal => it’s primary usually

76
Management:

Start by relieving the symptoms:

a. NSAIDs:
Mefenamic acid (N.B: if associated with excessive bleeding: tranexamic acid )
b. COCS: decrease pain by :
a. Regulation of the cycle
b. Shortening the bleeding time
c. Tocolytic action (progesterone): decrease uterine contraction => decrease
pain

Or Stop the cycle at all: Other Indications of GnRH :

1. Fibroid: 3-6 months before
• GnRH analogue => result in
surgery => to decrease size.
disappearance of dysmenorrhea and
2. endometriosis
result in inducible menopause S.E.:
3. menorrhagia
increase risk of osteoporosis.
4. management of subfertility -
• If doesn’t respond to GnRH:
ovulation induction
a. herbal medicine
5. pre-menstrual syndrome
b. Vitamin B1 (thiamine) and Mg
6. PCP (precocious Puberty )
=> decrease pain.
7. Prostatic CA
c. Surgical management: Uterine
nerve ablation.

Menorrhagia:
* Subjective Diagnosis. i.e. definition as bleeding > 80 ml/cycle is nonsense

a- Primary menorrhagia: DUB: a diagnosis of exclusion

RF:

• Early menarche
• +ve family history
• Obesity
• Smoking

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b- Secondary menorrhagia:

localized disease:

1. fibroid, polyps systemic disease:

2. endometrial hyperplasia
1. hypothyroidism
3. adenomyosis
2. bleeding tendency e.g.: VWD
4. Functional ovarian cyst
Presentation:

• Anemia due to iron deficiency

• Excessive bleeding, severe that is leading to social problems
• Associated with severe dysmenorrhea

Approach:

History: Assess the following:

• Length of the cycle, length of menstruation

• Amount of bleeding: (pads/day, clots, floods)
• Restriction of normal activity
• Symptoms of anemia: syncope, headache, palpitation, fatigue
• Possible cause, ask about:
- symptoms of hypothyroidism
- bleeding tendency
• Assess for a localized cause:
- Adenomyosis: severe abdominal pain, heavy menorrhagia, subfertility
- Polyps: irregular bleeding (metrorrhagia), it could be inter-menstrual or
postcoital if cervical polyps
- Possible symptoms of menopause: because DUB ia associated with
anovulatory cycle (i.e. at onset of menarche and approaching
menopause)

Investigations:

1. CBC

then according to suspected cause,

2. TFT
3. Abdominopelvic/TV USS
4. Coagulation profile

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Management:

- Correction of anemia: oral /I.V. iron Tranexamic acid also used in:
- Decrease bleeding: medical:
1. Management of VWD
1. NSAIDs: also decrease dysmenorrhea
2. Management of bleeding
2. Tranexamic acid: act as antifibrinolytic =
per-recatum due to
pro-coagulant
angiodyplasia
S.E.: increase risk of DVT and
3. Reversion of thrombolytics
pulmonary embolism
(given as combination with NSAID)
3. COCs
4. Mirena (IUS) progesterone, most effective non-invasive method
5. Danazole: androgenic side effect, no longer used
- Surgical: either:
1. Ablation: methods can be used:
▪ Trans-cervical resection of endometrium
▪ Radiofrequency
▪ Laser
▪ Heated saline in a balloon
Complications:
▪ induce Ashermann syndrome resulting in dysmenorrhea
▪ sub-fertility
▪ perforation of uterus
▪ TURB syndrome
2. Hysterectomy:
▪ Total: resolve bleeding completely, decrease risk of prolapse
▪ Subtotal: may not result in complete resolution of bleeding, but it
is associated with increased risk of prolapse
Recommended in woman who:
▪ Has completed her family
▪ Age > 35 years
▪ Or has another indication for hysterectomy

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 PCOS
Anovulatory disease that results from unopposed oestrogen secretion by the ovary.
Excessive oestrogen secretion and failure of ovulation + Low progesterone
→ no decedualization → Oligomenorrhea and irregular cycles

Diagnosis:

Rotterdam criteria: 2 of 3 to diagnose PCOS

1. Oligomenorrhea and anovulatory cycle

2. Clinical or biochemical hyperandrogenism
3. Presence of a polycystic ovary
USS finding in ovaries:
1. ovarian stroma increased
2. ovarian volume > 10 ml
3. presence of ≥ 12 subcapsular cysts, cyst never > 10 mm in size

Presentation: Long term complications:

- Oligomenorrhea (most common) Due to high unopposed estrogen:

- Amenorrhea (2nd common) - Endometrial hyperplasia and
- Subfertility increased risk of endometrial
- Obesity (½ pts) Carcinoma
- Acanthosis nigricans (least Obesity-associated:
common) - Type II DM
- Recurrent miscarriage (2nd - Hypertriglyceridemia
trimesteric) - Cardiovascular disease and HTN
- Dysfunctional uterine bleeding

Investigations:

To include or exclude other diagnoses and to detect complications

1. Abdominopelvic or TV USS => look for necklace sign

2. hormonal profile => LH: FSH ratio > 2
3. Free Androgen Index (FAI)
[FAI = total testosterone (nmol/L) x 100/sex hormone-binding globulin
(SHBG) (nmol/L)]
4. Prolactin level
5. lipid profile & GTT

