TYPES OF ABORTION

FEATURES
History Mild vaginal bleeding.
No abdominal pain or mild abdominal pain
2. Examination Good general condition.
The cervix is closed
The uterus is usually the correct size for date
3. U/S which is essential for the diagnosis Showed the
presence of fetal heart activity

THREATENED
ABORTION

1.

INEVITABLE
ABORTION

1. History
Heavy vaginal bleeding.
with no passage of products conception (inevitable)
with passage of products of conception (incomplete
abortion)
Severe lower abdominal pain which follows the
bleeding
2. Examinations
Poor general condition.
The cervix is dilating and products of conception may
pass thru the os
The uterus may be the correct size for date (inevitable
abortion) or small for date (incomplete abortion)
3. U/S Fetal heart activity may or may not present in
inevitable abortion or retained products of conception
(RPOC) in incomplete abortion
1. History
Heavy vaginal bleeding which has been stopped.
Lower abdominal pain which follows the bleeding
which has been stopped.

INCOMPLETE
ABORTION

COMPLETE
ABORTION

MANAGEMENT
1. Reassurance If fetal heart activity is
present, > 90% of cases will be
progressed satisfactorily
2. Advice: Decrease physical activity, avoid
intercourse
3. Hormones i.e. Progesterone & hCG to
support pregnancy, (no proven value)
4. Anti- D: Adequate dose of anti-D should
be given to all Rh ve, non-immunised
patients, whose husbands are Rh +ve
5. ANC as high risk patients
Coz liable to late pregnancy complications
such as APH and preterm labour.
1. CBC , blood grouping , XM 2 units of blood
2. Resuscitation large IV line, fluids &
blood transfusion
3. Oxytoxic drugs Ergometrine 0.5 mg IM
+
Oxytocin infusion (20-40 units in 500
cc saline)
4. Evacuation & curettage.
5. Post-abortion management.

1. Evacuation & curettage in the presence of

RPOC.
2. Post-abortion management.

MISSED
ABORTION

ANEMBRYONI
C
PREGNANCY
(BLIGHTED
OVUM)

2. Examination: The cervix is closed

3. U/S : Showed empty uterine cavity or PROP
1. Most are diagnosed accidentally
1. CBC , blood grouping, XM 2 units of blood
during routine U/S in early pregnancy. 2. Platelets count: to exclude the risk of DIC
In some cases there may be a history
NB : DIC does not occur before 5 weeks of missed abortion or
of:
IUFD and if occurred will be of mild grade
Episodes of mild vaginal bleeding 3. Options of treatment
Conservative treatment: if left alone spontaneous
Regression of early symptoms of
expulsion will occur
pregnancy.

Surgical evacuation of the uterus; by D & C: Indicated in 1 st

Stop of fetal movements after 20
trimester missed abortion
weeks gestation.
Medical termination of pregnancy: by Misoprostol (PGE1)
2. Examination: The uterus may be
small for date
Cytotec: Indicated in 1st & 2nd trimesters missed abortions.
3. U/S (essential for dx) diagnosed if
Cytotec vaginal ( is the best) or oral tab. 200 g, 2 tab/ 3
two ultrasound (T/V or T/A) at least
hrs/ up to 5 doses daily, which can be repeated next day if
7days apart showed an embryo of >7
there is no response in the first day
wks gestation (CRL >6mm in
Subsequent surgical evacuation is needed in cases of
diameter and gestational sac >20
RPOC
mm in diameter) with no evidence of
Main side effects of cytotec: Nausea, vomit & fever.
heart activity.
3. Post-abortion management.
It is due to an early death and resorption of the embryo with the persistence of the placental tissue
It is diagnosed if two ultrasound (T/V or T/A) at least 7 days apart showed after 7 weeks of gestation
i.e. gestational sac >20mm, an empty gestational sac with no fetal echoes seen.
It is treated in a similar way to missed abortion.

SEPTIC
ABORTION

Def: Incomplete abortion complicated by infection of the uterine

contents. May be due to criminal interference.
Features : Poor general condition
Features of incomplete abortion: Severe vaginal bleeding with
passage of product of conception, with/without hx of evacuation.
Features of pelvic infection: Pyrexia , tachycardia , general malaise
, lower ab pain, pelvic tenderness & purulent vaginal discharge.
Bacteriology : Mixed infection
The commonest organisms are :
1. Gram -ve: E.coli , strep & staph
2. Anaerobics: Bacteroides
Rarely Cl. tetani - potentially lethal if not treated adequately.
Types :
Mild the infection is confined to decidua : 80%
Moderate the infection extended to myometrium15%
Severe the infection extended to pelvis + Endotoxic shock +
DIC 5%

1. Investigations :
CBC, blood grouping, XM 2
units of blood.
Cervical swabs (not vaginal)
for culture and sensitivity
Coagulation profile , serum
electrolytes & blood culture
if pyrexia > 38.5
2. Antibiotics: IV Cephalosporin +
IV Metronidazole
3. Surgical evacuation of uterus
usually 12 hrs after
antibiotic therapy (until
reasonable tissue levels of
antibiotics achieved)
4. Post-abortion management.

RECURREN
T
ABORTION

Definition: 3 or more consecutive spontaneous abortions

It may presented clinically as any of other
types of abortions .
Types :
Primary: All pregnancies have ended in loss
Secondary: One pregnancy or more has proceeded
to viability (>24 weeks gestation) with all others
ending in loss.
Incidence: Occurs in about 1% of women of reproductive
age .
Causes
Idiopathic recurrent abortion, in about 50%, in which
no cause can be found .
The known causes include the followings :
1. Chromosomal disorders:
Fetal chromosomal abnormalities & structural
abnormalities
Parental balanced translocation
2. Anatomical disorders:
Cervical incompetence: congenital and
aquired
Uterine causes: submucous fibroids, uterine
anomalies & Ashermans syndrome
3. Medical disorders:
Endocrine disorders : diabetes , thyroid disorders ,
PCOS & corpus luteum insufficiency.
Immunological disorders: Anticardiolipin syndrome
& SLE.
Thrombophilia: congenital deficiency of Protein
C&S and antithrombin III, & presence of factor V
Leiden.
Infections
ToRCH - CMV may be a cause of recurrent

Diagnosis :
1. History :
Previous abortions : gestational age and place
of abortions & fetal abnormalities.
Medical history : DM , thyroid disorders,
PCOS, autoimmune diseases & thrombophilia.
2. Examination :
General : weight, thyroid & hair distribution
Pelvic: cervix (length & dilatation) and uterine
size.
3. investigations :
A. Investigations for medical disorders:
Blood grouping & indirect Coombs test in
Rh ve women
Endocrinal screening: Blood sugar , TFT &
LH /FSH ratio
Immunological screening: Anti
anticardiolipin antibodies & lupus inhibitor.
Thrombophilia screening: Protein C & S,
antithrombin III levels, factor V leiden, APTT
and PT.
Infection screening
High vaginal & cervical swabs
ToRCH profile (which scientifically is
unnecessary)
B. Investigations for anatomical disorders:
TV/US: fibroids, cervical incompetence &
PCOS.
Hysteroscopy or HSG, fibroids, cervical
incompetence, uterine anomalies &
Asherman's syndrome
C. Investigations for chromosomal disorders:
Parental karyotyping: Parental balanced

abortion, but ToRH are not causes of

recurrent abortion.
Genital tract infection e.g Bacterial
vaginosis
Rh isoimmunization

translocation.
Fetal karyotyping: Fetal chromosomal
anomalies.

Management
Idiopathic Recurrent Abortion
In the Presence of Cause
With support and good antenatal care , the chance of Treat the cause
successful spontaneous pregnancy is about 60-70%
Endocrine disorders
Support : from husband, family & obstetric
Control DM and thyroid disorders before
staff.
pregnancy
Advice : stop smoking & alcohol intake,

Ovulation induction drugs , ovarian drilling

or IVF in PCOS.
decrease physical activity

Progesterone or hCG in corpus luteum

Tender loving care
insufficiency
.
Drug therapy

In
anti-cardiolipin
syndrome:

Progesterone & hCG: start from the luteal

Low dose aspirin ( 75 mg/day ) & prednisilone
phase & up to 12 weeks.
( 20-30 mg / day), starting when pregnancy is
Low dose aspirin ( 75 mg/day ) start from
diagnosed till 37 weeks.
the diagnosis of pregnancy & up to 37
These drugs are not teratogenic.
weeks
In thrombophilia:
LMWH (20-40 mg/day) start from the
Low dose aspirin ( 75 mg/day) starting when
diagnosis of fetal heart activity & up to 37
pregnancy is diagnosed and low molecular weight
ws
heparin ie LMWH ( 20-40 mg/day) starting when fetal
heart activity diagnosed & to continue both till 37
weeks .
In uterine disorders
Cervical cerclage in cervical incompetence,
best time at the 14 weeks of pregnancy.
Myomectomy in submucus fibroid, excision of
uterine septum in septate & subseptate
uterus & adhesolysis in Asherman's
syndrome.
In infection:: treatment of the genital tract

infection.
In Rh isoimmunization: Repeated intrauterine
transfusion
In parental balanced translocation
Explain the risk of fetal chromosomal
disorders ( about 30% )
Encourage to try again or adoption.

COMPLICATIONS OF ABORTION
1. Haemorrhage .
2. Complication related to surgical evacuation ie E&C
and D&C.
Uterine perforation- which may lead to rupture
uterus in the subsequent pregnancy.
Cervical tear & excessive cervical dilatation
which may lead to cervical incompetence.
Infection may lead to infertility & Asherman's
syndrome.
Excessive curettage which may lead to
Adenomyosis
3. Rh- iso immunisation if the anti D is not given or
if the dose is inadequate .
4. Psychological trauma.

POST-ABORTION MANAGEMENT
In cases of incomplete, inevitable, complete, missed & septic
abortions
1. Support: from the husband, family& obstetric staff
2. Anti D to all Rh ve, nonimmunised patients, whose
husbands are Rh+ve
3. Counseling & explanation:
A. Contraception (Hormonal, IUCD, Barrier) Should start
immediately after abortion if the patient choose to
wait , because ovulation can occur 14 days after abortion
and so pregnancy can occur before the expected next
period .
B. When can try again :
Best to wait for 3 months before trying again . This time allow to
regulate cycles and to know the LMP, to give folic acid, and to
allow the patient to be in the best shape (physically and
emotionally) for the next pregnancy
C. Why has it happened
In the fiIn the majority of cases there is no obvious cause
In the first trimester abortion, the most common cause is fetal
chromosomal abnormality.
D. Can it happen again
As the commonest cause is the fetal chromosomal abnormality
which is not a recurrent cause, so the chance of successful
pregnancy next time in the absence of obvious cause is very
high even after 2 or 3 abortions
E. Not to feel guilty as it is extremely unlikely that
anything the patient did can cause abortion
No evidence that intercourse in early pregnancy is harmful
No evidence that bed rest will prevent it ..

MISCARRIAGE
(ABORTION)
Def: Expulsion or extraction of products of conception before fetal viability i.e. before 24 weeks of gestation.
Incidence :
Is the commonest gynaecological & obstetric disorder
About 15% of clinically recognized pregnancies end in abortion (this rise to 30% if unrecognized pregnancies are
included).
Most abortions occur between 8 and 12 weeks of pregnancy.
ETIOLOGY
1st Trimester Abortion
2nd Trimester Abortion
1. Fetal chromosomal abnormalities - particularly trisomy, triploidy & monosomy
1. Multiple pregnancy
- is the commonest cause of abortion
2. Cervical incompetence (congenital &
- 50 70 % of the first trimester abortions are due to chromosomal abnormalities
acquired )
- the incidence of these abnormalities increased with the increase in the maternal 3. Uterine anomalies and submucous
age
fibroid
2. Anembryonic pregnancy - Blighted ovum
4. Genital tract infection and PROM
3. Multiple pregnancy
4. Parental balanced translocation
5. Infections: genital tract infection , systemic infection with pyrexia & ToRCH
syndrome
6. Endocrine disorders : Diabetes, thyroid disorders , PCOS & corpus luteum
insufficiency
7. Uterine disorders: Uterine anomalies , submucus fibroid & Ashermans
syndrome
8. Thrombophilia: Congenital deficiency of protein C & S, & anti-thrombin III
9. Immunological disorders : Anticardiolipin syndrome and SLE
10. Cigarette smoking, anaesthetic agents & chemical agents.
11. Psychological disorders

LABOR PAIN
1ST STAGE
Uterine contractions
which cause myometrial
ischemia. The pain felt
Through hypogastric
plexuses, pre aortic
plexuses to spinal cord
through (T10-L1)
Cervical dilatation. Felt
through nerve entering to
sacral root.
At this stage this pain is
visceral pain, diffuse,
poorly localized, in lower
abdomen radiated to the
back.

SOURCES OF PAIN
2ND STAGE
1-Uterine contractions
2-Stretching of the vulval
orifice
3-Pressure on the pelvic floor
2+3 felt through pudendal
nerve (S2,3,4) mainly ilioinguinal, genitofemoral,
posterior femoral cutaneous
nerve.
This pain is somatic pain.

3RD STAGE
Is usually well
tolerated with
spontaneous placental
delivery.
Analgesia may be
necessary for manual
extraction.

PATHWAYS OF PAIN DURING LABOR

The body of uterus and cervix
are supplied by autonomic
nervous system (T10-L1)
through Hypogastric and Preaortic plexuses.
Vulva, perineum are supplied
by:-somatic nerve,
-Pudendal N S2-S4
-Genitofemoral N L1-L2
-Post. Femoral coetaneous N S1S3.

NON-PHARMALOGICAL
METHOD
Psychoprophylaxis (Lamaze
method): Emphasized
relaxation coupled with a
variety of patterned
breathing techniques.
Emotional support.
Massage.
Warm water baths.
Transcutaneous Electrical
Nerve Stimulation (TENS).
(works on blocking pain
fibers in the posterior
ganglia of the spinal cord).
Hypnosis.
Acupuncture.

No definitive evidence.

ANALGESIA IN LABOR
PHARMACOLOGICAL METHOD
Best Analgesics those that provide rapid onset, with Minimal to No impact on:
Progression of Labor, Maternal Vital Signs, Fetal Vital Signs, Maternal Passages, and
Uterine contractions
INTRATHECAL ANALGESIA
INHALATIONAL ANALGESIA
Provide better analgesia than
o More effective than opioids and is widely used.
parenteral opioids:
o Most commonly used mixture is Entonox (an
Provide rapid onset of relief.
equal mixture of NO & Oxygen).
Can have a long duration of
o Provides quick with short duration of effect.
action.
o Not suitable for prolonged use from early labor,
Typically cause no degree of
so most suitable is late in labor or while awaiting
motor blockade.
epidural analgesia.
Routinely cause no effect on
o Adverse effects include nausea & light
the fetus.
headedness.
Problems with Intrathecal Opiods.
o It is removed from the body unchanged via the
Pruritus (60-100%).
lungs, and does not accumulate under normal
conditions, explaining the rapid offset.
Nausea (25-60%).
o
Not suitable for prolonged use from early
Urinary retention (10-35%).
labor(bcoz hyperventilation may result in
hypocapnea , tetany , fetal hypoxia, so most
suitable is late in labor or while awaiting epidural
analgesia.

ANALGESIA IN LABOR
PHARMACOLOGICAL METHOD
PARENTERAL NARCOTICS
Easy administered.
Work best in early first stage, when pain is primarily visceral and less intense.
Cross placental barrier and so it affects fetus.
Narcotics can be given IV, IM or by Continuous infusion, in what is called PCA.
Naloxone is a narcotic antagonist, that is injected into the umbilical vein in Opioids toxicity cases
PETHIDINE
FENTANYL
BUTORPHANOL
One of the most widely used
Synthetic, more potent than other
Synthetic analgesic.
systemic opioids for labor analgesia.
opioids, so caution is necessary to
40 times more potent than
Work best in early 1st stage when
avoid serious respiratory
Pethidine.
depression.
pain is visceral.
Duration 2-4 hours.
Rapid onset , Short action.
T1/2(2-4 hour)
It antagonizes the narcotic effects of
Continuous pulse oximetry
Usually given IM
Pethidine, and therefore not given
monitoring and close nursing
Quick placental transfer
together.
surveillance
are
also
needed.
Causes drowsiness and dizziness.
Pethidine does not inhibit uterine
Side effect : nausea ,vomiting
Less nausea and vomiting.
contraction so has less adverse
,constipation ,drowsiness ,confusion. Less respiratory depression.
effects on baby.
Most serious side effect: delayed
Diamorphine is better analgesic
maternal gastric emptying (the
than pethidine but greater
danger to the mother when she
respiratory depressant effect on
require GA in the presence of full
newborn so we dont use it
stomach under GA regurgitation and
pulmonary aspiration can occur) tt
by: no solid food during labor ,
antiemetic ,H2 blocker.

INTRODUCTION
Anesthesia versus analgesia :
An analgesic drug such as aspirin
may relieve pain but the person
who takes aspirin still feels other
physical sensation such as
pressure , heat ,cold and
vibration , in contrast anesthetic
drugs blocks all these physical
sensation

ANESTHESIA IN LABOR
A] GENERAL
INTRODUCTION
GA isnt used in vaginal delivery.
GA Used in C/S in certain
circumstances.
Extreme emergency situations .
Any contraindication for regional
anesthesia e.g infection at needle
insertion site, prior back surgery,
increase intracranial pressure, etc.
Unexpected prolonged surgery.

ANESTHESIA
BENEFITS OF GENERAL
Help the obstetrician to deliver the
baby in fetal distress.
Situations where minutes may count
for the fetus e.g. ruptured uterus,
placental abruption, umbilical cord
prolapse.
Situations where rapid induction
maybe needed for maternal safety e.g.
uncontrolled hemorrhage as in cases
of: placenta previa, trauma, placental
abruption, ruptured vessels.

INTRODUCTION
Def: Introduction of a
local anesthetic into
the subarachnoid
space.
A short procedure
time.
Rapid onset of the
block, and limited
duration of action.
High success rate.
Used very late in
labor.

ANESTHESIA IN LABOR
B] REGIONAL ANESTHESIA
SPINAL ANESTHESIA
INDICATION
CONTRAINDICATION
(1) Operations below
Patient refusal,
umbilicus
uncooperative patients
(2) Any operation in perineum Hypovolemia
or genitalia
Clotting disorders
(3) All possible operation on
Septicemia
the leg except amputation Anatomical deformities in
(4) Very important to notice
the patient back
that spinal anesthesia is
Neurological disease
indicated for older patient
Inadequate resuscitative
with systemic disease .
drug and equipments

INTRODUCTION
Most effective form of labor pain relief, used
in the first and second stages of labor.
No direct effect on fetus & doesnt cross
placenta.
Injected into the epidural space between L2L3 or L3-L4 interspace.
A test dose is given to confirm the catheter
position, if no unwanted signs is observed
after 5 min of injection, a loading dose can
be administered.
Analgesia for the pain of labor and vaginal
delivery necessitates a block from the T10
to the S5 dermatomes.
For cesarean delivery, a block extending
from the T4 to the S1 dermatomes is

EPIDURAL ANESTHESIA
INDICATION
Pain.
Prolonged labor.
Maternal
hypertensive
disorder.
When there is high
risk of operative
intervention.
High risk fetus
group.

CONTRAINDICATION
Patient refusal.
Coagulopathy
disorders.

COMPLICATION
Hypotension, bradycardia if
block reachs T2-T4.
Post spinal headache
(postural)
Urinary retention
Failure of technique .
Epidural or subarachnoid
hematoma
Spinal cord trauma or
infection
Rarely, convulsions and
blindness

COMPLICATIONS
MATERNAL
IMMEDIATE
Hypotension
Complete motor and sensory paralysis.
LA-induced convulsions, uncommon but
serious.
LA-induced cardiac arrest.
DELAYED
Postural puncture headache.
Backache; there is good evidence that
epidural does not cause backache.
Urinary retention; To avoid this a catheter is
placed early.
Tingling in hands or fingers.
Epidural abscesses; extremely rare.

desired.
The spread of the anesthetic depends upon
the location of the catheter tip; the dose,
concentration, and volume of anesthetic
agent used, and whether the mother is
head-down, horizontal, or head-up.

Local or systemic
infection.
Hypovolemia.

FETAL
No direct adverse effect on fetus.
Fetal distress can occur if maternal hypotension
occurred.

SPINAL ANESTHESIA
ADVANTAGE
Faster, Technically easier
More reliable - Defined endpoint, Minimal
chance of patchy block
Denser block
Lower drug exposure for mother and fetus
No chance of systemic toxicity

EPIDURAL ANESTHESIA
ADVANTAGE
Can tailor duration to need
Lower chance of postdural
puncture headache
Beneficial in patients with
cardiac and hypertensive
disorders

DISADVANTAGE
Limited duration
Higher chance of postdural puncture headache

DISADVANTAGE
Slower onset
Higher risk of systemic
toxicity
Risk of high spinal
Risk of "patchy block
ANESTHESIA IN LABOR
C] LOCAL ANESTHESIA

PARACERVICAL BLOCK
INTRODUCTION
Def: Bilateral transvaginal local anestethetic
injection to block the frankhousers ganglion
lateral to cervix.
Provides satisfactory pain relief during the first
stage of labor.
Anesthetic agent is injected into the cervix
laterally at 3 and 9 o'clock.
Has a short duration of action, so paracervical
block may have to be repeated during labor.
Because the pudendal nerves are not blocked,
another analgesic procedure may be needed.
Usually, we use:
Lidocaine

COMPLICATION
Fetal bradycardia
(lasts up to 30 min)
Results from
decreased
placental perfusion,
due to the druginduced
vasoconstriction
and therefore
should not be used
in situations of
potential fetal
compromise.

PUDENDAL BLOCK
Def: Bilateral transvaginal LA injection to
block the pudendal nerve as it pass
through the ischial spine (originate from
S3-S4),
Relatively safe and simple method of
providing analgesia for spontaneous
delivery.
The successful pudendal block will allow
pinching of the lower vagina and
posterior vulva bilaterally without pain.
Pudendal block usually does not provide
adequate analgesia when delivery
requires extensive obstetrical
manipulation.
Complications: Intravascular injection,

 Chloroprocaine, 5 to 10 ml of a 1%
solution.
(Bupivacaine is contraindicated because of risk of
cardiotoxicity.)

hematoma, and rarely infection.

ANEMIA IN PREGNANCY
PHYSIOLOGICAL CHANGES IN PREGNANCY
ANEMIA
Progressive increase in plasma volume up till 32-34
Lower Hb normal values:
weeks, (50%).
Non-Pregnant 11.5-12 g/dl
Progressive increase in Red Cell mass, although the
Pregnant, change with gestation, but generally 10.5
pregnancy, (25%).
g/dl.
Maximum physiological anaemia occur at 32-34 weeks
Clinical features:
gestation.
Mostly detected on routine testing.
MCV, MCHC stay constant, i.e. dilutional anaemia.
Tiredness.
Progressive fall in platelet count, Low platelets only if
Lethargy.
Platelets are <100 or pathologically reduced count. 5 Dizziness.
10% will be 100-150*109/l
Fainting.
There is 2-3 fold increase in Iron requirements in
pregnancy
Hypercoagulable state.
IRON DEFICIENCY ANEMIA
FOLATE DEFICIENCY ANEMIA
The commonest in
Anemia results if
Second commonest in pregnancy.
Stores are depleted.
pregnancy.
The normal dietary Folate intake is
Increased demand by the
Iron intake is poor.
inadequate to prevent
developing fetus, leads to
Absorption is poor.
megaloblastic changes in the bone
increased absorption and
marrow in 25% of pregnant ladies.
Utilisation is reduced.
increased mobilisation from Demand is increased:
Prevalence varies according to :
stores.
Social class.
Multiple gestations.
IDA is more common in
Nutritional status.
Chronic blood loss.
multiple pregnancies.

Factors increasing the risk of FDA:

Haemolysis.
Blood loss at delivery will
Anticonvulsant therapy.
A lot of patients start pregnancy with
further increase maternal
Haemolytic anaemia.
already depleted stores.
anaemia, so it is not only a
Thalassemia.
Menorrhagia.

problem confined to
pregnancy period.

Inadequate diet.
Previous recent pregnancies
Conception while breast feeding.

Hereditary spherocytosis.

DIAGNOSIS
IRON DEFICIENCY ANEMIA
As it is the commonest, it
is always presumed to be
the diagnosis, but should
always be confirmed.
Changes in the indices as
follows:
MCV reduced.
MCH, MCHC reduced.
Serum iron fall,
<12mmol/l (normally
falls in pregnancy).
Total iron binding
capacity increased,
saturation <15%
indicate anaemia.
Serum ferritin, fall.

INTRODUCTION
Incidence
1/250 deliveries
20-30% of APH
Majority present as
painless vaginal bleeding
by 30 weeks of gestation
20% bleeding and
abdominal pain
Incidental discovery

FOLATE DEFICIENCY ANEMIA

MCV increased.
Megaloblastic changes in
the bone marrow.
Reduced serum and red
cell folate.

MANAGEMENT
Routine iron supplement, as demand is rarely met by
normal iron intake.
Oral supplementation is not without side effects:
Constipation.
Taste.
Diarrhoea.
Nausia and vomiting.
Alternate routes are available:
IM.
IV.
The maximum rate of rise in Hb is around 1g/dl/week.
Severe anaemia diagnosed in the later stages of
pregnancy may need transfusion.
Preconception advice for all women is to take folate
supplement of 0.4mg/day to reduce the risk of NTD, this
will increase to 5mg/day in cases of previous NTD baby,
or in case of intake of anti-folate medications

PLACENTA PREVIA
PREDISPOSING FACTORS
CLASSIFICATION
Multiparity
Related to internal os.
Increased maternal
Minor
age
Grade I, Low lying
Previous placenta
placenta
previa, recurrence
Grade II anterior,
rate 4-8%
marginal
Multiple gestation
Major
Previous cesarean
Grade II posterior
section
Grade III, partial
Uterine anomalies
Grade IV, central,
complete.

PRESENTATION
Painless vaginal bleeding,
more severe with major
degrees
Recurrent bouts of bleeding
may be from early
pregnancy
Malpresentation and high
presenting part
Uterus is soft and not
tender
Fetus is usually alive and

MATERNAL RISK
Maternal mortality 0.1%
mainly from hemorrhage
PPH
Anesthesia
Sepsis
Air embolism ??
DIC, late occurring, late

FETAL RISK
High perinatal
mortality ***
prematurity***
IUGR in 15-20%
Congenital
malformations
doubled
Umblical cord
complication
Malpresentation

*Expectant Management

Keep in hosp esp in major degree

Steroids

Correct anemia ? Blood transfusion

Cross-matched blood should be

available all the time

Assess fetal well-being

INTRODUCTION
Premature separation
of the placenta
(before delivery of the
fetus)
Incidence: 0.5-1.5%

DIAGNOSIS
Ultrasonography
*Abdominal 95% accurate
*Vaginal usually for post
placenta difficult to define by
abdominal ultrasound (done
in hosp)
* Double set up examination
rarely needed in patients not
actively bleeding

well
More serious for mother
than fetus
MANAGEMENT
Proper assessment of
maternal condition and
resuscitation
In severe bleeding,
emergency cesarean
delivery irrespective of
gestational age
If bleeding after 36-37
weeks, deliver.
If bleeding not severe and
early pregnancy, expectant
management, attempting to
reach fetal maturity (36-38
wks) without risking
maternal health

*Delivery

Delivery is by cesarean section

?? Anterior marginal placenta with

lower margin >2cm from the internal
os (by USS) may be delivered vaginally

Observe for PPH

Prophylaxis for Rh isoimmunization

PLACENTA ABRUPTION
PREDISPOSING FACTORS
CLASSIFICATION
Hypertension, mostly PET, in
Grade 0. Asymptomatic,
small retroplacental clot
pregnancy
after delivery
Previous placental abruption,
recurrence rate after one episode 8Grade 1. *External vaginal
17%, after two episodes 25%

CLINICAL FEATURES
Vaginal bleeding,
variable amount, no
bleeding in concealed
Abdominal pain,
discomfort and backache

CLINICAL
PRESENTATION
Concealed 25-30%
Revealed
65-80%
Other:
Mild
Moderate
Severe abruption

Trauma
Polyhydromnios
Premature rupture of memb.
Short cord
Smoking
High parity and low social class
Idiopathic
MANAGEMENT

Ressuscitation, IV canula, IV
crystalloid
Cross match blood and FFP
Assessment of mother, put fixed
catheter, CBC, KFT, Urine for
protein, and coagulation profile
Assessment of fetal wellbeing, CTG
Definitive treatment by delivery,
assess for labour, do ARM and
syntocinon infusion. Any fetal
distress or deterioration of maternal
condition deliver by C/S
DIC, packed RBC and FFP
Observe for PPH
Observe urine output, risk of renal
tubular or cortical necrosis

bleeding
*Uterine tetany and
tenderness may be
present
*No signs of maternal
shock
*No evidence of fetal
distress
Grade 2. *External vaginal
bleeding may or may not
be present.
*Uterine tender and
tetany
*No signs of maternal
shock.
*Signs of fetal distress
present.
Grade 3. &External
bleeding may or may not
be present.
*Marked uterine tetany.
*Persistent abdominal
pain.
*Maternal shock.
*Fetal death or distress.
*Coagulopathy in 30%

ANTEPARTUM HEMORRHAGE
Vaginal bleeding after age of viability

in 65% of cases
Uterine tetany and
tenderness over
placental site, more in
concealed
Normal lie and
presentation
High incidence of fetal
distress and fetal death.
Fetus is dead in 25-35%
of cases at admission
(perinatal mortality 4.467%)
Blood pressure may be
normal or elevated,
protein urea (IUGR
present in 80% of cases
delivered after 36 weeks
of gestation)
Over distended uterus,
rigid, difficult to feel
fetal parts in concealed
hemorrhage
Evidence of skin
ecchymosis in 13% of
cases usually those
admitted with fetal
death

Blood loss is a major cause of maternal death

Incidence
4%
CAUSES
o Placenta previa
20-30%
o Abruptio placentae 15-20%
o Unclassified
50%

Marginal separation

Show

Local causes

Vasa previa

Unknown cause

60%
20%
6%
0.05%

*Vasa Previa: Fetal bleeding presented as acute fetal distress after membranes ruptured
GENITAL PROLAPSE: APPROACH
HISTORY
PROFILE

Name, Age, Gravida, Para, Occupation, Ethnic

C/C: LUMP / SOMETHING PROTRUDYING THRU INTROITUS / COMING DOWN BELOW
HPI
Lump analysis: Duration. Present always/goes back in?
by long standing, at end of the day.
by lying dow
Impact on social & sexual life
Associated sx:
Back pain uterine prolapsed
Urinary sx, cant empty bladder, must reduce digitally Cystocele/urethrocele
Constip, Incomplete evacuation, must reduce digitally
Ulcer, blood stain, purulent vaginal discharge
Risk factors

DDx:
Congenital Gatners
cyst

Childbirth Multiparity? Vaginal delivery? Long labor?

Inclusion dermoid cyst

Menopause

Urethral diverticulum

Intra-ab pressure Obese, Chronic cough, constip,

Large cervical /
endometrial polyp

Pelvic surgery
Gynea Hx: Menopause, HRT, Pelvic surgeries

Chronic uterine

Past Hx: Chronic cough (COPD, Asthma, Pneumonia, CF), Constipation, Previous surgeries
Social Hx: Smoking
EXAM
Pelvic Exam
Inspection Vulva with cough & straining Demonstrate prolapse incontinence
Speculum
Rectal Exam to differentiate rectocele (finger goes thru) & enterocele (finger goes high up)

Rectocele
Procidentia

mass

INVESTIGATIONS
MSU analysis & culture
Renal US & IVU in procidentia & severe cystocele, to R/O hydroureter & hydronephrosis
Cystometry to R/O urge incontinence

PUERPERAL PYREXIA
Elevated temperature of more than 38.2C for a whole day within the first 10days postpartum.
History
Introduction
Permission
Complete patient profile: GA, GravidaPara, Address, Occupation, Blood group
Chief Complain
Analysis of chief complaint: Duration, onset, documented/not
R/O Endometritis: Offensive vaginal discharge, Ab pain
R/O Mastitis: Lactating or not, Abnormal breast discharge
R/O UTI: Urinary sx, Nausea, vomit, chills, rigors
R/O Wound infxn: Wound pus, bleeding from site
R/O URTI: Cough, SOB
R/O DVT: Leg swelling or redness
R/O Bacterial vaginosis: Vaginal discharge during pregnancy
Intrapartum Hx: Vaginal delivery/CS? Elective or emergency CS? Induction of labor? Instrumental delivery? PROM? Hx of
blood transfusion? Urine catheterization?
Hx of pregnancy: Anemic? Bacterial vaginosis during pregnancy?
Hx of the same problem in previous pregnancies?
PMH/PSH
Drug Hx. Family Hx. Social Hx.

Physical Examination:
Introduction
Permission
Privacy. Lighting. Hygiene.
General Exam:
-

Cannula site (superficial thrombophlebitis)

Catheter (uti)

Signs of anemia (anemia per se is risk factor)

Vital signs

Breast Exam (mastitis)

Chest Exam (urti)
Thyroid Exam
Abdominal Exam:
-

Uterine tenderness (endometritis)

Uterine subinvolution (endometritis)

Inspection of wound (wound infxn)

Pelvic Exam:
-

Cervix is open (endometritis)

Offensive vaginal discharge (endometritis)

Lower Limb Exam

-

Leg circumference (dvt)

Doppler (dvt)

URINARY INCONTINENCE APPROACH

HISTORY
Age, Parity
Analysis of Incontinence: Duration, frequency, amount
Precipitating factors
3Ps: Position, Protection, Problem
Progression
Urinary Diary
Association
Irritative sx (Freq, Urgency, Nocturia) urge
Obstructive sx (Poor stream, Incomplete void, Straining) overflow
Recurrent UTI urge
Past Obs Hx: Mode of Delivery. Instrumental?, Prolonged 2 nd stage? Baby birth W8.
Past Gynea Hx: Sx of Prolapse, Pelvic surgery, Hx of malignancy, Hx of radiotherapy
PHYSICAL EXAM
General Look
Abdominal Exam
Respiratory Exam
Neurological exam Mental status, Gait, Lower extremity, Perineal sensation & reflexes.
Pelvic Exam
Pelvic floor muscle tone
Stress test - >90% diagnostic for stress inc
Cotton swab @ Q-tip test
INVESTIGATIONS
1. Urine analysis & culture
2. Urodynamic studies
a. Non-invasive methods:

i.
ii.
iii.
iv.

3.
4.
5.
6.
7.

Uroflowmetry
Volume-frequency chart
Ultrasound: Residual Volume, Urethral cyst, Diverticulation of urethra
EMG by surface electrodes

b. Invasive methods
i. Cystometry
ii. Urethral Pressure Profilometry
iii. RV by Catheter
iv. EMG by needle electrodes
Ultrasound
VCU
IVU. Indication: Hematuria, Neuropathic bladder, Uterovaginal fistula.
Cystourethroscopy. Indication: Reduced bladder capacity, Short hx (<2yrs) of urgency & frequency, Persistent UTI,
High suspicion of tumors or stone.
MRI

UROFLOWMETRY
Normal flow curve: Bell shaped
Normal flow rate >15ml/sec
Normal voidal volume >150ml
CYSTOMETRY
Indications
1. Previous unsuccessful continency
surgery
2. Mixed incontinence
3. Voiding disorder
4. Neuropathic bladder

Normal Values
Residual Volume >50ml
1st Desire to Void: 150-200ml
Bladder Capacity: 400-600ml
Detrusor Pressure (Filling phase):
<15cmH20
Detrusor Pressure (Voiding phase): 4070cmH20
No leakage when coughing

MANAGEMENT
A. CONSERVATIVE
Success rate 40-60%. Mainstay in Stress Inc.
Stop smoking, alcohol, caffeine. Kegel exercise.
Intravaginal device to support bladder neck & urethra.
B. MEDICAL
Mild-Moderate Stress Incontinence
Alpha-Agonist
Pseudoephedrine
Phenylpropanolamine

Urge Incontinence
Anticholinergic Drugs
Oxybutynin chloride
Tolterodine
TCA: Imipramine

C. SURGICAL [Stress Incontinence]

Colposuspension

Tension-free Vaginal Tape (TVT)

PRE-INVASIVE & INVASIVE CERVICAL DISEASE

Dysplasia lesion in which part of the
epithelium is replaced by cells showing varying
degrees of atypia
Cervical Intraepithelial Neoplasia (CIN):

Intraepithelial dysplastic atypia occurring

within
the metaplastic epithelium of the
transformation
zone.

Bethesda system
ASCUS:
Atypical
squamous
cells of
undetermined
significance

LSIL: Low
grade
squamous
intraepithelia
l lesion

HSIL:High
grade
squamous
intraepithelia
l lesion

Cancer:
Squamous
cell
carcinoma

Original Squamocolumnar Junction(OSCJ): The junction in fetal

life between the Stratified SE of the vaginal and ectocervix,
and the CE of the end cervical canal.
New Squamocolumnar Junction (NSCJ): The upper margin of

Dysplasia / CIN System

Mild
dysplasia

Mod.dyspla
sia

Severe
dysplasia

CIN 1

CIN 2

CIN 3

CI
S

Canc
er

Cervical neoplasia originates within the TZ.

Low Risk HPV types (6 and 11), are associated lowgrade cervical lesions (condylomata acuminata,
and CIN1).
High Risk HPV types (16, 18, 31,33,or 35), are
associated
with high-grade cervical lesion (CIN2,3) and cervical
cancer.
HPV 16 is the type universally detected with
greatest
frequency in high grade lesion and cervical cancer,
50%
of SCC, 30% of Aden carcinoma, and in over 80% of
preinvasive lesions
At least 35%of patients with CIN3 will develop
invasive
cancer within 10years, whereas lower grades may
spontaneously regress.

Screening of asymptomatic women

the squamous metaplasia zone determined by the colposcopy

Transformation Zone (TZ): The area lying between the OSCJ
and the NSCJ

Risk factors for Cervical Cancer

1. Persistent HPV infection with high risk types
2. Young age at first coitus(20yr)
3. Multiple sexual partners
4. Sexual partner with multiple sexual partners
5. Young age at first pregnancy
6. High parity
7. Lower socioeconomic status
8. Smoking
9. Oral contraceptives use
10.Genital warts
11.Exogenous/endogenous immunosuppression

Papanicolaou Smear

Both the end cervical canal and

the ectocervix should be sampled
when taking the Pap smear
In US , the ACOG has
recommended that all women,
once they have become sexually
active, should undergo an annual
Pap smear, then 2-5 years
following two or three normal Pap
smears
In Australia, once sexually active
till the age of 65 year, routine
smear every 2 years
The false negative rate for Pap
smear for high grade lesions is
20%
New technologies (Thin prep,
AutoCyte PREP) are automated
liquid based slide preparation
systems to decrease the false
negative rate

Colposcopy

1.
2.

3.
4.
5.
6.

The colposcope is a
stereoscopic binocular
microscope of low
magnification, usually 10x
to 40x.
Indications for colposcopy:
Abnormal cervical smear
Abnormal findings on
adjunctive screening tests
such as HPV testing and
cervicography, particularly
in cases of ASCUS
If the cervix is clinically
abnormal or suspicious on
naked eye examination
Abnormal or unexplained
IMb or PCB
Persistent vaginal discharge
Personal history of in utero
DES exposure, vulvar or
vaginal
neoplasia

BEFORE Colposcopy
A complete medical history and general
examination
should be performed
A clinical and speculum examination of the
cervix, vagina
and vulva should be performed
A 3% to 5%acetic acid solution is liberally
applied to the
cervix using soaked swap
-The abnormal findings are acetowhite
epithelium and
abnormal vascular patterns (mosaicism and
punctuation)
Lugols iodine application to the cervix is
called shillers
test
-Normal ectocervix and vaginal squamous
epithelium
contains glycogen and stains mahogany-brown
-Normal columnar and squamous metaplasia
and neoplastic epithelium do not contain

glycogen, and appear mustard yellow

Satisfactory Colposcopic Examination: If the
new SCJ
and the entire TZ are seen
Evaluation of a patient with an abnormal Pap smear
Any patient with a grossly abnormal cervix should have a punch
biopsy performed regardless of the results of Pap smear
Patients with ASCUS found in their smear may have a repeat
smear in 6 months or HPV testing
About 6-10% of patients with an ASCUS smear will have highgrade CIN on colposcopy, 90% of these can be detected by HPV
testing for high-risk types
The colposcopic hallmark of CIN is an area of sharply delineated
acetowhite epitheilum, or/and abnormal vascular pattern:
punctuation and mosaicism

If colposcopic examination is satisfactory, punch

biopsy
from the suspicious area with end cervical curettage
specimen
Diagnostic cone biopsy of the cervix is indicated if:
1. colposcopic examination is unsatisfactory
2. Endocervical curettings show a high-grade
lesion
3. Pap smear shows a high-grade lesion that is not
confirmed on punch biopsy
4. Pap smear indicates Adenocarcinoma in situ
5. Microinvasion is present on punch biopsy

Micro invasive carcinoma: extremely irregular puncate and

mosaic patterns are found

Treatment of intraepithelial neoplasia CIN

Low grade lesions (CIN1) repeat smear in 6 month

interval until normal then back to the normal screening
program
High grade lesions (CIN 2,3):

4. Electrocoagulation, Requires general anesthesia, cervical

stenosis may occur, success rates up to 97%.

1. Loop Excision of The Transformation Zone

(LLETZ),relatively cheap, it can be performed on an
outpatient basis under local anesthesia, and tissue is
obtained for histologic evaluation.

5. Cervical conization: (cold knife or laser)

-mainly diagnostic but it may be used for treatment, cure
rates are as high as with hysterectomy for high grade
lesions.

2. LASER, destruction of the TZ by CO2 laser, ablation can

be performed as an outpatient procedure with local
anaesthesia, expensive.

