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O&G Compendium

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100% found this document useful (1 vote)
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O&G Compendium

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walefamous
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© © All Rights Reserved
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O&G COMPENDIUM

Olufemi Aworinde MBBS (Ogb)


Senior Registrar,
Department of Obstetrics and Gynaecology,
Obafemi Awolowo University Teaching Hospital Complex,
Ile-Ife, Osun state.

1
DEDICATION
This book is dedicated to the memory of my dear
friend Paulinus Omolere, whom I started residency
with but did not live to write his exams.

2
Acknowledgement
I am highly indebted to my dear wife
Omokehinde, who was there for me while
writing this compendium. My kids Darasimi
and Damilare who did not mind my
absence from home and my good friend
Marcel whose contributions and criticisms
were invaluable.
To everybody that contributed to this
compendium in one way or the other I say
thank you. 3
Foreword
While reading for my Part I examination, I realised the need
for a quick reference soft ware/hard copy for the topical
issues in Obstetrics and Gynaecology including definitions.
This led to the compilation of this materials as I read along.

It is a product of detailed internet search, morning review


jottings, extracts from update course materials and
departmental presentations.

I hope it would be a useful guide for medical and


postgraduate students alike. Comments and contributions
would be highly appreciated. Olufemi Aworinde
16th May, 2011 4
Lie: Refers to the relationship of the longitudinal axis
of the fetal spine to the longitudinal axis of the
uterus.
Presentation: Refers to the pole of the fetus overlying
the pelvic brim or occupying the lower uterine
segment.
Presenting part: part of the presentation that is felt
on vaginal examination (lowest part of a fetus
palpable on vaginal examination)
Malpresentation: any presentation other than vertex.
Unstable lie: occurs when there’s repeated change in
fetal lie and presentation at least on two occasions on
consecutive visits after 36weeks. 5
Attitude: The relationship of the different parts of a
fetus to one another in terms of flexion and
extension.
Position: The relationship of a reference point on the
fetal presenting part (denominator) to a fixed part
on the maternal pelvis.
Descent: The proportion of the fetal head palpable
above the pelvic brim.
Station: the relationship of the presenting part to the
maternal ischial spine.
Engagement: occurs when the widest diameter of the
presenting part has passed thru the pelvic brim.
6
•Caput succedaneum: oedema over the presenting
part of the head, crossing the suture lines.
(Cephalhaematoma is due to haemorrhage and is
limited by suture lines)
•Moulding: reduction in fetal skull diameter due to
relative movt across suture lines as it passes thru the
birth canal.
1+: reduction in gap btw suture lines with no overlap
2+: bony overlap along suture lines that are digitally
reducible
3+: bony overlap along suture lines that are not
digitally reducible
7
Grading of meconium stained liquor
1- diluted by a large volume of amniotic fluid; lightly
stained by meconium.
2-reasonable amount of amniotic fluid; with a heavy
suspension of meconium.
3- thick meconium ; undiluted with amniotic fluid.
*No AF has same risk as grade 3

• Mechanism of labour: series of changes in attitude


and position the fetus undergoes as it passes thru
the birth canal. (DEFIERE)
8
• Synclitism: relationship of the sagittal suture to the
plane of the inlet of the pelvis and to the sacrum
posteriorly and the symphysis pubis antly when the
fetal head is in the transverse position.
• Vertex: Area of the fetal skull bounded by the AF,
PF and laterally by the parietal eminences.
• Vertex presentation: area of the well flexed head
occupying the lower uterine pole.
• Crowning: when the largest diameter of the fetal
head has passed thru the pelvic outlet and does
not recede in btw contraction.

9
Fontanelle
• Posterior fontanelle, the two parietal bones adjoin
the occipital bone (at the lambda) triangular.
• Anterior fontanelle where the two frontal and two
parietal bones meet, diamond-shaped 
Two smaller fontanelles are located on each side of
the head, making 6 in all.
• More anteriorly the Sphenoidal fontanelle
(between the sphenoid, parietal, temporal, and
frontal bones)
• More posteriorly the Mastoid fontanelle(between
the temporal, occipital, and parietal bones).
10
Gynaecoid pelvis
Anteroposterio Oblique Transverse
diameter diameter diameter(cm)
Inlet 11 12 13.5
Midcavity 12 12 12
Outlet 13.5 12 11

Calculation of estimated fetal weight


• Ojwang’s rule:SFH x Abd girth at umbilical level(if <100cm)
• Johnson’s rule: {SFH – (11 or 12)} x155;
11 if engaged; 12 if unengaged
• 5% of booking maternal weight
• 10% of BMI
• USS estimation 11
Fetal Skull Measurements
Suboccipito-bregmatic (vertex) = 9.5cm
Suboccipito frontal diameter (Occipitoposterior) = 10cm
Occipitofrontal diameter (deflexed) = 11cm
Submento – bregmatic diameter (face) = 9.5cm
Occipito-mental = mento – vertical diameter (brow)
= 13cm

Vertex—96%; Breech---3-4%; Face---0.3%; Brow…rare;


Shoulder---0.4%
True conjugate: distance btw the upper border of the pubic
symphysis to the tip of sacral promontory (11cm).
Diagonal conjugate: dist btw the tip of sacral promontory
to the inferior border of the pubic symphysis (12.5cm).
Obstetric conjugate: distance from the tip of the sacral
promontory to the midpoint on the body of symphysis
pubis which is about 1cm below its upper border. It is the
shortest anteroposterior diameter (10.5cm).
External conjugate: from the depression below the last
lumbar spine to the upper anterior margin of the symphysis
pubis measured from outside by the pelvimeter . It does
not have a true obstetric importance (20cm).

13
• In the erect position,
the brim is normally
inclined at 60o .
• In Negroid women,
the angle of
inclination approach
90o - steep inclination
of the brim. The head
may be slow to engage
during labour.
• The pelvic outlet is
inclined at about 25 o
to the horizontal. 14
Angle of inclination: the angle sustained by an
imaginary line drawn btw the sacral promontory and
the upper border of the pubic symphysis and a line
drawn to the horizontal from the upper part of the
pubic symphysis.
Waste space of Moro: Space btw the sub pubic angle
and the fetal head during its passage thru the outlet.
High assimilation pelvis: Sacralisation of L5; angle is
btw L4 & L5; results in a deep pelvis.
Low assimilation pelvis: Lumbarlisation of S1; angle in
btw S1 & S2; results in shallow pelvis
Naegele’s pelvis- defective development of one side of the ala
of sacrum while both are defective in Robert pelvis. 15
MECHANISM OF NORMAL LABOUR
• Traditionally mechanism of labour has been focused on
3 participants viz- Powers( uterine contraction), passage
(birth canal), Passenger (fetus)
Cardinal points of mechanism of labour consists of:
• Descent
• Flexion
• Engagement
• Internal rotation
• Extension
• Restitution
• External rotation
Its pertinent to note that descent occurs throughout labour as a
prerequisite for birth of the baby.
• In the first stage and phase 1 of the
second stage of labour, descent is
dependent on the force of uterine
contractions.
• This means that descent would be
optimal when contractions are strong and
appropriate throughout 1st and 2nd stages
of labour.
• In phase 2 of 2nd stage labour descent is
facilitated by the voluntary use of
abdominal wall muscles.
ENGAGEMENT
• The head normally enters the pelvis in the transverse
position, so taking advantage of the widest diameter.
• Engagement is said to have occurred when the widest
part of the presenting part has successfully passed
through the inlet
• Engagement would have occurred in the vast majority of
white nulliparous women prior to labour but not so for
the majority of multiparous women.
• The number of fifths of the fetal head palpable per
abdomen is often used to describe whether engagement
has taken place. If more than two-fifths is palpable head is
not yet engaged.
flexion
• The fetal head may not be completely flexed when it
descends in to the pelvis.
• But when the head enters the narrower mid cavity, the
rigid pelvic floor muscles forces the chin in to contact
with the fetal thorax during contractions to create a
consequential flexion of the head.
This is because:
1 Any ovoid body being pressed through a tube tends to
adapt its long diameter to the long axis of the tube.
2 Of the so-called head lever.
The occipitospinal joint is nearer to the occiput than to the
sinciput, so the head can be regarded as a lever with a long
anterior and a short posterior arm.
When the breech is pressed on by the uterine fundus,
the fetus is subjected to axial pressure and the lever
comes in to play.
The long anterior arm meets with more resistance
than the short posterior arm and the head flexes.
• This produces a smaller diameter of presentation,
changing the occipito-frontal diameter of 11.5cm to
the suboccipito-bregmatic diameter of 9.5cm
• When contractions are weak or poor, this flexion
may not occur fully and the subsequent processes
in the MOL may not occur normally
Internal rotation
• As the head is flexed in its descent in to
the pelvic gutters, so also it has to
rotate from the lateral plane in which it
entered the pelvis in to the AP direction
because the pelvic outlet which the
head now approaches, has a much
wider AP than the transverse diameter.
• In a well flexed head,the leading
occiput is forced in to the AP direction.
Extension
• Following internal rotation and with further
descent,the sharply flexed head descends in to the
vulva and the base of the occiput comes in to
contact with the inferior rami of the pubis and the
bregma is near the lower border of the sacrum.
• With further push and descent,the only direction is
for the head to extend because the pubic rami acts
as a pivot and the head begins to crown.
• Delivery of the head occurs with the occiput often
directly anterior.
• RESTITUTION: When the head is delivering the
occiput is directly anterior.As soon as it escapes
from the vulva the head realigns itself with the
shoulders which has entered the pelvis in the
obligue position
• This slight rotation of the occiput through one-eight
of a circle is called restitution.
• EXTERNAL ROTATION:As the shoulder hit the pelvic
floor, it rotates into the roomy anteroposterior
plane as away to facilitate their delivery.
• The occiput also rotates through a further one-eight
of a circle to the transverse position so that the face
now looks at the maternal thigh.
DELIVERY OF THE SHOULDERS
• -Following restitution and external rotation, the
shoulder now at the outlet in A – P direction with
the anterior shoulder being under the pubic
symphysis.
• The anterior shoulder is delivered first followed by
the posterior shoulder
• DELIVERY OF THE FETAL BODY: After the delivery of
the shoulders, the fetal body is delivered easily,
aided by lateral movement.
Mechanism of labour in the occipito-
posterior position.
• The mechanism in this position,depends on the degree
of flexion,the strenght of uterine contractions,the tone
of the pelvic floor muscles and adequacy of the pelvis.
THE WELL FLEXED HEAD.
• If the head is well flexed (80%of OP),the occiput will be
in advance when the head meets the resistancs of the
pelvic floor.
• The occiput slides down the gutter formed by the
levator muscles,undergoing a long rotation through
three-eight of a circle,to reach the free space under the
pubic arch.
The long anterior arm meets with more resistance than
the short posterior arm and the head flexes.
This produces a smaller diameter of
presentation,changing the occipito-frontal diameter of
11.5cm to the suboccipito-bregmatic diameter of 9.5cm
When contractions are weak or poor,this flexion may not
occur fully and the subsequent processes in the MOL may
not occur normally
In the ROP positon,it rotates along the right side of the
pelvis to reach the front,the shoulders rotating with the
head from the left oblique diameter in to the AP
diameter.
From this point,the mechanism is the same as that of the
ROA position with the birth of the head by extension.
THE INCOMPLETELY-FLEXED HEAD
• When the occiput occupies the posterior part of one of
the oblique diameters of the pelvis, the BPD lies in the
bay to one side of the promontory
• When the head is pushed down into the pelvis in this
position, the BPD is hindered in descending if the pelvis
is small or the head is large and so the sinciput
descends more easily than the occiput and the head
enters the pelvis incompletely flexed.
• In this position, the larger occipito-frontal
diameter(11.5cm), has to pass thru the pelvis instead of
the suboccipito-bregmatic(9.5cm)
• Neither the occiput nor the sinciput is sufficiently in
advance of the other to influence rotation, so some
cases of OPP cause difficult and prolonged labor.
• However, delivery can take place by an alternative
mechanism viz- if the head is incompletely flexed
with an OPP the sinciput is as low as the occiput
and being at the anterior end of the oblique
diameter of the pelvis it meets the resistance of the
pelvic floor b4 the occiput.
• The sinciput rotates anteriorly to the free space
under the pubic arch turning thru 1/8th of a circle,
and the occiput posteriorly into the hollow of the
sacrum.
• The head may now be delivered with the face
towards the posterior surface of the symphysis
pubis
• The root of the nose is pressed against the bone
and head flexes abt this fixed point.
• Vertex is deliverd by flexion follwed by the occiput,
then the head extends with the face and chin
emerging from under the pubic arch.
DEEP TRANSVERSE ARREST OF THE HEAD
• In some cases the head becomes arrested with its
long axis in the transverse diameter at the level of
the ischial spines, the degree of extension being
such that neither the occiput nor synciput is
sufficiently advanced to influence rotation.
• Some of these cases are the result of an
incomplete ant rotation from an OPP
• Others, perhaps the majority, are the result of
descent of the head which originally lay in the
occipito-transverse position and failed to rotate
anterioirly.
MECHANISM OF LABOUR IN BREECH
• Four positions of the breech are conventionally
described:
1. Left sacroanterior 2. Rt sacroanterior
3. Rt sacroposterior 4. Lt sacroposterior
• In most cases, the bitrochanteric diameter(10cm)
engages in the transverse diameter of the brim with the
back to the front.
• During labor the breech descends into the pelvic cavity
and internal rotation brings the bitrochanteric diameter
into the AP diameter of the outlet
• The breech is born by lateral flexion of the trunk, the
anterior buttock appearing first.
• This movement is determined by the curve of the birth
canal and the more flexion is necessary with a rigid
perineum. It was initially thought that if the legs were
extended this splinted the trunk and prevented lateral
flexion, this is not the case.
• The frank breech usually descends easily, its conical
shape makes it a better dilator of the cervix than the
rounded head.
• The rest of the trunk is born by further descent
together with the arms which normally remains flexed
in front of it.
• The ant shoulder emerges 1st under the pubic arch
quickly followed by the posterior shoulder
• Pregnancy (gestation) is the maternal condition of having a
developing fetus in the body.
• The human conceptus from fertilization through the eighth
week of pregnancy is termed an embryo; from the eighth
week until delivery, it is a fetus.
• Gestational age: the estimated age of the fetus is
calculated from the first day of the last (normal) menstrual
period (LMP), assuming a 28-day cycle. Gestational age is
expressed in completed weeks.
• This is in contrast to developmental age (fetal age), which
is the age of the offspring calculated from the time of
implantation.
• The term gravid means pregnant, and gravidity is the total
number of pregnancies (normal or abnormal).
33
• Parity is the state of having given birth to an infant or
infants weighing 500 g or more, alive or dead. In the
absence of known weight, an estimated duration of
gestation of 20 completed weeks or more (calculated from
the first day of the LMP) may be used; a multiple birth is a
single parous experience.
• Live birth is the complete expulsion or extraction of a
product of conception from the mother, regardless of the
duration of pregnancy, which, after such separation,
breathes or shows other evidence of life (e.g., beating of
the heart, pulsation of the umbilical cord, or definite
movements of the involuntary muscles) whether or not the
cord has been cut or the placenta attached. (WHO 1950)
• An infant is a live-born individual from the moment of birth
until the completion of 1 year of life 34
• Birth rate is the number of live births per 1000 population.
• fertility rate is the number of live births per 1000 women
ages 15–49 years
• Neonatal interval is from birth until 28 days of life.
• Neonatal period I: birth through 23 hours, 59 minutes.
• Neonatal period II: 24 hours of life through 6 days, 23
hours, 59 minutes.
• Neonatal period III: seventh day of life through 27 days, 23
hours, 59 minutes.
• The perinatal period is the time from 28 weeks of
completed gestation to the first 7 days of life, spanning the
fetal and early neonatal interval.

35
• Presumptive Manifestations
Symptoms
• Amenorrhea
• Nausea and Vomiting
• Breasts
-Mastodynia, or breast tenderness, may range from tingling
to frank pain caused by hormonal responses of the
mammary ducts and alveolar system.
-Enlargement of Montgomery's Tubercles
-Colostrum secretion may begin after 16 weeks' gestation.
-Secondary breasts may become more prominent both in size
and in coloration..
• Quickening
• Urinary Tract: Bladder Irritability, Freq, and Nocturnal, UTI
36
Signs
• Increased Basal Body Temp: Persistent elevation of basal
body temperature over a 3-week period usually indicates
pregnancy if temperatures have been carefully charted.
• Skin- Chloasma, Linea Nigra, Stretch Marks, Spider
Telangiectases

• Probable Manifestation
• Symptoms are the same as those discussed under
Presumptive Manifestations, above.
• Signs
• Pelvic Organs
• Chadwick's Sign: Congestion of the pelvic vasculature
causes bluish or purplish discoloration of d vagina & cervix.
37
• Leukorrhea: increase in vaginal discharge consisting of
epithelial cells and cervical mucus due to hormone
stimulation. Cervical mucus that has been spread on a glass
slide and allowed to dry no longer forms a fernlike pattern
but has a granular appearance.
• Hegar's Sign: widening of the softened area of the isthmus,
resulting in compressibility of the isthmus on bimanual
examination. This occurs by 6–8 weeks.
• Bones and Ligaments of pelvis: There is slight but definite
relaxation of the joints. Relaxation is most pronounced at
the pubic symphysis, which may separate to an astonishing
degree.
• Abdominal Enlargement: progressive from 7–28 weeks. At
16–22 weeks, growth may appear more rapid as the uterus
rises out of the pelvis and into the abdomen 38
• Uterine Contractions: Braxton Hicks contractions are felt as
tightening or pressure; usually begin at about 28 weeks and
increase in regularity; disappear with walking or exercise.
Positive Manifestations
• Fetal Heart Tones: It is possible to detect FHT by hand held
Doppler as early as 10 weeks' gestation. It may be detected
by fetal stethoscope by 20 weeks' gestation.
• Palpation of Fetus: After 22 weeks, the fetal outline can be
palpated through the maternal abd wall. Fetal movts may
be palpated after 18 weeks. This may be more easily
accomplished by a vaginal examination.
• Ultrasound : Cardiac activity is discernible at 5–6 weeks,
limb buds at 7–8 weeks, and finger and limb movements at
9–10 weeks. At the end of the embryonic period (10 weeks
by LMP), the embryo has a human appearance. 39
• Pregnancy Tests: hCG is produced by the syncytiotrophblast
8 days after fertilization and may be detected in the
maternal serum after implantation occurs, 8–11 days after
conception; in urine by first missed period.
• Levels peak at 10–12 weeks of gestation; gradually decrease
in the 2nd& 3rd trimesters and increase slightly after 34 wks.
• The half-life of hCG is 1.5 days. After termination of
pregnancy, levels drop exponentially. Normally, serum and
urine hCG levels return to nonpregnant values (< 5 mIU/mL)
21–24 days after delivery.
• Urine pregnancy test is qualitative—+ve or -ve, based on
color change, with the level of hCG detectn btw5-50 mIU/mL
• Can be detected in the serum as early as a week after
conception. Serum preg test can be quantitative or
qualitative with a threshold as low as 2–4 mIU/mL 40
GROWTH OF THE PLACENTA
• Implantation starts day 6-7 and ends on day 10-12
• By the 12th week, the placenta has achieved its definitive
form and thickness. Further growth is circumferential.
• Initially, the placenta grows faster than the fetus and hence
larger
• By the 17th week, the weight of the placenta is equal to
that of the fetus
• By term, the weight of the placenta is 1/6th of that of the
fetus.
• It covers approximately 15-30% of the internal surface of
the uterus.
• Nitabuch’s Layer: A layer of continuous fibrinoid deposit at
the interphase where the trophoblast meets the decidua
basalis
CHANGES IN THE RELATIVE COMPOSITION OF THE PLACENTA
WITH GROWTH
• First Trimester: Large villi, rich in both syncitio- and
cytotrophoblasts
• Mid Trimester: Smaller villi. Less Cytotrophoblast
• Third Trimester: Much smaller villi. Very few
cytotrophoblastic cells (inconspicuous cytotrophoblast).
• The definitive placenta develops from both fetal and
maternal origins. However, at term, 4/5th of the placenta is
of fetal origin.
• Normal Anatomical Changes in the Placenta at Term include
Evidence of Infarction, Intervillous thrombosis and
Calcification.
• Functions are Respiratory, Excretory, Nutritional, Endocrine
ANATOMY OF THE PLACENTA
Type Haemochorial or Choriodecidual
Shape Discoid
Diameter 15-25cm
Thickness About 3cm
Weight 500-600g
No. of Lobes 15-20
No. of Surfaces 2- Maternal and Fetal.
Blood Supply Spiral arterioles terminate at the
orifices of the intervillous space
Umbilical Cord Inserted centrally.
Abnormalities Description

1. Circumvallate Placenta With central abnormal double folds of


amnion and chorion
2. Succenturiate Placenta Accessory lobe
3. Battledore Placenta Marginal insertion of the cord
4. Placenta Membranacea Villi of the chorion leave persist due
to unusual vascularisation. Hence,
the entire fetal envelope is
functioning placenta.
Morbidly adherent
placenta
a. Placenta accreta Abnormal trophoblastic invasion
beyond the Nitabuch's layer.
b. Placenta increta Invasion into the myometrium.
c. Placenta percreta Invasion through the serosa

44
The connective tissue of the umbilical cord is called
“ Wharton’s Jelly” and is derived from the primary
mesoderm.
Wharton’s jelly is a loose myxomatous tissue of
mesodermal origin.
This acts as a physical buffer and prevents kinking of
the cord and interference with circulation.
The amnion arises as a layer of epithelial cells btw
the ectodermal layer of the inner cell mass and the
trophoblast. Amniotic cavity is formed by day 7-8
It differentiates into 5 strata with further
development- Cuboidal epithelium, Basement
membrane, Compact, fibroblast & Spongy Layer. 45
Formation of amniotic fluid
Sources of Amniotic Fluid Route of amniotic fluid
loss
 Secretions from amniotic epithelial Swallowing by the
cells (in early embryonic life) fetus
 Decidual secretions (diffuses across
the amniochorionic membrane)
 Diffusion of fluid through the fetal
skin (reduceses with keratinisation)
 Secretion by the umbilical cord.
 Fetal urine (450-500ml per day at
term).
 Fetal respiratory tract secretions.

46
Amniotic fluid volume
EGA (weeks) Volume (mls)
10 30
15 150
20 300
30 600 - 750
36 900
38 1000
40 850
42 350
47
Oligo/polyhydramnios
Oligohydramnios Polyhydramnios
Amniotic fluid ≤400mls ≥2000mls
volume
Single vertical ≤2cm ≥8cm
pocket of AF
Amniotic fluid ≤5 ≥25
index

Poly hydramnios: Multiple pregnancy, Rh Isoimmunisation,


Hydrops fetalis, Aneceplaly, Oesophageal atresia,Duodenal atresia
Oligohydramnios: IUGR, Renal agenesis, Preeclampsia
48
• The chorion leave {has 4 strata-Fibroblast/ cellular
layer, Reticular Layer, Basement Membrane
&Trophoblast (2-10 cells thick)} is pushed against
the opposite wall of the uterus in the 4th month
• The decidua parietalis and capsularis fuse→
Obliteration of the original uterine cavity.
• The villi of the chorion leave atrophy,
• The amnion and chorion fuse to form the 2-layered
fetal (amniochorionic) membranes.
**The fetal membranes are devoid of blood vessels,
lymphatics and nerves.

49
USS pearls
• Diagnosis of an empty GS can only be made when
the mean GS diameter is >20 mm and CRL must be
≥6 mm before one can say for certain that fetal
heart activity is absent. If measurements are below
these thresholds a repeat TVS after at least a week
or TAB after 2weeks should be offered

Variable TVS picks it at TAB picks it at


Gestational sac 5weeks 6weeks
Fetal node 6weeks 7weeks
Fetal heart 7weeks 8weeks

50
• Preconception care: Specialised form of care given
to a woman of reproductive age group before onset
of pregnancy to detect, counsel or treat preexisting
medical and social conditions that may militate
against safe motherhood and the delivery of a
healthy infant.
Elements of pre-conception care
• Comprehensive health history: past medical, past
obstetric, drug and social history
• Thorough physical examination
• Ancillary screening tests
• Health promotion/intervention
51
Advantages of Pre-conception Care

• Improved pregnancy outcome


- improved maternal health
- significant reduction in neonatal
morbidity/mortality

• Cost-effectiveness

• Opportunity for counseling/health promotion

52
Obstacles to Pre-conception Care

• Lack of information
• Poor attitude by womenfolk
• High rates of un-planned
pregnancies
• Low level of acceptance by health
care providers
53
• Antenatal care: 1) Specialised pattern of care organised
for pregnant women to enable them attain and
maintain a state of good health throughout preg and to
improve their chance of having safe delivery of healthy
infants at term. (At least 1visit- 61%; 4+visits 47.4% in
Nigeria NDHS 2005)
• 2) Planned program of information, education and
medical mgt of the preg woman aimed at making preg
and childbirth a safe and satisfying experience

• Focused antenatal care: An evidence based, goal


oriented, family centred pattern of care with emphasis
on quality over quantity of care for the achievement of
safe motherhood. 54
• Antenatal care coverage (at least one visit) is the
percentage of women aged 15-49 with a live birth in
a given time period that received antenatal care
provided by skilled health personnel (doctors,
nurses, or midwives) at least once during
pregnancy, as a percentage of women age 15-49
years with a live birth in a given time period.
• Antenatal care coverage (at least four visits) is the
percentage of women aged 15-49 with a live birth in
a given time period that received antenatal
care four or more times with ANY provider
(whether skilled or unskilled), as a % of women age
15-49 years with a live birth in a given time period.
55
Aims of ANC
• Identification of pre-existing health conditions
• Screening /prevention of maternal problems
• Screening/prevention of fetal problems
• Management of maternal problems
• Management of fetal problems
• Preparation of the couple for childbirth and
childrearing
Booked woman: A woman is said to be booked if she
has had at least 2 antenatal visits or has had the
results of her investigations reviewed and has been
classified to high or low risk. If only one visit she is
registered. 56
Goals of Focused ANC

57
Prenatal diagnosis: It is the science of identifying
structural and functional abnormalities in the
developing fetus through invasive and non-invasive
techniques.
Genetic counselling: Is the screening procedure
designed to identify the individual having a greater
risk of producing an offspring with genetic
abnormalities.
Maternal serum alpha-fetoprotein (MSAFP): Done
15-18wks. 2.5 multiples of the median(MOM) when
adjusted to maternal weight, is taken as cut off point.
Triple test: AFP, hCG & uE3
Quadruple test: AFP, hCG, uE3 & inhibin A 58
Integrated test: Nuchal translucency (NT) + Preg
associated plasma protein (PrAP-A) in 1st trimester
+Quadruple test in 2nd trimester

Combined test: NT+ PrAP-A + free hCG + woman’s age

Nuchal translucency: sonographic measurement of


the subcutaneous collection of fluid in the nuchal
region of the fetus at 10- 13wks GA. Normal ≤3mm
and 6 mm for 1st and 2nd trimesters. Taken from
outer aspect of the occipital bone to the outer
aspect of the skin, and the section should pass via
the cerebellum and the cisterna magna. 59
Diagnostic Tests
Non Invasive Invasive

Maternal Serum Testing Amniocentesis

Ultrasonography & Foetal Chorionic Villus Sampling


Echocardiography (CVS)
Fetal Cells from Maternal Percutaneos Umbilical
Blood Blood Sampling
Preimplantation diagnosis Foetoscopy / Endoscopy

Foetal Tissue Sampling


USS “Soft Markers” of Chromosomal
Abnormalities:
• Common Markers:
Nuchal translucency
Hyperechogenic bowel
Choroid plexus cyst
Renal pelvi-calyceal dilatation
Cardiac echogenic foci
Short femur or humerus
2-vesel umbilical cord
USS “Soft Markers”
• Less Discriminatory Markers:
Sandal gap
Short ear length
Ventricular dilatation
5th digit mid phalanx hypolasia
Increased iliac length
short frontal lobe
ÞMajor structural abnormality: Significant ground to
offer Amniocentesis or CVS
ÞSoft Marker: Consider other factors before offering
Amniocentesis or CVS
Procedure Amniocentesis CVS PUBS

Gestation 15-40 10-40 20-40

Route TAB TAB/ TCER TAB

Cells sampled Fibroblasts Trophoblast Fetal WBC

Risk of 0.5-1% 1-3% 1%


miscarriage

DKR None 24-48hrs Not needed

CKR 2-3 weeks 1-2weeks 24-48hrs

Mosaicism None 1% None


rate
64
65
Physiuological changes in pregnancy
Uterus
 Increased size (7 cm/70 g ® 36 cm/1,100 g)
 Intraabdominal location after 12th week
 Thinning of muscular wall
 ↑ Blood flow (60 ml/minute ® 600ml/min)

Potential clinical consequences


 Increased susceptibility to injury
 Increased bleeding
 Compression of IVC in supine position 66
Genitourinary
 Dilated collecting system
 Displaced bladder intraabdominal
• ↑ renal blood flow 60-75%
• ↑ creatinine clearance 50% and GFR 50%
• ↓ glucose reabsorption
Potential clinical consequences
 Altered radiologic appearance and misdiagnosis
 Increased risk for injury
• Decreased BUN and serum creatinine
• Glucosuria
67
O&G: Olufemi Aworinde
Gastrointestinal
 Intestinal displacement into upper quadrant
 Decreased oesophageal sphincter tone.
 Peritoneal “stretching”

Potential clinical consequences


 Altered injury pattern
 ↓ peritoneal sensitivity &misleading P.E
 Increased risk for reflux and aspiration
68
O&G: Olufemi Aworinde
Gastrointestinal contd

• Decreased gastric emptying


• Increased gastric acid production
• Impaired gallbladder contraction

Potential clinical consequence


• Increased risk for acid reflux or aspiration
• Bile stasis or increased gallstone formation

69
O&G: Olufemi Aworinde
Respiratory
Elevated diaphragm (4 cm), ↑ excursion (1–2 cm)
Variable Change
PCO2 ↓ses 15-20%;
PO2 ↑ses 10%
Respiratory Rate ↑ses 15%

O2 consumption ↑ses 20%


FRC ↓ses 20%;
Tidal volume ↑ses 40%
Minute ventilation ↑ses 50%
Bicarbonate excretion ↑ses 70
Potential clinical consequence
• Altered anatomic landmark (e.g., misplaced
chest tube)
• ↓ Functional residual capacity (20%)
• Chronic respiratory alkalosis
• ↓ respiratory buffering capacity
• Altered response to inhalation anaesthetics
• Decreased tolerance of hypoxemia
71
Cardiovascular
Variable Change
Heart Rate ↑ses 10-20%;
Stroke Volume ↑ses 10%
PVR ↓ses 15%
Cardiac Output ↑ses 30-50%
BP (both sys & dias) ↓ses 5-15mmHg
MABP ↓ses 10%
Plasma volume ↑ses 45%
Blood volume ↑ses 30-50%

72
Haematologic
• ↓ haematocrit
• ↑WBC 18–25 WBC/mm3)
• ↑ Factor I, VII, VIII, IX, and X
• ↓ plasminogen activator levels

Potential clinical consequence


• Altered haematologic parameters
• Signs of ongoing hemorrhage delayed
• Hypercoagulability
73
Pituitary
Enlarged by 135%
Increased blood flow demands

Potential clinical consequences


Shock can cause necrosis of the anterior
pituitary gland, resulting in pituitary
insufficiency.
O&G: Olufemi Aworinde 74
Endocrine
Increased Progesterone and estrogen
↑sed prolactin concentration
↑sed corticosteroid concentration
Human growth hormone is supressed
Insulin resistance develops
↑sed transplacental calcium transport,
parathormone and calcitonin

75
O&G: Olufemi Aworinde
• Grandmultipara: woman who has carried 5 or more
pregnancies to the age of viability irrespective of the
outcome.
• Intermittent preventive therapy for malaria (IPT):
Administration of a therapeutic dose of an antimalarial to
an asymptomatic pregnant woman at predetermined time
and interval to prevent placental parasitization and
malaria in pregnancy. (Its given at least twice; 4weeks
apart from 16-36wks GA)
• Cervical incompetence: Cervical incompetence (CI) is the
inability of the cervix to maintain pregnancy to term due
to intrinsic structural or functional abnormalities.
• Partograph: graphical representation of the events in
labour 76
• Degree of resistance: Smears on day 2, 7,14 and 28 are
done to grade the resistance as R1 to R3.
• Sensitive (S): The asexual parasite count reduces to 25% of
the pre-treatment level in 48 hours after starting the
treatment and complete clearance after 7 days, without
subsequent recrudescence - Complete Recovery.
• RI, Delayed Recrudescence: The asexual parasitemia
(AP)reduces to < 25% of pre-treatment level in 48 hours,
but reappears between 14-28 weeks.
• RI, Early Recrudescence: The AP reduces to < 25% of pre-
treatment level in 48 hrs, but reappears earlier.
• RII Resistance: Marked reduction in AP (decrease >25% but
<75%) in 48 hrs, without complete clearance in 7 days.
• RIII Resistance: Minimal reduction in asexual parasitemia,
(decrease <25%) or an increase in parasitemia after 48 hrs.
77
Leopold's maneuvers
I: Fundus is palpated with the fingertips of both hands facing
toward the maternal xiphoid cartilage
II: the hands are placed at either side of the abd, the examiner
will be able to determine the location of the fetal back.
III: Using one hand, the examiner grasps the presenting part
btw the thumb and fingers (Paulik’s grip). This is done on the
lower abdomen, a few centimeters above the symphysis pubis.
This allows the examiner to develop a further identification of
the presenting part and assessment of its engagement. (This is
no more done or included)
IV: The examiner then faces the pelvis of the patient. The palm
of both hands are placed on either side of the lower abdomen,
with the fingertips facing toward the pelvic inlet. This allows
identification of the fetal parts in the lower pole of the uterus.
78
Estimated Date of Confinement (Näegele's Rule)
• Add 9months to the month of the LNMP, and
7days to the first day of the LNMP.
Example: With a LNMP of July 14, 2009; the EDD is
April 21, 2010. This rule is based on a normal 28-
day cycle. In women with a longer proliferative
phase, add to the first day of the LNMP the usual
7 days plus the number of days that the cycle
extends beyond 28 days and reverse for a shorter
proliferative period.
Prolonged Pregnancy: pregnancy at or beyond 42
completed weeks OR 294days or more from the
first day of Last menstrual period.(WHO/FIGO) 79
Ultrasound biometry margins of error
• Crown-rump length (CRL) till 12 weeks is 3-5 days,
• Biparietal diameter (BPD) at 12-20 weeks is 1 week,
• BPD at 20-30 weeks is 2 weeks, and
• BPD after 30 weeks is 3 weeks.
• If there is more than a ten days discrepancy between the
LMP and the ultrasound findings, the ultrasound data
should be used to determine the EDD.
• The use of early ultra­sound alone to calculate the rate of
postterm pregnancy in women who delivered
spontaneously significantly reduced the postterm rate
from 10 % to 1.5 %.
Transcerebellar diameter
• When composite biometry is not consistent in all of
the parameters (i.e. BPD, head circumference,
abdominal circumference, femur length), using the
transcerebellar diameter is a way to more
accurately date a pregnancy
• The diameter in millimeters corresponds
to weeks of gestation up to 24
weeks.
• Prelabour rupture of membranes: Leakage of
amniotic fluid thru the cervix in the absence of
uterine contractions irrespective of gestational age
• Preterm PROM: PROM < 37wk GA
• Term PROM: PROM ≥ 37 wk GA
• Latency interval: Time interval between PROM &
onset of uterine contractions ?1Hr
• Bad obstetric history: occurs if a woman has had at
least one previous adverse pregnancy or perinatal
outcome.
• High risk pregnancy: occurs when the likelihood of
adverse outcome is higher than in the general popn.
82
Bishop score (CPDES)
Parameters 0 1 2 3
Cervical dilatation 0 1-2 3-4 ≥5
Cervical length or >2cm 2-1 1-0.5 <0.5
Effacement <40% 40-50% 60-70% ≥80%
Station -3 -2 -1,0 <0
Consistency Firm Medium Soft
Position Posterior Central Anterior