80
Management:

depends on symptoms and fertility wish:

a. oligo/amenorrhea: cyclical progesterone (preferred) or COCS

b. hirsutism and acne:
1- local or topical Eflornithine cream
(N.B. it is also used for African trypanosomiasis) Or
2- Dianette (a combination of cyproterone acetate and
ethinylestradiol)
Or a combination of COCS and metformin
3- Antiandrogenic drugs:
a. Spironolactone
b. 5 α-reductase inhibitor
c. Flutamide
4- Mechanical: laser, shaving
c. fertility issues:
• Weight loss (most effective method)
• Ovulation induction:
- Clomiphene Citrate: estrogen receptor modulator, act in the pituitary gland.
It reduces the negative feedback of oestrogen => increase FSH and LH.
+ can be combined with metformin.
given in 5 days (day 2 to day 7) for 3 consequetive cycles, starting from 15 mg
up to 150 mg/day.
- if there still no conception after 3 cycles => give metformin combination,
if there were no conception after 1 year => Clomiphene resistant PCO, go for
- induction by GnRH analogue, this could be complicated by ovarian
hyperstimulation and multiple pregnancy.
If GnRH analogue failed, go for
• Laproscopic ovarian drilling by diathermy; it increases fertility for up to one and a
half year
• Assisted reproductive techniques
• Surrogacy
• Psychological support and tender loving care

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 Contraception
Contraception: methods used to prevent pregnancy.

Types: natural, chemical, mechanical, mixed (chemical & mechanical)

Chemical contraception:

COCS (Combined Oral Contraceptive Pills)

(ethinylestradiol (estrogen) + progesterone -1st, 2nd ,or 3rd generation-)

- 1st: historical
- 2nd: levonorgestrel
- 3rd: Norgestimate – Desogesterol
- 4th: Drospirenone

Yasmin: (ethinylestradiol + drospirenone) has a special characteristic; has an anti-

androgenic property and a more potent antidiuretic – compared to other progesterones
that cause fluid retention.

Method of action:

1. inhibition of ovulation – estrogen acts on pituitary gland => ↓ FSH & LH

2. thickening of cervical mucus => failure of sperm penetration
3. thinning of endometrium => failure of implantation

Side effects of COCS:

 Side effects are variable-according to generation of progestrone

- 2nd generation less thrombophilic (=> increased incidence of DVT, PE)
- 3rd generation more thrombophilic
a. GI upset (—progesterone) g. ↑ incidence of thromboembolism
b. Headache DVT/PE
c. Bloating h. Rare: psychotic manifestation,
d. Brest tenderness anxiety, depression
e. Fluid retention (—progesterone) i. Break-through bleeding in the 1st 3
f. Weight gain months (—progesterone)

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Extra-contraception benefits of COCS:
• regulate the cycle • Induce amenorrhea
• ↓ menorrhagia • ↓ incidence of ovarian,
• ↓ dysmenorrhea endometrial, colorectal Ca
• ↓ symptoms of endometriosis • ↓ risk of osteoporosis
• ↓ fibroid size • treatment of acne & hirsutism
• prevent development of PID • ↓ transmission of STD

Contraindications:
Absolute: Relative:

• Pregnancy • controlled DM
• undiagnosed genital tract • controlled HTN
bleeding • family history of
• uncontrolled HTN thromboembolism, CVA or
• acute liver failure heart disease
• previous CVA, MI • obesity
• active malignancy in breast or • age > 35
endometrium • smoking
• obesity - BMI > 30 + (smoking • chronic liver disease - stable
or age > 35) • gallbladder disease - stable
• uncontrolled DM > 20 years • sickle cell trait
• migraine with aura

How to give COCS:

▪ exclude absolute C/I ▪ to be taken for 21 days from the day 1 of the cycle
▪ measurement of BP ▪ last 7 days off for placebo (vitamins are given to assure
▪ proper counselling continuity)
▪ should be taken at the same time daily

Missed pills:
▪ 1st 7 pills and last 7 are the highest risky
▪ If 1 pill was missed at any time => take it as soon as possible and continue as usual
▪ If 2 pills or more use extra method of contraception for 7 days
- If this was in the 1st 7 days => emergency contraception
in the middle => no need for emergency contraception
in the last => no need for emergency contraception, but
skip the last placebo pills and start another pack without
placebo

83
Indications of continuous COCS:

• Pt has underwent total hysterectomy and has entered menopause

• endometriosis
• fibroid for myomectomy, but not > 6 months

Forms of Combined preparations:

Pills - transdermal patches - vaginal rings

* both patches and rings are also to be placed for 3 weeks of the cycle and removed in
the 4th.