-Major complications: Bleeding, infection, cervical stenosis

and incompetence.

3. Cryosurgery, relatively painless outpatient procedure

without anaesthesia, cheap, high failure rate for large
lesions, copious vaginal discharge for several weeks.

Simple hysterectomy is rarely necessary, it may be

applicable when sterilization is desired in a patient with CIN
III or when there is concomitant uterine or adnexal disease.

CERVICAL CANCER

Worldwide, cervical cancer is the most

common cause of death from cancer in
women.
In developed countries, regular screening
with Pap smear has markedly decreased
the incidence of the disease.
In US, cervical cancer now ranks only
eleventh among cancers in women.
The mean age for cervical cancer is 51.4
years, with the number of patients fairly
evenly divided
between the age groups 30 to 39 and 60
to 69 years
The most common type is SCC up to 80%,
adenocarcinoma and adenosquamous
account for 20% to 25%, other cell types
are rare.

Symptoms

Physical findings

1. Abnormal vaginal bleeding is

the most common presenting
symptom.
2. Postcoital bleeding in sexually
active women, IMB, and PMB
3. Asymptomatic until quite
advanced in women who are not
sexually active (unlike
endometrial cancer who bleed
early)
4. Persistent vaginal discharge,
pelvic pain, leg swelling, and
urinary frequency are usually
seen with advanced disease
5. Vesico-vaginal/recto-vaginal
symptoms

1. Usually normal general

examination
2. In advanced disease, enlarged
inguinal or supraclavicular lymph
nodes, edema of the legs, ascites,
pleural effusion or hepatomegaly.
3. The Pap smear may be normal in
up to 50% of cases (falsenegative rate)
4. Pelvic examination in early
disease may be normal,
especially if the lesion is
endocervical.
5. Visible disease may be,
ulcerative, exophytic ornecrotic

CERVICAL CANCER
Pattern of spread

Investigations

1.Direct invasion into the

cervical stroma, corpus,
vagina, and parametrium

1.
2.
3.
4.
5.
6.

2. Lymphatic permeation and

metastasis

CBC, LFT, KFT

Chest X-ray
Pelvic-abdominal CT Scan
Biopsy of the lesion
Cystoscopy and proctoscopy for clinical staging
PET Scan (positron-emission tomography) new technique has the potential more
accurately to delineate the extent of disease at the primary site and in lymph nodes.

3. Hematogenous
dissemination
Treatment
Stage IA ( Micro invasive
carcinoma)

Stage 1B

Radiation Therapy

A preoperative diagnosis can be

made only on the basis of a cone
biopsy of the cervix

May be treated by either radical

hysterectomy and bilateral pelvic
lymphadenectomy or radiation therapy.

Stage 1A1 :

The results of treatment by either

method are similar.

Total abdominal / vaginal

hysterectomy
Cone biopsy alone may suffice if
the patient desires to preserve her
fertility, as long as the cone
margins are free of disease and
the endocervical curetting are

The advantages of surgery is that the

ovaries may be spared in young women,
surgical staging may be carried out, and
chronic radiation therapy may be avoided.
Radical Hysterectomy: Removal of the
uterus along with the adjacent portions of

For patients with stage 1b2, most

centers use primary chemo radiation,
using weekly cisplatin as the
radiation sensitizer
Therapy usually begins with external
radiation to shrink the central tumor
and subsequent intracavitary
therapy.
External radiotherapy may also be
used postoperatively for patients with
lymph node mets, or inadequate
surgical margins
The addition of chemotherapy to
radiotherapy has been shown to
improve survival.

the vagina, cardinal ligaments ,

uterosacral ligaments, and bladder pillars.

Modified radical hysterectomy

and pelvic lymph node dissection.

The most common complication of

Rad/Hys is bladder dysfunction, 1% to 2%
have permanent dysfunction.

If childbearing is desired, largecone biopsy or radical

trachelectomy and pelvic lymph
node dissection may be offered

The most serious complication of

Rad/Hys is ureteric fistula or stricture,
which occurs in 1% to 2% of cases

negative.
Stage 1A2:

Lower limb lymphodema, 15% to 20%

due to pelvic
lymphadenectomy

CERVICAL CANCER
Complications of radiotherapy
Acute

Chronic

Stage IIa with minimal involvement of

the vaginal fornix, radical surgery or
chemo radiation may be employed.
Stage IIa to stage IVa: Pelvic chemo
radiation is the treatment of choice
Stage IVb Palliative radiotherapy or
palliative
chemotherapy

1. Acute cystitis: hematuria,

urgency and frequency.
2. Proctosigmoiditis:
manifested as tenesmus ,
diarrhea, and passage of
blood and mucus in the
stool
3. Enteritis: manifested by
nausea, vomiting,
diarrhea, and colicky
abdominal pain
4. Bone marrow depression

Radiation Enteropathy:
1. Proctosigmoiditis: pelvic pain, tenesmus,
diarrhea, and
rectal bleeding
2. Ulceration: manifested by rectal bleeding
and tenesmus
3. Rectovaginal fistula: manifested by
passage of stool
through the vagina
4. Rectum or sigmoid stenosis manifested by
progressive

Vaginal vault necrosis: associated with

severe pain
and tenderness of the vaginal vault and a
profuse
discharge.
Urologic Injuries:
1. Hemorrhagic cystitis which may need
frequent
blood transfusion and urinary diversion
2. Vesicovaginal fistula manifested by the
constant

large bowel obstruction

leakage of urine demonstrable by

cystoscopy

5. Small bowel injury usually present with

cramping

3. Ureterovaginal fistula which is manifested

by

abdominal pain and vomiting with

alternating diarrhea

constant leakage of urine and is

demonstrable by IVU

and constipation

4. Ureteric stenosis which is manifested by

progressive hydronephrosis.

Recurrent or Metastatic Disease

Prognosis

Chemotherapy: the effectiveness is limited, the most

active drug is the cisplatin
Pelvic exenteration: Reserved for patients who have
central recurrence following irradiation.

Prognosis is directly related to clinical stage

With higher stage , the frequency of nodal mets escalate,
and the 5-year survival rate diminishes.
Adenocarcinoma and adenosquamous carcinoma have a

Total exenteration involves removal of the pelvic

viscera,
including the uterus, tubes, ovaries, bladder and
rectum
Radiotherapy if the initial disease treated with surgery
alone

somewhat lower 5-year survival rate than do SCC, stage for

stage

PHYSIOLOGICAL CHANGES IN COAGULATION & FIBRINOLOYTICS SYSTEMS IN PREGNANCY

Coagulation system : Increase in levels of coagulation factors,
The result of these changes is hypercoagulable
mainly fibrinogen and factor VII, VIII, IX and X from the
state in pregnancy
beginning of the second trimester.
The benefit of these changes is protection of
Fibrinolytic system : Inhibition of the system, due to increase in
mother from severe haemorrhage after delivery
the levels of plasminogen inhibitors.
The risk of these changes is the increased risk of
Platelet count : No change
thromboembolism
Anticoagulant system : levels of anti-thrombin III, no change in
the levels of protein C & S
DISSEMINATED INTRAVASCULAR COAGULOPATHY
MAIN CAUSES IN
DIAGNOSIS
MANAGEMENT
PREGNANCY
Placental abruption Clinical observation
Insertion of at least 2 large infusion lines
Preeclampsia &
Vaginal bleeding, oozing from
Send at least 20ml of blood for cross-matching
eclampsia
venepuncture sites & surgical incisions.
& coagulation profile, and request at least 6
units of blood & 4 units of FFP.
Endotoxic shock
History of any of the above risk factors.
Correct hypovolaemia by fluids & whole
septic abortion,
Whole blood clotting time prolonged
blood
chorioamnionitis
( Normal 5-10 minutes)
and puerperal
Correct coagulation disorder by FFP
Coagulation profile :
sepsis
NB:- platelet transfusion only indicated in
Platelet count reduced (Normal
Amniotic fluid
presence of active bleeding if platelet count is
150,000 350,000)
embolism
Fibrinogen level reduced ( Normal 2-4 less than 50,000 , and if no active bleeding, if
platelet count less than 20,000.
Prolonged shock
gm/L)
Empty the uterus as rapidly as possible by
Prolonged retention
APTT prolonged (Normal 35-43
delivery or D&C.
of dead fetus
seconds)
NB- DIC is always a 2ry phenomenon to an
missed abortion or
PT prolonged (Normal 10-14 seconds)
underlying stimulus, and is usually self-limiting if
IUFD for >5 weeks
TT prolonged (Normal 10 seconds)

FDPs levels increased

the stimulus producing it is removed therefore

the uterus should be emptied as rapidly as
possible

THROMBOEMBOLISM
RISK FACTORS
Pregnancy hypercoagulate state .
Maternal age > 35 years.
Parity > 4
Obesity > 80 kg.
Caesarean section, particularly
emergency C.S
Previous history of
thromboembolism
*the risk of recurrence of
thromboembolism is 12%, & the
majority occur after delivery .
Prolonged hospital stay.
Family history of thromboembolism.
Thrombophilia ie. Congenital
deficiency of antithrombin III,
protein C or protein S, & presence
of factor V leiden.
Anti cardiolipin syndrome or
presence of lupus inhibitor
Cardiac disease such as valvular
prosthesis or atrial fibrillation.
Sickle cell disease.
Gross varicose veins.
Blood groups other than O
Suppression of lactation with
estrogen

DIAGNOSIS
DVT
PE
1- Sx: Pain & swelling in the leg
*There may be (50%) or may be not
(50%) prior clinical evidence of DVT.
2- Signs: temp of the leg, tender calf
1. Sx: Sudden onset of dyspnoea,
muscles, a difference of >2cm in the
chest pain, cough & haemoptysis,
circumference at identical sites of legs,
and sudden collapse in massive PE
and +ve Homan's sign.
*in 50% of patients there are no clinical 2. Signs: Cyanosis, rapid breathing &
jugular veins distention.
symptoms & signs referable to the
3.
Investigations:
limbs & pulmonary embolism may be
CXR: May be helpful ie.
the 1st indication of thromboembolism
Consolidation, infarction &
.
elevated hemidiaphragm on
*Over 80% of DVT are left-sided.
affected side, but can be totally
3-Investigations :
normal.
I.
Doppler U/S Noninvasive, safe,
ECG: Usually normal except when
accurate in 95%, more accurate if
the embolus is large.
DVT above the knee due to
absence of collaterals than if DVT
Respiratory alkalosis and low
below the knee due to presence of
Pco2 - due to hypoxia
collaterals.
hyperventilation with blowing off
II.
Ascending venography
of CO2 and respiratory alkalosis.
Contraindicated in the 1st
Ventilation & perfusion lung scan
trimester, and maybe indicated
Pulmonary angiography.
after that if Doppler U/S is not
informative.

ANTICOAGULANTS
HMWH HEPARIN
@ High molecular weight heparin
Rarely used ( if LMWH is not
available ).
Given by I.V route. The therapeutic
dose is 10,000 units bolus dose ,
followed by 24,000 units / day,
given via infusion pump.
Monitored therapeutic dose (1mg/kg/day 2x/day) by APTT; should be 2 times
of control.
Monitor maintenance (40mg/ml 1x/day) & prophylactic (20-40mg/ml 1x/day)
dose by plasma heparin level; should be 0.2-0.4 units/ml.
The action of therapeutic heparin is inhibition of thrombin & factors IX, X, XI &
XII.
Heparin DON'T cross the placental barrier & so can be used safely during
pregnancy
The side effect is bleeding.
If bleeding occur, stop the treatment, and in practice this is enough. Rarely if
bleeding not stopped, give specific antidote ie. Protamine sulphate.
The advantages of heparin compared to warfarin - are:1. Does not cross the placenta
2. Small dose prophylaxis- no haemorrhagic hazard
3. Easily and rapidly reversed as heparin disappears from the circulation in 6
hours.
The disadvantages:1. Osteoporosis if given for more than 6 months
2. Thrombocytopenia.
LMWH HEPARIN
Low molecular weight heparin (LMWH)
e.g Enoxaparin sodium (Clexane).
The preferred type used now.
Given by S.C route. The therapeutic
dose is 2 mg/kg/day, given in two
divided doses.

ORAL WARFARIN
The dose is 2.5-5 mg/twice daily
Monitored by International Normalized
Ratio ie. INR (which should be around
2 ) & by PT (which should be 2-2.5
times of control.)
MOA: Inhibition of the synthesis of Vit-K
dependent factors: II, VII, IX & X.
Disadvantages of warfarin are:
1. Bleeding
2. Teratogenic - if given in 1st trimester
during the period of organogenesis coz
warfarin cross the placenta:
chondrodysplasia punctata, cerebral
haemorrhage, calcification &
microcephaly.
3. Fetal & Neonatal cerebral
haemorrhage if given after 36 weeks.
4. Effect not easily or rapidly reversed
as warfarin disappears from the
circulation in 3 days.
In case of bleeding, antidote is FFP.
*Neither heparin nor warfarin are
excreted in breast milk, so that they are
safe to be used during lactation.

MEDICAL TREATMENT OF THROMBOEMBOLISM

ACUTE PHASE
Therapeutic dose of heparin. Either LMWH or HMWH.
LMWHs duration of acute phase therapy 2 3 months.
LMWH (Clexane)
HMWH
The therapeutic dose is 2 mg/kg/day, given in two
The therapeutic dose is 10,000 units bolus dose, followed by
divided doses
24,000 units / day, given via infusion pump.
LONG TERM THERAPY
Either LMWH (S/C) heparin or Oral Warfarin
- If thromboembolism occurs during pregnancy the best after acute phase therapy for 2-3 months, is to give S/C heparin
in the maintenance dose for the rest of pregnancy ( in order to avoid side effects of warfarin during pregnancy) & for 12
weeks postpartum of either S/C heparin or warfarin.
- If thromboembolism occurs after delivery S/C heparin in therapeutic dose for 4 weeks, then either S/C heparin in
maintenance dose or oral warfarin , for 3 months.
HEPARIN
WARFARIN
Given by SC route. The best is LMWH, if not available, HMWH.
Given orally.
Dose of LMWH (Clexane) 40mg/ 1x/day. HMWH 5000IU 2x/day.
Dose is 2.5-5mg 2x/day
Monitored by plasma heparin level; should be between 0.2-0.4 units/ml.
*Monitoring of maintenance or prophylactic dose of SC heparin by APTT is of no value,
coz maintenance & prophylactic dose doesnt level of coagulation factors & so
doesnt cause prolongation of clotting time.

1.
2.
3.
4.

COUNSELING AFTER AN ATTACK OF THROMBOEMBO DURING PREGNANCY

Explain the risk of recurrence in future pregnancies which is about 12 %
Explain the need for prophylactic anticoagulatnts in future pregnancies
Avoid the use of combined contraceptive pill.
Consider screening for thrombophilia in absence of other risk factors
POLICY OF PROPHYLAXIS

No hx.
Did c-section.
With 1 risk factor.
1 hx of DVT
No risk factor.

Delivery

1wk postpartum

Delivery
1 hx of DVT.
Other risk factor (e.g.
admitted to hospital)

Admission

Delivery

6wk postpartum

6wks postpartum

Hx of 2DVT or 1PE or
anticardiolipin or lupus
inhibitors presence or cardiac Pregnant
Delivery
2months
indication for prophylactic
postpartum
anticoagulants (eg AF,
valvular prosthesis)
*The policy of prophylactic anticoagulant during pregnancy in previous history of pulmonary embolism or DVT or
thrombophilia is by LMWH once daily throughout pregnancy up to 12 hours before delivery .
*The policy of prophylactic anticoagulant during pregnancy in cardiac indication : warfarin in the 1st trimester & up to 36
weeks and then by HMWH, I.V, 6000 units/6hrs up to 12 hours before delivery.
*S/C heparin is not effective in prevention of cardiac thrombosis, and so warfarin given in the 1st trimester in spite of its
known teratogenic effects.

CLASSIFICATION

DIABETES IN PREGNANCY
DIABETOGENIC
DEFINITIONS

PRESENTATION

Diabetes mellitus type I --insulin dependent (Ketosisprone)

Diabetes mellitus type II--non-insulin dependent
(Ketosis-resistant)
Impaired Glucose Tolerance
and Gestational Diabetes
(IGT)
SCREENING
Why.
30% have none of the
Above risk factors
Not all DM, IGT, have
persistent glucosuria
50% of pregnant women
have glucosuria at some
time

MATERNAL
Obstetric: Polyhydramnios,
pre-eclampsia (10-15%)
Diabetic Emergencies:
Hypoglycaemia, Ketoacidosis,
Diabetic coma
Vascular & End-Organs:
Renal,
Ophthalmic, Peripheral
vascular
Neurologic: Peripheral
neuropathy
GI disturbance

EFFECTS OF
PREGNANCY
Insulin resistance
Increased lipolysis
Altered maternal
gluconeogenesis

DM= Fasting venous glucose

concentration > 8.0 mmol/l
and 2 hrs (75 gm load ) > 11.0 mmol/l
(or) one of the above + Symptoms
IGT = Fasting < 8.00 mmol/l, but 2
hr (75 gm load) = (9.0-10.9)

-Symptoms
-Risk factors (hx &
examination)
-Blood tests-screening

RISK FACTORS
Age > 30
Family history of DM
Past history of: Diabetes in a previous pregnancy, Unexplained IUFD, Neonatal
death, Congenital abnormalities, Recurrent abortions, Large babies > 90 th centile
Obesity
HTN in multipara
Polyhydramnios
Recurrent infections: Urinary, Fungal
Significant Glycosuria

COMPLICATIONS
FETAL
(1) Macrosomia & Traumatic delivery (30% in seemingly controlled)
(2) Delayed organ maturity (RDS) 6 times
(3) Congenital malformations:
Cardiovascular: Transposition of great vessels, VSD, ASD,
Aortic coarctation
Central Nervous system: Anencephaly, Holoprosencephaly,
Encephalocele
Skeletal & spinal - Caudal regression
Genitourinary - Renal agenesis, ureteral dupliction
Gastrointestinal - anal atresia
** Note: when a two-vessel cord is found, suspect a high incidence of

NEONATAL
Hypoglycaem
ia
RDS
Hypocalcaem
ia
Polycythaemi
a

Infections: Urinary

congenital anomalies
(4) Intrauterine fetal Death
advanced DM)

(5) Growth restriction (in

MANAGEMENT

Start in preconception time

Specific during pregnancy
SPECIFIC

CONTROL

Diet:
16 x Wt. (pounds ) + 300 = CALORIES
Carbohydrates
60%
Fat
20%
Protein
20%
Insulin:
Regiment A
* 3 times sol.-with meals + lnt. Evening
Or
- Regiment B
* 2 types (short & intermediate)
Twice Daily
Dose (daily) = wt. (kg) x 0.6 first
x 0.7 second
x 0.8 third
2/3 in A.M.
2/3 1nt + 1/3 short
1/3 in P.M.
1/2 1nt + short.

Control :
Fasting < 5.0 mmol/1
2 hrs P.P. < 7.0 mmol/1
Adjustment when necessary
Glycosylated Hb A1c (retrospective) < 6
Fetal well being:
AFP 16-18 wks
Detailed scan 19-20 wks
Biophysical assay from 28 wks
Fetal wt. & growth two weekly (3rd)
Delivery:
- Timing depends on: (Around 38 wks)
Maternal factors
Biochemical control
Fetal status
- Method --- LSCS in any medical or obstetric complication.
**Insulin dose adjusted on hourly basis with caloric
requirements intravenously.

DRUGS IN PREGNANCY
Epidemiology

Maternal
Pharmacokinetics

Fetal pharmacokinetics

Placental pharmacokinetics

In pregnancy, it is
estimated that each
woman takes 1-3 drugs
beside vitamin
supplements or iron

Changes in body
fluid volume.
Changes in CVS
parameters.
Changes in

Plasma binding proteins

differ from maternal so
free fractions of basic
drugs are elevated.
Liver expresses

Blood flow through the placenta

(maternal side) increases
during gestation (50 ml/min at
10 weeks of pregnancy to 600
ml/min at 38 weeks)

 About 1/3 of women in

the UK take drugs at least
once during pregnancy.
Only 6% take a drug
during the first trimester.
There has been a
considerable reduction in
drugs used in pregnancy
since the mid-1960s
>>> Self-administered drugs
from 64% to 9%

pulmonary
functions.
Alteration in gastric
activity.
Changes in serum
binding protein
concentrations.
Alteration in kidney
function

Drug transfer
Most drugs have a molecular
weight below 1000 Daltons.
Drugs less than 100o Daltons cross
the placenta(less than 600 Daltons
cross easily)
Main determinant of the drug
concentration in the Embryo/Fetus
is the mothers blood
concentration.
Other factors:
>Lipid solubility and protein
binding.
> Degree of ionization at
physiologic pH.
>placental blood flow and surface
area available for transfer.

metabolizing enzymes,
but capacity less than the
mother.
Drugs transferred across
the placenta undergo 1st
pass hepatic effect
through the fetal liver.
Fetal kidneys are still
immature.
Fetal urine enters
amniotic fluid which may
be swallowed by the
fetus.

Compounds that alter blood

flow alter maternal drug
disposition and placental
transfer.
Placental metabolism
(dealkylation, hydroxylation,
demethylation) affects drugs
transfer across the placenta.
At term, the surface area of the
placenta is at its maximum and
nearly all substances can reach
the fetus.

The processes that govern the passage

of a drug into milk are similar to
placental condition:
Maternal serum concentration is
the main determinant.
The milk pH is slightly acidic
in comparison to serum pH;
so weak bases could become
trapped in milk ( ion trapping ).

Teratogenesis
It is defined as structural or
functional (e.g. renal failure)
dysgenesis of the fetal organs.
Typical manifestations include:
>congenital malformations with
varying severity.
>IUGR.
>Carcinogenesis.
>fetal demise.
In human, the critical time for druginduced congenital malformations is
in the first trimester.
Drug-induced toxicity can occur at
any time during gestation.

Type of effects on the fetus:

Barker hypothesis:

Teratogenecity- readily detected at,

or shortly after, birth (thalidomide).
Long term latency- ( DES- increased
risk of vaginal adenocarcinoma after
puberty, or abnormalities in
testicular function and semen
production).
Impaired intellectual or social
development (exposure to
phenobarbitone alters programming
of brain)
Predisposition to metabolic diseases
(Barker hypothesis: low birth weight
is associated with increased risk of
diabetes, hypertension and heart
disease in adulthood).
Malformations

The thrifty phenotype hypothesis

says that reduced fetal growth is
strongly associated with a number
of chronic conditions later in life.
This increased susceptibility results
from adaptations made by the fetus
in an environment limited in its
supply of nutrients. These chronic
conditions include coronary heart
disease, stroke, diabetes, and
hypertension

The overall incidence of:

> Major congenital malformations is
around (2-3)%
>minor malformations is 9%
It has been estimated that:
>25% are due to genetic or
chromosomal abnormalities
>10% due to environmental causes
including drugs.
>65% of unknown etiology.
The part played by drugs is probably
small.

The critical time for drug-induced

congenital malformations is usually
the period of organogenesis
>>about 20 to 55 days after
conception.
>>about 34 to 69 days (5-10
weeks) after the first day of the last
menstrual period.
Interference in this process causes a
teratogenic effect.
If a drug is given after this time it
will not produce a major anatomical
defect, but more of a functional one.

Organogenesis

Pregnancy Risk Categories

The drugs are classified according to their risk factor category, and the definitions for each category are used by the Food
and Drug Administration (FDA)
Category A

1)

2)
3)
4)

Controlled
studies in women
fail to demonstrate
a risk to the fetus
in the first
trimester, there is
no evidence of a
risk in later
trimesters, and a
remote possibility
of fetal harm
The only few
medications
classified as
category A are:
Each of the
vitamins when
used in the
recommended
doses (RDA)
Levothyroxine
Antiemetic
doxylamine
Electrolytes
potassium citrate,
potassium chloride,
and potassium

Category B

Animal
reproduction
studies have failed
to demonstrate a
risk to the fetus
and there are no
adequate and wellcontrolled studies
in pregnant women
OR Animal studies
have shown an
adverse effect, but
adequate and wellcontrolled studies
in pregnant women
have failed to
demonstrate a risk
to the fetus in any
trimester
The classical
example is
paracetamol

Category C

Animal
reproduction
studies have
shown an
adverse effect on
the fetus and
there are no
adequate and
well-controlled
studies in
humans, but
potential
benefits may
warrant use of
the drug in
pregnant women
despite potential
risks
These drugs
should only be
given if the
potential benefit
justifies the
potential risk to
the fetus

Category D

There is positive
evidence of human
fetal risk based on
adverse reaction data
from investigational
or marketing
experience or studies
in humans, but
potential benefits
may warrant use of
the drug in pregnant
women despite
potential risks
The benefits from use
in pregnant women
may be acceptable,
as if the drug is
needed in a lifethreatening situation
or for serious
diseases for which
safer drugs are
ineffective or cannot
be used
Examples include ACE
inhibitors and
diazepam

Category X

Studies in animals
or humans have
demonstrated fetal
abnormalities or
there is evidence of
fetal risk based on
human experience,
and the risk of the
use of the drug in
pregnant women
clearly outweighs
any possible benefit
These drugs are
contraindicated in
women who are or
may become
pregnant!
NEVER EVER
PRESCRIBE THEM!!
Examples include
statins and
misoprostol

gluconate

Diethylstilbesterol (DES)

Vitamin A analogues

Synthetic nonsteroidal estrogen that

was first synthesized in 1938, and
currently it is classified as Category
X drug
It was prescribed during 1940-1970
to prevent miscarriages in high risk
pregnancies by increasing the level
of estrogen and progesterone
synthesis by the placenta
In 1971, it was discovered that
women between 16-20 years old
developed vaginal adenocarcinoma,
that was linked to their intrauterine
fetal exposure
Approximately 1 in 1000
pregnancies were exposed, and 75%
of which resulted in girls with vaginal
and cervical carcinomas as well as
uterine anomalies
Male offspring had abnormal
genitalia and sperm defects
Thalidomide

The most common is isotretinoin,

used for the treatment of acne
Classified as category X
The teratogenic effects of retinoids
on animals were known for years
before their clinical use
The critical exposure time is between
3-5 weeks of pregnancy
Contraceptive measures are of
at least one month before,
during treatment, and no
pregnancy for 2 years after a
course of the drug
Fetal abnormalities have not been
associated with topical retinoids but
it is advised to avoid their use in
pregnancy

Teratogenic effects are seen in

up to 25% of babies
50% of affected children have
an IQ below 85
It was approximately recorded
that between 1982 and 1987:
o 900-1300 malformed children
o 700-1000 spontaneous
abortions
o 5000-7000 elective abortions
The embryopathy includes:
o CNS defects
o Craniofacial defects
o Cardiovascular defects
o Thymic defects
o Miscellaneous defects

It is no longer used as an antiemetic

It was used in the past by pregnant women in the 1 st trimester when they start having nausea and vomiting
The mechanism of action is thought to be partly due to antiangiogenesis
Fetal exposure caused high rates of abnormalities (20-30%) that include:
o Severe limb shortening defects (phocomelia)
o Loss of hearing, facial paralysis, anotia, microtia
o Renal malformations
o Congenital heart disease
It is now used for other diseases, such as drug-resistant multiple myeloma, cutaneous lupus erythematosis, erythema
nodosum leprosum, Behcets disease, and Kaposi sarcoma (care must be needed if the patient is a woman in
reproductive age or likes to become pregnant)

Antibiotics

Class of
Medication

Category B

Category C

Antibiotics

Azithromycin
Gentamycin
Aztreonam
Bacitracin
Cephalosporin Chloramphenicol
s
Clarithromycin
Clavulanate
Dapsone
Clindamycin
Erythromycin
Ethambutol
ImipenemMeropenem
ciliastatin
Metronidazole Isoniazid
Nitrofurantoin Linezolid
Penicillins
Pyrazinamide
Polymyxin B
Quinolones**
Sulbactam
Rifampin
Tazobactam
Spectinomycin
Vancomycin
Sulfonamides
Trimethoprim

Category D

Quinine
Streptomycin
Tetracyclines

** Although in category C, give concern for fluoroquinoloneinduced fetal cartilage damage, as most obstetricians avoid
their use in pregnancy

They are the most commonly prescribed

drugs in pregnancy
The safest being Penicillins (B) and
Cephalosporins (B)
Trimethoprim (C) is a theoretical
teratogen as it is a folic acid antagonist
Aminoglycosides can cause ototoxicity
(e.g., gentamyicn (C) and streptomycin
(D))
Erythromycin (C) is probably safe, but
not used from the start
Tetracyclines (D):
Safe during the first 18 weeks of
pregnancy
Minimal effect on bone but after 24
weeks of gestation, discoloration of
the teeth and enamel hypoplasia
occur
Maternal hepatotoxicity in the form of
acute fatty liver, leading to death in
some cases where pregnant women
were treated with large doses
Pregnancy is not terminated if the
women was found to take them

Trimethoprim (C/D) is a theoretical teratogen as it is a

folic acid antagonist
The aminoglycosides(D) can cause ototoxicity
Erythromycin (C) is probably safe
Metronidazole (B)
o Is a teratogen in animals but there is no evidence
of teratogenicity in humans and its benefit in
serious anaerobic sepsis probably outweighs any
risks
Ciprofloxacin (C)
o Results indicate that may affect joints, so caution
and suggest the need for more studies

Chloramphenicol (C)
o Should be avoided in late pregnancy and during
labour because of the potential for the grey
syndrome in the newborn infant
Nitrofurantoin (B)
o May be administered in pregnancy, but should be
avoided near term; may predispose fetal
hemolytic anemia
Vancomycin (B)
o Possible fetal ototoxic effect and should be
avoided unless benefit outweighs potential risk

Antifungals

Griseofulvin (C)
o Is a known teratogen in laboratory animals
o Has ben demonstrated to cross the human placenta
o Is contraindicated during pregnancy
o Pregnancy should be avoided for 1 month after
treatment
o Men should not attempt to father children within 6
months of treatment
Ketoconazole (C)
o Inhibits placental microsomal aromatase and
cytochrome P450
o Should be avoided during pregnancy as there is not
enough information to confirm its safety

Triazoles-fluconazole and itraconazole (C)

o If treatment of these conditions is clinically
indicated, other safer antifungal agents should
be used
Terbinafine (B)
o Approved for the treatment of onchomycosis
and it is estimated that 4 million patients
worldwide have been treated with oral
terbinafine
o Avoid as the adverse-effects profile of oral
terbinafine in pregnancy is limited

There is no obstacle in giving topical

antifungal agents, but systemic oral
medications are avoided

Class of
Medication

Category B

Category C

Antifungals

Amphotericin B
Clotrimazole

Caspofungi Ketoconazole
n
Nystatin
Fluconazole Terconazole
Griseofulvin

Antimalarial agents

Atovaquone/Proguanil (C)
o No fetal harm in pregnant rats and rabbits
o Proguanil is considered to be the least toxic
o Women taking the drug either alone or in
combination should be supplemented with FA
o Should be used with caution in the first trimester

Chloroquine (C)
o At high doses, it is embryo toxic and teratogenic
in rats
o Chloroquine should not be withheld during
pregnancy because the risk of comlications from
malarial infection in pregnancy is increased
o Safe to be breastfeed
(C) Hydroxychloroquine, Mefloquine, Primaquine,
Pyrimethamine, Dapsone, D.Halofantrine

Antiviral drugs

Acyclovir (B)
o Not fond to be teratogenic in pregnant mice, rats
and rabbits
o Probably safe in pregnancy and breastfeeding
Amantidine (C)
o Dose-related teratogenicity in rats at doses
equivalent to the human dose
o No fetal harm was observed in pregnant rabbits
o Birth defects have been observed in humans but
the data are very limited

Anti-retroviral agents
o Amprenavir (C), Indinavir (C), Nelfinavir (B/C),
Ritonavir (B/C) and Saquinavir (B/C) are protease
inhibitors used for the treatment of HIV infection
o No evidence of teratogenicity has been observed
in animals (exceptions of Indinavir)
o Benefit outweigh risks
Zidovudine (for HIV positive) category C, must be given
for the pregnant woman if she is HIV+ve

Avoid during lactation

Anticoagulants
Warfarin (D)

It is contraindicated in pregnancy, as
it crosses the placenta and may
cause bleeding in the fetus
Its use in pregnancy is commonly
associated in with spontaneous
abortions, stillbirth, neonatal death,
and preterm birth
Coumarins (such as warfarin) are
also teratogens; the incidence of birth
defects in infants exposed to
warfarin in utero appears to be
around 5%, although higher figures
(up to 30%) have been reported in
some studies
Warfarin administration in the second
and third trimesters is much less
commonly associated with birth
defects, and when they do occur, are
different from fetal warfarin
syndrome. The most common
congenital abnormalities associated
with warfarin use in late pregnancy

Fetal Warfarin Syndrome (FWS)

Aka dysmorphism due to warfarin,

warfarin embryopathy, or DiSala
syndrome
It occurs when warfarin (or
another 4-hydroxycoumarin
derivative) is given during the
first trimesterparticularly
between the sixth and ninth weeks
of pregnancy
Associated conditions include:
o Hypoplasia of nasal bridge
o laryngomalacia
o Pectus carinatum
o Congenital heart defects
o Ventriculomegaly
o Agenesis of the corpus
callosum
o Stippled epiphyses
o Telebrachydactyly

Associated with nasal hypoplasia

and chondrodysplasia in the first
trimester
CNS abnormalities in later
pregnancy
High incicence of hemorrhagic
complications toward the end of
pregnancy
Neonatal hemorrhage is difficult to
prevent because of the immature
enzymes in fetal liver and low stores
of vitamin K
Recent study doses >5mg had
significantly more fetal
complications independent of the
maternal INR

are central nervous system disorders,

including spasticity, seizures, and eye
defects

Growth retardation

Anticoagulants
Heparin (UFH & LMWH) (B)
Fast-acting anticoagulant with a high binding affinity for antithrombin III
Used in the prophylaxis and treatment of VTE and PE associated with pregnancy, which brings very high mortality to the
women if left untreated
Safe during pregnancy as it doesnt cross the placenta
The most significant side effect is heparin-induced thrombocytopenia, in addition to elevation of aminotransferase,
hyperkalemia, and osteoporosis in chronic use
Does not cross the placenta but may cause maternal osteoporosis and HIT
Cytotoxic drugs
Anticonvulsants

Cyclophosphamide (D) and

chlorambucil (D), are
teratogenic and
contraindicated in
pregnancy
Methotrexate (X) should be
discontinued at least 3
months prior to conception
and FA (5mg) given preconceptually
Azathioprine (D)
o Current evidence
indicates that
maternal use is not
associated wth an
increased risk of
impaired fetal
immunity, IUGR,

o
o
o
o
o

Class of
Medication

Category B Category C

Category D

Anticonvulsants

Magnesium Ethosuxamide
sulfate
Gabapentin
Lamotrigine
Levetiracetam
Oxcarbazepine
Topiramate
Zonisamide

Carbamazepine
Clonazepam
Diazepam
Phenytoin
Primidone
Valproic acid

All the anticonvulsants cross the placenta, and the four principal anti-epileptic drugs
are of category D, and so, most of them are teratogenic
Background risk = 3%
Untreated epileptic = 4%
1 drug = 7%
2 or more drugs = 15%
Val + Carb + Phenytoin = 50%

prematurity and
congenital
abnormalities
o Conflicting
information
regarding breastfeeding
Cyclosporin (D)
o Benefits outweighs
risk, so use with
caution

It is allowable to prescribe one drug, as an optimal treatment needed to stop the

fits rather than the required drug levels, as having a fit is more dangerous to the
mother and baby than the teratogenic effect.
So, this is a classical example of outweighing the benefits over the risks of
teratoegenesis , which the mother must be aware of
Folate has to be given to prevent neural tube defects (5mg/day)

Anti-inflammatory drugs

Aspirin and NSAIDS do not produce structural defects but

may increase the risk of neonatal hemorrhage (they are
considered in category C, but when used in large doses or
for prolonged duration, they will be in category D)
NSAIDS may also lead to oligohydraminos via effects on
the fetal kidney
Some are prescribed in early pregnancy in patients with
history of antiphospholipid syndrome, recurrent
miscarriages, or babies with IUGR
They are usually avoided in the last trimester as they may
cause premature closure of the ductus arteriosus, with
consequent neonatal primary hypertension

Cardiovascular drugs

COX-2 inhibitors
o Fetal COX-2 inhibitors can be resposible for
neonatal chronic renal failure
o Mternal uage should be avoided untl further
studies confirm the safety of this group of drugs
Colchicine (D)
o Given around conception may result in an
increased frequency of trisomy 21 by causing
chromosomal non-dysjnction
o Fetal karyotyping is recommended
o It is recommended that colchicine ingestion by
either parent be discontinued 3 months before
conception

Class of
Medication

Category B

Category C

Cardiovascular
drugs

Methyldopa
Acetazolamide
Hydrochlorothiazid Calcium-channel
e
blockers
Clonidine
Digoxin
Esmolol
Flecainide
Hydralazine
Isosorbides

Category D
Labetalol
Metoprolol
Minoxidil
Nitroglycerin
Nitroprusside
Prazosin
Propanolol
Terazosin

ACE inhibitors
Amiodarone
ARBs
Spironolactone
Atenolol

Cardiovascular drugs

If the treatment of hypertension

is required before 28 weeks,
Methyldopa (B) should be the
first drug of choice
There is concern for use of betablockers in the 2nd and 3rd
trimesters given reports of
intrauterine growth restrictions,
although labetalol has the most
safety data of the class
Calcium channel blockers mainly

Beta-adrenergic antagonists (C)

o Safety in pregnancy is not so well
established
o Guidelines of the ISSHP do not
recommend the use of oral betaadrenergic antagonists for mild
hypertension in pregnancy
Angiotension converting enzyme inhibitors
(D)
o Have been associated with
a. Prolonged renal failure and

Calcium channel blocker (C)

o Safe to use, caution with
MgSO2
Spironolactone (D)
o Anti-androgenic effects
were observed in exposed
male animal fetuses in one
study
o Is contraindicated in
pregnancy

used for severe pre-eclamptic

toxemia (PET)
Spironolactone , amiodarone,
and ACE inhibitors never
prescribed!
o

hypotension in the newborn

b. Decreased skull ossification ,
hypocalvaria, and renal
tubular dysgenesis
c. IUGR, oligohydromnios, PDA
Is not thought to produce structural
malformations, so it is acceptable to
cease treatment early in pregnancy
and not necessarily preconception

Amiodarone (D)
o Can reach the fetus by
transplacental passage and
induce fetal hypothyroidism
o Non-verbal Learning
Disability Syndrome
o Should be avoided during
the 1st trimester of
pregnancy

Endocrine drugs

Insulin is preferred over oral

hypoglycemic agents
Many women are taking
progesterons in the 2nd
trimester
Corticosteroids are relatively
safe, but they are not
prescribed, even if the woman
is breast-feeding

Class of
Medication

Category B Category C

Category D

Category X

Hormones

Acarbose
Adrenal
Desmopressi hormones
n
Calcitonin
Insulin
Glipizide
Metformin Glyburide
Somatostatin Melatonin
Troglitazone Repaglinide
Vasopressin Rosiglitazone
Micronized Tolbutamide
Progestero
ne

Methimazole
Propylthiouracil
Tamoxifen
Hydroxyprogest
-erone

Danazol
Estrogens
Iodide131
Leuprolide
Mifepristone
Testosterone

Endocrine drugs

Oral hypoglycemic drugs

o Suphonylureas (D) have been reported as direct
cause of neonatal hypoglycemia
o There is no firm evidence that these drugs are
teratogenic

Corticosteroids (C)
o Do not appear to give rise to any serious problems
o Transient suppression of the fetal HPAA has been
reported
o May affect growth later in life

Progestogens (D)
o Can masculinize the female fetus
o No evidence this occurs with the small amount in
the COCP

Danazol (X)
o Reports suggest virilization of the external genitalia of
female fetuses
o Should be avoided in pregnancy

Cases of neonatal withdrawal syndrome (usually selflimited) have been described in infants chronically exposed
to benzodiazepines in utero
If used in pregnancy, those benzodiazepines with a better
and longer safety record, such
as diazepam or chlordiazepoxide, are recommended over
potentially more harmful benzodiazepines, such
as alprazolam or triazolam
Using the lowest effective dose for the shortest period of
time minimizes the risks to the unborn child

Tranquilizers & antidepressants

In the United States, the FDA has categorized

benzodiazepines into categories D or X due to
potential harm to the fetus, SSRIs into category C,
and Lithium into D that is not commonly used
Their use by expectant mothers shortly before the
delivery may result in a floppy infant syndrome, with
the newborns suffering
from hypotonia, hypothermia, lethargy, and breathing
and feeding difficulties

Class of
medication

Category B

Antidepressants/ Buproprion
antipsychotics/
Buspirone
anxiolytics
Zolpidem

Bronchial Asthma

Category C
Aripiprazole
Chlorpromazi
ne
Clozapine
Haloperidol
Olanzapine
Quetiapine
Risperidone

Category D
SSRIs
TCAs
Thioridazine
Ziprasidone

Category X

Alprazolam
Other
Chlordiazepoxide BDZ
Clonazepam
Diazepam
Lithium
Lorazepam
Midazolam
Oxazepam

Treat as non-pregnant,
despite of the side effects of
drugs, as an asthma attack
(status asthmaticus) can be
very serious to the mother
and baby
In general, respiratory drugs
are either into category B or
C, and so are relatively safe
during pregnancy

Class of
Medication

Category B

Category C

Respiratory
drugs

Acetylcysteine
Budesonide
Cromolyn
sodium
Ipratropium
Montelukast
Zafirlukast

Albuterol
Corticosteroids (inhaled)
Dextromethorphan
Guaifenesin
Salmeterol
Theophylline

Summary
The decision to use any potentially harmful drug in pregnancy should be made on a case-by-case basis
There should be thorough counseling with the patient
Each case is an individualized case!
Before prescribing any drug, consideration must be given to any harmful effects on the fetus. However, no harm must
come to the mother or the baby because a disease is inadequately treated
To minimize the fetal risks, the lowest effective dose should be used
It is not a shame that you dont know exactly the possible side effects, search for them! To prevent any misinformation
about the teratogenicity of certain drugs
Keep always up-to-date with the drugs information, especially through the teratogen-information service

MENORRHAGIA

It is the most common gynecological case seen in the clinic.