*Modified BS used cervical length while original used


effacement. Used to assess the inducibility of the
cervix 83
• Labour: The process by which the fetus and
membranes are expelled through the birth canal
after the age of viability. It is xterised by regular,
painful, progressive uterine contraction leading to
cervical effacement and dilatation culminating in
descent of the presenting part and the eventual
delivery of the fetus and membranes.
• Normal labour: A retrospective diagnosis in which
there is spontaneous onset of uterine contraction at
term in a pregnancy with singleton fetus in vertex
presentation without operative intervention
leading to the delivery of the fetus and placenta
giving a well child and a satisfied mother.
84
• Trial of labour: Conduct of labour in a woman with
suspected borderline pelvis with the hope that with good
uterine contraction, flexion of the head and moulding
with pelvic give she will achieve vaginal delivery either
spontaneously or via assisted vaginal delivery.
• Induction of labour: artificial initiation of labour after the
age of viability with the aim of achieving vaginal delivery
• Failed induction: failure to achieve vaginal delivery
• Augmentation of labour: is the potentiation of an
ongoing labour.
• Prolonged labour:Active phase of labour lastn >12hrs.
• Stimulation of labour: membrane not intact b4 onset of
induction.
85
Active management of labour (AML): the strategic
approach to the management of labour already
established in the active phase aimed at preventing
prolonged labour based on anticipatn of normal
progress of the cervical os dilatatn of at least 1cm/
hour as the basis for the safe delivery of the mother
with no Cx to both mother and child. It involves:
 Early diagnosis of labour
 Artificial rupture of membrane once in active phase
 Partographic monitoring of labour
 Use of oxytocin especially in primigravida
 Adequate analgesia
 Companionship
 Review of indication for surgery by senior obstetrician
86
Theories of Onset of Labour
• It is unknown but the following theories were
postulated:
Hormonal factors
• Oestrogen theory:
– During pregnancy, most of the oestrogens are present in
a binding form. During the last trimester, more free
oestrogen appears increasing the excitability of the
myometrium and prostaglandins synthesis.
• Progesterone withdrawal theory:
– Before labour, there is a drop in progesterone synthesis
leading to predominance of the excitatory action of
oestrogens. 87
• Prostaglandins theory:
– Prostaglandins E2 and F2α are powerful
stimulators of uterine muscle activity. PGF2α was
found to be increased in maternal and foetal
blood as well as the amniotic fluid late in
pregnancy and during labour.
• Oxytocin theory:
– Although oxytocin is a powerful stimulator of
uterine contraction, its natural role in onset of
labour is doubtful. The secretion of oxytocinase
enzyme from the placenta is decreased near term
due to placental ischaemia leading to
predominance of oxytocin’s action. 88
• Foetal cortisol theory:
– Increased cortisol production from the foetal adrenal
gland before labour may influence its onset by
increasing oestrogen production from the placenta.
– Fetal CRH → fetal pituitary → fetal adrenals →
DHEAS → → DHEA → → → Estriol
• → → Placental sulphatase
• → → → Aromatase
Estriol stimulation increases sensitivity to oxytocin and
prostaglandin
Also cortisol is produced which acts on fetal lungs →
prostaglandin production.
89
•  Theory of aging placenta – (By 260 days, the
placenta begins to age) life span of placenta 42
wks. At 36 wks degenerates (leading to contraction
– onset labor).
Mechanical factors
• Uterine distension theory:
– Like any hollow organ in the body, when the
uterus in distended to a certain limit, it starts to
contract to evacuate its contents. This explains
the preterm labour in case of multiple
pregnancy and polyhydramnios.
• Stretch of the lower uterine segment:
– by the presenting part near term. 90
Structures Penetrated at lumbar
puncture
[1]Skin
[2]Subcutaneous fat
[3]Muscles
[4]Supraspinous ligament
[5]Interspinous ligament
[6]Ligamentum flavum
[7]Extradura space
[8]Dura mater and arachnoid.
91
• Skilled birth attendant: a health personnel trained
to proficiency in the mgt of normal labour and
diagnosis or referral of obstetric complications. 34%
in Nigeria (NDHS 2005)
• Traditional birth attendant: A person who assists a
woman during childbirth and initially acquired her
skills herself or via apprenticeship to another TBA.
• Hypersystole: Uterine contraction lasting longer
than 2minutes
• Tachysystole: more than 5 contractions in 10mins
for at least 20minutes
• Hyperstimulation syndrome:uterine hyperstimulatn
(any of 2 above) with FHR changes 92
BIRTH PREPAREDNESS
A COMPONENT OF FOCUSED ANC & INCLUDES A PLAN FOR:

• A skilled attendant at birth

• The place of birth and how to get there

• Items needed for the birth

• Money saved to pay the skilled provider and for any needed
mediations and supplies

• Support during and after the birth (e.g., family, friends)


COMPLICATION READINESS
• Required for effective BP & MM reduction. It Includes:

• Designated decision makers

• How to communicate with the skilled birth attendant

• provision for emergency transportation

• Funds

• Nearest 24 hr functioning EMOC facility

• Potential blood donors in case of emergency.


• Dystocia: difficult labour.
• Cervical dystocia: failure of cervical dilatation in the
presence of adequate uterine contraction due to
fibrotic disease in the cervix without CPD.
• Obstructed labour: An absolute condition in which
there is failure of labour to progress due to a
mechanical factor in the presence of adequate
uterine contraction in which an intervention is
needed to prevent maternal or fetal jeopardy.
• Cephalopelvic disproportion (CPD): a previously
unrecognized misfit btw the maternal pelvis and fetal
presenting part despite adequate uterine contraction
in the absence of fetal or maternal compromise.
95
• Shoulder dystocia: Documented difficulty in
extracting the shoulder after delivering the head
• A delivery that required additional OB maneuvers
following failure of gentle downward traction on the
fetal head to effect delivery of shoulders(ACOG)
• A prolonged head to body delivery interval >60secs.
• Routine traction: is ‘that traction required for
delivery of the shoulders in a normal vaginal
delivery where there is no difficulty with the
shoulders’
• Borderline pelvis: two out of the three planes of
the pelvis are normal.
96
Transfusion
• Massive blood loss may be defined as the loss of
one’s total blood volume within a 24-hour period.
Normal blood volume in the adult is approximately
7% of ideal body weight.
• Other definitions include 50% blood volume loss or
2500mls (1500mls is accepted by some) within 3
hours or a rate of loss of 150 ml/minute
• Clinically significant fibrinogen deficiency develops
after a loss of about 150% of bld vol – earlier than
any other haemostatic abnormality when packed
red cell concentrates are used in replacing major
blood loss. 97
• Essential obstetric care (EOC): Minimum health
intervention needed to prevent the cxs of preg,
labour and puerperium- basic & comprehensive.
Signal functions Basic EOC Comprehensive EOC
Parenteral antibiotics Elements in basic EOC plus
Parenteral oxytocic drugs Surgery
Parenteral anticonvulsants Blood transfusion.
for eclampsia
Manual removal of placenta **For the services at a facility to
be considered functional,
Manual vacuum aspiration EOC must have been provided
during the 6 months
Assisted vaginal delivery previous to data collection.
Newborn resusctation

98
• UN indicators for EmONC: 1 CEmONC facility/
500,000 popn; 4BEmONC centers/500,000 popn
• Comprehensive maternity care: consists of
preconception care; antenatal care; intrapartum care
and postpartum care.
• Application distance: dist btw the ant rim of the cup
and a line passing thru the post border of the AF,
perpendicular to the sagittal suture. Shld not be<3cm
• Superfecundation: Fertilization of more than one ova
released at about the same time by sperm released
at intercourse on different occasions.
• Superfetation: fertilization of ova released during
different menstrual cycle. 99
Oxytocin
• The mode of action involves stimulation of the upper
uterine segment
• Short plasma half-life (mean 3mins)
• Onset of action IV is 40seconds and plateau
concentration is achieved after 30 min.
• IM onset of action is 3–7 min but a longer lasting clinical
effect (up to 60 min).
• Metabolism of oxytocin is via the renal and hepatic
routes.
• Its antidiuretic effect, amounts to 5% of the antidiuretic
effect of vasopressin, can result in water toxicity if given
in large volumes of electrolyte-free solutions.
• Has mild vasodilatory effect 100
• Administration of ergometrine results in a sustained tonic
uterine contraction via stimulation of myometrial α-
adrenergic receptors. Both upper and lower uterine
segments are thus stimulated to contract in a tetanic
manner.
• Intramuscular injection results in an onset of action of 2–5
min while IV is about 40seconds.
• Metabolism is via the hepatic route and the mean plasma
half-life is 30 min.
• The clinical effect of ergometrine persists for about 3hrs.
• The co-administration of ergometrine and oxytocin
therefore results in a complementary effect, with oxytocin
achieving an immediate response and ergometrine a more
sustained action.
101
• Common SE include nausea, vomiting and dizziness
and these are more striking when given via the
intravenous route.
• As a result of its vasoconstrictive effect via
stimulation of α-adrenergic receptors, hypertension
• CI to use of ergometrine include hypertension,
heart disease and peripheral vascular disease.
• If given intravenously, it should be given over 60s
with careful monitoring of PR and BP.
• It is heat and light sensitive; should be stored at
temperatures below 8°C and away from light.
• Syntometrine® (5 units oxytocin and 0.5 mg
ergometrin) 102
Fetal distress: FHR < 100bpm for > 60seconds
• Significant and progressive hypoxemia, hypercapnia
and metabolic acidaemia that affects vital organ fxn
and may lead to permanent brain damage and death.
• A biochemical diagnosis in which fetal blood PH is
persistently < 7.20 in successive samples during labor.
• Deceleration of the FHR to 60 bpm for >2 minutes,
unresponsive to medical management such as a
change in maternal position, O2, or intravenous fluids,
in the face of a medically compromised fetus or
abnormal labor; or a deceleration of 60 bpm for
greater than 5 minutes, unresponsive to medical
management, in a normal fetus and normal labor. 103
The Treatment of Foetal Distress
• Change position of the patient [ left lateral best].

• Correct maternal hypotension.

• Decrease uterine activity; DC Oxytocin

• Administer O2 at 6-7L/min with a tight face mask.

• Prepare for operative delivery.

• If it persists for 30min terminate labor operatively.


• Fetal policing: refers to keeping a close watch on a
fetus that is suspected not to be doing well and
encompasses all measures taken in pregnancy to
determine the wellbeing of the fetus up to the
delivery of a healthy baby.

• Normal cardiotocography:
1.Baseline rate 120-160bpm
2.Variability 10-25bpm
3.Two accelerations in 30 minutes
4.No decelerations
105
• Threshold viability infants: infants born before 26
weeks gestation
• USA 20wks; WHO 22wks; UK 24wks age of
viability; Africa 28wks
• Perinatal mortality:
• In the least developed countries, a woman has a
lifetime risk of death during childbirth of 1 in 16,
or 6.25%. In the United States, this risk is 0.03%,
or 1 in 3500
• Nigeria makes up 1.7% of total world population
yet contributes 10% of global maternal mortality
106
APGAR SCORING
PARAMETER 0 1 2

Colour Blue/Pale Peripheral Pink


cyanosis
Respiratory No Irregular Regular resp
effort spontaneous resp effort effort
resp effort
Heart rate None <100 ≥100

Muscle tone Limp Some Active movt


movt
Reflex None Grimace Sneeze/cry

Virginia Apgar, (MD) 23rd/25th September 1952


Biophysical profile
Parameter Score 2 Score 0
Qualitative >1 pool of fluid in 2 Either no measurable
amniotic fluid perpendicular plane at least pool or a pool <1x1cm
volume 1cmx1cm

Gross body > 3 body/limb movt in 30 <3 body/limb movt in


movement mins 30 mins
Fetal breathing >1episode lasting 30s in Absent or episode
movt 30mins <30s in 30mins
Fetal tone >1 episode of body/limb Absent or slow
extension ffed by return to extension-flexion of
flexion or open-close cycle body or limbs
of hand
Reactive fetal > 2 FHR acceleration with <2acceleration or 1+
heart rate fetal movt in 30 mins deceleration in
30mins.
108
Score Clinical Risk of PNM Intervention strategy
significa within 1wk
8 Normal 0.7/1000 No intervention

6 Equivocal Variable •Assess for delivery if


37w
•Repeat test in 24h if
immature
4 Abnormal 89/1000 •Assess for delivery if
32w
•Repeat test in 24h if <
32w
2 Very 125/1000 If persistent on extended
abnormal testing assess for delivery
except in extreme
prematurity.
• Manning described the modified BPP in 1990, 10yrs
after describing FBPP
• less cumbersome than the original FBPP
• Utilizes amniotic fluid volume by the four quadrant
index (AFI) and the NST.
• The AFI - the indicator of long term uteroplacental
function (> 5 cm = adequate )
• AFI increase progressively up to 26weeks, remains
relatively constant (mean 16cm) until term.
• NST -short term indicator of fetal acid-base status.
Accuracy of USS for identifying SGA Foetus:
• Sensitivity - 70.1%; Specificity - 95.5%
• +ve predictive value - 49.5%; -ve predictive – 98.5%
Sequence of fetal deterioration
• Late decelerations appear (CST)
• Accelerations disappear (NST, BPP, CST)
• Fetal breathing movement stops (BPP)
• Fetal gross body movement stops (BPP)
• Fetal tone absent (BPP)
• Amniotic fluid decreases (chronic hypoxia
resulting in redistribution of cardiac output
away from the kidneys toward the brain)
CST=contraction stress test; NST=non stress test;
BPP=biophysical profile
CARDIOTOCOGRAPHY (CTG)
• Electronic monitoring of the FHR and rhythm,
either by external microphone or transducer or by
applying an electrode to the fetal scalp, recording
the fetal ECG and hence the heart rate.

• The procedure also includes measurement of the


strength and frequency of the uterine
contractions.

• The graphic print-out of the measurement


obtained is called a CARDIOTOCOGRAM
• Baseline FHR - is the fetal heart rate present when
(1) a patient is not in labor, or (2) in an interval
between uterine contractions in the labor patient.
A 1cm region where there are no accel/decel is used.
• PERIODIC FHR - is the fetal heart rate associated
with uterine contractions.
• The baseline FHR ranges are as follows:
Plus 2 tachycardia - > 180 bpm
Plus l tachycardia - 161-180 bpm
Normal - 120-160 bpm
Plus l bradycardia - 100-119 bpm
Plus 2 bradycardia - < 100 bpm
Clinical Significance of Zero/+1 Variability
Zero Variability
• Foetal immaturity -<30wk, autonomic n.s. imaturity
• Otherwise, a morbid sign
• Zero var. + late dec. + baseline tachy. = Hypoxia.
• Impending foetal demise = zero var. + bradycardia
preceded by tachycardia [decompensated foetus]
+ 1 Variability
• Resting/asleep foetus
• Effect of depressant drugs, Preeclampsia, MgSO 4
• Wake up foetus [external stimulation] and repeat test
over at least 10 minutes
Clinical Significance of +3/+4 Variability
+3 Variability
• Foetus waking up
• Over-active foetus
• Foetus recovering from deep variable deceleration
[increased compensatory activity]
+ 4 Variability
• Over-compensation of the foetal circulatory system.
• Sign of foetal hypoxia if associated with progressive
late or variable deceleration
• Foetus over-compensation on recovery from
increased stress [recurrent late or variable decel]
Early Decelerations
Causes
• Decrease in FHR with
onset of uterine • Compression of the
contraction (UC); returns fetal head during
to baseline with the end contraction
of UC thus the nadir of • Mild transient
the FHR coincides with hypoxia
the peak of UC.
Mx
• The amplitude of the – Relief of pressure
deceleration is 40 bpm or on the head
less – Changing maternal
position
Late Deceleration
• Decrease in FHR starts after a lag time from the
onset of UC and ends after a lag time from its end.
The nadir of FHR lags behind the peak of UC.
• It is u-shaped and the lag time is relatively long.
• It is almost always indicative of uteroplacental
insufficiency and decreased intervillous exchange
between the mother and the fetus resulting in fetal
hypoxia e.g IUGR, oligohydramnios
• During contraction, the intervillous blood flow is
limited and fetal oxygenation is impaired resulting
in late timing of the deceleration.
Variable Deceleration
• There is no constant relationship to the onset of
uterine contraction.
• Decelerations are of different intensity, pattern,
time of onset and offset.
• They are the commonest type of deceleration seen
during labour.
• They are generally caused by partial or complete
cord compression.
• It is a reflex-mediated by the vagal nerve.
• It is corrected by changing maternal position to
relieve cord compression.
• Worrisome when Rule of 60 is exceeded (i.e.
decrease of 60 bpm, or rate of 60 bpm and longer
than 60s)
Reactive NST: Interpretations
Baseline rate 120‑160 BPM
Baseline variability > 10 BPM
2‑5 accelerations with fetal movement (FM) with
variability > 15 BPM in a 20 minute period.
Nonreactive NST:
Baseline rate 120‑160 BPM
Baseline variability <5 BPM
Minimal accelerations with FM
Sinusoidal:
Baseline rate 120‑160 BPM
Baseline variability < 2 BPM
Superimposed periodic oscillations (2‑5 BPM; 5‑15 BPM)
Unsatisfactory:
Inadequate registration of FHR
Inadequate registration of FM
Categorization of FHR features
Feature Baseline Variability Deceleration Acceleration
(bpm) (bpm)

Reassuring 120-160 >5 None Present

Non- 100-119 <5 for >40 -Early deceleratn Absent with


reassuring 161-180 to <90 min -Variable decel otherwise
-Single prolonged normal CTG
del up to 3mins
Abnormal <100 <5 for >90 -Atypical variable CTG are of
>180 minutes decel. uncertain
Sinusoid -Late deceleratn significance.
pattern -Single prolonged
for ≥ del >3mins
10min

124
Categorization of FHR traces
Category Definition
Normal A CTG where all four features fall into the
reassuring category
Suspicious A CTG whose features fall into one of the
non-reassuring categories and the
remainder of the features are reasurring
Pathological A CTG whose features fall into two or more
non-reassuring categories or one or more
abnormal categories

125
Fetal scalp sampling
• ≥7.25 (Normal pH 7.25 – 7.35) Repeat if FHR abnormality
persists
• RANGE OF 7.21 – 7.24: Regarded as borderline and should
be repeated within 15 to 30 minutes or consider delivery if
rapid fall since last sample.
• ≤ 7.20: Should be regarded as acidosis and delivery is
indicated.
• <7.25 in first stage is abnormal
• <7.20 in second stage is abnormal
• All scalp pH estimation should be interpreted taking
into account the previous pH measurement, the
rate of progress in labour and the clinical features of
the mother and baby.
Quintero Staging of twin-twin transfusion
Stage I Polyhydramnios/Oligohydramnios

Stage II Absent donor bladder

Stage III Abnormal Doppler

Stage IV Hydrops

Stage VIUFD (one or both)


• FGM: All procedures involving partial or total
excision of the female external genitalia for cultural
or other non therapeutic reasons. 20% of Nigerian
women are circumcised (NDHS 2005)
• Type I: Excision of the prepuce with or without
excision of part or all of the clitoris.
• Type II: Excision of the prepuce and clitoris together
with partial or total excision of the labia minora.
• Type III: Excision of part or all of the labia majora
and stitching/narrowing of the vaginal opening
(infibulation)
• TYPE IV: Unclassified: Any other procedure that falls
under the defn of FGM e.g gishiri, angurya cuts. .128
• Infibulation: Excision of the clitoris, minora and
majora; the hole created is then closed.
Deinfibulatn is done in labour, ffed by
reinfibulation.

•  Chimerism the presence of two or more


different populations of genetically
distinct cells that originated in different zygotes.

• Mosaicism: the presence of two or more


different populations of genetically
distinct cells that emerged from the same zygote. 129
IMMEDIATE COMPLICATIONS OF FGM
• Pain
• Injury to adjacent tissue – urethra, vagina,
perineum, rectum – resulting in incontinence
• Haemorrhage
• Shock (neurogenic & haemorrhagic)
• Fracture or dislocation.
• Infection – pelvic infections, abscesses, tetanus,
gangrene, septicaemia, UTI, (HIV) hepatitis.
• Urinary retention
• Failure to heal.
• Death
LONG TERM COMPLICATIONS
• Haemotocolpos.
• Scarring and keloid formation.
• Recurrent urinary tract infections.
• Vulval epidermoid cysts
• Vulval abscess.
• Pelvic infection.
• Subfertility.
• Dysmenorrhoea.
• Recurrent urinary tract infection.
• Psychological (flashbacks, anxiety and depression).
131
LONG TERM COMPLICATIONS

• Difficulty in passing urine


• Clitorial neuroma – hypersensitivity and neuroma
• Calculus formation in the vagina
• Fistulae- VVF, RVF
• Development of false vagina
• Dyspareunia
• Difficulties in providing gynecological care
• Obstructed labour
• Caesarean section: A surgical procedure in which an
incision is made on the anterior abd wall and uterus
to deliver the products of conception after the age
of viability.
• Category 1 Emergency: Immediate threat to the life
of the woman or fetus (within 30mins)
• Category 2 Urgent: Maternal or fetal compromise
which is not immediately life-threatening (within
2hours)
• Category 3. Scheduled: No maternal or fetal
compromise but needs early delivery (within 2-
3days)
• Category 4. Delivery timed to suit woman or staff
133
• Assisted vaginal delivery: vaginal delivery requiring
manoeuvres that ordinarily are not carried out in an
uncomplicated vaginal delivery.
• Trial of IVD: use of mechanical devices when
delivery is indicated and the vaginal route remains a
possibility, but the outcome is uncertain.
• Sequential Instrument Use: forceps operation
followed by VE or vice versa no longer
recommended as this is associated with an increase
risk of fetal ICH.

134
• Instrumental vaginal delivery: vaginal childbirth
with the aid of mechanical devices.
• The application of an instrument to facilitate the
birth of a child per vagina
• Destructive operation: Mutilating and debulking
operations carried out on a dead or grossly
malformed fetus to achieve vaginal delivery.
• Hydrops fetalis: presence of fluid in two or more
potential spaces.

135
FACTORS FAVOURING SUCCESSFUL VBAC
• A hx of a previous vaginal birth before or after the
caesarean section.
• When the previous caesarean birth was for a non-
recurrent cause.
• When a lower segment uterine incision was used in
the previous caesarean section.
• No additional morbidity following the previous CS.
• When the Bishop score in the patient is 4 or more at
the time of assessment at term.
• Caesarean section performed in latent phase of
labour.
FACTORS THAT REDUCE THE SUCCESS OF VBAC
• Fetal macrosomia.
• IUGR.
• Fetal asphyxia.
• A short birth interval (especially when the inter-
pregnancy interval is less than 6 months; there is
increased risk of scar disruption)
• Grandmultiparity –have higher complication rates.
• Previous dysfunctional labour
• Non reassuring FHR tracing on admission.
• Induction Of labour
@Chances of successful planned VBAC is 60-80%
ACOG (72-76% RCOG)
ACOG & RCOG VBAC review
• There is agreement that factors associated with
unsuccessful VBAC include: IOL, no prior vaginal
birth, advanced GA (≥40 weeks), advanced maternal
age, high maternal BMI, high birth weight, CS for a
recurring indication, and non-white ethnicity.
• VBAC carries: a 22-74/10000 risk of uterine rupture;
1% additional risk of either blood transfusion or
endometritis compared with ERCS; an 8/10,000 risk
of the infant developing HIE; and a 2-3/10,000
additional risk of birth-related perinatal death when
compared with ERCS (comparable to the risk for
women having their first birth) 138
• A cautious approach is advised when considering
planned VBAC in women with twin gestation, fetal
macrosomia and short interdelivery interval, as
there is uncertainty in the safety and efficacy of
planned VBAC in such situations.(RCOG)
• IOL is an option in women undergoing TOLAC but
misoprostol should not be used. (ACOG)
• IOL& AOL 2-3fold increased risk of rupture and
around 1.5-fold increased risk of caesarean section
compared with spontaneous labour.
• Although augmentation is not CI it should only be
preceded by careful obstetric assessment, maternal
counselling and by a consultant-led decision (RCOG)
139
• Manual uterine exploration after VBAC and
subsequent repair of asymptomatic scar dehiscence
have not been shown to improve outcomes.
• Manual uterine exploration indicated following
excessive vaginal bleeding, manual removal of
placenta and instrumental vaginal delivery.

140
ACOG Classification of forceps Delivery
Outlet
• Fetal scalp visible without separating the labia
• Fetal skull has reached the pelvic floor
• Sagittal suture is in the AP diameter or right or left
occiput anterior or posterior position (rotation does
not exceed 450)
• Fetal head is at or on the perineum

Low
• Leading point of the skull (not caput) is at station +2
cm or more and not on the pelvic floor. Two
subdivisions:
– rotation of 450 or less -rotation more than 450
Mid
• Fetal head is 1/5 palpable per abdomen
• Leading point of the skull is above station plus 2 cm
but not above the ischial spines
• Two subdivisions:
– rotation of 450 or less -rotation more than 450
• High
When the head is unengaged. Not included in
classification anymore bcos of high morbidity.

142
Conditions to be fulfilled before application
of forceps.
• F –fully dilated cervix
• O –outlet adequate
• R –ruptured membranes
• C – cephalic presentation
• E –empty bladder
• P –position confirmed
• S –station 0
CHECKS FOR CORRECT FORCEPS
APPLICATION
• The sagittal suture lies in the midline of the
blades
• The operator is unable to place more than a
finger tip between the fenestration of the
blade and the foetal head on either side
• The posterior fontanelle of the fetal head is no
more than one finger breadth above the plane
of the shanks of the forceps
FORCEPS COMPLICATIONS
MATERNAL
• Extension of episiotomy and perineal tears
• Genital tract lacerations, i.e vaginal, cervix
• Ruptured uterus
• Fistulae – VVF, RVF
• Spinal sprain and nerve root damage due to
excessive traction force
• Anal sphincter damage
FORCEPS COMPLICATIONS
FETAL
• Asphyxia
• Scalp lacerations
• Supratentorial haemorrhage
• Subdural and subarachnoid haemorrhage
• Cephalhaematoma
• Facial nerve palsy
• Facial abrasion from undue compression or slipping
of the forceps
VACUUM COMPLICATIONS-MATERNAL

• Periurethral / Perineal laceration


• Vaginal / Cervical laceration
• Episiotomy expansion resulting in Trauma /
Morbidity
• Postpartum Haemorrhage
• Infections in the puerperium
• Annular detachment of the cervix
• Some cases of VVF reported.
FETAL/NEONATAL COMPLICATIONS
• Scalp trauma (abrasions)
• Subgaleal Haemorrhage (0.5%)
• Tentorial tear
• Intracranial Haemorrhage (0.35%)
• Cephalhaemtoma / N. jaundice (6%)
• Cerebral irritation and asphyxia
• Retinal Haemorrrhage (50%)
ADVANTAGES OVER FORCEPS
• Technique easily learnt, skill more easily acq.
• Vacuum cup does not occupy space in the
maternal pelvis
• Anaesthesia not required
• OCP and OCT with little complication
• In built safety mechanism, cap pulls off with
excessive traction
• Failed vacuum associated with fewer
complication
• Can be used in 1st stage of Labour
• Low maternal and fetal /neonatal complication
ADVANTAGES OF FORCEPS OVER
VACUUM
• Faster delivery in experienced and skilled
hand. Useful in cases of severe fetal distress
or cord prolapse
• Safely used to deliver premature infant with
birth weight < 1.5kg where the ventouse is
contraindicated.
• Deliver after coming head of foetus in breech
delivery
• Handy and does not easily develop faults.
Destructive operations
Why still relevant in the tropics
• High incidence of obstructed labour
• High risk of sepsis from surgery
• High risk of ruptured scar in subsequent pregnancy
• Aversion for caesarean section
• Shortage of manpower and materials
• Lack of access to skilled supervision in subsequent
deliveries
Low incidence in developed countries
• Rarity except for hydrocephalus
• High literacy rate
• Availability of wide range of antibiotics
• Good communication
• Availability of skilled manpower
151
Incidence
– UCH- 0.48% Otolorin & Adelusi 1980
– UCH Ibadan 1.65% Aimakhu 1975
– LUTH 0.2-0.3%
– Zaria 1.4% Harrrison 1980
Indication
– Obstructed labour with dead fetus
Prerequisites
– Confirmed that fetus is dead
– Competent operator
– Ruptured uterus excluded
– Resuscitative measures must be in progress
– Cervical dilatation should be full
152
Types of destructive operations
• Craniotomy

• Cleidotomy

• Embryotomy

• Decapitation

• Evisceration
153
Complications
• Ruptured uterus
• Cervical lacerations
• Vaginal lacerations
• Sepsis with its sequelae
• Vesicovaginal fistula
• Rectovaginal fistula
• Endotoxic shock
• Puerperal psychosis
• Maternal death
154
EPISIOTOMY
• Term coined by Carl Braun
• Deliberate surgical incision made on the perineum
to widen the introitus to facilitate vaginal delivery.

INDICATIONS
• Imminent perineal tear
• Rigid perineum
• Breech delivery
• Instrumental vaginal delivery – All forceps not all
vacuum
• Preterm labour
• Shoulder dystocia
155
3 types.
• Mediolateral episiotomy (commonest)cut at 450 from the
midline.
• Midline episiotomy to cut in centre of the perineum
separating the bulbocarvenous and superficial transverse
perineal muscles
• J-Shaped incision – made tangential to the top of the anus.
Midline Advantages And Disadvantages
• Easy to repair
• Heals well
• Less pain in the perineum
• Reduced dyspareunia
• Anatomical result almost always excellent
• Blood loss less
• Extension through anal sphincter common. 156
Mediolateral Advantages And Disadvantages
• More difficult to repair
• Faulty healing more common
• More painful in the puerperium
• Dyspareunia occassionally follows
• Blood loss greater
• Anatomical result not as satisfactory in 10% of
cases (depending on the operator)
• Anal sphincter extension less common

157
COMPLICATIONS OF EPISITOMY
Early
• Haematoma
• Dehiscence
• Infection – 0.05 to 3.0%
• Necrotising fasciatis / myorecrosis
Late
• Dyspareunia
• Psychosexual problem / morbid fear of subsequent
delivering
• Rarely endometrosis
• FETAL
• Lid Laceration .Castration (in breech birth)
• Increased risk of vertical transmission of HIV infection
• Hypersensitivity to local anaesthesia (xylocaine) 158
Symphysiotomy
• Artificial separation of the symphysis pubis to
enlarge the pelvis and facilitate delivery. Increases
AP diameter at outlet by widening the sub public
arch
• Enlarges capacity of pelvic by 25%  main
expansion in transverse diameter.
Indication
• Cephalopelvic disproportion
• Failed trial of vacuum extraction / forceps in 2nd
staged of labour.
• Trapped after coming head in breech
• Shoulder dystocia
159
• TECHNIQUE
– Zarate method- partial division of the symphysis no
longer done (forceful abduction)
– Seedat crichton’s method - complete division of the
symphysis now done.
– Avoid hyaline cartilage by strict adherence to midline
– Bladder emptied and patient catheterize
– Patient in the lithotomy position with angle between the
legs > 800 and avoid excessive abduction – strain on the
S.I. joint.
– Urethra guarded by the index and middle fingers of the
left hand.
– Scalpel applied on the fibro cartilage of symphyseal
joint, with process complete by inserting the thumb into
the divided joint.
160
COMPLICATIONS
• Damage to S.I. joints
• Permanent pelvic instability and pain
• Osteitis public and subsequent difficulty walking non
avoidance of Hyaline cartilage
• Vesico-Vaginal Fistula
• Osteitis pubis /retropubic abcess
• Stress in continence
• Perinatal mortality varies.
• Vaginal delivery rate postsymphysiotomy higher than after
previous C/Section 85% vs 44%

161
• Post-maturity syndrome refers to recognisable clinical
features in an infant that is attributable to placental
dysfunction/senescence.
- Occurs in 5 - 10% of cases
Complicates 20% of Prolonged pregnancy at 42wks
33% of Prolonged pregnancy at 44wks

• The presence of oligohydramnios in a postdate pregnancy


has been reported to substantially increase the incidence of
postmaturity {Trimmer et al,1990}

• The postmature infant is at increased risk of birth


asphyxia,meconium aspiration,early neonatal seizures and
neonatal demise.
Characteristic fetal appearance
– Wrinkled patchy peeling skin (skin because of loss
of vernix caseosa.)
– long nails
– Thin/Lean body (Decreased amount of
subcutaneous fat.)
– Old/Worried looking, Unusually alert
– Greenish or yellowish staining of the skin with
prolonged exposure to meconium.
– Fragile foetus, tolerate labour poorly and
frequently acidotic at birth.
Staging system used to quantify increasing severe
clinical manifestations of placenta dysfunction.
Stage 1 – Amniotic fluid is clear; long lean
infant with wrinkled peeling skin

Stage 2 - Stage 1 + Amniotic fluid, placental


membranes, fetal skin stained green

Stage 3 - High incidence of fetal distress +


yellowish – green/brown meconium
stained liquor

164
Intrauterine growth restriction(IUGR) occurs when
the :
• fetus is unable to achieve its genetic potential.
• when the fetus is at or below the 10th weight
percentile for age and sex.
• Fetus is > 2 SD below the mean for weight.
• Intrauterine fetal death (IUFD): Fetal death after
the age of viability but before onset of labour.
• Doppler principle “frequency shift”: states that
when energy is reflected from a moving boundary,
the frequency of the reflected energy varies in
relation to the velocity of the moving boundary.
165
• Abnormal findings on Doppler waveforms include the
following:
Highest uterine artery PI – lowest uterine artery PI >1.1
• Persistence of protodiastolic notch, unilateral or bilateral,
after 23 weeks is suggestive of IUGR or preeclampsia.
• Resistivity Index greater than 0.55 with bilateral notches
• RI greater than 0.65 with a unilateral notch
• RI greater than 0.70 with or without notches
• RI greater than 90th percentile for a given gestational age
regardless of notches
• An S/D ratio >3 after 30 weeks of gestation is abnormal.
• The reversal of flow in ductus venosus is suggestive of a
fetus with severely compromised IUGR and reflects fetal
metabolic acidemia. 166
Estimated average interval between onset of major obstetric
Cxs and death, in the absence of medical interventions

Complication Duration
Postpartum Haemorrhage 2 hours
Antepartum Haemorrhage 12hours
Ruptured uterus 1 day
Eclampsia 2 days
Obstructed labour 3 days
Infection 6 days
• Maternal mortality: The death of a woman while
pregnant or within 42 days of termination of
pregnancy irrespective of the duration or site of the
pregnancy from any cause related to or aggravated
by the pregnancy or its mgt and not from accidental
or incidental cause.
• Direct 80%/Indirect 20%
• Global- HITLA(25%, 15%, 12%, 8%, 13%, Others7%)
• Nigeria- HITLA(23%, 17%, 11%, 11%, 11%);
malaria11%, anaemia11%, others 5%.
(MCQ National) Haemorrhage 40%; Ectopic 2.5%
• Neonatal MR 47/1000; IMR 97/1000; U5MR
201/1000 (NDHS 2005)

168
Major Causes of Maternal Mortality in Nigeria

Haemorrhage 23%
Sepsis 17%
Eclampsia 13%
Abortion 11%
Anaemia 11%
Malaria 11%
Prolonged obstructed labour 11%

Others 3%
Source:FMOH
• Maternal mortality ratio: a measure of obstetric risks faced
by a woman each time she gets pregnant. Calculated as
maternal deaths during a given year per 100, 000 live birth
in same period. MMR in Nigeria previously 800-1100/100,
000 now 545/100,000 (2008 statistics)
• Maternal mortality rate: this measures both the obstetric
risk faced by a woman and the frequency with which
women are exposed to this risk. Calculated as maternal
deaths in a given period per 100, 000 women of
reproductive age group (usually 15-49yrs)
• Life time risk of maternal death: this takes into account
both the probability of becoming pregnant and the
probability of dying as a result of the pregnancy cumulated
across a woman’s reproductive years. (MMR X length of
reproductive period (35 years) 170
Burden of MM (2005 statistics)
• Maternal mortality is estimated to be 529 000 deaths per
year, a global ratio of 400 per 100 000 live births.