Progesterone

Preparations:

Pills - I.M. injections - subcutaneous implants - IUCD

POPS (Progesterone only contraceptive pills)

Indications:

If the women developed side effects of COCS or a contraindication to COCS (usually

thromboembolic disease, S.C. Trait, active gall bladder disease and Lactation)

Side effects: (progesterone is a vasodilator and smooth muscle relaxant)

1. fluid retention and edema 4. ovarian cyst

2. nausea and vomiting 5. ectopic pregnancy ( due to
3. breast tenderness relaxation of Fallopian tube)
Method of action:

=> same as COCS + relaxation of Fallopian tube

Contraindications of POPs - Absolute:

• pregnancy • previous ectopic pregnancy

• current breast Ca • undiagnosed vaginal bleeding
How POPs are used:

Pills are to be taken daily 28 or 35 days according to the length of the cycle

84
Missed pills:

• If more than 3 hours past the normal time => considered missed
 Take as soon as possible + extra contraception for 48 hours
• Except Cerazette (Desogestrel) > 12 hours past the normal time => considered
missed

I.M. Progesterone only injections:

• Medroxyprogesterone injections (Depo-Provera) – given every 12 weeks

• Norethisterone acetate injections – given every 8 weeks

Benefits: Side effects:

• For non-compliant women 1. Delay in resumption of fertility for

• More effective than POPs up to 1 year
• High risk of development of side 2. Excessive weight gain
effects 3. Fluid retention
4. Increase risk of osteoporosis

Subcutaneous implant (Implanon)

- Subcutaneous incision upper the arm

- Efficacy up to 3 years

Side effects:

• Irregular bleeding • Periods of amenorrhea

Progestin Intrauterine Device (IUD) (Mirena)

- Device coated with levonorgestrel

- Local effect => thickens the cervical mucus and thins the uterine lining => results in
atrophied endometrium and prevent the advancement of sperms
- Can be effective up to 5 years if implanted before the age of 35 years, and more
than 5 if implanted after the age of 45.

Side effects: (are less due to minimal absorption)

*Copper-coated IUD:

more advantages: spermicidal action, prevent zygote formation, can dislodge the
preformed embryo (emergency action). Can work up to 10 years.
85
Contraindications to IUD:

▪ Pregnancy ▪ Current malignancy

▪ Undiagnosed genital tract
infection
▪ Active infection, PID
▪ Allergy to copper - copper
Side effects:
▪ Wilson disease – copper
▪ Cardiac disease or valvular lesion
– risk of infective endocarditis
▪ Uterine anomalies

▪ Pelvic infection (at 1st 10 days)

▪ Irregular bleeding (more common with copper-coated)
▪ Dysmenorrhea (with copper-coated)

Generally,
COCs

▪ Start it in the 1st day of the cycle POPs

▪ Post-termination: in the 1st week
▪ Start it at any day of the cycle
▪ Postpartum: depend on lactation
▪ Post termination: within the 1st week
not before 6 months if lactating
▪ Postpartum: after 3 weeks (Best
If not lactating start after 3 weeks,
given at 3 weeks is I.M.
Why?
medroxyprogesterone)
- Interfere with uterine involution
- High risk of DVT in the 1st 3
weeks

 exclude pregnancy in all.

IUCD

▪ Inserted 3 days after bleeding has stopped (menses)

▪ At the time of termination
▪ Postpartum can be given at 3 weeks, but later at 6 weeks is better
▪ Complications: 1- vaginal discharge 2- perforation & bleeding
3- expulsion and proximal migration

86
Emergency Contraception

Contraception that given to a woman who is not planning for pregnancy after an un-
protected intercourse.

Chemical

1) Plan B
Levonorgestrel acetate
2 doses - every 12 hours
Very effective if given within 72 hours
2) Yuzpe method
using COCS at high doses
2 doses - 12 hours apart
S.E. (of COCS is more)
less effective than Plan B
3) Progesterone receptor modulator
Ulipristal acetate
can be given up to 5 days
effective as Plan B with less side effects

Mechanical:

• IUCD - copper:
Dislodge of implanted embryo
Can be given up to 5 days
More effective than chemical

 Note: Most effective contraceptive method: male vasectomy / implanon

87
 Subfertility
Def.: Failure of conception after 1 year of regular and un-protected intercourse.

Causes of subfertility:

same causes of amenorrhea + female factors (30%) / male factors (30%) / mixed factor
(30%) / Idiopathic (10%)

Female:

1. amenorrhea: look above

2. Tubal factor:
- PID
- Endometriosis 3. Cervical problem:
- Surgical ligation - Cervical stenosis
- Iatrogenic injury - Cervical anti-sperm antibodies
- Congenital abnormality

Male:

1. Sperm problem: 3. Hormonal effect:

- Klinefelter syndrome - Hypothalamus:
- Testicular torsion Kallmann syndrome,
- Cystic fibrosis => CBAVD => Craniopharyngioma
aspermia - Pituitary problem:
- Mump orchitis Vascular, inflammation,
- Tumors infective, malignancy
- Radiation 4. Systemic disease:
- Immunological problem – anti- - D.M. with vascular
sperm Abs (autoimmune complications,
orchitis) - psychological problems, SCD,
2. Obstruction of vas deference: liver, kidneys
- STD: gonorrhoea, chlamydia 5. Neural:
- Iatrogenic Vasectomy - M.S., spinal cord injury
- Cystic fibrosis CABVD 6. Drugs:
- Congenital anomaly - SSRI, B blockers, sulfasalazine
7. Idiopathic oligospermia
8. Occupation
9. Varicocele

88
Investigations:

Male investigations: start with it

Hx and examination.