It is the most common cause of anemia in developed countries.
And the 2nd common cause of iron deficiency anemia after poor diet in the developing countries.
Subjective: Prolonged or heavy Regular menstrual bleeding.
Objective: menstrual blood loss more than 80 ml (more accurate), but not used in practice , just in researches)
Thyroid: hypothyroidism.
* Normal menstrual blood loss range from 20 - 80 ml with average of 35 ml.
Coagulation disorder: ITP,
VWD, leukemia...
Advanced liver diseases.
Drugs: Warfarin, Heparin,
Aspirin, Tamoxifen, and

SYSTEMIC PATHOLOGY
(5%)

CAUSES OF
MENORRHAGIA
PELVIC PATHOLOGIC
(35%)

DYSFUNCTIONAL
UTERINE BLEEDING
(60%)

Fibroid (submucosal).
Endometriosis.
Adenomyosis.
Chronic PID.
Copper releasing IUCD.
Endometrial hyperplasia and
malignancy.
Ovarian tumors; Estrogen
producing.

DYSFUNCTIONAL UTERINE BLEEDING

FACTORS OF BLEEDING AMONG MENSES
ETIOLOGY
1- PG E2 and PG F2.
1. Endometrial dysfunction (Ovulatory DUB):
2- Fibrinolytic system.
- PGs imbalance (dec PGF2a : inc PGE2 ratio).
3- Blood Vessels of the endometrium.
- Increased fibrinolytic activity.
The most important is prostaglandin release and
- Ineffective contraction of myometrial vessels.
2. Hypothalamic Pituitary Ovarian hormonal
Fibrinolytic system any disturbance in them
axis: (Anovulatory DUB)
bleeding.
- Most common age at presentation is less than
Disturbance in prostaglandin release such as if
20 and more than 40.
PGE2 increased (it is a vasodilator) will lead to
bleeding and increased PG F2 which will cause
spasmodic or primary dysmenorrhea.
Also, if too much fibrinolytic system activity
menorrhagia.
HISTORY
PHYSICAL EXAM
INVESTIGATION
- Complaint: Assess the amount of blood
- General examination:
- CBC: Hb and platelets.
loss.
General condition (does she
- Pelvic ultrasound: Uterus; size, shape,
- Associated Gynecological problem:
look pale or not?), Vitals,
masses, and endometrial thickness. Adnexia
Congestive dysmenorrhea, deep
Weight, Thyroid, Lymph
- Cervical smear.
dyspareunia, chronic pelvic pain, pressure
nodes (axillary and
- Office biopsy: Pipelle, Novak
symptoms, and vaginal discharge.
inguinal), Breast, Abdomen
- Hysteroscopy and endometrial biopsy:
- Gynecological & Menstrual Hx: Last cx
(Pelviabdominal mass/
Mandatory
smear, previous gynae surgery,
ascites).
for women older than 40 years.
contraception, IMB, and PCB.
- Pelvic examination:
- Others, according to the suspected problem.
- Medical Hx: Thyroid symptoms,
Speculum examination,
Hematological disorders
Bimanual examination.
- Medications: The previous 4 drugs.
- Previous investigations and treatment.
DEFINITION
Menorrhagia in
the absence of
organic (pelvic,
systemic)
pathology.
Is a diagnosis of
exclusion.

TREATMENT
LESS THAN 20 YEARS OLD
Menorrhagia is a common cause of Gyn clinic visit in teenager, mainly due to DUB. (delayed maturation of HPO axis)
Treatment is simple and for short duration (few months) till the hormonal axis becomes mature.
Lines of management:
a) Reassurance and explanation.
b) Correction of anemia if present.
c) Medical treatment.
NON-HORMONAL
HORMONAL
ANTIANTIPROGESTOGENS
COMBINED OCP
DANAZOL
GnRH ANALOG
PROSTAGLANDIN
FIBRINOLYTICS
Most commonly
Tranexamic acid: Norethisterone
- 1tab daily for
- It is an androgen
- 3.75mg IM
used.
- 3 capsule daily,
and
21 days, from
analogue (17-
monthly, for 4
from day 1 to day
Medoxyprogest
day 5.
ethinyl
months.
Mefenamic acid 5 of the cycle.
erone acetate.
- menstrual
testosterone).
- Menstrual
(Ponstan):
- menstrual
- Most common
blood loss by
- Also
blood loss by 80- Is the most
blood loss by 50%. drug used for
50%.
antiestrogentic &
100%.
common drug
- Main S/E: nausea DUB.
- Less
antiprogestrogenic.
- Depression of the
used by
and vomiting, ~
- 5 mg twice daily, commonly used - Depression of the
HPO- axis;
adolescent
25% of patients
from day 5 to day due to its side
HPO- axis and has a
Menopausalsx.
female; for
stop it because of
25 of the cycle.
effects.
direct suppressive
- Major risk:
dysmenorrhea as
these side effects. - menstrual
- Minor S/E:
effect on
Osteoporosis if
well.
- Rarely, it may
blood loss by
Nausea,
endometrium.
used more than 6
- 3 capsules daily, cause cerebral
25%.
vomiting,
- menstrual blood
months.
from day 1 to day thrombosis, so it is - No serious S/E.
headache,
loss by 80 100%.
5 of the cycle.
contraindicated in - Safe to use.
- S/E:
*Although, these
irritability, in
- menstrual
patient with risk
Hoarseness of
drugs are
weight...
blood loss by
factors for
voice.
extremely
- Major side
25%.
thromboembolism.
Hirsutism
and
effective, but they
effects: HT,
-S/E: gastritis,
acne.
are no more used
thromboembolis
gastric ulcer.
nowadays due to
muscle mass.
m,
their serious side
cardiovascular
Cliteromegaly.
effects.
Breast atrophy.
Hypooestrogenic

Menopausal sx.

BETWEEN 20 & 40 YEARS OF AGE

Two lines of management:
A] Medical: same as for the teenagers.
B] Levonorgestrol releasing IUCD (Mirena) they
desire contraception; very effective.
- 20 mcg of levonorgestrol daily.
- It decreases menstrual blood loss by 8090 %.
- ~30% of women are amenorrhoeic after one year of
insertion.
- It decreases the incidence of PID.
- Doesnt increase risk of ectopic pregnancy.
- Side effects: breakthrough bleeding & spotting for the
first 3-6 months after insertion.

ABOVE THE AGE OF 40

Three lines of management:
A] Medical: Same, not OCP.
B] Mirena: Safely used.
C] Surgery:
1) Endometrial resection and ablation:
- Day case surgery under GA.
- Short stay in hospital, rapid recovery.
- Cure rate of 7080%.
- Risk of recurrence 2030%; Risk of endometrial
cancer exists.
2) Hysterectomy: Is the best, 100% cure rate.
No recurrence of the problem.

POSTCOITAL BLEEDING
Def: Bleeding during or after coitus.
Cervical Ectropion
The cause is almost always cervical:It is normal, physiological, it is not an ulcer.
- Cervical ectropion, the commonest cause.
- Occurs in high estrogenic state: Pregnancy or COCP users.
- Cervical ulcer, cervicitis.
- The estrogen will cause overgrowth of the columnar
- Cervical polyps.
epithelium of the endocervix into ectocervix postcoital
- Cervical cancer.
bleeding.
How to diagnose?
- C/C: PCB and excessive mucoid secretions.
- History
- In menopause, there will be inversion (the stratified layer
- Examination: General and pelvic, speculum.
of the ectocervix will move inwards).
Treatment: Should be directed toward the cause; Pap
- During pregnancy; Conservative treatment, after delivery
smear is mandatory before treatment.
it usually improves spontaneously.
- If on COCP, stop it, reassess again.

INTRODUCTION

ECTOPIC PREGNANCY
CAUSES

COMPLICATION

Def: Pregnancy that is implanted

outside the uterine cavity
The incidence nowadays is triple
the previously stated as 0.3%

SITES
Tubes 95%, Rt. > L
- 55% ampulla
- 25% Isthmic
Cervix, Rud. Horn
Ovaries
Peritoneal Abdominal

PRESENTATIONS
- Silent On routine
examination or
laparotomy
- Acute (often rupture)
- Subacute (Variable
presentations
DDX
Threatened
miscarriage
Corpus luteum cyst:
Amenorrhea, Unilateral
pain, Spotting, No
Pregnancy sx, Negative
HCG, If ruptured Same
treatment.
PID:
Bilateral, No amenorrhea
or pregnancy sx, Signs
of infection (50%)

Any delay in ovum passage until

implantation stage.
Tubal abnormalities: Diverticulae,
False passages, Endosalpingitis
ART
Endocrine disorders: Delayed
ovulation, Estrogen/Progesterone
Ratio.
Contraceptive failure: Minipill (46%), IUCD(4-9%), Tubal surgery
(lig., constr.)
Prior history (10-20% Recurrence)
Pathology: PID, Endometriosis
Others

-Tubal abortion
- absorption in tube
- Incomplete tubal abortion
- Tubal blood mole
- Tubal rupture
- intraperitoneal bleeding
- Broad ligaments
MANAGEMENT
- I.V. line (wide bore)
- Blood, Hb, group, cross- matching
- Once diagnosed laparatomy
laparoscopy
Expression
Salpingostomy
Salpingectomy

DIAGNOSIS
SYMPTOMS
INVESTIGATIONS
Amenorrhea (6-10 wks)
- Pregnancy test
Symptoms of pregnancy
Serum hCG correlates well with trophoblastCell
Abdominal pain (99%):
mass.
Generalised (45%), Unilateral
Ectopic rarely ruptures when cell mass is small or
(35%), Shoulder tip (25%)
hCG levels are low.
Abnormal uterine bleeding (75%) In normal pregnancy values, serum hCG > 1500
Any form
mlu/mL, must see gestational sac
Syncopal sx (35%)
In normal pregnancy, hCG Values doubles every
Adnexal tenderness (96%)
2.2 days. It doesnt occur in ectopic pregnancy.
Adnexal mass (90%)
- Blood Hb, grouping
Uterine size: Normal (70%)
- Transvaginal Ultrasound:
- 6 to 8 wks 25%
Intrauterine sac: - Pseudo sac (10-20%)
D&C curettings: -Proliferative,
- True sac (Yolk sac F.
secretory
Poles)
- Arias-stella
Adnexial mass (90%): - Sac with fetus or no
phenomenon
fetus
- Echogenic mass
(DDx. C.L)
Fluids in P.O.D: - in 80% of Ruptured ectopics

- In 20% of normal
pregnancy
** If Gest sac > 20 mm or (5-6 wk), must see yolk sac
& fetal pole. if not seen, suspect either ectopic or
blighted ovum
- Laparoscopy

Acute appendicitis

No sx of pregnancy
UTI

ENDOMETRIAL CARCINOMA
Malignant lesions of the body of uterus

Body of uterus composed of 3 layers (endometrium,

myometrium, serosa)
Myometrium
o Smooth muscle
o Malignant: Leiomyosarcoma

Endometrium
o Glands + Stroma
o Glands: Adenocarcinoma
o Stroma: Endometrial stromal sarcoma
o Glands + Stroma: Uterine
carcinomsarcoma/MMMR (mixed malignant
Mullerian tumor)

ENDOMETRIAL ADENOCARCINOMA

Disease of
menopause
Peak incidence
61.75% in
postmenopausal
women
There is marked
geographical and
racial variation in
the incidence, very
common in western
countries
Most common

Etiology

Pathology

Estrogen-dependent neoplasia

Estrogen-independent
neoplasia

Normally, endometrium is
exposed to estrogen in the 1st
half of the menstrual cycle and
progesterone in the 2nd half
Estrogen is bad, Progesterone is
protective
When endometrium exposed to
estrogen and not opposed by
Progesterone, will lead to
endometrial hyperplasia and
carcinoma
COCP & progesterone have

Younger, perimenopausal
women
History of chronic estrogen
exposure
Tumors initially endometrial
hyperplasia, progress to
carcinoma
Well differentiated
Favourable prognosis

Not associated with

endometrial
hyperplasia
Older,
postmenopausal, thin
women
Less differentiated

gynecological
cancer in the US
(obesity), rare in
Japan and China
Emigrant Japanese
in America gained
similar rates to
those of
Americans. So,
theres
geographical and
racial factors

protective effect against

endometrial CA
This can happen in:
1. Obesity (peripheral
conversion of androgens into
estrogen)
2. Nulliparous (unovulation)
3. Estrogen HRT
4. Estrogen secreting ovarian
tumor
5. Familial: HNPCC Lynch
Syndrome (ovarian, colon,
endometrial cancer)

Most common type of endometrial cancer: Endometrioid

adenocarcinoma (80%)
Other types: mucinous ca, clear cell ca, squamous ca,
papillary serous ca
Squamous cell in adenocarcinoma:adenosqumous ca
Small group of endometrial ca resembles ovarian ca:
Papillary serous & clear cell ca
o Elderly (>70), thin
o Not estrogen related
o Advanced stage at presentation

Commonest is the 1st type (estrogen related)

ENDOMETRIAL ADENOCARCINOMA

ENDOMETRIAL SARCOMA

Spread

Diagnosis

Direct invasion
Lymphatic
Blood (rarely)

Presentation

Postmenopausal bleeding
o Only in 10%
o 85%: atrophic dermatitis
o All PMB should do biopsy

Cervical smear
Transvaginal U/S
o Endometrial thickness of
postmenopausal women is
<4mm
o If >4mm, do biopsy
Biopsy: by hysteroscopy/D&C
If staging confirmed carcinoma, do
staging investigation: CBC, KFT,
LFT, CXR, pelvic MRI
Prognosis

Rare, very
aggressive
Pain &
bleeding
2 year suvival
LEIMYOSARCOMA

Most arise from normal endometrium

May arise from fibroid transformation
Abnormal bleeding, pelvic pain
Should be suspected in rapidly enlarge fibroid/
lesions keep enlarging after menopause
Diagnosis made after hysterectomy by

Premenopausal: IMB,
irregular periods
Pain (late presentation,
tumor has invaded locally
compressing pelvic plexus
and nerves)
Physical signs

Rarely suggest diagnosis

Uterine enlargement
Palpable LN (groin,
supraclavicular)
Vaginal nodule (in advanced
stage)

Stage
Grade
Myometrial invasion
Age
o Young: endmetriod type (good
px)
o Elderly: serous (bad px)

histological examination
Adjuvant raditherapy and chemotherapy is
questionable, not much benefit

Staging
Stage 1: confined to body of uterus
Stage 2: involvement of cervix
Stage 3: ovaries & tubes
Stage 4: Metastasis

Treatment
Stage 1 &2 (no bad prognostic factor): Hysterectomy + BSO +/- N
dissection
Stage 1 & 2 (with bad prognostic factor): adjuvant chemotherapy
Stage 3 & 4 (dissemination): combination radiotherapy, chemotherapy,
hormonal therapy
Endmetrial ca usually present in early stage
5 year survival rate is 70%
ENDOMETRIOSIS
Def: Presence of endometrial glands and stroma outside the endometrial cavity and walls.

Deposits proliferate during the menstrual cycle, break down & bleed, causing local inflammatory reaction.
Fibrosis & distortion of the tissue affected with dense scarring.
Benign.
EPIDEMIOLOGY
OVERVIEW
SITES
More commonly in the dependant
Disease of reproductive age
Hormone dependant
part of the pelvis
group
Responds to estrogen
Ovaries (2/3 of women)
Affect 5-15% of women
Regress after menopause, oopherectomy
Broad ligament
Diagnosed in 20-30% of
and during pregnancy
Peritoneal surface of Cul-de-sac
women investigated for
ETIOLOGY
and uterosacral ligaments
infertility
Unknown

Rectovaginal septum

More in women whose first

Theories
Rectosigmoid colon
degree relative have the
Retrograde menstruation
Distant and laparatomy scars
disease
Coelomic epithelium transformation
Often diagnosed incidentally
Lymphatic and vascular spread
High social class women in
Genetic and immunologic factors
their thirties and infertile!
Can be diagnosed in any type
of women and all age groups
PATHOLOGY
HISTOPATHOLOGY
Gross
Active endometrial glands and stroma
Hemorrhagic vesicle
Free
Blood filled cystic lesions
Papule and later nodule
Fibrosis with glands only no stroma
Enclosed
Adhesion formation
White nodules or flattened fibrotic scar
Healed
Ovarian endometrioma is an enclosed hemorrhagic cyst
of variable sizes

SYMPTOMS
According to site
No relation between extent of the disease and severity of the symptoms
Often discovered incidentally
FEMALE
Dysmenorrhea, Lower abdominal and pelvic pain, Dyspareunia, Accident to endometriotic cyst,
REPRODUCTIVE
Low back pain, Infertility, Menstrual irregularity
TRACT
URINARY TRACT
Cyclical haematuria / dysuria, Ureteric obstruction
GIT
Dyschezia, Cyclical rectal bleeding, Intestinal obstruction
SURGICAL SCAR &
Cyclical pain and bleeding
UMBILICUS
LUNGS
Cyclical haemoptysis, Haemopneumothorax
CLNICAL FINDINGS
INVESTIGATIONS
DDx
DIAGNOSIS
Often Negative
Ca 125 often
All causes of chronic pelvic
Direct visualization of the
elevated
pain
lesion
Suggested by
Laparascopy
Thickening and nodularity Ultrasonography for
Acute conditions
Laparatomy
of uterosacral L.
ovarian cyst
Ectopic pregnancy
Tenderness in POD
MRI
Acute PID
Histopathology to confirm
Ovarian mass/ masses
Complicated ovarian cyst
the diagnosis
Fixed retroverted uterus
Acute appendicitis and
Tender nodule in the
other surgical
cervix, umbilicus or scar
emergencies

TREATMENT
NSAIDS
PSEUDOPREGNANCY

- Combined OCP continuous

- Cyclical ?? of limited value
Side effect
- Synthetic progestogens: Medroxyprogesterone acetate and dydrogesterone high doses continuous
Side effect
- Levonorgestrel-releasing system reduces dysmenorrhoea and regress POD implants
PSEUDO Danazol androgen derivative 6-9 months
MENOPAUSE
Gestrinone, androgen derivative
Both drugs have androgenic side effects
GnRH agonists - Menopausal symptoms, Osteoporosis
? Add back therapy
SURGERY
CONSERVATIVE
Young patient, women seeking pregnancy, cysts >3cm in diameter
Surgical excision, Laser
HYSTERECTOMY &
Radical/Definitive surgery
BSO
FACTORS TO CHOOSE TREATMENT
ENDOMETRIOSIS & INFERTILITY
Certainty of diagnosis
Ovarian function
Severity of symptoms
Tubal function
Extent of the disease
Coital function
Fertility
Sperm function
Age
Early pregnancy failure
Damage to other organs

ADENOMYOSIS
Endometrial glands deep within the myometrium
Unknown etiology
Different type of patient and presentation
RISK FACTORS
TREATMENT
Multiparous women
Induce amenorrhea - sx recur once treatment is stopped.
Late thirties or early forties
Hysterectomy is the only definitive treatment
Severe spasmodic dysmenorrhea
Menorrhagia
Bulky uterus
Diagnosis often histological on examination of
hysterectomy sample

FETAL GROWTH ASSESSMENT

Obstetric Care
Objective

Fetal growth

The normal fetal growth pattern

Decrease the
maternal and
perinatal morbidity
and mortality

How to achieve these

objectives
1. Early confirmation of
dates
2. Detection of
congenital
malformations
3. Detecting fetal
hypoxia
4. Detecting abnormal
fetal growth
Small for gestational age

Fetal growth is
dependent on
genetic, placental
and maternal factors.
Fetal growth
restriction is the
second leading cause
of perinatal morbidity
and mortality.

Small for gestational age is defined as a fetal

birth weight below the 10th centile for the stated
gestational age.
The incidence of SGA fetuses is 5-10%

1/3 of the eventual birth is reached by 28 weeks , by 31 weeks ,

2/3 by 34 weeks

Constitutionally Small Fetus

Unfortunately, it can be concluded that a fetus

is constitutionally small only after pathologic
processes have been excluded.
Therefore, identification of a constitutionally
small infant is usually made in retrospect, after
the infant is born
Why is the fetus constitutionally small?

1.
2.
3.
4.
5.
6.

Determinants of fetal growth are multifactorial :

Race
Geographical area
Sex (M>F)
Maternal age
Maternal weight and height
Socioeconomic status

Assesing fetal growth

1.History

2.Examination

1. Mothers age
2. Accuracy of LMP date
3. Infections during
pregnancy
4. Multiple pregnancy

General examination
Obstetric examination
Uterine fundal ht

Uterus size

5. Antenatal care and visits

6. Supplements
7. Past obs. History
8. Past medical history
9. Drug history
10.Family history
11.Socioeconomic history

Obtaining serial uterine fundal height

measurements.
The Mcdonalds rule in pregnancy is
a rough determination of fetal age in
weeks

Evaluating the size of the uterus by pelvic

examination in the first trimester and
subsequent antenatal visits
Uterine size = Misleading in: Full bladder,
obesity, deep masses, uterine fibroids
&multiple pregnancy

Assesing fetal growth

3.Investigation: U/S
Uses of US

Diagnosis and Confirmation of Viability

Determination of GA and
assessment of fetal size
and growth

1. Diagnosis and
confirmation of viability in
early pregnancy
2. Determination of
gestational age and
assessment of fetal size
3. Intrauterine or Ectopic
pregnancy.
4. Multiple pregnancy
5. Diagnosis of fetal
abnormalities
6. Placental localization
7. Assessment of fetal wellbeing

Detection of :

a.
b.
c.
d.

Crown-Rump length
Biparietal diameter
Head circumference
Abdominal
circumference
e. Femoral length

Gestational sac (4-5 wks)

Yolk sac (5 wks)
Embryo (5-6 wks)
Visible heart beat (6 wks).

Up to 13 wks :
- Crown-Rump Length (CRL)
from 16 to 24 wks :
- Head circumference (HC)
- Biparietal Diameter (BPD)
- Femur length (FL)

a.Crown-Rump Length (CRL)

From Crown to Coccyx (Rump) (longitudinal

axis).
Accurate up to 14 wks (1st TM).
It is the most accurate parameter.
Provides accuracy of +/- 5 days from the GA.

3.Investigation: U/S
b. Bi-parietal Diameter (BPD)

The transverse width of the head at its

widest (the distance between the
parietal bones eminence of the skull).
Accurate up to 16-24 wks.
Provides accuracy of +/- 7 days.
It is affected by the shape of the head.

Not affected by the shape of the head.

c.Head circumference (HC)

3.Investigation: U/S
d. Femur length (FL)

e.Abdominal circumference (AC)

Better than BPD in accuracy and timing.

Accurate only when the image shows two blunted ends
of the femur.

 It is the most accurate single predictor of fetal weight.

IUGR
Is ..
Failure of the fetus to
achieve its growth
potential
True or False?

All SGA infants are

IUGR
False

All IUGR infants are

SGA

It is made at the widest points in the abdomen.

It is the most accurate single predictor of fetal weight.

IUGR and SGA

Incidence

3 - 10 % of all pregnancies.
20 % of stillborns are growth retarded.
9 - 27 % have anatomic and/or genetic
abnormalities.
Perinatal mortality is 8 - 10 times higher for
these fetuses.

False
Classification of
IUGR

Maternal causes

Physiological

Pathological

Multiple
pregnancy

1. Decrease Uteroplacental
blood flow:

Symmetrical growth
restriction: fetus
whose entire body
is proportionally
small.
Incidence : 20 %
Asymmetrical
growth restriction:
Decrease in
subcutaneous fat
and abdominal
circumference with
relative sparing of
head circumference
and femur length.
Incidence : 80 %

- Short stature
- Younger or
older age (<15
and >45)
- Low
socioeconomic
class
- Primiparity
- Grand
multiparity
- Low
pregnancy
weight
- Previous h/o
preterm IUGR
baby

Pre eclampsia /
eclampsia
chronic renovascular
disease
Chronic hypertension
2. Maternal malnutrition
3. Maternal hypoxemia
- Hemoglobinopathies
- High altitudes
4. Drugs
- Cigarettes, alcohol, heroin,
cocaine
- Teratogens, antimetabolites
and therapeutic agents such
as trimethadione, warfarin,
phenytoin
- Chronic illness ( DM, renal
failure, cyanotic heart disease

etc.)

Fetal causes
Physiological

Placental Causes
Pathological

Placental insufficiency ( most

- Genetic Factors:
- Race, ethnicity, nationality
- sex (male weigh 150 -200 gm more
female )
- parity (primiparous, weigh less than
subsequent siblings)

Genetic disorders (Achondroplasia,

Russell - silver syn.)
Chromosomal anomalies:
- Chromosomal deletions
- trisomies 13,18 & 21
Congenital malformations:
eg: Anencephaly, GI atresia, potters
syndrome, and pancreatic agenesis.

o
o
o
o

imp in 3rd trimester)

Anatomic problems:
Multiple infarcts
Aberrant cord insertions
Umbilical vascular thrombosis &
hemangiomas
Premature placental separation
Small Placenta

Fetal Cardiovascular anomalies

Congenital Infections:mainly TORCH
infections.
Inborn error of metabolism:
- Transient neonatal diabetes
- Galactosemia
- PKU
Diagnosis of IUGR
History
Physical examination
Investigations
U/S

Abdominal circumference is the single most effective

parameter for predicting fetal weight because its
reduced in both symmetrical & Asymmetrical IUGR .
In the presence of normal head and femur
measurements, abdominal circumference (AC)
measurements of less than 2 standard deviations below

Asymmetrical growth restriction: BPD is normal in the

3rd trimester , whereas ratio of HC/AC is abnormal .
Symmetrical growth restriction : HC/AC may be normal .
amniotic fluid volumes ( oligohydramnios is associated
with IUGR) .
Umbilical artery & fetal artery dopplar assessments :
increased resistance is associated with a greater risk of
IUGR as pregnancy progresses.

the mean appear to be a reasonable cut off to consider a

fetus asymmetric.

Complications of IUGR
Antenatal
Complications

Intrapartum
complications:

Neonatal complications

1- related to hypoxia
and acidosis:

Metabolic changes
(acidosis,..).
Oligohydramnios
(80%)
Abnormal fetal heart
patterns.
Abnormal Doppler
studies.
Intra uterine fetal
death.

Abnormal CTG.
Fetal death.
Meconium stained
liquor.
Increased incidence
of instrumental and
caesarean
deliveries.

a- meconium
aspiration.
b- persistent fetal
circulation.
c- hypoxic
ischemic
encephalopathy

2- metabolic:

3- related to the etiology:

ahypoglycemia

a- chromosomal abn.

bhypocalcaemia
chypothermia
dhyperviscocity

b- infection.
c- congenital anomalies.

syndrome
Management Principles
Pre-pregnancy

During pregnancy (Ante-partum)

Mode of delivery

Modify lifestyle
habits.
Detect and treat
medical disorders.

Regular antenatal care.

Serial fetal growth
assessment.
Serial fetal wellbeing
assessment
1-Biophysical profile
2-Computerized CTG
3-Umblical artery Doppler
Timing of delivery.
Mode of delivery.

Time & Mode of delivery

governed by:

Cesarean delivery without

a trial of labor:
1. in the presence of evidence
of fetal distress

maternal age
past obs. History
gestational age
fetal well being
status of cervix
availability of direct
monitoring during labor.
Ex: scalp PH sampling.

2. for traditional obstetrical

indications for cesarean
delivery
Induction of labor
continuous heart rate
monitoring and scalp pH
monitoring optimize success
of vaginal delivery

FIBROIDS

Fibroids(Leiomyomas
) are wellcircumscribed
benign uterine
tumors
Arise from the
overgrowth of
smooth muscle and
CT in the uterus
They are monoclonal

Frequency

Race

Age

Anatomy

It is the
commonest
tumor of the
female genital
tract
Being present in
at least 20% of
women over the
age of 35

Leiomyomas occur
more commonly in
black women than
white women, with
a black-to-white
ratio of 3-9:1
In Caucasian, but
not black women it
is associated with

Leiomyom
as occur
most
commonly
in women
older than
30 years
But they
may occur

Mostly occur in the fundus and

body of the uterus; only 3%
occur in the cervix
They may be solitary, multipe or
diffuse
o 95% are intramural
o Subserosal/ exophytic,
they can become
pedunculated

proliferation of
smooth muscle cells
which also contains
some fibrous CT
elements

The peak age of

incidence of
symptoms is
between 35-45
years

nulliparity or
relative infertility

in F of any
age

Hormonal effects

Mortality/Morbidity

Infertility

Growth may be related to

estrogen stimulation
o Both estrogen and
progestin receptors are
present in fibroids
o Elevated estrogens
levels my cause fibroid
enlargement. During
the 1st trimester of
pregnancy, 15-30% of
fibroids may enlarge
then shrink I
puerperium. Some
fibroids may decrease
in size during
pregnancy
o Fibroids may shrink
after menopause.
Some regrowth may
occur with hormonal
therapy

Clinical details

Malignant change to
become a sarcoma
o The true incidence
of malignant
transformation is
difficult to
determine because
leiomyomas are
common, whereas
malignant
leiomyosarcomas
are rare and can
arise de novo
o The incidence of
malignant
degeneration is less
than 1.0% and has
been estimated to
be as low as 0.2%

May occur as a result

of
o Narrowing of
the isthmic
portion of the
fallopian tube
o Or as a result of
interference
with
implantation,
especially
interference
caused by
submucosal
fibroids

Rarely, they may occur in

the broad ligament
Submucosal/
subendometrial fibroids
are the least common.
They can present as
fibroid polyp

Complications during
pregnancy
1. Spontaneous
miscarriage
2. IUGR
3. Pre-term labour
4. Uterine dyskinesia/
inertia during labour
5. Obstruction of the birth
canal
6. PPH
7. Hydronephrosis

 Most women with fibroids are asymptomatic

Only 10-20% of pt require txt
Symptoms of fibroids are related to the (location, size and the # of the tumors)
Symptoms may include the following
1.Bleeding
2.Pressure

3.Pain

Menorrhagia
o Increased amount & duration of
flow
o Is the most common symptom
May result in severe anemia and can be
life threatening, although this is rare
o Usually results from the erosion of
a submucosal fibroid into the
endometrial cavity
Rarely, dilated veins on the surface of a
subserosal pedunculated fibroid can
cause sudden massive intraperitoneal
bleeding

1. On bladder
o Frequency, urgency +/incontinence
2. On the colon
o Constipation
o Difficult defecation
o Rectal pain
3. Abdominal cramping results
from pressure on the small
bowel
4. Generalized pelvic &/ lower
abdominal discomfort may be
present

Women may experience

abdominal cramping
Pain usually is felt during
menstruation
Less often, pain occurs
intermenstrually
4.Others

Rare causes of secondary

polycythemia, cured with
hysterectomy are reported
Infertility and/or complications of
pregnancy may occur. Submucosal
fibroids may affect fertility

Complicated fibroids
1.
2.
3.
4.

Torsion of the pedicle

Hemorrhage
Infection (usually at the tip of the fibroid polyp)
Hyaline degeneration:
o present to some degree in most moderate
to large fibroids
o It becomes painful, enlarged and soft
5. Cystic degeneration

6. Red degeneration (necrobiosis)

o Occur typically in pregnancy
o Is due to infarction of the center of the tumor during midpregnancy
o Characteristically, the fibroid suddenly enlarges and is
painful & tender
o It can be mistaken with PA/ acute abdominal emergency
o In pregnancy it is treated conservatively
7. Calcification
o Usually seen in post-menopausal and/or pedunculated
fibroid

8. Malignant change

Investigations

U/S appearance

Treatment

1. Conservative
o The tumor is small and asymptomatic
in pregnancy
o Near menopause and asymptomatic
2. Medical (LHRH analogues), short term
o Contra-indication for surgery
o Adjunct to surgery in a large fibroids
3. Surgery
o Symptomatic fibroids
o Rapidly growing fibroids
o Diagnosis is in doubt
o Likely to complicate future pregnancy
4. Embolization

U/S is the preferred method

In some pt, MRI provides
additional information
The role of CT is limited
o Calcifications may be
more visible on CT
scans than on
conventional
radiographs because
of the superior
contrast
differentiation with CT

The most frequent is that of a

concentric, solid, hypoechoic mas
This appearance results from the
prevailing muscle
These solid masses absorb sound
waves and, therefore, cause a variable
amount of acoustic shadowing
Variable degree of echogenicity,
depending on the amount of fibrous
tissue and/or calcification
Fibroids may have anechoic
components resulting from necrosis
Fibroids in the lower uterine segment
may obstruct the uterine canal,
causing fluid to accumulate in the
endometrial canal
The echogenic endometrial striae may
be displaced by a fibroid. Calcifications
are hyperechoic, with sharp acoustic

Hysterectomy is the definitive txt

Myomectomy in women who are
subfertile/ those who refuse
hysterectomy

shadowing. Diffuse leiomyomatosis

GENITAL PROLAPSE
Genital prolapse is the downward descent of the uterus and /or the vagina towards or through the introitus
Occurr in about 10-30% of multiparous women and in 2% of nulliparous women .
TYPES
PELVIC SUPPORT
ETIOLOGY & PATHOPHYSIO
PREVENTION
UTERINE
VAGINAL
UTERUS
Weakening of and damage to the
Genital
supporting structures of the pelvic
prolapse is a
1st degree:
Cystocele: Prolapse i) Transverse @
organs:
preventable
Cardinal @
Descent of the
of the upper 2/3 of
1. Childbirth: (most imp)
disease
cervix within
the anterior vaginal Mackenrodts
Increasing parity, prolonged labour,
1. Prevention
cervical
the vagina.
wall and the
bearing down before full cervical
during
ligaments.
2nd degree:
bladder.
dilatation
and
difficult
instrumental
childbirth:
ii)
Uterosacral
Descent of the Urethrocele:
deliveries.
Good
labor
ligaments
cervix thru the
Prolapse of the
2. Chronic elevation in intramanagement,
iii) Pubocervical
introitus.
lowest 1/3 of the
abdominal pressure: Obesity,
postnatal pelvic
ligaments
3rd degree
anterior vaginal
smoking,
chronic
cough,
chronic
floor exercises,
wall and the
(Procidentia):
constip,
heavy
lifting
at
work,
abd
family planning.
Dont
give
urethra.
Descent of the
masses
and
ascites
.
2. Avoiding
cervix and the Rectocele: Prolapse support to the
3. Menopause: Weakness of the pelvic
uterus, ie broad
whole uterus
of the posterior
intra-abd
support
due
to

collagen
and
ligaments,
round
through the
vaginal wall and
pressure
weakness of the connective tissue
ligaments and the
introitus.
the rectum.
Obesity ,
4. Pelvic surgery :
levator ani
Enterocele: True
smoking,
Abd / vaginal hysterectomy
chronic cough
hernia of the pouch muscles
Vault
prolapse
and chronic
of Douglas through
VAGINA

the posterior
vaginal fornix - may
contain bowel or
omentum.
Vault prolapse:
Inversion of the
vaginal apex which
occur after
abdominal or
vaginal
hysterectomy.

Pelvic floor
muscles (the
levator ani
muscles mainly
and the
superficial and
deep transverse
perineal muscles)
and by the pelvic
floor fascia.

Composuspension Rectocele
and enterocele.
5. Congenital prolapsed - congenital
amount of collagen and weakness
of connective tissue of the pelvic
support. For the prolapse in 2% of
nulliparous women .
6. Racial variation .
Common in Caucasian women , less
common in Asians , and rare in Blacks .
Variation in the amount of collagen and
connective tissue in the pelvic support.

constipation
3. Prevention
postmenopa
usal:
Balanced diet,
exercise,
calcium & by
the increased
use of HRT.

DIAGNOSIS
EXAMINATION
DDx:
- Inspection of the vulva with cough and
Anterior
straining demonstrate severe prolapse and
vaginal wall
A feeling of something coming down below or a lump may demonstrate stress incontinence
prolapse:
(provided the bladder is full)
within the vagina or protruding from the introitus DDx: Congenital
- Speculum examination either dorsal
Gartners cyst,
worse at the end of the day, on standing and
position
(Bivalve)
or
left
lateral
position
inclusion dermoid
coughing, and by lying down.
(Sims).
cyst & urethral
- Other sx, depends on the organ which prolapsed into
- Rectal examination - differentiate between diverticulum.
the vagina.
rectocele (finger goes thru it) from
Uterine
Uterine prolapse: Low backache - central, worse at
enterocele (finger goes high up) .
prolapse:
the end of the day, on standing and by lying
DDx: large
down.
INVESTIGATIONS:
cervical or
Cystocele: Urinary sx, pt has to reduce the cystocele - MSU for analysis and culture.
endometrial
to empty her bladder.
- Renal ultrasound and IVU in cases of
polyp & chronic
Rectocele: Constipation, incomplete rectal
procidentia and severe cystocele to exclude
uterine inversion
evacuation and the patient has to reduce the
hydroureter & hydronephrosis.
rectocele digitally to empty her rectum.
- Cystometry in cases of incontinence, to
exclude urge incontinence
Procidentia: Ulcer, blood stained or purulent vaginal
discharge.
Coital problems - uncomfortable or difficult intercourse
in uterine and vaginal prolapse.
MANAGEMENT
CONSERVATIVE TREATMENT: PESSARY
INDICATIONS
TYPES
SIDE EFFECTS & THEIR MANAGEMENT
- Patient unfit for surgery .
Vaginal infection and discharge, ulceration and bleeding.
Ring pessary
- Patient refuses surgery .
commonly used
- During pregnancy and after delivery .
Precautions:
pessary.
- During waiting time for surgery.
Shelf pessary Use silicon pessary.
- As a therapeutic test to confirm that
Change the pessary yearly or earlier if infection or
rarely used
HISTORY
Sx depends on the site, type & degree of the prolapsed.

surgery may help.

ulceration occurred.
Use of vaginal estrogen cream in menopausal patients.

SURGICAL TREATMENT
PRE-OPERATIVE ASSESSMENT
TYPE OF SURGERY
Aims of surgery: Correct prolapse, maintain
Depends on: 1. Type of prolapsed, 2. Age and parity
UTERINE
VAGINAL
continence and preserve coital function.
i.
Vaginal
hysterectomy
the
i)
Cystocele
&
Success of the surgery depends on:
preferred operation in
Urethrocele:
1. Preoperative preparation of the patient such as
uterine prolapsed. For young Anterior
reduce weight in obese, stop smoking and
colporrhaphy.
treatment of chronic cough. (Gynaecologist cant do patients who complete the
family and in menopausal
ii) Rectocele:
his part unless the patient fulfills hers).
patients.
Posterior
2. Postoperative care
colpoperineorrhaphy
POST-OPERATIVE CARE
ii. Manchester (Fothergill)
.
Immediate postoperative care :
operation.
iii) Enterocele:
Vaginal pack remove within 24h.
Indicated
in
young
patients
Resection of
Foleys catheter - remove after 1- 2 days.
who not complete the
enterocele sac.
Prophylactic antibiotics: Metronidazole and
family.
iv) Vault prolapsed:
cephalosporin
Consisted
of
:
Abdominal
Instructions after discharge - to minimize recurrence
1. Partial amputation of
sacrocolpopexy.
Avoiding intercourse for 6 wks.
the cervix
Gradual return to normal activities over 2
2. Shortening of the
months.
transverse cervical
Avoiding smoking, obesity, constipation and
ligaments and suturing
lifting of heavy objects.
them to the front of cervical
Elective C.S. in the subsequent pregnancy.
stump.
RECURRENT PROLAPSE

of the patient
LEFORT
- Rarely
indicated in
elderly and
frail patients
who are unfit
for vaginal
hysterectomy
or pelvic floor
repair.
- Rectangular
strips of
vaginal
epithelium are
removed from
the anterior
and posterior
vaginal walls in
order to obtain
a partial
closure of the

Recurrence occur in about 20-25%

Even with expert surgery and good postoperative
care, recurrence can occur, esp in the presence
of obesity, smoking and constipation.

3. Anterior and posterior

repair.

vagina.

iii. Sacrohysteropexy
In patients who complete
the family and wish to
conserve the uterus

GESTATIONAL DIABETES MELLITUS (GDM)

Classification

Whites Classification

Diabetes mellitus
type I --- insulin
dependent
(Ketosis-prone)
Diabetes mellitus
type II--- noninsulin
dependent
(Ketosisresistant)
Impaired Glucose
Tolerance and
Gestational
Diabetes (IGT)
Diabetogenic
Effects of
Pregnancy

Insulin resistance
Increased
lipolysis
Altered maternal

DM= Fasting venous glucose

concentration > 8.0 mmol/l and 2
hrs (75 gm load ) > 11.0 mmol/l
(or) one of the above + Symptoms
IGT = Fasting < 8.00 mmol/l, but 2
hr (75 gm load) = (9.0-10.9)

How do diabetic pt present

Symptoms
Risk factors ( history &
examination)
Blood tests--screening

Screening

30% have none of the Above risk

factors
Not all DM, IGT, have persistent
glucosuria
50% of pregnant women have
glucosuria at some time

WHO recommended modified GTT ( 75 gm load)

Impaired glucose tolerance

Fasting

Normal

6.0-7.9

Hours 2

6.0 >

And

Or

9.0-10.9

9.0>

gluconeogenesis

Risk Factors
DM, IGT, must be suspected
in Pregnant women with
1. Age > 30
2. Family history of DM
3. Past history of:
- Diabetes in a previous
pregnancy

4.
5.
6.
7.