• Between 11% and 17% of maternal deaths happen during


childbirth itself and between 50% and 71% in the
postpartum period; with 25% occurring in pregnancy.

• About 45% of postpartum maternal deaths occur during


the first 24 hours, and more than two thirds during the first
week.

• Of the 20 countries with the highest maternal mortality


ratios, 19 are in sub-Saharan Africa. 172
Burden of MM (2008 statistics)
• The number of women dying due to complications during
pregnancy and childbirth has decreased by 34% from an
estimated 546 000 in 1990 to 358 000 in 2008, according to
a new report, Trends in maternal mortality, released by the
WHO, UNICEF, UNFPA and the World Bank.
• The 34% decline from 1990 translates into an average
annual decline of just 2.3% instead of 5.5% needed to
achieve MDG 5
• Every day, about 1000 women died due to complications in
2008. Out of the 1000, 570 lived in sub-Saharan Africa, 300
in South Asia and five in high-income countries.
• The risk of a woman in a developing country dying from a
pregnancy-related cause during her lifetime is about 36
times higher than in a developed country. 173
Classification of causes of PNM
• Smith Wigglesworth
• Noir Baltic
• ReCoDe: Relevant Condition at Death
• Tulip
• Multilayered: When, What and Why using
above four.

174
Burden of Newborn death
• 1 out of 5 African women loses a baby during her
lifetime, compared with 1 in 125 in rich countries.
• Each year 3.3 million babies are stillborn, and more
than 4 million others die within 28 days of birth.
• Newborn deaths now contribute to about 40% of all
deaths in children under five years of age globally,
and more than half of infant mortality.
• Each year over a million children who survive birth
asphyxia develop problems such as cerebral palsy,
learning difficulties and other disabilities.
175
Classification of causes of MM
A C
• Direct • Sociocultural factor
• Indirect • Health facility factor
• Fortuitous • Medical factor
• Late • Reproductive health factor

B D (Delays)
• Immediate (Medical) • Phase I, II and III
• Remote (Sociocultural) (delay in seeking; reaching/
accesing and
receiving/institutional)
176
Causes
• Medical factors: direct or indirect causes
• Non Medical Causes
– Socio-cultural factors; poverty, diet, religion,
harmful practices, low status
– Reproductive health factors; too young (<17yrs),
too many (>4), too often (<2yrs) , too late
(>35yrs)
– Health Service factors
• Access, inadequate personnel and supplies,
incorrect treatment and incessant industrial
actions
Phase 1 delay
Delay in decision to seek care maybe due to:
A. Socio-economic / Cultural Factors: Socio-legal
factors, Women status, Illness factors
B. Perceived Accessibility :Distance, Fees,
Transportation, Medications, poor road
condition, Opportunity cost, Cost, Transportation
C Perceived quality of Care: Previous experience,
Satisfaction with outcome, Satisfaction with
service i.e staff attitude, waiting time, availability
of supplies, fear of hospital procedures, privacy
etc
Phase 2 Delay: Delay arrival at a health facility

• Distribution and location of health facilities


• Cost may exceed ability to pay

Phase 3 Delay: Delay in the provision of adequate


care
• Actual quality of Care
– Poorly staffed facilities
– Poorly equipped facilities
– Inadequate management:
Delayed or incorrect treatment and action
Contribution of “Delays” to Maternal
Mortality in Nigeria
• No delay  10%

• Type I Delay  30%

• Type II Delay  20%

• Type III Delay 40%


• Direct obstetric death: Death resulting from obstetric
complications of pregnancy, labour and puerperium; from
interventions, omissions, incorrect treatment or from a
chain of events resulting from any of the above
• Indirect obstetric death: Those resulting from previously
existing dxes or dxes that devped during pregnancy, which
was not due to direct obstetric causes but which was
aggravated by physiological effects of preg.
• Late maternal death: Death of a woman from direct or
indirect obstetric causes more than 42 days but less than
one year after termination of pregnancy.
• Fortuitous death: deaths that were unrelated to the
pregnancy or puerperium and just happened to occur at
this time. Eg RTA, assault
181
• Pregnancy related death: Death of a woman while
pregnant or within 42days of termination of
pregnancy irrespective of the cause of death.
• Nigeria makes up 1.7% of total world population yet
contributes 10% of global maternal mortality.
• 11%-17% of maternal deaths occur during childbirth
• 50% -71% in the postpartum period (many
postpartum deaths are also a result of what
happened during birth)
• About 45% of postpartum maternal deaths occur
during the first 24 hours,
• More than two thirds during the first week.
182
• Near miss: acute obstetric complications that
immediately threaten a woman’s survival but do not
result in her death either by chance or because of
hospital care she receives, during pregnancy, labour
or within 42days of termination of preg or delivery.
• “a woman who nearly died but survived a cx that
occurred during pregnancy, childbirth or within 42
days of termination of pregnancy” (WHO)
• Sudden postpartum collapse: an acute emergency in
which there is sudden onset of prostration
(cardiorespiratory embarassment) in a recently
delivered woman who was previously
haemodynamically stable. 183
Criteria for Classifying Near-miss
1. Clinical Criteria related to disease entity
2. Organ-System dysfunction based criteria
3. Intervention-Based Criteria

Maternal mortality index = No of maternal deaths


No of maternal deaths and near miss.
It should be low if level of care is high.

Clinical
Done by Waterstone et al -2001
Criteria
• Carefully defined disease-specific morbidity namely
– Preclampsia
– Eclampsia
– Haemorrhage
– Uterine rupture etc
• Using this System he recorded morbidity of 12 per 1000 births in the
UK.
• Advantage
– Straight-forward to interpret
– Data can be obtained retrospectively from case notes,
register
– Quality of Care of a particular disease can be assessed
• Disadvantage
– The most direct cause of maternal mortality namely
pulmonary embolus may be missed because of difficulty in
diagnosing pulmonary emboli accurately when they are not
fatal
Organ-System dysfunction based criteria
• The system is based on the concept that there is a
sequence of events leading from good health to
death
• The sequence is:
»Clinical insult
»SIRS
»Organ dysfunction
»Organ failure
»Death
• Near miss would be those with organ dysfunction
and failure who survive
• The criteria for defining a near-miss are generic and
are defined per organ system
Intervention-Based Criteria
• In most developed countries, admission to an
ICU or the requirement for critical care has
been used as the criteria to classify near-miss.
• This system has the advantage that is simple
to identify the cases
• Disadvantage:
»Accessibility of ICU beds for patients
requiring them in UK
Proposed Clinical Criteria for a maternal near-
miss
Organ system-based Markers
Cardiac dysfunction Pulmonary edema: a clinical diagnosis
necessitating intravenous furosemie or
intubation
Cardiac Arrest
Vascular Dysfunction Hypovolemia requiring ≥ 5 units whole
blood or packed cells for resuscitation
Immunological Intensive care admission for sepsis
dysfunction Emergency hysterectomy for sepsis
Liver dysfunction Jaundice in the presence of pre-
eclampsia. Pre-eclampsia defined as
B.P≥140/90 together with≥1 +
proteinuria
Clinical Criteria (Contd)
Respiratory Intubation and ventilation ≥ 60min for any
dysfunction reason other for general anaesthesia
Oxy saturation on pulse oximetry < 90%
for more than 60 mins
Ratio of partial pressure of oxy in arterial
blood to the % oxy inspired air ≤3
Renal Oliguria (<400mls/ 24hrs) which doesn’t
dysfunction respond to either careful adequate
intravascular rehydration or attempts at
inducing a diuresis with frusemide or
dopamine.
Acute deterioration of urea to > 15mmol/L
or Cr to > 400mmol/L
Clinical Criteria (Contd)
Metabolic dysfunction Diabetic Ketoacidosis
Thyroid crisis
Coagulation dysfunction Acute thrombocytopaenia
requiring platelet transfusion
Cerebral dysfunction Coma in a patient lasting> 12 hrs
Subarachnoid or intracerebral
haemorrhage
Intervention- based
Intensive care admission For any reason
Emergency hysterectomy For any reason
Anaesthestic accident Severe hypotension associated
with spinal/ epidural anaesthetic
Hypotension = SBP<90mmHg
lasting >60mins
Failed tracheal intubation requiring
anaesthetic reversal
AVOIDABLE FACTORS, MISSED OPPORTUNITIES AND
SUBSTANDARD CARE?
• An avoidable factor is something which could have
caused the death and yet was potentially avoidable.
If that event or condition was not present, the
death may not have occurred.
• A missed opportunity is a potentially avoidable
maternal death where an opportunity was present
to prevent the death but the opportunity was
missed.
• Substandard care is poor care which may have
resulted in the woman's death.
191
192
Prevention of MM using MDG algorithm
• 1. Eradication of poverty which is linked to illiteracy,
ignorance, and poor nutrition as well as health education
about maternal mortality and its prevention.
• 2. Education of the girl child.
• 3. Promotion of female equity, equality and women
empowerment.
• 4. Care of the girl child vis a vis nutrition, immunization and
abortion of harmful traditional practices like female genital
mutilation
• 5. Encouragement of family planning, antenatal care, skilled
birth attendants and post abortal care.

193
• 6. Prevention of common diseases like malaria,
tuberculosis and HIV/AIDS.
• 7. Promotion of favourable government legislation
• appropriation of more resources to health funding,
• training and retraining of skilled health personnel
• provision of accessible and functional health
facilities providing essential obstetric care
• provision of necessary drugs
• improvement of infrastructural facilities like roads.

194
• Immediate: Provision of EmOC and essential drugs
• Short term: Family planning
Antenatal care
Clean and safe delivery
EmOC, training and retraining of skilled
birth attendants and providing health facilities.
• Long term: Education of females, adequate
nutrition of girl child, women empowerment, policy
change, abolition of harmful traditional practices.

@@The obstructed labor complex was characterized


by Arrowsmith, Hamlin, and Wall in 1996 195
Obstructed Labor Injury Complex (Arrowsmith complex)

2
• Anatomic / physiologic w.r.t. the recommended
surgical techniques and prognosis ( Kee Waaldjik)
- Class 1 – fistula not involving the closing
mechanism
- Class 2 – fistula involving the closing mechanism
A – without sub or total urethral involvement
a – without a circumferential defect
b – with circumferential defect
B – with sub or total involvement of the urethra
a – without a circumferential defect
b – with a circumferential defect
- Class 3 – Miscellaneous e.g. uretero- VF etc
Classification
Anatomical (Lawson-1968) HAMLIN CLASSIFICATION
• According to size -Simple
(Waaldjik) -difficult
Small-<2cm -total urethral loss
Medium 2-3cm -extensive scarring
Large 4-5cm
Extensive >6cm
VVF SCORE
• Scarring Score
– Mild 1
– Moderate 2
– Severe 3
• Urethral status
– Intact 0
– Partial damage 2
– Complete loss 3
83.5% who had a score <3 were dry at discharge & a 40% rate
for those with score of 3 or more
According to United Nations Population Fund survey of 2,500
repairs/annum, it will take >300yrs to restore all affected
women to urinary continence assuming no new OF occurs
Long-term Preventive Measures
Socio-Economic: Socio-Cultural:
• oppressive foreign and • early marriage and
domestic fiscal policies early childbirth
• widespread poverty
• inferior status of girls
• mass illiteracy and
ignorance and women
• inadequate transportation • harmful traditional
and communication practices and beliefs
systems • untrained TBAs
• inadequate health care
facilities
• insufficient trained health
care providers
Call for Comprehensive Care
Establish in each country at least one referral
service /centre for fistula treatment to ensure
high quality of care and training, so that all
women with fistula have access to
comprehensive treatment, including quality
medical care, rehabilitation, counselling,
mental health services and health education;
additionally, ensure access for all women to
social reintegration support.

Johannesburg Call to Action to Make Motherhood Safer by


Addressing Obstetric Fistula, October 2005
Adolescent pregnancy.
• Adolescents of today are attaining menarche earlier
• They are exposed to a longer period of schooling and are
getting married at a later age, thus long period of time in
which young people are sexually but not economically
mature.
• By 19years, most adolescents are sexually exposed
whether they are married or not (FMOH, 2003).
• Each year, 15-17million adolescent girls become pregnant
due to risky behaviors.
• About 4.4million resort to abortion.
• 40% of which take place under unsafe conditions.
• About 25% of adolescents have STIs yearly, Chlamydia is
the most common STI. HIV less than youths.
COMPLICATIONS OF ADOLESCENT PREGNANCY
• Not likely to enter healthcare system early for care.
• Increased risk of 1st and 2nd trimester bleeding.
• Poor nutrition with borderline iron stores – anaemia.
• Higher incidence of toxaemia of pregnancy (fulminant).
• High risk behavior – substance abuse increase risk of baby
with health problems.
• Undetected sexually transmitted disease.
• Premature labour.
• Low birth weight.
• Absence of perinatal care – Obstructed labour and sequelae.
• Increased risk of operative delivery (Small stature).
• Increased maternal morbidity and mortality.
• Increased perinatal morbidity / mortality
Safe Motherhood Initiatiave
•  International Safe Motherhood Conference,
convened in Nairobi in February 1987 by the World
Bank, World Health Organization (WHO), and United
Nations Fund for Population Activities (UNFPA)
• Safe Motherhood Inter-Agency Group (which
included the 3 sponsors of the conference plus
UNICEF, UNDP, IPPF and the Population Council) was
then formed
• Aim is to reduce maternal mortality by 50% by year
2000 and to increase antenatal attendance to 80%.

204
The Eight Pillars of Safe Motherhood in Nigeria

Safe Motherhood

Post-Abortion Care

STIs/ PMTCT-Plus
Clean and Safe del

Post-Natal Care
Family Planning

Emergency Obst.
Newborn Care
ANC

Care
Skilled Birth Attendants
Communication for Behavior Change +
Male involvement
Primary Health Care / Supportive Health Systems
205
Equity, Reproductive Health Rights and Education for Women
MPS and MDGs (Contd)
• MPS Initiative was launched by the WHO in
2005 Jan. in recognition of the need for further
progress and building on the experience of
more than a decade of SMI
• MPS Initiative sets out a way forward for making
pregnancy and child birth safer for women and
their newborns.
• MPS Initiative notes with great concern that at
current trends the International communities
would fail to meet MDGs 4 & 5
MDG (EAPRICED) SOME TARGET
1 Eradicate extreme poverty Target 2: half by 2015, the proportion of
and hunger people who suffer from hunger.
2 Achieve Universal Primary Ensure boys & girls alike complete full
Education course of primary schooling by 2015
3 Promote gender equality Eliminate gender disparity in 10 & 20
and empower women schools by 2005 and all levels by 2015.
4 Reduce Child Mortality Reduce U5 mortality rate by 2/3 by 2015,
5 Improve maternal health Target 6: reduce the MMR by ¾ by 2015
6 Combat HIV/AIDS, By 2015, to have halted and begin
Malaria, and other dxes reversing the spread of HIV/AIDS & co.
7 Ensure environmental Halve by 2015, the proportion of people
sustainability without access to potable water
8 Develop a global Provide by 2015 access to affordable
partnership for essential drugs and other health
development commodities on a sustainable basis
207
207
YAR’ADUA’S 7-POINT AGENDA
1.POWER AND ENERGY: Adequate power supply will ensure
Nigeria’s ability to develop as a modern economy and an
industrial nation by the year 2015.
2.FOOD SECURITY: primarily agrarian based
3.WEALTH CREATION:  through diversified production especially in
the agricultural and solid mineral sector
4.TRANSPORT SECTOR:  rehabilitatn and modernizatn.
5.LAND REFORMS:  release of lands for commercialized farming
and other large scale business by the private sector.
6.SECURITY: Niger delta is primary focus.
7.EDUCATION:   will ensure firstly the minimum acceptable
international standards of education for all, then  ensure
excellence in both the tutoring and learning of skills in science
and technology by students 208
Nigeria’s Immunization Schedule
Age Vaccine
At birth BCG OPV0 HBV1
6 weeks DPT1 OPV1 HBV2
10 weeks DPT2 OPV2
14 weeks DPT3 OPV3 HBV3
9 months Measles Yellow F Vit A1
15 mths Vit.A 2
• Tetanus immunization
Interval Protection
Contact 0
4 weeks 1 year
6months 3 years
1year 10years
1year Life

Vaccine Route
BCG Subdermal left deltoid 0.05ml
OPV Oral 0.5ml
HBV Intramuscular thigh 0.5ml
DPT Intramuscular thigh 0.5ml
Measles Intramuscular thigh 0.5ml
Yellow fever Intramuscular thigh 0.5ml
210
Olusanya et al social class
• Husband (type of job)
0- Professional
1- Skiled labour
2- Unskilled labour
• Wife (level of education)
1- Tertiary education
2- Secondary education
3- Primary or no formal education
*Social class- husband score + wife’s score
211
Ruptured uterus
• Total disruption of the wall of the pregnant
uterus with or without extrusion of its contents.

• Scar dehiscence: herniation of intact amniotic


membrane thru an existing uterine scar
(discontinuity does not extend beyond previous
scar and peritoneum is intact).

• Scar rupture: Separation of the scar along its


entire length often involving unscarred area with
rupture of the amniotic membrane.
212
• Obstetric haemorrhage: Abnormal bleeding from
the genital tract after the age of viability to 42days
of delivery (APH + PPH)

• APH: Bleeding from the genital tract after the age of


viability until delivery.

• PPH: Abnormal bleeding from the genital tract


within 42days of delivery.

• 10 PPH:1) ≥500mls or more (1000mls or more in


CS); 2) ≥10% of BMI; 3) ≥5% of maternal weight lost
213
Placenta praevia: placenta that is partially or wholly
inserted into the lower uterine segment.
Type I (P.P. lateralis; low-lying placenta): The lower edge
of the placenta reaches the lower uterine segment but
not the internal os. a- anterior; b- posterior
Type II( P.P. marginalis): The lower edge of the placenta
reaches the margin of the int os but does not cover it.
Type III (P.P. centralis): placenta covers the internal os
when it is closed or partially dilated but not when it is
fully dilated.
Type IV (P.P. centralis): The placenta covers the internal
os completely whether the cervix is partially or fully
dilated
214
Abruptio placenta: premature separation of a
normally situated placenta before delivery of
the fetus.
Shat and Stakler classification
• Grade I: Assymptomatic- Accidental finding on
USS or retroplacental clot on delivery
• Grade 2: Symptomatic fetus alive
• Grade 3: symptomatic fetus dead
a: No coagulopathy
b: presence of coagulopathy (DIC)

215
• Couvelaire uterus: extravasation of blood into the
myometrium thus inhibiting uterine contraction
(abruptio placenta and uterine rupture)
• Shock index: HR (bpm) /SBP (mmHg)
*Normal 0.5-0.7; if >0.9 likelihood of shock is high
*Sensitive indicator of left ventricular dysfxn
• Ponderal index: Birthwgt x 1000/[crown-heel
length(cm)]3
(Normal 1.8 at 28weeks; increases by 0.2 every 4weeks
to reach 2.4 by 40weeks)
• MABP: *(SBP+2DBP) / 3 or *1/3 Pulse Pressure + DBP

216
Shock
• The clinical manifestation of failure of cellular
function due to inadequate tissue perfusion
and consequent cellular hypoxia resulting
from a reduction in the effective circulating
blood volume.

• reduction in the effective circulating blood


volume inadequate tissue perfusion
cellular hypoxia failure of cellular function
217
• SIRS: The systemic inflammatory response to a wide
variety of severe clinical insults manifests by 2 or
more of the following conditions:

• Temperature greater than 38°C or less than 36°C


• Heart rate greater than 90 beats per minute

• Respiratory rate greater than 20 breaths per minute


or PaCO2 less than 32 mm Hg

• White blood cell count greater than 12,000/mm3 ,


less than 4000/mm3 or 10% immature (band) forms
Features of hypovolemic shock
Organ system Symptom/sign Cause
CNS Mental status ↓ cerebral
changes perfusion
Cardiac Tachycardia, Sympathetic
rapid thready stimulation
pulse
Systemic N/↓tensive, Initial , later
↓JVP, narrow PP ↓CO, SVR, VR
Renal Oliguria ↓perfusion
Respiratory N/tachypneic Sympathetic
stimulatn
Skin Cold & clammy Vasoconstriction
Features of septic shock
Organ system Symptom/sign Cause
CNS Subtle mental changes ↓cerebral perfusion
Leaky b-b barrier
Cardiac Tachycardia, bounding MI, ↓Cardiac fxn, CO,
pulse SVR
Systemic N/slightly ↓tensive, ↓CO, SVR, VR
↓JVP, widened PP
Renal Oliguria Afferent arteriolar
vasoconstriction
Respiratory Tachypneic Pulm edema, acidosis,
msl fatigue
Skin Warm CO, periph vasodilatn,
fever
Others Fever/ hypothermia Infectn, endotxns,
cytokines
Late features of shock
Organ system Symptom/sign Cause
CNS Disorientation, Hypoxia, worsening
obtundation cerebral edema
Cardiac Dysfxn, tachycardia, Irreversible
Dysrhythmias, ischemia, ↓CI, EF
Systemic N/↓tensive, RHF, EV pooling
Renal Oliguriaanuria ARF
Respiratory Tachypnea ARDS
Skin Cold, clammy Vasoconstrictn,
Sympa stimulatn
Other Lactic acidosis, Anaerobic meta,
coagulopathy hepatic dysfxn
Resuscitative priorities in mgt of
overt shock: Restore
ORDER
O Provide adequate oxygen delivery
R Restore circulatory vol (crystalloid & bld)
D Drug therapy (support BP, antibio, misc)
E Evaluate response to therapy
R Remedy underlying cause
FDA Classification of drug safety
A Safest. Well designed studies in people show no risks to the
fetus

B Studies in animal show no risk to fetus, & no well designed


studies in people have been done

C In animal studies, use of the drug resulted in harm to the


fetus, but no information about how drug affects the human
fetus is available

D Evidence shows a risk to the human fetus, but benefits of the


drug may outweigh risks in certain situations

X Risk to the fetus has been proved to outweigh any possible


benefit
FDA Categories
  A Controlled studies show no risk-Adequate, well-controlled
studies in pregnant women have failed to demonstrate a
risk to the fetus in any trimester of pregnancy.
  B No evidence of risk in humans-Adequate, well controlled
studies in pregnant women have not shown increased risk
of fetal abnormalities despite adverse findings in
animals, or
In the absence of adequate human studies, animal studies
show no fetal risk. The chance of fetal harm is remote, but
remains a possibility.
  C Risk can not be ruled out- Adequate, well-controlled
human studies are lacking, and animal studies have shown
a risk to the fetus or are lacking as well.

224
C Or There is a chance of fetal harm if the drug is
administered during pregnancy; but the potential
benefits may outweigh the potential risk.
  D Positive evidence of Risk-Studies in humans, or
investigational or post marketing data, have
demonstrated fetal risk. Nevertheless, potential benefits
from the use of the drug may outweigh the potential risk.
For example, the drug may be acceptable if needed in a
life threatening situation or serious disease for which
safer drugs cannot be used or are ineffective.
  X Contraindicated in Pregnancy- Studies in animals or
humans, or investigational or post-marketing reports,
have demonstrated positive evidence of fetal
abnormalities or risk which clearly outweighs any
possible benefit to the patient.

225
MECHANISM OF TERATOGENICITY
• DRUGS CAUSE :Mutation. Chromosome disruption.
Mitotic interference. Altered DNA structure.
Substrate deprivation. Altered membrane function.
etc.

• EFFECTS: Malformations. Growth retardation.


Functional disorder. Fetal death.
WHO classification of anaemia
Anaemia is a condition of low circulating
haemoglobin (Hb) in which the Hb conc has fallen
below a threshold lying at two standard deviations
below the median of a healthy population of the same
age, sex, and stage of pregnancy (WHO 1996)

Severity Hb conc (g/dl) PCV (%)


Mild 10 – 10.9 26-32 (29)
Moderate 7 – 9.9 19-25
Severe 4 – 6.9 14-18
Very severe <4 <14

** ( ) value for Nigeria 227


Severity Hb conc (g/dl) PCV (%)
Mild 9 – 9.9 27-29
Moderate 6.1 – 8.9 19-26
Severe 4 – 6.0 12-18
Very severe <4 <12

228
EFFECTS OF ANAEMIA
• Maternal • Fetal
– Reduced immunity to – Abortion
infection such as UTI – Preterm labour
– Congestive cardiac – Fetal distress
failure – IUGR
– Shock after losing – IUFD
relatively small
– Increased perinatal
quantity of blood
loss
– Increased morbidity
– Neural tube defects
& mortality
– Poor wound healing
IRON BALANCE IN PREGNANCY
Average Pregnancy Fe( mg)
-- basal iron loss ---280
--expansion of red cell mass ---570
--Fetus ---200-350
--Placenta ---50-150
-- Blood loss at delivery ---100-250
--Iron conserved by amenorrhea --240-480.
• Difference = 500-600 =4-6mg/day of absorbed iron.
• Achieved by -mobilizing iron stores & maximum iron
absorption from diet
• Average diet contains about 6mg of iron per 1000
calories and about 10% of dietary iron is absorbed
BLOOD FILM:BASED ON SIZE AND
HAEMOGLOBIN CONTENT
Hypochromic microcytic Macrocytic anaemia
MCV<76 fl N=75-96 Large RBC MCV>96
MCHC<30g/dl N=32-35 Well haemoglobinised
MCH<25pg N=27-33 Normal MCH &MCHC
Megaloblastic:
central palor seen in RBC
hypersegmented of
Normochromic Nomocytic neutrophil ≥ 4, (>4% of
• Leucocytosis the total wbc)
• Toxic granulation Macro-Ovalocytes
• Malaria parasite Nucleo-cytoplasmic
asynchrony
– Serum ferritin <12= IDA (N=15-300µg/L) 1st lab
test to be deranged in IDA
– Serum Iron<60µg/dl=IDA (N=60-120)
-Transferrin Saturation <15% =IDA Deficient iron
supply to the tissues
– TIBC>350µg/dl =IDA (N= 300-350)
– Free erythrocyte Protoporphyrin ↑ (FEP)
– Serum transferrin receptors: ↑ in IDA (best
indicator)
– Bone marrow stainable iron using potassium
ferrocyannate (Invasive, Aplastic anaemia, 4wks
no response
232
Preparations Molecular Iron Elemental Iron
(mg/tablets) (mg/tablets)
Ferrous 300 36
Gluconate
Ferrous Sulphate 300 60
Ferrous 200 66
Fumarate

• >180mg of Elemental Iron is required per day for treatment.


• Increase in reticulocyte count within 5-10days.
• Hb rises from 0.3g-1.0g per week.
• Increased formimoinoglutamic acid(FIGLU) in urine
following loading dose of histidine is found in folate
deficiency(rarely done) 233
• WHO recommends daily folate intake of 800ug in the
antenatal period and 600 ug during lactation.
• 5mg oral folate per day is administered for Rx
• Continued 4 weeks in puerperium
• Response indicated by fall in LDH levels within 3-4 days and
increase in reticulocyte count
• Parenteral folate is only indicated in gastric intolerance or
late pregnancy
• Serum homocysteine is elevated in folate and vit B12
• Deoxyuridine suppression test can differentiate between
vitamin B12 and folate
• Schilling test for diagnosing pernicious anaemia
• Monthly intramuscular injection of cyanocobalamin (250
microgramms for Rx 234
CLASSIFICATION OF ANTIMALARIAL DRUGS

 4- Aminoquinolines e.g. Chloroquine,


 8- Aminoquinolines e.g. Primaquine
 Quinoline methanols e.g., Mefloquine,
 Cinchona Alkaloids e.g. Quinine, Quinidine
 Phenanthrene-methanol e.g. Halofantrine
 Antifolates: Pyrimethamine, Sulphonamides
 Antibiotics: Tetracyclines, Azithromycin
 Sesquiterpene Lactones e.g. Artemisinin,
 Hydroxynaphthaquinone e.g.Atovaquone
235
236
237
Current National Antimalarial Policy In Nigeria

 ACT recommended as first line therapy for


Nigeria (Art/lum or Ast + AMQ)-January 2005.
 Rationale for combination:
 Worked in TB, Cancer and HIV therapy
 Increase cure rate beyond that of individual
components
 Delays emergence of resistance
 Reduces transmission
Roll Back Malaria: Abuja 2000
 Worldwide partnership
 Governments, private groups, research
organizations, civil society, media
 Aim to reduce malaria by half by 2010
 Free advocacy resources and tools:
http://www.rbm.who.int
 Priority: Prevent poor outcomes caused by malaria
in pregnancy
 Abuja declaration: Goal is for 60% of women in
Africa to be sleeping under insecticide-treated nets
(ITNs) and getting intermittent preventive treatment
(IPT) by 2005 239
INTEGRATED MATERNAL, NEWBORN &
CHILD HEALTH STRATEGY (IMNCH)
• Involves reorganization & reorientation of the
health system to ensure delivery of a set of
essential interventions for provision of
continuum of care for women, newborn &
children
• Initiated 2005
• Pursues MDG 4 & 5 (also 6 & 7)
• Launched in Nigeria in 2007

240
Malaria Prevention during Pregnancy
 Focused antenatal care (ANC) with health
education about malaria
 Use of insecticide-treated nets (ITNs)
 Intermittent preventive treatment (IPT)
 Case management of women with symptoms
and signs of malaria

241
Benefits of Insecticide-Treated Nets
 Prevent mosquito bites
 Protect against malaria, resulting in less:
 Anaemia
 Prematurity and low birthweight
 Risk of maternal and newborn death
 Help people sleep better
 Promote growth and development of fetus
and newborn
242
Indicators of Poor Prognosis in malaria
 Hyper parasitemia: - 5% erythrocytes infested.
 Peripheral schizotaemia.
 Leucocytosis 12,000/ cmm.
 Hb 7.1 gm%.
 PCV 20 %.
 Blood urea 60 mg / dL
 Creatinine 3 mg / dL.,
 Blood glucose 40 mg / dL.
 High lactate and low sugar in CSF.     
 Low antithrombin III level.
243
Malaria and HIV biologic interactions –
Summary 2004
 HIV-associated immunosuppression contributes to
more and worsen malaria and it’s consequences in
adults, pregnant women, and children.
 Malaria contributes to stimulus of HIV replication
and possibly to its consequences: disease
progression, transmission in adults, and MTCT.
 Co-infection with Malaria and HIV in pregnant
women contributes to anemia, low birth weight,
and their risk for poor infant survival.
 Malarial anemia in children too frequently requires
blood transfusion and may still lead to HIV
transmission 244
Malaria & HIV program overlap
 Population overlaps
 Anemic children; pregnant women; adults with
low CD4
 Intervention overlaps
 Diagnostics
 Treatments: complexity and costs of Tx,
resistance
 Protease inhibitors block endothelial CD36
binding of malaria-infected red blood cells
 OI prophylaxis with co-trimoxazole (an
antimalarial)
 HIV-infected persons need malaria prevention
245
Malaria & HIV program overlap
 Recommendations for coordinated program action
 Jointly strengthen health service delivery:
 Laboratories
 Antenatal and delivery care
 ITNs & IPT for malaria; VCT & MTCT 4 HIV
 Child care – anemia prevention
 Specific Interventions
 ITN distribution with ARV delivery
 Use highly efficacious antimalarials in HIV+
persons with malaria infection
 HIV+ persons on cotrimoxazole for OI prophylaxis
who get malaria should receive highly effective
antimalarials
246
• A National survey by the FMH, Abuja, in 2003,
revealed an average national Adequate
Clinical/Parasitological Response(ACPR) for
Chloroquine to be 39%. Consequently, the level of
resistance to CQ was 61%.

• ACPR for the South-Western geopolitical zone was


40.9%,with the level of resistance to CQ of 59.1%.

• The average national ACPR in 2003 to S-P was 57%.


CONSEQUENTLY, it’s level of resistance was 43%.

• ACPR of S-P in the South-western geo-political zone


was 75.6%. Consequently, the level of resistance to
S-P was 24.4%.
247
What is IPTp Strategy? - WHO definition
• At least two curative doses of SP administered
supervised after quickening (after 1st trim) at least
one month apart during pregnancy regardless of
whether the woman has malaria parasitemia or not.