1. Semen analysis (stop intercourse 2-7 days then collect sample)

Criteria:
- Volume > 1.5 ml
- Count > 15 million/ml
- Morphology > 4%
- Motility:
32 % progressive
≥ 40 % progressive and non-progressive

Repeated if normal or not after days (6 – 8 weeks)

2. Karyotyping
3. LH/Testosterone hormonal analysis (see interpretations below)
4. Testicular biopsy

Female investigations:

After Hx & relative Ex. Investigation is age-dependent:

• < 35 years investigate after 1 year

• 35 – 40 years => after 6 months
• Immediately if:
- > 40 years
- Previous fertility problem
- Active malignancy
- 2⁰ infertility due to: PID
- Hx of ectopic pregnany

Investigations:

1. Hormonal profile:
- FSH / LH / PRL / Testosterone:
Done in proliferative phase (2nd – 5th) day of start of cycle
- 21st day-progesterone level: (Mid-luteal phase progesterone)
in normal ovulation should be > 30 ng/dl (> 9 mmol/dl)
if abnormal -> luteal phase failure

68
2. Tubal investigations:
a. HSG: (Iodinated dye injected trans-cervical then X-ray) looking For:
i. Patency of tube (spillage of dye in peritoneum)
ii. Hydrosalpinx
iii. Stricture
iv. Peritubal adhesion (abnormal curvature of the tube)
v. Intrauterine adhesions (Asherman’s syndrome) – also can be seen
by hysteroscopy
vi. Fibroid / polyps
vii. Cervical stenosis / incompetence
• S.E.: -hypersensitivity reaction to iodine -nephrotoxicity
• Done in proliferative not luteal phase (to not damage a viable
embryo)
b. Hystero-contrast sonography:
Using Water-soluble contrast (Gastrografin). Seen with USS
Advantages:
▪ Avoid iodine
▪ No damage to fetus (recommended in proliferative phase)
▪ Submucus fibroid and polyp differentiation
c. Laparoscopy and dye test (Gold standard):
Methylene blue dye => in cervix => see it by laparoscope => s pillage from
fimbriae
Advantages: Therapeutics:
▪ Adhesolysis
▪ Laparoscopic Myomectomy (subserosal fibroid)
▪ Reconstruction of tubes
Disadvantages:
▪ Invasive
▪ Need GA
▪ Can’t see inside tube
▪ Dye allergy
3. Other investigations according to the case scenario:
o Kallmann syndrome: genetic analysis
o Craniopharyngioma: skull X-ray (calcification) then MRI
o Pituitary: hormonal analysis and MRI

90
Management:

Prolactinoma TTT: Bromocriptine or Cabergolin +/- surgery if there were pressure

symptoms

Neurological (MS) and other: control the underlying cause.

Localized causes:

o Testicular:

Azoospermia: ICSI after hormonal analysis and biopsy

N.B: biopsy should not be done unless there is a facility for ICSI available, for which
the biopsy can be used for fertility

Classification based on hormonal analysis:

- Primary testicular dysfunction: LH normal – Testosterone low/normal

- Primary testicular failure: LH normal – Testosterone low => Klinefelter →
karyotyping
- Secondary testicular dysfunction: LH high – Testosterone low/normal

If idiopathic:

Assisted reproductive techniques:

IUI (intra-uterine insemination) => pt. with antibodies problem, oligospermia

IFI (intra-fallopian insemination) => sperm motility problem

IVF (in vitro fertilization)

ICSI (Intracytoplasmic Sperm Injection)

IUI: => if mild male factor subfertility, mild motility problem, antibody present => IVF &
ICSI

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ART cycle:

1. Counselling
2. USS to exclude local abnormality
3. Urine analysis for infection
4. Suppress hypothalamus: GnRH analogue => -ve feedback of endogenous hormone
5. Ovarian stimulation: Give hMG (human menopausal gonadotropin) or FSH to
stimulate growth of follicle
6. Measure growth of follicle; Follicle Tracking Scan: To know the number and size of
stimulated follicles;
- we need dominant follicle > 11mm at the time of ovulation,
- if 5 follicles with size of > 11 mm → cancel the cycle, because ↑ risk of
ovarian hyper-stimulation syndrome and multiple pregnancy
- If 2 or less → induce ovulation by ß-hCG – collected from a pregnant woman
7. Once induce ovulation → provide luteal phase support by progesterone
8. Retrieval of the ovum outside and mix it with sperm
9. When to return them back to uterus?
2-3 days after fertilization (cleavage embryo)
better wait up to 5 days (blastomere)
10. Confirm pregnancy by ß-hCG (last step)

Problem of the cycle:

• Risk of multiple pregnancy

• Ovarian hyper-stimulation syndrome:
- growth of multiple dominant follicles, results in accumulation of fluid in 3rd space
(pleura, peritoneum,..)
- hemo-concentration, dehydration and hypercoagulability
- Risk factors:
1. GnRH analogue (use more than C. Citrate)
2. Young age
3. Low BMI
4. PCOS
-