Obesity
Hypertension in multipara
Polyhydramnios
Recurrent
infections:Urinary, Fungal
8. Significant Glycosuria

- Unexplained I.U.F.D.,
Neonatal death
- Congenital abnormalities
- Recurrent abortions
- Large babies > 90th centile
Risk factors

Complications

Complications
Maternal

Obstetric
- Polyhydramnios
- pre-eclampsia (1015%)
Diabetic
Emergencies
- Hypoglycaemia

- Ketoacidosis

Fetal
Neurol
ogic
- Peripheral
neuropathy

Gastrointestinal
disturbance

Infecti
ons

(1) Macrosomia &

Traumatic delivery

Central Nervous
system

(30% in seemingly
controlled)

- Anencephaly

** Note: when a two-vessel

cord is found, suspect a high
incidence of congenital
anomalies

Holoprosencephaly

(4) Intrauterine fetal

Death

(2) Delayed organ

maturity (RDS) 6x
(3) Congenital
malformations:

- Encephalocele
Skeletal & spinal

(5) Growth restriction (in

advanced DM)

- Diabetic coma
Vascular &
End-Organs
-Renal

- Ophthalmic

- Urinary

Cardiovascular :

Transposition of great
vessels
Ventricular septal defect
Aortic coarctation
Artial septal defect

-Caudal regression
Genitourinary
- Renal agenesis
- ureteral dupliction
Gastrointestinal

- Peripheral vascular

- anal atresia
Complications
(Neonatal)

Principles of management:

Start in preconception time

Specific during pregnancy

Specific

Hypoglycaemia
RDS
Hypocalcaemia

Control

Polycythaemia

Diet:

Control :

16 x Wt. (pounds ) + 300 = CALORIES

Fetal

Carbohydrates

60%

Fat

20%

Protein

20%

Insulin:
Regiment A
+ lnt. Evening

* 3 times sol.-with meals

Fasting < 5.0 mmol/1

2 hrs P.P. < 7.0 mmol/1
Adjustment when necessary
Glycosylated Hb A1c (retrospective) < 6
well being:

AFP 16-18 wks

Detailed scan 19-20 wks
Biophysical assay from 28 wks
Fetal wt. & growth two weekly (3rd)
Delivery:
- Timing depends on: (Around 38 wks)

Or
- Regiment B
intermediate)

* 2 types (short &

Twice Daily
Dose (daily) = wt. (kg) x 0.6 first
x 0.7 second

Maternal factors
Biochemical control
Fetal status
- Method --- LSCS in any medical or obstetric
complication.
**Insulin dose adjusted on hourly basis with caloric
requirements intravenously.

x 0.8 third
2/3 in A.M.

2/3 1nt + 1/3 short

1/3 in P.M.

1/2 1nt + short.

GESTATIONAL TROPHOBLASTIC NEOPLASIA

Classification of GTN
BENIGN
Hydatidiform mole
1. Complete mole
2. Partial mole

Genetics of GTN
MALIGNANT

Complete mole: the majority of HM are complete moles

and have a 46XX karyotype, both X chromosomes are
1. Invasive mole
paternally derived, result from fertilization of an empty
2. Choriocarcinoma
ovum by a haploid sperm
3. Placental-site
Partial mole: the karyotype is usually a triploid, often
trophoblastic tumor
69XXY, the remaining lesions are 69XXX or 69XYY
Choriocarcinoma: usually aneuploidy or polyploidy
typical for anaplastic carcinoma
HYDATIFORM MOLE (HM)

Clinical features

Diagnosis

Complete
Vaginal bleeding: the
most common
presenting symptom,
occurs in 97%of cases
Excessive uterine size:
large for date is one of
the classic signs,
occurs in 50% of cases
Toxemia: PET is
observed in 27%,
usually develops early
in the pregnancy
Hyperemesis
Gravidarum: Occurs in
25% of cases

Partial
Hyperthyroidism:
clinically evident
hyperthyroidism is
observed in 7%
Trophoblastic
Embolization:
respiratory distress
develops in
approximately 2%
Theca lutein ovarian
cysts: prominent cysts
>6cm develop in 50%
of cases
Lower abdominal pain,
expulsion of vesicles

Patients with Partial

HM usually do not
have the clinical
features of complete
HM
In general, these
patients present with
signs and symptoms
of incomplete or
missed abortion
The diagnosis may be
made only after
histologic review of
the curetting

Ultrasonography is a
reliable and sensitive
technique of Complete
HM, Snow storm
pattern
Serum B-HCG higher
than normal pregnancy
values
Chest film
Blood tests: FBC, BGRH,
Coagulation profile, LFT,
KFT

HYDATIFORM MOLE (HM)

FEATURES

PARTIAL HM

COMPLETE HM

Karyotype

Most
commonly
69,XXX

Most commonly
46,XX or 46,XY

Or 69,XXY
PATHOLOGY
Fetus

Amnion, fetal RBCs

Villous edema

Variable,
focal

Diffuse

Trophoblastic proliferation

Focal, slight
to moderate

Diffuse, slight
to severe

Diagnosis

Missed
abortion

Molar gestation

Uterine size

Small for
date

50% large for

date

Theca lutein cysts

Rare

15-25%

Post molar malignant

<5%

9-20%

CLINICAL PRESENTATION

Follow up
The B-HCG radioimmunoassay is the most reliable
assay available for the management of patients with
GTN
Following molar evacuation or hysterectomy ,
patients
should be followed by weekly determination of B-HCG
levels until these are normal for 3 consecutive weeks
and the by monthly determination until the levels are
normal for 6 consecutive months
CONTRACEPTION
Encourage to use effective contraception during the
entire interval of follow-up.
Intrauterine device should not be inserted until the
patient achieves a normal B-hCG level
If the patient does not desire surgical sterilization, the
choice is either hormonal contraception or barrier
methods

sequela

Treatment
SUCTION CURETTAGE

HYSTERECTOMY

PROPHYLACTIC CHEMOTHERAPY

The preferred method of evacuation , regardless

of uterine size in patients who desire to preserve
fertility, it involves the following steps:

If the patient desires

surgical sterilization, a
hysterectomy may be
performed with mole in
situ. The ovaries may be
preserved even though
theca lutein cysts are
present

Controversial
Not indicated in patients with molar
pregnancy because 90% have
spontaneous remissions
may be useful in the management of
high-risk complete HM, especially
when hormonal follow-up is
unavailable or unreliable

1. Oxytocin infusion- in the OR before the

procedure
2. Cervical dilatation then Suction curettage
followed by gentle sharp curettage
3. The specimens on suction and sharp
curettage should be submitted separately
for pathology

MALIGNANT GTN
Non-metastatic disease

Metastatic disease

FIGO staging

Locally invasive GTN

develops in 15% of
patients after evacuation
of a complete mole and
infrequently after other
gestations
The trophoblastic tumor
may perforate through
the myometrium, causing
intraperitoneal bleeding,
or erode into uterine
vessels, causing
hemorrhage
After molar evacuation,
persistent GTN may
exhibit features of either
HM or choriocarcinoma
After nonmolar pregnancy
, persistent GTN always
has the features of
choriocarcinoma

Metastatic GTN occurs in

4% of patients after
evacuation of a complete
mole and infrequent after
other pregnancies
Metastasis is usually
associated with
choriocarcinoma
Trophoblastic tumor
perfused by a network of
fragile hemorrhagic
vessels
Symptoms of mets may
result from spontaneous
bleeding at metastatic
sites
Relative incidence of
common metastatic sites

REVISED FIGO SCORING SYSTEM

Lung
s

80%

Liver

10%

Vagin
a

30%

5%

Pelvi
s

20%

Brain

10%

Bowe
l,
kidne
y,
splee
n
Other

5%

FIGO Score
4

Age (years)

<39

>39

HM

Abortion

Antecedent pregnancy
pregnancy

Term

Interval from index

Pregnancy(months)
>12

<4

4-6

7-12

Pretreatment hCG
level (mIU/ml)
100,000 >100,000
Largest tumor size
Metastatic site
Brain, liver
Number of mets
8
>8
Previous failed chemo
drug 2 or more

<1000

1000-10,000

3-4cm
lung, vagina
0

>10,000-

5
spleen, kidney

GI

1-4

4single

The total score for a patient is obtained by adding the

individual scoresfor each prognostic factor

Total score 0-6= low risk, 7 or more =high risk
,
FIGO STAGING FOR GTN
Stage I: patients with persistently elevated hGC levels and
tumor confined to the uterine corpus
Stage II: Patients with metastasis to the vagina or pelvis
Stage III: patients with pulmonary metastasis with or
without uterine, vaginal.or pelvic involvement
Stage IV: Patients with advanced disease and involvement
of the brain, liver, kidneys, or GIT
Diagnostic evaluation
1.
2.
3.
4.

A complete history and examination

Measurement of the serum hCG value
Hepatic, thyroid and renal function tests
Complete blood count

Metastatic work-up
1.
2.
3.
4.

A chest X-Ray
CT scan of the abdomen and pelvis
CT or MRI scan of the head
Measurement of CSF hCG level if any metastatic
disease is present and the head CT is negative
5. Selective angiography of abdominal and pelvic
organs if indicated
MALIGNANT GTN

Diagnosis of post HM trophoblastic neoplasia

1. Plateau of hCG lasts for four measurement over a period of 3 weeks or longer, i.e for days 1, 7,14 and 21
2. A rise in hCG level for three weekly consecutive measurements or longer, over a period of at least two weeks or more,
i.e on day 1,7and 14
3. Histological diagnosis of choriocarcinoma
When hCG level remains elevated for 6months or more
Management
Nonmetastatic (Stage I)

Stage II and III

Stage IV

Chemotherapy: Single agent

chemotherapy is the preferred
treatment in patients with stage I
disease who desire to retain fertility
Hysterectomy Plus
Chemotherapy: if the patient no
longer wishes to preserve fertility,
hysterectomy with adjuvant single
agent chemotherapy
Protocol for treatment of stage I
GTN

Low risk patients are

treated with primary
single-agent
chemotherapy, and the
High risk patients are
managed with primary
combination
chemotherapy
Protocol for treatment of
stage II and III GTN

All patients with stage IV disease should be

treated with primary combination
chemotherapy and the selective use of
radiation therapy and surgery
Protocol for treatment of stage IV GTN

Initial : MTX-FA; if resistant, switch to

Act-D or hysterectomy with adjuvant
chemotherapy
Resistant: Combination
chemotherapy or hysterectomy with
adjuvant chemo, local uterine
resection
Follow-up hCG: Weekly until normal
for 3 wk, then monthly until normal
for 12 mo
Contraception: 12 consecutive mo
of normal hCG values
Effective contraception during
the entire interval of hormonal
follow-up

LOW RISK:
Initial: MTX-FA; if
resistant , switch to Act-D
Resistant to both:
Combination
chemotherapy
High risk
Initial: Combination
chemotherapy
Resistant: Second-line
combination
chemotherapy
Follow up and
contraception are the
same as in stage I

Initial:
Brain
Combination chemotherapy,
Whole-head irradiation
Craniotomy to manage complications
Liver
Resection to manage complications
Resistant: Second-line combination
chemotherapy, Hepatic arterial infusion
Follow-up hCG Weekly until normal for
3wk, then monthly until normal for 24mo
Contraception Until there have been 24
consecutive mo of normal hCG

MALIGNANT GTN (Treatment-Chemotherapy)

Single agent

Combination

1. Methotrexate :
Usually given as a
daily dose for 5
consecutive days or
every other day for 8
days, alternating with
folinic acid rescue
(associated with less
bone marrow, GIT,
and liver toxicity )
2. Actinomycin D:
Given for 5
consecutive days or
every other week as a
single dose

EMA-CO Regimen for

patients with GTN
Course 1(EMA)
Day 1
Etoposide,
Actinomycin D and
Methotrexate
Day 2
Etoposide,
Actinomycin D and Folinic
acid 24hr after start of
MTX
Course 2 (CO)
Day 8
Vincristine and
Cyclophosphamide

MAC III : Methotrexate-FA, Act-D, and Cyclophosphamide

Duration of treatment :
Serum hCG is measured weekly after each course of
chemotherapy
Adequate response is defined as a falling the hCG level by
1log after a course of chemotherapy
Single and Combination chemotherapy should be given as
often as toxicity permits until the patient achieves three
consecutive normal hCG levels
After normal hCG levels are attained, at least two additional
courses of chemotherapy are undertaken to reduce the risk
of relapse
Secondary Tumors: Leukemia, colon cancer, melanoma and
breast cancer
Fertility outcome: No evidence that patients with GTN followed by
chemotherapy have an adverse pregnancy outcome
With each subsequent pregnancy : Pelvic USS in 1st trimester to
confirm normal gestation, histological review of the placenta, hCG
measurement 6 weeks after completion of the pregnancy to exclude
occult GTN

CHORIOCARCINOMA
Highly malignant tumor with a predisposition to

PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT)

PSTT is a very rare and unique form of GTN, represent a

haematogenous spread
Follows HM in 3-7% of cases
The organs most frequently affected by mets are, lung,
lower genital tract, brain, liver ,kidney and GIT
Some cases manifested by intraperitoneal bleeding
seconday to rupture liver or ruptured theca lutein cyst
Patients with pulmonary mets may present with
haemoptysis or resp failure
CNS mets presents with neurologic signs resulting from
spontaneous bleeding
50% of cases follow HM
Treatment with EMA_CO

GESTATIONAL HTN
BP reading 140/90
mmHg for the first
time after 20 weeks
of pregnancy
No proteinuria
BP returns to
normal within 12
weeks postpartum
(if the BP elevation
persists, the woman
is diagnosed as
having chronic
hypertension)
Final dx is only

neoplastic transformation of intermediate trophoblastic

cells
PSTT can occur after a normal pregnancy, abortion, term
delivery, ectopic pregnancy or molar pregnancy
Characterized by low B-hCG levels, expression of HPL is
incerased on histologic section and as well as in the
serum
Diagnosis is confirmed by dilatation and curettage and
hysterectomy
Most cases are confined to the uterus but mets has been
reported
Surgery is the primary treatment of choice
Good prognosis is anticipated in cases localized to the
uterus, with distant mets or delayed treatment the
outcome is dismal

HYPERTENSIVE DISORDERS IN
PREGNANCY-INDUCED HTN
PRE-ECLAMPSIA
ECLAMPSIA
Mild pre-eclampsia
CNS
BP 140/90 mmHg after
involvement
20 weeks gestation
with the
Proteinuria 1+ by urine occurrence of
dipstick or a total protein
convulsions that
level 300 mg/24 hours
cannot be
- Pre-eclampsia can develop attributed to
before the 20 week of
other causes
gestation in hydatidiform
mole and in the presence of
lupus anticoagulant
Severe pre-eclampsia
BP 160 mmHg systolic

PREGNANCY
PREGNANCY-AGGRAVATED
HTN
Development of PE or
eclampsia in pre-existing
hypertension detected by a
further increase of
> 30 mmHg in SBP or >15
mmHg in DBP
or
New onset proteinuria of
>300 mg/24 hours in
hypertensive women but
with no proteinuria before
20 weeks gestation
or
A sudden increase in

CHRONIC HTN WITH

PREGNANCY
Hypertension is
present before
pregnancy or
detected before 20
weeks Or
Hypertension first
diagnosed after 20
weeks gestation and
persisted after 12
weeks postpartum

made postpartum
May even be
associated with an
increased birth
weight

or 110 mmHg diastolic

Proteinuria 2+ by urine
dipstick or a total protein
level of 2 gm/24 hours

proteinuria or a drop in
platelet count to
<100,000/mm3 with HTN
and proteinuria before
20wk gestation

PREDISPOSING FACTORS
Age: PG<20, all women > 35
Parity: PG have double incidence
Lower socio-economic status
Genetic predisposition: Recessive trait
Obstetric complications: multiple and molar pregnancy, fetal hemolytic diseases (hydrops fetalis),
polyhydramnios
Existing medical conditions: chr BP, ren D, DM, SLE, antiphospholipid AS.
Previous PE. The recurrence rate for PE with the same male partner is ~ 20%, and usually
becomes apparent at later gestation than in the first pregnancy
Obesity: 4.3% for a women with a body mass index <19.8 kg/m2 to 13.3% for those > 35 kg/m2

FACTORS THAT PET

Prolonged exposure
to paternal Ag
Smoking, but if PE
occurs then perinatal
mortality triples
Placenta previa

PRE-ECLAMPSIA
CAUSE (UNKNOWN)

THEORIES
(I) Defective trophoblastic
invasion of the spiral arteries
(II) Immunologic factor
(III) Increased pressor
responses
(IV) Prostaglandins imbalance
(V) Genetic predisposition
(VI) Inflammatory factors
Ischemia could be due to:
- Underlying vascular changes (HTN/
Failure of physio chgs of spiral
arteries)
- Increased myometrial resistance of
the myometrial vessels, which could
be related to a heightened
myometrial tension produced by the
large fetus in a primiparous women,
by twins, or by polyhydramnios
The poorly perfused trophoblast
release factor X which enters
maternal circulation and causes
endothelial dysfunction Imbalance
between different classes of locally

PATHOPHYSIOLOGY
VASOSPASM
Excess
Decreased
production/
production/sensiti
sensitivity to
vity to
vasoconstrictors vasodilators
Angiotensin II
Prostacyclin
Serotonin
Nitric oxide
Endothelin
INTRAVASCULAR COAGULATION
Platelet activation
Thrombocytopenia
Reduced production of anti-thrombin
III
PLASMA VOLUME CONTRACTION
Redistribution of fluid from the intravascular to interstitial fluid spaces so
that total ECF volume remains
unaltered

ORGAN HYPOPERFUSION
Kidney: GFR, proteinuria,
hyperuricaemia, oliguria
Liver: SGOT, SGPT,
epigastric pain
Brain: visual scotomata due
to occipital lobe ischemia,
headache, convulsions
(eclampsia)
Placenta: IUGR, placental

Stimulation of the maternal immune system by the early

conceptus Produce blocking Ab to antigenic sites on the
placenta, thus preventing the rejection of the fetus and placenta.
Hypoimmune response results in damage of the placenta and
subsequent PE.
PE less common in previously stimulated immunity conditions as:
Previous pregnancy, Consanguineous marriages, Increased

PRE-ECLAMPSIA
DIAGNOSIS
INDICATIONS OF SEVERITY OF
INDICATIONS TO TERMINATE PREGNANCY
PRE-ECLAMPSIA
IN PRE-ECLAMPSIA
HISTORY
INVESTIGATION
Presence of symptoms
MATERNAL FACTORS
FETAL FACTORS
Persistent
headache
or
Personal hx
Completed 37 weeks
Obvious IUGR
CBC: PCV and
other cerebral or visual
Past hx
Abnormal liver/ renal

thrombocytopenia
disturbances
Menstrual hx
functions
Oligohydramnios
SGOT, SGPT:
- Persistent epigastric pain
Obstetric hx
Severe preeclampsia/
, IUFD
Elevated liver enzymes
Complaints and
eclampsia regardless of
Presence of
Creatinine clearance, Diastolic BP 110 mmHg

Proteinuria
of
2+
or
more
by
hx of present
the gestational age
congenital fetal
serum creatinine, uric
urine dipstick or a total protein
pregnancy
In selected cases of
malformations
acid, total protein in
level of 2 gm/liter in a 24-hour severe PET, where the
incompatible
urine, and blood urea:
urine sampling
expertise and
with life
impaired
PHYSICAL EXAM

Abnormal
lab
findings
equipment
are
available,

Coagulation
profile:
Hypertension
Obvious fetal growth
expectant management
PT, PTT, clot. and
Edema
restriction
may be undertaken for
bleed. time in DIC.
Obstetric exam
Neurological effects:
fetal indications
Fibrinogen and FDP to
Scotomata, hyperreflexia
diagnose DIC
Eclamptic convulsions
Fetal Surveillance
MANAGEMENT
CONVULSION
ANTIHYPERTENSIV TIMING OF DELIVERY FLUIDS
END-ORGAN COMPLICATIONS
PROPHYLAXIS
ES
Magnesium sulphate
Hydralazine
Once the dx of
Carefu Consumption coagulopathy: Administer
(MgSO4)
Nifedipine
severe preeclampsia l.
platelets/FFP only if clinical bleeding.
Blocks neuromuscular
Labetalol
has been
Colloid Intracranial hemorrhage:Severe
conduction through
Sodium
established,
s.
headache in the post partum with pre~ or
blocking the release of
nitroprusside
termination of
eclampsia. CT scan
acetylcholine at NMJ.
pregnancy becomes
Rx: Combined obstetric and neuro in 3
Toxicity: Neurotoxicity
mandatory after
hosp
(Loss of patellar reflex) ,
patient stabilization
Sub capsular hematoma:Severe
Resp depression (RR
Mode of delivery
epigastric pain+hepatomegaly. US.
<12/min), Cardiac toxicity
depends upon
Rx:Correct coagulopathy. If liver rupture,
(cardiac arrest)
whether: The woman
transfusion + liver surgery.
Antidote: Calcium
is in labor, The
HELLP syndrome: Abnormal vascular

gluconate

progress of labor,
The cervix is fit for
induction.

tone, vasospasm and coagulation defects.

Rx:Delivery regardless GA. Steroids.
Platelets only if <20k/ml. Csection in
platelets >50k/ml.

CLINICAL FEATURES
Premonitory phase
Tonic phase
Clonic phase
Coma

ECLAMPSIA
MANAGEMENT
EMERGENCY TREATMENT
MONITORING DURING HOSPITAL STAY
1. Clear airway passages
Close observation:
2. Apply an oxygen mask
Every 30 minutes assess pulse, BP and respiratory rate
3. Protect the patient from harm during
Maintain a fluid balance chart monitoring fluid intake
seizures
and urinary output
4. Control convulsions with MgSO4
Limit IV fluid administration unless excessive blood loss
5. Control high BP to avoid fatal
If convulsions occur despite MgSO4 therapy:
complications
CT scan should be performed
6. Deliver fetus
If severe respiratory insufficiency occurs:
7. Avoid diuretics and hyperosmotic
ICU admission and ventilation
agents
Measuring blood gases and blood pH levels
8. Close observation

HISTORY
Past history:
Hypertension treated before pregnancy
with various antihypertensive medication
Renal problems
Obstetric history:
Hypertension during previous pregnancies
Previous superimposed pre-eclampsia
Previous IUFD, IUGR and abortions
Family history of hypertension

CHRONIC HYPERTENSION
DIAGNOSIS
EXAM
Hypertension: Presenting before
20 weeks gestation
Cardiac enlargement: May be
present
Edema: Occurs when preeclampsia or heart failure occurs
as a complication of hypertension

INVESTIGATIONS
Urine analysis: Proteinuria indicates
occurrence of superimposed preeclampsia
Renal function: Serum creatinine, uric
acid and BUN
Fundus examination: Changes
indicating chronic hypertension

MANAGEMENT
ANTIHYPERTENSIVE THERAPY
- Antihypertensive therapy recommended when SBP > 160-170 and DBP > 105-110, as such treatment decreases the
maternal cerebral and cardiovascular complications.
- In acute control of severe HTN, the objective of therapy is a gradual reduction of blood pressure to a level of about 140150 / 90-100 mmHg
BP should be assessed every 15 minutes initially, once the blood pressure is stabilized the interval can be lengthened to 30
minutes
- Lowering the blood pressure rapidly over minutes abrupt and profound in BP cardiac output to the uterus with
possible fetal hypoxia. Continuous fetal heart rate monitoring should be performed during initial therapy to detect such
effect and allow early remedial action
HYDRALAZINE (Vasodilator), NIFEDIPINE (Ca Channel Blocker), LABETOLOL (Beta-blocker) - most commonly used.
Labetalol should be avoided in asthma. Atenolol, ACE inhibitor, ARB and diuretics should be avoided
Diuretics are not recommended
Angiotensin converting enzyme inhibitors are contraindicated with pregnancy

Termination if:
Fetal maturity reached
Fetal distress and severe IUGR
Additional complications occur (severe preeclampsia, abruptio placentae)

INDICATION
When delivery is safer to
mother & fetus than
continuation of pregnancy.
1. Postdate
2. Pre-eclampsia
3. PROM
4. Chorioamnionitis
5. IUGR
6. IUFD
7. Fetal anomalies
8. DM
9. Abruptio placenta
10. Rh isoimmunication

INDUCTION OF LABOR
Indicated in 10-20%
CONTRAINDICATION
ABSOLUTE
RELATIVE
1. Placenta previa
1. Severe pre2. Previous 2C/S, previous 1 due to eclampsia
recurrent cause, previous classical
2. Breech
C/S
presentation.
3. Abnormal antenatal CTG
3. Multiple pregnancy
4. Transverse/oblique lie
4. Grand multipara
5. Absolute contracted pelvis
5. Polydroamnios
6. Active genital herpes infection.
6. Presenting part
7. Tumor occupies pelvis
above pelvic inlet.
8. Cervical carcinoma
9. Successful pelvic floor repair &
successful surgical rx of stress
incontinence.

Bishop Score: Assess cervical condition & station of the head, in

13.
BISHOP SCORE
0
Cervical dilatation
Closed
Cervical length
>2cm
Cervical consistency
Firm
Cervical position
Station of the head

Posterio
r
-3

Bishop score <7 unfavorable cervix.

Bishop score 7 or more favorable cervix

COMPLICATION
1. Hyperstimulation fetal
distress & uterine rupture.
2. Failed induction
increased incidence of C/S.
3. Prolonged labour
instrumental delivery & PPH.
4. More painful more
analgesia
5. Prematurity
6. Infection

order to choose the best method for induction. Total score

1
1-2cm
2-1cm
Mediu
m
Centra
l
-2

2
3-4cm
1-0.5cm
Soft

3
>5cm
<0.5cm

Anterior
-1-0

Below ischial
spine

METHOD OF INDUCTION
Not reach effective contractions
Bish
op
<7

Vaginal
Prostaglandin

Bish
op
>=7

Artificial Rupture
of Membrane

Oxytocin

Indicated if effective uterine

contractions not obtained after 1-2 h
PG release from fetal
of AROM.
memb & decidua, & by
Complications:
mechanical descent of
1. Uterine hyperstimulation Uterine
fetal head
rupture & Fetal Distress
oxytocin from
2. Hypotension if given IV bolus dose.
3. Neonatal jaundice if total oxytocin
posterior pituitary
>20 units.
(Ferguson reflex)
4. Water intoxication if total amt of
Complications: Cord
fluids >1.5L confusion, convulsion,
prolapsed, placental
coma, death.
abruption, infection.
How given:
Start 2mU/min, double the dose every
30min.
Never exceed 32mU/min (multipara) &
64mU/min (primipara).
*Effective uterine contractions: 3-4 contractions, each lasting 50-60seconds in When
10minutes.
effective contractions reach,
keep lowest effective dose.

PGE2 (Prostin) most commonly

used.
PGE1 (Misoprostol)
Vaginal PGE2 pessory 3mg or
Intracervical PGE1 gel 0.5mg
Dose can be repeated every 4-6h
for a max dose of 3doses in 24h.
Main complication: Uterine
hyperstimulation Uterine rupture
& Fetal Distress.
If cervix remains unfavorable
despite max dose of PG
(3doses/24h), re-evaluate pt & if
theres no urgent indication for

Induces labor by

MANAGEMENT OF PATIENTS FOR INDUCTION OF LABOR

BEFORE INDUCTION
DURING INDUCTION
1. Counseling & explanation.
1. Good selection of method of induction (Bishop score)
2. Hx Assess GA & R/O contraindications of induction. 2. Proper dose of PG or Oxytocin.
3. Obstetrics exam Assess lie, presentation,
3. Monitoring of labor Fetal wellbeing, uterine activity, progress
engagement.
of labor & maternal wellbeing.
4. Vaginal exam: Assess Bishop score & pelvic
4. Adequate pain relief Best epidural
adequacy.
5. Ultrasound: Assess fetal age, wellbeing, amt of liquor
& placental site.
6. CTG: Assess fetal wellbeing.
TREATMENT OF HYPERSTIMULATION & FETAL DISTRESS
>7.25 Continue vaginal delivery
Fetal distress
7.2-7.25 Repeat pH after 30min
Stop oxytocin.
<7.2 Emergency c-section
Give oxygen by mask.
Lateral decubitus.
Rapid infusion normal
saline.
Uterine
Persist
hyperstimulation

Fetal scalp
Fetal
distress persist
blood
sampling

Terbutaline
Hyperstimulation
persist
0.25mg bolus
IV

Emergenc
y Csection

PROLONGED PREGNANCY
Post-date pregnancy: Continuation of pregnancy beyond 40 completed weeks
Post-term pregnancy: Continuation of pregnancy beyond 42 completed weeks
Incidence 5-10% pregnancies.
ETIOLOGY
Majority of cause no underlying cause i.e. physiological continuation of the pregnancy.
Extremely rare cases may be due to anencephaly, fetal adrenal hypoplasia or to placental sulphatase enzyme deficiency.
RISKS
A] Placental insufficiency & hypoxia which leads to:
1. Increased perinatal mortality (PNM)
2. Meconium aspiration syndrome
3. Oligohydroamnios & cord compression
B] Increased fetal weight & ossification of skull with decreased moulding, which leads to:
1. Prolonged labour and failure to progress which leads to incidence of C/S.
2. Shoulder dystocia with its neonatal & maternal risks.
a) Maternal risks vaginal & cervical lacerations & rupture uterus
b) Neonatal risks: neonatal asphyxia & death, cervical cord injury, brachial plexus injury (erbs palsy in C5&C6,
klumpks palsy in C8&T1, phrenic nerve injury in C4), clavicular & humeral fractures.
MANAGEMENT
BEFORE DELIVERY
DELIVERY
1. Counseling & explanation: explain risks on the fetus.
1. In uncomplicated postdate pregnancy, pt should be
2. Hx for accurate assessment of GA and to exclude C/I for delivered at 41wks + 3-7days.
induction.
2. Method of delivery either induction of labour (method of
3. Obstetric exam: Assess lie, presentation & engagement.
induction depends on Bishop score) or by C/S if there is C/I
4. Vaginal exam: Assess Bishop score & pelvic adequacy.
for induction.
5. Ultrasound: at 40.41 & 42 wks, to assess amt of liquor,
3. If delivery by induction of labour, a senior obstetrician
fetal wellbeing & w8.
should attend delivery due to risk of shoulder dystocia and a
6. CTG: every 3days after 40wks, to assess fetal wellbeing.
pediatrician should attend due to risk of meconium
aspiration.
ASSESSMENT OF GA

ANTENATAL METHODS
1. First day of LMP reliable in 50% of pregnancies.
2. Ultrasound best is CRL between 7-13wks, then BPD & FL between 1326wks & then BPD & FL after 26wks.
3. Clinical onset of early pregnancy sx, early bimanual exam, quickening
& serial fundal height.
INFERTILITY
INTRODUCTION
Def: Involuntary failure to conceive within 12 months of
commencing regular unprotected intercourse. (Old definition within
24 months)
Primary Infertility: No previous pregnancy
Secondary Infertility: With previous pregnancy ( whatever the
outcome)

POSTNATAL METHODS
1. Dubowitz score include an assessment of
the physical & neurological features of the
newborn.
2. Farr score which include an assessment of
the physical features of the newborn.

PHYSIOLOGY
Conception requires :
Oocyte, sperm, at optimal stage
Needs transportation
A receptive place for implantation
Intact Male and Female reproductive systems

Incidence:
10-15% of married couples
About 75% of couples conceive by 12 months,

About 85% of couples conceive by 24 months.

POSSIBLE CAUSES OF INFERTILITY

FEMALE
MALE
Ovulatory failure factor: (anovulation)
Coital factor: (psychological or
High centres - hypothalamic-pituitary axis
organic)
Thyroid
Spermatogenesis problem:
Adrenal
Azospermia, oligospermia
Ovarian - PCO(20%), premature failure( >30IU/L)
Ductus problem: Azospermia due
Genetic & Chromosomal
to obstruction (infection)
Tubal factor: PID,T.B
Uterine factor: Ashermans, congenital anomaly.
Cervical factor: infection, immunological
Endometriosis:
Coital factor: aparunia, dysparunia, vaginismus
Psychosomatic: ? Neurohormones

IDIOPATHIC
About 15-30% of Infertility. It
is a definition by exclusion,
and that depends on the
standard investigations
used.
(Ovulatory, Tubal, Male)

INFERTILITY WORK UP
HISTORY
EXAM
Male: Age, history of mumps, occupation, drugs, chemical,
Male: exam.vas deference -size of testicles ,
irradiation, hernia operations, varicocele
varicocele, endocrine stigmata
Female: Age, menstrual cycle (regularity) - previous pregnancies,
Female: B.P - Thyroid - galactorrhoea
Abortions and TOP, galactorrhoea - 1/2 - contraceptions ,
hirsutism. Abdominal and pelvic exam
Hirsutism.
genitalia (External & Internal)
Both: Coital history:- S.T.D - past med & surgical hx, smoking and
taking drugs
SPECIAL INVESTIGATIONS
OVULATION
CERVICAL FACTOR
TUBAL & UTERINE
MALE FACTOR
OTHERS
FACTORS
1. B.B.T.chart:
- Cx score (amount,
(CILIA, FERTILIZATION,
Semen analysis: by
CBC
Biphasic an increase
spinnbarkeit, ferning, os)
TRANSPORT)
coitus interruptus or
Urine analysis
of 0.5C, progesterone
- Cervical mucus alteration: - Tubal insufflation
masturbation after
S.T.D
effect
thin-clear-wateryelastic
(Rubins test) obsolete
abstinence of 3-5 days Chlamydia
2. Cx mucus
(subjective)
nowadays
delivered within 2 hours
Rubella titer
alteration:
- Elasticity (spinnbarkeit)
- Hysterosalpingogram:
to lab.
TFT
Mittelschmerz pain
- Fernning (arborization or
using radioopaque water
Skull x ray
3. Hormonal assay:
crystallization) of NaCl due
soluble, no G.A
Normal values: by WHO
CT Scan
S. progesterone d21
to unopposed action of
- Laparascopy +
criteria
X ray chest.
(20-30nmol/L),
estrogen
Methylene blue dye test: Volume: >2ml S. prolactin
- P.C.T:(post coital test):
under G.A, checks for
liquification in 20- 30
<20ng/ml
positive if: more than 5-10
endometriosis and D&C
minutes
S. FSH and LH first
sperm in (H.P.F) alive
in the same sitting
Density: >20-250 Mil/ml
days of period
forward progressive motility (when done in luteal
Motility: > 50% forward
4. Endometrial biopsy after 6-12 hours of sexual
phase)
motility within 2 h.
-d 21- secretory
intercourse at time of
- Hysteroscopy - in
Morpho: > 30% normal
endometrium. i.e.T.B
ovulation. Repeat 3 times if Ashemanns synd.
forms
5. U.S.S - monitoring
Negative (wrong timing,
congenital anomaly to
of follicles 18-22 mm,
cervical hostility due ?
visualize the uterine
Seminal fluid 90% of
d12=12mm
antibodies, severe oligo or
cavity (using CO2 or
ejaculate: 2\3 from
6. Laparascopy azospermia)
glyceine solution)
seminal vesicles
laparatomy - Cross hostility test
- Hy-co-sy
(fructose), 1\3 from

incidental findings
7. LH peak (LH home
kits): 26h later
ovulation occur
8. Pregnancy

(Kremer test) if P.C.T is

(hysterosalpingoprostate (zinc & acid ph.)
negative
contrast-sonagraphy)
In azospermia +
- Antisperm antibody titre using Echovist
oligospermia: hormonal
and MAR ( mixed
FSH,LH, prolactin &
agglutination reaction)
karyotyping
INFERTILITY MANAGEMENT
INDUCTION OF OVULATION
TUBAL FACTORS
CERVICAL FACTOR
A] Fertility agents:
Selective
improve cervical score: Treat
Oral agents: 90% induce ovulation, but 60% pregnancy
Hysterosalpingogra
infection, Cryocautery,
-In cases of hyperprolactinaemia :
m
Estrogen
Bromocriptine (ergot alkaloids, dopamine agonist)
Surgery:
immunological - ?
Lisuride 1x1
microsurgery: after
corticosteroids for the male
Cabergoline(Dostinex) 1mg weekly
falloposcopy:
during the luteal phase of
-Clomiphene citrate (clomid): 50mg _ 200mg _ (d2 - d6), for 6 Salpingolysis,
female ,Male use of condom
cycles. It is oral cyclical, synthetic, nonsteroidal, weak
for 6 months
salpingostomy,
estrogen with antiestrogenic activity
excision &
SIUI and SIVF
-Tamoxifen : 10-40mg (d2 - d6) for 6 cycles, in PCO
reanastom. (success
-Cyclofenil : 200mgb.d for 10 days
from 10-40%)
In PCOS :metformin (oral insulin sensitizers)

Uterine anomalies:
Side effects: ovarian cysts, twins 5%, hair loss, GIT, rarely
Myomectomy for
hyperstimulation syndrome (OHSS)
fibroids
Metroplasy in certain
Injectable agents
cases
Gonadotrophin therapy: urinary extracts, now recombinant
I.V.F program
- HMG: (FSH+LH) (Humegon-pergonal) injections 1-3
ENDOMETRIOSIS
MALE FACTOR

ampules daily or every other day till follicular maturation,

about 5-10 injections
- FSH: only (metrodin) in P.C.O
- H.C.G: (pregnyl,profasi) - 5000 - 10000 unit after
follicular maturation to release oocyte
- L.H.R.H-a: - ( Busserlin-Zoladex-superfact-Decapeptyl )
continuous (nasal or s.c. 4-6 times daily or depot IM) to
deplete endogenous FSH,LH
- L.H.R.H-a: - pulsatile infusion every 90 minutes, 15ug
- L.H.R.H.antagonist
Side effects: multiple pregnancy 25% - hyperstimulation
syndrome (if severe) -ascitis, large ovarian cysts,
hydrothorax, thromboembolic disease, multiorgan failure
B- Surgical: Ovarian drilling, wedge resection(obsolete)
Options of treatment: Oral fertility agents Injectables
SIUI,SIVF

Danazol, LHRH a
treatment (medical)
Conservative
surgery:
I.V.F. program

Treatment directed towards

cause.
Advice: stop smoking and
alcohol, avoid tight
underwear, take regular cold
baths, improvements in coital
practice.
Psychological therapy: for
sexual dysfunction
In severe oligospermia and
azoospermia, check for
karyotype (Klinefelters
syndrome, testicular atrophy)
hMG for hypothalamicpituitary failure.
Bromocriptine for
hyperprolactinemia.
Surgical treatment in
vasectomy reversal.
Varicocele ligation in
varicocele.
ART: SIUI,ICSI (by TESE or
MESA)

ARTIFICIAL INSEMINATION

Artificial insemination
(AI)
AIH: intravaginal,
intracervical and
pericervical,
intrauterine,
intraperitoneal
AIH(DI)
IUI and SIUI
The mostly used
nowadays: is SIUI
(stimulated
intrauterine
insemination:
- Proper selection of the
cases
- Controlled ovarian
stimulation
- Preparation of semen
- Timing of insemination

ASSISTED REPRODUCTION TECHNIQUES (ART)

IVF + ET (EMBRYO
VARIANTS OF IVF
TRANSFER)
Up to 35% could
o G.I.F.T: Gamete intra fallopian
transfer (indicated: unexplained
benefit from infertile
infertility, oligospermia,
couples
endometriosis. (C.I.tubal damage)
Candidates: Tubal
factor , endometriosis o Procedure: Laparascopy at ovulation retrieve oocycte mix with prepared
, oligospermia
semen - deposit both in tube
,unexplained infertility
o Z.I.F.T
It is expensive,
requires sophisticated o SUZI subzonal injection
lab. facilities, highly
o ICSI intracytoplasmic sperm injection
skilled medical,
o PESA percutaneous epididymal sperm
nursing, scientific and
aspiration
tech. personnel
o MESA
o TESE
OUTCOMES OF IVF PREGNANCIES
25% risk of miscarriage
2-5% risk of ectopics, heterotropic
pregnancy
25% risk of multiple pregnancy
Increase risk of prematurity, low birth
wt, Cs

RESULTS OF IVF

E.T (1) - 10% chance

of single pregnancy
E.T (3) - 25-30%
chance of single
pregnancy. 5% twins,
1%triplets
Efficiency: 25-35%
for each cycle - Take
home baby 15-20%
According to the
infertility factor and
the centre

RISKS OF IVF
Psychological trauma if
failed
(OHSS) ovarian
hyperstimulation
syndrome
Multiple pregnancy

INSTRUMENTS
1) Sims Speculum.
Uses: for visualising fistulae (abnormal holes or connections) and prolapse (protrusion) of the rectum orbladder into the
vagina

Uses: Pelvic exams.

2) Bivalve speculum
To take Pap smear. To take cone & punch biopsy.

3) Curette
Dilation & curettage. Evacuation & curettage.