• Number of doses was based on the average number


of ANC visits women had in African countries and on
results of earlier IPTp studies

• 3-4 doses found to be more effective in HIV +ve


women but no difference in HIV –ve women.
248
249

Rationale for the Timing of the SP Doses

Fetal growth
velocity 
Rx Rx

Quickening Last
month

10 16 20 30
Birth
Conception
Weeks of gestation
Source: WHO 2002.
Who should receive IPTp
• All pregnant women in malarious areas
– Though deleterious effects of MIP most pronounced in
Gravida 1 &2, all women suffer some deleterious effects

• Special needs for HIV +ve women


– MIP consequences more severe in HIV +ve women.
– Increased frequency of clinical and placental malaria.
– Patent parasitemia more frequent. Parasite densities
also much higher.
– Need for increased dosing of IPT
– Possible interference with sulpha - based prophylaxis of
opportunistic infections

250
Mefloquine as IPT
Relatively expensive. Resistance is rare in Africa.
– A retrospective study found an increased risk of
stillbirths. Not confirmed in a large prospective trial in
Malawi
– well tolerated at prophylactic dosages (5 mg/kg per
week),
– dose-dependent side- effects—dizziness in particular—
are very common when used for treatment (15 to 25
mg/kg).
– Low tolerability and the rare but more serious
neuropsychiatric adverse effects.
251
Vaccines to prevent malaria in preg.
• Pregnancy-specific vaccines that block cytoadherence
of infected red-blood cells from binding to chondroitin
sulphate A in the placental syncytiotrophoblast could
prevent placental sequestration of P falciparum.
– The success of such a vaccine would depend on whether
placental sequestration is either the only or the main
pathophysiological mechanism responsible for the harmful
effects of malaria in pregnancy.
• A pre- erythrocytic vaccine that effectively prevents
blood stage infections and is not strain specific could
also protect pregnant women.
– the pre-erythrocytic vaccine RTS,S/AS02A is in the most
advanced stage of development.
Malaria estimates
• Annual cases of malaria: Globally 247million
• Annual deaths Globally: 1.1-2.7 miliion
• 91% of deaths were in Africa; 85% in U5 children
• There are an estimated 30 million pregnancies per year in
malaria-endemic areas of Africa.  
• In subsaharan Africa; 10,000 pregnant women die annually
from malaria related causes and 200, 000 newborn die as a
result of their mother’s infection (source CDC 2010)
• 1 death every 45seconds (formerly 30seconds)
• Nigeria: 57,506,000 affected annually with 225,424 deaths
• Nigeria: direct loss to the economy is put at GBP530million

253
In heavily burdened countries the disease
accounts for:
• up to 40% of public health expenditures;
• 30% to 50% of inpatient hospital admissions;
• up to 60% of outpatient health clinic visits.
MDGs that could be impacted by addressing
malaria problem are MDG 1,2,4,5,6and 8

254
ROLL BACK MALARIA PARTNERSHIP
Initiated in 1998 by 4 partners WHO, UNICEF, UNDP, and the World Bank
Primary targets are that by 2010:
• 80% of people at risk from malaria are protected, thanks to locally
appropriate vector control methods such as insecticide-treated nets
(ITNs), and, where appropriate, indoor residual spraying (IRS) and, in
some settings, other environmental and biological measures;
• 80% of malaria patients are diagnosed and treated with effective
antimalarial medicines, e.g ACT within one day of the onset of illness;
• In areas where transmission is stable, 80% of preg women receive IPT;
• Malaria burden is reduced by 50% compared with 2000.
And by 2015:
• Malaria morbidity and mortality are reduced by 75% in comparison
with 2005, not only by national aggregate but particularly among the
poorest groups across all affected countries;
• Malaria-related MDGs are achieved, not only by national aggregate
but also among thepoorest groups, across all affected countries. 255
Global Malaria Action Plan (GMAP)
• Endorsed by RBM partnership at the 2008 MDG
Malaria Summit on 25/09/08
•  Consolidates the input of 30 endemic countries and
regions, 65 international institutions and 250
experts from a wide range of fields.
• The GMAP presents (i) a comprehensive overview
of the global malaria landscape,
• (ii) an evidence-based approach to deliver effective
prevention and treatment to all people at risk and
• (iii) an estimate of the annual funding needs to
achieve the goals of the RBM Partnership for 2010,
2015 and beyond. 256
The targets of the GMAP are to:
• Achieve universal coverage for all popns at risk with locally
appropriate interventions for prevention and case mgt by
2010 and sustain universal coverage until research suggests
that coverage can gradually be targeted to high risk areas
and seasons only, without risk of a generalized resurgence;
• Reduce global malaria cases from 2000 levels by 50% in
2010 and by 75% in 2015;
• Reduce global malaria deaths from 2000 levels by 50% in
2010 and to near zero preventable deaths in 2015;
• Eliminate malaria in 8-10 countries by 2015 and afterwards
in all countries in the pre-elimination phase today; and
• In the long term, eradicate malaria world-wide by reducing
the global incidence to zero through progressive
elimination in countries. 257
Strategy to achieve these targets are:
• control malaria to reduce the current burden and
sustain control as long as necessary,
• eliminate malaria over time country by country and
• research new tools and approaches to support
global control and elimination efforts.
The current tools to track implementation of GMAP
are so called Country roadmaps
 1+ : 1-10 parasites per 100 thick blood film
 2+: 11-100 parasites per 100 thick blood film
 3+: 1-10 parasites per 1 thick blood film
 4+: 11-100 parasites per 1 thick blood film 258
Life cycle Plasmodium
• In humans life cycle starts with inoculation of
sporozoites
• These disappears into the hepatocytes within 30-
60 minutes
• Development in the liver requires about 7-14* days
• The mature schizonts releases merozoites into
blood stream when erythrocytic stage begins
• The erythrocytic stage takes about 36-48 hours for
P. falciparum, P.vivax and P. ovale (and 72h for
malariae)
* ovale and vivax have hypnozoites
Life cycle Plasmodium
In the mosquito genus Anopheles:
• Life cycle begins with the fusion of ingested
gametocytes
• The formation of zygote and ookinette occurs
in the intestinal wall
• Oocyst subsequently undergoes nuclear
fission to produce sporozoites ( an average of 7
days is required)
Indicators of Poor Prognosis
• Hyper parasitemia: - 5% erythrocytes infested.
• Peripheral schizotaemia.
• Leucocytosis 12,000/ cmm.
• Hb 7.1 gm%.
• PCV 20 %.
• Blood urea 60 mg / dL
• Creatinine 3 mg / dL.,
• Blood glucose 40 mg / dL.
• High lactate and low sugar in CSF.     
• Low antithrombin III level.
261
Incidence and prevalence of infectious dxes
• Incidence of an infectious disease: number of new
cases in a given time period expressed as percent
infected per year (cumulative incidence) or
number per person time of observation (incidence
density).
• Prevalence of an infectious disease: number of
cases at a given time expressed as a percent at a
given time. Prevalence is a product of incidence x
duration of disease, and is of little interest if an
infectious disease is of short duration (i.e.
measles), but may be of interest if an infectious
disease is of long duration (i.e. chronic hepatitis B).
• Epidemic: “The unusual occurrence in a community
of disease, specific health related behavior, or other
health related events clearly in excess of expected
occurrence”

• Endemic: It refers to the constant presence of a


disease or infectious agent within a given
geographic area or population group. It is the usual
or expected frequency of disease within a
population.
Hyperendemic and holoendemic
• The term “hyperendemic” expresses that the
disease is constantly present at high incidence
and/or prevalence rate and affects all age
groups equally.

• The term “holoendemic” expresses a high level


of infection beginning early in life and
affecting most of the child population, leading
to a state of equilibrium such that the adult
population shows evidence of the disease
much less commonly than do the children
(e.g. malaria)
Pandemic and Exotic
• An epidemic usually affecting a large
proportion of the population, occuring over a
wide geographic area such as a section of a
nation, the entire nation, a continent or the
world, e.g. Influenza pandemics.

• Exotic diseases are those which are imported


into a country in which they do not otherwise
occur, as for example, rabies in the UK.
Sporadic
• “scattered about”. The cases occur irregularly,
haphazardly from time to time, and generally
infrequently. The cases are few and separated
widely in time and place that they show no or little
connection with each other, nor a recognizable
common source of infection e.g. polio,
meningococcal meningitis, tetanus….

• However, a sporadic disease could be the starting


point of an epidemic when the conditions are
favorable for its spread.
Gestational diabetes (GDM): Carbohydrate
intolerance of varying severity with onset or first
diagnosis during pregnancy.
Eclampsia: onset of generalized tonic-clonic
convulsion during pregnancy, labour and within 7 days
of delivery, excluding neurologic and metabolic causes
of seizures.
Epilepsy: recurring spontaneous seizures due to
sudden excessive and disordered electrical discharge
from the neurons of the cerebral cortex. It is
estimated that 7% of epileptic women become
pregnant and epilepsy affects about 0.5-1% of
pregnant women. 267
Potential DM
• A Hx of diabetes in a first degree relative or two
second degree relatives
• Glycosuria on two or more occasion
• Fasting glycosuria on one occasion
• Maternal weight ≥ 90kg
• A previous baby weighing 4kg or more
• Previous unexplained intrauterine death or early
neonatal death
• Congenital abnormality in a previous pregnancy
Priscilla White classification
• A- Chemical DM (Assymptomatic)
• B- Insulin Rxed DM onset >20yrs old ; duration < 10yrs
• C- Insulin Rxed DM onset 10-20yrs old ; durtn 10-20yrs
• D- Insulin Rxed DM onset <10yrs old ; durtn >20yrs
• F- Diabetic nephropathy
• H- diabetic ischaemic heart disease Banting and
Best discovered
• R- Proliferative retinopathy
insulin in 1921
• T- Renal transplant
Caudal regression syndrome: Abnormalities include sirenomyelia (the
most severe end of the spectrum with fusion of the lower extremitis,
sacral agenesis, anorectal stenosis, anal atresia, anal aplasia, renal
dysplasia, neurogenic bladder and malformed external genitalia.
1:60,000 269
Diagnostic Criteria outside
pregnancy
• Fasting Plasma Glucose of 126mg/dl (7mmol/L) or
more
• Random Plasma Glucose of 200mg/dl (11.1mmol/L)
or more
• 200 mg/dl or more at 2hrs following a 75gm OGTT
• Impaired Glucose Tolerance 140-199mg/dl
(7.8mmol/L-11.0mmol/L) at 2hr at OGTT
• Impaired Fasting Glucose 100-125mg/dl (5.6-
6.9mmol/L)
Diagnostic Criteria in Pregnancy
• No Universally agreed Diagnostic criteria
• Europe/WHO
– 75 gm 2hour OGTT
• North America
– 100 gm 3 hour OGTT
WHO CRITERIA FOR DIAGNOSIS
OF DIABETES
Venous plasma glucose level (mmol/l)

Fasting 2hr post prandial

Diabetes ≥ 8.0 ≥ 11.0

Impaired glucose 6.0 - <8.0 ≥ 8.0 to <11.0


tolerance
Normal <6.0 <8.0
RECENT WHO CRITERIA FOR DIAGNOSIS
OF DIABETES

273
3-hour 100gm GTT
Time ADA Thresholds* NDDG Thresholds*
hour
(mg/dl) (mg/dl)
Fasting 95 105
1 180 190
2 155 165
3 140 145
ADA. American Diabetic association.
NDDG. National Diabetic Data Group.
If two or more values meet or exceed these thresholds,
the diagnosis of gestational diabetes is made.
Effects of pregnancy on DM
• Hyperglycemia.
• Diabetic nephropathy.
• Diabetic retinopathy.
• Deterioration in those with
autonomic neuropathy & gastric
paresis.
Effects of DM on pregnancy
• Miscarriage.
• Pre-eclampsia
• Diabetic nephropathy & anaemia.
• Infections.
• 60% CS rates.
• Congenital anomalies. Sacral agenesis, heart, MSS,
& NTD.
• Increase in PNMR.
• IUD. Ketoacidosis, chronic hypoxia
• RDS
• NNJ
• Macrosomia
• Polyhydramnios
Preconceptional Care in DM
• To prevent excess spontaneous abortion and
congenital malformation in infants of diabetic
mothers
• Specific Goal is to lower HbA1c
• Unplanned pregnancies occur in 2/3 of
diabetic mothers even in developed countries
– effective contraception
• Evaluation of co-existing medical conditions
Evaluation for co-existing Medical conditions
Components of Antenatal
Management
Management of Diabetes in
Pregnancy
• The goals of management are
– Maintain FBS at 60-95mg/dl (whole blood)
– 2 hour post-prandial of <120mg/dl (whole blood)
– HbA1c of less than 6%
Dietary Management
• 30-35 Kcal/kg/day in Women of Normal
weight
• 30-40 Kcal/kg/day in women less than 90% of
desirable body weight
• 24 kcal/kg/day in women more than 120% of
desired body weight
Dietary Management
• 40-50% complex carbohydrates
• 20% proteins
• 30-40% unsaturated Fats
• 10-20% breakfast
• 20-30% lunch
• 30-40% dinner
Insulin Regimen
Dietary strategy for women with GDM.
Daily caloric requirements.
Current weight in relation Daily caloric
intake
to ideal body weight. (Kcal/kg)
<80% 35-40
80-120% 30
120-150 24
>150% 12-15
Risk Factors for Preeclampsia
Maternal-specific factors Pregnancy-associated factors
• >35 years or <20 years • Chromosomal abnmalities
• Black race • Hydatidiform mole
• FHx of preeclampsia • Hydrops fetalis
• Nulliparity • Multiple gestation
• Previous hx of preeclampsia • Oocyte donation or donor
• Medical conditions: DM, insemination
obesity, chronic HTN, renal • Structural congenital
dx, thrombophilias anomalies
• Stress • Urinary tract infection
• New male partner

286
Hypertension
– Single measurement of DBP  110mmHg.
– Two consecutive measurements of DBP  90mmHg taken
 4 hours apart.
– BP of 30/15mmHg above booking BP in the 1st trimester
– Mean arterial pressure > 105mmHg

Significant Proteinuria
– 300mg of total protein in 24hour urine .
– Two random clean-catch or one catheter urine specimen
with 2+ (1g alb/L) on reagent strip
– 1+ (0.3g albumin/L), if specific gravity is < 1.030 and pH
< 8.
287
Severe preeclampsia
• Blood pressure: 160 mm Hg or higher systolic or
110 mm Hg or higher diastolic on 2occasions at
least six hours apart in a woman at rest or
120mmHg on one occasion
• Proteinuria: 5 g or more of protein in a 24-hour
urine collection or 3+ or greater on urine dipstick
testing of two random urine samples collected at
least four hours apart
• Other features: oliguria (<500 mL of urine/24hrs),
cerebral or visual disturbances, pulmonary edema
or cyanosis, epigastric or right upper quadrant pain,
impaired LFT, thrombocytopenia 288
Diagnostic criteria for HELLP
The diagnosis is established by the presence of
preeclampsia and the following criteria:
• Microangiopathic hemolytic anemia with
characteristic schistocytes on blood smear
• Platelet count <100,000 cells/µL
• Serum lactate dehydrogenase (LDH) >600 IU/L or
total bilirubin >1.2 mg/dL
• Serum aspartate aminotransferase (AST) >70 IU/L

289
Urine dipstick for proteinuria
• Trace- 100mg
• 1+- 300mg
• 2+- 1g
• 3+- 3g
• 4+- 5g
• Puerperal pyrexia: occurrence of fever ≥380C twice
within 24hrs after delivery up to 14days excluding first
24hours.
• Puerperal sepsis: Puerperal pyrexia due to genital tract
infection.
• Puerperal infection: Puerperal pyrexia due to infection
other than genital tract infection. 290
• Pregnancy Induced Hypertension: Hypertension
with or without proteinuria developing after 20th
week gestation, during labour or puerperium in a
previously normotensive, non-proteinuric woman.
-Pregnancy induced hypertension (no proteinuria)
-Pregnancy induced proteinuria (no hypertension)
- Preeclampsia: Pregnancy induced proteinuric
hypertension.
• External cephalic version: Transabdominal
manipulation of a fetus presenting breech to
convert it to cephalic presentation with the aim of
achieving vaginal delivery.
291
NYHA Functional Classification for Congestive HF
• Class I: No breathlessness or limitation of physical
activity.

• Class II: breathlessness on severe exertion, slight


limitation of physical activity

• Class III: breathlessness on mild exertion or marked


limitation of physical activity.

• Class IV : breathlessness at rest, inability to carry


out physical activity without discomfort. 292
Newman scoring index
Used to predict success of ECV. Success rates is 0 %
with score < 2 and 100 % with score > 9
0 1 2
1 PARITY 0 1 2
2 DILATATION > 3 cm 2-1 cm 0 cm
3 EFW <2.5 kg 2.5 – 3.5kg > 3.5 kg
4 PLACENTA Anterior Posterior Lateral
5 STATION ≥-1 -2 ≤-3

Success rate in general is 35 – 86 % ( average58%)


improves with: Multiparity, Frank breech, Transverse
lie, Africa – American patient 293
Zatuchni Andros prognostic scoring index
0 1 2
1 Parity Primigravida Multigravida
2 GA (wks) ≥ 39 37-38 < 37
3 EFW (kg) >3.5 2.5 – 3.5 <2.5
4 Previous breech none 1 2
of average wgt
5 Dilatation 2 3 4
6 Station -3 -2 -1

Used to assess breech presentation presenting in


labour, to determine likelihood of vaginal delivery.
Good score ≥ 6 294
Obesity: Excess body fat OR
Imbalance between energy intake and expenditure

BMI Kg/M2 WHO CLASSIFICATION Description


Quetelet index
< 19 Underweight Thin
18.5 -24.9 Normal Healthy, normal
25.0 -29.9 Grade 1 Overweight Overweight
30.0-39.9 Grade 2 Overweight Obese
>40 Grade 3 overweigh Morbidly obese

Normal Waist Hip Ratio: 0.82–0.85

295
UTI in pregnancy
• True bacteriuria: >105 of bacteria of the same species
per ml of urine
• Asymptomatic bacteriuria: Presence of true bacteriuria
without subjective evidence of UTI eg frequency,
dysuria & urgency or detection of leukocyte esterase
using Nitrite dipstick on a clean urine catch. Occurs in 5
– 8% of patients
• Relapse: Recurrence of bacteriuria caused by the same
organism, usually within 6wks of the infection.
• Reinfection: Recurrence of bacteriuria involving a
different strain of bacteria after successful eradication
of the initial infection.
296
Nigeria and Global HIV Burden (2008)
• Nigeria has the second highest number of people living
with HIV in the world after South Africa.

• With about 2.98million PLHIV, accounts for about 9% of


the global HIV burden.

– 812, 001 require ARV drugs.


– home to one out of every 11 persons with the virus worldwide
[4],

• Home to 30% of the global PMTCT Gap burden


The AIDS epidemic in Nigeria
• Nigeria ( tenth largest country in the world,
the most populous country in Africa).
• Infection primarily- heterosexual transmission.
• HIV seroprevalence sentinel surveys involving
pregnant women attending antenatal clinics
by the FMOH.
• The results from 2008 showed a national
prevalence of 4.6%. -Generalized.
PREVALENCE OF HIV/AIDS IN NIGERIA

• 1.8% in 1991
• 4.5% in 1996
• 5.4% in 1999
• 5.8% in 2001
• 5.0% in 2003
• 4.4% in 2005
• 4.6% in 2008
Nigerian National HIV Prevalence Trend
1991 – 2008

7.0

6.0
5.8
5.4
5.0 5.0

4.5 4.6
4.4
Prevalence (%)

4.0
3.8

3.0

2.0
1.8

1.0

0.0
1991 1993 1995/96 1999 2001 2003 2005 2008
Year
Estimated Magnitude of MTCT in Nigeria
Population 140 million

Birth rate per annum 42/1000


Birth per annum 5,900,000
HIV prevalence in ANC women 4.4%
Estimated number of HIV exposed 260,000
infants at risk of MTCT annually

Estimated No. of HIV positive infants 65,000 to


per annum without intervention 117,500
Source: Nigerian National PMTCT Guidelines (2007)
The AIDS epidemic in Nigeria
• Some parts of the country are worse affected than others,
but no State or community is free from its scourge.

• 10.6% in Benue state to 1.0% in Ekiti state.


– 17 states and the FCT had a prevalence of 5.0%.

• Youths between the ages of 20 and 29 are more affected.


– Prevalence was generally higher in the urban than rural
areas.
303
Global impact of the HIV epidemic
on children
• 14 percent (370,000 of 2.7 million) of new
global HIV/AIDS infections

• 14 percent (270,000 of 2.0 million) of


HIV/AIDS deaths annually

• 6 percent (2.0 million of 33.0 million) of the


persons living with HIV

Over 90% of children acquire HIV through


mother-to-child transmission (MTCT)
2008 global HIV and AIDS estimates
Children (<15 years)
• Children living with HIV 2.1 million [1.2 – 2.9
million] -6.3% of 33.4 X 106

• New HIV infections in 2008 430 000 [240 000 – 610


000] - 14.3% of 3.0 X 106

• Deaths due to AIDS in 2008 280 000 [150 000 – 410


000] -14% of 2.0 X 106

• Over 90% of children acquire HIV through mother-to-


child transmission (MTCT)

December 2009
HIV INFECTION AND PREGNANCY
 Not a significant cause of congenital abnormalities or
spontaneous abortion.

 Late HIV disease may affect pregnancy outcome- poor


fetal growth, preterm del., LBW and prenatal and neonatal
death.

 Pregnancy appears to have little effect on the progress of


infection in asymptomatic HIV- positive women or in those
with early infection, although there may be more rapid
progression in women with late stage HIV infection.
Factors affecting mother-to-child transmission of HIV-1
VIRAL
 Viral load
 Viral genotype and phenotype
 Viral resistance
MATERNAL
 Maternal immunological status
 Maternal nutritional status
 Maternal clinical status
 Behavioural factors (Smoking, Alcohol, Injection
drug use)
 HIV infection acquired during preg or breastfeeding
 Genital tract infections ( STIs, Chorioamnionitis)
Factors affecting mother-to-child transmission of HIV-1
OBSTETRICAL
 Prolonged rupture of membranes ( > 4 hours )
 Mode of delivery
 Intrapartum haemorrhage
 Obstetrical procedures
 Invasive fetal monitoring
Factors affecting mother-to-child transmission of HIV-1

FETAL
 Prematurity
 Genetic
 Multiple pregnancy
 Placental malaria

INFANT
 Breastfeeding
 Gastrointestinal tract factors
 Immature immune system
Risk Factors for Postnatal Transmission
• Younger maternal age, lower parity
• Maternal sero-conversion during lactation
• Maternal immune status (CD4)
• Plasma and breast milk viral load
• Duration of breastfeeding
• Breast health:
– Mastitis (clinical and subclinical),
– Breast abscess
– Cracked nipples
• Infant factors (oral thrush)
• Pattern infant feeding – exclusive vs mixed
Components of PMTCT (UNGASS)
1. Primary prevention of HIV infection in
women of reproductive age
2. Prevention of unintended pregnancies
among women infected with HIV
3. Prevention of HIV transmission from
women infected with HIV to their babies
4. Provision of treatment, care, and support to
women infected with HIV, their infants, and
their families
Strategies of PMTCT
Strategies Thrusts
Prevention of HIV among •Abstinence
women of childbearing age •Being faithful
•Condom use
•Safe blood transfusion
•Safety of sharps

Prevention of unintended •Family planning counseling and services


pregnancy among HIV- •Abortion/postabortion services
positive women
Prevention of MTCT •Universal ANC patronage
•HIV Counseling & testing (opt-out approach)
•Anti retroviral drug prophylaxis/therapy
•Safe obstetric & delivery practices
•Infant feeding counseling and support

Provision of care & support •Mother/family’s HIV care/treatment


to HIV-infected women, •Early infant diagnosis & treatment
their infants & families •Support for OVC
•Strengthening of social/economic/nutritional support
312
Factors affecting mother-to-child
transmission of HIV(1)
VIRAL FACTORS Viral load, genotype and phenotype

MATERNAL FACTORS Immunological/ nutritional/clinical status ,


behavioral factors, antiretroviral treatment.

OBSTETRICAL FACTORS PROM(>4hrs), mode of delivery,


intrapartum hemorrhage, obstetrical
procedures, invasive fetal monitoring

FETAL FACTORS Prematurity, genetics (concordant


infant/maternal HLA), multiple pregnancy

INFANT FACTORS Breastfeeding, gastrointestinal tract


factors, immature immune system
Objectives of the
National PMTCT Program
• Reduce prevalence of risky behaviour that
promote transmission of HIV among women
and their partners by 50% by 2010

• Increase demand and uptake of VCT among


pregnant women by 75% of current level by
2010

• Prevent unintended pregnancy among HIV


positive women by 75% by 2010

• Ensure that 50% of HIV positive pregnant


Shittu 2006 1

women and their babies access ARV by 2010314


Objectives of the National
PMTCT Program - 2
• Increase access to obstetrics practices that
reduce risk of mother to child transmission of
HIV by 50% by 2010

• Ensure that 80% of HIV positive mothers


practise infant feeding options based on their
informed choice by 2010

• Ensure that all HIV positive mothers after


delivery, their partners and all HIV positive
infants access ARV and other care and
Shittu 2006 26
support services 315
• HIV testing: the process that determines whether a
person is infected with HIV or not.
• HIV counselling: the confidential dialogue btw
individuals and their health care providers to help
clients examine their risk of acquiring or transmitting
HIV infection and to make informed decisions based on
information available to them.
• Alpha response: A viral load drop that is ≥ 1.0 log10
suggesting that treatment is very likely to succeed
Checked about one month after starting treatment.
• Opportunistic infections (OIs): refer to disease
conditions, which ordinarily will not occur in a person
with competent immune system but thrive in persons
with a compromised immune response. 316
National PMTCT Protocol
ANC Clinic & ANC Side Laboratory:
• Group counseling
• Routine offer of HIV testing with option to decline.
• Testing algorithm using 2 Rapid tests and a tie breaker to
confirm positive cases
• Individual Post test counseling

Post test counseling for HIV Positive women


• Birth options and other preventive measures.
• Counseled on ARV interventions
• Counseled on infant feeding options
• Need to deliver in hospital
• Need for Partner notification
National PMTCT Protocol
Post test for HIV Negative
• Counsel on ‘ window period’
• Consider re-testing in labour
• Offer syndromic STI management
• Importance of partner testing

HAART: (Highly active antiretroviral therapy)


involves the use of three or more drugs, drawn
from at least two of the main classes of
antiretroviral (ie NRTIs, NNRTIs and PIs)
Clinical setting I :Pregnant woman who is HAART-
eligible but not currently receiving ARV prophylaxis
Clinical setting II: Pregnant woman not eligible for
HAART for her own disease
Clinical setting III: Pregnant woman receiving HAART
at the time of the current pregnancy
Clinical setting IV: HIV-infected woman who presents
in labour
Clinical setting V: HIV-infected woman who presents
after delivery
Clinical setting VI: HIV-infected woman with active TB
Clinical setting VII: HIV-infected women with
indication for ART, but required drugs are not
available. 319
CLINICAL STAGE 1
• Asymptomatic
• Persistent generalized lymphadenopathy
CLINICAL STAGE 2
• Moderate unexplained weight loss (under 10% of
presumed or measured body weight)
• Recurrent respiratory tract infections (sinusitis,
tonsillitis, otitis media, pharyngitis)
• Herpes zoster
• Angular cheilitis
• Recurrent oral ulceration
• Papular pruritic eruptions
• Seborrhoeic dermatitis
• Fungal nail infections
320
CLINICAL STAGE 3
• Unexplained severe weight loss (over 10% of presumed or
measured body weight)
• Unexplained chronic diarrhoea for longer than one month
• Unexplained persistent fever (intermittent or constant for
longer than one month)
• Persistent oral candidiasis
• Oral hairy leukoplakia
• Pulmonary tuberculosis
• Severe bacterial infections (e.g. pneumonia, pyomyositis)
• Acute necrotizing ulcerative stomatitis, gingivitis or
periodontitis
• Unexplained anaemia (<8 g/dl ), neutropenia (<0.5 x 109/l)
and/or chronic thrombocytopenia (<50 x 109 /l) 321
CLINICAL STAGE 4: HIV wasting syndrome; Pneumocystis
pneumonia; Recurrent severe bacterial pneumonia; Chronic
herpes simplex infection (orolabial, genital or anorectal of
>1month’s duration or visceral at any site); Oesophageal
candidiasis (or candidiasis of trachea, bronchi or lungs);
Extrapulmonary TB; Kaposi sarcoma; CMV infection (retinitis
or infection of other organs); CNS toxoplasmosis; HIV
encephalopathy; Extrapulmonary cryptococcosis including
meningitis; Disseminated non-TB mycobacteria infection;
Progressive multifocal leukoencephalopathy; Chronic
cryptosporidiosis; Chronic isosporiasis; Disseminated mycosis;
Recurrent septicaemia (including non-typhoidal Salmonella);
Lymphoma (cerebral or B cell non-Hodgkin); Invasive cervical
carcinoma; Atypical disseminated leishmaniasis; Symptomatic
HIV-associated nephropathy or HIV-associated
322
cardiomyopathy.
Nucleoside Non- Nucleotide
Reverse Nucleoside Reverse Fusion Protease
Transcriptase Reverse Transcriptase Inhibitors Inhibitors (PIs)
Inhibitor NRTIs Transcriptase Inhibitors
Inhibitors (NrRTI)
(NNRTIs)
Zidovudine Nevirapine Tenofovir Enfuvirtide Saquinavir-
(ZDV) (NVP) (TDF) ritonavir (SQV/r)
Didanosine Efavirenz Maturation (T-20) Ritonavir (RTV)
(ddl) (EFV) inhibitors Indinavir (IDV)
Zalcitabine Delavirdine Eg Bevirimat Nelfinavir (NFV)
(ddc) (DLV) Amprenavir
Stavudine(d4t) Etravirine (APV)
Lamivudine (ETV) Lopinavir-ritonavir
(3TC) Lersivirine (LPV/r)
Abacavir(ABC) Rilpivirine Atazanavir-
Emtricitabine ritonavir (ATV/r)
(FTC) Tipranavir

Integrase inhibitors eg Raltegravir, Elvitegravir


323
Chemokine co-receptor 5 (CCR5) blocker eg Mariviroc
ARV Drug Toxicity
DRUG TOXICITY MINOR MANAGEMENT
ZDV Anaemia, neutropoenia, Blue or black For severe anaemia,
thrombocytopoenia, discoloration reduce dose or change
myopathy, intolerance of nails, to d4T
nausea,
headache

3TC Pancreatitis, liver toxicity, Skin rash, If serum amylase


mild peripheral neuropathy headache elevated, discontinue
d4T Peripheral neuropathy, Insomnia, If severe peripheral
lipoatrophy, lactic acidosis, anxiety, panic neuropathy, abnormal
hepatitis, pancreatitis attacks serum amylase, and
transaminase, discntinue

NVP Skin rash (DRESS syndr), Do not give if CD4 >250


Stevens-Johnson because of severe
syndrome, hepatotoxicity hepatotoxicity
EFV Nightmares, rash, Dizziness If hepatitis, discontinue
hepatitis 324
Release of WHO Rapid Advice (Nov 2009)
• Release of WHO Rapid Advice (November 2009)
– “Rapid advice on the use of anti-retroviral drugs for
treating pregnant women and preventing HIV infection
in infants
– “Rapid advice on HIV and Infant feeding; revised
principles and recommendations”
• Adaptation of the Rapid Advice by PMTCT Task
Team (January/February 2010)
• Approval by Hon. Minister of Health (March 2010)
General Principles
Combination regimens are more effective than single or
double drug regimens.
Combination Highly Active Antiretroviral Therapy is
standard of care for treatment of maternal HIV infection
and prevention of mother to child transmission of HIV.
Pregnancy in the HIV positive woman is an indication for
prophylactic ART irrespective of CD4 count, viral load or
clinical stage of the disease.
All efforts should be made to ensure that all HIV positive
pregnant women have access to ART.
The normal CD4 count in a healthy adult is between 600
and 1,200 cells/mm3
General Principles (II)
All patients placed on ART should be monitored clinically,
biochemically and immunologically.
Pre-treatment evaluation should include:
Complete history and physical examination.
Checking laboratory parameters (FBC/ESR, FBS, LFT, E&U, Serum lipids,
CD4 count and viral load).
WHO clinical and immunological staging of the client.
Ensuring availability of supportive measures (nutritional and psychosocial).
Patient-specific adherence strategy
If facility for CD4count is not available, the client should be
referred or client’s specimen sent to the nearest centre with
such facility.
Where the patient is on AZT only for prophylaxis, the
minimum tests to be done will include HB /PCV, CD4 count and
urinalysis.
Eligibility criteria for ART or ARV prophylaxis in HIV
infected pregnant women (Ref: WHO 2009)

If facility for CD4count is not available, the client should be referred


or client’s specimen sent to the nearest centre with such facility. 328
Clinical Setting I
Pregnant woman who is HAART- eligible but not currently
receiving ARV prophylaxis Contd.
Alternative regimen:
 TDF+ (3TC or FTC) + (NVP++ or EFV**)
– *(Patients with HB≤ 8g/dl or PCV ≤ 24%),
– Hepatitis B co infection
• **EFV based regimen should NOT be used in the
first trimester

• Closely monitor for hepatotoxicity and systemic


toxicity ESPECIALLY women on NVP based regimen.
Caution :
The use of antiretroviral drugs in first trimester of pregnancy
requires caution:
Women already commenced on HAART; ZVD, 3TC and NVP
and found to react to NVP in first trimester pregnancy:
• Stop the NVP and replace with PI ***
• ***PIs include : Lopinavir/r, Saquinavir/r, Nelfinavir.
• **EFV use in early pregnancy is associated with congenital
malformations [Potential risk (probably <1%) of neural tube
defect with EFV use in first month of pregnancy (before 6
weeks of gestation)]
• ** Women on EFV based combination should be counselled
and offered effective contraception after delivery to avoid
conception while on EFV.
330
Special considerations on ART in PMTCT
Previous clinical or virological failure on NNRTI
PI* + 2 NRTIs
ZDV + 3TC + Abacavir
ZDV + 3TC + Tenofovir
Previous single-dose nevirapine
< 6months :
PI* + 2 NRTIs
> 6 months :
NVP + 2NRTIs
EFV + 2 NRTIs
ZDV + 3TC + Abacavir
ZDV + 3TC + Tenofovir
331
ARV Prophylaxis for the infant
 

All infants should receive daily NVP from birth until six
weeks of age.
This is irrespective of infant feeding practice.

Dose of daily NVP:


Birth weight < 2,500g : NVP 10mg(1ml) daily
Birth weight ≥ 2,500g : NVP 15mg(1.5ml) daily

332
Clinical Setting II :
For facilities with capacity (on – site or by linkage) to
provide and monitor Triple ARV medication:
• Triple ARV prophylaxis is the preferred regimen:
• Triple ARV prophylaxis should be started from 14 weeks
gestation or as soon as possible when the woman
presents during pregnancy
Any of the these regimens may be used as appropriate
AZT + 3TC + LPV/r
AZT + 3TC + EFV
AZT + 3TC (or FTC) + EFV
AZT + 3TC + ABC
TDF + 3TC (or FTC) + EFV 333
2. For facilities with limited capacity (on – site or
by linkage) to provide and monitor triple ARV
medication
The following ARV prophylactic regimen is
recommended:
 Zidovudine from 14 weeks gestation.
Sd NVP at onset of labour
AZT+3TC during labour and delivery
AZT+3TC for 7 days post partum

If haemoglobin is ≤ 8g/dl (PCV ≤ 24%), avoid


Zidovudine and refer to next level of care.
334
The Infant
• A For breastfeeding infants:
Commence daily NVP and continue until one
week after cessation of all breastfeeding.
• B For non-Breastfeeding infants:
Give daily NVP for 6 weeks only
All HIV exposed infants must receive daily NVP
for 6 weeks irrespective of infant practice

335
DOSAGE OF DAILY NVP FOR THE INFANT
From birth to 6 weeks of age:
Birth weight < 2,500g : NVP 10mg(1ml) daily
Birth weight ≥ 2,500g : NVP 15mg(1.5ml) daily
From 6 weeks to 6 months of age:
NVP 20mg(2ml) daily
From 6 months to 9 months of age:
NVP 30mg(3ml) daily
From 9 months to 12 months of age:
NVP 40mg(4ml) daily
336
Clinical setting III:
• HIV infected women receiving HAART who become
pregnant should continue with the therapy.