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- Presentation: mild/moderate/severe
1. pleural effusion -> SOB
2. abdominal distension
3. pelvic congestion and pain
4. dehydration: syncope, headache, fatigability, tachycardia, palpitation
5. DVT, PE, venous sinus thrombosis
6. MI
- Investigations:
CBC, coagulation profile, RFT with U&E, urine analysis, abdomino-pelvic USS =>
follow up the follicle
- Management:
1. stop cycle immediately, don’t induce ovulation
2. manage symptoms:
- chest tube
- paracentesis
- give albumin
- hydrate the pt
- anticoagulation
3. pt. may need more invasive method:
- intubation respiratory arrest
- inotropic agent hypotension

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 Infections
Vaginal discharge:

Physiological: Abnormal, pathological discharge:

At time of puberty, pregnancy, use of Infections, cervical ectropion, cervical

COCs, IUCD, mid cycle polyps, FB, endometrial hyperplasia

Infectious causes of pathological vaginal discharge:

1- vaginal candidiasis
2- bacterial vaginosis
3- Trichomonas vaginalis

Vaginal candidiasis:

By Candida Albicans

Risk Factors: usually immunocompromised pts, antibiotics usage, contraception, DM,

HIV, steroid use

Presentation:

1. vulvar itching,
2. cheese-like discharge (thick whitish)
3. vaginal erythema

Confirm:

- lower vaginal swab for microscopy, preparation by KOH media => to see pseudo-
hyphae and spores
- pH: low (normal 3.8 – 4.2) => reduction of no. of normal flora (lactobacilli)

Management:

- Topical azole drugs; Clotrimazole suppositories / gel for 5 days, Or

- Oral single dose Fluconazole

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Bacterial Vaginosis:

Not an inflammatory condition; occur as a result of growth of Gardenella vaginalis and

other anaerobic bacteria

Presentation:

1. pH change
2. no itching
3. offensive, fishy, grey-white discharge that occurs peri-menstrual
4. no inflamed red vagina

Investigation/diagnostic criteria: Amsel criteria (3 to make a diagnosis)

1. take sample and put KOH on it → it will result in a fishy smell (Whiff test)
2. pH ≥ 4.5
3. Presence of clue cells (by microscope => vaginal epithelium covered by
Gardenella vaginalis on its surface)
4. discharge that is grey-whitish or yellow semi-watery

Management:

Clindamycin or Metronidazole

Complications:

- high recurrence rate

- Risk of preterm labor, PPROM, 2nd trimester miscarriage

Trichomonas:

Sexually transmitted protozoal infection

No cyst stage.

Inflammation of the vagina and endocervix

Presentation:

1. Offensive yellowish greenish discharge

2. No itching
3. Inflamed red = Strawberry cervix

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Diagnosis: high vaginal swab

demonstration of motile trophozoite on wet mount preparation by normal saline

under microscopy.

Treatment:

- Metronidazole or Tinidazole
(treat for 5-7 days in case of infection outside pregnancy,
2 gm single dose during pregnancy)
- treat the partner to decrease the recurrence

Chlamydia Trichomatis:

Most common cause of PID

- inflammation of the urethra (non-gonococcal urethritis NGU)

- cervicitis
- Endometritis
- Tubo-ovarian abscess .
- Pelvic peritonitis

Presentation of PID:

thin watery whitish vaginal discharge not associated with itching

commonest presentation is asymptomatic (in male and female)

Diagnosis: endocervical swab

1. nucleic acid amplification test by PCR (diagnostic test of choice)

2. complement fixation test for detection of antibody.

Management:

- Tetracycline: doxycycline for 7 days, Or

- Macrolide: azithromycin single dose.
- and treat the sexual partner

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Neisseria gonorrhoea:

STD

Presentation:

Same presentation as chlamydia infection, but the vaginal discharge is thick leuko-
purulent (contain pus)

Diagnosis: endocervical swab

1. the gold standard test for diagnosis of neisseria is by microscopy

2. culture and sensitivity

Management:

- Most Neisseria infections are associated with chlamydia so treat chlamydia

empirically after diagnosis of Neisseria
- Treatment of Neisseria: single injection of ceftriaxone + 1 gm oral dose of
azithromycin.
- If ceftriaxone is contraindicated or not available you may give injection of an
aminoglycoside: spectinomycin + oral azithromycin.
- If IM injection is contraindicated give cefixime + oral azithromycin

PID:

Inflammation of an internal pelvic organ

75% mixed causative organisms, but the most common isolated cause is chlamydia
trachomatis

Risk factors:

1. multiple sexual partners

2. use of no barrier method

(Barrier and COCS are protectors)

3. IUCD

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PID divided as involvement of 4 structures:

1. Inflammation of endometrium.
2. ovaries.
3. fallopian tube.
4. pelvic peritoneum.

Complications:

Acute PID Chronic PID

• Tubo-ovarian abscess • Chronic pelvic pain

• Adhesion formation • Subfertality
(intrauterine adhesion, peritubal • Ectopic pregnancy
adhesion which may result in • Periappendicitis
diverticulum of the tube causing • Perihepatitis fitz-Huge-curtis
hydrosalpinx) syndrome
• Sepsis and septic shock
• Pelvic peritonitis

Clinical picture:

• fever, sweating, palpitation • dyspareunia

• abdominal pain • dysmenorrhea
• pelvic discharge • irregular bleeding (rare)
Acute PID investigation:

1. CBC: increase PMNL, high ESR and CRP

2. endocervical swab
3. abdominopelvic USS to localize abscess and hydrosalpinx.
4. urine analysis (concomitant urethritis)

Treatment of acute PID:

Admission if:

Severe toxicity, persistent vomiting, failure to respond to oral medication, tubo-ovarian

abscess, shock.