GLANDS: ADENOCARCINOMA
ENDOMETRIU
M

STROMA: ENDOMETRIAL STROMAL

GLANDS + STROMA: MMT
LEIOMYOSARCOMA

MYOMETRIUM
OTHERS
INTRODUCTION
Peak incidence is at
age of 61 years
75% occur in
postmenopausal
women
Only 5% occur before
age of 40
There is marked
geographical and
racial variation in the
incidence

ENDOMETRIAL
ETIOLOGY
Excessive unopposed estrogen
stimulation of the endometrium
Increase
Obesity, Nulliparity, Late
menopause, PCO, Estogensecreting ovarian tumors,
Unopposed estrogen therapy,
Family history of breast, ovary,
colon, endometrial tumors, DM
Decrease
OCCP, Progesterone

CARCINOMA
CLINICAL PRESENTATION
PMB
Intermenstrual
bleeding/irregular
periods
Heavy regular
periods
Watery
discharge/offensive
Pain
ENDOMETRIAL BIOPSY
SHOULD BE DONE IN
ALL PATIENTS WITH PMB

PATHOLOGY
Growth is usually
adenocarcinoma
Adeno-acanthoma/
adenosquamous
tumors
Serous papillary/

DIAGNOSIS
Always investigate PMB,
continuous or irregular
bleeding before assuming
benign cause for the bleeding
Cervical smear
TVS

PROGNOSIS
Stage
Grade
Myometrial invasion
Age
Tumor size
Assessment of these

PHYSICAL FINDINGS
Rarely suggest the diagnosis
Uterine enlargement
Palpable lymph node in the
groin. Supraclavicle.
Vaginal nodule

TREATMENT
Low risk stage I: TAH, BSO
High risk: postoperative
radiotherapy
Stage II: TAH,BSO+
radiotherapy/radical
hysterectomy

clear cell
Grade 1 grade 3
Spread: Direct
invasion, Lymphatic,
Blood

Endometrial biopsy
Hysteroscopy +curettage
If confirmed, CBC,KFT,URINE,
MRI.CXR

factors require
laparotomy and
histology (surgical
pathological staging)

Stage III /IV: individualized

.rarely surgery
usually chemo, radiotherapy
and hormonal
Follow up
Recurrence usually within 2
years (70%)
Overall 5 year survival is 60%

FIGO STAGING
Stage 1
Confined to the body of
uterus
Stage 2
Involvement of cervix
Stage 3
Extension into
adnexae,vagina or
positive L.N
Stage4
Distant mets

ENDOMETRIAL SARCOMA
Endometrial stromal sarcoma
Malignant mixed mullerian tumors
(carcinosarcoma)
More in black. Previous pelvic irradiation
Present with bleeding and pain
Poor prognosis

LEIOMYOSARCOMA
5-10% May arise from transformation of fibromyoma (0.2%)
Mostly arise from normal myometrium
Peak incidence is 10 years older than fibromyoma
Present with abnormal bleeding and pelvic pain and wt loss
Should be suspected in rapidly enlarging fibroids
In 80%,diagnosis is made after hysterectomy
Ideally should be treated by TAH, BSO, washing and full
staging
Adjuvant radiotherapy or chemotherapy?

BASIC CONCEPTS

PRESENTATION
Part of the fetus occupying the lower segment of the uterus
Cephalic (Head, 95%), Breech (Buttocks, 3-4%), Shoulder,
Cord, Compound.
Malpresentation is any presentation other than cephalic.
LIE
Relation of longitudinal axis of fetus to the mothers
longitudinal axis
Longitudinal (99%) Transverse Oblique

STATION
Relation between the lowest bony part of the presenting
part to the imaginary line between two ischial spines
-3, -2, -1, 0, +1, +2, +3 [if above line: -ve, if below line:
+ve]
Assessed through vaginal exam.
ENGAGEMENT
Passage of the widest diameter of the presenting part
through the pelvic inlet.
If <2 fingers needed to palpate fetal head in pelvic grip:
Engaged.
*Pelvic inlet: Upper border of symphysis pubis (ant), sacral
promontory (post), ileopectineal line of iliac crest (lateral).

POSITION
Relation between the dominator (bony landmark of the
fetus) to the internal pelvis.
8: Anteriorly (left, right, direct), Posteriorly (left, right,
direct), Transverse (left, right)
Most common: Left occipito-anterior.
Malposition is any position other than occipito anterior.
*Bony landmarks:
Vertex: Occipital
Face: Mental
Brow: Frontal
Shoulder: Scapula
Breech: Sacrum

FETAL ATTITUDE
Relation of fetus parts to each other
Well-flexed (normally), Extended

BREECH PRESENTATION
DEFINITION
CAUSES
DIAGNOSIS
Buttocks occupying
Maternal Causes: Nulliparity, Old age, Fibroid,
Hx: Subcostal pain (coz fetal head)
lower segment of
Polyhydroamnios, oligohydroamnios, Bicornuate Abd exam: Leopold maneuver solid ballotable
uterus.
/ septate uterus, Hx of breech, Uterine/pelvis
rounded mass in fundus; soft irregular mass in
Commonest
tumors.
pelvis.
malpresentation.
Fetal Causes: Prematurity, IUGR, Large babies,
Vaginal exam: 2 ischial tuberosities & tip of
Commonest cause is
Multiple gestations, Fetal abnormalities,
sacrum.
prematurity.
Congenital anomalies, Short umbilical cord,
US: Confirm dx, look placental site, uterine
Cephalo-pelvic disproportion.
abnormality, # of babies, liquor amount,
estimate fetal weight.
TYPES
FRANK @ EXTENDED
COMPLETE
FOOTLING
Hips flexed, knees
Feet present beside
Hip & knee extended in
extended.
buttocks. Both hips &
one or both sides.
Primigravida.
knees flexed.
Preterm singleton.
Multipara.
A] EXTERNAL CEPHALIC VERSION (ECV)
NOTES
METHOD
CONTRAINDICATIONS
COMPLICATION
S
Done at term
Prep her as if to do C-section NPO, cannula, conduct in Absolute: HTN, PET, Previous Labor, PROM,
(>37th wks)
OT, ultrasound, CTG.
2 C-sections, Multiple
Placental
coz may revert
Rotate the baby by direction of his nose until it becomes gestation with 1st twin
abruption,
to breech, or
cephalic.
breech, Abnormal CTG, HSV,
Cord
induce labor.
Repeat CTG.
Previa, Pt refusal.
compression &
Success rate
If Rh-ve mother, give antiD coz risk of fetomaternal
Relative: IUGR,
prolapsed,
60%.
hemorrhage.
Polyhydroamnios,
Fetal
Discharge waiting for spontaneous vaginal delivery.
oligohydroamnios, fetal
bradycardia.
anomaly.
B] ASSISTED VAGINAL BREECH DELIVERY
C] CAESEREAN SECTION
CRITERIA
ASSISTANCE
Absolute Indications:
Prematurity, Footling breech.
Normal baby weight 2.5-3.5kg
After delivery of buttocks, 1) Episiotomy
Superior to vaginal breech
>36wks GA. Good pelvimetry (roomy
2) Keep fetal back anterior
delivery.
pelvis). Fetal head flexed, Breech type
After appearance of scapula 3) Rotate 90 to
Frank or Complete. Experienced
deliver anterior shoulder & vice versa.
obstetrician. Anethetist (Epidural), No
After visible hair line 4) Either Liverpool

other indications for C-section,

Multiparous, Normal labor progress,
Uncomplicated pregnancy.

maneuver, or Mauriceau-Smellie-Veit maneuver

or forceps delivery.

FACE & BROW PRESENTATIONS

FACE
Vaginal Exam: Nose, cheeks, mouth.
Commonly misdiagnosed as breech.
TYPES
MENTO-ANTERIOR

Presenting
diameter: 9.5cm.
MENTOPOSTERIOR

MANAGEMENT
If fully dilated
Allow vaginal
delivery.
If not fully dilated
Can augment
labor with
oxytocin.
COMMON NOTES
Never attempt to
convert face to
vertex.
Never apply
vacuum.
Can use forceps.
Can augment with
syntocinon.
Large episiotomy.
If fully dilated Csection.
If not fully dilated
Monitor for
conversion into
vertex
presentation.
If fetus dead

BROW
Vaginal exam: Orbital
ridges & nose.
CAUSES
Grand
multiparous
Neck swelling
(cystic
hygroma, goiter
etc)
Anencephaly

SHOULDER PRESENTATION
Transverse or oblique lie.
Abd Exam: Head in one flank & buttock
in another. No vaginal exam till R/O
previa.
CAUSES
Placenta previa, Prematurity,
Polyhydroamnios, Multiple pregnancy,
Abnormal uterus, Fibroid, Cervical
cancer, Contracted pelvis, Relaxed ab
wall.
MANAGEMENT: C-section

Presenting diameter:
13cm.
C-section. Never
vaginal delivery.

Presenting
diameter: 13cm.

Craniotomy.

DEFINITION
Umbilical cord as the
presenting part, below any
part of the fetus.
Coz ill-fitting presenting part
into lower segment of uterus
cord can go into space
below presenting part mainly
when footling breech or
AROM.

UMBILICAL CORD PROLAPSE

RISK FACTORS
CONSEQUENCES
Multiparity
Cord compression &
Prematurity
Vasospasm Cutting
Macrosomia
blood from fetus Fetal
Breech
distress.
Polyhydroamnios
Outcome depends on GA
& duration of
compression.

MANAGEMENT
Emergency C-section
Vaginal delivery only if delivery is imminent
(when vaginal quicker than c-section: fully
dilated & presenting part very low)
While waiting for C-section
- Fill bladder with 1L
- Push presenting part up
- Tredelenburg position

ESSENTIAL HYPERTENSION
CLASSIFICATION
According to Severity:
A] Mild
B] Severe (>160/110)
According to Complications
A] Uncomplicated
B] Complicated. Any of the following:
Cardiomyopathy; Age >40; Duration of HTN >15yrs; Renal disease; DM,

MATERNAL RISK
Superimposed PET.
Abruptio.
Cerebral hemorrhage
Exacerbation of HTN
Renal failure
Congestive heart
failure.

FETAL RISK
IUGR.
IUFD.
Prematurity.
PNMM directly related
to HTN severity.

CT disease or coarctation of aorta; Previous hx of perinatal loss.

MANAGEMENT
PRENATAL
ANTENATAL
DURING LABOR
POSTNATAL
Assess cause & severity.
Mild uncomplicated HTN, stop drugs &
Observe BP.
Observe BP esp 48h
Look for risk factors.
observe 3months. If BP stayed mild,
Strict fluid control.
postpartum.
Review drugs.
dont give drugs.
Continue AHD if taking Observe for pulm edema.
Establish baseline CBC,
If BP >160/110, give drugs.
them.
Observe for hypertensive
urine analysis, 24h urine
Observe fetal growth (IUGR/IUFD)
Continuous fetal heart
encephalopathy.
collection test, KFT, Echo,
Observe maternal condition.
monitoring.
Reassess cardiac & renal
ECG, CXR.
No indication to induce labor before
f(x).
41wks.
CARDIAC DISEASES
Predictors (NYHA Functional Classification) #
Risk of
Complicates 1% of pregnancies.
predictors complications
Complications during pregnancy: HF,
Cardiac dysf(x) EF>60 or <40
0 3%
arrhythmia, stroke & death.
1 30%
Presence of pulm HTN
Assessment before pregnancy is essential.
2 60%
Presence of cyanosis (low Hb saturation)
Can be congenital, rheumatic & ischemic.
Presence of aortic or mitral valve stenosis
Hx of CHF, arrhythmia or TIA
MANAGEMENT
PRENATAL
ANTENATAL
DURING LABOR
Classify patients (predictors of
Monitor signs & sx of HF.
Avoid pain coz pain EF acute HF. Avoid
complications).
Serial Echo.
hypotension.
Investigations.
Serial fetal monitoring.
Left lateral position with oxygen mask.
Review drugs.
Continuous saturation monitoring.
Give predictions (safe to go thru
Shorten 2nd stage labor (instrumental?).
pregnancy?)
Prophylactic antibiotics.
Careful fluid therapy. Continuous CTG. Continuous
ECG.

HYPERTHYROIDISM
OVERVIEW
MANAGEMENT
95% cases due to Graves. 50% have +ve family hx.
Carbimazole & PTU are most commonly used drugs.
Clinical picture similar to non-pregnant.
Both cross placenta, to a lesser extent does PTU, so even in
Most discriminatory features in pregnancy are weight
moderate doses may cause fetal hypothyroidism.
loss, tremor & lid lag.
Both not teratogenic.
Thryotoxicosis usually improves in pregnancy as other
blockers used in thyroid crisis. Thyroidectomy rarely
autoimmune.
indicated in pregnancy.
Exacerbations may occur esp in 1st trimester ( subunit
Radioiodine contraindicated in pregnancy (also 4months
of hCG resembles TSH)
before) & during lactation.
Thyrotoxicosis associated with infertility, recurrent
Check for neonatal & fetal thyrotoxicosis.
pregnancy loss, IUGR, preterm labor, higher PNMM.
HYPOTHYROIDISM
OVERVIEW
MANAGEMENT
Commoner than thyrotoxicosis. Associated with other autoimmune like DM & pernicious
Thyroxine supplements are the
anemia.
only replacement therapy.
Clinical picture similar to non-pregnant.
Crosses placenta but only very
Most discriminatory feature are cold intolerance, slow pulse & delayed relax of tendon
little amount will reach fetus, so
reflexes.
fetus not at risk of dev
Pregnancy itself has no effect on hypothyroidism.
hyperthyroidism.
Associated with infertility, miscarriages, anemia, fetal loss, IUGR & PET.
Association b/w untreated hypothyroidism & reuced IQ & neurodev delay in offspring.
EPILEPSY
OVERVIEW
MANAGEMENT
Most cases are idiopathic and no underlying cause.
The lowest effective dose. Try with 1 drug & give full dose of folic
30% familial.
acid 5mg.
All types of seizures can occur in pregnancy.
Try stopping AED, if she is fit free for >2yrs.
Most AED are teratogenic.
Detailed anomaly scan at around 2owk gestation.
In majority of cases, frequency of seizure are not
Vit K supplement for the last 4wks of pregnancy for pts taking
altered by pregnancy.
valproic acid.
Risk of seizures are highest in peripertum period.
Avoid pain & long course of labor.
5-10% risk of transmitting epilepsy.
Major malformations caused by AED are NTD, orofacial defects &
The fetus is relatively resistant to short episodes of
congenital heart defects.
hypoxia.
Minor malformations are dysmorphic features, hypertelorism,

hypoplastic nails & digits.

MENOPAUSE

occurs secondary
to a genetically
programmed loss
of ovarian follicles
Defined as the
cessation of
menstrual periods
menopause
occurs at a mean
age of 51.4 years
in normal women

Epidemiology

The menopausal transition

variation in menstrual cycle

length (>7 days different from
normal menstrual cycle length,
which is 21 to 35 days)
2 skipped cycles and an
interval of amenorrhea 60
days
elevated serum FSH
concentration
Cessation menstrual period
(not recognized until after 12
months of amenorrhea).

Perimenopause "around the menopause," and begins

with the menopausal transition and ends 12 months after
the last menstrual period
Menopause Menopause is defined by 12 months of
amenorrhea after the final menstrual period. It reflects
complete, or near complete, ovarian follicular depletion and
absence of ovarian estrogen secretion.
Postmenopause is defined as (early) the first five years
after the final menstrual period. It is characterized by
further and complete dampening of ovarian function and
accelerated bone loss; many women in this stage continue
to have hot flashes. (late) begins five years after the final
menstrual period and ends with death
Endocrinology

Although the
average age at
menopause is
approximately 51
years, for 5
percent of
women, it occurs
after age 55 (late
menopause), and
for another 5
percent, between
ages 40 to 45
years (early
menopause).
Menopause
occurring prior to
age 40 years is
considered to be
premature
ovarian failure

The age of menopause is

reduced by about two years in
women who smoke
There is also a tendency for
women who have never had
children and for those with
more regular cycles to have an
earlier age of menopause
Other factors that may be
important include:
1. A family history of early
menopause
2. A history of type 1 diabetes
mellitus
3. The presence of a variant of
form galactose-1phosphate uridyl
transferase
4. Shorter cycle length during
adolescence (which is also
a predictor of higher basal
FSH).

Menstrual cycle and hormone patterns begin to change

many years prior to menopause.
In the late reproductive years, prior to the menopausal
transition, menstrual cycles are ovulatory, but follicular
phase length begins to shorten.
In the early menopausal transition, women begin to
experience some menstrual irregularity.
During this stage, inhibin B concentrations fall due to a
decline in follicular number, and as a result, serum FSH
levels begin to rise, with relative preservation of estradiol
secretion (normal or high estradiol levels), but with low
luteal phase progesterone concentrations .
The preservation of estradiol secretion appears to be due to
an increase in aromatase activity.
In the late menopausal transition, cycle variability
increases. High FSH and low estradiol values may be
suggestive of menopause, After menopause, when ovarian
follicles are depleted, the ovary no longer secretes
estradiol. However, it continues to produce and secrete
androgens under the continued stimulation of LH

Clinical Manifestations
1.Bleeding patterns

2.Hot flushes

3. Depression and mood

changes

Chronic anovulation and

Progesterone deficiency
in this transition period
may lead to long periods
of unopposed estrogen
exposure and therefore
anovulatory bleeding and
endometrial hyperplasia.
Oligomenorrhea (irregular
cycles) for six or more
months, or an episode of
heavy dysfunctional
bleeding.
Irregular or heavy
bleeding during the
menopausal transition
may be treated with lowdose oral contraceptives
or intermittent progestin
therapy
4.Sleep disturbance

A distressing feature of
hot flashes is that they
are often associated with
arousal from sleep. In
addition, primary sleep
disorders are common in
this population, even in
the absence of hot
flashes.

Clinical Manifestations

The most common acute

change during
menopause is the hot
flush, which occurs in up
to 75 percent of women
in some cultures, but only
about 20 percent of these
women seek medical
attention for treatment of
their flashes.
As noted above, hot
flushes are most common
in the late menopausal
transition and early
postmenopausal periods
They are self-limited,
usually resolving without
treatment within one to
five years, although some
women will continue to
have hot flushes until
after age 70.
The prevalence of
vasomotor symptoms is
quite variable across
cultures

Hot flushes typically

begin as the sudden
sensation of heat
centered on the upper
chest and face that
rapidly becomes
generalized.
The sensation of heat
lasts from two to four
minutes, is often
associated with profuse
perspiration and
occasionally palpitations,
and is often followed by
chills and shivering, and
sometimes a feeling of
anxiety.
Hot flushes usually occur
several times per day,
although the range may
be from only one or two
each day to as many as
one per hour during the
day and night. Hot
flashes are particularly
common at night.

However, a significant
association between the
menopausal transition
and risk for depression
seems apparent overall.
In the largest prospective
cohort study to date, the
Study of Women's Health
Across the Nation (SWAN)
reported that women in
early perimenopause had
a higher rate of mood
symptoms (14.9 to 18.4
percent) than
premenopausal women (8
to 12 percent)
These mood symptoms
primarily were irritability,
nervousness, and
frequent mood changes,
but not feeling "blue,"
and were more common
in women with lower
educational attainment.
Several studies have
reported that a prior
history of depression or
PMS is a strong predictor
of depressive recurrence
during the menopausal
transition .

5.Genitourinary symptoms
a.Vaginal dryness

b.Sexual dysfunction

c.Urinary symptoms

The epithelial lining of the vagina and

urethra are very sensitive to estrogen,
and estrogen deficiency leads to
thinning of the vaginal epithelium.
This results in vaginal atrophy
(atrophic vaginitis)
causing symptoms of vaginal dryness,
itching and often, dyspareunia.
The prevalence of vaginal dryness
was about 47 percent of women
On exam, the vagina typically
appears pale, with lack of the normal
rugae and often has visible blood
vessels or petechial hemorrhages.
Vaginal pH, which is usually <4.5 in
the reproductive years, increases to
the 6.0 to 7.5 range in
postmenopausal women not taking
estrogen. The increase in pH and
vaginal atrophy may lead to impaired
protection against vaginal and urinary
tract infection

Estrogen deficiency
leads to a decrease in
blood flow to the
vagina and vulva. This
decrease is a major
cause of decreased
vaginal lubrication and
sexual dysfunction in
menopausal women
This neuropathy
appears to be
completely reversible
with estrogen
replacement therapy
The cervix also can
atrophy and become
flush with the top of
the vaginal vault.
The elasticity of the
vaginal wall may
decrease and the
entire vagina can
become shorter or
narrower.

Low estrogen production after the menopause

results in atrophy of the superficial and
intermediate layers of the urethral epithelium
with subsequent atrophic urethritis, diminished
urethral mucosal seal, loss of compliance, and
irritation; these changes predispose to both
stress and urge urinary incontinence.
The prevalence of incontinence increases with
age. It has not been established, however, that
the frequency of urinary incontinence increases
across the menopausal transition
Although data are conflicting, systemic
estrogen therapy does not appear to be
effective for the treatment of urinary
incontinence.
Recurrent urinary tract infections are also a
problem for many postmenopausal women. In
addition to epithelial atrophy, estrogen
deficiency can increase vaginal pH and alter
the vaginal flora, changes which may
predispose to urinary tract infection

6.Others

Breast pain Breast pain and tenderness are common in the

early menopausal transition, but begin to diminish in the late
menopausal transition
Menstrual migraines Menstrual migraines are migraine

Balance Impaired balance in postmenopausal

women may be a central effect of estrogen
deficiency .Problems with balance may play a
major role in the incidence of forearm fractures in

headaches that cluster around the onset of each menstrual

period. In many women, these headaches worsen in frequency
and intensity during the menopausal transition .
Skin changes The collagen content of the skin and bones is
reduced by estrogen deficiency. Decreased cutaneous collagen
may lead to increased aging and wrinkling of the skin. The
collagen changes may be minimized with estrogen.
Joint pain Although the prevalence is not known, some
women experience diffuse joint pain during the menopausal
transition and postmenopausal period

Long-term issues

women. The incidence of Colles' fractures

increases markedly in women at age 50 but
remains stable in men up to the age of 80. A
mechanism other than osteoporosis must be
invoked to explain this observation because
osteoporosis occurs gradually.
The fracture is usually caused by falling on an
outstretched hand. The role of estrogen therapy on
falls is discussed elsewhere.

Diagnosis

Bone loss Bone loss

Menopause is defined clinically as 12 months of
begins prior to
amenorrhea in a woman over age 45 in the absence
menopause. The annual
of other biological or physiological causes.
rates of loss during
The best approach to diagnosing the menopausal
these phases were
transition is a longitudinal assessment of menstrual
approximately 1.8 to 2.3
cycle history and menopausal symptoms (vasomotor
percent in the spine and
flushes, mood changes, sleep disturbances).
1.0 to 1.4 percent in the Differential diagnosis Hyperthyroidism should
hip. Higher body mass
always be considered in the differential diagnosis
index was associated
pregnancy, hyperprolactinemia.
with slower bone loss;
Atypical hot flashes and night sweats may be due to
ethnicity had no effect.
other disorders, such as medications, carcinoid,
Cardiovascular
pheochromocytoma, or underlying malignancy.
disease
Dementia
Summary & recommendations

Hormone Replacement
Therapy (HRT)

Postmenopausal hormone
therapy is currently
recommended short-term for
the management of moderate
to severe vasomotor flushes.
Long-term use for prevention
of disease is no longer
recommended
Hormone preparations

Combined, continuous
conjugated estrogens e.g.
(0.625 mg) and
medroxyprogesteroneacetate
(MPA 2.5 mg).
Un-opposed estrogens (in

Most postmenopausal women, with the EXCEPTIONof women with breast cancer or
known cardiovascular disease, who have symptoms of vaginal atrophy and/or
vasomotor instability are good candidates for estrogen therapy (for the shortest
duration possible depending upon symptoms).
Vasomotor instability For postmenopausal women with moderate-to-severe
vasomotor symptoms (and no history of breast cancer or cardiovascular disease),
short-term estrogen therapy as the treatment of choice
Urogenital atrophy With the exception of women with breast cancer, almost all
postmenopausal women are candidates for vaginal estrogen.
Osteoporosis We currently do not consider estrogen to be a first-line therapy for
osteoporosis. Therefore, the management of women who choose not to or cannot
take estrogen is the same as for other postmenopausal women.
Cardiovascular disease prevention Estrogen is NO longer indicated for the
prevention of CHD in postmenopausal women. The best means of primary and
secondary prevention of cardiovascular disease involves attention to risk factors
such as smoking, hypertension, dyslipidemia, and diabetes mellitus

hysterectomised patients )
Oral preparations , local ,
injectables , vaginal
preparations and implants
Uses

Treat short term menopausal

symptoms
Disease prevention
Disease prevention

Coronary heart disease

Osteoporosis
Dementia

Women with POF

Women with breast cancer

Androgen replacement

In healthy women with

premature ovarian
failure, we continue
their hormone therapy
until their late 40s or
age 50 years. At that
point, the same
discussion of potential
risks and benefits of
postmenopausal
hormone therapy
should take place

Although women with breast cancer often

experience early menopause due to
adjuvant chemotherapy, and may have
vasomotor symptoms due to tamoxifen
therapy, estrogen therapy should NOT be
prescribed.
The epidemiologic data and clinical trial
data have been inconsistent, but the
increased risk of breast cancer recurrence
with estrogen therapy in one trial (HABITS),
is of great concern. We therefore do not
recommend estrogen for women with a
personal history of breast cancer.

The known decrease in ovarian androgen

production rates and serum androgen
concentrations has caused concern that
menopause might be associated with a
decline in libido. An age-associated
decline in sexual desire has been
observed in both men and women.
However, it is unclear whether the decline
in libido in women is age- or menopauserelated, since studies in women have not
shown a significant correlation between
libido and the serum estradiol or
testosterone concentration

MULTIPLE GESTATIONS
EPIDEMIOLOGY
Hellins rule: 1 in 80n-1 pregnancies
60% are Dizygotic (dichorionic and diamniotic)
40% are Monozygotic (one in 250 births, constant
worldwide)
- 10% (dichorionic and diamniotic)
- 20% (monochorionic and diamniotic)
- 10% (monochorionic and monoamniotic)

DEFINITION & TYPES

Any pregnancy in which two or more
fetuses exist simultaneously
Types
Dizygotic (dichorionic and
diamniotic), (fraternal)
Monozygotic
0-72 hr dichorionic and diamniotic
4-8 d monochorionic and diamniotic
Incidence varies with: Ethnic group (Blacks more),
9-12 days monochorionic and
Maternal age (Older more), Parity (Multi more),
monoamniotic
>12th day conjoined (Siamese) twins, Family Hx,
COH, 10 and 20% with CC & hMG res. (Only in
1:70,000 (thorcopagus is the
dizygotic twins)
commonest)
CHORIONICITY
UNIQUE COMPLICATIONS WITH IN MONOCHORIONIC
DETERMINATION
Ultrasound
TWIN-TWIN TRANSFUSION
ACARDIAC TWIN
- 30% of twins will be of
SYNDR (TTTS)
different sex
One baby will give blood to
Two growing fetuses but only
- 23% will have monochorionic the other baby through an
one heart beating
placenta
AV anastomosis.
Cause: Living cells in the
- 27% will have same sex,
deformed baby is sustained by
dichorionic placentas, but
the healthy twins circulation.
different blood grouping
- 20% have same sex,
dichorionic placentas, and
identical blood grouping that
will require HLA or DNA PCR
analysis

FETUS PAPYRACEOUS
Fetus in a multi-gestation
pregnancy dies in-utero &
then partially/completely
absorbed by the mother or
twin.
@Twin embolization
(vanishing) syndrome

PREGNANCY
COMPLICATIONS
Hyperemesis gravidarum
Hypertensive disease, 4x
more common than
singletons
Gestational diabetes
Anaemia
Hydramnios in 12%,
primarily in monozygotic
twins
Reflux, ab discomfort, back
pain, leg swelling, bladder
sx and haemorrhoids.
APH (PP and Abruptio, as
larger placental area and
PET)
Thromboembolic disease:
appropriate prophylaxis

and Rx

PRESENTATIONS
Four principal combinations of presentations
Cephalic/cephalic
60%
Cephalic/breech
20%
Breech/cephalic
10%
Breech/breech
10%
First two, many obstetricians will allow vaginal
delivery with the same contraindications as for
singleton pregnancies
The same applies for trial of vaginal delivery in
the presence of a previous lower segment
Caesarean Section
Complication
Abortion (12-12wk)
Premature labor (2432wk)
IUGR
Fetal defects

Singleto
n
1%
1%

Dichor
~
2%
5%

5%
1%

10%
2%

Anesthetic: Epidural

SECONDARY
PRIMARY

Labour management:
IV line, Delivery in theatre, Twin
CTG machine
2 resuscitation trolleys, 2
obstetricians, 2 paediatricians,
Inform SCBU
PPH: IV line, Blood grouped and
saved, Oxytocin infusion following
delivery

20%
8%
FOLLICULAR CYST
ANC: Consultant-led team. More
CORPUS LUTEAL CYST
GRANULOSA-THECA LUTEAL
POLYCYSTIC
ENDOMETRIOTIC
CYST

EPITHELIA
L
OVARIAN
NEOPLAS

LABOR MANAGEMENT

DIAGNOSIS OF MULTIPLE PREGNANCIES

Size and hormones
Diagnosis of multiple gestations
History, examination (4cm larger than
x1)
and investigations

Monochor
~
12%
10%

DEATH OF ONE FETUS IN A TWIN

NON-NEOPLASTIC
PREGNANCY.
FUNCTIONAL CYST
Dichorionic Preterm labor
Monochorionic Hypotension
Death / Handicap of the other.
Doesnt lead to DIC as readily as
singleton.

INDICATIONS FOR ELECTIVE CSECTION

- Malpresentation of the first twin
- Second twin larger than the first
- Evidence of IUGR in one or both
twins
- Monochorionic twins
- History of fertility treatment

BENIGN
BORDERLIN
E
MALIGNANT

MUCINOU
S
SEROUS
ENDOMETRIOI

CLEAR CELL
(MESONEPHROI
GERM CORD
GRANULOSA-THECA
NON-CELL
D)
CELL
(GONADAL
STROMAL)
DERMOID
CYST
BRENNET
TUMORS
SOLIDSAC
DYSGERMINO
GESTATIONAL
FIBROMA
(MEIGS
ANDROGEN
SECRETING
TUMOR
MALIGNANT
YOLK

FOLLICULAR CYST
- Usually less than 5 cm
- Benign and asymptomatic
- Thin wall, contain clear fluid
- Rescan in 4 weeks
- If enlarge or symptomatic,
consider surgery

OVARIAN NEOPLASM
NON-NEOPLASTIC FUNCTIONAL CYST
CORPUS LUTEAL CYST
GRANULOSA-THECA LUTEIN
CYST
Excessive bleeding into corpus - in molar pregnancy or part
luteum
of hyperstimulation
Cyst filled with blood
syndrome
- Due to excessive
Delayed period + pain
gonadotrophin
Usually the following period is
heavy

POLYCYSTIC OVARY
ENDOMETRIOTIC
CYST

PRIMARY OVARIAN TUMORS

A] EPITHELIAL
- Benign
- Borderline:
Epithelial tumors with no invasion of basement membrane
15% of epithelial tumors, mostly serous and stage 1 (70-85%).
10 year survival is 95%. Late recurrence.
Extensive histological sectioning is essential to exclude invasion.
- Malignant
MUCINOUS
SEROUS
ENDOMETRIOD
- Large tumors.
- Most common
- Few cases arise in
Multilocular filled with
endometriosis
- Contain clear fluid
mucin
- 30% coexist with
- Often bilateral.
- If ruptured
primary endometrial
Around age of
pseudomyxoma
cancer
menopause
peritonei
- Malignant type is
the commonest
ovarian cancer

BRENNER
- Usually benign.occur
in reproductive life
- May be associated
with endometrial
hyperplasia
- May coexist with
mucinous
cystadenoma

CLEAR CELL
@MESONEPHROID
- Associated with
endometriosis in 25%
- Worst prognosis

OVARIAN NEOPLASM
PRIMARY OVARIAN TUMORS
B] GERM CELL TUMORS
BENIGN
DERMOID CYST @ BENIGN CYSTIC
TERATOMA
- 25% of all ovarian neoplasm
- Contain tissue derived from two or
more germ cell layers
- Unilocular cyst. May contain teeth,
bone , cartilage, nerves, hair, thyroid,..
Tissues
- Almost always benign. Malignant
changes may occur in any component
- Occur at any age. Peak is 20-30 years.
- Bilateral in 20%

MALIGNANT
Rare. 3% of ovarian cancers
SOLID
TERATOMA
Peak
incidence in
second
decade

NONGESTATIONAL
CHORIOCARCINO
MA
- Secrete HCG
- May be
component of
solid teratoma

YOLK SAC @
ENDODERMAL
SINUS
- Highly malignant.
Affect young age
- Partly solid.
Secrete alpha fetoprotein

DYSGERMINOMA

- Most common.
Highly malignant
- Usually spread by
lymphatics
- Very radiosensitive
- Occur in young
women. May arise in
gonadal dysgenesis

C] GERM CORD @ GONADAL STROMAL @ SEX CORD TUMORS

GRANULOSA THECA CELL TUMOR
ANDROGEN-SECRETING TUMORS
FIBROMA
- Moderate to large size
- Androblastoma
- Solid tumor
- Solid, as enlarge may have cystic
- Sertoli-leydig
- May be associated with meigs
spaces
- Gynandroblastoma
syndrome
- Yellow tinge on cut surface
Cause virilization
- Tend to have long pedicle
- Thecoma is benign, but granulosa is
malignant
- Occur at any age .50%
postmenopausal
- Secrete estrogen
- Usually stage 1. Late recurrence
SECONDARY @ METASTATIC OVARIAN TUMORS
Always bilateral. From mucin secreting tumors, stomach and colon (Krukenberg tumors)
May be secondary to breast

INTRODUCTION
- Wide variety of tumors
- 25% of female genital tract
tumors
- In U.K, the most common
pelvic cancer
- Worst prognosis of all
female genital tract cancers
- Life time risk is 1%
- Spread by local spread,
lymphatic and rarely by blood

MALIGNANT EPITHELIAL OVARIAN TUMORS

ETIOLOGY
PRESENTATION
PHYSICAL FINDINGS
Risk Factors:
Silent disease 75%
Benign:
Nulliparity, Family
- Usually mobile. unless large or
present at advanced
history, Fertility
complicated
stage
drugs
- Dermoid cyst anterior to bladder
Symptoms of
Protective Factors:
Malignant:
abdominal
Number of
- Bilateral
involvement
pregnancies, OCCP,
- Ascites
Symptoms of distant
Tubal ligation.
- Hard deposit in pelvis
metastases
- Leg edema
General malaise,
- Signs of bowel obstruction of ureteric
weight loss
obstr
Hormonal production

COMPLICATION
Torsion
- common with dermoid/fibroma
- Severe abdominal pain/vomitting
Rupture
Haemorrhage
Impaction
infection

OVARIAN TUMOR IN PREGNANCY

Found incidentally
Corpus luteal/dermoid
2% are malignant
If discover early and persist ,
surgery around 16 weeks
If complicated, operate immediately

FIGO STAGING
Stage
Growth limited to one or both ovaries
1
Stage
Growth limited to one or both ovaries with
2
pelvic extension
Stage
Tumor involving one/both ovaries with
3
peritoneal implants outside pelvis/positive
retroperitoneal or inguinal nodes.

INVESTIGATION
Uss /CT scan
Tumor markers( ca125,CEA,
HCG,alpha FP
Urea and electrolyte
LFT
Chest X ray
Ascitic tap
Calculate risk malignancy index.

RISK MALIGNANCY INDEX

CA 125 estimation
Menopausal status
pre menopausal score = 1
post menopausal score= 3
Ultrasound score
Multi locular, solid areas, bilateral, ascitis, intra ab
mets.
if 0 or 1 score = 1
if 2-5
score= 3
RMI = CA125 x M x U

Stage
4

Growth involving one or both ovaries with

distant mets.

PRIMARY
- Primary cytoreduction
- TAH, BSO, OMETECTOMY,
WASHINGS, BOWEL SURGERY
- Optimal debulking: less
than 2 cm residual tumors
- Staging once histology is
available
- If confined to ovary and
young age, conservative
surgery
CHEMOTHERAPY
Indication stage 1c and
above
Platinium based
- Taxol
- 6 cycles at 3 weekly
intervals
- Monitoring:
examination
CA125
FBC, U&E

MALIGNANT EPITHELIAL OVARIAN TUMORS

MANAGEMENT
SURGICAL
INTERVAL DEBULKING
SECOND LOOK
SURGERY
- Alternative to primary surgery
- Assess response to
medically unfit
chemotherapy
large ascitis
- Plan future
severe malnutrition
management
- 3 cycles of chemotherapy surgery 3
- Only in research
more cycles of chemotherapy
context.
- Aim : to improve patient condition
less extensive surgery to achieve
optimal debulking
- May improve survival
FOLLOW UP
How aggressive?.
Three monthly for one year
then six monthly then yearly
History, examination and
CA125
Imaging if recurrence is
suspected clinically or by
CA125

PALLIATIVE SURGERY
- Removal of intestinal
obstruction
- Survival is very poor
- Quality of life
considerations

SCREENING
Life time risk is 1%
5% of tumors are genetic
History of breast cancer increases risk by factor of 2
History of ca ovary increases the risk by factor of 3
One first degree relative affected: risk 2.7%
2 first degree relatives affected : risk is 13%
If BRCA1 mutation carrier :
risk is 50%
Problems :
- no pre-cancerous stage
- unknown natural course
TVS AND CA125 ON YEARLY BASIS
ONGOING STUDY TO EVALUATE THIS.

Endometritis
Salpingitis
Oophoritis
Parametritis
Peritonitis
DDx
UTI
Early
pregnancy
complication,
Ectopic
pregnancy
Appendicitis,
diverticulitis
Complicated
ovarian tumor
Other causes of
lower ab pain

COMPLICATIONS
Tuboovarian
abscess,
polymicrobial,
50% bilateral
Tubal damage,
infertility and
future ectopic.
Fitz-Hugh-Curtis
syndr
Reinfection is
25%

PELVIC INFLAMMATORY DISEASE

PATHOLOGY
EPIDEMIOLOGY
CLINICAL FEATURES
Incidence variable
o Lower ab pain and
o Non specific, lack
Infection ascend to
tenderness
sensitivity and
10-13%,
the uterus resulting in
o Deep dysparunea
specificity
underestimated,
endometritis with
increasing
o Abnormal vaginal or o Positive predictive
plasma cell infiltration
Age, teens
value of clinical
cervical discharge
Tubes, mucosal
diagnosis is 65-90%
Sexual activity,
o Cervical excitation
inflammation with
as compared to
early coitus,
and adnexal
swelling, redness and
laparoscopy
multiple partners,
tenderness
deciliation, polymorph
o
Excess of WBC in
often
proceeded
by
o
Fever
>38C
infiltration of the
the vagina present
STD (chlamydia, GC) o Adnexal mass in
submucosa, exudate
in lower genital
with 2ndary invasion
fills the lumen,
20% of cases
tract infection also
with anaerobes
adhesions and spread
o Raised ESR, WBC,
o
Endometrial biopsy
to the serosal surface, Contraception
CRP
not recommended
pus from the fimbria
Pills? Protective
o Excess of
as routine
Ovaries and
Leukocytes in the
IUCD Cu releasing
investigation
formation of tubovagina
risk
ovarian abscess or
o General symptoms
Barrier protective
mass
depend on severity
Parity 75% are
nulliparous
INVESTIGATIONS
TREATMENT
CBC, CRP, Urine
Mild cases : Ambulatory Severe cases: Admit!
IV cephalosporin +
Antibiotic
metro till 24 h,
analysis and culture
Doxycycline 2x/day/14d Indications to Admit:
improvement oral
HVS, Endocervical
+ metronidazole
Surgical emergency
doxycycline and
swab
2x/day/5d
cannot
be
excluded,
metronidazole
USS, adnexal mass or
(if
GC
suspected
add
Clinically
severe
abscess
ciprofloxocine single
disease, Tuboovarian
Clindamycine
Laparoscopy if there
dose)
abscess,
PID
in
Ofloxocine+
is doubt about
pregnancy,
Lack
of
metronidazole
diagnosis or no
Or
response
to
oral
Clindamycine
improvement after
Ofloxocine
+
therapy,
Intolerance
to
24-48 hours of proper

Chronic PID,
adhesions,
pelvic pain,
dysparunea,
dysmenorrhea

treatment
BhCG

metronidazole

oral therapy

Supportive therapy

NOTES
*TUBERCULOSIS
POSTPARTUM HEMORRHAGE
Def1: Any
blood loss
>500mL (vaginal)
and >1000mL (caesarian) following
Patients
notofimproving
on antibiotic
Rare delivery. (Blood loss estimation inaccurate)
Def2: 10%therapy
drop ofshould
PCV. (Depends
on timing of test after onset)
have laparoscopy
Often secondary to pulmonary
Def3: Any
bleeding
which
result
in
the
signs
&
sx
of
hemodynamic
instability.
(Blood loss response differ from ppl esp
IUCD may be left in situ in women
TB
anemia, PET, cardiac diseases, dehydration)
with mild PID butHEMOSTATIC
should be MECH
May present as pelvi- RISK FACTORS
INCIDENCE
TYPE
removed
in
sever
cases
abdominal
The leading
At term, the estimated blood flow to Primary (Early)
PPH:
mass
Previous PPH
Laceration

Tuboovarian
abscess
may
be

Systemic
symptoms,
cause of
the uterus 500-800mL/min. 10-15%
Excessive blood loss
Abruptiomenstrual
Instrumental
maternal drainedof
Cardiac output.
abdominally,
within 24h of delivery
disturbance,
amenorrhoea,
delivery
Retained
mortality. lapaporoscopic
Natural hemostatic
mech:
(esp 1st 6h). infertility
or USS guided
LGA
placenta
Occur in 4%
of 1) Contraction
& retraction of
Secondary
(Late)
aspiration
on pelvic collection
Treated by antituberculous
Failure to
HTN disorders
deliveries.
myometrial fibers
PPH: Excessive blood
progress
Induction &
drugs
and
surgery
2) Hypercoagulable state in late
loss between 24hduring 2nd
Augmentation of
pregnancy
6wks postpartum
stage
labor
3) Integrity of the genital tract
(esp 2nd wk)
Placenta
accreta
ETIOLOGY
Bleeding mostly from endometrial spiral arterial arterioles & decidual veins that supplied & drain intervillous spaces of
placenta.
Causes of primary PPH: 1) Tone; 2) Trauma; 3) Tissue; 4) Thrombosis; 5) Uterine Inversion
TONE (ATONY, 75-80%)
TRAUMA
TISSUE
THROMBOSIS
UTERINE INVERSION
Failure of contraction & retraction of
Vascular beds in
- Retention of Preexistent: ITP,
Just after 2nd stage
myometrial muscle fibers.
genital tract are
part of
TTP.
of labor, due to
Predisposing factors:
engorged during
placenta.
Acquired:
uterine atony, cervix
1) Uterus overdistention Multiple
pregnancy.
50% cases of
1- Abruptio (Leak is open & placenta
gestation, LGA, Polyhydroamnios.
1) Laceration in
2ndary PPH.
AF)
attached.
2) Prolonged labor fatigue.
cervix & vagina
2- HELLP (low Plt) Inexperienced doc
3) Drugs Halogen anest, nitrate, NSAID,
spontaneous/
- Incomplete
3- Sepsis DIC
exert fundal

MgSO4, Nifedipine.
4) Placenta previa - content of
musculature of the wall.
5) Bacterial toxins chorioamnionitis,
endometritis & septicemia.
6) Fibroid esp intramural.
7) Grand multipara >5
8) Precipitous labor
9) Abruptio esp concealed coz interstitial
bleeding.
CLINICAL
MANIFESTATION
Heavy vaginal
bleeding
BP
HR
RBC count (Hct)
Swelling & pain in
tissues in the
vaginal & perineal
area.

instrumental/
manipulation of
fetus/ LGA/
precipitous labor.
2) Uterine rupture
intraperitoneal
bleeding.
3) Hematoma
perineal, vaginal or
broad ligament
hematoma.
COMPLICATION

4- Dilutional
coagulaopathy
5- Amniotic fluid
embolism
intravascular
infusion of small
amt of AF.

pressure while pull

umbilical cord before
complete placental
separation.
Inversion Traction
of peritoneal
structure
Vasovagal response
Vasodilation
Hypovolemic shock.