Zidovudine should be a component of the regimen


whenever possible [avoid if haemoglobin is < 8 g/dl
or PCV < 24%;
in this case use TDF + 3TC (or FTC) + NVP (or EFV) as
applicable]

• Efavirenz is contraindicated in the first trimester and


it should be replaced with NVP. 337
Clinical setting IV
1. For facilities with capacity (on – site or by linkage) to
provide and monitor Triple ARV medication:
Mother
 Commence triple ARV prophylaxis during labour and
continue until one week after all exposure to breast milk
has ended.
For details of regimen see clinical setting II.

 Clinically assess the mother for WHO staging of


maternal disease
 Determine maternal CD4 count as soon after birth as
practicable.
338
Clinical setting IV
2. For facilities with limited capacity to provide and
monitor triple ARV medication.
 Mother:
• Intrapartum:
sdNVP + ZDV + 3TC as soon as diagnosis is made
• Post partum:
ZDV + 3TC for 7 days
• Determine if mother is eligible (within 5 days of
delivery) for HAART for her own disease, and follow
appropriate guidelines including referral to ART
Care programme 339
Clinical setting IV:
Infant:
• Mother breastfeeding not commenced on HAART:
Give daily NVP to infants from birth until one
week after all exposure to breast milk.
• Mother breastfeeding (eventually on HAART)
Give daily NVP to infants from birth and continue
until six weeks after maternal commencement of
HAART
• Mother not breastfeeding:
Give daily NVP to infants from birth until 6 weeks
of age. 340
Clinical setting V:
Mother
• Determine if Mother is eligible for HAART for her own
disease, and follow appropriate guidelines including referral
to ART /Care programme
Infant: Mother breastfeeding not commenced on HAART:
Give daily NVP to infants from birth until one week after
all exposure to breast milk has ended. 
• Mother breastfeeding (eventually commenced on HAART)
Give daily NVP to infants from birth and continue until
six weeks after maternal commencement of HAART
•   Mother not breastfeeding:
Give daily NVP to infants from birth until 6 weeks of age.
341
Clinical setting VI:
• Delay ARV treatment until second trimester, if
possible.
Treatment regimens: These are in decreasing order
• If treatment is initiated in second trimester
EFV (800mg) + 2NRTIs
ZDV + 3TC + Abacavir
2 NRTIs + Ritonavir-boosted PI* (Saquinavir/r or
Lopinavir/r)
ZDV + 3TC + Tenofovir
Change rifampin to low dose rifabutin
342
Clinical setting VI:
Infant
 Give daily NVP to infant from birth until 6
weeks of age.
 Prophylactic INH from birth (5mg/Kg once
daily) until six (6) months of age.

• Dosage of NVP
• See Clinical Setting IV above.

Nigeria National PMTCT Training Slides


343
Module 4
Clinical Setting VII:

All efforts should be made to ensure that all HIV


pregnant women who need ART have access
to it either on site or by referral.

344
ARV Prophylaxis for Newborn Infants in all settings:
• Single dose NVP syrup (2mg/kg) as soon as possible
after birth(< 72 hours)
• Followed by ZDV syrup (4mg/kg/dose twice daily)
for 6 weeks. (Former regimen for infants)
NOTE: Lamivudine, emtricitabine & tenofovir are
effective against Hep B infection.
Post test counselling for HIV Negative
• Counsel on ‘ window period’
• Consider re-testing in labour
• Offer syndromic STI management
• Importance of partner testing 345
ANC Clinic & ANC Side Laboratory:
• Group counseling
• Routine offer of HIV testing with option to opt out.
• Testing algorithm using 2 Rapid tests and a tie breaker to
confirm positive cases
• Individual Post test counseling

Post test counseling for HIV Positive women


• Birth options and other preventive measures.
• Given prophylactic ART where available or
Nevirapine 200mg tab to take home for use in early
labor
• Counseled on infant feeding options
• Need to deliver in hospital
• Need for Partner notification
ADOPTION EMBRYO DONATION
• Risk free method • Donors must be
• Product is not a genetic confirmed to be HIV
child of male partner negative
• Difficult to obtain as HIV • Risk free method
status in the family may • Total protection from
be a legal reason for infection by partner
refusal • Product is not a genetic
• In Africa adoption is not child of both partners
popular
TIMED UNPROTECTED INTERCOURSE (TUI)
• Timed unprotected intercourse during ovulation reduces
but does not eliminate the risk of HIV transmission
• Risk of Male to female transmission without HAART is 0.1
– 0.3% per act of intercourse in stable monogamous
relationship without other risk factors
• Risk of Female to male transmission without HAART is 0.03
– 0. 09% per act of intercourse
• Factors that influence transmission include plasma viral
load, presence of STIs and frequency of intercourse
• With prolonged use of HAART (> 6 months) and
undetectable viral load transmission risk is reduced
• It is not recommended except if other options not
acceptable or accessible
DONOR INSEMINATION

• Donated semen must be confirmed to be HIV


negative
• Risk free method
• Total protection from infection by partner
• Product is not a genetic child of male partner
SPERM WASHING
• The practice is pioneered by Semprini et al.
• It is a risk reduction method
• It is based on the observation that HIV is present in seminal
fluid and as cell associated virus in leucocytes and non-
spermatozoa cells (NSC) but is not capable of attaching to
or infecting spermatozoa
• Involves density gradient centrifugation and swim-up to
separate progressively motile HIV-free sperm from NSC and
seminal plasma, which remain in the supernatant.
• As quality control for the procedure, and to protect the
service from medico – legal action, an aliquot of washed
sperm should be tested for detectable HIV RNA prior to
sample being used for treatment.
Hep C
• Irrespective of whether a patient has HIV infection, the
optimal treatment for hep C infection is pegylated
interferon alpha and ribavirin (RBV).
• These drugs are complex to deliver and costly.
• The initiation of ART in HIV/HCV-coinfected patients should
follow the same principles as in HIV-monoinfected patients.
• However, the pts should be ffed up more closely bcos of
the major risk of drug-related hepatotoxicity and for
specific drug interactns of some ARVs with anti-HCV drugs
• • Ribavirin and ddI –> pancreatitis/lactic acidosis (do not
give concomitantly).
• • Ribavirin and AZT –> anaemia (monitor closely).
• • Interferon and EFV –> severe depression (monitor closely351
Universal precautions: A concept of blood borne dx
control which requires that all human bld and other
potentially infectious materials be treated as if known to
be infectious for HIV, HBV, HCV or other bld borne
pathogens, regardless of the perceived “low risk” status
of a pt or pt popn.
Simple standard of infection control practices to be used
in the care of all pts at all times to reduce the risk of
transmission of bld borne infections. Components incld:
1.Hand washing with soap and water.
2.Use of protective barriers to prevent direct contact.
3.Safe handling and disposal of sharps
4.Safe decontamination of instruments and equipments.
5.Safe disposal of waste contaminated with body fluids.
352
• Puberty: the stage of physical maturation in which
an individual becomes physiologically capable of
sexual reproduction.
• Period when the endocrine and gametogenic fxns of
the gametes first devp to the point when
reproduction is possible. Av age in Nigeria: 13yrs

• Reproductive health: Reproductive health is a state


of complete physical, mental and social well-being
and not merely the absence of disease or infirmity,
in all matters relating to the reproductive system
and to its functions and processes.
353
 Reproductive health care: is the constellation of methods,
techniques and services that contribute to reproductive
health and well-being through preventing and solving
reproductive health problems. It also includes sexual health,
which includes healthy sexual devpt; equitable and
responsible relationships and sexual fulfilment; and
freedom from illness, diseases, disability, violence, and
other harmful practices related to sexuality.
Reproductive rights: include the basic right of all couples
and individuals to decide freely and responsibly the number,
spacing and timing of their children and to have the
information and means to do so. It also includes their right
to make decisions concerning reproduction free of
discrimination, coercion and violence, as expressed in
human rights documents. 354
The components of reproductive health
10/31/2022

 Safe Motherhood
 Infant and child survival, growth and devepment.
 Adolescent reproductive health and sexuality.
 Human sexuality.
 Family planning
 Abortion — including the prevention and
management of unsafe abortion.
 Infertility — prevention and management.
 Prevention and management of STIs & HIV/AIDS.
 Gender discrimination — gender inequity and
inequality.
 Traditional practices harmful to women
355
 Management of Reproductive tract malignancies, and other
non- infectious conditions of the reproductive system such
as genital fistula, cervical cancers and complications of
female genital mutilation.
 Reproductive health problems associated with menopause
& andropause.
RH Rights includes sexual rights which is:
• Right to sexual freedom – right to express full sexual
potential; excludes all forms of exploitation or abuse
• Right to sexual autonomy, integrity and safety within the
person’s personal and social ethics
• Right to sexual privacy – right for individual decisions and
behaviours about intimacy as long as they do not intrude
on the sexual rights of others
• " Sexual health is a state of physical, emotional,
mental and social well-being related to sexuality; it
is not merely the absence of disease, dysfunction or
infirmity. Sexual health requires a positive and
respectful approach to sexuality and sexual
relationships, as well as the possibility of having
pleasurable and safe sexual experiences, free of
coercion, discrimination and violence. For sexual
health to be attained and maintained, the sexual
rights of all persons must be respected, protected
and fulfilled.“

357
• Sexuality is a central aspect of being human
throughout life and encompasses sex, gender
identities and roles, sexual orientation, eroticism,
pleasure, intimacy and reproduction. Sexuality is
experienced and expressed in thoughts, fantasies,
desires, beliefs, attitudes, values, behaviours,
practices, roles and relationships. While sexuality
can include all of these dimensions, not all of them
are always experienced or expressed. Sexuality is
influenced by the interaction of biological,
psychological, social, economic, political, cultural,
ethical, legal, historical and religious and spiritual
factors."
358
• Gender based violence: Violence involving men and
women, in which the female is usually the victim;
which is derived from unequal power relationship
btw men and women.
• National health insurance scheme (NHIS): Social
security system that guarantees the provision of
needed health services to persons on the payment
of a premium (token contribution) at regular
intervals.
NHIS is a corporate body established under Decree
35 of 1999 by the FGN to improve the healthcare of
all Nigerians at a cost the government and the
citizens can afford. 359
International Planned Parenthood Federation
10/31/2022

(IPPF) Charter on Human Rights


Components of Women’s Sexual & Rep. Rights:
1. The right to Life.
2. The right to liberty and security of the person.
3. The right to equality and to be free from all
forms of discrimination.
4. The right to privacy.
5. Right to freedom of thought.

360
• 6. Right to information and education.
• 7. Right to choose whether or not to marry
and to found and plan a family.
• 8. Right to decide whether and when to have
children.
• 9. Right to healthcare and protection.
• 10. Right to benefits of scientific progress.
• 11. Right to freedom of assembly and political
participation
• 12. Right to be free from torture and ill
treatment
361
Ethics in PND
• Ethics
– Deals with decision making
– Making good choices, choices we can live
with….. That improve life and society
• Principles
– Relationship: based on trust
– Autonomy: choice and liberty issues
– Beneficence: act in best interest of others
– Non maleficence: do no harm
– Justice: do what’s fair
BIOETHICAL ANALYSIS
The Guiding Principles In Bioethics

1. RESPECT FOR PERSONS:


 Autonomy of capable persons - respect the right to self
determination and individual liberty. (Informed
voluntary consent and confidentiality).
 Overriding Autonomy – Medical Paternalism which is
divided into strong and weak.
 Protection of persons incapable of autonomy – children,
the mentally sub-normal and the unconscious.

2. NON-MALEFICENCE - Ethical duties to do no harm or


wrong.

363
3. BENEFICENCE- Responsibility to do and maximize good. (do good to
others and maintain a balance between benefits and acceptable
harms).

4. JUSTICE - Fairness and equity in Medicare to persons.


(Equitable distribution of potential benefits and risks).

Others include:

5. VERACITY- tell all the truth.

6. FIDELITY - do what is promised.

7. SCIENTIFIC VALIDITY- ensure professional competence and


scientific soundness.
364
The Nine Elements of Surgical Ethics

• Non-maleficence • Rescue
• Beneficence • Relational proximity
• Autonomy • Ordeal
• Justice • Aftermath
• Presence
• Steroidogenesis is a component of steroid
metabolism ; the latter encompasses steroid
synthesis, steroidogenesis and steroid
degradation

• Steroidogenesis is the biological process by


which steroids are generated from cholesterol
and transformed into other steroids

• ln humans, because the products of


steroidogenesis are basically steroid hormones,
steroidogenesis is widely equated to steroid
hormone biosynthesis.
Subclassification of steroids
• Can be subclassified based on their chemical
composition & structure
Class Example No of Carbon atoms
Cholestanes cholesterol 27
Cholanes cholic acid 24
Pregnanes progesterone, 21
corticosteroids
Androstanes testosterone 19
Estranes estradiol 18
Interactions between placenta and fetal adrenals(& liver)
Tanner Staging of Breast and Pubic Hair Development (1962)
Breast Development (From age 9;mean 9.8 yrs)
• Stage 1 – Infantile stage with no development, elevation
of papilla only
• Stage 2 – Breast bud stage. Elevation of breast and papilla
as small mound with enlargement of areola diameter
• Stage 3 – further enlargement and elevation of breast and
areola with no separation of their contour
• Stage 4 – projection of areola and papilla to form a
secondary mound above the level of the breast
• Stage 5 – mature stage : projection of papilla only caused
by recession of the areola to the general conduct of the
breast
Pubic Hair Development – 12- 15 yrs
• Stage 1 – no pubic hair
• Stage 2 – Scattered labial hair; sparse growth of long,
slightly pigmented downy hair straight or curled along
labia
• Stage 3 – Spread to mons pubis; the hair spreads
sparsely over the mons pubis and is darker in colour,
more coarse
• Stage 4 - Slight lateral spread ; hair – now adult like, but
area covered is still considerably smaller than adult-
now spread to lateral surface of thighs.
• Stage 5 – Adult appearance in quantity and type with
spread to medial surface of thighs.
Precocious puberty :
• Appearance of secondary sexual maturation at an
age greater than 2.5 SD below the mean.
• Breast and pubic hair before the age of 8years
• Menstruation before the age of 10 years.
It could be classified as:
1)GnRH – Dependent Precocious Puberty
• Constitutional – the commonest cause resulting
from premature activation of HPO axis.It’s a
diagnosis of exclusion – appearance in correct
order Gonadotrophins are adult level.
• Organic disorders e.g
 Harmatomas ventricular
 Tumours – craniopharyngioma, neuroblastoma, glioma,
Infections processes – brain abscess, meningitis,
encephalitis
 Other CNS processes – head trauma, hydrocephalus,
cerebral oedema often reversible, occurring 1-2 month
after insult.
2)GnRH – Independent precocious puberty 
• 10% of females with PP have ovarian tumour. Usually
gonadal- stromal in origin- and oestrogen secreting e.g
granulosa cell or theca cell; rarely- teratomas,
gonadoblastomas . Functional ovarian cysts.
• Adrenal tumours – usually with high DHEA, DHEAS
3) McCuine – Albright syndrome: polyostotic fibrous
dysplasia, Café –au- lait pigmentation,precocious
puberty
4)Exogenous oestrogens
• Medications
• Cosmetics and commercial production

Isolated Precocious Development 


• Premature Thelarche – Usually self limiting
• Premature Menarche- Infection, foreign body, abuse,
trauma, local neoplasm should be excluded.
• Premature Adrenarche – Adrenal tumour should be
excluded often idiopathic of no clinical significance.
Delayed Puberty -2.5 SD above mean age for puberty onset
• Constitutional delay – Anatomic or Genetic
• Hypogonadotrophic Hypogonadism
>CNS Tumours
>Congenital malfunctions:Isolated gonadotrophin deficiency,
Kallman syndrome, Idiopathic hypopituitary dwarfism
>Prader-willi syndrome
>Functional gonadotrophin deficiency
>Nutritional deficiency
>Hypothyroidism
>Exercise and stress induced amenorrhoea
>Diabetes, Cushing syndrome
>Marijuana use, hyperprolactinaemia
• Hypergonadotrophic hypogonadism
– Gonadal dysgenesis
– Turner syndrome
– Mosaicism
– True gonadal dysgenesis
– Primary Ovarian failure idiopathic
– Chemotherapy or Ovarian radiation
– Enzyme deficiencies.
• Pearl index: statistical estimation of the number of
unintended pregnancies in 100 woman-years of exposure
(e.g. 100 women over one year of use, or 10 women over
10 years).
There are two calculation methods:
• number of pregnancies in the study divided by the number
of months of exposure, multiplied by 1200.
• number of pregnancies in the study divided by number
of menstrual cycles experienced by women in the study,
multiplied by 1300. 1300 instead of 1200 is used on the
basis that the length of the average menstrual cycle is 28
days, or 13 cycles per year.
Usually two Pearl Indexes are published:
• Actual use Pearl Index, which includes all pregnancies in a
study and all months (or cycles) of exposure.
• Perfect use or Method Pearl Index, which includes only
pregnancies that resulted from correct and consistent use
of the method, and only includes months or cycles in which
the method was correctly and consistently used. 376
METHOD PEARL RATE
Contraceptive sponge 9 - 25  
Rhythm methods 6 - 25
Spermicide only 4 - 25
Coitus interruptus 8 - 17
Male condom (sheath) 2 - 15
Female condom 5 - 15
Diaphragm 4 - 20
IUCD (Coil) 0.2 - 2
Levonorgestrel intrauterine system Less than 0.5
Progestogen only pill 0.3 - 4
Combined pill 0.1 - 3
Subcutaneous implants  0- 0.1
Depo-Provera (injection) 0-1
Sterilisation - Female 0 - 0.5
                     - Male 0- 0.05

377
378
• Pearl Index assumes a constant failure rate over time. This
wrong bcos: 1.the most fertile couples will get pregnant
first. 2.Most birth control methods have better
effectiveness in more experienced users. So the longer the
study length, the lower the Pearl Index will be.
• PI provides no information on factors other than accidental
pregnancy which may influence effectiveness eg:
-Dissatisfaction with the method
-Trying to achieve pregnancy
-Medical side effects
-Being lost to follow-up
• A common misperception is that the highest possible PI is
100 - i.e. 100% of women in the study conceive in the 1st
year; if all the women conceived in the 1st month, the
379
study would yield a PI of 1200 or 1300.
• Family planning: A way of thinking and living that is
adopted voluntarily upon the basis of knowledge,
attitude and responsible decisions by an individual or
couple in order to promote health and welfare of the
family group and contribute effectively to the social
development of the country.
• Contraception: The voluntary prevention of pregnancy
by interrupting the chain of events that lead to
conception. The prevalence rate (PR) of modern
methods among all women in Nigeria is 8.9%; PR of all
methods is 12.6% (NDHS 2003).
• Medical regimen 4 abortion is 200 mg of mifepristone,
given orally, ffed 24–48 hours later by a PG– either 0.8
mg of misoprostol or 1 mg of gemeprost – vaginally. 380
World Health Organization (WHO) developed eligibility
criteria for the use of various contraceptive methods.
• Category 1: A condition for which there is no
restriction for the use of the contraceptive method.
• Category 2: A condition where the advantages of
using the method generally outweigh the theoretical
or proven risks.
• Category 3: A condition where the theoretical or
proven risks usually outweigh the advantages of
using the method.
• Category 4: A condition which represents an
unacceptable health risk if the contraceptive method
is used.
ABSOLUTE CONTRAINDICATIONS TO COCP
1. < 6 weeks postpartum if breastfeeding
2. Smoker over the age of 35 (≥ 15 cigarettes per day)
3. Hypertension (systolic ≥ 160mm Hg or diastolic ≥ 100mm Hg)
4. Current or past history of venous thromboembolism (VTE)
5. Ischemic heart disease
6. History of cerebrovascular accident
7. Complicated valvular heart disease
8. Migraine headache with focal neurological symptoms
9. Breast cancer (current)
10. Diabetes with retinopathy/nephropathy/neuropathy
11. Severe cirrhosis
12. Liver tumour (adenoma or hepatoma)
RELATIVE CONTRAINDICATIONS
1. Smoker over the age of 35 (< 15 cigarettes per day)
2. Adequately controlled hypertension
3. Hypertension (systolic 140–159mm Hg,
diastolic 90–99mm Hg)
4. Migraine headache over the age of 35
5. Currently symptomatic gallbladder disease
6. Mild cirrhosis
7. History of combined OC-related cholestasis
8. Users of medications that may interfere with
combined OC metabolism
NON-CONTRACEPTIVE BENEFITS OF COCP
1. Cycle regulation
2. Decreased menstrual flow
3. Increased bone mineral density
4. Decreased dysmenorrhea
5. Decreased perimenopausal symptoms
6. Decreased acne
7. Decreased hirsutism
8. Decreased endometrial cancer
9. Decreased ovarian cancer
10. Decreased risk of fibroids
11. Possibly fewer ovarian cysts
12. Possibly fewer cases of benign breast disease
13. Possibly less colorectal carcinoma
14. Decreased incidence of salpingitis
15. Decreased incidence or severity of moliminal symptoms
385
Instructions on the Use of OCP
Initiation of use (choose one):
• The patient begins taking the pills on the first day of
menstrual bleeding.
• The patient begins taking the pills on the first
Sunday after menstrual bleeding begins.
• The patient begins taking the pills immediately if
she is definitely not pregnant and has not had
unprotected sex since her last menstrual period.

386
MISSED PILLS
• A COCP is said to be missed if 12hours elapse from
the time the pill was to be taken and three hours for
a progestogen only pill.
• Missing pills at the beginning or end of the 21-day
cycle has the effect of lengthening the hormone-free
interval.
• If the hormone free interval exceeds 7 days, the risk
of ovulation and possible conception is increased.
• Forgetting tablets in the second or third week
of the 21-day cycle is unlikely to increase
the risk of ovulation if the hormone-free
interval does not exceed 7 days.
• If less than 12 hours late: Don't worry. Just take the
delayed pill at once, and further pills as usual .
• More than 12 hours late: Take the most recently
delayed pill now. Discard any earlier missed pills
• Use extra precautions (condom, for instance) for the
next 7 days
How many pills are left in the pack after the most
recently delayed pills?
• 7 or more Pills: When you have finished the pack,
leave the usual 7-day break before starting the next
pack
• Fewer than 7 Pills: When you have finished the
pack, start the next pack next day, without a break
388
Mgt of missed COCPs
Missed Progestin only Pills

• 3 or more hours late: Take a pill as soon as you


remember. Use a backup method for 48 hours.
INTRA-UTERINE CONTRACEPTIVES
• Interference with implantation
• Increase with sperm transport
• Inhibit capacitation
1. Non medicated (inert) e.g Lippes loop
2. Medicated - less bleeding and pain
Eficacy - 1.5 per 100 woman years
CU DEVICES
1st Generation Cu7, Cu T
2nd Generation Multiload 250, Nova T
3rd Generation Multiload 375, Cu T 380 A, Flexigard
330, Cu Fix PP 330
Progesterone Progestasert – levonorgestrel,
Releasing Devices Levonova - levonorgestrel
MIRENA (Levonova):
– Introduced in 1990
– Delivers levonorgestrel 20ug/day: use for 5 yrs
– As effective as sterilisation
– Preg: 0.1– 0.2 per 100 women in 1yr.
• In 5yrs : 0.5—1.1
• Causes less bleeding than Copper bearing IUCDs
• Can be used to treat heavy menstrual bleeding or
painful menstrual cramps
• May be a useful alternative to hysterectomy for some
women
INJECTABLE STEROIDS
•Depot Medroxyprogesterone Acetate (up john) Supplied in
aqueous microcrystalline suspension150mg/ml in 1ml and
3ml/vials. Must be well shaken before filling the syringe,
site of injection must not be rubbed because this disperses
the injection. Amorphous white deposit is left in the msl
which is slowly absorbed. I.M buttocks or upper arm.
Pregnancy rates of 0.0 - 1.2 per 100 women years reported
for 150mg 12wkly.

•Depot Norethisterone Oenanthate - derivative of 19


nortestosterone supplied as 200mg/ml in benzyl benzoate
and castor oil in 1ml vials. More difficult to inject and may
cause some discomfort. 0.01 - 1.3 per 100 woman years;
given every 8 weeks.
•Third may be in use in the near future: CYDCLOPROVERA
ONCE - A MONTH INJECTABLES IN USE
1. Dihydroxyprogesterone acetophenide (acetophenide
150mg and estradiol enanthate 10mg).
DHPA/E2-EN “Deladroxate” or Perlutal
2. Depot-Medroxyprogesterone acetate 25mg and
estraldiol cypionate 5mg DMPA/E2C; HRP11Z “Cyclofem” or
“Cycloprovera.
3. Norethisterone enanthate 50mg and estradiol valerate
5mg NET-EN/E2V; HRP102 “Mesigyna”
4. 17 & Hydroxyprogesterone caproate 250mg
andestraldiol valerate 5mg Chinese injectible No. 1
• Norigynon is a combined injectable contraceptive
that contains 5 mg Estradiol valerate + 50 mg
norethisterone enanthate. 12-month failure rates
are less than 0.4% (1/250)
Non-contraceptive Benefits of norigynon
• Decreases menstrual flow (lighter, shorter periods)
• Decreases menstrual cramps (dysmenorrhoea)
• May improve anaemia
• Favorable metabolic profile (lipid, carbohydrate, liver)
• Protects against ovarian and endometrial cancer
• Decreases benign breast disease and ovarian cysts
• Prevents ectopic pregnancy
• Protects against some causes of PID
SIDE EFFECTS
1. Menstrual Disturbances: Frequent and irregular
bleeding 71% women of 1st injection
2. Amenorrhoea: 54% of woman after 1 year of Rx. 35%
have complete Amenorrhoea during at least 1
injection cycle. Amenorrhoea cycles becomes less
frequent with Noristerat
Management of Irregular bleeding
With combined oral contraceptive
Premarin 1.25 - 2.5mg daily x 21 days.
3. Weight gain: Result of an increase appetite
4. Delayed return of fertility: 6 - 12 months. 2 years in extreme
cases. Quicker return of ovulation with DNO.
Women who have been treated for depression or have been
depressed while taking OCP should not use depot
contraceptive.
CONTRAINDICATIONS
ABSOLUTE
 Abnormal uterine bleeding
 Secondary amenorrhoea
 Arterial & liver disease
 Cancer of the breast (except where used to treat
endometrial cancer and breast cancer)
 Trophoblastic disease until HCG levels are normal.
RELATIVE
 Abnormal uterine bleeding - a definite established and
possibility of genital malignancy eliminated.
 Depression may be aggravated malignancy eliminated.
 Investigations of CHO metabolism may be distorted.
 Women with history of thrombembolism
 B.P before Rx once controlled, DMPA can be used.
• NET-EN and Mesigyna are oil-based solution.
Warming the vial to body temperature makes it
easier to draw into the syringe to prevent leakage.
• DMPA is an aqueous suspension, a DMPA vial
must be shaken vigorously before it is loaded into
the syringe, to resuspend any active ingredient in
the bottom of the vial.
• POI can be given: up to 2 weeks early or late
• Combined Injectables : Up to 3 days early or late
• Progestogen-Only Injectables :Suitable for
women who are breastfeeding at 6wks postpartum.
• Combined Injectables :Not suitable for women
fully breast feeding until 6 mths postpartum.
CONTRACEPTIVE IMPLANTS
(i) Norplant -6 soft capsules (36mg levonorgestrel each)
- Insertion is in the medial aspect of the upper part of
the non-dominant arm. Provides 5 years protection (same as
Jadelle)- efficacy 1st year rates 0.2% and cumulative 5-year
pregnancy rate 3.9%
- side effects are time dependent with the rate
declining
by about 50% after 1 yr. No delay in restoration of fertility
- no more available (used)
(ii) Jadelle 2 silicon capsules (75mg levonorgestrel each)
(iii) ST 1435 (Nestrone)-Lactation, less lipoprotein effects.
(iv) Uniplant (Nomegestrel Acetate) (1 year)
(v) Implanon - 3 Keto-Desogestrel (3 year) i.e 68mg
NuvaRing
• Releases 120µg of progestin etonogestrel and 15µg of
EE/day

• Left in vagina for three weeks. Removed for one week

• Can be re-inserted if it has been out for <3hours

• 8/10 partners do not feel the ring during intercourse

• A new NuvaRing is needed for each four week cycle

• Effectiveness: 1.2 pregnancies per 100women


Transdermal Patches (Ortho Evra)
• It delivers 150µg of the progestin norelgestromin
and 20µg of estrogen ethinyl estradiol per day
• 3 layers; outer protective polyester layer, middle
medicated adhesive layer and a clear polyester-
removable
• Delivers hormones thru skin
• Placed on any part of body
• Adheres to skin: normal activity even bathing
• Reduce adhesion: creams, oils powder, makeup.
• As effective as COC. Better compliance
• Experimental patch: 3.16 cm release 50ug
gestodene and 18ug of EE/day.
Indications for emergency contraception:

When no contraceptive has been used


• Contraceptive failure
• Condom breakage, slippage, incorrect use
• 2 or more consecutive missed COC pills
• Late taking of minipills
• More than 2weeks late for progestin-only injectable
contraceptive
• More than 7days late for a combined estrogen&
progestin monthly injection
• IUCD expulsion
• Sexual assault while not on contraception
Hormonal
• Levonorgestrel- only regimen: 1.5mg in a single dose or
in two doses of 0.75mg taken up to 12hours apart

• Combined estrogen-progestin (Yuzpe) regimen: two


doses of 100mcg ethinyl estradiol & 0.5mg of
levonorgestrel taken 12hours apart

Effectiveness:
• Levonorgestrel regimen: 60-93%
• Combined regimen: 56-89%
• New research indicates that ECPs can prevent
pregnancy up to five days (120hours) after
unprotected intercourse against the previous 72
hours timing

• The effectiveness of the single-dose regime (LNG


1.5 mg) is similar to that of split-dose LNG

• Its currently the recommended regime approved for


use up to 72 hours following unprotected sexual
intercourse
Mifepristone
• Progesterone receptor antagonists/modulators can
also be used for EC.

• Mifepristone is superior to LNG in efficacy

• Doses of 25-50 mg are very effective, and lower


doses (less than 25 mg) may be equally good.

• Menstrual delay is common with mifepristone.


Ulipristal acetate
• a selective progesterone receptor modulator

• One 30mg dose should be taken as soon as possible,


but no later than 120 hours after, unprotected
intercourse. 

• Randomised controlled trials show that it is more


effective than LNG (failure rate 1.4% versus 2.2%)

• Women on COC should use barrier method until the


next menses bcos it affects P4 metabolism.
MALE HORMONAL CONTRACEPTIVE
Still in the trial phase with four major groups
• Aim is to achieve azoospermia although studies have
shown that <1million/ml is functionally sterile.

• 99% effective

• 5-20% are non responders


TYPES
1. Androgen only
2. Progestin with androgen replacement
3. GnRH antagonist with androgen replacement
4. Androgen and progestin receptor modulators
• Abortion: Extraction of a fetus weighing 500g or
less corresponding to 20-22weeks gestation.
• Recurrent: 3 consecutive spontaneous abortion
• Residive: 2 consecutive spontaneous abortion
• Unsafe abortion: Termination of an unintended
pregnancy by a person lacking the necessary skills
or in an environment lacking the minimal medical
standards or both.
• Post abortal care: A composite care given to a
woman after an abortion process and the partner
where appropriate in order to prevent future risk
of unwanted pregnancy and its complications.
410
Statutory grounds for TOP in UK
A The continuance of the pregnancy would involve
risk to the life of the pregnant woman, greater than
if the pregnancy were terminated

B The termination is necessary to prevent grave


permanent injury to the physical or mental health
of the pregnant woman

C The pregnancy has not exceeded 24thweek and the


continuance of the pregnancy would involve risk,
greater than if it were terminated, of injury to the
physical or mental health of the pregnant woman 411
D The pregnancy has not exceeded its 24th week and
the continuance of the pregnancy would involve
risk, greater than if the pregnancy were terminated,
or injury to the physical or mental health of the
existing child (ren) of the family of the pregnant
woman
E There is a substantial risk that if thechild were born
it would suffer from such physical or mental
abnormalities as to be seriously handicapped
F To save the life of the pregnant woman
G To prevent grave permanent injury to the physical
or mental health of the pregnant woman
412
Types - Primary aborters – Women without a previous live
born infant
-Secondary aborters – Women with at least one live
born infant.
Recurrent pregnancy loss is the syndrome that causes
repeated abortion, stillbirth, premature delivery which
impair ability to have a live birth.
• 1- 2% of all pregnancies.
• 10 – 15% of all clinically recognized pregnancies end in
miscarriage.
• Theoretical probability of recurrent abortion is 0.3 – 0.4%
- This excess of over the probability suggests that there are
some pathological factors responsible (not by chance)
- Maternal age and previous number of miscarriages are two
independent risk factors for a further abortion.
- The rate of chromosomal aberrations in abortus decrease
with increasing number of past abortions.
Burden of unsafe abortion
• 211 million pregnancies occurred worldwide in 2008
• 46 million (20%) resulted in induced abortions; 60% of
which were safe abortion.
• 22 million of these women had an unsafe abortion; 99%
occurring in developing countries; with 25% occurring in
Africa (5.5million)
• 67 000 - 70 000 women die from complications of
unsafe abortion each year - all in developing countries
• With a woman dying every 8minutes worldwide
• 13%of MM in Nigeria= 5750 deaths/year
• 60% among aged 15-24 years in Africa
• 28/1000 women 15-44yrs in West Africa 414
• Unsafe abortion rate: the annual number of unsafe
abortions per 1000 women aged 15–44 years. This
measure describes the level of unsafe abortion in a
population.
• Unsafe abortion ratio: the number of unsafe
abortions per 100 live births. Indicates the
likelihood that a pregnancy will end in unsafe
abortion rather than a live birth.
• Unsafe abortion mortality ratio: the number of
deaths due to unsafe abortion per 100 000 live
births.
• Unsafe abortion case-fatality: estimated number
of deaths per 100 000 unsafe abortion procedures
415
UNINTENDED PREGNANCIES:
THE ROOT OF ABORTION
• Of the estimated 208million pregnacies in 2008,
33 million (16%) resulted in unintended births.
• 23 million pregnancies that occur in devped
countries, >40% are unintended, and 28% end in
induced abortion.
• Of the 185 million pregnancies that occur in
developing countries, 40% are unintended, and 19%
end in induced abortion.
• Average woman must use an effective contraceptn
for at least 20 years if she wants to limit her family
size to two children, and 16 years if she wants four.
416
• According to a 2009 report, an estimated 215 million
women in the developing world have an unmet need
for modern contraceptives, meaning they want to avoid
a pregnancy but are using a traditional family planning
method or no method.
• Some 82% of unintended pregnancies in developing
countries occur among women who have an unmet
need for modern contraceptive.
• The reasons why women do not use contraceptives
most commonly include concerns about possible health
and side-effects and the belief that they are not at risk
of getting pregnant.
• Unmet need for contraception in Nigeria is 16.7%-rural
and 17.3%-urban (NDHS 2003) 417
CRIMINAL CODE
Section 228: Any person who, with intent to procure the
miscarriage of a woman, whether she is or not with child,
unlawfully administers to her or causes her to take any
poison or other noxious thing or uses force of any kind or
uses any other means whatever, or permits any such thing
or means to be administered or used to her guilty of a
felony to imprisonment for 14 years.