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Inpatient Management:

1. Hydration: IV fluids
2. analgesia and antipyretics
3. broad spectrum antibiotic (IV ceftriaxone + oral metronidazole and doxycycline)
(Second choice IV ofloxacin + IV metronidazole)
*Change to oral when fever subsides
4. Laparoscopy aspiration of abscess or laparotomy

Outpatient management:

1. (ofloxacin + metronidazole) oral as first choice, at home.

2. ceftriaxone injection at hospital then oral metronidazole and doxycycline at home.

Management of chronic complications:

- Diagnostic and therapeutic laparoscopy.

- adhesiolysis and release of periheptic adhesion and treatment of hydrosalpinx .

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 Tumors
Uterine:

▪ Most common genital organ malignancy

▪ Age: 55 and above
▪ 2 types:
o Type I: endometrioid adenocarcinoma (commonest).
o Type II: serous or clear adenocarcinoma.

Type I: Endometrioid adenocarcinoma:

Risk factors for endometrioid adenocarcinoma:

1. Age more than 55 6. granulosa cell tumor (estrogen
2. Obesity secreting ovarian tumor)
3. DM 7. unopposed estrogen therapy
4. HTN 8. Tamoxifin
5. PCOS 9. Nulliparity
10. Early menarche
Protective factors: Smoking and COCS.

Presentation:
• usually present at stage 1: with post-menopausal bleeding
• post coital bleeding in advance (cervical involvement)
• pelvic pain (pelvic peritoneum deposition)
• metastatic spread.
 {post-menopausal bleeding is endometrial CA until prove otherwise}

Approach:
DDx of post-menopausal bleeding:
Investigation: To confirm and staging 1. urogenital atrophy.
2. endometrial polyp or
a- To confirm the diagnosis: hyperplasia.
A biopsy for histopathology: done by: 3. cervical polyp.

1. aspiration (by Pipelle or Vabra): not representative, blind.

2. D and C
3. Hysteroscopy biopsy (best approach), with local or general anaesthesia,
outpatient or inpatient procedure, => direct visualization + therapeutic (if you
find polyp can remove it)

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b- Staging: dependent upon biopsy:
Stage I: cancer confined to the uterus
Stage II: spread from the uterus to the cervix
Stage III: spread outside the uterus but not outside the abdomen
Stage IV: distant metastasis or involvement of bladder or rectal mucosa

*This malignancy can spread through Pelvic node to the Para aortic lymph node.

Treatment:
- No rule for chemotherapy.
- Mainly surgical management:
total abdominal hysterectomy +/- bilateral salpingo-oophorectomy
- Radical radiotherapy if the patient cannot tolerate surgery

Stage I and II: radical hysterectomy or radical radiotherapy

Stage III (locally advanced): radical surgery + adjuvant radiotherapy locally to prevent
the local recurrence.

Stage IV:

1. Palliative radiotherapy
2. Hormonal therapy (progesterone)

Type II: Serous adenocarcinoma

rare – not an exam Q.

Endometrial hyperplasia:

A precursor for malignancy

2 types: simple and complex. both of them can be typical and atypical.

- simple: there is stroma between the glands

- complex: no stroma between the glands

Management:

Progesterone, unless there is atypia

Atypia => hysterectomy

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Cervical:

- Anatomy: endo and ectocervix, junctional zone between them.

ectocervix: squamous epithelium (acidic)
endocervix: columnar (alkaline)
- During the reproductive age under the effect of estrogen the columnar zone extend
to the ectocervix and the squamous cells decrease, this will expose the alkaline
endocervix to the acidity of the vagina → leading to metaplasia = transformation
zone.
- The transformation zone is a suitable area for HPV 16 and 18 infection which will
result in metaplasia then dysplasia.

=> Precursor lesions for cervical cancer:

▪ Cervical Intraepithelial Neoplasia: According to the depth of the dysplasia:

CIN I involves only the lower 1/3
CIN II involves the lower 2/3
CIN III involves all thickness
▪ Other new classification:
1. High grade squamous intraepithelial lesion: CIN II and III.
=> higher risk of progression to malignancy.
2. Low grade squamous intraepithelial lesion: CIN I and infection with HPV.
=> most patients regress spontaneously.

presentation of cervical intraepithelial neoplasia is usually asymptomatic and detected

incidentally by pap smear.

changes by HPV in the cells:

1. change the shape of the nucleus (poikilocytosis)

2. change the density of the nucleus (koilocytosis)
3. perinuclear hallow (zone of clearance around the nucleus)

Pap smears for screening:

Age of 25-64 years in developed countries, as follows:

- 25-50 every 3 years

- 50-64 every 5 years

The Pap smear will detect the change in the transformation zone.

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The commonest type of cervical carcinoma is squamous cell carcinoma but other types
like adenocarcinoma also occur, but it cannot be detected via pap smear (cannot detect
glandular change).