DDx OF CAUSES

Hx: Ask risk factors of uterine atony & coagulopathy.

Exam:
Soft boggy & large uterus with profuse vaginal bleeding?

Atony.

Bright red bleeding b4 separation of placenta? Trauma.

Abdominal / vaginal mass increasing in size? Hematoma.

Bleeding severe, bright red, no clots but uterus contracts

well? Coagulopathy.
Cupping of fundus or non-palpable fundus? Uterine
inversion.
Fever & tenderness? Endomyometritis.
If no cause identified Manual exploration of genital tract.
MANAGEMENT OF PRIMARY POSTPARTUM HEMORRHAGE
Identification of those at risk of PPH. Start prophylactic measures during labor to minimize maternal mortality.
1. CBC Hb & Plt (correct anemia if present). 2. Blood typing & Ab screening (Xmatch 2-6units blood) 3. Insert large bore IV
line.
ROUTES OF MANAGEMENT
RESUSCITATION
EVALUATE
SURGICAL
PROGNOSIS
Oxygen by mask.
Monitor pulse, BP, 1. Laparotomy to drain
Depends on
2 large bore IV lines. Central venous line.
Urine output,
free blood & inspect any
cause of PPH,
Draw blood CBC, coagulation screen, urea, creatinine,
blood gases, level injury & repair.
duration,
electrolyte.
of consciousness. 2. Uterine artery ligation
amount of
Immediate fluid replacement with NS or RL.
Order regular CBS 3. Internal iliac (inferior
blood loss &

Anemia
Hypotension & hypovolumic shock
Renal failure
Risks of blood transf
Surgery complications & sepsis
Sheehan syndr
Venous thrombosis & embolic effects
(coz of surgery, bed rest &
hypercoagulable state)

separation of
accreta or
precreta.

Transfuse RBC as available & appropriate.

counts &
hypogastric) artery
effectiveness
FFP if abnormal coagulation test results & sites oozing.
coagulation tests
ligation.
of rx.
Cryoprecipitate if abnormal coagulation tests not
to guide blood
4. Total hysterectomy
Prompt dx &
corrected with FFP.
component
5. Selective arterial
rx.
Plt concentrates if plt count <50x10/L & bleeding
therapy.
embolization
continues.
MANAGEMENT OF UNDERLYING CAUSE
TONE
TRAUMA
TISSUE
COAGULOPATHY
Assess uterine size & tone.
Cervical & vaginal
Removed even if bleeding stopped Confirm by risk factors &
Bimanual express clots,
lacerations absorbable
with use of uretrotonics.
abnormal coagulation
stimulate uterine
continuous stitch.
Diffcult without GA.
test.
contractions.
Large lower genital tract,
Resuscitate adequately. Manual
FFP: 1U=1g fibrinogen
Empty bladder.
unstable broad lig &
explore.
Cryoprecipitate:VIII, XiII &
Uterine artery ligation,
retroperitoneal hematoma
Vaginal hand in situ to
fibrinogen.
selective arterial
incision, drain, ligation,
discomfort, infxn, trauma.
Plt concentrate: 1u 20embolization or subtotal/
packing.
Adherent? Curettage.
25k plt.
total hysterectomy.
Uterus rupture sub/TAH.
Packed RBC: 1U 1g/dL
Uterotonic drugs.

SECONDARY POSTPARTUM HEMORRHAGE

ETIOLOGY
RISK FACTORS
Retained products of conception (RPOC)
C-section
most common cause of 2ndary PPH
Prolonged ROM
Infection often 2ndary to RPOC. 1-3% after
Prolonged labor with multiple exams.
spontaneous vaginal delivery. Most common
Manual removal of placenta
cause of postnatal morbidity between day2Mothers age at extremes
10.
Low socioeco status
Maternal anemia
placental site - amt of bleeding. Lacerations includes episiotomy
Trauma

Rupture
of
vulval
hematoma
Internal fetal monitoring
Extent of bleeding less than
Pre-existing uterine disease Fibroids
Severe meconium staining in liquor
primary PPH.
Others (rare) Blood disorders, Carcinoma of
Prolonged surgery
cervix.
ASSESSMENT
INVESTIGATIONS
MANAGEMENT
Dx obtained clinically.
Crossmatch 2-4units of blood if
Mainstays: Bed rest & IV antibiotic
[Hx: Crampy ab pain? Passage of bits of placenta?
marked bleeding.
therapy.
Sx of infxn. Duration of labor. Smooth?
Coagulation profile as indicated. Curettage not performed outinely
Instrumental? Placenta complete? Complication?]
Speculum exam check status
(risk of uterus perforation)
Exam: Check temp, HR, BP.
of cervical os & obtain
No oxytocin.
Assess uterine size. Larger than appropriate?
endocervical swab.
Gentle digital evacuation of uterus
Assess clinical signs of blood loss. Estimate total
US may be used if RPOC
under GA performed with antibiotic
blood loss.
suspected. Blood clots may
coverage.
Establish IV line as indicated.
resemble RPOC.
Iron supplement if Hb low.
Oxygen via face mask as indicated.
CBC
OVERVIEW
Commonly presents as
prolonged or excessive bleeding
once woman has returned home
after 24h-6wks postpartum.
Most commonly at 2nd wk.
2ndary to sloughing of eschar on

DYSPLASIA
Def: Lesion in which part
of the epithelium is
replaced by cells showing
varying degree of atypia.

PREINVASIVE CERVICAL DISEASE

Cervical Intraepithelial Neoplasia (CIN)
BETHESDA SYSTEM
System
Intraepithelial dysplastic atypia occurring
ACSUS
LSIL
HSIL
CANCER
within the metaplastic epithelium of the
transformation zone.
Mild
Moder8 Severe CIN Cancer OSCJ Original squamocolumnar junction.

dysplasia

dysplasi
a
CIN 2

dysplas
ia
CIN 3

NSCJ New squamocolumnar junction

TZ Transfomation zone area between OSCJ &
NSCJ.
CIN 1
OVERVIEW
RISK FACTORS
Cervical neoplasia originates within TZ.
Persistent HPV infxn of high risk types.
Low risk HPV (types 6 & 11) are associated with low-grade
Young age at first coitus
cervical lesions (condyloma acuminata and CIN1)
Multiple sexual partners. Sex partner with multiple sex
High risk HPV (type 16, 18, 31, 33 or 35) associated with
partners.
high-grade cervical lesion (CIN2,3 and Cancer).
Young age at first pregnancy.
HPV type 16 is the type universally detected with the
Multiparity.
greatest frequency in high grade lesion & cervical ca. 50%
Low socioeco status
SCC, 30% adenoca, & >80% preinvasive lesions.
AT least 35% pt with CIN3 will dev invasive ca within 10yrs , Smoking & OCP
Genital warts
whereas lower grades may spontaneously regress.
Exogenous / endogenous immunosuppresion
SCREENING
PAP SMEAR
COLPOSCOPY
Before Colposcopy
Both the end
Stereoscopic binocular microscope of low
Complete hx and general exam.
cervical canal and
magnification, usually 10x to 40x.
A clinical and speculum examination of the cervix,
the ectocervix
vagina
should be sampled
Indications for colposcopy:
and vulva.
when taking the Pap - Abnormal cervical smear
A 3% to 5%acetic acid solution is liberally applied to
smear
- Abnormal findings on adjunctive
the
The false negative screening tests (HPV testing and
cervix using soaked swap
rate for Pap smear
cervicography)
- The abnormal findings are acetowhite epithelium &
for high grade
-If the cervix is clinically abnormal or
abnormal vascular patterns (mosaicism and
lesions is 20%
suspicious on naked eye exam.
punctuation)
New automated
- Unexplained IMB or PCB
Lugols iodine application to the cervix is called
liquid based slide
- Persistent vaginal discharge
shillers test
preparation systems - Personal history of in utero DES exposure, -Normal ectocervix and vaginal squamous epithelium
to decrease the false vulvar or vaginal neoplasia.
contains glycogen and stains mahogany-brown
negative rate
Normal columnar and squamous metaplasia and
neoplastic epithelium do not contain glycogen, and
appear mustard yellow
Satisfactory Colposcopic Examination: If the new SCJ
& entire TZ are seen.

EVALUATION FOR ABNORMAL PAP SMEAR

Any patient with a grossly abnormal cervix should have a punch biopsy performed regardless of the results of Pap
smear
Patients with ASCUS found in their smear may have a repeat smear in 6 months or HPV testing
About 6-10% of patients with an ASCUS smear will have high-grade CIN on colposcopy, 90% of these can be detected by
HPV testing for high-risk types
The colposcopic hallmark of CIN is an area of sharply delineated acetowhite epitheilum, or/and abnormal vascular
pattern: punctuation and mosaicism
Micro invasive carcinoma: extremely irregular puncate and mosaic patterns are found.
If colposcopic examination is satisfactory, punch biopsy from the suspicious area with end cervical curettage specimen.
Diagnostic cone biopsy of the cervix is indicated if:
- colposcopic examination is unsatisfactory
- Endocervical curettings show a high-grade lesion
- Pap smear shows a high-grade lesion that is not confirmed on punch biopsy
- Pap smear indicates Aden carcinoma in situ
- Microinvasion is present on punch biopsy
TREATMENT OF ABNORMAL INTRAEPITHELIAL NEOPLASIA CIN
Low Grade Lesions (CIN1) - Repeat smear in 6 month interval until normal then back to the normal screening program.
High grade lesions (CIN 2,3):
1. Loop Excision of The Transformation Zone (LLETZ), relatively cheap, it can be performed on an outpatient basis under
local anesthesia, and tissue is obtained for histologic evaluation.
2. LASER, destruction of the TZ by CO2 laser, ablation can be performed as an outpatient procedure with local anaesthesia,
expensive.
3. Cryosurgery, relatively painless outpatient procedure without anaesthesia, cheap, high failure rate for large lesions,
copious vaginal discharge for several weeks.
4. Electrocoagulation, Requires general anesthesia, cervical stenosis may occur, success rates up to 97%.
5. Cervical conization: (cold knife or laser)
-mainly diagnostic but it may be used for treatment, cure rates are as high as with hysterectomy for high grade lesions.
-Major complications: Bleeding, infection, cervical stenosis and incompetence.
Simple hysterectomy is rarely necessary, it may be applicable when sterilization is desired in a patient with CIN III or
when there is concomitant uterine or adnexal disease.

CERVICAL CANCER
INTRODUCTION
SYMPTOMS
FINDINGS
INVESTIGATIONS
Worldwide, cervical ca is the most
Abnormal vaginal bleeding is Usually normal general
CBC, LFT, KFT
common cause of cancer death in
the most common
exam.
CXR, Pelviwomen.
presenting sx.
In advanced disease,
abdominal CT
Mean age for cervical ca is 51.4yrs,
Postcoital bleeding in
enlarged inguinal or
Bx of lesion
with the number of pt evenly divided
sexually active women, IMB, supraclavicular LN, edema of Cystoscopy &
between age groups 30-39 and 60-69.
PMB.
the legs, ascites, pleural
proctoscopy for
Most common type is SCC (80%),
Asymptomatic until quite
effusion, hepatomegaly.
clinical staging.
adenocarcinoma & adenoquamous
advanced in women who are Pap smear may be normal in
PET scan to
account for 20-25%, others are rare.
not sexually active.
up to 50% of cases (false
delineate the
Persistent vaginal discharge, negative)
extent of disease
PATTERN OF SPREAD
pelvic pain, leg swelling &
Pelvic exam in early disease
at the primary site
1. Direct invasion into cervical stroma,
urinary frequency are
may be normal, esp if lesion
and in LN.
corpus, vagina and parametrium.
usually seen in advanced
is endocervical.
2. Lympathic permeation & mets.
disease.
Visible disease may be
3. Hematogenous dissemination.
Vesico-vaginal &
ulcerative, exophytc or
rectovaginal sx.
necrotic.
TREATMENT
Stage IA IA1 Total abdominal / vaginal hysterectomy.
- Cone bx alone may suffice if pt wants to preserve fertility, as long as cone margins free from disease &
endocervical curetting -ve.
IA2 Modified radical hysterectomy and pelvic LN dissection.
- If wants childbearing, large cone biopsy or radical trachelectomy & pelvic LN dissection are offered.
Stage IB a) Radical Hysterectomy & Bilateral pelvic lymphadenectomy Removes uterus, adjacent portions of vagina,
cardinal ligaments, uterosacral ligaments & bladder pillars. Spares ovaries, can surgically stage, prevent chronic
radiation. Most common complication: Bladder dysfunction, 1-2% permanent. Most serious complication: ureteric
fistula or stricture 1-2%. Lower limb lymphoedema 15-20%.
b) Radiation Therapy Begins by external radiation to shrink central tumor & cavitary lesion. Also done postop
for pt with LN mets, or inadequate surgical margins. Addition of chemo to radiotherapy improves survival.
Stage II
IIA with minimal involvement of vaginal fornix - Radical surgery or chemo radiation.
IIA IVA Pelvic chemo is the rx of choice.
Stage
Palliative radio or chemotherapy.
IVB
Recurre
Chemotherapy Limited effectiveness. Most active drug is cisplastin.
nt or
Pelvic exenteration Removal of pelvic viscera (uterus, tubes, ovaries, bladder, rectum) - For pt who have

Mets

central recurrence following irradiation.

Radiotherapy if initial disease treated by surgery only.
PROGNOSIS
Directly related to clinical staging. With higher stage, nodal mets escalate, & 5yr survival diminishes.
COMPLICATIONS OF RADIOTHERAPY

ACUTE
Acute cystitis Hematuria, urgency,
frequency.
Proctosigmoiditis Tenesmus, diarrhea,
passage of blood & mucus in stool.
Enteritis Nausea, vomit, diarrhea,
colicky ab pain.
BM depression.

CHRONIC
Radiation enteropathy: Proctosigmoiditis (pelvic pain, tenesmus, diarrhea,
rectal bleeding), ulceration (rectal bleeding & tenesmus), rectovaginal
fistula (stool thru vagina), Rectum or sigmoid stenosis (progressive large
bowel obstr), Small bowel injury (cramping ab pain, vomit, diarrhea)
Vaginal vault necrosis - Severe pain in vaginal vault & profuse discharge.
Urologic injury: Hemorrhagic cystitis, Vesicovaginal & Ureterovaginal
fistula (constant urine leakage), Ureteric stenosis (hydronephrosis)

PREMATURE RUPTURE OF MEMBRANE (PROM)

Definitions

Etiology

Clinical presentation

Premature rupture (PROM) denotes

spontaneous rupture of fetal membranes
before the onset of labor.
This can occur at term (PROM) or preterm
(PPROM).
Preterm premature rupture of membrane
(PPROM):
+\- Uterine contraction( preterm labor ? )

*It has been suggested that the term preterm

PROM (PPROM) should be used to define
those patients who are preterm with ruptured
membranes, whether or not they have
contractions.

Ascending Infection (vaginal \ cervical)

Abnormal membrane (deficient collagen
and minerals weakness)
Incompetent cervix
Nutritional deficiencies of copper,
ascorbic acid.
Smoking
Consider causes of preterm labor
a. multiple gestation.
b. Low socioeconomic class.
c. Ethnicity..etc

Sudden Gush of clear

vaginal fluid
Rule out :
o Episodic urinary
incontinence
o Leucorrhea
o loss of the mucus
plug
symptoms suggestive of
Chorioamnionitis ?

Method of diagnosis (Investigations)

Never do a digital vaginal exam on a patient who is not in labor, whether preterm or term
1. Sterile Speculum exam
Direct visualization of liquor Pooling
High Vaginal Swab (HVS) assess Chorioamnionitis
Nitrazine
Ferning
Sterile , not only to prevent infection but bcoz you may
take the swab from the speculum and get a false positive
Dx of PPROM involves first examining the abdomen
(assess the lie , position , ease of examination may
indicate oligohydramnios )

Bcoz we may face a case that we suspect PPROM but we dont

see the liquor ex. :
Severe oligohydramnios will appear in the abdominal exam
(small for GA on fundal height etc )
Fetal head closing the cervix manipulate the head and see
if liquor comes out
Theres No rupture of membranes think about other DDx
for the Gush of fluid (U. incontinence , leucorrhea ,loss of the
cervical mucous plug )

Method of diagnosis (Investigations)

1. Sterile Speculum exam
Direct visualization of liquor

Nitrazine blue test

False Positives
Cervical mucus
Blood
Vaginal infection
(BV)
Semen

Fern like

e positive
Cervical mucus
Blood
Urine

Fern and Nitrazine Tests

1. Insert speculum for sample collection, avoid the use of
lubricant.
2. Collect vaginal secretion from the posterior vaginal pool
with two cotton sterile swabs.
Do not touch the mucus plug in the cervix.
Do not contaminate the specimen with saline/koh.
3. After collection, immediately rub the swab against a glass
slide, creating a very thin smear, do not apply a
coverslip.
4.
Allow slide to dry for 5-10 minutes.
Fals
5. Using a microscope, examine the dried smear under 10X
power without a cover slip.
6. If present, saline in the amniotic fluid crystallizes to form
a fern-like pattern.

1.Tear off a 2-3 cm

piece of Nitrazine
paper.
2.Apply fluid
collected from the
vaginal pool
directly to the
paper.
3.A blue color
change is consistent
with amniotic
fluid pH of 7-7.5. The
Nitrazine paper
container includes a
chart of color change
and pH.
2.U/S

assess
gestational age ,
fetal growth and
wellbeing
Assess amniotic
fluid volume.
rule out fetal
anomalies

Saline

Complications

Chorioamnionitis

1. Depends on fetal age,

duration and liquor
volume lift
2. Prolonged PPROM
Chorioamnionitis
development and
neonatal infections
3. Prematurity related
complications (RDS , PDA
, IVH , NEC, ROP , BPD ,
CP )
4. Oligohydramnios : if
>24 weeks may lead to
pulmonary hypoplasia
5. Positional hypoplasia.
Suspect Chorioamnionitis
maternal fever and Uterine
tenderness in a confirmed
case of PROM and without
UTI or URI
Management : Vaginal
cultures , IV Antibiotics and
prompt delivery (not
necessarily CS)

Suspect Chorioamnionitis in the

presence of any change (rather
than absolute values) of:
1. Pulse rate
2. Temperature more than 38
(unexplained)
3. Tense or tender uterus
4. Color or smell of vaginal
secretions *
5. Fetal heart rate.
Management : take Vaginal
gram stain and cultures , give IV
Antibiotics

Deep infection , (in the uterus which is in the abdominal

cavity , not exposed to the omentum or other defense
mechanisms and the immune system )
So it could put the mother and the fetus at risk of sepsis

if gram stain positive

prompt delivery (not necessarily
CS) REGARDLESS of Gestational
Age

Any change of maternal HR ,

Temp , Tense tender uterus

WBC CRP may be high or low ,

so dont count on them as well
as the vaginal discharge (
may not be present)
Management

the main principle of the

management would be
conservative balancing
between prematurity and
infection (Unless
theres indications to
terminate preg)

Main risk is prematurity

First look if we have any

indication to terminate the
pregnancy :
1.Chorioamnionitis
2.Severe oligohydramnios
3.Congenital anomalies

Admit and give

Antibiotic use is
recommended
(Erythromycin and
Metronidazole)
but it may not
prevent fetal
infection* also may
mask
Chorioamnionitis.

PRETERM BIRTH

A birth that occurs before 37

Significance

Pathogenesis

Tocolytics : short term use

only
Steroids: Betamethasone

Blood doesnt reach the fetal

lung so we may face cases of
congenital pneumonia despite
Abx use

completed weeks of gestation.

Subclassifications of PTB are
variably and inconsistently
defined as:
Late preterm = 34 to 36
weeks

Moderately preterm = 32 to
34 weeks
Very preterm = <32 weeks
Extremely preterm = <28
weeks

PTB can also be defined by

birth weight (BW):
Low birth weight (LBW) BW
less than 2500 g

Taken together with its

sequelae, PTB is by far
the leading cause of
infant mortality in the
United States.
PTB is also a major
determinant of shortand long-term
morbidity in infants
and children.
INCIDENCE In the
United States, 12.8
percent of births in
2006 occurred preterm
and 3.66 percent were
less than 34 weeks of
gestation

Approximately 70 to
80 percent of PTBs
occur spontaneously.
preterm labor (PTL)
accounts for 40 to 50
percent of all PTBs
and preterm
premature rupture of
membranes (PPROM)
accounts for 20 to 30
percent.
The remaining 20 to
30 percent of PTBs
are due to
intervention for
maternal or fetal
problems

Clinical and laboratory

evidence suggest that a
number of pathogenic
processes can lead to a final
common pathway that results
in preterm labor and delivery.

The four primary processes

are:
1. Activation of the maternal
or fetal hypothalamicpituitary-adrenal axis
2. Infection
3. Decidual hemorrhage
4. Pathological uterine
distention

Very low birth weight (VLBW)

BW less than 1500 g
Extremely low birth weight
(ELBW) BW less than 1000
g
RISK FACTOR, CLINICAL MANIFESTATIONS AND DIAGNOSIS FACTORS

PTL is one of the most common reasons for

hospitalization of pregnant women.
In one systematic review, approximately 30
percent of preterm labors spontaneously
resolved.
Signs and symptoms of early PTL include

Uterine contractions are a normal finding at all stages of

pregnancy, thereby adding to the challenge of distinguishing
true from false labor. The frequency of contractions increases
with gestational age, the number of fetuses, and at night.
The diagnosis of PTL is generally based upon clinical criteria of
regular painful uterine contractions accompanied by cervical

menstrual-like cramping, constant low back

ache, mild uterine contractions at infrequent
and/or irregular intervals, and bloody show.
However, these signs and symptoms are nonspecific and often noted in women whose
pregnancies go to term.

Initial evaluation of
women with suspected
PTL should determine:
1. The presence and
frequency of uterine
contractions
2. Whether there is
uterine bleeding
3. Whether the fetal
membranes have
ruptured
4. Gestational age
5. Fetal well-being

Physical examination

The uterus is examined to

assess firmness,
tenderness, fetal size, and
fetal position.
A sterile speculum
examination is performed
to rule out ruptured
membranes, to visually
examine the vagina and
cervix
Obtain specimens for
laboratory testing .
A digital examination to
assess cervical dilatation
and effacement is
performed after placenta
previa and PPROM have
been excluded

dilation and/or effacement. Specific criteria, which were initially

developed to select subjects in research settings, include
persistent uterine contractions (four every 20 minutes or eight
every 60 minutes) with documented cervical change or cervical
effacement of at least 80 percent, or cervical dilatation greater
than 2 cm.
Digital cervical examination has limited reproducibility between
examiners, especially when changes are not pronounced;
therefore, some centers evaluate the cervix via transvaginal
ultrasound to confirm the diagnosis A short cervix has been
variously defined as a cervical length less than 2.0 cm, 2.5 cm,
or 3.0 cm.
Lab tests

Urine culture, since

bacteriuria and
pyelonephritis are
associated with PTB.
Rectovaginal group B
streptococcal culture, to
determine need for
antibiotic prophylaxis.
Tests for gonorrhea and
chlamydia.
Testing for gonorrhea and
chlamydia may be omitted
if previously performed, the
results were negative, and
the patient is not at high
risk of acquiring sexually
transmitted infections.

Fetal fibronectin (fFN),a

swab for fFN on all
symptomatic patients
considered at high risk for
PTB.
Perform transvaginal
sonographic
measurement of cervical
length.
We only send the swab to
the laboratory for FFN
determination if the
cervical length is 20 to 30
mm
Given the link between
cocaine use and placental
abruption, perform drug
testing in patients with
risk factors for drug
abuse

TRIAGE BASED UPON CERVICAL LENGTH

MANAGEMENT OF WOMEN WITH PRETERM LABOR

Cervical length >30 mm These women are at

low risk of PTB,
Regardless of fFN result. Discharge the patients home
after an observational period of four to six hours during
which confirm fetal well-being
Exclude the presence of an acute precipitating event
(eg, an abruption or overt infection),
Follow-up in one to two weeks
Cervical length 20 to 30 mm PTB is more likely in
women with cervices 20 to 30 mm than in women with
longer cervices, but most women in this group do not
deliver preterm. Therefore, send the swab for fFN
testing in this subgroup of women. If the test is positive
(level greater than 50 ng/mL), then actively manage
the pregnancy to prevent morbidity associated with
PTB.
Cervical length <20 mm .These women are at high risk
of PTB regardless of fFN result. Therefore, we do not
send their swabs for fFN testing to the laboratory and
actively manage them to prevent morbidity associated
with PTB.

Hospitalize women diagnosed with PTL at less than 34

weeks of gestation and initiate the following treatments:
Antenatal glucocorticoids to reduce neonatal morbidity
and mortality associated with PTB
Appropriate antibiotics for GBS chemoprophylaxis
Tocolytic drugs for up to 48 hours to delay delivery so that
glucocorticoids given to the mother can achieve their
maximum effect.
Appropriate antibiotics to women with positive urine
culture results or positive tests for gonorrhea or
chlamydia.

MANAGEMENT OF ASYMPTOMATIC WOMEN AT HIGH RISK OF PTB

Interventions to prevent PTB generally have not been successful, with some exceptions (eg, supplemental
progesterone).
Women with risk factors for PTB are sometimes followed with serial ultrasound measurement of cervical length. A
cervical length 35 mm is generally considered normal and reassuring; as cervical length decreases below 35 mm, the
risk of PTB increases
We manage asymptomatic patients at high risk of PTB similar to the way we manage symptomatic patients, but with a
higher cervical length threshold for intervention. This minimizes overtreatment of high risk asymptomatic patients and
undertreatment of symptomatic patients. Surveillance with serial cervical length measurements is begun at 22 weeks.
Cervical length 35 mm - The risk of PTB is low. See these patients in routine follow-up in one to two weeks.

Cervical length 25 to 34 mm - obtain a fFN concentration. If the test is positive (level greater than 50 ng/mL), then
actively manage the pregnancy to prevent morbidity associated with PTB.
Cervical length <25 mm - The risk of PTB is increased. We actively manage the pregnancy to prevent morbidity
associated with PTB, as described above.

PREMATURE RUPTURE OF MEMBRANE (PROM)

Refers to

Etiology & RF

Outcome

membrane rupture
before the onset of
uterine contractions;
preterm PROM
(PPROM) is the term
used when the
pregnancy is less than
37 completed weeks of
gestation.
PPROM occurs in 3
percent of pregnancies
and is responsible for,
or associated with,
approximately onethird of preterm births.
In management of
PPROM, Points of
contention include:

1. Expectant
management versus
intervention
2. Use of tocolytics
3. Duration of
administration of
antibiotic prophylaxis
4. Timing of
administration of
antenatal
glucocorticoids
5. Methods of testing for
maternal/fetal infection
6. Timing of delivery.

The pathogenesis of
PPROM is not
completely understood.
There are multiple
etiologies, mechanical
and physiological, that
probably share a final
common pathway
leading to membrane
rupture.
Risk factors for PPROM
are similar to those for
preterm labor
A history of PPROM in a
previous pregnancy
Genital tract infection
Antepartum bleeding
Cigarette smoking have a
particularly strong
association with PPROM
Although a small
randomized trial suggested
vitamin C
supplementation might
lower the risk of PPROM , a
larger randomized trial in
which both vitamin C and E
were given refuted this
finding and suggested the
risk of PPROM may actually
be increased with
antioxidant
supplementation .

1.
2.
3.
4.
5.

Approximately one-third of
women with PPROM develop
potentially serious infections,
such as intraamniotic
infection (chorioamnionitis),
endometritis, or septicemia.
Endometritis is more
common after cesarean than
vaginal delivery.
The fetus and neonate are at
greater risk of PPROM-related
morbidity and mortality than
the mother.
The majority of pregnancies
with PPROM deliver preterm
and within one week of
membrane rupture.

Preterm infants are especially

vulnerable to a variety of
problems, such as hyaline
membrane disease,
intraventricular hemorrhage,
periventricular leukomalacia
and other neurologic
sequelae, infection (eg,
sepsis, pneumonia,
meningitis), and necrotizing
enterocolitis. The rates of
these morbidities vary with
gestational age and are
higher in the setting of
chorioamnionitis

PPROM is also
associated with
increased risks of
abruptio placentae and
prolapse of the
umbilical cord. Fetal
malpresentation is
common, given the
preterm gestational age
and the frequent
occurrence of reduced
amniotic fluid volume.
The risk of cord
prolapse is especially
high (11 percent in one
study) in the setting of
both nonvertex fetal
presentation and
PPROM.
Early, severe,
prolonged
oligohydramnios can be
associated with
pulmonary hypoplasia,
facial deformation, and
orthopedic
abnormalities. Such
complications are most
likely when membrane
rupture occurs at less
than 23 weeks of
gestation.

RF for Pre-term birth

1. Stress Single women, Low socioeconomic status, Anxiety,

Depression, Life events (divorce, separation,
death)Abdominal surgery during pregnancy
2. Occupational fatigue Upright posture, Use of industrial
machines, Physical exertion, Mental or environmental
stress
3. Excessive or impaired uterine distention Multiple
gestationPolyhydramniosUterine anomalyUterine
leiomyomaDiethylstilbestrol
4. Cervical factors History of second trimester
abortionHistory of cervical surgeryPremature cervical
dilatation or effacement
Clinical Manifestation & Dx

5. Infection Sexually transmitted infections,

Pyelonephritis, appendicitis, pneumonia, Systemic
infection, Bacteriuria, Periodontal disease
6. Placental pathology Placenta previa, Abruption,
Vaginal bleeding
7. Miscellaneous Previous preterm delivery, Substance
abuse, SmokingMaternal age (<18 or >40), AfricanAmerican race, Poor nutrition and low body mass
index, Inadequate prenatal care, Anemia (hemoglobin
<10 g/dL)Excessive uterine contractility, Low level of
educational achievement, Genotype
8. Fetal factors Congenital anomaly, Growth restriction

History The classic clinical presentation of PPROM is a

sudden "gush" of clear or pale yellow fluid from the vagina.
However, many women describe intermittent or constant
leaking of small amounts of fluid or just a sensation of
wetness within the vagina or on the perineum. A clinical
history suggestive of PPROM should be confirmed by visual
inspection or laboratory tests to exclude other causes of
vaginal/perineal wetness, such as urinary incontinence,
vaginal discharge, and perspiration.
Physical examination The best method of confirming
the diagnosis of PPROM is direct observation of amniotic
fluid coming out of the cervical canal or pooling in the
vaginal fornix. If amniotic fluid is not immediately visible,
the woman can be asked to push on her fundus, Valsalva,
or cough to provoke leakage of amniotic fluid from the
cervical os. Digital examination should be avoided because
it may decrease the latency period (ie, time from rupture of
membranes to delivery) and increase the risk of
intrauterine infection
Nitrazine and fern tests If PROM is not obvious after
visual inspection, the diagnosis can be confirmed by testing
the pH of the vaginal fluid, which is easily accomplished
with nitrazine paper. Amniotic fluid usually has a pH range
of 7.0 to 7.3 compared to the normally acidic vaginal pH of
3.8 to4.
False-negative and false-positive nitrazine tests results
occur in up to 5 percent of cases.

False negative tests results can occur when leaking

is intermittent or the amniotic fluid is diluted by other
vaginal fluids. False positive results can be due to the
presence of alkaline fluids in the vagina, such as blood,
seminal fluid, or soap. In addition, the pH of urine can
be elevated to near 8.0 if infected with Proteus
species.
In the United Kingdom, an absorbent pad
(AmnioSense) that changes color at pH > 5.2 is used
as a panty liner and marketed to pregnant women. In a
study of 157 pregnant women, the sensitivity and
specificity of this device for diagnosis of membrane
rupture were 98 and 65 percent, respectively
Ultrasonography Ultrasound examination may be
of value in the diagnosis of PPROM. Fifty to 70 percent
of women with PPROM have low amniotic fluid volume
on initial sonography . A mild reduction of amniotic
fluid volume may have many etiologies. On the other
hand, the finding of anhydramnios or severe
oligohydramnios, combined with a characteristic
history, is highly suggestive of rupture of membranes,
although renal agenesis, obstructive uropathy, or
severe utero-placental insufficiency also can cause
marked reductions in amniotic fluid volume.
Instillation of indigo carmine One-half hour later,
the tampon is removed and examined for blue
staining, which indicates leakage of amniotic fluid.

Management

Initial evaluation

The management of pregnancies complicated by PPROM is based upon

consideration of several factors, which are assessed upon presentation
Gestational age

Expeditious delivery of women with

PPROM is indicated if intrauterine
infection, abruptio placentae, repetitive

1.
2.
3.
4.

Availability of neonatal intensive care

FHR decelerations, or a high risk of cord
Presence or absence of maternal/fetal infection
prolapse is present or suspected
Presence or absence of labor
In each of these conditions, fetal wellFetal presentation (Breech and transverse lies are unstable and may
being can deteriorate with expectant
increase the risk for cord prolapse)
management, and there are no
5. Fetal heart rate (FHR) tracing pattern
therapeutic interventions available other
6. Likelihood of fetal lung maturity
than delivery.
7. Cervical status (by visual, not digital, inspection unless induction is
planned or the woman is in labor)
Our simplified algorithm for management of other women with PPROM is shown in the

Antenatal glucocorticoids
Antibiotics
Treatment of overt infections
Tocolysis
Hospitalization
Tissue sealants (A variety of tissue sealants (eg, fibrin
glue, gelatin sponge) have shown some success in
stopping leakage in case reports. Neither the safety
nor the efficacy of these sealants has been established
).
Supplemental progesterone (There is no evidence that
administration of supplemental progesterone has any
beneficial effects in women with PPROM )

Maternal surveillance
Fetal surveillance
Timing of delivery
Gestational age <34 weeks In general,
prematurity is the greatest risk to the fetus with
PPROM. As discussed above, we administer a course
of antenatal glucocorticoids, prophylactic antibiotics
for seven days, and tocolytics for 48 hours, as
indicated.
Gestational age greater than 34 weeks
Method of delivery Cesarean delivery is
performed for standard indications; otherwise labor
is induced.
Favorable Cervix vs Unfavorable cervix

PRETERM LABOUR MANAGEMENT

Principles of management

Tocolytic agents

Contraindications to
Tocolysis

Initial assessment must

be done to ascertain
cervical length and
dilatation and the station
and nature of the
presenting part.*
Identify treatable causes
(such as a urinary tract or
vaginal infection)
Should be placed in the
lateral decubitus position,
monitored for the
presence & frequency of
uterine activity & cervical
changes..
High vaginal swab.(B
strep, Ureaplasma,
Mycoplasma,Gardnerella
vaginalis)*
Blood sugar, CBC, serum
electrolytes level,
urinalysis, and urine
culture and sensitivity.

Ultrasound (dates, cause,

growth).
Rest and fluids will
improve 50 % of cases.
HOW?
By the inhibition of the ADH
released from the post
pitutary gland from the
same site where oxytocin is
released..

Used to reduce and

stop uterine
Contraction .
We use them for 48-72
hours *..
1)corticosteroids work

1.
2.
3.
4.
5.
6.

2)in cases we dont have

good NICU facilities until we
transfer the pt. to another
hospital.

1.
2.

It is acceptable to
administer antibiotics *to
patients who are in
preterm labor (a 7-day
course of ampicillin
and/or erythromycin)..
**allergy use
clindamycin or
vancomycin ..
To prevent the
progression of a silent
infection to clinical
amnionitis

Tocolytic therapy
if the patient doesnt
respond to bed rest &
hydration

Tocolytics are routinely

used at less than 34
weeks gestation if there
are no contraindications
to treatment.
Treatment is
individualized from 34-37
weeks.

Severe PET
Severe APH
IUGR
Chorioamnionitis
Fetal anomalies
Cardiac disorders,
Arrhythmias.
7. Thyrotoxicosis.
Tocolytic agents
Magnesium sulfate
Calcium channel
blocker (nifedipine)
3.
Sympathomimetic
agents (ritodrine,
terbutaline)
4.
Prostaglandin
inhibitors
(indomethacin)
5.
Atosiban

TOCOLYTIC AGENTS

.
Sympathomimetic
agents

Action

Side effects

Notes

Decrease intracellular
Ca

1. Fetal and maternal

tachycardia.
2. Hypotension.
3. Rarely chest pain.
4. Hyperglycemia.
5. Hyperkalemia.
6. Right heart failure

Dose control by maternal response

and pulse

Competes with Ca+2

for entry into the cell
decrease free
intracellular Ca

Higher doses are required (1 gm 4

hourly orally) compared to
eclampsia
Useful in selected cases such as
diabetes, heart diseases
Strict serum levels should be
observed
It is used as an intravenous
medication to halt premature
labour..

Ritodrine
hydrochloride
Salbutamol

MgSO4

respiratory depression
and cardiac conduction
defect.

Atosiban

Oxytocin antagonist

PG synthetase
inhibitors

It prevents conversion
of arachidonic acid into

If prolonged use:
a. Oligohydramnios.

PG

Indomethacin
Aspirin
Flufenamic acid

Ca channel blockers

b. Premature closure of
ductus arteriosus(May
lead to neonatal PHTN &
CF)
c. Platelet dysfynction.

nifedipine inhibit slow

inward of calcium ions
Nifedipine
during the second
phase of action
potential of uterine
smooth muscle cell.
Is tocolytic therapy effective?

Has minimal side effect :

a.
b.
c.
d.

Headache
Flushing
hypotension
tachycardia

Animal studies showed fetal

acidosis

Failed to decrease preterm incidence in large population studies.

It did prolong gestation, decreased RDS , improved neonatal survival & increased birth weight.
Use after 34 weeks is limited.
All agents delayed labour by 72 hours in 80% of treated patients

Role of Glucocorticoids

Surfactant

Lung maturity

L/S ratio

Reduces the mortality, RDS &

IVH ..
It`s recommended use up to
34 weeks.
Dose consists of :
**2 doses of 12 mg of
betamethasone(Developmen
t of CNS), IM 24 hours apart or
** 4 doses of 6 mg of
dexamethasone, IM, 12 hours
apart.
SO ,It has both

Phospholipids
i.
Phosphotidyl
lecithin
ii.
Phosphotidylinositol
iii.
Phosphotidylglycerol
Proteins
Carbohydrate
Salts and neutral lipids
It is produced by
pneumocytes type II
(proliferates at 24
weeks and function by

Fetal lungs are

mature if:
1)Phosphatidylglycerol
is present in amniotic
fluid
or
2) Lecithin
sphingomyelin (L/S)
ratio is > 2

>2 indicates lung maturity.

Lecithin increases from 35
weeks onward while
sphyngomyline remains
constant after 35 weeks
Measured by liquid
chromatography.
2% of infant with L/S>2
develop RDS
Blood and meconium may
reduce the L/S ratio but has
no effect on PG detection.

prophylactic and
therapeutic use.

34 week)

PRETERM BIRTH
ETIOLOGY
CLINICAL FEATURES
1) Infection mostly subclinical
1. Cramping lower ab pain
infxn of choriodecidual space
that starts irregular & with
2) Overdistension of uterus
time in freq & intensity &
polyhydromnios, multiple
becomes more regular.
pregnancy
2. Low back ache
3) Vascular (placental
3. Bloody vaginal discharge
abnormalities)
4) Intercurrent illness
Extremely preterm: 24pyelonephritis, pneumonia. By
27th wk
either direct spread or indirect
chemical triggers eg endotoxins.
5) Cervical weakness
6) Idiopathic esp in mild preterm
births
7) Iatrogenic
MANAGEMENT
INVESTIGATIONS
1. Admit at least 24h
1. Sterile speculum exam amniotic fluid pooling
2. According to GA
2. Transvaginal USS asses cervical dilation.
<34wks antenatal steroids (given in 2 doses 12h apart)
Normal cervix ~3.5cm in length.
3. Prophylactic antibiotics (erythromycin until culture indicates
3. Vaginal swab for GBS
otherwise)
4. Urinalysis & culture (UTI main cause of preterm
4. Tocolytics for 48h until steroids works or till transfer to a hosp
labor)
with good NICU facility
6. fetal fibronectin (fFN)
When to ask?
- cervical length >3.5cm& not in labor no need
- cervical length <2n5cm & in labor no need
- 2.5 < cervical length < 3.5cm need fFN
CLASSIFICATION
GESTATIONAL AGE
BIRTH WEIGHT
Mild preterm
Low birth weight:
Late preterm: 34-36th wk <2.5kg
Very low birth weight:
Moderate preterm: 32<1.5kg
33rd wk
Extremely low birth
Very preterm: 28-31st wk Weight: <1kg

Braxton-Hicks contraction @ False Labor @ Practice Contractions - Sporadic uterine contractions that start around 6
weeks, to aid body in its preparation in birth. Infrequent, irregular, only mild cramping.