Section 229: Any woman who with intent to procure her own
miscarriage , whether she is or not with child, unlawfully
administers to herself any poison or other noxious thing or
uses force of any kind or uses any other means whatever, or
permits any such thing or means to be administered or
used to her guilty of a felony to imprisonment for 7 years.
Section 230: Any person who unlawfully supplies to or
procures for anything whatever, knowing that it is
intended to be lawfully used to procure the
miscarriage of a woman, whether she is or not with
child , is guilty of a felony and is liable to
imprisonment for 3 years.
Section 297: A person is not criminally responsible for
performing in good faith and with reasonable care
and skill a surgical operation upon for this benefit,
or upon an unborn child for the preservation of the
mother’s life, if the performance of the operation is
reasonable, having regard to patient’s state at the
and all the circumstances of the case.
PENAL CODE
Section 232: Whoever voluntarily causes a woman with child
to miscarry shall, if such a miscarriage be not caused in
good faith for the purpose of saving the life of the woman,
be punished with imprisonment for term which may extend
to fourteen years or with fine or with both
Section233: Whoever intent to cause the miscarriage of a
woman whether with child or not does any act which
causes the death of such a woman, shall be punished.
a) With imprisonment for a term which may extend to three
years or with fine with both; and
b) If the offender knew that the woman was with child, he
shall be punished with imprisonment for a term which
may extend to five years or with fine or with both.
Section 234:
• Whoever used force to any woman and thereby
unintentional causes her to miscarry, shall be
punished.
a) With imprisonment for a term which may extend
to three years or with fine with both; and
b) If the offender knew that the woman was with
child, he shall be punished with imprisonment for
a term which may extend to five years or with fine
or with both.

421
• Ectopic gestation: Implantation of a fertilized
ovum outside the endometrial lining of the uterus
• Arias Stella rxn: Exuberant endometrial response
to ectopic pregnancy. Diagnosed histologically by
hyperchromatic, hypertrophic, irregularly shaped
nuclei and foamy vacuolated cytoplasm.
• Heterotopic pregnancy: Extra-uterine pregnancy
co – existing with intra-uterine pregnancy
• Incidence in spontaneous conception: 1 in 30,000
• Incidence following ART: 1 in 100 pregnancies

422
• Bagel sign: Adnexal mass with a hyperechoic ring
around the gestational sac with an empty uterus
• Blob sign: Heterogeneous mass adjacent to and
moving separately from the ovary with an empty
uterus
• Galactorrhea: Inappropriate lactation outside of
pregnancy and one year after cessation of lactation.
• Substance abuse: Any substance or drug which when
used has a rapid effect on the CNS which alters the
consciousness or cause a change in the mental state of
the person.
• Endometriosis: a disorder in which hormonally
responsive endometrial tissue is found outside the
uterine cavity. 423
Ectopic in other sites
 Heterotopic: No room for expectant or medical mgt
• Ovarian
• Oophorectomy (localised surgical resection with
preservation of the ovary if detected early)
• Cervical
• Hysterectomy
• Tamponade with inflated Foley's catheter
• MTX administration avoids severe haemorrhage
• Abdominal: Diagnostic challenge; Surgery done.
 Placenta at laparotomy (Leave or remove)
 Give MTX or don’t give if placenta is left
Ovarian ectopic (Spiegelberg’s criteria)

• Tube on the affected side must be intact


• Gestational sac must be located in the ovarian
fossa
• Must be connected to the uterus by the ovarian
ligament
• Ovarian tissue must be found on its wall on
histology

31/10/22 06:38 PM Ectopic Pregnancy 425


Cervical ectopic criteria (Clinical)
• Soft, enlarged cervix equal to or larger than the
uterus

• Painless uterine bleeding following amenorrhea

• Products of conception entirely confined within


and attached to the endocervix

• Closed internal os with partially opened external os.


31/10/22 06:38 PM Ectopic Pregnancy 426
Cervical ectopic criteria (Rubins)
• Cervical gland must be present opposite placental
attachment.

• Attachment of placental to cervix must be intimate

• Placental must be below the entrance of uterine


vessels or below the peritoneal reflection on the
anteroposterior uterine surface

31/10/22 06:38 PM Ectopic Pregnancy 427


Abdominal ectopic criteria (Studdiford)
• Normal ovaries and tubes.

• Absence of uteroperitoneal fistula

• GS should be related exclusively to the


peritoneal surface and early enough to
eliminate 10 implantation in tube.
31/10/22 06:38 PM Ectopic Pregnancy 428
Genital prolapse
– Anatomical: protrusion of pelvic organs beyond its
anatomical boundaries.
– Functional: any symptomatic genital tract support
defect where the leading edge of the prolapse is
beyond the hymenal remnants.

429
SUPPORTS OF THE UTERUS AND VAGINA
The normal position of the uterus is maintained mainly by 3
factors:
1. The cervical ligaments: consist of 3 pairs:
• The Mackenrodt’s ligament; the most important part
• The uterosacral ligaments
• The Pubocervical ligaments
2. The pelvic floor muscles:
The levator ani muscles is the most important & consists of 3
parts:
– The ischio-coccygeus muscle
– The ilio-coccygeus muscle
– The pubo-coccygeus muscle; the most important part
3. The anteverted position of the uterus
430
Normal Vaginal Support
Three Levels of Support:
(DeLancey)
• Level I (upper level):
– Ischial spine & sacrospinous
ligaments
• Level II (middle level):
– Pubocervical fascia anteriorly
– Rectovaginal fascia posteriorly
– Levator ani muscles (through
the arcus tendineus fasciae
pelvis)
• Level III (lower level):
– Perineum
– Urogenital Diaphragm
431
Pathophysiology of Genital Prolapse
• Neuromuscular Dysfunction
– Delayed & Weakened Levator Contraction
– Damaged pelvic nerves
• Uterus:
– Weakness of the ligaments and Endopelvic Connective
Tissue holding the uterus
• Vagina:
– Detachment from the Pelvic Sidewall (Paravaginal
defects)
– Weakness/Tears of the Endopelvic Connective Tissue
(Central defects) 432
AETIOLOGY OF PROLAPSE
A) Predisposing Factors:
Weakness of the pelvic supports of the genital organs
• Weakness of the cervical ligaments and pelvic cellular
tissue
• Detachment of strategic fascial supports
• Injury of the pelvic floor muscles
B) Precipitating Factors
– Increased weight of the uterus: multiple small
fibroids.
– Raised IAP: chronic cough, constipation or abdominal
tumour.
– RVF; brings it in the axis of the vagina
– In vault prolapse; poor attention to vaginal vault
support at the time of hysterectomy. 433
Aetiology - Predisposing factors
I. Weakness of the cervical ligaments and pelvic cellular
tissue
A) Obstetric childbirth trauma:
• Straining during the first stage of labour.
• Wrong forceps application.
• Prolongation of the 2nd stage of labour leads to pressure
& stretching of levator ani
• Rapid succession of pregnancies, before involution of
the pelvic structures.
B) Congenital and developmental weakness:
• leads to the appearance of prolapse at an early age, the
so-called “nulliparous” or even “virginal” prolapse.
C) Postmenopausal atrophy:
• Oestrogen deficiency & ageing may lead to loss of
collagen and weakness in CT & fascia, particularly in
patients predisposed to by obstetric trauma. 434
Aetiology - Predisposing factors
II. Injury to the pelvic floor muscles:
A) Childbirth trauma;
Due to overstretching of the muscles causing deep
lacerations.

B) Perineal tears;
Especially when unsutured or badly repaired after labour.

C) Widening of the urogenital hiatus; Resulting in:


– Patulous introitus
– Increased tendency of the uterus and vagina to
prolapse through.
– Large baby may stretch and weaken the levator
muscles although the skin of the perineum remains
intact, the so-called “hidden perineal tear”.
435
BADEN-WALKER HALF-WAY SYSTEM
GRADE POSITION OF PROLAPSE SITE
0 No prolapse
1 Half-way to hymen
2 To hymen
3 Half-way past hymen
4 Maximum descent

436
PELVIC ORGAN PROLAPSE QUANTIFICATION (POPQ)
SYSTEM

STAGE POSITION OF PROLAPSE SITE


0 No prolapse
1 >1 cm above hymen
2 ≤ to 1cm proximal or distal to plane of hymen
3 > 1cm below plane of hymen, but protrudes
no further than 2cm less than the total length
4 Eversion of the lower genital tract is complete

• International Standard Classification System for Genital


Prolapse made by International Continent Society.
• Established in 1996. Is more accurate & objective 437
Pessary treatment
• Aim: To bring out temporary relief of symptoms in
cases were surgery is generally refused, risky, or
should be temporarily delayed.
• Indications of pessary treatment
1. Therapeutic test to confirm that presenting symptoms
are due to prolapse
2. Promote healing of decubital ulcers prior to surgery
3. Temporary contraindications to surgery as severe cough,
lactation, and patient refusal.
4. During pregnancy until the middle of second trimester
when the size of the uterus will be sufficient to prevent its
descent.
5. In young patients with mild degree of prolapse that wish
to avoid surgery
6. Medically unfit patients, as very old age, morbid obesity,
cerebrovascular accidents, etc. 438
Pessary treatment
• Types of Pessaries used in prolapse
Silicon-rubber-bases pessaries are the most popular form
of conservative therapy. They are inserted into the vagina,
and need replacements at variable intervals

A) The Ring pessary:


Introduced in the vagina, above the level of the levator ani
muscles. It stretches the redundant vaginal walls and
prevents descent of the uterus.
B) The shelf pessary:
Shelf pessaries are rarely used (Gelhorn pessary), but may
be useful in women who cannot retain a ring pessary due
to very weak pelvic floor muscles, especially those with 2nd
degree prolapse, old age and high risk for surgical
treatment.
C) The “cup and stem” pessary: is no more in use nowadays.
439
Colpexin™ Sphere
• New Intravaginal Device (IVD)
• Available in 5 sizes: 44, 42, 39,
36, & 32 mm
• Allows for prolapse elevation
while uniquely facilitating
the performance of
concomitant PFM exercises

440
Surgical treatment for genital prolapse
Surgery: The only curative approach in treatment of
prolapse
Aim: to restore both anatomy and function.
Indications:
– Most cases of moderate or severe degrees of
prolapse.

The type & extent of surgery: depend largely on


1. the type and degree of prolapse,
2. the patient’s general condition
3. Her plans for future fertility. 441
Traditional Operations for Genital Prolapse
• Cystocele and Cystourethrocele: Anterior Colporrhaphy
• Rectocele: Posterior Colpo-perineorrhaphy
• Enterocele
– Vaginal Repair: the commonest approach
– Abdominal repair: (rarely attempted, Moskowitch
operation)
• Uterovaginal prolapse
– Classical repair with shortening of the Mackenrodt's
ligaments Based on the
– Manchester (Fothergill’s) operation principle of
– Vaginal Hysterectomy and PF repair ‘Midline Plication’
– Le Fort’s operations of stretched &
• Vaginal Vault Prolapse torn fascia)
– Abdominal approach (abdominal sacro-colpopexy)
– Vaginal approach (sacrospinous ligament fixation) 442
CURRENT STRATEGY TO PROLAPSE
SURGERY
• Based on DeLancey’s anatomic
model of 3-level support for
normal vagina
• Strategy to:
– Restore all anatomic support
– Preserve desired function
• Sexuality
• Childbearing

443
SUSPENSION OPERATIONS FOR PROLAPSE

Current concepts
• Sling operations
• Closure or repair of enterocele
• Sacrocolpopexy
• Anterior Colpopexy
• Colposuspension
• Paravaginal repair

444
Abdominal Sling operations
• Indicated when the ligaments are extremely weak as in
nulipara & young women.
• Preserves reproductive function.
• Use fascial strip / prosthetic material (Merselene tape or
Dacron)
• Cervix is fixed to abdominal wall / sacrum / pelvis.
• Cervix amputated if Utereo-cervical length >12.5cm.
• Coexisting Cystocele/Rectocele repaired vaginally before
or after.
• Coexisting Enterocele repair done abdominally.

445
Abdominal
Colpopexy/Colposuspension
• Indicated at vault prolapse after hysterectomy or
vaginal laxity need correction at abdominal
hysterectomy.
• Major abdominal operation & technically difficult.
• Sexual function is preserved.
• Methods-.
– Sacrocolpopexy.
– Anterior Colpopexy.
– Colposuspension.
446
Laparoscopic Surgeries for Genital Prolapse
• Is minimal invasive surgery:
– small incision, better view, haemostasis, no packing,
minimal tissue & bowel handling, short recovery, less
pain, insignificant scar
• Permits treatment of most types of Prolapse
• Indicated Anterior/Posterior lower vaginal repairs can also
be done vaginally before or after laparoscopic Surgery
• But:
– Needs extended period of rest is essential
– Expertise is needed
– Not yet widely practised
– Is surgery of the future today
447
Laparoscopic Surgeries for Genital
Prolapse
• PROCEDURES:-
– Cervicopexy / Sling operations with/without
Laparospic Paravaginal repair / Vaginal repair
– VH / LAVH / LH / TLH + Colposuspension
– VH / LAVH /LH/TLH+ Laparospic Pelvic
reconstruction
– Rectocele repair & levatorplasty
– Enterocele repair with suturing of uterosacral
ligaments
– Anterior/Posterior Colpopexy 448
OTHER OPERATIONS
• Laser Vaginal Rejuvenation

• Designer Laser Vaginoplasty

• Vaginal approach to prolapse repair


incorporating mesh
• Sacrospinous ligament fixation entails
attachment of the vaginal apex to the
sacrospinous ligament, the tendinous
component of the coccygeus muscle

449
• Evidence based practice: The conscientious, explicit
and judicious use of current best evidence in making
decisions about the care of the individual patient
Involves integrating individual clinical expertise with
the best available external clinical evidence from
systematic research

• Communication: a process of transmitting and


receiving information on a particular issue between
two or more people (sender and receiver), through
a channel (medium), aimed at reaching mutual
understanding.
450
Evidence pyramid

interventional

observational

validity
Levels of Recommendations:
A: The recommendation is based on good and
consistent scientific evidence.

B: The recommendation is based on limited or


inconsistent scientific evidence.

C: The recommendation is based primarily on


consensus and expert opinion.
453
The GRADE approach
Grades of Recommendation Assessment
Development and Evaluation:
Clearly separates two issues:
1) Quality of the evidence (high, moderate, low, very
low)
– methodological quality of evidence
– likelihood of bias
– by outcome
2) Strength of recommendation: Strong or Weak/
Conditional (for or against)
– Quality of evidence is only one factor
Quality of the evidence
The extent to which one can be confident that an estimate of
effect or association is correct.

High, further research is very unlikely to change our


confidence in the estimate of effect
Moderate, further research is likely to have an important
impact on our confidence in the estimate and may change
the estimate
Low, further research is very likely to have an important
impact on our confidence in the estimate and is likely to
change the estimate
Very low, any estimate of effect is very uncertain
Strength of recommendations
A Good evidence to support the intervention

B Fair evidence to support the intervention

C Insufficient evidence to recommend for or


against the intervention, but recommendation
might be made on other grounds

D Fair evidence against the intervention

E Good evidence against the intervention


Strength of recommendation
Strong recommendation: guideline panel is confident
that the desirable effects of an intervention
outweighs its undesirable effects (recommendation
for an intervention) or that the undesirable effects
of an intervention effects outweighs its benefit
(recommendation against an intervention) –
implies that that most individuals will be best
served by the recommended course of action
Weak recommendation: desirable effects probably
outweigh the undesirable effects or undesirable
effects probably outweighs the desirable effects
but appreciable uncertainty exists
458
459
460
461
462
463
Ministry of health 2008 data
MMR 800/100 000
IMR 103/1000
U5MR 197/1000
Skilled attendant at del 34%
Malaria prevalence 1858/100 000
Malaria mortality 156/100 000
HIV prevalence in >15yrs 2886/100 000
Doctor : patient 0.28/1000
Patient/doctor 3571pt/ doctor
Likelihood of death before 40yrs 33.7%

464
465
Primitive structure Female Male
Gonad Ovary Testis
Mullerian system Uterus, fallopian Appendix testis,
(paramesonephric) tubes, upper 4/5 of prostatic utricle
vagina
Wolffian system Paroophoron, Epididymis, vas
(mesonephric) epoophoron, part of deferens, trigone
bladder and urethra of bladder &
prostatic urethra

Genital tubercle Clitoris Penis


Genital folds Labia minora Penile urethra
Genital swellings Labia majora, Scrotum, bulbo
bartholin’s glands urethral glands
• Intersex: An individual in whom there is
discordance between chromosomal, gonadal,
internal genital, and phenotypic sex or the sex
of rearing.

• Intersexuality: Discordance between any two


of the organic sex criteria

• Transsexuality: Discordance between organic


sex and psychological sex components
467
Congenital adrenal hyperplasia
• CAH: commonest form of female intersex; can also
present as male intersex (macrogenitosomia
precox).

• Autosomal recessive

• 21hydroxylase commonest, located on xsome 6p


btw HLA-B & HLA-DR. 90%

• Incidence 1:5000 -1:15000.Mild CAH occurs in


1:100. Classical occurs in 1:13000-16000.
Male intersex
Failure to produce Failure to utilize
testosterone testosterone
• Pure XY gonadal • 5-alpha-reductase
dysgenesis (Swyer’s deficiency
syndrome) • Androgen receptor
• Anatomical testicular deficiency
failure (testicular
regression syndrome) * Complete androgen
• Leydig-cell agenesis Insensitivity
(TFS)
• Enzymatic testicular
failure * Partial androgen
Insensitivity
• Rape: forced, unlawful carnal knowledge of an
individual.

• Sexual assault: any non-consensual sexual act


performed on an individual by another.

• Faecal incontinence: involuntary loss of faeces at


anytime after toilet training has been achieved.

• Fistula: an abnormal connection between two


epithelial surfaces
470
• Fecundability: the likelihood of conception per month of
exposure. (20% in normal couple)
• Fecundity: probability of achieving a live birth In one
menstrual cycle.
• Infertility: Failure of a couple to achieve pregnancy after
1yr of regular, unprotected, ejaculatory sexual
intercourse.
• Infecundity: Inability of a couple to achieve a live birth
after 12mths of unprotected intercourse.
• Sterility: an intrinsic inability to achieve pregnancy.
• Anovulation: Failure to discharge ova over a long
period, usually defined as longer than 3months.
• Oligovulation: Failure of female gonads to discharge ova
in a monthly, repetitive manner. 471
Contributions of Partners to Infertility
SOURCE OF THE PROBLEM
• Sole cause in the male - 30% - 40%
• Sole cause in the female - 30% - 40%
• Combined cause - 10% - 20%
• No recognizable cause - 5% - 10%

CHANCES OF PREGNANCY (Normal Couples)


• 60-75% of couples conceive in 6 months
• 85-90% in 1 year
• 95% in 24 months, and
• 10% - 15% -- infertile.

472
Etiologic Agents of tubal infertility
Primary
1. Neisseira Gonorrhea
2. Chlamydia Trachomatis
3. Mycoplasma Hominis
4. Mycobacterium Tuberculosis
5. Others.
Secondary
6. Bacteroides
7. Peptostreptococcus
8. Escherichia Coli.
9. Group B Streptococcus
• ART includes “all fertility treatments in which both
eggs and sperm are handled.” They do not include
procedures in which only sperm are handled(e.g
IUI) or procedures in which a woman takes
medicine to stimulate egg production without the
intention of having eggs retrieved”
• Methods, procedures, techniques employed to
increase the chances of conception, and to achieve
conception usually in infertile couples.
• Active management of infertility: Full investigation
or completion of investigation within one menstrual
cycle.
474
What is Assisted Reproductive Technology?
• Definition used by CDC is based on the 1992 Fertility Clinic
Success Rate and Certification Act
• ART includes all fertility treatments in which both eggs and
sperm are handled.
• In general, ART procedures involve surgically removing
eggs from a woman’s ovaries, combining them with sperm
in the laboratory, and returning them to the woman’s body
or donating them to another woman.
• They do NOT include treatments in which only sperm are
handled (i.e., intrauterine—or artificial—insemination) or
procedures in which a woman takes medicine only to
stimulate egg production without the intention of having
eggs retrieved.
475
ASSISTED CONCEPTION TECHNIQUES
• IVF --- In vitro fertilization
• DI --- Donor insemination
• GIFT --- Gamete intrafallopian transfer
• ZIFT --- Zygote intrafallopian transfer
• SUZI --- Subzonal insemination
• ICSI --- Intracytoplamic sperm injection
• TESA --- Testicular sperm aspiration
• PESA --- Percutanous sperm aspiration
• MESA --- Micro-epididymal sperm aspiration.

476
Tubal patency tests.
• Tubal insuflation.
• Hysterosalpingography.
• Laparoscopy and dye test.
• Sonohysterosalpingography.
• Transvaginal Hydrolaparoscopy .
• Salpingoscopy
• Falloposcopy.
Procedure of IVF + ET
• Initial consultation: PE, invx, counselling
• Pituitary down regulation-natural cycle, long or short prt
• Ovarian stimulation (Superovulation) – FSH/HMG
• Ovulation trigger- urinary hCG 10,000iu/recombinant hCG
150ug subcutaneously.
• Follicular Aspiration
• Sperm processing
• Insemination- 4-6 hrs after retrieval, 100,000sperms /ml
/oocyte for 16-18hrs at 370C with 5% CO2.
• Embryo culture
• Embryo transfer- day2 (4 cell)or day 5(blastocyst)
• Luteal phase support- hCG and progestogens
• Pregnancy test- 12-14 days after ET
Monitoring protocol
• Baseline uss and E2 on day 23 b/4 GnRH
• Uss and E2 after 10 days on GnRH to confirm down
regulation & exclude cysts
• Uss and E2 on day 5-6 of FSH stimulation
• Uss on day 8-9 –intermediate follicles
• Uss alternate day till size of 15mm
• Then uss daily till day of hCG & E2 also check on day
of hCG.
Women with poor response
Def: failure to produce adequate no of mature follicles and /or
peak E2 <cut-off
• Predicting poor response
– Age >35yrs
– Baseline FSH (day3-5) >15mIU/mL
– E2 (day 3-5) >80pg/ml
– Baseline LH (day 3) <3mIU/mL
– FSH/LH >3
– Low level of Inhibin in early follicular phase.
– Low level of GnSAF/IF
– Dynamic test; leuprolide test, hMG test
– Uss ovarian volume and vascular supply, uterine artery
pulsatility index >3
Strategies for poor responders
• Long protocol of GnRH agonist
• Rec-FSH
• IVF using natural cycle
• Use of low dose clomiphene
• OCP for 28-42 days
• Use of growth hormone along with hMG; GH
↑intraovarian IGF which in turn amplifies
granulosa cell response to gonadotrophin. Dose 4-
24IU every 2 days x 7. this reduces the dose of
gonadotrophin required and some patients
responded.
Problems of ovulation induction
• Multiple pregnancy
• Ovarian hyperstimulation syndrome (OHSS)
• Risk of ovarian cancer

Note: no increase risk of abortion or congenital


abnormality. There is increase risk of ectopic
pregnancy.
PATHOPHYSIOLOGY OF OHSS
• Its moderate to severe manifestations complicate
1-2% of ovulation induction protocols.
• The underlying factor in OHSS is thought to be the
abnormally high oestrogen levels resulting from the
multiplicity of developing ovarian follicles.
• There is associated excessive VEGF production,
altering the permeability of the capillaries leading
to leakage of fluid.
• Other implicated factors include interleukins, nitric
oxide and angiotensin II.
CF of OHSS
• MILD OHSS: <8cm ovarian enlargement,
abdominal pain, distension, weight gain.
• MODERATE OHSS: 8-12cm sized ovaries, USS
ascites, nausea, vomiting and/or diarrhoea.
• SEVERE OHSS: Appearance of hydrothorax,
clinical ascites, anasarca, haemoconcentration
(PCV>45%, WBC>15000/μl), oliguria with normal
serum creatinine, liver dysfunction.
• CRITICAL OHSS: Appearance of tense ascites,
PCV>55%, WBC>25000/ μl, thromboembolism,
shock, renal failure.
MANAGEMENT
• Outpatient management for mild cases
• Moderate to critical cases are managed in
hospital
– Bed rest.
– Adequate analgesia, avoiding NSAIDs.
– Consider cyst complication in acute abdomen
– Fluid replacement; colloids if PCV>44% and serum
albumin<30mg/dl
– Abdominal paracentesis may be useful.
– Diuretics contraindicated
– Multidisciplinary ICU care for critical cases.
RISK FACTORS
• PCOS (Diagnostic criteria)
• Young age
• Thin bodily habitus
• Treatment resulting in pregnancy
• Use of hCG for luteal support

PREDICTION
• Serum oestradiol>3000pg/ml
• >20 Antral follicles
• >4 mature follicles
SFA Reference values (WHO 1999) 4th edition
• Volume - ≥ 2ml Motility:
• pH - 7.2-7.8 • Grade A : >25 μm/s
• Liquefaction time: 30mins • Grade B : 10-25μm/s
• Sperm conc- ≥ 20x106/ml • Grade C : < 10 μm/s
• Total count ≥40x106/ejaculate (or shaking on the spot)
• Motility - ≥ 50% motile • Grade D : immotile
• Morphology- ≥30% N ≥ 50% motile(grade A+B)
Strict criteria- >14%N or
• Viability--- ≥75% live forms ≥25% (grade A) within
• WBC - < 1million /ml 60mins of ejaculation
487
SFA Reference values (WHO 2010) 5th edition
• Volume - ≥ 1.5ml
• pH - 7.2-7.8 • These values were
• Liquefaction time: 30mins generated from a study by
• Sperm conc- ≥ 15x106/ml Cooper et al, 2009
• Total count involving 4500 recent
≥39x106/ejaculate fathers from 14 countries
• Motility - ≥ 40% motile on 4 continents.
• Morphology- ≥4% N
• Viability--- ≥58% live forms
• WBC - < 1million /ml

488
SEMEN VARIABLES
• Normozoospermia: Normal ejaculates as defined
by the reference values.
• Oligozoospermia: Sperm Concentration less than
the reference value.
• Asthenozoospermia: Less than the reference
value for motility.
• Teratozoospermia: Less than the reference value
for morphology
• Oligoasthenoteratozoospermia: Signifies
disturbance of all three variables.
• Azoospermia: No spermatozoa in the ejaculate.
• Aspermia: No ejaculate.

489
• Ovarian dysgenesis – failure to develop or maintain
normal number of oocytes in a state of devpmental
arrest until puberty usually due to a genetic defect.

• Premature Ovarian failure: menopause b4 age 40


(due to accelerated depletion (atresia) of ovarian
follicles or reduced number during development)

• Poor response to ovulation induction: failure to


produce adequate no of mature follicles and /or
peak E2 less than cut-off

490
WHO classification of Ovulatory Disorders
● Group Ι: Hypothalamic-pituitary failure: are estrogen
deficient with non elevated FSH and prolactin levels and no
SOL in the hypothalamic pituitary region. They typically
have amenorrhea and do not bleed in response to
progestin challenge.

● Group ΙΙ: Hypothalamic pituitary dysfunction (e.g. PCOS);


not estrogen deficient. FSH and prolactin levels are not
elevated. They typically experience oligomenorrhea, but
they may have anovulatory cycles or amenorrhea with
bleeding in response to a progestin challenge.

● Group ΙΙΙ: Ovarian failure


Clomiphene challenge test
• A clomiphene challenge test is a dynamic type of test that
can discover some cases of poor ovarian reserve that are
still showing a normal day 3 FSH. This test is done by:
• Obtaining a day 3 FSH and estradiol
• Take 2 tablets of clomiphene (100 mg) on days 5-9 of the
cycle
• Repeat an FSH level on day 10 of the cycle
• The normal Clomid challenge test result is a low FSH on day
3, a low estradiol on day 3 and a low FSH on day 10 with
increased estradiol.
• Cut off values for the day 3 and the day 10 FSH values are
assay dependent and must be determined by experience
with the lab being used. 492
• Urinary incontinence: involuntary loss of urine which
is a social or hygienic problem and is objectively
demonstrable.
• Fistulous incontinence (bypass incontinence):
occurrence of urinary incontinence in the presence of
intact sphincteric mechanism.
• Urge incontinence: involuntary leakage of urine
immediately preceded by or accompanied by marked
urinary urgency as a result of involuntary detrusor
contraction.
• Genuine stress incontinence: involuntary loss of urine
that occurs when the intravesical pressure exceeds the
maximum urethral closure pressure in the absence of
detrusor activity. 493
• Detrusor instability: Involuntary loss of urine either
spontaneously or provoked during the filling phase when the
individual is unwilling to void.
• Overflow incontinence: Involuntary loss of urine due to
overdistension of the bladder in the absence of detrusor
activity.
• Total incontinence: Constant diurnal and nocturnal
incontinence without normal voiding. It can be differentiated
from overflow incontinence by catheterization.
• Functional incontinence: Normal urinary organs, with
inappropriate urination with respect to social norms of time
and place. Psychiatric dx, physical problems with mobility
and dexterity
• Post void dribbling: Due to urethral diverticulum.
494
Classification of stress incontinence.
– Type I: Defect in pelvic support of the
bladder neck, hence hypermobile, urethra moves down
less than 2 cm when stressed. Type I patients have little or
no sign of cystocele
– Type II: Defect in pelvic support of both the
bladder neck and the urethra, hence hypermobile, the
urethra moves down more than 2cm when stressed
IIA :Patients who have cystocele inside the vagina .
IIB When cystocele is outside the vagina
– Type III: Intrinsic urethral defect (sphincteric
insufficiency) e.g. due to trauma, denervation,
radiation No urethral hypermobility
• Amenorrhea: absence of menstrual periods.
• Primary amenorrhea:
– absence of menarche by age 14 with no 20 sex changes
– absence of menarche by age 16 regardless of 20 sex
changes
– no periods by 2 years after the start of 20 sex cgs
• 20 amenorrhea: is the absence of menses for over 3 cycles
or 6 consecutive months in a previously menstruating
woman with a regular cycle ; or the absence of menses for
12months in a patient with history of oligomenorrhoea.
• Regular cycle: variation usually within 5days
• Fertile period: Shortest cycle minus 18days to longest cycle
minus 11days.
496
Asherman's syndrome (AS)
• Intrauterine adhesions (synechiae) may be asymptomatic or
have menstrual irregularity with or without infertility with a
broad spectrum of severity
• Also known as Fritsch or Fritsch-Asherman syndrome
• First described in 1894 by Heinrich Fritsch and further
xterized by the gynecologist Joseph Asherman in 1948.
• Occurs in 1-5% 0f D&Cs in general populace
•  25% of D&Cs 1–4 weeks post-partum; up to 30.9% of D&Cs
for missed abortion and 6.4% ffing incomplete abortions.
• Diagnosis is primarily by hx and a high index of suspicion.
• Direct visualization of the uterus via hysteroscopy confirms
it. Other methods are sonohysterography (SHG) and
hysterosalpingogram (HSG). 497
• Causes include postpartum curettage; any infection or
inflammation of the endometrial tissue eg TB,
schistosomiasis; surgery or trauma eg CS, myomectomy.
• Rx is aimed at lysis of the intrauterine adhesions (preferably
hysteroscopically), restoration of normal endometrium and
prevention of subsequent adhesion formation
• Following treatment, prognosis is good with pregnancy
rates of 70-80%; this is influenced by the cause and degree
of initial problem as well as the method of adhesiolysis.
• There is a high incidence of recurrent abortion, PROM,
premature labour, abnormal presentation, placenta accreta
and praevia and PPH ffing pregnancy

498
499
Grades AS European Society for Hysteroscopy (1989)
• I - Thin or filmy adhesions easily ruptured by hysteroscope
sheath alone, cornual areas normal;
• II - Singular firm adhesions connecting separate parts of the
uterine cavity, visualization of both tubal ostia possible,
cannot be ruptured by hysteroscope sheath alone;
• III - Multiple firm adhesions connecting separate parts of
the uterine cavity, unilateral obliteration of ostial areas of
the tubes;
IIIa - Extensive scarring of the uterine cavity wall with
amenorrhea or hypomenorrhea;
IIIb - Combination of III and IIIa;
• IV - Extensive firm adhesions with agglutination of the
uterine walls. Both tubal ostial areas occluded
500
Grading of AS (Valle and Sciarra's table of 1988)

• Mild- Filmy adhesions composed of basal


endometrium producing partial or complete uterine
cavity occlusion;
• Moderate - Fibromuscular adhesions that are
characteristically thick, still covered by
endometrium that may bleed on division, partially
or totally occluding the uterine cavity;
• Severe - Composed of connective tissue with no
endometrial lining and likely to bleed upon division,
partially or totally occluding the uterine cavity.
501
• PCOS: The Rotterdam consensus (2003): Presence of 2 of 3
criteria by American Society .for Reproductive Medicine and
the European Society of Human Reproduction and
Embryology (ASRM/ESHRE)
-oligo-and/ or anovulation
-clinical and/or biochemical sign of hyperandrogenism
-polycystic ovary morphology on USS:
12 or more follicles, 2-9mm,and/or increased
ovarian volume > 10ml3. (Adam’s criteria)
• Other causes for hyperandrogenism that mimic
PCOS (eg. CAH, Cushing syndrome, androgen
secreting tumours) should be excluded
502
CLINICAL FEATURES/ INVESTIGATIONS

• Menstrual abn.- Oligomenorhea/ 20 amenorhea


attributed to chronic anovulation.
• Hyperandrogenism – Excess terminal body hair
in testosterone dependent hair distribution
areas.
• Others- Muscle mass, deepening voice,
clitorimegaly.(VIRILIZATION)
• Infertility
Clinical Features (Contd.)
• Obesity- BMI> 30Kg/M2. Waist circumference>
88cm.
• DM- Approx. 10% PCOS women have type II DM.
30-40% - IGT @ 40 yrs.
• Sleep Apnea Syndromes
• Acanthosis Nigricans- Dark pigmented skin- nape
of the neck, skin folds, Knuckles & elbows
• Acne Vulgaris.
• May be asymptomatic
Clinical Features (Contd.)
Metabolic syndromes.
• 3 of the following
• 1. Waist circumference >88cm
• 2. Triglycerides >150 mg/dl
• 3. HDL <50 mg/dl
• 4. Blood pressure > 130/85
• 5. Fasting Blood glucose 110-126 &/or 2-h glucose 140-
199 mg/dl
Suggested routine testing for PCOS
• Pelvic ultrasound (preferably TVS)
– endometrial thickness (to exclude endometrial pathology
including endometrial hyperplasia)
– ovaries (presence of polycystic ovaries, exclude ovarian
androgen producing tumours)
• Hormone assays (time for days 2–5 if oligomenorrhea)
– ßHCG if amennorrhea (exclude pregnancy)
– FSH, LH, E2 (raised LH in up to 50% of patients, exclude other
causes of anovulation such as hypogonadotropic
hypogonadism or premature ovarian failure)
– thyroid function tests (exclude hypothyroidism, another cause
of anovulation)
506
• prolactin (exclude hyperprolactinaemia, another cause of
anovulation, with the caveat that some PCOS patients may
have slightly high prolactin levels)
– 17 hydroxyprogesterone (exclude CAH)
– androgens (DHEAS, total testosterone, SHBG, free androgen
index (FAI) to possibly help confirm PCOS and exclude
androgen producing tumours)
• Metabolic screening
– 2 hour 75 g OGTT if BMI 28 kg/m2 (exclude IGT and type 2
diabetes mellitus)
– fasting lipids (exclude dyslipidaemia such as total
cholesterol, LDL cholesterol, triglycerides, HDL cholesterol)

507
Treatment.
OBJECTIVES OF MANAGEMENT
Depends on presenting complaint
• Prevent endometrial hyperplasia/ Carcinoma
• Restore menstruation, ovulatory cycles &
fertility
• Improve Acne & Hirsutism.
Treatment
• Figure 8
Treatment
• Figure 9
Differential Diagnoses + R/O Labs

􀂃 Idiopathic hirsutism
􀂃 Thyroid disorder(TSH)
􀂃 Hyperprolactinemia(PRL)
􀂃 Cushing’s syndrome(Cortisol elevated)
􀂃 Premature ovarian failure (FSH/LH)
􀂃 Adrenal hyperplasia : DHEA/S (very elevated)
ACTH (normal), 17‐hydroxyprogesterone
􀂃 Androgen‐producing adrenal or ovarian neoplasm (CA-
125)
Long term sequelae of PCOS
• Non- insulin dependent diabetes.
-OGTT indicated, recheck once preg
• Cardiovascular disease.
-fasting lipid profile indicated.
• Endometrial ca
-intermittent progestin indicated
• Hirsutism: the excessive growth of terminal hair on
the face and body of a female in a typical male
pattern to a degree that worries the patient.
• Primary dysmenorrhoea: Cramping lower abd
pain before the onset of menstruation and persists
throughout the first 12 to 48 hrs in the absence of
other dx (Nulliparous and cycles are usually ovulatory)
• Secondary dysmenorrhoea
Pain occurs at time of menstruation which is due to
associated with organic pelvic disease
• Premenstrual Syndrome: Cyclic recurrence of
physical, psychological or behavioural symptoms
that appear after ovulation and resolve with the
onset of menstruation 513
• Abnormal Uterine Bleeding: Any alteration of normal
pattern of menstrual flow.
1.Menorrhagia-prolonged&increased flow.
2.Metrorrhagia-regular intermenstrual bleeding.
3.Polymenorrhea-menses at < 21days interval.
4.Hypomenorrhea-unusually light menstrual flow.
5.Hypermenorrhea-excessive regular menstrual flow
6.Menometrorrhagia-prolonged menses & intermenstrual
bleeding.
7.Oligomenorrhea-menses @interval >35days.