Results of Pap smear:

i. CIN I: screen for high risk HPV:

+ve => go for colposcopy
-ve or low risk HPV => repeat smear every 6 months for 3 times
if no regression => go for colposcopy
ii. CIN II and III or abnormal glandular epithelium => go for colposcopy

Colposcopy:

Device with magnifying lens, visualizes the area of the transformation zone and allows
the following:
▪ Looking for gross abnormalities like;
- Irregular surface of cervix in invasive malignancy
- Easily bleed mucosa in invasive malignancy

What changes you see in colposcopy?

1. abnormal blood vessels,

2. blood vessel could be mosaic in shape with punctuation (coma shape).
3. invasive carcinoma.
▪ Application of acidic acid => abnormal cell will take it up, resulting in white (aceto-
white epithelium)
▪ Application of Lugol's iodine stain => abnormal cells will not be colrized. While the
high glycogen content of normal cells take the color of the iodine.
▪ biopsy/punch biopsy of cervix.

Management of CIN:

CIN I: have a chance of regression => watch and wait.

CIN II and III: large loop excision of transformation zone

*in the past the management was conization and destruction by gamma knife, but it has
the disadvantage of inability to do re-biopsy looking for recurrence

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Cervical cancer:

- Squamous cell carcinoma (commonest)

- Pap smear decrease the incidence of squamous cell carcinoma not adenocarcinoma

Risk factors:

1. HPV infection (high risk) 5. Early age of the first sexual

2. Smoking intercourse
3. Immunosuppression 6. multiple sexual partner
4. Multiparity (the only genital 7. COCS
malignancy associated with
multiparity)

Peak of incidence:

1. at reproductive age group (35-45 years)

2. after 70 years

Presentation:

1. Incidentally
2. Postcoital and intermenstrual bleeding or post-menopausal bleeding
3. Advance malignancy:
- acute renal failure (commonest cause of death due to compression of the
ureter → hydroureter → hydronephrosis)
- The dissemination of cervical cancer into the surrounding tissue result in the
formation of fistula (cervico-vesical fistula or vagino-vesical fistula).
- Uterus, intra-pelvic and intra-abdominal spread of metastasis.

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Diagnosis of cervical cancer:

a- Confirmation: Punch biopsy.

b- Staging:
1. examination under anaesthesia
2. Cystoscopy
3. Hysteroscopy
4. Sigmoidoscopy
c- Other investigations; RFT, Abdominal USS (kidneys and lymph nodes)

Staging with MRI (if available):

- Stage I: localized to the cervix

- Stage II: has involved the cervix and the uterus
- Stage III: spread outside the uterus and cervix to the perimetrium and the
upper 1/3 of the vagina.
- Stage IV: distant metastasis or involvement of rectal and bladder mucosa

Management:

1. Radiotherapy to all stages

2. Chemotherapy not effective
3. Surgery is the main form of management

N.B: Stage I and II are considered: early. Stage III: locally advanced. Stage IV: advanced.

Stage Ia or if she want to conceive: remove the affected part only => Trachelectomy.

Stage Ib and early II: surgery in form of modified radical hysterectomy => remove the
uterus, cervix, upper part of the vagina, and nearby ligaments and tissues. Nearby lymph
nodes may also be removed, if L.N. samples were suspicious. + ligate the uterine artery
+/- give adjuvant radiotherapy (if L.N were affected).

Late stage II and stage III: chemoradiotherapy

Stage IV: Palliative chemoradiotherapy

Locally advanced malignancy of the cervix: exenteration

Anterior exenteration: remove the uterus, cervix and bladder

Total exenteration: remove the uterus, cervix, bladder and the lower part of the
rectum – this operation is now avoidable due to resultant severe psychological
trauma.

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Ovarian Tumors:

Malignant ovarian tumors are considered

as leading cause of death.

Benign:

Follicular cyst:

- Due to atresia of dominant follicle

or failure of atresia of non-
dominant follicle.
- Occur in follicular phase i.e. in
reproductive age group
- Size up to 6-8 cm
- Detected by ultrasound but no symptoms usually

Management:

▪ If smaller than 6 cm => ignore

▪ if larger than 6 cm => repeat USS after 6 weeks
if not resolved rescan and reassure the patient but you can
remove it if the patient want to
▪ If symptomatic => laparoscopic cystectomy

Corpus luteal cyst:

- Failure of regression of corpus luteum

- The normal size of corpus luteum is less than 3 cm
- The corpus luteal cyst is more than 3 cm and can reach up to 15 cm
- In > 90% of cases, it occurs in the right ovary
- Occur late in cycle and it may need analgesia
- Can be complicated by haemorrhage or rupture.
- Management: Whether symptomatic or asymptomatic => Remove it by laparoscopy

Benign neoplastic cysts:

1. Germ cell (most common is dermoid cyst)

2. Stroma cell
3. Epithelial cell

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Dermoid cyst (Mature Cystic Teratoma)

- Occur at young age

- Bilateral
- Size up to 10 cm
- Histology: All types of cells can be found in it
- Effects: mechanical or non-mechanical
Mechanical:
1. Torsion
2. rupture and chemical peritonitis
3. chronic granulomatous peritonitis.
Non-mechanical:
o malignancy (in endoderm derivative, in form of squamous cell cancer)
o Struma Ovarii (contains thyroid tissue lead to high levels of T3 and T4)
o carcinoid syndrome (by production of bradykinin and serotonin)
- Note: Mature Solid Teratoma is difficult to differentiate from malignant so it is
managed as malignant.