(Preterm labor progressively & becomes more intense & regular with time)

PREMATURE RUPTURE OF MEMBRANE

Amniorrhexis (spontaneous rupture of membranes) before the onset of uterine contractions.
Preterm PROM (PPROM) preterm (<37 wks) with ruptured membrane, with or without contractions.
RISK FACTOR
HX & PE
LAB TESTS
CONSIDERATIONS
o Hx of previous
Hx: Vaginal loss of fluid
Pulm
Management depends a
R/O episodic urinary incontinence, leukorrhea or
maturation
lot to GA at time of memb
PPROM
loss
of
cervical
mucus
plug.
studies.
rupture.
o Vaginal & cervical
PE: Pooling of amniotic fluid in posterior vaginal
Gram stain & Also quantity of remaining
infxn
culture.
amniotic fluid.
o Antepartum bleeding fornix.
Confirm
by:
o Cigarette smoking
1) NItrazine paper (alkali blue)
Amniotic fluid index (AFI):
have a particularly
2)
Microscopic
exam
(ferning)
Vertical axis of amniotic
strong association
Sterile vaginal speculum.
fluid present in four
with PPROM
*No
digital
vaginal
exam!!
quadrants. Abnormal is
o Abnormal memb
USS:
R/O
fetal
anomalies,
assess
GA
&
amniotic
<5cm.
physiology
fluid
volume.
o Incompetent cervix
o Nutritional
deficiencies
MANAGEMENT
GA <24 wks (Pre24wks > GA > 36wks (Preterm PROM)
GA 36wks or
viable PROM)
more
(PROM)
Risk of dev of
A] Conservative Expectant Management - To continue pregnancy until the lung profile is Induce labor
pulmonary
mature. Diagnose chorioamnionitis at an early stage to minimize fetal & maternal risks. after 6-12h
hypoplasia due
Chorioamnionitis Maternal temp >38C with no other sites of infxn, fetal tachy,
if no
to fetal crowding
tender uterus, uterine irritability on NST. Presence of bacteria by Gram/culture.
spontaneous
with thoracic
Ampicillin/erythromycin prolongs interval of delivery in pt with PPROM.
contractions

compression,
restriction of fetal
breathing and
disturbances of
pulm fluid
production & flow.
Positional skeletal
abnormality eg
talipes
equinovarus.

When diagnosed, ampicillin + gentamycin after taken enough cultures. Then induce
labor.
C-section if cervix unfavorable, fetal involvement or presence of active genital herpes.
B] Tocolytic Therapy To gain time for pulm maturation. Unsuccessful if with infection.
C] Cortisteroids Use - Given to pt with PPROM only up to 32 wks GA.
D] Outpatient Management
Can consider after inpatient observ for 2-3d without any evidence of infxn.
Rules of eligibility: Pt reliable, fully informed of risks, prepared to participate in her own
care. Fetus vertex. Cervix closed.
Restrict physical activity. No coitus. Monitor temp at least 4x/d. Rush to hosp if >37.8C.
Seen weekly to measure temp, NST after 28wk, evaluate baseline fetal heart rate & AFI.
Contraindicated in oligohydramnios.

occur.

PROLONGED PREGNANCY
Definitions

RISKS

Post date pregnancy: continuation of

pregnancy beyond 40 completed weeks

Placental insufficiency and

hypoxia

Increased fetal wt, ossification of skull &

decreased moulding

Post term pregnancy: continuation of

pregnancy beyond 42 completed weeks

1. Increased perinatal
mortality: Doubled for
each week after 42 weeks
2. Meconium aspiration
syndrome
3. Oligohydromnios
4. Cord compression

1. Prolonged labour and failure to progress:

increase incidence of C/S
2. Shoulder dystocia:
Maternal risks: vaginal & cervical lacerations
& rupture uterus
Neonatal risks:
i.
Neonatal asphyxia & death
ii.
Cervical cord injury
iii.
Brachial plexus injury: Phrenic N.
injury (C4 injury), Erbs palsy (C5&C6
injury), Klumpks palsy (C8 & T1)
iv.
Clavicular & humeral fractures

Incidence
5-10% of pregnancies
Aetiology

In majority of cases there is no

underlying cause (its a physiological
continuation of pregnancy)
Extremely rare, due to
i.
Anencephaly
ii.
Fetal adrenal hypoplasia

iii.

Placental sulphatase enzyme

deficiency

How to manage pt in Post-date & Post-term pregnancy

Assesment of GA:

Before delivery

During delivery

A.Antenatal methods

1. Counselling and explanation

Explain the risk of post-date and post
term on the fetus
2. History
For accurate assessment of GA
To exclude contraindications for
induction
3. Obs exam
To assess lie, presentation and
engagement
4. Vaginal exam
To assess Bishop score and pelvic
adequacy
5. U/S (at 40, 41 and 42 weeks)
To assess amount of liquor, fetal
wellbeing and wt
6. CTG (every 3 days after 40 weeks)
To assess fetal wellbeing

1. 1st day LMP (reliable in 50% of

pregnancy)

Uncomplicated post-date
pregnancy: deliver at
40+3-7 days
Method of delivery:
a. Induction of labour
(depends on Bishop
score)
b. C/S if theres
contraindication for
induction
If delivery by induction of
labour, senior obs(risk of
shoulder dystocia) and
paed(risk of meconium
aspiration) should attend
the delivery.

2. U/S: CRL (7-13 weeks), BPD & FL (1326 weeks & >26 weeks)
3.Clinical:
i.
ii.
iii.
iv.

early pregnancy symptoms

early bimanual exam
quickening
serial fundal ht

B.Postnatal methods
1. Dubowit score: assessment of physical
and neurological features of the newborn

2. Farr score: assessment of physical

features of the newborn

PUERPERIUM
PHYSIOLOGIC CHANGES DURING PUEPERIUM
The period following delivery of the baby and placenta to about 6-8 weeks postpartum.
During that the reproductive organs and the maternal physiology return toward the non-pregnant status.
LOCAL
UTERUS

Uterine involution.
Structure
- autolysis of excess muscle fibers
- obliteration & thrombosis of blood vessels, then degeneration &
transformation into elastic tissue
- separation of the decidua
Weight - reduced (1kg after delivery 70-100g end of puerperium)
Size
- after delivery the length of the uterus is 20 cm and felt at the level
of umbilicus
- after one week it is midway between umbilicus and symphysis pubis
- after 2 weeks it is at the level of symphysis
- by the end of the 6th week it is 7.5 cm long
Uterine ligaments - are involuted
Subinvolution predisposes to prolapse and retroversion.
Endometrial lining rapidly regenerates, so that by the 7th day the
endometrial glands will be evident. By the 16th day, the
endometrium is restored throughout the uterus, except at the
placental site.
The contractions of the arterial smooth muscle and compression of
the vessels by contraction of the myometrium result in homeostasis.
The size of the placental bed decreases by half, and the changes in
the placental bed result in the quantity and quality of the lochia that
is experienced.

Lochia
Bloodstained uterine discharge that is composed of
cervical mucous, vaginal transudate, and products
of necrosis and sloughing of the superficial layer of
the decidua
- Lochia rubra (red): consists mainly of blood and
decidua. It lasts for 5 days.
- Lochia serosa (pale): due to relative in RBCs and
predominance of leukocytes. It lasts for 5 days.
- Lochia alba (white): consists mainly of leukocytes
and mucus. It lasts for 5 days.
- Persistence of red lochia means subinvolution.
- Offensive lochia means infection.
- In severe infection with septicaemia, lochia is
scanty and not offensive
- The period of time the lochia can last varies,
although it averages approximately 5 weeks.
- Often, women experience an increase in the
amount of bleeding at 7-14 days secondary to the
sloughing of the eschar on the placental site.

CERVIX
The cervix begins to rapidly revert
to a non-pregnant state (less
elastic, more firm) but it never
returns to the nulliparous state.
By the end of the first week, the
external os is closed to the extent
that a finger could not be easily
introduced.
By the end of the second week the
internal os should be closed.
VAGINA
In the first few days the streched
vagina is smooth & edematous,
but by the end of the third week
rugae begin to appear, but never
completely return to its prepregnant size

PUERPERIUM
PHYSIOLOGIC CHANGES DURING PUEPERIUM
LOCAL
OVARIES
PERINEUM
The resumption of normal
The perineum has been stretched and
function by the ovaries is highly
traumatized, and sometimes torn or cut, during
variable and is greatly influenced the process of labor and delivery. The swollen and
by breastfeeding the infant.
engorged vulva rapidly resolves, and swelling and
The woman who breastfeeds her
engorgement are completely gone within 1-2
infant has a longer period of
weeks.
amenorrhea and anovulation
Most of the muscle tone is regained by 6 weeks,
than the mother who chooses to
with more improvement over the following few
bottle-feed.
months. The muscle tone may or may not return to
Mother who does not breastfeed
normal, depending on the extent of injury
may ovulate as early as 27 days
after delivery.
ABDOMINAL WALL
Most women have a menstrual
The abdominal wall remains soft and poorly toned
period by 12 weeks; the mean
for many weeks. The return to a prepregnant state
time to first menses is 7-9 weeks. depends greatly on exercise

WEIGHT
Decreased due to
- evacuation of
uterine content.
- more fluids loss
through urine and
sweat

TEMPERATURE
A reactionary
increase may
occur following
difficult
delivery, but it
does not exceed
38C and drops
within 24 hrs.
A slight rise may
occur in the 3rd
day due to breast
engorgement.

PHYSIOLOGIC CHANGES DURING PUERPERIUM

GENERAL
BREAST
BOWEL
BLOOD
Changes that prepare the mother for Tendency to
Increase
breastfeeding occur throughout
constipate
coagulability of
pregnancy:
Causes :
blood continue
- Lactogenesis is triggered initially
- Atony of bowel
during the first 2
by the delivery of placenta
- Laxity of ab and
weeks despite of
- Falling level of Estrogen and
perineum
decrease in a
Progesterone
- Anaroxia
number of
- Continue presence of PRL
- Loss of fluids
coagulation factor
- If mother is not lactating, the
- Fear of evacuation: This may increase
Pain from stretched
incidence of PE
Prolactin level and return to
perineum, prolapse
and DVT.
normal within 2-3 weeks
Hb concentration
- Colostrum secreted during the first hemorrhoid, or anal
fissure
tends to fall in the
3 days
first 2-3 days
URINE
Colustrum - yellowish, high protein
concentration (IgA), protects against Increase in urine production by the 2nd4th day
infection, replaced by milk at the
Retention of urine is not uncommon
3rd-4th day postpartum
Causes:
- Atony of bladder neck
- Engorgement of the breast
- Laxity of ab
- Large and painful breast
- Compression of urethra by vulval edema
But, suckling relieve the discomfort
or hematoma
Suckling PRL (milk secretion) +
Oxytoxin (milk ejection)

CARDIOVASCULAR
- Immediately
following delivery,
there is marked
increase in
peripheral vascular
resistance due to
the removal of the
low-pressure uteroplacental
circulatory shunt
- The cardiac output
and plasma volume
gradually return to
normal during the
first two weeks of
puerperium
- Pulse is normal
but may increase if
there is infection or
hemorrhage

PATHOLOGIC CHANGES DURING PUERPERIUM

POST PARTUM HEMORRHAGE
PSYCHOLOGICAL
It is an excessive (>500 mL at vaginal and >1000 mL at
POSTPARTUM BLUES
cesarean) blood loss after delivery.
Complicates 50% of deliveries
First 24 h primary
Mild, transient, self-limited disorder.
Up to 6 weeks secondary
Mood swings, with change in appetite and sleep.
First 2 weeks after delivery, often resolves by postpartum
day 10.
No pharmacotherapy is indicated.
PRIMARY
SECONDARY
POSTPARTUM DEPRESSION
Causes:
Causes:
- Complicates 5% of pregnancies
1) Uterine atony
1) Retained products of
- Sx: Sadness, fatigue, changes in sleeping and eating
Risk Factors:
conception
patterns, reduced libido, crying episodes, anxiety, and
chorioaminionitis, multiple
Management:
irritability.
gestations, macrosomic
Heavy bleedingIV infusion
- Usually in the first few months, and may last up to several
fetus, fibroid.
months or even a year.
and X-match of blood.
Rx: Massage and bimanual
- Treatment is recommended for 9-12 months beyond
Syntocinon (synthetic
compression, then
remission of symptoms.
oxytocin).
oxytocin infusion,
POSTPARTUM PSYCHOSIS
Examination under
ergometrin, prostaglandin F2 anesthesia.
Rare but serious.
If bleeding persists despite
Evacuation of the uterus.
Sx: Restless agitation, confusion, delusions, hallucination,
uterine contraction, suspect
Antibiotics given if placental
thoughts of self harm.
2) Genital tract trauma
tissue is found, even without Rarely presents before the 3rd postpartum day but
Cervical and vaginal
evidence of overt infection.
usually does so before 4 weeks.
lacerations
If blood loss is not excessive, Recovery occurs over 4-6 weeks.
use pelvic US to exclude
Patient should be referred urgently to a psychatrist and
retained products.
will usually require admission to a psychiatric unit.
2) Endometritis
Pathophysiology
3) Bleeding disorders
Poorly understood, but may be due to rapid changes in
estrogen, progesrtone and prolactin in postpartum
patients.
Stress - Responsibilities of child rearing
Postpartum thyroid dysfunction (psychiatric disorders).
Seen in higher rates in patients with history of

depression or other mental illnesses.

PATHOLOGIC
ENDOCRINE
SHEEHANS SYNDROME
Anterior pituitary gland enlarges during pregnancy
due to an increase in the size and the number of
prolactin secreting cells
If significant hemorrhage occur during the
peripartum period, ischemic necrosis of the gland
will happen.
Full clinical picture apparent after 95% destruction
1) PRL Failed lactation
2) FSH & LH Anovulation & 2ndary
amenorrhea
3) Hypothyroidism Brady, cold intolerance,
constip
4) ACTH Hypotension & weight
Rx: Replacement therapy
-cortisone & thyroxine for life.
-HMG for induction of ovulation if pregnancy is
desired.
POSTPARTUM THYROIDITIS
Transient destructive inflammation of Thyroid
gland occuring within the 1st year after delivery.
Believed to result from modif to the immune
system necessary in pregnancy.
2phases: 1) Thyrotoxicosis 2) Hypothyroidism
The process is normally self-limiting, but when
conventional antibodies are found there is a high
chance of this proceeding to permanent
hypothyroidism.
POSTPARTUM GRAVES DISEASE
Less common than PPT.
Similar to Graves disease in other settings.
Autoimmune Ab against TSH receptors

CHANGES DURING PUERPERIUM

NEURO OBSTETRIC PALSY
BLADDER PROBLEMS
One or both of the lower
*Urinary retention, voiding difficulty,
limbs may develop signs &
and bladder over-distension are
sx of motor and/or sensory
common.
neuropathy following
*The baby's exit may have traumatized
delivery.
it
leading to temporary paralysis.
Causes:
*Loss of bladder sensation due to
1- Compression or
regional anesthesia.
stretching of the
*Swelling and pain in the perineal area.
lumbosacral plexus as it
*Psychological (fear) factors
crosses the sacroiliac joint
during decent of the fetal
Over-distention will lead to :
head.
1. Dampen bladder sensation, render it
2- Herniation of the
hypo-contractile and lead to fibrous
lumbosacral discs (L4/L5)
replacement of smooth muscle.
may also occur in the
2. Over flow incontinence.
exaggerated lithotomy
position and during
It's important to urinate within 6-8h of
instrumental delivery.
delivery.
This rate of UTI and prevent any
Features: Sciatic pain,
damage and bleeding that can happen
unilateral foot drop,
when bladder gets overly full.
hypoaesthesia, muscle
If the female didnt urinate during this
wasting.
period, we insert a catheter.
-Most cases resolve
spontaneously in a matter
of days or weeks, or
managed orthopaedically.
URINARY INCONTINENCE
Vaginal delivery strongly implicated in
the development of stress
incontinence.

Excess production of thyroid hormones.

Needs treatment, like any other graves
disease.

- Delivery weakens muscles around the

bladder and pelvis, which makes it
harder to control when urine starts.
- Hormonal changes

PATHOLOGIC CHANGES DURING PUERPERIUM

BOWEL FUNCTION DISORDERS
THROMBOEMBOLISM
PUERPERAL PYREXIA
CONSTIPATION
* The risk of thromboembolic
Def: Temperature of 38C or higher on
disease rises 5 fold during
It is a common problem during puerperium
any two of the first 10 days
pregnancy
periods.
postpartum, exclusive of the first 24h
* The majority of deaths occur in
There are three main causes:
measured orally by a standard
the
puerperium and are more technique
1. Interruption of normal diet, dehydration
common after caesarean section.
during labor.
* If DVT or pulmonary embolism is
2. Fear of evacuation due to pain from
Causes of pyrexia:
suspected, a full anticoagulant
sutured perineum, prolapsed hemorrhoid,
* Genital tract infection; upper tract
therapy should be commenced & a (bulky tender uterus) , or perineal
anal fissures.
bilateral venogram or lung scan
3. Atony of intestinal, abdominal, perineal
infection only
should be carried out within 24
muscles.
* UTI.
48 hours.
Management:
* Breast infections e.g. mastitis.
*Adequate fluid intake and increase in fiber
* Resp tract infection - more common
intake.
after anesthesia.
*Stool softener (laxatives) if necessary.
* Thrombophlebitis and deep vein
Laxatives: lactulose, ispaghula
thrombosis.
ANAL INCONTINENCE & FECAL URGENCY
* Wound infections; Anemia.
Incontinence of stool and flatus are frequent
* Non-puerperal related causes e.g.
complications of childbirth.
appendicitis.
Anal incontinence is associated with:
- Anal sphincter damage especially
operative delivery.
- Following repair of third or fourth degree
tear.
- Stool impaction.
- Dev of the anovaginal or rectovaginal
fistula.
- Pelvic floor dysfunction

PUERPERAL INFECTIONS
Infections are among the most prominent puerperal complications.
Fever remains the hallmark of puerperal infection, and the patient with fever can be assumed to have genital infection until
proven otherwise.
ENDOMETRITIS
MASTITIS
URINARY TRACT INFECTION
Def: Infection of the endometrium or
Def: Inflammation of the mammary gland
2-4 % of women dev UTI
decidua, with extension into the
Could be :
postpartum.
myometrium and parametrial tissues.
- Congestive mastitis (breast engorgement).
Causes: Bladder and the lower
Usually develops on the 2nd or 3rd
- Infectious mastitis
urinary tract remains
postpartum.
Both are more common in Primigravidas.
hypotonic, Catheterization, Birth
Etiology: PROM > 24 hours, Cesarean
Infectious mastitis and breast abscess are
trauma, Conduction anesthesia,
section, Chorioamnionitis, Excessive
uncommon complications of the breastfeeding. Frequent pelvic exam.
number of digital pelvic exam,
Almost certainly occur as a result of trauma to
Commonest m/o: E.coli and
Prolonged labor > 12 hour, Low
the nipple and the subsequent introduction of
Proteus spp.
socioeconomic status, Toxemia,
the Organisms from the infants nostrils.
intrauterine monitoring devices, PreMost common m/o: Staph aureus.
Sign & sx: Dysuria, Frequency,
existing vaginitis and cervicitis.
Loin pain if pyelonephritis,
Bacteriological findings: Anaerobic
Rx: isolation. Cease breast feeding from
Systemic sx, May be
strep, Gram negative coliforms,
affected breast. Expression of milk. Culture &
asymptomatic and recognized
Bacteroid spp., Aerobic strep,
sensitivity. Flucloxacillin commenced while
on routine mid-stream urine
Chlamydia and Mycoplasma (difficult to awaiting sensitivity result. 10% with breast
(MSU) sample.
culture)
abcess need surgical incision & drainage.
(performed on all patients who
INFECTIOUS
CONGESTIVE
DDx: UTI, Acute pyelonephritis, Lower
have been catheterized in
Usually occur on the
genital tract infection, Wound infection, 1 wk or more after
labor)
nd
rd
delivery.
2
or
3
postpartum
Atelectasis, Pneumonia,
Exam: Raised temperature,
Usually
one
breast
is
day.
Thrombophlebitis, Mastitis,
Supra-pubic and/or renal angle
involved.
Breast swollen,
Appendicitis.
tenderness.
Tender,
redness,
tender,
tense
and
Management:
Investigation: MSU, White cell
swollen
and
hot.
warm.
Admit, Evacuation of retained products
count, Nitrites and leucocytes
Temp may be mildly
of conception under antibiotics cover, Pt is febrile and
on dipstick.
appears
ill.
elevated.
Parenteral broad-spectrum antibiotics,

usually stopped once the patient is

afebrile for 24-48 hours, tolerating a
regular diet, and ambulating without
difficulty.

Purulent discharge may

be present.

Axillary adenopathy
can be seen.

Rx: Broad-spectrum antibiotics

until the results of culture and
sensitivity are known, then be
specific. Bed rest. High fluid,
light solid diet.

PUERPERIUM
Definition

Physiological changes during puerperium

Local changes

General changes

1.
2.
3.
4.

1. Weight
2. Temperatu
re
3. Bowel
habit

The period following delivery of the baby and placenta to

about 6-8 weeks postpartum.
During that the reproductive organs and the maternal
physiology return toward the non-pregnant status
Family support

Uterus
Cervix
Vagina
Ovaries

5. Perineum
6. Abdominal
wall
7. Breast

4. Blood
5. Urine
6. CVS

Local physiological changes

1.Uterine Involution
Structure
Autolysis , enzymatic digestion of
the cytoplasm
obliteration & thrombosis of blood
vessels, then degeneration &
transformation into elastic tissue.
separation of the decidua
Weight - reduced from 1000gm
-after delivery- into 70-100gm by the
end of puerperium

Size
after delivery the length of the

Within 2 to 3 days postpartum,

the remaining decidua become
differentiated into two layers:
1. Superficial layer becomes
necrotic sloughs off as vaginal
discharge = lochia
2. Basal layer (adjacent to the
myometrium) becomes new
endometrium

The endometrial lining rapidly

regenerates, so that by the 7th

Lochia
Lochia is the bloodstained uterine discharge
that is composed of cervical mucous, vaginal
transudate, and products of necrosis and
sloughing of the superficial layer of the
decidua
- Lochia rubra (red): consists mainly of blood
and decidua. It lasts for 5 days.
- Lochia serosa (pale): due to relative decrease
in RBCs and predominance of leukocytes. It

uterus is 20 cm and felt at the level

of umbilicus.
after one week it is midway
between umbilicus and symphysis
pubis.
after 2 weeks it is at the level of
symphysis.
by the end of the 6th week it is 7.5
cm long
Uterine ligaments - are involuted
and subinvolution predisposes to
prolapse and retroversion

day the endometrial glands will

be evident. By the 16th day,
the endometrium is restored
throughout the uterus, except
at the placental site.
The contractions of the arterial
smooth muscle and
compression of the vessels by
contraction of the myometrium
result in homeostasis. The size
of the placental bed decreases
by half.

lasts for 5 days.

- Lochia alba (white): consists mainly of
leukocytes and mucus. It lasts for 5 days.

Persistence of red lochia means

subinvolution (arrested involtion)
Offensive lochia means infection , it may
be accompanied by pyrexia and tender
uterus.
- In severe infection with septicaemia, lochia
is scanty and not offensive.

The period of time the lochia can last

varies, although it averages approximately
5 weeks
Often, women experience an increase in
the amount of bleeding at 7-14 days
secondary to the sloughing of the eschar
on the placental site

Local physiological changes

2.Cervical changes

4.Ovaries

5.Perineum

The cervix begins to rapidly

revert to a non-pregnant state
(less elastic, more firm) but it
never returns to the
nulliparous state.
Before childbirth, the os is a
small, regular, oval opening.
After childbirth, the orifice is a
transverse slit.
The external os of the cervix
contracts slowly and is
narrowed by the end of the
first week to the extent that
a finger could not be easily
introduced.
By the end of the second
week the internal os should
be closed.
3.Vaginal changes
In the first few days the streched
vagina is smooth & edematous,
but by the end of the third week
rugae begin to appear, but never
completely return to its prepregnant size.

The resumption of normal function by the ovaries is

highly variable and is greatly influenced by breastfeeding
the infant. The woman who breastfeeds her infant has a
longer period of amenorrhea and anovulation than the
mother who chooses to bottle-feed. The mother who does
not breastfeed may ovulate as early as 27 days after
delivery. Most women have a menstrual period by 12
weeks; the mean time to first menses is 7-9 weeks

In the breastfeeding woman, the resumption of menses is

highly variable and depends on a number of factors,
including how much and how often the baby is fed and
whether the baby's food is supplemented with formula.
The delay in the return to normal ovarian function in the
lactating mother is caused by the suppression of
ovulation due to the elevation in prolactin. Half to three
fourths of women who breastfeed return to periods within
36 weeks of delivery.
The lactational amenorrhea method is 98% effective for
up to 6 months if:

The mother is not menstruating

The mother is nursing > 2 to 3 times per night, and
every 4 hours during the day without other
supplementation.
The baby is < 6 months old

The perineum has been

stretched and traumatized,
and sometimes torn or cut,
during the process of labor
and delivery. The swollen
and engorged vulva
rapidly resolves, and
swelling and engorgement
are completely gone within
1-2 weeks.
Most of the muscle tone is
regained by 6 weeks, with
more improvement over
the following few months.
The muscle tone may or
may not return to normal,
depending on the extent of
injury
6.Abdominal wall
The abdominal wall remains
soft and poorly toned for
many weeks. The return to a
prepregnant state depends
greatly on exercise

General physiological changes

1.Weight

2.Temperature

3.Breast changes

Decreased due to

The changes to the breast

that prepare the mother for
breastfeeding occur
throughout pregnancy

- evacuation of uterine
content.
- more fluids loss through
urine and sweat.
4.Bowel changes
Theres tendency to
constipate
Causes :
1. Atony of the intestine
2. Laxity of abdomen and
perineum
3. Aneroxia
4. Loss of fluids
5. Fear of evacuation; pain
from stretched
perineum,prolapse
hemorrhoid, or anal
fissure

A reactionary increase
may occur following
difficult delivery, but it
does not exceed 38C and
drops within 24 hours
A slight rise may occur in
the 3rd day due to breast
engorgement
5.Urine

Increase in urine
production by the 2nd-4th
day
Retention of urine is not
uncommon
Causes:
1. Atony of bladder neck
2. Laxity of abdomen
3. Compression of urethra by
vulval edema or
hematoma

Lactogenesis is triggered
initially by the delivery of
placenta
At delivery, the abrupt,
large decrease in
progesterone and
estrogen levels leads to
increased production of
alpha-lactalbumin
stimulates lactose
synthase increased milk
lactose
Continue presence of
Prolactin
If the mother is not
lactating, the Prolactin
level decreases and return
to normal within 2-3
weeks.

6.Blood changes

7.Cardiovascular changes

Leukocytosis occurs during and after labor up to

Colostrum yellow-colored
liquid secreted by the
breasts that contains
minerals, protein, fat,
antibodies, complement,
macrophages,
lymphocytes, lysozymes,
lactoferrin, and
lactoperoxidase. It is
secreted during the first 35 days.
Engorgement of the breast
with milk is common on
days 2 to 3 postpartum
Often painful
Often accompanied by
transient temperature
elevation
suckling relieve the
discomfort.
Suckling
oxytocin
ME cell contraction and milk
expulsion.

Immedietely following delivery, there is marked increase

30,000/L
Increase coagulability of blood continue during the first 2
weeks despite of decrease in a number of coagulation
factor
This may increase incidence of PE and DVT
Hemoglobin concentration tends to fall in the first 2-3
days

in peripheral vascular resistance due to the removal of the

low-pressure utero-placental circulatory shunt
The cardiac output and plasma volume gradually return to
normal during the first two weeks of puerperium
Pulse is normal but may increase if there is infection or
hemorrhage

Management
1. Observation
Pulse, T, BP
Breast, lochia, urine
output, bowel motion
2. Rest and Exercise
Rest in bed for 2 days
after uncomplicated
vaginal delivery
Complicated/ operation
needs a few days longer
Movement in and outside
the bed are advised to
minimized the risk of DVT

Problems in the
puerperium
3. Diet
Food rich in proteins,
vitamins, mineral and
fluid
4. Care of the breast
Wash the nipple and
areola with warm water
and soap before and after
each feed
5. Local Aseptic
The vulva and perinuem
are washed with
antiseptic lotion after
each micturation and
defecation
Then, use sterile vulval
pad
Add local antibiotic if
perineal stitch is present

6. Care of the bladder

1. Patient is encouraged to
micturate frequently
2. If retention present,
catheter is applied under
aseptic condition
7. Care of the bowel
Uptake of vegetables are
highly advisable to
prevent constipation
Sufficient fluid intake and
the use of glycerine
suppositories if needed

1. Postpartum
hemorrhage.
2. Neurological Problems.
3. Psychological
problems.
4. Endocrine problems.
5. Miscellaneous problems.
6. Puerperal Pyrexia &
Sepsis.
7. Infections.
8. Pelvic septic
thrombophlibitis.
9. Thromboembolism

POST-PARTUM HEMORRHAGE

It is an excessive blood
loss after delivery
First 24 h=primary

Primary PPH

Secondary PPH

Management

1.Uterine atony

3.Retained products of
conception

1. Heavy bleeding, IV
infusion and X-match of
blood.
2. Syntocinon (synthetic
oxytocin).
3. Examination under
anesthesia.
4. Evacuation of the uterus.
5. Antibiotics given if
placental tissue is found,
even without evidence of
overt infection

-R.F: chorioaminionitis,
multiple gestations,
1.
macrosomic fetus, fibroid.2.
-Trt: massage and
bimanual compression, 3.
then oxytocin infusion,
ergometrin, prostaglandin
F2

Up to 6 weeks=secondary
>500 mL at vaginal delivery
and >1000 mL at cesarean
delivery.

2. Genital tract trauma

-if blood loss is not excesive,

-Associated more with
secondary PPH.
-use pelvic US to exclude
retained products.
4.Others
Endometritis , bleeding
disorders.

-cervical and vaginal

lacerations.

PSYCHOLOGICAL PROBLEMS
Postpartum Blues

Postpartum Depression.

Postpartum Psychosis

Pathophysiology

Complicates 50%
of deliveries
Mild, transient,
self-limited
disorder.
Mood swings, with

complicates 8-15% of pregnancies

symptoms include sadness, fatigue,
changes in sleeping and eating
patterns, reduced libido, crying
episodes, anxiety, and irritability.
usually in the first few months, and

Rare but serious.

Symptoms include
restless agitation,
confusion, delusions,
hallucination, thoughts
of self harm.

Poorly undertood, but

may be due to rapid
changes in estrogen,
progesterone and
prolactin in postpartum
patients.

change in
appetite and
sleep.
First week after
delivery.
often resolves by
postpartum day
10.
No
pharmacotherapy
is indicated.

may last up to several months or

even a year.
TREATMENT

Pharmacologic intervention is typically

required:

1.
2.
3.
4.

Antidepressants
Anxiolytic agents
Electroconvulsive therapy
Mother should be co-managed with
a psychiatrist

Rarely presents before

the 3d postpartum day
but usually does so
before 4 weeks.
Recovery occurs over 46 weeks
The patient should be
referred urgently to a
psychatrist and will
usually reqiure
admission to a
psychatric unit.

Stress
Responsibilities of child
rearing
Postpartum thyroid
dysfunction (psychiatric
disorders).
These psychological
disorders are seen in
higher rates in patients
with history of
depression or other
mental illneses.

ENDOCRINE DISORDERS
Sheehans syndrome

Postpartum Thyroiditis

Postpartum Graves
disease

Anterior Pituitary gland enlarges during pregnancy due to an

increase in the size and the number of prolactin secreting cells

If significant hemorrhage occur during the peripartum period

ischemic necrosis of the gland will happen.
The full picture is seen with destruction of 95% of the gland
1.Decreased prolactin: causes Failed Lactation (commonly the
first symptom).
2. Decreased FSH & LH: causes anovulation & secondary
amenorrhea
3. Hypothyroidism: causes bradycardia , cold intolerance,
constipation,
4. Decreased ACTH: causes hypotension & loss of weight

Transient destructive
inflammation of Thyroid
gland occuring within the
1st year after delivery.
it is believed to result from
the modifications to
the immune
system necessary
in pregnancy
2 phases
1. Thyrotoxicosis. 2.
Hypothyroidism.

The process is normally selflimiting, but when

conventional antibodies are
found there is a high chance
of this proceeding to

Less common than

PPT.
Similar to Graves
disease in other
settings.
Autoimmune
antibodies against
TSH receptors
leading to excess
production of
thyroid hormones .
Needs treatment,
like any other
graves disease.

Treatment

permanent hypothyroidism.

REPLACEMENT THERAPY
-cortisone & thyroxine for life.
-HMG for induction of ovulation IF pregnancy is desired.

NEUROLOGICAL
PROBLEMS

BLADDER FUNCTION
PROBLEMS

BOWEL FUNCTION DISORDER

Thromboembolism

Obstetric palsy

Bladder problems

Constipation

Condition by which one or

both of the lower limbs
may develop signs &
symptoms of motor
and/or sensory
neuropathy following
delivery.

Urinary retention, voiding

difficulty, and bladder overdistension are common.

-May be due to:

1- compression or
stretching of the
lumbosacral plexus as it
crosses the sacroiliac joint
during decent of the fetal
head.
2 -Herniation of the
lumbosacral discs (L4/L5)

*The baby's exit may have

traumatized it leading to
temporary paralysis.
*loss of bladder sensation due
to regional anesthesia.
*Swelling and pain in the
perineal area.
*psychological (fear) factors
Over-distention will lead to :
1. dampen bladder sensation,
render it hypo-contractile and

It is a common problem
during puerperium periods.
There are three main causes:
1. Interruption of normal diet,
dehydration during labor.
2. Fear of evacuation due to
pain from sutured perineum,
prolapsed hemorrhoid, anal
fissures.
3. Atony of intestinal,
abdominal, perineal muscles.
Management:
1. adequate fluid intake and
increase in fiber intake.
2. stool softener (laxatives) if
necessary.
3. Laxatives:lactulose,
ispaghula
Anal incontinence and fecal
urgency

The risk of
thromboembolic
disease rises 5 fold
during pregnancy
The majority of
deaths occur in the
puerperium and are
more common after
caesarean section.
If DVT or pulmonary
embolism is
suspected, a full
anticoagulant therapy
should be commenced
& a bilateral
venogram or lung
scan should be carried
out within 24 48
hours

may also occur in the

exaggerated lithotomy
position and during
instrumental delivery.
Features include:
-sciatic pain.
-unilateral foot drop.
-hypoaesthesia.
-muscle wasting.
-Most cases resolve
spontaneously in a matter
of days or weeks, or
Managed orthopaedically.

lead to fibrous replacement of

smooth muscle.

2. Over flow incontinence.It's

important to urinate within (6)
to (8) hours of delivery.

This decrease rate of UTI

and prevent any damage
and bleeding that can
happen when your bladder
gets overly full.
If the female didnt urinate
during this period, we insert
a catheter.
Urinary incontinence

1.
2.
3.
4.
5.

Incontinence of stool and

flatus are frequent
complications of childbirth.
Anal incontinence is
associated with:
Anal sphincter damage
especially operative
delivery.
following repair of third or
fourth degree tear.
Stool impaction.
Development of the
anovaginal or rectovaginal
fistula.
Pelvic floor dysfunction

Vaginal delivery strongly

implicated in the development
of stress incontinence.
*Delivery weakened muscles
around the bladder and pelvis,
which make it harder to control
when urine starts.
*Hormonal changes

Puerperal pyrexia

PUERPERAL INFECTIONS

puerperal pyrexia is
defined as a
temperature of 38
or higher on any two
of the first 10 days
postpartum,
exclusive of the first
24h measured orally
by a standard
technique
causes e.g.
appendicitis.

Causes
1. genital tract infection; upper tract (bulky tender
uterus) , or perineal infection only
2. urinary tract infection.
3. Breast infections e.g. mastitis.
4. respiratory tract infection - this is more common after
anesthesia.
5. thrombophlebitis and deep vein thrombosis.
6. wound infections ; Anemia.
non-puerperal related

Infections are among the most

prominent puerperal complications .
Fever remains the hallmark of
puerperal infection , and the patient
with fever can be assumed to have
genital infection until proven
otherwise.
1. Endometritis
2. Mastitis
3. UTI

PUERPERAL INFECTIONS
1.Endometritis

Endometritis is an infection of
the endometrium or decidua,
with extension into the
myometrium and parametrial
tissues .
Usually develops on the 2nd or
3rd postpartum day .
Etiology
1.
2.
3.
4.
5.
6.
7.
8.
9.

PROM > 24 hours

Cesarean section
Chorioamnionitis
Excessive number of digital
pelvic examination
Prolonged labor > 12 hour
Low socioeconomic status .
Toxemia .
intrauterine monitoring devices .
pre-existing vaginitis and

Sign & symptoms

Differential diagnosis

1. Urinary tract infection.

2. Acute pyelonephritis.
3. Lower genital tract infection.
4. Wound infection.
5. Atelectasis.
6. Pneumonia.
7. Thrombophlebitis.
8. Mastitis.
9. Appendicitis
Management

Body temp. >38c in two

occasion 6h apart or once
>38.5
Lower abdominal pain
Change in Lochia : more
profuse, Foul smelling or
purulent
Leukocytosis which may be
difficult to interrupt because
of the physiological
leukocytosis seen
postpartum
Investigations
(Bact.findings)
Anaerobic streptococci .

1. Admit to hospital.
2. Evacuation of retained products of conception
under antibiotics cover.
3. Parenteral broad-spectrum antibiotics, usually
stopped once the patient is afebrile for 24-48
hours, tolerating a regular diet, and ambulating

cervicitis

1.
2.
3.
4.

Gram negative coliforms

Bacteroid spp.
Aerobic streptococci
Chlamydia and Mycoplasma
(difficult to culture)

without difficulty.

PUERPERAL INFECTIONS
2.Mastitis

3.Urinary tract infection

Definition

Incidence

Examination

Approximately 2-4 % of women

develop UTI postpartum .
During and Following delivery:
1. the bladder and the lower urinary
tract remains somewhat
hypotonic .
2. Catheterization .
3. Birth trauma .
4. Conduction anesthesia
5. Frequent pelvic examination
The commonest organisms are
E.coli and proteus spp.
Sign & Symptoms

-Raised temperature.

1.
2.
3.
4.

1. Broad-spectrum antibiotics until the

results of culture and sensitivity are
known, then be specific .
2. Bed rest .
3. High fluid, light solid diet .

Inflammation of the mammary gland

Could be :
a. Congestive mastitis ( breast
engorgement).
b. Infectious mastitis
Both are more common in
Primigravidas
Infectious mastitis and breast
abscess are uncommon
complications of the breastfeeding .
Treatment
1. isolation of the mother & baby
2. ceasing breast feeding from affected
breast.
3. Expression of milk either manually
or by electric pump.
4. microbiological culture & sensitivity
of a sample of milk.
5. flucloxacillin can be commenced
while awaiting sensitivity result.

Dysuria.
Frequency of micturition.
Loin pain if pyelonephritis occurs.
Systemic symptoms such as
pyrexia and tachycardia.
5. May be asymptomatic and
recognized on routine mid-stream

-Supra-pubic and/or renal angle

tenderness .
Investigation
-MSU.
-White cell count.
-Nitrites and leucocytes on dipstick.
Management

6. 10% of woman with mastitis

develop breast abcess which need
surgical incision & drainage under
general anesthesia.

urine (MSU) sample.

6. (This should be performed on all
patients who have been
catheterized in labor)

RHESUS ISOIMMUNIZATION
FETOMATERNAL
HEMORRHAGE
Leakage of Rh+ve fetal cells
in Rh-ve maternal circulation
during pregnancy
Examples: Spontaneous
abortion, Induced abortion,
APH, E.C.V, Cordocentesis,
CVS, amniocentesis, Severe
preeclampsia, Ectopic
pregnancy, Caesarean
section, Manual removal of
placenta, Silent feto-

1- If ABO is incompatible:
RBC easily destroyed, so not
reaching enough immunological
component to cause antibody
response and reaction
2- If ABO is compatible:
Rh +ve fetal cells remain in
circulation (life span) until removed
by R.E.S destroyed liberating
Ag (D) isoimmunization.

Mild Cases:
Fetal RBC destruction from IgG anti D anaemia
It takes
time:

compensating
hemopoiesis excess of
1st pregnancybilirubin.
is almost always not
unconjugated
affected:
Severe
Cases:
1% duringdestruction
labour or 3rd
stageRBC severe
Excessive
of fetal
10%
6
months
after
delivery
anemia Tissue Hypoxia Cardiac / circulatory
and15%
the 2nd pregnancy
failure
by
Generalized
edema Heart Failure
Ascites -Intrauterine Fetal Death
With excessive unconjugated bilirubin >310-350
mol/L Passes BBB kernicterus permanent
neuro and mental disorders.
FETAL & NEONATAL EFFECTS
- Haemolytic anaemia of newborn Hb 14-18g/dl
- Icterus gravis neonatorum Hb 10-14g/dl
- Hydrops fetalis (Erythroblastosis fetalis)

Factors Affect Dev of Rhesus

antibodies:
1- Inborn ability to respond
2- Protection if ABO
incompatible1\10
3- Strength of Rh Ag stimulus
(CDe=R1)
4- Volume of leaking feta
blood (0.25ml)
IgM (7 days) doesnt cross
placenta, then IgG 21 days crosses placenta)

INTRODUCTION
Rhesus factor: Agglutinogen
(C,D,E) mainly D
C,D,E dominant antigen
d,e recessive antigen
- Rh +ve about 85%
(homozygous DD35% or
heterozygous Dd 50%

MANAGEMENT
A) Prophylaxis
1- Prevention of Rhesus isoimmunization: Anti D (RhoD IgG)
Standard dose for >20w, and standard dose for <20weeks. Given within 72h of
the incident.
SD: I.M. injection: 500 iu = 100 ugm (UK) - neutralize 5ml (4ml + 1ml) = 100fetal
cells
SD in USA 300ugm=1500iu - neutralize 15ml

- Rh negative about 15%.