Virilism- the presence one or more of the following: clitoral


hypertrophy, breast atrophy; male- type baldness and
deepening of the voice ± Amenorrhoea 514
• AUB is any form of uterine bleeding that is irregular in
amount, duration, or timing.
• Dysfxnal uterine bleeding (DUB):Abnormal bleeding
from the uterus in the absence of organic disease of
the genital tract OR
• Excessive bleeding of uterine origin which is not due
to demonstrable pelvic disease, complications of
pregnancy or systemic disease
• Postmenopausal bleeding: bleeding from the female
genital tract after one yr of cessation of menses.
• Gynaetresia: refers to the narrowing of the female
genital tract. This may involve part or whole of the
vaginal or confined to the vulva orifices. 515
AETIOLOGY OF POSTMENOPAUSAL BLEEDING
-- SYSTEMIC FACTORS
-- LOCAL FACTORS
SYSTEMIC
---Unopposed estrogen stimulation of endometrial lining
• Exogenous estrogen e.g. HRT
• Endogenous e.g. thecoma, adult granulosa cell tumour and
peripheral conversion of androstenedione
• Simple Hyperplasia :Increased glandular/stroma
ratio.Nuclear atypia absent. Risk of progression to cancer
0.4 – 1.1%
• Complex : Increased crowding of glands with less
intervening stroma.Nuclear polarity preserved.Risk of
progression 0.3 – 4% 516
Bleeding disorders
• Disturbances in the haemostatic mechanism e.g.
thrombocytopenia,disseminated intravascular
coagulation,chronic liver diseases, anticoagulants.
(Associated with bleeding from other parts of the
body)

517
LOCAL CAUSES
• BENIGN
• PREMALIGNANT
• MALIGNANT
BENIGN:
-UTERINE:
• Polyps : small pink or red tumours projecting from
the endometrial and endocervical surfaces
• Atrophic endometritis : Estrogen deficiency leads
to atrophy of glands and stroma with large dilated
venules under a thin endometrium.Venules rupture
easily and cause bleeding.
518
CERVICAL CAUSES:
• Cervical polyp : Single or multiple small red
swelling.Inflammation and ulceration lead to blood stained
discharge and postcoital bleeding
• Atrophic cervicitis :Cervix also involved in menopause
induced genital atrophy.This leads to increased vulnerability
to trauma, dyspareunia and postcoital bleeding
VAGINAL CAUSES
• Atrophic vaginitis and vaginal polyps
VULVAL LESIONS
• Dystrophy: Lesions such as lichen sclerosus
• Dermatitis : Contact dermatitis due to allergic response to
deodorants, topical antihistamines and antibiotics etc.
519
PREMALIGNANT CAUSES:
ENDOMETRIAL HYPERPLASIA:

• Proliferative lesions of the endometrial glands and,


to a lesser extent , the endometrial stroma. Result
from unoppossed estrogen stimulation.
• 3 types namely Simple, Complex and Atypical
• Cause bleeding due to erratic shedding of
hyperplastic epithelium

Atypical Hyperplasia : Cytologic atypia with loss of


polarity, increased nuclear/cytoplasmic ratio,a large
nuclei of varying sizes.Risk of progression to
carcinoma 22 – 33% 520
MALIGNANT CONDITIONS
• Cervix, endometrial, vulva, vaginal,fallopian tube
• Secondary deposits from the rectum, anus,breast
and upper gastrointestinal tract

Other documented causes include;


• Extraovarian granulosa cell tumour
• Arteriovenous malformation in the uterus
• Endometrial sarcoidosis and tuberculosis
• Pinworm infestation of the uterus

521
Epidemiology of DUB
• DUB accounts for 50% of all cases of AUB
• Common in extremes of reproductive age
• 20% of DUB are in adolescents.
• 95% of AUB in adolescents is DUB due to anovulation.
• 55% of cycles in the 1st year after menarche are
anovulatory & up to 1/3 of adolescents still have
anovulatory cycles in the 5th yr after menarche
• The earlier the onset of menarche, the shorter the
duration of anovulatory cycles
• If menarche before 12, 50% of cycles are ovulatory
after 1yr, but if menarche occurs after 13 yrs it may
take 4-5yrs before cycles are ovulatory
• 40% - 50% are aged >40yrs
• Ovulatory DUB is more common than anovulatory DUB
• Chronic pelvic pain (CPP): a noncyclical pain of >6
months’ duration that is localised to the pelvis,
anterior abdominal wall at or below the umbilicus,
the lumbosacral area, or buttocks, and is of
sufficient severity as to cause functional disability or
lead to medical care
• Pelvic inflammatory disease (PID): ascending
infection of the upper genital tract from the lower
gt that is not due to pregnancy, trauma or tumour.
• Unplanned preg: Conceived while the woman was
not aware of her fertile period.
• Unwanted preg: Conceived while the interest of
one or both parties were in jeopardy. 523
Risk factors for PID
• Low socioeconomic class • Termination of
• Black race pregnancy
• Young age (<25 years) • Insertion of IUCD in the
• Multiple sexual partners past 6 weeks
• Previous PID • In-vitro fertilization
• IUCD procedure
• Hysterosalpingography • Bacterial vaginosis
• Past history of STI (in the • A recent new sexual
patient or her partners) partner (within the
• Postpartum endometritis previous 3 months)
Aetiology of PID
1.Exogenous agents:
-Neisseria gonorrhoea
-Chlamydia trachomatis
-Mycoplasma hominis
2.Endogenous organisms usually coliforms:
-E.coli
-Streptococcus faecalis
-Enterococcus
-Bacteroides
-Actinomyces, especially associated with
IUCD (Dalkon shield).
Aetiopathogenesis
Theories for ascent from lower genital tract:
a.Uterine muscular activity
b.Role of vectors:
Spermatozoa & Trichomonas vaginalis
c.Association with intrauterine manipulation:
.IUCD
.HSG
.D&C
d.Association with cervical dilation:
.Menstruation
.Miscarriage & Childbirth
Diagnosis of PID
Major (Minimum) criteria
 Lower abdominal pain and tenderness
 Adnexal tenderness
 Cervical excitation tenderness
The above 3+ any of these minor criteria
 ESR >15 mm/hr
 Abnormal vagina discharge
 Temp >380C
 WBC >10,000 X109/L
 Gram stain of endocervix swab yielding Gram
negative intracellular diplococci.
 Elevated C-reactive protein
 Pelvic ultrasound: fluid in POD
Laparoscopic classification
Mild PID
• Erythema of the fallopian tubes without pus
formation
• Oedema & swelling of fallopian tubes that are
otherwise freely mobile
Moderate PID
• Sero-purulent exudates from fimbriated end or
serosal surface of fallopian tubes
Severe PID.
• Inflammatory mass
• Pyosalpinx or Abscess
Treatment

• Empirical treatment should begin immediately


with broad-spectrum antibiotics to cover
– Gonococcus
– Chlamydia
– Anaerobic organisms
• These can be replaced with antibiotics
recommended by sensitivity patterns when
available, if there’s no response
 Oral Ofloxacin 400 mg b.d. +
 Oral Metronidazole 400 mg b.d for 14 days
OR
 IM Ceftriaxone 250 mg stat / IM Cefoxitin 2g
stat with oral probenecid 1 g, then:
 Oral doxycycline 100 mg b.d. +
 Oral metronidazole 400 mg b.d. for 14 days.
OR
 Oral Azithromycin 1g stat +
 Oral metronidazole 400 mg b.d. for 14 days.
Inpatient therapy
 Surgical emergency (eg. Acute appendicitis,
ectopic pregnancy) cannot be excluded
 Clinically severe disease
 Tuboovarian / pelvic abscess
 PID in pregnancy
 Lack of response to oral therapy after 48hrs
 Intolerance to oral therapy
 Nulliparous patient to preserve compliance to
treatment & fertility
Other highlights of treatment
• Inpatient (intravenous) therapy should be contd
until 24hrs after clinical improvement, before
changing to oral
• Partners should be evaluated & treated as
appropriate
• Surgery may be required for abscesses
• PID is extremely rare in pregnancy; only use safe
antibiotics
• IUCD can be left in situ in mild cases. If severe,
remove after commencement of antibiotics
Complications
• Repeat infections • Septicaemia
• Chronic pelvic pain • PID in pregnancy
• Infertility-the risk • Marital disharmony
increases with each • Low productivity
episode • Hysterectomy
• Ectopic pregnancy • Death
• Fitz-Hugh-Curtis
syndrome: Chlamydial
perihepatitis
• Pelvic abscess
PREVENTION
Primary
• Health education
• Barrier contraception
• Vaccination
Secondary
• Prompt and accurate diagnosis
• Early and effective treatment
• Contact tracing
• STI – presence of a sexually transmissible infection
without symptoms
• STD – presence of symptoms associated with a STI
• Syndromic Management of STI: the presumptive
clinical diagnosis based on identification of
consistent group of symptoms and signs of the STI.
• Syndrome-based management: is a process where,
after a syndromic diagnosis has been made,
treatment dealing with a majority of the organisms
responsible for producing each syndrome is given.
This may mean treating for one or more specific
infections.
• Expedited partner therapy: practice of treating the
sexual partner of a person with STI without an
intervening medical evaluation; usually patient
delivered partner therapy(PDPT).
• High risk sex: Sex with a non-marital, non-
cohabiting partner in the last one year.
535
ADVANTAGES OF SYNDROMIC MGT
• Highly sensitive when used to detect infection among
symptomatic patients
• Treatment is given at first visit so delays in treatment are
avoided and the patient is not lost to follow-up b4 Rx
• Opportunity and time for education and counseling
• Avoids expensive laboratory tests
• Can be implemented at primary care level because it is easy
to use, does not require highly trained STI specialists
• Limits referral to specialist centres
• Problem-orientated (based on patient’s symptoms)
• High rates of cure, provided that the effectiveness of the
drugs selected is adequate and properly monitored
• The use of flow charts standardises diagnosis & treatment 536
DISADVANTAGES
• Over-diagnosis and over-treatment may result in increased
drug costs, side-effects of multiple drugs, alterations in
vaginal flora and potential for increased drug resistance
• Does not detect infections among asymptomatic individuals
• Poorly predictive of the presence of cervical chlamydial
and/or gonococcal infection
• OverRx of partners of women with vaginal discharge, most
of whom do not have an STI, may lead to serious social and
physical consequences for the female index case
• Not easily accepted by doctors as thought of as inferior
quality
• Does not address the issue of poor treatment-seeking
behaviour by symptomatic individuals
537
Advantages
• Makes treatment more readily available, accessible and
affordable to a large majority of the population.
• Does not require sophisticated equipment
• Eliminates high cost of lab investigations and offers prompt
treatment to patients.
• Reduces inconvenience, ensures compliance and prevents
missed opportunities for treatment.
Limitations include: ●Over treatment
• Every flow chart represents a compromise between
diagnostic accuracy, technical and financial realities
• Treating when there is no STI may lead to marital
discordance or serious embarrassment to an unmarried
patient whose symptoms are not due to STI
• Can easily be misused or abused by untrained personnel
Causes of vaginal discharge
 Physiological  Cervicitis
 In children › Gonococcus
› Infection 20 to atrophic › Chlamydia
vaginitis  Atrophic vaginitis
› Foreign body  Miscellaneous causes
› Thread worm › Foreign body e.g.
› Trauma/abuse tampon
› Ectopic ureter › Tumours in genital tract
 Infective vaginitis › Rarely, fistula involving
› Candida bladder or rectum
› Trichomonas
› Bacterial vaginosis
Physiological discharge
 Normal vaginal secretion is white, yellowish on
contact with air (due to oxidation) & acidic
 It is a transudate containing
› Desquamated vaginal and cervical epithelial cells
› Cervical gland mucus
› Endometrial gland secretion
› Bacteria-mostly (95%) lactobacilli
 Increases in mid-cycle, during pregnancy & COC
use
 Physiological’: Sexual arousal, ovulation, lochia.
Vaginal flora
• Mostly lactobacilli
• Mixed flora, especially in hypoestrogenic states
– Gardnerella vaginalis (commonest cause of
bacterial vaginosis)
– Mobiluncus spp.
– Peptostreptococcus
– Bacteroides
– Prevotella
– Mycoplasma hominis
– Ureaplasma urealyticum
• Normal flora is altered when there’s bacterial
vaginosis, there’s overgrowth of these organisms
Pathological discharge: evaluation
• Discharge is considered abnormal if
– There’s an increase in volume
– It is foul-smelling
– Change in colour or consistency
– Associated irritation (pruritus, dysuria,
dyspareunia)
• Speculum examination
• Determine pH of secretion
• Place on 2 slides
– Normal saline: trichomonads, clue cells, Candida
– 10% KOH: transient fishy smell (Sniff/Whiff test)
in vaginosis. Also, candida more visible
Features Candida Bact. Trichomo Cervicitis
vaginosis niasis
Itching/ ++ - +++ -
soreness
Smell None/ Offensive/ offensive -
Yeasty fishy
Colour White White/ Yellow/ Clear/
yellow green coloured
Consistency Cheesy/ Thin / homogeneous Mucoid
curdy
pH <4.5 4.5-7.0 4.5-7.0 <4.5

Further tests Microsc/ Microscop M&C Chlamydia


culture y , Gono.
Candidiasis
• Factors predisposing to vaginal candidiasis include:
Immunosuppression- HIV, steroids use; DM, vaginal
douching, bubble bath, shower gel, tight clothing, increased
oestrogen, pregnancy, high-dose COC, underlying
dermatosis, e.g. eczema; broad spectrum antibiotic therapy

• Spores & pseudohyphae are seen on microscopy


Rx: Clotrimazole vaginal tablets (with topical cream for
irritation)
– Nystatin 100,000 units for 2wks, vaginally
– Oral fluconazole 150mg stat
• Asymptomatic women from whom Candida is grown on
culture do not require treatment.
Trichomonas vaginalis
• Symptoms worse after menstruation or during pregnancy
• Punctate haemorrhages can occur on the cervix, giving the
appearance of a 'strawberry cervix'.
• Diagnosis is confirmed by culture, preferably in a specific
medium such as Fineberg-Whittington.
• Microscopy of vaginal secretions mixed with saline
has 60% sensitivity for detecting the organism.
• Numerous polymorphonuclear cells are seen and the
unicellular motile organism is identified from its shape, four
moving flagellae and terminal spike.
Rx: Metronidazole 2g stat OR 400mg b.d. for7days (+partners)
• In persistent trichomoniasis a higher dose e.g 400 mg tds or
more is used.
Bacterial Vaginosis
• Commonest cause of abnormal vaginal discharge in women
of childbearing age. Risk- blacks, STI and IUCD
• Often arises spontaneously around the time of
menstruation and may resolve spontaneously in midcycle.
• Gardnerella vaginalis, Bacteroides (Prevotella) spp.,
Mobiluncus spp. and Mycoplasma hominis are common.
• 'Clue cells' are vaginal epithelial cells so heavily coated with
bacteria that the border is obscured.
• Large numbers of G+ve & G-ve cocci are seen, with reduced
or absent large G+ve bacilli (lactobacilli) on gram staining.
• Are at risk of 2nd trimester miscarriage, preterm delivery,
upper genital tract infection following termination TOP,
gynaecological surgery (vaginal cuff cellulitis) and CS.
546
Amsel's Diagnostic Criteria for Bacterial Vaginosis
3 of 4 criteria must be met; sensitivity is 90%
• Homogeneous vaginal discharge (color and amount
may vary)
• Amine (fishy) odor when 10%KOH is added to
vaginal secretions ("whiff test")
• Presence of clue cells (>20%) on microscopy*
• Vaginal pH greater than 4.5
* Highly significant criterion.
Rx: Metronidazole or Clindamycin
• Metronidazole 400 mg twice a day for 7days, or 2g
stat. 547
• Other causes of vaginal discharge include atrophic vaginitis,
toxic shock syndrome, Bartholin's abscess and infestations
like pubic lice and scabies.
• Atrophic vaginitis: Treat with estrogen cream
• TSS has 10% mortality rate
• Streptoccocal and other organisms may cause discharge.
They respond to appropriate antibiotics.
• Vaginal discharge in children may be due to: foreign body,
pin worm (Enterobius vermicularis), sexual assault
(Gonorrhea & Chlamydia); streptococcal & shigella
infection.
• Lice are Rxed by application of topical agents eg malathion,
carbaryl or permethrin. Repeat after 7 days.
• Scabies responds to malathion or permethrin. 548
The philosophy of
Minimal Access Surgery
• Less trauma
- Major trauma vs surgery.
patho-physiologically similar ?
→ Stress response (metabolic, endocrine, immune)

• Better visualisation due to magnification

• More comfort
- Pain, fatigue & convalescence
- Hospital stay, recovery
- Body image.
Principles of Microsurgical Technique
1. Use of magnification by microscope or head loupes.
2. gentle handling of tissues.
3. meticulous tissues dissection.
4. precise haemostasis.
5. careful approximation of tissues.
6. Irrigation of the field with heparinized Ringer's
lactate.
7. The use of non - or delayed absorbable suture
material , cat gut should be avoided as it is irritant
to the tissue.
8. Contamination of the pelvis with foreign
material as talc powder from gloves should be
avoided as it provokes inflammation .
9. Intra - operative dextran 70.
10. postoperative corticosteroids and
prophylactic antibiotics may be used .

@@Uterine contraction palpation- 15cmH20


@@Pain of uterine contraction- 40cmH20
Indications for diagnostic laparoscopy
• Acute or chronic pelvic pain
• Ectopic pregnancy
• Pelvic inflammatory disease (including TB)
• Endometriosis
• Adnexal torsion
• Subfertility
• Congenital pelvic abnormality
• Abnormal pelvic scan
• Unexplained pelvic mass
• Staging for ovarian and cervical malignancy
• Missing IUCD 552
Therapeutic laparoscopy
• Ectopic pregnancy
• Ovarian accident: torsion, haemorrhagic
• Tubo-ovarian abscess not responding to antibiotics
• Endometriosis
• Ovarian cyst- dermoid, simple, endometrioma
• Oophorectomy
• hysterectomy
• Urogynaecology- Sacrocolpopexy
• Removing lost coil.
• Abdominal cerclage.
• Myomectomy
Absolute and relative contraindications
• Mechanical or paralytic bowel obstruction
• Generalized peritonitis
• Diaphragmatic hernia
• Major intraperitoneal haemorrhage (e.g. shock)
• Severe cardiorespiratory disease
• Massive obesity
• Inflammatory bowel disease
• Large abdominal mass
• Advanced pregnancy
• Multiple abdominal incisions
• Irreducible external hernia 554
• Wound contamination: the presence of non-
replicating organisms in the wound.
• Wound colonization: the presence of replicating
microorganisms adherent to the wound in the
absence of injury to the host.
• Wound Infection: the presence of replicating
microorganisms within a wound that cause host
injury.
• Surgical Site Infection (SSI) includes all infections
related to the incision at any depth. Occurs within
30 days after surgery; when there is purulent
drainage from the incision or growth on culture of
material from the surgical site. 555
• Clean Operations ( 5%) in which no inflammation , the
respiratory, alimentary / genitourinary tracts not
entered; no break in aseptic operating technique.
• Clean-contaminated Operations (10%) the respiratory,
alimentary / genitourinary tracts entered but no
significant spillage
• Contaminated Operations (15%) acute inflammation
(no pus) /visible contamination of the wound; i.e. gross
spillage from a hollow viscous during the operation
open injuries operated on in four hours.
• Dirty Operations (30%)+pus; previously perforated
hollow viscous, open injuries > four hours old.

556
• Primary wound closure: wound completely closed
intra-operatively
• Secondary intention: fascia closed but skin and
subcutaneous tissue left open
• Delayed Primary Closure: closure using Steri-strips
or intra-operatively placed sutures at bedside
approximately 3-5 days post-op if tissue healthy and
free of exudates
• Many studies indicate the choice of closure should
be determined by risk subsequent infection

557
National Nosocomial Infections
Surveillance System (NNIS)

Classification Wound Class SSI Risk

Clean 0

Clean- Lower
1
contaminated:

Contaminated: 2
Higher

Dirty-infected: 3
558
• Menopause: Permanent cessation of
menstruation resulting from the loss of ovarian
follicular activity. (The North American Menopause Society)

• Climacteric: Transition period from reproductive


stage of life to non-reproductive stage. ( Occupies
about a decade: 45-55 years)

• Perimenopause: The period immediately prior to


menopause and the 1st year after menopause. It
lasts average of 4 years.

560
STAGES OF REPRODUCTRIVE AGING
(STRAW, 2001)
-5 Menarche
-4 early reproductive phase
-3 late reproductive phase
-2 early perimenopause
-1 late perimenopause
0 menopause
+1 early post menopause (< 5 years)
+2 late menopause (> 5 years).
• Screening: is a systematic application of a test to
person in order to detect pre-clinical stage or early
stage of a disease for the purpose of identifying
those likely or unlikely to have a disease.
• Primary screening: This is the screening that is
done for asymptomatic people without a disease.
What is done is behavioral modifications like
promotion of healthy living, tobacco cessation,
safe sexual practices, prophylactic HPV vaccination
• Secondary screening: This form of screening is
applied to asymptomatic patients with the
presence of the disease e.g. Pap smear, Visual
Inspection Techniques, HPV Testing 562
CRITERIA FOR SCREENING
• The disease must have serious public health
consequences.
• The disease must have a detectable preclinical stage
(without symptoms).
• The screening test must be simple, non-invasive,
sensitive, specific, inexpensive and acceptable to the
target audience.
• Rx at the preclinical stage must favourably influence
the long-term course and prognosis of the disease.
• Any further testing and treatment needed must be
available, accessible and affordable for those who
have a positive screening test.
• Sensitivity: The proportion of all those with disease
that the test correctly identifies as positive.
• Specificity: The proportion of all those without
disease (normal) that the test correctly identifies as
negative.
• Pap smear’s sensitivity ≥ 70%,specificity is abt 92%

564
Risk Factors for uterine fibroid
• 2-9 times more common in black compared to white
• Nulliparity
• Overweight (Obesity)
• Early Menarche => long reproductive period
• Positive Family History
• Consumption of red meat
Decreased risk
• Increasing parity and age at last term birth
• Having at least one pregnancy beyond the gestational age
of 20 weeks is protective; 2 gives 50% protection.
• Consumption of vegetables
• Smoking
• OCP
TREATMENT OPTIONS

• Expectant management
• Medical management
• Uterine artery embolisation.
• Endometrial ablation with or without myomectomy
• In-situ destructive techniques (MRI-guided focused
ultrasound and cryotherapy)
• Myomectomy (abdominal, laparoscopic,
hysteroscopic)
• Hysterectomy (abdominal, laparoscopic, vaginal)
EXPECTANT MANAGEMENT
Indications:-
Small fibroid 6-8cm in diameter
Fibroid outside endometrium
Asymptomatic fibroid
Myoma co-existing with pregnancy
Post menopausal woman
Follow up by;
• Reviewing patient quarterly
• Postmenopausal women should be seen regularly.
Medical Management

• Control of symptoms – Androgens eg. Danazol


• Reducing size – Aromatase inhibitors eg.
• Awaiting Menopause Fadrozole
– GnRH Analogues – Mifepristone
– GnRH Antagonist e.g – Selective oestrogen
Ganirelix, Cetrirelix receptor modulator eg.
Raloxifene
– Progestogens eg.
– LNG-IUS (Mirena®)
Gestrinone,
– Combined OCP
depomedroxy
– Progesterone receptor
progesterone acetate
modulator eg CDB 4124
– Anti-prostaglandins
(NSAIDs)
GnRH-a
• Preoperative Use as adjunct
Reduced uterine and fibroid volume reduces
intraoperative blood loss.
Improvement in pre-operative haemoglobin.
Reduced operating times and hospital stays.
Facilitate use of pfannestiel incision for both
hysterectomy and myomectomy thus avoiding
vertical incisions with its drawbacks.
Also allows conversion of planned abdominal
hysterectomy to vaginal hysterectomy.
• Temporary treatment for perimenopausal women.
• GnRH antagonists – Direct suppression of
endogenous GnRH without initial flare
resulted in more rapid response
• Ganirelix subcutaneously daily, reduced
uterine volume and fibroid size by about 43%
within 3 weeks.
• However, long acting drugs not yet available
• PROGESTERONE- MEDIATED MEDICAL
TREATMENT.
Mifepristone (RU – 486) a progesterone blocking
drug used for 1 year (5 or 10mg) achieved about
48% reductions in uterine size comparable to
GnRH agonist.
Side effects
• Endometrial hyperplasia because of unopposed
estrogen action
• Hot flushes
• Elevated liver enzymes.
Asoprisnil, a selective progesterone receptor
modulator binds to P receptors which are
increased in myoma tissue with fewer side
effects
MYOLYSIS
• Cauterization of uterine tumours (myolysis)
– Destruction of fibroid or its blood supply using cryo or
laser through a laparoscope; or using ultrasound
– The advantage of myolysis is that the treatment of the
tumour is done under direct vision,
– and is limited only to the desired area compared to
embolization.
– If myolysis is done too vigorously, it can cause a similar
problem as uterine artery embolization, that is,
adversely affect the chances of conception and increase
complications at the time of delivery.
– shrinks tumour and reduces symptoms
ENDOMETRIAL ABLATION
Techniques of Ablation
• Electrosurgical Transcervical resection of
endometrium (TCRE)
• Endometrial laser ablation (ELA)
• Thermochoice Balloon Ablation (TBA)
• Microwave Endometrial Ablation (MEA)
• Hydrothermal Ablation of endometrium (HTA)
• Cryo-ablation of endometrium (CAE)
• Photodynamic endometrial Ablation (PDT)
• Intra-uterine surgery using a coaxial bipolar
electrode (Versapoint)
Endometrial Ablation (Resection)
• It has been postulated that the endometrium is a
potent source of growth factors which have been
implicated in myoma growth.

• It has been observed that endometrial resection is


associated with inhibition of fibroid growth and in
patients with menorrhagia resulted in amenorrhoea
or hypomenorrhoea in up to 90% of cases.

• This is a relatively minor procedure which can be


performed under local anaesthesia or conscious
sedation. The patient satisfaction rating is high.
Uterine Artery Occlusion
• This is a minimally invasive interventional
radiological procedure in which embolisation of the
uterine artery and its branches is accomplished by
injecting gelatin sponges, polyvinyl alcohol particles
or tris-acryl gelatin microspheres via a catheter until
occlusion or slow – flow is documented.

• The advantages over surgical management include


fewer complications, faster recovery and shorter
hospitalization periods
Prerequisites for UAE
• Highly qualified interventional radiologists
• Availability of in suite fluoroscopy machine
• Availability of angiographic catheters, specific
embolisation materials
Contraindications to UAE include active genitourinary
infection, genital tract malignancy, reduced immune
status, severe vascular disease limiting access to uterine
arteries, contrast allergy or impaired renal function.
• Presently the effects of UAE on premature ovarian
failure, fertility and pregnancy are unclear and therefore
women considering future fertility are not encouraged.
• Reported complications though rare include sepsis
which may necessitate life –saving hysterectory,
Ischemic sequalae such as necrosis of bowels, vulva,
radiation injuries and pulmonary embolism
• Complications:
– Post embolisation syndrome
– Allergy to iodinated contrast medium
– Inadvertent embolization of other vessels
– Fetal Pulmonary embolism
– Infection
– Ischemic injury of uterus
– Inadvertent end organ damage
– Post procedure amenorrhoea
Alternative Uterine artery occlusion methods
• Laparoscopic uterine artery occlusion under
anaesthesia invasive and requiring skilled
laparocopic surgeon
• Uterine artery ligation at caesarean section
• Incisional transvaginal uterine artery ligation
• Non – incisional transvaginal uterine artery
occlusion using specially designed clamps in the
vaginal fornices guided by Doppler ultrasound
auditory signals.
• Results are comparable to UAE and further work is
in progress.
MRI– GUIDED FOCUSED ULTRASOUND.
• Relies on the use of MRI to precisely focus
ultrasound energy to a predetermined depth of
tissue causing denaturation of protein and cell
death.
• Advantage of very low morbidity and very rapid
recovery often within 24 hours.
• Application limited by size and number of myomas,
and current regulations limits exposure to
approximately 10% of myoma volume.
GENE THERAPY
• A normal gene may be inserted into a nonspecific
location within the genome to replace a non-
functional gene. This approach is most common.
• An abnormal gene could be swapped for a normal
gene through homologous recombination.
• The abnormal gene could be repaired through
selective reverse mutation, which returns the gene
to its normal function.
• The regulation (the degree to which a gene is
turned on or off) of a particular gene could be
altered.
PREVENTION OF HAEMORRHAGE
1)Correct anaemia before surgery with iron supplement or
induce anaemia: Progestogens, danazol, GnRH analogue,
GnRH antagonist
2)Schedule the operation in the follicular phase to prevent
inadvertent rupture of fresh corpus luteum; blood supply to
uterus reduced then.
3)Moderate trendelenburg position
4)Controlled hypotensive anaesthesia-keep the mean arterial
blood pressure at 60mmHg e.g. epidural/spinal anaesthesia
5)Intraoperative autotransfusion and normovolemic
haemodilution
6)Use of clamps e.g foley’s catheter or bonney’s clamp
PREVENTION OF HAEMORRHAGE
7)Local injection of vasoconstrictive agents
-vasopressin induces smooth muscle contraction at vascular
bed; 20units of vasopressin is diluted with 20mls of N/S (not
more than 30mls is recommended); SE include water
intoxication, angina, MI and late postoperative bleeding.
-Plasma half life 10-20 mins
-Current evidence indicates vasopressin is as effective as
mechanical occlusion of the vessels in controlling blood loss
at myomectomy
8)CO2 laser-Increases surgical precision, decreases bleeding
tissue injury and adhesion
PREVENTION OF HAEMORRHAGE
9)Good surgical techniques
-minimal number of incision in the anterior uterine corpus
and in the midline when feasible to avoid vascular areas
and broad ligament
-meticulous closure of the myoma bed
-haemostasis must be ensured and blood pressure restored
to normal
PREVENTION OF ADHESIONS
• GnRH analogue preoperatively reduces adhesions in clinical
and animal studies
• Build up patient PCV & nutrition wise to fight infection
• Use of talc free gloves (wash off)
• Perioperative antibiotics
• Adequate exposure e.g Maylard incision with proper
retraction and good lighting
• Gentle and minimal handling of tissues to avoid
unnecessary trauma to serosal surface
• Any previous adhesion should be released so that intestines
could be packed away in upper abdomen
• Liberal use of suction to remove blood from field instead of
sponges because it is less traumatic
PREVENTION OF ADHESIONS
• Lintless laparotomy packs or laparotomy packs in plastic
bags to minimise microtrauma to peritoneal surfaces
• Operative field is kept moist and free of clots with a
solution of ringers lactate containing heparin:5000iu in 1
litre ringers lactate (prevent dessication)
• Non traumatic instruments should be used with meticulous
closure of the myoma bed;
• Fine non reactive monofilament absorbable sutures eg
vicryl should be used on the serosal surface
• Continuos sutures are preferred to avoid extra knots
minimal number of incisions
• Avoid incision on the posterior surface of the uterus
• Bonney’s hood incision to remove fundal fibroid
PREVENTION OF ADHESIONS
• Use of Barrier
a. interceed(oxidized regenerated cellulose) absorbable-
placed on the incision
b. Gore—tex(polytetrafluoroethylene surgical membrane)It
can be sutured over uterine incisions with 7/0 absorbable
suture, it prevents new adhesion formation
c. Seprafilm bioresorbable membrane(aodium hyaluronate
and carboxymethylcellulose)
• Second look laparoscopy
-Indicated in multiple incision or posterior incision
-early adhesion can be lysed and additional barrier
membrane placed
-clinical role of second look lapatotomy is not well known
FIGO staging system for ovarian cancer.
Stage I Growth limited to ovaries
Ia Growth limited to one ovary, no malignant cells in
ascitic fluid or peritoneal washings; no tumour on
external surface; capsule intact
IbGrowth limited to both ovaries, no malignant cells
in ascitic fluid or peritoneal washings; no tumour on
external surface; capsule intact
Ic As with 1a or 1b but with tumour on the surface of
one or both ovaries; or with malignant cells in
ascitic fluid or peritoneal washings

587
Stage II Growth involving one or both ovaries with pelvic
extension
IIa Extension and/or metastases to the tubes and/or
uterus No malignant cells in ascitic fluid or peritoneal
washings
IIb Extension to other pelvic tissues No malignant cells
in ascitic fluid or peritoneal washings
IIc As with 2a or 2b but with tumour on the surface of
one or both ovaries; or with malignant cells in ascitic
fluid or peritoneal washings
Stage III Tumour involving one or both ovaries with
peritoneal implants outside the pelvis and/or positive
retroperitoneal or inguinal lymph nodes Superficial
liver metastases equals stage 3 588
IIIa Tumour grossly limited to true pelvis with negative nodes
but histologically confirmed microscopic seeding of
abdominal peritoneal surfaces
IIIb Histologically confirmed tumour implants of abdominal
peritoneal surfaces, none exceeding 2 cm in diameter
Nodes negative
IIIc Abdominal tumour implants exceeding 2 cm in greatest
dimension and/or +ve retroperitoneal or inguinal Lnodes
Stage IV Growth involving one or both ovaries with distant
metastases, positive pleural effusions and/or parenchymal
liver disease
• Para-aortic lymph node metastases are considered regional
lymph nodes (Stage IIIC).