Epithelial cell tumors (derived from celomic epithelium):

Serous cystadenoma

- Most common benign epithelial cell tumor

- Cyst is unilocular.
- Contains Psammoma bodies (also found in meningioma and papillary thyroid
cancer)

Mucinous cystadenoma

- large and multilocular, secretes a lot of mucous

- Can cause abdominal distention and urinary tract symptoms
- Contents can be spelled in the peritoneum leading to pseudomyxoma peritonei
- These cells can differentiate into Endometrioid adenocarcinoma
- It is said to be associated with endometriosis

Brenner’s tumor

- Originate from transitional epithelium of urinary tract

- Non cystic, i.e. solid
- Secrete hormones

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Stromal cell tumor

In females :

Granulosa cell Tumor:

- Low malignant potential but not benign

- Post-menopause
- Secretes estrogen (this can lead to premature puberty if occurred early, or
endometrial hyperplasia and endometrial cancer if occurred later in life)

Fibroma.

- Solid
- Can lead to Meigs' syndrome: right-sided pleural effusion + ascites

In males:

Leydig and sertoli cell tumor:

- Low malignant potential

- Secrete androgens and lead to virilization

Investigations (for ovarian tumor):

Abdominopelvic USS to visualize the tumor (unilocular or multilocular , unilateral or

bilateral, homogenous or heterogenous)
Features that may suggest benign tumor: less than 6 cm, unilateral, unilocular,
homogenous, not calcified (and the opposite is most likely malignant)

Management of benign ovarian tumors:

- if the patient is in reproductive age group < 45 years => remove the cyst
- if the cyst is more than 10 cm -regardless the age of the patient-, there is malignant
features and CA-125 is high => unilateral oophorectomy by laparoscopy
- postmenopausal age > 45 years => it is unlikely to be benign so no rule for
conservative management
- features of benign tumor => follow up by CA-125 and USS with Color Flow Doppler
every 3-6 months
- high suspicious of malignancy => total abdominal hysterectomy + bilateral
salpingoopherectomy

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  Staging of ovarian cancer is by surgical laparotomy

Malignant:

Risk factors:

- Increase age
- Nulliparity
- Early menarche late menopause
- Family history of: ovarian cancer, breast cancer, colorectal cancer, uterine cancer
- Subfertility
- Ovulation induction medication, especially clomiphene citrate usage
✓ Multiparty and combined oral contraceptives are protective

Germ cell tumors:

▪ Differentiated:
• Embryonic differentiation
o Immature Solid Teratoma:
Usually < 20 years of age
High capacity to disseminate hematogenously
Tumor markers: can secrete both α-fetoprotein and ß-hCG
Different tissues inside can underwent further malignant transformation
Associated with para-neoplastic syndromes: autoimmune encephalitis
• Extra-embryonic differentiation
o Choriocarcinoma:
Compose of 2 types of cells: cytotrophoblasts and syncytiotrophoblast
Highest malignant potential with the highest metastatic potential
To Liver, lung… via hematogenous spread
Tumor marker: ß-hCG
o Yolk-sac tumor (epidermal sinus tumor):
Age: as early as 4-6 years
Usually male baby
Tumor marker: α-fetoprotein

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▪ Undifferentiated:
• Dysgerminoma:
Solid mass
Tumor marker: Lactate dehydrogenase (as seminoma)
Germ cell tumors are the most likely curable tumors

Epithelial cell tumors:

▪ Serous cystadenocarcinoma
▪ Mucinous cystadenocarcinoma
▪ Brenner’s adenocarcinoma
▪ Endometrioid adenocarcinoma
▪ Clear cell adenocarcinoma
 The last two are associated with endometriosis

Stromal cell tumors:

▪ Granulosa cell tumor

▪ Sertoli and Leydig cell tumor

Management of ovarian Malignancy:

o No rule for radiotherapy

o Mainly surgical management: Achieved by maximum debulking procedure:
Laparotomy → total abdominal hysterectomy + bilateral salpingoopherectomy +
infra colic-omentectomy + lymph node dissection + peritoneal washing
o For locally advanced tumors (involving pelvic wall) => neoadjuvant chemotherapy,
followed by maximum debulking procedure, followed by adjuvant chemotherapy
 Second look procedure is not done now
o Chemotherapy used in ovarian cancer:
- platinum-based drug such as cisplatin
- taxane such as paclitaxel
o Management of germ cell tumors is usually achieved by minimal surgical procedure
laparoscopy or laparotomy for unilateral oophorectomy, followed by chemotherapy
(they are highly responsive to chemotherapy)

*********

110
..‫تم بحمد هللا‬

These notes were typed and revised from voice records of Dr. M. Tmbool

Credits:

Abdelraheem Farah

Hiba Basheer

Lamees Mohammed

Aya Kambal

Samar Moawia

Yusra Elsiddig

Duaa Fadlalah

Ahmed Omer

Eman Saeed

Walaa Basheer

Romaisaa Ismail

Ahmed Shadad

Israa Alrayah

Aya Salah

Hala Abdelaziz

Nanaa’ Abdelwakeel

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