Incidence of Rh -ve in far east is
about 1%
Examples of Rh factor:
(CDe=R1) , (Cde=r) (cDE=R2)
Other systems: kell-antikell,
luther, Duffy, etc .
Introduction of foreign protein
(Ag) production of Ab to
neutralize the Ag.
In ABO and other non Rhincompatibility: It usually causes
mild anemia, mainly as there is
no intrapartum boosting .
In Rhesus isoimmunization:
mainly (D), but C,E can produce
antibodies.
Kleihauer-Betke technique (acid
elution test): Measure amount of
feto-maternal haemorrhage.
If 0.1- 0.25ml of fetal blood leaks
(critical volume) this will produce
isoimmunization represented by
5 fetal cells in 50 low power
microscopic field of peripheral
maternal blood.
So 1ml is represented by 20 fetal
cells

K-B test if large amount of leaking another SD if mother is Rh -ve, baby Rh +ve
with no isoimmunization (checked by indirect or direct coombs test)
2- A.P administration of anti D
SD at 28w or at 28 and 36w will reduce Rh isoimmunization
B)
1- Antibody Screening: for all pregnant women in ANC for irregular antibodies
(mainly for Rhesus Negative women) then start at 20w, and every 4 weeks
2- Management following detection of Rh antibodies
- Should be treated in specialized centers
- Quantitative measures of antibodies + husband genotype
- Repeat titration (indirect coombs, detecting of antibodies) titer or specific
enzymes for antibodies IU
- Amniocentesis once necessary
- Obstetrical management based on timing of I.U trans-fusion (Now
cordocentesis + fetoscopy) versus delivery
3- Amniocentesis: should be performed under ultrasound guidance if titer >
1\16 = 0.5-1 ugm = > 2.5-5 I.U
- timing: 1st amniocentesis 10 weeks before previous IUFD
- Start from 20-22 weeks, 2-4 weekly or more frequent if needed
- Amniotic fluid analysis: spectrophotometry: optical density at the height of
optical density deviation at wave length 450 nM.

IU transfusion (cordocentesis, in the past intraperitoneal transfusion) versus

delivery of the baby:
- Using Lilys chart
- Prediction chart (Queenan curve)
- Whitefields action line
-Alternatively follow up with doppler study for the fetal middle cerebral artery.
Prognosis depends on: Obstetric hx, paternal genotype, maternal history (blood

transfusion, antibody titre) amniocentesis results.

Delivery: Vaginal versus Cs
Intensive plasmaphoresis: when severe cases anticipated, using continous flow
cell separator, as early as 12 w
Postnatal management: for the neonate
- direct coombs test, Blood group, Rh type, Hb, bilirubin .
- Mild cases: phototherapy, correction of acidosis
- Severe cases :exchange transfusion

SMALL FOR GESTATIONAL AGE

INTRODUCTION
- Fetal growth is dependent on genetic, placental and maternal factors.
- Fetal growth restriction is the second leading cause of perinatal morbidity and mortality.
ASSESSING FETAL GROWTH
HISTORY
PHYSICAL EXAM
USES OF ULTRASOUND
- Mothers age
a) General Exam
- Diagnosis and confirmation
- Accuracy of LMP
b) Obstetrical Exam
of viability in early pregnancy
date
Uterine Fundal Height
- Determination of gestational

FETAL VIABILITY
Detection of :
Gestational sac (45wks)

- Infections during
pregnancy
- Multiple
pregnancy
- ANC and visits,
Supplements
- Past obs. Hx, Past
Med Hx, Drug Hx,
Family Hx,
Socioeconomic Hx.

- Obtaining serial uterine fundal height

age and assessment of fetal
measurements.
size
- The Mcdonalds rule in pregnancy is a
- Intrauterine or Ectopic
rough determination of fetal age in weeks
pregnancy.
Uterus size: by pelvic examination in the
- Multiple pregnancy
first trimester and subsequent antenatal
- Diagnosis of fetal
visits.
abnormalities
Misleading in: Full bladder, obesity, deep
- Placental localization
masses, uterine fibroids & multiple
- Assessment of fetal wellpregnancy
being
DETERMINATION OF GA AND ASSESSMENT OF GROWTH
UP TO 13TH WEEKS GA
FROM 16 24 WEEKS GA
CROWN-RUMP LENGTH
BIPARIETAL DIAMETER
HEAD CIRCUMFERENCE
FEMUR LENGTH
(CRL)
(BPD)
(HC)
(FL)
From Crown to
The transverse width Not affected by the
- Better than BPD
shape of the head.
in accuracy and
Coccyx (Rump)
of the head at its
timing.
(longitudinal axis).
widest (the distance
- Accurate only
Accurate up to 14
between the parietal
st
when the image
bones eminence of
wks (1 TM).
shows two blunted
the skull).
It is the most
ends of the femur.
Accurate up to16-24
accurate
wks.
parameter.
Accuracy of +/- 7
Accuracy of +/- 5
days.
days from the GA.
It is affected by the
shape of the head.

Yolk sac (5wks)

Embryo (5-6wks)
Visible heart beat
(6wks).

ABDOMINAL
CIRCUMFERENCE (AC)
Made at the widest
points in the
abdomen.
Most accurate
single predictor of
fetal weight.

SMALL FOR GESTATIONAL AGE (SGA)

Small for gestational age is defined as a fetal birth weight below the 10 th centile for the stated gestational age.
The incidence of SGA fetuses is 5-10%
CONSTITUTIONAL
(70%)
SGA

PREMATURITY (10%)
INTRAUTERINE
GROWTH
RESTRICTION (20%)

SYMMETRICAL IUGR
(20%)
ASYMMETRICAL IUGR
(80%)

A] CONSTITUTIONALLY SMALL FETUS

Unfortunately, it can be concluded that a fetus is constitutionally small only after pathologic processes have
been excluded.
Therefore, identification of a constitutionally small infant is usually made in retrospect, after the infant is born.
Causes (Multifactorial): Race, Geographical area, Sex (M>F), Maternal age, Maternal weight and height,
Socioeconomic status

B] INTRA-UTERINE GROWTH RESTRICTION

Failure of the fetus to achieve its growth potential
INCIDENCE
TYPES
3 - 10 % of all pregnancies.
Symmetrical growth restriction: fetus whose entire body is
proportionally small. (20%)
20 % of stillborns are growth retarded.
Asymmetrical growth restriction: Decrease in subcutaneous fat and
9 - 27 % have anatomic and/or genetic
abdominal circumference with relative sparing of head circumference
abnormalities.
and femur length. (80%)
Perinatal mortality is 8 - 10 times higher for
these fetuses.
CAUSES OF IUGR
MATERNAL
MATERNAL
FETAL
FETAL PATHOLOGICAL
PLACENTAL CAUSES
PHYSIOLOGICAL
PATHOLOGICAL CAUSES
PHYSIOLOGICAL
CAUSES
CAUSE
CAUSES
Multiple pregnancy Uteroplacental
Genetic disorders
Placental
Genetic Factors:
blood flow:
(Achondroplasia,
insufficiency
Short stature
Race, ethnicity,
- PET/eclampsia
Russell
silver
synd)
(most imp in 3rd
Younger or older
nationality
trimester)
Chromosomal
age (<15 and >45) - chronic renovascular
sex (male weigh
anomalies:
Anatomic
Low socioeconomic disease
150 -200 gm
- Chronic HTN
Chromosomal
deletions
problems:
class
more than
Maternal malnutrition
Trisomies
13,18
&
21
Multiple
infarcts
Primiparity
female)
Aberrant
cord
Maternal hypoxemia

Congenital
Grand multiparity
Parity
insertions
Hemoglobinopathies
malformations:
Low pregnancy
(primiparous,
- Umbilical
- High altitudes
Ex: Anencephaly, GI
weight
weigh less than
vascular thrombosis
atresia, Potters
Drugs
Previous h/o
subsequent
& hemangiomas
syndrome, and
preterm IUGR baby - Cigarettes, alcohol,
siblings)
- Premature
pancreatic agenesis.
heroin, cocaine
placental
separation
- Teratogens,
Fetal Cardiovascular
- Small Placenta
antimetabolites and
anomalies
therapeutic agents such
Congenital Infxn:
as trimethadione,
mainly TORCH.
warfarin, phenytoin.
Inborn error of
Chronic illness (DM,
metabolism:
renal failure, cyanotic
- Transient neonatal
heart disease etc.)
diabetes

- Galactosemia
- PKU
DIAGNOSIS
History, Physical examination, Investigations
Ultrasound
Abdominal circumference is the single most
effective parameter for predicting fetal weight
because its reduced in both symmetrical &
Asymmetrical IUGR .
In the presence of normal head and femur
measurements, abdominal circumference (AC)
measurements of less than 2 standard deviations
below the mean appear to be a reasonable cutoff to
consider a fetus asymmetric.
COMPLICATIONS
ANTENATAL
NEONATAL
Metabolic changes 1- Related to hypoxia and
acidosis:
(acidosis etc).
a- Meconium aspiration.
Oligohydramnios
b- Persistent fetal
(80%)
circulation.
Abnormal fetal
c- Hypoxic ischemic
heart patterns.
encephalopathy.
Abnormal Doppler
2- Metabolic: Hypoglycemia,
studies.
HypoCa, Hypothermia,
IUFD
Hyperviscocity syndrome
INTRAPARTUM
3- Related to the etiology:
Abnormal CTG.
a- Chromosomal
Fetal death.
abnormalities.
Meconium stained
b- Infection.
liquor.
c- Congenital anomalies.
incidence of
instrumental and
caesarean
deliveries.

Asymmetrical growth restriction : BPD is normal in the 3rd

trimester , whereas ratio of HC/AC is abnormal .
Symmetrical growth restriction : HC/AC may be normal .
Amniotic fluid volumes ( oligohydramnios is associated with
IUGR) .
Umbilical artery & fetal artery dopplar assessments : increased
resistance is associated with a greater risk of IUGR as pregnancy
progresses.

PRE-PREGNANCY
Modify lifestyle
habits.
Detect and
treat medical
disorders.

MANAGEMENT
ANTEPARTUM
Regular antenatal care.
Serial fetal growth assessment.
Serial fetal wellbeing assessment
1- Biophysical profile
2- Computerized CTG
3- Umbilical artery Doppler
Timing of delivery.
Mode of delivery.

Time & Mode of delivery governed by: Maternal

age, Past obs. History, GA, Fetal well being,
Status of cervix, Availability of direct
monitoring during labor (Ex: scalp PH
sampling).
Mode of Delivery
Cesarean delivery without a trial of labor:
1. in the presence of evidence of fetal distress
2. for traditional obstetrical indications for
cesarean delivery

 Induction of labor
Continuous heart rate monitoring and scalp pH
monitoring optimize success of vaginal delivery
SHOULDER DYSTOCIA
Risk Factors
1. Fetal macrosomia
2. Maternal DM
3. Others:
- Antepartum: Obesity, Multiparity,
Post-term gestations, Short
stature, Previous hx of
macrosomia, Previous hx of
shoulder dystocia
- Intrapartum: Labor induction,
epidural analgesia, Prolonged
labor, Operative vaginal delivery

Def: Difficult
delivery of the
shoulder.
Arrest of normal
labor after the
delivery of the head
by the impaction of
anterior shoulder
against symphysis
pubis.
Posterior shoulder
may also be
obstructed by
sacral promontory.
Complications
Fetal risks
- Asphyxia
- Birth trauma: Brachial
plexus injuries (Erbs &
Klumpkes), Frx humerus &
clavicle
- Death

Maternal risks
Genital tract
trauma
risk of PPH
Uterine rupture

Clinical Manifestations
Fetal shoulder fails to deliver
after delivery of fetal head
despite routine maneuvers.
Impaction of fetal shoulder
behind pubic symphysis.
Turtle sign: Retraction of
fetal head into perineum
after its delivery and before
the shoulders can be
delivered.

Pregnancies at Risk
Cannot accurately predict (50%
without risk factors)
ACOG recommends CS for EFW 5kg in
nonDM mothers and 4.5kg in DM
mothers.

HELPER

HUMAN
H: Call for
Help.PAPILLOMAVIRUS (HPV)
OVERVIEW
PREVALENCE & TRANSMISSION
CLINICAL PRESENTATION
Mostly asymptomatic; no visible
There are about 200 HPV genotypes, 30 Common viral STI with an
E: Evaluate for Episiotomy
to 40 types of HPV are typically
estimated 20 million infected
lesions (latent infection).
transmitted through sexual contact
and
persons
in
the
US
and
5
million
Characterized by readily visible
Midline episiotomy.
infect the anogenital region.
new cases every year.
"warty" growths (condylomata
F(x): Facilitates delivery of posterior
The most clinically evident results of
About 75% of sexually active
acuminata) on the vulva,
infection with human papillomavirus shoulder.
adults will be infected sometime in
vagina, cervix, urethra, and
L: Legs @
(HPV) are condyloma acuminata
orMcRoberts
their Maneuvre
life.
perianal area, that can be pruritic
genital warts.
Transmission
HPV canlegs.
occur
Hyperflexion, abduction & external
rotation of of
maternal
or cause bleeding.
Majority of genital
warts
are
caused
by
even
when
there
are
no
visible

HPV infection usually clears

F(x): Straightens maternal lordosis, remove sacral promontory as
HPV types 6 and 11 which have little
lesions (latent).
spontaneously within 2 years, but
obstr, open pelvis to max dimension, pelvic inlet into plane
oncogenic potential.
During pregnancy, condylomata
recurrences are common.
to maxmay
expulsive
force.
HPV types 16 and 18 mayperpendicular
cause flat
increase
in number and size,
Suprapubic
Pressure @
Mazzanti
Technique from
warts and have beenP:linked
with the
however,
transmission
dev of cervical ca. Direct suprapubic pressure
mother
tofetal
infant
is very rare.
against
anterior
DIAGNOSIS
TREATMENT
shoulder to dislodge from under symphysis pubis.
Clinical exam
Provider-applied topical therapies include: podophyllin resin 10% to
Biopsy of the lesion (uncertain of
25% in tincture of benzoin and trichloroacetic acid (TCA) or
E:lesions
Enter @
Rubin
Maneuvres
bichloracetic
acid (BCA) 80% to 90%.
diagnosis or for
that
are & Wood-Corkscrew

Patient-applied
topical
therapies
include: podofilox solution or gel and
unresponsive
to
therapy)
Rubin: Digital pressure to the posterior aspect of anterior shoulder,
pushing
towards
fetal chest. imiquimod cream.
Surgical therapies include: cryotherapy, manual excision,
Woods: Digital pressure applied to anterior aspect of posterior shoulder, pushing
electrocautery, laser vaporization, and intralesional interferon.
towards fetal
back.
Reasons for treating visible genital warts are to relieve symptoms
(pain and/or bleeding) and sometimes for cosmetic concerns of the
R: Release of posterior shoulder @ Jacquemier
Maneuvre
patient
Hand inserted into vagina, and the posterior arm is grasped and pulled
resulting delivery in posterior shoulder & displacement of anterior
shoulder.
Gaskin All-Fours
Put patient on all fours (knee-chest position) and repeat
maneuvers.
Last Resorts:
Zavanelli Maneuvre: Replace head back into pelvis &
deliver CS.
Deliberate fracture of clavicle.

OVERVIEW
STD caused by the HSV type I
or type 2.
HSV-1 is most commonly
associated with oral lesions
(cold sores), but about 30% of
primary GH is due to HSV-1.
HSV-2 is the cause of 70% of
primary GH and 95% of
recurrent GH.
Characterized by repeated
eruptions of small, painful
blisters on the genitals,
around the rectum, or
covering adjacent areas of
skin (genital ulcer).

HERPES SIMPLEX VIRUS (HSV)

PREVALENCE
TRANSMISSION
Genital herpes (GH) is the Virus enters body thru
most prevalent STD in the
mucosa or microabrasions
US.
in the skin and follows the
Although only about 5% of
sensory nerves to the
dorsal spinal ganglion
women report a history of
where it remains dormant
genital herpes infection,
until reactivated.
as many as 25% to 30%
Transmission occurs
have antibodies on
serologic testing
through intimate genital,
(asymptomatic).
oral or anal contact.
Transmission from an
An infected mother can
infected male to his
transmit the virus to her
female partner is more
infant during delivery
likely than from an
resulting in significant fetal
infected female to her
mortality and morbidity.
male partner.

COMPLICATION
Psycho distress.
(counseling)
Neuro involvement
(aseptic meningitis,
transverse myelitis
or autonomic
neuropathy).
Herpes keratitis
(corneal scarring
and blindness).
risk of HIV
infection
Neonatal herpes
(vertical
transmission)

PRIMARY
Typically asymptomatic
Presents up to 3 weeks after
acquisition
Begins with flulike symptoms
(malaise, myalgias, nausea,
diarrhea, and fever).
Vulvar burning and pruritus
followed by multiple bilateral
vesicles that appear next and
usually remain intact for 24 to
36 hours before evolving into
painful genital ulcers.
Inguinal adenopathy, dysuria
and acute urinary retention
may occur.
Require a mean of 10 to 22
days to heal, with no scarring.

DIAGNOSIS
Clinical diagnosis
Viral culture from vesicular
fluid (the gold standard; low
sensitivity)
DNA PCR assays for HSV
(experimental)
A Tzanck smear (cytology)
Type- specific antibodies for
HSV-1 and HSV-2 IgG
(diagnose the primary
infection and the serotype of
the causative organism).

RECURRENT
When the virus becomes
reactivated and travels down
the sensory nerve to the
mucoepithelial surface.
Can occur as frequent as 16x/yr.
Trigger factors include fever,
menses, emo stress, or local
trauma.
Usually occur in the same
area, unilateral, may be less
painful than those of the first
episode but can still be
uncomfortable.
Systemic sx are uncommon
with recurrences.
By the 7-9th day, most
lesions are healed without
scarring.
TREATMENT
The goals of treatment for
GH are sx relief, acceleration
of lesion healing, and a in
frequency of recurrences.
Antiviral - acyclovir,
famciclovir, and valacyclovir
are safe and effective for
treating primary and
episodic outbreaks, and
suppressive therapy for
patients with chronic
disease.

NEONATAL
85% of cases occur during birth, 5% are infected
in utero, and10% of cases are acquired
postnatally.
Risk of transmission to the newborn is 30-57% in
cases where the mother acquired a primary
infection in the 3rd trimester of pregnancy, risk of
transmission by a mother with existing antibodies
for both HSV-1 and HSV-2 is about 1-3%.
Neonatal herpes may take three forms:
1) Disseminated (with the high morbidity and
mortality despite appropriate treatment)
2) CNS only (high morbidity, some mortality
despite treatment)
3) Skin/Eye/Mouth involvement only (low
morbidity and almost no mortality with
treatment)

MANAGEMENT FOR NEONATAL HERPES

Acyclovir may be administered orally to pregnant
women with mild or moderate outbreaks, but for
primary infections or severe recurrent outbreaks,
IV therapy should be administered.
At the onset of labor, all women should be
questioned carefully about symptoms of genital
herpes, and should be examined carefully for
herpetic lesions.
Patients with typical prodromal symptoms or
active lesions in labor should be delivered by
cesarean section.
Preventing is difficult because 70-80% of afflicted

 No treatment completely
eradicates virus.
Education and supportive
counseling.

newborns are born to mothers with no hx of prior

infection or signs or sx at or around the time of
delivery.

INTRODUCTION
o Most common bacterial STI in US.
o Obligate intracellular bacteria that
grows in vitro only in tissue culture.
o Infects columnar epithelium of
endocervix, urethra, endometrium,
fallopian tubes & rectum.
o No vaccine. Antibodies doesnt
protect against reinfection.
RISKS
For pregnant women: Preterm labor,
Chorioamnionitis, Postpartum
endometritis.
30% untreated chlamydial cervicitis
progress to PID.
For infant: Neonatal conjuntivitis &
pneumonia

CHLAMYDIA TRACHOMATIS
CLINICAL FEATURES
Hx : Most (70% women + 50% men)
are asymptomatic!
o Mucopurulent cervicitis or mucopus
o Acute urethritis with dysurea but
minimal frequency & urgency &
negative urine culture.
Examination: Mucopurulent cervical
discharge & Cervical Erythema
Lab tests
o Tissue culture - expensive
o Antigen tests
o DNA hybridization & nucleic acid
amplification tests NAATs (PCR or
ligase chain reaction)

SCREENING
Selective screening.
All sexually active female <26yrs
All women with risk factors
(unmarried, multiple sexual
partners, inconsistent use of
barrier contraception, previous
hx of STI, pregnant)
DNA amplification test
TREATMENT
1. Presumptive treatment with
appropriate antibiotics
o Azithromycin 1g orally single dose,
or
o Doxycycline 100mg 2x/day for a
week
o Pregnant? Amoxicillin or
erythromycin
2. Treat all sexual contacts within the
past 60 days of diagnosis. PDPT.
3. Testing for other STI
4. Abstinence from sexual contact for 7
days after starting treatment.

GONORRHEA
INTRODUCTION
SIGNS & SYMPTOMS
o Gram negative diplococcus Neisseria o Asymptomatic (Most women, but 5%
Gonorrhea
men)
o Infects cuboidal & columnar
o Increased vaginal discharge with
epithelium in endocervical & urethral
lower ab/pelvic pain.
mucosa.
o Dysurea with urethral discharge.
o Also rectal & nasopharyngeal mucus o Proctitis with rectal bleeding,
memb.
discharge, pain.
o Coinfection with Chlamydia &
o Endocervical mucopurulent
Trichomonas.
discharge & contact bleeding.
o No vaccines.
o Mucopurulent urethral discharge.
o 15% untreated gonococcal cervical
o Pelvic tenderness with cervical
infxn progress to PID.
excitation.
RISKS
TREATMENT GUIDELINES
To pregnant women: Preterm
1. Treatment with appropriate antibiotics.
labor & delivery,
2. Simultaneous treatment for chlamydia
chorioamnionitis, postpartum
(1g azithromycin in single oral dose)
endometritis.
3. Treatment of all sexual contacts within 60days
To infants: Neonatal
before diagnosis.
conjunctivitis (ophthalmia
4. Abstinence from sexual activity for 7 days.
neonatorum).
5. Testing for other STIs.
6. Counselling regarding long-term
complications: Chronic pelvic pain, tubal
infection, subfertility.

DIAGNOSTIC TESTS
o Gram staining: Gram ve
diploccocci in leukocytes.
Very sensitive in men. In women, 50%
sensitive.
o Culture: Thayer-Martin or
Transgrow media. Sensitive &
specific but takes time.
o Nucleic acid amplification tests
(NAATs): PCR & LCR. More
expensive but rapid & high
sensitivity & specificity.
o Nucleic acid hybridization tests
TREATMENT
o Single oral dose of cefixime, or
o Single IM dose of ceftriaxone, or
o Single IM dose of spectinomycin,
or
o Single oral dose of ciprofloxacin,
or
o Single dose of oral (Ampicillin 2g
or Amoxycillin 1g) + Probenicid 2g
Pregnant? Penicillin & cephalosporin
are safe!

o
o

INTRODUCTION
Treponema pallidum,
motile anaerobic
spirochete.
Can be eradicated,
yet can reinfect.
Spread: STD or
Congenital

o
o

SYPHILIS
DIAGNOSIS
History and physical examination
Lab investigations: Blood tests
Non-specific VDRL, rapid
plasma reagin test
Treponema-specific TPHA, FTAAbs
Dark-field microscopy

PRIMARY SYPHILIS
o

1st stage after infxn.

Appear 2-3wks after
contact.
Chancre - Firm,
painless, non-itchy
ulcers with rolled edges
most commonly on
vulva, vagina or cervix.
Spontaneously
disappear.

SECONDARY SYPHILIS
o
o
o

2-3 months after contact

Systemic sphirochetemia.
Fever, malaise, general
adenopathy, maculopapular skin
rash money spots. Broad
exophytic excrescences
condyloma lata on vulva.
Spontaneously disappear.

TREATMENT
o Mode of delivery: Vaginal delivery; C-section only
for obstetric indications.
o STD Prevention: Avoid multiple sexual partners,
promote use of barrier contraceptives.
o Treatment: Benzathine penicillin (G) in pregnancy
o Allergy? Full penicillin dose with oral
desensitization regimen under controlled
conditions.
LATENT
TERTIARY SYPHILIS
SYPHILIS
Absence of sx
o Necrotic, ulcerative nodules
or physical
gumma
findings.
o Sx dependent on which organ
affected.
CVS: Aortitis, saccular aneurysm
CNS: Meningitis, Tabes dorsalis,
Dementia, Ataxia
MSS: Osteitis

CONGENITAL SYPHILIS
Transmission: Transplacental passage from mother to fetus during delivery. Or, at birth.
Birth outcomes in congenital syphilis: Low birth weight, prematurity, congenital anomaly, miscarriage or death of baby.
Early Manifestation (<2 yrs)
Late Manifestation (>2 yrs)
Non-immune hydrops,
Hutchinson teeth
macerated skin, anemia,
mulberry molars
thrombocytopenia,
saber shins
hepatosplenomegaly.
saddle nose
Fetal death rates high
8th nerve deafness.

Perinatal mortality rate 50%.

Placenta typically large &
edematous.

VDRL
FTA-Abs
Dark
field
CSF

Primar
y
+
+

Seconda
ry
+
+
+

Laten
t
+
+
+

Tertiar
y
+
+
+
+ if
CNS
involve
d

VAGINAL DISCHARGE
NORMAL VAGINAL DISCHARGE

Discharge is common to all women and helps vaginas

stay healthy by regularly flushing them out and
maintaining their pH.
A normal vaginal discharge consists of about a
teaspoon (4 milliliters) a day that is white or
transparent, thick to thin, and odorl
This is formed by the normal bacteria and fluids the
vaginal cells put off. The discharge can be more
noticeable at different times of the month depending
on ovulation, menstrual flow, sexual activity and birth
control.

It is not uncommon for the normal discharge to be dark,

brown or discolored a day or two following the menstrual
period.
The following situations can increase the amount of normal
vaginal discharge:
1-Emotional stress
2-Ovulation (the production and release of an egg from your
ovary in the middle of your menstrual cycle)
3-Pregnancy
4-Sexual excitement

ABNORMAL VAGINAL DISCHARGE

When is vaginal discharge a sign
of an infection?
Your vaginal discharge might be a sign
of an infection if it:

Here are some key ways to determine if your vaginal discharge is normal
or if you have cause for concern:
Normal

Cause for concern

Colour

Clear or whitish discharge (may

be yellowish when dried)

Yellow or greenish discharge, or

discharge that suddenly
changes color

Scent

Mild scent or none at all

A strong, foul, sometimes

"fishy" odor, or a sudden
change in odor

Texture

Can vary from "paste" like and

somewhat sticky to clear and
stretchy, depending on where you

Clumpy or lumpy discharge,

with "cottage cheese" like

1-Causes itching
2-Causes swelling
3-Has a bad odor
4-Is green, yellow, or gray in color
5-Looks foamy or like cottage cheese

Volume

ABNORMAL VAGINAL DISCHARGE

May be due to:

are in your cycle and whether you

are aroused

texture

Can vary from very little to quite a

lot (particularly when ovulating or
aroused)

Sudden changes in volume,

particularly if other symptoms
are present

1. Atrophic vaginitis (seen in

women who have gone through
menopause and have low
estrogen levels)
2. Bacterial vaginosis (BV) -Bacteria that normally live in the
vagina overgrow, causing a grey
discharge and fishy odor that
worsen after sexual intercourse.
BV is usually not sexually
transmitted.
3. Cervical or vaginal cancer
(rarely a cause of excess
discharge)
4. Chlamydia
5. Desquamative vaginitis
and lichen planus
6. Forgotten tampon or foreign
body
7. Gonorrhea
8. Other infections and sexually
transmitted diseases
9. Trichomoniasis
10.
Vaginal yeast infection
11.
Allergic reactions,Cervical
polyp,Cervicitis, Genital
Warts (HPV), Pelvic
inflammatory disease

CANDIDAL VAGINITIS
common vaginal infection in

Risk factors

Clinical Presentation

the United States.

Etiology

The etiologic agent is a

yeast (fungi) organism,
usually Candida albicans.
The organism is a
common inhabitant of the
bowel and perianal region
Thirty percent of women
may have vaginal
colonization and have no
symptoms of infection.

Contraceptive
practices (e.g., birth
control pills and vaginal
spermicides, which
influence vaginal pH)
Use of systemic
steroids, which influence
the immune system
Use of antibiotics, which
alters the microbiology of
the vagina; 25% to 70%
of women report yeast
infections after antibiotic
use. Any antibiotic,
particularly a broadspectrum agent, may play
a causative role.
Tight clothing, panty
hose, and bathing
suits (yeast thrives in a
dark, warm, moist
environment)
Undiagnosed or
uncontrolled diabetes
mellitus

Another reason for a

refractory monilial
infection may be
compromised immune
status; with recurrent
monilial vaginitis, an HIV
test is indicated, along
with a fasting serum
glucose level.
There has been a recent
increase in the number of
infections caused by nonalbicans species. Up to
20% of infections maybe
caused by organisms
such as Candida tropicalis
and Torulopsis glabrata.
These organisms may be
resistant to standard
treatment regimens

Patients with monilial

vaginitis characteristically
complain of a thick,
white discharge and
extreme vulvar
pruritus. The vulva may
be red and swollen,
fissures may occur
Symptoms may recur and
be most prominent just
before menses or in
association with
intercourse
Yeast infections may
occur more frequently
during pregnancy
Patients with infections
caused by C. tropicalis
and T glabrata may have
an atypical presentation.
Irritation may be
paramount, with little
discharge or pruritus.

Diagnosis

Diagnosis is made by history,

physical examination, and
microscopic examination of the
vaginal discharge in saline and 10%
KOH.
On examination, excoriations of the
vulva may be noticeable; the vulva

Infection with C. tropicalis and

T glabrata may not be
associated with the classic
discharge; discharge may be
white-gray and thin.
#Vaginal pH may be normal or
slightly more basic than

Wet mount microscopic examination

reveals hyphae or pseudohyphae with
budding yeast in 50% to 70% of women
with yeast infections.
Cultures are not necessary to make the
diagnosis except in some cases of
recurrent infections.

and vagina may be erythematous,

with patches of adherent cottage
cheese-like discharge. Candidal
infections of the vulva are
characterized by classic satellite
lesions.

normal (4.0 to 4.7).

CANDIDAL VAGINITIS
Treatment

Many agents are available for the

treatment of vulvovaginal
candidiasis. These include topical
agents, which may be available
over the counter (OTC) or by
prescription, and oral agents, which
are available by prescription only.
1. Antifungal intravaginal agents
are administered as suppositories
or creams. These drugs are
available in three regimens: a
single dose, 3-day course, or 7-day
course. Agents include
butoconazole, clotrimazole,
miconazole, tioconazole, and
terconazole. OTC regimens should
be used only by women who have
been diagnosed with a yeast
infection in the past and are
experiencing identical symptoms.

Chronic yeast infection

2. Oral Agents:
Ketoconazole,
Fluconazole
Fluconazole is available as a
single-dose (150 mg)
treatment for uncomplicated
vaginal candidiasis.
-Ketoconazole is used
effectively for the treatment of
chronic and recurrent
candidiasis; a 5% incidence of
hepatotoxicity limits more
widespread use. The dosing
schedule is 200 mg twice a
day for 5 days, then 100 to
200 mg daily for 6 months
3. Boric acid capsules
intravaginally, 600 mg for
14 days, may be effective.

(5% of women). In most cases, no exacerbating

factor can be found; however, the following
possibilities should be considered
1-Failure to complete a full course of
therapy.
2-HIV infection. Recalcitrant candidiasis may be
a presenting symptom in women with HIV
infection. HIV testing should be considered and
offered to the patient.
3-Chronic antibiotic therapy.
4-Infection with a resistant organism such as
C. tropicalis or T glabrata.
5-Sexual transmission from the male
partner.
6-Allergic reaction to partner's semen or a

vaginal spermicide.
7-Diabetes. Patients should have a fasting
serum glucose level if they have recurrent
infections.

TRICHOMONAS VAGINALIS
Trichomonas vaginalis vaginitis (trichomoniasis) is the third most common vaginitis, accounting for 25% of cases.
Etiology

trichomonad can be recovered from 70% to 80% of the

male partners of the infected patient; therefore,
Trichomonas vaginitis is an STD.
#This infection is the most prevalent nonviral STD in the
United States (Van der Pol, 2005, 2007). Unlike other
STDs, its incidence appears to increase with age in some
studies. Trichomoniasis is more commonly diagnosed in
women because most men are asymptomatic. However,
up to 70 percent of male partners of women with vaginal
trichomoniasis will have trichomonads in their urinary
tract.

This parasite is usually a marker of high-risk sexual

behavior, and co-infection with other sexually
transmitted pathogens is common, especially Neisseria
gonorrhoeae. Trichomonas vaginalis has predilection for
squamous epithelium, and lesions may increase
accessibility to other sexually transmitted species.
Vertical transmission during birth is possible and may
persist for a year.

TRICHOMONAS VAGINALIS
Clinical presentation

Diagnosis

Trichomonas vaginitis is a multifocal infection involving

the vaginal epithelium, Skene glands, Bartholin glands,
and urethra.
No symptoms may be noted in up to one-half of women
with trichomoniasis. However, in those with complaints,
vaginal discharge is typically described as foul, thin, and
yellow or green. Additionally, dysuria, dyspareunia,
vulvar pruritus, and pain may be noted. At times,
symptomatology and physical findings are identical to
those of acute pelvic inflammatory disease.
Laboratory tests
1-The vaginal pH is usually between 5.0 and 7.0.

2-Saline wet mount of the vaginal discharge reveals

numerous leukocytes and the highly motile, flagellated
trichomonads (as many as 75% of cases).
3-Cultures are not usually necessary to make the diagnosis.
They should be obtained when the diagnosis is suspected
but cannot be confirmed by wet mount examination.

4-Pap smears may be positive in as many as 65% of cases.

Positive Pap smears should be confirmed by wet mount
examination because of the high false-positive rate.

Incubation with T vaginalis requires 3 days to 4 weeks,

and the vagina, urethra, endocervix, and bladder can be
infected, such colonization may persist for months or
years in some women.
With trichomoniasis, the vulva may be erythematous,
edematous, and excoriated. The vagina contains the
above-described discharge, and subepithelial
hemorrhages or "strawberry spots" may be seen on the
vagina and cervix. Trichomoniasis is typically diagnosed
by microscopic identification of parasites in a saline
preparation of the discharge.
Trichomonads are anteriorly flagellated, and therefore
mobile, anaerobic protozoa. They are oval and slightly
larger than a white blood cell (WBC). Trichomonads
become less motile with cooling, and slides should be
read within 20 minutes. Inspection of a saline preparation
is highly specific, yet sensitivity is not as high as hoped
(60 to 70 percent). In addition to microscopy, vaginal pH
is often elevated
The most sensitive diagnostic technique is culture, which
is impractical because special media (Diamond media) is
required and few laboratories are equipped. Moreover,
nucleic acid amplification tests (NAAT) for trichomonal
DNA are sensitive and specific, but not widely available.
Alternatively, the OSOM Trichomonas Rapid Test
(Genzyme, Cambridge, MA) is an
immunochromatographic assay, which has 88 percent
sensitivity and 99 percent specificity. It is available for
office use, and results are available in 10 minutes
(Huppert, 2005). Trichomonads may also be noted on Pap
smear screening and sensitivity approximates 60 percent.
Women with trichomonal infection should be tested for
other sexually transmitted infections. Additionally, sexual
contact(s) should be evaluated or referred for evaluation

TRICHOMONAS VAGINALIS
Treatment

Because Trichomonas is sexually transmitted, both partners require therapy; 25% of women will be reinfected if their
partner does not receive treatment.
A-Vaginal therapy alone is ineffective because of the multiple sites of infection, and systemic agents are necessary.
B-If both partners are treated simultaneously, cure rates of 90% are achieved with treatment with metronidazole. Patients
should be warned that a disulfiram-like reaction may occur and that they should abstain from alcohol use during treatment.
1-The preferred regimen is 2g in one dose because of ease of compliance. As many as 10% of patients may experience
vomiting.
2-An alternative regimen is 500 mg twice daily for 7 days.
C-Resistant cases may require treatment with intravenous metronidazole. Because resistance is rare, other causes, such as
noncompliance of the patient or partner, should be considered.
D-Metronidazole is contraindicated for use during the first trimester of pregnancy. After this time, it can be used to treat
Trichomonas infections.
E-Infected patients should be screened for other STDs.
BACTERIAL VAGINOSIS
Bacterial vaginosis is the

Etiology

Risk factors

most common vaginal

infection in the United States
today. In the past, bacterial
vaginitis was known as
nonspecific vaginitis and
Gardnerella vaginitis.

Bacterial vaginosis is a
polymicrobial clinical syndrome
caused by an overgrowth of a
variety of bacterial species,
particularly anaerobes, often
found normally in the vagina.
Organisms most often involved
include Bacteroides,
Peptostreptococcus, Gardnerella
vaginalis, and Mycoplasma
hominis.
The anaerobic bacteria produce
enzymes that break down
peptides to amino acids and
amines, resulting in compounds
associated with the discharge
and odor characteristic of this
infection.

This condition is not considered by the Centers

for Disease Control and Prevention (CDC)
consensus group to be a sexually transmitted
disease (STD), and it is seen in women without
previous sexual experience. Many risk factors,
however, are associated with sexual activity, and
an increased risk of acquiring STDs has been
reported in affected women
1-Oral sex
2-Douching
3-Black race
4-Cigarette smoking
5-Sex during menses
6-Intrauterine device
7-Early age of sexual intercourse
8-New or multiple sexual partners
9-Sexual activity with other women

BACTERIAL VAGINOSIS
Clinical presentation

Diagnosis

Fifty percent of women

with bacterial vaginosis
are asymptomatic.
In symptomatic patients,
the most common
presentation is a
malodorous, gray
discharge.

Three of the following four criteria must be present:

A-The vaginal pH is generally between 5.0 and 5.5.
B-Wet mount preparations with saline reveal a CLUE CELL background with minimal or no
leukocytes, an abundance of bacteria, and the characteristic clue cells. The clue cells are
squamous cells in which coccobacillary bacteria have obscured the sharp borders and
cytoplasm.
C-Application of 10% KOH to the wet mount specimen produces a fishy odor, indicating a
positive WHIFF test.
D-A gray, homogenous, malodorous discharge is present

Treatment
Therapy is based on the use of agents with anaerobic activity and involves both topical and systemic agents. The
combination appears to be 90% effective
A-Vaginal preparations:
1-Intravaginal 2% clindamycin cream is used at bedtime for 7 days.
2-Intravaginal metronidazole is applied once a day for 5 days.
B-Oral regimens:
1-Metronidazole may be administered two ways: 500 mg twice daily for 7 days or a single, 2-g dose.
2-Clindamycin, 300 mg twice daily for 7 days (may be associated with diarrhea, especially Clostridium difficile)
C-Sexual partners should be treated in cases of repeated episodes of bacterial vaginosis. Routine treatment
of partners has not been shown to improve cure rates or lower reinfection rates.
D-Treatment during pregnancy is critical; data suggest an association of adverse maternal and fetal
outcomes with bacterial vaginosis.

1-Clindamycin may be used throughout pregnancy.

2-Metronidazole may be used after the first trimester.
E-Patients with recurrences should be screened for STDs

PREVENTION

To help prevent and treat

vaginal discharge:
1-Keep your genital area
clean and dry.
2-Do not douche. While
many women feel cleaner if
they douche after
menstruation or intercourse,
it may actually worsen
vaginal discharge because it
removes healthy bacteria
lining the vagina that are
there to protect you from
infection. It can also lead to
infection in the uterus and
fallopian tubes, and is never
recommended.
3-Use an over-the-counter
yeast infection treatment
cream or vaginal
suppository, if you know
that you have a yeast
infection.
4-Eat yogurt with live
cultures or take
Lactobacillus acidophilus
tablets when you are on
antibiotics to avoid a yeast
infection.

5-Use condoms to avoid

catching or spreading
sexually transmitted
diseases.
6-Avoid using feminine
hygiene sprays, fragrances,
or powders in the genital
area.
7-Avoid wearing
extremely tight-fitting
pants or shorts, which may
cause irritation.
8-Wear cotton underwear
or cotton-crotch
pantyhose. Avoid
underwear made of silk or
nylon, because these
materials are not very
absorbent and restrict air
flow. This can increase
sweating in the genital area,
which can cause irritation.
9-Use pads and not
tampons.
10-Keep your blood sugar
levels under good control
if you have diabetes

If the discharge is caused by

a sexually transmitted
disease, your sexual
partner (or partners)
must be treated as well,
even if they have no
symptoms. Failure of
partners to accept treatment
can cause the infection to
keep coming back and may
lead to pelvic inflammatory
disease or infertility.

Also call if:

Call your doctor rightaway if:

#Your symptoms worsen or

last longer than 1 week
despite home care
measures.

#Your discharge is
associated with fever or pain
in your pelvis or abdomen.
#You have been exposed to
a sexual partner with
gonorrhea, chlamydia, or
other sexually transmitted
disease.
#You have increased thirst or
appetite, unexplained weight
loss, increased urinary
frequency, or fatigue - these
may be signs of diabetes

#A child who has not

reached puberty has vaginal
discharge.
#You think that your
discharge may be related to
a medication.
#You are concerned that you
may have a sexually
transmitted disease or you
are unsure of possible
exposure.

#You have blisters or other

lesions on your vagina or
vulva (exterior genitalia).
#You have burning with
urination or other urinary
symptoms -- you may have a
urinary tract infection.