589
Criteria for Potential Fertility-Sparing Surgery in Ovarian Ca
• Patient desirous of preserving fertility
• Patient and family consent and agreement to close ff-up
• No evidence of dysgenetic gonads
Specific situations
•    Any unilateral malignant germ cell tumor
•    Any unilateral sex cord-stromal tumor
•    Any unilateral borderline tumor
•    Stage IA invasive epithelial tumor
• The optimal candidate for conservative surgical
management is a young patient who has stage IA disease.

590
Risk factors for Ca ovary
Definite cause not yet ascertained
Factors investigated:
1. Incessant ovulation: risk from frequent, regular
breaches in epithelium
2. Pregnancy and Parity: 13 – 19% risk reduction per
pregnancy
3. Breastfeeding: protective
4. Oral contraceptive use: 50% risk reduction when
taken for 5 or more years, present till 15 years after
use
5. Ovulation inducing drugs: no increased risk
591
6. Infertility
nulliparity: multiparity 2.42 : 1.00
infertility >5 years: < 1 year 2.70 : 1.00
7. Hormone replacement therapy. Non significant
increase in risk
8. Diet: High saturated animal fat intake increases risk
9. High BMI, height: Increased risk
10.? Alcohol, ? Milk product, ?Talc, ?Asbestos
11.BTL, hysterectomy: protective
12.Sunlight: protective
592
Risk of malignancy index for ovarian Ca (RMI)
Ultrasound score (U) (0 for 0 points; 1 for 1 point; 3 for 2-5 points)
• Multilocular cyst
• Evidence of solid areas <25 (low risk)- gen gynaecologist
• Evidence of metastases 25- 250- in a cancer unit
• Presence of ascites >250 (high risk)- gynaecological
• Bilateral lesions oncologist in cancer centre
Menopausal status score (M) Normal Ca125 <35u/L
• Premenopausal 1
• Postmenopausal 3
RMI = U x M x serum CA125 level
A sensitivity of 85% and specificity of 97% was reported
with a RMI score of 200 or more in predicting ovarian Ca.
593
594
Types of transformation zone
01 Type I Fully visualised
02 Type II In to canal but visualised
03 Type III Not fully visualised
99 Not known

The probability for a patient to have a type 1


transformation zone declined with age, parity, and smoking
status whereas it increased with the use of combined oral
contraception. There is no statistically significant effect of
the time of cycle on the visibility of the transformation
zone.
595
Cervical Cancer – FIGO Staging
I Cervical carcinoma confined to uterus (extension to corpus
should be disregarded)
IA Invasive carcinoma diagnosed only by microscopy.
IA1 Stromal invasion ≤ 3.0mm in depth and ≤ 7.0mm in
horizontal spread
IA2 Stromal invasion >3.0mm and not >5.0mm with a
horizontal spread ≤ 7.0 mm

IB Clinically visible lesion confined to the cervix or microscopic


lesion greater than IA2. All macroscopically visible lesions –
even with superficial invasion – are Stage IB
IB1 Clinically visible lesion ≤4cm in greatest dimension
IB2 Clinically visible lesion >4 cm in greatest dimension
II Tumour invades beyond the uterus but doesnt extend to the
pelvic sidewall or to the lower 1/3 of the vagina
IIA Without parametrial invasion
IIA1 Clinically visible lesion ≤4 cm in greatest dimension
IIA2 Clinically visible lesion >4 cm in greatest dimension
IIB With parametrial invasion
III Tumour extends to pelvic side wall (PSW) &or involves
lower 1/3 of vagina &or causes hydronephrosis or non-
functioning kidney
IIIA Tumour involves lower 1/3 of vagina but no PSWE
IIIB Tumour extends to PSW and/or causes hydronephrosis or
non-functioning kidney
IVA Tumour invades mucosa of bladder or rectum and/or
extends beyond true pelvis
IVB Distant metastasis
Risk factors for Ca cervix
• Major Risk factors:
– Early Coitarche, Multiple sexual partners in the
woman & Male partner with multiple sexual
partners.
• Other Risk factors:
– Cigarette smoking, High parity, family hx, Oral
contraceptives, genital infection, Lack of
circumcision & Low socioeconomic status.
• 95% Squamous cell and 5% adenocarcinoma.
• Necrosis and erosion of blood vessels result in
hemorrhage, foul-smelling vaginal discharge
HPV SEROTYPES
o HPV 16 is most prevalent with Squamous Cell Cancers
o HPV 18 is the most prevalent type in Adenocarcinomas
o HPV 16 & 18 responsible for 70% of Ca cervix
o HPV 6 & 11 responsible for 90% of genital wart
o Commonest in Nigerians: 16, 31, 35, 56 & 58
o Gardasil- quadrivalent (6,11,16 &18); Cervarix- bivalent
(16 &18) vaccine
o 9-25years both male and female are immunised
o The most common HPV types in all cervical cancers are
HPV 16, 18, 45, 31 and 33
o HPV 16, 18, 45 and 31 are responsible for > 90% of
cervical adenocarcinoma cases2,3
HPV vaccines and cross-protection
• Antibodies generated in response to vaccine antigens may
provide protection against other closely related antigens
• HPV 16 and 31 and 18 and 45 are closely related
phylogenetically
– > 90% of adenocarcinoma result from these four HPV
types
Cumulative presence of HPV in cervical adenocarcinoma
HPV types Cumulative %
16 48.4
16 + 18 84.7
16 + 18 + 45 90.5
16 + 18 + 45 + 31 91.2
HPV transmission
• Transmission by non-sexual routes is thought to be
rare but possible routes include:
– Via the fingers
– Transmission from mother to newborn (vertical
transmission)
– Transmission via fomites and environmental
surfaces
• Vertical transmission together with other non-sexual
routes may contribute to the low prevalence of
anogenital HPV infections in children.
Risk of HPV infection
• HPV infections are very common
• The cumulative risk of acquiring cervical HPV infection in
women with only one sexual partner is 46% (3 years after
first sexual encounter)
• The risk of oncogenic HPV infection is high even after first
intercourse and continues throughout a woman’s sexually
active lifetime
• Up to 80% of women will acquire an HPV infection in their
lifetime.
• While most infections are cleared, women are less likely to
clear infections as they get older
• ~11% of cervical cancers are adenocarcinoma and ~76% are
squamous cell carcinoma but percentages vary by region
Pathogenesis of Ca cervix
• E6 and E7 are oncogenes and produce E6 and E7 prteins
• The key action of the E6 protein of high-risk HPV is to cause
immortalization of the infected cell, a process that may
eventually lead to malignant transformation.
• It does this by enhancing the degradation of p53 protein, a
protein that promotes apoptosis
• The E6 protein also activates the enzyme telomerase, which
counteracts the shortening the chromosome telomeres — a
cell-aging process.
• The continued actions of E6 and E7 in a cell persistently
infected with HPV lead to increasing genomic instability,
accumulation of oncogene mutations, further loss of cell-
growth control, and ultimately cancer
Viral persistence
• HPV prevalence and incidence appears to peak in
women under 20 years of age, with a decline noted
in women 30 or older which is secondary to the
clearance of HPV.
• Persistence can be broadly defined as detection of
the same HPV type two or more times with a given
time interval between the examinations.
• Although time to clearance may vary between
studies, almost all show that approximately 90%
clear a specific HPV type after two years of
observation
• With longer HPV persistence of a given type, the
probability of clearance decreases and the risk of
pre-cancer diagnosis increases.

• Prevalent infections in older women persist longer


than in younger women, probably because they are
more likely to represent infections already of long
duration

• The median time to clearance of HPV infections


detected during screening studies is 6–18 months
Summary: HPV pathogenesis
• Protein products of the early HPV genes E6 and E7 are
responsible for immortalizing and transforming cells, which
may lead to the development of cervical cancer in women
• Viral proteins E6 and E7 interact with central molecules in
cell cycle control, pRB and p53
– pRB- Tumour suppressor protein, inhibited by E7
• Loss of cell cycle control and activation of specific genes for cell
cycle progression
– p53
• Tumour suppressor protein, inhibited by E6
• Regulation of cell response to mitogenic events
• Acts as ‘guardian’ of the genome
• Loss of cell cycle control, anti-apoptotic events
Natural History of CIN

Progression Progression to
Degree of Regression Persistence to CIN 3 Invasive Cancer
Dysplasia (%) (%) (%) (%)
CIN I 60 30 10 1
CIN II 40 40 15 5
CIN III 33 55 N/A > 12
Sensitivity and Specificity of Screening Tests

TEST SENSITIVITY SPECIFICITY


VIA/VIAM 79% (95% CI 73 - 85%) 85% (95% CI 81-89%)
VILI 10% more than VIA Same as VIA
PAP 57%(95% CI 38-76%) 93%; (95% CI 89-97%)
HC2 (Care 62% (95% CI 56-68%) 94% (95% CI 92-95%)
HPV test)
REPORTING PAP SMEAR
BETHESDA BRITISH SOCIETY FOR HISTOLOGICAL
SYSTEM CERVICAL CYTOLOGY EQUIVALENT

ASCUS Borderline
LGSIL Mild dyskaryosis Mild dysplasia
(CIN 1)
HGSIL Moderate dyskaryosis Moderate
dysplasia (CIN 2)
HGSIL Severe dyskaryosis Severe dysplasia
(CIN 3)
PREVENTION OF CERVICAL CANCER?
PRIMARY PREVENTION-
Avoid risk factors for HPV infection
• Avoid early sexual debut
• Avoid multiple sexual partners
• Avoid sex with men who have multiple sex partners
Avoid co-factors that modulate oncogenic potential of HPV
• Smoking tobacco/cigarettes
• First pregnancy/delivery at early age (teens)
• Limit the number of pregnancies: women who have had 5 or more
children have a higher chance of developing cervical cancer
• HIV
• Other STIs
HPV VACCINE
SCREENING – pap smear, VIA, VILLI
TREATMENT OF CIN
ABLATIVE All women treated for CIN
• Cryotherapy should be followed for life
• Laser with annual smears.
• Diathermy Ablative are quick, cheap and
easy to learn but no histology
• Cold coagulation
is available for review.
• Electrocoagulation diathermy
EXCISIONAL
• Large Loop Excision of the Transformation Zone (LLETZ) also
called Loop Electrosurgical Excision Procedure(LEEP)
• Laser cone biopsy
• Cold knife cone biopsy
HYSTERECTOMY-performed when there are other uterine
conditions e.g fibroids or uterine prolapse
Stages of cervical cancer
Stage 5-year
survival
Ia 90–100

Ib 80–90

IIa 75
IIb 50–60
IIIa 20–40
IIIb 20–40
IVa 5–10
IVb 0
HIV and Cervical Cancer
• HIV-infected (HIV+) women who present with
cervical cancer are significantly younger than non-
HIV-infected
• Higher risk of squamous intraepithelial lesions (SIL)
among HIV-infected women, especially women with
low CD4+ lymphocyte counts, was identified.
• HIV-1 and HIV-2 were also shown to be associated
with an increased risk for high-grade SIL (HSIL).
• This risk appears to be related primarily to
increased HPV persistence resulting from
immunosuppression due to HIV-1 and/or HIV-2
infection.
614
615
FIGO, 2009 staging system for Ca of corpus uteri
Stage IA* - No or less than half myometrial invasion
Stage IB* - Invasion equal to or more than half myometrium
Stage II* - Tumor invades cervical stroma but does not extend
beyond the uterus**
Stage III - Local and/or regional spread of the tumor
Stage IIIA* - Tumor invades the serosa of the corpus uteri
and/or adnexa †
Stage IIIB* - Vaginal metastasis and/or parametrial
involvement †
Stage IIIC* - Metastases to pelvic &or para-aortic lymph nodes
Stage IIIC1* - Positive pelvic nodes
Stage IIIC2* - Positive para-aortic lymph nodes with or
without positive pelvic nodes 616
Stage IV* - Tumor invasion of bladder and/or bowel mucosa
and/or distant metastases
Stage IVA* - Tumor invasion of bladder &/or bowel mucosa
Stage IVB* - Distant metastases, including intra-abdominal
and/or inguinal lymph node
Graded according to degree of histological differentiation.
Class G1 - Nonsquamous or solid growth pattern of 5% or less
Class G2 - Nonsquamous or solid growth pattern of 6-50%
Class G3 - Nonsquamous or solid growth pattern of > 50%
*Either G1, G2, or G3
**Endocervical glandular involvement only should be
considered as Stage I and no longer as Stage II
† Positive cytology has to be reported separately without
changing the stage 617
Endometrial Ca 5-year survival
Dependent on stage and histological grade.
81-91%  Stage I
61-77%  II
31-60%  III
5-20%  IV
Factors that increase 8.Personal hx of
incidence breast/ovarian cancer
1. Obesity [truncal] 9.Family hx of [8] above
2. Carbohydrate 10.Tamoxifen therapy
intolerance & 11.Pelvic irradiation
Hypertension 12.High socio-economic
3. Nulliparity class
4. Late menopause Factors that decrease incid
5. PCOS •High parity,
6. Unopposed •usage of COC
oestrogen therapy •cigarette smoking
7. Functional ovarian
•breast feeding
•dairy products
tumours
• active lifestyles
TYPES OF HYSTERECTOMY
• SUBTOTAL
• TOTAL
– CLASS 1
EXTRAFASCIA HYSTERECTOMY
URETERS REMAINED UNDISTURBED

– CLASS 2 (Te Linde modified radical)


– Hysterectomy
– Pelvic lymphadenectomy
– Removal of paracervical tissues
– Lateral retraction of the ureters
– Removal of half of the uterosaccral ligament.
• CLASS 3 (Meigs-Wertheim)
– Hysterectomy
– Pelvic lymphadenectomy
– Vaginectomy(upper one-third to half)
– Excision of the uterosaccral ligaments close to their
origin
– Ligation of the uterine arteries close to their origin
• CLASS 4
– CLASS 3
– Dissection of the ureters from their bed
– Ligation of the superior vesical artery.
• CLASS 5- Ureteric and/or bladder resection with
anastomosis and re-implantation
Staging Ca Vulva
• Stage I Tumor confined to the vulva
IA Lesions ≤2 cm in size, confined to the vulva or
perineum and with stromal invasion ≤1.0 mm, no
nodal metastasis
IB Lesions >2 cm in size or with stromal invasion >1.0
mm, confined to the vulva or perineum, with
negative nodes
• Stage II Tumor of any size with extension to
adjacent perineal structures (1/3 lower urethra, 1/3
lower vagina, anus) with negative nodes
Ca Vulva
• Stage III Tumor of any size with or without
extension to adjacent perineal structures (1/3 lower
urethra, 1/3 lower vagina, anus) with positive
inguino-femoral lymph nodes
IIIA (i) With 1 lymph node metastasis (≥5 mm), or
(ii) 1–2 lymph node metastasis(es) (<5 mm)
IIIB (i) With 2 or more lymph node metastases(≥5mm)
or (ii) 3 or more lymph node metastases (<5 mm)
IIIC With positive nodes with extracapsular spread
Staging Ca Vulva
• Stage IV Tumor invades other regional (2/3 upper
urethra, 2/3 upper vagina), or distant structures
IVA Tumor invades any of the following:
(i) upper urethral and/or vaginal mucosa, bladder
mucosa, rectal mucosa, or fixed to pelvic bone, or
(ii) fixed or ulcerated inguino-femoral lymph nodes
IVB Any distant metastasis including pelvic lymph
nodes
Complete Partial

Karyotype 46 XX(90%), 46 XY(10%) 69XXY,69XXX

Fetal tissue Absent Present

Hydropic villi Diffuse Focal

Trophoblastic Diffuse Focal


hyperplasia
Scalloping of villi Absent Present

Trophoblastic stromal Absent Present


inclusions
Β –hCG >50,000 <50,000

Classic symptons Common Rare

Risk of persistence 20-30% (8-20%) <5% (0.5%)


Staging (Revised FIGO, 2000)
I – confined to uterus
II – extending outside uterus, but limited to genital
structures (adnexa, vagina, broad ligament)
III – extending to lungs with/without known genital
tract involvement
IV – other metastatic sites.
Substage: A – no risk factors
B – one risk factor
C – two risk factors
Staging
Risk factors
• hCG >100,000 mIU/ml
• Duration from antecedent pregnancy to
diagnosis >6 months

Note following in reporting:


• Prior chemotherapy given for GTD
• Report PSTT separately
• Histological verification not required
PROGNOSIS
• Level of HCG @ Presentation
• Presence of distant metastasis
• Response to chemoRx
• 86% EMACO respond, 17% resistance
• 4% trophoblastic dx have Cerebral metastasis
@ diagnosis. Have 86% cure rate
• Fertility: age of menopause 1yr earlier for
MonoRx & 3yrs for Multi-drug Rx.
FIGO/WHO prognostic scoring system (2002)
0 1 2 4
Age (yrs) ≤39 >39
Antecedent preg Mole Abortion Term
Interval (mths) <4 4–6 7 – 12 >12
Pre-Rx hCG <103 103-104 104-105 >105
Largest tumour <3cm 3-5 >5
Metastasis Spleen, GIT Brain
kidney liver
No of metastases 1-4 4-8 >8
Prior chemo Single ≥2

Low risk → ≤6; Requires single agent chemotherapy


High risk → ≥7; Requires combined agent chemotherapy
Follow-up after evacuation
• Serum hCG :
• weekly after Rx till normal for 3 consecutive assays
• Then monthly for a year (Most normal by 14 weeks)
• Pelvic examination: uterine size, presence of
adnexal masses & mets. One week post-Rx, if
normal, then 4 weekly.
• CXRs: if mets seen in baseline film. 4-weekly till
remission, then 3-monthly
• Contraception: during entire follow-up.
Sterilization, barrier are safest
OCPs: Attenuates BHCG level.
IUCDs: not used before hCG is normal, because of risk
of perforation
INDICATIONS FOR CHEMOTHERAPY
• Raised HCG levels 6mths after evacuation
• HCG plateau in 3 consecutive samples.
• Rising HCG in 2 consecutive samples.
• HCG> 20,000iu 4wks after evacuation.
• Pulmonary, vulva or vaginal met unless HCG is
falling
• Brain,liver GI met or pulm met >2cm on CXR
• Histological evidence of Choriocarcinoma
• Heavy vaginal bleeding or evidence of GI or
Intraperitoneal Haemorrhage
RISK FACTORS FOR PERSISENT GTD
• Increasing maternal age

• Uterine enlargement beyond date

• Clinically detected theca lutein cysts

• Pulmonary complications

• Uterine subinvolution
DIAGNOSIS OF PERSISTENT GTD
• Serum hCG >20,000IU/L (>4month post evacuation)

• Progressively increasing hCG

• Histologic evidence of choriocarcinoma

• Plateau of serial hCG


CHEMOTHERAPY- LOW RISK
Drug Administration Cycle

• Methotrexate 1mg/kg(70mg) 14days


IM /IV days 1,3,5,7

• Folinic acid 0.1mg/kg


IM /IV days 2,4,6 OR

• Methotrexate 0.4mg/kg im or iv 14days


daily x 5days
Combination chemotherapy
• EMACO most successful and least toxic.
Salvage regimens: MAC, MAC-III
• 2nd line: Cisplatin with MTX & Vincristine
repeat cycles as soon as toxicity clears.
Give cycles until complete remission; defined
as 3 consecutive normal hCG levels is
obtained, then commence surveillance.
Follow-up after chemotherapy
hCG:
• 1-2 wks for 1st 3 months
• 2-4 wks for next 3 months
• 1-2 months to complete 1st year of
surveillance
• 6-monthly indefinitely
Change drugs if:
• Titre does not drop by ≥25% after a cycle
• If toxicity does not permit adequate dose or
frequency of administration.
Follow-up (contd)
• In subsequent pregnancies:
• Early USS to confirm normal pregnancy
• Histologic examination of placenta or products
of conception
• hCG level 6-8 weeks after termination of
pregnancy
Metastatic, good prognosis
• The last pregnancy was less than 4 months ago.
• The level of beta HCG in the blood is low.
• Cancer has not spread to the liver or brain.
• The patient has not received chemotherapy
earlier.
Metastatic, poor prognosis
• The last pregnancy was more than 4 months
ago.
• The level of beta HCG in the blood is high.
• Cancer has spread to the liver or brain.
• The patient received chemotherapy earlier
and the cancer did not go away.
• The tumor began after the completion of a
normal pregnancy.
Tumour Markers: -
• Biochemical indicators selectively produced by the
neoplastic tissue and released into blood and
detected in blood or in other body fluids.
• It may be used to: -
– Detect the presence of a tumour
– Monitor the progress of disease
– Monitor the response to treatment
• They cannot be constructed as primary modalities
for diagnosis of tumours
640
Tumour Markers: -
• Types of Tumour markers
– Cell surface antigens e.g CA125, CEA
– Cytoplasmic proteins e.g AFP,
– Enzymes e.g human placental Alkaline
phosphatase, serum lactate dehydrogenase
– Hormone e.g BHCG, estrogen, progesterone,
androgens
• Criteria of an Ideal Tumour Marker: -
-Specific -Sensitive
– The method of assay must be cheap & easy 641
Classification
• Class 1: -
– Antigens unique to a neoplasm not shared by
other tumours of same histological type .
• Class 2: -
– Antigens expressed by many or most tumours of
a specific histological type and of other
histological type, but not expressed by normal
adult tissue.
• Class 3: -
– Antigens expressed by both cancer and normal
adult tissue. 642
Gynaecological Tumour Markers
1. Human Chorionic Gonadotrophin (HCG)
2. Alfa Feto Protein (AFP)
3. Cancer Antigen-125 ( CA125)
4. CA 19-9
5. Carcino Embryonic Antigen (CEA)
6. Placental Alkaline Phosphtase (PLAP)
7. Squamous Cell Carcinoma Antigen (SCCA)
8. CA15-3, ( Also known as HER-2neu, OVX1, OVX2).
643
Gynaecological Tumour Markers
9. Macrophage Colony Stimulating Factor
(MCSF)
10. Tumour Associated Trypsin Inhibitor (TATS)
11. Galactosyl Transferase Associated with
Tumour ( GAT)
12. Alfa Amylase
13. Lactate Dehydrogenase (LDH)
14. Tumour Associated Glycoprotein-72 (TAG-72
644
HCG: -
• Selectively produced by syncytiotrophoblast,
normal titre 20 to 30 mIU /ml,
• A glycoprotein having molecular weight 36,000 to
40,000, half life 32 to 37 hours
• It has two fractions alpha and beta.
• There is immunological and biological similarity
between alpha fraction and pituitary
gonadotrophins.
• So beta fraction of HCG is specific which is
measured by immunological & biological methods,
RIA and enzyme immunoassay.
645
HCG: -
• Can be detected in serum a day after implantation, 8 days
after ovulation and 9 days after LH surge .
• Concentration rises exponentially until 9 to 10 wks of
gestation with a doubling time of 1.3-2 days; peak of around
105 IU/ml.
• Decreases from peak level to plateau value of 103 -203IU/ml,
which is maintained for the remainder of the pregnancy.
• HCG level comes to non pregnant level of less than
5mU/ml, 21 to 24 days after delivery.
• A 66% rise in the HCG level over 48 hours represents the
lower limit of normal value of viable intrauterine pregnancy
• in 15% of cases of viable intrauterine pregnancy, & ectopic
its reversed 646
HCG: - in Hydatidform Mole
• Hydatidiform mole is very much suggestive if:-
– urine in dilution of 1 in 200 to 1 in 500 is positive
for HCG beyond 100 days of gestation.
– If HCG in urine in 24 hours is around 0.3 to 3
million IU during similar period of amenorrhoea.
• Molar pregnancy patients are more prone to
develop Choriocarcinoma:
– If excreting HCG > 100,000 IU in urine in 24 hrs
– If serum level of HCG is > 40,000 mIU/ml.
647
HCG: - in Choriocarcinoma
• A single tumour cell produces HCG around 5x10-5 to
5x10-4 IU/24 hours.
• If a patient excretes 106 IU of HCG in 24 hours, it
indicates presence of 1011 viable tumour cells.
• Normally with functioning gonads a woman excretes
HCG less than 4 IU in 24 hours.
• During methotrexate, treatment
– Serum level of HCG is measured at weekly
intervals and
– The HCG regression curve serves as an indicator to
determine the need for second course of
chemotherapy. 648
HCG: - in Choriocrcinoma

• A second course of chemotherapy is to be administer under


the following conditions: -
– If HCG level plateaus for more than 3 consecutive weeks
or begins to rise again
– If the HCG level doesn’t decline by one log within 18
days of the completion of first course of treatment.
• During second course of chemotherapy,
– The dose of methotrexate is kept unaltered if the
patient’s response to the first course of chemotherapy is
adequate.
– If response is inadequate the dose of methotrexate is
increased from 1mg/kg body wt. to 1.5mg/kg body wt. 649
HCG: - in Choriocrcinoma
• An adequate response is, when serum level of HCG
falls by one log.
• If the response to two consecutive courses of
chemotherapy is inadequate the patient is
considered resistant to methotrexate-folic acid and
then Actinomycin-D is given.
• Subsequently the response to Actinomycin-D is
estimated by measuring serum HCG level.
• If the patient is resistant to Actinomycin-D then
combination chemotherapy is indicated.
650
HCG: - in Choriocarcinoma
• False +ve test for serum and urinary HCG can occur
– When a patient is taking drugs like
phenothiazines, antidepressants & antiepileptics,
– In proteinuria / protinemia, menopause, pelvic TB
associated with amenorrhoea.

651
Alfa Feto Protein:-
• A major foetal serum protein, resembles
albumin.
• AFP exists in a number of isoforms which can
be separated by their differential binding to
lectins.
• Physiologically AFP is produced by
– The yolk sac of human foetus more than 4
weeks old and
– Later by liver & GI tract.
• AFP attains peak values i.e. 4mg/ml at 34
weeks of gestation. 652
Alfa Feto Protein:-
• After birth AFP usually falls, within 8 to 12 months
of delivery to a very low conc.of 10mcg/ml and
persists at this low level throughout life.
• Unexplained and persistent elevation of AFP in
nonpregnant state should be screened, as it may be
due to-
– Hepatocellular Ca, germ cell tumour, hereditary
persistence of AFP, viral hepatitis and cirrhosis .
• In addition to its role in prenatal diagnosis, it is also
widely used in the diagnosis, therapeutic
monitoring and follow up of patients with germ cell
tumours. 653
CA-125: -
• A mullerian differentiated antigen identified by a
monoclonal antibody ovarian cancer 125.
• Gotten at 125th attempt; developed by Bast et al.
• It is a mucin like glycoprotein having MW >200 kDA.
• It is expressed by
– 80% of nonmucinous ovarian tumours including serous,
endometroid, & clear cell & undifferentiated ovarian
tumours
– Endometriosis (luteal phase and menstruation)
• The cut off level of CA-125 is 35 u/ml.
• It is detected in serum by RIA.
• It is useful as a marker for Ovarian tumours and
Endometriosis
654
CA-125: -
• It can also be positive in
– 0.2% of healthy blood donors and 1% of normal
healthy women and 5% Benign gynaecological
disorder like endometriosis & PID.
– 16% of woman in 1st trimester of pregnancy
– 25% of non gynaecological conditions like cancers
of GI tract and breast cancer.
– High levels of CA-125 is detected also in advanced
cases of Adenocarcinoma of Cervix, endometrium
& fallopian tube.
– Menstruation, pregnancy, acute PID, fibroid,
adenomyosis, smoking 655
CA-125: - in Ovarian Cancer
• It is useful for the screening for ovarian cancer, along with
bimanual examination & USS, in high risk groups like-
– Family history of breast, ovarian, endometrial cancer
– History of removal of benign ovarian and breast tumour.
– Postmenopausal palpable ovary.
– Woman workers in asbestos industries.
• Sensitivity –
– It can detect Ca.Ovary in 50% of Stage I and in 60% in
Stage II.
– Its specificity increases if it is combined with USG or is
measured over a period of time
656
CA-125: - in Ovarian Cancer
• The predictive value of a +ve test is 100% and indicates
presence of tumour tissue
– because when the level of ca125 was >35u/ml, disease
was always detected during second look surgery.
• The predictive value of a -ve test is only 56% and does not
exclude the presence of tumour
– because when the level of ca125 was <35u/ml, disease
was still detected in 44% during second look surgery.
• Persistently high levels of CA125 after treatment with cycles
of chemotherapy indicates presence of resistant clones of
tumour tissue.

657
CA-125: - in Endometriosis
• In minimal to mild endometriosis serum CA125 is normal
but in moderate to severe endometriosis the level rises.
– In normal person with out endometriosis level is : -
8 to 22 u/ml (non-menstrual phase)
– In minimal to mild endometriosis level is: - 14 to 31 u/ml
(non-menstrual phase)
– In moderate to severe endometriosis level is: -
13 to 95 u/ml (non-menstrual phase)
• The specificity in endometriosis is about 80%
• The sensitivity is around 66%.
• If the ratio during menstrual phase to follicular phase is
more than 1.5, then it is a better sensitive marker. 658
CA-19-9: -
• Carbohydrate determinant 19-9.
• Mainly expressed by colonic CA.
• Also expressed by most mucinous ovarian tumours.
• It can also be expressed by a significant proportion
of serous and other non-mucinous ovarian tumours.
• Used in combination with CA125 for clinical
monitoring.

659
CEA:-
• It is a glycoprotein of mol.wt 200kda.
• Though it is a tumour marker for GI cancers, it is
also expressed by
– malignant mucinous tumor (100%),
– 100% cases of atypical hyperplasia of
endometrium,
– 60% cases of endometrial Ca,
– 50-80% cases of squamous cell of Cervix,
– 75-100% cases of adenocarcinoma of Cervix.
• It is also produced in pneumonia, hypothyroidism
and pancreatic tumours. 660
• BRCA1 is located on chromosome 17q
• encodes a protein of 1863 amino acids which
appears to be involved in the transcription-coupled
repair of DNA damage. Mutations in BRCA1:
• account for about 75% of families with inherited
ovarian cancer
• carried by 0.11% of women in the general popn
• have a higher carrier frequency in Ashkenazi Jewish
population where about 1 in 100 women.
• cumulative risk for ovarian cancer is 29% by age 50
and 44% by age 70.
• 51% developing breast cancer by 50 and 85% by 70
661
• BRCA2 chromosome13qand
• encodes a protein of 3418 aa.Mutations in BRCA2:
• account for about 10% of breast/ovarian cancer
• carried by 0.12% of women in the general popn
• The risk of developing ovarian cancer with BRCA2 is
less than for BRCA1.The cumulative risk is 0.4% by
age 50 and 27% by age 70
• There appears to be a genotype/phenotype
correlation for mutations in BRCA1&2 with the
highest ovarian cancer risk being associated with
mutations in the five prime third and central
portion of the gene respectively.
662
Palliative Care
• Palliative Care can be defined as an Interdisciplinary
Model of Care that is Patient and Family-Centred
and that focuses on the management of Physical,
Psychological, and Social Distress with its major goal
being to Improve the Quality of Life of Patients.

• WHO 2002 - “An approach which improves the


quality of life of patients and families facing life-
threatening illness thru the prevention and relief of
suffering by means of early identification and
impecable asessment & treatment of pain & other
problems physical, psychosocial and spiritual.”
Clotting Factor Synonyms
Fibrinogen Factor I
Prothrombin Factor II
Tissue factor Factor III; tissue thromboplastin
Calcium Factor IV
Factor V Proaccelerin; labile factor
Factor VII proconvertin; stable factor
Factor VIII Antihemophilic globulin (AHG); antihemophilic factor A
Factor IX Christmas factor; antihemophilic factor B
Factor X Stuart factor; Stuart-Prower factor
Factor XI Plasma thromboplastin antecedent; AHF factor C
Factor XII Hageman factor
Factor XIII Fibrin-stabilizing factor
Prekallikrein Fletcher factor
HMWkininogen Fitzgerald factor; HMWK

664
Coagulation Cascade

665
666
NORMAL COAGULATION VALUES
• PT: 11-16secs.
• APTT: 30-45secs.
• TT: 15-19secs.
• Fibrinogen assay: >200mg/ml
• Platelet count: 150- 450 x 109/L
• Bleeding time: 1-6mins
• Clotting time: 5-11mins
• ↑sed in pregnancy: Factors 1,8,9 and 10
• ↓sed in pregnancy: Protein S and Antithrombin III
Virchow’s triad
1. Stasis
2. Endothelial injury
3. Hypercoagulability

668
Endometriosis
“Presence of endometrial tissue outside the lining of
the uterine cavity” or
“Proliferation of endometrium in any site other than
the uterine mucosa”
• Age: common in reproductive period
• True Incidence Unknown: ? 1-5% & 30 – 50 %
infertility.
• Does NOT Discriminate by Race.
• Histology: Endometrial Glands with Stroma +/-
Inflammatory Reaction.
• Hereditary (↑↑ among sisters).
 Uterine= • The cause is unknown.
Adenomyosis • Theories of causes:
(50%).  Transplantation theory.
 Extra Uterine: Retrograde
- Ovary 30%a Vascular and lymphatic
- Pelvic peritoneum Mechanical
10%.  Coelomic metaplasia.
- Fallopian tube.  Embolisation theory: spread
- Vagina. by haematogenous or
-Bladder & rectum. lymphatic embolisation.
- Pelvic colon.  Immunological and genetic
- Ligaments.  Composite theory
Predisposing Factors
1. Hyperoestrinism:
a) Fibroid & metropathia hemorrhagica.
b) Delayed marriage, infertility.
c) Oestrogen secreting tumours of the
ovary e.g. granulosa & theca cell tumours,
or with prolonged oestrogen therapy.
2. Cervical Stenosis.
3. Insufflation.
4. Curettage.
Adenomyosis Extra uterine
endometriosis
Age About 40 years About 30 years
Parity Multipara nullipara
Socioeconomic Low high

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1. Laparoscopy .

2. Cystoscopy and proctosigmoidoscopy.

3. Histopathological examination.

4. Imaging.

5. Serum CA – 125 (cancer antigen 125).


6. ? IL-8 (Interleukin 8) & CEA.
Revised American Fertility Society Classification
of Endometriosis rAFS 1985

• Stage I (minimal) 1 – 5.

• Stage II (mild) 6 – 15.

• Stage III (moderate) 16 – 40.

• Stage IV (severe) > 40.


Feeding option should Goals should be SMART:
be AFASS: • Specific
• Acceptable • Measurable
• Feasible • Attainable
• Affordable • Realistic
• Safe • Time bound
• Sustainable

BMS is:
• Breast
• Milk
• Substitute 676

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